Congestive Heart Failure Flashcards
ACEIs
Captopril
Enalapril
Lisinipril
ARBs
Losartan
Valsartan
Positive Inotropes
Digoxin
Doubtamine
B-Blockers
Carvedilol
Metaprolol
Diuretic
Spironolactone
Eplerenone
ACEI and ARBs are…
DOC in HF
Heart failure
Decrease in cardiac contractility which results in decrease CO
Pharmacotherapy aimed at
Increase contractility of the heart (increase CO)
Decrease preload
Decrease afterload
Decrease remodeling of cardiac muscle
Angiotensin Antagonists
- MOA
Decreased preload and afterload
Angiotensin Antagonists
- Reduces
Cardiac remodeling and improve left ventricular function
Morbidity and mortality in CHF
ACEIs
- Captopril, enalapril, lisinopril
Used as first-line therapy in patients with HF
Slow the progress of ventricular dilation by decreasing preload and afterload
ARBs
- losartan, valsartan, telmisartan
Block AT1 recetpors
Produce beneficial clinical effects similar to ACEIs
ARBs do not interfere with bradykinin degradation (DO NOT INDUCE DRY COUGH)
ARBs
- Block AT1 receptors
Effective against hypertension and CHF
Diuretics
Spironolactone
Loop diuretics
Thiazide diuretics
Diuretics
- Spironolactone
Used to decrease remodeling (decrease aldosterone-induced remodeling)
Diuretics
- Loop diuretics
Furosemide
Carefully monitor K+ levels
Diuretics
- Thiazide diuretics
Hydrochlorothiazide
Monitor K+ levels
Metoprolol and Carvedilol
Decrease HR and renin release
Decrease remodeling (by decreasing catecholamine-induced mitogensis)
Improve left ventricular function and exercise time, and reduce mortality and morbidity post-CHF
Positive Inotropic Drugs
- Digoxin
Increase contractility of heart (increase CO)
Digoxin
- MOA
Inhibition of cardiac Na+-K+ ATPase, increasing calcium activity within the cardiac myocyte
Digoxin
- Results in:
Increased intracellular Na+
Affects Na+/Ca2+ exchange
Increase intracellular Ca++
Increase Ca2+ released from sarcoplasmic reticulum
Increase actin-myosin interaction
Increase contractile force
Digoxin indirect effect
Inhibition of cardiac Na+-K+ ATPase
Inhibition of cardiac Na+-K+ ATPase
- Results in
Increase vagal activity (therapeutic doses)–> slows HR and AV nodal conduction-treats atrial flutter/fibrillation and supraventricular tachycardia
Positive Inotropic Drugs
- Pharmacokinetics
Narrow therapeutic index
Long t1/2: 30-40 hours
Renal clearance (digoxin)
Positive Inotropic Drugs
- Uses
CHF
Supraventricular tachycardias
Side effects of Digoxin
Anorexia
Nausea
Vomiting
ECG changes (AV block)
Bradycardia
Disorientation
Visual effects (halos)
Increase (toxic) doses–> increase sympathetic activity (ventricular arrhythmias)
Management of Digoxin toxicity
Use antidote
Supportive therapy
Management of Digoxin toxicity
- Antidote
Digoxin antibodies (Fab fragments) known as Dgibind, DigiFab
