Boron Cardiac Physio Review III Flashcards
response to hypoxia and resp acidosis
tachycardia
bainbridge reflex
tachycardia caused by increased venous return
volume loading and volume depletion
both cause an increased heart rate
heart rate minimum
when effective circulating volume is normal
bainbridge - high volume
baroreceptor - low volume
stroke volume changes
low volume - starling law - short fiber decreased SV - but baroreceptor increases sympathetics
high volume - baroreceptor - increased stretch - decreases sympathetics - flattens starling response
cardiac output changes
low at low volume
high at high volume
venous return
blood returning to heart
vasoconstrictors
epinephrine - alpha1 serotonin ANG II AVP endothelin
vasodilators
epinephrine - beta1 histamine ANP bradykinins PGE2, PGI2 NO
angina pectoris
hypoxia in myocardium
coronary sinus
emptying of coronary flow to right atrium
blood flow to heart
contraction compresses coronary aa
left -majority of left coronary blood flow - during diastole - when aortic pressure still high
right - majority during systole - bc lower wall tension on right side during systole doesn’t compress vessels during contraction
adenosine
rise with:
- increased metabolic activity of heart
- insufficient coronary flow
- fall in myocardial PO2
-induces vasodilation of coronary vessels
sympathetics on coronary vessels
constrict - but overpowered by metabolic adenosine affects
-with drugs that block beta1 - prevent increased metabolism - results in vasoconstriction
collateral coronary vessels
if narrows gradually over time - can have collateral vessels grow
coronary steal
ischemic coronary vessels - max dilation downstream of blockage
vasodilatory drugs result in diameter increase in nonischemic vessels
result - reduction in flow to area down stream of ischemic region (BAD)
skeletal m blood flow
extreme range
-can increase 50x
vasodilation occurs to all vessels in series
orthostatic response
stand up
-increased HR and peripheral vascular resistance - to restore MAP
four factors reducing pooling and maintaining RAP when stand up
anatomical
1 non-uniform blood distribution - most central - near heart
2 non-uniform distensibility of vessels - leg veins stiffer
physiological
3 muscle pumps - this with valves - pushes blood upward
4 autonomic reflex - decreased venous return - baroreceptors increase sympathetic output - vasoconstriction and increased HR
temp and orthostatic response
warm - vasodilation in legs - more pooling to legs - more likely to faint
fight or flight response
skeletal muscle blood flow increase - sympathetics to beta2
little sympathetic change to cutaneous blood flow
vasoconstriction of kidney and splanchnic (alpha1)
veins constrict - sympathetic
heart - increased CO
vasovagal syncope
decreased perfusion to brain
- massive vasodilation
- decreased CO - vagal to heart
- decreased MAP
- decreased cerebral blood flow
- sweating, nausea, pupil dilation all occur as well
skeletal muscles during exercise
increased venous return
local vasodilation - CO2, lactic acid, K, adenosine
central command during exercise
increased CO - sympathetics
vasoconstriction - sympathetics - inactive muscles, renal, splanchnic, cutaneous
vasodilation - active muscles early (later reinforced by chemical local factors)
exercise pressor reflex
from exercising muscle - reinforces central input - sustains sympathetic flow
arterial baroreceptor during exercise
resets so heart slows only at very high arterial pressures
core body temp and exercise
temp sensitive cells in hypothalamus
- inhibit sympathetics to skin - increased cutaneous blood flow
- stimulate sweat glands
hypovolemic shock
loss of 30% or more of blood
-sighs - narrow pulse pressure, cold, moist skin, rapid and weak pulse
response to hemorrhage
decreased firing of high P baroreceptors - increases sympathetics - increase HR, contractility, veno and arterioconstriction
low P baroreceptors - decreased activity - increased sympathetics - also increase ADH release
peripheral chemoreceptors - hypoxia - increase firing rate - increased sympathetics
central chemoreceptors - hypotension - brain ischemia - POWERFUL sympathetic response
degree of tachycardia
proportional to severity of hemorrhage
hemorrhage and arteriolar constriction
extremities, skin, skeletal m, abdominal viscera
-precapillary dominates
renal blood flow falls rapidly - recovers after a few minutes (autoregulation)
hemorrhage and venous constriction
larger veins constrict with sympathetic activity
transcapillary refill
movement of fluid from interstitium to blood plasma
- important during blood loss
- starling forces altered - decreased cap hydrostatic P - net movement of fluid and electrolgytes from interstitium into capillaries
- precapillary resistances increases more than postcap - movement into caps
- alters other starling forces - resulting in transcapillary refil stopping
also - increased plasma proteins - causes increased uptake of fluid into caps (liver more albumin)
renal conservation of salt and water
with blood loss - decreased excretion of water and salt
irreversible hemorrhagic shock
with failure of vasoconstriction, cap refill, cardiac response, and CNS response
vasoconstriction fail - desensitization - with new set point
cap refill fail - precap constrictor response decreases
cardiac fail - acidosis - decreased contractility - and necrosis makes it nonfunctional
CNS fail - prolonged cerebral ischemia depresses neural activity in brain - decreased sympathetic output
