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Lecture 4

Lecture 4.docx

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University of Otago
Regis Lamberts

Intrinsic Control of Cardiac Function Objectives:  Intrinsic control of cardiac function by heart rate (Treppe effect)  Intrinsic control of cardiac function by Frank-Starling mechanism  The length dependent activation  Concepts of preload, afterload and contractility Physiological Factors of the CVS: MAP = CO x TPR  Controls originating from within the heart: intrinsic  Heart rate  Stroke volume (dictated by preload, afterload, contractility)  Input from outside the heart: extrinsic  Hormonal and nervous control  Cardiac cycle: closed loop  Both of these operate continuously to adjust the heart and vessels to maintain MAP Cardiac Output:  CO = SV x HR Intrinsic Control of Heart Rate:  Overall intrinsic control of heart rate seems very limited  Extrinsic parasympathetic and sympathetic nervous system control seems to be much more important  Increased heart rate = increased developed force/pressure  Treppe effect: Bowditch effect: positive pressure/force-frequency relationship: myocardial contraction increases with frequency.  Mechanism: Increase in Ca per unit time (increase in Na due to slower Na/K pump).  Negative force/frequency relationship is the hallmark of heart failure. o Increases HR o Stronger contraction o Faster contraction Intrinsic control of stroke volume:  Determined by pre-load (input), afterload (resistance to output), and contractility (force produced).  Increase in preload produces a larger stroke volume: ‘starling’s law of the heart’ or the ‘Frank-Starling mechanism’  Increase in venous return = ventricle is filled more = increased pre-load  Increased end-diastolic volume (EDV) consequently the ventricle is stretched- increase in sarcomere length therefore increase in contraction which leads to an increased stroke volume.  The heart regulates ventricular output in response to ventricular filling. Frank-Starling mechanism: increased volume = increased length of cardiomyocytes = produces more force.  This is called length-dependent activation: need less Ca to produce larger forces (compared to a shorter cardiomyocyte).  At the same Ca concentration at different lengths, you have different amounts of force produced.  Overlap of actin/m
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