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69 Cards in this Set
- Front
- Back
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3 factors that influence cardiac perfusion:
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1) metabolic demand=sympathetic stimulation of Beta-1's, cardial musclulature stimulation causes increased demand
2)pressures generated by the muscluature during contraction 3) aortic hydrostatic blood pressure |
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pressures in the heart are greatest in/when?
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systole in the left ventricle and the endocardium (more pressure than epicardium)
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what part of the heart is most likely to be ischemic?
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endocardium of the left ventricle
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effect of vent pressure on coronary flow. As left Ventricular pressure increases...
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there is a drop in flow to coronary arteries near the left ventricle. this is more evident in the Left ventricle because the right ventricle doesn't have as much pressure.
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ionic changes that occur inside the cell during ischemia
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increased Na and Ca, Decreased K
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ionic changes that occur outside the cell during ischemia
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decreased Na, decreased Ca and increased K
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impact of ischemia within 10 minutes..
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membrane potential begins to depolarize increasing permeability to Na and Ca. this causes predisposition to arrythmias.
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Explain why ST segment appears elevated in STEMi
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no current flow during phase 4 rest. It appears ST segment is elevated but in reality the rest of the EKG is depressed because of increased Ca and Na permeability.
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reperfusion injury can occur due to...
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inflammatory process producing an invastion by macrophages and secretion of cytokines. Mechanical damage when ATP is returned.
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ischemic blood vessels will
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maximally dilate
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extracellular tissue is more_____ in response to intracellular ischemic tissue
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more negative. this is why the ST segment appears elevated.
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Non-stemi shows depressed ST segment because:
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ischemia is limited to the endocardial surface of the heart.So the epicardial surface is positive at rest compared to the endocardial surface. Causes the ST depression.
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coronary flow influence by 3 factors
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1) metabolic demand (sympathetic stimulation of heart, increased metabolism)
2) pressures generated by musclulature during cardiac cycle 3) aortic hydrostatic BP (higher pressure causes more blood to enter coronaries) |
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what does sympathetic stimulation due to coronary vasculature?
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nothing! but the muscle will increase metabolism.
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pressures generated by contracting heart reduce coronary blood flow. pressures are greatest during?
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1) systole
2) in the left ventricle (because it squeezes hardest) 3) in the endocardium (because it's physical pressure clampind down is harder) |
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what part of heart is most likely to be region of ischemia?
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Left ventricle, endocardium
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as left ventricular pressure rises what happens to flow in left coronary artery?
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flow drops as the left ventricle contracts, most deep drop occurs during isovolemic contraction of ventricle
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our greates perfusion in the left ventricle occurs..
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when we get relaxation of L ventricle. (the aortic pressure is still high right at this second)
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right coronary artery (correlates to pulmonary flow) doesn't show the drop in flow during isovolemic contraction that the left does..why?
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because the right ventricle doesn't contract as forcibly. so the flow during isometric contraction doesn't change, no visible change in contour of flow on his graph. (contour parallels the aorta pressure)
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effect of HTN on ischemia to the heart.
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it increases the afterload and therefore increases the work of the heart. PLUS it is squeezing off vasculature to the ventricles more than in normotensive pt. (HTN causees increased need for blood and decreasd flow) also increases thrombus formation and atherosclerosis
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stroke work is
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stroke volume x mean aortic pressure (dictates the metabolic needs of the heart)
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significant obstruction from atherosclerosis is considered___. We don't get concerned until it reaches ___%
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40% or greater occlusion.. Not concerned clinically until occlusion is 70%.
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70% occlusion reduces blood flow by____
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a much lower % than 70%. It is not equal
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effect of ischemia on ion pumps in cardiac muscle
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ischemia reduces amout of ATP available within minutes-->lack of ATP causes pumps to slow. (Na/K, Ca++ pump, Na/Ca++ exhanger slows) causes less effective contraction (hypokinetic heart)
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What happens specifically to Ca and Na and K ions during ischemia?
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1) lose ability to resequester Ca++ in SR
2) lose ability to get rid of Na and bring K back in to cell 3) lose ability to actively pump Ca out of the cell 4) lose the Na/Ca exchanger |
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intracellular ion changes in ischemia***
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1) Increased Na+
2) increases Ca++ 3) Decreased K+ |
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extracellular ion changes in ischemia
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the opposite of what happens inside the cell. we will have less Na and Ca outside the cell and have more K+ outside the cell.
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what is the impact of ischemia within 10 minutes?
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the membrane potential begins to depolarize, increaseing permeability to Ca++ and partially activates fast Na+ gates.
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explain the changes in EKG baseline related to current flow of ions.
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current flow occurs during phase 4 (not normal) there is no current flow during phase 2 (ST segment) because entire heart depolarized about the same potential. depolarized tissue in ischemic area causes a current flow between the ischemic, depolarized tisse and normal tisse causing the EKG changes. refered to as ST elevation or depression even though it's actually the rest of the cycle which is not at the normal level.
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normal heart tissue can repolarize to -90 and the ischemic area only repolarizes to -50. What will this cause?
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a current flow which will make the ST segment appear elevated on the EKG. It should normally all depolarize at the same level.
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increased intracellular Na+ and Ca++ as well as loss of K+ has what effect on polarization of phase 4?
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reduces polarization. it is less negative. AP amplitude is reduced because the Na gates are no longer present and because we are already starting at a depolarized state before phase 0 is initiated.
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coronary flow influence by 3 factors
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1) metabolic demand (sympathetic stimulation of heart, increased metabolism)
2) pressures generated by musclulature during cardiac cycle 3) aortic hydrostatic BP (higher pressure causes more blood to enter coronaries) |
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what does sympathetic stimulation due to coronary vasculature?
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nothing! but the muscle will increase metabolism.
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pressures generated by contracting heart reduce coronary blood flow. pressures are greatest during?
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1) systole
2) in the left ventricle (because it squeezes hardest) 3) in the endocardium (because it's physical pressure clampind down is harder) |
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what part of heart is most likely to be region of ischemia?
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Left ventricle, endocardium
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as left ventricular pressure rises what happens to flow in left coronary artery?
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flow drops as the left ventricle contracts, most deep drop occurs during isovolemic contraction of ventricle
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our greates perfusion in the left ventricle occurs..
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when we get relaxation of L ventricle. (the aortic pressure is still high right at this second)
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right coronary artery (correlates to pulmonary flow) doesn't show the drop in flow during isovolemic contraction that the left does..why?
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because the right ventricle doesn't contract as forcibly. so the flow during isometric contraction doesn't change, no visible change in contour of flow on his graph. (contour parallels the aorta pressure)
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effect of HTN on ischemia to the heart.
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it increases the afterload and therefore increases the work of the heart. PLUS it is squeezing off vasculature to the ventricles more than in normotensive pt. (HTN causees increased need for blood and decreasd flow) also increases thrombus formation and atherosclerosis
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stroke work is
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stroke volume x mean aortic pressure (dictates the metabolic needs of the heart)
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within 10 min what happens to membrane potential in cardiac muscle
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the membrane potential begins to depolarize increaseing permeability to Ca++ and partially activates fast Na+ gates.
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what causes the changes in the EKG baseline in ischemic tissue?
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current flow is occuring in phase 4 (not normal) and there is no current in phase 2 (ST segment/normal) this causes a current flow between ischemic/depolarized tissue and normal tissue. reffered to as ST depression or elevation even though it's actually the rest of the cycle that's not at it's normal level.
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What happens to the AP of ischemic tissue?
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during rest (phase 4) the ischemic tissue AP amplitude is reduced. increased intracellular Na and Ca as well as loss of K reduces polarization (less negative) reduces polarization of phase 4
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what does the electrode 'see'
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see's the extracellular potential (not intracellular) since the extracellular potential of ischemic tissue is less postive than normal tissue it is recorded/seen as negative. (depressed ST segment)
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Is the extracellular membrane potential of ischemic tissue negative or positive compared to normal tissue?
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Negative, since elecrodes see the extracellular potential differences. (Na and Ca rush in so the extracellular tissue is more neg)
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what happens to the resting membrane potential of ischemic tissue
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there is a decreased resting membrane potential, it is much closer to threshold and prone to arrythmias
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hypokinetic heart
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because of lack of ATP, the tissue cross bridge interaction is inhibited, so this decreases contractile force
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what happens to the amplitude of the AP and phase 0 in ischemic tissue?
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the action potential is slower to be generated (phase 0 has less steep slope) and the AP amplitude is much less. this alters speed of conduction and favors reentry arrhthmias.
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a decreased speed of conduction favors what kind of arrythmias?
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reentry arrhytmias. decreased additional amt of Ca enters during phase 2 (systole) causes weaker conracion, decreased CO, decreased BP and now the non-ischemic heart is working harder.
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exercise stress test can produce a depressed (or elevated) ST segment. what happens to ions in the ischemic tissue
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1) intracellular K+ is decreased
2) intracellular Ca is increased 3)peak Na conduction is decreased 4)intracellular Na concentration is increased 5) Ca conduction is increased in phase 4 (it's partially depolarized and Ca conductance is voltage dependent) |
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exercise would produce ischemia most easily in which part of myocardium?
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endocardial portion of the left ventricle
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how long does it take for cell death to occur in ischemia?
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20-30 minutes. then adjacent regions are at risk due to increase metabolic demand.ischemic and infarcted tissue is hypokinetic.
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how long does it take for remodeling to occur in heart after ischemia/infarct
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one week. it can become dilated or hypertrophic.
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reperfusion injury can occur due to
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inflammatory process produces invasion by macrophages and secretion of cytokines. mechanical damage happens when ATP is returned. reactive hyperemia can potentiate the harmful effects of sudden reperfusion.(influx of inflammatory elements hits ischemic tissue that is completely dilated) All this Calcium is present and no ATP, then all of a sudden there is ATP present, and we get mechanical tears in cardiac muscle.
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baroreceptor reflex response to cardiac failure
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carotid baroreceptors increase TPR, short term control, can cause tissue ischemia
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TPR hormonal response to cardiac failure
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adrenal secretion of Norepi and epi causes vasoconstriction and increases TPR. angiotensin causes vasoconstriction, vasopressin (ADH) secretion stimulated by angiotensin.
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ADH secretion is stimulated by....
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angiotensin
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angiotensin causes
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vasoconstriction
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vasopressin causes....it's stimulated by,..
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vasoconstriction. it's secreted in response to angiotensin and also in response to low osmotic or hydrostatic pressures.
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baroreceptor reflex response to cardiac failure
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increases preload. short term control.
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renin is produced in response to...renin causes...
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lowering BP. renin causes production of angiotensin I-->angiotensin II-->vasoconstriction and salt/fluid retention.
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what causes aldosterone secretion and what does aldosterone do?
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angiotensin causes aldosterone secretion and aldosterone causes additional salt/fluid retention
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natriuretic factor
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atrial natruretic factor is secreted by atrium in response to atrial stretching .causes renal Na+ and fluid excretion. limits increase in blood volume being caused by other reflexes and helps prevent overstretching and excessive preload. (natriuretic factor B is secreted by the ventricles)
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STEMI is generally considered to effect how much of heart?
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transmural infarct. spans the width of the myocardium.
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NSTEMI infarct is restricted to what area of the heart?
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endocardial region most commonly. recording electrode reads a positive value on epicardial region (compared to the endocardial region) shows ST depression. (goes from + to = voltage)
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cocaine's effect on the heart
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blocks reuptake of norepi from sympathetic nerve endings. this causes increase stimulation of beta receptors of heart (tachycardia, increased inotrophy, increased BP) also increased stimulation of alpha receptors (coronary vascular smooth muscle contraction, decreased myocardial perfusion)
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chronically elevated BP can lead to
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arteriosclerosis, endothelial toxic effects of cocaine probably facilitates arteriosclerosis
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myocardial effects of cocaine use
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similar to and can lead to an MI. increased metabolic demand, decreased coronary perfusion, cardiac ischemia=chest pain, ECG changes. long term use can cause LVH
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BP =
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TPR x CO also TPR (HR x SV)
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