Hypertensive crises

• A hypertensive emergency is severe high blood pressure (above about 180/120 mm Hg) with new or worsening organ damage; it needs urgent, careful reduction.
• A severe rise without organ damage is now managed slowly, usually with tablets, and is not a reason for rapid intravenous lowering.
• The damaged organ decides the target blood pressure, the drug and how fast to lower it: brain, heart, lungs, aorta, kidney, retina and pregnancy each have different rules.
• Lowering too fast can harm; ischaemic stroke is the clearest example. The exception is acute aortic dissection, where the systolic pressure is taken below 120 mm Hg quickly.
• Follow-up matters: a hypertensive emergency carries high risks of recurrence, chronic kidney disease and stroke, and is often triggered by not taking antihypertensive medication.

By the end of this page you should be able to:

1. Define a hypertensive emergency and explain why the term "hypertensive urgency" is being abandoned.
2. List common causes and precipitants of a sudden severe blood-pressure rise.
3. Match each presentation (encephalopathy, stroke, acute coronary syndrome, pulmonary oedema, aortic dissection, acute kidney injury, eclampsia/pre-eclampsia, retinal haemorrhage) to its blood-pressure target, first-line drug and speed of reduction.
4. Recall intravenous drug doses with routes, monitoring and contraindications, and know which drugs to avoid in which situation.
5. Plan hospital and outpatient follow-up, and describe care when advanced tests and drugs are unavailable.

Hypertensive crisis is the point at which high blood pressure becomes an acute, organ-threatening emergency rather than a chronic risk. The deciding factor is not the height of the pressure but target-organ damage (also called hypertension-mediated organ damage, HMOD): the same severe pressure may be harmless in one person and sight- or life-threatening in another. Target-organ damage means new injury to the brain, eyes, heart, lungs, aorta, kidneys or, in pregnancy, to the placenta and fetus. That distinction separates patients who need intravenous drugs in a high-dependency setting from those who can be treated with tablets and observed.

A hypertensive emergency is the combination of a very high pressure and acute injury to one of the key organs: heart, retina, brain, kidneys or large arteries such as the aorta. ^[2] There is no single threshold, because at the same pressure one patient may have acute organ damage and another may not; the rate of rise matters more than the absolute value. ^[2]

Historically, severe pressures without acute organ damage were called hypertensive urgency. The ESC Task Force considers it preferable not to use that term, because "hypertensive urgency" is a diagnosis of exclusion and there is no evidence that these patients are treated differently from patients with asymptomatic uncontrolled hypertension. ^[2] The Task Force's exact statement is that "the term hypertensive crisis ... becomes obsolete." ^[2] The 2017 AHA/ACC guideline still uses both terms. ^[1] The 2024 ESC guidelines use severe hypertension with or without acute HMOD, while the 2023 ESH guidelines retain "hypertensive urgency". ^[3] In practice, the 2024 ESC document requires that a hypertensive emergency be ruled out in anyone with blood pressure at or above 180/110 mm Hg. ^[4]

Malignant hypertension is a severe hypertensive emergency: a very high pressure (usually above 200/120 mm Hg) with advanced retinopathy, meaning bilateral flame-shaped haemorrhages, cotton-wool spots and sometimes papilloedema. ^[2] It reflects acute microangiopathy (microvascular damage), and an alternative term, "acute hypertensive microangiopathy", has been proposed because retinal lesions can be absent even when the kidney or brain is involved. ^[2]

Hypertensive encephalopathy is a hypertensive emergency with severe hypertension and one or more of seizures, lethargy, cortical blindness and coma, with no other explanation. ^[2]

The common themes are discontinuing or not taking antihypertensive medication, chronic uncontrolled hypertension, and sudden sympathetic surges. ^[5]

• Chronic or inadequately treated hypertension, often with missed doses or running out of tablets.
• Renal parenchymal disease and renal artery stenosis.
• Drugs and toxins: cocaine, amphetamines, phencyclidine, monoamine oxidase inhibitors, cyclosporin, anti-angiogenic agents, steroids and NSAIDs; sudden withdrawal of clonidine or similar sympatholytics can also precipitate a crisis. ^[5]
• Endocrine causes, especially pheochromocytoma, and hyperaldosteronism.
• Pregnancy (pre-eclampsia and eclampsia).
• Perioperative hypertension, including severe postoperative rises.
• Aortic dissection, acute coronary syndromes, intracerebral haemorrhage and subarachnoid haemorrhage are both causes and presentations.
• Secondary hypertension is found in an important minority (20-40%) of patients presenting with malignant hypertension, most often renal parenchymal disease or renal artery stenosis; endocrine causes are comparatively rare. ^[2]

A hypertensive emergency begins with loss of the normal autoregulation of blood flow: once pressure rises beyond the range the arterioles can buffer, endothelial damage, oedema and ischaemia follow, and the renin-angiotensin system is activated. Pressure natriuresis causes volume depletion, which drives further renin release. Autoregulation failure and microcirculatory damage underlie the organ injury of malignant hypertension and produce hypertensive retinopathy, thrombotic microangiopathy and encephalopathy, damage that is not seen in stable chronic hypertension. ^[2]

Severe blood pressure rises also produce retinal haemorrhage and cotton-wool spots (Grade III retinopathy), with or without papilloedema (Grade IV). ^[2] Ten to 15% of patients with malignant hypertension develop hypertensive encephalopathy, and advanced retinopathy may be absent in about one-third of these patients, so the diagnosis relies on neurological features and brain imaging. ^[2]

Thrombotic microangiopathy can accompany severe hypertension: Coombs-negative haemolysis (high LDH, unmeasurable haptoglobin, schistocytes) with thrombocytopenia, improving within 24-48 hours of blood-pressure lowering. ^[2]

Symptoms are those of the failing organ: severe headache, visual disturbance or loss, chest pain, dyspnoea, reduced urine output, nausea, and focal or general neurological symptoms. ^[5] Dizziness from impaired cerebral autoregulation and gastrointestinal complaints (abdominal pain, nausea, anorexia) are common and less specific. ^[2]

Ask about medications and whether they have been stopped or changed; a missed prescription is the most common, reversible cause. ^[2] Ask about drugs of abuse (cocaine, amphetamines), other chronic medications (steroids, NSAIDs, cyclosporin, anti-angiogenic therapy), renal disease, previous blood-pressure control, pregnancy and headache severity. Ask someone who lives with the patient for a collateral history.

Measure blood pressure in both arms and, if aortic dissection is possible, at the lower limb; repeat it over time because a significant fall can occur without treatment. ^[2] Perform a focused cardiovascular and neurological examination. Fundoscopy is essential when malignant hypertension is suspected. A pregnancy test and a bedside urine dipstick for blood and protein are indispensable in a woman of childbearing age.

The 2017 AHA/ACC guideline approach and the ESC position document support a standard minimum set. ^{[1] [2]}

• Electrocardiogram for ischaemia, arrhythmia and left-ventricular hypertrophy; chest X-ray or point-of-care ultrasound to distinguish cardiac from non-cardiac dyspnoea.
• Metabolic panel with creatinine and electrolytes, full blood count with platelets, LDH, haptoglobin and urinalysis (protein, blood, casts).
• Troponin if cardiac chest pain or ECG changes.
• Brain imaging (CT or MRI) for acute neurological symptoms.
• Transthoracic echocardiography if cardiac structure or function is in doubt.
• CT angiography of the thorax and abdomen if acute aortic disease is possible.
• Renal ultrasound for suspected obstructive or advanced renal disease.

The urgent question is whether the patient has a hypertensive emergency (organ damage) or severe uncomplicated hypertension. The second question, once a mass of very high pressure is present, is which organ is injured.

There is no substitute for a careful bedside assessment: organ damage is diagnosed clinically and with basic tests, not by the blood pressure number alone. The brain targets (stroke, encephalopathy), the lungs (cardiogenic pulmonary oedema), the heart (acute coronary syndrome), the aorta (dissection), the kidneys (acute injury or TMA), the retina and pregnancy each create a different risk matrix. The table below maps each presentation to its management.

The organ that is damaged determines the target, the drug and the speed. The table summarises the consensus targets of the ESC Council on hypertension. ^[2]

For most hypertensive emergencies the standard approach is to reduce blood pressure by about 20-25% in the first hour, then to roughly 160/100 mm Hg over the next 2-6 hours, and then to normalise within 24-48 hours. ^[5] This applies to malignant hypertension, acute kidney injury and hypertensive encephalopathy. ^[2] Aortic dissection is the exception.

• Aortic dissection (and acute aortic rupture): reduce the systolic pressure to below 120 mm Hg and the heart rate to below 60 bpm as soon as possible; a beta-blocker (esmolol, metoprolol or labetalol) should be used before or with a vasodilator, so that heart rate control accompanies the pressure fall. ^{[2] [5]}
• Ischaemic stroke: do not lower blood pressure acutely unless it is very high (above 220/120 mm Hg), or lowering is needed for another reason, because an acute fall worsens neurological outcome. ^{[2] [6]} If BP-lowering is indicated, a fall in mean arterial pressure of no more than about 15% in the first 24 hours is reasonable. ^[2] When thrombolysis is intended, blood pressure must be below 185/110 mm Hg before alteplase is given, and maintained below 180/105 mm Hg for the first 24 hours afterwards. ^{[6] [7]} The prevailing strategy is permissive: allow pressures up to those thresholds without aggressive lowering. ^[6]
• Intracerebral haemorrhage: the 2024 ESC guidelines advise against lowering blood pressure by more than 70 mm Hg in the first hour when the starting systolic pressure is above 220 mm Hg, and target 140-160 mm Hg within the first few hours to limit haematoma expansion. ^[4] The consensus target of the ESC Council on hypertension is a systolic pressure of 130-180 mm Hg. ^[2] These values differ; use the one applied in your unit.
• Acute coronary syndrome: reduce systolic pressure to below 140 mm Hg. ^[2] Avoid excessive diastolic hypotension; some consensus documents put the floor at about 70 mm Hg (BIHS) and older reviews at below 60 mm Hg. Sodium nitroprusside is avoided in acute coronary syndromes because it reduces regional coronary blood flow. ^[2]

The 2024 ESC document also recommends blood-pressure-lowering treatment before discharge for patients with ischaemic stroke. ^[4] After stroke, the target becomes 120-129 mm Hg. ^[4]

• This is hypertension above about 180/120 mm Hg with no evidence of acute organ damage; it is a diagnosis of exclusion. ^{[1] [2]}
• Most patients can be managed with oral drugs and an adaptation of their existing regimen; observation for at least 2 hours after a change in treatment is suggested to judge safety and effect. ^[2]
• Rapid blood-pressure lowering is not recommended; it is the same approach as for asymptomatic uncontrolled hypertension. ^[2]
• Short-acting nifedipine (immediate-release capsules) is specifically not recommended because it can cause sudden falls. Delayed-release preparations, captopril or labetalol are the usual oral agents. ^[2]
• In pregnancy the rules change (see below): this is an emergency needing immediate treatment.

Oral agents for severe uncomplicated hypertension: captopril, labetalol and modified-release nifedipine are the options with the best limited evidence; non-selective short-acting nifedipine should be avoided. ^[2]

Intravenous drugs. The dosing below is from the ESC Council on hypertension position document, supplemented by standard review doses. ^{[2] [5]} Check your local formulary and drug availability; labels and units differ between countries.

Notes on specific situations:

• Acute pulmonary oedema: intravenous nitroglycerin, clevidipine or nitroprusside are used; beta-blockers are generally avoided in the acute phase, and a loop diuretic (intravenous furosemide) is added. ^[5]
• Acute coronary syndrome: nitroglycerin and labetalol are used; nitroprusside is avoided. ^[2]
• Acute aortic disease: esmolol (loading dose 500-1000 mcg/kg, equivalent to 0.5-1 mg/kg, given over 1 minute) plus a vasodilator, then switch to oral therapy as tolerated with a long-term systolic target of 120 mm Hg or less. ^[5]
• Pheochromocytoma or sympathomimetic crisis: phentolamine or nitroprusside; nicardipine can be used; labetalol is relatively contraindicated because it is not effective against coronary vasoconstriction; treat cocaine or amphetamines with benzodiazepines first. ^[2]
• Pregnancy: pre-eclampsia and eclampsia are treated with labetalol or nicardipine, and magnesium sulphate for eclampsia; hydralazine is less used because of adverse perinatal outcomes, and sodium nitroprusside is contraindicated because of fetal cyanide risk. ACE inhibitors, ARBs and direct renin inhibitors are avoided in pregnancy. ^{[1] [2]} Hydralazine is still used in some settings: up to 20 mg initially, then 0.3-1.0 mg/kg to a total of 300 mg. ^[5]
• Renal dysfunction: nicardipine and labetalol are commonly used; in one comparison, 92% of patients given nicardipine achieved target systolic pressure within 30 minutes, versus 78% given labetalol. ^[5]

• Rapid or excessive lowering in most patients, especially in ischaemic stroke, where it worsens outcome.
• Short-acting (immediate-release) nifedipine, because of unpredictable, abrupt falls in pressure.
• Beta-blockers in acute pulmonary oedema in the acute phase.
• Sodium nitroprusside in pregnancy (fetal cyanide toxicity) and in acute coronary syndromes (reduced coronary flow), and with caution in renal or hepatic impairment.
• ACE inhibitors, ARBs and direct renin inhibitors in pregnancy.
• Hydralazine as first-line in eclampsia in current ESC guidance, because it is less available and has been associated with adverse perinatal outcomes.
• Thrombolysis in stroke should not be delayed while waiting for an excessive blood pressure fall; the threshold of <185/110 mm Hg should be met and then maintained. ^[7]
• Induced hypotension for ischaemic stroke is investigational, not routine care.

Pregnancy and the postpartum period. Hypertension in pregnancy is a leading cause of maternal morbidity. Treat chronic hypertension in pregnancy with methyldopa, labetalol or long-acting nifedipine, and switch ACE inhibitors, ARBs or direct renin inhibitors to these agents. ^[1] In pre-eclampsia the diagnostic threshold is tighter (at least 140/90 mm Hg) and the ESC 2023/2024 documents broaden the diagnosis to include gestational hypertension with proteinuria or other organ dysfunction. ^[3] Severe pre-eclampsia or eclampsia is an emergency: reduce systolic pressure below 160 mm Hg and diastolic below 105 mm Hg without delay, using labetalol or nicardipine plus magnesium sulphate, and deliver once the mother is stable. ^[2]

Older adults. Use caution with aggressive targets and big pressure falls, particularly if frail or symptomatic with postural hypotension; aim for the "as low as reasonably achievable" principle. Children are outside the scope of this page; paediatric hypertensive emergencies follow paediatric protocols and drugs.

A hypertensive emergency is not a single event: survival has improved, but survivors remain at higher cardiovascular and renal risk than hypertensive patients who have never had an emergency, and hospital mortality in those admitted to coronary care is 4.6% versus 0.8% in hypertensive patients without an emergency. ^[2] Poor adherence and under-treatment drive recurrence.

Follow-up, from the ESC position document: ^[2]

• Frequent, at least monthly, visits in a specialist setting until the target blood pressure is reached; longer follow-up while hypertension-mediated organ damage (renal function, proteinuria, left-ventricular mass) regresses.
• Review and simplify the regimen, intensify treatment (including adding a diuretic and fixed-dose combination), reinforce sodium restriction and check adherence; motivational interviewing and family support help.
• Investigate secondary causes and quantify organ damage.
• Treat acute drug-induced emergencies by withdrawing the offending drug, and discuss any chemotherapy changes with oncology.

In hospital, monitor blood pressure every 5-15 minutes during initial treatment and every 30-60 minutes after stabilisation. ^[5] Switch to oral agents once the pressure is controlled, usually 8-24 hours after achieving the target intravenous regimen.

• The diagnosis rests on clinical assessment plus basic tests: careful repeated blood-pressure measurement, fundoscopy, urine dipstick, creatinine and ECG. ^[2]
• The ESC Task Force states that labetalol and nicardipine should appear on the essential-drug list of every hospital that has an emergency room or intensive care unit, because they treat most hypertensive emergencies; urapidil, clevidipine, fenoldopam and advanced imaging are often unavailable. ^[2]
• Severe uncomplicated hypertension should be managed with inexpensive oral agents (modified-release nifedipine, captopril, labetalol) and at least 2 hours of observation. ^[2]
• Only stabilise, then transfer when urgent imaging or surgery (for dissection) or an intensive-care bed is required. A transthoracic echocardiogram and a plain CT brain, where available, are the investigations that most change management.
• Short-acting nifedipine should be avoided at all levels of care.

• Heart failure (acute pulmonary oedema, cardiogenic shock)
• Atrial fibrillation and flutter
• ECG interpretation
• Cardiac physical examination
• Ventricular arrhythmias
• Bradyarrhythmias and AV block
• Supraventricular tachycardias
• Approach to tachyarrhythmias
• Stroke, acute aortic syndromes, acute kidney injury, pre-eclampsia/eclampsia, thrombotic microangiopathy and retinal vascular disease are the other key linked areas.

• A hypertensive emergency is severe hypertension with new or worsening target-organ damage; the organ injured determines management.
• There is no single blood-pressure threshold; the rate of rise and new organ damage matter more than the number.
• Terms are changing: "hypertensive urgency" and "hypertensive crisis" are falling out of favour in European guidance, which prefers "hypertensive emergency" (with acute HMOD) and severe uncomplicated hypertension.
• Most emergencies: reduce mean arterial pressure by 20-25% in the first hour, then to about 160/100 mm Hg, then normalise within 24-48 hours.
• Aortic dissection is the exception: systolic pressure below 120 mm Hg and heart rate below 60 bpm as soon as possible, with a beta-blocker.
• Ischaemic stroke: do not lower acutely unless above 220/120, or thrombolysis/aortic dissection requires it; meet and hold <185/110 mm Hg before alteplase.
• Intracerebral haemorrhage: avoid a fall of more than 70 mm Hg in the first hour when starting above 220 mm Hg; target 140-160 mm Hg in the first hours (consensus 130-180 mm Hg).
• Acute coronary syndrome or pulmonary oedema: target systolic pressure below 140 mm Hg; beta-blockers are avoided in acute pulmonary oedema.
• Eclampsia/pre-eclampsia: below 160/105 mm Hg with labetalol or nicardipine plus magnesium sulphate.
• Avoid immediate-release nifedipine, beta-blockers in pulmonary oedema, nitroprusside in pregnancy and acute coronary syndromes, and ACE inhibitors/ARBs in pregnancy.
• Survivors need monthly specialist follow-up, adherence work and investigation of secondary causes; prognosis is worse than in uncomplicated hypertension.

See the reference list in the page front matter. All values in this topic are from the sources cited in the text.