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Coronary Circulation


Objectives

  • 1.

    Delineate the physical, neural, and metabolic factors that affect coronary blood flow.

  • 2.

    Explain the relative importance of these factors in the regulation of the coronary circulation.

  • 3.

    Compare the oxygen requirements of the heart during pressure work versus volume work.

  • 4.

    Discuss the metabolic changes caused by ischemia and the role of interstitial adenosine in ameliorating the effects of ischemia.

  • 5.

    Describe the development of coronary collateral vessels.

Functional Anatomy of the Coronary Vessels

The right and left coronary arteries, which arise at the root of the aorta behind the right and left cusps of the aortic valve, respectively, provide the entire blood supply to the myocardium. The right coronary artery supplies principally the right atrium and ventricle. The left coronary artery, which divides near its origin into the anterior descending and the circumflex branches, supplies principally the left ventricle and atrium, but there is some overlap. In humans, the right coronary artery is dominant in 50% of individuals, and the left coronary artery is dominant in another 20%. The flows delivered by the two main arteries are about equal in the remaining 30%. The epicardial distribution of the coronary arteries and veins is illustrated in Fig. 11.1 .

Fig. 11.1, Anterior and posterior views of the heart, illustrating the location and distribution of the principal coronary vessels.

The microcirculatory unit of coronary vessels consists of terminal arterioles, precapillary sinuses, capillaries, and venules. Cardiac myocytes are surrounded by capillaries that, in general, are aligned with them. The average length of the microcirculatory unit is about 350 μm. During diastole, precapillary sinuses may serve as a blood reservoir. During systole, these sinuses disgorge the blood so as to sustain myocyte perfusion.

After the blood passes through the capillary beds, most of the venous blood returns to the right atrium through the coronary sinus. However, some of the blood reaches the right atrium by way of the anterior coronary veins. There are also vascular communications between the vessels of the myocardium and the cardiac chambers. These constitute the arteriosinusoidal , arterioluminal, and thebesian vessels . The arteriosinusoidal channels consist of small arteries or arterioles. These vessels lose their arterial structure as they penetrate the chamber walls and divide into irregular, endothelium-lined sinuses (50 to 250 μm). These sinuses anastomose with other sinuses and with capillaries, and they communicate with the cardiac chambers. The arteriosinusoidal vessels are small arteries or arterioles that open directly into the atria and ventricles. The thebesian vessels are small veins that connect capillary beds directly with the cardiac chambers, and they also communicate with cardiac veins and other thebesian veins. On the basis of anatomical studies, intercommunication appears to exist among all the minute vessels of the myocardium in the form of an extensive plexus of subendocardial vessels. However, the myocardium does not receive significant nutritional blood flow directly from the cardiac chambers.

Coronary Blood Flow is Regulated by Physical, Neural, and Metabolic Factors

Physical Factors

The principal factor responsible for perfusion of the myocardium is the aortic pressure, which is generated by the heart itself. Changes in aortic pressure generally evoke parallel changes in coronary blood flow. If a cannulated coronary artery is perfused by blood from a pressure-controlled reservoir, perfusion pressure can be altered without changing aortic pressure and cardiac work. Under these conditions, abrupt variations in perfusion pressure produce equally abrupt changes in coronary blood flow in the same direction. However, maintenance of the perfusion pressure at the new level is associated with a return of blood flow toward the level observed before the induced change in perfusion pressure ( Fig. 11.2 ). This phenomenon is an example of autoregulation of blood flow . As discussed in Chapter 9 , autoregulation in coronary arteries is mediated by a myogenic mechanism, by the metabolic activity of cardiac muscle, and by the endothelium. Thus autoregulation depends on the interplay of activities of vascular smooth muscle and cardiac muscle. Under normal conditions, blood pressure is kept within relatively narrow limits by the baroreceptor reflex mechanisms.

Fig. 11.2, Pressure-flow relationships in the coronary vascular bed. At constant aortic pressure, cardiac output, and heart rate, coronary artery perfusion pressure was abruptly increased or decreased from the control level indicated by the point where the two lines cross. The closed circles represent the flows that were obtained immediately after the change in perfusion pressure; the open circles represent the steady-state flows at the new pressures. There is a tendency for flow to return toward the control level (autoregulation of blood flow), which is most prominent over the intermediate pressure range (about 60–180 mm Hg).

However, alterations of cardiac work, produced by an increase or decrease in aortic pressure, have a considerable effect on coronary resistance. Increased metabolic activity of the heart decreases the coronary vascular resistance, and a reduction in cardiac metabolism increases the coronary resistance. The position of the autoregulatory region is affected by the metabolic state of cardiac muscle ( Fig. 11.3 ). Hence changes in coronary blood flow are caused mainly by caliber changes of the coronary resistance vessels in response to metabolic demands of the heart. Coronary flow reserve is the difference between maximal flow as caused by a vasodilator drug and the flow in the physiological range.

Fig. 11.3, Illustration of autoregulation in coronary vasculature and the effect of metabolic activity on the position of the auto-regulatory region. When cardiac metabolism increases, as during exercise, autoregulation persists as the pressure-flow relation shifts upward.

In addition to providing the head of pressure to drive blood through the coronary vessels, the heart also influences its blood supply by the squeezing effect of the contracting myocardium on the blood vessels that course through it ( extravascular compression or extracoronary resistance ). This force is so great during early ventricular systole that blood flow, as measured in a large coronary artery that supplies the left ventricle , is briefly reversed. Maximal left coronary inflow occurs in early diastole, when the ventricles have relaxed and extravascular compression of the coronary vessels is virtually absent. This flow pattern is seen in the phasic coronary flow curve for the left coronary artery ( Fig. 11.4 ). After an initial reversal in early systole, left coronary blood flow follows the aortic pressure until early diastole, when it rises abruptly and then declines slowly as aortic pressure falls during the remainder of diastole.

Clinical Box

The minimal extravascular resistance and absence of left ventricular work during diastole can be used to improve myocardial perfusion in patients with damaged myocardium and low blood pressure. The method, called counterpulsation , consists of the insertion of an inflatable balloon into the thoracic aorta through a femoral artery. The balloon is inflated during ventricular diastole and deflated during systole. This procedure enhances coronary blood flow during diastole by raising diastolic pressure at a time when coronary extravascular resistance is lowest. Furthermore, it reduces cardiac energy requirements by lowering aortic pressure (afterload) during ventricular ejection.

Fig. 11.4, Comparison of phasic coronary blood flow in the left and right coronary arteries.

Left ventricular intramural pressure ( pressure within the wall of the left ventricle ) is greatest near the endocardium and least near the epicardium. However, under normal conditions this pressure gradient does not impair endocardial blood flow, because a greater blood flow to the endocardium during diastole compensates for the greater blood flow to the epicardium during systole. In fact, when radioactive spheres, 10 μm in diameter, are injected into the coronary arteries, their distribution indicates that the blood flows to the epicardial and endocardial halves of the left ventricle are approximately equal (slightly higher in the endocardium) under normal conditions. The equality of epicardial and endocardial blood flows indicates that the tone of the endocardial resistance vessels is less than the tone of the epicardial vessels because extravascular compression is greatest at the endocardial surface of the ventricle.

Clinical Box

Under abnormal conditions, when diastolic pressure in the coronary arteries is low (such as in severe hypotension, partial coronary artery occlusion, and severe aortic stenosis ), the ratio of endocardial to epicardial blood flow falls below a value of 1. This change indicates that blood flow to the endocardial regions is more severely impaired than that to the epicardial regions of the left ventricle. Reduced blood flow to the endocardium is also reflected in an increase in the gradient of myocardial lactic acid and adenosine concentrations from epicardium to endocardium. Thus the myocardial damage observed in the left ventricle after occlusion of a major coronary artery is greater in the inner wall than in the outer wall of the ventricle.

Flow in the right coronary artery shows a similar pattern (see Fig. 11.4 ). However, because of the lower pressure developed during systole by the thin right ventricle, reversal of blood flow does not occur in early systole, and systolic blood flow constitutes a much greater proportion of total coronary inflow than it does in the left coronary artery.

The extent to which extravascular compression restricts coronary inflow can readily be detected when the heart is suddenly arrested in diastole, or with the induction of ventricular fibrillation. Fig. 11.5 illustrates the changes in mean left coronary flow when the vessel was perfused with blood at a constant pressure from a reservoir. At the arrow in Fig. 11.5A , ventricular fibrillation was electrically induced, and blood flow increased immediately and substantially. Subsequent increase in coronary resistance over a period of 30 minutes reduced myocardial blood flow to below the level that existed before induction of ventricular fibrillation (see Fig. 11.5B , before stellate ganglion stimulation).

Fig. 11.5, (A) Unmasking of the restricting effect of ventricular systole on mean coronary blood flow by induction of ventricular fibrillation during constant pressure perfusion of the left coronary artery. (B) Effect of cardiac sympathetic nerve stimulation on coronary blood flow and coronary sinus blood O 2 tension in the fibrillating heart during constant pressure perfusion of the left coronary artery.

Tachycardia and bradycardia have dual effects on coronary blood flow. A change in heart rate is accomplished chiefly by shortening or lengthening of diastole. During tachycardia, the proportion of time spent in systole, and consequently the period of restricted inflow, increases. However, this mechanical reduction in mean coronary flow is overridden by the coronary vasodilation that is associated with the greater metabolic activity that prevails when the heart is beating rapidly. When bradycardia prevails, the opposite is true. Coronary inflow is less restricted (more time in diastole), but the metabolic (O 2 ) requirements of the myocardium are also diminished.

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