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CV II Exam 1 > Boron Cardiac Physio Review III > Flashcards

Boron Cardiac Physio Review III Flashcards

1
Q

response to hypoxia and resp acidosis

A

tachycardia

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2
Q

bainbridge reflex

A

tachycardia caused by increased venous return

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3
Q

volume loading and volume depletion

A

both cause an increased heart rate

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4
Q

heart rate minimum

A

when effective circulating volume is normal

bainbridge - high volume
baroreceptor - low volume

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5
Q

stroke volume changes

A

low volume - starling law - short fiber decreased SV - but baroreceptor increases sympathetics

high volume - baroreceptor - increased stretch - decreases sympathetics - flattens starling response

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6
Q

cardiac output changes

A

low at low volume

high at high volume

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7
Q

venous return

A

blood returning to heart

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8
Q

vasoconstrictors

A 
epinephrine - alpha1
serotonin
ANG II
AVP
endothelin
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9
Q

vasodilators

A 
epinephrine - beta1
histamine
ANP
bradykinins
PGE2, PGI2
NO
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10
Q

angina pectoris

A

hypoxia in myocardium

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11
Q

coronary sinus

A

emptying of coronary flow to right atrium

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12
Q

blood flow to heart

A

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

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13
Q

adenosine

A

rise with:

  • increased metabolic activity of heart
  • insufficient coronary flow
  • fall in myocardial PO2

-induces vasodilation of coronary vessels

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14
Q

sympathetics on coronary vessels

A

constrict - but overpowered by metabolic adenosine affects

-with drugs that block beta1 - prevent increased metabolism - results in vasoconstriction

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15
Q

collateral coronary vessels

A

if narrows gradually over time - can have collateral vessels grow

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16
Q

coronary steal

A

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)

17
Q

skeletal m blood flow

A

extreme range
-can increase 50x

vasodilation occurs to all vessels in series

18
Q

orthostatic response

A

stand up

-increased HR and peripheral vascular resistance - to restore MAP

19
Q

four factors reducing pooling and maintaining RAP when stand up

A

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

20
Q

temp and orthostatic response

A

warm - vasodilation in legs - more pooling to legs - more likely to faint

21
Q

fight or flight response

A

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

22
Q

vasovagal syncope

A

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
23
Q

skeletal muscles during exercise

A

increased venous return

local vasodilation - CO2, lactic acid, K, adenosine

24
Q

central command during exercise

A

increased CO - sympathetics
vasoconstriction - sympathetics - inactive muscles, renal, splanchnic, cutaneous
vasodilation - active muscles early (later reinforced by chemical local factors)

25
Q

exercise pressor reflex

A

from exercising muscle - reinforces central input - sustains sympathetic flow

26
Q

arterial baroreceptor during exercise

A

resets so heart slows only at very high arterial pressures

27
Q

core body temp and exercise

A

temp sensitive cells in hypothalamus

  • inhibit sympathetics to skin - increased cutaneous blood flow
  • stimulate sweat glands
28
Q

hypovolemic shock

A

loss of 30% or more of blood

-sighs - narrow pulse pressure, cold, moist skin, rapid and weak pulse

29
Q

response to hemorrhage

A

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

30
Q

degree of tachycardia

A

proportional to severity of hemorrhage

31
Q

hemorrhage and arteriolar constriction

A

extremities, skin, skeletal m, abdominal viscera

-precapillary dominates

renal blood flow falls rapidly - recovers after a few minutes (autoregulation)

32
Q

hemorrhage and venous constriction

A

larger veins constrict with sympathetic activity

33
Q

transcapillary refill

A

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)

34
Q

renal conservation of salt and water

A

with blood loss - decreased excretion of water and salt

35
Q

irreversible hemorrhagic shock

A

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

CV II Exam 1 (10 decks)

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