Acute Hypertension

Overview – Acute Hypertension

Acute hypertension refers to a sudden, severe elevation in blood pressure that may present with or without target organ damage. While most chronic hypertension is asymptomatic, acute hypertensive episodes—especially hypertensive crises—can be life-threatening. Early recognition and careful blood pressure control are essential to reduce the risk of cerebral, cardiac, and renal complications.

Aetiology

Primary (Essential) Hypertension – ~95%

• Idiopathic origin; likely multifactorial and not curable
• Risk factors:
  • Family history, age
  • High-salt and high-cholesterol diet
  • Obesity, diabetes mellitus
  • Smoking and alcohol use
  • Stress

Subtypes

• Isolated Diastolic Hypertension
  • More common in older men
• Isolated Systolic Hypertension
  • In young adults: Often due to increased sympathetic drive and elevated cardiac output
  • In older adults: Due to decreased arterial compliance (e.g. fibrosis, calcification)

Secondary Hypertension – ~5%

• Cardiovascular: Coarctation of the aorta, hypervolaemia, rigid vessels
• Renal:
  • Acute glomerulonephritis
  • Chronic kidney disease
  • Polycystic kidney disease
  • Renal artery stenosis
• Endocrine:
  • Hyperadrenalism (e.g. Cushing’s syndrome)
  • Acromegaly
  • Thyroid dysfunction
  • Phaeochromocytoma
• Neurological:
  • Raised intracranial pressure
  • Psychogenic causes
  • Sleep apnoea
  • Acute stress
• Pregnancy-related:
  • Pre-eclampsia: Placental ischaemia triggers release of vasoactive mediators → maternal hypertension as compensation

Hypertensive Crisis (Malignant Hypertension)

Definition

A hypertensive crisis is a medical emergency characterised by severely elevated blood pressure (>200/120 mmHg) accompanied by signs of end-organ damage.

End-Organ Manifestations

• Retinopathy:
  • Papilloedema
  • Flame haemorrhages
  • Optic disc swelling
• Brain:
  • Hypertensive encephalopathy
  • Mental status changes
  • Risk of stroke or cerebral oedema
• Kidneys:
  • Acute kidney injury (elevated creatinine)
• Heart:
  • Pulmonary oedema
  • Congestive heart failure

Common Triggers

• Abrupt withdrawal of antihypertensive therapy
• Sympathetic overactivity
• Drug use (e.g. cocaine, amphetamines)
• Glomerulonephritis
• Head trauma
• Tumours (e.g. phaeochromocytoma)
• Pre-eclampsia

Pathophysiology

• Thought to involve failure of vascular autoregulation
• Sudden spike in systemic vascular resistance
• Vicious cycle of escalating vascular damage, ischaemia, and organ dysfunction

Symptoms

• Severe headache
• Confusion or drowsiness
• Visual disturbances (e.g. blurred vision due to papilloedema)
• Nausea and vomiting

Management

• Goal: Gradual reduction of BP to ~150/90 mmHg over 24–36 hours
• Rapid BP drops can precipitate ischaemia in coronary, cerebral, or renal circulations
• Management must be guided by local protocols and the presence of end-organ damage

Disclaimer: Always refer to local or hospital-specific guidelines when managing hypertensive crises.

Summary – Acute Hypertension

Acute hypertension may be due to primary or secondary causes and can escalate into a hypertensive crisis with rapid-onset vascular damage. Recognising high-risk features such as altered mental status, retinopathy, and renal dysfunction is essential. Management focuses on controlled blood pressure reduction to prevent organ ischaemia. For a broader context, see our Emergency Medicine Overview page.