Hypertensive Emergencies
KEY POINTS
1 Most cases of severe hypertension in the ICU do not stem from an exotic cause but are the result of patients interrupting previously efficacious treatment for essential hypertension. Initial episodes of severe hypertension clearly should be investigated for a secondary cause.
2 When organ failure accompanies severe hypertension, blood pressure generally should be reduced within minutes; in the absence of organ failure, reduction over hours to days is not only acceptable but also desirable.
3 If immediate parenteral therapy is indicated for hypertensive crises with associated organ failure, sodium nitroprusside is in most cases the initial drug of choice. Nicardipine and labetalol are reasonable alternatives with niche advantages.
4 Oral therapy should be initiated early in the hospitalization to minimize the duration of parenteral therapy and ICU stay.
5 For most hypertensive crises requiring treatment, a mean arterial pressure of 110 mm Hg represents a reasonable initial BP target.
6 Patients with chronic severe hypertension often do not tolerate rapid, profound BP reductions, because cerebral autoregulation is reset by chronic hypertension. More harm can be done by hypotension than persistent hypertension.
▪ DEFINITIONS
Historically, the term “malignant hypertension” was defined by severe elevations of blood pressure (BP) and advanced retinopathy and papilledema. For patients meeting this definition, accompanying organ dysfunction was common but not universal. Similarly, “accelerated hypertension” was traditionally defined by comparable elevations of BP with lesser degrees of retinopathy in patients not exhibiting other organ damage. Unfortunately, this distinction is artificial and not very clinically useful. A simpler and more useful approach is to classify hypertensive crises by the presence or absence of life-threatening organ damage and hence, the urgency for treatment. When organ failure accompanies severe hypertension, interventions to reduce BP toward normal should be accomplished within minutes to hours, whereas in cases of hypertension without organ failure, more gradual BP reduction over hours to days is prudent.
▪ PATHOPHYSIOLOGY
Organ damage in hypertension is caused largely by a small vessel (arteriolar) necrotizing vasculitis that results in platelet and fibrin deposition and loss of vascular autoregulation raising systemic vascular resistance (SVR). In most patients, the pathophysiology of a hypertensive emergency is elevated SVR, not volume overload or elevated cardiac output. In reality, absent renal failure, ongoing hypertension results in natriuresis and intravascular volume contraction. Therefore, the most efficacious hypertension treatments reduce afterload, not preload and in some cases, intravenous volume expansion may even be necessary.
Although hypertension with a specific etiologic cause is rare in the general population, as many as half of all patients presenting for the first time with hypertension-induced organ failure are discovered to have an identifiable cause of hypertension. Young patients (<30 years of age) and those of African descent are more likely to have one of these secondary (usually, renovascular or endocrine) causes. Most hypertensive crises seen in the intensive care unit (ICU) are not, however, these newly discovered patients with secondary hypertension but rather patients, more commonly men, with known “essential” hypertension noncompliant with previously effective medical therapy. Oftentimes, these days cocaine use is a contributing factor. Regardless of the etiology, hypertension-induced organ failure is a serious problem. Historically, more than 90% of patients presenting with organ failure from hypertension were dead within a year of the diagnosis. Although the causes of death from
hypertension have not changed, (heart failure, myocardial infarction, stroke, and renal failure) mortality rates are now less than 10% provided the patient will simply take prescribed medications.
hypertension have not changed, (heart failure, myocardial infarction, stroke, and renal failure) mortality rates are now less than 10% provided the patient will simply take prescribed medications.
▪ HISTORY AND PHYSICAL EXAMINATION
The goals of the history and physical are to distinguish hypertension that requires immediate treatment from that to be corrected more gradually and to define the reason for the crisis. Obtaining a history of long-standing hypertension, antihypertensive drug use, or illicit or over-the-counter drug use is critical. Knowledge of preexisting organ failures also helps define the urgency of therapy. (Patients with well-established chronic renal failure do not require the same haste for BP control as patients acutely developing a similar elevation in serum creatinine.) Most patients with hypertensive crises are symptomatic but have nonspecific complaints. Headache occurs in approximately 85% of patients and blurred vision occurs in more than 50%. Cardiac symptoms (e.g., angina, congestive heart failure) and dyspnea are frequent, whereas nausea, vomiting, and focal neurological deficits are distinctly uncommon.
BP should be measured in all four limbs using an appropriate-size cuff. Failure to compare upper to lower extremity BP risks missing aortic coarctation or distal dissection, whereas failure to detect asymmetrical arm BP risks missing proximal aortic dissection. Surprisingly, many patients presenting with severe hypertension exhibit orthostatic symptoms because of pressure-induced diuresis. Physical examination should devote special attention to inspection of the ocular fundus and to examination of the neurologic and cardiopulmonary systems. Retinopathy is a sensitive indicator of hypertensioninduced organ injury. Papilledema, exudates, flame hemorrhages, and arteriolar constriction characterize the retinopathy traditionally associated with “malignant hypertension” and correlate well with renal involvement. After control of BP, retinal hemorrhages and papilledema resolve or heal over weeks to months. Confusion can be an important sign of hypertensive encephalopathy or ischemic or hemorrhagic stroke. Examination of the heart can reveal enlargement and a fourth heart sound with longstanding hypertension and a third heart sound in the presence of left ventricular decompensation. Murmurs of aortic or mitral insufficiency are important to identify as potential causes of pulmonary edema. Detection of an abdominal bruit, suggestive of renal artery stenosis, is an uncommon but critical physical finding.
Laboratory examination should include urinalysis, electrocardiogram, chest radiograph, blood smear, and determinations of electrolytes and creatinine. Evidence of left ventricular or atrial enlargement is common, occurring in about a quarter of patients. Renal insufficiency (i.e., serum creatinine > 3.5 mg/dL) is also present in about one fourth of cases. In patients with an elevated creatinine, urinalysis commonly shows proteinuria, hematuria, and red cell cast formation. The peripheral blood smear may demonstrate microangiopathic hemolysis. Hypokalemic alkalosis frequently occurs as a result of secondary hyperaldosteronism consequent to diuretic usage, but could be a clue to primary hyperaldosteronism.
▪ TREATMENT PRINCIPLES
Hypertension with Organ Failure (Hypertensive Emergency)
The aggressiveness of therapy should be guided by chronicity of the condition and evidence for organ damage, not by BP values alone. In fact, most patients with “severe hypertension” defined as a systolic BP greater than 160 mm Hg or a diastolic BP greater than 100 mm Hg have no acute organ dysfunction, and it is uncommon to see organ injury until the values exceed 220/130 mm Hg. A significant exception to this rule is the pregnant patient, in whom end-organ effects may be seen with diastolic values as low as 100 mm Hg. (Children can also have noteworthy end-organ damage at seemingly low BPs.) Patients requiring immediate treatment should be admitted to an ICU for closely monitored therapy. If there are doubts regarding the accuracy of noninvasive measurements, an arterial catheter can be inserted, but one is not routinely necessary.
Surprisingly, given the incidence of severe hypertension, there are no studies which demonstrate superiority of one drug class over another with regard to organ protection or survival. Given lack of proven advantage of a particular treatment, drug selection is typically made based on patient characteristics, drug cost, and physician preference. The ideal emergency antihypertensive would be potent, titratable, intravenous, rapid but short-lived, and would act by reducing afterload. Sodium nitroprusside, nicardipine, and to a lesser degree, nitroglycerin best fit this description. The advantages and disadvantages of commonly used drugs for severe hypertension treatment are shown in Table 22-1. Whenever possible, oral therapy should be initiated concurrently to minimize the duration of IV therapy and ICU stay.
TABLE 22-1 PARENTERAL DRUG THERAPY FOR SEVERE HYPERTENSION | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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As a general rule, when acute myocardial infarction, aortic dissection, pulmonary edema, cerebral hemorrhage, or hypertensive encephalopathy complicates severe hypertension, the goal should be to reduce diastolic BP by roughly 15% to 20% or achieve a diastolic BP near 110 mm Hg as quickly as possible (typically, within an hour). Slowly progressive renal insufficiency or mild left ventricular failure present less-threatening problems and mandate less-urgent treatment. In such cases, the goal should be to reduce the BP more gradually.
Hypertension Without Organ Failure (Hypertensive Urgency)
Although important, hypertension occurring in the absence of organ failure does not present the same urgency as that when organ failure is present. In this setting, a reasonable goal is also reduction in mean arterial BP by approximately 15% to 20%, usually to a diastolic value near 110 mm Hg but over a longer (24 to 48 h) period. Subsequent normalization of BP over days to weeks is safe and averts complications associated with rapid or excessive reductions.
An elevated BP alone does not necessarily require invasive monitoring or parenteral treatment. In fact, when hypertension is the result of cocaine, amphetamine, or phencyclidine ingestion, antihypertensive drugs may not even be needed; withholding the offending agent and providing judicious benzodiazepine sedation often suffices. In hypertensive urgencies, oral therapy can be successfully used (Table 22-2). Because many of these cases are the result of noncompliance with a previously effective regimen, merely restarting the patient’s outpatient medications is often effective. It is important to identify the reasons for noncompliance for if it is due to prohibitive drug costs or intolerable side effects (e.g., sedation, fatigue, or impotence), the problem is likely to be repeated. Currently, as there are so many choices for antihypertensive treatment, such problems can almost always be surmounted. In previously untreated patients, oral clonidine and nifedipine have been used as initial treatment. Of the two, clonidine reduces BP more gradually (over 30 to 120 min) and is less likely to result in hypotension. However, many physicians are reluctant to use clonidine because of its propensity to cause sedation and potential for bradycardia and high-grade atrioventricular block. Short-acting nifedipine should be used very cautiously if at all. Patients with the highest BP usually show the largest declines, and occasionally disastrous results occur when BP plummets to dangerous levels.
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