![]() Decades of research in the interim, however, have been unable to demonstrate the role of adenosine in physiologic coronary vasodilation conclusively. The thinking was that adenosine then acted on vascular smooth muscle adenosine receptors to result in increased coronary flow. The hypothesis was that decreased oxygen tension stimulated the release of adenosine due to the consumption and degradation of adenosine triphosphate (ATP). In the 1960s, adenosine was a proposed possible metabolite responsible for triggering coronary vasodilation. ![]() While it is likely that localized hypoxemia and hypercarbia have a role in coronary regulation during pathophysiologic states, it is not yet clear whether an intermediary molecule is involved in the process. Indeed, multiple studies have demonstrated that the concentrations of both oxygen and carbon dioxide are insufficient in explaining the majority of the total extent of coronary vasodilation in response to increased oxygen demand. Measurements of coronary venous pO2 and pCO2, however, show little, if any, change during states of physiologically increased demand (i.e., exercise.) This situation suggests that alternative factors must contribute to coronary regulation under normal conditions that prevent hypoxemia and hypercarbia. ![]() Meanwhile, localized hypoxia, along with the resultant release of vasodilatory substances, likely contributes to coronary vasodilation during various physiologic and pathophysiologic states of mismatched oxygen supply and demand.Īt the most basic level, local hypoxemia and hypercarbia have shown to correlate with coronary vasodilation. Downstream metabolites of oxygen consumption, such as carbon dioxide, are thought to be the primary determinant of coronary flow under physiologic conditions at rest. Current evidence suggests a multifactorial model of coronary regulation. The majority of this demand must be met by increased coronary flow, the mechanisms of which are only partially understood. Due to the high baseline oxygen consumption of the myocardium, increased oxygen extraction provides only a limited buffer capacity. Myocardial oxygen demand can increase several-fold depending on ventricular rate, contractility, and pressures. It also highlights the importance of increasing overall coronary flow during times of increased myocardial oxygen demand. This degree of oxygen extraction is a testament to the high metabolic activity of the myocardium. Due to this pattern of blood flow, tachycardia - and the resultant decrease of time spent in diastole - can decrease the efficiency of myocardial perfusion.Īt rest, approximately 60% to 70% of oxygen is extracted from blood in the coronary arteries. When the ventricles relax during diastole, the coronary vessels are no longer compressed, and normal blood flow resumes. Of note, this compression can be significant enough to reverse coronary flow, particularly in the intramuscular vessels of the thicker left ventricle. The most significant compressive force is felt by the vessels in the endocardial layer, with little force felt by the vessels of the epicardium. This unusual pattern is a result of external compression of coronary vessels by myocardial tissue during systole. Bloodflow through the coronary vessels, however, is seemingly paradoxical and peaks during ventricular diastole. In most tissues, blood flow peaks during ventricular systole due to increased pressure in the aorta and its distal branches. The latter are smaller and course within the myocardium their various branches and arterioles provide higher resistance but more fine-tuned control of blood flow. ![]() The former are larger and more superficial, and they serve as conductors for blood flow. The coronary arteries can broadly classify as epicardial vessels and intramuscular vessels. There is substantial overlap in these blood supplies due to the existence of collateral vessels and variant anatomy, but these intricacies are beyond the scope of the current discussion. The left coronary artery (LCA) arises from the left posterior aortic sinus and quickly bifurcates into the left circumflex artery (LCX) and left anterior descending artery (LAD), which supply blood to the left atrium and left ventricle. The right coronary artery (RCA), arising from the anterior aortic sinus, supplies blood to the right atrium, right ventricle, sinoatrial node, atrioventricular (AV) node, and select portions of the left ventricle. The coronary arteries arise from the sinuses of Valsalva, just past the origin of the aortic root. ![]()
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