Cardiology > Hypertensive Emergency   

Background 

 A hypertensive emergency is defined as a severe elevation in blood pressure (typically ≥180/120 mm Hg) associated with acute target-organ damage such as encephalopathy, myocardial infarction, pulmonary edema, aortic dissection, or acute renal failure. Unlike hypertensive urgency, it requires immediate blood pressure reduction with intravenous (IV) medications to limit morbidity and mortality. 

II) Classification/Types

By BP Measurement (AHA/ACC Guidelines): 

• • Normal BP: <120/80 mm Hg 

• • Elevated BP: 120–129/<80 mm Hg 

• • Stage 1 Hypertension: 130–139/80–89 mm Hg 

• • Stage 2 Hypertension: ≥140/90 mm Hg 

• • Hypertensive Crisis: ≥180/120 mm Hg 

• • Hypertensive Urgency: No end-organ damage 

• • Hypertensive Emergency: With acute end-organ damage 

By Target-Organ Involvement: 

• • Neurologic: Hypertensive encephalopathy, ischemic/hemorrhagic stroke 

• • Cardiac: Acute coronary syndrome, heart failure, aortic dissection 

• • Renal: Acute kidney injury 

• • Ocular: Retinal hemorrhages, papilledema 

• • Obstetric: Eclampsia, HELLP syndrome 

III) Pathophysiology 

 Acute and severe hypertension overwhelms autoregulatory mechanisms in vital organs, causing endothelial injury, increased vascular permeability, fibrinoid necrosis, and microvascular thrombosis. This leads to acute ischemia or hemorrhage in critical tissues, especially the brain, heart, and kidneys. 

IV) Epidemiology

• • Occurs in ~1–2% of all hypertensive patients 

• • More prevalent in African American populations 

• • Common in patients with medication non-adherence, undiagnosed secondary hypertension, or abrupt withdrawal of antihypertensives 

• • High morbidity and mortality if not treated promptly 

Etiology 

I) Causes

• • Poorly controlled or undiagnosed chronic hypertension 

• • Abrupt withdrawal of antihypertensives (especially clonidine, beta-blockers) 

• • Secondary causes: Pheochromocytoma, renal artery stenosis, glomerulonephritis 

• • Drug-induced: Cocaine, amphetamines, NSAIDs, cyclosporine 

• • Pregnancy-related: Eclampsia, preeclampsia 

• • Postoperative states or trauma 

• • Acute stress response 

II) Risk Factors

• • History of chronic hypertension 

• • Non-compliance with medications 

• • Illicit drug use 

• • Underlying renal or endocrine disease 

• • Recent surgery, trauma, or acute stress 

Clinical Presentation 

I) History (Symptoms)

 Depends on the affected organ: 

• • CNS: Severe headache, visual changes, confusion, seizures, focal deficits 

• • Cardiac: Chest pain, dyspnea, palpitations 

• • Renal: Oliguria, hematuria, back/flank pain 

• • Ophthalmic: Blurred vision, papilledema 

• • Pregnancy: Seizures, right upper quadrant pain (eclampsia) 

II) Physical Exam (Signs)

• • BP typically ≥180/120 mm Hg 

• • Retinal changes: hemorrhages, exudates, papilledema 

• • Neurologic deficits or altered mental status 

• • S3 gallop, rales (heart failure) 

• • Diminished urine output, edema 

• • Signs of aortic dissection: unequal pulses, mediastinal widening 

Differential Diagnosis (DDx) 

• • Hypertensive urgency (no target-organ damage) 

• • Stroke (ischemic vs hemorrhagic) 

• • Preeclampsia/eclampsia 

• • Acute coronary syndrome 

• • Drug-induced hypertensive crisis (e.g., cocaine) 

• • Anxiety or pain-induced BP elevation (transient) 

• • Intracranial hemorrhage or encephalitis 

Diagnostic Tests 

Initial Work-Up 

• • BP measurement in both arms (look for dissection) 

• • Fundoscopy 

• • Basic metabolic panel: electrolytes, renal function 

• • Urinalysis: hematuria, proteinuria 

• • ECG: LVH, ischemia, arrhythmias 

• • Cardiac enzymes: Troponins 

• • Chest X-ray: Pulmonary edema, widened mediastinum 

• • Head CT: Rule out hemorrhagic stroke if neurologic symptoms 

• • Echocardiogram: Suspected aortic dissection, heart failure 

• • Toxicology screen: Cocaine, amphetamines 

• • Pregnancy test in women of childbearing age 

Treatment 

I) Initial Approach

• • Admit to ICU for continuous monitoring 

• • Start IV antihypertensive therapy immediately 

• • Target BP reduction: 

• • Reduce MAP by ~10–20% in first hour 

• • Further 5–15% over next 23 hours (unless aortic dissection or eclampsia) 

• • Treat underlying cause and organ-specific complications 

II) IV Antihypertensive Medications

III) Oral Therapy 

• • Transition to oral medications once BP is controlled and stable for 24–48 hours. 

Patient Education, Screening, Vaccines 

Education 

• • Importance of medication adherence 

• • Home BP monitoring 

• • Recognizing warning signs of hypertensive crisis 

• • Avoid sudden discontinuation of antihypertensives 

• • Avoid substances that raise BP (NSAIDs, cocaine, etc.) 

Screening 

• • Regular BP checks for high-risk populations 

• • Monitor for end-organ damage 

• • Screen for secondary causes if appropriate 

Vaccinations 

• • Keep up with adult immunizations 

• • Emphasize influenza, pneumococcal, and COVID-19 

• • Special focus in patients with CKD or heart failure 

Consults/Referrals 

• • Neurology: Suspected stroke or encephalopathy 

• • Cardiology: Acute coronary syndrome, dissection, heart failure 

• • Nephrology: Acute kidney injury or CKD 

• • Obstetrics: Eclampsia or hypertensive disorders of pregnancy 

• • Toxicology: Drug-induced hypertension 

• • Surgery/Vascular: Aortic dissection requiring intervention 

Follow-Up 

Short-Term 

• • Close outpatient follow-up within 1 week post-discharge 

• • Monitor for recurrence or rebound hypertension 

• • Titrate long-term oral therapy as needed 

Long-Term 

• • Lifelong BP control 

• • Regular labs: renal function, electrolytes, lipid profile 

• • Assess adherence and lifestyle modifications 

Prognosis 

• • Favorable if recognized early and treated aggressively 

• • Poor outcomes include stroke, MI, acute renal failure, and death if left untreated or undertreated