PHYSIOLOGY OF THE HEART

Introduction

The heart is essentially two different pumps, a right heart pumping blood
through the lungs and a left heart pumping blood through the systemic circulation
supplying blood supply to the other organs and body tissues. It is a pulsatile, two-
chamber pump consisting of an atrium and a ventricle. An atrium is a weak ventricle
priming pump that helps move blood into the ventricle. The ventricles then provide
the key pumping force that propels the blood either (1) through the pulmonary
circulation via the right ventricle or (2) through the systemic circulation via the left
ventricle. The heart is protected by a two-layer membrane, called the pericardium,
which covers and retains the heart in position.

The human heart has a special mechanism for rhythmic self-excitation and
repeated contraction about 100,000 times a day, or 3 billion times a day in the
normal human life. This remarkable feat is achieved by a system that does the
following: (1) produces electrical impulses to activate the heart muscle's rhythmic
contraction; and (2) executes these impulses quickly through the heart. As this
mechanism usually functions, the atria contracts about one-sixth of a second ahead
of ventricular contraction, which enables the ventricles to fill before circulating
blood through the lungs and peripheral circulation. Another particularly important
feature of the system is that it allows for almost simultaneous contraction of all
portions of the ventricles, which is necessary for the most efficient pressure
generation in ventricular chambers.

This rhythmical and conductive system of the heart is susceptible to damage

by heart disease, especially by ischemia resulting from inadequate coronary blood
flow. The effect is often a bizarre heart rhythm or an abnormal sequence of
contraction of the heart chambers, and the pumping effectiveness of the heart can
be affected severely, even to the extent of causing death.
 This unit will allow you to understand the function of the heart, cardiac
cycle, rhythmic conducting system of the heart including the heart control and
waveforms of the normal electrocardiogram.

Learning Outcomes

✓ Explain the cardiac cycle.

✓ Explain how the specialized cardiac conduction system coordinates the
synchronized contraction and relaxation of the atria and ventricles.
✓ Explain how cellular mechanisms, calcium ions, and adenosine
triphosphate work together to bring about myocardial contraction and
relaxation.
✓ Describe how Frank-starling mechanism helps the heart adjust pump
varying amounts of blood.
✓ Explain the timing and sequence of all mechanical events in the cardiac
cycle.

Topic 1: Cardiac Cycle

Learning Objectives

✓ Determine the function of atria and ventricle.

✓ Differentiate the different heart valves.
✓ Explain the aortic pressure curve.
✓ Explain how heart sounds being produce.
✓ Determine the normal and abnormal heart sounds.

Presentation of Contents

The cardiac events that occur from the start of one heartbeat to the start of
the next are called the cardiac cycle. The spontaneous generation of an action
potential inside the sinus node initiates each cycle. This node is in the upper lateral
wall of the right atrium near the opening of the superior vena cava, and the action
potential travels easily from here through both atria and then through the A-V
bundle into the ventricles. Because of this special arrangement of the conducting
system from the atria into the ventricles, the cardiac impulse from the atria into the
ventricles is delayed by more than 0.1 seconds during the flow. This delay helps
the atria to contract ahead of ventricular contraction, pumping blood into the
ventricles before the beginning of the strong ventricular contraction. The atria serve
as primer pumps for the ventricles and, in turn, the ventricles provide the central
power source for moving blood through the body's vascular system.
The cumulative duration of the heart cycle, including the systole and the
diastole, is the heart rate reciprocal. For eg, if the heart rate is 72 beats per minute,
the cardiac cycle length is 1/72 min / beat — around 0.0139 min / beat, or 0.833
sec / beat.

The figure indicates the numerous events to the left side of the heart during
the cardiac cycle. The top
three curves reflect
changes in pressure in the
aorta, left ventricle, and
left atrium, respectively.
The fourth curve depicts
the changes in the left
ventricular volume, the
fifth depicts the
electrocardiogram, and
the sixth depicts a phonocardiogram, which is a recording of the sounds created by
the heart as it pumps — mainly by the heart valves.

As heart rate rises, the length of each cardiac cycle decreases, including the
phases of contraction and relaxation. The length of the action potential and the
systole also decreases, but not by a percentage as high as the diastole. At average
heart rate of 72 beats / min, systole constitutes approximately 0.4 of the entire
cardiac cycle. The systole is about 0.65 of the entire cardiac cycle at three times the
normal heart rate. This means that the heart beating very quickly does not stay
relaxed long enough to allow the cardiac chambers to fill fully before the next
contraction.

Blood normally flows continually from the great veins into the atria; about
80% of the blood flows directly through the atria into the ventricles, even before
the atria contract. Then, atrial contraction usually causes an additional 20% filling
of the ventricles. Blood usually flows continuously from the great veins into the
atria; about 80 percent of the blood passes through the atria into the ventricles, even
before the atria contract. Then atrial contraction normally allows the ventricles to
be filled by an additional 20 per cent.

The atria act as primary pumps, which increases the effectiveness of

ventricular pumping by up to 20 percent. However, even without this additional 20
percent efficacy, the heart will continue to function in certain circumstances
because it usually has the capacity to pump 300 percent to 400 percent more blood
than the rest body needs.

Read Chapter 10 of Egan’s Fundamental of Respiratory Care 11th

edition by Kacmarek, R., Stoller, J., Heuer, A. and Chapter 5 & 12 of
Cardiopulmonary Anatomy & Physiology Essentials by
Respiratory Care 7th edition by Terry des Jardins and answer the
following questions.

1. What do you think will happen when the atria fail to function?

2. What do you think will happen if the atrial septum does not form or
fuse?

3. Can aging or diseases such high blood pressure or diabetes mellitus

affects the filling of blood to the ventricles? Why or why not?
 Large volumes of blood collect in the right and left atria during ventricular
systole because of the closed A-V valves. Therefore, once the systole is over and
the ventricular pressures fall again to their low diastolic values, the moderately
increased pressures that formed in the atria during the ventricular systole
immediately force the A-V valves open and allow blood to flow rapidly into the
ventricles; as shown by the rise of the left ventricular volume curve in the first
figure. This period is called the period of rapid filling of the ventricles.

The rapid filling cycle lasts for the first third of diastole roughly. Just a small
amount of blood usually flows into the ventricles during the middle-third of the
diastole. This is blood that keeps emptying into the Atria from the veins, flows
directly through the ventricles via the atria. The atria contracts during the last third
of diastole and gives an extra thrust to blood inflow into the ventricles. During each
heart cycle, this process accounts for around 20 percent of the ventricles fill.

Immediately after ventricular contraction begins, as seen in the figure

above, the ventricular pressure increases suddenly causing the A-V valves to close.
A 0.02 to 0.03 second is then needed for the ventricle to build up adequate pressure
to push open the semilunar (aortic and pulmonary) valves against the aorta and
pulmonary artery pressures. There is contraction in the ventricles during this time,
but no emptying occurs. This period is called period of isovolumic or isometric
contraction, indicating cardiac muscle tension is increasing but there is little or no
shortening of the muscle fibers.

As the left ventricular pressure rises slightly above 80 mm Hg (and the right
ventricular pressure rises slightly above 8 mm Hg), the ventricular pressure forces
open the semilunar valves. Immediately, blood is pumped to the aorta and
pulmonary artery out of the ventricles. During systole, approximately 60 percent of
the blood in the ventricles at the end of the diastole is ejected; approximately 70
percent of that portion flows out during the first third of the ejection cycle, with the
remaining 30 percent emptying over the next two thirds. Therefore, the first third
is called the period of rapid ejection, and the last two thirds is called the period of
slow ejection.

Ventricular relaxation starts abruptly at the end of the systole, allowing for
rapid reduction of both right and left intraventricular pressures. In the distended
large arteries, the elevated pressures that have just been filled with blood from the
contracted ventricles quickly force back the blood into the ventricles, which snaps
the closed aortic and pulmonary valves. The ventricular muscle continues to relax
for another 0.03 to 0.06 seconds, but the volume of the ventricle does not change,
giving rise to isovolumic or isometric relaxation. The intraventricular pressures
rapidly decline back to their low diastolic levels during this time. The A-V valves
then open to start a new ventricular pumping cycle.

Standard filling of the ventricles during diastole increases each ventricle 's
volume to around 110 to 120 ml. This volume is called volume end diastolic. Then,
when the ventricles empty during systole, the volume diminishes by around 70 ml,
which is called the stroke volume output. The remaining volume in each ventricle
is called the end-systolic volume, about 40 to 50 ml.
The fraction of the expelled end-diastolic volume is called the ejection
fraction, generally equal to approximately 0.6 (or 60 per cent). The percentage of
the ejection fraction is also clinically used to test cardiac systolic (pumping)
capability. The end-systolic volume may decrease to as little as 10 to 20 ml as the
heart contracts strongly. By comparison, when large quantities of blood flow into
the ventricles during diastole, the ventricular end-diastolic volumes in the healthy
heart can increase to as much as 150 to 180 ml. By both increasing the end-diastolic
volume and decreasing the end-systolic volume, the output of the stroke volume
can be increased to more than double what is usual.
 Read Chapter 10 of Egan’s Fundamental of Respiratory Care 11th
edition by Kacmarek, R., Stoller, J., Heuer, A. and Chapter 5 & 12 of
Cardiopulmonary Anatomy & Physiology Essentials by Respiratory
Care 7th edition by Terry des Jardins and answer the following questions.

1. What are the functions of the following?

a. Atrioventricular Valves.

b. Papillary Muscles.

c. Aortic and Pulmonary Artery Valves.

2. What is the relationship of the heart sounds to heart pumping?

3. What produces heart sounds?

4. What are the normal and abnormal heart sounds? Explain your answer.
5. What is the normal heart rate for newborn? pediatric? adult? Explain
why a neonate 's heart rate is higher than an adult.
 The ventricular pressure rises rapidly as the left ventricle contracts before
the aortic valve opens. Then the pressure in the ventricle increases much less
quickly after the valve opens, so blood instantly flows out of the ventricle into the
aorta, and then into the systemic circulation arteries. During systole, blood entry
into the arteries causes the walls of these arteries to stretch, and the pressure to rise
to around 120 mm Hg. Then, after the left ventricle ceases ejecting blood at the end
of the systole and the aortic valve closes, the artery 's elastic walls sustain a high
pressure in the arteries, even during diastole.

An incisura occurs at closure of the aortic valve in the aortic pressure curve.
This is triggered by a brief burst of backward blood flow immediately prior to valve
shutdown, accompanied by a rapid cessation of backflow. After the aortic valve is
closed, pressure throughout the aorta steadily reduces in the diastole, since the
blood contained in the stretched elastic arteries continuously flows back to the veins
through the peripheral vessels. The aortic pressure has normally dropped to around
80 mm Hg (diastolic pressure) before the ventricle contracts again, which is two-
thirds the maximum pressure of 120 mm Hg (systolic pressure) that occurs in the
aorta during ventricular contracture. The pressure curves in the right ventricle and
pulmonary artery are like those in the aorta, except that the pressures are only about
one-sixth as great.

Work Output of the Heart

The heart's stroke work output is the amount of energy the heart uses to
work at each heartbeat when pumping blood into the arteries. The heart's work
output comes in two ways. First, the main proportion is used to transfer the blood
to the high-pressure arteries from the low-pressure veins. This is called volume-
pressure work or external work. Second, a minor proportion of the energy is used
to accelerate the blood to its velocity of ejection through the aortic and pulmonary
valves, which is the kinetic energy of blood flow component of the work output.
Because of the six-fold difference in systolic pressures pumped by the two
ventricles, the right ventricular external work output is usually around one-sixth of
the left ventricle. The additional work output needed for each ventricle to produce
kinetic blood flow energy is proportional to the mass of blood ejected times the
square of ejection velocity. Ordinarily, the work output of the left ventricle required
to create kinetic energy of blood flow is only about 1% of the total work output of
the ventricle and therefore is ignored in the calculation of the total stroke work
output

Read Chapter 10 of Egan’s Fundamental of Respiratory Care 11th

edition by Kacmarek, R., Stoller, J., Heuer, A. and Chapter 5 & 12 of
Cardiopulmonary Anatomy & Physiology Essentials by Respiratory
Care 7th edition by Terry des Jardins and answer the following questions.

1. What is the approximate amount of blood the heart pumps each minute
when at rest? During strenuous exercise?

2. What are the basic mechanisms by which heart pumping is regulated?

Explain your answer.

3. Explain how sympathetic and parasympathetic nerves affects cardiac

output.
 One of the best ways to
express the functional ability of
the ventricles to pump blood is
by ventricular function curves.
The 2nd figure shows a type of
ventricular function curve
called the stroke work output
curve. Note that as atrial
pressure for each side of the
heart increases, stroke work
output for that side increases until it reaches the limit of the ventricle’s pumping
ability.

One of the best ways of describing the ventricles' capacity to pump blood.
The 2nd figure shows a kind of ventricular function curve called the stroke work
output curve. Notice that as atrial pressure rises on each side of the heart, the stroke
work output of that sided increases until it exceeds the limit of the pumping
capacity of the ventricle. On
the 3rd figure, it shows another
type of ventricular function
curve called the ventricular
volume output curve. The two
curves of this figure depict
activity of the two human
heart ventricles based on data
extrapolated from
experimental animal studies. As the right and left atrial pressure rises, so does the
corresponding ventricular volume outputs per minute.

Ventricular function curves show that as the ventricles fill in response to

higher atrial pressures, each ventricular volume and strength of cardiac muscle
contraction increase, causing the heart to pump increased quantities of blood into
the arteries.

Topic 2: Rhythmic Heart Excitation

Learning Objectives

✓ Explain the conducting system of the heart.

✓ Describe SA Node, AV Node, Bundle Branch Block and Purkinje Fibers.
✓ Explain how the ventricular muscle transmits cardiac impulse.
✓ Determine how Sympathetic and Parasympathetic Nerve affects the heart
rate.

Presentation of Content

The sinus node is about 3

mm wide, 15 mm long, and 1 mm
thick, a thin, smooth, ellipsoid strip
of specialized cardiac muscle. It is
situated directly below the superior
posterolateral wall of the right
atrium, and slightly lateral to the
opening of the superior vena cava. In
comparison to a diameter of 10 to 15
μm for the surrounding atrial muscle fibers, the fibers of this node have almost no
contractile muscle filaments and are each just 3 to 5 micrometers (μm) in diameter.
The sinus nodal fibers, however, attach directly with the atrial muscle fibers, so that
any action potential that begins in the sinus node immediately extends through the
atrial muscle wall.

Some cardiac fibers have the ability of self-excitation, a mechanism that can
trigger automatic rhythmic discharge and contraction. This capacity is particularly
true for the specialized conductive system of the heart, including sinus node fibers.
For this reason, the sinus node usually regulates the entire heart's beat rate.

The second figure shows the action potential of three heartbeats and, by
contrast, a single ventricular
muscle fiber action potential
reported from within a sinus
nodal fiber. The sinus nodal
fiber's resting membrane
potential between discharges is
around – 55 to – 60 millivolts,
compared to – 85 to – 90
millivolts for the ventricular
muscle fiber. The cause of this
lower negativity is that the cell membranes of the sinus fibers are normally leaky
to sodium and calcium ions and some of the intracellular negativity is neutralized
by positive charges of the entering sodium and calcium ions.

The rapid spike of the action potential observed in the ventricular muscle
due to the rapid influx of positive sodium ions into the interior of the fiber is
responsible for 10,000ths of a second. Then, the plateau of the ventricular action
potential is mainly triggered by slower opening of the slow sodium-calcium
channels, which lasts around 0.3 second. Finally, the opening of potassium
channels enables large quantities of positive potassium ions to be diffused through
the fiber membrane in the outward direction and returns the membrane potential to
its resting level. However, in the sinus nodal fiber there is a disparity in the function
of these channels since the resting potential is much less negative — only – 55
millivolts in the nodal fiber instead of the – 90 millivolts in the ventricular muscle
fiber.
 The fast sodium channels have already mainly become inactivated or
blocked at this stage of -55 millivolts. This is because at any point for more than a
few milliseconds the membrane potential remains less negative than around – 55
millivolts, the inactivation gates on the inside of the cell membrane that close the
fast sodium channels are closed and remain so. Only the slow sodium-calcium
channels can open (i.e., can activate) and thus trigger the potential for action. As a
result, the potential for atrial nodal action is slower to develop than the ventricular
muscle's potential for action. And, after the potential for action occurs, the potential
return to its negative state still happens slowly, rather than the sudden return for the
ventricular fiber.

Due to a higher concentration of sodium ions in the extracellular fluid

outside the nodal fiber and a moderate number of already open sodium channels,
positive sodium ions from outside the fibers usually appear to leak through inward,
"funny" currents to the inside. Hence the influx of positively charged sodium ions
during heartbeats induces a gradual increase in the positive direction of the resting
membrane potential.

As shown in the 2nd figure, the resting potential thus steadily increases and
becomes less negative between each and every two heartbeats. When a threshold
voltage of around – 40 millivolts exceed the limit, the calcium channels of the L-
type become activated, thereby triggering the potential for action. Thus, the
intrinsic leakage of the sinus nodal fibers to sodium and calcium ions causes their
self-excitation.
 Read Chapter 10 of Egan’s Fundamental of Respiratory Care 11th
edition by Kacmarek, R., Stoller, J., Heuer, A. and Chapter 5 & 12 of
Cardiopulmonary Anatomy & Physiology Essentials by Respiratory
Care 7th edition by Terry des Jardins and answer the following questions.

1. Why does the leakiness to sodium and calcium ions not cause the sinus
nodal fibers to remain depolarized all the time?

2. What is hyperpolarization?

3. What is the resting membrane potential of hyperpolarization?

4. Why is the new state of hyperpolarization not maintained forever?

The atrial conductive system is structured in such a way that the cardiac
impulse does not move too quickly from the atria to the ventricles; this delay
enables the atria to empty their blood into the ventricles before ventricular
contraction starts. In the ventricles it is mainly the A-V node and its neighboring
conductive fibers that interrupt this transmission.
 The A-V node is located immediately behind the tricuspid valve in the right
atrium's posterior wall,
as shown in the first
figure. The 3rd figure,
the different sections of
this node, plus its
connections to the
internodal pathway
fibers entering the
atrium and to the exiting
A-V bundle. This figure
also demonstrates the
average time intervals
(in fractions of a
second) in the sinus
node between the initial onset of the cardiac impulse and its subsequent presence
in the A-V nodal system. Note that after traveling the internodal pathways, the
impulse reaches the A-V node about 0.03 seconds after it originates in the sinus
node. Then in the A-V node itself, there is a delay of another 0.09 second before
the impulse reaches the penetrating portion of the A-V bundle, where it passes into
the ventricles.

A final delay of another 0.04 second occurs mainly in this penetrating A-V
bundle, which consists of several small fascicles passing through the fibrous tissue
separating the atria from the ventricles. In the A-V nodal and A-V bundle system,
the cumulative delay is thus around 0.13 seconds. This delay, in addition to the
initial delay in conduction of 0.03 seconds from the sinus node to the A-V node,
results in a cumulative pause of 0.16 seconds before the excitatory signal enters the
ventricle contracting muscle.
 Read Chapter 10 of Egan’s Fundamental of Respiratory Care 11th
edition by Kacmarek, R., Stoller, J., Heuer, A. and Chapter 5 & 12 of
Cardiopulmonary Anatomy & Physiology Essentials by
Respiratory Care 7th edition by Terry des Jardins and answer the
following questions.

1. What is the key explanation why the transitional, nodal, and penetrating
A-V bundle fibers are slow conduction?

2. What is the origin of rapid cardiac impulse transmission in the

ventricular Purkinje system?

3. What is the unique characteristic of A-V bundle? Explain your answer.

4. Describe the distribution of the Purkinje Fibers in the Ventricles— Left

and Right Bundle Branches.
5. Explain the transmission of the cardiac impulse in the ventricular
muscle.

6. Why does the sinus node regulate the rhythm of the heart, rather than
the A-V node or the Purkinje fibers?

7. What is the role of the Purkinje system in causing the ventricular muscle
to synchronously contract?

8. Explain the function of Parasympathetic (Vagal) and Sympathetic Nerve

in Cardiac Rhythm and Conduct Stimulation?
 9. Explain possible effect of temperature on heart function.

Summary
The heart's SA node depolarizes spontaneously and cyclically faster than
any cardiac fibers; hence, the SA node is the natural pacemaker of the heart. Any
other than the SA Node Pacemaker is an ectopic pacemaker. If the SA Node is
suppressed or other foci become more excitable than the SA Node, an ectopic
pacemaker may develop. Ectopic foci are the result of premature atrial or
ventricular contractions. The AV Node's slight delay in cardiac impulse usually
allows sufficient ventricular filling time. Parasympathetic stimulation speeds down
the heart rate and force of contraction, while sympathetic stimulation has the
opposite effect.

Reflection:

How will you apply your knowledge from this unit to help the following
clienteles?

a. Smoker

b. Obese

c. Hypertensive patient
d. Diabetic patient

e. Geriatric

f. Pediatric

g. Patient recovered from Covid-19