Biomedical Engineering Reference
In-Depth Information
vessel can no longer maintain normal cardiac contractions, this region will become
infarcted. Without a blood supply for 1 to 2 hours, cardiac muscle cells begin to die. As
stated above, collateral blood flow can return to the infarcted area. However, as tissue
damage has been done, this blood has little purpose there because the damaged cells can-
not contract as strongly as before. Blood that enters an infarcted region stagnates because
the major vessels have been closed off from circulation, and eventually the blood becomes
deoxygenated. In extreme cases, the endothelial cells become very permeable and leak
blood into the heart wall.
With a minor block in the coronary vessels, it is unlikely that cardiac tissue will become
infarcted. Cardiac tissue is supplied with approximately 4 times as much blood as it needs
to survive. So even with a blockage that reduces blood flow by half, it is unlikely that muscle
tissue will die immediately, if collateral circulation does not take up the slack of the blocked
vessel. However, if the blockage is severe enough or the collateral circulation does not sup-
ply the newly infarcted region with enough blood, the muscle tissue will begin to die.
Once a large region of the heart becomes infarcted, there are four likely outcomes that
can each lead to death. The first two outcomes are consequences of the heart not pumping
enough blood to the systemic circulation. As stated above, an infarcted region of the heart
does not contract as strongly as is necessary. If the region of the heart that is infarcted is
large, it is possible that the total cardiac output reduces. A lower cardiac output can and
does affect many locations throughout the body. A decreased blood supply to any organ
will change its function and potentially lead to death. Also, when the ventricular muscle
mass is not moving enough blood, the blood must be pooled somewhere. Because the total
blood volume does not change and the arterial system is not highly compliant, the excess
blood is typically held within the veins and the pulmonary circulation. When the blood
volume in the venous and pulmonary circulation systems increases significantly, the over-
all pressure of the cardiovascular system increases (see Section 5.11.1). This especially
becomes detrimental when the capillary pressure increases and blood cannot be delivered
to the body.
The remaining two outcomes are problems associated with the heart due to the lack of
nutrients being supplied to the infarcted region. A common cause of death associated with
myocardial infarction is ventricular fibrillation. With no or small quantities of blood being
supplied to the cardiac tissue, there is a rapid reduction of potassium ions from the muscle
cells. Without potassium ions, a cell cannot become repolarized after an action potential
has passed. This leads to a basic breakdown in the membrane potential because the ionic
concentration gradients are incorrect, causing the cells to not function properly. All of
these processes lead to fibrillation of the tissue. The last major possible occurrence is rup-
ture of the cardiac tissue. An infarcted region by definition is composed of dead muscle
cells. A few days after the infarction occurs, the tissue will begin to degenerate and thin. If
the majority of the heart is functioning at its optimal capacity, then it is likely that the
thinned region will become unable to withstand the pressure generated by cardiac contrac-
tion. At the onset of this process, the infarcted region begins to bulge outward, and even-
tually, if not corrected, the infarcted region can burst. Blood would then pool in the
pericardial space and begin to compress other regions of the heart. In a short time,
the weaker atria will collapse and little to no blood will be pumped out by the ventricles.
The patient would die from a reduction in cardiac output.
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