Cardiology · Hypertension
The facts most likely to be tested
Hypertensive emergency is defined as severe hypertension (typically systolic BP >180 mmHg or diastolic BP >120 mmHg) accompanied by acute end-organ damage.
The most common clinical presentation of hypertensive emergency is hypertensive retinopathy, characterized by papilledema, flame-shaped hemorrhages, or cotton-wool spots on funduscopic exam.
Hypertensive encephalopathy presents with altered mental status, seizures, or focal neurologic deficits due to loss of cerebral autoregulation.
Labetalol or nicardipine are the preferred first-line agents for most hypertensive emergencies, except in cases of aortic dissection or acute pulmonary edema.
Esmolol is the drug of choice for aortic dissection because it provides rapid control of both heart rate and blood pressure to reduce aortic wall shear stress.
Nitroglycerin is the preferred agent for hypertensive emergency associated with acute pulmonary edema or myocardial ischemia due to its potent venodilation properties.
Blood pressure should be reduced by no more than 25% within the first hour to prevent cerebral hypoperfusion and ischemic stroke.
Vignette unlocked
A 58-year-old male with a history of poorly controlled hypertension presents to the emergency department with a severe, throbbing headache and blurred vision. On physical exam, his blood pressure is 210/130 mmHg. Funduscopic examination reveals bilateral papilledema and flame-shaped retinal hemorrhages. The patient is alert and oriented, and his neurological exam is non-focal. Serum creatinine is 1.4 mg/dL, and urinalysis shows microscopic hematuria.
What is the most appropriate initial management for this patient?
Intravenous administration of nicardipine or labetalol with a goal of reducing mean arterial pressure by no more than 25% in the first hour.
The patient exhibits signs of end-organ damage (retinopathy and renal involvement) in the setting of severe hypertension, confirming a hypertensive emergency; rapid but controlled reduction of blood pressure is required to prevent further damage while avoiding hypoperfusion.
Full handout
High yield triage
Etiology / Epidemiology
Occurs when BP >180/120 mmHg with acute end-organ damage. Common in patients with uncontrolled hypertension or medication non-adherence.
Clinical Manifestations
Presents with end-organ damage including encephalopathy, acute coronary syndrome, or aortic dissection. Look for papilledema.
Diagnosis
Diagnosis requires BP >180/120 mmHg plus evidence of acute target organ damage. Funduscopic exam is mandatory.
Treatment
Reduce MAP by max 25% in first hour. Use IV Labetalol or Nicardipine. Avoid rapid BP drops to prevent cerebral ischemia.
Prognosis
High risk of stroke or myocardial infarction. Requires ICU admission and continuous arterial line monitoring.
Full handout
Epidemiology & Etiology
Most common in patients with chronic hypertension who are non-compliant with therapy. Secondary causes include renal artery stenosis, pheochromocytoma, or cocaine use. It is defined by the presence of acute end-organ damage rather than an absolute BP value.
Pertinent Anatomy
The retina serves as the primary window for assessing microvascular damage. The aorta is susceptible to dissection under high shear stress. The brain and kidneys are the most frequent sites of acute failure.
Pathophysiology
Acute, severe elevation in systemic vascular resistance leads to fibrinoid necrosis of arterioles. This triggers a cycle of endothelial dysfunction, activation of the coagulation cascade, and ischemia. The loss of autoregulation in cerebral and renal beds results in rapid, irreversible tissue damage.
Clinical Manifestations
Patients present with altered mental status, hypertensive encephalopathy, or chest pain. Physical exam must include funduscopic exam for papilledema or flame hemorrhages. Red flags include focal neurologic deficits, dyspnea, or oliguria indicating acute kidney injury.
Diagnosis
Diagnosis is clinical, confirmed by BP >180/120 mmHg and evidence of organ dysfunction. Gold standard for aortic dissection is CT Angiography. Urinalysis and Creatinine are essential to assess renal involvement.
Treatment
Goal is a 10-20% reduction in MAP in the first hour, then 5-15% over the next 23 hours. IV Nicardipine or Labetalol are preferred. Contraindicated: rapid lowering of BP can cause watershed infarcts. Use Esmolol specifically for aortic dissection.
Prognosis
Untreated, mortality is high due to intracranial hemorrhage or heart failure. Patients require ICU admission for titration of IV antihypertensives and continuous monitoring of MAP.
Differential Diagnosis
Hypertensive Urgency: No evidence of acute end-organ damage
Acute Ischemic Stroke: BP is often elevated as a compensatory mechanism
Pheochromocytoma: Paroxysmal hypertension with palpitations and sweating
Aortic Dissection: Tearing chest pain radiating to the back
Acute Pulmonary Edema: Severe dyspnea with bilateral rales