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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
how to change conduction velocity?
aka dromotropy** amplitude of action potential rate of membrane potential change (depolarization)
26
extrinsic factors increasing conduction velocity?
``` sympathetic muscarinic antagonist beta agonist catecholamines hypokalemia hyperthyroidism ```
27
extrinsic factors decreasing conduction velocity?
``` parasympathetic muscarinic agonist beta antagonist (beta-blocker) ischemia hyperkalemia Na/Ca channel blocker ```
28
SV?
stroke volume = HR x SV = EDV - ESV end diastolic volume - end systolic volume
29
how to increase SV?
increase EDV | increase contractility of heart
30
how to decrease SV?
afterload increases
31
what can promote increased EDV?
``` 1 filling pressure 2 decreased heart rate 3 increased ventricular compliance 4 increased atrial contractility 5 increased aortic pressure 6 pathological conditions ```
32
filling pressure?
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
decreased heart rate?
more filling time - more EDV
34
increased ventricular compliance?
increased chamber filling volume - EDV
35
increased atrial contractility?
sympathetic stimulation | increased ventricular filling (EDV) from atria
36
increased aortic pressure?
increased afterload - increased ESV, decreased SV - secondary increase in preload for next cycle not a good way**
37
pathological conditions?
systolic failure -valve defects not a good way
38
what can promote decreased EDV?
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
factors affecting ESV?
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
bowditch effect?
increased heart rates, you see an increase of calcium causing increased contractility
41
frank-starling relationship?
stroke volume vs EDP with increased afterload, increased stroke volume
42
inotropy?
contractility independent of preload*** -increased contractility: increased SV and ejection fraction decreased ESV
43
lusitropy?
rate of relaxation
44
increased contractility?
decreased ESV
45
ESPVR
end-systolic pressure volume relationship indicator of contractility*** -more slope, more contractility and vice versa lowest ESV possible independent of preload/EDV
46
increased contractility?
sympathetic output | -beta-1 adrenergic receptors
47
how to increase contractility?
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
phospholamban
inhibitory in SERCA
49
five positive inotropics?
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
adrenergic agonist?
beta1 -increased contractility E and NE
51
cardiac glycosides?
digitalis derivatives inhibit Na/K ATPase -increase sodium decreased sodium gradient, decrease Na/Ca exchanger -decrease Ca extrusion increase calcium (increased contractility)***
52
decreased ECF Na
decreased sodium gradient - decrease Na/Ca exchanger - decreased Ca extrusion, increase calcium increased contractility***
53
increased ECF Ca?
increased Ca infux increased contractility**
54
increased HR?
staircase phenomenon (bowditch) increased APs, increased Ca over time increased phospholamban P -increased SERCA, more Ca2+ storage for later release
55
anrep affect
increased afterload leads to increased inotropy compensation for increased ESV and decreased SV caused by the increased afterload**
56
negative inotropic effects?
``` 1 muscarinic agonist 2 decreased ECF Ca 3 Ca channel blocker 4 increased ECF Na 5 decreased affinity of troponin for Ca -acidosis ```
57
muscarinic agonist?
ACh decreases adenylyl cyclase - decreased Ca - decreased contractility**
58
decreased ECF Ca?
decreased L-type Ca influx - increased Na/Ca exchanger - decreased contractility**
59
calcium channel blockers?
decreased L-type Ca influx decreased contractility**
60
decreased affinity of troponin for Ca?
ex/ acidosis decreased contractility**
61
rate of relaxation?
lusitropy
62
beta-1 agonists and lusitropy?
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
negative lusiptropy?
elevated Ca impaired SERCA increased affinity of troponin C pH changes
64
increased MSFP?
increased blood volume | increased vasoconstriction
65
decreased MSFP?
decreased blood volume | increased venous compliance
66
increased inotropy?
increased contractility | increased CO
67
decreased inotropy?
decreased contractility | decreased CO
68
Net filtration = ?
(Pc + #if) - (Pif + #c)
69
PP = ?
pulse presure SBP - DBP
70
MAP = ?
DBP + 1/3 (SBP - DBP)
71
Q = ?
CO = VO2 / A - V O2 difference

MSS - CV Exam 2 (7 decks)

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