How should I manage a hemodynamically stable adult with rapid‑ventricular‑response atrial fibrillation (heart rate ~150 bpm), fever 38.5 °C from pneumonia, normal blood pressure, known severe pulmonary hypertension, and bilateral lung opacities on chest X‑ray, without using aggressive resuscitation?

Management of Atrial Fibrillation with RVR Secondary to Pneumonia

Treat the Underlying Infection First

The most critical step is aggressive antimicrobial therapy for pneumonia, as treating the underlying infection will often resolve the tachycardia without requiring rate-control agents. 1, 2

• Fever and infection drive sympathetic tone, which sustains the rapid ventricular rate; rate-control medications are less effective during active infection and may cause harm in this hemodynamically stable patient. 2
• With temperature 38.5°C and bilateral lung opacities, initiate appropriate antibiotics immediately based on community-acquired pneumonia guidelines (e.g., ceftriaxone plus azithromycin or respiratory fluoroquinolone). 1
• Provide supplemental oxygen to maintain SpO₂ ≥90%, as hypoxemia worsens pulmonary hypertension and increases right ventricular afterload. 1

Avoid Aggressive Rate Control in This Clinical Context

Do not pursue aggressive pharmacologic rate control in a hemodynamically stable patient (BP 130/80) with secondary AF driven by acute illness. 1, 2

• The heart rate of 150 bpm represents an appropriate physiologic response to fever, infection, and increased metabolic demand; suppressing this response may compromise cardiac output and tissue perfusion. 1
• Severe pulmonary hypertension creates right ventricular strain; negative inotropic agents (beta-blockers, calcium channel blockers) can precipitate acute right heart failure and hemodynamic collapse. 2, 3
• A "lenient" rate-control target of <110 bpm at rest is acceptable in stable patients; this patient's rate will likely decrease as the infection resolves. 2

If Rate Control Becomes Necessary

Only pursue pharmacologic rate control if the patient develops hemodynamic instability (hypotension, pulmonary edema, chest pain, altered mental status) or if the rate remains >110 bpm after fever resolves. 1, 2, 3

First-Line Agent: Low-Dose Diltiazem

• If rate control is required, use low-dose IV diltiazem 0.13 mg/kg (approximately 10 mg for a 70-kg patient) over 2 minutes, as this achieves comparable rate control to standard 0.25 mg/kg dosing but produces significantly less hypotension. 2, 4
• Diltiazem is preferred over beta-blockers in patients with severe pulmonary hypertension because it causes less negative inotropy and may provide mild pulmonary vasodilation. 2, 5
• Avoid standard-dose diltiazem (0.25 mg/kg or 20 mg) in this patient with severe pulmonary hypertension and borderline blood pressure, as hypotension can precipitate right ventricular failure. 2, 4

Avoid Beta-Blockers

• Do not use IV metoprolol in this patient despite its Class I recommendation for AF with RVR, because beta-blockers worsen pulmonary hypertension by blocking β₂-mediated pulmonary vasodilation and can precipitate acute right heart failure. 2
• Beta-blockers are contraindicated in severe pulmonary hypertension unless the patient has concurrent left ventricular systolic dysfunction with proven mortality benefit. 2

Avoid Digoxin

• Digoxin is ineffective for acute rate control during periods of heightened sympathetic tone (fever, infection, hypoxia) and should not be used as monotherapy in this setting. 2, 6

Critical Safety Exclusions

Before any pharmacologic intervention, verify the ECG does not show pre-excitation (delta waves, short PR interval, wide QRS) suggesting Wolff-Parkinson-White syndrome. 1, 2

• If pre-excitation is present, all AV-nodal blocking agents (beta-blockers, calcium channel blockers, digoxin, amiodarone) are absolutely contraindicated because they can precipitate ventricular fibrillation. 1, 2
• In pre-excited AF, use IV procainamide 15 mg/kg over 20–30 minutes or perform immediate synchronized cardioversion if unstable. 1

Anticoagulation Strategy

Initiate therapeutic anticoagulation immediately unless contraindicated, as this patient has AF of unknown duration and likely has CHA₂DS₂-VASc score ≥2 (age, hypertension, pulmonary hypertension). 1, 2

• Start IV heparin bolus 80 units/kg followed by infusion 18 units/kg/hour, or subcutaneous enoxaparin 1 mg/kg twice daily if renal function permits. 1
• Continue anticoagulation for at least 4 weeks regardless of whether sinus rhythm is restored, then determine long-term anticoagulation based on CHA₂DS₂-VASc score. 1, 2

Avoid Cardioversion

Do not perform elective cardioversion in this patient with secondary AF driven by acute infection, as the arrhythmia will likely recur until the underlying pneumonia resolves. 1, 7

• Cardioversion is only indicated if the patient becomes hemodynamically unstable (hypotension, pulmonary edema, ongoing chest pain, altered mental status). 1, 3
• If cardioversion becomes necessary, perform synchronized electrical cardioversion at 200 joules biphasic without awaiting anticoagulation, as the risk of death from hemodynamic collapse outweighs the risk of thromboembolism. 3

Common Pitfalls to Avoid

• Never combine more than two AV-nodal blocking agents (beta-blocker, calcium channel blocker, digoxin, amiodarone) due to risk of severe bradycardia, high-grade AV block, or asystole. 2, 8
• Do not use amiodarone for rate control in this hemodynamically stable patient; amiodarone is reserved for patients with severe left ventricular dysfunction or when beta-blockers and calcium channel blockers are contraindicated. 2, 8
• Avoid aggressive fluid resuscitation in a patient with severe pulmonary hypertension and bilateral lung opacities, as volume overload can precipitate acute right heart failure and pulmonary edema. 3

Monitoring and Reassessment

• Reassess heart rate, blood pressure, and oxygen saturation every 15–30 minutes after any intervention. 2
• Expect the heart rate to decrease by 10–20 bpm for every 1°C reduction in body temperature as the infection resolves. 2
• If the rate remains >110 bpm 24–48 hours after fever resolution and infection control, then pursue more aggressive rate control or consider rhythm-control strategies. 2, 7