Which manifestation is an indication that a patient is having a hypertensive emergency?

1 What is a hypertensive crisis?

The term hypertensive crisis generally is inclusive of two different diagnoses, hypertensive emergency (HE) and hypertensive urgency. Distinguishing between the two is important because they require different intensities of therapy. It should be noted that older and less specific terminology, such as “malignant hypertension” and “accelerated hypertension,” should no longer be used. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7) defines HE as being “characterized by severe elevations in blood pressure (BP) (>180/120 mm Hg), complicated by evidence of impending or progressive target organ dysfunction.” JNC-7 defines hypertensive urgency as “those situations associated with severe elevations in blood pressure without progressive target organ dysfunction.” The updated JNC-8 did not change these definitions. The important thing to remember is that there is no absolute value of BP that separates the two syndromes. Instead, the most important distinction is whether there is evidence of impending or progressive end-organ damage, which defines an emergency, or other symptoms that are felt referable to the BP.

PATHOPHYSIOLOGY

The underlying pathophysiology of hypertensive crises still is not fully understood. The transition from mild hypertension or normotension to a hypertensive crisis usually is precipitated by an event that leads to an abrupt increase in blood pressure. Situations associated with this event may include cessation of hypertensive medications with potential rebound effects, consumption of illicit drugs, and severe pain, as well as several clinical syndromes. Blood pressure is determined by the product of cardiac output and systemic vascular resistance (BP = CO × SVR). In most hypertensive crises, the initial rise in blood pressure is secondary to increased systemic vascular resistance. The rise in systemic vascular resistance is believed to be caused by humoral vasoconstrictors.6 With the increase in blood pressure, mechanical stress on the arteriolar wall leads to endothelial damage and fibrinoid necrosis of the arterioles.6,7 Vascular damage leads to loss of autoregulatory mechanisms, ischemia, and acute end-organ damage, which prompts further release of vasoconstrictors, thereby initiating a vicious circle6,7 (Fig. 35-2).

Epidemiology and Etiology

Approximately 3% to 5% of patients who come to the emergency department because of symptoms of extreme hypertension will have a hypertensive crisis; of those, up to one third will have a hypertensive emergency.5,6 Men are more likely than women to come to medical attention with a hypertensive emergency, although the risk is also increased in women who are postmenopausal.6 Racial and ethnic factors mirror the prevalence of poorly controlled hypertension, with non-Hispanic blacks having the highest risk for a hypertensive emergency, followed by non-Hispanic whites and, lastly, Hispanics.7 Other risk factors for the development of hypertensive crisis include older age, increasing degrees of obesity, prior history of heart failure, hypertensive or coronary heart disease, the need for multiple antihypertensive medications, and a history of nonadherence to medications.8,9 The development of hypertensive crisis has also been linked to several social and socioeconomic factors, including cigarette smoking, lack of a primary care physician, and lack of medical insurance.9,10

Hypertensive emergency more commonly affects adults, but it can occur at any age. It can affect neonates with congenital renal artery hypoplasia, children with acute glomerulonephritis, pregnant teenage girls with eclampsia, middle-aged or older patients with treatment nonadherence, or elderly people with atherosclerotic renal artery stenosis. Such individuals are not typically accustomed to significant elevations in BP and may come to medical attention with signs and symptoms of hypertensive emergency at much lower BP levels than patients with long-standing, poorly controlled hypertension, in whom severe elevation in BP can be tolerated with less risk of target organ damage.

Hypertension

Hypertensive crises usually occur when monoamine oxidase inhibitors are combined with other drugs or foods that cause interactions, but in a few cases, a hypertensive crisis appears not to have been provoked by known drug or dietary precipitants [18]. From a review of 12 reports of spontaneous hypertension in patients taking tranylcypromine or phenelzine, it has emerged that a family history of hypertension may be a risk factor [19]. A significant increase in supine blood pressure without similar changes in standing blood pressure after the administration of tranylcypromine has also been described [20].

Hypertensive crisis

Hypertensive crises can manifest as severe headache, visual disturbances, acute myocardial infarction, congestive heart failure or cerebrovascular accident. It is a true medical emergency and should be treated as such in preferable setting of the intensive care unit that allows continuous monitoring of the patient’s haemodynamic parameters. Phentolamine (Regitine) is one of the choice medications, used as repeated (every 2 minutes) intravenous 5 mg boluses or as a continuous infusion (100 mg of phentolamine in 500 ml of 5% dextrose in water). Alternatively, nifedipine (10 mg orally or sublingually) can also be used to control hypertension, while labetalol should be used with caution (see above). Some drugs (e.g. tricyclic anti-depressants, metoclopramide and naloxone) can cause hypertensive crisis in patients with pheochromocytoma.

Management of a Hypertensive Crisis During Sedation or General Anesthesia

Hypertensive crises can be divided into hypertensive emergency or hypertensive urgency according to the presence or lack of acute target organ damage.33 In general medical practice a hypertensive crisis is said to exist when the SBP is 220 mm Hg or greater and/or the diastolic blood pressure (DBP) is 120 mm Hg or greater.34

In the area of sedation and general anesthesia no set blood pressure reading can be used to establish the presence of a hypertensive crisis. An acute rise in blood pressure is more significant than the actual numbers, but a systolic BP of >220 or a diastolic BP of >120 must be treated promptly.34 Sustained blood pressure elevations of 20% to 30% or greater during dental treatment, whether with or without sedation or general anesthesia, require immediate cessation of the treatment and management. Hypertensive crises are most likely to occur in patients with chronic, stable hypertension. The goal in management is to avoid rapid changes in blood pressure without compromising cerebral perfusion.35 To this end, antihypertensive therapy is not recommended in any patient unless there is severe hypertension (>220/120 mm Hg).36 Hypertensive crisis must be distinguished from a modest and transient elevation in blood pressure from causes previously listed. Deepening of the anesthesia or eliminating pain through the readministration of local anesthetics will often bring with it a return of the elevated blood pressure toward baseline values. However, when elevated blood pressure does not return to acceptable levels within a few minutes of onset, or if it continues to increase, the possibility of a hypertensive crisis must be considered and steps initiated to manage it.

Among the possible acute causes of the hypertensive crisis are cardiovascular complications, such as MI and dissecting aortic aneurysm; recreational drug use (e.g., cocaine); monoamine oxidase inhibitor use; pheochromocytoma; and thyroid crisis.35 It is important when evaluating the hypertensive crisis to distinguish whether the cause is cardiac or noncardiac.2 When significant elevation is noted in the patient's blood pressure, proceed as follows.

Step 1: Terminate dental treatment and P-Position the patient. Position the patient in an upright position (45 degrees or more upright).

Step 2: Assess C-Circulation, A-Airway, B-Breathing (basic life support), as indicated. Airway, breathing, and circulation are usually adequate.

Step 3: D-Definitive care.

Step 3a: Monitor blood pressure and heart rate and rhythm every 5 minutes and administer oxygen.

Step 3b: Activate EMS. Emergency medical personnel should be summoned.

Step 3c: Establish an IV infusion, if not already present. Where the cause of the hypertensive crisis is cardiac, such as HF, proceed as follows.

Step 3d: Administer nicardipine (Cardene). Start at 5 mg/hour and increase by 2.5 mg/hour every 5 to 15 minutes. Maximum dose is 15 mg/hour.

Step 3d: Titrate nitroprusside (Nipride) for acute, life-threatening hypertension at an infusion rate of 0.3 mcg/kg/min and increase slowly. The maximum dose is 10 mcg/kg/minute until the blood pressure is lowered to a desired point.

Step 3e: Administer beta-blockers (labetalol 5 mg every 2 minutes is preferred because it has both alpha- and beta-blocking properties).

When a noncardiac cause of the hypertensive crisis is present (e.g., anxiety, allergy, CVA), proceed as follows:

Step 3d: IV diazoxide (Hyperstat) should be administered in doses of 1 to 3 mg/kg up to 150 mg. This dose may be repeated every 5 to 10 minutes up to 600 mg.

Step 4: When anxiety is a major component of the hypertensive crisis, midazolam or diazepam, titrated intravenously, may be of some utility in managing the hypertension. Table 34.5 summarizes the drugs employed in management of the hypertensive crisis.

Situations may arise in which an IV infusion cannot be started and/or the appropriate parenteral antihypertensive drugs are not available for administration. In such instances the following regimen is suggested:

Step 1: Terminate dental treatment and P-Position the patient. Position the patient in an upright position (45 degrees or more upright).

Step 2: Assess C-Circulation, A-Airway, B-Breathing (basic life support), as indicated. Airway, breathing, and circulation are usually adequate.

Step 3: D-Definitive care.

Step 3a. Monitor blood pressure and heart rate and rhythm every 5 minutes and administer oxygen.

Step 3b. Oxygen should be administered.

Step 3c. Activate EMS. Emergency medical personnel should be summoned.

Step 3d. Sublingual nitroglycerin tablets (2 tablets of 0.4 mg) or two doses of Nitrolingual spray should be administered (spray medication onto the mucous membrane of the tongue). This dose may be repeated every 5 to 10 minutes if necessary.

Step 3e. On arrival of emergency medical assistance, an IV infusion will be established and appropriate antihypertensive drugs administered. The patient usually requires a period of hospitalization to ensure stabilization of blood pressure.

In summary, transient elevations in systolic and diastolic blood pressure can occur during dental procedures utilizing sedation or general anesthesia. These transient spikes in blood pressure are usually secondary to inadequate pain control and/or sedation. Another factor is inadequate maintenance of a patent airway, leading to the development of hypoxia and/or hypercarbia. Transient elevations in blood pressure do not usually require management employing antihypertensive drug administration.

Extremely rare is the situation in which sustained blood pressure elevations are encountered. When such occur following evaluation of the aforementioned etiologies, the administration of antihypertensive drugs may be indicated.

CONCLUSIONS

Hypertensive “crises” can be viewed as a spectrum, from nonurgent, to urgent, to truly emergent. Most instances of severe but asymptomatic hypertension need not be treated urgently unless required by underlying conditions. Hypertensive urgencies can be treated with oral or intravenous agents, whereas true emergencies require short-acting intravenous agents such as sodium nitroprusside. The treatment of accelerated or malignant hypertension is usually sufficiently urgent to preclude the use of agents that can help identify pathogenetic mechanisms and guide subsequent treatment (see Fig. 55-1). Therapeutic restraint, particularly in patients with severe but asymptomatic BP elevation, is required to avoid complications from unnecessary and overzealous lowering of BP.

MEDICAL HISTORY, PHYSICAL EXAMINATION, AND LABORATORY EVALUATION

Hypertensive crisis is a syndrome that usually develops in the setting of essential hypertension but is also seen in the setting of secondary hypertension. Hypertensive crisis may also develop in previously normotensive individuals who acquire preeclampsia, a pheochromocytoma, or acute glomerulonephritis or who experience drug withdrawal. The medication history detailing use of over-the-counter medications and illicit drugs is important to discuss with every patient. Risk factors associated with the development of malignant hypertension include age between 30 and 50 years, male gender, African-American ethnicity, and smoking (increases the risk by 2.5- to 5-fold).

The clinical presentation of hypertensive crisis is variable and related to end-organ damage (see Fig. 32.1). One of the most common complaints is headache, often increased in the morning, sudden in onset, and usually different in character from the patient's usual headache. Symptoms of hypertensive encephalopathy include headache, visual changes, and seizures. Individuals with hypertensive crisis may also complain of ischemic chest pain, renal symptoms, and GI problems (see Fig. 32.1). Early on, many patients experience spontaneous diuresis and often have intravascular volume depletion.

To exclude coarctation, the BP is measured in both arms. It is also important to exclude “pseudohypertension.” Pseudohypertension (caused by stiffening of the vascular wall that prevents vessel compression by a BP cuff) refers to an artificial increase (at times extreme) in the systolic and diastolic BP. Pseudohypertension can occur in atherosclerosis, Monckeberg's medial calcification, and metastatic calcification as experienced in end-stage renal disease. Pseudohypertension should be suspected when severe hypertension is noted in an individual without evidence of end-organ damage. The diagnosis is suggested by a palpable radial artery after proximal compression (Osler's maneuver).

There are distinct funduscopic changes in hypertension. Funduscopic changes in chronic hypertension include arteriolar thickening (manifested by increased light reflex), vascular tortuosity, and arteriovenous nicking (grades I and II). Increased arteriole damage results in decreased blood flow manifested by a silver wire pattern to the vessels. These funduscopic changes seen with chronic hypertension do not impact prognosis or treatment with regard to hypertensive crisis. On the other hand, with loss of cerebral autoregulation in malignant hypertension, evidence of vasculitis occurs in the retinal arteriolar and venous circulation. Acute changes including flame-shaped hemorrhages, white cotton-wool spots, yellow-white exudates, and eventually papilledema may be seen.

Other important physical examination findings include evidence of left ventricular hypertrophy (suggesting chronic hypertension), and the abdomen should be examined to exclude aortic aneurysm. A careful neurologic examination, including a mental status evaluation, should be done to rule out a cerebrovascular insult. Hypertensive neuroretinopathy is usually present but may be absent in patients in whom the pressure increase has been very abrupt, such as in cases of acute glomerulonephritis or catecholamine excess states.

The initial laboratory evaluation should include a serum sodium, chloride, potassium, bicarbonate, creatinine, blood urea nitrogen, complete blood count (with a peripheral smear to identify schistocytes), electrocardiogram, and urinalysis. Evidence of microangiopathic hemolysis may make it difficult to distinguish hypertensive crisis from primary vasculitis with secondary hypertension. Hypokalemic metabolic alkalosis suggests activation of the renin-angiotensin-aldosterone system. The blood urea nitrogen and creatinine levels are often elevated. The acute development of proteinuria and hematuria (20% of patients have gross hematuria, 50% microhematuria) is often found on urinalysis with occasional erythrocyte casts.

The differential diagnosis of hypertensive encephalopathy is shown in Figure 32.3. Several important diagnostic considerations help narrow the diagnosis: (1) symptoms of generalized brain dysfunction usually develop slowly (12–24 hr) with hypertensive encephalopathy and more acutely with ischemic stroke or cerebral hemorrhage; (2) focal neurologic findings are less common with hypertensive encephalopathy than with a CNS bleed; (3) papilledema is almost always noted with hypertensive encephalopathy and, if absent, should raise suspicion of another etiology; and (4) in comparison with an acute CNS bleed, mental status with hypertensive encephalopathy generally improves within 24 to 48 hours of treatment. Ultimately, an MRI should be performed. With hypertensive encephalopathy, edema may occur in the posterior regions of the cerebral hemispheres, particularly in the parieto-occipital regions, a finding called posterior leukoencephalopathy on MRI. However, brainstem involvement on MRI has also been reported.

SUMMARY

Hypertensive crisis is defined as a severe elevation in BP, such as a diastolic BP above 120 to 130 mmHg, and can be subclassified into either emergency or urgency (Figure 63-1). Hypertensive emergencies are relatively rare, and are said to be present only when BP elevation confers an immediate treat to the integrity of the cardiovascular system. In this setting immediate reduction in BP is required, generally by intravenous therapy in an intensive care unit. Unlike emergencies, urgency is said to be present when severe elevation in BP is not associated with end-organ injury. Outcome data attesting to benefits of acutely lowering BP in this condition are not available.

Clearly, patients with hypertensive crises are not good candidates for prospective randomized trials. Therefore, the accepted approach for patients with hypertensive urgency is to lower the BP more gradually over 24 to 48 hours with oral antihypertensive agents. In many patients, panic or anxiety may be the precipitating factor for the BP elevation, and therefore anti-anxiety treatment may be initiated. If anxiety is not the cause, or an anti-anxiety agent does not lower the BP, then oral antihypertensive agent should be started. Any drug that lowers BP precipitously should be avoided. The efficacy of nifedipine, captopril, clonidine, labetalol, nicardipine, and nitroglycerin seems to be similar. Choice of the appropriate agent should be based on the underlying pathophysiologic and clinical findings, mechanism of action, and the potential adverse effects.