Lifesaving Value of Collateral Circulation in the Heart

degree of damage to the heart muscle caused either by slowly developing atherosclerotic constriction of the coronary arteries or by sudden coronary occlusion is determined to a great extent by the degree of collateral circulation that has already developed or that can open within minutes after the occlusion.

In a normal heart, almost no large communications exist among the larger coronary arteries. But many anastomoses do exist among the smaller arteries sized 20 to 250 micrometers in diameter, as shown in Figure 21-6.

When a sudden occlusion occurs in one of the larger coronary arteries, the small anastomoses begin to

Minute anastomoses in the normal coronary arterial system.

Cardiac Collateral Circulation

Minute anastomoses in the normal coronary arterial system.

Figure 21-6

Figure 21-6

dilate within seconds. But the blood flow through these minute collaterals is usually less than one half that needed to keep alive most of the cardiac muscle that they now supply; the diameters of the collateral vessels do not enlarge much more for the next 8 to 24 hours. But then collateral flow does begin to increase, doubling by the second or third day and often reaching normal or almost normal coronary flow within about 1 month. Because of these developing collateral channels, many patients recover almost completely from various degrees of coronary occlusion when the area of muscle involved is not too great.

When atherosclerosis constricts the coronary arteries slowly over a period of many years rather than suddenly, collateral vessels can develop at the same time while the atherosclerosis becomes more and more severe. Therefore, the person may never experience an acute episode of cardiac dysfunction. But, eventually, the sclerotic process develops beyond the limits of even the collateral blood supply to provide the needed blood flow, and sometimes the collateral blood vessels themselves develop atherosclerosis. When this occurs, the heart muscle becomes severely limited in its work output, often so much so that the heart cannot pump even normally required amounts of blood flow. This is one of the most common causes of the cardiac failure that occurs in vast numbers of older people.

Myocardial Infarction

Immediately after an acute coronary occlusion, blood flow ceases in the coronary vessels beyond the occlusion except for small amounts of collateral flow from surrounding vessels. The area of muscle that has either zero flow or so little flow that it cannot sustain cardiac muscle function is said to be infarcted. The overall process is called a myocardial infarction.

Soon after the onset of the infarction, small amounts of collateral blood begin to seep into the infarcted area, and this, combined with progressive dilation of local blood vessels, causes the area to become overfilled with stagnant blood. Simultaneously the muscle fibers use the last vestiges of the oxygen in the blood, causing the hemoglobin to become totally de-oxygenated. Therefore, the infarcted area takes on a bluish-brown hue, and the blood vessels of the area appear to be engorged despite lack of blood flow. In later stages, the vessel walls become highly permeable and leak fluid; the local muscle tissue becomes edematous, and the cardiac muscle cells begin to swell because of diminished cellular metabolism. Within a few hours of almost no blood supply, the cardiac muscle cells die.

Cardiac muscle requires about 1.3 milliliters of oxygen per 100 grams of muscle tissue per minute just to remain alive. This is in comparison with about 8 milliliters of oxygen per 100 grams delivered to the normal resting left ventricle each minute. Therefore, if there is even 15 to 30 per cent of normal resting coronary blood flow, the muscle will not die. In the central portion of a large infarct, however, where there is almost no collateral blood flow, the muscle does die.

Subendocardial Infarction. The subendocardial muscle frequently becomes infarcted even when there is no evidence of infarction in the outer surface portions of the heart. The reason for this is that the subendocar-dial muscle has extra difficulty obtaining adequate blood flow because the blood vessels in the subendo-cardium are intensely compressed by systolic contraction of the heart, as explained earlier. Therefore, any condition that compromises blood flow to any area of the heart usually causes damage first in the subendo-cardial regions, and the damage then spreads outward toward the epicardium.

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