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Year 2 CV > Exam 3, drugs used in HF DSA > Flashcards

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
Q

what can reduce toxic effects of digoxin

A

hyperkalemia

26
Q

what can potentiate toxic effects of digoxin

A

hypokalemia

27
Q

What ion levels increase risk of digoxin induced arrhythmia

A

hyperCa and hypoMg

28
Q

how do bipyridines work

A

selective inhibition of phosphodiesterase isozyme 3 PDE3 which increases cAMP
directly stimulating myocardial contractility and acceleartaion of releaxation

29
Q

how does increased cAMP levels affect vasculature

A

balanced arterial and venous dilation with fall in systemic and pulmonary vascular R
L and R filling P

30
Q

What are Sx of inamrinone toxicity

A

nausea, vomiting, arrhythmias, thrombocytopenia, liver enzyme changes

31
Q

what are Sx of Milrinone toxicity

A

arrhythmias

32
Q

When are bipyridines used

A

short term therapy

33
Q

what are dopamine and dobutamine used for

A

short term support for acute decompensated HF

34
Q

what are the hemodynamic effects of dobutamine

A

increase in SV from + ionotropic action and increased CO

35
Q

side effects of dobutamine

A

tachy and arrhythmias

36
Q

describe dopamine effects at low, intermediate and high doses

A

low- vasodilation
intm- increases contractility and neural NE release
high- peripheral arterial and venous constriction via alpha stimulation

37
Q

What are loop diuretics used to Tx

A

heart failure

38
Q

what are thiazide diuretics primarily used for

A

systemic HTN

39
Q

what are negative effects of increased aldosterone in system

A

increased Na and water retention

may also cause myocardial and vascular fibrosis and baroR dysfunction

40
Q

What is conivaptan used for, MOA?

A

HF, SIADH

antagonist at ADH R V1a and V2 in cortical collecting tubule

41
Q

how does tolvaptan differ from conivaptan

A

selective antagonist of V2 ADH R

42
Q

which diuretic decreases mortality in HF

A

aldosterone antagonist

43
Q

What is a big difference os ACEI and ARB

A

ACEI block degradation of bradykinin

ARBs are downstream of that

44
Q

what are sideeffects of ACEI

A

angioedema, cough, mild hyperkalemia

45
Q

what ACEI have been approved for use in patients with HF

A

captopril, enalapril, ramipril, lisinopril, quinapril, fosinopril

46
Q

Which R do ARBs selectively block

A

AT1 R

47
Q

how are vasodilators effective in acute HF

A

reduce preload and reduce afterload

48
Q

how does isosorbide dinitrate work

A

NO released when drug is metabolized, NO activates guanylyl cyclase
reduce preload and ventricular stretch

49
Q

when is isosorbide dintrate used and what are side effects

A

used in acute and chronic HF as well as angina and HTN emergencies
adverse effects= postural hypotension, tachy and HA

50
Q

How does hydralazine work

A

stimualtes release of NO from endothelium causing direct vasodolation of arterioles with little effect on vv
dec BP and afterload, inc CO

51
Q

how does nitroprusside work

A

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
Q

How does nesiritide work

A

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
Q

what beta blockers have been shown to reduce mortality

A

bisoprolol, carvedilol, metoprolol, nebivolol

54
Q

why are beta blockers started on low doses

A

acutely antagonize the supportive effects of catecholamines and can worsen HF

55
Q

how can hypokalemia be treated

A

ACEI or K sparing diuretic

56
Q

patients with high filling pressures with dyspnea what drug class would be most helpful

A

venous dilators

Year 2 CV (31 decks)

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