What is a hypertensive emergency, its etiology, pathophysiology, signs, symptoms, diagnosis, treatment, potential complications, and relevant red flags?

Hypertensive Emergency: Definition, Etiology, Pathophysiology, Diagnosis, and Management

A hypertensive emergency is defined as severely elevated blood pressure (often >180/120 mmHg) associated with acute hypertension-mediated organ damage requiring immediate intervention to prevent progressive organ failure. 1, 2

Definition

• Hypertensive emergency is characterized by the presence of target organ damage rather than by specific blood pressure thresholds 1, 2
• Distinguished from hypertensive urgency, which involves severely elevated blood pressure without evidence of acute end-organ damage 3
• Without treatment, hypertensive emergencies carry a 1-year mortality rate >79% and median survival of only 10.4 months 2

Etiology & Pathophysiology

• Common causes include medication non-adherence, inadequate therapy, or abrupt discontinuation of antihypertensive medications 2
• Secondary causes are found in 20-40% of patients with malignant hypertension 1
• Contributing factors include use of sympathomimetics, cocaine, NSAIDs, steroids, immunosuppressants, and antiangiogenic therapy 1
• Pathophysiologically involves failure of autoregulatory mechanisms leading to endothelial injury, increased vascular permeability, activation of coagulation cascade, and fibrinoid necrosis of arterioles 4
• Renin-angiotensin system activation is highly variable in malignant hypertension, making blood pressure response to medications unpredictable 2

Signs & Symptoms

• Presentations vary based on the affected organ systems 1
• Common symptoms include headache, visual disturbances, chest pain, dyspnea, neurological symptoms, and dizziness 1
• Specific clinical presentations include:
  • Malignant hypertension: Severe BP elevation with advanced bilateral retinopathy (hemorrhages, cotton wool spots, papilledema) 1
  • Hypertensive encephalopathy: Severe BP elevation with lethargy, seizures, cortical blindness, and coma 1
  • Hypertensive thrombotic microangiopathy: Severe BP elevation with hemolysis and thrombocytopenia 1
  • Other presentations: Cerebral hemorrhage, acute stroke, acute coronary syndrome, cardiogenic pulmonary edema, aortic dissection, and severe preeclampsia/eclampsia 1

Diagnosis & Evaluation

• Diagnosis requires evidence of acute target organ damage in the setting of severely elevated blood pressure 2
• Thorough history should assess preexisting hypertension, onset and duration of symptoms, and potential causes 1
• Physical examination should focus on cardiovascular and neurological assessment 1
• Essential laboratory tests include:
  • Complete blood count (hemoglobin, platelets) 1, 2
  • Renal function tests (creatinine, BUN, electrolytes) 1, 2
  • Lactate dehydrogenase (LDH) and haptoglobin to detect hemolysis 1, 2
  • Urinalysis for protein and urine sediment examination 1, 2
  • Troponins in patients with chest pain 1, 2
• Additional investigations based on clinical presentation:
  • Fundoscopy to assess for hypertensive retinopathy 1
  • ECG to evaluate for cardiac involvement 1, 2
  • Chest X-ray for congestion/fluid overload 1
  • Echocardiogram for cardiac structure and function 1
  • CT/MRI brain for cerebral hemorrhage/stroke 1
  • CT-angiography thorax/abdomen for acute aortic disease 1

Interventions / Treatments

• Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous blood pressure monitoring and parenteral antihypertensive administration. 2, 3

• Treatment goals vary by specific organ damage:

  • General approach: Reduce mean arterial pressure by 20-25% within the first hour, except in specific conditions 3
  • Avoid excessive BP reduction which can precipitate ischemic events 2

• First-line IV medications based on specific presentations:

  • Malignant hypertension: Labetalol, nicardipine, or clevidipine with target MAP reduction by 20-25% over several hours 1, 2, 5
  • Hypertensive encephalopathy: Immediate MAP reduction by 20-25% using labetalol or nicardipine 1, 2
  • Acute ischemic stroke with BP >220/120 mmHg: MAP reduction by 15% within 1 hour 1, 3
  • Acute coronary event: Nitroglycerin with target SBP <140 mmHg immediately 1, 3
  • Acute cardiogenic pulmonary edema: Nitroprusside or nitroglycerin with target SBP <140 mmHg immediately 1, 3
  • Acute aortic disease: Esmolol plus nitroprusside/nitroglycerin with target SBP <120 mmHg and heart rate <60 bpm immediately 1, 3
  • Eclampsia/severe preeclampsia: Labetalol or nicardipine plus magnesium sulfate with target SBP <160 mmHg and DBP <105 mmHg immediately 1, 3

• Transition to oral antihypertensive therapy once stabilized 2, 3

• Avoid short-acting nifedipine due to risk of unpredictable blood pressure reduction 2, 3

Potential Complications

• Cerebral complications: Hypertensive encephalopathy, ischemic or hemorrhagic stroke 1, 2
• Cardiac complications: Acute myocardial infarction, acute left ventricular failure 1, 2
• Renal complications: Acute kidney injury, thrombotic microangiopathy 1, 2
• Vascular complications: Aortic dissection or rupture 1, 2
• Ocular complications: Advanced retinopathy with potential vision loss 1, 2
• Excessive BP reduction can lead to organ hypoperfusion, particularly cerebral, coronary, or renal ischemia 2, 3

Relevant Red Flags & CVICU Tips

• The actual BP level may not be as important as the rate of BP rise; patients with chronic hypertension often tolerate higher BP levels than previously normotensive individuals 2
• Volume depletion from pressure natriuresis may occur, requiring intravenous saline to prevent precipitous BP falls 2
• Avoid excessive acute drops in systolic BP (>70 mmHg) as they may be associated with acute renal injury and early neurological deterioration 2
• Screen for secondary hypertension after stabilization, as patients with hypertensive emergencies remain at high risk 2, 3
• In acute ischemic stroke, avoid BP reduction within the first 5-7 days unless BP exceeds 220/120 mmHg 2
• For intracerebral hemorrhage, immediate BP lowering (within 6 hours of symptom onset) to a systolic target of 140-160 mmHg is recommended to prevent hematoma expansion 2
• Patients should be advised to contact healthcare professionals immediately for any signs of a new hypertensive emergency: neurological symptoms, visual changes, or evidence of congestive heart failure 5