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. Progressive ischemic coronary artery disease results in the growth of new vessels termed angiogenesis and collateralization within the myocardium.
Collateralization increases myocardial blood supply by increasing the number of parallel vessels, thereby reducing vascular resistance within the myocardium. Extravascular compression shown to the right during systole markedly affects coronary flow; therefore, most of the coronary flow occurs during diastole. Because of extravascular compression, the endocardium is more susceptible to ischemia especially at lower perfusion pressures.
Furthermore, with tachycardia there is relatively less time available for coronary flow during diastole to occur — this is particularly significant in patients with coronary artery disease where coronary flow reserve maximal flow capacity is reduced. In the presence of coronary artery disease , coronary blood flow may be reduced. This will increase oxygen extraction from the coronary blood and decrease the venous oxygen content.
Phasic changes in blood flow to the right ventricle are less pronounced because of the lesser force of contraction. Central venous pressure may be a more appropriate choice for downstream pressure to calculate the right-sided coronary perfusion pressure. Any increase in heart rate impinges on diastolic time more than systolic time and reduces the perfusion time. Vasomotor tone and deposits inside the vascular lumen determine the vessel wall diameter.
The interplay of various mechanisms that regulate the coronary vasomotor tone usually favours vasodilatation Fig. Factors affecting coronary vasomotor tone. Vasomotor tone is ultimately mediated by the vascular endothelium, which secretes vasodilators; endothelium derived relaxant factor EDRF , nitric oxide and endothelin, a potent vasoconstrictor. Vasomotor tone is almost exclusively determined by local metabolic oxygen demand. Hypoxia causes coronary vasodilatation directly but also releases adenosine and opens ATP-sensitive potassium channels.
Pre-capillary sphincters are relaxed and more capillaries recruited. Under resting conditions, coronary blood flow remains constant between mean arterial pressures of 60— mm Hg. Beyond this range, flow becomes pressure-dependent.
Probable mechanisms include the myogenic response to intraluminal pressure changes fast and metabolic regulation slow. The myocardial oxygen tension and presence of vasoconstrictors or vasodilators influence the range of coronary autoregulation.
Autonomic influences are generally weak. It is difficult to tease out the role of neural control on coronary blood flow, as the metabolic effects of any change in blood pressure, heart rate and contractility dominate the subsequent response. Alpha stimulation may play a role in the distribution of blood flow within the myocardium by restricting metabolically mediated flow increase and exerting an anti-steal affect.
Parasympathetic influences are minor and weakly vasodilatory. The vasodilatory effect of acetylcholine depends on an intact endothelium. Most vasoactive hormones require an intact vascular endothelium. The peptide hormones include antidiuretic hormone, atrial natriuretic peptide, vasoactive intestinal peptide, and calcitonin gene-related peptide.
Antidiuretic hormone in physiological concentration has little effect on the coronary circulation but causes vasoconstriction in stressed patients. The other peptides cause endothelium-mediated vasodilatation. Angiotensin II causes coronary vasoconstriction independent of sympathetic innervation. It also enhances calcium influx and releases endothelin, the strongest vasoconstrictor peptide yet identified in humans. Angiotensin-converting enzyme inactivates bradykinin, a vasodilator.
The vascular endothelium is the final common pathway regulating vasomotor tone. It modulates the contractile activity of the underlying smooth muscle through synthesis and secretion of vasoactive substances in response to blood flow, circulating hormones and chemical substances.
Vasorelaxants are endothelium-derived relaxing factor, nitric oxide, prostacyclin and bradykinin. Vasoconstrictors include endothelin and thromboxane A2. The net response depends on the balance between the two opposing groups. Oxygen delivery is the product of arterial oxygen carrying capacity and myocardial blood flow.
The diastolic pressure time index DPTI is a useful measure of coronary blood supply and is the product of the coronary perfusion pressure and diastolic time. Similarly, oxygen demand can be represented by the tension time index TTI , the product of systolic pressure and systolic time. The EVR is normally 1 or more. Such a value may be reached in a patient with the following physiological data: Note that systolic time is typically fixed at ms, with diastole occupying the remaining time.
The coronary circulation functions in a state of active vasodilatation. Abnormal endothelial nitric oxide production may play a role in diabetes, atherosclerosis and hypertension. Deposits of lipids, smooth muscle proliferation and endothelial dysfunction reduce the luminal diameter. With increasing stenosis, distal arterioles dilate maximally to preserve flow up to the point where the vascular bed is maximally dilated.
Further stenosis leads to a drop in flow and flow becomes pressure dependent. Flow diverted into a dilated parallel bed proximal to a stenosis is called coronary steal and can aggravate ischemia. Flow in collaterals is also often pressure dependent. The left ventricle undergoes hypertrophy in response to raised afterload.
The myofibrillar growth outstrips the capillary network, resulting in decreased capillary density. Raised intramyocardial pressure lowers the subendocardial blood flow. The pressure load increases myocardial work and oxygen demand. Typically the right coronary artery courses along the right anterior atrioventricular groove just below the right atrial appendage and along the epicardial surface adjacent to the tricuspid valve annulus.
It traverses along the tricuspid annulus until it reaches the posterior surface of the heart, where it then commonly becomes the posterior descending artery and runs toward the apex of the left ventricle. Along its course, a number of branches emerge, most notably those that supply the sinus node and the atrioventricular node; hence blockage of such vessels can lead to conduction abnormalities. Additionally, several marginal branches run to the right ventricular and right atrial epicardial surfaces.
The left main coronary artery typically bifurcates quickly upon exiting the ascending aorta into the left circumflex and left anterior descending arteries. The left circumflex artery runs under the left atrial appendage on its way to the lateral wall of the left ventricle.
Along the way, it spawns a number of branches that supply the left atrial and left ventricular walls. In some cases, a branch will course behind the aorta to the superior vena cava such that it can supply the sinus node.
The left anterior descending artery supplies a major portion of the ventricular septum, including the right and left bundle branches of the myocardial conduction system, and the anterior and apical portions of the left ventricle.
Figure 7. Drawing of the coronary arterial circulation in the human heart. The normal human hears does not typically elicit collateralization; each area of myocardium is usually supplied by a single coronary artery. Coronary arteries are so vital to the function of heart; whenever disease states are associated with flow restriction through the coronary arteries, and subsequently the remainder of the coronary circulations capillaries and veins , the effects on cardiac performance are quite dramatic and often fatal.
Coronary artery disease CAD is generally defined as the gradual narrowing of the lumen of the coronary arteries due to coronary atherosclerosis. Atherosclerosis is a condition that involves thickening of the arterial walls from cholesterol and fat deposits that build up along the endoluminal surface of the arteries. With severe disease, these plaques may become calcified and so large that they produce stenoses within the vessels, and thus permanently increase the vascular resistance which is normally low.
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