Cardiovascular Physiology
383
SECTION B SUMMARY
Anatomy
I. The atrioventricular (AV) valves prevent fl ow from the
ventricles back into the atria.
II. The pulmonary and aortic valves prevent backfl ow from the
pulmonary trunk into the right ventricle and from the aorta
into the left ventricle, respectively.
III. Cardiac muscle cells are joined by gap junctions that permit
the conduction of action potentials from cell to cell.
IV. The myocardium also contains specialized cells that constitute
the conducting system of the heart, initiating the cardiac
action potentials and speeding their spread through the heart.
Heartbeat Coordination
I. Action potentials must be initiated in cardiac cells for
contraction to occur.
a. The rapid depolarization of the action potential in atrial and
ventricular muscle cells is due mainly to a positive-feedback
increase in sodium permeability.
b. Following the initial rapid depolarization, the cardiac
muscle cell membrane remains depolarized (the plateau
phase) for almost the entire duration of the contraction
because of prolonged entry of calcium into the cell through
plasma-membrane L-type calcium channels.
II. The SA node generates the action potential that leads to
depolarization of all other cardiac cells.
a. The SA node manifests a pacemaker potential, which brings
its membrane potential to threshold and initiates an action
potential.
b. The impulse spreads from the SA node throughout both
atria and to the AV node, where a small delay occurs. The
impulse then passes into the bundle of His, right and left
bundle branches, Purkinje fi bers, and ventricular muscle
cells.
III. Calcium, mainly released from the sarcoplasmic reticulum
(SR), functions as the excitation-contraction coupler in cardiac
muscle, as in skeletal muscle, by combining with troponin.
a. The major signal for calcium release from the SR is
extracellular calcium entering through voltage-gated L-type
calcium channels in the T-tubular membrane during the
action potential.
b. This “trigger” calcium opens ryanodine receptor calcium
channels in the sarcoplasmic reticulum membrane.
c. The amount of calcium released does not usually saturate all
troponin binding sites, so the number of active cross-bridges
can increase if cytosolic calcium increases still further.
IV. Cardiac muscle cannot undergo summation of contractions
because it has a very long refractory period.
Mechanical Events of the Cardiac Cycle
I. The cardiac cycle is divided into systole (ventricular
contraction) and diastole (ventricular relaxation).
a. At the onset of systole, ventricular pressure rapidly exceeds
atrial pressure, and the AV valves close. The aortic and
pulmonary valves are not yet open, however, so no ejection
occurs during this isovolumetric ventricular contraction.
b. When ventricular pressures exceed aortic and pulmonary
trunk pressures, the aortic and pulmonary valves open, and
the ventricles eject the blood.
c. When the ventricles relax at the beginning of diastole,
the ventricular pressures fall signifi cantly below those
in the aorta and pulmonary trunk, and the aortic and
pulmonary valves close. Because the AV valves are also still
closed, no change in ventricular volume occurs during this
isovolumetric ventricular relaxation.
d. When ventricular pressures fall below the pressures in
the right and the left atria, the AV valves open, and the
ventricular fi lling phase of diastole begins.
e. Filling occurs very rapidly at fi
rst so that atrial contraction,
which occurs at the very end of diastole, usually adds only a
small amount of additional blood to the ventricles.
II. The amount of blood in the ventricles just before systole is the
end-diastolic volume. The volume remaining after ejection is
the end-systolic volume, and the volume ejected is the stroke
volume.
III. Pressure changes in the systemic and pulmonary circulations
have similar patterns, but the pulmonary pressures are much
lower.
IV. The fi rst heart sound is due to the closing of the AV valves, and
the second to the closing of the aortic and pulmonary valves.
V. Murmurs can result from narrowed or leaky valves, as well as
from holes in the interventricular septum.
The Cardiac Output
I. The cardiac output is the volume of blood each ventricle
pumps and equals the product of heart rate and stroke volume.
a. Heart rate is increased by stimulation of the sympathetic
nerves to the heart and by epinephrine; it is decreased by
stimulation of the parasympathetic nerves to the heart.
b. Stroke volume is increased mainly by an increase in end-
diastolic volume (the Frank-Starling mechanism) and
by an increase in contractility due to sympathetic-nerve
stimulation or to epinephrine. Afterload can also play a
signifi cant role in certain situations.
Measurement of Cardiac Function
I. Methods of measuring cardiac function include
echocardiography, for assessing wall and valve funcion, and
cardiac angiography, for determining coronary blood fl ow.
Additional Clinical Examples
I. Hypertrophic cardiomyopathy is a disease caused by a genetic
mutation in genes coding for cardiac contractile proteins. It
can lead to heart failure, as well as sudden death caused by
arrhythmia.
SECTION B KEY TERMS
afterload
379
aortic valve
366
atrioventricular (AV)node
368
atrioventricular (AV) valve
365
automaticity
370
bicuspid valve
365
bundle of His
369
cardiac cycle
373
cardiac output (CO)
378
chordae tendineae
365
conducting system
367
contractility
380
coronary artery
367
coronary blood fl ow
367
cusp
365
diastole
373
ECG lead
371
ejection fraction (EF)
380
electrocardiogram (ECG)
371
end-diastolic volume
(EDV)
375
endothelial cell
365
endothelium
365
end-systolic volume (ESV)
375
epicardium
365
Frank-Starling mechanism
379
F-type sodium channel
370
heart rate
368
heart sounds
377
interventricular septum
365
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