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Cardio 2 > drugs used in heart failure > Flashcards

drugs used in heart failure Flashcards

1
Q

inotropic agents

A

byryridines
cardiac glycosides
beta-adrenergic receptor agonists

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2
Q

bypyridines

A

-rinone

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3
Q

beta-adrenergic receptor agonists

A

dobutamine

dopamine

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4
Q

agents w/o inotropic effects

A 
diuretics
ACE inhibitors
ARBs
vasodilators
beta-adrenergic receptors blockers
natriuetic peptide
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5
Q

loop diuretics

A

-bumatanide
furosemide
torsemide

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6
Q

thiazide diuretics

A

HCL

chlorathiadone

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7
Q

aldosterone antagonists

A

eplerenone

spirolactone

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8
Q

ASH antagonists

A

conivaptan

tolvaptan

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9
Q

ACE inhibitors

A

-pril

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10
Q

ARBs

A

-sartan

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11
Q

vasodilators

A

isosorbide dinitrate (venous)
hyralazine (arterial)
nitroprusside (aa and vv)

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12
Q

beta blockers

A

-olol

carvediol

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13
Q

natriuretic peptide

A

nessiritide

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14
Q

diuretics and inotropic agents

A

increase quality of life and treat symptoms

do not decrease mortality

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15
Q

reduce mortality

A

ACE inhibitors, ARBs, beta-blockers, aldosterone recepotr antagonists

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16
Q

systolic failure

A

reduced CO and contractility
reduced EF (<45%)
typical of acute failure
responds to positive inotropic effects

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17
Q

diastolic failure

A

occurs as a result of hypertophy and stiffening myocardium
CO reduced
EF may be normal
does not typically respond to positive inotropic agents

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18
Q

digoixin

A 
only glycoside available in US
HF and Afib
enters CNS
normal renal fnx- 1/day
vasodilators can increase clearance
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19
Q

digoxin pharmacodynamics

A

inhibits membrane-bound NA/K ATPase-> blocks Na/Ca exchanger -> more intracellualr Ca ->increases contraction of cardiac mm

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20
Q

effects of digoxin

A

improves contractility and prolongs refractory period of AV for treatment of supraventricular arrhythmia’s

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21
Q

digoxin and ANS

A

increases parasympathetics and reduces sypathetics

increases refractory period of AV node

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22
Q

digoxin toxcity

A 
AV junctional rhythm
PACs
bigeminal rhythm
second degree AV block
tachycardia-> Vfib -> death

at toxic levels increases sympathetics

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23
Q

digoxin SA node

A

therapeutic dose- decrease rate

toxic dose-decrease rate

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24
Q

digoxin atrial mm

A

therapeutic dose- decrease refracotry period

toxic dose-decrease refractory period, arrythmias

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25
Q

digoxin AV node

A

therapeutic dose- decrease condcution velocity, increase refractory period
toxic dose- decrease refractory period, arrythmias

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26
Q

digoxin purkinje system and ventriuclar mm

A

therapeutic dose- slight decrease in refractory period

toxic dose- extrasystoles, tachycardia, fibrillation

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27
Q

digoxin EKG

A

therapeutic doses: increased PR interval, decreased OT

toxic doses- tachycardia, fibrillation, arrest

28
Q

digoxin toxicity GI

A

anorexia, nausea, vomiting, diarrhea

29
Q

digoxin toxicity CNS

A

vagal and chemoreceptors trigger zone stimulation -> GI, disorientation, hallucinations, visual disturbances

30
Q

other digoxin toxicity effects

A

gynocomastia rare in men

31
Q

digoxin toxicity Tx

A

antidigoxin immunotherapy

32
Q

digoxin and K

A

bind to competing sites on Na/K ATPase
hyperkalemia can reduce effects of digoxin
hypokalemia can potentiate toxic effects

33
Q

digoxin and Ca and Mg

A

hypercalcemia and hypermagnesemia increase risk of digoxin-induced arrhythmias

34
Q

byridines

A

short term support of circulation in acute decompensated HF
may increase mortality if used long term
only parenteral

35
Q

byridines MOA heart

A

selective inhibition of PDE3 -> increase cAMP -> direct stimulation of myocardial contraction and accelerated relaxation -> increased CO

36
Q

byridines MOA vessels

A

inhibit PDE3 -> increase cAMP -> balances aa and vv dilation w/decrease in TPR and pulmonary resistance -> less work of left and right heart

37
Q

caffeine

A

nonspecific PDE inhibitors -> limited by side effects

38
Q

byridines toxicity

A

inamrinone- nausea, vommiting, arrhythmias, thrombocytopenia, liver enzyme changes
milirinone- arrhythmias

39
Q

beta adrenergic and dopaminergic agents MOA

A

short term use (long term may increase mortality)
stimulate cardiac myocyte D1 R and beta 1 R
Gs -> AC -> cAMP -> PKA -> Ca -> increase contraction and speed relaxation

40
Q

dobutamine

A 
stimulates beta 1 
choice drug for systolic dysfunction and HF
increase in SV and CO
can cause excessive tachycardia 
parenteral
41
Q

dopamine low doses

A

vasodilation via D1 on smooth m and D2 on presynaptic sympathetics

42
Q

dopamine intermediate doses

A

directly stimulated beta Rs on heart and vasculature sympathetics -> increased CO and increased NE release

43
Q

dopamine high doses

A

peripheral aa and vv constriction via alpha 1

may be desirable in patients where circulatory failure is result of vasodilation

44
Q

loop diuretics

A

heart failure

45
Q

thaizide diuretics

A

systemic HTN

more effective in treating HF when combined w/loop

46
Q

K sparring diuretics

A

relatively weak, but shown to improve survival in advanced HF via a mechanism other then diuresis

47
Q

aldosterone antagonists

A

aldosterone may cause mycardial and vascular fibrosis and baroreceptors dysfunction
antagonism improves survival

48
Q

ADH antagonists toxicity

A

hypernatremia, nephrogenic DI

49
Q

ADH antagonists and HR

A

use is controversial

50
Q

ACE inhibitors

A
  • reduce TPR -> reduce afterload
  • decrease sympathetics
  • reduce long term remodeling of heart and vessels (ACE is same enzyme as kinase II) therefore increases bradykinin levels
  • potentiate effects of diuretics in HF
51
Q

ACE inhibitors adverse effects

A

angioedema, cough, hyperkalemia

52
Q

ARBs

A

angiotensin II R blockers
block AT1, but beneficial effects of AT2 intact
ARBs do not alter bradykinin metabolism
should be considered in patients intolerant to ACE inhibitors

53
Q

isosorbide dinitrate

A

NO released when drug metabolized -> increased cGMP-> venodilation and reduces preload and ventricular stretch
used in acute and chronic HF, angina, and HTN emergencies
long term limited by tolerance

54
Q

isosobide dinitrate adverse effects

A

orthostatic hypotension, tachycardia, headache

55
Q

nitroglycerin

A

venodilator used for acute decompensated heart failure

56
Q

hydralazine

A

stimulates release of NO from endo -> vasodilation aa -> reduces BP and afterload -> increased CO
used in combo w/nitrates to reduce mortality in HF and HTN emergencies

57
Q

hydalazine toxicity

A

tachycardia, fluid retention, lupus like syndrome

58
Q

nitroprusside

A

spontaneously converted to NO -> marked vasodilation of aa and vv -> reduces preload and afterload
used for acute cardiac decompensation and HTN emergencies

59
Q

nesiritide

A

recombinant form of BNP for acute decompensated HF w/dyspnea at rest
cases smooth mm relaxation and reduced endothelin production
vasodilation, natiuresis, diuresis counter acts effects of angtiotensin and NE
IV

60
Q

adverse effects of nesirtide

A

excessive hypotension

61
Q

beta blockers

A

improve contractile function
attenuation of maladaptive catecholamine induced cardiomyocyte toxicity
favorable effects on remodeling
reduce myocardial O2 consumption
decrezse frequency of unstable angina
may take several months before benefit is seen

62
Q

Na removal

A

thiazide or loop diuretics cause loss of Na which leads to secondary loss of K
dangerous if on digoxin

63
Q

hypokalemia Tx

A

addition of ACE inhibitor or K sparring diuretic, or supplementation

64
Q

HF w/o edema first line Tx

A

ACE inhibitors w/diuretics

ARBs should be used if patients intolerant to ACE inhibitor

65
Q

vasodilators in african americans

A

hydralazine and isosorbide dinitrate if they cannot tolerate or standard therapy no effective

Cardio 2 (17 decks)

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