Coronary autoregulation

A primary advantage of etomidate is its ability to preserve cardiovascular and respiratory stability both cardiac output and diastolic pressure are well maintained. Use of etomidate may offer some advantage to the patient with compromised myocardial oxygen or blood supply or both, since it produces mild coronary vasodilation. Thus, coronary vascular resistance decreases with no change in perfusion pressure. Preservation of diastolic perfusion pressure may be particularly important when myocardial blood supply cannot be increased by autoregulation. 

The caliber of arteriolar resistance vessels controls blood flow through the coronary bed. Arteriolar caliber is determined by myocardial 02 tension and local concentrations of metabolic products, and is automatically adjusted to the required blood flow (B, healthy subject). This metabolic autoregulation explains why anginal attacks in coronary sclerosis occur only during exercise (B, patient). At rest, the pathologically elevated flow resistance is... 

Q3 The major control in the coronary circuit is autoregulation, predominantly hypoxia. A small degree of hypoxia dilates coronary vessels and produces a large increase in blood flow increased arterial PC02 and decreased pH also dilate coronary arteries and increase blood flow. 

Blood flow to the coronary arteries arises from orifices located immediately distal to the aorta valve. Perfusion pressure is equal to the difference between the aortic pressure at an instantaneous point in time minus the intramyocardial pressure. Coronary vascular resistance is influenced by phasic systolic compression of the vascular bed. The driving force for perfusion therefore is not constant throughout the cardiac cycle. Opening of the aortic valve also may lead to a Venturi effect, which can slightly decrease perfusion pressure. If perfusion pressure is elevated for a period of time, coronary vascular resistance declines, and blood flow increases however, continued perfusion pressure increases lead, within limits, to a return of coronary blood flow back toward baseline levels through autoregulation. 

Myogenic control (also known as the Bayliss effect) of coronary artery tone occurs when the vessel is stretched secondary to an increase in pressure and contracts to return blood flow to normal. It is thought that the myogenic response to stretching in coronary arteries is a modest one and that metabolic factors such as nitric oxide play a much larger role in autoregulation. 

At perfusion pressures below 60 mm Hg, since the coronary arteries are maximally dilated and the buffering effect of autoregulation has reached its capacity, further reduction in coronary blood flow will decrease perfusion pressure and tissue oxygenation. It is thought that autoregulation works more efficiently in the epicardial layers than in the subendocardial layers, and this may contribute to coronary steal. 

Wong, A.Y. and Klassen, G.A. 1991. Vasomotor coronary oscillations a model to evaluate autoregulation. Basic Res. Cardiol. 86 461 75. 

Critical coronary perfusion pressure. As stated above, flow is related to the pressure gradient. However, in stenotic vessels, flow will remain disproportionaUy low, as autoregulation cannot cause the maximal vasodilation in the healthier vessels. This may exacerbate regional hypoxia, the build up... 

The zero flow pressure, a well known phenomenon in the coronary bed, is commonly known in other vascular beds as the critical closing pressure . Many theories attempt to explain the reason for the existance of the critical closing pressure (Hoffman, 1978 Archie, 1978 Bellamy, 1978). Is this a real physical closure of the micro vessel lumen, or is it a function of the yield stress of the blood attributed to its cassonian rheological properties The zero flow pressure, Pjf, is in fact a combination of the critical closing pressure, the compressive effects and the autoregulating effects. 

FigureS.Time dependent coronary blood flow distribution with (lower) and without (upper) introduction of an algorithm for autoregulation. These calculated results are based on integrated model combing mechanical with coronary perfusionarameters (Beyar and Sideman, 1984c)...

Space and time integration of the coronary perfusion flow yields the total blood flow to the LV. A classical experiment relating the total blood flow to the coronary pressure is simulated in Figure 9. The calculated classical autoregulating range are shown for two metabolic demands. The curvilinearity of the coronary flow pressure relationship, above and below this range, is due to the modification of the resistance by the increase of the coronary transmural pressures. 

The analysis of the nonisotropic nonhomogeneous asymmetric mechanical 3-D problem is an important step to be accomplished. Independent of the precise method which will be selected for the solution of the mechanical problem, a time dependent field of mechanical parameters s(y, qp,d,t),e y,q>,6, t),P (y, local energy demand will be related to the local coronary perfusion, autoregulated by local metabolic autoregulatory functions as well as by general control systems. 

Arnold G, Morgenstern C, Lochner W (1970) The autoregulation of the heart work by the coronary perfusion pressure. Pflugers Archiv. 321 34-55... 

Intravenous infusion of dipyridamole blocks the cellular re-absorp-tion of adenosine and, in turn, increases the concentration of adenosine, an endogenous vasodilator that can activiate specific receptors (72). Coronary blood flow is autoregulated by adenosine to meet myocardial metabolic demands (72). In patients without CAD, dipyridamole or adenosine infusion creates vasodilatation and increases coronary blood flow three to five times above baseline levels. In patients with coronary disease the resistance vessels distal to the stenotic area are already dilated, often maximally, to maintain normal coronary flow at rest. In these patients (coronary patients) dipyridamole IV or adenosine IV (78) does not (cannot) cause further vasodilatation in the atherosclerotic vascular... 

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