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CARDIOVASCULAR PHYSIOLOGY (Gloria Marie M. Valerio, MD) Outline: 1. 2. 3. 4. 5. 6. 7. 8.

Functional Anatomy of the Heart Properties of the Myocardial Cells Electrical Events Cardiodynamics Characterics, Properties, Functions of the Different Types of Blood Vessels Hemodynamics Microcirculation Mechanisms that Regulate Cardiovascular Function

the different organs of the body. This is made possible by the pumping action of the heart, so when the heart contracts, it will pump blood to the arteries. The arteries in turn will distribute blood at a high pressure to the different organs of the body. And from the different organs of the body, blood then will be collected by the veins and returned to the heart. So the arteries are distributing blood vessels while the veins are collecting blood vessels. The capillaries will allow the exchange of fluid and solutes between intravascular and interstitial fluid compartments. The human heart is divided into two pumps: right and left and they are connected in series. The left heart pumps blood to the systemic or peripheral circulation by way of the aorta. The right heart pumps blood to the pulmonary circulation by way of the pulmonary artery. Systemic or peripheral circulation includes blood flow to all organ systems of the body except for the lungs. When the cells of the systemic or peripheral circulation are metabolizing, they consume oxygen and produce carbon dioxide that will now be collected by the veins and will have a low oxygen tension and a high carbon dioxide tension called unoxygenated/deoxygenated/venous blood. This blood will be emptied by way of vena cava to the right side of the heart. When the right heart contracts, this same blood will be ejected to the pulmonary circulation by way of pulmonary artery. Unlike the other arteries of the body, the pulmonary artery carries deoxygenated or venous blood. This same blood will then reach the pulmonary capillaries and this is where exchange of gases will take place between the alveoli in the lungs and blood in pulmonary capillary across respiratory membrane. The blood from the pulmonary capillaries will come from the right side of the heart low oxygen tension, high carbon dioxide tension. The opposite is true with regards to air in alveoli - increase oxygen tension, low carbon dioxide tension. Movement or transport of these gases across the respiratory membrane is a passive process. It occurs by simple diffusion brought about by pressure gradient. So the transport of movement of oxygen will take place from alveoli to pulmonary capillary, the carbon dioxide goes in opposite direction. So the blood that will enter the Alveoli Increase pO2 Decrease pCO2 Decrease pO2 Increase pCO2 Pulmonary capillary

Functional Anatomy of the Heart The normal position of the heart inside the thoracic cavity is slightly tilted to the left, pointing downwards. When the heart contracts, it has a wringing action, meaning to say, when the heart contracts, it rotates slightly to the right and that will now expose the cardiac apex, so that when you place the diaphragm of the stethoscope over the chest wall particularly on the fifth intercostal space, left mid-clavicular line, that is where you will heartbeat the loudest called apex beat or point of maximum impulse. Fifth intercostal space: Start palpating below the clavicle and first rib the second intercostal space, and move three spaces down. The midclavicular line: left of the left clavicle, take note of the mid-point then move five spaces below. In males, it is easily located because it is exactly below the left nipple. In females, the location may be variable so you need to palpate.

pulmonary vein is already oxygenated. Unlike the other veins in the body, the pulmonary vein carries oxygenated or arterial blood which will then be emptied on the left side of the heart which means the left heart pumps blood to the systemic circulation and receives blood from the pulmonary circulation while the right heart pumps blood to the pulmonary circulation and receives blood from the systemic circulation. The circulatory system is a closed system whatever amount of blood will be pumped by the blood per minute will be equal to the volume of blood that will return to the heart per minute. Structures of the Human Heart

PHOTO: Schematic diagram of the parallel and series arrangement of the vessels composing the circulatory system. The capillary beds are represented by thin lines connecting the arteries (on the right) with the veins (on the left). The crescent-shaped thickenings proximal to the capillary beds represent the arterioles (resistance vessels).

The cardiovascular system consists of the heart at the center and the different blood vessels which are arranged in parallel and in series with each other. The red are the arteries, the blue are the veins, and the capillaries are the smallest vessels in the body. The major function of the cardiovascular system is to transport nutrients including oxygen to the different organs of the body and to remove the waste products of metabolism including carbon dioxide from 1 Shannen Kaye B. Apolinario, RMT The heart is divided into two pumps: the right and the left. The two pumps in turn are made up of two chambers: atrium and ventricle. The right heart is made up of the right atrium and right ventricle while the left heart is made up of the left atrium and left ventricle.

The two atria are separated by a band of connective tissue forming the interatrial septum. The two ventricles are also separated by a band of connective tissue forming the interventricular septum. The two atria are separated from the two ventricles by a mass of connective tissue. The four chambers of the heart are separated by connective tissues.

Other important structures in the heart are the valves and there are two sets of cardiac valves. Between the atria and ventricles are the atrioventricular valves - tricuspid valve on the right side and mitral valve on the left side. The tricuspid valve is between the right atrium and right ventricle while the mitral valve is between the left atrium and left ventricle. The other sets of cardiac valves are between the ventricles and the arteries the pulmonary valve between the right ventricle and pulmonary artery; the aortic valve between the left ventricle and aorta. Functions of the valves: first, when they open, they allow blood to flow from one chamber of the heart to another when the atrioventricular valves are open, blood flow from the atria to the ventricles and when the semilunar valves are open, blood ejects from the ventricles to the arteries. When they close, they will prevent regurgitation or backflow of blood. However, there are no cardiac valves between the atria and veins so when there is atrial contraction, small amount of blood backflows to the veins. There is only small amount of backflow because when the atria contracts, there is increase in pressure and the tendency is to push blood downwards to the ventricles and at the same time, when it contracts, the orifice of the veins becomes smaller. Structure of Cardiac Valves

The wall of the atria and ventricles is made up of cardiac muscle. The atrial wall/musculature is thinner compared to the ventricular wall or musculature. The two atria functions as a primer pumps for the ventricles and as conduits of blood from veins to ventricles. It is therefore the ventricles with the thicker wall that are the major pumps in the heart with the left ventricular wall thicker than the right ventricular wall. The left ventricular wall is thicker because it pumps blood to the systemic circulation with an average pressure of 70-130 mmHg. On the other hand, the right ventricle will pump blood to the pulmonary circulation with an average pressure of only 4-25 mmHg. The left ventricle will have to pump blood against a higher pressure resistance in the systemic circulation compared to the right ventricle that will pump blood against a lower pressure in the pulmonary circulation. Since the opposing force is higher in the left ventricle, the tendency is to contract more forcefully because of increased workload resulting to hypertrophy of the muscle fibers. Although the left ventricular wall is thicker, contract more forcefully, higher workload and higher opposing force than the right, the output of the two ventricles is the same. Whatever amount will be ejected by the left ventricle per minute is the same with the amount of blood ejected by the right ventricle per minute. Aside from the cardiac muscles, the atrial and ventricular wall also contains a fair amount of elastic tissues that will enable the different chambers of the heart to dilate when the volume of the blood inside increases. Also present in the atrial and ventricular wall is a fair amount of connective tissue and this connective tissue in turn will prevent overstretching or distension of cardiac muscles when the cardiac size increases.

PHOTO: Drawing of a heart split perpendicular to the interventricular septum to illustrate the anatomic leaflets of the atrioventricular and aortic valves.

The three cardiac valves tricuspid, pulmonary and aortic contains three cusps. It is only the mitral valve that contains only two cusps. For the atrioventricular valve, the cusps are attached by strong ligaments called chordae tendinae to the papillary muscle and the papillary muscle arises from the ventricular wall. Mitral valve has two cusps attached by the chordae tendinae to the papillary muscle. The semilunar valve aortic valve has no chordae tendinae. Tricuspid valve has chordae tendinae attached to the papillary muscle and arises from the ventricular wall. Each cusp has an orifice or opening covered by leaflets which are made up of loose fibrous tissue. One end of the leaflets is attached to the border of the orifice while the central part is freely movable. Since it is thin and freely movable, it can open. However when they close, they close completely because there is extensive overlapping of the leaflets that cover the orifice of the cusp. Opening and closing of the cardiac valve is a passive process brought about by pressure differences between the two chambers of the heart. In the case of tricuspid valve for example, if the right atrium is contracting, the right ventricle is in a relaxed state. When the right atrium is contracting, the pressure increases and that will push open the tricuspid valve so that blood will flow from the right atrium and right ventricle. On the other hand, if it now the right ventricle contracting and the right atrium is relaxed, the high pressure in the right ventricle will close the tricuspid valve to prevent back flow of blood to the right atrium. It is also a passive process due to the pressure gradient. Same things happen with regards to the mitral valve as well as to the semilunar valves. When the ventricle is contracting, the papillary muscle also contracts but the contraction of the papillary muscle is not essential in closing the atrioventricular valves. Remember that when the ventricle is contracting due to the thick musculature, the pressure is high. So the high pressure will tend to push the AV valves to bulge into the atria

PHOTO: Four cardiac valves as viewed from the base of the heart. Note how the leaflets overlap in the closed valves.

Shannen Kaye B. Apolinario, RMT

however, when the papillary muscle contracts, it will pull the chordae tendinae to prevent eversion or over-bulging of the AV valves during ventricular contraction.

the leaflets. In insufficient or incompetent cardiac valve, the leaflets do not close completely allowing back flow of the blood either from the ventricles to the atria or from the arteries to the ventricles. In normal mitral valve, when the left atrium is contracting, that is the amount of blood that will be ejected to the left ventricle. In stenotic mitral valve, even if the left atrium is contracting, there will be less amount of blood that will be ejected to the left ventricle. There will be now pooling of blood in the left atrium causing the left atrium to dilate. In stenotic aortic valve, the leaflets hardened so that during contraction, the amount of blood ejected in the aorta will be decreased. There will be pooling of blood in the left ventricle causing the left ventricle to dilate. An example of an insufficient or incompetent cardiac valve is a prolapsed mitral valve. When the left ventricles contract, it does not close even if there is blood ejected in the aorta, it will be lessened because of the backflow of blood in the left atrium. Presence of a stenotic or an incompetent cardiac valve will produce abnormal heart sounds called a murmur.

PHOTO: Mitral and aortic valves (the left ventricular valves)

Valve Mitral Aortic

Heart Sounds Closing of the cardiac valves will produce the normal heart sounds. The first heart sound is at the onset of ventricular contraction with closing of AV valve. That closing of AV valve produces the first heart sound. Compared to the second heart sound, closing of the AV valve is said to be louder and longer in duration. The sound produced by the closing of the tricuspid valve is heard best on the fifth intercostal space, left of the sternum while the sound produced by closing of the mitral valve is heard best on the fifth intercostal space at the cardiac apex - left mid-clavicular line. The second heart sound occurs at the onset of ventricular relaxation with closing of the semilunar valves. And because of the pressure in the arterial system, when the semilunar valves close, they close abruptly and that will make the duration of the heart sound shorter. The sound produced by the closing of the pulmonary valve is heard best on the second intercostal space left of the sternum while the sound produced by the closing of the aortic valve is heard best on the second intercostal space right of the sternum. The quality of the second heart sound can be affected by respiratory phase expiration and inspiration. During expiration, you will hear only one second heart sound there is simultaneous closure of the aortic and pulmonary valves. During inspiration, there is a physiological splitting of the second sound with closing of the aortic valve occurring a little ahead of the pulmonary valve and the sound produced by closing of aortic valve is louder than that produced of the closing of the pulmonary valve except in patients with pulmonary hypertension. The pressure inside the thoracic cavity is negative or below atmospheric pressure causing a suction effect on structures that can be dilated. (In positive or above atmospheric pressure, it will compress the structures in the thoracic cavity.) The more negative the intra-thoracic pressure is, the more the heart and lungs are dilated. When the heart is dilated, it allows more blood to return especially to the right heart more blood will return from the systemic circulation. There will be an increase volume of blood to the right heart causing a delay of the closing of the pulmonary valve during inspiration. In children with thin chest wall or patients suffering from left ventricular failure, a third heart sound can be heard and that will coincide with filling of blood in the ventricles. Rarely, there is a fourth heart sound that can be heard and that will coincide with atrial contraction. In some abnormal conditions, the third and fourth heart sounds may be accentuated so that what you will hear in the stethoscope will be triplets of sounds resembling the sound that is produced by galloping horses called a gallop rhythm. Certain abnormal conditions like an infection in the heart may damage the cardiac valves and there are two types of lesions that may occur in the cardiac valve: stenosis and incompetent cardiac valve. In stenosis, the valve cannot open completely because of the hardening of 3 Shannen Kaye B. Apolinario, RMT

Type of lesion Stenosis Incompetent Stenosis Incompetent

Timing of murmur Diastole Systole Systole Diastole

Diastole ventricular relaxation Systole ventricular contraction The Pericardium

Pericardial fluid Parietal pericardium Visceral pericardium The heart is covered by a membrane which is made up of connective tissue the pericardial sac or pericardium. This connective tissue that makes up the pericardium is less distensible. Presence of this will also prevent overstretching of the cardiac muscle when the cardiac size increases. The pericardium is made up of two membranes: visceral and parietal pericardium. The visceral pericardium is the membrane directly attached to the anterior surface of the myocardium. When the visceral pericardium is reflected back, it forms the parietal pericardium. The space in between the two membranes is filled with 30cc of pericardial fluid. The importance of the pericardial fluid is to lubricate the heart facilitating the movement of the heart when it contracts. (2) Groups of Myocardial Cells 1. Automatic Cells An automatic cell is a cell that is capable of spontaneously generating its own action potential independent of extrinsic nervous stimulation. In the case of myocardial cells, it is independent of automatic stimulation. Aside from generating its own action potential, the cells of the heart are capable of transmitting or conduction action potentials throughout the heart. Structures that make up the hearts conduction system: Synoatrial (SA) node = located at the junction of superior vena cava and right atrium. Atrioventricular (AV) node = located posteriorly on the right side of interatrial septum. It is divided into three zones: o Atrionodal (AN) zone most proximal zone, a transitional zone between the right atrium and AV node o Nodal (N) zone - middle

Nodal His (NH) zone most distal, connects with the bundle of His

Purkinie system/ventricular conduction system = made up of bundle of HIS and purkinje fibers o Bundle of HIS located at the interventricular septum. The bundle of HIS forms right and left bundle branches. The left bundle branch will divide to form the posterior and anterior fascicles. The left posterior and anterior fascicles as well as the right bundle branch will then connect with the Purkinje fibers that are present mostly at the apex of the heart.

0 4

-90 mv

Skeletal muscle action potential: 5-30 millisecond Phase 4 Resting Membrane Potential (-90mv) membrane is highly permeable to potassium because of the presence of many potassium leak channels. Since there are many potassium leak channels on the membrane of the skeletal muscle and there is a concentration gradient for potassium, the tendency is for potassium to move out decreasing the amount of positively charged ions inside. Also present inside the cell are negatively charged molecules including proteins which are large molecules so they remain inside. The main extracellular cation is sodium, there is a concentration gradient for sodium but the membrane is only slightly permeable to sodium ions because of there are only few sodium leak channels most sodium will remain outside. The membrane is permeable to chloride at rest, it allows the chloride ions to move in but because of the presence of the negatively charged ions inside the cell, chloride will eventually get out. To maintain the concentration of Na and K inside the cell, you have the activity Na-K pump (3 Na out, 2 K in). These things stabilize the RMP of the cell to -90mv.
PHOTO: The cardiac conduction system

All of these cells are automatic cells and can generate own action potential. But in a normally functioning heart, all action potentials are generated by the sinoatrial (SA) node and is referred as the primary pacemaker of the heart while the other automatic cells are latent pacemakers. They are called latent pacemakers because although they do not normally generate action potential, in some abnormal conditions, they can be stimulated to generate their own action potential. The primary pacemaker of heart is the one that determines the heart rate number of heart beats per minute. The average heart beats per minute is 75-80 beats per minute. The SA node is the primary pacemaker of the heart because it is the fastest that can generate an action potential. Overdrive suppression is the increase frequency of discharge of an action potential from an automatic cell will diminish the automaticity of other automatic cells. The SA node will fire at a high rate of 75-80 beats per minute with each action potential that will depolarize other automatic cells. With each depolarization, a certain amount of sodium ions will enter the cell that will create a concentration gradient for sodium that will activate the Na-K exchange pump. The Na-K pump will extrude sodium ions. The more frequent the other automatic cells are depolarized, the more sodium ions will enter the cell, the more Na-K pump will be activated, the more sodium ions will be extruded from the cell that would cause the cell to be hyperpolarized. If the other automatic cells are hyperpolarized, they will become less excitable. When the overdrive stops, the activity of Na-K pump will not stop immediately; it will remain active, continuing to extrude sodium ions, the more the other automatic cells will become hyperpolarized, the more they will become less excitable, and the more their automaticity will be diminished. (44m) 2. Non-automatic cells Non-automatic cells cannot generate own AP and are specialized mainly for contraction. The presence of non-automatic cells in the heart, even if you cut the automatic innervation to the cardiac muscle, it can still contract. Non-automatic cells are the cardiac muscle cells present in the atrial wall and ventricular wall.

Intracellular Increase K+ Negatively charged proteins Decrease Na+ Decrease Cl-

Extracellular Decrease K+ Increase Na+ Increase Cl-

Resting Membrane Potentials: Neurons = -70mv Skeletal muscle = -90 mv SA node = -60mv Ventricular muscle = -90mv Gastrointestinal smooth muscle = -60mv The resting membrane potential is different in each cells because of the potassium leak channels. The more potassium leak channels present on the membrane, more K+ will move out of the cell, making the membrane potential more negative and vice versa. Phase O depolarization opening of fast voltage gated Na+ channels Phase 1,2,3 repolarization re-establishing the RMP, brought about by the closure of fast voltage gated Na channels and opening of slow voltage gated K channels. Since these K channels are slow, they remain open for a long time allowing K+ to continuously move out so that at some point, the MP will go below the resting level = hyperpolarization. When the K+ gated are closed, the RMP will be restored Automatic Fiber Action Potential 1

4 Properties of Myocardial Cells 1st Property: Automaticity generation of action potentials 4 Shannen Kaye B. Apolinario, RMT -60 mv

250-300 milliseconds hyperpolarization Action potential of an automatic cell- SA node

Difference from the AP of skeletal muscle: Duration is longer 250-300 millisecond RMP is less negative - -60 mv Phase 4 slow rise in membrane potential and is unstable. The slow rise in membrane potential is called the pre-potential or slow diastolic depolarization. There is more Na leak channels, membrane potential increases. Phase 0 Depolarization. Somewhat inclined, depolarization occurs slowly Phase 1,2,3 Repolarization. Inclined, occurs slowly, there is hyperpolarization like in the skeletal muscle The increase in sodium leakage and a decrease in the membrane permeability to potassium will account for the automaticity of the SA node. Voltage gated K channels will open allowing K efflux. But repolarization cannot occur rapidly because of the long lasting Ca channels are still open. Ca influx and K efflux Midway of repo: Ca channels close, K channels open Na leakage, Decrease K -40 mv -50 mv -60 mv 250-300 milliseconds Action potential of an automatic cell (same thing happens in SA node, AV node, bundle of HIS) With parasympathetic or vagal stimulation, the neurotransmitter released (NTA) released is acetylcholine (Ache). When Ache binds with muscarinic 2 receptors in the SA node, it increases permeability to K+, allowing more K+ efflux. Parasympathetic or vagal stimulation will hyperpolarize the SA node. If it is hyperpolarized, it is less excitable and the duration of the membrane pre-potential is longer or delayed generation of action potential. In parasympathetic or cholinergic stimulation, SA node is inhibited, heart rate decreases. The opposite happens with sympathetic stimulation, norepinephrine released by sympathetic nerves will bind with the B1 receptor in the SA node resulting to an increased permeability to Na and Ca causing hypopolarization of the SA node, making it more excitable and the heart rate increases. Hyper: prolonged opening of K channels

Non-automatic Fiber Action Potential (ventricular muscle)

PHOTO: Action potential in the ventricle (250-300 milliseconds)

Activation of slow (inclined) voltage gated long lasting Ca++ channels allowing Ca influx with some Na influx = MP will become less negative

RMP - -90, straight line, it is stable Phase 0 depolarization, straight line. Occurs rapidly due to opening of fast voltage-gated Na channels = Na influx then reaches the threshold voltage of -60 mv resulting to depolarization. When the membrane potential reaches -20 mv, it will open up slow, long lasting voltage gated Ca channels = Ca influx. (The main factor responsible for depolarization is Na influx) Peak of the spike Na channels closes, K channels open. Ca++ channels are still open Phase 1 initial phase of repolarization brought about mainly by slow voltage gated K+ channels Phase 2 plateau the amount of K+ that goes out is equal to the amount of Ca++ that goes in. no electrical activity. At the end of the plateau, the Ca++ channels will close leaving only the K+ channels open that will bring about the final phase of repolarization Phase 3 final phase of repolarization Phase 4 - -90 RMP is re-established. The increase membrane permeability to potassium is responsible for the -90 mv RMP. No hyperpolarization Although the K+ channels can remain open for a long time, because of the plateau, it is open for a long period of time thus it does not reach hyperpolarization Similarities and differences with the action potential of skeletal and cardiac muscles: Similarities: -90 mv RMP, fast-paced depolarization Differences: repolarization, no hyperpolarization, duration

PHOTO: Action potential of the SA node

PHOTO: Action potential of the atrium

Shannen Kaye B. Apolinario, RMT

Similarities and differences between the ventricle and atrium: Similarities: same, RMP, depolarization, phase 1 Differences: o phase 2 plateau. In the atrium, the membrane is more permeable to K+ than to Ca++. More K+ conductance than Ca++ conductance that will make the duration of the plateau shorter and not sustained as compared to that of the ventricle. o Repolarization phase is shorter in atrium than in the ventricle Periods of Refractoriness ARP RRP

The importance of prolonged duration of refractoriness is for the ventricles to be filled with blood resulting to a more effective pumping action, no fatigue, no tetanic contractions. One cannot elicit successive action potentials or contractions without tetanic or sustained contractions in the cardiac muscle = allow more time for ventricular filling. The musculature of the ventricle is thick so when it contracts, it compresses the coronary arteries. The coronary arteries supply blood and oxygen to the cardiac muscle thus when it is compressed, there is poor perfusion of cardiac muscle and less oxygen supply, this happens if there is tetanic contractions but in the cardiac muscle, there are no tetanic contractions. There is longer period of relaxation, when the ventricles are relaxed, there will be better perfusion of the cardiac muscle. Duration Action potential ARP RRP Heart rate of 75 beats per min 0.25 sec 0.20 sec 0.05 sec Heart rate 200/min 0.55 sec 0.13 sec 0.02 sec Skeletal muscle 0.005 sec 0.004 sec 0.001 sec

In Absolute or Effective Refractory Period (ARP), no amount of stimulus intensity will be able to re-excite the membrane of that cell. It covers the whole of depolarization until 1/3 of the repolarization phase. At phase 0, it is absolute refractory because all the voltage gated sodium channels are open and it is not able to re-open the already open sodium channels. In phases 1 and 2, the Na channels are already close but it is still absolute refractory because Na channels are voltage gated and they only open at a certain voltage or membrane potential near the critical firing level of about -60mv more so if the membrane potential is at its resting level. It is far from the CFL. In Relative Refractory Period (RRP), its level is near the critical firing level and resting level, the membrane becomes more excitable so that a stronger than threshold stimulus can be able to open up the voltage gated sodium channels and elicit a second action potential.

PHOTO: Changes in action potential amplitude and upstroke slope as action potentials are initiated at different stages of the relative refractory period of the preceding excitation

As the membrane potential reaches the relative refractory period as well as the RMP, if there is stimulus later in the RRP, that will open up more and more voltage gated Na channels so that its depolarization increases its amplitude, same thing happens in the SA node. 2nd Property: Rhythmicity It is said that the SA node generates the action potentials at regualr intervals. Even if the heart rate increases, if the impulses are still generated at regular intervals, that is still called the sinus rhythm.

Photo: Normal sinus rhythm

PHOTO: Relationship between action potential and contraction in the ventricle

A contraction cannot be elicited unless the ventricle is almost completely relaxed.


Photo: Normal ECG

Shannen Kaye B. Apolinario, RMT

P wave represents atrial depolarization QRS complex represents ventricular depolarization When seeing a normal sinus rhythm, take note of the interval between successive P waves regular interval, take note of the interval between successive QRS complex regular interval.

With regards to the right and left atrium, transmission of impulses can occur locally through gap junctions. When the impulse reaches the AV node, there is a delay in the transmission of impulses so the velocity of conduction decreases at the AV node and this is called the AV nodal delay. Most of the delay will take place between the AN and N zones of the AV node. There is a delay in the transmission of impulses in the AV node because it has a small fiber diameter and few gap junctions spaces or channels between the membranes of the muscle fibers that will allow ions to flow freely from one muscle fiber to the next. The smaller fiber diameter and fewer gap junction causes increased resistance to impulse conduction - the AV nodal delay. The importance of AV nodal delay is for the ventricles to remain in a relaxed state for a longer period of time allowing more time for the ventricular filling and to ensure that the atria and ventricles will not contract simultaneously. From the AV node, the impulse will then travel to the bundle of His then to the left and right bundle branches then to the Purkinje fibers then it would stop (from antero-basal apex end). Transmission of impulse in heart: basal. Conduction Speed in Cardiac Tissue SA node Atrial muscle AV node Bundle of His Purkinje fibers Ventricular muscle Conduction rate (m/sec) 0.05 1 0.05 1 4 1 antero-basal apex postero-basal

Photo: Sinus tachycardia

The heart rate may increase with sympathetic stimulation, during moderate to heavy exercise, and increase temperature during fever. In these three conditions, the heart rate will increase but if the impulses are generated at regular intervals, that is still sinus rhythm. But since the rate will increase, it is now called sinus tachycardia.

The part of the heart that will depolarize last is the postero-

Photo: Sinus bradycardia

On the other hand, in cold temperatures or if there is vagal over stimulation that inhibits the SA node, the rate of firing will decrease but if the impulses are generated at regular intervals, that is still sinus rhythm but this time, it is now called sinus bradycardia. If there is no rhythm or if it is irregular, it is now called arrhythmia. 3rd Property: Conductivity

Conduction speed is lowest in the AV node (not in the SA node because it is generation). Fastest is in the Purkinje fibers because of the large fiber diameter. In the atria and ventricles, conduction of impulses may occur locally through gap junctions. Reentry

Photo: Transmission of the cardiac impulse through the heart, showing the time of appearance (in fractions of a second after initial appearance at the sinoatrial node) in different parts of the heart.

All impulses from a normal functioning heart will come from the SA node. From the SA node, the impulse will be transmitted to the AV node and transmission of impulses from the SA node to the AV node is facilitated by means of three internodal tracts: anterior internodal tract of Bachmann, middle internodal tract of Wenckeback and posterior internodal tract of Thorel. Take note that the tips of the fibers of the SA node are directly connected to the right atrial muscle cells so there is direct transmission of impulses from the SA node to the right atrium. 7 Shannen Kaye B. Apolinario, RMT

Photo: The role of unidirectional block in re-entry. In A, an excitation wave traveling down a single bundle (S) of fibers of continues down the left (L) and right (R) branches. The depolarization wave enters the connecting branch (C) from both ends and is extinguished at the zone of collision. In B, the wave is blocked in the L and R branches. In C, a bidirectional block exists in branch R. in D, a unidirectional block exists in branch R. the antegrade impulse is blocked, but the retrograde impulse is conducted through and re-enters bundle S.

A Normal direction. Coming from the SA node to the AV node to the bundle of His. From the bundle of His, the impulse will be transmitted to the left and right bundle branches. From the left and right bundle branches to the apex of the heart but there is a connecting fiber between the right and left bundle branches. B Both left and right bundle branches are blocked so there is no impulse transmission to the apex of the heart as well as to the connecting fiber. C Only one bundle branch is blocked (right bundle branch). The impulse that is supposed to go the right bundle branch is blocked but the left bundle branch goes to its normal route to the apex and to the connecting fiber. The one that goes to the connecting fiber can now go to the apex but can also go back to the area that is blocked; this is called reentry or circus movement. D Since the right bundle branch is blocked, the transmission of impulse is blocked while that coming from the left will re-enter the area where the impulse came from, it goes round and round thats why it is called circus movement. Reentry or circus movement is possible because the distance travelled by this impulse is longer compared to other one which is blocked so it becomes refractory. Since the distance is longer, when it reaches the area that is blocked, it becomes out of refractory/out of refractoriness so it can go back. Because of this phenomenon, this is the path that is responsible for atrial or ventricular fibrillation/flatter. In the synchronised contraction, the whole atria or the whole ventricle, there is an area that will contract and there is an area that will relax. Ectopic Tachycardias Atrial contraction Ventricular contraction AV nodal delay Most of the blocks takes place in the AV node so that it will produce the 1st degree, 2nd degree and 3rd degree heart block, all of these are abnormal conditions. The normal ratio between atrial and ventricular depolarization is 1:1, so that during atrial and ventricular contraction, if the atria will contract three times, the ventricles will also contracts three times but atrial contraction happens first than ventricular contraction causing an AV nodal delay.

1st degree heart block Incomplete heart block. All impulses from the SA node can still be transmitted to the ventricles. Based on the spacings in the photo, there is atrioventricular depolarization happening. The ratio of ventricular depolarization is still 1:1. So that when it contracts three contractions in the atria, there will also be three contractions in the ventricles. The difference from the normal is that it has a longer duration of the AV nodal delay. 2nd degree heart block Not all impulses from the SA node will reach the ventricles. What happens is P-P-QRS, P-P-QRS. This time, the ratio of the atrial to ventricular depolarization is 2:1 or 3:1. Not all the impulses reach the ventricles but since there are impulses that can reach the ventricles, this is still an incomplete heart block. 3rd degree heart block Complete heart block. No impulses from the SA node will be able to reach the ventricles. What happens is P-P-P-P. The atria will be contracting normally at a rate that is dictated by the SA node; that is 75 beats per minute. Initially, the ventricle will not contract because no impulses will reach the ventricles but there are pacemaker cells in the ventricles the bundle of His and Purkinje fibers. The two are latent pacemakers and they are also automatic cells. For 20 seconds, there will be no impulse coming from the SA node, the latent pacemaker in the ventricle specifically the Purkinje fibers will be activated, it will escape from the overdrive suppression and this is called the ventricular escape. When activated, the Purkinje fibers will generate its own impulse causing the ventricles to contract at a rate that is dictated by the Purkinje fibers. If the contraction in the atria is 75 beats per minute, in the ventricle, it is 30-40 beats per minute. The firing of Purkinje fibers is slower than the SA node. Another abnormal condition is the presence of a premature contraction or an extrasystole wherein another contraction happens in response from an impulse that will not come from the SA node. For example, there is atrial contraction that is initiated by the impulse from the SA node, other parts of the atria will be activated, and there will be an ectopic fossi impulse coming from other sources. So when it contracts, if there is another impulse, there will be another contraction and this is premature contraction or extrasystole.

PHOTO: Frequency summation and tetanization

In wave summation in the skeletal muscles, if three maximal stimuli is applied successively, the magnitude of the 2nd contraction is higher than the first because in the muscle, calcium ions have not yet returned to the sarcoplasmic reticulum and when another stimuli is applied, there will be more releasing of calcium ions that will increase the force of contraction. In cardiac muscle, the magnitude of the 2nd contraction is lower than the first. Take note that extrasystole can only be elicited during the mid or late diastole. It is not able to elicit an extrasystole during systole or early diastole because of the long duration of the Absolute Refractory Period. Another contraction can be produced only during the mid or late diastole when the muscle is almost completely relaxed (Note: almost but not yet relaxed).

PHOTO: AV blocks. A, First-degree block; the PR interval is 0.28 second (normal: <0.20 sec). B, Second-degree block (2:1). C, Third-degree block; note the dissociation between the P waves and the QRS complexes

Shannen Kaye B. Apolinario, RMT

Remember that one of the important factors that will determine the force of cardiac muscle contraction is the volume of blood that will stretch the muscle before contraction. The longer the relaxation phase, the more blood will be filled in the ventricles, the greater the stretch of the cardiac muscle will be and the greater the force of contraction will be. There is a decrease in the magnitude of the 2nd contraction because the relaxation phase is not yet complete so the filling of the blood is less resulting to less stretch of the muscle and less force of contraction. 4th Property: Contractility Important characteristic of a cardiac muscle: Involuntary. Activity of the heart is not controlled by the cerebral cortex, it is controlled by the autonomic nervous system although there are automatic cells present in the heart. Smaller. Compared to skeletal muscle cell, the cardiac muscle cell is smaller Either binucleated or mononucleated Striated. Just like the skeletal muscle cell, the cardiac muscle is striated. Striated means that the muscle fibers are distinctly separated from one another. What separates the individual muscle fibers is the Z line that is why the area between two Z lines will form a sarcomere. The difference between the skeletal and cardiac muscle cell is that the membrane of the cardiac muscle branches out to reconnect with the membrane of the next muscle fiber so that the force generated with one muscle fiber can be transmitted to the other muscle fibers as well.

Nebulin forms the scaffold of the thin filament actinin will connect the thin filament to the Z line Titin connects the thick filament to the Z line Tropomodulin regulates the length of the thin filament

Elastic tissue. Fair amount of elastic tissue that will enable the chambers of the heart to dilate to accommodate a greater volume of blood. Connective tissue. Presence of connective tissue that will prevent over distension or overstretching of a cardiac muscle when the cardiac size increases. More mitochondria and active capillaries. Compared to the skeletal muscle, there are more mitochondria as well as active capillaries in the cardiac muscle and that is important because the main source of energy for cardiac muscle contraction is oxidative metabolism. Sarcoplasmic reticulum. The sarcoplasmic reticulum in the cardiac muscle is less well developed. Meaning to say, it cant store large quantities of calcium ions that will provide for full contraction so there has to be another source of Ca++ for the cardiac muscle contraction and that is the extracellular fluid (ECF). And because the transverse tubular system in the cardiac muscle is more developed it has a bigger diameter; it can allow more Ca++ from the ECF to enter the cardiac muscle cell.

PHOTO: Syncytial, interconnecting nature of cardiac muscle fibers.

Presence of the intercalated disk. The intercalated disk is present on the Z line. Its function is to separate one muscle fiber from another but at the same time, to connect one muscle fiber to another by means of gap junctions. Present in the intercalated disk are channels that will allow ions to flow freely from one muscle fiber to the next so that when an action potential is generated anywhere in a bundle, it can be transmitted rapidly causing the whole bundle to be depolarized at the same time and to contract as a single unit and this is called a syncytial type of arrangement of muscle fibers. The cardiac muscle cell anatomically is striated but functionally or physiologically, it is a syncytium. The syncytial arrangement of muscle fibers is important because it will provide synchronized contraction of the atria and ventricles that is important for the pumping action of the heart. It will also provide synchronized relaxation of the atria and ventricles that is important for filling of blood in the different chambers of the heart. Contractile proteins present: Thick filament - myosin Thin filament actin, troponin, tropomyosin Meromyosin, C protein forms the scaffold or suport of the thick filament 9 Shannen Kaye B. Apolinario, RMT

PHOTO: Cardiac muscle (panel A) has high resistance to stretch when compared with skeletal muscle (panel B). When either cardiac or skeletal muscle is stretched, there is an increase in resting tension (RT). If the muscle is then stimulated to contract maximally, it generates more tension (termed total tension TT). The difference between total tension and resting tension at any given length is the force produced by contraction (e.g. active tension AT). The bell-shaped dependence of active tension on muscle length is consistent with the sliding filament theory of cardiac and skeletal muscle. It is, however, difficult to stretch cardiac muscle beyond its optimal sarcomere length, as evidenced by the rapid rise in resting tension in the middle of the bell-shaped AT curve.

Above is a graph that shows the importance of the presence of elastic tissue in the cardiac muscle. The blue line represents the resting tension tension that develops in the muscle before contraction. The red line represents active tension tension that develops in the muscle during contraction. Because of the many elastic tissue in the cardiac muscle, even in the resting state or resting length, passive tension increases in the muscle and it can dilate so that when the cardiac muscle fiber contracts, the difference between active and passive tension is smaller compared to skeletal muscle. The importance of that is the different chambers of the heart can accommodate a large volume of blood with little increase in pressure. Excitation-Contraction Coupling

potassium ions pumped into the cell so that it will create a concentration gradient for sodium increased concentration outside, low concentration on the inside. That will now activate the sodium-calcium exchange pump that will pump three Na+ in, in exchange for one Ca++ that is pumped out of the cell and that is the main means by which Ca++ is extruded from the cardiac muscle cell. In patients suffering from heart failure, the main problem is poor force of contraction of the ventricle. This poor force of contraction has to be made strong by giving cardiac glycosides (e.g. digitalis). The main mechanism of action of cardiac glycosides is to inhibit the sodiumpotassium pump. If this pump is inhibited, Na+ will not be extruded so that will not create a concentration gradient for Na+. If there is no concentration gradient for Na+, nothing will activate the sodium-calcium pump so Ca++ will remain inside the cell and that can be utilize to increase the force of ventricular contraction. Arrangement of Muscle Fibers When the heart contracts, it rotates slightly to the right and that will expose the cardiac apex. The heart can rotate when it contracts because of the arrangement of muscle fibers. The arrangement of muscle fibers is synospiral and bulbospiral. Autonomic Innervation of the Heart How does the Autonomic Nervous System (ANS) regulates the cardiac activity? Sympathetic: T3 T4 T5 SA node AV node Purkinje system Atrial muscle Ventricular muscle

Norepinephrine + 1 receptor

PHOTO: Excitation-contraction coupling in the heart requires Ca++ influx through L-type Ca++ channels in the sarcolemma and T tubules.

Present on the membrane or sarcolemma is a calcium pump, calcium-sodium exchange pump, sodium-potassium exchange pump and the last two are antiporters. Invagination of the sarcolemma will form the T-tubules. Present on the membrane of the T-tubules are voltage-gated calcium channels. Inside the cell, there are myofilament and sarcoplasmic reticulum (SR). On the membrane of the sarcoplasmic reticulum is another calcium pump. Also on the membrane of SR are ryanodine receptors and these receptors are calcium-gated calcium channels. What happens is when a membrane is depolarized, this will activate the voltage-gated calcium channels of the membrane of the T tubule and that will allow Ca++ to enter from the extracellular fluid (ECF) to the inside of the cardiac muscle cell. Some of this Ca++ will immediately bind with troponin C forming the calcium-troponin C complex that will initiate muscle contraction but some of the Ca++ will bind with the ryanodine receptors on the membrane of SR activating the calcium-gated calcium channels that will allow Ca++ to move out from the SR to the cytoplasm to bind with troponin C. The difference of this from the skeletal muscle is that the Ca++ from the SR will not move out unless there is a trigger that will cause the Ca++ to move out. The trigger is also Ca++ from the ECF that will bind with ryanodine receptors hence it is called calcium-gated calcium channels. It needs Ca++ from ECF to trigger movement of Ca++ from SR into the cytoplasm. That is why it has two sources of Ca++ compared to skeletal muscle the SR and ECF. If there already many Ca++, the force of contraction is stronger. With repolarization, it is expected that the muscle will relax but for the muscle relax; Ca++ has to be removed. Ca++ is removed by the activity of calcium pump on the membrane of the SR that will actively transport Ca++ back into the SR. Another means to remove Ca++ is through the activity of the calcium pump on the sarcolemma that will actively transport Ca++ back into the ECF. But the most important means by which calcium is extruded from the cardiac muscle cell is through the activity of the sodium-calcium antiporter. Initially, with repolarization, the sodium-potassium pump is activated that will pump three sodium ions out in exchange for two 10 Shannen Kaye B. Apolinario, RMT

First, the sympathetic nerves that innervate the heart originate from T3, T4, and T5 segments (T = thoracic). Pre-ganglionic fibers from T3, T4 and T5 will synapse with the sympathetic ganglia and this is called the sympathetic chain. Post-ganglionic fibers from the sympathetic chain will bind with 1 receptors in the heart and the neurotransmitter agent (NTA) released by these sympathetic nerves is norepinephrine (NE). The effect of NE at the myocardial cells is to increase membrane permeability to Ca++ and Na+ so that will make the myocardial cell more excitable and therefore increased cardiac activity. Sympathetic nerves innervate ALL structures in the heart either automatic and non-automatic so that will include the sinoatrial (SA) node, atrioventricular (AV) node, ventricular conduction system or the Purkinje system as well as the atrial and ventricular muscle. Parasympathetic: CN 10 Acetylcholine + M2 SAN AVN Atrial muscle

On the other hand, parasympathetic innervation to the heart is carried by the vagus nerve which originates from the medulla. So the vagus nerve will bind with muscarinic 2 receptors in the heart and the NTA released is acetylcholine (Ache). The effect of Ache on the myocardial cells is to increase membrane permeability to K+ so that will hyperpolarize the myocardial cells inhibiting them or decreasing cardiac activity. The structures in the heart that receive parasympathetic or vagal innervation are the SA node, AV node, only the proximal part of the bundle of His, atrial muscle, and there is very little, if any, vagal innervation to the ventricles. Chronotropic regulation: Sympathetic Increased frequency of discharge of the SA node Increased the heart rate Parasympathetic Decreased frequency of discharge by the SA node Decreased the heart rate

In relation to this, lets look at how the autonomics regulate cardiac activity: First, regulation of heart rate is called chonotropic regulation. The sympathetic nervous system will increase the activity of the SA node so that this stimulation will increase the frequency of discharge of action potentials from the SA node, increasing the heart rate. On the other hand, parasympathetic or vagal stimulation will inhibit the SA node, decreasing the heart rate. Dromotropic regulation Sympathetic Increased velocity of conduction Decreased duration of AV nodal delay Parasympathetic Decreased velocity of conduction Increased duration AV nodal delay Regulation of the velocity of conduction of impulses in the heart is called dromotropic regulation. Sympathetic stimulation will increase the velocity of conduction of impulses in the heart so it will decrease the duration of the AV nodal delay. In contrast, parasympathetic stimulation decreases the velocity of conduction of impulses in the heart prolonging the duration of the AV nodal delay. *** In parasympathetic or VAGAL stimulation, buma-VAGAL ang heart rate and velocity of conduction. Inotropic regulation Sympathetic Increased force of atrial and ventricular contraction Parasympathetic Decreased force of atrial contraction Regulation of the force contraction of the myocardial cells or inotropic regulation is by increasing membrane permeability to Ca++. Sympathetic stimulation increases the force of contraction of both the atria and ventricles. As for parasympathetic stimulation, it decreases the force of atrial contraction and it has no direct effect on the force of ventricular contraction. It has no direct effect but it has an indirect effect, that is, parasympathetic stimulation will prolong the duration of the AV nodal delay allowing more time for ventricular filling so the more the ventricles are filled with blood, the more the ventricular wall is stretched, and the greater will be the force of ventricular contraction. Cardiac Cycle Cardiac cycle is the sequence of events - electrical and mechanical events taking place in the heart from the beginning of one heart beat initiated by an impulse from the SA node to the beginning of the next heart beat also initiated by an impulse from the SA node. Electrical events depolarization, repolarization of the atria and depolarization and repolarization of the ventricle Mechanical events contraction or relaxation of the atria and ventricles Electrical events The electrical events will precede the mechanical events. All the electrical events taking place in the heart can be recorded by the electrocardiogram (ECG). To get an ECG tracing, electrodes are placed on the four extremities of the subject as well as on different locations on the chest wall. This electrodes act as sensors so that it will be able to pick up electrical potentials produced by the myocardial cells so that what is seen on the ECG tracing will represent electrical potentials and electrical activities of the myocardial cell. By placing electrodes particularly on the four extremities, bipolar limb leads are formed or standard limb leads. There are three bipolar limb leads Lead I, II and III. These leads will represent electrical potential difference between two electrodes placed on two different extremities. In order to have an electrical potential difference between two electrodes, one electrode is arbitrarily designated as the negative electrode and the other one is the positive electrode.

Lead I represent electrical potential difference between electrodes that are placed on the right arm and on the left arm. In lead I, the electrode that is on the right arm is the negative electrode that of the left arm is the positive electrode. Lead II represents electrical potential difference between electrodes that are placed on the right arm and on the left leg. The electrode of the right arm is designated as the negative electrode that of the left leg as the positive electrode. Lead III represents electrical potential difference between electrodes that are placed on the left arm and on the left leg. The electrode of the left arm is designated as the negative electrode that of the left leg as the positive electrode.

PHOTO: Einthoven triangle illustrating the electrocardiographic connections for standard limb leads I, II, and III.

The electrode that is placed on the right arm is always negative and on the left leg, it is always positive. In one lead, the electrode is positive when it is located nearer on the apex of the heart. Lead II will approximate the direction of impulse transmission in the heart. So that when asked to measure the duration of the different ECG waves, the amplitude of the different ECG waves, it is preferable to use lead II because it approximates the direction of impulse transmission in the heart right arm is negative, left leg is positive (from base to apex).

Right arm (negative)

Left leg (positive)


Lead II

11

Shannen Kaye B. Apolinario, RMT

repolarization, it will appear as a downward or negative deflection because the direction of repolarization in the atria follows the direction of depolarization repolarization is toward a positive electrode. This means that in the atria, the first part to depolarize is also the first part to repolarize and the last to depolarize is also the last part to repolarize. When the impulse reaches the AV node, there will an AV nodal delay ad that is represented by the straight line called a P-Q or P-R segment. The P-R segment starts at the end of P up to the beginning of the QRS complex. It is a straight or isoelectric line because of the delay on the impulse transmission at the AV node. From the beginning of P to the beginning of the QRS complex is the P-R interval. The P-R interval will cover the P wave representing atrial depolarization and the P-R segment that represents AV nodal delay.

P-R segment (isoelectric)

S-T segment (isoelectric)

PHOTO: Depolarization of interventricular septum from the left to right bundle branch PHOTO: Important deflections and intervals of a typical scalar ECG.

Above is an example of an ECG tracing that shows electrical events in the heart in one cardiac cycle. The P wave represents atrial depolarization, QRS wave or complex represents ventricular depolarization, and T wave represents ventricular repolarization. ECG Rules: Depolarization (+) electrode = upward

QRS complex will represent ventricular depolarization. It is a complex made up of three waves. In the QRS complex, there is an initial negative or downward deflection that represents depolarization of the interventricular septum which will occur from left bundle branch to right bundle branch. The positive electrode is in the left leg [it is moving from the left to right bundle branch] so it is moving away from a positive electrode that is why the Q wave which represents the depolarization of the interventricular septum and is recorded as a downward or negative deflection. R wave is a very high positive deflection that represents depolarization of the cardiac apex that is definitely towards a positive electrode. Then there is a second downward deflection which is the S wave. So which part of the heart will depolarize last? Usually it goes from the anterobasal apex posterobasal so when the wave of depolarization moves from the apex to posterobasal part, again it is moving away from a positive electrode so the S wave which represents depolarization of the posterobasal part of the ventricle is recorded as negative or downward deflection. T wave is only a part of ventricular repolarization because ventricular repolarization starts at the end of QRS complex. So from the end of S wave to the beginning of T wave, there is an isoelectric line or the S-T segment. Recall the action potential generated in the ventricle, the phase of repolarization that represents the S-T segment is the plateau or phase II. There is a straight line because of the equal conductance of Ca+ and K+; there is no change in membrane potential. The T wave will represent only the phase III of repolarization or the final phase of repolarization and it is a positive or upward deflection. In the ventricles, the repolarization does not follow the direction of depolarization, unlike in the atria. Repolarization will occur in the opposite direction: from posterobasal apex anterobasal. It is moving away from a positive electrode because from the apex, it will go up hence it is recorded as an upward or positive deflection. So in the ventricles the first part of the ventricles that will depolarize is the last part to repolarize and the last part to depolarize will be the first part to repolarize. So when it is said ventricular repolarization, it is actually the S-T interval, from the end of S to the end of T, not just the T wave. Mechanical events Following depolarization, the atrial and ventricular muscles will contract and it is called the systole. During systolic phase of the

Depolarization away from (+) electrode = downward Repolarization (+) electrode = downward

Repolarization away from (+) electrode = upward Why is there an upward or positive deflection and a downward or negative deflection? The rule in ECG is that if depolarization will move towards a positive electrode, it is recorded as an upward or positive deflection. On the other hand, if depolarization will move away from a positive electrode, it is recorded as a downward or negative deflection. In repolarization, if the electrode moves toward a positive electrode, it is recorded as positive or downward deflection and if repolarization will move away from a positive electrode, it is recorded as an upward or positive deflection. Remember that in lead II, the positive electrode is on the left leg.

P wave

P wave - atrial depolarization, it is a positive deflection. Remember that the impulse is generated from the SA node transmitted to the AV node so the direction of impulse transmission in the atria is it moves towards a positive electrode. That is why the P wave is recorded as an upward deflection. There is no ECG wave that represents atrial repolarization because atrial repolarization occurs simultaneously with ventricular depolarization. If ever there is an ECG wave that will represent atrial 12 Shannen Kaye B. Apolinario, RMT

cardiac cycle, blood is ejected from the different chambers of the heart. Following repolarization, the muscles will relax and it is called diastole. During diastolic phase, there will be filling of blood in the different chambers of the heart. The average duration of one cardiac cycle is 0.8 second. The duration of the systolic phase is 0.27 second and that of the diastolic phase is longer which 0.53 of a second and this happens at the heart rate of 75 beats per minute. When the heart rate increases, the duration of the cardiac cycle will decrease so the duration of the systole and diastolic phases is also decreased. But there is a greater decrease in the duration of the diastolic phase and there is a constant duration in the systolic phase when the heart rate increases. Correlation of the Electrical and Mechanical Events in the Heart in One Cardiac Cycle SAN atr. depo (P wave) AVN VCS delay (P-R segment) vent. depo (QRS) atr. repo VP > AP atr. systole inc. VF vent. systole atr. diastole inc. VP dec. AP 20% VF inc. AP (a wave)

An impulse will be generated from the SA node transmitted to the AV node. Transmission of the impulse from the SA node to the AV node is facilitated by the three internodal tracts: Bachman, Wenckeback and Thorel. In the process, the atria will undergo depolarization recorded in the ECG as the P wave. The response of the atrial muscle to depolarization is to contract so there will be atrial systole. When the atria contracts, although it is a weak pump, there is still blood ejected to the ventricles and that will account for only 20% of ventricular filling. When the atria are contracting, atrial pressure increases and remember that there are no cardiac valves between the atria and veins so that any increase in atrial pressure can be transmitted to the veins so that in the recording of the jugular venous pressure curve will show increase atrial pressure during atrial systole and this is called A wave. A wave is not an ECG tracing, it is only a label to the increase atrial pressure during atrial systole. When the impulse reaches the AV node, there will be a delay called the AV nodal delay, in the ECG that is recorded as the P-R segment. The importance of the AV nodal delay is that it will provide more time for ventricular filling. From the AV node, the impulse will now be transmitted to the ventricular conduction system (VCS) or Purkinje system and that will cause ventricular depolarization in the ECG recorded as the QRS complex. The response of the ventricular muscle to depolarization is to contract so following ventricular depolarization will be ventricular systole. When the ventricles contract, the ventricular pressure increases. Simultaneous with ventricular depolarization is atrial repolarization and no ECG wave represents atrial repolarization. The response of the atrial muscle to repolarization is to relax so atrial diastole happens. Since the atria is relaxed, there will be a decrease in the atrial pressure. When the ventricular pressure exceeds atrial pressure, there will be a pressure gradient and that will now close the AV valves therefore the first heart sound will be heard. There will be a condition wherein the SL are still closed and the AV valves are now closed, there is no change in ventricular volume because all the cardiac valves are closed but since the ventricles are contracting, there is increase in ventricular pressure and this is called isovolumic or isovolumetric contraction phase of the cardiac cycle. When the ventricles are contracting, ventricular pressure still increases and this high pressure may push the AV valves to bulge into the atria and that will cause a slight increase in atrial pressure which is now called the C wave. But remember that the AV valves does not over-bulge into the atria when the ventricular pressure is increased because when the ventricles contract, the papillary muscles will contract pulling the chordae tendinae which will prevent over-bulging of the AV valves into the atria resulting to only a slight increase in the atrial pressure. When ventricular pressure exceeds 80 mmHg, this will push open the SL valves and following the opening of the SL valves is the period of rapid ejection of blood from the ventricles to the arteries: aorta and pulmonary arteries. But when it is ejecting more and more blood, the volume of the blood in the ventricles as well as ventricular pressure will start to decrease. So the period of rapid ejection will now be followed by a period of reduce ejection of blood from the ventricles to the arteries and at the same time, the blood that is contained in the aorta will drop off to the arteries to the different organs of the body and the veins are also collecting blood so that little by little, there will be atrial filling. The ventricles will undergo repolarization so this is the S-T interval in the ECG. The response of the ventricular muscle to repolarization is to relax so there will be ventricular diastole therefore ventricular pressure will start to decrease. Pressure in the aorta or in the arterial system is always high so that when arterial or aortic pressure now exceeds ventricular pressure, this will close the semilunar valves and that will produce the second heart sound. But there is a short interval of time between ventricular diastole and closure of SL valves which is called protodiastole. There will be a condition again wherein the SL valves are now closed, the AV valves are still closed so there is no change in ventricular volume but since the ventricles are in a relaxed state, ventricular pressure decreases and this is called isovolumic relaxation. At the same

close AV valves (1st heart sound)

isovolemic contractions: slight inc. AP (C wave) VP > 80 mmHg open SL valves rapid ejection reduced ejection; atrial filling vent. repo vent. diastole dec. VP (S-T interval) AP > VP protodiastole close SL valves (2nd heart sound) isovolemic relaxation; inc. atr. filling; inc. AP (V wave) AP > VP open AV valves rapid inflow diastasis reduced inflow of blood to the ventricles atr. atrial AV - antrioventricular AVN atrioventricular node dec. - decrease depo depolarization inc. - increase repo repolarization SAN sinoatrial node SL - semilunar vent. ventricular/ventricle VF- ventricular filling VP ventricular pressure

At the beginning of one cardiac cycle, before an impulse is generated from the sinoatrial (SA) node, the atrium and ventricles are all relaxed atrial systole and ventricular diastole. The semilunar (SL) valves are closed but the atrioventricular (AV) valves are open so that will allow blood to flow from the atria to the ventricles. In fact, 80% of ventricular filling (VF) takes place when all four chambers of the heart are in a relaxed state. It is not needed for the atria to contract to have ventricular filling because its contraction is weak primer pump, so whenever the AV valves are open, there is 80% of ventricular filling. 13 Shannen Kaye B. Apolinario, RMT

time as isovolumic relaxation, the atrial filling increases which will again increase atrial pressure and is called the V wave. When atrial pressure exceeds ventricular pressure, this will now open the AV valves which will be followed by a period of rapid inflow of blood to the ventricles and this event will account for the 80% of ventricular filling. When there is more blood filled in the ventricle, it will be slightly stabilized so that the period of rapid inflow will be followed by a period of reduced inflow of blood to the ventricles called diastasis. From that, there will be another impulse from the SA node beginning another cycle. All of these events take place in the heart for 0.8 second. Cardiac Cycle

Ventricular pressure is initially low. It will increase slightly during atrial systole because of the additional volume of blood that will be ejected by the atria to the ventricles. Ventricular pressure will actually increase during isovolumic contraction and still high during the period of ejection of blood. But as the volume of blood in the ventricles decreases, ventricular pressure will also decrease. It will continue to decrease during the period of isovolumic relaxation. It will remain low during the periods of rapid inflow of blood to the ventricles and diastasis. Again, slight increase with atrial systole because of the additional volume of blood ejected from the atria to the ventricles. Closing of the AV valves will mark the onset of isovolumic contraction. Remember that in isovolumic contraction, all the cardiac valves are closed so there will be no change in the volume of ventricles. So that means at that point, the first heart sound will be heard. Opening of the AV valves mark the end of isovolumic relaxation so there will be period of ventricular filling. What will happen at the end of isovolumic contraction? There will be opening of the SL valves. While at the beginning of isovolumic relaxation, the SL valves close so the second heart sound will be heard. Atrial Pressure Curve incisura

Phases:

as atrial systole ic isovolumic contraction ejection rapid and reduced ejection phase ir isovolumic relaxation R inflow rapid inflow of blood to the venticles diastasis as atrial systole

The period of ventricular systole covers from the beginning of isovolumic contraction until the end of the ejection phase while the ventricular diastole will start with isovolumic relaxation up to the end of atrial systole. Ventricular Pressure Curve SL valves open SL valves close 2nd heart sound ***Atrial pressure curve yellow dotted line Aortic pressure or arterial pressure is always high. It will continually increase during the period of rapid ejection because of the increased volume that will be ejected from the ventricle to the aorta. So if the volume of blood in the aorta is greater, there will be greater force exerted by that volume of blood on the aortic wall. During the period of reduced ejection, the aortic pressure decreases because there will be peripheral run-off blood, meaning to say, blood that is contained in the aorta will now be distributed to the arteries, to the arterioles, and to the different organs of the body so the volume of blood in the aorta will decrease and that will now cause the aortic wall to recoil. When the aortic wall recoils, there is a slight vibration of blood inside so there will be slight increase again in aortic pressure which is called a dichotic notch or incisura. All throughout the period of ventricular diastole, the aortic pressure is stable and is slightly low but it is still higher compared to the ventricular pressure. The pressure difference between the aorta and the ventricles will cause the closing of the SL valves when aortic pressure exceeds ventricular pressure.

*** Ventricular pressure curve green line 1st heart sound 14 AV valves open

Shannen Kaye B. Apolinario, RMT

Ventricular Volume Curve

The 3rd heart sound heard in abnormal conditions is due to ventricular filling. There is an increase in ventricular filling coinciding with the appearance of the 3rd heart sound.

At the start, there is additional increase in volume with atrial systole additional 20% of ventricular filling. During isovolumic contraction, all cardiac valves are closed so there is no change in the ventricular volume. During period of rapid ejection, blood is ejected from the ventricles so the ventricular volume will decrease. In the period of isovolumic relaxation, all cardiac valves are closed so there is no change in ventricular volume. During the period of rapid inflow, there is a very high increase in ventricular volume. It is somewhat stabilized in diastasis and a slight increase again during atrial systole. Atrial Pressure or Central Venous Pressure (CVP) Curve

c c

PHOTO: Left atrial, aortic, and left ventricular pressure pulses correlated in time with aortic flow, ventricular volume, heart sounds, venous pulse, and the electrocardiogram for a complete cardiac cycle.

Ventricular Volume Pressure Curve (Ejection Loop) A wave is increase in atrial pressure during atrial systole. C wave is slightly increased in atrial pressure during isovolumic contraction when the increased ventricular pressure pushes the AV valves to bulge into the atria. The V wave is increase atrial pressure during isovolumic relaxation where it is simultaneous with the increase in atrial filling. Heart Sounds The 1st heart sound is due to closure of the AV valves. Closure of the AV valves will mark the onset of the period of isovolumic contraction so when seen at the ventricular volume curve, it is a straight line no change in ventricular volume. The 2nd heart sound is due to the closure of the SL valves that will now mark the onset of the period of isovolumic relaxation. Again, there is no change in the ventricular volume. 15 Shannen Kaye B. Apolinario, RMT

PHOTO: Relationship between left ventricular volume and intraventricular pressure during diastole and systole. Also shown by the heavy red lines is the volume-pressure diagram, demonstrating changes in intraventricular volume and pressure during the normal cardiac cycle. EW, net external work.

Reduced ejection

Rapid ejection

Volume of blood remain on ventricles after contraction

PHOTO: Pressure-volume loop

The vertical axis will represent changes in ventricular pressure, the unit is mmHg. The horizontal axis represents changes in ventricular volume and the unit is either cc or mL. In relation to changes in ventricular volume and pressure, the cardiac cycle is divided into four phases. The letters represent each point. Point A - ventricular volume is 50 mL. This 50 mL is actually the volume of blood remaining in the ventricles after contraction. At 50 mL, the pressure is low a little above 0 mmHg. At point A, the atrioventricular valves open. Phase I from 50 mL, the volume of blood in the ventricles increased to 120 or 130 mL but there is little increase in pressure. Phase I is ventricular filling. Point B - the volume of blood is 130 mL. There is closing of the AV valves so the first heart sound is heard. Phase II the volume of blood is 130 mL and the pressure continues to increase. At phase II, there is period of isovolumic contraction. Point C opening of SL valves. When the SL valves open, the ventricular pressure still increases but the volume is already decreasing. From C prime, it is the period of rapid ejection. Phase III in the latter part of Phase III the volume decreases and the pressure decreases, this is now the reduced ejection. Point D closing of the SL valves so the second heart sound is heard. Phase IV the volume of blood is still 50 mL but the pressure is decreasing and decreasing. This is isovolumic relaxation. I can do EVERYTHING through Him who gives me strength -Philippians 4:13 GOD BLESS YOU!

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Shannen Kaye B. Apolinario, RMT