In a patient with acute myocardial infarction who develops hypotension, which vasopressor or inotrope should be started to raise blood pressure?

Vasopressor Management in Myocardial Infarction with Hypotension

Norepinephrine should be started as the first-line vasopressor to elevate blood pressure in a patient with myocardial infarction who develops hypotension, targeting a mean arterial pressure ≥65 mmHg. 1

Initial Vasopressor Selection

Norepinephrine is the mandatory first-choice agent for hypotension complicating acute myocardial infarction, particularly when cardiogenic shock develops. 1 The 2021 American Heart Association scientific statement explicitly recommends norepinephrine as first-line therapy for acute myocardial infarction complicated by cardiogenic shock (AMICS). 1

Dosing and Administration

• Start norepinephrine at 0.02 mcg/kg/min (or 2-3 mL/min of standard dilution containing 4 mcg/mL), titrating to maintain mean arterial pressure >65 mmHg. 1, 2
• Administer through a central venous catheter whenever possible, though peripheral administration can be initiated while awaiting central access. 2
• Place an arterial catheter as soon as practical for continuous blood pressure monitoring. 1
• Use the minimum necessary dose to maintain adequate perfusion; average maintenance ranges from 0.5-1 mL/min (2-4 mcg base). 2

Alternative Agents Based on Clinical Context

The choice of vasopressor or inotrope may need modification based on specific clinical circumstances in myocardial infarction:

When Bradycardia is Present

• Dopamine or epinephrine may be preferred over norepinephrine when unstable bradycardia accompanies hypotension, as their increased chronotropic effect can address both heart rate and blood pressure. 1
• Dopamine dosing: 5-15 mcg/kg/min, though note this agent carries higher arrhythmia risk. 1

When Dynamic Left Ventricular Outflow Tract Obstruction Exists

• Phenylephrine or vasopressin should be used instead of norepinephrine when dynamic LV outflow tract obstruction is present, as pure vasopressors without inotropic effects are preferred in this scenario. 1
• Phenylephrine: 0.5-2.0 mcg/kg/min. 3
• Vasopressin: 0.03 units/min (never as monotherapy, only as adjunct). 1

When Refractory Hypoxemia or Acidosis is Present

• Vasopressin may be preferred when catecholamine vasopressor efficacy is attenuated by severe acidosis or hypoxemia, as its mechanism does not depend on adrenergic receptors. 1

Second-Line Vasopressor Options

If target blood pressure cannot be achieved with norepinephrine alone:

• Add vasopressin 0.03 units/min to either raise MAP or reduce norepinephrine requirements. 1, 4
• Add epinephrine (0.05-2 mcg/kg/min) as an alternative second agent, particularly beneficial when myocardial dysfunction is present due to its inotropic effects. 1, 4

Inotropic Support Considerations

Inotropic agents (dobutamine, milrinone, levosimendan) have limited value for initial stabilization in AMICS because of increased risk for worsening myocardial ischemia. 1

However, consider adding dobutamine 2.5-10 mcg/kg/min when: 1, 5

• Evidence of low cardiac output persists despite adequate MAP and fluid resuscitation
• Myocardial dysfunction is documented with elevated filling pressures
• Signs of hypoperfusion continue despite vasopressor therapy

Critical Management Principles

Blood Pressure Targets

• Maintain mean arterial pressure >65 mmHg as the minimum target. 1
• This target is not well-established and requires attentiveness to clinical perfusion status beyond just the number. 1
• In previously hypertensive patients, avoid raising blood pressure more than 40 mmHg below pre-existing systolic pressure. 1, 2

Fluid Resuscitation First

• Ensure adequate volume resuscitation before or concurrent with vasopressor initiation—hypotension in MI may have a hypovolemic component. 1, 2
• Occult blood volume depletion should always be suspected and corrected when present, especially if requiring escalating vasopressor doses. 2

Monitoring Requirements

• Assess clinical perfusion continuously: lactate levels, urine output, mental status, skin perfusion. 1, 4
• Document LV end-diastolic pressure, as elevated values are associated with increased mortality. 1
• Monitor for arrhythmias, particularly with dopamine use. 1, 6

Common Pitfalls to Avoid

• Do not use dopamine as first-line therapy in cardiogenic shock—it is associated with higher mortality and more arrhythmic events compared to norepinephrine. 1, 6
• Avoid progressive escalation of vasopressor and inotrope therapy without reassessing volume status and considering mechanical circulatory support. 1
• Do not delay early intubation and mechanical ventilation when respiratory failure accompanies cardiogenic shock, as worsening hypoxemia and acidosis increase susceptibility to ventricular fibrillation. 1
• Caution with positive pressure ventilation in right ventricular infarction, as it can abruptly lower systemic arterial pressure. 1

When to Consider Mechanical Circulatory Support

If persistent hemodynamic instability continues despite vasopressor therapy, consider early mechanical circulatory support (MCS) in patients with: 1

• High-risk coronary anatomy
• Severe ventricular dysfunction
• Persistent electrical or respiratory instability despite initial measures

The decision requires individualized assessment balancing institutional experience, vascular access availability, and potential delay to primary reperfusion therapy. 1