cardiovascular: control of cardiac output Flashcards
3 things that directly influence CO
preload/afterload/ cardiac contractility
whats preload
degree of stretch of heart right before contraction; EDV; CVP
whats afterload; what is it influenced by
force against which LV pumps
TPR and aortic stiffness
frank starling relationship crux; implications; shape of graph
the fuller the heart, the more it will pump
EDV/EDP and stroke volume are correlated;
stroke volume of LV=RV
upward sloping, plateauing
mechanism behind frank starling relationship
cross bridge theory: maximum tension generated when cardiac sarcomeres are stretched to 2micrometres
cardiac cells are very sensitive to stretch
CO vs stroke volume
CO: vol of blood pumped per minute
Stroke vol: vol of blood pumped per heartbeat
how does heart failure change the frank starling curve? how does the compensated/decompensated heart failure curve look? explain compensatory mechanism
heart failure: lower amplitude
compensated: higher than HF, lower than normal
decompensated: lower than HF
pt has heart failure-> BP drops-> water + salt excretion drops/ SNS activated/ RAAS activated-> blood volume rises/ cardiac contractility increased/ HR increases/ venoconstriction -> EDP/EDV rises-> CVP rises-> Stroke volume increases
decompensated heart failure curve kicks in as heart failure continues
how does afterload affect CO? does it affect it to a large extent?
afterload does not affect CO much within physiological range.
+ afterload-> stroke volume/ ejection fraction falls-> more blood remains in heart at end of systole-> EDV and EDP rises-> stoke volume restored by frank starling mechanism
ANREP response-> Ca release-> cardiac contractility rises
HOWEVER, increased BP-> baroreceptor reflex causes BP and CO to decrease
what is CVP affected by; what does it affect
volume of blood and vein capacitance
affects preload
how does increased SNS activation affect frank starling curve
increased contractility + venoconstriction-> upward and rightward shift