Molecular structure pattern

Hypertensive Crisis Disease Background

Last updated: 28 August 2026
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Introduction

Hypertensive crisis refers to a severe, acute increase in blood pressure (BP) and is classified as hypertensive emergency and acute severe hypertension (formerly hypertensive urgency). It is important to note that the clinical differentiation between hypertensive emergency and acute severe hypertension is dependent on the presence of target organ damage rather than the level of BP.  For successful management of patients, it is necessary to differentiate hypertensive emergency from acute severe hypertension.

Hypertensive Emergency

Hypertensive emergency is severely elevated BP (systolic BP [SBP] >180 mmHg and/or diastolic BP [DBP] >120 mmHg) that is complicated by progressive or worsening target organ damage of the central nervous system (CNS), heart, kidneys, lungs, large arteries, retina, or the gravid uterus. There is no definite BP threshold for the diagnosis of hypertensive emergency.  Most target organ damage happens with DBP ≥130 mmHg. This is a potentially life-threatening condition requiring prompt diagnosis, immediate treatment (eg usually with titratable intravenous [IV] antihypertensive therapy) and hospital admission for close monitoring. 

Clinical Conditions or Associated Target Organ Damage that Meet the Diagnostic Criteria for Hypertensive Emergency

  • Acute left ventricular (LV) failure with pulmonary edema
  • Acute coronary syndrome (ACS)
  • Acute renal failure
  • Crisis associated with pheochromocytoma
  • Dissecting aortic aneurysm
  • Hypertensive encephalopathy
  • Intracranial hemorrhage or cerebrovascular accident (CVA)
  • Illicit drug use (eg amphetamines, cocaine)
  • Perioperative hypertension
  • Severe preeclampsia/eclampsia
  • Symptomatic microangiopathic hemolytic anemia
  • Malignant hypertension with advanced retinopathy, with or without thrombotic microangiopathy or acute renal failure

 

Acute Severe Hypertension

Acute severe hypertension refers to patients with severely elevated BP (>180 mmHg/120 mmHg) but with no evidence of acute hypertension-mediated organ (HMOD) damage, usually asymptomatic with a mild headache. Frequently associated with non-compliance with or discontinuing or decreasing treatment, as well as anxiety, acute pain, emotional stress, or non-adherence to a low-sodium diet. Management generally consists of gradually lowering BP with oral antihypertensive medications over several hours to days in a controlled outpatient setting.

Epidemiology

Hypertension affects approximately 1.3 billion individuals worldwide, yet only about 17-20% achieve adequate BP control.  It is estimated that approximately 1-2% of individuals with hypertension will experience a hypertensive crisis because of untreated or inadequately controlled BP.  Findings regarding gender differences among patients with hypertensive emergencies have been inconsistent. Most published studies report a higher prevalence of hypertensive crisis among women; however, many of these studies included patients with eclampsia. Other studies indicate that men account for a slightly higher proportion of hypertensive emergency cases than women.

Black patients comprise the largest proportion of hospital admissions for hypertensive emergency, followed by White and Hispanic patients. The prevalence of hypertensive emergencies in Asia differed across countries and regions and was lower compared to Western countries. Cross-sectional and retrospective studies in South and Southeast Asia report that hypertensive emergencies in emergency departments occur in approximately 0.1–0.5% of cases.

Pathophysiology

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Chronic uncontrolled hypertension causes long-term endothelial injury characterized by oxidative stress and reduced nitric oxide production. Progressive arteriolar thickening and atherosclerosis result in vascular narrowing and decreased arterial compliance, including within the cerebral circulation. In hypertensive emergency, the loss of vascular autoregulation increases peripheral vascular resistance and causes microcirculatory damage. The activation of the renin-angiotensin system, vasoconstriction, pressure-induced natriuresis and volume depletion further amplify BP elevation, creating a self-perpetuating cycle that ultimately leads to acute HMOD.

Etiology

The etiology of hypertensive crisis includes non-adherence to, withdrawal of, or inadequate response to antihypertensive therapy; drug interactions, overdose, or exposure to sympathomimetic agents; and secondary hypertension caused by renal (eg renovascular diseases, renal parenchymal disorders), endocrine (eg pheochromocytoma, Cushing disease, primary hyperaldosteronism, renin-secreting tumors), cardiovascular (eg coarctation of the aorta), or neurologic disease (eg cerebral infarction, intracerebral hemorrhage, head injury). It may also result from physiologic or psychosocial stressors, including acute pain, severe emotional stress, and anxiety, as well as substance use and withdrawal and excessive alcohol consumption.

Risk Factors

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Risk factors for hypertensive crisis largely overlap with those of cardiovascular disease, including chronic kidney disease, renovascular hypertension, coronary artery disease, heart failure, prior stroke, alcohol consumption, and recreational drug use. Hypertensive emergencies are also commonly associated with comorbid conditions such as diabetes, hyperlipidemia, and chronic kidney disease. Among patients with acute severe hypertension, the presence of advanced age (>60 years old), male sex, chronic kidney disease, and proteinuria are risk factors necessitating close monitoring, though management can be done in an outpatient setting.