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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
digoxin AV node
therapeutic dose- decrease condcution velocity, increase refractory period toxic dose- decrease refractory period, arrythmias
26
digoxin purkinje system and ventriuclar mm
therapeutic dose- slight decrease in refractory period | toxic dose- extrasystoles, tachycardia, fibrillation
27
digoxin EKG
therapeutic doses: increased PR interval, decreased OT | toxic doses- tachycardia, fibrillation, arrest
28
digoxin toxicity GI
anorexia, nausea, vomiting, diarrhea
29
digoxin toxicity CNS
vagal and chemoreceptors trigger zone stimulation -> GI, disorientation, hallucinations, visual disturbances
30
other digoxin toxicity effects
gynocomastia rare in men
31
digoxin toxicity Tx
antidigoxin immunotherapy
32
digoxin and K
bind to competing sites on Na/K ATPase hyperkalemia can reduce effects of digoxin hypokalemia can potentiate toxic effects
33
digoxin and Ca and Mg
hypercalcemia and hypermagnesemia increase risk of digoxin-induced arrhythmias
34
byridines
short term support of circulation in acute decompensated HF may increase mortality if used long term only parenteral
35
byridines MOA heart
selective inhibition of PDE3 -> increase cAMP -> direct stimulation of myocardial contraction and accelerated relaxation -> increased CO
36
byridines MOA vessels
inhibit PDE3 -> increase cAMP -> balances aa and vv dilation w/decrease in TPR and pulmonary resistance -> less work of left and right heart
37
caffeine
nonspecific PDE inhibitors -> limited by side effects
38
byridines toxicity
inamrinone- nausea, vommiting, arrhythmias, thrombocytopenia, liver enzyme changes milirinone- arrhythmias
39
beta adrenergic and dopaminergic agents MOA
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
dobutamine
``` stimulates beta 1 choice drug for systolic dysfunction and HF increase in SV and CO can cause excessive tachycardia parenteral ```
41
dopamine low doses
vasodilation via D1 on smooth m and D2 on presynaptic sympathetics
42
dopamine intermediate doses
directly stimulated beta Rs on heart and vasculature sympathetics -> increased CO and increased NE release
43
dopamine high doses
peripheral aa and vv constriction via alpha 1 | may be desirable in patients where circulatory failure is result of vasodilation
44
loop diuretics
heart failure
45
thaizide diuretics
systemic HTN | more effective in treating HF when combined w/loop
46
K sparring diuretics
relatively weak, but shown to improve survival in advanced HF via a mechanism other then diuresis
47
aldosterone antagonists
aldosterone may cause mycardial and vascular fibrosis and baroreceptors dysfunction antagonism improves survival
48
ADH antagonists toxicity
hypernatremia, nephrogenic DI
49
ADH antagonists and HR
use is controversial
50
ACE inhibitors
- 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
ACE inhibitors adverse effects
angioedema, cough, hyperkalemia
52
ARBs
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
isosorbide dinitrate
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
isosobide dinitrate adverse effects
orthostatic hypotension, tachycardia, headache
55
nitroglycerin
venodilator used for acute decompensated heart failure
56
hydralazine
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
hydalazine toxicity
tachycardia, fluid retention, lupus like syndrome
58
nitroprusside
spontaneously converted to NO -> marked vasodilation of aa and vv -> reduces preload and afterload used for acute cardiac decompensation and HTN emergencies
59
nesiritide
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
adverse effects of nesirtide
excessive hypotension
61
beta blockers
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
Na removal
thiazide or loop diuretics cause loss of Na which leads to secondary loss of K dangerous if on digoxin
63
hypokalemia Tx
addition of ACE inhibitor or K sparring diuretic, or supplementation
64
HF w/o edema first line Tx
ACE inhibitors w/diuretics | ARBs should be used if patients intolerant to ACE inhibitor
65
vasodilators in african americans
hydralazine and isosorbide dinitrate if they cannot tolerate or standard therapy no effective

Cardio 2 (17 decks)

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