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MSS - CV Exam 2 > Regulation of Cardiac Output > Flashcards

Regulation of Cardiac Output Flashcards

1
Q

what can affect CO?

A

age
body size (cardiac index)
basal metabolic rate
rest/exercise

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2
Q

oxygen consumption?

A

parallels cardiac output with increasing work output during exercise

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3
Q

two determinants of CO?

A

heart rate and stroke volume

CO = HR x SV

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4
Q

phase 0

A

inward Ca2+ influx

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5
Q

phase 3

A

outward K+ efflux

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6
Q

phase 4

A

funny current

outward K+ decreasing
sodium (funny) increasing
calcium increasing influx

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7
Q

three ways to change pacemaker potential?

A

1 change in slope of phase 4 (slow depolarization)
2 change in the maximum diastolic potential
3 change in threshold potential

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8
Q

parasympathetic input?

A

ACh on M2 receptors

results in negative chronotrophy (decreased HR)

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9
Q

sympathetic input?

A

NE on beta-1 receptors

resultsin positive chronotrophy (increased HR)

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10
Q

sympathetic effect on HR?

A

beta-1 agonists (NE)

changes:
increased funny current (sodium)
-more steepness

increased I-Ca (calcium)

  • more steepness
  • threshold more negative
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11
Q

changes in funny current with sympathetics results in ?

A

more steepness

faster rate

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12
Q

changes in I-Ca with sympathetics results in?

A

more steepness AND threshold more negative

faster rate

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13
Q

parasympathetic effect on HR?

A

M2 muscarinic agonist (ACh)

increased K + permeability
-hyperpolarize - more negative max diastolic potential

decreased funny current
-decreased slow depolarization rate

decreased I-Ca

  • decreased slow depolarization rate
  • more positive threshold
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14
Q

increased potassium permeability in PS results in?

A

more negative maximum diastolic potential

slows heart rate

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15
Q

decreased funny current in PS results in?

A

decreases slow depolarization phase

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16
Q

decreased I-Ca in PS results in?

A

decreases slow depolarization rate AND threshold more positive

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17
Q

effects of ACh on HR?

A

1 change in slope
2 negative shift in maximum diastolic potential (K+)
3 threshold is more positive

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18
Q

hyperthyroidism?

A

increases heart rate

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19
Q

hypothyroidism?

A

decreases heart rate

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20
Q

catecholamines?

A

increase heart rate

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21
Q

hyperkalemia

A

decrease heart rate

more K+ in ECF, effects concentration gradient that normally promotes efflux

  • repolarization phase, efflux is slowed phase 3
  • longer AP
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22
Q

hypokalemia

A

increases heart rate

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23
Q

nodal ischemia/hypoxia

A

decreased heart rate

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24
Q

drugs that influence HR?

A

antiarrhythmic drugs
calcium channel blockers
beta-1 adrenoreceptor agonists/antagonists

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25
Q

how to change conduction velocity?

A

aka dromotropy**

amplitude of action potential
rate of membrane potential change (depolarization)

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26
Q

extrinsic factors increasing conduction velocity?

A 
sympathetic
muscarinic antagonist
beta agonist
catecholamines
hypokalemia
hyperthyroidism
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27
Q

extrinsic factors decreasing conduction velocity?

A 
parasympathetic
muscarinic agonist
beta antagonist (beta-blocker)
ischemia
hyperkalemia
Na/Ca channel blocker
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28
Q

SV?

A

stroke volume = HR x SV = EDV - ESV

end diastolic volume - end systolic volume

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29
Q

how to increase SV?

A

increase EDV

increase contractility of heart

30
Q

how to decrease SV?

A

afterload increases

31
Q

what can promote increased EDV?

A 
1 filling pressure
2 decreased heart rate
3 increased ventricular compliance
4 increased atrial contractility
5 increased aortic pressure
6 pathological conditions
32
Q

filling pressure?

A

filling pressure: increase CVP

  • decrease venous compliance, forces veins to return blood to right heart
  • sympathetic venoconstriction
  • increase thoracic blood volume
  • increased total blood volume
  • increased venous return
  • muscle pumps,gravity, increased CO

increased EDV***

33
Q

decreased heart rate?

A

more filling time - more EDV

34
Q

increased ventricular compliance?

A

increased chamber filling volume - EDV

35
Q

increased atrial contractility?

A

sympathetic stimulation

increased ventricular filling (EDV) from atria

36
Q

increased aortic pressure?

A

increased afterload

  • increased ESV, decreased SV
  • secondary increase in preload for next cycle

not a good way**

37
Q

pathological conditions?

A

systolic failure
-valve defects

not a good way

38
Q

what can promote decreased EDV?

A

1 decreased filling pressure (CVP)
2 increased heart rate
3 decreased atrial contractility
4 decreased afterload - increased ejection
5 diastolic failure - decreased V compliance
6 mitral or tricusid valve stenosis

39
Q

factors affecting ESV?

A

1 preload

  • greater EDV - lesser ESV
  • starlings law of heart

2 afterload
-greater afterload - greater ESV

3 contractility
-increased calcium - greater contractility - decreased ESV

4 heart rate (mixed)

  • increased HR - decreased EDV - increased ESV
  • also bowditch
40
Q

bowditch effect?

A

increased heart rates, you see an increase of calcium causing increased contractility

41
Q

frank-starling relationship?

A

stroke volume vs EDP

with increased afterload, increased stroke volume

42
Q

inotropy?

A

contractility

independent of preload***
-increased contractility:
increased SV and ejection fraction
decreased ESV

43
Q

lusitropy?

A

rate of relaxation

44
Q

increased contractility?

A

decreased ESV

45
Q

ESPVR

A

end-systolic pressure volume relationship

indicator of contractility***
-more slope, more contractility and vice versa

lowest ESV possible independent of preload/EDV

46
Q

increased contractility?

A

sympathetic output

-beta-1 adrenergic receptors

47
Q

how to increase contractility?

A

beta1 adrenergic agonist

1 more calcium influx
2 increase sensitivity of RyR channel
3 increased SERCA activity (more Ca2+ storage)
4 increase ECF Ca2+ influx

48
Q

phospholamban

A

inhibitory in SERCA

49
Q

five positive inotropics?

A

1 adrenergic agonists
-catcholamines (E and NE)

2 cardiac glycosides

  • inhibits Na/K pump
  • more sodium in cell than normal
  • decreased Na/Ca exchanger pump
  • decreased Ca extrusion

3 decreased ECF sodium

  • decrease Na/Ca exchanger pump
  • decreased Ca extrusion

4 increased ECF Ca

5 increased HR

50
Q

adrenergic agonist?

A

beta1
-increased contractility

E and NE

51
Q

cardiac glycosides?

A

digitalis derivatives
inhibit Na/K ATPase
-increase sodium

decreased sodium gradient, decrease Na/Ca exchanger
-decrease Ca extrusion

increase calcium (increased contractility)***

52
Q

decreased ECF Na

A

decreased sodium gradient

  • decrease Na/Ca exchanger
  • decreased Ca extrusion, increase calcium

increased contractility***

53
Q

increased ECF Ca?

A

increased Ca infux

increased contractility**

54
Q

increased HR?

A

staircase phenomenon (bowditch)

increased APs, increased Ca over time

increased phospholamban P
-increased SERCA, more Ca2+ storage for later release

55
Q

anrep affect

A

increased afterload leads to increased inotropy

compensation for increased ESV and decreased SV caused by the increased afterload**

56
Q

negative inotropic effects?

A 
1 muscarinic agonist
2 decreased ECF Ca
3 Ca channel blocker
4 increased ECF Na
5 decreased affinity of troponin for Ca
-acidosis
57
Q

muscarinic agonist?

A

ACh decreases adenylyl cyclase

  • decreased Ca
  • decreased contractility**
58
Q

decreased ECF Ca?

A

decreased L-type Ca influx

  • increased Na/Ca exchanger
  • decreased contractility**
59
Q

calcium channel blockers?

A

decreased L-type Ca influx

decreased contractility**

60
Q

decreased affinity of troponin for Ca?

A

ex/ acidosis

decreased contractility**

61
Q

rate of relaxation?

A

lusitropy

62
Q

beta-1 agonists and lusitropy?

A

P of phospholamban - increased SERCA
-leads to faster relaxation

also P of troponin I

  • enhances Ca2+ dissociation from troponin C
  • leads to faster relaxation
63
Q

negative lusiptropy?

A

elevated Ca
impaired SERCA
increased affinity of troponin C
pH changes

64
Q

increased MSFP?

A

increased blood volume

increased vasoconstriction

65
Q

decreased MSFP?

A

decreased blood volume

increased venous compliance

66
Q

increased inotropy?

A

increased contractility

increased CO

67
Q

decreased inotropy?

A

decreased contractility

decreased CO

68
Q

Net filtration = ?

A

(Pc + #if) - (Pif + #c)

69
Q

PP = ?

A

pulse presure

SBP - DBP

70
Q

MAP = ?

A

DBP + 1/3 (SBP - DBP)

71
Q

Q = ?

A

CO = VO2 / A - V O2 difference

MSS - CV Exam 2 (7 decks)

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