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Pharmacy > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

an impairment of the contraction of the left ventricle. SV is reduced. EF is reduced (<45%)

A

systolic dysfunction

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2
Q

heart failure with preserved left ventricular systolic function

A

diastolic dysfunction

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3
Q

ventricular filling rate and extent of filling (EDV) are reduced. Normal EF is maintained

A

diastolic dysfunction

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4
Q

CO=?

A

CO=HRxSV

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5
Q

left ventricular end diastolic pressure

A

preload

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6
Q

systemic vascular resistance

A

afterload

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7
Q

Causes of ischemic heart failure

A

coronary artery disease (myocardial ischemia and infarction)

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8
Q

causes of non-ischemic heart failure

A

HTN, primary myocardial muscle dysfunction, valvular abnormalities, structural damage to valvular walls, dilated cardiomyopathy

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9
Q

what are compensatory mechanisms for heart failure

A

increased SNS activity (increase HR, BP)
Frank starling (increase preload= increase SV)
Activation of RAAS
myocardial remodeling (concentric and eccentric hypertrophy)

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10
Q

direct toxic effects of NE and AT2

A

arrhythmias, apoptosis

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11
Q

Symptoms include SOB, DOE, orthopnea, cough, PND, fatigue and weakness, memory loss and confusion, anorexia. Signs include tachy, rales, diaphoresis, S3 and S4 gallops

A

LVF

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12
Q

Symptoms include weight gain, transient ankle swelling, abdominal distention, anorexia, nausea. Signs include JVD, edema, hepatomegaly, ascites, and maybe hepatojugular reflux

A

RVF

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13
Q

this class of drugs has no data regarding morb or mort of HF. Class I- indicated in pts with current or prior symptoms of HF and reduced LVEF w evidence of fluid retention (level of evid- C)

A

diuretics

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14
Q

this diuretic can be useful if GFR > 30 ml/min and work on the distal tubule

A

thiazides

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15
Q

these diuretics work on the ascending LOH and are more of a DOC for HF

A

loops

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16
Q

what should you monitor for a pt on diuretics

A

K, Mg, BUN, SCr

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17
Q

this drug is class IIa and can be beneficial in pts with current or prior symptoms of HF and reduced LVEF to decrease hospitalization for HF (level of evidence B)

A

Digoxin

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18
Q

Hemodynamic effects in HF include increased CO, decreased wedge pressure, and increased LVEF

A

digoxin

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19
Q

neurohormonal effects in HF include vagomimetic action, improved baroreceptor senitivity, decreased NE, decreased RAAS activation, direct sympathoinhibitory effect

A

digoxin

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20
Q

this drug results in increased sympathetic CNS outflow at high doses, decreased cytokine concentration, and increased release of ANP and BNP

A

Digoxin

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21
Q

electrophysiological effects of this drug include slowing sinus rate (SA node), slowed conduction (AV node), decreased refractory period (atrium) and no effects of the ventricles and Purkinje fibers

A

digoxin

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22
Q

a low dose of this drug is sufficient. Inotropic effects can be seen at low concentrations, but women may not derive benefit

A

digoxin

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23
Q

this drug inhibits ATPase pump which acts to increase intracellular calcium leading to increased contractility

A

digoxin

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24
Q

Conditions likely to alter serum concentrations of this drug include changing renal function, drug interactions, and hypokalemia

A

digoxin

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25
Q

amniodarone and quinidine increase clearance of this drug (empirically by 50%)

A

digoxin

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26
Q

Drug interaction include diltiazem, verapimil, abx, azole antifungals, propafenone- all of these decrease clearance of the drug. Also interacts with furosemide

A

digoxin

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27
Q

pt comes in with ventricular arrhythmias, heart block. also complaining of visual changes, anorexia, N/V/D, abdominal pain, confusion, and HA

A

digoxin toxicity

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28
Q

treat digoxin toxicity

A

digoxin immune Fab

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29
Q

these classes are recommended for all pts with current or prior symptoms of HF and LVEF class I LOE A

A

ACE I

beta blockers

30
Q

how is dosing of ACEI different for HTN and HF

A

higher for HF

31
Q

what should you monitor when someone is on ACEI

A

SCr, K, BP, symptoms

32
Q

this drug may interfere with the efficacy of ACEI

A

aspirin

33
Q

side effects of this class include renal impairment, hyperkalemia, hypotension, and cough

A

ACEI

34
Q

intolerance to this class includes cough, angioedema

A

ACEI

35
Q

two alternatives for pts who cant take ACEI

A

ARBs or a combo of isosorbide dinitrate and hydralazine

36
Q

effects of chronic adrenergic activation

A

myocardial remodeling, apoptosis, arrhythmias, impaired diastolic filling, increased myocardial energy demand

37
Q

contraindications to the class include documented allergy, RAD, symptomatic bradycardia or > 1st degree heart block, fluid overload or on IV inotropic agents

A

beta blockers

38
Q

monitor pts taking this class for HR, BP, weight, symptoms (SOB, edema, DOE, dizziness)

A

beta blockers

39
Q

hemodynamic effects of aldosterone in CHF

A

sodium and water retention
increased plasma fluid volume
elevated BP

40
Q

Non hemodynamic effects of aldosterone in CHF

A

myocardial/vascular fibrosis, impaired arterial compliance, baroreceptor dysfunction, K and Mg excretion, elevated ANP, parasympathetic inhibition

41
Q

you can ADD this class in selected patients with moderately severe to severe symptoms of HF and reduced LVEF who can carefully be monitored for preserved renal function and normal K

A

aldosterone antagonists

42
Q

can only use this class is SCr < 2.5 in men and 2.0 in women, K 30

A

aldosterone antagonists

43
Q

this drug reduces the risk of CV events in pts without CHF but has not been demonstrated in CHF patients

A

ASA

44
Q

this class reserved for patients with afib or previous TE

A

anticoagulants

45
Q

this combo trio is never recommended for patients with HF

A

ACE I
ARB
aldosterone antagonists

46
Q

can combine these two in a persistently symptomatic patient who is already being treated with conventional therapy

A

ACEI plus ARB

47
Q

use this drug for post MI patients with LV dysfunction or those with gynecomastia from spironolactone

A

eplerenone

48
Q

cardiac index

A

CI= CO/BSA

49
Q

pulmonary artery wedge pressure

A

estimate of left ventricular end diastolic pressure (PRELOAD)

50
Q

systemic vascular resistance

A

pressure the left ventricle must overcome to eject its blood volume (AFTERLOAD)

51
Q

myocardial hypertrophy: systolic failure

A

excessive elongation of fibers so ventricle is unable to contract effectively

52
Q

myocardial hypertrophy: diastolic failure

A

hypertrophy of ventricles affects ability to relax, does not fill properly

53
Q

this diuretic can be administered for ADHF and acts through venodilation and Na/H2O excretion

A

Furosemide

54
Q

this drug is a potent beta 1 and beta 2 receptor agonist and a weak alpha 1 agonist

A

dobutamine

55
Q

this drug has positive inotropic and chronotropic effects, which increases CO and vasodilation (thereby decreasing SVR)

A

dobutamine

56
Q

monitor vitals, urine output, K, and telemetry when giving these drugs

A

dobutamine
dopamine
phosphodiesterase inhibitors
epi, norepi, isoproterenol

57
Q

this drug affects beta, alpha, and dopaminergic (DA1) receptors

A

dopamine

58
Q

what dose of dopamine is most often used for HF

A

MEDIUM (increases CO)

high dose has alpha 1 effects, increase SVR and make you worse

59
Q

these drugs increase intracellular cAMP, which increases intracellular calcium, which increases contractility and CO

A

phosphodiesterase inhibitors

60
Q

this positive inotrope does not reduce incidence of sudden death or prolong survival in patients with CHF

A

amniodarone

61
Q

these inotropes increase CO and SVR because they are beta 1, beta 2, and alpha 1 agonists

A

epi and norepi

62
Q

this inotrope is a beta 1 and beta 2 agonist. It increases CO and decreases SVR

A

isoproterenol

63
Q

this class reduces preload and therefore PCWP. Can cause HA, dizziness, reflex tachycardia, hypotension, thiocyanate toxicity

A

venodilators (thio tox is with nitroprusside)

64
Q

this venodilator is preferred when CO is not severely compromised or when other inotropic agents are administered

A

nitroglycerin

65
Q

this venodilator is also an arterial vasodilator and is preferred in patients with an increased SVR

A

nitroprusside

66
Q

this venodilator reduces preload (PWCP) and reduces heart rate

A

morphine

67
Q

taper this venodilator to avoid rebound HTN

A

nitroprusside

68
Q

this venodilator is typically used in the early stage of tx esp if the pt has anxiety, restlessness, or dyspnea

A

morphine

69
Q

monitor vitals for this class

A

venodilators

70
Q

this venodilator increases intracellular cGMP which leads to smooth muscle relaxation

A

nesiritide

71
Q

this venodilator promotes vasdilation, naturesis, and diuresis. It reduces PCWP, SVR, and increases CO

A

nesiritide

72
Q

this drugs use is controversial, it should be limited to patients presenting to the hospital with ADHF and dyspnea at rest

A

nesiritide

Pharmacy (22 decks)

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