Physiology 3120 Lecture Notes - Lecture 18: Pulmonary Artery, Pulmonary Circulation, Circulatory System

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Stavraky Lecture 18
-filling of heart – 70% during ventricular diastole 30% during atrial systole
-so an increase in EDV = more blood going into heart ie: higher preload that stretches out
ventricular muscle more
-when contractile cells stretch more, they contract more forcefully ie: increase in SV
-in volume graph, black shows normal EDV and blue shows increased EDV
-increased EDV results in increased SV
-in pressure graph, shows that when stretch more, need to contract just as much so contractile
force increases which ejects more blood = higher stroke volume
-graph shows that an increase in EDV causes an increase in SV (will plateau at some point)
-sarcomeres increase in length which are then able to generate more force due to max overlap
of actin/myosin (RMR from Org Phys – overlap = more cross-sectional area = more force
generated)
-when ventricular contractile cells stretch, stretch-sensitive Ca channels open, letting in more
Ca which increases contraction force of contractile cells
-troponin will bind more easily to Ca taking off tropomyosin from actin so actin-myosin can
form more cross-bridges to generate more force of contraction
-this is because will not always get the same amount of blood coming into ventricles
-so the heart needs to be able to deal with changing loads
-activate SNS, NE secreted on contractile cells, open Ca channels allowing more Ca to come into
cell, plus due to stretch in ventricular muscle cells, increase SV for given EDV
-activate PNS, takes away SNS input, less Ca comes into cell, decrease SV for given EDV
Ie: how do you increase the amount of blood in heart before it contracts?
-increase amount of blood that returns to heart by increasing venous return (RMR most of
blood sitting in veins that takes blood back to heart)
-very low BP in veins thus very easy to squeeze veins
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