What is the diagnosis for an adult or elderly patient with severe bradycardia who responded to atropine (antimuscarinic agent) with an increased pulse rate to 60 beats per minute?

Diagnosis: Symptomatic Bradycardia with Partial Response to Atropine

The diagnosis is symptomatic bradycardia that responded partially to atropine, indicating the underlying conduction disturbance is likely at the AV nodal level (such as sinus bradycardia, first-degree AV block, or Mobitz type I second-degree AV block) rather than infranodal pathology. 1, 2

Diagnostic Reasoning

Why Atropine Response Matters

• Atropine works by blocking vagal (parasympathetic) activity at the AV node, which means a positive response indicates the bradycardia originates from increased vagal tone or AV nodal-level conduction problems 1, 2

• The fact that heart rate increased from severe bradycardia to 60 bpm demonstrates atropine effectiveness, suggesting the conduction block is at the AV node where cholinergic blockade can improve conduction 1, 3

• Atropine is typically ineffective or contraindicated in infranodal blocks (Mobitz type II second-degree AV block, third-degree AV block with wide QRS complex) because these blocks occur below the AV node in the His-Purkinje system where vagal tone has minimal influence 1, 3, 4

Most Likely Underlying Diagnoses

The atropine response pattern suggests one of these conditions:

• Sinus bradycardia with increased vagal tone - most responsive to atropine 1, 2
• First-degree AV block - generally benign and atropine-responsive 1
• Mobitz type I (Wenckebach) second-degree AV block - block at AV node level, often transient and atropine-responsive 1
• Symptomatic bradycardia in the setting of acute inferior MI - right coronary artery occlusion can cause vagally-mediated bradycardia that responds to atropine 1

What This Rules Out

• Mobitz type II second-degree AV block is unlikely because atropine is typically ineffective and can paradoxically worsen this condition 1, 3, 4

• Third-degree (complete) AV block with wide QRS escape rhythm is unlikely because atropine is contraindicated and can precipitate ventricular asystole in this setting 3, 4

• Post-cardiac transplant bradycardia is unlikely because atropine causes paradoxical high-degree AV block in denervated hearts 1, 2

Critical Next Steps

Immediate Assessment Required

• Obtain a 12-lead ECG immediately to identify the specific rhythm and determine PR interval, QRS width, and presence of dropped beats 1, 2

• Assess for signs of ongoing hemodynamic compromise including altered mental status, chest pain, acute heart failure, hypotension, or shock despite heart rate of 60 bpm 1, 2

• Identify underlying causes such as acute MI (especially inferior), medications (beta-blockers, calcium channel blockers, digoxin), electrolyte abnormalities (hyperkalemia), or hypoxia 1, 2

If Heart Rate of 60 is Inadequate

• A heart rate of 60 bpm may still be inadequate if the patient continues to show signs of poor perfusion, as bradycardia definition is based on clinical context, not just absolute numbers 1

• Consider additional atropine (can repeat 0.5-1 mg IV every 3-5 minutes up to maximum 3 mg total) if symptoms persist 1, 2

• Prepare for transcutaneous pacing if patient remains unstable despite maximum atropine dosing 1, 2

• Consider IV chronotropic agents (dopamine 5-10 mcg/kg/min or epinephrine 2-10 mcg/min) as bridge to definitive therapy if atropine fails 2

Common Pitfalls to Avoid

• Do not assume heart rate of 60 is adequate - assess clinical status and perfusion, not just the number 1

• Do not give additional atropine if 12-lead ECG shows Mobitz type II or third-degree AV block with wide QRS - this can cause paradoxical worsening or asystole 1, 3, 4

• Do not delay transcutaneous pacing in unstable patients while giving multiple atropine doses 2

• Use atropine cautiously if acute coronary ischemia or MI is suspected as increased heart rate may worsen ischemia or increase infarct size 1, 2