Manual of Cardiovascular Diagnosis and Therapy

Previous Chapter | Next Chapter >

CHAPTER 13. Hypertensive crisis

Quick Links to Sections in this Chapter

–Definition. Hypertensive crisis is a medical emerg...

–Incidence. The true incidence of hypertensive cris...

–Pathophysiology. The most significant lesion assoc...

–Diagnosis. The initial diagnostic workup should be...

–Therapy. Once the diagnosis of hypertensive crisis...

–Selected Readings

  1. Definition. Hypertensive crisis is a medical emergency requiring immediate action. Hypertensive crises are often categorized into emergencies and urgencies (Table 13-1). This chapter focuses on hypertensive emergencies. A hypertensive emergency is characterized by some or all of the following signs: (i) sudden or sustained blood pressure rise to diastolic greater than 120 mm Hg, (ii) papilledema (not always present), (iii) evidence of progressive decrease in renal function, (iv) presence of heart failure or dissection of the aorta, and (v) presence of neurologic dysfunction.

    An alternative term for hypertensive crisis is malignant hypertension. In this chapter, the terms are used interchangeably.

    Hypertensive crisis may present in a variety of ways demanding emergency treatment (Table 13-1). Treatment should assume higher priority than diagnostic procedures. Many of the complications of hypertensive crisis can be avoided or diminished by prompt and effective treatment. Management of hypertensive crisis is often performed in the hospital and by means of intravenous drugs. However, potent oral antihypertensive agents can be used, and under specific, carefully controlled circumstances, some patients can be managed as out-patients.

  2. Incidence. The true incidence of hypertensive crisis is difficult to assess. In patients with previously diagnosed hypertension, it is estimated that malignant hypertension arises in 2% to 7% of patients at some time during the course of their illness. Those at highest risk are 40 to 60 years old with a 2-to 10-year history of poorly controlled blood pressure. Malignant hypertension arising in a previously normotensive patient is extremely rare, although isolated cases exist.

  3. Pathophysiology. The most significant lesion associated with malignant hypertension is focal necrosis of arteries and arterioles known as "fibrinoid necrosis." Although this pathologic change may be found in any end organ, it is most common and significant in the kidney, retina, and brain.

    Hypertensive crisis may be associated with a variety of underlying and intercurrent conditions and illnesses (Table 13-2).

  4. Diagnosis. The initial diagnostic workup should be minimal, with emphasis placed on blood pressure reduction. Parts of the detailed diagnostic plan presented in this section may be performed during the patient's hospitalization.

    1. History. A brief history should be taken on admission (Table 13-3). Of particular importance is a history of hypertension and the drugs have been used for its treatment. The history should focus on neurologic, renal, and cardiac symptoms, both to assess the degree of end organ damage and to rule out other cardiac, renal, or neurologic emergencies.

    2. Physical examination. Physical examination (Table 13-4) should focus on accurate assessment of blood pressure and evidence of end-organ damage (particularly funduscopic and neurologic examinations). It is important to attempt to distinguish complications of hypertensive crisis from other neurologic emergencies or other causes of congestive heart failure and pulmonary edema. Evidence of significant intercurrent disease (such as coronary artery disease [CAD]) should be noted. Intercurrent diseases will influence how rapidly and with which agents blood pressure can be treated.

    3. Laboratory tests. Laboratory tests in the workup of hypertensive crisis are divided into two categories: (i) emergency (a rapidly obtainable laboratory profile should be made) and (ii) further diagnostic laboratory tests based on clinical impression and initial laboratory results (should be obtained after therapy is in progress). Valuable time should not be wasted on detailed diagnostic tests before therapy to reduce blood pressure is undertaken. The recommended laboratory tests are outlined in Table 13-5.

    4. ECG. It is essential to examine the ECG carefully, because evidence of myocardial ischemia may influence the choice of therapy. In patients with CAD, blood pressure reduction must proceed cautiously (see Section V.). Evidence of left ventricular hypertrophy is of prognostic value (left ventricular hypertrophy carries a poor prognosis in hypertensive crisis particularly if ST–T wave changes are present). Serial ECGs should be taken as therapy is initiated (particularly during the first half-hour; when rapid-acting vasodilators are used, patients should have continuous ECG monitoring). Daily ECGs should be obtained for a short period of time to assist in the diagnosis of myocardial necrosis.

    5. Chest x-ray examination. A good quality posteroanterior chest x-ray film to examine cardiac chamber size and lung fields should be taken once therapy has commenced. Except for rare cases of coarctation of the aorta, the film will not yield a diagnosis in patients with hypertensive crisis.

    6. Other radiologic studies. Other radiologic studies should be undertaken only for specific clinical reasons, namely, intravenous pyelogram, renal angiography, and computed tomography scanning (Table 13-5).

    7. Catheterization and angiography. Cardiac catheterization and angiography have no role in the diagnostic workup of hypertensive crisis with two exceptions.

      First, catheterization and aortography are important in the rare instance in which one suspects that coarctation of the aorta underlies hypertensive crisis. Aortography may be undertaken later after therapy has reduced blood pressure. Second, when dissection of the aorta is suspected as a complication of hypertensive crisis, emergency aortography is important. Renal catheterization and angiography may be undertaken with a high clinical suspicion that renal artery embolization underlies hypertensive crisis. These procedures, however, usually have no role in the initial diagnostic workup.

    8. Protocol for the diagnosis of hypertensive crisis

      1. Criteria for the diagnosis. At least two of the following must be present: (i) sudden or sustained blood pressure rise to greater than 120 mm Hg diastolic, (ii) papilledema, (iii) evidence of progressive decrease in renal function, (iv) evidence of neurologic dysfunction, and (v) evidence of pulmonary edema.

      2. Differential diagnosis. Two critical issues arise in the differential diagnosis of hypertensive crisis: (i) distinguishing between hypertensive crisis and other entities for which the treatment would be markedly different and (ii) recognizing intercurrent diseases and conditions that would modify the course of treatment. These two categories are outlined in Table 13-6 and discussed here.

      3. Entities that must be distinguished from hypertensive crisis

        1. Severe hypertension. It has been clearly established that one may have blood pressure elevations as high as 180/120 mm Hg or more without the end-organ damage associated with hypertensive crisis. Although such elevations also require urgent medical attention, they should be distinguished from hypertensive crisis, in which delay of even a few hours may be disastrous. Both severe hypertension and hypertensive crisis are most frequently the result of uncontrolled essential hypertension. Both may demand immediate hospitalization, possibly in a coronary care unit or intensive care unit. As noted earlier, selected, stable patients may be managed with meticulous and frequent out-patient visits. The rapidity with which the blood pressure must be lowered, and hence, the choice of therapeutic agents differs. In hypertensive crisis, an attempt is made to achieve significant blood pressure reductions within minutes to hours, whereas in severe hypertension, bed rest plus immediate two- or three-drug therapy administered orally will usually bring blood pressure under control within 24 to 48 hours.

        2. Surgically correctable neurologic emergencies. Neurologic emergencies can occur both as a result of hypertensive crisis and independently of it.

          All patients with neurologic changes that are possibly secondary to hypertensive crisis must receive a careful neurologic examination and appropriate laboratory studies to rule out potentially correctable neurologic disease of other origin. Neurologic disorders that must be ruled out include (i) infiltrating and rapidly growing cerebral and glial tumors, (ii) pseudotumor cerebri, (iii) significant intracerebral bleeding, (iv) seizure disorders secondary to cortical scars in patients with hypertension, (v) edematous cerebral infarcts, and (vi) high brainstem lesions causing elevated blood pressure. In each of these conditions, headache, convulsions, or focal neurologic signs may be present. The key distinction between these conditions and neurologic dysfunction based on severe hypertension is that, in the latter, reduction in blood pressure results in symptomatic improvement. Spinal tap may be warranted in some settings. Cerebrospinal fluid findings in hypertensive crisis include elevated pressure and elevated protein; gross blood is rare. Computed tomography scanning is usually helpful in ruling out mass lesions or acute central nervous system bleeding.

        3. Anxiety with labile hypertension. Occasionally, it is necessary to distinguish between hypertensive encephalopathy and anxiety accompanying labile hypertension. The distinction is significant because anxiety will respond to sedatives, tranquilizers, or both, whereas hypertensive encephalopathy requires immediate blood pressure control. In general, the patient with anxiety expresses multiple complaints, often including dizziness. Physical examination of this patient shows normal retinal vasculature, normal cardiac findings, and no focal neurologic findings. Treatment should be directed toward relief of anxiety. As the patient's psychological distress recedes, blood pressure returns to lower levels, at times, even normalizing.

        4. Pulmonary edema with left ventricular failure. Patients with pulmonary edema secondary to cardiac disease occasionally present with marked elevation of blood pressure. In this situation, blood pressure will respond to the standard therapy as outlined in Chapter 5.

      4. Intercurrent diseases for which special precautions must be observed in the treatment of hypertensive crisis

        1. Toxemia of pregnancy. The diagnosis of toxemia will be apparent from the clinical setting. This diagnosis has important treatment implications, discussed in Section V.A.5.

        2. Pheochromocytoma. The presence of a pheochromocytoma is suggested by elevated catecholamines, metanephrine, or vanillylmandelic acid in a 24-hour urine. Treatment is discussed in Section V.A.5.b.

        3. Stroke. The diagnosis of stroke is important because it will influence the rate of blood pressure reduction (slower if a stroke is thought to have occurred or to be in process). Diagnosis is made by history, either from patient or family, or by complete neurologic examination. Computed tomography scan and spinal tap are often helpful.

        4. Dissecting aortic aneurysm. Diagnosis is largely by history, with sudden onset of severe thoracic, back, or abdominal pain. Chest x-ray films usually show a widened mediastinum. Emergency transesophageal echocardiography and/or aortography is essential to confirm the diagnosis. Treatment is discussed in Section V.A.5.d.

        5. Renal insufficiency. Patients presenting with severely elevated blood pressure and blood urea nitrogen greater than 60 have a poor long-term prognosis. Some investigators believe that these patients have irreversible renal insufficiency with progressive renal dysfunction despite blood pressure reduction and dialysis. Others point out that renal function may return after long periods of dialysis (up to 6 months). The return of renal function is a rare phenomenon. There is no evidence that rapid reduction of blood pressure contributes to long-term deterioration of renal function.

        6. CAD. The increased afterload that accompanies marked elevation of blood pressure increases myocardial oxygen demand and can exacerbate the symptoms of CAD. Chest pain generally diminishes when blood pressure is brought under control. The diagnosis is made by history and ECG.

          Agents such as hydralazine and diazoxide should be avoided because of the added cardiac work load owing to sympathetic reflex stimulation with resultant increased heart rate (see Section V.A.5.f.).

  5. Therapy. Once the diagnosis of hypertensive crisis has been established and initial laboratory work rapidly completed (within 30 minutes), the first priority is to reduce the blood pressure as rapidly and safely as possible. A good general target is reduction of diastolic blood pressure to 100 to 110 mm Hg. A wide variety of drugs with different properties, times of onset, and durations of action are available for use in hypertensive crisis. Furthermore, the intercurrent conditions outlined in the previous section may dictate different approaches.

    1. Medical treatment

      1. Drugs. The clinical properties, dosage schedules, and side effects of the drugs discussed here are listed in Table 13-7. There are basically two types of drugs available: (i) rapid-acting agents (nitroprusside, nitroglycerin, diazoxide), which act quickly but require close monitoring, and (ii) slower acting drugs (hydralazine, methyldopa), which are more gradual but smoother in onset of action, thus requiring less monitoring.

        The drugs most commonly used are all administered parenterally. An important goal of therapy is to switch to long-term oral antihypertensive therapy as soon as the clinical situation allows. Selected patients may be managed with oral agents alone (Table 13-7).

        1. Hydralazine. Hydralazine can be employed either intramuscularly or intravenously. It works by directly dilating peripheral resistance vessels (arterioles). The onset of action of hydralazine is approximately 15 minutes. Its chief disadvantages are that (i) it is not predictably effective in blood pressure reduction, and (ii) it provokes reflex cardiac sympathetic stimulation (this reflex arc can be blunted by administering intravenous beta-blockade [metoprolol, atenolol, propranolol] or pretreating with reserpine or methyldopa).

        2. Diazoxide. Acting through the same mechanism as hydralazine, diazoxide is more powerful and more predictably effective. It may be less effective in severely uremic patients. It must be administered intravenously and rapidly (10 to 20 seconds) and if not effective may be readministered in 30 minutes. The reflex tachycardia it provokes may be blunted by intravenous beta-blockade. Because it causes sodium retention, diazoxide should always be coadministered with a diuretic (intravenous furosemide 10 to 40 mg).

        3. Nitroprusside. Nitroprusside is a potent and predictably effective drug for hypertensive emergency. It works primarily through arteriolar dilatation but has some venous effects as well. It acts immediately and requires constant blood pressure monitoring (arterial line). Thiocyanate toxicity may be a problem in long-term use.

        4. Nifedipine. Oral nifedipine is a potent arteriolar vasodilator that can rapidly control marked hypertension. The drug is a calcium channel blocker. Some patients experience an excessive drop in blood pressure that may be dangerous. Therefore, nifedipine is not advised for the therapy of patients with hypertensive crisis.

        5. Labetalol. Although several beta-blockers can be given parenterally (e.g., propranolol, esmolol, metoprolol and atenolol), labetalol is one of the most commonly employed beta-blockers in the intensive care unit for hypertensive emergencies. Labetalol is a racemic mixture of a selective alpha1 agonist and a nonselective beta-blocker. It promptly reduces both peripheral vascular resistance and cardiac contractility. Because the beta-blocker component of labetalol prevents significant changes in cardiac output or reflex tachycardia, it is particularly valuable when CAD and hypertensive crisis coexist.

      2. Activity. During the acute phase of a hypertensive crisis, the patient should be confined to strict bed rest. For many of the parenteral therapies just outlined, 30-degree elevation of the head of the bed is beneficial. Activity may be increased once blood pressure is controlled.

      3. Diet. In the acute phase of hypertensive crisis, patients are given nothing by mouth. Once pressure is controlled, only moderate salt restriction, used as part of long-term antihypertensive therapy, is necessary. In patients with renal failure complicating hypertensive crisis, protein restriction may also be necessary.

      4. Environmental support. Patients with a hypertensive crisis are acutely ill and often extremely anxious. A quiet supportive atmosphere is beneficial.

      5. Specific diseases with accelerated or malignant hypertensive potential. A number of disease states can be complicated by severe or accelerated hypertension. These entities may require special diagnostic or therapeutic intervention.

        1. Toxemia of pregnancy. Two drugs are as a rule contraindicated: (i) reserpine, tends to increase the likelihood of seizures; and (ii) trimethaphan, causes fetal ileus and stops labor.

        2. Pheochromocytoma. Phentolamine (Table 13-7) is the treatment of choice for paroxysmal hypertension in previously diagnosed pheochromocytoma. Oral phenoxybenzamine (10 to 40 mg per day) should also be begun immediately. Oral and/or intravenous beta-blockade is a useful adjunct to blunt tachycardia and prevent angina in patients with CAD.

        3. Stroke. Blood pressure should be diminished more gradually if the possibility of an intercurrent stroke exists. The risk of "completing" an occlusive stroke may be decreased by using drugs that increase cardiac output such as hydralazine or diazoxide.

        4. Dissecting aortic aneurysm. Agents that either leave cardiac output unchanged or reduce it (beta-blockade, methyldopa, reserpine, trimethaphan) are recommended for lowering blood pressure when aortic dissection is suspected. Agents that increase cardiac output and hence pulse pressure (hydralazine, diazoxide, nitroprusside) are contraindicated unless the patient is first treated with intravenous beta-blockade, for example, metoprolol, atenolol, propranolol, or esmolol.

        5. Renal insufficiency. Treatment for renal insufficiency complicating hypertensive crisis may include dialysis and may rarely include nephrectomy and transplantation. The drug of choice in the acute setting is diazoxide (which increases cardiac output and renal perfusion). Calcium channel blockers are also indicated in this setting. ACE inhibitors are contraindicated.

        6. CAD. Hydralazine and diazoxide are contraindicated because of their effect on heart rate (reflex tachycardia). The drugs of choice are beta-blockers, alone or in combination with nitroprusside or ACE inhibitors.

    2. Surgery. Surgery has little role in the acute management of hypertensive crisis. With two conditions, however, surgical intervention is necessary: (i) pheochromocytoma and (ii) dissection of the aorta.

      1. Pheochromocytoma (see Chapter 11 for details). Surgery should be undertaken under pharmacologic coverage of both alpha- and beta-adrenergic blockade.

      2. Dissecting aortic aneurysm. Some controversy exists over the relative merits of surgical versus medical therapy for acute dissection of the thoracic aorta (see Chapter 26). Evidence seems to support surgical treatment for ascending aortic dissections or any dissection complicated by acute bleeding. Stable descending aortic dissections can often be treated medically but eventually may require surgery.

    3. Protocol for acute treatment of hypertensive crisis. The following sequence is recommended:

      1. Brief history (special attention paid to cardiovascular and neurologic systems, renal function, and medications)

      2. Physical examination (look for end-organ damage—central nervous system, cardiac, renal)

      3. 12-Lead ECG

      4. Intravenous line started (central venous pressure obtained if possible)

      5. Arterial line needed if trimethaphan or nitroprusside is to be given

      6. Baseline blood and urine (complete blood cell count, blood urea nitrogen, creatinine, electrolytes, glucose levels, urinalysis, urine culture)

      7. Parenteral (occasionally oral) therapy begun based on clinical situation (Table 13-7)

      8. Chest x-ray study (posteroanterior)

      9. Admission to hospital usually indicated. ECG monitoring necessary.

      10. Reassessment and alteration of therapy on the basis of initial clinical response and laboratory studies

      11. Further laboratory investigation considered to elucidate the cause of the hypertensive crisis or the resultant end-organ damage

Selected Readings

Back to Quick Links

Heyka RJ. Evaluation and management of hypertension in the ICU. In: Rippe JM, Irwin RS, Fink MP, et al., eds. Intensive care medicine. Boston: Little, Brown and Company, 1995.

A thorough and up-to-date summary of treatment options for hypertensive crisis.

Kincaid-Smith, P. Malignant hypertension: mechanisms and management. Pharmacol Ther 1980;9:245–269.

Updates Dr. Kincaid-Smith's classic article of 1958.

Kincaid-Smith P, McMichael J, Murphy E. The clinical course and pathology of hypertension with papilledema (malignant hypertension). Q J Med 1958;27:117.

The classic article on malignant hypertension; describes clinical characteristics and natural history in detail; out of date in terms of therapy.

The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med 1997;157:2413–2446.

Consensus recommendations on all aspects of hypertension by the Joint National Committee supported by the National Institutes of Health, Bethesda, Maryland.

Varon J, Marik PE. The diagnosis and management of hypertensive crises. Chest 2000;118:214–227.