Exam 3, drugs used in HF DSA Flashcards Preview

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Flashcards in Exam 3, drugs used in HF DSA Deck (56):
1

What are the drugs with positive ionotropic effects

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

2

What cardiac drugs do not have a positive ionotropic effect

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

3

what are the loop diuretics

bumetanide
furosemide
torsemide

4

what are the thiazide diuretics

HCTZ

5

what are the aldosterone antagonists

eplerenon and spironolactone

6

what are the vasopressin (ADH) antagonists

conivaptan, tolvaptan

7

What drug class ends in "pril"

ACEI

8

what drug class ends in "sartan"

ARB

9

what drugs specifically venodilate

isosorbide dinitrate

10

what drug is an arteriolar dilator

hydralazine

11

what drug is a combined arteriolar and venodilator

nitroprusside

12

what drug class ends in "olol"

beta blockers

13

what drug do we have that is a ntriuretic peptide

nesiritide

14

what drugs for HF have been proven to reduce HF mortality

ARB, ACEI, beta blocker, aldosterone R antagonist

15

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

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

16

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

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

17

What are signs and dx of HF

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

18

what is digoxin used to Tx

HF and Afib

19

How does digoxin work

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

20

how does digoxin change myocardial electrical potentials

brief prolongation of AP followed by shortening
increased potassium conductance(rapid repolarization)

21

what are common cardiac manifestations of digoxin toxicity

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

22

What are the therapeutic effects of digoxin on AV node

decrease conduction velocity
increase refractory period

23

how does digoxin change EKG

increase PR interval and decrease QT interval

24

where in the body are digoxin toxicity signs seen

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