What are the first‑line inotropes and vasopressors for treating cardiogenic shock in an adult with acute severe left‑ventricular failure (e.g., post‑myocardial infarction)?

First-Line Inotropes and Vasopressors for Cardiogenic Shock

Dobutamine is the first-line inotrope for cardiogenic shock, and norepinephrine is the preferred vasopressor when blood pressure support is needed despite adequate fluid resuscitation and inotropic therapy. 1, 2, 3

Initial Management Algorithm

After immediate ECG and echocardiography to confirm cardiogenic shock (hypotension with SBP <90 mmHg plus signs of hypoperfusion), the treatment sequence is: 1, 3

1. Fluid challenge first (250 mL over 10 minutes) if no overt fluid overload is present 3, 4
2. Start dobutamine at 2-3 μg/kg/min without loading dose, titrating up to 15-20 μg/kg/min based on clinical response 1, 2
3. Add norepinephrine if SBP remains <90 mmHg or mean arterial pressure <65 mmHg despite dobutamine 1, 3

Why Dobutamine is First-Line

Dobutamine is explicitly recommended by the European Society of Cardiology as the most commonly used adrenergic inotrope for cardiogenic shock. 1 The drug increases cardiac output and stroke volume through β1-adrenergic stimulation without excessive chronotropic effects compared to alternatives, making it ideal for dilated, hypokinetic ventricles typical of cardiogenic shock. 2, 5

The FDA label confirms dobutamine is indicated for short-term inotropic support in cardiac decompensation due to depressed contractility. 5 Start at 2-3 μg/kg/min and titrate progressively according to symptoms and clinical status, with most patients responding at doses up to 15 μg/kg/min. 2 Patients on chronic beta-blockers may require higher doses (up to 20 μg/kg/min) to overcome receptor blockade. 2

Why Norepinephrine is the Preferred Vasopressor

When mean arterial pressure needs pharmacologic support despite inotropic therapy, norepinephrine is the recommended vasopressor. 1, 3 This recommendation is based on evidence showing norepinephrine causes fewer arrhythmias than dopamine (12% vs 24%) and is associated with lower mortality in cardiogenic shock. 2

Norepinephrine should be administered through a central line, starting at 2-3 mL/min (8-12 μg/min of base) and titrating to maintain SBP >90 mmHg and MAP ≥65 mmHg. 6 The average maintenance dose ranges from 0.5-1 mL/min (2-4 μg/min). 6

Why NOT Dopamine

Dopamine should only be considered if the patient has significant bradycardia or as a second-line option. 1 While the FDA label indicates dopamine for shock due to myocardial infarction 7, contemporary guidelines have moved away from dopamine as first-line therapy because it causes more arrhythmias and higher mortality compared to norepinephrine. 2 Dopamine is particularly problematic because it increases myocardial oxygen demand and arrhythmia risk in an already ischemic myocardium. 3

Why NOT Epinephrine

Epinephrine is explicitly NOT recommended as an inotrope or vasopressor in cardiogenic shock and should be restricted to cardiac arrest only. 3 This is a critical caveat—despite epinephrine's potent inotropic and vasopressor effects, it significantly increases myocardial oxygen consumption and arrhythmia risk, making it dangerous in the setting of acute myocardial injury. 3

Monitoring Parameters During Treatment

Establish invasive arterial line monitoring (Class I recommendation) to continuously track: 1, 3

• Blood pressure targets: SBP >90 mmHg, MAP ≥65 mmHg 3, 6
• Cardiac output/index: Target cardiac index >2 L/min/m² 2
• Organ perfusion markers: Urine output, lactate clearance, mental status, mixed venous oxygen saturation 1, 4
• Pulmonary capillary wedge pressure: Target <20 mmHg if pulmonary artery catheter is placed 2
• Heart rate and rhythm: Watch for tachyarrhythmias, which are dose-related adverse effects 2

Alternative Agents for Refractory Cases

If the patient fails to respond adequately to dobutamine plus norepinephrine, consider levosimendan rather than adding additional catecholamines. 1, 3, 4 Levosimendan works through calcium sensitization and phosphodiesterase-3 inhibition, making it particularly useful in patients on chronic beta-blocker therapy where dobutamine may be ineffective. 1, 2

Milrinone (a phosphodiesterase-3 inhibitor) is another alternative, especially in patients with significant beta-blocker therapy, as its mechanism is independent of beta-adrenergic receptors. 1, 2

Critical Caveats and When to Escalate

Rather than combining multiple inotropes, mechanical circulatory support should be considered when pharmacologic therapy is inadequate. 1, 3 All inotropes increase myocardial oxygen demand and arrhythmia risk, so they should be used at the lowest effective doses for the shortest duration. 1, 3

The routine use of intra-aortic balloon pump (IABP) is NOT recommended based on the IABP-SHOCK II trial, which showed no mortality benefit. 1 However, IABP may still be considered for specific mechanical complications like acute mitral regurgitation or ventricular septal rupture before surgical correction. 1

All patients with cardiogenic shock should be rapidly transferred to a tertiary center with 24/7 cardiac catheterization capabilities and mechanical circulatory support availability. 1, 4 In cardiogenic shock complicating acute coronary syndrome, immediate coronary angiography (within 2 hours) with intent to revascularize is mandatory, as this provides the greatest mortality benefit. 1, 4

Duration and Weaning

Tolerance to inotropes develops after 24-48 hours of continuous infusion. 2, 3 Wean dobutamine gradually by decreasing in steps of 2 μg/kg/min while simultaneously optimizing oral vasodilator therapy. 2 Continue vasopressor and inotropic support until adequate blood pressure and tissue perfusion are maintained without therapy, then reduce gradually to avoid rebound hypotension. 6