Inotropes
This infographic provides a detailed breakdown of inotropes, including their mechanisms, clinical applications, and adverse effects.
What are Inotropes?
- Inotropes increase the force of myocardial contraction.
- Their effects vary depending on which adrenergic receptors they activate:
- Alpha-1: Vasoconstriction
- Beta-1: Increases inotropy (contractility) and chronotropy (heart rate)
- Beta-2: Vasodilation
Why Use Inotropes?
- Cardiogenic shock: Maintain perfusion and preserve organ function (Class 1a recommendation)
- Bridge therapy: For patients awaiting mechanical circulatory support (MCS) or heart transplant (Class 2a)
- Palliative care: Improve symptoms and functional status in advanced heart failure (Class 2b)
4 Main Classes of Inotropes
- Catecholamines (e.g., norepinephrine, epinephrine)
- Activate beta-1 adrenergic receptors to increase heart rate and contractility.
- PDE-III Inhibitors (e.g., milrinone)
- Increase calcium influx by inhibiting cAMP degradation, enhancing contractility.
- Calcium Sensitizers (e.g., levosimendan)
- Enhance myocardial sensitivity to calcium, improving tension development (not available in the US).
- Digoxin
- Inhibits Na/K ATPase, increasing intracellular calcium to promote contraction.
Adverse Effects of Inotropes
- Norepinephrine: Reflex bradycardia, peripheral ischemia, hypertension
- Epinephrine: Splanchnic vasoconstriction, hyperglycemia
- Dopamine: Tissue ischemia, gangrene
- Dobutamine: Fever, headache, ischemia
- Milrinone: Hypotension, Torsades de Pointes
- Digoxin: AV block, visual disturbances
Hemodynamics Overview
This table summarizes the effects of key inotropes on cardiac output (CO), heart rate (HR), systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR).
| Inotrope | CO | HR | SVR | PVR |
|---|---|---|---|---|
| Norepinephrine | ↑ | → | ↑↑ | ↑ |
| Epinephrine | ↑↑ | ↑ | ↑↑ | ↑ |
| Dopamine | ↑↑ | ↑ | ↔ | ↔ |
| Dobutamine | ↑↑ | ↑ | ↓ | ↓ |
| Isoproterenol | ↑ | ↑↑ | ↓ | ↓ |
Created by: Dr. Cali Clark
Reviewed by: Dr. Eunice Dugan
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