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Physiology of the Coronary Blood flow

*Normal coronary blood flow: The resting coronary blood flow in human being averages about 225 ml /min, which is about 4 to 5 percent of the total cardiac output. The cardiac output (CO) can be increased to fourfold up to sevenfold in young adults during strenuous exercises, and it pumps this blood against a higher than normal arterial blood pressure, in other words, the cardiac output under severe conditions may increase six fold to nine fold. While, the coronary blood flow increases three fold to fourfold during exercise to supply the extra nutrients needed to the heart, such increases is not as much as the increase in work load, which means that O2 supply to the myocardium could not meet its energy requirement

The energy requirements of the myocardium are provided almost aerobically with little capacity for anaerobic metabolism. During resting condition, 70 to 80 % of oxygen carried by coronary blood is extracted by the myocardium. Because of the limited capacity to increase oxygen availability by further increasing oxygen extraction, increases of myocardial demands during exercise or other stress must be met by equivalent increases of the coronary blood flow. Myocardial ischemia results from imbalance between O2 supply to the myocardium and its O2 requirement.

Collateral channels are blood vessels (usually small) which allow blood to flow directly from one artery to another; hence if an artery becomes obstructed, and the collateral channels exist they can allow the arterial blood to enter the blocked vessel beyond the site of obstruction. Under normal conditions such collateral channels appear to have a little function, but they can undergo substantial enlargement when atherosclerotic disease involves the coronary arteries

Blood flow in the coronaries is usually regulated almost exactly in proportion to the need of the cardiac musculature for oxygen, mainly by local arterial and arteriolar vasodilatation in response to cardiac muscle's need for nutrition. This mechanism works equally well even when the nerves to the heart are intact or when they are removed. So, whenever the force and/or the rate of myocardium contraction are increased, regardless of cause; the coronary blood flow simultaneously increases. Conversely, decreased myocardium activity is accompanied by decreased coronary flow

The decrease in oxygen concentration in the heart causes vasodilator substances to be released from the muscle cells that in turn dilate the arterioles. One of the substances which have the greatest vasodilator propensity is adenosine. In the presence of a very low concentration of oxygen in heart muscle, a large proportion of cell's ATP degrades to adenosine monophosphate; then a small portion of this are further degraded to release adenosine into the tissue fluids of the heart muscle. After the adenosine causes vasodilatation, much of it is reabsorbed into the cardiac cells to be reused. Adenosine is not the only vasodilator product that has been identified, while others include adenosine phosphate compounds, potassium ions, hydrogen ions, carbon dioxide, and possibly, prostaglandins

*Local influences from endothelial cells;


Endothelial cells cover the entire inner surfaces of the cardiovascular system. It has been reported that blood vessels could respond in a different or abnormal way to different physiological stimuli, if its endothelial lining are damaged or injured as occurs in atherosclerosis. For example, Acetylcholine, cause vasodilatation of intact vessels but cause vasoconstriction of the vessels with damaged endothelial lining. The endothelial cells respond to various stimuli by producing a local factors that can decrease the tone of the overlying smooth muscle layers, as the EDRF(endothelial derived relaxing factor),which is known now as nitric oxide

The nitric oxide easily diffuses to adjacent smooth muscle cells where it causes its relaxation. Acetylcholine and several other agents (including bradykinin, and vasoactive intestinal peptide) stimulate endothelial cells nitric oxide production because their receptors on endothelial cells are linked to receptor-operated Ca2+ channel. This is in addition to the flow related shear stresses on endothelial cells which occur during exercise, as increased blood flow during exercise stimulate the production of endothelial cell nitric oxide. Endothelial cells have been also shown to produce several other locally acting vasoactive agents including the vasodilators e.g. (endothelial-derived hyperpolarizing factor "EDHF", and prostacycline ("PGI2") and the vasoconstrictors, endothelin

Determinants of myocardium oxygen consumption The oxygen consumption of the whole heart (MVO2) can be determined using fick equation, provided the arteriovenous (AV) O2 difference across the coronary bed, and the coronary blood flow (CBF) are known, where MVO2= CBF X AVO2. There are four main factors that mainly determine the myocardial oxygen consumption as they are related to the performance of the myocardium; these are the heart rate, peak systolic

blood pressure, wall tension, and the level of inotropic state.

The heart rate, the frequency of cardiac

contraction is a very important determinant of MVO2, as there is a linear relation between increases in heart rate and increases in cardiac O2 requirement. Under controlled experimental conditions when the heart is contracting isovolumetrically (stroke volume is heled constant), if the heart rate is doubled by electrical pacing, the MVO2 approximately doubles to match the increased number of beats per minutes (Guyton,"2000").

Another important determinant of MVO2 is

the peak systolic blood pressure (SBP) or the peak systolic tension

developed by the left ventricle. It has been determined that there is a linear relation between MVO2 and peak systolic blood pressure, which occurs either in ventricles made to contract isovolumetrically or in beating heart .Under normal conditions, the product of systolic blood pressure by the heart rate has been found to adequately reflect changes in MVO2

One of the common methods used to estimate the myocardial workload (and resulting oxygen consumption) is the product of peak systolic blood pressure and the heart rate. It is considered as an index of relative cardiac work, termed the double product, or rate-pressure product (RPP).It relates closely to the directly measured myocardial oxygen consumption and coronary blood flow in healthy subjects over a wide range of exercise intensities. RPP=SBP X HR. Changes in heart rate and blood pressure contribute equally to changes in RPP. Typical values for RPP range from 6,000 under resting conditions e.g. (HR=50 bpm, and SBP=120 mm Hg) to 40,000 during strenuous exercise, e.g. (HR=200 bpm, and SBP = 200 mmHg) or higher depending on intensities and mode of exercise

Research with heart disease patients has shown a physiologic correlation between the RPP, the onset of angina pectoris, and the elecrocardiographic abnormalities during exercise. In this regard, the RPP provides an objective yardstick to evaluate the effect of cardiac performance in various clinical, surgical, or exercise intervention. The well documented lowering of exercise heart rate and systolic pressure (hence lower RPP and lower myocardial O2 requirement) with training help to explain improved exercise capacity of cardiac patients