CORONARY CIRCULATION. The coronary circulation supplies the myocardium, a tissue that rivals the...

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Transcript of CORONARY CIRCULATION. The coronary circulation supplies the myocardium, a tissue that rivals the...

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CORONARY CIRCULATION Slide 2 Slide 3 The coronary circulation supplies the myocardium, a tissue that rivals the brain in terms of its nutritional demands and the critical importance of continued flow for normal function. Slide 4 Anatomy The myocardium is supplied by left and right coronary arteries that originate from the root of the ascending aorta immediately above the aortic valve. The right coronary artery generally supplies the right heart, whereas the left coronary artery supplies the left. The arteries course over the hearts surface and then dive down through the muscle layers. The vasculature is notable for numerous collaterals connecting adjacent arteries and also for the presence of precapillary sphincters. Slide 5 Coronary Circulation Only 1/10 mm of the endocardial surface can obtain nutrition from the blood inside the cardiac chamber Left coronary artery supplies mainly anterior and lateral portions of the left ventricle Right coronary artery supplies most of the right ventricle and some posterior part of the left ventricle Most coronary venous blood returns to the right atrium by coronary sinus (75% of total coronary flow) Anterior cardiac veins from right ventricle open directly into the right atrium Thebesian veins empty directly into chambers of the heart Slide 6 Regulation At rest, the coronary circulation receives 5% of CO. Cardiac muscle extracts 70% of available O 2 from blood, and it has a very low capacity for anaerobic metabolism, much like the brain. This O 2 dependence means that any increase in work must be matched by an increase in coronary flow, achieved entirely through local control mechanisms. Slide 7 1.Local controls: Coronary resistance vessels are exceptionally sensitive to adenosine. Local control mechanisms allow for a fourfold to fivefold increase in coronary flow when CO increases, a phenomenon called coronary reserve. 2. Central controls: Coronary resistance vessels are innervated by both branches of the ANS, but their influence is overridden by local controls. Slide 8 Coronary Circulation Right and left coronary arteries Slide 9 External Heart: Anterior View Slide 10 External Heart: Posterior View Slide 11 Coronary Circulation: Arterial Supply Slide 12 Coronary Circulation: Venous Supply Slide 13 Slide 14 Coronary reserv Slide 15 Precapillary sphincters Precapillary sphincters comprise single smooth muscle cells wrapped around the inlets to individual capillaries. They contract and relax with changes in local metabolite concentrations and function as on/off switches to capillary flow. Slide 16 When CO is minimal, most sphincters are contracted (off), and flow is inhibited. They relax intermittently as local metabolite levels rise but again contract when the increased flow washes the metabolites away. At rest, only a small proportion (20%) of sphincters is relaxed, and capillaries are actively perfused, but the pattern of capillary flow shifts continually (vasomotion). When cardiac workload increases, levels of metabolic waste products rise, and the sphincters spend a much greater percentage of time in the on position. At maximal levels of CO, all sphincters are open all the time, and coronary flow rises to maximal levels also. Slide 17 Vasomotion and basis of coronary reserve Slide 18 Extravascular compression Blood flow through most systemic vascular beds follows the aortic pressure curve, rising during systole and falling during diastole. Flow through the left coronary artery drops sharply during systole and then rises sharply with the onset of diastole. This unique flow pattern occurs because ventricular myocytes collapse the arterial supply vessels as they contract (extravascular compression). The effect is felt strongest during early systole because aortic pressure, the main force maintaining vascular patency, is at a low point. During diastole, the compressive forces are removed, and blood surges through the musculature at peak rates. Slide 19 Left coronary blood flow. Slide 20 Normal Coronary Blood Flow Resting coronary blood flow (CBF) is about 225 ml/min CBF increases in proportion to exercise or work output Phasic changes in CBF during systole and diastole Slide 21 Extravascular compression in the left ventricular wall. LV= left ventricle; P= pressure. Slide 22 Slide 23 Coronary Blood Flow Epicardial vs subendocardial CBF (intramyocardial pressure) Epicardial arteries in the outer surface supply most of the muscle Subendocardial arterial plexus is beneath the endocardium Slide 24 Aort kapa Sol koroner arter Sa koroner arter Slide 25 Control of Coronary Blood Flow Local muscle metabolism is the primary controller of CBF Oxygen demand as a major factor in local CBF regulation Normally about 70% of O 2 is removed as the blood flows Role of adenosine in vasodilation And other substances Slide 26 Nervous Control of Coronary Blood Flow Autonomic nerves can affect the CBF both directly and indirectly Direct stimulation of coronary blood vessels Indirect effects result from secondary changes in CBF caused by increased or decreased activity of the heart Direct effects of nervous stimuli on coronary vasculature Parasympathetic fiber distribution is not great There is more sympathetic innervation of coronary vessels Constrictor receptors are alpha adrenoreceptors (more epicardial) Beta receptors are vasodilatory (more in the intramuscular arteries) Slide 27 Special Features of Cardiac Muscle Metabolism At rest, cardiac muscle normally consumes fatty acids to supply most of its energy instead of carbohydrates About 70% of total energy from fatty acids However, under anaerobic or ischemic conditions, glycolytic mechanism is required Glycolysis consumes tremendous amounts of blood glucose and forms large amounts of lactic acid Hypoxia, release of adenosine and dilation of coronary artery Slide 28 Ischemic Heart Disease The most common cause of death Insufficient coronary blood flow Coronary ischemia, coronary occlusion and myocardial infarction congestive heart failure Atherosclerosis as a cause of ischemic heart disease Consumption of large amounts of cholesterol and lack of mobility Development of atherosclerotic plaques in major coronary arteries Slide 29 Acute Coronary Occlusion Acute coronary occlusion occurs frequently in atherosclerotic heart 1) Atherosclerotic plaque can cause a local blood clot called a thrombus Unsmooth surface, adherence of blood platelets 2) Local muscular spasm of coronary arteries may occur Spasm may result from irritation of smooth muscle Or from local nervous reflexes plaque Spasm may lead to secondary thrombosis of the vessel Slide 30 Value of Collateral Circulation in the Heart In normal heart, there is no communication between large coronary arteries But many anastomoses do exist among the smaller arteries (20-250 micrometre in diameter) This collateral circulation may delay appearance of ischemic heart symptoms Slide 31 Collaterals: Collaterals are vessels that connect adjacent arterioles. They are usually constricted in a healthy heart, but, if a supply vessel becomes occluded, they dilate in response to rising metabolite levels. Flow through collaterals may prevent infarction if the occluded vessel is small. In time, these channels enlarge to provide near-normal flow to the ischemic area. Slide 32 Flow interruption Because the ventricular myocytes extract such high levels of O 2 from the blood, a delicate balance exists between myocardial workload and coronary supply. If the balance is disturbed, then myocytes become ischemic and infarcted. Most commonly, this occurs due to atherosclerosis and coronary artery disease. Slide 33 Atherosclerosis: Atherosclerotic lesions appear at an early age in the populations of most Western countries. They evolve to become complex plaques of lipids, hypertrophied myocytes, and fibrous material. Plaques enlarge at the expense of the vascular lumen and impair blood fl ow. This causes an imbalance between coronary supply and myocardial demand, resulting in ischemia. Ischemic myocytes release large quantities of vasoactive compounds, such as adenosine, but vasodilators have no effect on plaque. As the O 2 deficit continues, the myocytes release lactic acid, which stimulates pain fibers within the myocardium and causes angina pectoris. Slide 34 Slide 35 Slide 36 Slide 37 Slide 38 Slide 39 Slide 40 Slide 41 Coronary angiography Slide 42 Coronary angioplasty Slide 43 Myocardial Infarction After coronary occlusion, blood flow ceases beyond the blockage Cardiac muscle has little or no blood flow The overall process is called myocardial infarction After the onset of MI, small amounts of collateral blood begin to seep into the infarcted area Progressive dilation of local blood vessels In later stages, the vessel walls become highly permeable and leak fluid Cardiac muscle tissue becomes edematous Subendocardial infarction and systolic contraction Slide 44 Acute Myocardial Infarction Infarction In the common heart attack a thrombus form in a coronary artery. Death of more than 1/3 of the left ventricle will lead to severe heart failure. Slide 45 Causes of Death After Coronary Occlusion 1) Decreased cardiac output 2) Damming of blood in the pulmonary edema 3) Fibrillation of the heart 4) Rupture of the heart Slide 46 Causes of Death After Coronary Occlusion 1) Decreased cardiac output (Systolic stretch and cardiac shock) Systolic stretch Incapable heart to pump sufficient blood into the peripheral arterial tree Coronary shock, cardiogenic shock, cardiac shock or low cardiac output failure Cardiac shock occurs when >40% of the LV is infarcted Death occurs in 85% of patients once they develop cardiac shock Slide 47 Causes of Death After Coronary Occlusion 1) Decreased cardiac output (Systolic stretch and cardiac shock) Slide 48 Causes of Death After Coronary Occlusion 2) Damming of blood in the bodys venous system Acutely redu