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Hypertensive Emergency

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Definition

• Severe BP elevation: SBP > 180 mmHg and/or DBP > 120 mmHg
• WITH evidence of acute target organ damage (TOD)

• Lippincott Pharmacology, p. 316
• Comprehensive Clinical Nephrology, 7th ed., p. 540

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Hypertensive Urgency vs. Emergency

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Target Organs Involved (Approximate Incidence)

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Pathophysiology

1. Abrupt rise in BP overwhelms autoregulation
2. Endothelial injury → fibrinoid necrosis of arterioles
3. Activation of RAAS → further vasoconstriction
4. Increased vascular permeability → end-organ ischemia
5. In the brain: failure of cerebral autoregulation → vasogenic edema → hypertensive encephalopathy
6. In the kidney: "onion skin" concentric intimal thickening + glomerular collapse
7. In the heart: increased afterload → pulmonary edema or ischemia

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Clinical Features / Target Organ Assessment

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Investigations

• CBC with peripheral smear (microangiopathic hemolytic anemia - schistocytes, TMA)
• Serum creatinine, urea, electrolytes
• Urinalysis (hematuria, RBC casts)
• Urine albumin/creatinine ratio
• ECG (LVH, ischemia)
• Chest X-ray (pulmonary edema, widened mediastinum)
• Troponin, CK-MB, NT-proBNP (cardiac involvement)
• CT brain (stroke, hemorrhage, encephalopathy)
• Plasma catecholamines (if pheochromocytoma suspected)

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General Principles of Treatment

Goals of BP Reduction (ACC/AHA 2017)

• Aortic dissection: Target SBP < 120 mmHg within 1 hour
• Eclampsia/Pheochromocytoma: SBP < 140 mmHg within 1 hour
• Ischemic stroke (for thrombolysis): BP < 185/110 mmHg
• Ischemic stroke (no thrombolysis): Only treat if BP > 220/120; reduce by ~15%

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Drugs Used in Hypertensive Emergency (IV Agents)

1. Sodium Nitroprusside

• Mechanism: NO donor → direct arterial + venous dilator
• Onset: Seconds; Duration: 1-2 min
• Dose: 0.3-10 mcg/kg/min IV infusion
• Advantage: Instantly titratable
• Toxicity: Cyanide/thiocyanate toxicity with prolonged use, raised ICP
• Use: ACS, aortic dissection (after beta-blocker), severe encephalopathy
• Avoid: Renal failure (thiocyanate accumulation), pregnancy, isolated ICH

2. Nicardipine (Dihydropyridine CCB - 3rd gen)

• Mechanism: Selective L-type Ca²⁺ channel blockade → arterial vasodilation
• Onset: 5-10 min; Duration: 15-30 min
• Dose: 5-15 mg/hr IV infusion
• Use: Most hypertensive emergencies including stroke, encephalopathy, renal crisis
• Advantage: Minimal reflex tachycardia; titratable

3. Clevidipine (Dihydropyridine CCB - 4th gen)

• Mechanism: Selective arteriolar dilator (no venodilation)
• Onset: 2-4 min; Duration: ~5-15 min
• Dose: 1-6 mg/hr IV
• Advantage: Ultra-short acting, renal/hepatically independent metabolism (esterases in blood)
• Use: Cardiac surgery HTN, acute heart failure, ACS

4. Labetalol (α₁ + β blocker)

• Mechanism: Reduces cardiac output + peripheral resistance
• Onset: 5-10 min IV bolus; Duration: 4-6 hours
• Dose: 20-80 mg IV bolus q10 min OR 1-2 mg/min infusion
• Use: Most emergencies, especially aortic dissection, eclampsia
• Avoid: Acute heart failure (↓CO), bronchospasm, bradycardia

5. Esmolol (Cardioselective β₁-blocker)

• Mechanism: Reduces HR and CO
• Onset: 60 sec; Duration: 10-20 min (ultra-short)
• Dose: Bolus 500 mcg/kg IV, then 0.05-0.2 mg/kg/min
• Use: Aortic dissection (first-line to reduce dP/dt before vasodilator), perioperative HTN
• Advantage: Titratable; safe in renal/hepatic failure

6. Nitroglycerin

• Mechanism: NO donor → predominantly venodilation (venous > arterial)
• Dose: 5-100 mcg/min IV
• Use: ACS, acute hypertensive heart failure/pulmonary edema
• Avoid: Used alone in aortic dissection; causes reflex tachycardia

7. Hydralazine

• Mechanism: Direct arteriolar vasodilator
• Onset: 10-20 min; Duration: 1-4 hours (unpredictable)
• Dose: 10-20 mg IV bolus
• Use: Eclampsia/pregnancy-induced hypertension (drug of choice)
• Disadvantage: Unpredictable response; reflex tachycardia; avoid in ACS/dissection

8. Phentolamine (α-blocker)

• Mechanism: Competitive α₁ and α₂ blockade
• Use: Pheochromocytoma crisis, MAOI-tyramine interaction, cocaine-induced HTN
• Dose: 5-15 mg IV bolus

9. Fenoldopam (Dopamine D₁ agonist)

• Mechanism: Renal and systemic vasodilation; natriuresis
• Dose: 0.1-0.3 mcg/kg/min IV
• Use: Hypertensive emergency with renal impairment (preserves/improves renal perfusion)
• Advantage: Increases renal blood flow

10. Enalaprilat (IV ACE Inhibitor)

• Mechanism: ACE inhibition → reduced angiotensin II
• Use: Acute HF, scleroderma renal crisis (drug of choice for scleroderma crisis)
• Avoid: Bilateral renal artery stenosis, pregnancy, acute MI

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Condition-Specific Drug Selection

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Drugs Used for Hypertensive URGENCY (Oral)

Sublingual nifedipine is CONTRAINDICATED - causes precipitous, uncontrolled BP drop with risk of stroke, MI, and death due to excessive reflex tachycardia and coronary steal.

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Key Points (KDT Exam Perspective)

1. Emergency = TOD present → IV mandatory; Urgency = no TOD → oral acceptable
2. Never reduce MAP >25% in the first hour (except aortic dissection and eclampsia)
3. Nitroprusside = most titratable; watch for cyanide toxicity in prolonged use/renal failure
4. Aortic dissection: Beta-blocker (esmolol) FIRST, then vasodilator; target SBP <120 mmHg
5. Pheochromocytoma: Alpha-blockade FIRST (phentolamine), never give beta-blocker alone
6. Eclampsia: Hydralazine/labetalol IV + MgSO₄; no ACE-I/ARBs (teratogenic)
7. Scleroderma renal crisis: ACE-I is the exception - actually beneficial here
8. Sublingual nifedipine is CONTRAINDICATED in all hypertensive crises
9. Fenoldopam is preferred when renal protection is needed
10. Most patients are volume-depleted - avoid diuretics unless pulmonary edema is present

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