integrated CV responses: orthostasis and exercise Flashcards
what happens to pressure in feet when upright vs lying down?
when lying down arterial end is ard 96, venous is 10, diff is 86
when standing up arterial end is 186, venous is 100, diff is 86
pressure increases equally on both sides -> increased capillary pressure-> increased filtration-> feet swell
flow increases
what happens to CO and pressure in veins of legs when u stand up after lying down
VEINS ARE DISTENSIBLE
stand up-> venous valves in veins shut transiently-> outflow of heart > inflow-> excess CO builds up in veins in legs-> veins distend-> pressure in veins rise-> valves open and blood flow into heart recommences
CVP drops transiently, therefore CO too (frank starling)
what happens to plasma volume when you stand up after lying down
in lower extremities, net hydrostatic pressure increases from arterial-venous end-> increased filtration-> oedema -> plasma volume drops
how are the effects of orthostasis limited
- baroreceptor reflex-> vasoconstriction
- veno-arteriolar axon reflex (baroreceptors in veins sense distension-> arteriolar constriction)
- skeletal muscle pumping (skeletal muscle contracts-> blood pumped up-> skeletal muscle relaxes-> low pressure created-> blood sucked up from lower extremities)
what happens to venous pressures above heart+ cranium upon standing
veins collapse
fall in pressure in arteries> veins -> arteriovenous pressure gradient driving cerebral profusion falls
veins in cranium dont collapse-> internal pressures become negative-> pressure gradient driving flow through veins falls-> cerebral flow drops -> fainting with prolonged standing
why dont veins in cranium collapse upon standing, what risk does this pose during neurosurgery
surrounded by CSF-> CSF is displaced downwards when standing -> negative intercranial pressure
air embolism
vasovagal faint
when you stand up for too long, blood pools in lower extremities -> TPR and HR drop-> BP and cerebral flow fall-> fainting-> horizontal position restores venous return and CO
energy sources during exercise (from most immediate)
immediate: muscle ATP and phosphocreatine (very quickly depleted)
anaerobic
aerobic
formula for oxygen consumption; how do these factors change with exercise
oxygen consumption= CO (arterial-venous o2 content)
CO rises; arterial is unaffected; venous falls progressively as more o2 is used
change in vasculature @ active muscle/splanchnic circulation/skin during exercise; net effect on TPR
active muscle: vasodilation by local metabolites eg pCO2 rise/ pO2 fall/ H+ rise
splanchnic circulation: SNS vasoconstriction
skin: vasoconstriction (SNS)-> vasodilation (lose heat)-> vasoconstriction (at max exercise)
TPR falls
TPR/systolic/diastolic during dynamic exercise vs static exercise
dynamic: TPR falls/systolic rises/diastolic no change/BP plateaus
static: TPR rises/systolic rises/diastolic rises/BP rises more and falls sharply
TPR rises due to compression of blood vessels in contracting muscle