In a patient with ST‑elevation myocardial infarction receiving a fibrinolytic infusion who develops hypotension, what is the appropriate management?

Management of Hypotension During Fibrinolytic Infusion in STEMI

If hypotension develops during fibrinolytic infusion in a STEMI patient, immediately assess for cardiogenic shock versus other causes, provide volume loading if hypovolemia is suspected, and initiate vasopressor support (dopamine or norepinephrine) if hypotension persists after volume resuscitation. 1

Immediate Assessment and Differential Diagnosis

When hypotension occurs during fibrinolytic therapy, you must rapidly distinguish between several potential etiologies:

• Cardiogenic shock from extensive myocardial damage, mechanical complications (ventricular septal rupture, acute mitral regurgitation, free wall rupture), or right ventricular infarction 1
• Hypovolemia from inadequate preload
• Bleeding complications including intracranial hemorrhage or gastrointestinal bleeding 1
• Allergic/anaphylactic reaction (particularly with streptokinase) 1
• Reperfusion arrhythmias causing hemodynamic compromise 1

Stepwise Management Algorithm

Step 1: Volume Assessment and Resuscitation

• Administer intravenous fluids to achieve a central venous pressure of 10-15 cm H₂O or pulmonary wedge pressure of 14-18 mm Hg before initiating vasopressors 1
• This initial volume loading distinguishes true cardiogenic shock from relative hypovolemia and optimizes preload 1

Step 2: Vasopressor Support for Persistent Hypotension

Vasopressor therapy should be initiated when hypotension does not resolve after adequate volume loading. 1

• Dopamine is the recommended first-line vasopressor, starting at 2-5 mcg/kg/min and titrating upward in 5-10 mcg/kg/min increments to achieve adequate blood pressure 1, 2
• For doses exceeding 20-50 mcg/kg/min, monitor urine output closely; if oliguria develops without hypotension, consider reducing the dopamine dose 1, 2
• Norepinephrine may be used as an alternative vasopressor when dopamine is insufficient or contraindicated 1

Step 3: Mechanical Circulatory Support

Intra-aortic balloon counterpulsation (IABP) is recommended when cardiogenic shock is not quickly reversed with pharmacological therapy alone. 1

• IABP serves as a stabilizing bridge to urgent coronary angiography and revascularization 1
• Consider alternative left ventricular assist devices for refractory cardiogenic shock 3

Step 4: Diagnostic Evaluation

• Obtain urgent echocardiography to assess left and right ventricular function, detect mechanical complications (ventricular septal defect, papillary muscle rupture, free wall rupture), and exclude pericardial tamponade 1, 3
• Establish intra-arterial blood pressure monitoring for accurate hemodynamic assessment in cardiogenic shock 1
• Consider pulmonary artery catheter monitoring to guide therapy, though this carries a Class IIa recommendation 1

Decision Point: Continue or Abort Fibrinolysis?

The guidelines do not explicitly recommend stopping the fibrinolytic infusion for hypotension alone. However:

• If intracranial hemorrhage is suspected (altered mental status, severe headache, focal neurological deficits), immediately stop fibrinolysis and obtain emergent head CT 1
• If major bleeding is identified, discontinue fibrinolysis and initiate appropriate hemostatic measures 1
• If hypotension is due to cardiogenic shock without bleeding, fibrinolytic therapy should be completed while simultaneously providing hemodynamic support 1

Urgent Revascularization Strategy

Immediate transfer to a PCI-capable center for rescue angiography and revascularization is indicated when cardiogenic shock develops after fibrinolysis. 1

• This recommendation carries Class I, Level B evidence for patients with cardiogenic shock or acute severe heart failure developing after initial presentation 1
• Early revascularization (PCI or CABG) is recommended for patients <75 years who develop shock within 36 hours of MI, when revascularization can be performed within 18 hours of shock onset 1
• For patients ≥75 years, revascularization is reasonable (Class IIb) if they have good prior functional status and agree to invasive care 1

Critical Pitfalls to Avoid

• Do not delay vasopressor support while waiting for volume resuscitation to take effect; hypotension in STEMI rapidly worsens myocardial ischemia through reduced coronary perfusion pressure 1
• Avoid beta-blockers or calcium channel blockers in patients with frank cardiac failure, pulmonary congestion, or low-output state, as these agents will worsen hypotension and cardiogenic shock 1
• Do not administer morphine excessively in hypotensive patients, as it can further reduce blood pressure and mask evolving shock 1
• Recognize that aggressive simultaneous use of hypotensive agents (nitrates, ACE inhibitors, morphine) can precipitate iatrogenic cardiogenic shock and create a cycle of hypoperfusion-ischemia 1

Monitoring During Vasopressor Therapy

• Continuously monitor arterial blood pressure, preferably via intra-arterial catheter 1
• Assess urine output hourly; diminishing urine flow despite adequate blood pressure suggests excessive vasoconstriction and warrants dopamine dose reduction 1, 2
• Watch for new or worsening tachyarrhythmias, which may indicate excessive catecholamine stimulation and require dosage adjustment 2
• Evaluate peripheral perfusion (skin temperature, capillary refill, lactate levels) to ensure adequate tissue oxygen delivery 1

Special Consideration: Failed Reperfusion

If hypotension develops in the context of persistent ST-elevation 60-90 minutes after fibrinolytic administration, this indicates failed reperfusion and mandates urgent transfer for rescue PCI (Class IIa, Level B). 1, 4 The combination of hemodynamic instability and failed fibrinolysis carries particularly high mortality and requires immediate mechanical revascularization. 4, 5