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pathophysiology Lecture 24 Determinants of Myocardial oxygen demands (MVO2): a-HR(increase demands because of the increase of Number of contractions per minute). b-contractility (as it increases, MVO2 will increase) c- Intramyocardial wall tension during systole (most important)we can represent myocardial wall tension by(tension time index TTI) which is measured by :measuring the area under the curve of the left ventricular pressure curve. Intramyocardial wall tension during systole is determined by 3 parameters: 1)intraventricular pressure (IVP) 2)Radius of ventricle (R) 3)Thickness of the wall those parameters are linked with Laplace law Laplace lowintramyocardial wall tension=(Radius* IVP)/(Thickness*2) It states that: Intramyocardial wall tension is directly related to the product of intraventricular pressure multiplied by radius( R) and inversely related to the thickness multiplied by factor 2 . If systemic pressure increasedIntraventricular pressure increaseincrease ventricular dilationincrease radius of the 1 ventriclesincrease intramyocardial wall tensionincrease MVO2 Hypertrophyincrease thickness of the ventricular walldecrease intramyocardial wall tension-decrease MVO2 Hypertrophy, as process; was initiated due to chronic increasing in hemodynamic load (not acute increase in hemodynamic laod), it is a reversible process, it will increase the thickness of myocardial wall , and by this it will reduce the tension on the walls (because the tension will spread on larger area on the wall) and by this it will reduce the MVO2again;here we are talking about reversible process for short period of time (and the attempt to decrease hemodynamic load will be initiated at the same time. e.g; ANF) BUT when we talk about hypertrophy as chronic process (for long period of time)we need to understand that it will increase the myocardial oxygen demand MVO2 and it will aggravate ischemia as well) Regulation of coronary blood flow (regulation of supply): How heart is supplied? By epicardial vessels then to the intramyocardial ones then capillaries then to the myocytes. Parameters control blood flow: A) Arteriolar resistance (inversely related)---most important factor B) Coronary driving pressure(directly related) If pressure increasesfilling increasesblood flow into these epicardial vessels increases as a result. Epicardial vesselson the surface of the heart (bigger ones) 2 Intramyocardial vesselsinside myocardium(smaller ones) Resistanceit will be determined by intramyocardial vessels(smaller) .If I want to calculate total resistance in the coronary artery ,we will sum the resistance due to epicardial R1 and intramyocardial R2 vessels : Rt=R1+R2 (in normal situation R2< R1) In case of atherosclerosis, the most common sites are epicardial vessels. In case of IHD (the most common cause of atherosclerotic lesions in the epicardial vessels) it will result in shift of resistance to the epicardial vessel rather than intramyocardial ones R1<R2 The distribution of blood between epicardial and intramyocardial vessels is normally kept 1:1 even when we do exercise, because of “Auto regulation” Autoregulation: when intramyocardial vessels sense a drop in blood flow, they will vasodilate ,at the same time when they sense an increase in blood flow they will vasoconstrict to maintain normal perfusion .(So when we do exercise what will keep blood distribution 1:1 between epicardial and intramyocardial vessels is autoregulation, these intramyocardial vessels will vasodilate) In case we have atherosclerotic lesion in epicardial vessels it will result in decrease blood flow in intramyocardial vessels , and this will initiate autoregulation (vasodilate) and they keep on doing that until reaching a state where this vasodilation is no longer sufficient to prevent Ischemia(to maintain normal perfusion to myocytes) 3 As we said, the most important factor is Resistanceincreasing diameter of the atherosclerotic lesion decrease in the diameter of the lumenincrease the resistanceas a result blood flow will decrease Notes: 1)When autoregulation occurs, vasodilation of intamyocardial vessels occur, but when this vasodilation is insufficient to keep perfusion we have what we call Coronary reserve. At severe stenosis (<70%) ,coronary blood flow will decrease dramatically and this result in ischemia and symptoms even at rest. 2)Remember the important determinant for resistance is Diameter of the vessel. 3)if obstruction in epicardial vessels is huge this is called coronary steal. The anatomy of vascular bed will affect: A) Oxygen supply B) Myocardial metabolism C) Mechanical function . Other factors also affect coronary blood flow and function of the collateral circulation: 1)length of the lesion 2)the influence of the pressure drop across an area of stenosis The resistance to flow in a vessel is directly related to length of the obstructing lesion but resistance is inversely related to the diameter of the vessel to the fourth power(the most important) This relationship can dramatically affect collateral blood flow and its response to exercise , resulting in what has been called coronary steal. 4 A similar situation may also occur when the epicardial or subepicardial vessel “steal” blood flow from the endocardium in the presence of a stenotic lesion. 5