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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2] Hafiz M. Ahmed, M.D.[3] James Nasr[4]

Synonyms and keywords: Hypertensive emergency; hypertensive urgency; severe hypertension (previously termed hypertensive urgency)

Overview

Hypertensive emergency is a severe elevation in blood pressure, usually systolic blood pressure (SBP) >180 mm Hg and/or diastolic blood pressure (DBP) >120 mm Hg, accompanied by evidence of new or worsening acute target organ damage.[1] The diagnosis depends on acute organ injury rather than the blood pressure value alone. Acute target organ damage may involve the brain (hypertensive encephalopathy, intracranial hemorrhage, ischemic stroke, posterior reversible encephalopathy syndrome), heart (acute coronary syndrome, acute heart failure, pulmonary edema), aorta (aortic dissection), kidney (acute kidney injury), retina (retinal hemorrhage, papilledema), or systemic microvasculature (thrombotic microangiopathy).[2]

Hypertensive emergency must be distinguished from severe hypertension without acute target organ damage, because hypertensive emergency generally requires emergency evaluation, close monitoring, and titratable intravenous antihypertensive therapy, whereas asymptomatic markedly elevated blood pressure should generally not be treated with rapid intravenous blood pressure reduction.[2] Patients with hypertensive emergencies have high short-term and long-term risk. Untreated malignant hypertension historically carried a 1-year death rate exceeding 79%, with a median survival of 10.4 months.[3]

Epidemiology

Acute severe hypertension is common in emergency and inpatient settings, but only a minority of patients with markedly elevated blood pressure have hypertensive emergency. A systematic review and meta-analysis of emergency department presentations reported that among patients with hypertensive emergency, the most common acute target organ injuries were ischemic stroke (28.1%), pulmonary edema or acute heart failure (24.1%), hemorrhagic stroke (14.6%), acute coronary syndrome (10.8%), acute renal failure (8.0%), subarachnoid hemorrhage (6.9%), hypertensive encephalopathy (6.1%), and aortic dissection (1.8%).[4] Hypertensive emergencies are more frequent among patients with preexisting uncontrolled hypertension, medication nonadherence, chronic kidney disease, diabetes mellitus, limited access to longitudinal care, and secondary causes of hypertension.[5]

Historical Perspective

The older term malignant hypertension referred to severe hypertension associated with advanced bilateral hypertensive retinopathy, including retinal hemorrhages, cotton-wool spots, and often papilledema. Before effective antihypertensive therapy, malignant hypertension carried a poor prognosis.[6] Because systemic microcirculatory damage is the pathologic hallmark of malignant hypertension and retinal lesions can be absent in some patients with acute renal injury, the term "acute hypertensive microangiopathy" has been proposed as a more mechanistically descriptive term.[6]

Modern terminology emphasizes acute target organ damage rather than blood pressure number alone. The term hypertensive urgency is less favored because it may imply a need for immediate aggressive blood pressure lowering despite the absence of acute target organ damage. The 2024 American Heart Association scientific statement instead uses terms such as asymptomatic markedly elevated blood pressure for severe blood pressure elevation without new or worsening target organ damage.[2]

Classification

Hypertensive emergency can be classified by the affected target organ system.

Category Target organ Common clinical syndromes
Neurologic Brain Hypertensive encephalopathy, posterior reversible encephalopathy syndrome, intracranial hemorrhage, subarachnoid hemorrhage, ischemic stroke
Cardiac Heart Acute coronary syndrome, acute heart failure, pulmonary edema, myocardial injury
Aortic / vascular Aorta and large vessels Aortic dissection, acute aortic syndrome, penetrating aortic ulcer
Renal Kidney Acute kidney injury, acute glomerular injury, malignant nephrosclerosis
Microangiopathic / retinal Microvasculature, retina Thrombotic microangiopathy, microangiopathic hemolytic anemia, retinal hemorrhage, papilledema
Pregnancy-related Maternal-fetal unit and maternal organs Severe preeclampsia, eclampsia, HELLP syndrome
Catecholamine-mediated Multiple organs Pheochromocytoma crisis, cocaine toxicity, amphetamine toxicity, clonidine withdrawal
Term Blood pressure pattern Acute target organ damage Usual management implication
Hypertensive emergency Usually SBP >180 mm Hg and/or DBP >120 mm Hg Present Emergency evaluation, parenteral titratable therapy, monitored setting or intensive care unit
Asymptomatic markedly elevated blood pressure Usually SBP >180 mm Hg and/or DBP >110-120 mm Hg Absent Confirm measurement, assess causes, restart or adjust oral therapy, arrange follow-up, avoid rapid intravenous lowering
Elevated inpatient blood pressure SBP ≥130 mm Hg and/or DBP ≥80 mm Hg Absent Reassess technique and clinical context; avoid reflexive acute treatment unless clinically indicated

Causes

Most hypertensive emergencies occur in patients with chronic hypertension, especially when long-term blood pressure control is poor. Common precipitants include medication nonadherence, inadequate antihypertensive regimen intensity, excess dietary sodium, pain, anxiety, volume overload, withdrawal of antihypertensive drugs during hospitalization, use of nonsteroidal anti-inflammatory drugs, high-dose glucocorticoids, sympathomimetic drugs, cocaine, amphetamines, and abrupt withdrawal of clonidine or beta blocker therapy.[7] Medication nonadherence is a common precipitating factor; rates of nonadherence for patients with treatment-resistant hypertension and hypertensive crisis range from 50% to 80%.[5]

Secondary causes should be considered when hypertensive emergency occurs in a young patient, in a patient without known hypertension, in recurrent hypertensive emergencies, or in apparent resistant hypertension. Important secondary causes include renovascular hypertension, primary aldosteronism, pheochromocytoma, Cushing syndrome, coarctation of the aorta, acute glomerulonephritis, scleroderma renal crisis, obstructive sleep apnea, and drug-induced hypertension.[1] Among hospitalized patients, common inpatient precipitants include mobilization of infused intravenous fluids, withholding of antihypertensive medications, pain, and urinary retention.[2]

Differentiating Hypertensive Emergency from Other Diseases

The most important diagnostic distinction is whether the patient has acute target organ damage. A markedly elevated blood pressure alone does not establish hypertensive emergency. The BARKH acronym (Brain, Arteries, Retina, Kidney, Heart) may assist in quickly identifying potential target organs at risk.

Condition Key distinguishing features Clues against hypertensive emergency
Hypertensive emergency Severe blood pressure elevation with new or worsening acute target organ damage None; requires syndrome-specific evaluation and treatment
Asymptomatic markedly elevated blood pressure Severe blood pressure elevation without symptoms or objective acute organ injury Normal neurologic examination, no pulmonary edema, no ischemic symptoms, no acute kidney injury, no retinal emergency findings
Pain-, anxiety-, or withdrawal-associated blood pressure elevation Blood pressure elevation temporally associated with pain, agitation, alcohol withdrawal, opioid withdrawal, or medication withdrawal Blood pressure improves after treating the precipitating condition; no objective acute organ injury
White coat hypertension Office blood pressure elevated with normal out-of-office readings Confirmed by home or ambulatory blood pressure monitoring
Pseudohypertension Falsely elevated cuff pressure, usually from noncompressible calcified arteries in older adults Symptoms of hypotension despite high cuff readings; consider confirmation in selected cases

Differential diagnosis by presentation

Presentation Hypertensive emergency syndrome Alternative diagnoses to consider
Altered mental status, headache, seizure, visual symptoms Hypertensive encephalopathy, posterior reversible encephalopathy syndrome Intracranial hemorrhage, ischemic stroke, subarachnoid hemorrhage, meningitis, encephalitis, seizure, hypoglycemia, toxic-metabolic encephalopathy
Focal neurologic deficit Ischemic stroke or intracranial hemorrhage with severe hypertension Stroke from embolic, thrombotic, hemorrhagic, or structural causes; blood pressure elevation may be reactive
Chest pain Acute coronary syndrome, aortic dissection Pulmonary embolism, pericarditis, pneumothorax, esophageal disease, musculoskeletal pain
Dyspnea Pulmonary edema, acute heart failure Pneumonia, pulmonary embolism, asthma, chronic obstructive pulmonary disease exacerbation, acute respiratory distress syndrome
Acute kidney injury, hematuria, proteinuria Hypertensive renal emergency, malignant hypertension, thrombotic microangiopathy Acute glomerulonephritis, vasculitis, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, scleroderma renal crisis, obstructive uropathy
Severe hypertension in pregnancy or postpartum period Severe preeclampsia, eclampsia, HELLP syndrome Chronic hypertension, gestational hypertension, acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura, antiphospholipid syndrome

Pathophysiology

The pathophysiology of hypertensive emergency involves abrupt failure of vascular autoregulation, endothelial injury, inflammatory activation, and microvascular ischemia. A rapid rise in blood pressure increases shear stress on the vascular wall, producing endothelial dysfunction, increased vascular permeability, platelet activation, fibrin deposition, and tissue ischemia.[8] Activation of the renin-angiotensin-aldosterone system further increases vasoconstriction and sodium retention, while angiotensin II promotes oxidative stress, inflammatory signaling via nuclear factor-κB (NF-κB), and additional vascular injury.[8]

Microvascular Injury

In the kidney, myointimal thickening of afferent arterioles results in luminal narrowing and further activation of the renin-angiotensin-aldosterone system, which increases blood pressure and aggravates vascular injury. Hallmarks of malignant hypertension include myointimal proliferation of arterioles and fibrinoid necrosis caused by leakage of fibrin through a necrotic vessel wall. Activation of prothrombotic and proinflammatory pathways may give rise to thrombotic microangiopathy.[6]

Cerebral Autoregulation

In chronic hypertension, the cerebral autoregulation curve shifts to the right. This adaptation allows tolerance of higher perfusion pressures but increases vulnerability to cerebral hypoperfusion if blood pressure is reduced too quickly. In hypertensive encephalopathy, severe pressure elevation exceeds autoregulatory capacity, leading to blood-brain barrier disruption, vasogenic edema, and neurologic symptoms. The lower limit of cerebral autoregulation may be reached when blood pressure is reduced by approximately 25%, and cerebral ischemia or infarction may be precipitated by more rapid or excessive reductions.[9]

Diagnosis

Diagnosis requires confirmation of markedly elevated blood pressure and systematic assessment for acute target organ damage. Blood pressure should be repeated using an appropriately sized cuff and correct technique. Testing should be guided by symptoms and the suspected organ system involved. Routine broad testing in asymptomatic patients without signs of target organ damage is not always necessary, but suspected hypertensive emergency warrants urgent evaluation.[2]

History

The history should assess prior hypertension diagnosis, usual and recent blood pressure readings, prescribed antihypertensive medications, missed doses, recent medication changes, over-the-counter drugs, recreational drugs, pregnancy or postpartum status, symptoms of organ injury, and possible secondary causes. Symptoms suggesting acute target organ damage include severe headache, confusion, seizure, visual disturbance, focal weakness, chest pain, tearing chest or back pain, dyspnea, orthopnea, oliguria, hematuria, and severe epigastric or right upper quadrant pain in pregnancy.

Physical Examination

The physical examination should include repeated blood pressure measurement using correct cuff size and technique, blood pressure measurement in both arms when feasible, assessment for pulse deficits, cardiopulmonary examination, volume status assessment, neurologic examination, pregnancy assessment when applicable, and fundoscopy to evaluate for retinal hemorrhage, cotton-wool spots, or papilledema.

Diagnostic Workup

Test Purpose
Basic metabolic panel Evaluate creatinine, acute kidney injury, potassium, sodium, metabolic abnormalities
Urinalysis and urine protein assessment Evaluate proteinuria, hematuria, urinary casts, renal parenchymal injury
Complete blood count Evaluate anemia, leukocytosis, thrombocytopenia
Lactate dehydrogenase, haptoglobin, bilirubin, peripheral blood smear Evaluate hemolysis, schistocytes, and thrombotic microangiopathy
Troponin Evaluate myocardial injury or acute coronary syndrome
BNP/NT-proBNP Evaluate for heart failure
Electrocardiogram Evaluate myocardial ischemia, arrhythmia, left ventricular hypertrophy
Chest radiograph Evaluate pulmonary edema, cardiomegaly, widened mediastinum
Echocardiography Evaluate ventricular function, regional wall motion abnormality, severe valvular disease, selected aortic pathology
Computed tomography of the head Evaluate acute neurologic symptoms for intracranial hemorrhage, mass effect, or stroke mimics
Computed tomography angiography of the chest, abdomen, and pelvis Evaluate suspected aortic dissection or acute aortic syndrome
Pregnancy testing Evaluate pregnancy-related hypertensive emergency in persons of reproductive potential

Treatment

Treatment depends on the type of acute target organ damage. Excessively rapid blood pressure reduction can cause cerebral, myocardial, or renal hypoperfusion, especially in patients with chronic hypertension. Selection of treatment should be driven by the clinical syndrome, the desired speed of reduction, contraindications, and drug pharmacology.[2]

Initial Management

Patients with hypertensive emergency should generally receive care in a monitored setting, often an intensive care unit, with frequent or continuous blood pressure monitoring and titratable intravenous antihypertensive therapy.[1] Intra-arterial blood pressure monitoring may be used in patients receiving potent vasodilators or in whom accurate continuous measurement is required.

Blood Pressure Targets

Clinical scenario Initial blood pressure target Timeframe / comments
Hypertensive emergency without a compelling condition Reduce SBP by no more than 25% First hour
Hypertensive emergency without a compelling condition, after initial reduction If stable, reduce toward approximately 160/100 mm Hg Next 2-6 hours
Hypertensive emergency without a compelling condition, after stabilization Cautiously reduce toward usual long-term goals Next 24-48 hours
Aortic dissection or acute aortic syndrome SBP <120 mm Hg and heart rate 60-80 beats/min, while maintaining end-organ perfusion As rapidly as tolerated, usually within the first hour; beta blockade before vasodilator therapy is preferred[10]
Intracerebral hemorrhage with presenting SBP 150-220 mm Hg Smoothly lower SBP to a target range of 130-140 mm Hg when clinically appropriate; avoid lowering SBP below 130 mm Hg Early treatment with careful titration is reasonable in mild-to-moderate spontaneous ICH[11]
Intracerebral hemorrhage with presenting SBP >220 mm Hg Use careful, titratable intravenous therapy and avoid excessive reduction Consider continuous infusion and frequent monitoring; avoid blood pressure variability[11]
Ischemic stroke eligible for intravenous thrombolysis Lower BP to <185/110 mm Hg before thrombolysis; maintain BP <180/105 mm Hg for the first 24 hours after treatment Avoid intensive SBP lowering to <140 mm Hg after intravenous thrombolysis[12]
Ischemic stroke not receiving thrombolysis or thrombectomy Usually permissive hypertension unless BP is >220/120 mm Hg or another emergency indication exists If treatment is needed, lower cautiously, often by approximately 15% during the first 24 hours[12]
Severe hypertension in pregnancy or postpartum period Treat persistent SBP ≥160 mm Hg or DBP ≥110 mm Hg; commonly target SBP 140-150 mm Hg and DBP 90-100 mm Hg during acute treatment Treat as soon as reasonably possible, ideally within 30-60 minutes after confirmed severe hypertension[13]
Severe hypertension without acute target organ damage Avoid rapid intravenous BP lowering Confirm BP, evaluate for symptoms or organ injury, restart or adjust oral therapy, and arrange follow-up[2]

Excessive BP reduction can cause harm. If excessive BP reduction occurs, intravenous antihypertensive therapy should be reduced or discontinued, and selected patients may require intravenous fluids, vasopressors, or other supportive measures.[2]

Medical Therapy

To achieve rapid BP control and avoid large swings in BP, continuous infusion of short-acting titratable antihypertensive agents is often preferable in the intensive care setting. Hydralazine has unpredictable effects and may lead to excessive BP lowering; it is generally not preferred outside pregnancy-related severe hypertension.

Intravenous Antihypertensive Agents

Drug Class Common dosing approach Useful situations Important cautions
Nicardipine Dihydropyridine calcium channel blocker 5 mg/hour IV infusion; increase by 2.5 mg/hour every 5-15 minutes; maximum 15 mg/hour Most hypertensive emergencies, neurologic emergencies Avoid or use caution in advanced aortic stenosis; may cause reflex tachycardia
Clevidipine Ultra-short-acting dihydropyridine calcium channel blocker 1-2 mg/hour IV infusion; titrate rapidly until near target; maximum 32 mg/hour; maximum duration 72 hours Rapid titration, perioperative hypertension, neurologic or cardiac settings Contraindicated in soy or egg allergy and disorders of lipid metabolism; use low-end dose range for older adults
Labetalol Combined alpha-1 and nonselective beta blocker 10-20 mg IV bolus, then 20-80 mg every 10 minutes as needed, or 0.5-2 mg/min infusion; maximum cumulative 300 mg/24 h Pregnancy, neurologic emergencies, adrenergic hypertension, aortic dissection when appropriate Avoid in asthma, bradycardia, heart block, or decompensated heart failure
Esmolol Short-acting beta-1 blocker 500 mcg/kg loading dose over 1 minute, then 50-300 mcg/kg/min infusion Aortic dissection, perioperative hypertension, tachycardia-driven hypertension Avoid in decompensated heart failure, severe bradycardia, heart block
Nitroglycerin Venous and coronary vasodilator 5-10 mcg/min IV infusion; titrate by 5 mcg/min every 3-5 minutes; maximum 200 mcg/min Acute coronary syndrome, pulmonary edema Headache, tachyphylaxis, hypotension; limited arterial effect at low doses; contraindicated with recent PDE-5 inhibitor use
Sodium nitroprusside Direct arterial and venous vasodilator 0.3-0.5 mcg/kg/min IV infusion; titrate carefully; usual maximum 10 mcg/kg/min for short duration; thiosulfate can be coadministered for high-dose or prolonged infusion Selected refractory cases requiring immediate titration Cyanide and thiocyanate toxicity; avoid or use extreme caution in renal/hepatic failure and pregnancy; invasive monitoring often preferred
Hydralazine Direct arterial vasodilator 5-10 mg IV or IM; repeat every 4-6 hours as needed; maximum 200 mg/24 h Pregnancy-related severe hypertension when selected Unpredictable and prolonged response; reflex tachycardia; generally not preferred outside pregnancy
Fenoldopam Dopamine-1 receptor agonist 0.1 mcg/kg/min IV infusion; increase by 0.05-0.1 mcg/kg/min every 15 min; maximum 1.6 mcg/kg/min Hypertensive emergency with renal dysfunction in selected patients Avoid in glaucoma and sulfite allergy; may cause tachycardia, headache, hypokalemia
Phentolamine Nonselective alpha-adrenergic blocker 5 mg IV bolus; repeat every 10 min as needed; maximum 50 mg/24 h Pheochromocytoma crisis, catecholamine excess, cocaine or amphetamine toxicity Tachycardia, orthostatic hypotension

Preferred Agents by Clinical Scenario

Clinical scenario Preferred or commonly used agents Agents to avoid or use cautiously
Aortic dissection Esmolol or labetalol first; add nicardipine or sodium nitroprusside only after heart rate control if SBP remains high Avoid vasodilator monotherapy because reflex tachycardia can increase aortic shear stress
Acute coronary syndrome Nitroglycerin, labetalol, esmolol when no contraindication Avoid excessive DBP reduction that may impair coronary perfusion; avoid beta blockers in acute decompensated heart failure or shock; avoid hydralazine
Acute pulmonary edema Nitroglycerin, sodium nitroprusside, clevidipine, nicardipine depending on context; loop diuretics are often needed when volume overload is present Avoid beta blocker initiation during acute decompensated heart failure unless otherwise indicated and stable
Hypertensive encephalopathy / posterior reversible encephalopathy syndrome Nicardipine, clevidipine, labetalol Avoid rapid overcorrection; avoid hydralazine when possible
Intracerebral hemorrhage Nicardipine, clevidipine, labetalol Avoid blood pressure variability and avoid lowering SBP below 130 mm Hg in mild-to-moderate ICH with presenting SBP 150-220 mm Hg
Ischemic stroke eligible for reperfusion therapy Nicardipine, clevidipine, labetalol Avoid intensive post-thrombolysis SBP lowering to <140 mm Hg
Ischemic stroke not receiving reperfusion therapy Generally permissive hypertension unless BP >220/120 mm Hg or another emergency indication exists If treatment is needed, lower cautiously by approximately 15% during the first 24 hours
Diffuse microvascular injury / malignant hypertension Labetalol, nicardipine, clevidipine Avoid overly rapid lowering because renal, cerebral, and myocardial hypoperfusion may occur
Pheochromocytoma crisis or sympathomimetic toxicity Phentolamine, nicardipine, clevidipine; benzodiazepines for agitation in sympathomimetic toxicity Avoid beta-blocker monotherapy before alpha blockade in suspected pheochromocytoma crisis; avoid unopposed beta blockade in cocaine toxicity
Severe hypertension in pregnancy/postpartum IV labetalol, IV hydralazine, oral immediate-release nifedipine Avoid ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors, spironolactone, eplerenone, and sodium nitroprusside when possible[14]
Perioperative hypertension Clevidipine, esmolol, nicardipine, nitroglycerin Avoid agents with prolonged duration of action when rapid titration is needed
Acute kidney injury Clevidipine, fenoldopam, nicardipine Avoid sodium nitroprusside in significant renal impairment due to thiocyanate accumulation

Transition to Oral Therapy

Resumption or initiation of long-acting oral antihypertensive drugs should take place once the patient is clinically stable and able to tolerate oral therapy. Oral therapy is commonly started while intravenous therapy is being tapered to provide a smoother transition, reduce the need for intravenous drugs and intensive care, and minimize rebound hypertension.[2]

Procedural / Surgical Therapy

Procedural or surgical therapy is required when hypertensive emergency is caused by a condition that cannot be definitively treated with blood pressure reduction alone:

  • Aortic dissection: Emergent open surgical or endovascular repair may be required depending on anatomy and Stanford type. Stanford type A dissections generally require emergent surgery, in addition to aggressive BP and heart rate control.[10]
  • Pheochromocytoma: Definitive treatment is surgical resection after adequate alpha-blockade and volume repletion.
  • Renovascular hypertension: Percutaneous transluminal angioplasty or stenting may be considered in selected patients with hemodynamically significant renal artery lesions.
  • Coarctation of the aorta: Surgical repair or balloon angioplasty/stenting may be indicated in selected patients.
  • Intracerebral hemorrhage: Neurosurgical intervention may be required for selected patients with cerebellar hemorrhage, hydrocephalus, mass effect, or clinical deterioration.[11]

Long-Term Management

After stabilization, intravenous therapy should be transitioned to an appropriate oral antihypertensive regimen. Long-term management includes:

  • Identification and treatment of the precipitating cause
  • Assessment of medication adherence
  • Simplification of the drug regimen when possible, including single-pill combination therapy and once-daily dosing
  • Home blood pressure monitoring
  • Evaluation for secondary hypertension when indicated
  • Close outpatient follow-up, often within 1 week of discharge
  • Team-based care, patient education, and medication reminder systems to improve adherence and blood pressure control[15]
  • Long-term control of blood pressure to prevent recurrent hypertensive emergencies and improve overall prognosis[16]

Special Populations

Pregnancy and postpartum period

Systolic BP ≥160 mm Hg or diastolic BP ≥110 mm Hg persisting for at least 15 minutes is an obstetric emergency requiring urgent antihypertensive therapy to reduce the risk of maternal stroke. Treatment should be initiated as soon as reasonably possible after confirmation, ideally within 30-60 minutes.[13] Preferred agents include intravenous labetalol, intravenous hydralazine, and oral immediate-release nifedipine. ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors, spironolactone, and eplerenone are contraindicated in pregnancy.[14] Magnesium sulfate is used for seizure prevention and treatment in preeclampsia with severe features and eclampsia. Definitive treatment of severe preeclampsia and eclampsia is delivery of the fetus and placenta when clinically indicated, after maternal stabilization.[17]

Older adults

Older adults may be more vulnerable to excessive blood pressure reduction because of impaired baroreceptor sensitivity, vascular stiffness, frailty, orthostatic hypotension, and reduced cerebral or renal reserve. Therapy should be titrated carefully with attention to mental status, urine output, symptoms of hypoperfusion, and orthostatic blood pressure after stabilization.

Chronic kidney disease

Patients with chronic kidney disease are at higher risk for hypertensive emergency and may have volume overload, secondary hypertension, or medication accumulation. Clevidipine and nicardipine generally do not require dose adjustment in renal impairment. Sodium nitroprusside should be avoided or used with extreme caution in significant renal impairment because of thiocyanate accumulation. Evaluation should include urinalysis, kidney function, electrolytes, and assessment for glomerular disease or renovascular disease when indicated.

Acute stroke

Blood pressure management in acute stroke depends on stroke type and reperfusion eligibility. In spontaneous intracerebral hemorrhage, smooth and sustained control of BP is preferred, and excessive BP variability or lowering below SBP 130 mm Hg should be avoided in patients with mild-to-moderate ICH and presenting SBP 150-220 mm Hg.[11] In ischemic stroke, patients eligible for intravenous thrombolysis should have BP reduced to <185/110 mm Hg before treatment and maintained at <180/105 mm Hg for the first 24 hours after treatment; intensive lowering to <140 mm Hg after thrombolysis is not recommended.[12] Patients not receiving reperfusion therapy are usually managed with permissive hypertension unless BP exceeds 220/120 mm Hg or another hypertensive emergency indication exists.[12]

Prevention

Primary Prevention

Prevention of hypertensive emergency centers on effective long-term management of hypertension. Major preventive strategies include lifestyle modification, pharmacologic therapy when indicated, and reliable follow-up. Lifestyle interventions include a Dietary Approaches to Stop Hypertension (DASH)-style dietary pattern, sodium reduction, regular physical activity, moderation of alcohol intake, weight management when appropriate, and avoidance of substances that raise blood pressure.[1] Home blood pressure monitoring can improve detection of uncontrolled hypertension and support medication titration.[1]

Secondary Prevention (Preventing Recurrence)

Medication nonadherence is a common precipitant of hypertensive emergency, with nonadherence rates of 50% to 80% in patients with treatment-resistant hypertension and hypertensive crisis.[5] Evidence-based adherence strategies include:

  • Once-daily dosing when possible
  • Single-pill combination therapy to reduce pill burden
  • Medication reminder aids
  • Education and coaching by pharmacists and other health professionals
  • Electronic or home blood pressure monitoring with feedback
  • Shared decision-making that incorporates patient preferences and values
  • Medication synchronization
  • Screening for low health literacy and providing targeted education
  • Addressing cost, access, transportation, and other social determinants of health barriers[15]

Avoidance of Precipitants

Special Populations

Population Key considerations
Pregnancy and postpartum period Persistent SBP ≥160 mm Hg or DBP ≥110 mm Hg requires urgent treatment; assess for preeclampsia, eclampsia, and HELLP syndrome.[13]
Chronic kidney disease Evaluate for renal parenchymal disease, volume overload, renovascular disease, and thrombotic microangiopathy; avoid nephrotoxic precipitants and avoid nitroprusside when possible in advanced renal dysfunction.
Acute neurologic symptoms Determine whether severe hypertension is the cause of neurologic injury or a physiologic response to stroke; treatment targets differ by stroke subtype and reperfusion plan.[11][12]
Catecholamine excess Treat agitation, pain, and catecholamine-mediated vasoconstriction; avoid beta-blocker monotherapy when pheochromocytoma crisis is suspected.
Older adults and frail patients Lower blood pressure cautiously and monitor for orthostatic hypotension, renal hypoperfusion, and neurologic change.
Black patients and underserved populations Higher burden of uncontrolled hypertension and hypertensive crises is linked to structural barriers, access to care, medication cost, and comorbidity burden; prevention requires longitudinal blood pressure control and adherence support.

Prognosis

Untreated malignant hypertension historically had very poor survival, with a 1-year death rate exceeding 79% and median survival of 10.4 months.[3] Modern treatment has improved prognosis, but hypertensive emergency remains associated with substantial morbidity and mortality. In a systematic review and meta-analysis, neurologic and cardiopulmonary presentations accounted for a large proportion of emergency department hypertensive emergencies.[4] Poor prognostic features include older age, higher creatinine, lower hemoglobin, thrombotic microangiopathy, intracerebral hemorrhage, aortic dissection, acute heart failure, and multiorgan involvement.[16] Prevention of recurrence depends on sustained outpatient blood pressure control, medication adherence, treatment of secondary causes, and timely follow-up after discharge.[15]

Indications for Referral

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Jones DW, Ferdinand KC, Taler SJ, Johnson HM, Shimbo D, Abdalla M, Bello NA, Charchar FJ, Khera A, Lambert E, Lloyd-Jones DM, Ndumele CE, Thomas G, Van Spall H, Wozniak G (2025). "2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults". Hypertension. 82 (10): e212–e316. doi:10.1161/HYP.0000000000000249. PMID 40811516 Check |pmid= value (help). Vancouver style error: initials (help)
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Bress AP, Anderson TS, Flack JM, Garg R, Gidding SS, Kramer HJ, Lackland DT, Muntner P, Rakotz MK, Rosendorff C, Schwartz JE, Smith SC Jr, Taler SJ, Wozniak G, Whelton PK (2024). "The Management of Elevated Blood Pressure in the Acute Care Setting: A Scientific Statement From the American Heart Association". Hypertension. 82 (4): e94–e118. doi:10.1161/HYP.0000000000000238. PMID 38804130 Check |pmid= value (help).
  3. ↑ 3.0 3.1 Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC Jr, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA Sr, Williamson JD, Wright JT Jr (2018). "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". J Am Coll Cardiol. 71 (19): e127–e248. doi:10.1016/j.jacc.2017.11.006. PMID 29133356.
  4. ↑ 4.0 4.1 Siddiqi TJ, Usman MS, Rashid AM, Khan MS, Sreenivasan J, Greene SJ, Butler J, Mamas MA, Fonarow GC (2023). "Clinical Outcomes in Hypertensive Emergency: A Systematic Review and Meta-Analysis". Journal of the American Heart Association. 12 (14): e029213. doi:10.1161/JAHA.123.029213. PMID 37421281 Check |pmid= value (help).
  5. ↑ 5.0 5.1 5.2 Krämer BK, Krämer RM, Benck U, Krüger B (2019). "Nonadherence in patients with hypertensive emergency or hypertensive urgency". Journal of Clinical Hypertension. 21 (1): 36–43. doi:10.1111/jch.13464. PMID 30548984.
  6. ↑ 6.0 6.1 6.2 Boulestreau R, Śpiewak M, Januszewicz A, Prejbisz A, Williams B, Amar L, Azizi M, Lorthioir A (2024). "Malignant Hypertension: A Systemic Cardiovascular Disease: JACC Review Topic of the Week". Journal of the American College of Cardiology. 83 (17): 1660–1673. doi:10.1016/j.jacc.2024.02.024. PMID 38359858 Check |pmid= value (help).
  7. ↑ Peixoto AJ (2019). "Acute Severe Hypertension". N Engl J Med. 381 (19): 1843–1852. doi:10.1056/NEJMcp1901117. PMID 31657794.
  8. ↑ 8.0 8.1 Vaughan CJ, Delanty N (2000). "Hypertensive emergencies". Lancet. 356 (9227): 411–417. doi:10.1016/S0140-6736(00)02539-3. PMID 10917387.
  9. ↑ Calhoun DA, Oparil S (1990). "Treatment of hypertensive crisis". N Engl J Med. 323 (17): 1177–1183. doi:10.1056/NEJM199010253231707. PMID 2215562.
  10. ↑ 10.0 10.1 Isselbacher EM, Preventza O, Hamilton Black J 3rd, Augoustides JG, Beck AW, Bolen MA, Braverman AC, Bray BE, Brown-Zimmerman MM, Chen EP, Collins TJ, DeAnda A Jr, Fanola CL, Girardi LN, Hicks CW, Hui DS, Jones WS, Kalahasti V, Kim KM, Milewicz DM, Oderich GS, Ogbechie L, Promes SB, Rodriguez-Lopez JA, Ross EG, Schermerhorn ML, Schofield RS, Shih T, Thourani VH, Tseng EE, Wang GJ, Woo YJ (2022). "2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease". J Am Coll Cardiol. 80 (24): e223–e393. doi:10.1016/j.jacc.2022.08.004. PMID 36322642 Check |pmid= value (help).
  11. ↑ 11.0 11.1 11.2 11.3 11.4 Greenberg SM, Ziai WC, Cordonnier C, Dowlatshahi D, Francis B, Goldstein JN, Hemphill JC 3rd, Johnson R, Keigher KM, Mack WJ, Mocco J, Newton EJ, Ruff IM, Sansing LH, Schulman S, Selim MH, Sheth KN, Sprigg N, Sunnerhagen KS (2022). "2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the American Heart Association/American Stroke Association". Stroke. 53 (7): e282–e361. doi:10.1161/STR.0000000000000407. PMID 35579034 Check |pmid= value (help).
  12. ↑ 12.0 12.1 12.2 12.3 12.4 Prabhakaran S, Rabinstein AA, Ackerson T, Adeoye OM, Bambakidis NC, Becker K, Biller J, Brown M, Demaerschalk BM, Hoh B, Jauch EC, Levine SR, Lyden PD, Mack WJ, Madsen TE, Messé SR, Powers WJ, Schwamm LH, Sheth KN, Southerland AM, Tirschwell DL (2026). "2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association". Stroke. doi:10.1161/STR.0000000000000513. PMID 41582814 Check |pmid= value (help).
  13. ↑ 13.0 13.1 13.2 American College of Obstetricians and G (2019). "ACOG Committee Opinion No. 767: Emergent Therapy for Acute-Onset, Severe Hypertension During Pregnancy and the Postpartum Period". Obstet Gynecol. 133 (2): e174–e180. doi:10.1097/AOG.0000000000003075. PMID 30575639. Vancouver style error: initials (help)
  14. ↑ 14.0 14.1 Halpern DG, Weinberg CR, Pinnelas R, Mehta B, Garan H, Landy DC, Siu SC (2019). "Use of Medication for Cardiovascular Disease During Pregnancy: JACC State-of-the-Art Review". J Am Coll Cardiol. 73 (4): 457–476. doi:10.1016/j.jacc.2018.10.075. PMID 30674457.
  15. ↑ 15.0 15.1 15.2 Choudhry NK, Kronish IM, Vongpatanasin W, Ferdinand KC, Pavlik VN, Egan BM, Schoenthaler A, Houston Miller N, Hyman DJ (2022). "Medication Adherence and Blood Pressure Control: A Scientific Statement From the American Heart Association". Hypertension. 79 (1): e1–e14. doi:10.1161/HYP.0000000000000203. PMID 35766033 Check |pmid= value (help).
  16. ↑ 16.0 16.1 Miller JB, Hrabec D, Krishnamoorthy V, Kinni H, Brook RD (2024). "Evaluation and Management of Hypertensive Emergency". BMJ. 386: e077205. doi:10.1136/bmj-2023-077205. PMID 39059997 Check |pmid= value (help).
  17. ↑ American College of Obstetricians and G (2020). "Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin, Number 222". Obstet Gynecol. 135 (6): e237–e260. doi:10.1097/AOG.0000000000003891. PMID 32443079 Check |pmid= value (help). Vancouver style error: initials (help)


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