Hypertensive Crisis in an Era of Escalating Health Care Changes

Theresa P. Yeo; Sherry A. Burrell

Journal for Nurse Practitioners. 2010;6(5):338-346.

Epidemiology of Hypertensive Crisis

It is estimated that between 1% and 5% of persons with HTN will develop a hypertensive crisis at some point in their lifetime.^[12,13,17] The prevalence of hypertensive crisis mirrors that of essential HTN in the United States, in which the incidence is higher in older adults, blacks and African Americans, and men.^[18,19] The majority of patients presenting in hypertensive crisis have a prior history of HTN and have been prescribed antihypertensive medications at some point.^[20] Sudden escalation of essential, chronic HTN (also called accelerated HTN) is a common precipitant of hypertensive crisis, though drug interactions and/or withdrawal of treatment are also frequently factors.

Uncontrolled BP is a major risk factor for hypertensive crisis with an accompanying cardiovascular event and TOD. Predictors of uncontrolled BP are advancing age, persistent stage I HTN, use of fewer antihypertensive agents, uncontrolled diabetes, hyperlipidemia, HF, and nephropathy.^[4] A 1996 study on the prevalence of hypertensive crisis found that it accounts for 25% of all emergency department visits.^[17] A quarter of these patients experienced cerebral infarction, 37% had pulmonary edema or heart failure, 12% had acute coronary syndromes, 4.5% had intracerebral or subarachnoid hemorrhage, 13% had unsuspected cocaine use,^[21] 4.5% had eclampsia, and 2% had an acute aortic dissection.^[22]

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Table 1. Manifestations of Target Organ Damage
Papilledema, retinal hemorrhage, and exudates Headache, somnolence, confusion, and changes in mental status Oliguria or proteinuria Chest pain, shortness of breath, rales, and pulmonary edema Signs of stroke Encephalopathy

Table 2. Evaluation of Severely Elevated Blood Pressure
	Hypertensive Emergency > 220/140 mmHg	Hypertensive Urgency > 180/120 mmHg
Clinical manifestations
	Shortness of breath	Headache
	Chest pain	Shortness of breath
	Nocturia	Epistasis
	Dysarthria	Edema
	Weakness	Often asymptomatic
	Altered LOC
Physical examination
	Encephalopathy	May have TOD
	Pulmonary edema	Clinical CVD present
	Renal insufficiency	Stable, often no TOD/CVD
	Cerebrovascular accident
	Acute coronary syndrome
Therapy
	Baseline laboratory tests	Observe
	Intravenous line	Initiate/resume medication
	Monitor BP	Increase dose of
	May initiate therapy in ED	inadequate agent
Plan
	Immediate admission	Arrange follow-up < 24 hours to several days if no prior evaluation
	Monitored unit
	Parenteral agents	Schedule appointment
	Treat to goal BP
	Other diagnostic studies

Table 3. Keith-Wagener-Barker System of Retinopathy ^[28]
Grade of Retinopathy	Clinical Features
Grade 1	Moderate arterial constriction, referred to as "silver-wiring"
Grade 2	Blood vessel tortuosity with arterial-venous crossing changes
Grade 3	Hard exudates and retinal flame hemorrhages
Grade 4	Papi Edema with disc margin blurring and optic disc edema

Table 4. Dosing Recommendations for Selected Parenteral and Oral Antihypertensive Agents Used in Hypertensive Crises ^[29]
Agent	Indication for Use Hypertension With	Route of Administration	Dose
Enalaprilat	Pulmonary edema, HF, Hemorrhagic stroke	IV	1.25 mg every 6 hours
Esmolol	Aortic dissection, Hemorrhagic stroke, Post-cardiac surgery HTN	IV	Loading dose 500 μ/kg over
			1 minute, then 25–200 μ/kg/min
Fenoldopam	Acute or chronic renal failure, HF with renal impairment	IV	0.1–1.6 μ/kg/min
Hydralazine	Pre-eclampsia/eclampsia	IV, IM	5–20 mg; may repeat after 20 minutes
Labetolol	Hypertensive urgency, (except in HF, COPD or diabetic patients), Aortic dissection, Hemorrhagic stroke, Ischemic stroke	Oral, IV	Oral: 20 mg
			IV: 20–40 every 10 minutes to 300 mg or 2 mg/min
			infusion. Can transition from IV to oral dosing
Magnesium sulfate	Pre-eclampsia-eclampsia	IV	4–6 grams load; followed by 2–3 grams/hour
Nicardipine	Aortic dissection, Hemorrhagic stroke	IV	5 mg/hour; may titrate to 15 mg/hour
Nitroglycerine	Acute MI	IV	0.25–5 μ/kg/min
Nitroprusside	Pulmonary edema, HF, Aortic dissection, Cocaine use, Post-cardiac surgery HTN, Hypertensive encephalopathy	IV	0.25–10 μ/kg/min
Clonidine	Hypertensive urgency	Oral	0.1–0.2 mg, then 0.1 mg every hour to a maximum of 0.8 mg
Enalapril	Hypertensive urgency	Oral	12.5–25 mg

Table 5. Nitroprusside Cautions ^[20,30]
Nitroprusside is metabolized to cyanide and binds with a sulfate group to become thiocyanate, which is excreted by the kidneys. Excess, unbound cyanide attaches to cytochromes, thus preventing participation in oxidative metabolism, resulting in cell death and hypoxia. If the rate of infusion of nitroprusside exceeds the rate of clearance of cyanide, the patient will be poisoned. Bright red venous blood is a sign of cyanide poisoning and indicates that O₂ cannot be extracted from blood. Thiocyanate levels must be checked during administration. Use Nipride cautiously in renal patients, as the half-life of thiocyanate increases from 3 days to 9 to 12 days with renal failure.