Hypertensive Emergencies
Last Updated: January 21, 2002 |
Background: Patients with
hypertension in the ED can be classified into 3 categories based upon their
symptoms and the organ systems that are affected at the time of
presentation.
Hypertensive emergency
Hypertensive emergency, also called hypertensive crisis, is severe
hypertension with acute impairment of an organ system (eg, central nervous
system [CNS], cardiovascular, renal). In these conditions, the blood
pressure (BP) should be lowered aggressively over minutes to hours.
Hypertensive urgency
This is distinguished from hypertensive urgency, in which the BP is a
potential risk but has not yet caused acute end-organ damage. These patients
require BP control over several days to weeks.
Severe hypertension
The third category, severe hypertension, is elevated BP not yet leading
to significant organ damage. In these patients, the hypertension does not
necessarily require treatment during the ED visit but does require close
follow-up with a primary care physician for long-term BP control. In these
cases, beginning antihypertensive therapy in the ED may be appropriate and
should be done in consultation with the patient's primary care physician,
who will be caring for the patient after the ED visit.
Emergency department considerations
Optimal control of hypertensive situations balances the benefits of
immediate decreases in BP against the risk of significant decrease in
end-organ perfusion. The emergency physician must be capable of the
following:
Appropriately evaluating patients with an elevated BP
Correctly classifying the hypertension
Determining the aggressiveness and timing of therapeutic interventions
Making disposition decisions
An important point to remember in the management of the patient with any
degree of BP elevation is to "treat the patient and not the number."
Pathophysiology: The 3 major organ systems affected by
high BP are the CNS, cardiovascular system, and renal system.
Central nervous system
The CNS is affected as the elevated BP overwhelms the normal cerebral
autoregulation. Under normal circumstances, with an increase in BP, cerebral
arterioles vasoconstrict and cerebral blood flow (CBF) remains constant.
During a hypertensive emergency, the elevated BP overwhelms arteriolar
control over vasoconstriction and autoregulation of CBF. This results in
transudate leak across capillaries and continued arteriolar damage.
Subsequent fibrinoid necrosis causes normal autoregulatory mechanisms to
fail, leading to clinically apparent papilledema, the sine qua non
of malignant hypertension. The end result of loss of autoregulation is
hypertensive encephalopathy.
Cardiovascular system
The cardiovascular system is affected as increased cardiac workload leads
to cardiac failure; this is accompanied by pulmonary edema, myocardial
ischemia, or myocardial infarction.
Renal system
The renal system is impaired when high BP leads to arteriosclerosis,
fibrinoid necrosis, and an overall impairment of renal protective
autoregulation mechanisms. This may manifest as worsening renal function,
hematuria, red blood cell (RBC) cast formation, and/or proteinuria.
Frequency:
- In the US: More than 60 million Americans, about
25-30% of the population, have hypertension. Of these individuals, 70%
have mild disease, 20% moderate, and 10% severe hypertension (diastolic BP
[DBP] >110 mm Hg). Approximately 1-2% develop a hypertensive emergency
with end-organ damage.
Mortality/Morbidity: Morbidity and mortality depend on
the extent of end-organ damage on presentation and the degree to which BP is
controlled subsequently. BP control may prevent progression to end-organ
impairment.
- One-year mortality rate for an untreated hypertensive emergency is
greater than 90%.
- Five-year survival rate among all patients presenting with a
hypertensive crisis is 74%.
- Median survival is 144 months for all patients presenting to the ED
with a hypertensive crisis.
Race: African Americans have a higher incidence of
hypertensive emergencies than Caucasians.
Sex: Males are at greater risk of hypertensive
emergencies than females.
Age: Hypertensive emergencies occur most commonly in
middle-aged patients. The peak incidence occurs in those aged 40-50 years.
CLINICAL
History: Focus history on the
presence of end-organ damage, the circumstances surrounding the
hypertension, and any identifiable etiology.
- Use of hypertensive medications and compliance
- Use of illicit drugs (specifically alpha-adrenergic agents)
- Duration of current symptoms
- Other medical problems (eg, prior hypertension, thyroid disease,
Cushing disease, systemic lupus, renal disease)
- Date of last menstrual period
- Headaches (85%): Mild headache alone in association with elevated BP
does not indicate a hypertensive crisis.
- New-onset blurred vision (60%)
- Weight loss (75%)
- Nausea and vomiting
- Weakness and fatigue (30%)
- Confusion and mental status changes
- Cardiovascular manifestations
- Symptoms of congestive heart failure (CHF)
- Angina
- Dissecting aneurysm
- History of hematuria
- Oliguria
- Abdominal pain
- Shortness of breath
Physical: Use an approach based on organ systems to
identify signs of end-organ damage.
- Focal neurologic findings
- Papilledema, hemorrhages, exudates, or evidence of closed-angle
glaucoma
- Lung auscultation for evidence of pulmonary edema
- Signs of CHF, including extra heart sounds
- Jugular venous distension
- Check for equal and symmetric BP and pulses bilaterally.
- Check for abdominal masses and bruits.
Causes: The most common hypertensive emergency is a
rapid unexplained rise in BP in a patient with chronic essential
hypertension.
- Renovascular hypertension
- Antihypertensive withdrawal syndromes
- Head injuries and CNS trauma
- Drug-induced hypertension
- Thrombotic thrombocytopenic purpura
- Postoperative hypertension
DIFFERENTIALS
Acute Coronary Syndrome
Aneurysms, Abdominal
Anxiety
Congestive Heart
Failure and Pulmonary Edema
Cushing Syndrome
Delirium Tremens
Encephalitis
Glomerulonephritis,
Acute
Headache, Cluster
Headache, Migraine
Headache, Tension
[Hyperthyroidism, Thyroid Storm and Graves Disease]
Myocardial Infarction
Pregnancy, Eclampsia
Pregnancy,
Preeclampsia
Stroke, Hemorrhagic
Stroke, Ischemic
Subarachnoid
Hemorrhage
Systemic Lupus
Erythematosus
Other Problems to be Considered:
Steroid use
Use of over-the-counter or recreational sympathomimetic drugs
Pheochromocytoma
Acute vasculitis
Serotonin syndrome
Other CNS pathology
Coarctation of the aorta
|
WORKUP
Lab Studies:
Electrolytes, BUN, and creatinine for evidence
of renal impairment
- Dipstick urinalysis to detect presence of hematuria or proteinuria as
evidence of renal impairment
- Microscopic urinalysis, evaluating for RBCs or RBC casts as evidence
of renal impairment
Imaging Studies:
- Chest x-ray - Signs of CHF, pulmonary edema, or coarctation of aorta
- Head CT scan - Indicated with abnormal neurologic exam to look for
intracranial bleeding, edema, or infarction
- Chest CT scan, transesophageal echo, or aortic angiogram - May be
indicated for clinical suspicion of aortic dissection
Other Tests:
- Electrocardiogram (ECG) to assess for evidence of ischemia or
infarction
TREATMENT
Prehospital Care:
- Address the manifestations of a hypertensive emergency, such as chest
pain or heart failure. Reduction of BP may not be indicated in the
prehospital setting.
- Oxygen, furosemide (Lasix), and nitrates all may be appropriate.
- Under most circumstances, attempting to treat hypertension directly in
the prehospital setting is unwise. In particular, rapid lowering of BP can
critically decrease end-organ perfusion.
Emergency Department Care: The fundamental principle in
determining the necessary ED care of the hypertensive patient is the
presence or absence of end-organ damage.
- Initial considerations (if the patient is not in distress)
- Place patient who is not in distress in a quiet room and reevaluate
after an initial interview. In one study, 27% of patients with an
initial DBP >130 mm Hg had their DBP fall below critical levels after
relaxation without specific treatment.
- Consider the context of the elevated BP (eg, severe pain often
causes increase in BP).
- Screen for end-organ damage
- Use historical criteria, physical examination steps, lab studies,
and diagnostic tests outlined in
Workup.
Patients with end-organ damage usually require admission and rapid
lowering of BP using intravenous (IV) medications. Suggested medication
depends on the affected organ system.
Patients without evidence of end-organ effects may be discharged
with follow-up.
- The misconception remains that a patient never should be
discharged from the ED with elevated BP. As a result of this belief,
patients are given oral medicines, such as nifedipine, in an effort to
lower BP rapidly before discharge. This is not indicated and may be
dangerous.
- Attempts to temporarily lower BP by using these medicines may
result in a precipitous and difficult-to-correct drop in BP. Should
this occur, end-organ hypoperfusion may result. Furthermore, patients
who present with high BP may have had this elevation for some time and
may need chronic BP control but may not tolerate rapid return of BP to
a "normal" level.
- Acute lowering of BP in the narrow window of the ED visit does not
necessarily improve long-term morbidity and mortality rates. The
follow-up recommended for these situations by The Joint National
Committee on High Blood Pressure is outlined in
Follow-up.
Rapid BP reduction is indicated in the following circumstances:
- Acute myocardial ischemia
- Nitroglycerin IV
- Beta-blockers IV
- Angiotensin-converting enzyme (ACE) inhibitors IV
- CHF with pulmonary edema
- Nitroglycerin IV
- Lasix IV
- Morphine IV
- Acute aortic dissection
- Nitroprusside IV plus beta-blockers IV
- Alternative - Trimethaphan IV plus beta-blockers IV
- Cerebral vascular accident: Lowering BP is indicated in cardiac or
renal compromise, DBP >130 mm Hg, hypertensive encephalopathy, or
subarachnoid hemorrhage (may require BP control to prevent rebleeding
even without other evidence of end-organ damage).
- Nitroprusside IV
- Labetalol IV
- Nimodipine IV
- Monoamine oxidase (MAO)-tyramine interactions with acute
hypertension - Phentolamine IV
- Reduce BP quickly (over minutes to hours) in the following settings:
- Pheochromocytoma
- Phentolamine IV
- Nitroprusside IV
- Labetalol IV
- Hypertensive encephalopathy
- Nitroprusside IV
- Trimethaphan IV
- Beta-blockers IV
- Eclampsia
- Hydralazine IV
- Labetalol IV
- Magnesium IV
- Lowering of BP acutely in the ED in clinical situations other than
those listed here is controversial and generally should be avoided.
Consultations:
- Consultations may be indicated for comorbid conditions and their
definitive treatment.
- Since hypertension is usually a chronic problem, access to a primary
care physician and long-term follow-up are essential for all patients.
MEDICATION
Once the diagnosis of a true hypertensive
emergency is established and end-organ damage confirmed, the BP should be
lowered by up to 25% of the mean arterial pressure (MAP) over minutes to
hours. Treat a diastolic reading of 120 mm Hg or greater with an IV
antihypertensive medication to prevent cerebral hemorrhage.
Drug Category: Beta-blockers -- These
agents are used for hypertensive emergency, especially with aortic
dissection and myocardial infarction. They may be used alone or in
combination with sodium nitroprusside. Pure beta-blockers should not be used
alone in cases that are the result primarily of alpha stimulation (eg,
pheochromocytoma, MAOI -tyramine interaction).
Drug Name
|
Labetalol (Normodyne) -- Alpha-,
beta1-, and beta2-blocker, especially useful with aortic dissection.
Lowers BP, reduces incidence of myocardial infarctions and death.
|
Adult Dose |
2 mg/min continuous infusion to
start; titrate up to 5-20 mg/min; not to exceed 300 mg/dose |
Pediatric Dose |
0.4-1 mg/kg/h; not to exceed 3
mg/kg/h |
Contraindications |
Documented hypersensitivity;
cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block;
uncompensated CHF; reactive airway disease; severe bradycardia
|
Interactions |
Decreases effects of diuretics;
increases toxicity of methotrexate, lithium, and salicylates; may
diminish reflex tachycardia resulting from nitroglycerin use without
interfering with hypotensive effects; cimetidine may increase blood
levels; glutethimide may decrease effects by inducing microsomal enzymes
|
Pregnancy |
C - Safety for use during pregnancy
has not been established. |
Precautions |
Caution in impaired hepatic
function; discontinue therapy if signs of liver dysfunction; in elderly
patients, response rate may be lower and incidence of toxicity higher |
Drug Name
|
Esmolol (Brevibloc) -- Ideal for
use in patients at risk for complications from beta-blockers, especially
patients with mild to moderately severe LV dysfunction or peripheral
vascular disease. Has short half-life of 8 min; thus, easily titratable
to desired effect. In addition, therapy may be stopped quickly if
necessary. |
Adult Dose |
Loading dose: 250-500 mcg/kg
infused over 1 min
Maintenance infusion: 50 mcg/kg/min over 4 min
If adequate effect not observed within 5 min, repeat loading dose and
follow with maintenance infusion using increments of 50 mcg/kg/min (for
4 min); this regimen may be repeated up to 4 times if necessary
As desired BP approached, skip loading infusion and reduce dose
increments in maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min.
If necessary, may increase interval between titration steps from 5-10
min.
|
Pediatric Dose |
Suggested dose: 100-500 mcg/kg
administered over 1 min |
Contraindications |
Documented hypersensitivity;
uncompensated CHF; bradycardia; cardiogenic shock; atrioventricular
conduction abnormalities |
Interactions |
Aluminum salts, barbiturates,
NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may
decrease bioavailability and plasma levels, possibly resulting in
decreased pharmacologic effect; sparfloxacin, astemizole, calcium
channel blockers, quinidine, flecainide, and contraceptives may increase
cardiotoxicity; digoxin, flecainide, acetaminophen, clonidine,
epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and
catecholamine-depleting agents may increase toxicity |
Pregnancy |
C - Safety for use during pregnancy
has not been established. |
Precautions |
Beta-adrenergic blockers may mask
signs and symptoms of acute hypoglycemia and clinical signs of
hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm,
may worsen when medication abruptly withdrawn; withdraw drug slowly and
monitor patient closely |
Drug Category: Alpha-adrenergic blockers
-- At low doses, alpha-adrenergic receptor blockers may be used as
monotherapy in treatment of hypertension. At higher doses, they may cause
sodium and fluid retention. As a result, concurrent diuretic therapy may be
required to maintain the hypotensive effects.
Drug Name
|
Phentolamine (Regitine) -- Alpha1-
and alpha2-adrenergic blocking agent, effective for pheochromocytoma and
hypercatecholaminergic-induced hypertension. |
Adult Dose |
Load 5-20 mg IV q5min or infuse
0.2-0.5 mg/min |
Pediatric Dose |
0.05-1 mg/kg/dose IV/IM and repeat
q2-4h prn until hypertension controlled |
Contraindications |
Documented hypersensitivity;
coronary or cerebral arteriosclerosis; renal impairment |
Interactions |
Epinephrine or ephedrine may
decrease effects; ethanol increases toxicity |
Pregnancy |
C - Safety for use during pregnancy
has not been established. |
Precautions |
Caution in tachycardia, peptic
ulcer, and gastritis; cerebrovascular occlusions and myocardial
infarctions can occur |
Drug Category: Antihypertensive agents --
Sodium nitroprusside is DOC for most hypertensive emergencies. It is potent,
rapid in onset, and has a relatively short duration.
Drug Name
|
Nitroglycerin (Nitro-Bid) --
Decreases coronary vasospasm, which increases coronary blood flow. Also
induces vessel dilatation, decreasing cardiac workload. |
Adult Dose |
400 mcg SL tab or spray q5min up to
3 doses
Alternatively, 5-10 mcg/min IV titrating upward to keep SBP >90 mm Hg or
to decrease MAP by 25%
|
Pediatric Dose |
Continuous 0.1-1 mcg/kg/min IV
infusion |
Contraindications |
Documented hypersensitivity; severe
anemia; shock; postural hypotension; head trauma; closed-angle glaucoma;
cerebral hemorrhage |
Interactions |
Aspirin may increase serum nitrate
concentrations; calcium channel blockers may cause marked symptomatic
orthostatic hypotension (dose adjustment of either agent may be
necessary) |
Pregnancy |
C - Safety for use during pregnancy
has not been established. |
Precautions |
Caution in coronary artery disease
and low SBP |
Drug Name
|
Sodium nitroprusside (Nitropress)
-- Reduces peripheral resistance by acting directly on arteriolar and
venous smooth muscle. |
Adult Dose |
0.3-0.5 mcg/kg/min IV initial
infusion, increase in increments of 0.5 mcg/kg/min; titrate to desired
effect
Average dose: 1-6 mcg/kg/min; rates >10 mcg/kg/min may lead to cyanide
toxicity
|
Pediatric Dose |
Administer as in adults
|
Contraindications |
Documented hypersensitivity;
subaortic stenosis, idiopathic hypertrophic; atrial fibrillation or
flutter |
Interactions |
None reported
|
Pregnancy |
C - Safety for use during pregnancy
has not been established. |
Precautions |
Caution in increased intracranial
pressure, hepatic failure, severe renal impairment, and hypothyroidism;
in renal or hepatic insufficiency, nitroprusside levels may increase and
can cause cyanide toxicity; sodium nitroprusside has ability to lower BP
and thus should be used only in those patients with MAP >70 mm Hg |
Drug Name
|
Hydralazine (Apresoline) --
Principal indication is treatment of eclampsia. Decreases systemic
resistance through direct vasodilation of arterioles. |
Adult Dose |
5-20 mg IV q4-6h prn initial dose;
increase dose prn; change to PO ASAP |
Pediatric Dose |
0.1-0.2 mg/kg/dose IV q4-6h prn;
not to exceed 20 mg or 1.7-3.5 mg/kg/d divided in 4-6 doses |
Contraindications |
Documented hypersensitivity; mitral
valve rheumatic heart disease |
Interactions |
MAOIs and beta-blockers may
increase toxicity; pharmacologic effects may be decreased by
indomethacin |
Pregnancy |
B - Usually safe but benefits must
outweigh the risks. |
Precautions |
Has been implicated in myocardial
infarction; caution in suspected coronary artery disease |
FOLLOW-UP
Further Inpatient Care:
Patients with a true hypertensive emergency
require the careful titration of IV medications for good control and a
smooth reduction of their BP.
- Close monitoring is required; therefore, an intensive care unit is the
most suitable place for admission.
- Other problems or comorbid conditions need to be addressed
appropriately (ie, surgery for aortic dissection).
Further Outpatient Care:
- Hypertension is a chronic problem. The most important factor in a
patient's overall risks of morbidity and mortality is appropriate
long-term care.
- If a patient presents with a high BP but ED evaluation reveals no
evidence of end-organ damage, the patient does not need immediate
treatment in the ED. Patient does require proper follow-up.
- The Joint National Committee on High Blood Pressure has published a
series of recommendations for appropriate follow-up, assuming no end-organ
damage.
- For a systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg, confirm BP
within 2 months.
- For systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg,
evaluate/refer within 1 month.
- For systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg,
evaluate/refer in 1 week.
- For systolic BP greater than 210 mm Hg/diastolic greater than 120 mm
Hg, evaluate/refer immediately.
Transfer:
- Transfer requirements are based on the ability of the institution to
care for the patient and the patient’s associated comorbid conditions.
- A patient with uncomplicated hypertensive emergency needs only an
ICU setting and a physician.
- Patients with comorbid conditions, such as aortic dissection or
subarachnoid hemorrhage, may require transfer to a higher level of care.
Deterrence/Prevention:
- Good long-term control of hypertension is the best method for
prevention of acute hypertensive emergencies.
- Patient education and close follow-up in patients who have had a
hypertensive crisis are essential to prevent recurrent hypertensive
emergencies.
- Proper use of antihypertensive medications by primary care physicians
is the major tool in avoiding development of hypertensive emergencies.
Complications:
- Abrupt lowering of the BP may result in inadequate cerebral or cardiac
blood flow, leading to stroke or myocardial ischemia.
Prognosis:
- The 1-year mortality rate is higher than 90% for patients with
untreated hypertensive emergencies.
- Median survival duration is 144 months for all patients presenting to
the ED with a hypertensive emergency.
- Five-year survival rate among all patients presenting with
hypertensive crisis is 74%.
Patient Education:
- Patients need continuing education about antihypertensive medications
and complications arising from inadequate BP control.
- Dangers of uncontrolled hypertension must be stressed, including
associated serious morbidity and death.
- Education and maintenance of BP control are important to help prevent
further complications.
MISCELLANEOUS
Medical/Legal Pitfalls:
- Administering long-acting oral/sublingual medications to acutely lower
nonurgent elevations in BP
- Failure to arrange timely and appropriate follow-up
- Failure to recognize the serious complications of severe hypertension
BIBLIOGRAPHY
- Bennett NM, Shea S: Hypertensive emergency: case criteria,
sociodemographic profile, and previous care of 100 cases. Am J Public
Health 1988 Jun; 78(6): 636-40
[Medline].
Calhoun DA, Oparil S: Treatment of hypertensive crisis [see comments].
N Engl J Med 1990 Oct 25; 323(17): 1177-83[Medline].
Danish Multicenter Study: Emergency treatment of severe hypertension
evaluated in a randomized study. Effect of rest and furosemide and a
randomized evaluation of chlorpromazine, dihydralazine and diazoxide.
Danish Multicenter Study. Acta Med Scand 1980; 208(6): 473-80[Medline].
Ferguson RK, Vlasses PH: Hypertensive emergencies and urgencies. JAMA
1986 Mar 28; DA - 19860418(12): 1607-13[Medline].
Houston M: Pathophysiology, Clinical Aspects, and Treatment of
Hypertensive Crises. In: Progress in Cardiovascular Diseases 1989; XXXII:
99-148.
JNCV: The fifth report of the Joint National Committee on Detection,
Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1993 Jan
25; 153(2): 154-83[Medline].
Lavin P: Management of hypertension in patients with acute stroke.
Arch Intern Med 1986 Jan; 146(1): 66-8[Medline].
Ledingham J: Management of Hypertensive Crisis. In: Hypertension 5
1983; supp III: 114-118.
Lip GY, Beevers M, Beevers DG: Complications and survival of 315
patients with malignant-phase hypertension. J Hypertens 1995 Aug; 13(8):
915-24[Medline].
McRae RP Jr, Liebson PR: Hypertensive crisis. Med Clin North Am 1986
Jul; DA - 19860724(4): 749-67[Medline].
Murphy C: Hypertensive emergencies. Emerg Med Clin North Am 1995 Nov;
13(4): 973-1007[Medline].
Panacek E: Controlling Hypertensive Emergencies: Strategies for
Prompt, Effective Therapeutic Intervention. In: Emergency Medicine Reports
1992; 13: 53-61.
Ram CV: Management of hypertensive emergencies: changing therapeutic
options. Am Heart J 1991 Jul; 122(1 Pt 2): 356-63[Medline].
Reuler JB, Magarian GJ: Hypertensive emergencies and urgencies:
definition, recognition, and management. J Gen Intern Med 1988 Jan-Feb;
3(1): 64-74[Medline].
Strandgaard S, Paulson OB: Cerebral autoregulation. Stroke 1984
May-Jun; DA - 19840709(3): 413-6[Medline].
|