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CV Pharmacology > CHF Treatment > Flashcards

CHF Treatment Flashcards

1
Q

What is the mechanism of action of Digoxin?

A

Inhibits the Na+/K+ ATPase to increase intracellular Na+ and decrease intracellular K+.

Prevents the NCX from effluxing Ca2+ .

Causes a buildup of Ca2+ in the cell to increase inotropy.

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2
Q

How is digoxin eliminated?

A

Excreted unchanged in the urine.

Reduce dose in renal disease and elderly.

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3
Q

What are the toxic effects of Digoxin?

A
  • Very narrow therapeutic window
    • serum levels roughly correlate with therapeutic effect but vary between patients
  • atrial & ventricular arrhythmias
  • visual changes - blurring, yellow-green halo
  • headache, fatigue, drowsiness, confusion, seizures
  • Digibind - Ab that can neutralize serum digoxin
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4
Q

What are the drug interactions with Digoxin?

A
  • quinidine and amiodarone increases plasma digoxin concentration by reducing elimination
  • verapamil can slow heart and cause toxicity
  • diruetics increase chance of arrhythmias by causing hypokalemia
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5
Q

How does Digoxin affect mortality with CHF?

A

Study compared digoxin + ACEI and diuretic with placebo + ACEI and diuretic. Overall mortality was unchanged, mortality from CHF was reduced while other cardiac mortality increased. Benefit greatest in pts with EF < 0.25.

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6
Q

What is the mechanism of action of Captopril and other -prils?

A

Block ACE to prevent conversion of Ang I to Ang II in endothelial cells of lung. Causes reduction in TPR, natriuresis, water excetion, and decreased aldosterone.

Decreases blood volume which decreases cardiac output by reducing preload.

Also increases bradykinin levels by inhibiting metabolism.

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7
Q

What is the mechanism of action of Losartan and other -tans?

A

Block the AT1 angiotensin II receptor to prevent vasoconstriction and stimulating of aldosterone (so Na+ excretion and water excretion).

Decreases blood volume which decreases cardiac output by reducing preload.

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8
Q

What is the mechanism of action of Aliskiren?

A

Directly inhibits protease activity of renin. Decreases blood volume which decreases cardiac output by reducing preload.

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9
Q

What are the benefits of ACEI?

A
  • decreases mortality after an MI
  • does not effect lipids or sexual function
  • preserves renal function in diabetics
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10
Q

Which population does not respond as well to ACEI?

A

African-Americans and low-renin hypertensives

Thiazide + ACEI are highly effective.

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11
Q

What are the adverse effects of ACE inhibitors?

A
  • 1st dose hypotension
  • Na+ depletion
  • dry cough
  • hyperkalemia
  • angioedema (more common in AA)
  • renal insufficiency
  • fetotoxicity
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12
Q

What are the adverse effects of angiotensin receptor antagonists?

A
  • 1st dose hypotension
  • hyperkalemia
  • hepatic dysfunction
  • fetotoxicity
  • (Olmesartan - spruelike enteropathy)
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13
Q

What are the side effects of Aliskiren?

A
  • 1st dose hypotension
  • hyperkalemia
  • angioedema
  • fetotoxicity
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14
Q

What are the drug interactions with Aliskiren?

A

Inhibits p-glycoprotein (careful with erythromycin, amiodarone)

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15
Q

What are the common adverse effects of the drugs affecting the renin-angiotensin system?

A
  • fetotoxicity
  • hyperkalemia
  • 1st dose hypotension
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16
Q

What are the effects of angiotensin II binding to the AT1 receptor?

A
  • vasoconstriction - increased TPR - increased BP
  • stimulates aldosterone production - increases sodium and water retention - increases BP
  • cell growth - left ventricular hypertrophy, vascular remodeling
    • worsening of CHF
17
Q

Why are beta-blockers used as a treatment for CHF?

A
  • CHF involves chronically high levels of Epi and NE to try and maintain CO
    • causes worsening hypertrophy and increases oxygen comsumption, arrhythmias, receptor downregulation, myocyte apoptosis and fibrosis
  • beta-blockers reverse desensitization, increase receptor number, and restore fast signaling modes over slow signaling modes
    • long-term effect: increased CO, decreased LVEDP (preload) for better coronary artery perfusion
18
Q

What is the mechanism of acute adrenergenic signaling in the heart?

A
  • overall mechanism increases chronotropy and inotropy
    • increase of cAMP to activate PKA
    • PKA phosphorylates many proteins to increase Ca+ influx, relaxation of the sarcomeres, reuptake into the sarcomeres
  • ​requires a high number of receptors and spikes of SNS activity
19
Q

What is the mechanism of chronic adrenergenic signaling in the heart?

A
  • requires lower number of beta receptors and chronically low levels of Epi and NE
  • receptors undergo desensitization and internalization
    • also causes gene expression leading to cardiac hypertrophy
    • cells no longer respond as well to NE and Epi
20
Q

What are the contraindications for beta-blocker use in CHF?

A
  • heart block
  • bradycardia
  • decompensated CHF/need for IV inotropes
  • volume overload
21
Q

What beta-blockers are approved for CHF?

A
  • Metoprolol
  • Carvedilol (also an alpha1-antagonist)
  • Bisoprolol
  • (Nebivolol increases NO, not approved but used)
22
Q

Describe the Stage A classification of CHF.

A
  • at risk for developing CHF
    • HTN, dyslipidemia, smoking, diabetes, alcohol usage, valve dysfunction, IHD
  • Treated with preventative measures and ACEI/ARBs
23
Q

Describe the Stage B classification of CHF.

A
  • no symptoms
  • ejection fraction < 50%
  • Treated with ACEI/ARBs, beta-blockers
24
Q

Describe the Stage C classification of CHF.

A
  • symptoms on exertion
    • dyspnea, orthopnea, edema, PND
  • treated with ACEI/ARBs, beta-blockers, diuretic/digoxin/spironolactone
25
Q

Describe the Stage D classification of CHF.

A
  • symptoms at rest
    • refractory edema
  • treated with ACEI/ARBs, beta-blockers (sometimes withdrawn), diuretic/digoxin/spironolactone, IV inotropes, transplant
26
Q

What is the mechanism of action of diuretics?

A
  • cause Na+ and water excretion
  • reverse edema and pulmonary congestion
  • reduce preload
  • treat symptoms, do not improve survival or prognosis
27
Q

What are the different classes of diuretics?

A
  • Loop diuretics: Furosemide, Bumetanide
  • Potassium sparing, aldosterone antagonists: spironolactone, eplerenone (usually used with loop diuretic)
28
Q

What are the adverse effects of diuretics?

A
  • electrolyte disturbances
  • hypokalemia, hyponatremia
  • arrhythmias
  • metabolic acidosis
  • azotemia
  • dehydration
  • hypotension
  • ototoxicity for loop diuretics
29
Q

Drug interactions with diuretics.

A
  • NSAIDs promote fluid retention and decrease efficacy
  • ACEI and ARBs have mild diuretic effects - reduce dose of diuretic
30
Q

What vasodilators are used in CHF and why?

A
  • Hydralazine - decreases afterload to increase cardiac output
    • used in pts unable to take ACEIs
    • causes nausea, anorexia, anti-nuclear Abs, exacerbate angina (coronary steal)
  • Nitrates - venodilates to cause a decrease in preload and wall stress and vasodilates to reduce afterload
31
Q

What drugs are used in advanced stage CHF?

A
  • IV nitrates
  • IV inotropic agents, short-term use
    • Dobutamine
    • Milrinone: PDE inhibitor (prevents cAMP breakdown)
  • Nesiritide: B-type natriuretic peptide
32
Q

What are the mechanisms of the natriuretic peptides?

A
  • released from heart in response to volume/pressure expansion and naturally increased in CHF
  • causes vasodilation, venodilation, natriuresis
  • reduces preload, inhibits renin/aldosterone, reduces blood volume
  • anti-mitogenic effects
33
Q

When is Nesiritide used in CHF?

A

Limited ot pts that don’t respond to nitroglycerin. Similar benefit but more persistent hypotension.

CV Pharmacology (5 decks)

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