In a patient with third-degree atrioventricular block and new inferior-wall T-wave inversions but no chest pain, what is the appropriate diagnostic work-up and management?

Management of Third-Degree AV Block with Inferior T-Wave Inversions and No Chest Pain

Immediate Diagnostic Priorities

This patient requires urgent evaluation for acute myocardial infarction despite the absence of chest pain, as third-degree AV block with inferior T-wave inversions strongly suggests inferior wall MI with conduction system involvement. 1

Critical Initial Work-Up (Within 10 Minutes)

• Serial cardiac troponins at presentation, 3 hours, and 6 hours—a single measurement is insufficient to exclude myocardial injury 1, 2
• Immediate 12-lead ECG to assess for ST-segment elevation, Q-waves, or other ischemic changes beyond the T-wave inversions 1
• Continuous cardiac monitoring to track heart rate, escape rhythm characteristics, and hemodynamic stability 3
• Transthoracic echocardiography to evaluate for regional wall motion abnormalities (particularly inferior wall hypokinesis), assess ventricular function, and exclude mechanical complications 1

ECG Pattern Recognition

• T-wave inversions in inferior leads (II, III, aVF) without chest pain may represent "inferior Wellens sign"—a pattern indicating critical stenosis of the right coronary artery or left circumflex artery that can precede inferior STEMI 4
• Third-degree AV block associated with inferior wall infarction is typically supra-Hisian and usually resolves spontaneously after reperfusion, but requires immediate attention due to increased mortality risk 1, 5
• The depth of T-wave inversion matters: inversions ≥1 mm in two or more contiguous inferior leads warrant investigation; ≥2 mm depth indicates high-risk pathology 1, 2

Risk Stratification and Hemodynamic Assessment

High-Risk Features Requiring Urgent Intervention

• Hemodynamic instability (hypotension, altered mental status, pulmonary edema, or signs of shock) 1
• Ventricular escape rhythm with wide QRS and rate 20-40 bpm (indicates infra-Hisian block with higher mortality) 3
• Recurrent chest pain or dynamic ECG changes despite initial absence of symptoms 4
• Elevated cardiac biomarkers confirming acute myocardial injury 1, 5

Intermediate-Risk Features

• Junctional escape rhythm with narrow QRS and rate 40-60 bpm (supra-Hisian block, better prognosis) 3
• Stable hemodynamics but persistent complete AV block 1
• T-wave inversions without ST-segment elevation but positive troponins 4

Immediate Management Algorithm

Step 1: Hemodynamic Stabilization

If hemodynamically unstable:

• Intravenous atropine 0.5-1 mg as first-line therapy 1
• If atropine fails, initiate transcutaneous pacing immediately 1
• Consider dopamine or epinephrine infusion as bridge therapy if pacing unavailable or while awaiting transvenous pacemaker 5

If hemodynamically stable:

• Close monitoring with transcutaneous pacing pads in place 1
• Avoid AV-nodal blocking agents (beta-blockers, calcium channel blockers, digoxin, amiodarone) 1

Step 2: Determine Need for Revascularization

Urgent coronary angiography with view to revascularization is indicated if the patient has not received previous reperfusion therapy 1

• Revascularization should be considered in patients with AV block who have not yet received reperfusion therapy (e.g., late arrival) 1
• AV block associated with inferior wall infarction usually resolves spontaneously or after reperfusion 1
• Revascularization will often reverse both the T-wave inversion and wall-motion disorder in ischemic cases 2

Step 3: Pacing Decision

Temporary transvenous pacing is indicated in cases of failure to respond to positive chronotropic medication 1

Permanent pacemaker considerations:

• Second-degree type II (Mobitz II) AV block and complete AV block may be indications for pacing 1
• AV sequential pacing should be considered in patients with complete AV block, RV infarction, and hemodynamic compromise 1
• A transvenous pacing electrode should be inserted in the presence of advanced AV block with a low escape rhythm 1

Critical Differential Diagnoses to Exclude

Non-Ischemic Causes of Complete AV Block

• Myocarditis (particularly post-viral or post-COVID-19) 2
• Electrolyte disturbances (hyperkalemia, hypomagnesemia) 1
• Medication toxicity (beta-blockers, calcium channel blockers, digoxin, tricyclic antidepressants, phenothiazines) 1, 2
• Infiltrative cardiac disease (sarcoidosis, amyloidosis) 1
• Infectious endocarditis with perivalvular abscess 3

Alternative Causes of Inferior T-Wave Inversions

• Central nervous system events (intracranial hemorrhage can cause deep T-wave inversions with QT prolongation) 2
• Pulmonary embolism (may produce T-wave inversions in inferior leads) 1
• Pericarditis (typically shows diffuse ST elevation and PR depression, not isolated T-wave inversions) 2
• Hypertensive emergency with rapid blood pressure reduction (can cause asymptomatic T-wave inversions without ischemia) 6

Disposition and Ongoing Management

Immediate admission to intensive care unit with continuous telemetry monitoring 3

Consultation with interventional cardiology for:

• Urgent coronary angiography if troponins positive or high clinical suspicion for ACS 1
• Transvenous pacemaker placement if temporary pacing required 1
• Permanent pacemaker evaluation if AV block persists beyond 48-72 hours post-reperfusion 1

Serial monitoring:

• Repeat ECGs every 6-8 hours or with any symptom recurrence to detect dynamic changes or evolution to STEMI 4
• Serial troponins at 3 and 6 hours from presentation 1, 2
• Daily echocardiography to assess for mechanical complications (papillary muscle rupture, ventricular septal defect, free wall rupture) 1

Common Pitfalls to Avoid

• Do not dismiss the absence of chest pain as excluding acute MI—up to 30% of inferior MIs present without typical angina, particularly in elderly, diabetic, or female patients 1, 5
• Do not rely on a single negative troponin—myocardial injury may not be detectable until 6 hours after symptom onset 1, 2
• Do not assume inferior T-wave inversions are benign—they may represent "inferior Wellens sign" preceding STEMI 4
• Do not administer AV-nodal blocking agents (beta-blockers, calcium channel blockers) in the setting of complete AV block, as this can precipitate hemodynamic collapse 1
• Do not delay revascularization in patients with complete AV block and evidence of acute MI, as reperfusion often resolves the conduction abnormality 1