Beruflich Dokumente
Kultur Dokumente
General principles
Brain
a ventricle that expels blood: from the right ventricle, to the pulmonary artery to enter the lungs from the left ventricle to the aorta, in the direction of the other organs. The main function of the heart is to maintain blood ow.
Lungs
Heart
Other organs
Inferior limbs
resistance in the systemic arterioles, the pressure is not the same in the two networks. Both sides of the heart have: an atrium (once known as oriellette) that receives blood
At rest
At rest, cardiac output is around 56L/min. The blood arrives in the tissues with the same average arterial pressure and approximately the same force. The blood ow within each organ depends solely on the extent of the vascularization and local arterial resistance. At rest, the digestive system and the kidneys attract about 50% of the blood distributed, whereas the heart brings in only 34% (Table 1.1 & Fig. 1.3).
Lungs 9%
Capillaries 5%
Veins 64%
Heart 7%
General principles
With exertion
During heavy muscle work, the cardiac output increases to 1725L/min. Distribution to various tissues is modied, with the exception of the brain, whose supply remains remarkably constant (Table 1.2 & Fig. 1.3).
Table 1.1 Resting blood ow Organs Digestive Kidneys Brain Skin Heart % total 25 20 13 9 4
Table 1.2 Blood ow on exertion Organs Heart Brain Kidney Skeletal muscle Skin Other organs % total 4 14 20 22 8 12
750
Skin
500
Kidneys
1100
Abdomen
1400
1900
Others
600
Fig. 1.3 Blood output at rest and with exertion. Adapted from Marieb (2005).
Arterioventricular valves Each arterioventricular valve is formed by a fold of endocardium, reinforced by brous tissue. The right arterioventricular valve comprises of three valvules or cuspids (tricuspid valve), whereas the left arterioventricular valve has just two (bicuspid or mitral valve). They prevent the blood from owing back during contraction of the ventricles. Arterial valves The valves of the aorta and the pulmonary trunk are located at the base of the aorta and the pulmonary trunk. Each of these valves, also called sigmoid, have there semilunar
Chambers
The hollow muscle of the heart is divided into right and left parts by the interatrial septum. Each side of the heart has two chambers, an
General principles
Aortic arch
Pulmonary veins Right atrium Pulmonary valvule Left atrium Aortic valve Mitral valvule Tricuspid valvule Interventricular septum Left ventricle Right ventricle Myocardium Inferior vena cava
valvules in the form of a crescent or a pocket. They open when the ventricles contract to pump the blood into the arterial trunk. They close and prevent blood from returning to the ventricles, during ventricular relaxation when the ventricles are relling.
Myocardium The myocardium is made up of: striated muscle bers anchored to a brous framework differentiated bers forming the nodal tissue or conducting system of the heart.
Fibrous skeleton The brous framework or brous skeleton of the heart denotes the four rings of dense collagen that surround the orices of the auriculoventricular and arterial valves. The two auriculoventricular rings and the aortic ring are located in the same brous body. The
Muscular bers The heart is composed of ventricular and auricular bers (Fig. 1.5). The ventricular bers consist of: bers specic to each ventricle whose oblique moorings attach to the brous rings of the skeleton Common bers that envelop and join the two sacs formed by the individual bers. The ventricular heart is composed of two muscular sacs contained in a third muscular sac (Winslow, cited by Bouchet & Cuilleret).
Fibrous ring of the ostium of the aorta Muscle fibers of the left ventricle (middle layer)
General principles
Left atrium Sinoatrial node Internodal tract Right atrium Auriculoventricular node Auriculoventricular bundle (bundle of His) Cardiac conducting muscle fibers Interventricular septum Purkinje fibers (branches of AV bundles)
The atrioventricular (AV) node (Aschoff Tawara) is a smaller collection of nodal tissue situated in the interauricular septum, near the atrioventricular valves. It functions as a secondary pacemaker. The atrioventricular (AV) bundle (of His) is a collection of specialized muscle bers beginning at the AV node and dividing into right and left bundles at the junction of the membranous and muscular parts of the interventricular septum. The AV bundles proceed on either side of the septum, deep to the endocardium, and then ramify into the subendocardial branches (Purkinje network), which extend into the walls of the respective ventricles. Endocardium The endocardium is a thin internal layer lining all cardiac cavities and continuous with the endothelium of the vessels. This ne
smooth glistening membrane permits the blood to circulate easily inside the heart. A fold of endocardium forms the valvules of the orices anchored on the brous skeleton, arising from the perioricial ring. Pericardium The pericardium is a broserous sac surrounding the heart and the roots of the great vessels at the base of the heart. Extending 1214cm in height with a width of 13 14cm, it comprises two layers: The serosal pericardium: this glistening serous membrane facilitates all manner of movements, glidings, and deformations of the heart, in relation to its neighboring organs. The brous pericardium clothes the serous pericardium. The heart is protected and somewhat tethered in place inside this brous sac.
10
Fibrous pericardium
The brous pericardium is the external layer of the brous serous sac that encloses the heart. The internal layer of the brous pericardium is lined with the parietal serous pericardium. Its exterior surface is reinforced by a layer of sturdy intertwined collagen bers. Thus, its elasticity is reduced and this unyielding quality is what protects the heart from overexpansion. The brous pericardium is attached to the thorax wall and neighboring organs by ligaments (Fig. 1.7, Box 1.1): Caudally: to the central tendon of the diaphragm, by the phrenicopericardial ligaments Ventrally: to the sternum by the sternopericardial ligaments Dorsally: to the vertebral column by the vertebropericardial ligaments. Several more modest bers connect the pericardium to the bifurcation of the trachea, the thoracic esophagus, and laterally to the pulmonary veins and bronchi. Vestiges of the pleuropericardial membrane unite the mediastinal pleura and the brous pericardium.
Serous pericardium
Between the parietal and visceral layers of the serous pericardium is a virtual space called the pericardial cavity. The visceral layer, or epicardium, covers the myocardium, the coronary vessels, and the structural fat layer on the surface of the heart, and is reected onto the aorta, pulmonary trunk, veins, and vena cavae. The parietal layer covers the visceral layer and lines the internal surface of the brous pericardium. The pericardial cavity is contained between the two layers of serous pericardium. It is a space designed for the frictionless gliding of the heart, lubricated by several cubic centimeters of pericardial uid. The large pericardial cavity surrounds the heart and expands over the vascular trunks. The transverse pericardial sinus, or sinus of Theile, is a reection of the large cavity,
Box 1.1 Pericardial ligaments Physicians and surgeons are often surprised to hear us use the term ligament to describe structures mooring the pericardium. The anatomy is nevertheless very clear on the subject, and we are not inventing this. Several authors, such as Testut, Cruveilher, Paturnet, and a few contemporary anatomists such as Kamina, have given excellent descriptions of these structures and the individual ligament ber directions identiable within the intrathoracic connective tissue. Curiously, description of these ligaments is lacking in most English-language anatomy texts. It is true that very often surgeons do not nd them, or in any case do not look for them, in the course of operations. However, the dissections we have performed on unpreserved fresh cadavers clearly show the organization of the pericardial ligaments. We would draw the readers attention to the fact that descriptive anatomy is a science of observation, and a somewhat biased procedure. In effect, to view certain discrete structures clearly, it is necessary to clean and remove certain parasitic structures that obstruct their observation. For example, to render the arterial tree clearly visible, all surrounding tissues must be cleared off: fascia, nerves, veins, muscle, Continued
11
General principles
Box 1.1 Pericardial ligamentscontd aponeurosis, etc. In the case of muscles, they must be divested of their aponeurotic envelopes It is generally from what anatomists justiably call a preparation that anatomical schematics and descriptions have been developed to facilitate the teaching of anatomy. The same applies in the observation of visceral ligaments: the connective tissue must be exposed and all the rest discarded. It is not usual to dissect away what are termed noble structures with the sole aim of conserving connective tissue, reputed to be uninteresting and generally the rst discarded in any dissection. However, it is only under these conditions that these ligaments can be observed. Bear in mind, as well, that visceral ligaments are not exposed to the same mechanical strain to which articular ligaments are subjected. As a consequence, their development and sturdiness are not comparable to those of the cruciate ligament of the knee or lateral ligaments of the elbow, for example! Visceral ligamentous structures are tenuous arrangements that play a suspensory and stabilizing role for the viscera, within a precise mechanical context and a particular pressure system. The visceral mechanism is a subtle and singular mechanism, a system of mutually adaptive parts working together for optimal cohabitation of the organs. To summarize, it is necessary to carry out dissection research biased towards making these ligaments clearly visible, and, if some anatomists fail to nd them, it is simply because they are not looking for them. This holds true for the uterine ligaments, prostatic ligaments, and, in a general way, for all visceral ligaments, whose existence is sometimes contested or called into question.
Esophagus Trachea
Vertebropleural ligament Aorta Vertebropericardial ligaments Right bronchus Superior sternopericardial ligament
12
Cardiac vessels
The heart has many vascular connections. They can be described anatomically as vasa publica and vasa privata. Vasa publica These are the great vessels at the base of the heart, such as the aorta and the pulmonary artery which depart the left and right ventricles. Here also we nd the vena cavae and the pulmonary veins, connected to the right and left atria respectively. Vasa privata These are the coronary arteries (Fig. 1.8A,B) that feed the heart. The left and right coronary arteries are the rst collateral branches of the aorta. They transport nutrients and oxygen to the myocardium. The coronary veins eliminate waste and collect in the coronary sinus. This main drainage vessel of the heart empties into the right atrium. The coronary arteries function almost only during diastole (especially at the left ventricle) because the vessels are compressed by the contractile cardiac muscle during systole. The small anastomoses between them are not quite sufcient to constitute a collateral circulation. These branches are considered functional terminals. In case of obstruction, the part of the myocardium affected is supplied inadequately and a myocardial infarction results. Apart from obstructive causes such as atheroma or atherosclerosis, coronary arteries can spasm due to: cold anxiety physical exercise.
The efferent cardiac nerves, via which the function of the heart can be modied, are sympathetic and parasympathetic bers (Fig. 1.9).
Sympathetic system
The sympathetic cardiac bers derive from the cervical sympathetic system. They reach the organ by three pairs of cardiac nerves: superior, middle, and inferior (right and left). These nerves issue from the lateral vertebral chain arising from the superior, middle, and inferior cervical ganglia (also called the stellate ganglion) respectively. Note that the middle ganglion is not always present, in which case it is fused to the inferior ganglion. In these postganglionic bers, the relay occurs in the paravertebral ganglia. The cell bodies of the preganglionic neurons are located in the lateral horn of the cervicothoracic spinal cord, between C4 and T4. After passage in the cardiac plexus, the sympathetic bers are distributed to all the nodal and myocardial tissues.
Parasympathetic system
The major cardiac parasympathetic supply runs from the right and left vagus (X) nerves, where again they descend by three paired branches, arising above the recurrent nerve, from the recurrent nerve itself, and below the recurrent nerve. These are preganglionic bers that derive essentially from the dorsal vagal nucleus. After passage in the cardiac plexus, they relay in the atrial wall and end in the atrioventricular (AV) and sinoatrial (SA) nodes. This innervation is composed of very short postganglionic neurons that do not invade the ventricle (Buser & Imbert 1994). As such, they differ notably from sympathetic system innervation.
Cardiac plexus
Sympathetic and parasympathetic bers unite to compose two cardiac plexuses. 13
General principles
Aortic valve
A. Anterior view
Coronary sinus
Fig. 1.8 Coronary arteries. (A) Anterior view. (B) Superior view after removal of the atria.
14
Stellate ganglion
Vagus nerve
Sympathetic Parasympathetic
15
General principles
The arterial plexus is formed from the superior part of the sympathetic and vagus nerves. The bers descend in front of and behind the arterial trunk, and constitute the ganglion of Wrisberg, situated beneath the aortic arch and in front of the right pulmonary artery. The cardiac plexus gives rise to the periarterial coronary plexus, from which the subpericardial and subendocardial plexuses originate. The venous plexus originates below the arterial plexus, descending behind the pulmonary artery to reach the atrial part of the heart. On the posterior surface of the right atrium, it forms the central ganglion of Perman. norepinephrine (noradrenaline). Norepinephrine reacts with type 1 adrenoreceptors, which represent about 80% of all heart receptors, the remaining 20% being type 2. Circulating catecholamines, norepinephrine and epinephrine (adrenaline), secreted by the adrenal medulla, have the same effect on the heart as sympathetic innervation. Sympathetic stimulation increases cardiac output by: increasing the heart rate (tachycardia, from the Greek tachus, meaning rapid) by acting on the sinoatrial node (positive chronotropic effect) stimulating conduction towards the AV node (positive dromotropic effect) increasing the power of the ventricular contraction (positive inotropic effect) increasing cardiac and vascular tonus (positive tonotropic effect) accelerating the speed at which the heart muscle relaxes following contraction (positive lusitropic effect) increasing myocardial excitability (positive bathmotropic effect). The sympathetic nervous system comes into play in the course of everyday life, such as during physical exercise, when under stress or hemorrhaging. Parasympathetic action Parasympathetic bers innervate the sinoatrial node, the atrioventricular node, and the myocardium of the atria. There is virtually no parasympathetic supply to the ventricles. The neurotransmitter of the major postganglionic sympathetic cardiac bers is acetylcholine. The cardiac receptors for acetylcholine are the muscarinic type. At the sinoatrial node, the muscarinic receptors are seven times more plentiful than sympathetic receptors. The action of the parasympathetic system is opposite to that of the sympathetic, and its effects are more limited. The lowering of cardiac output is achieved by: lowering the heart rate by vagal bers that terminate on the sinoatrial node
Actions
Although there is much intermingling of the sympathetic and parasympathetic bers in the cardiac plexus, it is possible to systematize their actions. Two categories of ber, centrifugal (visceromotor) and centripetal (viscerosensory), can be isolated. Both types are designed to regulate the heart rhythm and adapt the cardiovascular tone to the changing needs of the body. Adaptation of cardiac activity The following aspects of cardiac activity can be modied: the frequency of contractions (chronotropism) the force of contraction (inotropism) muscle tone (tonotropic effect) muscular excitability (bathmotropism) the speed of muscle relaxation following contraction (lusitropic effect). Sympathetic action Sympathetic bers innervate all regions of the heart: the sinoatrial node, atrioventricular node, atrial myocardium, ventricular myocardium (particularly the left) and coronary arteries. Postganglionic sympathetic cardiac bers mediate by way of their neurotransmitter,
16
1.3 VESSELS
Vessels can be divided in three main categories: arteries, capillaries, and veins. Laid end to end, the blood vessels of a human adult would measure about 100000km. The arteries, which transport the blood from the heart, branch out or divide into smaller and smaller vessels. The veins, which carry the blood towards the heart, merge or converge to form larger and larger trunks.
17
General principles
Tunica adventitia
Tunica media
Elastic membrane
Valve
bers and the greater the quantity of smooth muscle bers. Tunica adventitia The outer coat is essentially made up of connective tissue bers. The cells and the brous network of this layer are laid out along the vessel axis. This layer allows the vessel to adapt to its environment, and to resist outside inuences, notably vessel strain, such as overstretch. In the large vessels, the vasa privata, called the vasa vasorum, is encountered at this layer. These tiny vessels supply the outermost layers of the vessel wall. Autonomic nerve bers, called the nervi vasorum, supply the musculature of the blood vessels that penetrate the tunica adventitia.
18
Endothelium
Blood vessels are lined with endothelium, made of very smooth attened cells designed to reduce blood friction. This barrier between the blood and the rest of the vessel produces these vasoactive factors. nitrogen monoxide endothelin angiogenic stimulants (formation of neovessels) histamine, a local mediator found in connective tissue (mastocytes) and some blood cells.
Anastomoses
Anastomoses are numerous and varied. This natural communication between arteries permits the constant supply to the bodys countless tissues (Fig. 1.11). The different types of arterial anastomosis are described below. Inosculation Two vessels of the same caliber can bend towards each other to cross-connect. The left and right gastric arteries are good examples. Transversal When two arteries run parallel, they can exchange cross-pieces that run perpendicular to them.
19
General principles
Convergence Two arteries that are oblique in relation to each other can converge into a single trunk; this happens, for example, with the vertebral arteries and the basilar trunk. Plexus The term plexus signies interlacing or braiding. Arterial plexuses are rare in the large trunks, but common nearer the capillaries.
Angiogenesis
Angiogenesis is the formation of new blood vessels. During embryological development, it is a primary activity; after birth, it continues in various situations: the scarring of wounds regeneration of the uterine lining after ovulation the make-up of the corpus luteum after ovulation vessel development around obstructed coronaries arteriole formation in the adipose tissue during weight gain the proliferation of arterioles to feed tumor cells. Malignant tumor cells secrete a protein, called tumor angiogenesis factor (TAF), that stimulates the development of blood vessels.
1.3.3 Capillaries
Capillaries are very thin-walled structures with no contractile properties. They divide and branch, without their caliber diminishing. They contain no more than 5% of the
20
1.3.4 Veins
Veins are blood vessels that return blood from the capillary bed to the heart, under low pressure.
Capillary bed
Capillaries are generally arranged in networks called capillary beds (Fig. 1.12). There are between 10 and 100 true capillaries in a capillary bed, depending on the organ or tissue supplied. In most regions of the body, the capillary beds are made up of two types of vessel: Vascular diversion vessels which consist of a metarteriole and a thoroughfare channel directly linking the arteriole and the venule, on either side of the bed The true capillaries, where blood and interstitial uid are exchanged.
Walls
The walls of veins are thinner than those of their companion arteries. Although vein walls are comprised of the same three tunica, there is less muscular and elastic tissue in the middle coat. Veins atten when empty. Very extensible transversally, their diameter can be multiplied by ve, as opposed to just two for the arteries.
Number
Veins are about twice as numerous as arteries, giving them a network approaching 200000km. There are two veins for every artery, except in regions where vessels are of large caliber: the knee, armpit, thoracic inlet. Veins have many anastomoses. The large veins are rectilinear (straight lines).
Microcirculation
The circulation of blood from an arteriole to a venule across a capillary bed is called microcirculation. Blood ow slackens in the capillaries to permit the exchange of nutrients and other cellular material between the blood and the surrounding tissue. Red blood cells can pass through only singly, by deforming. By altering the degree of tonus in their smooth muscle walls, arterioles can regulate blood pressure and thus the perfusion of a given region. A cuff of smooth muscle called a precapillary sphincter surrounds the root of each true capillary that detaches itself from the metarteriole. Like a tiny valve, it controls the ow of blood through the capillary.
Capacity
Venous tributaries converge into larger and larger trunks, and the total venous surface diminishes as veins approach the heart. Like a tree, the total volume of peripheral branches is greater than that of the terminal trunk.
Valves
Certain veins have valves that permit blood to ow towards the heart but not in a reverse direction. These ap valves are folds of the
21
General principles
Vascular diversion
Sympathetic innervation Thoroughfare channel Metarteriole Precapillary sphincters Terminal arteriole Postcapillary venule
Pericyte
True capillaries
Sphincters open
Vascular diversion
Sympathetic innervation Thoroughfare channel Metarteriole Precapillary sphincters Terminal arteriole Postcapillary venule Pericyte
B
True capillaries
Sphincters closed
22
Venous sinus
A venous sinus is a vein with a thin wall of endothelium that is devoid of smooth muscle to regulate its diameter. The thick connective tissue surrounding it lends the support normally provided by the tunica media and tunica adventitia. For example, the cranial venous sinuses, reinforced by dura mater, convey the venous blood from the brain to orices at the base of the skull. The coronary sinus of the heart has the same kind of arrangement.
Transport
In the service of metabolism, blood transports: oxygen from the lungs to the tissues, and carbon dioxide from the tissues to the lungs products of digestion absorbed by the intestines and conveyed to the liver and other tissues metabolic waste from tissues towards the lungs and kidneys. Blood participates in intercellular communication and systemic interactions via its role as an endocrine carrier or in the transport of neurotransmitters.
Properties
Veins are called capacitance vessels (low pressure). Thanks to their wide lumina and ability to expand, they have the capacity to contain a large proportion of the bodys blood. At any given time, veins contain as much as twothirds of corporeal blood, and constitute a blood reservoir. The vascular system is able to absorb most changes in blood volume. In case of hemorrhage, for example, the veins contract to avoid a sudden drop in blood pressure.
Regulation
The blood intervenes in several regulatory activities: It participates in the exchange of water and mineral salts between various parts of the organism, thus contributing to the equilibrium of the internal environment in terms of pH and hydroelectrolytic balance. It maintains vital homeothermia, by distributing heat from the deep organs towards the supercial tissues of the body.
1.4 BLOOD
Thanks to the constant exchange between blood and interstitial uids, the cells of various tissues are brought into relationship
Defense
The blood contributes to immune defense through the phagocytes and antibodies contained in its plasma.
23
General principles
he
nc
an
ie
ch s in ve C av
2 3.2 18 250 4.41
es
te r
ra
br
ar
lb
le
ri e
illa
ia
io
us
le
rta
nu
no
te r
te r
rg
C ap
Ao
Ve
Ve
La
Number
Crossed
0.16109
510
0.510
Uncrossed
Common cross-sectional area cm3 550 180 250 250 300 125 1550 900
24
La
Ar
Ar
rg
ve
in
Hemostasis
Hemostasis describes several biological phenomena involved in the cessation of bleeding. Platelet clumping occurs at the site of bleeding and then coagulation takes over, whereby circulating brinogen is converted to a mesh of insoluble brin, called a clot.
Red blood cells are one-third water. Their solid part is 90% hemoglobin. Hemoglobin carries oxygen to the cells. This respiratory pigment of the blood transports oxygen and carbonic anhydride, regulates pH balance, gives rise to bilirubin, and gives the blood its red color. An erythrocyte normally lasts for 100120 days, before being broken down in the spleen. Leukocytes, or white blood cells White blood cells are found in blood and lymph, cerebrospinal uid, lymphatic ganglions, connective tissue, and inammatory effusions, as they are mobile and migratory. Their average dimension varies between 9 and 18 m. Normal blood values are about 8000 leukocytes per cubic millimeter. This increases during digestion and with pathology. Leukocytes are classied in two groups according to the shape of their nuclei; about one-third are mononuclear and two-thirds are polynuclear. White blood cells are able to squeeze through intercellular spaces by way of diapedesis, and migrate by ameboid movements. Cellular movement is initiated by pleudopods. This distinctive motility is controlled by chemotaxis and is especially well developed in the polynuclear neutrophils. Leukocytes are able to glide in the interstitium and migrate to all tissues, especially at sites of inammation. Phagocytosis is the ability of white blood cells to engulf and destroy microorganisms and cellular debris. Some leukocytes, such as granulocytes, live for only a few hours. Platelets or thrombocytes Platelets are the smallest cells in the blood. Colorless and fusiform, they measure 23 m in diameter. Normally between 200000 and 300000 are found per cubic millimeter of blood, and they live for 810 days. Platelets are essential for the coagulation of blood and are rich in serotonin. 25
1.4.3 Composition
Blood consists of several elements (blood cells), suspended in a clear uid called plasma.
Plasma
Plasma is what remains once the cellular components of blood that has been rendered incoagulable have been centrifuged off. It contains about 7080g protein/L. When blood coagulates, the clot is the result of brin, a protein that precipitates out and immobilizes blood cells, and blood serum in an insoluble network.
Blood cells
Erythrocytes or red blood cells Under the microscope, erythrocytes appear like biconcave discs. The surface area of all erythrocytes is estimated at 3000m2. The diameter of a single cell is 7.2 m, slightly larger in venous blood than in arterial blood. In a normal adult, there are approximately 5 million cells per cubic millimeter of blood. Erythrocytes are elastic and deformable. When crossing a capillary, their caliber is sometimes less than their diameter.
General principles
1.4.4 Hematocrit
Hematocrit denes the relative volume occupied by red blood cells in a given volume of whole blood. Normal hematocrit is about 45% and varies depending on the quantity of plasma or red blood cells in circulation.
cohesion of a liquid. The ability or inability of a uid to ow easily is determined by several factors, among which is the adhesive effect of adjacent molecules. In a normal state and at 37C, global blood viscosity relative to water (being 1 unit) is equal to about 5. In fact, in vivo, blood ows more easily than its viscosity and complex composition would indicate.
Clinical notes An increase in red blood cells is called polycythemia; a decrease signies anemia. In an anemic patient the cellular volume falls and consequently the viscosity of the blood decreases. Conversely, a patient whose blood cell volume is abnormally high will have thicker and slower-moving blood. These pathologies have hemodynamic repercussions (see section on Reynolds number in Chapter 2).
1.4.6 Viscosity
Blood is a concentrated suspension of red blood cells. Viscosity is what characterizes uid cohesion. Plasma viscosity can be differentiated experimentally from blood viscosity. The viscosity coefcient determines the
26
Circulatory physiology
If the laws of uid dynamics were applied, the cardiovascular system would form an unusually complicated hydraulic system. Our biological vascular plumbing arrangement is a much more difcult study and is harder to conceptualize than the circulation of water through central heating pipes! This system comprises a far greater number of variables than those governing the function of most systems of pumps, pipes, and uids to be found in the industrial world.
the cardiovascular system has some porous tubes (capillaries) the cardiovascular system is made up of elastic tubular elements and not rigid structures the volume of its contents is subject to changes depending on digestive absorption, as well as renal and digestive elimination. These characteristics fundamentally complicate any more basic conceptualization.
Arterial pressure
Arterial pressure results from the pressure exerted by the blood in the large arteries. Blood pressure depends on cardiac output and total peripheral resistance. Arterial pressure uctuates with each heart beat, according to the pumping of the heart. It: increases during the emptying phase (ventricular systole) decreases during the lling phase (ventricular diastole). Systolic pressure Systolic pressure is the blood pressure measured during the period of cardiac contraction.
27
General principles
Tubing
Pave = Pd + 1/3(PS Pd )
For example, in a person whose arterial pressure is 140/80mmHg, the average pressure is: 80 + 1/3 (140 80) = 100 mmHg
Control system
Double pump
Fluid
According to the law of HagenPoiseuille, it depends on three factors: 1 cardiac output 2 elasticity of the large arteries 3 viscosity of the blood. Diastolic pressure Diastolic pressure corresponds to the arterial pressure during the cardiac relaxation phase. It depends on the speed of blood ow and therefore on the total peripheral resistance. This attests to the resistance provided by vessels to blood ow. It is a good indicator of arterial wall elasticity. Average blood pressure Blood pressure values oscillate between a maximum (Ps) and a minimum (Pd) value. The average arterial pressure (Pave) is obtained by integrating the pressure curve in the course of a cardiac cycle. In practice, for the peripheral arteries, take one-third of the difference between maximum and minimum pressures, and add to the minimum pressure.
Values Normal arterial blood pressure in a healthy 40-year-old man is 140mmHg during systole at the maximum and 80mmHg during diastole at the minimum. According to the World Health Organization, pressure is considered pathological (arterial hypertension) if systole pressure is greater than 160mmHg and/or diastolic pressure is higher than 95mmHg. Arterial pressure varies with: Sex: up to the age of 40 years males have higher arterial values than women, becoming lower than women after age 50 (DAlch 2008). Age: on average blood pressure rises with age. Measurement circumstances. Cardiac output: a rise in output tends to increase blood pressure. For example, during physical exertion, arterial pressure increases. By contrast, blood pressure falls during sleep. Systolic pressure comes down as much as 10 to 30mmHg, and diastolic pressure lowers 5 to 10 mmHg. (DAlch 2008). Blood volume: increased blood volume increases blood pressure. An injection of 250mL water causes blood pressure to rise by 10mmHg within 60min. Blood ow to individual organs depends on the degree of vasoconstriction of the arteries supplying the particular organ. Digestion modies arterial pressure.
Clinical note With arterial hypertension the heart must work harder and consume more energy to supply the same output. Arterial hypertension therefore represents a form of energy squandering for both the heart and the organism.
28
Circulatory physiology
The regular recurring expansion and contraction of an artery (the pulse) is produced by waves of pressure and is not the same as the sensation of uid pulsation linked to a rhythmic blood ow, passing under the ngers (pulse taking). Moreover, the pulse wave velocity is much higher (from 5 to 15m/s) than the speed of blood!
T Pe
Pi
Heart rate
The functioning of the cardiac pump is discontinuous. Heart rate is intermittent and 29
General principles
0.1 s Auricular systole
Auricular diastole
0.3 s
pulsatile. The heart beats normally about 70 times per minute (bpm). In mammals, cardiac frequency is much more rapid if the heart is small. For example, the heart rate of a mouse is on average 500bpm, whereas that of an elephant is only about 25bpm. In mammals, the relationship between the resting heart rate and life expectancy is indubitable. The lower the heart beat, the longer the lifespan. In humans, many studies show a relationship between a raised resting heart rate and an increased mortality rate in subjects at cardiovascular risk. A low resting heart rate seems to be associated with longevity. Bradycardia is a slower than normal heart rate, whereas tachycardia describes a faster than normal heart rate. Many factors can alter heart rate such as age, sex, physical exertion, and stress.
Together they constitute the cardiac cycle (Fig. 2.3). When the heart rate changes, diastole is shortened or extended, whereas the duration of the systole remains relatively unchanged, at least on a broad scale frequency. At 75bpm, the duration of systole is 0.27s, whereas that of diastole is 0.53s, giving a systole to diastole relationship of about 1 to 2. The resting time between heart beats is about twice that of a contraction.
Terminology
Cardiovascular literature can be daunting in its use of prexes. Notions such as telediastolic or even protosystolic are encountered. Although they are brief events in the cardiac cycle, diastole and systole are of a particular duration nonetheless. Sometimes it is necessary to be more specic about a particular moment during these occurrences or, in contrast, it can be helpful to refer to the overall
Cardiac cycle
30 The contraction of the heart, or systole, is followed by a period of rest, called diastole.
Circulatory physiology
Table 2.1 Meaning of prexes with regard to the cardiovascular system Diastole Beginning Protodiastolic Holodiastolic total Middle Mesodiastolic End Telediastolic Systole Beginning Protosystolic Holosystolic total Middle Mesosystolic End Telesystolic
Cardiac cycle
The heart can be likened to a hollow muscle that propels blood by alternately contracting and relaxing. This sequence affects the size of various cavities, especially the ventricles. During ventricular contraction (systole) the walls thicken and the cavity size diminishes, whereas during ventricular relaxation the walls thin and the cavity enlarges (Fig. 2.4). The cardiac cycle is a repetitive sequence of systole (period of myocardial contraction) and diastole (period of myocardial relaxation). Within this sequence the cardiac valves open and close at key moments, to manage the ow of blood. The adult human heart beats about 70 times per minute, which means the four action phases of the heart are accomplished in less than 1s. The four phases (Fig. 2.5) are: The ventricular lling phase, during which the atrioventricular valve is open. Blood ows from the atrium towards the ventricle, while the aortic valve (for the left ventricle) and the pulmonary valve (for the right ventricle) remain closed. During this phase, blood ow rst ows passively from the atrium to the ventricle, and then more actively during auricular diastole. In the isovolumetric contraction phase, myocardial ventricular contraction increases the pressure in the ventricle, and all valves are closed.
Diastole
Systole
Fig. 2.4 Ventricular cross-section in diastole and systole.
Systolic ejection begins when pressure in the ventricle (ventricular pressure) overtakes the pressure in the aorta (aortic pressure) or the pulmonary artery, during the course of which the blood is expelled
31
General principles
Right atrium
Right ventricle
1. Ventricular filling
2. Isovolumetric contraction
3. Systolic ejection
4. Isovolumetric relaxation
32
from the ventricle. The semilunar valves are opened. Isovolumetric relaxation begins at the end of the ventricular contraction. Ventricular pressure falls below that of the aorta and the pulmonary artery causing closure of the semilunar valves. The atrioventricular valve remains closed.
Circulatory physiology
a cardiac output of 5.6L. A man weighing 70kg possesses about 6L of blood, which means that his total blood mass is pumped in about 1min. 1 The pre-charge corresponds to the volume of blood present in the left ventricle just before ejection. Volume depends on the pressure of venous return to the heart, called central venous pressure (CVP). 2 The contractility of the myocardium, regulated by the autonomic nervous system. 3 The post-charge represents those factors that oppose the work of the heart: Parietal resistance of the ventricle Impedance of the aorta (aortic resistance, inertia of the blood column, reection waves aortic compliance) Peripheral vascular resistance, also controlled by the autonomic nervous system. The activity of the heart is dependent on vascular activity, and vice versa. Pre-charge Pre-charge is the degree of ventricular myocardial stretch just before contraction. It refers to the accumulated blood load imposed on the left ventricle. It equals ventricular lling, represented by the telediastolic volume. When the pre-charge increases, this stretches the heart muscle bers, and this leads automatically to an increase in the force of contraction in the left ventricle. The stretch of the cardiac muscle depends on the venous return. The quantity of blood returned to the heart by the veins distends the ventricles. Everything that increases the volume or the speed of the venous return raises: the telediastolic volume the force of ventricular contraction the systolic volume. This is what happens during physical exercise. Post-charge The post-charge is the counterpressure exerted by the arterial blood. It is the brake on ejection. It comprises all the forces against which
Regulation of output
The right and left heart can be likened to two pumps arranged in series. This implies that the two ventricles have the same output. Suppose that the right ventricular output is 5.1L/min and that of the left ventricle only 5L/min. After 10min, 1L of blood will have accumulated in the lungs, causing pulmonary edema. As the two pumps operate at the same rate, output regulation can occur only through a change in the volume ejected from the two ventricles, dependent on the force of contraction of the ventricle itself.
FrankStarling law
Each ventricle must be able to change its force of contraction and therefore stroke volume in response to changes in venous return. The FrankStarling law describes the mechanism by which changes in pressure alter stroke volume. It states that the force of ventricular contraction is increased when the ventricle is stretched prior to contraction. The myocardial bers experience an increase in load due to the extra blood entering the heart. And the force of contraction of the cardiac muscle is proportional to its initial length. The capacity of the stretched heart to contract is a quality shared by all striated muscles. The FrankStarling law allows the heart to be synchronized with the venous return without depending on external regulation to make alterations. It is vital that stroke volume of both ventricles match so exactly that neither stagnation nor total emptying of the pulmonary circulation can occur, either of which would be fatal.
33
General principles
the right ventricle must struggle to eject its blood. The post-charge corresponds to the charge displaced by the left ventricle and is directly dependent on aortic resistance expressed by the size of telesystolic volume. In simple terms it refers to aortic resistance. For example, the post-charge is increased by clamping of the aorta when the volume of systolic ejection falls; as a result the residual volume (telestolic volume) rises. In healthy people, the post-charge has no signicant inuence on the systolic volume because it is relatively constant. However, in the case of arterial hypertension, the postcharge can reduce the capacity of the ventricles to eject blood, and blood remains in the heart following the systole phase (augmentation of telestolic volume). To summarize: The pre-charge refers to all the forces that work towards ventricular lling. The post-charge describes all the forces that run counter to ventricular ejection. synthesized by the adrenal medulla, have the same effects as the sympathetic nervous system. All of these elements increase cardiac output. By contrast, vagal parasympathetic activity stimulated by acetylcholine, causes: lowering of the heart rate (negative chronotropic effect) decreased contractility (negative inotropic effect) reduced cardiac and vascular tone (negative tonotropic effect) decreased speed of cardiac muscle relaxation (negative dromotropic effect) reduced myocardial excitability (negative bathmotropic effect). These factors lower cardiac output.
Output adaptation
Cardiac output can also be modied by extrinsic factors, such as the autonomic nervous system. Stimulation of the sympathetic cardiac nerves through the intermediary of norepinephrine (noradrenaline) has the following effects: increase in the heart rate (positive chronotropic effect) increase in cardiac and vascular tone (positive tonotropic effect) increase in the force of contraction (positive inotropic effect) increase in the speed of cardiac muscle relaxation (positive lusitropic effect) increase in the speed of conduction of excitation of the cardiac muscle (positive dromotropic effect) increase in excitability via alteration in the excitation threshold (positive bathmotropic effect). Circulating catecholamines, norepinephrine and epinephrine (adrenaline),
2.3 HEMODYNAMICS
It is useful to review several denitions pertaining to the circulation of blood. As a liquid, blood is subject to certain physical and biophysical laws: Hydrostatic law because of discrepancy in height between the head, the heart and the lower extremities Hydrodynamic law because of the ow impulse from the heart. However, blood is also one of a kind on account of: Heterogeneity, by which special macromolecules (proteins) and
34
Circulatory physiology
deformable cells (red and white blood cells) confer various properties to whole blood and isolated plasma Its vascular container that has walls with their own tension, elasticity, and inertia. Blood has very special circulatory properties in relation to uids as a whole. Outputspeed relationship With V being the speed of a uid owing in a tube of cross-section S, the ow of uid is calculated to be equal to the product of its speed multiplied by the cross-section (Fig. 2.6). Principle of continuity When an incompressible uid circulates in a static state through a conduit, the product is cross-section speed. That is to say, the output remains constant all along the conduit (Fig. 2.7). Cross-section effects From the above it is clear that, assuming output is constant, when the cross-section varies, the speed of the liquid changes proportionally. If the cross-section increases, speed diminishes. If the cross-section diminishes, speed increases.
Output
The ow of a uid across a canalization is dened as the volume of uid that crosses in a unit of time. It is denoted by the sign Q, and it is expressed in cubic meters per second (m3/s). Denitions Blood ow is the volume of blood circulating in a tissue in a given period of time. Total blood ow is the volume of circulating blood at each minute in the pulmonary circulation. It is the cardiac output. Blood ow is generally expressed in liters per minute (L/min) or milliliters per second (mL/s).
Q=SV
The principle of continuity of output when an incompressible static fluid circulates. section speed, corresponds to output which remains constant along the conduit.
S1
V1 V2
S2
V3
S3
S1 V1 = S2 V2 = S3 V3 = constant = output
35
General principles
S1 = 1 cm2
S2 = 10 cm2
S3 = 2 cm2
Q 10 ml/s
Q 10 ml/s
V1 = 10 cm/s
V2 = 1 cm/s
V3 = 5 cm/s
This principle extends to conditions in which tubes of owing uids subdivide into smaller tubes, or the inverse, when several tubes converge into one (Fig. 2.8). Thus, the speed of blood ux is inversely proportional to the area of the transverse cross-section of the blood vessel, or, more precisely, to the vascular sector being considered. In the aorta, the area of the transverse cross-section is no more than 35cm2 and the average blood ux speed is from 40cm/s. In the capillaries, the total transverse cross-sectional area is between 4000 and 6000cm2 and the blood ux rate is less at 0.1cm/s (Fig. 2.9).
3500
2700 100 30 18
Effects on pressure
When the cross-section changes, the lateral pressure of liquid exerted on the tube walls also modies. If you have horizontal ow with a constant cross-section and speed, the lateral pressure is constant (Fig. 2.10A). If you consider a horizontal ow in a tube of variable cross-section, when the crosssection diminishes speed increases, and pressure declines beyond the zone of the stricture (Fig. 2.10B).
Circulation time
Circulation time approaches that of cardiac output. We have seen that, at rest, the totality of the blood is pumped in about 1min, which matches the time theoretically required for a drop of blood to complete the circuit from left ventricle to left atrium.
Blood ow
Circulatory gradients The term gradient expresses the level with which a physical property increases or
36
Circulatory physiology
S V Lateral pressure P
V A
V B
diminishes in magnitude as observed in passing from one point to another. There is no life without gradient. A dead system has homogeneous properties, without gradient or ux. In this state equilibrium is true, stable, and non-excited. A living system requires, by necessity, heterogeneous properties. Life demands incessant disequilibrium and permanent ux of matter or energy. A continuous supply of energy is required to maintain gradients and generate the passive ux indispensable to it. A constant expenditure of energy is needed to sustain excitement and instability in a system, despite apparent equilibrium. Active blood ux can insure the passive exchanges necessary to the life of every tissue and cell. It is not until death that all ux ceases and the gradients disappear. The notion of vascular charge At any given point along a hydraulic conduit, the energy of an incompressible uid comprises: potential energy, linked to the effects of gravity on the liquid pressure energy, linked to volume and pressure of liquid on walls kinetic energy, linked to the speed of the uid: E hydraulic = E potential + E pressure + E kinetic The energy restored to the unit of volume is also called a charge.
V1
V2
V3
In waterworks, it is common usage to express charge in meters of columns of water. This is also referred to as hydraulic charge. When considering uid in a pipe, hydraulic energy corresponds to the total mechanical energy, and is also called charge or total charge. The energy consumed by friction constitutes loss of charge. A liquid always ows from the most elevated charge towards the weakest charge. To understand blood circulation, it is better to consider differences in charge, rather than differences in pressure. Charge gradients established all along the circulatory circuit are the true motor of the overall movement of the blood mass.
Blood viscosity Two moving solids have friction between them when they are in contact, and displace at different speeds. In a viscous liquid, two adjacent ow layers also have friction (Fig. 2.11). These forces oppose movement by tending to slow the faster layer and accelerate the slower layer. In vivo, blood behaves much like plasma. Accordingly it can:
37
General principles
either increase its viscosity by the aggregation of red blood cells or diminish its viscosity by the deformation and change in direction of its hematies. This is called uid rheouidifying. Because of this, blood is sometimes considered to be a perfect (ideal) uid. Loss of charge Owing to its viscosity, blood does not have the same characteristics as a perfect uid, in the sense that physics understands it to be. In a perfect uid there is no molecular friction, and the uid ows without energy loss. However, there is a loss of usable hydraulic energy during blood ow. This loss of charge is linked to the dissipation of energy in heat due to the viscosity of the liquid. These charge losses result from friction against vascular walls and friction within blood tissue itself. Venturi effect From the above, it is possible to envisage how a stricture affects pressure and ow velocity. This is what happens with arterial stenosis (Fig. 2.12). S Blood ow is conserved on either side of the stenosis, but the velocity must change. Blood ow accelerates as it passes through the restriction (Fig. 2.12A). Globally the charge is conserved, and the total energy does not change. As a result, if the speed increases, kinetic energy augments proportionately. This results in a pressure change through the restriction. What follows is (Fig. 2.12B): suppression upstream of the stenosis that can cause dilation or fatigue of the vessel wall. depression downstream of the stenosis that can lower the lling pressure of vessels downstream (as a function of squaring the percentage of stenosis).
Nature of the ow
Velocity prole Molecules of a uid that ow at identical speeds are called a uid let. Each let can be represented by a vector proportional to its ow velocity. The arrangement of these different vectors is called the velocity prole (Fig. 2.13).
38
Circulatory physiology
Flow velocities Depending on its velocity prole, a viscous uid can have various ow speeds (Fig. 2.14). wall. An extremely thin layer adheres to the vessel wall and essentially does not move. A parabolic prole develops (Fig. 2.16). In this type of ow, all the energy consumed is used to overcome uid viscosity. There is a linear relationship between pressure and ow.
Laminar ow
If the average speed of a viscous uid is low, the ow is described as laminar (Fig. 2.15). The uid remains coherent and ows in concentric uid layers. Adjacent layers of blood move at different speeds. Fluid velocity is maximal at the center of the stream and decreases towards the vessel
Turbulent ow
If the average speed of a viscous uid increases, ow becomes turbulent. Viscosity ceases to be a cohesive factor and the uid molecules become turbulent, owing in a disrupted manner, with no systematic distribution of speeds. In this type of ow, energy is wasted in propelling blood in a disorderly manner. Flow is no longer proportional to pressure. This is a very inefcient type of ow. Reynolds number The boundary between laminar and turbulent ows depends on four factors: 1 diameter of the blood vessel 2 mean velocity of ow 3 viscosity of the blood 4 density of the blood. Reynolds number is a dimensionless number, used to predict whether blood will be laminar or turbulent. Blood ow loses its laminar characteristic and becomes turbulent when Reynolds number passes a critical value. Empirically it is known that: if Reynolds number is less than 2400, ow remains laminar if Reynolds number is greater than 10000, ow is always turbulent.
Laminar flow
Intermediate flow
Turbulent flow
V3 V4
V2
V1
Parabolic velocity profile is linked to viscosity. Speed is maximal at the center of the stream and an infinitely small layer in contact with the wall moves at zero speed
39
General principles
Between the two there exists a zone of uncertainty, in terms of critical uid speed. In this zone, we nd intermediate ow. Blood ow is laminar except where the great vessels branch off and turbulence occurs. Blood ow is turbulent in the heart and the arch of the aorta during a great part of systolic ejection. At rest, Reynolds number in the aorta is about 1650 and ow is laminar. However, in certain physiological or pathological circumstances, the calculated values can change. This is the case, for example: on exertion: output, and consequently blood velocity, increases anemia associated with lowered hemoglobin and decreased velocity. Moreover diminishing levels of blood oxygen cause a compensatory increase in ow in stenosis: the diameter diminishes and speed increases through the stricture resulting in an unchanged ow. In all these examples, Reynolds number rises and blood ow becomes turbulent. Turbulent ow is often accompanied by audible vibrations called vascular murmurs. These murmurs are normal with exertion, but pathological in the case of stenosis or anemia. If Reynolds number remains higher than the critical value during the entire cardiac cycle, these murmurs are permanent. If Reynolds number is higher during only part of the cardiac cycle, the murmurs are not permanent. If Reynolds number is higher than the critical value only at certain moments in the cycle, the murmurs are intermittent or transitory.
Elastic arteries
The intermediate layer (tunica) of elastic arteries is rich in elastic bers, conferring compliance. These are the major arteries of large diameter located near the heart. They are distributing arteries like the pulmonary artery, the aorta and its branches, such as the brachiocephalic trunk, the subclavian and renal arteries. Windkessel effect Thanks to their elastic bers, the aorta and the large arteries convert the intermittent blood ow to a smooth continuous ow. The dampening effect on pulsatile ow is similar to the action of an air chamber in a bottle. The artery is somewhat like an elastic reservoir. This effect is called the Windkessel effect, from the German Kessel meaning bottle and Wind, meaning air (Fig. 2.17). As the heart contracts and blood pressure increases, the arteries stretch and store potential energy. When the heart relaxes, blood pressure decreases and the stretched arteries rebound (Fig. 2.18). This keeps blood owing
Circulatory physiology
during diastole even though the aortic valve is closed. Aortic compliance saves the heart work. Thanks to its softening effect on pulsation, blood ow is normalized. Reduced aortic compliance leads to increased systolic pressure. This explains age-related hypertension. Pressure wave It is not possible for the total volume of systolic ejection (about 80mL blood) to ow across the entire vascular tree during a single ventricular contraction. We will see that a large part of blood is temporarily stored, thanks to aortic compliance. Flow is determined by the interaction of stroke volume and compliance. The Windkessel mechanism produces a sort of arterial wave that propagates the length of the arterial tree at several meters per second. This rate is proportional to the thickness and rigidity of the arterial wall. It increases when the arterial wall becomes thicker (in the lower extremities for example) or abnormally rigid (as in patients suffering from hypertension, arteriosclerosis, atheroma, or diabetes).
The universal tangible manifestation of this wave of arterial pressure is none other than the pulse, palpable at the peripheral arteries.
Muscular arteries
The arterial media becomes richer in smooth muscle bers and poorer in elastic bers the further the distance from the heart. Arteries of medium and small diameter are considered muscular arteries. These are the coronary, splenic, and mesenteric arteries. These vessels are capable of dilation or constriction. They distribute the blood mass. In addition they are known as resistance arteries. Resistance to blood ow depends essentially on the caliber of these vessels. Peripheral vascular resistance Vascular resistance is the force that opposes blood ow in the vessels. It results from blood friction against the vessel wall. As resistance is weak in the elastic arteries, the blood rubs up very little against the walls. By contrast, it is much higher in the muscular
41
General principles
arteries, whose diameter is considerably smaller. Law of HagenPoiseuille According to the law of HagenPoiseuille, vascular resistance is proportional to: the viscosity of the blood the length of the vascular segment. It is inversely proportional to the radius of the vessel lumen. The higher the resistance, the weaker the blood ow. Resistance depends on the viscosity of the uid and is inversely proportional to the fourth power of the radius. This relationship constitutes the law of HagenPouiseuille. The radius is thus the principal determinant of blood ow resistance. For example, if the radius of a tube is doubled, the ow is multiplied 16-fold! In hemodynamics, vasomotion plays a very important role in peripheral territory irrigation. Put another way, when the diameter of a vessel decreases by half, its resistance to ow becomes 16 times greater. For this reason atheromatous plaques are injurious, not just because of their local consequences, but also because of the general health of the person as they contribute to arterial hypertension. Arterioles and circulatory resistance The arterioles are the main site of circulatory resistance (Fig. 2.19). Arteriole vasoconstriction causes total peripheral resistance to rise. In the face of unchanged cardiac output, high blood pressure results.
Exchanges
Circulation exchanges across the capillary wall occur though different mechanisms. Pores are orices whose number and dimension vary according to the organ. They afford passage of lipid-insoluble molecules. Flow is limited by size, number of available pores, and blood ow. Lipid-soluble molecules can diffuse across the same capillary wall, which is itself made up largely of lipids. Water movement across the capillary wall is by osmosis, driven by the sum of hydrostatic and osmotic pressures. Starlings curve (Fig. 2.20) shows that in the initial part of a capillary hydrostatic pressure overcomes osmotic pressure, resulting in
Capillaries 27%
42
Fig. 2.19 Peripheral resistance distribution (after Silbernagl & Despopoulos 1985).
Circulatory physiology
Lymph vessel Arteriole Venule
~ 10% ~ 90%
Resorption Filtration
venous cross-section, the dispensability of the wall coming into play only when pressure is increased. From a functional point of view, it is convenient to distinguish two large venous categories: 1 Postcapillary venules are resistant vessels, whose muscular component inuences blood pressure and blood ow. 2 Systemic veins, called collector veins, are rich in elastic bers. Their increased capacitance makes them potential blood reservoirs.
Venous return
Venous circulation collects blood and returns it to the heart. The difference in charge between the aorta and the vena cava is sufcient to explain the return of blood to the heart. Nevertheless, three categories of force (vis) can be conceived that participate in venous return, depending on whether the force is acting from behind (a tergo) on the sides (a latere) or in front (a fronte) of the blood mass. Vis a tergo corresponds to the residual force of propulsion in the left ventricle. Vis a latere involves: the attening of the plantar venous sole (plantar veins) the venous muscular pump of the calf muscle action of the venous wall tunica, reinforced by the valvules the abdominodiaphragmatic pump and the pressure gradients of the visceral column. Vis a fronte refers to the force of thoracic aspiration during inspiration. Also note that gravity favors the veins situated above the heart and is unfavorable to those below.
Arterial extremity
Capillary length
ltration, with the result that the uid moves out of the capillary into the interstitial uid. In the second part of the capillary, osmotic pressure (derived from blood proteins, particularly albumin) prevails, drawing the water towards the capillary vascular lumen.
Abdominothoracic pressure
The pressure gradients of the trunk (Fig. 2.21) are fundamental factors in subdiaphragmatic venous return. Whereas the veins of the lower
43
General principles
10 cmH2O
5 cmH2O
Heart
+10 cmH2O
+15 cmH2O
+20 cmH2O
+25 cmH2O
44
Circulatory physiology
extremities are endowed with valves, vessels above the inguinal ligament, such as the iliac vessels and the inferior vena cava are no longer equipped with these devices. In the trunk, regularity of blood ow towards the right atrium rests on differences in venous charge, to which thoracoabdominal pressure gradients contribute in a major way. Because of the force of gravity, intraabdominal pressure is not homogeneous in the standing or sitting position. Instead, craniocaudal pressure applies. The greatest pressures are located at the pelvic level, while weaker pressures prevail just below the diaphragm. In the thorax, pressure is even subatmospheric and known as negative pressure. Blood moves from areas of stronger charge to areas of weaker charge. Normal, harmonious, and balanced pressure gradients are a vital component of venous return. In order for these gradients to be well tiered and regular, a balanced and free visceral mechanism is essential. Fixation, ptosis, dysfunction, or irritation can all create areas where the blood slows down in the collector vessels. This causes venous stasis in the territories located upstream of the slowing down, usually the pelvis and lower extremities. Numerous venous problems, such as pelvic weightiness or heaviness in the lower limbs, are the consequence of deregulation of this thoracoabdominal pressure system.
45
Regulation of the circulatory function ensures that sufcient blood is provided to all parts of the body, whether the individual is resting or working and whatever the ambient conditions. It must: Ensure a minimal perfusion to each organ Control cardiac function and arterial pressure Provide for blood to be distributed to active organs, at the expense of resting ones. Silbernagl & Despopoulos (1985) emphasize that maximal and simultaneous perfusion of all the organs would overtax the heart. To maintain vital circulatory homeostasis for optimal organ function, the cardiovascular system must continually adapt itself to variations in hemodynamic parameters. These adjustments depend upon cardiac output and vascular resistance. Cardiac output changes constantly and instantaneously, in accordance with demand. Cardiac activities that can be modied include the frequency with which impulses are initiated by the pacemaker, and the volume of systolic ejection. Adaptations in heart rate are described as chronotropic, and alterations in the volume of systolic ejection as inotropic (inuencing muscular contractility). Peripheral resistance plays a major role in cardiovascular exibility, essentially
through vasomotion, which controls blood vessel diameter. Changes in vascular diameter regulate perfusion to a particular body part or organ. The smooth muscle tone of the vessels depends on local factors, as well as neural and hormonal signals. Circulatory function regulation includes three levels of control: local vascular control mechanisms, the autonomic nervous system, and the endocrine system. Each system has a particular time limit and duration.
Vascular self-regulation
If the vascular system were passive, there would be a linear relationship between debit and pressure: an increase in the pressure
46
Mechanisms of autoregulation
Myogenic effects Myogenic stretch response means that, when a vascular smooth muscle is stretched, it contracts. If arterial pressure rises, the arteriole muscle responds with increased myogenic activity. This passive stretch depends upon the volume of blood reaching the arterioles. The lessening of the stretch prompts the reduction of myogenic tone. Temperature In most tissues, a rise in temperature causes vasoconstriction. This is because cutaneous circulation is rich in 2 receptors, whose
47
General principles
5-Hydroxytryptophan (5-HTP) is produced by blood platelets, the central nervous system, and some cells of the digestive tube wall. Prostaglandins are made by macrophages, broblasts, leukocytes, and vascular endothelium. These compounds have an array of signicant effects. Prostaglandin F (PGF) is a vasoconstrictors, whereas, for example, prostaglandin E (PGE) and prostacyclin are vasorelaxants, very much involved in inammatory phenomena. Leukotrienes are released by leukocytes during the inammatory response. They are vasoconstricting and also increase the permeability of the capillary wall. Platelet activating factor (PAF) is produced by macrophages as part of the inammatory response. It causes vasodilation and increased capillary permeability. Vascular endothelium The endothelium lining the lumina of the vascular wall plays an important role in vasomotion. It constitutes a mechanical barrier, guaranteeing relative vessel water tightness and controlling permeability, especially at the capillary level. It is a true interface between the blood and the vascular wall, ensuring the transmission and translation of chemical messages. It is involved in variation of the vascular diameter. By way of its surface characteristics and secretions, it is able to limit platelet aggregation. These various endothelial functions are carried out only when the structural integrity of the endothelium is protected. Consequently any factor altering endothelial cell morphology or physiology (e.g. nicotine, cholesterol, or mechanical overload accompanying arterial hypertension) changes the permeability of the endothelium, diminishing its antithrombogenic capacity as well as its secretion of vasorelaxing factors. This is how endothelial changes are implicated in numerous pathological processes, and even lie at the heart of the physiology of atherothrombosis.
Results
In functional or metabolic hyperemia, blood ow to an organ is proportional to its metabolic activity. Changes in arteriole diameter achieve this result. Every tissue adapts its blood ow to its own metabolic requirements. By the mechanism of ux-dependent vasodilation, involving nitrous oxide and prostaglandins, there is an adjustment in arterial diameter and in the distribution of the blood ow that they transport. Every vessel adapts its diameter to its ow. Local factors are depicted in Table 3.1.
Table 3.1 Local factors Local vasodilators Produced by blood-decient tissues Vasodilation of smooth muscles of the precapillary sphincters Local vasoconstrictors Produced as a reaction to a rise in systemic arterial pressure Vasoconstriction of pre-capillary sphincters. At high concentration, a narrowing of arterioles and reduced blood ow to the tissue Endothelin Prostaglandins Thromboxanes Leukotrienes
Hypoxia CO2 (carbon dioxide) K+ (potassium) ADP, AMP Histamine Acidity (lactic acid) Nitrous oxide (N2O) Warmth
48
cause more or less stretch on the baroreceptors. Some receptors respond to increased stretch whereas others are designed to detect decreased stretch.
Receptors
Arterial pressure is under the constant surveillance of arterial baroreceptors. These receptors stimulate a short-term response in a matter of seconds. Baroreceptors modify heart rate and total systemic resistance via autonomic nervous system activity at the heart and the smooth arteriole muscles. Long-term adaptations are made by adjustments in blood volume, in response to thirst and urine volume. Arterial receptors Baroreceptors and chemoreceptors are essential to homeostasis.
Chemoreceptors Chemoreceptors are sensitive to chemical changes and are located in the corpuscles of the carotid glomus and the aortic arch. Fibers issuing from the carotid glomus travel the length of the IXth pair of cranial nerves. Fibers from the aortic corpuscle accompany the Xth cranial nerves along their pathway. They join together at the brainstem. Chemoreceptors are sensitive to hypoxia and hypercapnic acidosis. In response to these stimuli, chemoreceptors signal an increase in sympathetic activity, resulting in peripheral arterial vasoconstriction and splanchnic venoconstriction. They signal an increase or decrease in respiration during extreme conditions such as asphyxia or severe hemorrhage. Chemoreceptors help keep arterial pressure constant in cases of grave hypertension, when the limits of baroreceptor reexes are overcome.
Other receptors Beyond aortic and carotid receptors are receptors that contribute to cardiovascular regulation. Venous baroreceptors situated in the wall of the right atrium detect variations in central venous pressure. In addition, stretch receptors are located in the pulmonary vessel walls. These mechanisms relay information to the brainstem, signaling the autonomic nervous system to adapt to variations in intrathoracic venous pressure due to respiration. Venoatrial receptors are involved in the hormonal response of atrial natriuretic peptide, which aids in regulating mean arterial pressure. Striated skeletal muscles have muscular or ergo receptors, sensitive to metabolic perturbation and mechanical actions. They inform
Baroreceptors Baroreceptors are pressure-sensitive free nerve endings found in the adventitia of the carotid sinus and the aortic arch. Carotid baroreceptors are optimally located to monitor the pressure in arteries supplying the brain, whereas the aortic baroreceptors relay information about the major arteries that furnish the rest of the body. Information from the carotid sinus baroreceptors is carried to the brainstem on the carotid sinus nerve, which joins the glossopharyngeal nerve. Fibers issuing from the baroreceptors of the aortic arch form the aortic nerve, which merges with the vagus nerve. These two nerves ascend to the nucleus of the tractus solarius at the brainstem. Baroreceptors are mechanoreceptors that are sensitive to pressure or stretch of the vascular wall. Thus, changes in arterial pressure
49
General principles
the central nervous system about muscle activity. vasomotor nerves in peripheral vessel smooth myocytes. Systemic arterial pressure can be lowered by changing cardiac output and altering peripheral resistance. Base adjustment notwithstanding, during physical activity arterial pressure rises. It is as if the baroreceptors increase their sensitivity threshold. Should arterial pressure not rise on exertion, a left ventricular problem is indicated.
Central control
Pathways from the various receptors terminate in the medullopontine region of the brain. Cardiovascular motor centers in the brainstem The cardiovascular centers receive information continuously. The baroreceptors constantly relay information about arterial pressure. In turn, vasomotor centers coordinate responses to pressure variations. Impulses are sent to the sympathetic system, the heart, and vessels to create a relaxed vascular tone (relaxed vasoconstriction). Apart from messages coming from different receptors, the cardiovascular center receives stimuli from the higher cerebral centers: the cortex, hypothalamus, and limbic system. For instance, the limbic system can engender cardiovascular modications before a physical test or at the time of a particular emotion such as when taking an exam. It will stimulate the cardiovascular center to increase the heart rate. During physical activity, internal body temperature rises. In this case, the hypothalamus, which governs the internal thermostat, sends impulses to the cardiovascular center, whereupon the vessels of the skin dilate to give off heat. Responses The cardiovascular center adjusts sympathetic and parasympathetic activity at the heart and the vessels. Groups of neurons scattered through the cardiovascular system direct changes in: heart rate ventricular contraction blood vessel diameter. Arterial pressure must be maintained at a level satisfactory to the metabolic needs of every organ. For example, to lower systemic arterial pressure, the cardiovascular center reduces sympathetic inux from the
Electrical pathway
The two efferent branches of the autonomic nervous system have antagonistic effects and operate in different timeframes. The sympathetic outow accelerates the heart rate by about ten beats. The parasympathetic outow decreases the heart rate in the order of a single heart beat. This is called a vagal brake. Increases or decreases in outow from the sympathetic and parasympathetic nervous systems have three actions: 1 An effect on the heart rate, either by rhythm modication by the pacemaker, or by changing the speed of the transmission of electrical impulses in the heart wall. 2 An effect on cardiac muscle to increase contractility either directly on the speed of contraction, or on the tension and relaxation of these bers. 3 Action on peripheral vascular resistance: vasoconstriction or vasodilation. Sympathetic system A premier contingent of sympathetic bers emerges from the spinal cord between C6 and C7, joining the sympathetic ganglions (superior, middle, and inferior cervical ganglions), distributing to the walls of the large vessels and the heart, and innervating the entire myocardium. Another sympathetic contingent arises from the spinal cord between T1 and T3, destined for the arteries, arterioles, and the splanchnic veins.
50
Mediators
The mediators and receptors of the autonomic cardiovascular innervation supplement and modulate vessel responses.
Effects on nodal tissue: Chronotropic, Dromotropic Parasympathetic system Neurotransmitter: acetylcholine The heart Salivary glands Vasodilation Special vessels Pancreas Erectile tissues
Heart rate
51
General principles
hormonal effects
Sympathetic system
Postganglionic neurofibers
Heart receptors 1
vasorelaxation
Vessels
vasoconstriction
52
Postganglionic neurons of the sympathetic system that innervate the heart and the vessels release a hormonal signal called norepinephrine. Norepinephrine stimulates receptors on the smooth vascular muscles and 1 receptors on the cardiac cells. Note, however, that certain vessels are equipped with 2 type receptors whose stimulating effects are opposite to the rst (Fig. 3.2). The 1 receptors are most common on the membrane of the vascular smooth muscles; they are vasoconstrictors. The 2 receptors are located mainly on the walls of the cutaneous vessels. They create a phenomenon of neuromodulation.
The principal role of 1 receptors is increasing the frequency (positive chronotropic effect) and the myocardiac contractility (positive inotropic effect) of the heart. The 2 receptors are situated at the arteriole level of striated skeletal muscles, of the liver, and of the coronary arteries. They have a vasorelaxing effect (see Fig. 3.2). Adrenal gland innervation comes from sympathetic bers sent without relay in the sympathetic ganglions. The second neuron is thus represented by the adrenal medullary cells themselves. These cells secrete epinephrine (adrenaline) into the bloodstream.
Vasopressin
Production Antidiuretic hormone (ADH), or vasopressin, is a hormone secreted by the hypothalamus,
53
General principles
Carotid bifurcation Baroreceptors Chemoreceptors Subclavian artery Baroreceptors Aortic arch Baroreceptors Chemoreceptors
Baroreflex
CN IX CN X
Adrenal medulla
1 heart receptors
Vessels Heart
Vasoconstriction
Heart rate
54
Sympathetic system
General effects: Lipolysis Glycogenolysis b2: vasodilation Hepatic Striated skeletal muscles Coronary b2: heart + Inotropic + Chronotropic
Adrenal medulla
Epinephrine Norepinephrine
a: vasoconstriction Systemic
Hypothalamus
Vasopressin (ADH)
and sent by axonal transport to the posterior pituitary gland where it is released into the bloodstream. Effects Circulating ADH acts on the kidney and the cardiovascular system. ADH decreases the volume of urine by increasing the reabsorption of water in the kidneys. ADH causes contraction of vascular smooth muscles, constriction of arterioles, and peripheral
vasoconstriction. This manifests at the skin as palor and brings about vasodilation of the coronary and cerebral arteries (Fig. 3.5). This action, which explains its name vasopressin, occurs only when ADH is present in high, non-physiological concentrations. Application ADH is concerned with the regulation of body uid osmolarity. An increase in blood osmolarity is detected by central osmoreceptors, connected with the hypothalamus.
55
General principles
It reinforces contractility of the heart (positive inotropic effect) At the level of the peripheral nervous system, it favors the release of norepinephrine by the process of neuromodulation. In the central nervous system it reinforces sympathetic command. Application The production of renin is initiated with any drop in arterial pressure, whether this is a lowering of systemic arterial pressure or a local diminution of intrarenal arterial pressure. This secretion can also be triggered by the renal sympathetic system or by circulating epinephrine, in the framework of a baroreex, for example. Lowered renal tubule sodium charge increases renin production. Under normal conditions, renin levels determine the activity of the renin angiotensinaldosterone system. This mechanism can be upset during chronic hepatic
Vascular endothelium
Juxtaglomerular apparatus
Renin
Conversion enzyme
Pulmonary circulation
Liver
Inactive angiotensinogen
Inactive angiotensin I
Active angiotensin II
Vessels: Vasoconstriction
Heart: + Inotropic
56
Volume increase
Kidney: Increased water elimination Natriuretic atrial peptide (NAP) Vessels: Vasorelaxation
Atrial receptors
constant in the short term. While baroreceptors instigate changes in heart rate, cardiopulmonary receptors adjust peripheral vasomotor tone. If the nervous and hormonal systems provide overall equilibrium to the cardiovascular apparatus, local or regional circulatory variations respond rst to local mechanisms. However, when local circulatory changes alter general circulatory parameters, systemic arbitration is required. For example, during physical exercise, vasodilation in the striated muscle bellies is essentially the result of local mechanisms, linked to metabolic changes that result from effort. Systemic control intervenes by way of reexes only when the total muscle mass implicated in the effort is such that the muscular vasorelaxation reduces total peripheral vascular resistance, lowering arteriole pressure and triggering a baroreex.
57
General principles
1 The circle of Willis 2 The extracranial and intracranial anastomoses notably between branches of the external and internal carotid arteries via the ophthalmic artery or internal maxillary artery 3 The anastomosis between adjoining cortical territories unites branches of the anterior, middle, and posterior cerebral arteries, although branches feeding the cerebral parenchyma are terminal. The brain does not possess any signicant energy reserves and therefore any interruption in blood supply causes a nearly instantaneous loss of consciousness. The brains intolerance of hypoxia means that a constant oxygen supply is imperative. Average cerebral blood ow is on the order of 55mL/min for every 100g brain tissue, which represents 1215% of cardiac output. The gray matter requires even more oxygen, up to 100mL/min per 100g tissue. Intellectual cerebral activity does not entail any notable change in total cerebral blood ow, but rather prompts a change in its distribution. For example, visual observation of a scene or an image requires an increase in blood in the occipital cortical areas. Listening to a recital draws more blood ow to the temporal lobes. Variations in cortical blood ow distribution depend on metabolic vasodilation. Local blood ow adapts to the needs of local tissues by way of metabolic hyperemia. The brain is dense with capillaries. As cerebral arteries are short, circulatory resistance is located more at the level of the arteries than the arterioles. Likewise, sympathetic innervation predominates at the extracerebral arteries rather than the arterioles. The brain has some measure of control over the constancy of its blood supply, independent of systemic vasomotor commands, which it is capable of escaping. In this way it can resist systemic vasomotor control, which is beholden to the needs of the central nervous system. Cerebral circulation is thus endowed with very effective autoregulation, permitting it to maintain a stable blood ow as long as the systemic arterial pressure remains between 60 and 180mmHg: the cerebral arteries react with constriction to a rise in systemic arterial pressure and, conversely, by relaxation to a drop in pressure. When the pressure falls below 60mmHg or rises above 180mmHg, cerebral blood ow varies. Cerebral autoregulation also occurs in response to chemical changes, notably to carbon dioxide. This is why voluntary hyperventilation is triggered by alkalosis hypocapnia, and causes immediate cerebral vasoconstriction. By contrast, apnea occurs with hypercapnic acidosis and results in vasodilation. Cerebral circulation is distinguished by the watertightness of its epithelial lining. The bloodbrain barrier is watertight, as there are no pores on its endothelial surface. Because the adult brain is located in a rigid box, increased intracranial pressure can alter cerebral perfusion. Cerebral edema is an example. When intracranial pressure approaches systolic arterial pressure, it opposes blood ow causing ischemia. Ischemia itself promotes acidosis, which results in more edema, leading to an accumulation of uid in the interstitial spaces.
58
59
General principles
only arteries in the body that carry deoxygenated blood. In the pulmonary capillary beds, carbon dioxide is removed from the circulation and added to alveolar gas, while oxygen is added to the blood from lung alveolar gas. The oxygen-rich blood is then returned to the left side of the heart through the four pulmonary veins. Pulmonary circulation has weak resistance, thereby facilitating higher blood ow. Blood pressure is relatively low and the arterial walls are quite thin. The pressure in the right ventricle and the pulmonary trunk is six to eight times lower than in the left ventricle and the aorta. Although their pressures are different, the two ventricles eject the same quantity of blood. When cardiac output rises, resistance in the pulmonary vessels falls. The great dispensability of the pulmonary vessels allows signicantly more ow without any marked rise in pressure, thus protecting the fragile alveolar capillary barrier. The volume of the pulmonary circulation represents about 1012% of the total blood volume and is subject to very little variation. In cross-section, the pulmonary arteries appear oval and do not become circular until the pulse wave passes through. Because of their compliance, the large arteries are able to convert the intermittent blood ow coming from the heart to the smoother ow of the pulmonary capillaries (Windkessel effect). Due to their great dispensability, gravity has an effect on the pulmonary circulation. In upright posture, which creates differences in hydrostatic pressure, the vessels at the base of the lungs are wide open, while the vessels at the apex can be collapsed. Perfusion is more evenly distributed when lying down. In contrast to all other circulatory territories, the pulmonary circulation responds by vasoconstriction to hypoxia, histamine, and bradykinin. Finally, recall the big role played by the pulmonary circulation in systemic circulatory regulation, via the production of conversion enzyme.
60
People are not at equal risk for heart disease. Atherosclerotic lesions can develop early, sometimes even in adolescence. However, they form even earlier in the presence of known cardiovascular risk factors. Risk factors include behaviors, situations, or antecedents that inuence the frequency of heart problems. A predisposing factor can be dened as a physiological state (e.g. age), pathological condition (e.g. hypertension), or a habit (smoking, for example) that is associated with a higher rate of occurrence. Cardiovascular risk factors are: age and sex: over age 50 years in men, and age 60 years in women smoking: current or having quit for less than 3 years diabetes: treated or not arterial hypertension: treated or not heredity an excess of bad cholesterol, insufcient good cholesterol, or both obesity or overweight sedentary lifestyle stress alcohol.
The probability of cardiac disorders or cerebral vascular accident rises sharply after the age of 50 years in men and 60 years in women. The variation in cardiovascular rates between the sexes is most likely explained by hormonal differences. Before menopause, women have a reduced risk. After menopause, when estrogen falls, cardiovascular disease rises sharply in women and reaches that of men of the same age. Several years after the menopause, women are at higher risk than men.
4.2 SMOKING
Smoking is directly or indirectly responsible for many deaths. Aside from the numerous lung pathologies it causes, tobacco is a key factor in cardiovascular disease. Smoking is linked particularly to the sudden death associated with myocardial infarction. Smoking 10 cigarettes a day doubles the risk of a heart attack. Smoking 20 cigarettes daily increases the risk threefold compared with that in a non-smoker. Passive smoke inhalation presents the same health risk. It has been demonstrated than a nonsmoking spouse married to a smoker has a 25% increased risk of infarction. The benets of quitting are progressive. Two to three years after quitting, the coronary
61
General principles
risk is still not signicantly different from that of a smoker. However, in the case of myocardial infarction, the risk of recurrence or death diminishes signicantly after the rst year of quitting and eventually falls to the same risk level as that in nonsmokers. hypertension is particularly high in industrialized countries. Often it has no identiable origin and for this reason is called essential hypertension. Nevertheless, in some cases there are known causes (alcohol, drugs such as corticosteroids, oral contraceptives, cocaine, ecstasy, and certain illnesses, notably renal disease), in which case the term secondary hypertension applies. Arterial hypertension is usually silent; it has no symptoms or visible sign and is therefore called the silent killer. It is detectable only through regular blood pressure testing. Large-scale epidemiological studies show that the relationship between arterial pressure and cerebral risk is greater than the relationship between arterial pressure and coronary risk. Arteriosclerosis (hardening of the arteries) linked specically to high blood pressure (HBP) and aging is distinguished from the process of atherosclerosis (formation of plaque) in which HBP does not intervene except as a general risk factor. Arteriosclerosis is mainly a pathology of the intima of the large arterial vessel walls, notably in the areas of turbulent ux. In the brain, arteriosclerosis is implicated in at least 50% of cardiovascular accidents. It is responsible for the small cerebral infarcts resulting from the occlusion of perforating arteries. Atherosclerosis is responsible for one-third of cerebral lesions in people with hypertension. It causes large cerebral infarcts. Hemorrhage occurs in only 20% of cases. In the heart HBP: favors the formation of atheromatous plaque in the large coronary trunks responsible for organic cardiac insufciency contributes, in collaboration with various neurohormonal factors, to hypertrophy of the left ventricle. This hypertrophy then contributes to structural and functional anomalies of the small coronary arteries, further contributing to coronary insufciency.
4.3 DIABETES
The consequences of diabetes carry numerous health risks. Excess blood glucose over many years is toxic to the arteries and the nervous system. In terms of small arteries, diabetes chiey affects the eyes and the kidneys: In the eyes, the disease creates retinopathy, which manifests as visual disturbances and can eventually cause blindness. Diabetes is the principal cause of adult blindness. In the kidneys, arteriopathy disease of the artery can evolve into chronic renal insufciency requiring dialysis, and even renal transplantation. In large arteries, diabetes favors the formation of atheromatous plaque, greatly increasing cardiovascular risk. The three target areas are: 1 The heart: coronary heart disease and angina pectoris 2 The brain: affected carotid arteries can be the source of cerebrovascular accidents 3 The lower extremities: there is a predisposition to the development of arteriosclerosis obliterans of the lower extremity. Nerves can suffer diabetic neuropathy, bringing with it intractable leg pain. Frequency increases with the duration of the diabetes and the age of the person affected. Such neuropathy linked with afiction to the smaller vessels can cause wounds to the foot leading to amputation.
4.5 HEREDITY
Heredity is a major risk factor for cardiovascular disease. Illness in the immediate family (father, mother, or sibling) is especially signicant. Even one such family member suffering from heart disease increases the chances of it developing. Nevertheless, only cardiovascular accidents occurring early are taken into consideration: sudden death from myocardial infarcts: before age 55 in the brother or father before age 65 in the mother or sister. Cerebrovascular accidents in a member of the family before age 45.
(French recommendation) or 0.4g (American recommendation) is thus considered an additional cardiovascular risk factor.
63
General principles
lowers triglyceride levels, increases HDL concentrations, diminishes plaque aggregation, lowers the sympathetic stress response, and stimulates brinolysin (an enzyme that promotes the dissolution of thrombi). For the majority of urban dwellers, energetic expenditure is limited to leisure activities. A meta-analysis (Berlin & Colditz 1990) combining the results of several studies found that a sedentary lifestyle increases the risk of dying from heart trouble 1.9-fold. As therapists, it is important that we recommend that patients practice at least 30min of moderate physical exercise daily, which amounts to 30min of brisk walking. demands arising from the environment, ourselves, our daily responsibilities, and extraneous events) and our capacity to face these difculties. This imbalance bring with it signs of stress in our feelings, thoughts, behavior, and body, which can aggravate and maintain the problem. Stress increases sympathetic activity and causes a rise in the blood levels of catecholamines such as epinephrine (adrenaline). Raised catecholamine levels contribute to an increase in cholesterol and blood sugar concentrations, in turn causing blood pressure to rise and reducing the exibility of uctuations in cardiac rhythm (Black & Garbutt 2002). The most common alarm signs of stress are difculty falling asleep and/or early waking, persistent fatigue, muscle tension in the jaw, neck, and shoulders, diminished power of recuperation, reduced ability to concentrate, failing short-term memory, and agoraphobia.
4.9 STRESS
It has taken the scientic community a number of years to admit that stress is an integral part of cardiovascular risk. Stress is an interaction between the individual and the constraints of their environment. Cardiovascular risk is linked more to the response of the individual than to the circumstances themselves. Stress can be divided in two categories: 1 Emotional factors such as anxiety, depression, relationship problems, or the inability to express anger. 2 Chronic stress, connected with low socioeconomic status, overwork, or a weak social network. Psychosocial stress develops when there is an imbalance between the stress load (all the
4.10 ALCOHOL
In a person suffering from hypertension, excessive alcohol consumption is calculated to be: more than three glasses of wine per day in men and two glasses in women (Haute Autorit de Sant 2005). Taking into account the cumulative effect, three glasses of wine per day adds up to about 120 bottles per year!
64
5.1 ATHEROMA
5.1.1 Pathological anatomy
Atheromatous plaque (atheromas) can develop on the intima of large- and mediumcaliber arteries. Plaque is an accumulation of cholesterol and other lipid compositions that forms on the inner walls of vessels. This deposit is covered by a cap of brosity. These fatty deposits extend the length of the arterial wall and protrude on the vessel lumen. Sometimes the entire thickness and very long segments of the vessel wall can be affected. Plaque may break off, stimulating the production of blood clots created when the material beneath the intima comes in contact with the blood. This can cause a thrombus and a vasospasm, impeding blood ow. The most commonly affected arteries are those of the heart, brain, kidneys, small intestine, and lower extremities.
5.1.2 Etiology
Arterial obstruction is considered a disease of old age, as it is usually in this age group that clinical signs appear. However, plaques have been found in infancy in the developed world. The origin of atheromatous plaque is uncertain, but it seems that predisposing factors exert their effects over a long period of time. These include: family history higher incidence in men than in women until menopause
aging arterial hypertension diabetes smoking excessive stress food rich in rened carbohydrates, cholesterol, and saturated fatty acids obesity sedentary lifestyle excessive alcohol consumption. Most of the time, a combination of factors underlies the formation of plaque. Arterial obstruction by deposits in an arterial wall may be partial or total. These deposits can reduce or abolish blood supply. Their effects depend on the location and caliber of the associated artery, as much as on the available collateral circulation. Incomplete arterial stenosis causes ischemia in the tissues downstream of the stenosis. The tissues can still receive adequate blood to meet their minimum requirements, but not enough to cope with increased metabolic activity. For example, when muscular activity increases, ischemic pain can occur, similar to a muscle cramp. The heart muscle and the skeletal muscles of the lower extremities are those most commonly affected by this phenomenon. Ischemic heart pain is called angina pectoris; ischemia of the lower extremity is called intermittent claudication. In cases of complete occlusion of an artery, the tributary tissues degenerate rapidly and die. The extent of tissue lesions depends on the caliber of the occluded artery, the extent and type of tissue affected, and the degree of collateral circulation.
65
General principles
If the occlusion impacts: a coronary artery, myocardial infarction results a cerebral artery, the resulting cerebral ischemia leads to cerebral infarction. clot may form in the aorta and migrate as an embolism to a distant area, or the disease may manifest as an abdominal aneurysm. Usually there are no symptoms until one or several arteries have been obstructed by atheromatous plaque, and blood ow is severely reduced provoking ischemia. Atherosclerosis progresses quietly and remains asymptomatic for a long time. For example, a coronary artery can gradually become 75% occluded and remain asymptomatic or produce episodes of angina sine dolore (painless episode of coronary insufciency). The rst symptom may be myocardial infarction, caused by obstruction of the residual lumen, from either atherosclerosis or a blood clot. Typical symptoms of atherosclerosis are thoracic pain, when the coronary artery is involved, or leg pain, when an artery of the lower extremity is diseased. Arterial hypertension often accompanies atherosclerosis.
Hemorrhage
If calcium salts deposit in plaque, the arterial wall becomes fragile, rigid, and responds poorly to high blood pressure. Plaque can break off and cause a hemorrhage.
5.2 ARTERIOSCLEROSIS
Arteriosclerosis is a progressive degeneration of the arterial wall that develops with aging and hypertension.
Arterial aneurysm
A localized dilation of a blood vessel wall can be caused by atherosclerosis and hypertension.
5.1.4 Symptomatology
In atherosclerosis, the vessel lumen narrows as a result of atheromatous plaque lesions. Certain vessels are especially vulnerable to this arterial disorder and all may be involved by atheroma in the same patient. The most frequent locations are: the coronary arteries the carotid bifurcations the iliac and femoral arteries. The pulse provides important information. An obliterated pulse in the lower extremity can be found in cases of extreme stenosis. Atherosclerosis may be present in the aorta for some time before symptoms are noticed. Symptoms may not appear in the aorta itself owing to its large caliber. However, a blood
66
Fusiform aneurysm
5.3.2 Etiology
Although the pathogenesis of an aneurysm is unclear, there are several predisposing factors: atherosclerosis trauma atheroma arterial hypertension congenital anomalies in blood vessel formation defective collagen formation in the artery wall syphilis.
Saccular aneurysm
Dissecting aneurysm
5.3.3 Forms
Types of aneurysm (Fig. 5.1) include: Fusiform distensions occur in the entire circumference of the vessel wall, affecting mainly the aorta and sometimes the iliac arteries. These aneurysms present with atheromatous lesions. Saccular aneurysm is a localized dilation of a vessel wall in which a small area, rather than the entire circumference, is distended, forming a sac-like swelling. These aneurysms can be due to defective collagen, atheromatous lesions, or congenital weakness. Dissecting aneurysm is a localized dilation, most commonly in the arch of the aorta.
It is characterized by an inltration of blood between the outer and middle layers of the vessel wall. It begins as an endothelial tear and extends little by little to become a longitudinal dissection along the artery. Microaneurysms occur in small arteries and arterioles of the brain. They are linked to hypertension. Transitory ischemic accidents are often the result of a thrombus or hemorrhage of these aneurysms.
67
General principles
Unfortunately, the onset of symptoms is delayed in relation to the initial weakness. Often the aneurysm is not discovered until it has increased considerably in size. Aneurysms that grow rapidly are most susceptible to rupture. In any event, it is important to be vigilant in the presence of cardiovascular risk factors, together with the following signs and symptoms: When cerebral aneurysms begin to dilate, the following symptoms can appear: headache (worsening headache can indicate minor bleeding) double vision loss of vision or visual eld trembling or uncontrollable movement of the eye or eyelid strabismus facial pain. In the case of thoracic aneurysm, symptoms are rare but can include: thoracic pain, pain at the cervicothoracic junction, or both wheezing coughing tinged with blood hoarseness of voice dysphyagia (difculty swallowing) Claude BernardHorner syndrome (oculosympathetic palsy). Ptosis (drooping of the upper eyelid) Enophthalmos (impression that the eye is sunken in) Miosis (constricted pupil) Decreased sweating on one side of the face Abdominal aneurysms present as: abdominal pulsation pain in the upper abdomen pain at the thoracolumbar junction, the lumbar column, or both. In the event of a rupture, symptoms vary according to location. A ruptured abdominal aneurysm causes intense pain and sensitivity in the stomach or lower back. Rupture of a thoracic aneurysm provokes excruciating pain in the upper chest,
Compression
Even when an aneurysm does not rupture, the swelling of the artery can compress adjacent tissues causing: an interruption of blood ow due to the compression of other vessels compression exerted on neighboring organs, nerves, and bones.
5.3.6 Symptomatology
Generally aneurysms are not painful. Sometimes even large ones are entirely asymptomatic and detected only by accident through imaging tests. Cerebral, thoracic, and abdominal aneurysms are the most likely to produce symptoms if they grow large enough to exert pressure on neighboring structures, or because they stimulate nociceptive nerve endings.
68
5.6.2 Symptomatology
In about 50% of cases, venous thrombosis produces no symptoms, especially at the beginning when the clot is still small and localized. Frequently symptoms appear only once the clot has obliterated the vein. Symptoms are diverse: Local and distal edema: swelling is more or less pronounced in one leg only, at the ankle, calf, or thigh, sometimes with pain on exing the foot Pain: spontaneous calf or thigh pain that worsens with walking Sensitivity: the leg can become sensitive, with tenderness and warmth of the skin Cyanosis: bluish discoloration of the skin. Other warning signs: Arrhythmia: redness or pallor in the limbs Persistent ankle cramps Pins and needles Venous distension: with supercial thrombosis, the vein just under the skin forms a red, hardened cord that is sensitive to pressure Light fever Warmth. The symptoms are numerous, but none is really specic to venous thrombosis. In effect, lymphangitis, an infection of the skin or leg, or even a kidney problem, gives the same signs. The loss of accidity of the calf and the pain on dorsiexion at the ankle are the classic diagnostic signs. Unfortunately they are often absent. For this reason, in the presence of symptoms or simply when in doubt, it is vital to send the patient for an immediate medical consultation and a Doppler examination to conrm what you suspect on palpation. Note that smoking, obesity, and estrogen supplementation can predispose a person to deep vein thrombosis.
5.4 ANGIOMA
Angiomas are benign tumors of blood vessels (hemangioma) or of lymph vessels (lymph angioma). The latter are rarer to the extent that the sufx angioma commonly refers to hemangioma. Angiomas are an excessive growth of blood vessels arranged in a nontypical fashion and separated by collagen bers. They are not true tumors but are classed as such because of their resemblance to tumors.
69
General principles
of the heart) or myocardial infarction can result. In the brain, sustained hypertension causes cerebrovascular accidents. Small or large cerebral arteries rupture causing hemorrhage. The kidneys are also targeted by hypertension. Lesions are found in the renal arterioles. Sustained high blood pressure causes the renal arterioles to thicken with a consequent narrowing of their lumen. Renal blood ow is gradually reduced and in response the kidneys secrete renin, which aggravates hypertension compounding the problem. Reduced blood ow to renal cells can cause cell death and an attendant loss of kidney function, which may progress to renal insufciency.
5.7.1 Consequences
Untreated hypertension is an important cause of heart, brain, and kidney damage. In most cases, the heart is affected by hypertension. When blood pressure is raised, the heart expends more energy to carry out its work of propulsion and overcome the extra demands created by the rise in blood pressure. With sustained hypertension the arteries thicken and the left ventricle becomes hypertrophied in its effort to maintain normal circulation. The heart requires increased oxygen. If this demand is not met, angina pectoris (inadequate blood supply to the left side
70
71
General principles
conditions (rhizomelic pseudo-polyarthritis with shoulder and hip pain), etc. One in three patients presents with visual disturbances: diplopia, blurred vision, ptosis, etc. Moreover, the main risk linked to this arteritis is loss of vision should the central retinal artery becomes occluded. This is a medical emergency; treatment involves massive doses of corticosteroids, which are generally effective in preventing otherwise permanent blindness. kidneys. Edema in the lower extremities and ascites may be part of the picture. This problem can be due to increased vascular resistance in the lungs, myocardial weakness, stenosis, and/or insufciency of the tricuspid or pulmonary valves.
72
73
This book is not a medical treatise. It has neither the attributes nor the competence to provide the elements necessary for a complete medical diagnosis. As manual therapists, we must continue to train our hands, and this is no small thing. It demands a long, complex, and never ending apprenticeship. On the other hand, some patients misguidedly attribute their symptoms to purely mechanical causes, when they may in fact be of some other origin. We have had patients consult us for thoracic pain, neglecting to mention their previous myocardial infarctions. Because of this, it is necessary to appreciate the terrain of the patient. The explanation of common pathologies reveals that cardiovascular symptoms can be far from specic, are often absent, or remain quiet for a long time, and that it is sometimes necessary to have a bit of a nose to avoid pitfalls in daily practice. Be rigorous in your work by relying on objective ndings such as risk factors, a detailed interview, and a thorough clinical examination. The evaluation of risk factors provides an initial and fairly accurate picture of the quality of the vascular terrain of a patient and at the same time, the advisable level of vigilance. The interview, tailored to cardiovascular symptoms, provides more detail as to the possible existence of underlying pathology. Finally, the clinical examination can reveal an established illness, or one still in the early stages, prompting referral to a specialist.
6.1 INTERVIEW
Find out whether the patient has had: an infarction coronary insufciency a pneumothorax a cardiopulmonary intervention. Ask whether they have any of the following: cardiac malformation arterial malformation valve anomalies hiatus hernia. Ask whether they have: an articial valve an endovascular prosthesis (stent) a pacemaker (heart stimulator). Ask whether they have ever had one of the following diseases: acute articular rheumatism (risk of valve problem) diabetes or other systemic illness (connective tissue disorder, lymph or reticuloendothelial system disorders, etc.) congenital or acquired vascular fragility recurrent tonsillitis. Inquire about lifestyle: sedentary lifestyle eating habits (excess sugar, fat, alcohol) toxic habits (smoking, addictions, etc.) escalating psychoemotional tension. Ask patients: whether they know what their normal blood pressure is whether they take antihypertensive medication.
74
75
General principles
may be dry or damp, if accompanied by sweating. This is a transitory erythema of the face that can extend to the neck and upper thorax or even the abdomen. Vasodilation of neurogenic origin or vasoactive circulating substances can cause this increased blood ow to the skin. The causes of ashes are numerous: susceptibility to alcohol, some food additives, certain medications, systemic illnesses, and some cancers. Cyanosis of the face can indicate right ventricular insufciency or mitral valve constriction.
6.2.2 Eyelids
The eyelids should be looked at closely, by having the patient rmly close their eyes. Some systemic diseases can be diagnosed by this simple inspection. Xanthelasmata are yellow spots appearing at the inner angle of the eye or on the lid close to the bridge of the nose. This nding indicates raised levels of cholesterol. Cholesterol levels should be determined, and evaluated for chronic hepatic cholestasis. Eyelid edema is notably present in the nephrotic syndrome.
6.2.3 Pupils
The most frequent iris anomaly is an opaque ring surrounding the periphery of the cornea (gerontoxon or arcus senilis). It can be limited to one part of the circumference of the iris, or appear as a full circle. This sign indicates high cholesterol but is also observed in patients with atheromatous plaque and no hyperlipidemia. It is advisable to be wary when this sign appears together with hypertension. In view of arcus senilis, it is advisable to look for lipid deposits in other areas (xanthelasma of the eyelids, xanthoma tendinosum).
76
Lichstein's sign
6.2.6 Gums
Bleeding gums can mean trouble with hemostasis. They are common in patients undergoing anticoagulant treatment.
6.2.7 Ears
An oblique incisura in the earlobe (Fig. 6.1) indicates the need to ask the patient about vascular risk factors and signs of coronary insufciency. Also called Lichtsteins sign or Franks sign, this oblique groove often bilateral seen on the earlobe indicates premature aging of the connective cutaneous tissue of the heart. Frequently observed in patients over 50 years of age, this sign is a more or less reliable indicator of coronary disease. A study carried out in Sao Paulo on 1500 people demonstrated the correlation between this anomaly and coronary disease (Tranchesi etal 1992). In the event of somewhat atypical thoracic pain, this mark in the earlobe is strongly suggestive of angina.
6.2.5 Lips
Cyanosis of the lips should prompt a blood gas test to check for possible hypoxia and verify hemoglobin levels. This bluish discoloration is seen in cases of polycythemia, cardiopathy, or chronic bronchiopathy. In telangiectasia there are small vascular dilations of supercial capillaries and venules. Very red, these can be found on the tongue as well. If telangiectasia is observed in a female suffering from Raynauds phenomenon, consider the possibility of scleroderma.
77
General principles
dilation of abdominal veins (compression of the inferior vena cava or right ventricular insufciency).
6.3 PALPATION
6.3.1 Arterial test
As a rule, an artery is supple, and regular on palpation. Feel for the possibility of: sclerosis or hardening of the arteries Mussets sign: head nodding in time with the heart beat (aortic insufciency or, more rarely, aneurysm) Cardarellis sign: an abnormal pulsation of the trachea when the head is thrown back (aneurysm or dilation of the aortic arch) an abnormal dilation of a main artery (investigate for aneurysm).
Palmar erythema
This redness of the palm of the hand is classically linked to jaundice. It is also implicated with the cardiovascular system. It is seen in cases of: polycythemia thrombocythemia infectious endocarditis at the periphery of the palm (Janeway lesion) tricuspid insufciency vasculitis. Remember that palmar erythema is also seen in rheumatoid arthritis, pregnancy, and Basedows goiter.
78
Systolic pressure
The systolic index is the relationship between the systolic pressure at the ankle to the systolic pressure at the humerus. This ratio is normally equal to 0.9. Any inferior value is evidence of a perfusion decit, more serious when the arterial lesion is not well
79
General principles
though they have fallen asleep, and shakes the hands and ngers. Thoracic inlet compression usually occurs at night, when the patient is in a restricted position. Depending on how long it took the ngers to fall asleep, the sensation will take more or less time to disappear. palpitations slightly raised arterial systolic pressure
Digestive system
dyspepsia inhibited secretions (saliva, gastric juice) solar plexus tension (emotional pain) meteorism (intestinal gas) frequent constipation postprandial pain
Vagotonia
Behavior sadness depression discouragement melancholy Vasomotor symptoms pallor abundant sweating cyanosis of the extremities overcautiousness decient peripheral circulation Digestive system hypersecretion hypersialorrhea (excessive production of saliva) hyperchloridia (excessive secretion of hydrochloric acid) heartburn vomiting sea-sickness, motion sickness colic intestinal spasm hyposthenia Ocular system miosis Circulatory system bradycardia extrasystole hypotension lipothymia (profound melancholy: malaise, profuse sweating, nausea,
Sympathicotonia
Behavior nervousness hypermotility instability irritability aggressiveness anxiety pessimism hyperactivity insomnia Neurological (general) hyperreexia tremors weight loss Ocular system mydriasis mild exophthalmia Circulatory system tachycardia precordial pain
80
Box 6.1 Precautions to take before viscerovascular manipulation 1. Take the patients blood pressure. 2. Look for anisotension. This can reveal stenosis of large vessels, innate or acquired atherosclerosis, or indicate problems of the following origins: homolateral visceral thoracic inlet cervical cervicobrachial plexus. 3. Perform the AdsonWright test. It is positive in cases of: thoracic inlet syndrome pleurocervical system acromioclavicular or sternoclavicular ligamentous system corococlavicular ligaments (conoid and trapezoid) PancoastTobias syndrome (pulmonary tumor). 4. Analyze the radial pulse for: arrhythmia dysrhythmia tachycardia bradycardia. 5. Check the condition of the lower extremities, looking for edema. Take the blood pressure of the lower extremities to check the systolic index. 6. Palpate the main abdominal pulses, especially those of: abdominal aorta splenic artery common hepatic artery superior mesenteric artery. These pulses serve as evidence and landmarks for manipulation.
thoracic constriction or obstruction bronchial spasm Box 6.1 shows the precautions to be taken before viscerovascular manipulation.
81
the entire circulatory system. Also, bear in mind that hormones must travel through the circulation to stimulate their target organs. A balanced nervous system. Good health depends in large measure on a balance between the sympathetic and parasympathetic nervous systems. Their complementary actions are responsible for constant adjustments in local, regional, and central functions. These modulations represent the eternal search for balance between more and less. Visceral vascular manipulations allow us access to this autonomic balance. Anatomically, numerous laments of the nervous plexus accompany the arterial tree. Thus, in manipulating the arteries, our ngers are in contact with the nervous system and promote central autoregulation. A harmonious electromagnetic eld. Experiments carried out by scanning thermal detectors a short distance from the body demonstrate that visceral manipulation can change the infrared wavelength emitted by an organ. An organ in dysfunction gives off more heat. Infrared wavelengths are a component part of the electromagnetic eld. A thermal change almost always accompanies a reaction in one of the other wavelengths, such as ultrasound, short waves, radio waves, and electrical waves. Visceral manipulation has a regulating effect on the harmony of the electromagnetic eld.
85
Some examples
Described below are several examples of vascular interdependence. The stomach The left gastric artery comes directly off the celiac trunk. The right gastric artery arises from the proper hepatic artery. The left gastroepiploic artery is a branch of the splenic artery. The gastroduodenal artery gives off the right gastroepiploic artery. All of this makes up the vascular circle of the stomach. The pancreas The superior anterior pancreaticoduodenal artery arises from the gastroduodenal artery. The superior posterior branch of the superior pancreaticoduodenal artery given off the gastroduodenal artery. The inferior pancreaticoduodenal artery arises from the superior mesenteric artery. The splenic artery. The right gastric artery has anastomoses with the right gastroepiploic artery via the splenic artery. The small intestine The superior mesenteric artery has branches to the cecum and jejunal loops. The inferior mesenteric artery. The inferior pancreaticoduodenal artery arises from the rst jejunal branch of the superior mesenteric artery. The duodenum The anterior superior pancreaticoduodenal artery divides off the gastroduodenal artery. The posterior superior pancreaticoduodenal artery divides off the gastroduodenal artery.
86
87
89
90
SECTION 1
VESSELS OF THE THORAX
First test The palms are placed one on top of the other, over the angle of the sternum. Begin by compressing the sternum in a posterior and slightly caudal direction (Fig. 8.1). Move your palms towards the left and towards the right to appreciate the chondrosternal and chondrocostal elasticity. Perform the same maneuver below the angle of the sternum. This is a test to nd anterior chondrosternal xations. These restrictions offer a distinctive resistance in the thoracic cage on compression. Second test Slide the at of your palm under the dorsal spine. Using your ngers, push the costovertebral and costotransverse junctions, and the posterior rib angles (the most prominent part of the posterior ribs) anteriorly while externally rotating the upper extremity with your free hand.
91
In procubitus position
The patient lies face down with their forehead on the back of their hands. With both palms,
Position
The patient is supine with both hands placed on the abdomen. The practitioner is beside the patient.
Fig. 8.1 Sagittal evaluation of the thorax.
92
Test
Place a palm against the lateral part of the thorax and exert pressure in the direction of the sternum, rst towards its cephalad part, then middle, and nally towards its caudal aspect. Position your elbow against your own chest to be able to apply powerful but not painful pressure, and with no effort to yourself. In our experience, the more we use force, the more we feel our own ngers, and risk not being able to feel the true xation. All techniques that tire us are to be banished. After all, the road is long and, whats more, such fatigue makes us feel our own body rather than that of the patient. With the other palm, exert an anterior posterior pressure at the sternum or the anterior ribs. You must feel the two pressures meet and thereby identify an area of rmness. You will be surprised by this double compression test as it will reveal new zones of rigidity that were not apparent in the initial tests. Thoroughly test the different anterior posterior planes by applying fairly deeply from both sides.
First time
With one palm compress the thorax laterally, and with the other palm exert a sagittal pressure on either the sternum or the anterior ribcage.
Second time
The two pressures should meet at the restricted zone. Compress several times to stimulate the mechanoreceptors and then perform the induction technique with both palms. Next, exert a second anteriorposterior pressure on the sternum or the ribs, the other palm compressing the lateral thorax. When the two pressures meet at the most rigid area of the thorax, treat again with induction. At this stage it is sometimes necessary to go slightly past the limit of induction. Finally, you must feel for the melting of the thorax, and that it presents no more distinct areas of resistance. You feel as though there is a hard ball gradually deating. This technique not only gives good results, but also permits you to feel the treatment in three dimensions.
93
The heart
The heart is often described in the form of a clenched st resting on the diaphragm. The average heart weighs about 275g. It has a height of 10cm, a width of 11cm, and a circumference of 25cm. It is inclined to the left in relation to midline of the body, its apex is oriented anteriorly and to the left, with its base (its cephalad part) facing posteriorly and to the right. The heart is of great interest to us, because it is the point of arrival and departure of the great vessels and thus the whole vascular system.
the left atrium. The anatomical landmark for the left border is a little medial of the left mid-clavicular line. In our techniques, it is mostly the ventral part that we contact through the intermediary of the ribcage.
94
The heart
effect on autonomous auricularventricular sinus interdependence. heart contractions, and result in a slowing of the heart rate. As a general rule, compression of the upper part of the heart stimulates the vagal parasympathetic response. We will revisit this concept in later chapters.
Vagosympathetic actions
These systems have a strong action on the vasomotor system and vascular pressure. The sympathetic system is vasoconstrictive and hypertensive. The parasympathetic system is vasodilatory and hypotensive.
Carotid sinus
The carotid sinus is a baroreceptor that responds to changes in blood pressure. When intracarotid blood pressure rises, it triggers bradycardia resulting in a lowered heart rate. A technique for the carotid sinus is described in Chapter 23.
95
Right common carotid artery Left common carotid artery Right subclavian artery Left subclavian artery
Aortic arch Superior vena cava Ascending aorta Pericardium Left superior pulmonary vein Right atrium Left atrium Left pulmonary artery
Right ventricle
Left ventricle
Apex of heart
96
complex framework of dense collagen conguring four brous rings which surround the orices of the valves (Fig. 9.3). The rmest areas on compression are formed by the valves (aortic, tricuspid, and mitral) and the brous connective tissue that unites them. The brous skeleton functions as a stable but deformable base for attachment of the leaets and cusps of the valves. NB: The pulmonary valve is not anchored to the brous skeleton of the heart, and it is less rm on compression palpation.
Nevertheless we are beginning to be able to palpate its distinctive area of resistance. When compressing different parts of the heart, some areas are clearly more rm and resistant than others. These are located towards the upper heart, which is the base. It is understandable that some are skeptical of the ability to differentiate particular parts of the heart by manual compression. Nevertheless, there is a methodical protocol of approach that allows such subtlety of perception.
The heart
Aortic arch Pulmonary valve Aortic valve True ribs (1st to 7th) Mitral valve
Tricuspid valve
Diaphragm
Pulmonary valve Fibrous ring of the ostium of the pulmonary trunk Aortic valve Left fibrous trigone Fibrous ring of the ostium of the right atrioventricular valve Right atrioventricular valve Fibrous ring of the ostium of the aorta
97
Dyspnea
With dyspnea, the patient has the impression that: Even routine activity is accompanied by shortness of breath. In the night, for no reason, the patient feels an oppression that makes them sit up or remain upright in bed with pillows supporting the back, or impels the patient to sit astride a chair with the chest leaning forward against the back of the chair. The patient feels their heart beating strongly in the chest to the point of discomfort. The patient feels as though a peach stone has been swallowed and lodged in the esophagus.
Circumstances of onset
Did the symptoms appear: spontaneously and randomly? during physical activity? after a meal? on exposure to cold? when lying down? during sleep?
Location of pain
Is the pain is located: at the intercostal level? behind the sternum? on one side only? Does the pain radiate to: the inner arm? the left little nger?
Discussion
In general, pain of mechanical, vertebral, or intercostal origin:
98
The heart
follows a strain or trauma is relieved by changing position is intensied by coughing, sneezing, or by leaning on the ribs or sternum is identied by a mobility test in the case of a costal, sternocostal, chondrocostal, or costovertebral xation in the area of complaint is usually unilateral does not cause dread or a subjective sense of being in danger. It is advisable to pay attention to pains that are: random disordered triggered by cold occur at night, unrelated to movement accompanied by a feeling of suffocation or oppression set off by activity or exertion postprandial generate anxiety independent of osteoarticular xations. causes hyperchlorhydria and spasm of the gastric musculature, creating a sort of air pocket. The vagus nerves provide a large part of the hearts innervation. Sometimes the brain cannot tell the difference between what is digestive and what is cardiac.
The esophagus
The vagus nerve provides both sensitivity and the motor control for the esophageal musculature. Although not the only nerve innervating this region, its role is considerable. Because of its anatomical position so near to the heart, a spasm or irritation in the esophagus can alarm the patient into thinking there is a heart problem. In addition, hiatus hernia and gastroesophageal reux can provoke chest pain.
Costovertebral neuralgia
This pain typically occurs after a fall onto the back, rib, or upper extremity. Several months later the patient feels mild left thoracic discomfort accompanied by the impression of small stabs to the chest. These various symptoms lead the patient to believe they have a heart condition. Costovertebral xations can give respiratory discomfort and the impression of the thorax being in the grip of a vice. Little by little, rather insidiously, the patient senses danger and the smallest additional symptom gives the feeling of an imminent heart attack. It is imperative to refer this patient to their family physician or cardiologist, for his brain is in a state of hypervigilance with regard to the cardiac region. It literally waits for the slightest physical manifestation in the thorax to transform it into a message of danger. We like to give our patients the following illustration of this phenomenon. You might live in an apartment whose neighbors above are so noisy that they disturb your tranquility and cause stress. One day you no longer hear noise. Hold on, how is it that they are not making any noise today? Your brain was on
The stomach
Precordial pains are frequently due to gastric dilation caused by air in the stomach. In this instance, on percussion one hears a very clear hollow sound in the left subcostal region. Often, the patient burps to relieve the discomfort, to the point of having a tic: the more the patient belches, the more they need to belch. Note, however, that a heart problem can also trigger belching. We think that, in addition to producing local mechanical discomfort, gastric tension stimulates the vagus nerves abnormally. This
99
9.3.2 Indications
The following are indications for manual therapy of the heart: Major thoracic trauma. Recall that it is not the osseous framework itself but rather the intrathoracic organs that provide, by virtue of their viscoelastic resistance, the solidity of the thorax Following cardiopulmonary surgery Thoracic hypersensitivity due to anxiety. We have worked in departments of pneumology and cardiac surgery. It is astonishing to see how many patients experience fear when we touch the exact part of the thorax where surgery was necessary A patients subjective sensation of heart disease when all objective examinations are negative. Cardiophobia Arterial hypertension Tachycardia Dysrhythmia.
Other causes
Numerous organs can cause patients to believe that they have a cardiopathy. The following list, inevitably incomplete, is founded on our clinical observations: the bronchi, notably during bronchospasm the gallbladder, perhaps because of its relationship to the phrenic nerve the spleen, due to the left-side intercostal neuralgia it can provoke kidney stones vertebral and rib xations.
9.3.3 Contraindications
Manual therapy should not be undertaken following cardiac surgery where a foreign object has been placed. Stents, articial valves, and pacemakers are all contraindications. It is advisable to be wary of patients who have never consulted their doctor and who present with: non-positional vertigo the impression of having weak legs or legs that give way from under the patient violent and random headaches a weak femoral pulse. These various signs and symptoms can indicate an aortic aneurysm. Finally, it is important to pay attention to signs of mediastinal compression: retrosternal pain cough dysphonia due to compression of the recurrent nerve dysphagia.
The heart
Protocol
The patient is in decubitus, with hands folded on the abdomen. Place yourself beside the patient. Place your palms one over the other on the sternum, in the space between the sternal angle and the sternoxiphoid junction (avoid putting pressure on the xiphoid process). Sagittally compress the sternocostal framework to pass beyond the rst osteocartilaginous barrier. Think in three dimensions; as we have said before, the thorax is a solid volume that contains other, more supple, volumes. When you perceive the heart beat, your hands are on a second barrier consisting of the heart and its attachments. Without releasing your pressure, overtake this second barrier slightly, to appreciate the rmer parts of the heart. NB: This approach need not ever be painful or anxiety provoking. Perform the maneuver softly and very gradually, with the impression that each time that you open a barrier, you enter into another space. During the compression, you initially feel the elasticity of certain parts of the heart. It is also possible to appreciate the viscoelasticity of the structure by releasing your compression very gradually and evaluating the gradual return of the structures to their original form.
The brous skeleton is strongest at the junction of the aortic, mitral, and tricuspid valves. Anatomically this part is called the central brous body of the heart (trigonum brosum). Adjoining this area, the orice of the pulmonary artery and the tricuspid valve can be found. The tricuspid and mitral valves are surrounded by a brous demi-ring encircling the insertion of these valves. The pulmonary valve is not anchored to the brous skeleton of the heart. Apart from its mechanical role of muscular support, the brous skeleton forms an electrical insulator by separating the myenterically conducted impulses of the atria and the ventricles, so that they contract independently (Dauzat etal 2002).
101
Diaphragm Harder parts of the heart Barrier of the heart and its system of attachments
Osteo-cartilaginous barrier
induction, all the while allowing the gradual viscoelastic return of the indurated zones. Repeat this maneuver several times until you feel a marked release, rst in the quality of a full viscoelastic return and then by conrming through Listening the Listening no longer attracts your hand. Double pressure technique Do not hesitate to apply the double pressure technique (Fig. 9.6) that we employ for both
102
the thoracic cage and intrathoracic structure. Double pressure allows you to release very deeply situated areas with great precision. The heart beat is an objective indicator of the effectiveness of our techniques. When all mechanical tensions have been resolved, heart beats are more distinct, fuller, and more harmonious. It is important to differentiate cardiac viscoelasticity from other elements surrounding the heart.
The heart
The mechanical test of the aorta demands long and fairly difcult practical experience, as it is not easy to perceive. The quality of change detected at the radial pulse is what veries the effect of visceral vascular manipulation. When the technique succeeds, one feels a progressive slowing and a regulation of the cardiac rhythm. We have demonstrated this numerous times with the aid of an oximeter.
103
Esophagus Trachea
T2
T3 Aortic arch T4
Sternum
T5
T9
Diaphragm
T10
T11
T12
104
The heart
As stated above, we have had several patients who have been hospitalized following precordial pain where the suspicion of an infarction or coronary insufciency was strong and all tests proved negative. It turned out that the patients had either chondrocostal xations, pericardial connective tissue tension, or coronary spasm. With these types of functional problem we obtain excellent results.
Position The patient is in decubitus, with their hands on the abdomen. Place yourself to one side.
Technique Place your two palms, one over the other on the sternal angle (Fig. 9.8). Compress the sternum softly and gradually to pass beyond the osseous barrier, until you feel the heart beat. Still in compression, direct your palms cephalad and slightly left. Beneath and to the left of the sternoclavicular junction, change direction tipping caudally to follow the curvature of the aorta. The goal is to stimulate the mechanoreceptors that constantly discharge central information. These receptors ensure optimal vascular circulation
for the body. Finish with the induction technique. Learn to appreciate the quality of the heart beat to rene the direction of your manipulations.
105
10
The thymus
10.2.2 Vascularization
The thymus is supplied mainly by the internal thoracic artery, a branch of the subclavian artery (Fig. 10.4). The thymus sometimes receives small branches from the inferior thyroid and pericardial arterioles.
10.2.3 Innervation
As with all organs of the thorax, the thymus is innervated by the vagus nerves and the sympathetic chain. It exchanges bers with the phrenic nerve and the cardiac plexus.
10.2.4 Structure
The thymus is composed of reticular epithelial cells, enclosed in connective tissue bers and surrounded by a protective capsule.
10.2.1 Evolution
In the newborn, the thymus weighs about 10g. By puberty, at 40g, it has reached its maximum development (Fig. 10.2). The thymus has two lobes which normally extend superiorly to the lower edge of the thyroid gland and in the adult can migrate inferiorly as far as the fourth intercostal space. During dissections with Professor Arnaud, we have rarely seen the adult thymus present as anything more than small islands, imbedded in connective tissue. Professor Arnaud maintained that the gland evolves into a ligament of the heart, reinforcing the pericardium. As a result it is impossible to gauge its weight in the adult. Because of the numerous possibilities of involution, the thymus displays multiple morphological variations (Fig. 10.3).
106
The thymus
10
Thymus
Thymus in a newborn.
Thymus in an adult
107
Pericardial sac
108
Fig. 10.4 Vascularization of the thymus.
The thymus
capable of distinguishing between the bodys own components and foreign cells. T lymphocytes pass through the circulation across the capillary endothelium. viscoelasticity induction technique. Refer to the preceding chapter and to the points concerning the brous skeleton of the heart and the arch of the aorta.
10
109
11
11.1.1 Origin
The importance of the subclavian arteries cannot be overstressed, as they are located at strategic crossroads in the human body. The thoracic inlet is one of the weak points of the human body. It was certainly better protected and more functional when our ancestors walked with four points of contact on the ground.
subclavian artery is 9cm long and the right one is 6cm long.
11.1.3 Pathway
The subclavian artery runs laterally, following a concave bend posteriorly. It passes above the rst rib, between the scalene muscles. In its cervical segment, the artery is described in three parts: prescalene, interscalene, and postscalene.
11.1.2 Dimensions
The subclavian artery has an average caliber of 912mm. It is a bit smaller on the left, and on the right it is slightly narrower at its middle section by the isthmus. The left
Interscalene segment
The artery arches between the anterior and middle scalene muscles. The main trunks of the brachial plexus are found posterior
110
1 1
and superior to the artery. The subclavian vein runs in front of the anterior scalene muscles.
111
11.1.6 Termination
The subclavian artery extends to the outer border of the rst rib, where it becomes the axillary artery.
11.2.2 Indications
The indications for subclavian artery manipulations are numerous in view of the large territory supplied by these vessels. The main indications are: vertigo and instability tinnitus hypoacousis numbness of the upper extremity carpal tunnel syndrome recurrent capsulitis or tendinitis of the upper extremity.
11.2.1 Contraindications
112 An aneurysm of the subclavian artery is rare. When it does occur, it is more often found on
1 1
Axillary artery Deltoid branch Deltoid muscle Coracoid process Thoracoacromial artery Pectoral branch
Biceps brachii muscle Medial cutaneous nerve of arm Deep artery of arm Median nerve Brachial artery Medial cutaneous nerve of forearm Ulnar nerve Long head of triceps brachii muscle Radial recurrent artery Superior ulnar collateral artery Medial head of triceps brachii muscle Inferior ulnar collateral artery
Muscular branch
113
the upper extremities to maintain their internal rotation. You are seated on the side of the subclavian artery to be treated. Maneuver The thumb on the subclavian artery creates lateral traction on the artery by drawing it laterally, distal and very slightly caudal; the thumb does not glide on the artery (Fig. 11.4). This subclavian contact serves as an indicator to nd the ideal brachial traction the place that increases the intensity of the beats. With the ngers on the brachial artery, draw the vessel distally and slightly laterally to create a longitudinal tension that can be felt at the subclavian artery. To coordinate your hands well, close your eyes and imagine a long pipe that you are trying to stretch between your thumb and ngers. Repeat this technique about ten times and, as you proceed, you will have the impression of continuity between your two contacts. This is a marvelous feeling.
Second method
Sweeping the subclavian artery Like all large arteries, the subclavian is surrounded by nerve bers that inform the hypothalamus and the cerebellum about blood pressure and heart rate. The technique described below has two steps:
114
1 1
1 The rst is to release the pleurocervical attachments. 2 The second is to sweep the subclavian artery (Fig. 11.5).
Pleurocervical attachments The patient is in lateral decubitus on the side opposite the subclavian artery to be treated. Position yourself behind the patient. Your goal is to penetrate deeply into the thoracic inlet without pain, following two steps.
Step one The ngers of one hand are placed just behind the clavicle, near the clavicular attachment of the sternocleidomastoid muscle. Bring the shoulder forward without trying to direct it cephalad. Place the ngers of the other hand
Sweeping During the nal pleurocervical maneuver to free the subclavian artery from its mechanical constraints, gently move your ngers along the length of the artery to feel the pulsations. Next run your ngers along the surface of the length of the artery, looking for small hardened neural bers. This palpation requires a long apprenticeship. Nevertheless, even without individually identifying them, one can have an effect on the quality and frequency of the pulse.
Third method
Position The patient is prone, shoulders and arms in chandelier position resting on the table; arm
115
Fig. 11.6 Manipulation of the subclavian artery third method (aortobrachial induction).
116
12
12.1 ANATOMY
The pulmonary vasculature can be divided into two circulatory pathways: the vasa publica part of the circulation serving the interests of the whole body the vasa privata arising from the systemic circulation and serving an organ.
On the right, the pulmonary hilum is larger but not as high as on the left. The hilum projects posteriorly and superiorly to the cephalad edge of the fourth rib, and inferiorly as far as the cephalad border of the sixth rib.
12.1.4 Comments
One can note three features when viewing the pulmonary vascular trunks: 1 They are located anterior to the trachea and the bronchi. 2 They are covered in large part by the heart. 3 They are clearly transverse in orientation. For these reasons: We avoid the cardiac region with our two points of contact. We stretch the pulmonary hilum laterally.
12.2 PRECAUTIONS
One must be cautious of osteoporosis when applying costochondral pressure. In the case of vascular fragility, especially venous, it is advisable to observe the facial coloration of patients during the maneuver. At no time should the patient feel ill at ease. In addition, the following elements call for circumspection before vascular pulmonary manipulations: fever weight loss subcutaneous emphysema
117
12.5.1 Comments
Before manipulating the pulmonary vascular tree: perform the AdsonWright test evaluate the pleural cervical attachments test the subclavian arteries.
12.3 CONTRAINDICATIONS
The main contraindications to manipulation are the following: accidental or spontaneous pneumothorax cardiac material (i.e. material medica) pacemakers: these are frequently placed beneath the right clavicle, where one would exert the action of the palm. It is best to abstain from this maneuver, to avoid moving the pacemaker. Among thoracic pains, it is important to emphasize that spontaneous pneumothorax can occur during exertion or without reason. We have seen this in athletes practicing windsurng and skiing, whose only complaint was neck pain or scapular discomfort. The most common symptoms are a sudden sharp chest pain, sometimes accompanied by suffocating dyspnea, bouts of dry coughing, and unaccustomed anxiety.
12.5.2 Position
The patient is in decubitus, hands crossed over the stomach (Fig. 12.2). You are standing behind the patient, your palms placed on the thorax of the patient. On the right side: the right border of the heart is about one ngerwidth lateral to the edge of the sternum. The main right bronchus lies obliquely along a line running from the right second rib to the left fourth rib. To ne-tune your contact over the lungs, place your right palm in alignment with the right mid-clavicular line. On the left side: the left border of the heart is just inside the vertical left midclavicular line: position your palm outside this line.
12.4 INDICATIONS
The indications for manipulations are the following: pleural pulmonary pathology chronic bronchitis, asthma, dyspnea frequent stitch in the side allergies (treat in conjunction with the liver and pancreas).
118
12
Left internal jugular vein Left subclavian artery Trachea Aortic arch Left pulmonary artery Left pulmonary vein Pulmonary trunk
thorax and the muscles attached to it. To reach the deep structures, such as the heart, it is necessary to pass through different barriers. At the beginning of palmar sagittal compression, you will rst feel the strong resistance of the hard frame of the thorax. Continue softly and gradually without ever releasing your pressure, as you go past this barrier. You will then feel a second, less marked, impression of resistance. Here it feels like a soft pillow under your pressure. You are now in contact with the lung. Without releasing your pressure, move your palms laterally, maintaining the pressure for about 15s. Keeping the sagittal pressure, allow the tissues to return medially, and smoothly commence
another round of lateral pressure. Repeat this several times. It is as though you want to separate the lung from its hilum. It is important to have a mental picture of the lungs and their pulmonary roots so as to exert the pressures in the correct direction.
Pulmonary arterioles
To affect the arterioles, work with the pulmonary viscoelasticity of each lung individually. Palm over palm, sink to the level of the lung in a sagittal direction. Take care to return to the starting position very slowly and gradually following induction. It is at this level that the hand has the sensation of a sponge that you are squeezing and releasing several times. You can also place one hand posterior in relation to the anterior hand to perform a
119
double compressioninduction. Be sure that the posterior hand has passed through the posterior osteocartilaginous barrier (hard frame) of the thorax.
Make two points of contact, one anterior and one posterior, directly opposite each other (Fig. 12.3). Together, the two hands will stretch the thorax and the lungs laterally and cephalad. During this movement you must have the impression of lifting the hemi-thorax laterally.
120
13
121
13.3 ANATOMY
13.3.1 Container
The breasts, located between the third and seventh ribs, are supported by collagen bers called the suspensory mammary ligaments (of Astley Cooper) (Fig. 13.1). The ligaments are found between the dermis and the connective tissue of the breast. They can extend towards the axillary fossa, overlying the pectoral muscle. The suspensory ligaments of the breast are comprised of numerous septa,
Deltoid muscle
Coracobrachialis muscle Triceps brachii muscle Teres major muscle Subscapularis muscle Axillary process of breast Serratus anterior muscle Mammary lobe Latissimus dorsi muscle Pectoralis major muscle
122
13
13.3.2 Contents
The breast is composed of glandular lobes and adipose tissue surrounded by connective tissue (Fig. 13.2). The adipose tissue makes up the shape and size of the breast. Surrounding the areola are
Parietal pleura
123
breast, whereas the anterior cutaneous branches pass through the pectoralis major muscle to reach the medial breast.
13.3.4 Vascularization
We emphasize again the fact that vascular manipulations will involve the venous system. The breast has a rich venous supply (Fig. 13.4).
Tegumentary innervation
The areola and nipple have a dense nerve plexus, carrying genital corpuscles. These mechanoreceptors are nerve endings in the skin. Once called Golgi and VaterPacini corpuscles, these receptors are responsive to
124
13
Axillary artery
Brachiocephalic trunks
Lateral thoracic artery Lateral mammary branches Circular areolar plexus Internal thoracic vein
cerebellum, medulla oblongata, spinal cord, breast, and arm. Internal thoracic artery
Interesting relationship As it enters the thorax, the phrenic nerve crosses the internal thoracic artery obliquely from its lateral side. Collaterals The anterior intercostal arteries perforate the intercostal muscle and pectoralis major at the third, fourth, and fth intercostal spaces. These branches then reach the mammary gland, becoming the medial mammary arteries. Posterior branches go to the thymus and the pericardium. Lateral branches, which form the anterior arteries, are distributed in pairs in each intercostal space.
Origin The internal thoracic artery arises from the anterior surface of the rst part of the subclavian artery, opposite the thyrocervical trunk, one ngerwidth lateral to the sternoclavicular joint. Pathway Posterior to the sternal end of the clavicle, the internal thoracic artery descends posteriorly to the costal cartilages, close to the lateral sternal border.
125
Origin The axillary artery, a continuation of the subclavian artery, begins inferior to the clavicle at the outer border of the rst rib. Pathway The axillary artery descends caudally and laterally. Termination The axillary artery ends nominally at the insertion of the latissimus dorsi muscle, where it becomes the brachial artery. Relations The pectoralis minor muscle is the most important landmark for the axillary artery. The muscle crosses the artery and divides it into three parts: Proximal to the pectoralis minor muscle: The axillary artery runs between the clavicle and the rst rib anterior to the brachial plexus. Lying against the anterior wall of the axilla, the artery runs anterior to the serratus anterior, where it is covered by the clavicular bers of pectoralis major and the clavipectoral fascia. The pectoralis minor muscle crosses the artery at right
Collaterals Thoracoacromial artery The thoracoacromial artery arises from the second part of the axillary artery immediately posterior to the pectoralis minor muscle. The superior thoracic artery sometimes arises from it.
Superior thoracic artery This artery derives from the rst part of the axillary artery and passes between the pectoralis major and pectorals minor muscles, near the lower border of the subclavius. It anastomoses with the internal thoracic artery and the rst intercostal artery. Its pulse can be felt two ngerwidths beneath the clavicle on the mid-clavicular line. It reaches the breast at the level of the third intercostal space. Lateral thoracic artery The lateral thoracic artery curves between the pectoralis major muscle and the serratus anterior as far distally as the fth intercostal space. It anastomoses with the intercostal arteries and distributes branches to the mammary gland. It projects on the thorax on a vertical line passing one thumbwidth outside the coracoid process.
126
13
Areolar network
Mammary plexus
Comments All of these branches have shared anastomoses in the adipose layer of the breast, forming an arteriovenous net. This rich perimammary network gives off very ne cutaneous branches and more important glandular branches. Numerous branches divide in the interlobular connective tissue to supply the tiny acinar glands (Fig. 13.5).
Posterior drainage The intercostal veins drain into the azygos veins on the right and the accessory hemiazygos veins on the left. This is the metastatic route to the lung, bone, and ovaries. The azygos vein drains the vertebral, pelvic, shoulder, and proximal femur veins.
13.4 MANIPULATIONS
We concentrate our breast techniques around the pectoralis minor and its tendinous insertion. The goal is to softly and gently to free up all the elements superior, inferior, and posterior to this tendon and muscle.
13.4.1 Preamble
Before any vascular breast manipulation, be sure to have freed up any mechanical constraints in the surrounding structures:
127
Manipulation
Position In decubitus, the persons hands are placed either on the abdomen or behind the lower back, to open the intercostal spaces.
128
Fig. 13.6 Manipulation of the axillary artery (via the subclavian muscle).
13
129
Position
The patient is in decubitus, with both hands around the breast to be treated. Through their hands, compress the breast several times to wake up its mechanoreceptors. Then carry out the induction technique until the Listening ceases. It is possible at the outset to do these compressiondecompression techniques without the patients hands to free the breast from its thoracic attachments. Show the patient how to do the technique herself, 20 times once a day for 1 month, and repeat if need be.
organ that frequently has circulatory problems. A breast bruise or hematoma takes a long time to resorb. In our experience with infrared scanners, we nd the breast is an organ of lower temperature than the others. The two coldest regions in the body are the buttocks and the breasts, from where hematoma and bruises are the slowest to disappear. The breast is a veritable sponge and responds well to our viscoelasticity technique (Fig. 13.8).
First method
Contact the periphery of the breast with the ngerpads of both hands (Fig. 13.9). Place your thumbs together in line with the nipple to create a xed point between your hands, and nd a comprehensive contact. Exert light compression towards the center of the breast to delicately to contact the mammary gland. Maintain this contact as you traction the breast as though gradually and lightly ungluing the breast from the chest wall. Be alert for small spontaneous movements of the mammary gland as you mobilize it, and slowly amplify these movements with induction. Generally, when the Listening stops, the consistency of the mammary gland changes. As a rule, it becomes more yielding and more uid between your ngers.
Precaution
To remove any ambiguity about this technique, we begin by working over the patients own hands placed on the breast. Very often the patient herself asks whether the viscoelasticity technique would not be more efcient 130
13
Second method
The second method addresses specically the superior lateral quadrant, which is situated towards the axilla (the axillary tail). Place two thumbs on the superior lateral quadrant (Fig. 13.11). First spread your thumbs apart, and then push the gland anteriorly and medially. This technique can also be done in sidelying position.
131
index nger against the caudal border of the cephalad rib. Direct your pressure rst a little medially to better contact the pedicle better, and perform a gliding induction in a posterior and then anterior direction (Fig. 13.12).
132
SECTION 2
VESSELS OF THE HEAD AND NECK
14
14.1.2 Pathway
The common carotid artery ascends along the tracheoesophageal axis, inside the sternocleidomastoid muscle. It follows a more or less straight line from the sternoclavicular joint to a point just behind the condyle of the mandible.
14.1.6 Features
The common carotid artery, internal jugular vein, and vagus nerve are enveloped in a common brous sheath. Because of this, it is difcult not to include the nervous system in carotid artery manipulation, especially knowing the sympathetic bers neighboring the vagus nerve are in the direct vicinity.
14.1.3 Termination
The common carotid artery ends where it bifurcates into internal and external branches, between the hyoid bone and the thyroid cartilage, between C3 and C4. Note that: 67% of bifurcations occur cephalad of the thyroid cartilage at C4 20% appear at the level of the hyoid bone, approximately C3.
14.1.4 Relations
The common carotid arteries are covered by the following muscles: omohyoid sternohyoid
Sternocleidomastoid muscle
towards the artery being palpated. Palpate the artery with two or three ngerpads. The sternocleidomastoid muscle crosses the common carotid artery like an X. Palpation varies depending on whether your ngers are cephalad, medial, or caudad in relation to this muscle crossing (Fig. 14.3).
Progressively glide your ngers cephalad to check the pulse of the artery.
Medial part
The medial part is palpated two to three ngerwidths from the lateral border of the trachea, outside the sternal head of the sternocleidomastoid. Do not hesitate to mobilize this muscle to better perceive the carotid pulse better. In the carotid triangle, the common carotid artery is covered only by skin, platysma, and supercial fascia. Here the carotid artery relates: medially to the trachea, esophagus, larynx, and thyroid laterally to the internal jugular vein and vagus nerve.
Caudad part
At this level the common carotid artery can be palpated between the two heads of the sternocleidomastoid muscle by pushing the clavicular head laterally just above the clavicle. Place two or three ngerpads immediately outside the trachea, inside the sternal head of the sternocleidomastoid. Due to the obliqueness of this muscle, the common carotid artery approximates its anterior border.
134
14
Parotid gland Digastric muscle Stylohyoid muscle Internal jugular vein Sternocleidomastoid muscle Trapezius muscle Brachial plexus Sternohyoid muscle Submandibular gland Common carotid artery
135
Cephalad part
The common carotid artery ascends free of the sternocleidomastoid 2cm beneath the upper border of the thyroid cartilage. Feel for the carotid pulse below the hyoid bone. Remember that the common carotid divides at the level of C3 or C4.
often indicate a respiratory or food allergy. Small retrocervical or laterocervical ganglia the size of a hazelnut, often more evident on one side, are the result of infection or inammation. It is usually on the side where they are more developed that a gingival, dental, or ear, nose, and throat (ENT) problem exists. Always be prepared to ask the patient when they last visited the dentist, especially when they have neck pain of nontraumatic origin. Submental and maxillary ganglia arise with infections of the face and mastication system. In adolescents, multiple ganglia often appear at the neck and cervical region. Usually, they signify a general state of exhaustion. Nevertheless, consider mononucleosis in the presence of tonsillitis, sizable adenopathies, and ganglia that are painless, rm, and smooth.
14.2.3 Contraindications
The contraindications for manipulation of the common carotid artery are: arterial hypertension higher than 150/90mmHg drop attack (sudden fall caused by vertebral basilar insufciency) vascular fragility (diabetes, connective tissue disease, and other systemic illness). If in the slightest doubt, refer the patient to a physician an aneurysm of the common carotid artery feels like a large pulsation that lifts the sternocleidomastoid muscle slightly. It is fairly soft and compressible. The enlargement is longitudinal and easily mobilized transversely. The dilation increases in size with distal compression of the artery, and diminishes with proximal compression. Aneurysm of the common carotid artery can accompany a bitonal voice (laryngeal compression), irritating cough, or neck pain.
14.2.2 Precautions
It is advisable to proceed with caution in these instances: signicant arterial hypertension atheromatous plaque raised cholesterol levels unexplained vertigo or instability. Pay attention with female smokers who are taking contraceptive hormones and who have high cholesterol levels. Adenopathy is very common at the neck. Often benign, these ganglia are indicators of an immune response to serious disease challenges. Some things to keep in mind include: Small riziform (rice-shaped) and easily mobilized ganglia at the back of the neck
136
14
Often our colleagues question us about the risk of dislodging atheromatous plaque. Those who have done cadaver dissection know that such a plaque is generally very hard and not easily detached certainly not by our technique.
14.2.4 Indications
Due to the large territory supplied by the common carotid artery, there are many treatment indications: headache vertigo instability arterial hypertension tachycardia cardiac arrhythmia precordial pain gastroesophageal reux pain in the solar plexus region vagotonia sympathicotonia thyroid dysfunction ocular dysfunction hemiplegia cerebral deciency following craniofacial trauma after surgery.
Bidigital technique
We perform these techniques either by stretching or by using induction. With one thumb, lightly take a xed point on the carotid artery, within the triangle separating the two heads of the caudal insertion of the sternocleidomastoid muscle (Fig. 14.4). With the other thumb, take another xed point lightly on the medial part of the carotid artery at its cephalad part. Several times, traction the areas where you felt a less distinct pulse during the initial evaluation. Next stretch the carotid artery by following the Listening and encouraging the Listening with induction. NB: It is always good to do this technique on both common carotid arteries to obtain a central stimulating effect.
137
slide smoothly. On any areas that appear to scrape or rub your ngers, execute a glideinduction. The ngers are placed on the artery as above. Encourage and amplify the movements you feel with Listening. The objectives of the technique are: to balance the vascular tone of the two common carotid arteries to release hardened zones impeding the harmonious and balanced arterial ow to affect the bers of the glossopharyngeal nerve in order to provide central benet.
Glideinduction technique
Glide your ngerpads lightly along the length of the artery. Your ngers should
138
15
The external carotid artery is very much the true artery of the neck. Manipulation of this artery and its branches (studied in subsequent chapters) improves the function of the thyroid, parotid, trachea, face, and the entire mastication system, once the other tissue xations are resolved.
Only the lingual and pharyngeal arteries are omitted from our description. They are difcult to access and respond poorly to our manipulations.
15.1.2 Course
The external carotid artery is initially oblique, adopting a vertical course after the angle of the mandible.
15.2.2 Precautions
Be careful and do not hesitate to direct patients to medical care in case of: recurrent vertigo without antecedent trauma instability unsteady gait.
15.1.4 Collaterals
The external carotid artery has six collateral branches: three anterior: superior thyroid, lingual, and facial two posterior: occipital and posterior auricular one medial: pharyngeal.
15.2.3 Contraindications
Contraindications to treatment of the external carotid artery include: drop attack (sudden fall without loss of consciousness, generally due to vertebral basilar insufciency) sudden, localized, and unexpected headache alerts you to the possibility of aneurysm
139
Thyrocervical trunk
Subclavian artery
140
15
Glidinginduction technique
The initial point of contact is the same as above, at the level of the thyroid cartilage. The other thumb or index nger carries out the glidinginduction technique, departing along the artery from the xed point. It is important to feel all small sections where you have the impression that the nger does not glide as well. This technique has an effect on the wall of the external carotid artery and also on the bers of the hypoglossal nerve.
15.2.4 Indications
The indications are the following: headache facial paralysis thyroid dysfunction problems affecting the face, alveolar dental and pharyngeal laryngeal junction cervical trauma with associated functional signs such as vertigo, instability, tinnitus, and headache.
Digital spreadinggliding technique 15.2.5 Manipulations Common position for three techniques
The patient is in decubitus, elbows on the table, hands resting on the abdomen. The head is turned slightly away from the external carotid artery in question. Keep to the treatment side of the patient. Carry out this maneuver with two or three ngerpads of each hand, positioned as described in the palpation test above (Fig. 15.3). Focus the action of the ngers where the gliding is not smooth. Remember that gliding is the key component, and any compression must be minimal. The maneuver is complete
141
when the ngers can move over the artery easily without any sense of roughness along the vessel wall. In addition to affecting the elasticity of the artery itself, the ngers act on the periarterial nervous system (cervical sympathetic, hypoglossal, and glossopharyngeal bers). At
the end of treatment you should feel a regular, smooth arterial pulse, with no weak areas. NB: Remember to examine the part of the external carotid artery located where the sternocleidomastoid muscle crosses the vessel. Fixations of hypoglossal nerve bers are common here.
142
16
16.1 ANATOMY
16.1.1 Origin
The facial artery arises between the hyoid bone and the base of the mandible. It winds its way in front of the external carotid, from which it originates (Fig. 16.1).
16.1.5 Function
The facial artery supplies the palatine tonsils, soft palate, pterygoid, mylohyoid, and digastric muscles, the submandibular gland, and all of the face.
16.1.6 Anastomoses
The facial artery is joined with the internal carotid via the intermediary of its terminal branch, the angular artery.
16.1.2 Course
The facial artery winds its way forward and upwards towards the submandibular gland, passing onto the face where its pulse can be felt as it crosses the mandible. It courses over the face, emerging by the edge of the lips and ascending between the nostril and cheek.
16.1.3 Termination
The terminal branch of the facial artery is the angular artery, at the inner corner of the eye.
16.1.4 Collaterals
The facial artery supplies eight branches: In the cervical region: ascending palatine artery pterygoid artery submental artery submaxillary artery. Its named branches on the face are the: masseteric artery superior labial artery inferior labial artery lateral nasal artery.
Comments
The facial artery serves as an indicator of the effect of our manipulation of the common carotid and external carotid arteries.
143
Supraorbital artery Supratrochlear artery Angular artery Dorsal nasal artery Lateral nasal artery Facial artery Occipital artery Maxillary artery
Fig. 16.2 Locating the pulse of the facial artery at the mandible.
144
16
Supratrochlear artery Supraorbital artery Superficial temporal artery Dorsal nasal artery
Angular artery
Facial artery
145
16.2.2 Indications
Indications for manipulation of the facial artery are: facial paralysis chronic rhinopharyngeal infection cerebral lesions
146
17
17.1 ANATOMY
17.1.1 Origin
The occipital artery arises in the neck anterior to the mastoid protuberance from the posterior aspect of the carotid. It branches from the carotid just a little above the facial artery (Fig. 17.1).
17.1.2 Course
The occipital artery passes posteriorly, parallel and deep to the posterior belly of the digastric muscle, and passes in a groove on the temporal bone medial to the mastoid process. It then runs towards the external occipital protuberance where it ascends the scalp. It perforates the trapezius muscle and the nuchal fascia between the cranial insertions of the trapezius and sternocleidomastoid muscles.
17.2.2 Indications
Indications for manipulation of the occipital artery are: aftereffects of otitis tinnitus facial paralysis hearing dysfunction cranial trauma (especially posterior) following rabbit punch blow to the back of the head cervical pain cerebellar problems.
17.1.3 Collaterals
The occipital artery has these branches: muscular branches supplying the sternocleidomastoid, digastric, splenius capitis, and semispinalis capitis of the head stylomastoid artery that accompanies the facial nerve in the stylomastoid foramen to run in the tympanum and mastoid cavities, as well as the semicircular canals meningeal artery supplying the dura mater of the mastoid and the diplo. The artery penetrates the mastoid foramen, usually accompanied by an emissary vein.
Epicranial aponeurosis
148
17
Technique
With one or two ngers, palpate the occipital arterial pulsations mid-distance between the external occipital protuberance and the lateral border of the occiput (Fig. 17.2). Alternately compress and decompress to create a viscoelastic suction phenomenon. Next contact the occipital artery as it emerges from the trapezius muscle attachment. Take a second contact on the artery a little medially or laterally, depending on the direction of the Listening. Begin by releasing the fascia that surrounds the artery, as well as the fascial ring surrounding the emissary vein. Then treat the artery itself with induction.
Comment
When you do this technique, you obtain an effect on the greater occipital nerve. Moreover, thanks to the emissary vein that connects the interior of the skull with the extracranial veins, our manipulation extends to the occipital and mastoid dura mater.
Fig. 17.2 Manipulation of the occipital artery.
149
18
18.1.1 Origin
The posterior auricular artery is not the most important branch of the external carotid. However, because of its anastomoses, treating it improves the results on the occipital and supercial temporal arteries.
an auricular branch supplying the medial and lateral cranial surfaces of the auricle a mastoid branch.
18.1 ANATOMY
The posterior auricular artery (Fig. 18.1A,B) arises from the dorsal side of the external carotid artery, just above the occipital artery. These arteries sometimes share a common trunk. It is the most superior of the posterior branches of the external carotid artery.
18.1.5 Anastomoses
The posterior (mastoid) branch anastomoses with the occipital and supercial temporal arteries.
18.1.2 Pathway
The posterior auricular artery penetrates the parotid gland, and ascends between the auricle and the mastoid process.
18.1.3 Collaterals
The posterior auricular artery supplies branches to the parotid gland and the skin covering it. The stylomastoid branch orginates from the posterior auricular artery.
18.2.2 Indications
Indications are similar to those for the occipital artery: sequelae of otitis tinnitus facial paralysis auditory problems following posterior cranial trauma rabbit punch blow (to the back of the head).
150
18
Parietal artery
Occipital artery
Posterior auricular artery Facial artery Internal carotid artery A External carotid artery Common carotid artery
Perforant branches
Fig. 18.1 (A) Posterior auricular artery. (B) Arteries behind the ear pavilion.
151
18.2.3 Manipulations
Treatment is with viscoelasticity and then stretchinduction. This same technique (Fig. 18.2) serves to evaluate changes in the pulse following manipulation of the occipital and supercial temporal arteries.
18.2.4 Position
The patient is in lateral decubitus, on the side opposite the artery concerned.
18.2.5 Technique
Place one or two ngers (space permitting) on the pulse of the posterior auricular artery. Stretch the artery in induction.
152
19
19.1 ANATOMY
The maxillary artery (Fig. 19.1) cannot be palpated at its origin, as it is located behind the mandible. Of interest is its terminal infraorbital branch that accompanies the maxillary nerve and, to a lesser degree, its mental branch, which accompanies the mandibular nerve.
19.1.1 Origin
The maxillary artery is the largest branch of the external carotid, arising just above the posterior auricular artery. It is hidden behind the zygomatic arch.
ophthalmic artery, arising from the internal carotid. Descending branches: The inferior alveolar artery gives off alveolar dental branches, before passing through the mental foramen as the mental artery. The mental artery serves as an indicator of the effects of maxillary and mandibular manipulations. It can also be used to evaluate the impact of dental apparatus. When braces are too tight, for example, the mental pulse on the side of the mechanical tension is either strained or diminished.
19.1.2 Pathway
The maxillary artery runs between the two heads of the lateral pterygoid muscle to penetrate the pterygopalatine fossa.
The patient is in decubitus, hands crossed over the abdomen. Position yourself at the patients head in order to compare the left and right arteries.
Infraorbital artery
The infraorbital foramen is familiar to us as the location where we manipulate the maxillary nerve, the second branch of the trigeminal nerve. It is not really possible to separate treatment of the maxillary nerve and the maxillary artery. Palpate the artery in the infraorbital foramen found beneath the orbital rim,
153
Superficial temporal artery Supraorbital artery Supratrochlear artery Transverse facial artery Angular artery Infraorbital artery Facial artery Internal carotid artery External carotid artery Middle temporal artery Occipital artery Maxillary artery
154
Fig. 19.2 Manipulation of the infraorbital artery.
19
Mental artery
Take the mental pulse at the mental foramen, in line with the second premolar. The mental foramen is approximately on the extension of an imaginary vertical line passing through the infraorbital and supraorbital foramina.
19.2.2 Indications
The indications for the maxillary artery are:
155
20
20.1.1 Origin
20.1 ANATOMY
The supercial temporal artery (Fig. 20.1) is the smaller terminal artery of the external carotid. It arises at the neck of the mandibular condyle and has several named branches.
20.1.5 Features
The supercial temporal artery, a branch of the external carotid, anastomoses with the supraorbital artery, a branch of the internal carotid. Here, once again, is an example of the entanglement of these arteries. Moreover, the orbital branch of the supercial temporal artery anastomoses with a branch of the internal carotid artery.
20.1.2 Pathway
The supercial temporal artery passes over the zygomatic tubercle and the external pore, to run up the scalp in the temporal region. At the zygomatic arch it is covered by the parotid gland.
20.1.3 Collaterals
The principal branches of the supercial temporal artery are: a transverse artery that courses across the cheek an anterior articular branch supplying the temporomandibular joint branches for the side of the face and the ear pavilion an orbital branch supplying muscles of the eyelids and anastomosing with the superior palpebral artery, arising from the ophthalmic artery (a branch of the internal carotid).
20.2.1 Position
The patient is in decubitus, hands on the abdomen, with the head turned slightly away from the side of the manipulation.
Technique
Perform this technique where you best perceive the facial artery pulse as described above (Fig. 20.2).
20
Lateral branch
Medial branch Frontal branch Middle temporal artery Transverse facial artery Facial artery Occipital artery Maxillary artery
Labial branches
157
Technique
Treat this artery with a small stretchinduction (Fig. 20.3).
Technique
Treat with maneuvers. small stretchinduction
Fig. 20.3 Manipulation of the zygomatico-orbital artery.
158
20
20.2.6 Comments
All the arteries have their contralateral partners, allowing us to compare pulses on both sides. Often the problem artery is on the side where the pulse is weakest or most tenuous. More rarely the problem side is indicated by a bounding or stretched (tense or pulled) pulse. Cranial suture xations often affect the pulse of the neighboring artery. Finally, it is helpful to show your patients how to do skin rolling over hardened or sensitive cutaneous areas of the temporal fossa.
Technique
Undertake microstretchinduction movements, using two or more ngers (Fig. 20.4).
159
21
21.1.1 Origin
The internal carotid artery is very difcult to feel at its origin and impossible to palpate along its intracranial course. Happily, some of its terminal branches appear on the face where they are fairly easily palpated. These branches serve mainly to direct us to the side of reduced cerebral blood ow, and enable us to evaluate our results.
21.1.4 Comment
The ophthalmic artery provides an indication of the internal carotid dysfunction.
21.1.5 Relations
In the neck, the internal carotid artery has the same positioning as the external carotid, although it is slightly lateral and posterior to it. The internal carotid is initially supercial, covered only by skin, the platysma, and the supercial cervical aponeurosis. At the base of the skull the glossopharyngeal, vagus, and hypoglossal nerves are positioned posterior to the internal carotid artery. They then circumvent it and are lateral to the internal carotid artery.
21.1 ANATOMY
The internal carotid (Fig. 21.1) begins at the bifurcation of the common carotid, between the hyoid bone and the superior border of the thyroid cartilage, at the level of C3 or C4. It is located lateral and posterior to the external carotid artery as it ascends the neck.
21.1.2 Pathway
The internal carotid runs superiorly and medially towards the pharynx. It enters the skull through the carotid canal in the petrous part of the temporal bone (foramen lacerum).
21.2.2 Contraindications
The contraindications are: violent and random headache general vascular fragility cerebral hemorrhage.
21.2.3 Indications
Indications for manipulation are cerebral disorders in general, such as:
160
21
Parkinsons disease arteriosclerosis cerebrovascular accidents motor decits consequences of paralysis vertigo instability.
161
Glossopharyngeal nerve
Internal carotid artery External carotid artery Carotid glomus Nerve of the carotid sinus Carotid sinus
Carotid glomus
Supraorbital nerve Orbital septum Lacrimal gland Superior tarsus Lateral palpebral ligament Inferior tarsus
Ophthalmic artery Angular vein Medial palpebral ligament Angular artery Lacrimal sac
Facial artery
162
21
Manipulation
Position The subject is in decubitus, eyes closed. Technique Place the pad of one index nger on the eyeball (Fig. 21.4). Superimpose the other index nger. With the overlaid nger creating the movement, delicately push the eyeball posteriorly and medially. Release your pressure and allow its gradual viscoelastic return. This is the same technique we apply to the optic nerve. It has the effect of pleating and then unpleating the artery.
As a preliminary assessment, take the supraorbital and supratrochlear pulses. Apply the technique on the side of the weaker pulse. Afterwards verify your treatment with the same pulses. In any event, always treat both left and right arteries. This general rule applies to all paired organs. The ophthalmic artery follows the trajectory of the superior oblique muscle. To stretch it, draw the eyeball laterally and caudally. Normally the pulse is more marked when this muscle is stretched. This technique can be combined with induction of the supraorbital artery, described below.
Indications
Manipulation of the supraorbital artery is used for all circulatory problems involving the brain, whether of traumatic, infectious, or degenerative origin. The aftermath of vascular cerebrovascular accidents is a good indication for treatment.
Fig. 21.5 Manipulation of the supraorbital artery.
Contraindication
There are no formal contraindications. Our techniques are so soft and respectful of the tissues that it is difcult to believe they could be iatrogenic. You have only to remember that coughing, sneezing, and straining on the toilet all increase intracranial pressure far more than any pressures we might exert with our ngers.
which it originates. Keep this in mind when choosing the direction of the manipulation. The supraorbital artery divides into small branches supplying the soft tissue of the eyebrow, and also sends a branch to the diplo of the frontal bone.
Manipulation
This technique has two components: one directed to the supraorbital artery and the other to the optic nerve (Fig. 21.5). Step one With the pad of one nger, compress the supraorbital artery. Gently release your pressure and follow the decompression with induction. Step two With the index nger of the opposite hand, compress the eyeball in a posteromedial direction to manipulate the optic nerve. Allow the eyeball to gradually return to its neutral position.
164
21
21.2.8 Exercise
If you nd a difference in the quality of the supratrochlear and supraorbital pulses, consider a possible cranial problem. This nding can be of osseous, sutural, meningeal, or encephalic origin. As a rule, the restriction will be on the side of the weak pulse.
Cranial Local Listening is the best way to detect the restriction. Effective cranial treatment often resolves the pulse difference. An overly tight dental appliance frequently manifests as a weakened supratrochlear or infratrochlear pulse, on the side of the constraint.
165
22
consistency is rather soft, and its parenchyma is slightly granular. Its surface, when lightly palpated, appears somewhat irregular.
The thyroid
Lobes The thyroid lobes have the shape of a pear or a triangular pyramid, and are largely covered by the sternothyroid, sternohyoid, and omohyoid muscles. A perfectly normal thyroid is difcult to palpate. The medial surfaces of the lobes are adapted to the lateral surfaces of the rst ve or six tracheal cartilages, the lateral surface of the cricoid cartilage, and the inferior part of the thyroid cartilage. Posteriorly, the lobes relate to the carotid sheath and its neurovascular contents, as well as to the parathyroid glands. Isthmus The isthmus is a at lamina connecting the lobes, usually over the second, third, and fourth tracheal cartilages. It measures about 10mm in width, 15mm in height, and 5mm in thickness. The superior border of the isthmus often gives rise to a vertical prolongation called the pyramidal lobe. This extra lobe is sometimes joined to the hyoid by a bromuscular band, the levator of the thyroid gland.
Stability
The thyroid parenchyma is surrounded by a thin brous capsule, a dependency of the visceral sheath of the neck. The capsule is held in place by ligaments of the trachea and the
166
22
Thyroid cartilage Pyramidal lobe (of Lalouette) Superior parathyroid gland Thyroid isthmus Inferior parathyroid gland
Trachea
Anterior view
Posterior view
Fig. 22.1 (A) Frontal view and prole of the thyroid. (B) Posterior view of the thyroid.
vascular sheath called the thyrotracheal ligaments, one medial and two lateral. These are also referred to as the ligaments of Grber. The thyroid compartment is in the shape of a U, open at the back. The thyroid sheath enclosing it is made up: posteriorly by the visceral sheath medially and the carotid sheath laterally anteriorly by the pretracheal layer of the deep cervical fascia, which also surrounds the infrahyoid strap muscles. The pretracheal lamina inserts on the inferior border of the hyoid bone and splits into two layers: a pretracheal lamina covers the sternohyoid and omohyoid muscles a deep lamina covers the thyrohyoid and sternothyroid muscles.
Physiology
The thyroid gland secretes two hormones that stimulate cellular metabolism, and one hormone concerned with phosphate and calcium metabolism. Thyroxine and triiodothyronine Iodine is essential in the formation of the thyroid hormone thyroxine (T4) and tri iodothyronine (T3). The abbreviations T4 and T3 denote the number of iodine atoms the hormone contains. These hormones are initially synthesized as the precursor thyroglobulin. The release of hormones into the blood is controlled by TSH (thyroid stimulating hormone), secreted by the anterior pituitary gland. The secretion of TSH is stimulated by
167
Table 22.1 Symptoms of thyroid dysfunction Hyperthyroid Symptoms Sympathicotonia Nervousness Irritability, intense emotion Fatigue, lethargy Apathy, sleepiness Memory problems, poor hearing Peripheral neuropathy, carpal tunnel syndrome Excessive sweating, thirst Intolerance to heat Palpitations Frequent stools, diarrhea Weak muscles, fatigue Trembling Oligomenorrhea, amenorrhea Weight loss despite increased appetite Signs Tachycardia Increased systolic and diminished diastolic pressure Leucopenia, thrombopenia Hot, smooth, moist skin Trembling, proximal muscle weakness Basedows disease: ocular signs (xed gaze, oculopalpebral asynergy, exopthalmia) Bradycardia Decreased systolic and increased diastolic pressure Anemia Dry, rough, cold skin Edema (nonpitting) Dull hair, fragile nails, hair loss Weight gain despite decreased appetite Constipation Muscle cramps, myotonia Arthralgia, paresthesia Hypothermia, chills Intolerance to cold Hypothyroid
Swelling of the face, hands, and feet; pufness around the eyes
168
22
Physiology
The parathyroids secrete parathyroid hormone (parathormone) and play an important role in calcium metabolism. Secretion is regulated by blood calcium levels. When calcium concentration falls, parathyroid hormone secretion increases, and vice versa. The main function of the parathyroid hormone is to maintain a constant concen tration of calcium in the extracellular uid. Thus, when blood calcium levels falls, parathyroid hormone: increases the amount of calcium absorbed in the small intestine increases the amount of calcium reabsorbed in the renal tubule.
Palpation
The supercial location of the thyroid suggests that palpation will be easy. However, in the absence of pathology, palpation of the gland is hampered by the thickness of the infrahyoid and sternocleidomastoid muscles covering it. Ideally, palpation is done with a patient seated with their back leaning against the therapist, who stands behind the patient. To begin, either the patients head is in the standard neutral position or the cervical thoracic junction is slightly exed to reduce tension on the anterior neck muscles. With practice it is possible to perform this palpation in supine. You might want to provide a glass of water for the patient if he or she needs to swallow repeatedly. Identify the cricoid cartilage and then, with the pad of your index and middle ngers, search caudally to feel the isthmus, located about 1cm below. To palpate the isthmus from the sternal notch, glide your ngers upwards using a light touch, and short back and forth
169
Infrahyoid region
170
movements. Your ngers will run into the substance of the isthmus. Have the patient swallow and feel the elastic isthmus elevate under your nger (Fig. 22.3). Move laterally to palpate the right and left lobes, which are somewhat easier to nd. Palpate in a symmetrical manner using the ngers of both hands simultaneously. The palpation can be facilitated by asking the patient to swallow, in order to mobilize the thyroid cephalad, making the inferior part more accessible. To access the medial part of each lobe with precision, maintain the trachea with one hand and palpate the internal border of the lobe with the other hand. To palpate the main and lateral aspects of each lobe, glide the trachea towards the side being examined. With the other hand, encircle the sternocleidomastoid by placing your ngers and thumb around it. Ask the patient to swallow once more and palpate the whole lobe. This technique is particularly useful in cases of glandular hypertrophy.
This exploration is sometimes difcult, especially when the neck is short and thick or the person is obese. You can always ask the patient to tilt the neck toward and away from the side of the examination. If you still feel nothing, when the patient swallows make soft vertical up and down movements with the ngers just below the thyroid cartilage. Occasionally thyroid palpation requires extension and rotation of the neck towards the side being examined. This relaxes the sternocleidomastoid so that it can be moved out of the way. Palpation allows you to check the shape, size, structure, mobility, and sensitivity of the thyroid parenchyma, and to look for lymph nodes in the area of thyroid drainage. Form The lateral lobes lie anterior and lateral to the trachea and larynx, and posterior to the isthmus, which crosses the anterior surface of the trachea (Fig. 22.4). It is helpful to
22
Epiglottis
Thyroid
Trachea
Anterior jugular vein Sternothyroid muscle Sternocleidomastoid muscle Omohyoid muscle External jugular vein Inferior laryngeal nerve Lymph nodes Sternohyoid muscle Thyroid Internal jugular vein Common carotid artery Vagus nerve Inferior thyroid artery Vertebral artery and vein
171
172
22
Multinodular goiter
Fig. 22.5 Anomalies in thyroid volume and consistency (after Bates 1993).
Diffuse hypertrophy of the thyroid. A diffusely enlarged gland or goiter engulfs the isthmus and the lateral lobes, but has no palpable nodes. This is found in Basedows disease, Hashimotos disease, and endemic goiter linked to iodine deciency. Sporadic goiter refers to hypertrophy with no apparent cause. Multinodular goiter. This term applies to a swollen thyroid containing two or more identiable nodules. Multiple nodules cause more metabolic problems than does a malignant lesion. In any case, exposure to radiation in infancy, a family history of cancer, or a rapid increase in the volume of one of the nodules makes one suspicious of a malignant lesion. Isolated thyroid nodule. An isolated nodule found during examination may be a cyst, a benign tumor, a nodule within an atypical multinodular goiter, or a malignant lesion. Again, factors such as anterior irradiation, a rapid or recent increase in nodule size, xations to neighboring tissues, the hardness of the nodule, irregularity of contour, or enlarged cervical lymph ganglia raise the
173
Relations The superior thyroid artery passes under the omohyoid, sternohyoid, and thyrohyoid muscles. Collaterals The main branches of the superior thyroid artery are the laryngeal arteries supplying the tissues of the larynx. Function The superior thyroid artery supplies the superior two-thirds of the gland. Terminal branches The superior thyroid artery divides into three branches relating to the three surfaces of the lobes: 1 a lateral branch for the anterior lateral surface 2 a medial branch which crosses above the isthmus to anastomose with its partner on the opposite side 3 a posterior branch descending on the posterior border to supply the medial and lateral surfaces (anastomoses with the posterior branch of the inferior thyroid artery). Distinctive feature The superior thyroid artery follows the superior laryngeal nerve, branch of the vagus nerve (see Barral & Croibier 2006). Needless to say, any manipulation of the laryngeal artery has an effect on the superior laryngeal nerve.
Inferior thyroid artery
Arteries
The arterial blood supply relies on two main trunks: 1 the superior thyroid artery, arising from the carotid artery 2 the inferior thyroid artery, a branch of the subclavian artery. These two trunks are large and, because their branches anastomose frequently, their manipulations are complementary. There is also an accessory pedicle called the middle thyroid artery. This collateral branch comes from the arch of the aorta and ascends the trachea to reach the inferior border of the isthmus. Superior thyroid artery
Origin This is the rst branch of the external carotid artery; it arises just beyond the carotid bifurcation (Fig. 22.6). Pathway Beginning just below the greater cornu of the hyoid bone, the superior thyroid artery descends vertically along the lateral border of the thyrohyoid muscle, to reach the upper lobe of the gland.
Origin The inferior thyroid artery (Fig. 22.7) arises from the thyrocervical trunk, which branches from the subclavian artery on the pleural dome, in front and a little lateral of the vertebral artery. Course The inferior thyroid artery has three segments: 1 A vertical part beginning just outside the vertebral artery.
174
22
External carotid artery Suprahyoid artery Superior laryngeal artery Internal carotid artery Superior thyroid artery Common carotid artery Cricothyroid artery
2 A curved segment that runs medially above the transverse process of C6, passing in front of the vertebral artery and behind the carotid sheath. Here it intersects with the sympathetic cervical chain. 3 Curving again, the artery ascends obliquely in an anteromedial direction. It intersects the lateral border of the esophagus and the trachea, and passes anterior to the recurrent laryngeal nerve
Relations The inferior thyroid artery reaches the posterior surface of the thyroid gland at C5. It winds around the: internal jugular vein common carotid artery vagus nerve sympathetic trunk.
175
At the level of C5, the inferior thyroid artery passes anterior to the vertebral artery and posterior to the carotid sheath. Manipulation of the inferior thyroid artery at its origin affects the homolateral vertebral artery.
medially behind the carotid sheath. It supplies the adjacent muscles and gives off spinal branches to supply vertebral bodies and the spinal cord, owing to its anastomoses with the spinal arteries.
176
Collaterals The inferior thyroid artery divides into several branches to supply the: esophagus trachea larynx. The ascending cervical artery is a small branch that arises as the inferior thyroid turns
Terminal branches The inferior thyroid artery reaches the thyroid body at the junction of the superior twothirds and inferior one-third of the gland. It divides into three terminal branches: 1 A posterior branch forms an anastomosis with the posterior branch of the superior thyroid artery, along the
22
Superior parathyroid gland Supraisthmic arcade Deep branch Inferior thyroid artery Infraisthmic arcade
posterior medial border of the thyroid lobe. 2 A deep branch anastomoses with its contralateral partner. 3 An inferior branch anastomoses with its counterpart, along the inferior border of the isthmus (Fig. 22.8). NB: The inferior thyroid artery is subject to numerous variations from its origin and along its trajectory. To keep it simple, just remember that it reaches the thyroid body at C5.
The middle thyroid veins are short horizontal branches that arise from the posterior surface of the lobes, drain the middle of the lobe, and empty directly into the inferior jugular vein. The inferior thyroid veins collect blood from the inferior pole of the lobe and inferior border of the isthmus. They descend obliquely inferiorly to let into either the brachiocephalic or the internal jugular vein.
Function The inferior thyroid artery supplies the inferior third of the thyroid gland.
Nerves
The thyroid receives nerve supply from: parasympathetic bers arising from the superior and inferior laryngeal nerves sympathetic bers from the superior and middle cervical ganglia, as well as from the superior cardiac nerve. The parathyroid nerve supply is sympathetic, from the cervical ganglion. Innervation reaches the thyroid through the periarterial plexus on the inferior thyroid
Veins
Three pairs of veins drain the thyroid. The superior thyroid veins drain the superior pole of the thyroid and accompany the superior thyroid artery. They empty into the internal jugular vein via the thyro-lingual-facial trunk.
177
22.5.2 Manipulations
Manipulation of the superior laryngeal artery
178
Position The patient is in decubitus, hands crossed on the abdomen, head turned slightly away from the artery in question (Fig. 22.9).
Techniques Once the artery is perceived, compress and release it a few times. Using a very light contact, treat it with induction. One or two ngerwidths from the lateral border of the thyroid cartilage, below the hyoid bone, the superior laryngeal artery perforates the thyrohyoid membrane (Fig. 22.10). This piercing is often surrounded by a small fascial ring, which must be released for two reasons: to free the perineurovascular tension to obtain an effect on the superior laryngeal nerve. This, along with the external auditory canal, is a key point for manipulation of the vagus nerve. Next, locate the superior laryngeal artery where it arises from the superior thyroid artery. Stretch the artery in a superior and medial direction, with induction. It is also important to perform skin rolling in regard to this artery, both vertically and transversally.
22
Fig. 22.10 Manipulation of the superior laryngeal artery at the thyroid membrane.
Stretch maneuver With one nger x the superior thyroid artery where it arises from the carotid. With the other ngerpad placed atly just beneath the rst nger, stretch this artery caudally and medially on the anterior surface of the thyroid cartilage. NB: Always remember to treat both the left and right inferior and superior thyroid arteries. Viscoelasticityinduction This technique is applied where the superior laryngeal artery passes through the thyrohyoid
membrane. Compress, release, and follow the Listening. Be careful to stay light with your palpation because of the superior laryngeal nerve.
Multidigital fanning Depending on the size of the neck, this technique is recommended because it benets several small branches of the artery. Throughout the maneuver, keep one ngerpad on the origin of the superior thyroid artery as you spread small branches towards the substance of the gland. Pulse variations guide you in determining the optimal orientation of the fanning (Fig. 22.11).
179
Manipulation of the inferior thyroid artery The inferior thyroid artery is located behind the common carotid and just above the subclavian arteries. It is very difcult, not to say impossible, to differentiate its pulse at its origin. Take the pulse as it courses superiorly along the medial surface of the scalene muscle.
lobe medially at the same time, to assist the stretch. Complete the technique with induction, following the same protocol as for the superior thyroid artery, extending your action as caudally as possible to affect the anastomoses between the paired arteries.
Decubitus position The patient is in decubitus, elbows on the table, hands placed under the lower back to open the thoracic inlet (Fig. 22.12).
Maneuver Locate the pulse of the common carotid artery inside the sternal head of the sternocleidomastoid. Next, direct your ngers laterally and posteriorly to the common carotid to nd the second, less distinct, pulse of the inferior thyroid artery. Locate the pulse of the subclavian artery beyond the sternoclavicular junction in order to distinguish it from the inferior thyroid artery, whose caliber is clearly smaller. Place one thumb on the subclavian artery, and either x it or push it slightly caudally. At the same time, place the other thumb in the direction of the inferior thyroid artery, and stretch it medially and a little cephalad. You can mobilize the corresponding thyroid
Lateral decubitus position The patient is in lateral decubitus on the side opposite the manipulation. Place yourself directly behind the patient. Pass your arm under the patients forearm to support the upper extremity with your forearm. Place your thumb under the clavicle, and your index or middle nger just above the sternoclavicular junction. Your free cephalad hand pushes the shoulder anteriorly; this allows your ngers to penetrate against the pleural dome. Next, bring the shoulder cephalad. This position allows the index or middle nger easily to reach the medial surface of the anterior scalene muscle, in order to search for a small arterial pulse. Sweep your nger along the short course of this artery to discover any lack of elasticity or a hard part.
Maneuver Following the same principles, carry out induction on the inferior thyroid artery by
180
22
supinating the nger that is in contact with the artery (Fig. 22.13). Strumming The patient is in decubitus, hands on abdomen. This technique involves strumming on the thyroid lobes to nd small hardened areas, which are different from cysts. These hardened areas are less compressible than cysts, and have limited elasticity and viscoelasticity. By working with these parameters in mind, you will feel these zones gradually soften. Search carefully for hardened areas located behind the sternocleidomastoid, as they are often found here. In addition, with your free hand, you can bring the lateral lobe medially
to increase its thickness and make it easier to feel for, and work with, variations in elasticity and viscosity. Indications The indications for treating the thyroid are: thyroid dysfunction tracheal or laryngeal dysfunction vertebral artery problems, because of the contiguity of the two arteries and the anastomoses between the cervical branch and spinal arteries. Results It is difcult to objectify our results. However, clinically, we have seen notable improvements in certain thyroid dysfunctions.
181
23
Neurovascular techniques
One of the key propositions of the neck is that it allows free passage of numerous nerve bers arising from the skull and the cervical column. These nerve bers help to regulate the cardiovascular system, viscera of the neck such as the thyroid, and organs of the thorax, such as the heart and the lungs (Fig. 23.1). In a somewhat simplied manner, we will describe a few manipulations for the neurovascular system of the neck. We will focus primarily on the glossopharyngeal, hypoglossal, vagus, and sympathetic cervical chain.
superior cervical ganglion vagus nerve phrenic nerve cardiac plexus rst two cervical nerves
182
Neurovascular techniques
23
First cervical nerve Second cervical nerve Third cervical nerve Fourth cervical nerve Ansa cervicalis (XII)
Superior laryngeal nerve Common carotid artery Recurrent laryngeal nerve (X) Sympathetic trunk
feeling the precise micro-zone of neural xation, and not to decide for ourselves the outcome of the technique. The organism can self-regulate, as long as the manipulation is subtle, precise, and not painful.
Carotid sinus
This small dilation rich in mechanoreceptors (Fig. 23.3) is located between the hyoid bone and the superior border of the thyroid cartilage. By analyzing intracarotid pressure it responds to changes in blood pressure.
Carotid glomus
The Latin word glomus means pellet or little ball. Located at the carotid bifurcation, this chemoreceptor monitors the oxygen, carbon dioxide, and pH of the blood.
183
Second cervical nerve Hyoid bone Third cervical nerve Ansa cervicalis (XII) Common carotid artery Sympathetic trunk
Note that the carotid glomus receives nerve bers from the vagus, glossopharyngeal, and sympathetic cervical nerves. With regard to manipulation, it is difcult to separate the sinus and the glomus, and so we treat them together.
184
As a preliminary, take the pulse at the radial artery or use a pulse-taking devise at the index nger. After several manipulations, the pulse will diminish in intensity and rapidity, because of stimulation to the vagus and hypoglossal nerves. These manipulations cause reactive bradycardia. We like to use the skin rolling technique in the area of the carotid sinus. It is an effective technique with no risk of vagotonia (Fig. 23.5). NB: Be very gentle. This region of the neck is extremely sensitive. It is not the force of the maneuver that counts, but its precision.
Neurovascular techniques
23
Glossopharyngeal nerve
Carotid body
185
Fig. 23.5 Skin rolling at the carotid sinus and carotid body.
23.6.2 Indications
Indications for manipulation of the carotid sinus and glomus are: arterial hypertension tachycardia arrhythmia
anxiety attack precordial pain gastroesophageal reux pain in the solar plexus vagotonia sympathicotonia gingival or dental problems.
186
SECTION 3
VESSELS OF THE ABDOMEN
24
ngerwidths above the umbilicus. This slightly variable point is more or less symmetrical with the duodenojejunal junction. Remember that the sphincter of Oddi is in the posterior medial wall of the duodenum. Manipulation of this sphincter affects both the hepatopancreatic ampulla and the major duodenal papilla (of Vater).
24.1.5 Pylorus
The pylorus is usually found just to the right of the xiphoid umbilical line, a handswidth superior to the umbilicus. If the person is stressed or the pylorus is active, this sphincter could move more towards the right. Despite its mobility, it is easily palpated.
24.1.2 Gallbladder
The gallbladder is located where the right mid-clavicular umbilical line meets the ninth costal cartilage. The gallbladder is only pal pable under the ribs and in the seated position.
187
RMCUL
1 2 5 3 4
6 ASIS 1/3 7
2/3
8 1/3
2/3
1. Gastroesophageal junction (esophagocardio-tuberosity) 2. Gallbladder 3. Sphincter of Oddi (hepatopancreatic ampulla) 4. Duodenojejunal junction 5. Pylorus 6. Ileocecal valve 7. Ovary 8. Ovary
188
pancreas. Never place your ngers in an anteroposterior direction. Commence lateral of the artery to avoid picking up the beat of the superior mesenteric artery. Proceed towards the aorta, delicately and gradually. It is only by placing your ngers on either side of the aorta that you can feel an abdominal aortic aneurysm. Beware if you have the impression that the aorta is more than 45cm wide. Its normal dimension is no more than 3cm. Sometimes, for emotional reasons, the abdominal pulse is very powerful and distinct. This can worry the patient, even though it is a normal somatic reaction. One of the rst signs of aortic aneurysm is lumbago or low back pain. If the slightest
24
Celiac trunk (superior border of L1) Superior mesenteric artery (superior border of L2) Renal artery (L2) Inferior mesenteric artery (L3)
Transtubercular plane Aortic bifurcation (L4) Confluence of the common iliac veins (L5)
Pubic symphysis
doubt arises, refer the patient to their physician. As a preliminary, compare the blood pressure of the upper and lower extremities. The systolic index normally sits at about 0.9mmHg (see Chapter 6). Check that both femoral pulses are clearly perceptible. Some aneurysms are located higher up by the renal arteries. These are very difcult to feel manually.
189
MCUL
1 5 6
3 4
7 Bi-iliac line 9 8 10
11
1. Celiac trunk 2. Hepatic artery 3. Left gastric artery 4. Splenic artery 5. Superior mesenteric artery 6. Inferior mesenteric artery 7. Right colic artery 8. Common iliac artery 9. External iliac artery 10. Internal iliac artery 11. Left colic artery
more pressure you apply, the greater your chances of mistaking the abdominal aorta for the celiac trunk. This confusion is common (Fig. 24.3). This pulse is an indicator of the vascular effects of our manipulations with regard to the liver, stomach, spleen, and pancreas.
190
24
mistaken for the transverse colon. This pulse is fairly easy to feel. Palpate for it to the left, beyond the abdominal aorta.
191
Diaphragm
Right inferior phrenic artery Celiac trunk Common hepatic artery Right renal artery Abdominal aorta Right ovarian and testicular artery Right lumbar artery Right common iliac artery
Left gastric artery Left inferior phrenic artery Splenic artery Superior mesenteric artery Inferior mesenteric artery
192
24
24.2.13 In summary
The most perceptible pulses are those of the: aorta hepatic artery splenic artery iliac arteries superior mesenteric artery.
the aortic mechanoreceptors. Complete the treatment with induction. Always think in three dimensions, picturing the aorta as a pipe that might have a xation on any part of its contour.
193
25
Origin Course
The arteries described in this chapter serve as witnesses before and after liver lifting maneuvers. These gauges are the celiac trunk and hepatic artery.
manipulations, not only of the liver, but also of the spleen and pancreas. Because it is surrounded by the solar plexus, the celiac trunk is very sensitive to the glideinduction technique.
25.1 ANATOMY
25.1.1 Celiac trunk
The celiac trunk (Fig. 25.1) arises just below the aortic hiatus, at the caudal part of the 12th vertebral body, two ngerwidths below the xiphoid process.
Course
The hepatic artery passes almost horizontally anteriorly and laterally toward the pylorus. It passes between layers of the lesser omentum, medial to the common bile duct, to reach the porta hepatis.
The celiac trunk is 1.52cm long, passing almost horizontally anteriorly and slightly to the right. It divides into the hepatic, splenic, and left gastric arteries. This is referred to as a tripod division (ad modum tridentis). Usually the left gastric artery arises cephalad of the others.
Branches
The branches of the hepatic artery are: the pyloric artery the right gastroepiploic artery the pancreaticoduodenal arteries the gastric and omental branches the cystic artery the proper hepatic artery.
Relations
The celiac trunk relates: anteriorly and slightly to the right to the caudate (Spiegel) lobe of the liver posteriorly to the superior border of the pancreas on the left, to the stomach.
Remarks
There is an arterial interrelationship between the liver, stomach, pancreas, and spleen. As we shall see, it is not possible to select just one artery to treat an organ fully.
Comments
194 The celiac trunk is an excellent indicator to verify the effects of our vascular
25
Gallbladder Cystic artery Portal vein Celiac trunk Common hepatic artery Right gastric artery Gastroduodenal artery Superior pancreaticoduodenal artery Duodenum
Pancreas
to the right. This ligament determines the axis for manipulating the liver.
195
196
Fig. 25.3 Lifting irrigation of the liver (left lateral decubitus position).
25
25.2.4 Indications
We have performed this technique on patients suffering from hepatitis B or C. Although biological tests did not change much, many patients felt better, often regaining appetite and experiencing a desire to be more intellectually and physically active. The most common indications for treating the hepatic vessels are: fatty liver aftermath of alcohol or alimentary intoxication hepatitis sequelae
Fig. 25.4 Lifting irrigation of the liver (decubitus position).
allergies eczema psoriasis following infectious disease psychasthenia (phobias, obsessions) digestive disorders.
197
26
Origin
26.1 ANATOMY
The vascular circle of the stomach is composed of the left and right gastroepiploic (gastro-omental) arteries, and the left and right gastric arteries. The left gastroepiploic artery is a branch of the splenic artery that passes through the gastrosplenic ligament and then the gastrocolic ligament. It anastomoses with the right gastroepiploic artery, arising from the gastroduodenal artery. The left gastric artery joins with the right gastric artery, itself a branch from the common hepatic artery.
Course
The right gastric artery runs between the layers of the lesser omentum and crosses in front of the gastroduodenal artery.
Termination
The right gastric artery anastomoses with the left gastric artery.
Course
The left gastroepiploic artery follows the greater curvature of the stomach. Its direction varies depending on the fullness and shape of the stomach. For this reason it is fairly sinuous.
Course
The left gastric artery runs along the superior end of the lesser curvature of the stomach.
Termination
The left gastric artery anastomoses with the right gastric artery near to the pylorus.
Termination
The left gastroepiploic artery anastomoses with the right gastroepiploic artery.
26
Right gastric artery Superior pancreaticoduodenal artery Right gastroepiploic artery Inferior pancreaticoduodenal artery Superior pancreaticoduodenal artery Epiploic (omental) arteries
Left gastroepiploic artery Splenic artery Dorsal pancreatic artery Greater omentum
manipulation of the abdominal organs must take the entire ensemble into consideration.
Course
The right gastroepiploic artery runs to the left, posteriorly and inferiorly to the pylorus, along the greater curvature of the stomach to anastomose with the left gastroepiploic artery.
Comment
In studying the distribution of these arteries, it is clear that the arterial blood supply of the stomach is related to that of the liver and pancreas. This means that any effective
199
2 1
pancreas. The left gastric pulse is located more superiorly, toward the caudal part of the gastroesophageal junction. Confusion between the two pulses is essentially unimportant because the purpose is to feel a change in the quality of pulsation following treatment. Due to their vascular interrelationship, manipulating any of the organs brings change to any or all of the pulses in the area. Take the pulse of the common hepatic artery, to the right of the celiac trunk, perpendicular to the aorta.
mobilizing to the left. During this maneuver, place a at nger on the splenic artery, whose pulse is easy to feel. This enables you to pick up variations in the pulse, as a function of the direction of your manipulations. Step two: Bring the lesser curvature caudad and maintain this position for about 20s.
200
26
Fig. 26.3 Manipulation of the left gastric artery (right lateral decubitus position).
201
Fig. 26.5 Manipulation of the gastroepiploic artery (left lateral decubitus position).
at on the splenic artery, whose pulse variation will allow you to ne-tune the axis of your maneuvers. Move your hands in the direction where the pulse strengthens. This technique can be combined with the maneuver for the left gastric artery (Fig. 26.7).
202
the spleen via the left gastro-omental artery the liver via the right gastro-omental artery the pancreas via the right gastro-omental artery the esophagus and hiatal region via the left gastric artery. The structures concerned are: the right and left vagus nerves, and the celiac plexus, in the region of the esophagus the gastric veins the portal vein.
26
Fig. 26.7 Combined manipulation of the left gastric artery and the gastroepiploic artery (decubitus position).
Hepatic branch of the anterior vagal trunk Anterior vagal trunk Left gastric artery and plexus
Lesser omentum
Hepatic plexus Celiac ganglion and plexus Right gastric artery and plexus
Anterior gastric branch of the anterior vagal trunk Splenic artery and plexus
Gastroepiploic artery
203
26.2.6 Indications
Indications for manipulation of the stomach vessels include: gastric dysfunction (especially slow digestion) gastric ptosis hyperchloridia sequelae of ulcers gastroesophageal reux hepatopancreatic dysfunctions.
The celiac plexus is the largest major autonomic nerve plexus. It surrounds the celiac trunk and the origin of the superior mesenteric artery near the duodenojejunal junction, in front of the aorta. The plexus is comprised of the celiac, superior mesenteric, and aorticorenal ganglia. It exchanges bers with the vagus, and greater and lesser splanchnic nerves indeed with all the nerves arising in the abdomen.
26.2.8 Contraindications
An active ulcer and previous gastric bypass surgery are contraindications for manipulations. It is advisable to be particularly cautious with a patient suffering with stomach pain together with low systolic pressure. It is advisable to determine the color of the stools. Black stools are a sign of gastric or upper intestinal hemorrhage.
204
Pancreaticoduodenal vessels
27
It is difcult to separate the duodenum from the pancreas because their arterial systems are intertwined. In our opinion, the duodenum merits more medical attention than it receives because, embryologically, it is the origin of the liver and the pancreas. In medicine the duodenum is rarely cited, as it is obscured by gastric pains.
intraperitoneal and very dependent on the mobility of the liver. The second part of the duodenum is retroperitoneal and is almost always implicated in any right renal xations. One could almost speak of a duodenorenal irtation. It is at the duodenojejunal exure that the small intestine becomes intraperitoneal.
27.1 ANATOMY
We will see that the arteries common to the duodenum and pancreas arise from the gastroduodenal artery (Fig. 27.1).
205
Inferior vena cava Proper hepatic artery Right adrenal gland Portal vein Duodenum Superior mesenteric artery and vein Abdominal aorta Right iliac artery and vein
Pancreas Splenic artery Celiac trunk Left renal artery and vein
Note that this artery gives off a great number of small branches, perpendicular to it.
Position
The patient is seated, legs hanging free, hands on thighs. Position yourself behind the patient.
One hand lifts the liver while the other hand pushes the duodenum towards the back. It is often easier to push back the junction of the second and third parts of the duodenum than it is to move the sphincter of Oddi. Maintain this stretchinduction position for about 20s.
Technique
Begin with a hepatoduodenal lift (Fig. 27.2). Place the ngers of your right hand medial to the projection of the fundus of the gallbladder (right mid-clavicularumbilical line). Direct your ngers rst posteriorly and then cephalad to capture the liver. With the thumb of the other hand, contact the second part of the duodenum, below the sphincter of Oddi.
206
Pancreaticoduodenal vessels
27
Technique
The pancreaticoduodenal arteries run along a main vertical axis and their perpendicular branches run transversely.
The technique consists of pushing the lateral border of the second part of the duodenum across the xiphoidumbilical line, and maintaining the push while stretching it longitudinally. Progressing from cephalad to caudad, along the tube of the duodenum. Hold each pushinduction for about 20s (Fig. 27.3). This technique is good for the pancreaticosplenic arteries, which we will learn about in Chapter 28.
207
Portal vein Common hepatic artery Superior posterior pancreaticoduodenal vein Splenic artery Gastroduodenal artery Dorsal pancreatic artery
Superior posterior pancreaticoduodenal artery Inferior posterior pancreaticoduodenal artery Inferior anterior pancreaticoduodenal artery Superior anterior pancreaticoduodenal artery
Technique
Your two hands work simultaneously (Fig. 27.4). Exert a light perpendicular traction along the main axis of the second part of the duodenum, as if wanting softly to separate
208
the second part of the duodenum from the pancreas. Perform a couple of rotations on the frontal plane, clockwise and counterclockwise. While the second part of the duodenum is brought
Pancreaticoduodenal vessels
clockwise, move the pancreas reciprocally counterclockwise. While performing the clockwise or counterclockwise rotations, add induction of all the tiny movements that spontaneously arise. You will be able to feel a release and often a warming of the tissues under your hands. This maneuver has an effect on both the inferior and inferior posterior pancreaticoduodenal arteries, their anastomoses, and the short perpendicular branches arising from them and going to the vertical part of the duodenum (Fig. 27.5).
27
209
28
Pancreaticosplenic vessels
28.1 ANATOMY
28.1.1 The pancreas
We have seen that the arterial supply of the pancreas derives mainly from branches of the gastroduodenal artery (via the superior anterior and superior posterior pancreaticoduodenal arteries as intermediaries) and the splenic artery (Fig. 28.1). These two arteries anastomose with the inferior pancreaticoduodenal artery, which runs transversely from the superior mesenteric artery. Remember that the vascular arrangement between the abdominal organs allows the body to compensate for any irrigation decit.
xations, especially in the face of unusual, and sometimes disconcerting, symptoms. We have seen, for example, several cases of posttraumatic iron deciency where the spleen is the cause.
210
Pancreaticosplenic vessels
Reflected stomach
28
Left and right inferior phrenic arteries Celiac trunk Common hepatic artery Proper hepatic artery Dorsal pancreatic artery Superior posterior pancreaticoduodenal artery Left gastroepiploic artery Great pancreatic artery Inferior pancreatic artery Splenic artery Superior mesenteric artery
Superior anterior pancreaticoduodenal artery Inferior pancreaticoduodenal artery Duodenum Inferior anterior pancreaticoduodenal artery
Comments
Two things can be concluded about these arterial arrangements: 1 It is important to stretch these arteries transversely. 2 It is also necessary to carry out stretches perpendicular to the transverse arteries. Caution: Do not compress the pancreas! The pancreas is a fragile gland that cannot rebuild itself like the liver can. At all costs one must avoid compressing it anterior to posterior, against the vertebral column. This is the only organ where there is a real risk of creating a direct irritation or inammation. Also, take
special care with diabetic patients, who might have vascular fragility.
211
Short gastric arteries Abdominal aorta Posterior gastric artery Splenic artery Great pancreatic artery Inferior pancreatic artery Dorsal pancreatic artery
Cystic artery Inferior vena cava Celiac trunk Common hepatic artery Gastroduodenal artery Portal vein Superior posterior pancreaticoduodenal artery Superior anterior pancreaticoduodenal artery Inferior pancreaticoduodenal artery
212
Pancreaticosplenic vessels
28
Position
The patient is in decubitus, legs exed, hands placed on the thorax. Position yourself to the right of the patient.
lateral surfaces of the left ribcage, ribs eight, nine, and ten. Place your thumb under the left costal margin to keep the spleen from slipping away during the manipulation. Depending on the size of your hand or the body of the patient, this may not be possible. In such a case simply clasp the abdominal costal junction with your left hand. Gradually approximate your hands to shorten the pancreas along its main axis. Then release your palms, allowing the organ to regain its original length gradually in viscoelasticity. Depending on the morphology of the patient, it is possible to perform the same technique by placing a ngerpad on the splenic artery. The pulse variations allow you to monitor the effectiveness of the maneuver.
Technique
Place your right palm against the lateral border of the second part of the duodenum, level with the sphincter of Oddi. The duodenum will serve to protect the pancreas. With your left hand, encompass the posterior
213
Position
The patient is in decubitus, hands alongside the body with a pillow placed under the thoracolumbar region. Position yourself either behind the patient or to the side, to be able to stretch the superior border of the pancreas in a caudad direction.
214
Pancreaticosplenic vessels
28
Fig. 28.5 Manipulation of the pancreatic arteries in left lateral decubitus position.
Technique
For the left part, place your thumb against the most lateral portion of the transverse colon. For the right part, place your other thumb as cephalad as possible on the second part of the duodenum. Delicately direct your thumbs posteriorly to nd the upper part of the pancreas. Using your thumbs, gently stretch the upper border
of the pancreas caudally. Maintain the stretch for about 20s. This technique, of course, affects the transverse mesocolon, which is rmly attached to the pancreas. The difference in this version is that pressure is applied to the right side of the duodenum, whereas for the mesocolon technique the right hand contact is close to the hepatic exure of the colon.
215
28.2.7 Indications
The indications include: digestive problems allergies asthma psoriasis faintness postprandial fatigue immune system deciency hyperhidrosis.
216
29
29.1 ANATOMY
29.1.1 Generalities Irrigation
At rest, intestinal irrigation represents 27% of total body irrigation. This percentage is very important considering that the heart, for example, draws on only 34% of total blood ow.
Hormonal control
The more that is learned about the physiology of the small intestine, the more complex it appears to be. In addition to local autonomic nervous system control, hormones regulate the organ as it adapts to the workings of the digestive tract. For example, vasoactive intestinal peptide (VIP) releases the smooth muscles and increases circulation. Acetylcholine levels rise considerably in the circulating blood after eating.
217
Celiac ganglion and plexus Aorticorenal plexus Superior mesenteric ganglion Intermesenteric (aortic) plexus Middle colic plexus Superior mesenteric artery and plexus Mesenteric branches
218
29
Subserous plexus Myenteric plexus Longitudinal muscle layer Circular muscle layer
Muscular
Mucosal
Reflected liver Left gastric artery Proper hepatic artery Portal vein Gastroduodenal artery Right colic artery Splenic artery Abdominal aorta Left renal artery Superior mesenteric artery Jejunal arteries Ileal arteries Posterior cecal artery Anterior cecal artery
Ileocolic artery
219
Greater omentum Transverse colon Right colic artery Superior mesenteric artery Duodenum Descending colon Inferior vena cava Right common iliac artery Ileocolic artery Posterior cecal artery Anterior cecal artery Abdominal aorta Inferior mesenteric artery Left colic artery Sigmoid artery Aortic bifurcation Superior rectal artery Sigmoid colon
junction projects on the mid-clavicular umbilical line, about three ngerwidths above the umbilicus. Origin and course The superior mesenteric artery: originates from the abdominal aorta opposite L1 is about one vertebral body height lower than the celiac trunk runs beneath the caudal border of the pancreas, where it is easily located is situated higher and to the right of the inferior mesenteric artery is more supercial than the inferior mesenteric artery, and thus easier to palpate. Collaterals The superior mesenteric artery gives off these branches: middle colic right colic ileocolic jejunal and ileal.
Termination The superior mesenteric artery terminates by innumerable arterioles that irrigate the small intestine and colon. These arterioles often run perpendicular to the various parts of the small intestine and colon they perfuse. Comments The superior and inferior mesenteric arteries anastomose with the middle colic and left colic arteries (Fig. 29.3). The rst jejunal artery, branching from the superior mesenteric artery, anastomoses with the pancreaticoduodenal artery. This illustrates the vascular interdependence of these organs and shows that vascular manipulation of the pancreas engages the small intestine. Aorta mesenteric clamp In certain cases, the superior mesenteric artery can clamp the left renal vein against the aorta and produce lumbago and lumbar sciatic pain more commonly on the left (Fig. 29.4). The left kidney can also be affected by constriction of the superior mesenteric artery. In addition to local pain, lymphatic venous
220
29
Esophagus
Renal vein
problems can involve the urogenital system. When the compression is severe, surgery is indicated.
the left. It originates at the level of the third or fourth lumbar vertebra. Course As the inferior mesenteric artery descends from the aorta, it makes a large curve to the left. It then runs caudally and to the right, ending at the anterior surface of the sacrum, at the level of the third sacral segment. It is covered by the peritoneum and rests in succession on the:
221
Locate the duodenojejunal exure about three ngerwidths above the umbilicus on the left mid-clavicularumbilical line. Glide one at nger along the medial border of the duodenojejunal junction until you feel the pulse of the superior mesenteric artery. This artery is smaller than your little nger. If you go too deep you will be on the wall of the aorta. This pulse will serve as a reference (Fig. 29.5).
Manipulations
Bidigital technique Standing to the right of your patient, place your at thumb where you feel the pulsation of the superior mesenteric artery. This will serve as a xed point (Fig. 29.6). Place your other thumb at the ileocecal valve, located on the lateral third of the right umbilicalanterior superior iliac spine line. Direct your ileocecal thumb caudally and laterally, virtually drawing a convex line between your two thumbs. The idea is to create a curved line between your thumbs, rather than to stretch in a straight line. Maintain this convex stretch for about 20s to irrigate the small intestine, and then evaluate the difference in the pulsations of the superior mesenteric artery.
Distinctive techniques
Because of the anatomical arrangement of the mesenteric arteries, manipulation of the small intestine and the colon are considered separately: One technique concerns the more supercially located superior mesenteric
222
29
Fanning technique Again the left thumb serves as a xed point. The ngers of the right hand spread like a fan, following the contour of the superior mesenteric artery (Fig. 29.7).
Manipulation in decubitus
The patient rests on their back, the arms alongside the body, with a soft cushion placed under the thoracolumbar region (Fig. 29.8). Place yourself to the right of the patient. Your ngers stretch the colon to the right, moving in sequence from the cecum towards the hepatic exure of the colon. Perform a spreadinginduction maneuver to open the medial and lateral sides of the colon. Do this several times, maintaining each stretch for about 20s. You can also employ the fanning technique here.
223
digestion. It is highly placed when full, but found much lower in the abdomen when empty. Remember that the greater omentum hangs inferior from the greater curvature of the stomach, as part of the gastrocolic ligament that connects the transverse colon to the stomach. The variable position of the transverse colon leads us to focus our vascular manipulations near the hepatic and splenic exures. Here, we can be certain not to make a mistake.
29
Fig. 29.9 Manipulation of the right colic and ileocolic arteries in left lateral decubitus.
CannonBhm zone
This is a zone that particularly interests us, as it is the location of the anastomoses 225
Liver
CannonBhm zone Superior mesenteric artery Vagus nerve Inferior mesenteric artery Sacral parasympathetic nerve
226
between the superior and inferior mesenteric arteries. It is found midway between the mid-transverse colon and the left colic exure (Fig. 29.11). In the CannonBhm zone, the transverse colon is innervated by the vagus nerve, whereas beyond this interchange it is innervated by nerve bers arising from the sacral parasympathetic nerves (S2, S3). In this region the left colic artery branch of the inferior mesenteric artery irrigates the left part of the transverse colon, and other
branches contribute to the descending colon and the rectosigmoid. To review: The right half of the colon is innervated by the vagus nerve and irrigated by the superior mesenteric artery. The left half of the colon is innervated by the sacral parasympathetic nerves and fed by the inferior mesenteric artery. This transition zone is a key area for neural and vascular manipulation of the intestines.
29
Manipulation in decubitus
The patients arms lie alongside the body, a soft cushion under to the thoracolumbar junction. Stand to the right of the patient (Fig. 29.12). Place the sides of your thumbs along the mesenteric artery. In step one, your ngers bring all the loops of the small intestine from left to right, with the goal of sinking gradually deeper with your thumbs, without causing pain.
227
Fig. 29.13 Manipulation of the jejunal and ileal arteries in lateral decubitus.
Manipulation in decubitus
The subject is in decubitus, arms alongside the body, with a soft cushion under the lumbar region. Position yourself to the right of the patient (Fig. 29.15). The left thumb is placed on the origin of the inferior mesenteric artery with the ngers of the other hand above the symphysis pubis, very slightly to the left of the median line. The caudal ngers are located on the rectosigmoid
228
29
junction. Anchor the inferior mesenteric artery with your thumb and push the recto sigmoid junction in a posterior direction. Either maintain this distal pushinduction maneuver for 20s, or separate your ngers like a fan and maintain the stretch for 20s.
descending colon and sigmoid colon, and bring the tubes towards you, in liftinduction to increase the vascularization of the left colon. When you reach the rectosigmoid junction, stretch the sigmoid in an almost purely caudal direction.
229
When the liver is overworked, hemorrhoids are a frequent complaint. Apart from local discomfort, hemorrhoids have an undeniable effect on the urogenital region. In women, pelvic venous congestion can be a factor in uterine malposition and associated functional disturbances. The urogenital system is supported not only by ligaments and fascias, but also by a rich venous plexus (of Santorini). Lymphatic and venous rectal congestion contributes to absent or reduced mobility of the urogenital system. In men, the prostate suffers the most from venous disturbances and, more rarely, so does the erectile system.
then push the tube of the sigmoid colon in the direction of the iliac crest.
Advice
In the case of venous problems, ask the patient to avoid pepper, mustard, peppers, cooked fats, strong sauces, and aspirin, antiinammatory, antianxiety, and antidepressant medications.
29.2.8 Indications
The indications are as follows: postabdominal pelvic surgery irritable bowel syndrome constipation chronic muscular contracture Crohns disease bromyalgia, spasmophilia pancreatic dysfunction muscular cramps postpartum constipation bladder ptosis pelvic lymphatic venous congestion.
230
SECTION 4
UROGENITAL VESSELS
Renal vessels
30
Method
Your cephalad hand contacts the paravertebral mass opposite the renal area, in the neighborhood of the 12th rib, and maintains a posteroanterior pressure throughout the duration of the search (Fig. 30.2). Place three or four ngers of your caudal hand juxtaposed to the lateral border of the rectus abdominis muscle, slightly above the umbilicus. Slowly progress towards the anterior surface of the lumbar wall, rst in a purely sagittal direction and then slightly oblique and medial, until you meet the anterior lateral surface of the psoas muscle. Glide your ngers longitudinally along the psoas, looking for an arterial pulse, perpendicular to the main axis of the psoas. As a rule you will capture this pulsation under one ngerpad only. Stay sufciently lateral to the abdominal aorta. You will feel a distinct pulse, almost perpendicular to the aortic axis. Oriented posterior and lateral to the psoas, the artery is of a signicant caliber. It is obviously larger than the pancreaticoduodenal branches of the celiac trunk and the middle colic artery accompanying the transverse colon. Palpation of the renal artery clearly illustrates the phenomenon referred to as principle of the concealing pulse. In this particular region, the hand is easily dazzled by the pulsations of the larger vessels. Typically the biggest
30.1 ANATOMY
30.1.1 Renal arteries
The direction of the renal arteries is essentially perpendicular to the aorta (Fig. 30.1). Due to their retroperitoneal location, these arteries are the most problematic to mobilize. The right renal artery arises from the abdominal aorta at the level of L1. The left shorter renal artery originates slightly higher up. The vessels branch laterally from the aorta, just below the origin of the superior mesenteric artery.
231
Right inferior phrenic vein Hepatic veins Inferior vena cava Esophagus Diaphragm Left gastric artery Celiac trunk Right kidney Superior mesenteric artery Abdominal aorta Ovarian artery and vein Ureter Common iliac artery External iliac artery and vein Inferior phrenic artery Left renal artery Left renal vein Left kidney Duodenum Inferior mesenteric artery Median sacral artery Internal iliac artery and vein
232
Renal vessels
pulse can be felt clearly, even when it lies deep to the more slender ones.
30
Rightleft differences
Relatively speaking, the right renal artery pulse seems a little easier to perceive than the left. On the right, the renal artery is located behind the second part of the tube of the duodenum, whereas on the left it lies above and slightly lateral to the duodenojejunal junction, making it particularly difcult to feel in heavier set subjects. In cases of severe kidney ptosis, especially right ptosis, you can sometimes pick up the artery near the umbilicus. In this case it is certainly easier to feel.
Palpation limit
Palpating the renal artery has taken us a good deal of time, perseverance, and patience in return for rather inconsistent results. Even today, with as many patients as we have seen, it is not always possible to be absolutely sure of our palpation. Nevertheless, in certain circumstances the pulse is relatively easy to feel and has enabled us to standardize our approach. These are: thinness hypotonic abdominal muscles (postpartum, old age) diastases recti abdominis. By contrast, plumpness, abdominal fat, obesity, and hypertonic abdominal musculature are all unfavorable to this approach.
Place your ngers three ngerwidths below the right costal margin (Fig. 30.3). Direct them initially posteriorly and then cephalad. Next, draw the liver laterally, while maintaining a cephalad traction. With this technique, you have an effect on the hepatic and duodenal arteries, as well as innumerable small nerve bers that make up the celiac and renal plexuses. Left renal artery Place your ngers below the duodenojejunal junction. Direct them rst deeply posterior and then exert a cephalad traction. At the end of the cephalad traction, stretch the entire gastric, omental, enteric, and pancreatic ensemble laterally. As with the right kidney, this is not a specic technique. Maintain traction of this viscerovascular group for about 20s. It is difcult to prove the effect on the renal arteries, which are not directly palpable.
233
However, before carrying out these maneuvers, take the arterial pressure of the patient in both arms. It is frequently possible to remedy a difference in blood pressure, and to lower elevated tension.
Manipulation in decubitus
The patient lies on their back. Position yourself to the side of the renal artery in question (Fig. 30.4). Place the index and middle nger of both hands on either side of the location where you have palpated the renal pulse. Place your
thumbs on the posterior lateral part of the ribs and on the lumbar wall. Manipulation of the renal artery is done with two hands. Draw your ngers towards your thumbs in an obliquely posterolateral direction. Gently take the renal hilum laterally and posteriorly, distancing it gradually and progressively from the aorta in a stretchingListening of the renal artery. Repeat a few times to be sure that you have indeed mobilized the kidney. Once the elasticity of the renal artery seems satisfactory, maintain the stretch for 2030s in order to irrigate the organ.
234
Iliac vessels
31
31.1.3 Internal iliac artery Course
Formerly called the hypogastric artery, the internal iliac artery (Fig. 31.2) separates from the common iliac artery at the sacroiliac junction and descends posteriorly towards the greater sciatic foramen.
31.1 ANATOMY
The aorta divides into the median sacral artery and the two common iliac arteries, to the left side of L4 and L5 intervertebral disc.
Pelvic collaterals
At the greater sciatic foramen the internal iliac artery gives off about ten branches. We have selected the most important among them. They can be divided into two groups: parietal branches for the walls of the lesser pelvis visceral branches for the pelvic organs. Parietal branches Parietal branches are divided in accordance with their function. The iliolumbar artery often sends a small spinal branch to penetrate the intervertebral foramen, between the fth lumbar and rst sacral vertebrae. The lateral sacral artery supplies branches to the cauda equina and smaller vessels that penetrate the vertebral canal. The obturator artery passes out of the pelvis through the obturator canal. Of special note is the acetabular branch, which enters the hip joint at the acetabular notch and sends a branch
Noteworthy relationships
The ureter crosses the common iliac arteries like an X. These small tubes are covered with peritoneum and run along the medial border of the psoas. The common iliac arteries diverge at an angle of 65 in men, and 75 in women, whose pelvis is wider.
Terminals
The common iliac arteries divide into the internal and external iliac arteries.
235
Renal vein
Aorta
Renal artery
Ureter
Common iliac artery External iliac artery External iliac vein Bladder
along the ligament of the femoral head. The inferior gluteal artery runs in the buttock between the piriformis and adjacent muscles. Together with the comitans artery of the sciatic nerve, the inferior gluteal branch supplies the vascularization of the sciatic nerve. NB: Osteopaths are now well aware that the fascial mechanics of the lesser pelvis affect coxofemoral articulations. They cannot obscure the pelvic vascular connections, particularly the pelvic arteries that nourish the femoral head.
Visceral branches Uterine artery Internal pudendal artery Inferior vesical artery Middle rectal artery Vaginal artery
236
Iliac vessels
31
Aorta
Common iliac artery Iliolumbar artery Superior gluteal artery Middle rectal artery External iliac vein Bladder Superior vesical arteries Median sacral artery Internal iliac artery
Uterine artery
when you no longer feel its pulse, direct your ngers laterally at a 6575 angle. The new pulse you feel will be the beat of the common iliac arteries. Second way to locate the artery Place your thumbs midway along the puboumbilical line (Fig. 31.4). Direct your thumbs cephalad. You will feel the aortic pulse and, from there, orient your thumbs laterally to feel the common iliac arteries.
resting on the chest. Stand near to the patients pelvis (Fig. 31.5).
Manipulation
Position The patient is in decubitus, with a soft pillow placed beneath the lumbar spine, hands
Technique Identify the pulse of the abdominal aorta by palpating it above the umbilicus. Move your ngers caudally until the pulse disappears, and you will nd yourself at the level where the aorta bifurcates into the common iliac arteries. Place one thumb beneath the umbilicus at the bifurcation, and the other thumb on the iliac vessel. Draw your distal thumb in a caudal and lateral direction to stretch the artery following induction. Recall that we
237
Fig. 31.3 Palpation of the common iliac arteries (rst way to locate artery).
238
Fig. 31.4 Palpation of the common iliac arteries (second way to locate artery).
Iliac vessels
31
Manipulation
Manipulation in decubitus The patient has a pillow supporting the lumbar spine, with both hands resting on the thorax. Position yourself next to the patients pelvis (Fig. 31.6). Starting at the common iliac artery, glide your ngers along the internal iliac artery, searching for brous or adhered tissues.
This is really a perivascular technique to release the soft tissue around the artery and veins. Manipulation in lateral decubitus This position allows easier digital penetration. Perform the same technique as above, rst on one side then on the other. Begin midway along the umbilicalanterior superior iliac spine (ASIS) line.
239
32
Course
Uterine vessels
32.1 ANATOMY
32.1.1 Uterine artery
The uterine artery (Fig. 32.1) arises from the internal iliac artery and travels caudally and anteriorly to reach the uterus a little above the uterine cervical junction. It ascends the border of the uterus, where its branches anastomose with the ovarian artery. The twists and turns of the uterine vessels allow them to adapt to manifold uterine movements. Keep in mind the following: Just beyond its origin, the artery crosses the ureter anteriorly. Along its caudal journey, the uterine artery rests on the aponeurosis of the obturator internus. Just before reaching the isthmus, it is in line with the base of the broad ligament.
Technique
Glide the ngers of both hands along the iliac fascia in the direction of the pubic symphysis. Try to sink as deeply and posteriorly as possible before gliding in the direction of the symphysis. Once you feel the body of the uterus, rst stretch it cephalad and then medially. The uterine arteries run along a cephalocaudal longitudinal main axis, but also divide into innumerable arterioles that run perpendicular to its main axis. To stretch the small ramications, glide the uterus bilaterally. Repeat on the other side.
Collaterals
Among the numerous arterioles arising from the uterine artery, we cite branches for the: ureter vagina ovary uterine tube.
Terminal branches
Near the cephalad part of the uterus, the uterine artery anastomoses with the ovarian artery, which descends from the abdominal aorta.
240
Uterine vessels
32
Ovarian artery and vein Ureter Common iliac artery Common iliac vein
Uterine artery
Uterine tube
Uterus (retracted)
241
Technique
Following the same principle as in decubitus, endeavor to go posterior rst, then medially and nally caudad. Surround the vesicouterine unit with both hands and draw it cephalad several times. Maintain the traction for about 20s and follow the Listening with induction. Some patients feel an immediate benet from this manipulation. It is as if a weight has been lifted from my belly, they tell us.
systems. The vesicouterine adnexa is surrounded by a rich venous plexus. For example, the venous plexus of Santorini plays an important role in bladder continence. Many women have pelvic varicosities involving pelvic and lower extremity problems. To have an effect on the venous system, stretch the vesicouterine unit superiorly and posteriorly several times. This movement is benecial for arterial, venous, and lymphatic circulation. We advise our patients to place two feet on the wall with a large pillow supporting their buttocks, and to bring the soft tissues of the pelvis cephalad, beginning at the pubic symphysis. The technique is effective when performed for 23min once a day. This maneuver is very effective for the small intestines, which play a considerable role in visceral pelvic mechanics.
Uterine vessels
32
32.3.1 Dysmenorrhea
In women with sudden onset dysmenorrhea, consider: genital infection endometriosis cervicouterine malposition benign or malignant tumor.
The following are strong contraindications: undiagnosed pelvic mass sharp pains on pelvic palpation sudden amenorrhea inguinal lymph ganglia coupled with edema of the lower extremities.
In young women, premenstrual pains are often due to spasm of uterine muscle bers, owing to hormonal hyperstimulation. However, consider falls on the sacrum or coccyx as causative factors.
32.4 INDICATIONS
The indications for uterine vessel manipulation are: premenstrual syndrome dysmenorrhea pelvic varicosities venous deciency of the lower extremities infertility lumbago sciatica (often worse on the left) femoral neuralgia (cruralgia).
32.3.3 Hemorrhages
Until they are fully understood, diagnosed, or explained, hemorrhages are formally contraindicated for manipulations. Apart from occurring as pregnancy complications, other possible causes of hemorrhage are: broma endometriosis uterine polyps cervical cancer hormonal insufciency.
243
244
Ovarian vessels
33
33.1 ANATOMY
The ovaries are irrigated by: the ovarian arteries arising from the abdominal aorta the ovarian branch of the uterine artery (Fig. 33.1). The left ovarian vein drains directly into the left renal vein, whereas the right ovarian vein drains into the inferior vena cava. When treating the ovary it is imperative to include manipulation of the left kidney, along with viscerovascular manipulation. Originating just below the renal arteries, the ovarian arteries descend along the psoas in an oblique lateral and caudal direction. They rst cross the ureter just above the aortic bifurcation, and again in front of the sacral promontory.
anterior superior iliac crests. Softly direct the thumb deeply; you will clearly feel the rmness of the ureter. Bring the thumb caudally and medially, carrying out several transverse glideinduction maneuvers. To include the venous and lymphatic systems, stretch the thumb cephalad and slightly laterally. NB: This technique is meant to have both a vascular and a ureteral effect. However, it is here where kidney stones are found. Any precise, sharp pain demands that you lighten your pressure, discontinuing the manipulation if pain persists. This technique also serves the inferior mesenteric artery.
33.2.1 Technique
Place one thumb on the abdominal aorta, slightly above the umbilicus, to serve as a counterbalance. Position the other thumb where the ureter crosses the common iliac artery at the level of the sacral promontory. This is on an imaginary line joining the
Uterine tube
246
suprarenal, spermatic, and left ovarian. This basic anatomical data has implications for all urogenital manipulations. The left kidney goes hand in hand with the genital system, whereas the right spermatic and ovarian
veins drain directly into the inferior vena cava. It is difcult to conceive of any effective genital manipulation without including the left kidney, and vice versa.
34
34.1 ANATOMY
At its origin in the pelvis, the internal pudendal artery (Fig. 34.1) crosses anterior to the piriformis and the sacral plexus. It leaves the pelvis by the inferior rim of the greater sciatic foramen below the piriformis. It then curves around the lateral surface of the ischial spine to enter the perineum by the lesser sciatic foramen. The pudendal artery accompanies the obturator internus muscle contained between it and its aponeurosis, to x on the medial surface of the ischium. Finally it runs forward towards the genital organ. The artery can serve to locate the pudendal nerve, when this nerve is slender and difcult to palpate.
34.1.2 Collaterals
Many arterioles joining the rectum, prostate and bladder arise from the internal pudendal artery. Also given off are the: inferior rectal artery the supercial and deep perineal arteries.
247
Internal iliac artery Piriformis muscle Inguinal ligament Internal obturator muscle
Sacrotuberous ligament
Effects of manipulation
In women. The pudendal artery gives off numerous branches to the clitoris, labia majora, rectum, and the perineum in general. Thus the entire genital sphere benets from its treatment. In men. The perineum, scrotum, rectum, bulbospongiosus muscle, prostate, spongiosum, and the corpora cavernosa of the penis can benet from the improved circulation provided by this technique. In any case, when there are urogenital problems, it is seldom possible to isolate any one area. The whole of the urogenital system, as well as the kidneys, must be considered. This includes osteoarticular xations of the lumbar spine, sacrum, and coccyx.
Position
The patient is in decubitus, hands on thorax, the leg of the treatment side exed and somewhat spread. Facing the patient, position yourself on the side of the artery in question (Figs 34.3 & 34.4).
Technique
Place your ngers against the medial aspect of the ischial tuberosity.
248
34
Common iliac artery Common iliac vein Internal iliac artery Iliolumbar artery Lateral sacral artery External iliac artery External iliac vein Obturator artery Superior gluteal artery Piriformis muscle Inferior gluteal artery Obturator muscle Symphysis pubis Iliococcygeus muscle Sacrotuberous ligament
Vestibule of vagina Ischiocavernosus muscle Superficial perineal fascia Perineal artery Perineal nerve Obturator fascia Pudendal canal (Alcocks) Inferior rectal artery Inferior fascia of pelvic diaphragm Central perineal tendon Superficial transverse perineal muscle Internal pudendal artery and vein Pudendal nerve Inferior rectal nerve Levator ani muscle External anal sphincter muscle Anococcygeal ligament
Anus
249
Fig. 34.3 Landmarks for manipulation of the internal pudendal artery.
250
35
35.1 ANATOMY
We have studied the inguinal canal (Fig. 35.1) for the manipulation of the peripheral nerves (Barral & Croibier 2004). Contained within the canal are the iliohypogastric, ilioinguinal, and genitofemoral nerves. Supercial to the canal is the external pudendal artery, arising medially from the femoral artery to enter the saphenous hiatus. In the inguinal fold, above the supercial inguinal canal, the anterior cutaneous branch of the iliohypogastric nerve appears. Caudally and laterally one nds the ilioinguinal nerve, which joins either the round ligament of the uterus or the spermatic cord, accompanied by a small artery. NB: Although it is fairly easy to penetrate a nger in the male inguinal canal, this is next to impossible in the case of a woman. These techniques apply to men, for the most part. In any case, it seems the effect is greater on the intrainguinal nervous system than on the vascular system.
exed. Place yourself to one side, facing the patient (Fig. 35.2).
35.2.2 Technique
Place one thumb just to the side of the pubic spine and direct it laterally and cephalad to push into the inguinal canal. At the same time, the free hand brings the skin and external oblique, internal oblique, and transversus abdominis muscles to bear against the thumb in the canal. With experience, and thanks to their pulsations, it is possible to distinguish the testicular artery, arising directly from the aorta, and the artery of the round ligament from the nerves that accompany them. The maneuver consists of glideinduction and small cephalocaudad stretches, carried out with the thumb.
251
Inguinal ligament
Superficial epigastric artery Superficial circumflex iliac artery Superficial external pudendal artery
Iliohypogastric nerve Deep inguinal ring Superficial inguinal ring Spermatic cord Femoral artery
252
Bibliography
Aboa-Eboul C, Brisson C, Maunsell E, et al. Job strain and risk of acute recurrent coronary heart disease events. JAMA 2007; 98(14): 16521660. Ader JL. Physiologie. Paris: Elsevier Masson; 2006. Anderson RM. The gross physiology of the cardiovascular system. Tucson: Racquet Press; 1993. Barral JP, Croibier A. Manipulations des nerfs priphriques. Paris: Elsevier; 2004. Barral JP, Croibier A. Manipulations des nerfs crniens. Paris: Elsevier; 2006. Bates B. Guide de lexamen clinique (3rd edn). Paris: Arnette; 1993. Berlin JA, Colditz GA. A meta-analysis of physical activity in the prevention of coronary heart disease. Am J Epidemiol 1990; 132(4): 612628. Bestel J, Clairambault J, Medigue C, et al. Le systme cardiovasculaire et sa rgulation par le systme nerveux autonome: modlisation et mesures. ESAIM Proceedings 2000; 9: 6592. Black PH, Garbutt LD. Stress, inammation and cardiovascular disease. J Psychosom Res 2000; 52(1): 123. Boccalon H, Lehert P. Diagnostic prcoce de lartriopathie des membres infrieurs laide de mesures adaptes la pratique gnraliste: lindex systolique et la perception des pouls. Journal des Maladies Vasculaires 1995; 20(1): 2837. Bouchet Y, Cuilleret J. Anatomie topographique, fonctionnelle et descriptive. Lyons: Simep; 1983. Buser P, Imbert M. Commandes et regulations neurovgtatives. Neurobiologie V. Paris: Hermann; 1994. Chevrel JP, Fontaine C. Anatomie clinique. 3: Tte et cou. Paris: Springer; 1994. Coumel P, Maison Blanche P, Catuli D. Heart rate and heart variability in normal young adults. J Cardiovasc Electrophysiol 1994; 5(11): 899911. Coumel P. Cardiac arrhythmias and the autonomic nervous system. J Cardiovasc Electrophysiol 1993; 4(3): 338355.
Croibier A. Diagnostic ostopathique gnral. Paris: Elsevier; 2005. Cruveilhier J. Trait danatomie humaine. Paris: Octave Doin; 1852. DAlch EP. Comprendre la physiologie cardiovasculaire (3rd edn). Paris: Flammarion Mdecine-Sciences; 2008. Dauzat M, et al. Manuel de physiologie intgre. Montpellier: Sauramps Mdical; 2002. Farisse J, Argme M, Di Marino V, Brunet C. La glande thyroide les glandes parathyroides le thymus. In: Chevrel JP (ed.), Anatomie clinique, volume 3: Tte et cou. Paris: Springer; 1996: 371397. Haute Autorit de Sant (HAS). Prise en charge des patients adultes atteints dhypertension artrielle essentielle. Actualisation. Argumentaire. 2005. Online. Available: http://www.has-sante.fr/ portail/upload/docs/application/pdf/HTA_2005_ rap.pdf 28 Nov 2010 Hittinger L. Hormones, coeur et vaisseaux. Paris: INSERM; 1997. Kamina P. Anatomie. Introduction la clinique. Fascicule 10: Tte et cou. Nerfs crniens et organes des sens. Vol. 2. Paris: Maloine; 1996. Laborit H. Physiologie humaine, cellulaire et organique. Paris: Masson; 1961. Marieb EN. Anatomie et physiologie humaines. Paris: Pearson Education France; 2005. Roche. ObEpi 2003: 3e enqute pidmiologique nationale sur lobsit et le surpoids en France. 2003. Online. Available: http://www.sante.gouv. fr/htm/pointsur/nutrition/poli_nutri122.pdf 28 Nov 2010 Oppert JM. Rle de la sdentarit et des apports alimentaires dans le gain de poids chez ladulte. Cah Nutr Diet 2000: 35(5); 317326. Paturet G. Trait danatomie humaine. Paris: Masson; 1951. Peto R, Lopez AD, Boreham J, et al. Mortality from smoking in developed countries 19502000
258
Bibliography
(2nd edn). Oxford: CTSU, University of Oxford; 2006. Seippel L, Bckstrm T. Luteal-phase estradiol. J Clin Endocinol Metab 1998; 83: 1988 1992. Shapiro PA, Sloan RP, Bagiella E, et al. Cerebral activation, hostility, and cardiovascular control during mental stress. Journal of Psychosomatic Research 2000: 48(45): 485491. Silbernagl A, Despopoulos D. Atlas de poche de physiologie. Paris: Flammarion; 1985. Thomas Y. Hmodynamique. PCEM1. Biophysique du systme cardiovasculaire. Paris: Vuibert Suprieur; 1999. Testut L. Trait danatomie humaine. Paris: Doin; 1896. Testut L, Jacob O. Anatomie topographique. Paris: Doin; 1935. Testut L, Latarjet A. Trait danatomie humaine (9th edn). Paris: Doin; 1948. Tortora GJ, Grabowski SR. Principes danatomie et de physiologie (2nd edn). Brussels: De Boeck University; 1994. Tranchesi B, Barbosa V, Piva de Albuquerque C, et al. Diagonal earlobe crease as a marker of the presence and extend of coronary atherosclerosis. Am J Cardiol 1992; 70: 14171420. Waugh A, Grant A. Ross et Wilson: Anatomie et physiologie normales et pathologiques (trans, 9th English edn). Paris: Maloine; 2003.
259
Conclusion
We are rst and foremost therapists, who work everyday in the eld. There may be tens of thousands of techniques to apply to an organism, and new ones all the time. Even if one mastered them all, it is more important to have soul in order fully to grasp osteopathic or manual therapy concepts and philosophies. The hand gives information to the head, and then the head returns information to the hand. In this way, we pass from the technique to the art, and this makes a world of difference.
For any osteopath or manual therapist to be a specialist is nonsense. In all the Listening techniques, it is the body that expresses its tensions, and you can be sure it does not specialize! All tissues deserve our attention. It is for us to understand them, and help them. Osteopathy and manual therapy are disciplines of generalists, whose foundation is anatomy. Their motto could be: the hands at the service of anatomy. Let us try to keep this spirit.
253
Glossary
AdsonWright test evaluation of the radial pulse while moving the arm in abduction and external rotation (arm and forearm in the chandelier position). The test is deemed positive if the radial pulse diminishes or obliterates. This can be due to an osseous callus on the clavicle or rib, a redundant rib, bony outgrowth, an anterior scalene muscle insertion problem, brosis of the pleurocervical ligaments, or a pulmonary apex tumor. Adventitia the outermost layer of a blood vessel wall, made up of connective tissue and smooth muscle bers. Alcocks canal a canal containing the pudendal vessels (once called the internal shame vessels). This passage is formed from the obturator internus aponeurosis, located along the inferior pubic ramus, where it is palpable externally. Aneurysm a localized dilation of the blood vessel wall. Aneurysms may ssure or rupture. A dissecting aneurysm occurs as a result of degeneration of the artery wall, creating a tear in the intima. Angina the word derives from the Greek strangling. A condition marked by severe constrictive pain in the chest and often spreading to the left arm and jaw. The patient experiences anxiety and has the impression they might die. Angina is provoked by physical activity, running or exertion.
Angiogenesis the development of new blood vessels. Angiotensin this peptide maintains volume and arterial tension and thus can cause intense vasoconstriction of the peripheral arterioles (especially splanchnic) and arterial hypertension. Anisotension a difference in systolic tension (blood pressure) between the two arms, due to osseous or muscular compression in the thoracic inlet, or a cervical, brachial, or visceral restriction. Arterial tension also called arterial pressure, this is the elastic force exerted by the arterial walls on their blood contents. It represents the resistance of the vessel walls to blood pressure. Atheroma fatty deposits that form on the internal artery wall and can create calcication or ulceration. Atherosclerosis arterial scarring due to the deposit of fatty material on the intima that progressed towards the media. It promotes the proliferation, thickening, and calcication of elastic bers. This condition is often found on large and medium-sized arteries, such as the aorta, femoral artery, coronary artery, etc. Bradycardia abnormally slow heart rate. Bradykinin a polypeptide formed in the plasma that causes contraction of smooth
254
Glossary
muscle bers, an increase in capillary permeability, and a lowering of arterial pressure. Carotid glomus small nerve ganglion located at the carotid bifurcation containing chemoreceptors that monitor oxygen and carbon dioxide blood levels. Carotid sinus small dilations in the carotid arteries, just above the common carotid bifurcation. They contain baroreceptors whose principal sensory innervation comes from the glossopharyngeal and vagus nerves. Catecholamine any of a class of sympathomimetic vasoconstrictive amines such as epinephrine (adrenaline), norepinephrine (noradrenaline), and their precursor dopamine, and some metabolic derivatives. These compounds are produced by the adrenal medulla and other chromafn cells found in the coccygeal and carotid ganglia, the sympathetic nerves, and organs containing catecholamines. Circle of Willis a circular anastomosis at the base of the brain comprised of the internal carotid, the anterior and posterior cerebral, and the posterior and anterior communicating arteries. Coccygeal glomus a cluster of nerve cells with an epinephrine (adrenaline)-secreting endocrine function. They lie against the anterior surface of the coccyx, near its caudal extremity on the ansa which unites the two intermediate cords of the pelvic sympathetic chain. It is also known as the ganglion impar, and played an important role earlier in human evolution. Coronary thrombosis the formation of a thrombus in a coronary artery that can cause ischemia and myocardial infarction. Dopamine a neurotransmitter synthesized in various neurons. It is a vasodilator for the kidneys, the intestine, and the coronary arteries, and increases the force of contraction of the heart, without altering its rhythm. Embolus an obstacle on the inner vessel wall (blood clot, fatty deposit, air bubble, bacterial growths, etc.) that can lead to an embolism. Endothelium a very thin membrane that lines the intima of blood vessels and the heart. It secretes various vasoactive substances such as angiogenesis stimulants. Epinephrine (adrenaline) a hormone released by the adrenal medulla that stimulates the sympathetic system, accelerates the heart, raises arterial pressure, and contracts the arteries (except the coronary and muscular arteries). It is responsible for mydriasis, dilates the bronchioles, lowers digestive motor control, and increases blood glucose levels. General circulation so-called systemic circulation serving all the organs except the lungs. Hepatic steatosis excessive liver triglycerides; this is foie gras. Histamine a substance found in almost every tissue. It is involved in the immune response and regulation of physiological function. It stimulates gastric secretion, contraction of smooth arterial bers, and capillary dilation, and makes the vascular wall more permeable. This neurotransmitter is elicited in response to allergic and inammatory reactions such as asthma and anaphylactic shock, for example. Inosculation the direct anastomosis of two vessels of the same caliber or the surgical joining together of two vessels of the same diameter. Intima the innermost coating of an artery or vein that allows frictionless gliding and facilitates gaseous, liquid, and oxygen exchange. Kallikrein a polypeptide enzyme present in plasma, salivary glands, sweat glands, urine, and the pancreas. It produces bradykinin. Law of HagenPoiseuille the resistance in a tube depends on the length of the tube
255
Glossary
and the viscosity of the liquid running through it. Manual induction a treatment that consists of treating the tissues in the direction of the Listening, by augmenting its force and amplitude. Manual tissue Listening manual evaluation whereby the hand is allowed to be drawn passively towards the xation. Listening is an evaluation, not a treatment. Maximum arterial tension (or systole) this measure indicates the pressure in the arteries during systole (normal range is 120140mmHg). Media the intermediate arterial layer, composed of smooth muscle cells and elastic bers. Minimum arterial tension (or diastole) arterial pressure between cardiac contractions. It depends on blood ow velocity, and thus on total peripheral resistance. Miosis excessive constriction of the pupil. Muscle of Trietz (suspensory muscle of the duodenum) a muscle consisting of smooth muscle bers running from the duodenojejunal junction to the crus of the diaphragm and its aortic aperture. It neutralizes the pull of the duodenojejunal junction on the adjacent vessels and nerves, notably the superior mesenteric artery. We believe that this muscle also orients the duodenojejunal junction so as to facilitate transit. Mydriasis abnormal dilation of the pupil. Myocardial infarction necrosis of a part of the heart muscle, following coronary thrombosis or embolism. Nervi vasorum autonomic nerve bers that innervate the arteries. Orthostatic hypotension a transient drop in arterial pressure when a person stands suddenly. A head rush or dizzy spell. Vagotonia is a possible cause. Pulse the propagation of a shockwave along the arteries, generated by the impact of the ascending aorta on blood ejected from the left ventricle. It is a vibratory, not a uid, event. The pulsatile wave is more rapid than the speed of blood. Reclining hypotension a transient drop in arterial pressure when moving from a vertical position to lying down. Among the numerous causes, cerebellar hypocirculation due to a vertebrobasilar artery problem can be the underlying etiology. It is interesting to note that this cerebellar hypocirculation does not occur in the prone position. Renin an enzyme produced by the kidney that, after diverse transformations, produces vasoconstriction and, as a consequence, hypertension. Serotonin (5-hydroxytryptamine, 5-HT) a substance synthesized in the cerebral tissue and in the digestive tube. Transported by blood platelets, it is vasoconstrictive and stimulates intestinal peristalsis. It also acts during immediate hypersensitivity reactions. Neurovascular chemoreceptors are located in the jugular fossa (a depression in the petrous temporal bone, behind the carotid canal, in which the beginning of the jugular vein is found). Small circulation the pulmonary circulation. Splanchnic concerning the viscera. Subclavian steal syndrome this condition arises in patients whose subclavian artery or brachiocephalic trunk is compromised by a stenosis or thrombus, often of atheromatous origin. The origin can be a mechanical obstruction such as osseous callus, clavicular malobliquity, or osteochondroma. Blood is stolen by the ipsilateral subclavian artery from the contralateral vertebral artery, to feed the upper extremity. This ow reversal deprives the cerebellum of circulation, and can result in a sudden fall during arm exercise, especially with the head thrown back.
256
Glossary
Systolic pressure index the relationship between systolic arterial pressure in the superior and inferior limbs. Humeral pressure compared with dorsal pedis or posterior tibial artery pressure. The index must be 0.90. A reduction indicates arteriopathy of the inferior limb, arterial obliteration, or a lumbosacral problem (narrowing of the lumbar canal, for example). Tachycardia accelerated heart rate. Thrill a ne vibration felt by an examiners hand on an artery due to arterial restriction or narrowing, or even an intra- or periarterial obstruction. Thrombus a blood clot that forms in a vessel or in the heart. It is made up of plaque and agglutinated leukocytes. Tract an assembly of ducts and viscera belonging to the same anatomophysiological system. Triglycerides a variety of lipids found in adipose tissues and blood serum. They are synthesized in the small intestine from digested dietary fat, and in the liver where they are converted to glucose for brain fuel. Vasa nervorum small arteries that supply blood to peripheral nerves. Windkessel effect elasticity of arteries that allows them to distend under the effect of blood pressure exerted against the vessel wall. This blood pressure is stored by the arteries during systole and returned during diastole, guaranteeing continuity of blood ow.
257
Index
Page numbers followed by f indicate gures, t indicate tables, and b indicate boxes. Abdominal aorta, 188189, 189f, 193f Abdominal fat, 63 Abdominal landmarks, 187193 aorta, branches, 192f pulses, 188193 visceral, 187188, 188f Abdominothoracic pressure, 4345, 44f Accordion technique, 88 Acetylcholine, 16, 34 Acidic ions, 47 Active hyperthermia, 5 Addisons disease, 76 Adenosine diphosphate (ADP), 47 Adenosine monophosphate (AMP), 47 Adrenal medullary hormones, 53, 55f Adrenaline (epinephrine), 16, 19, 34, 5253 Adrenomedullin, 19 AdsonWright test, 7980 Age arterial pressure, 28 cardiovascular risk, 61, 7273 Alcocks canal, 247, 249f Alcohol, cardiovascular risk, 64 Alternating pulse, 78 Amenorrhea, secondary, 243 Anastomoses, 1920, 20f breast, 127f cerebral, 5758 facial artery, 143 interpancreatic, 208f intrathyroid, 177f posterior auricular artery, 150 superior/inferior mesenteric arteries, 220, 220f supratrochlear-angular, 146 Anemia, 26b, 76 Aneurysms, abdominal aortic, 188189 Angina pectoris, 65 Angiogenesis, 20 Angiogenic stimulants, 19 Angioma, 69
260
Angiotensin, 19 Angular artery, 145f Antidiuretic hormone (ADH) (vasopressin), 19, 5355, 55f Antihypertensive agents, 71 Aorta, 13, 19 branches, 192f mesenteric clamp, 220, 221f narrowing, 70 Aortic arch technique, 103105, 104f105f Aortic receptors, 49 Aortic resistance, 34 Areola, 124 Arterial aneurysm, 6669 complications, 68 etiology, 67 forms, 67, 67f pathological anatomy, 67 symptomatology, 6869 treatment, 68 Arterial hemodynamics, 4042 Arterial hypertension, 28, 28b, 62, 7071 consequences, 70 signs, 75 treatment, 7071 Arterial plexus, 16 Arterial pressure, 17, 2728, 50, 79 classical measurement, 79 systolic pressure, 79 Arterial pulse, 29 Arterial receptors, 49 Arterial smooth muscle bers, 1819 Arterial tension, 28, 29f Arterial test, palpation, 78 Arterial valves, 78 Arterial waves, 41 Arteries, 1920 arterial network, 19 elastic, 19, 4041, 41f manipulation, 8990 muscular, 4142 pain and, 87 unpleating, 89
Index
Arterioles, 5, 19 adaptation, 46 arteriosclerosis, 6667 blood pressure, 21 circulatory resistance, 42, 42f pulmonary, 119120 Arteriosclerosis, 62, 6667 large/medium-caliber arteries, 66 small arteries/arterioles, 6667 Arteriovenous axis, 8889 Arterioventricular valves, 7 Atheromas (atheromatic plague), 6566 complications, 66 etiology, 6566 pathological anatomy, 65 symptomatology, 66 Atherosclerosis, 62 Atrial natriuretic peptide, 53 Atrioventricular (AV) node (Tawaras node), 10, 10f, 94 Atrioventricular bundle, 10, 10f Atrium (oriellette), 4, 7 Autacoids, 4748 Autonomic nervous system, 4953 electrical pathway, 5051 Autoregulation cerebral, 58 mechanisms, 4748 Axillary artery, 126127 manipulation, 128129, 128f Bainbridge reex, 45 Baroex, 53, 54f Baroreceptors, 49 Beta-blockers, 71 Bidigital stretch technique common carotid artery, 137, 137f external carotid artery, 141, 141f superior mesenteric artery, 222, 223f Blood, 2326 composition, 25 distribution, 56, 5f functions, 2325 physical properties, 26 see also Hemodynamics Blood cells, 25 Blood ow, 3538 arterial pressure, 28 dened, 35 nature of, 3839 output-speed relationship, 35, 35f total, dened, 35 Blood lipids, cardiovascular risk, 63 Blood pressure, 27 arterioles, 21 average, 28 blood ow and, 36, 37f Blood speed, 35 cross-section effects, 3536, 36f output-speed relationship, 35, 35f Blood viscosity, 26, 3738, 37f Blood volume, 5f, 25 arterial pressure, 28 Body mass index (BMI), 63 Brachial artery, 112, 113f114f manipulation, 129 Bradycardia, 1617, 30 Bradykinin, 47 Brain arterial hypertension, 62 central control, 50 cerebral circulation, 5758 Brainstem, motor centers, 50 Breasts, 121132 anatomy, 122127, 122f cancer, 121122 container, 122123, 122f contents, 123, 123f innervation, 123124, 124f mammary pain, 87, 121 manipulation, 127132 vascularization, 124127, 125f, 127f Bundle of HIS, 10, 10f Calcitonin, 168 Calcium, 169 Calcium channel blockers, 71 CannonBhm zone, 217, 225227, 226f Capacitance, 45, 43 Capillaries, 5, 2021 Capillary beds, 19, 21, 22f Capillary pulse, 78 Carbon dioxide, 47 Cardarellis sign, 78 Cardiac activity, 16 Cardiac arrest, 51 Cardiac cycle, 3032, 30f32f Cardiac bers, excitability, 9495 Cardiac insufciency, 72 left chronic, 72 right chronic, 72 Cardiac mass, 2932 Cardiac output, 3234 adaptation, 34 arterial pressure, 28 with exertion, 6, 6f, 6t homeostasis, 46 lowering, 1617 regulation, 33 at rest, 5, 6f, 6t stimulation, 16 Cardiac physiology, 2934 terminology, 3031, 31t Cardiac plexus, 1316 Cardiac vessels, 45, 13 Cardiovascular system, 326 blood, 2326 diseases, 6573 function, 37 heart, 717
261
Index
Cardiovascular system (continued) risk factors, 6164, 74 semiology, 7481 vessels, 45, 13, 1723 see also Homeostasis, cardiovascular system Carotid bifurcation, palpation, 161, 162f Carotid body, 185f186f Carotid glomus, 183186 Carotid receptors, 49 Carotid sinus, 95, 183186, 184f186f Carotid sinus nerve, 49 Carotid triangle, 133, 135f Catecholamines, 16, 34, 53, 55f Celiac plexus, 203f, 204 Celiac trunk, 189190, 190f, 194, 195f Central nervous system see Nervous system Central venous pressure (CVP), 33, 45 Centrifugal (visceromotor) bers, 16 Centripetal (viscerosensory) bers, 1617 Cephalad to caudad technique, 214216, 215f Cerebral circulation, 5758 Chambers, heart, 78, 8f Chemoreceptors, 49 Chest pain, 98 onset, 9899 Circulatory system, 3, 4f balance, 8081 uid, 85 function, 2729, 28f gradients, 3637 time, 36 types, 67 see also Blood; Hemodynamics Clotting, 25 Coagulation, 25 Colic artery left, 191 right, 191, 223224, 223f, 225f Common carotid artery, 133138 anatomy, 133, 134f135f contraindications, 136137 evaluating, 136 indications, 137 manual approach, 133138 precautions, 136 Common hepatic artery, 190, 191f Common iliac arteries, 235, 236f Common iliac artery, 191, 236238, 238f239f Complexion, inspection, 76 Compliance, 29 Compression, arterial aneurysm, 68 Compression-decompression technique, 88 occipital artery, 149 supratrochlear artery, 164 supratrochlear-angular anastomoses, 146 Compression-palpation, heart, 101 Conducting arteries, 19 Continuity, principle of, 35, 35f Convergence, 20, 20f Conversion enzyme inhibitors, 7071 Coopers ligaments, 122, 122f Coronary arteries, 13, 14f Coronary circulation, 5859 Coronary heart disease, 69 Coronary insufciency, 69 Coronary sinus, 7 Coronary veins, 13 Costovertebral neuralgia, 99100 Counter-rotation, pancreaticoduodenal arteries, 207209, 208f Cranial Local Listening, 165 Cranial nerves, 49 Cranial venous sinuses, 23 Cushing syndrome, 76 Cyanosis face, 76 lips, 77 Cysts, 181 Deep vein thrombosis, 69 pathophysiology, 69 symptomatology, 69 Diabetes, cardiovascular risk, 62 Diapedesis, 25 Diastole, 31f Diastolic pressure, 28 Diffuse thyroid hypertrophy, 173, 173f Digestive system, 80 Digital clubbing (hippocratism), 78 Diseases, cardiovascular, 6573 Dissecting aneurysm, 67, 67f Distributing arteries, 19 Diuretics, 70 Double compression, thorax evaluation, 9293, 92f treatment, 93 Double pressure technique, heart, 103f Drop attack, 136 Duodenojejunal junction, 187 Duodenum, 205, 206f vascular interdependence, 8687 Dysmenorrhea, 243 Dyspnea, 98 Ears, inspection, 77 Edema, eyelid, 76 Elasticity, 29 arteries, 19, 4041, 41f veins, 43 see also Viscoelasticity entries Electrochemical coupling, 18 Electromagnetic eld, 85 Embolism, 68 Emotional discharge, 86 Endocardium, 10 Endocrine disease, 70 Endocrine function, 34 Endothelin, 19
262
Index
Endothelium, vascular, 19, 48 Enteric nervous system, 217, 218f219f Epinephrine (adrenaline), 16, 19, 34, 5253 Ergo receptors, 4950 Erythrocytes see Red blood cells Esophagus, precordial pain, 99 Essential hypertension, 62, 70 Estradiol, 121 Estrogen, 121 Euthyroid goiter, 172 Exhalation, 17 External carotid artery, 139142 anatomy, 139, 140f contraindications, 139141 indications, 141 manual approach, 139142 precautions, 139 External iliac artery, 191 Eyelids edema, 76 inspection, 76 Eyes pupils, 76 white of, 77 Face, inspection, 76 Facial artery, 143146 anatomy, 143, 144f indications, 146 manual approach, 143146 pulse landmarks, 143146, 144f145f Fanning technique sigmoid vessels, 230f superior mesenteric artery, 223, 224f superior thyroid artery, 179, 179f Fibers, muscular, 9, 9f Fibrogen, 25 Fibrous pericardium, 1011, 12f Flow velocities, 39, 39f Fluid let, 38 Franks sign, 77, 77f FrankStarling law, 33 Functional circulation, 7 Fusiform distensions, 67, 67f Gallbladder, 187 Gastric artery left, 190, 198, 199f201f, 200, 203f right, 198, 199f, 201 Gastroepiploic (gastro-omental) artery, 201202, 202f 203f left, 198, 199f right, 198199, 199f Gastroesophageal junction, 187 Gate control, pain, 88 Glide-induction technique, 8788 common carotid artery, 138 external carotid artery, 141 recurrent laryngeal nerve, 182 Glossopharyngeal nerve, 49, 182 Goiter, 172 multinodal, 173, 173f Granulocytes, 25 Gums, inspection, 77 HagenPoiseulle law, 2728, 42 Hand, inspection, 78 Heart, 717, 94105 activity, 33 anatomy, 713, 9496 conduction system, 911, 10f contraindications, 100 extrinsic innervation, 1317, 15f brous skeleton, 89, 9596, 97f, 101102, 102f103f form/orientation, 7 function, 34 great vessels, 95, 96f high blood pressure (HBP), 62 indications, 100 innervation, 1317, 15f landmarks, 95, 97f manual approach, 100105 precautions, 100 precordial pain evaluation, 98100 structure, 89, 9f Heart rate, 1617, 2930 resting, 30 Hematocrit, 26 Hemodynamics, 3445 arterial, 4042 venous, 4345 see also Blood Hemorrhage arterial aneurysm, 68 atheroma, 66 uterine vessels, 243 Hemostasis, 25 Hepatic arterial buffer response, 59 Hepatic artery, 194 Hepatic pulse, 78 Hepatopancreatic ampulla, 187 Heredity, cardiovascular risk, 63 Heterogeneity, 3435 High blood pressure (HBP), 62 High compliance, 5 High density lipoprotein (HDL), 63, 7273, 121 High pressure system, 45 High resistance, 4 Hippocratism, 78 Histamine, 19, 47 Homeostasis, cardiovascular system, 4660 adaptation factors, 4657 local circulatory adaptation, 5760 Homeothermia, 23 Hormonal system, 5357, 87 complementary, 57 control, 217
263
Index
Hortons arteritis, 7172 Hydraulic charge, 37 loss of, 38 Hydraulic circuit principle, 27, 28f Hydrodynamic law, 34 Hydroelectrolytic balance, 23 Hydrostatic law, 34 5-Hydroxytryptophan (5-HTP), 48 Hyperpigmentation, 76 Hyperthermia, 5 active, 5 Hypogastric (internal iliac) artery, 192f, 193, 235236, 237f, 238239, 239f Hypoglossal nerve, 182, 184f Ileal artery, 227, 227f228f Ileocecal valve, 187 Ileocolic artery, right, 223224, 225f Iliac vessels, 235239 anatomy, 235236, 236f manual approach, 236239 Iliolumbar artery, 235 Immune defense, 23, 217 Infarction, 66 Inferior cardiac nerve, 13 Inferior gluteal artery, 236 Inferior mesenteric artery, 219f, 221222, 228229, 228f229f Inferior pancreatic artery, 210 perpendicular branches, 210211 Inferior thyroid artery, 174177, 176f, 180181, 180f 181f Inferior thyroid veins, 177 Inferior vena cava, 7 Infraorbital artery, 153155, 154f Inguinal canal, 251 anatomy, 251, 252f manual approach, 251, 252f precautions/contraindications, 251 Inhalation, 17 Innervation, vasculature and, 20 Inosculation, 19, 20f Intercostal nerves, 123124, 124f Intercostal pedicle, 132, 132f Intermediate ow, 39f, 40 Intermittent claudication, 65 Internal carotid artery, 160165 anatomy, 160, 161f contraindications, 160 indications, 160161 manual approach, 160165 precautions, 160 Internal iliac artery, 192f, 193, 235236, 237f, 238239, 239f Internal pudendal artery, 247250 anatomy, 247, 248f indications, 247248 manual approach, 247250, 249f250f Internal thoracic artery, 125126, 128 Interview technique, 7475 Intestine, vessels of, 217230 anatomy, 217222, 218f221f indications, 230 manual approach, 222230 Iron deciency, 76 Irrigation, 8889 intestinal, 217 jejunoileum, 222 liver, 195197, 196f197f organs affected, 89 principles, 8889 subclavian arteries, 112 technique, 89 uterus, 242 Ischaemia, 5 Isolated thyroid nodule, 173, 173f Isovolumetric contraction, 31, 32f Isovolumetric relaxation, 32, 32f Isthmus, 166 Jejunal artery, 227, 227f228f Jejunoileum, arterial irrigation, 222 Jugular pulse, 79 Laminar ow, 39, 39f Laplaces law, 29 Large pericardial cavity, 11 Larynx, 171f Lateral elevation, thorax, 92, 92f Lateral sacral artery, 235 Lateral thoracic artery, 126, 129 Left chronic cardiac insufciency, 72 Left colic artery, 191 Left gastric artery, 190, 198, 199f201f, 200, 203f Left gastroepiploic (gastro-omental) artery, 198, 199f Left ovarian vein, 245246 Left renal artery, 233234 Left renal vein, 245246 Leukocytes, 25 Leukotrienes, 48 Lichsteins sign (Franks sign), 77, 77f Lifestyle, cardiovascular risk, 6364, 74 Lift experimentation, 89 lateral/sagittal, thorax, 9192, 92f liver irrigation, 195197, 196f197f maintained, 89 uterus irrigation, 242 Ligaments Coopers, 122, 122f of Grber, 166167 pericardial, 11, 11b12b, 12f thyrotracheal, 166167 Lips, inspection, 77 Liver, 194197 anatomy, 194195 indications, 197 manual approach, 195197
264
Index
Local circulatory regulation, 4648, 48t Longitudinal anastomosis, 20f Low compliance, 4 Low density lipoprotein (LDL), 63, 7273, 121 Low pressure system, 5 Lymphatic ganglia, 172 McBurneys point, 187, 191 Malignant tumor cells, 20 Mammary pain, 87, 121 Manipulation see Visceral vascular manipulation Manual Therapy for the Cranial Nerves (Barral & Croibier), 87 Marginal artery, transverse colon, 225, 225f Maxillary artery, 153155 anatomy, 153, 154f indications, 155 manual approach, 153155 Mechanical pain, 75 Median sacral artery, 235, 236f Mediators, 5153 Mental artery, 155 Metabolic hyperemia, 58 Metabolic waste, transport, 23 Metabolites, 47 Microaneurysms, 67 Microcirculation, 21, 4243 Middle cardiac nerve, 13 Middle thyroid veins, 177 Migraine, 87 Mixed circulation, 7 Mobility, 85 Multinodal goiter, 173, 173f Muscarinic receptors, 16 Muscle of Trietz, 222 Muscular arteries, 19, 4142 Muscular bers, 9, 9f Mussets sign, 78 Myocardium, 89 Myogenic stretch response, 47 Natriuretic atrial peptide (NAP), 19, 34, 57, 57f Nervi nervorum, 20 Nervi vasorum, 18 Nervous system, 4953, 9495 balance, 85 celiac plexus, 203f, 204 complementary, 57 enteric, 217, 218f219f Neurological system, 80 Neurotransmitters, transport, 23 Neurovascular techniques, 182186, 183f Nitrogen monoxide, 19, 47 Nodal escape, 51 Norepinephrine (noradrenaline), 16, 19, 34, 5253 Nourishing circulation, 6 Nutrients, 5 Obesity, cardiovascular risk, 63 Obturator artery, 235236 Occipital artery, 147149 anatomy, 147, 148f indications, 147 manual approach, 147149, 149f Ocular system, 80 Ophthalmic artery, 163, 163f Oriellette, 4 Ovarian artery, 246f Ovarian vessels, 245246 anatomy, 245, 246f manual approach, 245246 vein, left, 245246 Ovaries, 188 Oxygen, 5 transport, 23 Oxygen deciency, 47 Pain arteries, 87 chest, 98 costovertebral neuralgia, 99100 duration, 75, 98 intensity, 98 location, 75, 98 mammary, 87, 121 mechanical, 75 onset, 9899 precordial, 98100 pudendal nerve neuralgia, 247 type, 75 Palmar erythema, 78 Palpation, 7881 abdominal aorta, 189f carotid bifurcation, 161, 162f common carotid artery, 133136, 135f common iliac artery, 236237, 238f external carotid artery, 139 internal iliac arteries, 238 maxillary artery, 153155 occipital artery, 147 posterior auricular artery, 150 renal artery, 231233, 232f subclavian arteries, 112 supraorbital foramen, 161, 162f supratrochlear arteries, 162f, 163 thyroid, 169173, 171f Pancreas, 205, 206f anatomy, 210, 211f vascular interdependence, 86 Pancreaticoduodenal arteries, 205206, 206f207f counter-rotation, 207209, 208f perpendicular branches, 206207, 207f Pancreaticoduodenal vessels, 205209 anatomy, 205, 206f, 208f manual approach, 205209 Pancreaticosplenic vessels, 210216 anatomy, 210211, 211f indications, 216 manual approach, 211216, 212f213f, 215f organs, associated, 216
265
Index
Paradoxical pulse, 79 Parasympathetic cardiomoderator tone, 51 Parasympathetic system, 13 action, 1617 cardiovascular effects, 51, 51f Parathyroid glands, 168169 Parathyroid hormone (parathormone), 169 Pectoralis minor muscle, 126, 129, 129f Pericardial cavity, 11 Pericardial ligaments, 11, 11b12b, 12f Pericardium, 1011 Peripheral resistance, vascular, 4142, 42f homeostasis, 46 Periphlebitis, 244 Peyers patches, 217 Phagocytosis, 25 Phlebitis, 244 Physiological venous pulse, 79 Plasma, 25 Platelet activating factor (PAF), 48 Platelets, 25 clumping, 25 Pleurocervical attachments, 115 Plexus, 20 Polycythemia, 26b Post-charge, 3334 Posterior auricular artery, 150152 anatomy, 150, 151f indications, 150 manual approach, 150152 Potassium, 47 Precapillary sphincter, 21 Precautions, 81b Pre-charge, 33 Precordial pain evaluation, 98100 non-cardiac origin, 99100 Premenstrual syndrome, 243244 Pressure gradients, trunk, 4345, 44f Pressure waves, 41 Pressure-induction maneuver, carotid bifurcation, 184, 185f Principle of concealing pulse, 231233 Principle of continuity, 35, 35f Prostaglandins, 48 Prostate symptoms, 243b Psychoemotional factors, 100 Pudendal nerve neuralgia, 247 Pulmonary arteries, 13 techniques, 118119 Pulmonary arterioles, techniques, 119120 Pulmonary circulation, 5960 Pulmonary hilum, 117 Pulmonary (small) circulation, 3, 4f Pulmonary vessels, 117120 anatomy, 117, 119f contraindications, 118 indications, 118 manipulation, 118120, 120f precautions, 117118 veins, 7, 13 Pulse analysis, 7879 principle of concealing, 231233 Pupils, inspection, 76 Purkinje network, 10, 10f Pylorus, 187 Pyramidal lobe (pyramid of Lalouette), 166, 172 Rabbit punch accidents, 112 Radiotherapy, 121 Raynauds disease, 71 Raynauds phenomenon, 71 Receptors, 4950 receptors, 52 receptors, 5253 Recurrent laryngeal nerve, 182 Red blood cells composition, 25 hematocrit, 26 increase/decrease, 26b microcirculation, 21 Reddened face, 76 Referrals, 75 Regulation, blood, 23 Renal arteries, 231234, 232f, 234f anatomy, 231, 232f left, 233234 right, 233234, 233f Renal disease, 70 Renal veins anatomy, 231, 232f left, 245246 Renal vessels, 231234 anatomy, 231, 232f manual approach, 231234 Renin-angiotensin-aldosterone system, 53, 5657, 56f Reservoir vessels, 45 Resistance, 45 Respiratory pulse, 79 Respiratory sinoatrial arrhythmias, 17 Respiratory system, balance, 81 Retrosternal techniques, thymus, 109 Reynolds number, 3940 Right chronic cardiac insufciency, 72 Right colic artery, 191, 223224, 223f, 225f Right gastric artery, 198, 199f, 201 Right gastroepiploic (gastro-omental) artery, 198199, 199f Right ileocolic artery, 223224, 225f Right lateral traction technique, pancreas, 211, 212f Right renal artery, 233234, 233f Saccular aneurysm, 67, 67f Sagittal elevation, thorax, 9192, 92f
266
Index
Secondary amenorrhea, 243 Secondary hypertension, 62, 70 Sedentary lifestyle, cardiovascular risk, 6364 Semiology, cardiovascular system, 7481 Serosal pericardium, 10 Serous pericardium, 11 Sex arterial pressure, 28 cardiovascular risk, 61 Sigmoid vessels, 230, 230f Sinoatrial (SA) node, 9, 10f excitation, 94 Skin rolling, carotid sinus, 186f Small intestine, vascular interdependence, 86 Smoking, cardiovascular risk, 6162 Sphincter of Oddi (hepatopancreatic ampulla), 187 Sphincters, 85 Splanchnic circulation, 59 Spleen, 213 anatomy, 210, 211f Splenic artery, 190191, 191f, 210, 212f Spreading-gliding technique, external carotid artery, 141142, 142f Starlings curve, 4243, 43f Stomach, 198204 anatomy, 198199 contraindications, 204 indications, 204 manual approach, 199204 organs/structures, associated, 202 precordial pain, 99 vascular interdependence, 86 Stress, cardiovascular risk, 64 Stretch maneuver combination, 88 common carotid artery, 138, 138f maintained, 89 superior thyroid artery, 179 see also Bidigital stretch technique Stretch receptors, 49 Stretch-induction technique, 88 posterior auricular artery, 152, 152f Stroke volume, 33 Strumming, inferior thyroid artery, 181 Subclavian arteries, 110116, 124125 anatomy, 110112, 111f contraindications, 112 indications, 112 interscalene segment, 110111 irrigation territories, 112 manual approach, 112116, 113f116f postscalene segment, 111 prescalene segment, 110 Subclavian muscle, 128129, 128f Supercial temporal artery, 156159 anatomy, 156, 157f manual approach, 156159 Superior cardiac nerve, 13 Superior laryngeal artery, 178181, 178f179f Superior mesenteric artery, 191, 217223, 219f, 223f Superior thoracic artery, 126, 129 Superior thyroid artery, 174, 175f176f, 178179, 179f Superior thyroid veins, 177 Superior vena cava, 7 Supraorbital artery, 163164, 164f Supraorbital foramen, palpation, 161, 162f Supratrochlear arteries, 162f, 163164, 165f palpation, 162f, 163 Supratrochlear-angular anastomoses, 146 Sweeping, subclavian arteries, 114115, 115f Sympathetic chain, 182183 Sympathetic system, 13, 95 action, 16 cardiac nerves, 34 cardiovascular effects, 5051, 52f Sympathicotonia, 80 Syndrome X, 63 Systemic (great) circulation, 3, 4f Systole, 31f Systolic ejection, 3132, 32f volume, 3334 Systolic pressure, 2728, 79 Tachycardia, 16 Telangiectasia, 7778 Temperature, 47 Temporal arteritis, 7172 Tendinomuscular structure, heart, 9f Thoracoacromial artery, 126 Thorax, 9193 container, 91 contents, 93 rigid components, 9193 Thready pulse, 78 Thrombocytes see Platelets Thrombosis, 66, 68 Thymus, 106109 anatomy, 106, 107f evolution, 106, 107f108f innervation, 106 manual approach, 109 physiology, 106109 structure, 106 vascularization, 106, 108f Thyroid, 166181 anatomy, 166169, 167f, 171f, 174178, 177f contraindications, 168t, 174 dysfunction, symptoms, 168t examination, 169174, 170f manipulation, 174178 manual approach, 178181 physiology, 167168 Thyroid gland, 166168 Thyroid hypertrophy, 172173, 173f
267
Index
Thyroid releasing hormone (TRH), 167168 Thyroid stimulating hormone (TSH), 167168 Thyrotracheal ligaments, 166167 Thyroxine, 167168 Toxicity, 76 Traction-induction technique, breast, 130131, 131f132f Transport blood, 23 metabolic waste, 23 neurotransmitters, 23 oxygen, 23 Transverse accordion technique pancreas, 213214, 213f spleen, 214 Transverse anastomosis, 19, 20f Transverse colon arteries, 224227 marginal artery, 225, 225f Transverse facial artery, 156, 157f Transverse pericardial sinus, 11 Trigeminal cervical system, 87 Triiodothyronine, 167168 True capillaries, 21 Tubes, 85 Tucina intima, histology, 17, 18f Tucina media, histology, 1718, 18f Tumor angiogenesis factor (TAF), 20 Tunica adventitia, 18, 18f, 20 Turbulent ow, 3940, 39f Unpleating arteries/veins, 89 Unstable pulse, 79 Uterine artery, 245 anatomy, 240, 241f manipulation, 240242, 241f242f Uterine vessels, 240244 anatomy, 240 common venous complaints, 244 indications, 243244 precautions/contraindications, 242243 Uterus, lifting irrigation, 242 Vagal brake, 50 Vagal cervicothoracic depressor nerve, 95 Vagal parasympathetic nerves, 34, 95 Vagal sympathetic tone, 17 Vagosympathetic actions, 95 Vagotonia, 8081 Vagus nerves, 13, 182 Values, blood, 28 Valves heart, 78 vein, 2123 Vasa privata, 13, 14f, 117 Vasa publica, 13, 117 Vasa vasorum, 18, 20 Vascular activity, 33 Vascular axis, direction, 89 Vascular charge, 37 Vascular diversion vessels, 21 Vascular endothelium, 48 Vascular interdependence, 8687 Vascular murmurs, 40 Vascular myocytes, 1819 Vascular network, 3, 4f, 23, 24f Vascular resistance, peripheral, 4142, 42f homeostasis, 46 Vascular sections, 45 Vascular self-regulation, 4647 Vascular shortening, 89 Vascular supply, 8687 Vascular walls, histology, 1718, 18f Vasculature, innervation and, 20 Vasoconstriction, 5, 19, 47, 48t Vasodilation, 19, 48, 48t Vasodilators, 71 Vasomotor symptoms, 80 Vasopressin (antidiuretic hormone (ADH)), 19, 5355, 55f Vasosympathetic balance, 8081 Veins common complaints, 244 elastic, 43 manipulation, 8990 properties, 23 unpleating, 89 Veins, histology, 2123 capacity, 21 number, 21 valves, 2123 walls, 21 Velocity prole, uid, 38, 38f Vena cavae, 13 Venoatrial receptors, 49 Venous baroreceptors, 49 Venous hemodynamics, 4345 Venous plexus, 16 Venous pulse, physiological, 79 Venous return, 43 vis a fronte, 43 vis a latere, 43 vis a tergo, 43 Venous sinus, 23 Ventricles, 7 Ventricular diastole, 27 Ventricular bers, 9 Ventricular lling phase, 31, 32f Ventricular systole, 27 Venturi effect, 38, 38f Vesicouterine venous system, 242 Visceral vascular manipulation, 8590 arteries and veins, 8990 global concept, 8687 precautions, 81b principles of, 8586 techniques, 8789 Visceromotor bers, 16 Viscerosensory bers, 1617
268
Index
Viscoelasticity techniques, 85 breast, 129130, 130f capillary function, 21 posterior auricular artery, 152 supratrochlear-angular anastomoses, 146 Viscoelasticity-induction infraorbital artery, 154f, 155 superior thyroid artery, 179 Visual inspection, 7678 Weak resistance, 5 Weight, cardiovascular risk, 63 White blood cells, composition, 25 White of eye, 77 Windkessel effect, 4041, 40f41f, 60 Wiry pulse, 78Xanthelasmata, 76 Zygomatico-orbital artery, 158, 158f
269
Commissioning Editors: Sarena Wolfaard, Alison Taylor Development Editor: Fiona Conn Project Manager: Anita Somaroutu Designers: Charles Gray, Sarah Russell Illustrator: lnore Lamoglia
Alain Croibier
D.O., MRO(F)
Member of the Registre des Ostopathes de France Member of the Academie dOsteopathie de France Lecturer in Visceral Manipulation and Osteopathic Diagnosis at the Osteopathic College, A.T. Still Academy, Lyon, France Lecturer in Visceral Manipulation and Nerve Manipulation for The Barral Institute Translated by Annabel Mackenzie, RST
EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY TORONTO 2011
2011 The Barral Institute First published in French under the title Manipulations vasculaires viscrales 2009 Elsevier Masson SAS Paris. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elseviers Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail: healthpermissions@elsevier.com. You may also complete your request online via the Elsevier website at http://www.elsevier. com/permissions. First published 2011 ISBN 978 0 7020 4351 2 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Notice Neither the Publisher nor the Authors assume any responsibility for any loss or injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. It is the responsibility of the treating practitioner, relying on independent expertise and knowledge of the patient, to determine the best treatment and method of application for the patient. The Publisher
Printed in China
Preface
The human body is incredibly complex. It is practically impossible to imagine the myriad of cells that contribute to our survival and to our good health. Each must play its note in the grand concert that is our life. The osteopathic concept is global in its approach. Each component part of the living human structure is of vital importance. The notion that an osteopath specializes in one part of the body is sheer nonsense. It is not for any of us to choose, by virtue of our education, our culture, or our life, what is important for the patient. Rather, it is the organisms own vast memory store that must always guide our hand. Knowing how to listen to a body is essential; the hand must design a therapeutic response according to the messages it receives. A. T. Still declared the rule of the artery to be supreme and fundamental. In order to function well, an organism requires optimal circulation. Few manual therapists concern themselves with the circulatory function directly. We acknowledge, however, that our excellent friend and colleague, Paul Chauffour, has pursued a keen interest in the vascular system. In this book we share the fruits of our research and experience. The visceral system requires especially plentiful circulation and it is therefore natural that we have, little by little, sought out ways to improve vascular function. Our endeavor has been to perfect simple and effective maneuvers for the visceral vascular network. About 100000km of
arteries and 250000km of veins run through our bodies an impressive quantity! For an individual weighing 70kg, this amounts to about 1500km of arteries per kilogram. In this text we describe the precise location of the principal visceral pulses. These key pulses are a reliable witness by which to gauge the changes that treatment brings. We have studied, according to artery type the most effective techniques for increasing the irrigation of given organs. The experiments have been duplicated by way of Doppler effect tests. Even if for some deeply situated arteries we have not always been able to prove an augmentation of blood ow, clinical improvements have demonstrated the effectiveness of this type of manipulation. In the case of some arteries, only a momentary variation in circulation has been observed, with no ascertainable long-term effect. Even with that, the patient felt an improvement and this is the essential thing. Our work is somewhat empirical and somewhat subjective, but why be ashamed of it? Our hands possess the magnicent privilege of improving the major functions of the human body. This remains true provided practitioners continually work to augment and broaden their knowledge, and to rene their manual applications. Knowledge of the anatomy and function of the vascular system is what determines the quality of care that patients receive. We hope that this book will become indispensable to you in meeting this objective. xxi
Acknowledgments
The authors would like to thank Annabel Mackenzie, RST, for her superb translation from the French version. Thanks also to Gail
Wetzler, RPT, and Dawn Langnes for their editorial support. JP Barral A Croibier
xxiii