3 CORONARY CIRCULATIONThe 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.
4 AnatomyThe 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 heart’s 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 .
5 Coronary CirculationOnly 1/10 mm of the endocardial surface can obtain nutrition from the blood inside the cardiac chamberLeft coronary artery supplies mainly anterior and lateral portions of the left ventricleRight coronary artery supplies most of the right ventricle and some posterior part of the left ventricleMost 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 atriumThebesian veins empty directly into chambers of the heart5
6 Regulation At rest, the coronary circulation receives 5% of CO. Cardiac muscle extracts 70% of available O2 from blood, and it has a very low capacity for anaerobic metabolism, much like the brain.This O2 dependence means that any increase in work must be matched by an increase in coronary flow, achieved entirely through local control mechanisms.
7 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.
8 Coronary CirculationRight and left coronary arteries8
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.
16 When CO is minimal, most sphincters are contracted (“off”), and flow is inhibited. They relax intermittentlyas 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.
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.
23 Coronary Blood FlowEpicardial vs subendocardial CBF (intramyocardial pressure)Epicardial arteries in the outer surface supply most of the muscleSubendocardial arterial plexus is beneath the endocardium23
25 Control of Coronary Blood Flow Local muscle metabolism is the primary controller of CBFOxygen demand as a major factor in local CBF regulationNormally about 70% of O2 is removed as the blood flowsRole of adenosine in vasodilationAnd other substances25
26 Nervous Control of Coronary Blood Flow Autonomic nerves can affect the CBF both directly and indirectlyDirect stimulation of coronary blood vesselsIndirect effects result from secondary changes in CBF caused by increased or decreased activity of the heartDirect effects of nervous stimuli on coronary vasculatureParasympathetic fiber distribution is not greatThere is more sympathetic innervation of coronary vesselsConstrictor receptors are alpha adrenoreceptors (more epicardial)Beta receptors are vasodilatory (more in the intramuscular arteries)26
27 Special Features of Cardiac Muscle Metabolism At rest, cardiac muscle normally consumes fatty acids to supply most of its energy instead of carbohydratesAbout 70% of total energy from fatty acidsHowever, under anaerobic or ischemic conditions, glycolytic mechanism is requiredGlycolysis consumes tremendous amounts of blood glucose and forms large amounts of lactic acidHypoxia, release of adenosine and dilation of coronary artery27
28 Ischemic Heart Disease The most common cause of deathInsufficient coronary blood flowCoronary ischemia, coronary occlusion and myocardial infarction – congestive heart failureAtherosclerosis as a cause of ischemic heart diseaseConsumption of large amounts of cholesterol and lack of mobilityDevelopment of atherosclerotic plaques in major coronary arteries28
29 Acute Coronary Occlusion Acute coronary occlusion occurs frequently in atherosclerotic heart1) Atherosclerotic plaque can cause a local blood clot called a thrombusUnsmooth surface, adherence of blood platelets2) Local muscular spasm of coronary arteries may occurSpasm may result from irritation of smooth muscleOr from local nervous reflexes – plaqueSpasm may lead to secondary thrombosis of the vessel29
30 Value of Collateral Circulation in the Heart In normal heart, there is no communication between large coronary arteriesBut many anastomoses do exist among the smaller arteries ( micrometre in diameter)This collateral circulation may delay appearance of ischemic heart symptoms30
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.
32 Flow interruptionBecause the ventricular myocytes extract such high levels of O2 from the blood, a delicate balance exists between myocardial workload and coronary supply. If the balance is disturbed, then myocytes becomeischemic and infarcted. Most commonly, this occurs due to atherosclerosis and coronary artery disease.
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 O2 deficit continues, the myocytes release lactic acid, which stimulates pain fibers within the myocardium and causes angina pectoris.
43 Myocardial Infarction After coronary occlusion, blood flow ceases beyond the blockageCardiac muscle has little or no blood flowThe overall process is called myocardial infarctionAfter the onset of MI, small amounts of collateral blood begin to seep into the infarcted areaProgressive dilation of local blood vesselsIn later stages, the vessel walls become highly permeable and leak fluidCardiac muscle tissue becomes edematousSubendocardial infarction and systolic contraction43
44 Acute Myocardial 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.Acute Myocardial InfarctionInfarction
45 Causes of Death After Coronary Occlusion 1) Decreased cardiac output2) Damming of blood in the pulmonary edema3) Fibrillation of the heart4) Rupture of the heart45
46 Causes of Death After Coronary Occlusion 1) Decreased cardiac output (Systolic stretch and cardiac shock)Systolic stretchIncapable heart to pump sufficient blood into the peripheral arterial treeCoronary shock, cardiogenic shock, cardiac shock or low cardiac output failureCardiac shock occurs when >40% of the LV is infarctedDeath occurs in 85% of patients once they develop cardiac shock46
47 Causes of Death After Coronary Occlusion 1) Decreased cardiac output (Systolic stretch and cardiac shock)47
48 Causes of Death After Coronary Occlusion 2) Damming of blood in the body’s venous systemAcutely reduced cardiac output leads to diminished blood flow to the kidneysThe kidneys fail to excrete enough urineThis adds to progressively to the total blood volume and congestive symptomsDevelopment of pulmonary edema48
49 Causes of Death After Coronary Occlusion 3) Fibrillation of the ventricles after myocardial infarctionSudden ventricular fibrillationFour factors into tendence for the heart to fibrillate:a) Acute loos of blood supply to the cardiac muscle and increased K ions in the extracellular space* irritability of cardiac muscleb) Ischemia of the muscle causes “injury current”* ischemic muscle cannot completely repolarizec) Powerful sympathetic reflexes develop after massive infarction – irritability increasesd) Cardiac muscle weakness causes the ventricles to dilate excessively.* This increases the pathway length for impulse conduction49
50 Causes of Death After Coronary Occlusion 4) Rupture of the infarcted areaDead heart muscle bulges outward with each contractionSystolic stretch becomes greater and the heart may ruptureLoss of blood into the pericardial space and development of cardiac tamponade50
51 Stages of Recovery from Acute Myocardial Infarction Small or large ischemic areaReplacement of dead muscle by scar tissueAfter a few days to three weeks, most of the nonfunctional muscle becomes functional again or dieFibrous tissue begins developing among the dead fibers, ischemia stimulates growth of fibroblasts51
52 Prolonged ischemia of the heart leads to myocardial infarction Prolonged ischemia of the heart leads to myocardial infarction. Cells begin to die approximately 20 min after the onset of a coronary occlusion and killing is complete after 6 hr.A heart slice with a fresh infarct
53 Recovery from MI Value of rest in treating myocardial infarction Effect of exercise or emotional strainFunction of the heart after recovery from MIOccasionally a heart that has recovered from a large MI returns almost to full functional capabilityMore frequently its pumping capability is permanently decreased below that of a healthy heartCardiac reserve – reduction to 100%Pain in coronary heart diseaseFeeling the heartIschemic cardiac muscle often causes pain sensationHistamine, kinins, cellular proteolytic enzymes, lactic acid etc53
54 Angina PectorisProgressive constriction of coronary arteries, cardiac pain, angina pectorisIt appears when the load on the heart increasesUsually felt beneath the sternum and often referred to left arm, shoulder and neckExercise or emotional stress increases anginaTreatmentVasodilator drugsNitroglycerin and other nitrate drugsBeta adrenergic blockers – inhibition of sympathetic activity of the heartPropranolol54
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