ICU · cardiovascular
Acute hypertensive emergency — comprehensive ICU management (hypertensive encephalopathy, ICH, dissection, pre-eclampsia, phaeochromocytoma, cocaine)
Also known as Hypertensive emergency · Hypertensive crisis · Malignant hypertension · Hypertensive encephalopathy · Hypertensive urgency · Pre-eclampsia and eclampsia · Phaeochromocytoma crisis · Cocaine-induced hypertensive crisis · Cerebral autoregulation · PRES (posterior reversible encephalopathy syndrome) · INTERACT2 · STAT registry · Sublingual nifedipine (avoid)
Hypertensive emergency = a severe elevation of blood pressure (typically SBP 180 and/or DBP 120 mmHg) accompanied by ACUTE ongoing target-organ damage (cerebral — encephalopathy, intracerebral haemorrhage, ischaemic stroke; cardiac — acute coronary syndrome, acute pulmonary oedema, aortic dissection; renal — acute kidney injury with proteinuria/microangiopathy; retina — papilloedema and flame haemorrhages; pregnancy — pre-eclampsia/eclampsia). It is distinguished from hypertensive URGENCY (severe BP but NO acute end-organ damage), which is managed with ORAL agents over 24-48 h. The central pathophysiological principle is the cerebral autoregulation curve: in chronic hypertension the curve shifts to the RIGHT, so the brain depends on a higher mean arterial pressure (MAP) to maintain perfusion. Reducing BP too rapidly or to 'normal' values drops cerebral blood flow below the autoregulatory threshold and causes ISCHAEMIC stroke — hence the safe target for most emergencies is a 10-20% MAP reduction in the first hour, then gradual reduction to ~160/100 mmHg over 2-6 h. EXCEPTIONS requiring aggressive, immediate reduction are aortic dissection (SBP to 100-120 mmHg, beta-blocker FIRST to lower dP/dt) and ischaemic stroke pending thrombolysis decision. MANAGEMENT is in ICU/HDU with an arterial line and a titratable IV agent; drug selection is dictated by the SPECIFIC emergency: labetalol (alpha + beta-blocker, versatile, safe in pregnancy and post-stroke), nicardipine (smooth titratable calcium-channel blocker, the preferred agent for most), clevidipine (ultra-short-acting dihydropyridine), nitroglycerin (ACS and pulmonary oedema), esmolol (aortic dissection — titratable beta-blockade), hydralazine (pregnancy), phentolamine (phaeochromocytoma — alpha-blockade), and fenoldopam (renal-protective). AVOID sodium nitroprusside where possible (cyanide/thiocyanate toxicity, increases intracranial pressure, coronary steal) and NEVER give sublingual nifedipine (unpredictable precipitous fall - stroke/MI). SPECIAL CASES: intracerebral haemorrhage - lower SBP to 140 mmHg (INTERACT2 — intensive lowering to 140 improved functional outcome); pre-eclampsia/eclampsia - MAGNESIUM SULPHATE FIRST for seizure prevention/treatment, then labetalol/hydralazine; phaeochromocytoma - ALPHA-blockade (phentolamine/phenoxybenzamine) BEFORE any beta-blocker (unopposed alpha-1 stimulation - catastrophic hypertension); cocaine-induced - BENZODIAZEPINES first (calm sympathetic surge), avoid pure beta-blockers (unopposed alpha).
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Red flags
- Hypertensive EMERGENCY (severe BP + acute end-organ damage) needs immediate IV therapy in ICU; URGENCY (no end-organ damage) gets oral agents over 24-48 h.
- Do NOT reduce BP too rapidly or to 'normal' in chronic hypertension — cerebral autoregulation is shifted right; rapid reduction -> cerebral hypoperfusion -> ischaemic stroke. Reduce MAP by 10-20% in the first hour.
- Aortic dissection is the EXCEPTION — rapid reduction to SBP 100-120 mmHg, beta-blocker FIRST (lower dP/dt before vasodilation).
- Phaeochromocytoma: ALPHA-blockade (phentolamine/phenoxybenzamine) BEFORE any beta-blocker — beta-blocker first causes unopposed alpha-1 stimulation -> catastrophic hypertension.
- Eclampsia: give MAGNESIUM SULPHATE FIRST (seizure prevention and treatment), then BP control with labetalol/hydralazine.
- NEVER give sublingual nifedipine — unpredictable precipitous BP fall -> stroke/MI. It is withdrawn from guidelines.
- Avoid sodium nitroprusside where possible — cyanide/thiocyanate toxicity, increases ICP, causes coronary steal.
- Cocaine-induced crisis: BENZODIAZEPINES first; avoid pure beta-blockers (unopposed alpha).
Meet the patient
A 58-year-old man with chronic hypertension arrives with tearing interscapular pain, SBP 220, unequal blood pressures in his two arms, and a widened mediastinum on the chest film. Another patient — a 52-year-old, also hypertensive — arrives confused and seizing with papilloedema and a BP of 224/138. Same blood pressure, same chronic disease, opposite drugs and opposite targets. One gets a beta-blocker first and a rapid drop; the other gets a titratable vasodilator and a gradual one.[1]
The skill the round tests is not lowering blood pressure — it is naming which organ is failing, then matching the drug, the order, and the target to that organ. The number alone never decides it.[2]
References20ShowHide
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- [19]Zawadzka K, Pisarska-Adamczyk M, Hubalewska-Dydejczyk A, et al. Prolonged alpha-blockade and doxazosin are associated with hypertensive crisis in pheochromocytoma surgery Front Endocrinol (Lausanne), 2025.PMID 41573200
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