The Heart - Biofluidmechanics: An Introduction to Fluid Mechanics Macrocirculation and Microcirculation - page 101

contractions, there is a specialized conduction pathway between these two chambers. This
conduction pathway slows the action potential so that the atria can completely contract
and eject all of the blood into the ventricles before the ventricles begin to contract. Also,
the conduction pathway brings the action potential to the apex of the heart, so that ventri-
cle contraction proceeds from the bottom of the heart toward the top of the heart. This
forces blood toward the aorta and the pulmonary arteries to exit the heart (see Section 4.2
for a detailed discussion on the cardiac conduction system).
Another difference between cardiac muscle cells and skeletal muscle cells is that the car-
diac action potential differs from skeletal muscle action potential, allowing for the cardiac
myocytes to contract as a whole system, instead of as independent fibers ( Figure 4.3 ). As
with normal skeletal muscle action potentials, there is a rapid depolarization of the cells
caused by an influx of sodium ions through rapid sodium channels. This depolarization
increases the membrane potential from approximately negative 85 mV to approximately
positive 15 to 20 mV. In a nerve cell, this is followed by a rapid repolarization (the duration
of the action potential is less than 0.1 sec) of the nerve cell. Cardiac action potentials, how-
ever, exhibit an elongated plateau phase in which the cells remain depolarized for approxi-
mately 0.25 seconds. This elongated plateau region is caused by a constant influx of calcium
ions through slow calcium channels. During the plateau phase, the permeability of potas-
sium ions decreases, significantly slowing the efflux of potassium ions out of the muscle.
This process is also not seen in skeletal muscle action potentials, where potassium efflux
causes the rapid repolarization discussed above. After the slow calcium channels close, the
cell membrane permeability toward potassium ions is increased, allowing for the rapid
repolarization of the cell. After the cell has repolarized, there is a latent period of about
0.25 seconds, in which it is difficult to excite the cardiac myocytes again. After this latent
period, the myocytes are able to contract again as normal. Except for the slow movement of
calcium ions, the ion movement during the cardiac and skeletal action potentials is similar.
This entire discussion has arrived at a point where it should be understood how the car-
diac muscle contracts to effectively move blood throughout the cardiovascular system and
the heart (see Figure 4.1 ). To begin its path through the heart, deoxygenated blood enters
from the superior vena cava or the inferior vena cava into the right atrium. The superior
vena cava collects blood from the head, neck, and arms, while the inferior vena cava col-
lects blood from the trunk and legs. Once the atrium contracts, blood passes through the
right atrioventricular (AV) valve, also known as the tricuspid valve, into the right ventri-
cle. This valve acts to prevent the backflow of blood into the right atrium, when the right
ventricle contracts. Once the right ventricle contracts, blood is ejected through the right
semilunar valve (also known as the pulmonary valve) into the respiratory circulation to
become oxygenated. Blood is transported to the pulmonary circulation via the pulmonary
arteries. Oxygenated blood returns into the left atrium via the pulmonary veins. As the
atria contract, blood passes through the left AV valve, also known as the mitral valve, into
the left ventricle. This valve also acts to prevent the backflow of blood during ventricular
contraction. Upon left ventricle contraction, oxygenated blood is ejected into the systemic
circulation, through the left semilunar valve (also known as the aortic valve). Note that all
of the valves in the heart open and close passively, in response to pressure changes.
During atrial contraction, the fluid pressure within each atrium becomes greater than the
fluid pressure within the ventricles. This change in the pressure gradient direction forces