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Understanding Inotropes and Cardiac Care

Apr 20, 2025

Lecture Notes: Inotropes

Objectives

  • Describe the usage and effects of inotropes
  • Outline how inotropes affect practice, cardiac status, and patient care

Definition

  • Inotropes: Agents influencing the contractility of muscle tissue
    • Positive Inotropes: Increase force of contractility
    • Negative Inotropes: Decrease force of contractility

Focus on Positive Inotropes

Digoxin

  • Category: Inotrope

  • Effects:

    • Increases force and velocity of myocardial contraction
    • Inhibits sodium pump; increases intracellular calcium
    • Decreases conduction in the AV node
    • Decreases ventricular response in atrial fibrillation
    • Prolongs slope of phase IV diastolic depolarization, decreasing heart rate
    • Acts as a vasodilator, reducing afterload
  • Indications:

    • Atrial fibrillation with uncontrolled ventricular response (ventricular HR > 100 bpm)
    • Heart failure due to systolic dysfunction (NYHA class II-IV)
    • Failure of diuretics and vasodilator therapy
    • Severe heart failure with reduced EF and hypotension
  • Drug Interactions:

    • Antiarrhythmics, beta-blockers, clonidine, methyldopa, certain antibiotics, atorvastatin
  • Sensitivity Factors:

    • Elderly (>70), low skeletal mass, electrolyte imbalances
    • Acute MI, fibrotoxic heart disease, renal failure, COPD
  • Risks:

    • Anorexia, restlessness, insomnia, drowsiness
    • Arrhythmias: PVCs, AV block, junctional/ventricular tachycardia, bradyarrhythmias

Mechanism Reflection

  • Digoxin as Positive Inotrope: Increases cardiac output in heart failure
  • Digoxin as Negative Chronotrope: Controls atrial fibrillation with rapid ventricular rate

Acute Heart Failure and Inotropes

Clinical Conditions

  • Chronic heart failure
  • Acute heart failure with pulmonary edema
  • Cardiogenic shock

Importance of Acute Support

  • Necessary to prevent worsening of condition
  • Cardiogenic Shock: Inadequate cardiac output to maintain circulation

Catecholamine-like Agents

  • Provide acute inotropic stimulation, vasodilation, or vasoconstriction

Sympathetic Nervous System Receptors

  • Alpha Receptors: Vasoconstriction in blood vessels
  • Beta-1 Receptors: Increase heart contractility and rate
  • Beta-2 Receptors: Bronchodilation and vasodilation
  • Dopaminergic Receptors: Dilation of renal and mesenteric arteries

Key Inotropic Agents

Dobutamine

  • Receptors: Mostly beta-1, moderately beta-2, little alpha
  • Effects: Increases heart contractility, causes vasodilation

Dopamine

  • Receptors: Beta-1 and alpha
  • Effect: Dose-dependent

Epinephrine

  • Receptors: Stimulates all SNS receptors
  • Response: Fight-or-flight-like

Norepinephrine

  • Receptors: Mostly alpha and beta-1

Usage of Sympathomimetic Drugs

  • Purpose: Augment SNS, especially post-depletion of endogenous catecholamines
  • Result: Increased contractility, stroke volume, vasoconstriction/dilation, heart rate, BP, cardiac output, and tissue perfusion

Inotropic Effects Table

  • Tool for study: Listing inotropic agents and effects on various parameters

Reflection on Inotropes and Cardiogenic Shock

  • Purpose: Increase cardiac output through HR, vasoconstriction, and contraction force

Conclusion

  • End of presentation on inotropes