Cardiovascular Emergencies
CARDIOPULMONARY ARREST
Prevalence
The value of early CPR and immediate defibrillation has been proved in many community-based studies.1–4 Additionally, among adults in whom ventricular tachycardia, ventricular fibrillation, or both is more common, the increased use of automated external defibrillators (AEDs) by emergency medical services (EMS), businesses, and airports has improved survival.5–8 Without defibrillation, mortality from ventricular tachycardia, ventricular fibrillation, or both increases by approximately 10% per minute.9–12
Diagnosis and Therapy
The American Heart Association, in collaboration with the International Liaison Committee on Resuscitation, has established guidelines for resuscitation of cardiac arrest patients.13,14 In each resuscitation scenario, four concepts should always apply:
Ventricular Tachycardia or Ventricular Fibrillation
Pulseless Electrical Activity
Bradycardia
HYPERTENSIVE EMERGENCY
Definition
A hypertensive emergency is an acute, severe elevation in blood pressure accompanied by end-organ compromise. In newly hypertensive patients, a hypertensive emergency is usually associated with a diastolic blood pressure higher than 120 mm Hg. Nephrosclerosis that causes acute renal failure frequently complicates hypertensive emergencies, with resultant hematuria and proteinuria. Nephrosclerosis also may perpetuate the elevation of systemic pressure through ischemic activation of the renin-angiotensin system. Ocular involvement with retinal exudates, hemorrhages, or papilledema connotes a worse prognosis.15,16
Complications of particular concern include hypertensive encephalopathy, aortic dissection, and eclampsia. Hypertensive encephalopathy signals the presence of cerebral edema and loss of vascular integrity. If left untreated, hypertensive encephalopathy may progress to seizure and coma.17,18 Aortic dissection is associated with severe elevations in systemic blood pressure and wall stress, requiring immediate lowering of the blood pressure and emergent surgery to reduce morbidity and mortality. Eclampsia, the second most common cause of maternal death, occurs from the second trimester to the peripartum period. It is characterized by the presence of seizures, coma, or both, in the setting of preeclampsia. Delivery remains its only cure.19
Etiology
Hypertensive emergencies result from an exacerbation of essential hypertension or have a secondary cause, including renal, vascular, pregnancy-related, pharmacologic, endocrine, neurologic, and autoimmune causes (Box 1).
Prevalence
The prevalence of hypertension rises substantially with increasing age in the United States and is greater among blacks than among whites in every age group.20,21 Based on the third National Health and Nutrition Examination Survey (NHANES III), the prevalence of hypertension in those older than 70 years was found to be approximately 55% to 60% of the U.S. population.22,23 A British study has revealed that less than 1% of patients with primary hypertension progress to hypertensive crisis.24 This study also showed that despite increasingly widespread therapy, the number of patients presenting with hypertensive crises did not decline between 1970 and 1993.
Clinical Evaluation
The symptoms and signs of a hypertensive emergency vary widely. Symptoms of end-organ involvement include headache, blurred vision, confusion, chest pain, shortness of breath, back pain (e.g., aortic dissection) and, in severe end-organ involvement, seizures and altered consciousness.15,16 Physical examination should assess end-organ involvement, including detailed fundoscopic, neurologic, and cardiovascular examinations, with emphasis on the presence of congestive heart failure and bilateral upper extremity blood pressure measurements. Laboratory evaluation should include measurement of the complete blood count with differential and smear evaluations, measurements of electrolyte, blood urea nitrogen, and creatinine levels, and electrocardiography, chest radiography, and urinalysis.
Treatment
No large randomized clinical trials have assessed therapy in hypertensive emergency; therapeutic intervention is largely a result of expert opinion. All patients with end-organ involvement should be admitted for intensive monitoring and have an arterial blood pressure line placed.16
Pharmacologic Therapy
Intravenous vasodilator therapy to achieve a decrease in mean arterial pressure (MAP) of 20% to 25% or a decrease in diastolic blood pressure (DBP) to 100 to 110 mm Hg in the first 2 hours is recommended. Decreasing the MAP and DBP further should be done more slowly because of the risk of decreasing perfusion of end-organs.16 Several drugs have proved beneficial in achieving this goal (Table 1).
Table 1 Intravenous Vasodilator Therapy for Hypertensive Crisis
| Drug | Dosage | Half-Life |
|---|---|---|
| Nitroprusside | 2.5-10 µg/kg/min | 1-2 min |
| Labetalol | 20- to 80-mg bolus, 2 mg/min maintenance | 2-6 hr |
| Fenoldopam* | 0.1-0.5 µg/kg/min | 10-20 min |
| Enalaprilat† | 1.25- to 5-mg bolus | 4-6 hr |
* Recommended starting dose is 0.1 µg/kg/min, with a slow increase to a maximum rate of 0.5 mcg/kg/min and/or target blood pressure.
† Use specifically for angiotensin-converting enzyme-mediated hypertensive crises, such as scleroderma renal crisis. It is contraindicated in pregnancy.
Medical Economics Staff, Physician’s Desk Reference, 57th Edition, 2003.
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