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PMCOL 343 > 4-cardio > Flashcards

4-cardio Flashcards

1
Q

what type of vessels is the main location of resistance in circulation

A

arterioles

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2
Q

where is renin released

A

kidneys

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3
Q

what is afterload

A

the resistance that the heart has to pump against

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4
Q

what determines afterload

A

arteriolar pressure and peripheral resistance

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5
Q

what is preload

A

the stress on ventricular wall before systole

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6
Q

in the shovel snow example, what is preload and afterload

A

preload=how much snow on shovel

afterload=how high lift snow

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7
Q

what happens to afterload when you increase peripheral resistance

A

it increases

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8
Q

what happens to afterload when you increase BP

A

it increases

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9
Q

how do you find left ventricle end diastolic pressure / what is another name for it

A

pulmonary wedge pressure, it is the preload

weird question

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10
Q

how do you find cardiac output

A

stroke volume x heart rate

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11
Q

is left or right ventricular pressure bigger

A

left because it has to pump to the whole system

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12
Q

what is venous return

A

rate of return of blood to the heart

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13
Q

what does cardiac output equal in terms of vein

A

cardiac output=venous return

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14
Q

are veins or arteries more rigid

A

arteries

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15
Q

are veins or arteries more elastic

A

veins

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16
Q

what is capacitance

A

ability to store blood

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17
Q

is venous capacitance bigger or smaller than arterial capacitance

A

venous>arterial

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18
Q

what is another name for the intrinsic relationship in the heart

A

the Frank Starling relationship

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19
Q

what does the frank starling relationship tell us

A

that the force of contraction is proportional to initial fibre length (aka more blood in heart means more contraction)

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20
Q

what does left ventricular end diastolic pressure =

A

=preload

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21
Q

what is the measure of initial fibre length

A

left ventricular end diastolic pressure

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22
Q

what happens during heart failure in the Frank Starling relationship

A

more blood in the heart doesnt make more contraction

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23
Q

what is the extrinsic regulation of the heart contractility

A

baroreceptor reflex

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24
Q

what happens if BP increases in BR reflex

A

carotid sinus baroreceptors - CNS- enhances vagal flow- bradycardia

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25
Q

what happens if BP decreases in BR reflex

A

carotid sinus baroreceptors - CNS- decrease vagal flow- tachycardia +vasoconstriction

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26
Q

what are 4 causes of congestive heart failure

A

infarction
ischemia
increase presure
increase volume load

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27
Q

what is ischemia

A

inadequate blood supply to an organ or part of the body, dead tissue

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28
Q

what is infarction

A

obstruction of the blood supply to an organ or region of tissue, causing local death of the tissue.

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29
Q

what are 5 sings of congesttive heart failure

A

reflex tachycardia, enlarged heart, oedema, dyspnea(shortness of breath), elevated venous pressure (swollen neck veins+ankles)

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30
Q

what is dyspnea

A

shortness of breath

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31
Q

what is a main force that keeps circulation moving

A

the large pressure between arteries and veins

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32
Q

what causes venous distention

A

heart is too weak to pump

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33
Q

what happens to venous return in heart failure

A

decreases

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34
Q

what happens to cardiac output in heart failure

A

decreases

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35
Q

what happens to sympathetic outflow in heart failure

A

increase (accumulate fluid)

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36
Q

what happens to glomerular filtration in heart failure

A

decrease

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37
Q

what does the “congestive” in congestive heart failure mean +what does it come from

A

enhanced sympathetic outflow leads to the circulatory congestion

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38
Q

what does increased sympathetic outflow do to HR

A

increase

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39
Q

what does congestive heart failure do to arterial pressure

A

maintain!

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40
Q

why is there edema in congestive heart failure

A

elevated venous pressure, fluid expelled from capillaries

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41
Q

what happens to heart size in congestive heart failure

A

becomes large

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42
Q

what happens to sympathetic outflow in congestive heart failure

A

increase

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43
Q

what happens to renal blood flow in congestive heart failure

A

decrease

44
Q

what happens to cardiac output in congestive heart failure

A

decrease

45
Q

why is renal blood flow decreased in congestive heart failure

A

because less cardiac output

46
Q

what does low renal blood flow cause

A

increase in renin release

47
Q

what happens to renin release in congestive heart failure and why

A

increase renin release because there is less renal blood flow

48
Q

what does renin cause the conversion of

A

angiotensinogen to angiotensin 1

49
Q

what happens to angiotensin 2 in congestive heart failure

A

increase

50
Q

what does angiotension 2 do to preload in congestive heart failure

A

increase

51
Q

what does angiotension 2 do to afterload in congestive heart failure

A

increase

52
Q

what are 3 ways to treat heart failure (broad)

A

enhance contractility
diuretic+reduce fluid intake
reduce cardiac work load

53
Q

what are 2 ways(drug types) to enhance contractility in congestive heart failure

A

cardiac glycosides and positive inotropic agents

54
Q

how can you reduce fluid intake and increase fluid loss in congestive heart failure

A

diuretics

55
Q

what are 2 ways(drug types) to reduce cardiac work load

A

vasodilators and beta-blockers

56
Q

what is an example of a positive inotropic gent

A

cardiac/digitalis glycosides / digoxin

57
Q

what do positive inotropic agents do

A

increase force of contraction

58
Q

what do negative inotropic agents do

A

decrease force of contraction

59
Q

what are 2 things that positive inotropic agents cause via the increased force of contraction

A

circulatory improvement and preserved arterial blood pressure

60
Q

what are 3 things that negative chronotropics agents cause

A
  • reflex tachycardia & vasoconstriction eliminated
  • venous return increased
  • circulatory improvement lowers ventricular filling pressure
61
Q

what happens to the heart size when you use cardiac glycosides

A

smaller

62
Q

what happens to edema with cardiac glycosides

A

it becomes reduced

63
Q

what do cardiac glycosides do to baroreceptors

A

sensitize (indirect)

64
Q

what do cardiac glycosides do to vagal tone

A

increase (indirect)

65
Q

what are the indirect effects of cardiac glycosides like

A

ACh

66
Q

what are the 2 indirect effects of cardiac glycosides on supraventricular tissue

A

sensitization of baroreceptors, increased vagal tone

67
Q

where are the 2 direct effects of cardiac glycosides on the heart (which parts of the heart)

A

purkinje fibres and ventricular myocardium

68
Q

what do cardiac glycosides do to ventricular myocardium

A

increase force of contraction (positive inotropic effect),

ERP and APD reduced

69
Q

what do cardiac glycosides do to SA node + net effect

A

increase vagal outflow, decease sinus rate (indirect) -bradycardia

70
Q

where are the 2 indirect effects of cardiac glycosides on heart tissue

A

SA node and AV node

71
Q

what do cardiac glycosides do to SA node + net effect

A

increase vagal outflow (indirect) - promotes AV block!

72
Q

what is the net effect of cardiac glycosides on the SA node

A

bradycardia

73
Q

what is the net effect of cardiac glycosides on the AV node

A

promotes AV block

74
Q

what do cardiac glycosides do to purkinje fibres

A

increase automaticity and excitability

75
Q

what do cardiac glycosides do to ERP

A

reduce

76
Q

what do cardiac glycosides do to APD

A

reduce

77
Q

what is the TI of cardiac glycosides

A

low, 2-3 of TI

78
Q

what are some cardiotoxic effects of cardiac glycosides (5)

A
  • arrhythmias
  • enhancement of effects seen with therapeutic dose
  • generation of after-depolarization
  • AV block
  • ectopic pacemakers in Purkinje fibres or ventricles
79
Q

what causes the contractile machinery during AP

A

ca++ entry through ca channels

80
Q

which ion exchange channel is occuring during phase 2 AP

A

Na+/Ca++ exchange (plateau)

81
Q

which gradient provides evergy for the extrusion of Ca++

A

Na+ gradient

82
Q

what is the mechanism of action of digitalis

A

inhibits the Na+/K+ ATPase pump

83
Q

what happens to intracellular Na+ with digitalis

A

accumulation due to the AP

84
Q

what happens to Na+ gradient with digitalis

A

it is decreased

85
Q

what happens to Na+/Ca+ exchange with digitalis

A

it is reduced

86
Q

what happens to the amount of Ca++ that leaves the cell during plateau phase of AP with digitalis

A

less leaves

87
Q

what kind of dysrhythmia are cardiac glycosides good for

A

atrial and supraventricular

88
Q

what is the role for cardiac glycosides in atrial dysrhythmias + How!?

A

control ventricular rate by impeding transmission through AV node

89
Q

are cardiac glycosides good for ventricular dysrhythmias

A

bad

90
Q

are cardiac glycosides good for do supraventricular dysrhythmias

A

good

91
Q

are cardiac glycosides good for atrial dysrhythmias

A

good

92
Q

how do cardiac glycosides help atrial dysrhythmias

A

impede transmission through AV node

93
Q

what do cardiac glycosides do to AV node

A

impede transmission

94
Q

are catecholamines positive or inotropic agents

A

positive

95
Q

are phosphodiesterase inhibitors positive or inotropic agents

A

positive

96
Q

what are 2 examples of catecholamines

A

dopamine and dobutamine

97
Q

what are dopamine and dobutamine used for

A

acute heart failure

98
Q

how do dopamine and dobutamine work

A

stimulate b1 adrenoceptors (increase force) so they increase Ca++ influx through L-type Ca++ channel (increase force more so than rate)

99
Q

is the inotropic or chronotropic effect bigger in dopamine and dobutamine

A

inotropic (more force rather than rate)

100
Q

what are two examples of phosphodiesterase inhibitors

A

amrinone and milrinone

101
Q

what are amrinone and milrinone used for

A

chronic heart failure

102
Q

what does phosphoodiesterase do

A

breaks down cAMP

103
Q

what would a phosphodiesterase inhibitor do to cAMP level

A

increase

104
Q

what does amrinone and milrinone do to contractility and how

A

increases because it increases Ca++ through L-type channels

105
Q

what does amrinone and milrinone do to arteries

A

vasodilates

106
Q

what does amrinone and milrinone do to force

A

increase

107
Q

what does amrinone and milrinone do to afterload

A

lower

PMCOL 343 (31 decks)

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