Congestive heart failure positive inotropics

Congestive Heart Failure Microchapters
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Acute Pharmacotherapy
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Chronic Pharmacotherapy in HFrEF Diuretics ACE Inhibitors Angiotensin receptor blockers Aldosterone Antagonists Beta Blockers Ca Channel Blockers Nitrates Hydralazine Positive Inotropics Anticoagulants Angiotensin Receptor-Neprilysin Inhibitor Antiarrhythmic Drugs Nutritional Supplements Hormonal Therapies Drugs to Avoid Drug Interactions Treatment of underlying causes Associated conditions
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Surgical Therapy: Biventricular Pacing or Cardiac Resynchronization Therapy (CRT) Implantation of Intracardiac Defibrillator Ultrafiltration Cardiac Surgery Left Ventricular Assist Devices (LVADs) Cardiac Transplantation
ACC/AHA Guideline Recommendations Initial and Serial Evaluation of the HF Patient Hospitalized Patient Patients With a Prior MI Sudden Cardiac Death Prevention Surgical/Percutaneous/Transcather Interventional Treatments of HF Patients at high risk for developing heart failure (Stage A) Patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms (Stage B) Patients with current or prior symptoms of heart failure (Stage C) Patients with refractory end-stage heart failure (Stage D) Coordinating Care for Patients With Chronic HF Quality Metrics/Performance Measures
Implementation of Practice Guidelines
Congestive heart failure end-of-life considerations
Specific Groups: Special Populations Patients who have concomitant disorders Obstructive Sleep Apnea in the Patient with CHF NSTEMI with Heart Failure and Cardiogenic Shock
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

1. Agents that increase intracellular cAMP
   • Alpha-adrenergic agonists
   • Phosphodiesterase inhibitors
2. Agents that affect sarcolemmal ion pumps/channels
   • Digoxin
3. Agents that modulate intracellular calcium mechanisms by either:
   • Release of sarcoplasmic reticulum calcium (IP3)
   • Increased sensitization of the contractile proteins to calcium
4. Drugs having multiple mechanisms of action
   • Pimobendan
   • Vesnarinone

Digoxin

• Inhibits Na,K+-ATPase resulting in an increase in intracellular Na+, extracellular Ca2+ exchange increasing the velocity and extent of sarcomere shortening.
• ACC/AHA recommend digoxin for symptomatic patients with left ventricular systolic dysfunction.
• Commonly used in patients with heart failure and atrial fibrillation to reduce the ventricular response rate.
• Mortality has not been shown to be improved with use of digoxin, but the use of digoxin has been associated with a reduction in hospitalization in the RALES study.
• There is no need to load a CHF patient with digoxin. For the majority of patients with normal renal function, a daily dose of 0.25 mg of digoxin is usually adequate. In the older patient or in those patients with renal impairment, a dose of 0.125 mg per day may be adequate.
• Drugs that increase the concentration of digoxin include antibiotics and anticholinergic agents as well as amiodarone, quinidine and verapamil.
• In the RALES study, a level of < 1 ng/ml was associated with efficacy. Levels above 1 ng/ml were not associated with greater efficacy and were associated with higher mortality.

Dobutamine

• Activates beta-1 receptors resulting in enhanced cardiac contractility.
• Long-term dobutamine infusions are arrhythmogenic and increase mortality.
• Dobutamine also slightly reduces afterload

Dopamine

• Unique dose dependent mechanism of action.
• At low doses: (≤2 µg/kg/min), selective dilation of splanchnic and renal arterial beds. assists in increasing renal perfusion.
• At intermediate doses: (2 to 10 µg/kg/min), increased norepinephrine secretion results in increased cardiac contractility, heart rate and systemic vascular resistance.
• At higher doses: (5 to 20 µg/kg/min), direct alpha-adrenergic receptor stimulation increases systemic vascular resistance.

Milrinone

• Phosphodiesterase-III inhibitor that enhances cardiac contractility by increasing intracellular cyclic adenosine monophosphate (cAMP).
• Potent pulmonary vasodilator that may benefit some patients with pulmonary hypertension.
• Unlike dobutamine milrinone is beneficial in decompensated heart failure patients who are on beta-blocker therapy.
• Long term milrinone infusions are arrhythmogenic, and increase mortality.

References

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