What is the management for a patient with chest pain, back pain, diaphoresis, nausea, pallor, urinary retention, bradycardia, and hypotension, suspected of having acute coronary syndrome (ACS) with bradycardia and hypotension?

Management of ACS with Bradycardia and Hypotension

Atropine is the first-line treatment for bradycardia with hypotension in acute coronary syndrome, as it rapidly increases heart rate and blood pressure while potentially reducing ventricular ectopy. 1

Immediate Recognition and Differential Diagnosis

This clinical presentation—chest pain, back pain, diaphoresis, nausea, pallor, and urinary retention combined with bradycardia and hypotension—requires urgent differentiation between:

• Inferior/posterior STEMI with vagal activation (most common cause of bradycardia-hypotension in ACS) 1
• Aortic dissection (back pain + hypotension is a red flag) 2
• Right ventricular infarction (hypotension with inferior MI) 2
• Cardiogenic shock (requires immediate invasive strategy) 3

The combination of back pain with chest pain significantly raises concern for aortic dissection, which must be excluded before administering antithrombotic therapy. 2

Critical First 10 Minutes

Obtain a 12-lead ECG within 10 minutes of presentation to differentiate STEMI from NSTE-ACS and identify the infarct territory. 2, 4

Key ECG findings to identify:

• ST-elevation in inferior leads (II, III, aVF) suggests right coronary artery occlusion with vagal activation causing bradycardia 1
• ST-depression in anterior leads with ST-elevation in posterior leads suggests posterior MI 2
• Right-sided leads (V4R) should be obtained if inferior STEMI is present to assess for RV involvement 2

Immediate Pharmacologic Management of Bradycardia-Hypotension

Administer atropine 0.5-1.0 mg IV bolus for symptomatic bradycardia with hypotension in the setting of suspected ACS. 1

The bradycardia-hypotension syndrome occurs in approximately 17% of acute MI patients within the first 24 hours and responds favorably to atropine in 90% of cases. 1 In the landmark study, atropine increased heart rate from 46±14 to 79±12/min and systolic blood pressure from 70±15 to 105±13 mm Hg. 1

Key benefits of atropine in this setting:

• Increases heart rate and blood pressure simultaneously 1
• Reduces ventricular premature complexes (decreased from 9.4±3/min to 2.4±0.7/min in patients with ectopy) 1
• Minimal complications when appropriately dosed 1

Avoid excessive atropine dosing (>2-3 mg total), as this can precipitate tachycardia and increase myocardial oxygen demand. 1

Hemodynamic Support Strategy

If hypotension persists after atropine:

• Consider temporary transcutaneous pacing for persistent symptomatic bradycardia unresponsive to atropine 2
• Cautious IV fluid bolus (250-500 mL) if RV infarction is suspected (inferior MI with clear lung fields) 2
• Avoid nitrates in the setting of hypotension, as they can precipitate cardiovascular collapse, especially with RV infarction 2
• Inotropic support (dobutamine) may be needed if cardiogenic shock develops despite heart rate correction 2

Antithrombotic Therapy Considerations

Once aortic dissection is excluded and STEMI is confirmed:

• Aspirin 150-300 mg oral loading dose (or 75-250 mg IV if unable to swallow), chewed and swallowed for faster absorption 3
• P2Y12 inhibitor loading: Ticagrelor 180 mg or prasugrel 60 mg (if proceeding to PCI and age <75, weight >60 kg) 3
• Parenteral anticoagulation: Unfractionated heparin 70-100 IU/kg IV bolus (preferred in hemodynamically unstable patients due to short half-life and reversibility) 3

Critical pitfall: Do not administer antithrombotic therapy until aortic dissection is excluded, as the combination of back pain, chest pain, and hemodynamic instability raises significant concern for this diagnosis. 2 If blood pressure differential exists between arms or pulse deficits are present, obtain emergent CT angiography of the chest before antiplatelet/anticoagulation. 2

Reperfusion Strategy

Patients with hemodynamic instability require immediate invasive strategy regardless of STEMI vs. NSTE-ACS classification. 3

• STEMI with bradycardia-hypotension: Immediate cardiac catheterization for primary PCI (door-to-balloon <90 minutes) 2
• Cardiogenic shock: Emergent angiography with consideration for mechanical circulatory support 3
• Persistent ischemia despite medical therapy: Urgent angiography within 2 hours 2

High-Risk Features Requiring Intensive Monitoring

This patient has multiple high-risk features mandating CCU-level care: 2

• Hemodynamic instability (hypotension) 2
• Bradyarrhythmia 2
• Signs of heart failure or shock (pallor, diaphoresis) 2
• Urinary retention (suggests severe autonomic dysfunction or cardiogenic shock with end-organ hypoperfusion) 2

Special Considerations

Atypical presentations are common in elderly patients, women, and diabetics, who may present with nausea, diaphoresis, and hemodynamic compromise without classic chest pain. 2 This patient's constellation of symptoms (diaphoresis, nausea, pallor) represents a high-risk ACS presentation despite potentially atypical pain characteristics. 2

Urinary retention in this context likely reflects:

• Severe vagal activation (common with inferior MI) 1
• Cardiogenic shock with renal hypoperfusion 2
• Autonomic dysfunction from extensive myocardial injury 2

Do not delay cardiac evaluation to address urinary retention—this is a secondary issue that will resolve with hemodynamic stabilization. 2