TRIPASS XR تري باس

Hypertensive Emergencies

Erik K. Nordqu ist, MD

Key Points

• Hypertension is a very common fi nding in emergency

department patients. Evidence of acute end-organ

dysfunction in the setting of hypertension is rare but

requires emergent diagnosis and treatment.

• Depend on the history and physical to guide the clinical

eva luation of patients with severe hypertension.

INTRODUCTION

Hypertension affects up to 30% of the total adult population and is one of the most common medical conditions in

the United States. Of these individuals, nearly 75% have

inadequately controlled blood pressure (BP) (beyond normotensive limits of 140/90 mmHg), and only half are taking their medications correctly as prescribed. That said,

fewer than 1% of all patients with hypertension will ever

develop a hypertensive emergency.

Patients presenting with a systolic BP :?: 180 mmHg or a

diastolic BP :?:l l O mmHg are classified as having severe

hypertension. Evaluating a patient with severe hyperten ­

sion should focus on the rapid distinction between hypertensive emergency or hypertensive urgency, as the

treatment and disposition differ dramatically. Hypertensive

emergency is defined as an acute elevation in BP ( :?: 180/l lO

mmHg) associated with active end-organ damage, specifically ongoing injury to the brain, heart, aorta, kidneys,

and/or eyes. Hypertensive urgency is less clearly defined,

but can be thought of as a severe elevation in blood pressure without evidence of acute end-organ dysfunction.

The suggested mechanism behind hypertensive emer ­

gency requires a sudden increase in systemic vascular

75

• Emergent blood pressure control is contraindicated

in asymptomatically hypertensive patients without

evidence of end-organ dysfunction.

resistance due to an unregulated surge in circulating vasoconstrictors. This spike in BP causes undo stress on the

vascular wall with consequent endothelial injury. The

injured endothelium produces pathologic increases in vascular permeability, activation of the platelets and coagulation cascade, and the localized deposition of intraluminal

fibrin. Secondary fibrinoid necrosis of the arteriolar endorgan circulation results in significant tissue hypoperfusion and consequent organ system dysfunction.

Most individuals presenting with hypertensive emer ­

gency will carry a previous diagnosis of hypertension. When

determining the goals for BP treatment, it is important to

understand the effects of longstanding hypertension on the

cerebral circulation. Chronic hypertension forces a shift in

cerebral autoregulation, allowing patients to tolerate significant elevations in blood pressure without any signs of cerebral end-organ damage. Consequently, the overaggressive

reduction of systemic BP in this setting, even if only

decreased to normotensive limits, may lead to secondary

hypoperfusion and ischemia of the central nervous system

(CNS). Always remember that treating blood pressure based

on numbers alone, without considering the clinical context,

can be altogether quite harmful for the patient.

CLINICAL PRESENTATION

� History

CHAPTER 18

Patients with severe hypertension require a rapid evaluation for evidence of end-organ damage. Start with a

focused history and comprehensive review of systems,

inquiring about the presence of chest pain, back pain,

shortness of breath, hematuria or decreased urine output,

and neurologic complaints including numbness, weakness, headache, confusion, and visual disturbances.

A more detailed history related to specific diagnoses

follows.