1. Introduction
A hypertensive emergency is defined as severe hypertension (usually systolic BP ≥180 mmHg or diastolic BP ≥120 mmHg) with evidence of acute target organ damage, such as:
- Acute heart failure or pulmonary edema
- Myocardial infarction or unstable angina
- Acute aortic dissection
- Stroke or encephalopathy
- Acute kidney injury
Management requires rapid but controlled blood pressure reduction, typically with intravenous (IV) agents that have rapid onset and titratable effects.
2. Principles of Management
- Immediate goal: Reduce mean arterial pressure (MAP) by no more than 25% within the first hour, unless in aortic dissection (target SBP <120 mmHg)
- Route: IV preferred for rapid titration; oral agents may be used once stable
- Choice of agent: Depends on target organ involvement and patient comorbidities
- Monitoring: Continuous BP and cardiac monitoring, frequent neurologic assessment, urine output
3. Pharmacologic Agents
3.1 Nitroprusside
- Class: Direct-acting vasodilator
- Mechanism: Releases nitric oxide → arterial and venous dilation → ↓ BP
- Onset/Duration: Immediate (1–2 min) / short duration
- Clinical Use:
- Most hypertensive emergencies
- Acute heart failure with elevated BP
- Adverse Effects: Cyanide toxicity (especially prolonged use), reflex tachycardia, headache
- Monitoring: Continuous BP; limit duration; monitor thiocyanate in renal impairment
3.2 Nicardipine
- Class: Dihydropyridine calcium channel blocker (IV)
- Mechanism: Arterial vasodilation via L-type calcium channel inhibition
- Onset/Duration: 5–15 min / 2–4 h
- Clinical Use: Hypertensive emergencies in stroke, encephalopathy, perioperative settings
- Adverse Effects: Reflex tachycardia, headache, flushing
- Advantage: Easy titration, safe in renal impairment
3.3 Labetalol
- Class: Mixed α1 and non-selective β-adrenergic blocker
- Mechanism: ↓ peripheral resistance (α1) and cardiac output (β1), modest HR reduction
- Onset/Duration: 5–10 min IV / 2–4 h
- Clinical Use:
- Aortic dissection
- Stroke (if not ischemic thrombolysis candidate)
- Pregnancy (safe option)
- Adverse Effects: Bradycardia, heart block, bronchospasm (avoid in asthma)
3.4 Esmolol
- Class: Short-acting β1-selective blocker
- Mechanism: ↓ HR and cardiac output
- Onset/Duration: 1–2 min / 10–20 min
- Clinical Use:
- Aortic dissection (used with nitroprusside)
- Perioperative hypertension
- Adverse Effects: Bradycardia, hypotension, fatigue
3.5 Fenoldopam
- Class: Dopamine D1 receptor agonist
- Mechanism: Arteriolar vasodilation, promotes renal perfusion
- Onset/Duration: 5 min / 30–60 min
- Clinical Use:
- Hypertensive emergencies with renal dysfunction
- Adverse Effects: Reflex tachycardia, headache, flushing
3.6 Nitroglycerin
- Class: Nitrate vasodilator
- Mechanism: Venodilation (reduces preload) and some arterial dilation
- Onset/Duration: 2–5 min / 3–5 min IV
- Clinical Use:
- Acute coronary syndrome
- Acute pulmonary edema with hypertension
- Adverse Effects: Headache, hypotension, reflex tachycardia
3.7 Clevidipine
- Class: Ultra-short-acting dihydropyridine CCB (IV)
- Mechanism: Rapid arterial vasodilation
- Onset/Duration: 2–4 min / 5–15 min
- Clinical Use: Rapid BP control in perioperative or ICU settings
- Adverse Effects: Hypotension, reflex tachycardia
- Advantage: Rapid titration, favorable in renal or hepatic impairment
4. Clinical Pearls
- Aortic dissection: Labetalol or Esmolol first-line; nitroprusside adjunct
- Acute pulmonary edema: Nitroprusside, nitroglycerin preferred; avoid excessive beta-blockade
- Acute ischemic stroke: Lower BP cautiously; nicardipine preferred if needed
- Pregnancy: Labetalol or hydralazine are first-line
5. Monitoring Parameters
| Parameter | Frequency |
|---|---|
| Blood pressure | Continuous (invasive arterial line if available) |
| Heart rate | Continuous |
| ECG | Continuous in cardiac patients |
| Urine output | Hourly |
| Electrolytes, renal function | Baseline and daily |
| Cyanide/thiocyanate | If using nitroprusside >24–48 h |
6. Adverse Effects Summary
- Hypotension → tissue hypoperfusion if overcorrected
- Reflex tachycardia → common with vasodilators
- Bradycardia/heart block → beta-blockers
- Organ-specific toxicity → cyanide (nitroprusside), headache, nausea, flushing
7. Summary
Hypertensive emergencies require rapid, controlled blood pressure reduction to prevent further target organ damage. IV agents are first-line therapy, and choice depends on:
- Target organ involvement
- Comorbidities (cardiac, renal, pregnancy)
- Drug pharmacokinetics and safety profile
Key agents: Nitroprusside, Nicardipine, Labetalol, Esmolol, Fenoldopam, Nitroglycerin, Clevidipine.
Important: Avoid rapid BP reductions to prevent ischemic complications; titrate carefully and monitor continuously.
8. References
- Whelton PK, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Hypertension. 2018;71:e13–e115.
- Chobanian AV, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA. 2003;289:2560–2572.
- Varon J, Marik PE. The diagnosis and management of hypertensive crises. Chest. 2000;118:214–227.
- Katz JN, et al. Acute management of hypertensive emergencies. N Engl J Med. 2016;374:1355–1364.
- Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 14th Edition, 2021.
