BIOL 1119 Lecture Notes - Lecture 1: Heart Valve, Inotrope, Afterload
3 Oct 2017
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Governed by three factors: preload, contractility, afterload. Increase afterload decreases sv: amount of tension in ventricular myocardium before it contracts. Moderate stretch enables myocytes to generate more tension during contraction. The more a muscle is stretched, the better the overlap between filaments and the stronger the contraction. Frank-starling law of heart: sv edv. Ventricles eject as much blood as they receive: more they are stretched, the stronger the contraction. Contractility: contraction force for a given preload, sympathetic nervous system and chemicals affect contractility, the parasympathetic system via the vagus nerve has no significant effect on strength of ventricular contraction because it does not innervate the myocardium. Afterload: pressure in arteries above semilunar valves opposes opening of valves. Any restricting of arterial circulation increases afterload (lung disease, atherosclerosis, etc. : continuous increases in afterload causes hypertrophy of ventricular myocardium, may lead to weakening and failing of ventricles. Positive inotropic chemicals: catecholamines increases calcium levels in cardiocyte via camp mechanisms.
