## Hypertensive Crisis in Pheochromocytoma: Acute Management **Key Point:** In suspected pheochromocytoma with hypertensive emergency, alpha-blockade MUST precede beta-blockade to prevent unopposed alpha-mediated vasoconstriction and paradoxical hypertension. ### Pathophysiology Pheochromocytoma releases catecholamines (epinephrine and norepinephrine) causing: - Alpha-1 mediated: vasoconstriction, hypertension - Beta-1 mediated: tachycardia, palpitations - Beta-2 mediated: hyperglycemia, tremor **Clinical Pearl:** Beta-blockers alone cause unopposed alpha-receptor stimulation, worsening hypertension—the classic "catecholamine paradox." ### Correct Management Sequence 1. **Alpha-blockade first:** Phentolamine (short-acting, 5 mg IV bolus, repeat as needed) or phenoxybenzamine (longer-acting, 10 mg PO daily, titrate over 7–10 days for elective surgery) 2. **Then beta-blockade:** Only after alpha-blockade is established; esmolol or metoprolol to control reflex tachycardia 3. **Vasodilator:** Sodium nitroprusside or nicardipine for ongoing hypertensive control **High-Yield:** The mnemonic is **"Alpha first, beta second."** This is the single most tested principle in pheochromocytoma management. ### Why This Patient Needs Immediate Alpha-Blockade - Severe hypertension (210/120 mmHg) with catecholamine excess - Dilated pupils, diaphoresis, and elevated metanephrines confirm diagnosis - Hypertensive emergency requires rapid, controlled reduction; phentolamine achieves this safely **Tip:** In the exam, any pheochromocytoma question with hypertensive crisis will have a distractor offering beta-blocker monotherapy—this is a classic trap.
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