I.

Introduction
Myocardial Infarction

Death of myocardial cells as a result of coronary artery occlusion

The irreversible necrosis of heart muscle secondary to prolonged ischemia
AKA Heart Attack
The damage and death of heart muscle from the sudden blockage of a coronary artery by a blood
clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen

Classification of myocardial infarction

Spontaneous Myocardial Infarction (MI Type 1)

This is an event related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or

dissection with resulting intraluminal thrombus in one or more of the coronary arteries, leading to
decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The
patient may have underlying severe CAD but, on occasion (5 to 20%), non-obstructive or no
CAD may be found at angiography, particularly in women.

Myocardial Infarction Secondary to an Ischemic Imbalance (MI Type 2)

In instances of myocardial injury with necrosis, where a condition other than CAD contributes to
an imbalance
between myocardial
oxygen supply
and/or demand, the
term 'MI type 2' is
employed. In
critically ill patients,
or in patients
undergoing major
(non-cardiac)
surgery, elevated
values of cardiac
biomarkers may
appear, due to the
direct toxic effects of
endogenous or
exogenous high
circulating
catecholamine
levels. Also coronary
vasospasm and/or
endothelial dysfunction have the potential to cause MI.

Cardiac Death Due to Myocardial Infarction (MI Type 3)

Patients who suffer cardiac death, with symptoms suggestive of myocardial ischemia
accompanied by presumed new ischemic ECG changes or new LBBBbut without available
biomarker valuesrepresent a challenging diagnostic group. These individuals may die before
blood samples for biomarkers can be obtained, or before elevated cardiac biomarkers can be
identified. If patients present with clinical features of myocardial ischemia, or with presumed new
ischemic ECG changes, they should be classified as having had a fatal MI, even if cardiac
biomarker evidence of MI is lacking.

Myocardial Infarction Associated With Revascularization Procedures (MI Types 4 and 5)

Periprocedural myocardial injury or infarction may occur at some stages in the instrumentation of
the heart that is required during mechanical revascularization procedures, either by PCI or by
coronary artery bypass grafting (CABG). Elevated cTn values may be detected following these
procedures, since various insults may occur that can lead to myocardial injury with necrosis. It is
likely that limitation of such injury is beneficial to the patient: however, a threshold for a
worsening prognosis, related to an asymptomatic increase of cardiac biomarker values in the
absence of procedural complications, is not well defined. Subcategories of PCI-related MI are
connected to stent thrombosis and restenosis that may happen after the primary procedure.

Definition of terms

II.

Coronary artery occlusion The sudden complete occlusion of a coronary artery causes death of
the area of muscle served by that artery (a myocardial infarct).
Necrosis Death of a body tissue. It occurs when there is not enough blood flowing to the tissue,
whether from injury, radiation, or chemicals.
Ischemia an inadequate blood supply to an organ or part of the body, especially the heart
muscles.
Myocardial cells Cardiac muscle cells or cardiomyocytes (also known as myocardiocytes or
cardiac myocytes) are the muscle cells (myocytes) that make up the cardiac muscle.
Epidemiology

HTN is the most prevalent CVD in the United States and one of the most powerful contributors to
cardiovascular morbidity and mortality. HTN occur when the systolic blood pressure is
consistently greater than 140 mm Hg or the DBP is equal to or greater than 90 mm Hg.
CVD remains the leading cause of death and disability in the United States. According to the
American Heart Associations Heart Disease and Stroke Statistics 2011 Update, an estimated
82,600,000 American adults (more than 1 in 3) have one or more types of CVD. Currently, HTN
occurs in 76,400,000 individuals, CHD affects 16,300,000, and heart failure is seen in 5,700,000
patients. The average annual rates of first cardiovascular events rise from 3 per 1,000 men at age
35 to 44 years to 74 per 1,000 at age 85 to 94. For women, comparable rates occur 10 years later
in life with a narrowing gap with advancing age. On average, 2,200 Americans die of CVD each
day with an average of 1 death every 39 seconds. In every year since 1900 except 1918, CVD
accounted for more deaths than any other major cause in the United States.
It is also important to note that the United States is in the midst of a demographic shift with a
remarkable increase in the diversity of the American population. By 2050, there will be a
decrease in the white non-Hispanic population to 52.5% from 75.7% in 1990. The Hispanic
population will increase to 22.5%, a change in African Americans to 15.7%, and Asian and

Pacific Islanders will account for 10.3% of the population. These statistics will have a major
impact on the epidemiology, pathophysiology, and treatment of CVD in the forthcoming years.
Thus, within the United States and worldwide, we are faced with major challenges as CVD
dominates as a major cause of death and disease. This chapter provides a review of normal
anatomy and physiology of the cardiovascular system and its relevance to physical therapist
practice followed by a discussion of various pathologies and pertinent physical therapy
implications.
III.

Anatomy, Physiology and

Kinesiology

Heart
The heart is a hollow
muscular organ that is
somewhat pyramid shaped
and lies within the
pericardium in the
mediastinum. It is connected
at its base to the great blood
vessels but otherwise lies free
within the pericardium. The
heart lies within the left
thoracic cavity.
The heart is composed of
three major types of cardiac
muscle: atrial muscle,
ventricular muscle, and
specialized excitatory and
conductive muscle fibers. The
atrial and ventricular types of
muscle contract in much the
same way as skeletal muscle,
except that the duration of
contraction is much longer. Conversely, the specialized excitatory and conductive fibers contract
only feebly because they contain
few contractile fibrils; instead, they
exhibit either automatic rhythmical
electrical discharge in the form of
action potentials or conduction of
the action potentials through the
heart, providing an excitatory
system that controls the rhythmical
beating of the heart.

Surfaces of the heart

The heart has three surfaces:
sternocostal (anterior),

diaphragmatic (inferior), and a base (posterior). It also has an apex, which is directed downward,
forward, and to the left.
The sternocostal surface
is formed mainly by the
right atrium and the right
ventricle, which are
separated from each other
by the vertical
atrioventricular groove.
The right border is formed
by the right atrium; the left
border, by the left ventricle
and part of the left auricle.
The right ventricle is
separated from the left
ventricle by the anterior
interventricular groove.
The diaphragmatic
surface of the heart is
formed mainly by the right
and left ventricles
separated by the posterior
interventricular groove.
The inferior surface of the
right atrium, into which the
inferior vena cava opens,
also forms part of this
surface.
The base of the heart, or the posterior surface, is formed mainly by the left atrium, into which
open the four pulmonary veins. The base of the heart lies opposite the apex.
The apex of the heart, formed by the left ventricle, is directed downward, forward, and to the
left. It lies at the level of the fifth left intercostal space, 3.5 in. (9 cm) from the midline. In the
region of the apex, the apex beat can usually be seen and palpated in the living patient.

* Note that the base of the heart is called the base because the heart is pyramid shaped; the base lies
opposite the apex. The heart does not rest on its base; it rests on its diaphragmatic (inferior) surface.
Borders of the heart

The right border is formed by the

right atrium; the left border, by
the left auricle; and below, by the
left ventricle. The lower border is
formed mainly by the right
ventricle but also by the right
atrium; the apex is formed by the
left ventricle. These borders are
important to recognize when
examining a radiograph of the
heart.
Chambers of the heart

The heart is divided by vertical

septa into four chambers: the
right and left atria and the right
and left ventricles. The right
atrium lies anterior to the left
atrium, and the right ventricle lies
anterior to the left ventricle. The
walls of the heart are composed
of cardiac muscle, the
myocardium; covered externally with serous pericardium, the epicardium; and lined internally
with a layer of endothelium, the endocardium.

The right atrium

The right atrium consists of a main cavity and a small outpouching, the auricle. On the outside of
the heart at the junction between the right atrium and the right auricle is a vertical groove, the
sulcus terminalis, which on the inside forms a ridge, the crista terminalis. The main part of the
atrium that lies posterior to the ridge is smooth walled and is derived embryologically from the
sinus venosus. The part of the atrium in front of the ridge is roughened or trabeculated by bundles
of muscle fibers, the musculi pectinati, which run from the crista terminalis to the auricle. This
anterior part is derived embryologically from the primitive atrium.

Openings of the
right atrium
o

o
o
o

The
superior
vena cava
opens into
the upper
part of the
right
atrium; it
has no
valve. It
returns the
blood to
the heart
from the
upper half
of the
body. The
inferior
vena cava
(larger than
the superior vena cava) opens into the lower part of the right atrium; it is guarded by a
rudimentary, nonfunctioning valve. It returns the blood to the heart from the lower half of
the body.
The coronary sinus, which drains most of the blood from the heart wall, opens into the
right atrium between the inferior vena cava and the atrioventricular orifice. It is guarded
by a rudimentary, nonfunctioning valve.
The right atrioventricular orifice lies anterior to the inferior vena caval opening and is
guarded by the tricuspid valve.
Many small orifices of small veins also drain the wall of the heart and open directly into
the right atrium.

The right ventricle

The right ventricle communicates with the right atrium through the atrioventricular orifice and
with the pulmonary trunk through the pulmonary orifice. As the cavity approaches the pulmonary
orifice, it becomes funnel shaped, at which point it is referred to as the infundibulum.

The walls of the right ventricle are much thicker

than those of the right
atrium and show several internal
projecting
ridges formed of muscle bundles. The projecting
ridges give the
ventricular wall a spongelike
appearance
and are known as trabeculae
carneae.
The tricuspid valve guards the
atrioventricular orifice and consists
of three
cusps formed by a fold of endocardium with some
connective
tissue enclosed: anterior, septal, and inferior
(posterior)
cusps.
The pulmonary valve guards the
pulmonary orifice and consists of three semilunar cusps
formed by folds of
endocardium with some connective tissue enclosed. The
curved lower margins
and sides of each cusp are attached to the arterial wall. The open mouths of the cusps are directed
upward into the pulmonary trunk.
The three semilunar cusps are arranged with one posterior (left cusp) and two anterior (anterior
and right cusps). (The cusps of the pulmonary and aortic valves are named according to their
position in the fetus before the heart has rotated to the left. This, unfortunately, causes a great deal
of unnecessary confusion.) During ventricular systole, the cusps of the valve are pressed against
the wall of the pulmonary trunk by the outrushing blood. During diastole, blood flows back
toward the heart and enters the sinuses; the valve cusps fill, come into apposition in the center of
the lumen, and close the pulmonary orifice.

The left atrium

Similar to the right atrium, the left atrium consists of a main cavity and a left auricle. The left
atrium is situated behind the right atrium and forms the greater part of the base or the posterior
surface of the heart. Behind it lies the oblique sinus of the serous pericardium, and the fibrous
pericardium separates it from the esophagus. The interior of the left atrium is smooth, but the left
auricle possesses muscular ridges as in the right auricle.

Openings of the left ventricle

o

The four pulmonary veins, two from each lung, open through the posterior wall and have
no valves. The left atrioventricular orifice is guarded by the mitral valve.

The left ventricle

The left ventricle communicates with the left atrium through the atrioventricular orifice and with
the aorta through the aortic orifice. The walls of the left ventricle are three times thicker than
those of the right ventricle. (The left intraventricular blood pressure is six times higher than that
inside the right ventricle.)

In cross section, the left

ventricle is circular; the
right is crescentic because
of the bulging of the
ventricular septum into
the cavity of the right
ventricle. There are
welldeveloped trabeculae
carneae, two large
papillary muscles, but no
moderator band.
The part of the ventricle
below the aortic orifice is
called the aortic
vestibule.
The mitral valve guards
the atrioventricular
orifice. It consists of two
cusps, one anterior and
one posterior, which have
a structure similar to that
of the cusps of the
tricuspid valve.
The anterior cusp is the larger and intervenes between the atrioventricular and aortic orifices. The
attachment of the chordae tendineae to the cusps and the papillary muscles is similar to that of the
tricuspid valve.
The aortic valve guards the aortic orifice and is precisely similar in structure to the pulmonary
valve. One cusp is situated on the anterior wall (right cusp) and two are located on the posterior
wall (left and posterior cusps). Behind each cusp, the aortic wall bulges to form an aortic sinus.
The anterior aortic
sinus gives origin to
the right coronary
artery, and the left
posterior sinus gives
origin to the left
coronary artery.

Structures of the heart

The walls of the

heart are composed
of a thick layer of
cardiac muscle, the
myocardium,
covered externally by
the epicardium and
lined internally by
the endocardium.
The atrial portion of the heart has relatively thin walls and is divided by the atrial (interatrial)

septum into the right and left atria. The septum runs from the anterior wall of the heart backward
and to the right.
The ventricular portion of the heart has thick walls and is divided by the ventricular
(interventricular) septum into the right and left ventricles.
The septum is placed obliquely, with one surface facing forward and to the right and the other
facing backward and to the left.
Its position is indicated on the surface of the heart by the anterior and posterior interventricular
grooves. The lower part of the septum is thick and formed of muscle.
The smaller upper part of the septum is thin and membranous and attached to the fibrous
skeleton.
The so-called skeleton of the heart consists of fibrous rings that surround the atrioventricular,
pulmonary, and aortic orifices and are continuous with the membranous upper part of the
ventricular septum.
The fibrous rings around the atrioventricular orifices separate the muscular walls of the atria from
those of the ventricles but provide attachment for the muscle fibers.
The fibrous rings support the bases of the valve cusps and prevent the valves from stretching and
becoming incompetent. The skeleton of the heart forms the basis of electrical discontinuity
between the atria and the ventricles.

Conducting system of the heart

The normal heart contracts rhythmically at about 70 to 90 beats per minute in the resting adult.
The conducting system of the heart consists of specialized cardiac muscle present in the
sinuatrial node, the atrioventricular node, the atrioventricular bundle and its right and left
terminal branches, and the subendocardial plexus of Purkinje fibers (specialized cardiac muscle
fibers that form the conducting system of the heart).

Sinuatrial node
o

The sinuatrial node is

located in the wall of the
right atrium in the upper
part of the sulcus
terminalis just to the right
of the opening of the
superior vena cava.
The node spontaneously
gives origin to rhythmic
electrical impulses that
spread in all directions
through the cardiac muscle
of the atria and cause the
muscle to contract.

Atrioventricular node
o

The atrioventricular node

is strategically placed on

o
o
o

the lower part of the atrial septum just above the attachment of the septal cusp of the tricuspid
valve.
From it, the cardiac impulse is conducted to the ventricles by the atrioventricular bundle.
The atrioventricular node is stimulated by the excitation wave as it passes through the atrial
myocardium.
The speed of conduction of the cardiac impulse through the atrioventricular node (about 0.11
seconds) allows sufficient time for the atria to empty their blood into the ventricles before the
ventricles start to contract.

Atrioventricular bundle
o

o
o
o

The atrioventricular bundle (bundle of His) is the only pathway of cardiac muscle that connects
the myocardium of the atria and the myocardium of the ventricles and is thus the only route along
which the cardiac impulse can travel from the atria to the ventricles. The bundle descends through
the fibrous skeleton of the heart.
The right bundle branch (RBB) passes down on the right side of the ventricular septum to reach
the moderator band, where it crosses to the anterior wall of the right ventricle. Here, it becomes
continuous with the fibers of the Purkinje plexus.
The left bundle branch (LBB) pierces the septum and passes down on its left side beneath the
endocardium. It usually divides into two branches (anterior and posterior), which eventually
become continuous with the fibers of the Purkinje plexus of the left ventricle.
It is thus seen that the conducting system of the heart is responsible not only for generating
rhythmic cardiac impulses, but also for conducting these impulses rapidly throughout the
myocardium of the heart so that the different chambers contract in a coordinated and efficient
manner.
The activities of the conducting system can be influenced by the autonomic nerve supply to the
heart. The parasympathetic nerves slow the rhythm and diminish the rate of conduction of the
impulse; the sympathetic nerves have the opposite effect.

Arterial supply of the heart

The arterial supply of the heart is provided by the right and left coronary arteries, which arise
from the ascending aorta immediately above the aortic valve. The coronary arteries and their
major branches are distributed over the surface of the heart, lying within subepicardial connective
tissue.

The right
coronary
artery arises
from the
anterior aortic
sinus of the
ascending
aorta and runs
forward
between the
pulmonary
trunk and the
right auricle.
It descends
almost
vertically in
the right

atrioventricular groove, and at the inferior border of the heart it continues posteriorly along the
atrioventricular groove to anastomose with the left coronary artery in the posterior
interventricular groove.
The following branches from the right coronary artery supply the right atrium and right ventricle
and parts of the left atrium and left ventricle and the atrioventricular septum.
Branches
1. The right conus artery supplies the anterior surface of the pulmonary conus (infundibulum
of the right ventricle) and the upper part of the anterior wall of the right ventricle.
2. The anterior ventricular branches are two or three in number and supply the anterior
surface of the right ventricle. The marginal branch is the largest and runs along the lower
margin of the costal surface to reach the apex.
3. The posterior ventricular branches are usually two in number and supply the diaphragmatic
surface of the right ventricle.
4. The posterior interventricular (descending) artery runs toward the apex in the posterior
interventricular groove. It gives off branches to the right and left ventricles, including its
inferior wall. It supplies branches to the posterior part of the ventricular septum but not to the
apical part, which receives its supply from the anterior interventricular branch of the left
coronary artery.
5. The atrial branches supply the anterior and lateral surfaces of the right atrium. One branch
supplies the posterior surface of both the right and left atria. The artery of the sinuatrial node
supplies the node and the right and left atria; in 35% of individuals it arises from the left
coronary artery.
6. The anterior interventricular (descending) branch runs downward in the anterior
interventricular groove to the apex of the heart. In most individuals, it then passes around the
apex of the heart to enter the posterior interventricular groove and anastomoses with the
terminal branches of the right coronary artery. In one third of individuals, it ends at the apex
of the heart. The anterior interventricular branch supplies the right and left ventricles with

numerous branches that also supply the anterior part of the ventricular septum. One of these
ventricular branches (left diagonal artery) may arise directly from the trunk of the left
coronary artery. A small left conus artery supplies the pulmonary conus.
7. The circumflex artery is the same size as the anteriorinterventricular artery. It winds around
the left margin of the heart in the atrioventricular groove. A left marginal artery is a large
branch that supplies the left margin of the left ventricle down to the apex. Anterior
ventricular and posterior ventricular branches supply the left ventricle. Atrial branches
supply the left atrium.
*The left coronary artery, which is usually larger than the right coronary artery, supplies the major part
of the heart, including the greater part of the left atrium, left ventricle, and ventricular septum. It arises
from the left posterior aortic sinus of the ascending aorta and passes forward between the pulmonary
trunk and the left auricle. It then enters the atrioventricular groove and divides into an anterior
interventricular branch and a circumflex branch.
Variations in the coronary arteries

Variations in the blood supply to the heart do occur, and the most common variations affect the
blood supply to the diaphragmatic surface of both ventricles. Here the origin, size, and
distribution of the posterior interventricular artery are variable. In right dominance, the posterior
interventricular artery is a large branch of the right coronary artery. Right dominance is present in
most individuals (90%). In left dominance, the posterior interventricular artery is a branch of the
circumflex branch of the left coronary artery (10%).

Coronary artery anastomoses

Anastomoses between the terminal branches of the right and left coronary arteries (collateral
circulation) exist, but they are usually not large enough to provide an adequate blood supply to
the cardiac muscle should one of the large branches become blocked by disease. A sudden block
of one of the larger branches of either coronary artery usually leads to myocardial death
(myocardial infarction), although sometimes the collateral circulation is enough to sustain the
muscle.

Venous drainage of the heart

Most blood from the heart wall drains into the right atrium through the coronary sinus, which lies
in the posterior part of the atrioventricular groove and is a continuation of the great cardiac vein.
It opens into the right atrium to the left of the inferior vena cava. The small and middle cardiac
veins are tributaries of the coronary sinus. The remainder of the blood is returned to the right
atrium by the anterior cardiac vein and by small veins that open directly into the heart
chambers.

Nerve supply of the heart

The heart is innervated by sympathetic and parasympathetic fibers of the autonomic nervous
system via the cardiac plexuses situated below the arch of the aorta. The sympathetic supply
arises from the cervical and upper thoracic portions of the sympathetic trunks, and the
parasympathetic supply comes from the vagus nerves.
The postganglionic sympathetic fibers terminate on the sinuatrial and atrioventricular nodes, on
cardiac muscle fibers, and on the coronary arteries. Activation of these nerves results in cardiac
acceleration, increased force of contraction of the cardiac muscle, and dilatation of the coronary
arteries.

The postganglionic parasympathetic fibers terminate on the sinuatrial and atrioventricular nodes
and on the coronary arteries. Activation of the parasympathetic nerves results in a reduction in the
rate and force of contraction of the heart and a constriction of the coronary arteries.
Afferent fibers running with the sympathetic nerves carry nervous impulses that normally do not
reach consciousness. However, should the blood supply to the myocardium become impaired,
pain impulses reach consciousness via this pathway. Afferent fibers running with the vagus nerves
take part in cardiovascular reflexes.

Action of the heart

The heart is a muscular pump. The series of changes that take place within it as it fills with blood
and empties is referred to as the cardiac cycle. The normal heart beats 70 to 90 times per minute
in the resting adult and 130 to 150 times per minute in the newborn child. Blood is continuously
returning to the heart; during ventricular systole (contraction), when the atrioventricular valves
are closed, the blood is temporarily accommodated in the large veins and atria. Once ventricular
diastole (relaxation) occurs, the atrioventricular valves open, and blood passively flows from the
atria to the ventricles.
When the ventricles are nearly full, atrial systole occurs and forces the remainder of the blood in
the atria into the ventricles. The sinuatrial node initiates the wave of contraction in the atria,
which commences around the openings of the large veins and milks the blood toward the
ventricles. By this means, blood does not reflux into the veins. The cardiac impulse, having
reached the atrioventricular node, is conducted to the papillary muscles by the atrioventricular
bundle and its branches.
The papillary muscles then begin to contract and take up the slack of the chordae tendineae.
Meanwhile, the ventricles start contracting and the atrioventricular valves close. The spread of the
cardiac impulse along the atrioventricular bundle and its terminal branches, including the
Purkinje fibers, ensures that myocardial contraction occurs at almost the same time throughout
the ventricles.
Once the intraventricular blood pressure exceeds that present in the large arteries (aorta and
pulmonary trunk), the semilunar valve cusps are pushed aside, and the blood is ejected from the
heart. At the conclusion of ventricular systole, blood begins to move back toward the ventricles
and immediately fills the pockets of the semilunar valves. The cusps float into apposition and
completely close the aortic and pulmonary orifices.

Action potentials in cardiac muscle

The action potential recorded in a

ventricular muscle fiber, averages
about 105 millivolts, which means
that the intracellular potential rises
from a very negative value, about -85
millivolts, between beats to a slightly
positive value, about +20 millivolts,
during each beat. After the initial
spike, the membrane remains
depolarized for about 0.2 second,
exhibiting a plateau as shown in the
figure, followed at the end of the
plateau by abrupt repolarization. The
presence of this plateau in the action
potential causes ventricular
contraction to last as much as 15
times as long in cardiac muscle as in
skeletal muscle.

Velocity of Signal Conduction in Cardiac

Muscle

The velocity of conduction of the

excitatory action potential signal along both atrial and ventricular muscle fibers is about 0.3 to
0.5 m/sec, or about 1/250 the velocity in very large nerve fibers and about 1/10 the velocity in
skeletal muscle fibers. The velocity of conduction in the specialized heart conductive systemin
the Purkinje
fibersis as great
as 4 m/sec in
most parts of the
system, which
allows reasonably
rapid conduction
of the excitatory
signal to the
different parts of
the heart.

Refractory Period of
Cardiac Muscle

Cardiac muscle,
like all excitable
tissue, is
refractory to
restimulation during the action potential. Therefore, the refractory period of the heart is the
interval of time, as shown to the left in Figure 94, during which a normal cardiac impulse cannot

re-excite an already excited area of cardiac muscle. The normal refractory period of the ventricle
is 0.25 to 0.30 second, which is about the duration of the prolonged plateau action potential.
There is an additional relative refractory period of about 0.05 second during which the muscle is
more difficult than normal to excite but nevertheless can be excited by a very strong excitatory
signal, as demonstrated by the early premature contraction in the second example of Figure 9
4. The refractory period of atrial muscle is much shorter than that for the ventricles (about 0.15
second for the atria compared with 0.25 to 0.30 second for the ventricles).
Control of the Heart by the Sympathetic and
Parasympathetic Nerves

The pumping effectiveness

of the heart also is controlled
by the sympathetic and
parasympathetic (vagus)
nerves, which abundantly
supply the heart. For given
levels of input atrial
pressure, the amount of
blood pumped each minute
(cardiac output) often can be
increased more than 100 per
cent by sympathetic
stimulation. By contrast, the
output can be decreased to as
low as zero or almost zero
by vagal (parasympathetic)
stimulation.

Mechanisms of Excitation of the

Heart by the Sympathetic Nerves

Strong sympathetic
stimulation can increase the
heart rate in young adult
humans from the normal rate of 70 beats per minute up to 180 to 200 and, rarely, even 250 beats
per minute. Also, sympathetic stimulation increases the force of heart contraction to as much as
double normal, thereby increasing the volume of blood pumped and increasing the ejection
pressure.
Conversely, inhibition of the sympathetic nerves to the heart can decrease cardiac pumping to a
moderate extent in the following way: Under normal conditions, the sympathetic nerve fibers to
the heart discharge continuously at a slow rate that maintains pumping at about 30 per cent above
that with no sympathetic stimulation.
Therefore, when the activity of the sympathetic nervous system is depressed below normal, this
decreases both heart rate and strength of ventricular muscle contraction, thereby decreasing the
level of cardiac pumping as much as 30 per cent below normal.

Parasympathetic (Vagal) Stimulation of the Heart

Strong stimulation of the parasympathetic nerve fibers in the vagus nerves to the heart can stop
the heartbeat for a few seconds, but then the heart usually escapes and beats at a rate of 20 to 40
beats per minute as long as the parasympathetic stimulation continues. In addition, strong vagal
stimulation can decrease the strength of heart muscle contraction by 20 to 30 per cent.
The vagal fibers are distributed mainly to the atria and not much to the ventricles, where the
power contraction of the heart occurs. This explains the effect of vagal stimulation mainly to
decrease heart rate rather than to decrease greatly the strength of heart contraction.
Nevertheless, the great decrease in heart rate combined with a slight decrease in heart contraction
strength can decrease ventricular pumping 50 per cent or more.

Effect of Temperature on
Heart Function

Increased body temperature, as occurs when one has fever, causes a greatly increased heart rate,
sometimes to as fast as double normal. Decreased temperature causes a greatly decreased heart
rate, falling to as low as a few beats per minute when a person is near death from hypothermia in
the body temperature range of 60 to 70F. These effects presumably result from the fact that heat
increases the permeability of the cardiac muscle membrane to ions that control heart rate,
resulting in acceleration of the self-excitation process.
Contractile strength of the heart often is enhanced temporarily by a moderate increase in
temperature, as occurs during body exercise, but prolonged elevation of temperature exhausts the
metabolic systems of the heart and eventually causes weakness. Therefore, optimal function of
the heart depends greatly on proper control of body temperature by the temperature control
mechanisms.

Electrical conduction of the heart

It is important to note that mechanical contraction of the ventricles only occurs with appropriate
electrical conduction through the heart. Effective contraction depends on an intact electrical
conduction system that results in depolarization of the myocardium and timely repolarization.
In normal sinus rhythm (NSR) the impulse begins in the sinus node and travels through the atria,
the AV node, bundle of His, Purkinje fibers, septum, and ventricles.
o
o
o
o
o

The P wave depicts sinus node and atrial depolarization.

The PR segment demonstrates conduction through AV node.
The QRS complex denotes electrical flow through the ventricles causing ventricular
depolarization.
The ST segment describes the initiation of ventricular repolarization.
The T wave illustrates the completion of ventricular repolarization.

Each ECG complex represents one cardiac cycle or one heartbeat. In a series of ECG complexes
representing sinus rhythm, each QRS complex should be preceded by a P wave and the QRS
complexes should be equally spaced apart, indicating a regular rhythm. ECG interpretation
enables the clinician to differentially diagnose the cause of reduced CO that may occur from a
true mechanical problem versus that occurring from an electrical problem disrupting mechanical
activity of the heart.

Blood pressure

Standard Units of Pressure

Blood pressure almost always is measured in millimeters of mercury (mm Hg) because the
mercury manometer has been used since antiquity as the standard reference for measuring
pressure. Actually, blood pressure means the force exerted by the blood against any unit area of
the vessel wall. When one says that the pressure in a vessel is 50 mm Hg, one means that the
force exerted is sufficient to push a column of mercury against gravity up to a level 50 mm high.
If the pressure is 100 mm Hg, it will push the column of mercury up to 100 millimeters.
Occasionally, pressure is measured in centimeters of water (cm H2O). A pressure of 10 cm H2O
means a pressure sufficient to raise a column of water against gravity to a height of 10
centimeters. One millimeter of mercury pressure equals 1.36 cm water pressure because the
specific gravity of mercury is 13.6 times that of water, and 1 centimeter is 10 times as great as 1
millimeter.

Resistance to Blood Flow

Units of Resistance

Resistance is the impediment to blood flow in a vessel, but it cannot be measured by any direct
means. Instead, resistance must be calculated from measurements of blood flow and pressure
difference between two points in the vessel. If the pressure difference between two points is 1 mm
Hg and the flow is 1 ml/sec, the resistance is said to be 1peripheral resistance unit, usually
abbreviated PRU.

Total Peripheral Vascular Resistance and Total Pulmonary Vascular

Resistance

IV.

The rate of blood flow through the entire circulatory system is equal to the rate of blood pumping
by the heartthat is, it is equal to the cardiac output. In the adult human being, this is
approximately 100 ml/sec. The pressure difference from the systemic arteries to the systemic
veins is about 100 mm Hg. Therefore, the resistance of the entire systemic circulation, called the
total peripheral resistance, is about 100/100, or 1 PRU. In conditions in which all the blood
vessels throughout the body become strongly constricted, the total peripheral resistance
occasionally rises to as high as 4 PRU. Conversely, when the vessels become greatly dilated, the
resistance can fall to as little as 0.2 PRU. In the pulmonary system, the mean pulmonary arterial
pressure averages 16 mm Hg and the mean left atrial pressure averages 2 mm Hg, giving a net
pressure difference of 14 mm.Therefore, when the cardiac output is normal at about 100 ml/sec,
the total pulmonary vascular resistance calculates to be about 0.14 PRU (about one seventh that
in the systemic circulation).
Causes/Etiology

Causes of myocardial infarction by atherosclerosis

Modifiable risk factors for atherosclerosis include the following:

Smoking or other tobacco use

Diabetes mellitus
Hypertension

Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders

Obesity
Sedentary lifestyle and/or lack of exercise
Psychosocial stress
Type A personality

Causes of myocardial infarction other than atherosclerosis

Nonatherosclerotic causes of myocardial infarction include the following:

Coronary occlusion secondary to vasculitis

Ventricular hypertrophy (eg, left ventricular hypertrophy, idiopathic hypertrophic subaortic

stenosis [IHSS], underlying valve disease)

Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis

Congenital coronary anomalies

Coronary trauma

Primary coronary vasospasm (variant angina)

Drug use (eg, cocaine, amphetamines, ephedrine)

Arteritis

Coronary anomalies, including aneurysms of coronary arteries

Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism

Factors that decrease oxygen delivery, such as hypoxemia of severe anemia

V.

Pathophysiology

Thrombus
formation

Area of the
myocardium is
permanently
destroyed

Plaque rupture
and subsequent
thrombus
formation

Complete
occlusion of the
artery

Vasospasm of
the coronary
artery

Decrease
oxygen supply

Increased
demand for
oxygen supply

Oxygen
deprivation of
the cells

Ischemia
develops

Cellulary
injuries occur

Infarction of the
cells

VI.

Physical Dysfunction/Impairments

Clinical Signs and Symptoms

May be silent (smokers, diabetics: reduced sensitivity to pain)

Sudden cardiac death
Prolonged or severe substernal chest pain or squeezing pressure
Pain possibly radiating down one or both arms and/or up to the throat, neck, back, jaw, shoulders,
or arms
Feeling of indigestion
Angina lasting for 30 minutes or more
Angina unrelieved by rest, nitroglycerin, or antacids
Pain of infarct unrelieved by rest or a change in position
Nausea
Sudden dimness or loss of vision or loss of speech
Pallor
Diaphoresis (heavy perspiration)
Shortness of breath
Weakness, numbness, and feelings of faintness

Clinical Signs and Symptoms of MI for women

Heart pain in women does not always follow classic patterns

Many women do experience classic chest discomfort
Older female: mental status change or confusion may be common
Dyspnea (at rest or with exertion)

Weakness and lethargy (unusual fatigue; fatigue that interferes with ability to perform activities of
daily living)
Indigestion, heart burn, or stomach pain; mistakenly diagnosed or assumed to have
gastroesophageal reflux disease (GERD)
Anxiety or depression
Sleep disturbance (woman awakens with any of the symptoms listed here)
Sensation similar to inhaling cold air; unable to talk or breathe
Isolated, continuous mid-thoracic or interscapular back pain
Isolated right biceps aching
Symptoms may be relieved by antacids (sometimes antacids work better than nitroglycerin)

Mechanical complications

Free wall rupture: acute free wall rupture is almost always fatal within minutes. In some cases
of sub-acute free wall rupture, only a small quantity of blood initially reaches the pericardial
cavity and begins to cause signs of pericardial tamponade.
Ventricular septal rupture: A ventricular septal defect (VSD) caused by myocardial infarction
and septal rupture occurred in 1% to 2% of all patients with infarction in older series, though the
incidence in the fibrinolytic age is 0.2% to 0.3%. Patients may complain of a chest pain
somewhat different that their MI pain and will usually develop cardiogenenic shock.
Papillary muscle rupture: Papillary muscle rupture leads to acute and severe mitral
regurgitation. It occurs in approximately 1% of STEMIs. Because of the abrupt elevation in left
atrial pressure, there may not be an audible murmur of mitral regurgitation. Pulmonary edema and
cardiogenic shock usually develop.

Ischemic complications

Angina
Reinfarction
Infarct extension

Arrhythmic complications

Atrial or ventricular arrhythmias

Sinus or atrioventricular node dysfunction

Embolic complications

Central nervous system or peripheral embolization

Inflammatory complications

VII.

Pericarditis
Differential Diagnosis

1. Coronary artery disease

The major disorders caused by insufficient blood supply to the myocardium are angina
pectoris and myocardial infarction.
These disorders are collectively known as coronary artery disease (CAD), also called
coronary heart disease or ischemic heart disease.
CAD includes atherosclerosis (fatty buildup), thrombus (blood clot), and spasm (intermittent
constriction).
2. Atherosclerosis
The disease process often called arteriosclerosis or hardening of the arteries.
It is a progressive process that begins in childhood.
3. Angina
Acute pain in the chest, called angina pectoris, results from the imbalance between cardiac
workload and oxygen supply to myocardial tissue.
Angina is a symptom of obstructed or decreased blood supply to the heart muscle primarily
from a condition called atherosclerosis.
4. Pericarditis
Pericarditis is an inflammation of the pericardium, the sac-like covering of the heart.
Specifically, it affects the parietal pericardium (fluid-like membrane between the fibrous
pericardium and the epicardium) and the visceral (epicardium) pericardium

5. Congestive heart failure or Heart failure

Heart failure, also called cardiac decompensation and cardiac insufficiency, can be defined as
a physiologic state in which the heart is unable to pump enough blood to meet the metabolic
needs of the body (determined as oxygen consumption) at rest or during exercise, even
though filling pressures are adequate.
6. Right ventricular failure
Failure of the right ventricle may occur in response to left-sided CHF or as a result of
pulmonary embolism.
Right ventricular failure results in peripheral edema and venous congestion of the organs.
7. Aneurysm
An abnormal dilatation (commonly a saclike formation) in the wall of an artery, a vein, or the
heart.
Aneurysms occur when the vessel or heart wall becomes weakened from trauma, congenital
vascular disease, infection, or atherosclerosis.
VIII.

Diagnostic tools

Cardiac Imaging

Magnetic resonance imaging (MRI) is a safe, noninvasive test that creates detailed pictures of
your organs and tissues. "Noninvasive" means that no surgery is done and no instruments are
inserted into your body.
MRI uses radio waves, magnets, and a computer to create pictures of your organs and tissues.
Unlike other imaging tests, MRI doesn't use ionizing radiation or carry any risk of causing cancer.
Stress echocardiography can be used to rule out myocardial ischemia in patients, who come to the
emergency department with chest pain.

Electrocardiogram

As recommended by the most recent ACC/AHA guidelines for the management of unstable
angina/NSTEMI, patients with active on-going symptoms suggestive of an acute coronary
syndrome should have early risk stratification by checking cardiac enzyme levels and undergoing
a 12-lead ECG within 10 minutes of presentation of the emergency department.
For patients with on-going symptoms, serial ECGs should be performed to look for dynamic
changes in the ST segment.
The ECG is the most important tool in the initial evaluation and triage of patients in whom an
ACS is suspected. It is confirmatory of the diagnosis in approximately 80% of cases.

Pharmacologic treatment

The goals of pharmacotherapy for myocardial infarction are to reduce morbidity and to prevent
complications. The main goals of ED medical therapy are rapid IV thrombolysis and/or rapid
referral for PCI, optimization of oxygenation, reduction of cardiac workload, and pain control.

Antiplatelet agents

Aspirin
Clopidogrel
Vorapaxar
Ticagrelor

Beta-adrenergic blockers

Metoprolol
Esmolol
Atenolol

Analgesics

Morphine

Vasodilators

Nitroglycerin

Angiotensin-converting enzyme inhibitors

Captopril
Enalapril
Quinapril
Lisinopril

Thrombolytics

Alteplase, t-PA
Tenecteplase

PT Management
Cardiac Rehabilitation
PHASE I: (In-hospital Phase)

Whether you are in the ICU, private room or ward, the physical therapy and ward activities are
started to encourage early sitting, standing and walking. These prevent the harmful effects of
prolonged bed rest. Initial health education and psychosocial evaluation is performed or done.

PHASE II: (Out - Patient Phase)

This phase starts 1-2 weeks after hospital discharge. Group exercises are done 3 times a week
(Tuesdays, Thursdays and Saturdays) for a period of 6 weeks.
Exercises

Emphasis on Risk Stratification

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.

Calisthenics
Aerobics
Flexibility
Telemetrymonitored exercise training
Prescription or instruction for independent maintenance of exercises (e.g. home
exercises)
Professionally supervised exercise training
Resistance/ Strength training
Submaximal fitness testing
Stress testing
Stress management

Education, Counseling and Behavioral Services

1.
2.
3.
4.
5.
6.
7.
8.
9.

Orientation to cardiac rehabilitation

Risk factors for heart disease and lifestyle modification
Anatomy of the Heart
Psychological Referral
Understanding your medications
Benefits of exercise and the heart
Dietary education
Diabetes, Hypertension and Smoking Cessation
Weight loss program, Return to work, Spiritual Counseling (optional)

PHASE III: (Out-Patient Maintenance)

1. Continuation phase lasting for three months
2. Group exercises at 3 times a week
3. Focus on risk factors and lifestyle modification

Home Exercise Program

Ambulation exercises
Walking exercise
Combination of rest and low-level activity including ambulation and LE and UE mobility
Energy conservation techniques
Position change or activity for every 1-2 hours

Reference:
Physical Rehabilitation - Schmitz, Thomas, O'Sullivan, Susan, Fulk, George
Brunner and Suddarth's Textbook of Med.-Surg. Nursing 12th ed. (2 vols) - S. Smeltzer, et al.,
(Lippincott, 2010) BBS
Snell's Clinical Anatomy by Regions 9th Edition
Cardiology Secrets by Glenn N. Levine Third Edition
Differential Diagnosis for Physical Therapists 2007 by Goodman and Synder
http://emedicine.medscape.com/article/155919-overview
http://www.medicinenet.com/heart_attack/article.htm
http://www.medscape.com/viewarticle/772514_5
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/complication
s-of-acute-myocardial-infarction/Default.htm