Key Points
- Stabilize ABCs; begin targeted evaluation without delaying life-saving therapy.
- Use system-specific risk tools to guide testing and disposition.
- Order high-yield tests first; escalate imaging when indicated.
- Start evidence-based initial therapy and reassess frequently.
Algorithm
- Primary survey and vitals; IV access and monitors.
- Focused history/physical; identify red flags and likely etiologies.
- Order system-appropriate labs and imaging (see Investigations).
- Initiate guideline-based empiric therapy (see Pharmacology).
- Reassess response; arrange consultation and definitive management.
Clinical Synopsis & Reasoning
AF evaluation focuses on hemodynamic stability, symptom burden, and secondary precipitants (thyrotoxicosis, infection, PE, alcohol). Classify as first‑detected, paroxysmal, persistent, or long‑standing, and determine stroke risk via CHA₂DS₂‑VASc. ECG confirms diagnosis and helps identify pre‑excitation or flutter; echocardiography informs structural disease and guides rhythm‑control choices.
Treatment Strategy & Disposition
For unstable patients, perform immediate synchronized cardioversion. In stable patients, choose rate vs rhythm control based on symptoms, duration, and substrate; employ β‑blockers or non‑DHP CCBs for rate control, and consider antiarrhythmics or ablation for rhythm strategies. Anticoagulate according to thromboembolic risk and timing around cardioversion. Disposition hinges on control of rate/rhythm and comorbidities; ensure follow‑up for anticoagulation and risk‑factor modification (BP, OSA, obesity).
Epidemiology / Risk Factors
- Atherosclerotic risk (HTN, DM, HLD, smoking)
- Age/family history of premature CAD
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| EKG | Rhythm/ischemia | ST-T changes/arrhythmia | Serial |
| Troponin | Myocardial injury | Dynamic rise/fall | Trend |
| CXR | Pulmonary edema/size | Cardiomegaly/edema | |
| BMP/Mg2+ | Electrolytes/renal | Derangements | |
| CBC/Coags | Bleeding risk | Abnormal/INR |
CHA₂DS₂-VASc (Abbrev.)
| Factor | Points |
|---|---|
| CHF/LV dysfunction | 1 |
| HTN | 1 |
| Age ≥75 | 2 |
| DM | 1 |
| Stroke/TIA/TE | 2 |
| Vascular disease | 1 |
| Age 65–74 | 1 |
| Female sex | 1 |
Pharmacology
| Medication | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Amiodarone | Multi-channel blockade | Hours | Rhythm control in HFrEF/critically ill | QT prolongation, interactions |
| Diltiazem | Non-DHP calcium-channel blockade | Minutes | Rate control (avoid in HFrEF) | Hypotension; avoid HFrEF |
| Metoprolol | β1 blockade | Minutes | Rate control without decompensated HF | Bradycardia/hypotension |
| Flecainide/Propafenone | Na-channel (class IC) | Hours | Rhythm (pill-in-pocket) without structural heart disease | Proarrhythmia; avoid CAD/HFrEF |
| Apixaban | Factor Xa inhibition | Hours | Anticoagulation per CHA₂DS₂-VASc | Bleeding; renal dosing |
Prognosis / Complications
- Prognosis by ischemic burden/LV function
- Arrhythmias and HF are complications
Patient Education / Counseling
- Explain red flags and when to seek emergent care.
- Reinforce medication adherence and follow-up plan.
Notes
Anticoagulate ≥3 weeks before and 4 weeks after elective cardioversion unless TEE-guided strategy is used. Choice of antiarrhythmic depends on structural heart disease.