The coronary circulation consists of the blood vessels that supply blood to, and remove blood from, the heart muscle itself. Although blood fills the chambers of the heart, the muscle tissue of the heart, or myocardium, is so thick that it requires coronary blood vessels to deliver blood deep into the myocardium. The vessels that supply blood high in oxygen to the myocardium are known as coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle are known as cardiac veins.
The coronary arteries that run on the surface of the heart are called epicardial coronary arteries. These arteries, when healthy, are capable of autoregulation to maintain coronary blood flow at levels appropriate to the needs of the heart muscle. These relatively narrow vessels are commonly affected by atherosclerosis and can become blocked, causing angina or a heart attack. (See also: circulatory system.)
The coronary arteries are classified as "end circulation", since they represent the only source of blood supply to the myocardium: there is very little redundant blood supply, which is why blockage of these vessels can be so critical.
Contents
1 Coronary anatomy
1.1 Variations
1.2 Coronary artery dominance
2 Blood supply of the papillary muscles
3 Coronary flow
Coronary anatomy
The exact anatomy of the myocardial blood supply varies considerably from person to person. A full evaluation of the coronary arteries requires cardiac catheterization or CT coronary angiography.
In general there are two main coronary arteries, the left and right.
Right coronary artery
Left coronary artery
Both of these arteries originate from the beginning (root) of the aorta, immediately above the aortic valve. As discussed below, the left coronary artery originates from the left aortic sinus, while the right coronary artery originates from the right aortic sinus
Variations
Four percent of people have a third, the posterior coronary artery. In rare cases, a patient will have one coronary artery that runs around the root of the aorta.
Occasionally, a coronary artery will exist as a double structure (ie there are two arteries, parallel to each other, where ordinarily there is one). Dana Carvey has this variation, which led to a mishap during his CABG operation.
Coronary artery dominance
The artery that supplies the posterior descending artery (PDA) and the posterolateral artery (PLA) determines the coronary dominance.
If the right coronary artery (RCA) supplies both these arteries, the circulation can be classified as "right-dominant".
If the left circumflex artery (LCX) supplies both these arteries, the circulation can be classified as "left-dominant".
If the RCA supplies the PDA and the LCX supplies the PLA, the circulation is known as "co-dominant".
Approximately 70% of the general population are right-dominant, 20% are co-dominant, and 10% are left-dominant. [1]
Blood supply of the papillary muscles
The papillary muscles tether the mitral valve (the valve between the left atrium and the left ventricle) and the tricuspid valve (the valve between the right atrium and the right ventricle) to the wall of the heart. If the papillary muscles are not functioning properly, the mitral valve leaks during contraction of the left ventricule. This causes some of the blood to travel "in reverse", from the left ventricle to the left atrium, instead of forward to the aorta and the rest of the body. This leaking of blood to the left atrium is known as mitral regurgitation.
The anterolateral papillary muscle receives two blood supplies: the LAD and LCX, and is therefore somewhat resistant to coronary ischemia. On the other hand, the posteromedial papillary muscle is supplied only by the PDA. This makes the posteromedial papillary muscle significantly more susceptible to ischemia. The clinical significance of this is that a myocardial infarction involving the PDA is more likely to cause mitral regurgitation.
Coronary flow
During contraction of the ventricular myocardium (systole), the subendocardial coronary vessels (the vessels that enter the myocardium) are compressed due to the high intraventricular pressures. However the epicardial coronary vessels (the vessels that run along the outer surface of the heart) remain patent. Because of this, blood flow in the subendocardium stops. As a result most myocardial perfusion occurs during heart relaxation (diastole) when the subendocardial coronary vessels are patent and under low pressure. This contributes to the filling difficulties of the coronary arteries.
The primary determinant of coronary blood flow is the level of myocardial/cardiac oxygen consumption. As the heart beats more vigorously, ATP is consumed at a greater rate due to the increased force and/or frequency of contraction and the depolarization and repolarization of the cardiac membrane potential. The increase in oxygen consumption results in the release of a vasodilator substance, the identity of which remains unknown. The vasodilator reduces vascular resistance and allows more blood to flow through the heart during each diastole. Systolic compression remains the same. Failure of oxygen delivery via increases in blood flow to meet the increased oxygen demand of the heart results in tissue ischemia, a condition of oxygen debt. Brief ischemia is associated with intense chest pain, known as angina. Severe ischemia can cause the heart muscle to die of oxygen starvation, called a myocardial infarction. Chronic moderate ischemia causes contraction of the heart to weaken, known as myocardial hibernation.
In addition to metabolism, the coronary circulation possesses unique pharmacologic characteristics. Prominent among these is its reactivity to adrenergic stimulation. The majority of circulation in the body constrict to norepinephrine, a sympathetic neurotransmitter the body uses to increases blood pressure. In the coronary circulation, norepinephrine elicits vasodilation, due to the predominance of beta-adrenergic receptors in the coronary circulation. Agonists of alpha-receptors, such as phenylephrine, elicit very little constriction in the coronary circulation.
Tuesday, December 19, 2006
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