Sustained ischemia within a given myocardial region will most likely result in an infarction. As noted above, as in any microcirculatory bed, the greatest resistance to coronary blood flow occurs in the arterioles.
Blood flow through such vessels varies approximately with the fourth power of these vessels' radii; hence, the key regulated variable for the control of coronary blood flow is the degree of constriction or dilatation of coronary arteriolar vascular smooth muscle.
As with all systemic vascular beds, the degree of coronary arteriolar smooth muscle tone is normally controlled by multiple independent negative feedback loops. These mechanisms include various neural, hormonal, local non-metabolic and local metabolic regulators. It should be noted that the local metabolic regulators of arteriolar tone are usually the most important for coronary flow regulation; these feedback systems involve oxygen demands of the local cardiac myocytes.
In general, at any one point in time, coronary blood flow is determined by integrating all the different controlling feedback loops into a single response i. It is also common to consider that some of these feedback loops are in opposition to one another.
Interestingly, coronary arteriolar vasodilation from a resting state to one of intense exercise can result in an increase of mean coronary blood flow from approximately 0.
As with all systemic circulatory vascular beds, the aortic or arterial pressure perfusion pressure is vital for driving blood through the coronaries, and thus needs to be considered as another important determinant of coronary flow. More specifically, coronary blood flow varies directly with the pressure across the coronary microcirculation, which can be essentially considered as the aortic pressure, since coronary venous pressure is near zero.
However, since the coronary circulation perfuses the heart, some very unique determinants for flow through these capillary beds may also occur; during systole, myocardial extravascular compression causes coronary flow to be near zero, yet it is relatively high during diastole note that this is the opposite of all other vascular beds in the body.
Oxygenated blood is pumped into the aorta from the left ventricle. This is where it enters the right and left main coronary arteries, and subsequent branching feeds the myocardial tissue of all four chambers of the heart see Figure 7. The ascending portion of the aorta is where the origins ostia of the right and left coronaries reside; specifically, they exit the ascending aorta immediately superior to the aortic valve at the sinus of Valsalva.
Blood flow into the coronary arteries is greatest during ventricular diastole when aortic pressure is highest and it is greater than in the coronaries. There are also anterior cardiac veins and thesbesian veins drain directly into the cardiac chambers. Although there is considerable heterogeneity among people, the following table indicates the regions of the heart that are generally supplied by the different coronary arteries. This anatomic distribution is important because these cardiac regions are assessed by lead ECGs to help localize ischemic or infarcted regions, which can be loosely correlated with specific coronary vessels; however, because of vessel heterogeneity, actual vessel involvement in ischemic conditions needs to be verified by coronary angiograms or other imaging techniques.
Flow is tightly coupled to oxygen demand. In non-diseased coronary vessels, whenever cardiac activity and oxygen consumption increases there is an increase in coronary blood flow active hyperemia that is nearly proportionate to the increase in oxygen consumption.
Good autoregulation between 60 and mmHg perfusion pressure helps to maintain normal coronary blood flow whenever coronary perfusion pressure changes due to changes in aortic pressure. Adenosine is an important mediator of active hyperemia and autoregulation.
It serves as a metabolic coupler between oxygen consumption and coronary blood flow. Nitric oxide is also an important regulator of coronary blood flow. Therefore, sympathetic activation to the heart results in coronary vasodilation and increased coronary flow due to increased metabolic activity increased heart rate, contractility despite direct vasoconstrictor effects of sympathetic activation on the coronaries.
This is termed "functional sympatholysis. Parasympathetic stimulation of the heart i. However, if parasympathetic activation of the heart results in a significant decrease in myocardial oxygen demand due to a reduction in heart rate, then intrinsic metabolic mechanisms will increase coronary vascular resistance by constricting the vessels.
The heart muscle, like every other organ or tissue in your body, needs oxygen-rich blood to survive. Blood is supplied to the heart by its own vascular system, called coronary circulation. The aorta the main blood supplier to the body branches off into two main coronary blood vessels also called arteries.
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