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Define the term "cardiac output" and describe how it can be calculated.
CO: the volume of blood pumped by each ventricle per minute. (~5L/min).
CO= SV x HR
Draw a typical SA node pacemaker potential and describe how increasing or decreasing sympathetic and parasympathetic input alters the heart rate.
Increasing sympathetic input increases the heart rate: it increases the number of Na and Ca T-type channels that are open, causing the membrane potential to reach threshold faster. NE causes influx of Ca and Na. Epi can stimulate beta adrenergic receptors, increasing HR also. Sympathetic innervation can also activate a quicker conduction of the action potential through the AV node.
Increasing parasympathetic input decreases HR: it decreases the number of Na and Ca channels open, causing the membrane potential to drag and take longer to reach threshold. The cell hyper polarizes after depolarization, which increases the distance it must go to reach threshold again. ACh causes Na and Ca channels to stay closed. Parasympathetic innervation can further inhibit the conduction of an AP throughout the AV node.
Draw a ventricular function curve and describe the Frank-Starling mechanism for increasing stroke volume. On that same diagram, show the effect of increasing the activity of cardiac sympathetic nerves.
Frank-Starling mechanism: when the ventricle has increased blood volume during diastole filling, then its walls have been stretched a little bit more than normal. With this increased stretching of the walls, that stores energy and the energy is real eased during the systole contraction, increasing SV. We are effecting the EDV.
Sympathetic nerve activity: this has an effect on the contractility of the muscle cells, or the strength of the contraction, not EDV.
List the three mechanisms that seem to be responsible for producing increases in cardiac contractility.
Opening more Ca L-type channels during plateau phase.
Stimulating Ca reabsorption into the SR.
Altering the binding of Ca to troponin.
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