Most Likely Diagnosis: Supraventricular Tachycardia (SVT) with Hemodynamic Compromise
This 75-year-old woman with coronary artery disease, hypotension (BP 90/60), and a heart rate of 180 bpm requires immediate synchronized cardioversion without attempting vagal maneuvers or pharmacologic therapy. 1, 2
Immediate Assessment and Diagnosis
Why This Is Hemodynamically Unstable SVT
- Hypotension (BP 90/60 mmHg) in the setting of tachycardia (pulse 180) defines hemodynamic instability, even though oxygen saturation is preserved at 99%. 1, 2
- The combination of severe hypotension with extreme tachycardia in a 75-year-old with known coronary artery disease places her at immediate risk for myocardial ischemia, cardiogenic shock, and cardiac arrest. 1
- A heart rate of 180 bpm is most consistent with supraventricular tachycardia (AVNRT or AVRT) rather than ventricular tachycardia, particularly given the preserved oxygen saturation. 1, 2
Critical Differential Considerations
- Atrial fibrillation with rapid ventricular response is possible but less likely to produce such a regular rate of exactly 180 bpm. 1
- Ventricular tachycardia must be excluded with a 12-lead ECG during the tachycardia, as treatment differs fundamentally if VT is present. 1, 2
- Atrial flutter with 2:1 conduction (atrial rate 360, ventricular rate 180) is a key consideration in elderly patients with coronary disease. 1, 2
Immediate Treatment Protocol
Step 1: Synchronized Cardioversion (First-Line)
- Proceed directly to synchronized cardioversion with appropriate sedation; this restores sinus rhythm in nearly 100% of hemodynamically unstable SVT cases. 1, 2
- Do not attempt vagal maneuvers or pharmacologic therapy when hypotension is present, as this delays definitive treatment and risks deterioration. 1, 2
- Initial energy: 50–100 joules synchronized. 1, 2
Step 2: Obtain 12-Lead ECG During Tachycardia (If Time Permits)
- A 12-lead ECG obtained while the heart rate is 180 bpm is essential to differentiate SVT from ventricular tachycardia and to identify pre-excitation (Wolff-Parkinson-White syndrome). 1, 2
- If the rhythm is wide-complex or uncertain, treat as ventricular tachycardia until proven otherwise. 1, 2
Step 3: Supportive Measures During Preparation
- Establish large-bore IV access immediately. 2
- Administer IV fluid bolus (250–500 mL normal saline) to support blood pressure while preparing for cardioversion. 1
- Apply supplemental oxygen if not already done, though SpO₂ 99% suggests adequate oxygenation. 2
- Have a defibrillator and crash cart immediately available. 2
If Cardioversion Fails or Is Delayed
Pharmacologic Options (Second-Line Only)
- Intravenous amiodarone is the preferred agent for hemodynamically unstable tachycardia when cardioversion is delayed or unsuccessful: 150 mg IV over 10 minutes, followed by 1 mg/min infusion for 6 hours, then 0.5 mg/min. 1, 3
- Critical warning: Amiodarone causes hypotension in 16% of patients and can worsen existing hypotension; monitor blood pressure closely and slow the infusion if hypotension worsens. 3
- Avoid adenosine in hemodynamically unstable patients, as it is indicated only for stable SVT. 2
- Avoid calcium-channel blockers (diltiazem, verapamil) and beta-blockers in the setting of hypotension, as they will worsen hemodynamic compromise. 1, 2
Post-Conversion Management
Immediate Monitoring
- Continuous cardiac monitoring is essential immediately after conversion, as premature atrial or ventricular complexes frequently trigger recurrent SVT within seconds to minutes. 2
- Repeat blood pressure measurement every 5 minutes for the first 30 minutes post-conversion. 2
- Obtain a 12-lead ECG in sinus rhythm to assess for pre-excitation (delta waves suggesting WPW syndrome). 1, 2
Prevent Recurrence
- If immediate recurrence occurs, administer a longer-acting AV-nodal blocker such as oral diltiazem or a beta-blocker (if blood pressure has normalized) to prevent re-initiation. 2
- In elderly patients with coronary artery disease, beta-blockers are preferred for long-term rate control and secondary prevention. 1
Investigate Underlying Triggers
- Check electrolytes (potassium, magnesium, calcium) and correct any abnormalities, as hypokalemia and hypomagnesemia predispose to arrhythmias. 1
- Assess for acute coronary syndrome: obtain serial troponins and ECGs, as the combination of hypotension and tachycardia may have precipitated myocardial ischemia. 1, 4
- Review medications for QT-prolonging drugs or recent changes that may have triggered the arrhythmia. 1
Long-Term Management
Definitive Therapy
- Catheter ablation should be offered as first-line definitive therapy for recurrent symptomatic SVT, with single-procedure success rates of 94–98%. 2
- If ablation is declined or unsuitable, oral beta-blockers (e.g., metoprolol 25–50 mg twice daily) are first-line for prevention in patients with coronary artery disease. 1, 2
Secondary Prevention for Coronary Artery Disease
- Ensure the patient is on aspirin 75–150 mg daily for secondary prevention of coronary events. 1
- Initiate or optimize high-intensity statin therapy (atorvastatin 80 mg or rosuvastatin 40 mg daily). 4, 5
- Optimize blood pressure control with target <130/80 mmHg in patients with coronary disease. 1
- Counsel on smoking cessation, exercise, and weight loss as the most important lifestyle modifications. 5
Critical Pitfalls to Avoid
- Do not delay cardioversion in hemodynamically unstable patients to attempt vagal maneuvers or drug therapy. 1, 2
- Do not administer calcium-channel blockers or beta-blockers when hypotension is present, as this may precipitate cardiovascular collapse. 1, 2
- Do not assume the rhythm is benign simply because oxygen saturation is preserved; hypotension with tachycardia is a medical emergency regardless of SpO₂. 1, 2
- Do not miss acute coronary syndrome as a precipitant or consequence of the arrhythmia; obtain serial troponins and ECGs. 1, 4