Stroke Volume

Mathematically, stroke volume is equal to end diastolic volume (EDV) minus end systolic volume (ESV). End diastolic volume represents the preload, which is defined as the tension on the muscle fibers at the beginning of contraction; in other words, the degree to which the muscle fibers are stretched. End systolic volume is determined by: a) Contractility, the ability of cardiac muscle cells to produce force, and, b) Afterload, the force opposing muscle contraction. Set up the graph: – The x-axis tracks left ventricular volume from 40-120 mL. – The y-axis tracks left ventricular pressure from 0-120 mmHg. Begin with ventricular diastole, when pressure is ~10 mmHg and volume is ~ 50 mL. We call this point A. Now, show that the mitral valve opens and allows passive ventricular filling. Thus, volume increases, even as pressure continues to fall due to muscle relaxation during diastole. At point B, pressure begins to increase, slightly, due to continued filling. Ultimately, the rise in pressure closes the mitral valve (point C), and diastole is complete; highlight that end-diastolic volume is approximately 120 mL. At this point, isovolumetric contraction raises ventricular pressure; notice that this is isovolumetric contraction because volume remains the same. At point D, when pressure is approximately 80 mmHg; the aortic valve is pushed open and allows blood ejection. Thus, contraction decreases blood volume and raises ventricular pressure to 130 mmHg (Point E). Because of blood ejection, both pressure and blood volume fall to point F, which permits aortic valve closure and marks the end of systole; highlight that end-systolic volume is 50 mL. Isovolumetric relaxation brings left ventricular pressure back to point A. Stroke volume is equal to the distance between the end systolic volume and end diastolic volume. First, we show the normal pressure-volume loop. Then, we show another loop, this time with an increased end-diastolic volume. We can see that, when preload, aka, end diastolic volume is increased, so, too, is stroke volume. This makes sense, according to the Frank-Starling mechanism: there is more blood in the heart at the end of diastole, therefore, more blood is ejected in a heartbeat; we'll return to this concept. We show the original loop plus a new pressure volume loop to illustrate that increased contractility shifts Points E and F to the left, which reduces end systolic volume. We can see that, because contractility reduced end-systolic volume without altering end-diastolic volume, stroke volume is increased. This occurs when aortic pressure rises, for example. We show the original loop, then we show that changes in afterload increase the ventricular pressure needed to open the aortic valve and eject blood (Points D, E, and F). Less blood can be ejected against the higher pressure, so end systolic volume is increased. Recognize that if we also increased the contractility of the cardiac muscle, the heart could eject the same volume of blood, despite the increased afterload, to maintain stroke volume. This brings us to an important point about our diagrams: we've shown independent effects of preload, contractility, and afterload. However, in real life, these variables are interdependent, so that the effects of one parameter are often partially offset by changes in another. For example, an increase in preload can ultimately increase afterload. Remember that higher stroke volume increases cardiac output; in turn, arterial pressure, aka, afterload, will rise (which means that the hypothetical increase in stroke volume will be partially offset by increase in afterload). Or, consider that increased afterload lowers stroke volume; however, it also increases preload, which, thanks to the Frank-Starling mechanism, increases contractility. The increased contractility can partially offset the initial decrease in stroke volume. Increased contractility and stroke volume ultimately decreases end-systolic volume; decreased contractility ultimately increases end-systolic volume and decreases stroke volume. Exercise is a good example of these interdependent mechanisms. When compensatory mechanisms fail, the heart cannot pump blood effectively. The Frank-Starling Law of the heart predicts the relationship between changes in end diastolic volume, i.e., preload, and stroke volume. As left ventricular end-diastolic volume increases, so, too, does stroke volume. This is because the volume of blood in the ventricle determines the degree of myofibril stretch; In turn, the degree of myofibril stretch, aka, the tension on the myofibril, determines the mechanical force produced by the myofibril during contraction. And, as we know, the force of contraction determines how much blood is ejected from the ventricle. Changes in contractility shift the Stroke Volume – End Diastolic Volume curve to the Right or Left. The sympathetic nervous system Adrenergic agonists Cardiac glycosides (such as digoxin) Angiotensin II Reduced sodium levels Increased heart rate Several these agents act by increasing the intracellular calcium concentration; in their presence, stroke volume is increased at any given end diastolic volume. The parasympathetic nervous system Beta blockers Reduced intracellular calcium (and, therefore, calcium channel blockers) Some antiarrhythmics High sodium concentrations Reduced heart rate Thus, in the presences of these agents, stroke volume is decreased at any given end diastolic volume.