Exam 3, drugs used in HF DSA Flashcards

1
Q

What are the drugs with positive ionotropic effects

A

cardiac glycosides- digoxin
Bypyridines- inamrinon and milrinone
beta adrenergic R agonists- dobutamine and dopamine

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2
Q

What cardiac drugs do not have a positive ionotropic effect

A

diuretics, ACEI, ARBs, vasodilators, Beta blockers, Natriuretic peptide

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3
Q

what are the loop diuretics

A

bumetanide
furosemide
torsemide

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4
Q

what are the thiazide diuretics

A

HCTZ

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5
Q

what are the aldosterone antagonists

A

eplerenon and spironolactone

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6
Q

what are the vasopressin (ADH) antagonists

A

conivaptan, tolvaptan

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7
Q

What drug class ends in “pril”

A

ACEI

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8
Q

what drug class ends in “sartan”

A

ARB

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9
Q

what drugs specifically venodilate

A

isosorbide dinitrate

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10
Q

what drug is an arteriolar dilator

A

hydralazine

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11
Q

what drug is a combined arteriolar and venodilator

A

nitroprusside

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12
Q

what drug class ends in “olol”

A

beta blockers

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13
Q

what drug do we have that is a ntriuretic peptide

A

nesiritide

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14
Q

what drugs for HF have been proven to reduce HF mortality

A

ARB, ACEI, beta blocker, aldosterone R antagonist

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15
Q

What occurs in systolic heart failure and what drug class is used

A

reduced CO and contractility
redced EF
typical of acute failure
responds to positive ionotropic agents

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16
Q

What occurs in diastolic heart failure and what drug class is used

A

results from hypertrophy and stiffening of myocardium
CO is reduced
EF is normal
does not typically respond optimally to + ionotropic agents

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17
Q

What are signs and dx of HF

A

tachy, decreased exercise tolerance, SOB, peripheral and pulmonary edema, cardiomegaly, decreased exercise tolerance is major direct consequence of diminished cardiac output while other manifestations result from compensatory adaptations

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18
Q

what is digoxin used to Tx

A

HF and Afib

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19
Q

How does digoxin work

A

inhibits Na K ATPase causing increased contraction of cardiac sarcomere
reduce Na extrusion and Ca efflux then is decreased too. more Ca in sarcoplasmic reticulum for more contractility

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20
Q

how does digoxin change myocardial electrical potentials

A

brief prolongation of AP followed by shortening

increased potassium conductance(rapid repolarization)

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21
Q

what are common cardiac manifestations of digoxin toxicity

A

AV junctional rhythm, premature ventricular depolarization, bigeminal rhythm, second degree AV block

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22
Q

What are the therapeutic effects of digoxin on AV node

A

decrease conduction velocity

increase refractory period

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23
Q

how does digoxin change EKG

A

increase PR interval and decrease QT interval

24
Q

where in the body are digoxin toxicity signs seen

A

GI - nausea, vomiting, diarrhea
and CNS - vagal and chemoR trigger zone stimulation can cause GI symptoms, disorientation, hallucinations and visual changes
can cause gynecomastia in men

25
what can reduce toxic effects of digoxin
hyperkalemia
26
what can potentiate toxic effects of digoxin
hypokalemia
27
What ion levels increase risk of digoxin induced arrhythmia
hyperCa and hypoMg
28
how do bipyridines work
selective inhibition of phosphodiesterase isozyme 3 PDE3 which increases cAMP directly stimulating myocardial contractility and acceleartaion of releaxation
29
how does increased cAMP levels affect vasculature
balanced arterial and venous dilation with fall in systemic and pulmonary vascular R L and R filling P
30
What are Sx of inamrinone toxicity
nausea, vomiting, arrhythmias, thrombocytopenia, liver enzyme changes
31
what are Sx of Milrinone toxicity
arrhythmias
32
When are bipyridines used
short term therapy
33
what are dopamine and dobutamine used for
short term support for acute decompensated HF
34
what are the hemodynamic effects of dobutamine
increase in SV from + ionotropic action and increased CO
35
side effects of dobutamine
tachy and arrhythmias
36
describe dopamine effects at low, intermediate and high doses
low- vasodilation intm- increases contractility and neural NE release high- peripheral arterial and venous constriction via alpha stimulation
37
What are loop diuretics used to Tx
heart failure
38
what are thiazide diuretics primarily used for
systemic HTN
39
what are negative effects of increased aldosterone in system
increased Na and water retention | may also cause myocardial and vascular fibrosis and baroR dysfunction
40
What is conivaptan used for, MOA?
HF, SIADH | antagonist at ADH R V1a and V2 in cortical collecting tubule
41
how does tolvaptan differ from conivaptan
selective antagonist of V2 ADH R
42
which diuretic decreases mortality in HF
aldosterone antagonist
43
What is a big difference os ACEI and ARB
ACEI block degradation of bradykinin | ARBs are downstream of that
44
what are sideeffects of ACEI
angioedema, cough, mild hyperkalemia
45
what ACEI have been approved for use in patients with HF
captopril, enalapril, ramipril, lisinopril, quinapril, fosinopril
46
Which R do ARBs selectively block
AT1 R
47
how are vasodilators effective in acute HF
reduce preload and reduce afterload
48
how does isosorbide dinitrate work
NO released when drug is metabolized, NO activates guanylyl cyclase reduce preload and ventricular stretch
49
when is isosorbide dintrate used and what are side effects
used in acute and chronic HF as well as angina and HTN emergencies adverse effects= postural hypotension, tachy and HA
50
How does hydralazine work
stimualtes release of NO from endothelium causing direct vasodolation of arterioles with little effect on vv dec BP and afterload, inc CO
51
how does nitroprusside work
spontaneously converted to NO which activate guanylyl cyclase and causes vasodilation and profound reduction in preload and afterload used for acute cardiac decompensation and HTN emergencies
52
How does nesiritide work
bindes to natriuretic peptide R on vascular smooth muscle and endothelial cells, increasing intracell cyclic GMP resulting in smooth muscle cell relaxation and endothelin production
53
what beta blockers have been shown to reduce mortality
bisoprolol, carvedilol, metoprolol, nebivolol
54
why are beta blockers started on low doses
acutely antagonize the supportive effects of catecholamines and can worsen HF
55
how can hypokalemia be treated
ACEI or K sparing diuretic
56
patients with high filling pressures with dyspnea what drug class would be most helpful
venous dilators