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RCS > L18- Heart Failure Drugs > Flashcards

L18- Heart Failure Drugs Flashcards

1
Q

define HF and list its symptoms

A

Defn: CO is inadequate to provide needed O2 to the body

Sxs: tachycardia, dec exercise tolerance, dyspnea, cardiomegaly, peripheral / pulmonary edema

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2
Q

list the risk factors for HF

A
  • MAINLY: HTN, CAD

- MI, CM, FHx of cardiomyopathy, use of cardiotoxins, obesity

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3
Q

compare HFrEF v HFpEF

A

r = reduced EF, Systolic HF, loss of contractility / pumping action (heart can’t squeeze as well)

p = preserved EF, relaxation is inadequate for ventricular filling (stiff heart can’t relax normally - still reduced CO)

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4
Q

define and list the symptoms of CHF

A

(congestive heart failure)
-Defn: abnormal inc in BV, interstitial fluid

-Sxs: dypnea via pulmonary edema via LHF, peripheral edema via RHF

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5
Q

The main pathogenesis of HF includes the chronic activation of (1) and (2).

  • (1) will result in an increase in (3), (4), (5), (6)
  • (2) will result in an increase in (5), (6) and is critical in (7)
  • the end result is a vicious cycle of (1) and (2)
A 
1- SNS activation (3, 4, 5, 6)
2- RAAS activation / angiotensin II (5, 6, 7)
3- inc heart force / contraction
4- inc HR
5- inc preload
6- inc afterload
7- cardiac remodeling
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6
Q

cardiac performance is based on the following, describe….

A
  • preload
  • afterload
  • contractlility
  • HR
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7
Q

list the many lifestyle and medication recommendations** for chronic HF patients

A
  • *ACE inhibitors, diuretics, β-blockers, inotropic agents
  • light aerobic exercise, low Na intake (<2g), fluid restriction (2L), smoking cessation, achieve ideal weight
  • Tx comorbidities
  • avoid NSAIDs, EtOH, Ca channel blockers**
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8
Q

list the drugs used to treat HFrEF (systolic HF)

A
  • *diuretics (loop / furosemide)
  • spironolactone (aldosterone antagonist)
  • *ACEIs or ARBs
  • direct vasodilators
  • *β-blockers
  • inotropic agents
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9
Q

list the drugs used to treat HFpEF (diastolic HF)

A
  • diuretics
  • ACEIs or ARBs
  • β-blockers
  • Ca channel blockers
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10
Q

In HFrEF (systolic), describe how to choose diuretic type and how it will be useful

A

i) Thiazides: pts w/ HTN HD w/ congestive Sxs
ii) Loops: more effective, useful if edema is present

  • NO evidence of mortality benefit if used alone
  • Reduces Sxs of volume overload: peripheral / pulmonary edema (dec preload / afterload)
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11
Q

In HFrEF (systolic), describe when to start ACEIs (ARBs) and how it will be useful

A
  • Recommended for symptomatic HF and asymptomatic Pts w/ dec LVEF / h/o MI
  • (suggested for Pts at risk for development of HF due to atherosclerosis, obesity, DM, HTN)
  • dec afterload: dec PVR and BP via dec angiotensin II
  • dec preload: dec Na/H2O retention via dec aldosterone
  • dec long-term remodeling of the heart
  • *dec incidence of hospitalization, MI and prolongs survival
  • *use ARBs if Pt cannot tolerate ACEIs (cough / angioedema)
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12
Q

In HFrEF (systolic), describe what direct vasodilators to use, when to use them, and how it will be useful

A
  • Hydralazine (arterial dilation), Isosorbide Dinitrate (venous dilation) [note- ACEIs do both]
  • **use in BLACK pts, or those who can’t tolerate ACEIs/ARBs
  • venous dilation - dec preload
  • arterial dilation - dec afterload / PVR
  • Can produce a sustained improvement in LVEF
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13
Q

list the main vasodilators and their adverse effects

A

Hydralazine (arterial): HA, dizziness, tachycardia, peripheral neuritis, lupus-like syndrome

Nitrates / isosorbide dinitrate: HA, dizziness

***DO NOT USE Nitrates with Sidenafil/Viagra

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14
Q

In HFrEF (systolic), describe when to start β-blockers and how it will be useful

A

-In addition of ACEIs: use in symptomatic HF or in asymptomatic Pts w/ dec LVEF, h/o MI

  • dec HR, dec contractility, dec renin release (dec afterload/preload) via β1 antagonist
  • reverses cardiac remodeling (+hypertrophy), reduces hospitalization and mortality

-NOTE- several week to start working, may get initial exacerbation of Sxs

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15
Q

list the main ACEIs and ARBs used in HF

A

ACEIs: captopril, enalapril, lisinopril

ARBs: valsartan, candesartan

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16
Q

list the main β-blockers used in HF

A
  • carvedilol

- metoprolol

17
Q

In HFrEF (systolic), describe when to use Spironolactone and how it will be useful

A

(K+ sparing diuretic / aldosterone inhibitor)
-use in adjunct with ACEIs –> dec morbidity and mortality

-dec aldosterone –> dec Na/H20 retention –> prevents myocardial hypertrophy and hypokalemia

18
Q

what are the adverse effects of spironolactone

A
  • hyperkalemia
  • GI disturbances: gastritis, peptic ulcer
  • CNS effects: lethargy, confusion
  • Endocrine effects: ANDROGEN analog; gynecomastia, dec sperm. dec libido in men; menstrual abnormalities, dec libido in women
19
Q

(1) is a cardiac glycoside that is widely used in the treatment of HF. It will decrease (2) and (3) seen in HF patients and will increase (4). Despite this, it will have no effect on (5).

A 
1- digoxin
2- dec sxs of HF
3- dec hospitalizations
4- exercise tolerance
5- survival rate / mortality
20
Q

describe the disadvantages of digoxin

A

Narrow therapeutic window with complicated pharmacokinetics where drug sensitivity varies from patient to patient and from day to day in patients on therapy — its adverse effects may be lethal

-very potent, widely distributed (CSF) + accumulates in muscle => large Vd – large loading dose, half life 36-40 hrs

21
Q

describe the MOA of digoxin

A

Positively Inotropic: inc heart contraction by blocking Na/K ATPase – less Ca efflux – inc intracellular Ca to inc contraction force –> inc CO

Negatively Inotropic: dec HR by inc vagal tone (reduces SNS –> dec PVR => dec myocardial O2 demand)

22
Q

the main application of Digoxin is for (1), but may also be used for (2)

A

1- HF w/ AFib

2- in addition to ACEI, β-blocker to dec HF Sxs, HF hospitalizations, and inc exercise tolerance (no direct effect on mortality)

23
Q

list the adverse effects of digoxin

A

Cardiac: arrhythmias, slows AV conduction (atrial arrhythmias)

GI: n/v, anorexia

CNS: HA, fatigue, confusion, blurred vision + ***altered color perception (world with yellow-green hue)

24
Q

describe the interactions electrolytes have with digoxin use

A

K+: digoxin and K+ compete for Na/K ATPase binding => hypokalemia will potentiate effects, hyperkalemia will reduce effects

Ca2+: hypercalcemia potentiates effects

Mg2+: antagonizes Ca effects, hypomagnesia potentiates effects

25
Q

list the predisposing factors for digoxin toxicity (include drugs)

A
  • K+ depleting diuretics (loop, thiazides), corticosteroids
  • hypothyroidism, hypoxia, renal failure, myocarditis

-quinidine, verapamil, amiodarone

26
Q

list the contraindications of Digoxin

A
  • diastolic HF or RHF
  • uncontrolled HTN
  • bradyarrhythmias
  • non-responders / intolerant patients
27
Q

briefly describe the general treatment of HFpEF (diastolic)

A
  • little evidence drug Tx improves clinical outcomes

- largely treatment is for associated conditions and symptoms (HTN, edema)

28
Q

describe the benefit of diuretics in HFpEF (diastolic HF)

A
  • treats pulmonary edema

- use cautiously, don’t want to dec SV

29
Q

describe the benefit of ACEIs/ARBs in HFpEF (diastolic HF)

A
  • dec afterload: dec PVR via dec angiotensin II
  • dec preload: dec Na/H2O retention via dec aldosterone
  • dec cardiac remodeling
30
Q

describe the benefit of Ca channel blockers in HFpEF (diastolic HF)

A
  • INOTROPY is normal in diastolic HF, so Ca channel blockers won’t impair SV
  • improves ventricular relaxation and reduces HR
31
Q

describe the benefit of β-blockers in HFpEF (diastolic HF)

A

improves ventricular relaxation and reduces HR

32
Q

list the 4 inotropic drugs used in acute HF

A
  • PDE (phosphodiesterase) III inhibitors (inamrinone, milrinone)
  • dobutamine
  • dopamine
  • glucagon
33
Q

PDE III inhibit, aka (1), includes (2) drugs. They function on the heart to inhibit (3) resulting in (4) overall.

A

1- phosphodiesterase III inhibitor
2- inamrinone, milrinone
3- myocardial cAMP PDE activity –> inc cAMP levels => positive inotropic effect / inc CO
4- inc CO; dec preload/afterload, inc AV conduction slightly

34
Q

describe the effects of dopamine at different doses (and in terms of acute HF)

A

Low: D1 stimulation, renal and mesenteric vasodilation

Intermediate: D1, β1 receptors –> cardiac stimulation, renal vasodilation

Large: D1, β1, α1 receptors –> vasoconstriction

HF: in shock Tx, also promotes diuresis

35
Q

dobutamine has (1) and (2) forms (include functions), and is used to (3) in acute HF

A

(racemic mixture)
1- (-) isomer, α1 antagonist, weak β1 agonist
2- (+) isomer, α1 antagonist, potent β1 agonist, mild β2 agonist

3- stimulates β1 –> positive inotropic effects, little change in HR (mild vasodilation) –> inc CO in acute HF

36
Q

glucagon will increase (1) in the heart, leading to a (2) effect; used as (3)

A

1- cAMP
2- potent inotropic, chronotropic effects (inc contractility)
3- cardiac stimulant in severe cases of β-blocker overdosage + acute HF

RCS (29 decks)

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