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.

Evaluation of Hypertensive Crises

Successful management of a patient with severely elevated BP depends on the ability to immediately differentiate hypertensive urgency from hypertensive emergency,^[20] as treatment is dependent on the presence or absence of target-organ involvement (Table 2). The initial evaluation begins with obtaining a targeted, but accurate previous medical history, including a history of HTN and CVD, usual medications taken, and previous episodes of hypertensive crisis. The BP should be taken in all extremities with an appropriately sized BP cuff, and pulses assessed in all extremities. Lung auscultation includes assessment for the presence of rales and pulmonary edema. It is essential to listen over both renal arteries for bruits, to perform a focused neurological and fundoscopic examination. Hypertensive retinal changes are classified using the Keith-Wagener-Barker System (Table 3).^[28] A complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, urinalysis with specific gravity, plasma renin levels, catecholamine levels, and cardiac enzymes including troponins should be obtained on all patients. Imaging studies such as a chest radiograph (to assess heart size and presence of HF or pulmonary edema), head CT scanning (to assess for intracerebral hemorrhage or subarachnoid hemorrhage [SAH]), an EKG (electrocardiogram) (to look for evidence of acute MI, unstable angina, or left or right ventricular hypertrophy), and possibly an echocardiogram (to assess for global akinesis) are appropriate. While other diagnostic tests may be indicated depending on the patient's history, the BP must be addressed while awaiting the results of diagnostic testing.

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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.