this lecture introduces one major idea in hemodynamics; venous return and its influence on CO. venous pressure is explained to be caused by three factors: contraction of skeletal muscle during movement which squeezes blood up a series of valves, venoconstriction, and thoracic pressure from breathing. venous pressure in turn affects CO by increasing the end diastolic volume and hence the stroke volume and hence the cardiac output. the venous pressure's relationship to cardiac output follows the frank starling law (although i thought this applied to the active tension curve, but i guess not) and is pictured as an ascending curve in the graph of cardiac output vs. venous pressure.
the "cardiac function" is then introduced as a secondary mechanism that affects / is affected by venous flow / cardiac output. as cardiac output increases, blood is drawn from the veins into the arteries, thereby reducing venous pressure. as cardiac output decreases, equilibrium between the pressures of arteries and veins is reached and more blood is pooled into the veins due to the higher compliance; venous pressure is increased. thus, this relationship is pictured by a curve that descends on the same output vs. venous pressure graph.
the intersection of the two curves represents the equilibrium point, the specific venous pressure and cardiac output that the body has reached as a balance of the two functions. these curves can both be shifted due to different factors: for example, increasing the contractility or heart rate will shift the ascending (frank starling) curve, while vasoconstriction or decreasing vascular resistance will shift the descending curve upwards. both of these actions can potentially shift the cardiac output upwards, and the most efficient increase in cardiac output is created from the combination of increased contractility plus decreased vascular resistance.
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