MANAGEMENT OF AHF

AIM OF MANAGEMENT:

• Decreasing congestive symptoms (with diuretics).
• Increasing contractility (with positive inotropic agents).

1. Diuretics:

Pathophysiology:

• In heart failure, fluid accumulation in lungs & peripheral organs –> Causes congestive symptoms.

MOA: 

• Diuretics decrease congestive symptoms by edema fluid mobilization.
• DOC – Loop diuretics (furosemide & bumetanide)

Drug effects:

• Possess high ceiling diuretic effect.
• Decrease preload.
• Reduce congestive symptoms. 
• Produce venodilation prior to diuresis –> Immediate relief from dyspnea in pulmonary edema.

Adverse effects:

• Development of tolerance (chronic use) – Prevented by combination with thiazides or spironolactone.
• Spironolactone decreases mortality.

2. Inotropic drugs:

• Important drugs: Dobutamine, dopamine, inodilators & cardiac glycosides.
• Used for short-term management of acute CHF (except digoxin used orally for maintenance also).

Dobutamine

• Selective ß1 agonist.
• No effect on dopamine receptors.
• Given as i.v. infusion.

Drug actions:

• Increases cAMP in heart –> increases cardiac contractility –> increases output.

Dopamine

• Acts on dopamine, ß and α receptors depending on drug concentration.
• At dose 1-2µg/kg/min – Stimulates only dopamine receptors & causes renal vasodilation.
• Intravenous infusionrate of 2-10µg/kg/min –  Stimulates heart by ß1 agonistic action.
• Higher dose (>10µg/kg/min) – Intense vasoconstriction.

3. Cardiac Glycosides

Drugs included: 

• Digoxin, digitoxin, strophanthin & ouabain.
• Collectively known as digitalis.

Digitalis – 

• Only oral inotropic drug.
• Positive inotropic drug.

Uses:

• Treatment of atrial fibrillation, atrial flutter & paroxysmal supraventricular tachycardia.
• Used as acute treatment of CHF & for maintenance (digoxin).

Disadvantages:

• Decreases heart rate or oxygen consumption (unlike other inotropic drugs).
• Do not alter basic pathology.
• Inability to decrease mortality.

4. Inodilators

• Drugs included: Inamrinone (previously amrinone), milrinone & vesnarinone.

MOA: 

• Inhibits phosphodiesterase III enzyme –> increases cAMP in heart & blood vessel –> cAMP increases transmembrane Ca+ influx in myocardial cells –> increases contractility –> vascular smooth muscle relaxation (vasodilation/inotrophic).

Uses: 

• Severe & refractory CHF – Short term i.v. use.

Adverse effect:

• Thrombocytopenia – Mainly with inamrinone.
• Less with milrinone (hence preferred).
• Both cause arrhythmias.

5. Levosimendan:

• Inhibits phosphodiesterase & sensitizes myocardium to Ca+.

6. Nesiritide:

• Recombinant BNP.

BNP:

• Brain-derived natriuretic peptide.
• Secreted by ventricles.
• Used as i.v. for acute CHF associated with dyspnoea at rest.
• Helps differentiating cardiac from pulmonary causes of dyspnoea.
• Increases cGMP & causes vasodilation.
• Increases renal sodium excretion.

Metabolism:

• Short half-life.
• Limiting factor: Its breakdown by neutral endopeptidase (NEP) enzyme.
• Ecadotril – NEP enzyme inhibitor.

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