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Cardiovascular > Heart Failure Pharmacology > Flashcards

Heart Failure Pharmacology Flashcards

1
Q

goals of HF treatment

A

prevent patients from ever getting symptomatic HF

focus on stage A and B HF for prevention

once symptomatic, prevent hospitalization

prevent progression to stage D HF

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2
Q

Stage A HF treatment

A

treat hypertension

encourage smoking cessation

treat lipid disorders

encourage regular exercise

discourage alcohol intake and illicit drug use

control metabolic syndrome

drugs: ACEI or ARB in appropritae patients

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3
Q

Stage B HF treatment

A

all measure under A

drugs: ACEI or ARB as well as beta-blockers in appropriate patients

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4
Q

Stage C HF treatment

A

all measures under stages A and B

dietary salt restriction

drugs for routine use: diuretics for fluid retention, ACEI, beta-blockers

drugs in selected patients: aldosterone antagonist, RBs, digitalis, hydralazine/nitrates

devices in selected patients: biventricular pacing, implantable defibrillators

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5
Q

Stage D HF treatment

A

appropriate measures under stages A, B, or C

decide on appropriate level of care

options are end-of-life care/hospice

extraordinary measures include heart transplant, chronic inotropes, permanent mechanical support, experimental surgery or drugs

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6
Q

symptoms of HF

A

low exercise capacity - decreased CO

dyspnea - pulmonary edema

orthopnea - increased venous return when supine

nocturia - increased venous return when supine

swelling, weight gain - salt and water retention

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7
Q

signs of HF

A

increased JVP - elevated RA pressure

rales - pulmonary edema

S3 - elevated LV filling pressures and stiff LV

hepatomegaly - systemic venous congestion

edema - transudation of fluid from capillaries

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8
Q

NYHA class I

A

no limitations of physical activity

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9
Q

NYHA II

A

slight limitation of activity

dyspnea and fatigue with moderate physical activity

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10
Q

NYHA III

A

marked limitation of activity

dyspnea with minimal activity

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11
Q

NYHA IV

A

severe limitation of activity

symptoms are present at rest

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12
Q

precipitating factors of HF

A

medication non-compliance

dietart indiscrtion

increased metabolic demands (fever, infection, anemia, tachycardia, hyperthyroidism, pregnancy)

increased circulating volume (increased preload)

increased afterload (uncontrolled systemic hypertension, pulmonary embolism)

reduced CO due to either reduced contractility or reduced stroke volume/abnormal heart rate

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13
Q

principles of HF treatment

A

identify underlying etiology

eliminate precipitating cause

ameliorate HF symptoms

modulate maladaptive neurohormonal response

improve long-term survival

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14
Q

steps to prevent heart failure

A

control blood pressure

control diabetes

control lipids

smoking cessation

weight control

early recognition and treatment of acute coronary syndromes

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15
Q

treatment of symptomatic HF

A

identify and treat the underlying etiology of HF

eliminate precipitating factors

ameliorate HF symptoms

modulate maladaptive neurohormonal response

improve long-term survival

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16
Q

treatment of heart failure with reduced EF (systolic HF)

A

improve Frank-Starling relationship in acute and asymptomatic patients

neurohormonal antagonists - reverse remodel and prolong life, pharmacogenomics is a possibility

devices to preevent sudden death

inotropic devices

heart replacement/support

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17
Q

treatment of heart failure with preserved EF (diastolic HF)

A

so far randomized controlled trials have been disappointing

find and treat underlying etiology

agggressively treat hypertension

coronary revascularization

if atrial fibrillation - control rate and/or convert to normal sinus rhyth

treat comorbidities

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18
Q

treatment of acute pulmonary edema in acute decompensated HF

A

LMNOP

L - loop diuretics, acutely venodilate and then natriuresis

M - morphine, venodilator to decrease sensation of dyspnea

N - nitrates, venodilator to increase pulmonary venous capacitance

O - oxygen, increased supply at a time when oxygen demand is high

P - positive pressure ventilation, improve oxygenation and decrease venous return, increases contractility

after acute stabilization, medicate underlying problem

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19
Q

hemodynamic goals for achieving symptom relief and stabilization in acute decompensated EF

A

reduce right and left heart filling pressures

reduce systemic vascular resistance

increase cardiac output

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20
Q

signs of congestion

A

orthopnea, increased JVP, rales, ascites, leg swelling

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21
Q

signs of poor perfusion

A

cool extremities, decreased BP, decreased pulse pressure, sleepy/obtunded, worsening renal function, decreased urine output

22
Q

cold and wet

A

congested with poor perfusion

use vasodilators first and then inotropes

warm up and then diurese

23
Q

cold and dry

A

no congestion but poor perfusion

end-stage HF vasodilators, inotropes

LVAD

heart transplant

24
Q

warm and wet

A

congested but well-perfused

diurese and uptitrate HF meds

25
Q

warm and dry

A

reconsider HF diagnosis

26
Q

diuretics

A

most comonly used are secreted into the nephron via the proximal tubule (except aldosterone antagonists)

therefore doses need to be increased in patients with chronic kidney disease

categorized by site of action

27
Q

types of diuretics

A

proximal tubule - acetazolamide, rarely used

thick ascending limb of loop of henle - loop diuretics

distal convoluted tubule - thiazide diuretics

collecting ducts - potassium-sparing diuretics

28
Q

loop diuretics

A

improve symptoms but increase neurohormones

ex. furosemide, torsemide, bumetanide, ethycrinic acid (important, ototoxicity)

29
Q

thiazide diuretics

A

HCTZ, chlorthalidone, chlorhiazide, metolazone

less potent than loop diuretics but can be very potent in combination

30
Q

potassium sparing diuretics

A

triamterene and amiloride

rarely used

aldosterone-antagonists, improve mortality

31
Q

deleterious effects of aldosterone

A

prothrombotic effects

vascular inflammation and injury

potassium and magnesium loss

central hypertensive effects

endothelial dysfunction

ventricular arrhythmias

cardiovascular disease

sodium retention

catecholamine potentiation

myocardial fibrosis

32
Q

types of vasodilators

A

intravenous

hydralazine

nitrates

ACE-inhibitors and angiotensin receptor blockers (ARBs)

33
Q

intravenous vasodilators

A

nitroglycerin

nitroprusside

nesiritide

34
Q

nitroglycerine

A

primarily a venodilator

good for patients who are warm and wet but not patients who are cold because they can acutely worsen hypotension

35
Q

nitroprusside

A

mixed venous and arterial vasodilator

vesodilator of choice if a patient is cold because it won’t decrease preload as much as other agents

36
Q

nesiritide

A

recombinant BNP natriuretic peptide that also dilates veins and some arteries

do not use in hypotensive patients because it may increase mortality or renal failure

37
Q

oral vasodilators

A

hydralazine

nitrates

ACE inhibitors

ARBs

38
Q

hydralazine

A

pure arterial vasodilator

reduces SVR, thereby increasing CO and can paradoxically increase BP

39
Q

nitrates

A

venodilator

increased pulmonary venous capacitance, decreased pulmonary venous pressure, decreased hydrostatic pressure, decreased pulmonary edema

use with caution in hypotensive patients who may be preload-dependent

40
Q

ACE inhibitors

A

block deleterious effects of angiotensin II

increases bradykinin, which leads to vasodilation and cough

41
Q

angitensin receptor blocekrs (ARBs)

A

block angiotensin II receptor

no cough, but no bradykinin-induced vasodilation

better than ACE inhibitors because they block the receptor completely

there is no cough, but benefits of high bradykinin is gone

42
Q

inotropes

A

all IV inotropes increase mortality in acute decompensated heart failure, so use with caution

beta-adrenergic agonists

phosphodiesterase inhibitors

calcium sensitizers

digitalis (digoxin)

43
Q

digoxin

A

decreases hospitalization but not mortality

optimal concentration between 0.5 and 0.8 ng/ml

higher dizes increases mortality

blocks Na/K-ATPase which increases calcium in the cell due to the sodium/calcium pump

adrenergic modulation

44
Q

beta-blockers

A

indicated for all classes of systolic HF

use after stabilization of the patient, can cause acute decompensation, so start low and be cautious

if a patient is on chronic beta-blocker therapy and gets admitted for ADHF, try to keep on beta-blocker if possible

reduce mortality

45
Q

beta-adrenergic agonists

A

ex. dobutamine, dopamine, and norepinephrine

can cause increased contractility, increaed HR, peripheral vasodilation, and peripheral vasoconstriction depending on the drug

dobutamine is most commonly used

46
Q

phosphodiesterase inhibitors

A

amrinon and milrinone

milrinone is the only one clinically used

these work intracellularly and bypass the beta-receptor by increasing cAMP

also increase contractility and cause peripheral vasodilation

47
Q

calcium sensitizers

A

levosimendan

sensitizes myocytes to calcium, which increases contractile force

no evidence of outcome benefits

48
Q

limitation of drugs in heart failure

A

too many

need to be taken without specified periodicity

side effects/toxicity

drug/drug interactions

costly

49
Q

non-pharmacologic therapies

A

lifestyle / dietary chagnes / exercise

treatment of comorbidities

ultrafiltration - alternative to diuretic therapy

cadiac resynchronizatino therapy (CRT)

implantable cardiac defibrillator (ICD) therapy - used in patients in class I-III HF but not patients with class IV

surgical therapies - mitral valve repair, ventricular assist device, cardiac transplantation

50
Q

cardiac resynchronization therapy (CRT)

A

indicated in symptomatic patiwhts with NYHA class III or IV with persistent symptoms despite optimal medical management

patients who most likely have intraventricular and interventricular electrical and mechanical dyssynchony

by pacing RV and LV simultaneously, cardiac function can improve in these patietns

51
Q

ventricular dyssynchrony

A

uncoordinated electrical and mechanical contraction of the ventricles

may involve disruption of collagen matrix - impairs electrical condcution and mechanical contraction or efficiency

associated with woprse prognosis and impaired hemodynamic function

Cardiovascular (46 decks)

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