Volume I:
First Thirty Minutes
- Section 1
  Acute Care Algorithm/ Treatment Plans/ Acronyms
- Section 2
  Universal Approach
  - CALS Universal Approach To Emergency Advanced Life Support
- Section 3
  Steps 1-6
- Section 4
  Preliminary Impression/Focused Clinical Pathways
Volume II:
Resuscitation Procedures
Volume III:
Definitive Care

Cardiovascular 13: Hypertensive Crises Portal

Incidence/Epidemiology
For reasons that are unclear, hypertensive crises occur in 1% to 2% of cases of untreated essential hypertension.

Risk Factors for Hypertensive Crises

African American heritage
Use of oral contraceptives
Secondary hypertension (renovascular, pheochromocytoma)
Sudden withdrawal from alpha 2 stimulants (Clonidine [Catapres])
Cigarette smoking
Low socioeconomic class
Alcohol withdrawal (Non-compliance with treatment)
Sudden withdrawal from beta blockers

Definitions: Urgencies vs. Emergencies

Hypertensive emergencies require immediate reduction of BP (not necessarily to normal) to prevent or limit target organ damage. (Examples: hypertensive encephalopathy, intracranial hemorrhage, acute left ventricular failure with pulmonary edema, aortic dissection, eclampsia or severe pregnancy-induced hypertension, unstable angina, and acute MI)

Hypertensive urgencies require lowering BP within 24 hours. (Examples: accelerated or malignant hypertension without symptoms or progressive target-organ complications, severe post-operative hypertension)

Absolute BP level is not used to define whether a situation is urgent or emergent. Elevated BP alone, without symptoms or target organ damage, does not require emergency therapy. Rate of rise of BP may be more important than absolute BP level.

Patients in Hypertensive Crisis
History

If possible, determine the patient's duration of hypertension, current drug therapy, and history of onset of the present crisis.
Is the patient experiencing chest pain, dyspnea, headache, visual changes, loss of consciousness?
Is the patient pregnant?
Is there a possibility of alcohol or drug intoxication (especially methamphetamine or other stimulant) or withdrawal? See Vol III—Toxicology Portals

Physical examination

Focus assessment on target organ damage.
Perform a neurological exam to determine change in mental status or any loss of motor or sensory function.
Carefully examine the optic fundi for evidence of papilledema, hemorrhage, or evidence of chronic retinopathy of diabetes.
Perform cardiac and pulmonary exams looking for signs of CHF.
Examine the abdomen and peripheral pulses with attention to symmetry of pulses.

Pertinent diagnostic studies

Draw blood samples for CBC, electrolytes, BUN, creatinine, and transaminase; obtain a urinalysis.
Order an ECG for all patients.
A chest x-ray is also advisable.
If there are any abnormal neurologic findings, obtain a head CT to rule out intracranial hemorrhage.
Select patients may need thyroid function studies, pheochromocytoma studies, and/or renovascular evaluation (after BP is stabilized).

General treatment principles

In a true emergency, the timing of treatment of the elevated BP is after obtaining the ECG but before the lab and x-ray results are available.
Most patients in hypertensive crises cannot tolerate a rapid BP reduction to normal levels. Many patients develop cerebral hypoperfusion at normal BP levels due to impaired autoregulation in the cerebral circulation. The lower level of cerebral autoregulation is approximately 25% below the resting mean arterial pressure (MAP). Therefore, the goal of treatment in hypertensive crises is to reduce the MAP by 20% to 25% over a period of minutes to hours.

MAP=diastolic BP + 1/3 (systolic pressure—diastolic pressure)
For all patients in hypertensive crisis, monitor urine output carefully. Most patients in hypertensive crisis are volume depleted, probably from pressure-induced diuresis. Therefore, reserve diuretics and fluid restriction for patients who are clinically fluid-overloaded. In fact, if a patient is severely volume depleted (as evidenced by marked orthostatic fall in BP or prerenal azotemia), an infusion of isotonic saline solution may be needed to improve renal function.
If using intravenous medications to obtain rapid BP reduction, begin oral medications as early as practical to allow for IV therapy discontinuation as soon as possible.

Management of Specific Hypertensive Emergencies

Central Nervous System Conditions or Complications

1. Hypertensive encephalopathy

Symptoms of hypertensive encephalopathy include a severe headache (of somewhat gradual onset and progression), nausea, vomiting, visual changes, and varying degrees of obtundation. Usually the BP is high (> 250/150). There is usually a history of untreated hypertension, inadequately treated hypertension, or discontinuation of antihypertensive medication (often without medical advice.) The symptoms have an insidious onset over 48 to 72 hours.
Other clinical findings may include retinopathy (including papilledema), disorientation, focal neurologic signs, generalized or focal seizures, asymmetric reflexes, and nystagmus.
Hypertensive encephalopathy is a diagnosis of exclusion that requires ruling out stroke, subarachnoid hemorrhage, intracranial mass, seizure disorder, vasculitis, and encephalitis.
The preferred drug for treating hypertensive encephalopathy is sodium nitroprusside. (Labetalol is an alternative.)
The goal of treatment is to reduce BP over 2 to 3 hours by no more than 25% reduction in MAP.
Relief of headache and clearing of the sensorium should accompany BP reduction. If these particular symptoms do not improve, reconsider the diagnosis and examine for concurrent medical problems.

2. Subarachnoid hemorrhage

In contrast to the headache of hypertensive encephalopathy, the headache of subarachnoid hemorrhage is of sudden onset, is very severe, and may be accompanied by nuchal rigidity. Diagnosis may be made from a CT scan of the head or, if the CT is non-diagnostic, by finding bloody CSF from lumbar puncture.
There is no consensus at present regarding the wisdom of attempting BP reduction for these patients. Angiography has demonstrated that there is severe vasospasm around the hemorrhage site. Lowering the BP may increase the area of ischemia and lead to cerebral infarction.
Reduce severe hypertension gradually over 6 to 12 hours by 20% to 25% of the MAP using sodium nitroprusside. (However, reduce no lower than about 180/100.) If BP reduction worsens the clinical status of the patient, discontinue the infusion. The BP should return to pretreatment values in 2 to 4 minutes. Do not use long-acting agents; inadvertent hypotension may be disastrous.
If the patient has signs of increased ICP (either on CT scan or clinically), treat the patient with mannitol, dexamethasone, hyperventilation, or surgery.

3. Intraparenchymal intracranial hemorrhage

Again, there is no consensus regarding when to treat BP elevations in patients. Cerebral edema may cause an increase in ICP, which results in a requirement for a higher MAP in order to perfuse the brain adequately.
No treatment is recommended if the BP is < 180/105.
If the BP range has been from 180/105 to 230/120 persistently for over 1 hour, initiate treatment with oral labetalol, nifedipine, or captopril. Labetalol may also be given IV if the patient cannot take medications by mouth.
If the BP is > 230/120 for more than 20 minutes, use labetalol 20 mg IV every 10 to 20 minutes as needed.
If the diastolic BP is > 140, use a sodium nitroprusside infusion. If the patient's neurologic deficit or mental status worsens, the infusion may be decreased or discontinued.

4. Acute ischemic stroke¹

Treatment guidelines for hypertension in the setting of acute ischemic stroke differ depending on the patient’s eligibility for fibrinolytic treatment. (See Vol III—NEU2 Treatment of Stroke)

For patients not eligible for fibrinoytics or for whom fibrinolytic therapy is not the selected management strategy:

For patients with systolic BP >220 and/or diastolic BP >120, regardless of symptoms, the goal is to lower BP 15% to 25% over 24 hours.
For patients with BP in the hypertensive range but <220 systolic BP and/or <120 diastolic BP, withhold treatment if the patient is asymptomatic. If end-stage organ involvement (myocardial infarction, pulmonary edema, or encephalopathy) is present, treat to lower BP 15% to 20% over 24 hours or as dictated by the patient's clinical condition.

For stroke patients for whom fibrinolytic therapy is planned:

For patients with systolic BP >185 and/or diastolic BP >110, reduce BP below these levels in order to administer fibrinolytics. This must take place in the 3-hour window between symptom onset and planned fibrinolytic administration.

For all these scenarios, a variety of agents may be used including labetalol, nicardipine, nitroglycerin intravenous, and sodium nitroprusside. For doses, see the table Drugs Used to Treat Hypertensive Crisis, at the end of this portal.

Cardiac Complications

1. Acute left ventricular failure (See Vol III—CV 12, Acute Heart Failure.)

For patients with acute left ventricular failure due to uncontrolled hypertension, lower the BP immediately to decrease the workload on the left ventricle.
Agents useful for BP control in this setting include intravenous nitroglycerin, sodium nitroprusside, and ACE inhibitors, such as intravenous enalapril [enalaprilat]. For doses, see the table Drugs Used to Treat Hypertensive Crisis, at the end of this portal. If fluid overload is suspected, give furosemide 40 to 80 mg IV.
Start an oral ACE inhibitor (such as captopril or enalapril) so that IV drug therapy may be discontinued as soon as possible.

2. Unstable angina and/or MI

The preferred antihypertensive drug is nitroglycerin IV. Remember however that the BP reduction is ancillary to measures to improve or restore coronary patency with heparin, fibrinolytics, angioplasty, or surgery.

3. Thoracic aortic dissection

Symptoms of thoracic aortic dissection include sudden onset of severe pain in the chest, back, or abdomen. The pain is persistent and may migrate downward as the dissection extends. The pain is often described as ripping or tearing.
Physical findings may include discrepancies between pulses, a murmur of aortic insufficiency, and neurologic deficits. A chest x-ray, which shows mediastinal widening, may suggest the diagnosis. Echocardiography or CT scanning may be helpful in confirming the presence of a dissection.
If the dissection involves the aortic arch, in conjunction with efforts to lower the BP, emergent surgery is the preferred treatment.
If the dissection is distal to the left subclavian artery, antihypertensive drugs are the preferred treatment. In aortic dissection, the treatment goal is to reduce the BP rapidly (within 15 to 30 minutes) to a systolic pressure of 100 to 120 or a MAP of less than or equal to 80 mm Hg.
Use labetolol 20 to 80 mg as IV bolus every 5 to 10 minutes.
Alternatively, pretreat the patient (initially) with a beta blocker, reserpine, or methyldopa (to decrease reflex adrenergic stimulation from vasodilators). Next, use sodium nitroprusside to rapidly lower BP to the desired range.
Diazoxide and hydralazine are contraindicated in aortic dissection.
After initiating treatment and instituting appropriate monitoring (in an intensive care unit), transfer the patient to the angiography suite to confirm the diagnosis and to locate the site and extent of the dissection

Hypercatecholaminemia States

These hypertensive conditions (which include pheochromocytoma, MAO inhibitor interactions, clonidine withdrawal syndrome, and cocaine ingestion) are usually handled as hypertensive urgencies and can be treated with oral medications. The appropriate treatment may consist of prazosin (Minipress), resumption of clonidine (Catapres), or nifedipine (Procardia and other) PO.

Preeclampsia/Eclampsia: (Vol III—OB8 Hypertension in Pregnancy)

Summary of Treatment Time Frames for Hypertensive Emergencies

Clinical Setting	Time Goal to Achieve Target BP Reduction
Aortic dissection Pulmonary edema	15 to 30 minutes
Hypertensive encephalopathy	2 to 3 hours
Acute cerebral infarction Intracranial hemorrhage (decrease no lower than 170 to 180/100)	6 to 12 hours

Drugs Used to Treat Hypertensive Crises

Parenteral Vasodilators

Drug Cautions	Dose	Onset	Cautions
Sodium nitroprusside	0.25 to 10 µg/kg/min as IV infusion; maximal dose for 10 minutes only	Instantaneous	Nausea, vomiting, muscle twitching; prolonged use may cause thiocyanate intoxication, methemoglobinemia, cyanide poisoning
Nitroglycerin	5 to 100 µg/min as IV infusion	2 to 5 minutes	Headache, flushing, tachycardia, vomiting, methemoglobinemia
Diazoxide (Hyperstat)	1 to 3 mg/kg IV bolus one 15 to 30 sec, repeat q 5 to 15 minutes until desired effect, or 15 to 30 mg/min by IV infusion	1 to 2 minutes	Hypotension, N/V tachycardia, aggravation of angina, hyperglycemia
Hydralazine (Apresoline)	10 to 20 mg as IV bolus; may repeat in 30 minutes	10 minutes	Tachycardia, headache, vomiting, aggravation of angina
Enalapril (Enalaprilat [Vasotec])	0.625 to 1.25 mg IV every 6 h	15 to 60 minutes	Renal failure in patients with bilateral renal artery stenosis; hypotension

Parenteral Adrenergic Inhibitors

Drug Cautions	Dose	Onset	Cautions
Phentolamine (Regitine)	5 to 15 mg as IV bolus	1 to 2 minutes	Tachycardia, orthostatic hypotension
Labetalol (Trandate, Normodyne)	20 to 80 mg as IV bolus every 10 minutes 2 mg/min as IV infusion	5 to 10 minutes	Bronchoconstriction, heart block, orthostatic hypotension
Methyldopa (Aldomet)	250 to 500 mg as IV infusion every 6 h	30 to 60 minutes	Drowsiness

Oral Agents

Drug Cautions	Dose	Onset	Cautions
Captopril (Capoten)	25 mg PO; repeat prn	15 to 30 minutes	Hypotension, renal failure in bilateral artery stenosis
Clonidine (Catapres)	0.1 to 0.2 mg PO; repeat every hour prn to total dose of 0.6 mg	30 to 60 minutes	Hypotension, dry mouth, drowsiness
Labetalol (Trandate, Normodyne)	200 to 400 mg PO; repeat every 2 to 3 h	30 min to 2 h	Bronchoconstriction, heart block, orthostatic hypotension

Reference