22. Regulation of Arterial Blood & CPR Endo Flashcards
What is mean arterial P (MAP)
driving force for blood flow (around 100 mmHg)
how do you calculate MAP
CO * TPR aka HR * SV * TPR or (2/3) DBP +(1/3) SBP
what 3 systems is Pa regulated by
baroreceptors, RAAS (endocrine) ADH & ANP
where are baroreceptors located
carotid sinus (respond to increase/decrease in MAP) –> use CN IX to get to brainstem
aortic arch (respond to mostly increase) –> use CN X to get to brain stem
what kind of receptors are baroreceptors
mechanoreceptors- respond to change in stretch/pressure &&& rate of change of P
chemoreceptors - respond to PO2,PCO2 & pH
when are baroreceptors most responsive
rapid change in arterial P
where do baroreceptors send signals
medulla (vasomotor center) –> then integrate into nucleus tractus solitarius
where do efferents travel
cerebral cortex & hypothalamus
what parts of the brain assist in parasym activity in the CV system
dorsal motor nucleus of CN X
nucleus ambiguus
what part of the brain causes sym activity in CV system
rostral ventrolateral medulla
what happens to MAP during hemorrhage
decrease bc decreased BV
how can a strength of AP be increased
increase freq up to certain point (around 200 mmHg in carotid bodies)
until what point can you decrease AP w/ decreased freq of firing
40-60 mmHg
how does the threshold of aortic bodies compare to carotid bodies
higher threshold
-continue to respond above saturation
BUT less sensitive to rate & less effective for decreases in pressure
what is the result when sym NS is triggered
-triggered when Pa decreases -
constrict arterioles & Vs (alpha receptor) –> increase TPR & VR
- increase HR & contractility (beta 1 receptors)
- fluid retention by kidney bc afferent arteriole constriction & renin secretion
what is result when parasym NS is triggered
- triggered when Pa increases
- decrease HR - vagus N to SA node via mAChR
- indirect vasodilation on blood vessels
what happens to baroreceptors during HTN
baroreceptors reset - adjust to the constant increase in P & now respond to higher set point
what is the difference btn baroreceptors & RAAS/ADH/ANP
baroreceptors are quick to respond RAAS/ADH/ANP - long term adjustments - take longer to respond and last longer
when is RAAS triggered
decrease Pa
what occurs with RAAS stimulation
renin –> convert angiotensinogen to angiotensin I –> use ACE to convert to angiotensin II –> 1. stimulate aldosterone –> increase Na reabsorption –> increase ECF –> increase BV –> 2. stimulate ADH production –> increase h2o reabsorption –> decrease urine production –> 3. global vasoconstriction of arterioles –> increase TPR & BP
when can ADH secretion be stimulated
angiotensin II
atrial receptor (low preload)
increased osmolality
sym NS activation
what does ADH do
increase TPR & water retention
what are the types of natriuretic peptides &when are they secreted
ANP -atrial
BNP -brain
CNP -c-type
excessive preload of atria &ventricles
what is the role of natriuretic peptides
protect against overdilation or overstretching of cardiac chambers
when will the vascular fxn curve shift left
hemorrhage
dehydration/loss of body fluid
decreased VR, preload, SV, CO and/or MAP
do chemoreceptor activator/inhibitors change with aerobic exercise?
no (if so, very very little)
what occurs during anticipation of exercise
central command response 1. increase sym (beta-1) & decrease parasym 2. increase HR & contractility & VR 3. selective arteriolar vasoconstriction (alpha-1) to make sure blood goes to Ms
what is orthostatic hypotension
decreased Pa upon standing -lightheaded, faint quick compensatory effects not working to quick change in P
what happens to blood when you go from lying to standing
blood accumulate in Vs in LE –> increase capillary pressure –> edema &/or hypotension
what is the compensatory mechanism for changes of position
stand –> decrease Pa –> baroreceptor detect change –> increase sym & decrease parasym –> increase HR, contractility & CO –> increase TPR (constrict arterioles) –> increase VR (constrict Vs)
