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A 48-year-old man with no remarkable medical history was sent to the emergency department from a local urgent care facility because of cough, dyspnea, mild chest discomfort, lower extremity edema, and a blood pressure (BP) of 210/150 mm Hg. He had no fever, constitutional symptoms, blurry vision, headaches, back pain, weakness, palpitations, or tremors and no personal or family history of hypertension. He did not use alcohol, tobacco, or illicit drugs.
Physical examination at the emergency department revealed an overweight man with a BP of 222/167 mm Hg, pulse rate of 123 beats/min, temperature of 36.7°C, respiratory rate of 16 breaths/min, and oxygen saturation of 91% while the patient received 2 L/min of oxygen by nasal cannula. Peripheral pulses were equal and synchronous. Findings on cardiac examination were notable for a sustained laterally displaced apical impulse and a third heart sound with no murmurs. Pulmonary examination revealed bibasilar crackles and reduced breaths sounds at the right lung base. No masses or bruits were noted on abdominal examination. Pitting lower extremity edema was present to the knees bilaterally. There were no focal neurologic deficits. A funduscopic examination was not performed.
Initial laboratory studies yielded the following results (reference ranges shown parenthetically): hemoglobin, 16 g/dL (13.5-17.5 g/dL); creatinine, 2.0 mg/dL (0.8-1.3 mg/dL); sodium, 137 mEq/L (135-145 mEq/L); potassium, 3.8 mEq/L (3.6-5.2 mEq/L); and serum urea nitrogen, 38 mg/dL (8-24 mg/dL). The N-terminal pro-B-type natriuretic peptide level was 12,629 pg/mL (≤56 pg/mL). The troponin T value was 0.4 ng/mL at baseline, 0.2 ng/mL at 3 hours, and 0.3 ng/mL at 6 hours after presentation (<0.01 ng/mL). Urinalysis revealed no abnormalities. Findings on electrocardiography included sinus tachycardia, rightward axis, left atrial enlargement, and left ventricular hypertrophy with secondary ST-T abnormalities. Chest radiography showed notable cardiac enlargement as well as mild pulmonary vascular congestion and a small right pleural effusion.
Although accelerated/malignant hypertension may present with severely elevated BP, it cannot be diagnosed in the absence of documented funduscopic findings of retinal exudates, hemorrhages, or papilledema. Hypertensive urgency refers to severe elevation in BP without symptoms or evidence of acute or progressive target organ injury. In this patient, the clinical and laboratory findings suggest acute target organ damage with involvement of the heart and kidneys. Hence, hypertensive emergency is the most accurate diagnosis at this time. The clinical presentation and electrocardiographic findings are not consistent with acute coronary syndrome in the absence of typical chest pain, specific ST-T changes, or a marked increase in cardiac biomarker levels. Flash pulmonary edema refers to acute hypertensive pulmonary congestion in the setting of severe diastolic dysfunction, especially in elderly women with systemic hypertension.
The patient continued to have mild shortness of breath with a nonproductive cough but had no new symptoms suggestive of additional target organ damage.
Computed axial tomography of the chest with PE protocol is premature at this time in the absence of features concerning for aortic dissection or high probability for PE. Given the strong evidence of target organ damage, it is vital to address the underlying elevated BP precipitating the cardiac emergency; therefore, an IV antihypertensive infusion should be initiated immediately. Although oral medications are used to lower BP in hypertensive urgency, the presence of target organ damage in this case renders the use of oral β-blockers alone inadequate. No immediate surgical concerns warrant consultation at this time. Intensive care is required, and transfer to a lower level of care is inappropriate.
The patient received 3 IV boluses of metoprolol, and IV nitroglycerin infusion was initiated before transfer to the cardiac intensive care unit.
Hypertensive emergencies must be treated expediently to prevent progression of target organ damage. The goal at presentation is to carefully reduce the diastolic BP by 15% to 20% or to about 110 mm Hg over the first hour while monitoring for evidence of worsening target organ injury. In hypertensive crises without target organ damage, BP can be gradually reduced to baseline over the next 24 to 48 hours. The only indication for immediate reduction of BP within 10 minutes is aortic dissection, which is not present at this time. There is no evidence of ischemic stroke, which would require thrombolytic therapy and a prerequisite BP of less than 185/110 mm Hg. After the initial reduction of diastolic BP by 15% to 20%, systolic BP is gradually reduced by 25% over the next 6 hours.
The patient's BP on arrival at the cardiac intensive care unit was 199/105 mm Hg. He was transitioned to IV labetalol infusion with a plan for additional IV hydralazine boluses as needed for optimal control.
Computed axial tomography of the abdomen and pelvis may be useful to identify underlying causes of the severe hypertension. In particular, it would be helpful to rule out potential causes such as pheochromocytoma, primary aldosteronism, or renal cell carcinoma. However, it would be inappropriate as the immediate next step because the priority should be to correct target organ damage before undertaking a search for the underlying cause. Moreover, it would be relatively contraindicated by the presence of acute kidney injury. Transthoracic echocardiography would help characterize the type and severity of heart failure and differentiate potential causes of heart failure such as valvular disease, ischemia, and cardiomyopathy. Renal angiography would be premature at this time in the absence of evidence of renal artery stenosis. Although measurement of urinary metanephrine would be important to exclude pheochromocytoma as a cause of the hypertensive crisis, it should not take priority over characterizing the extent of target organ damage. No information obtained thus far provides any evidence to support an indication for right upper abdominal ultrasonography.
The patient underwent urgent TTE, which revealed severe left ventricular hypokinesis with an ejection fraction of 10% to 15%, grade 3/4 left ventricular diastolic dysfunction, and moderately increased concentric left ventricular wall thickness. There were no regional wall motion abnormalities. He had a sustained clinical response overnight in response to IV labetalol with systolic BP in the range of 180 to 200 mm Hg. He was transitioned to oral carvedilol at 6.25 mg twice daily and low-dose hydralazine at 10 mg thrice daily with further reduction in systolic BP to the mid 150 mm Hg range. Renal ultrasonography showed normal echogenicity, size, and cortical thickness of both kidneys and no focal mass, hydronephrosis, or renal artery stenosis. He was given a 40-mg dose of furosemide for diuresis with a resultant urine output of 2.3 L over the course of the night. He was transferred to the cardiology service the next day for further workup. However, progressive dyspnea developed over the course of the day, and an additional 20 mg of IV furosemide was administered. He was subsequently noted to have mild right arm weakness, right facial droop, and slurred speech. His systolic BP at that time ranged from 130 to 140 mm Hg. Hydralazine was withheld, and the dose of carvedilol was decreased. An urgent neurology evaluation was requested.
Although traditional risk factors for thromboembolism such as diabetes mellitus, hyperlipidemia, or arrhythmia were absent, the severely decreased left ventricular function raises the possibility of left ventricular thrombus. However, the recent TTE did not demonstrate an intraventricular thrombus, which makes an embolic stroke less likely. The neurologic deficits in this case were not preceded by a severe sudden headache, which is the classic presentation of a subarachnoid hemorrhage. The patient has no signs or symptoms that suggest the presence of an intracranial tumor. It is unlikely that he has an intracerebral hemorrhage because this disorder is typically associated with extremely high BP. Given his normalized BP at the time of onset of his neurologic deficits, cerebral hypoperfusion from impaired autoregulation in the setting of aggressive treatment of severe hypertension best explains the new findings.
Emergent computed axial tomography of the head was negative for intracranial hemorrhage, mass effect, or signs of acute stroke but demonstrated features consistent with chronic small-vessel ischemic disease as well as old lacunar infarcts in the thalamus and the corona radiata. The patient was transferred back to the cardiac intensive care unit for closer monitoring of his BP and frequent neurologic evaluations. Further neurologic examination on arrival was notable for improvement in his neurologic deficits with only a residual pronator drift in the right hand and diminished alternating movements. Antihypertensive medications were withheld, and a target systolic BP was set at 150 to 160 mm Hg for a period of 2 to 4 weeks. Magnetic resonance imaging and angiography of the head and neck without contrast showed no high-grade carotid stenosis or features suggestive of posterior reversible encephalopathy syndrome. Previously observed white matter infarcts and features of chronic ischemic changes were again seen. Over the next 4 days of hospitalization, carvedilol was reintroduced at low dose and was slowly titrated upward to maintain the new target BP. A diuretic regimen was initiated to correct the peripheral edema.
An evaluation for secondary causes of hypertension such as pheochromocytoma or hyperaldosteronism yielded negative findings because serum metanephrine, plasma aldosterone, and renin activity were all within normal limits. The urinary metanephrine level was mildly elevated but on repeated studies was found to be normal. The patient underwent an adenosine sestamibi stress test, which showed severe global hypokinesis but no evidence of infarction or stress-induced ischemia. Overnight oximetry obtained for evaluation of suspected sleep apnea yielded abnormal results, suggesting a sleep-associated breathing disorder. The patient was scheduled to undergo formal polysomnography in the outpatient setting. He was discharged in clinically stable condition a week after admission with a regimen of carvedilol, 6.25 mg twice daily, lisinopril, 5 mg/d, and oral furosemide, 80 mg/d.
More than a billion people worldwide are affected by systemic hypertension. It is estimated that 1% to 2% will develop severe acute elevations of BP requiring immediate medical therapy.1 Elevations of systolic BP greater than 179 mm Hg or diastolic BP greater than 109 mm Hg are usually referred to as hypertensive crisis.2 Such elevations are classified as hypertensive emergencies when target organ damage is present and as hypertensive urgencies when it is absent. Hypertensive crises are thought to result from a sudden increase in systemic vascular resistance. The ensuing ischemia and hypoperfusion of critical arterial beds (cerebral, coronary, and renal) result in a hypertensive emergency.
Common manifestations of hypertensive emergency are shortness of breath, chest pain, headache, altered mental status, and focal neurologic deficits. Hence, a comprehensive evaluation at presentation must be expedient and targeted toward identifying and preventing the progression of target organ damage. After elicitation of a complete history and a thorough physical examination (including funduscopic examination), initial studies should include a complete metabolic panel, a cardiac biomarker panel, a complete blood cell count with peripheral smear, urinalysis, chest radiography, and electrocardiography. Imaging studies such as computed tomography of the head and chest, magnetic resonance imaging, and echocardiography should be tailored to the appropriate clinical scenario. A blood sample should be obtained for evaluation of plasma renin activity and measurement of aldosterone and catecholamine levels when secondary hypertension is suspected.3
Immediate reduction of BP in a controlled manner should be accomplished in a monitored setting using a continuous infusion of a short-acting antihypertensive that can be titrated to prevent additional target organ damage, which may arise from hypoperfusion due to rapid and excessive correction of BP. It has been suggested that most patients in hypertensive crises are treated inappropriately.4,5 Only 15% of patients in the Studying the Treatment of Acute Hypertension registry received a continuous IV infusion of antihypertensive as first-line treatment.6 In hypertensive urgencies, gradual lowering of BP over a 24- to 48-hour period using oral medications is the recommended approach. Only in hypertensive emergencies should IV antihypertensive drugs be administered, with the goal of reducing mean arterial BP by no more than 25% within minutes to 1 hour and then, if BP is stable, to 160/100 to 160/110 mm Hg within the next 2 to 6 hours.7 A more practical goal may be to reduce diastolic BP by 15% to 20% or to about 110 mm Hg over a period of 30 to 60 minutes.8 Oral therapy can then be initiated as IV agents are titrated downward after BP control has been achieved. Volume expansion may be indicated to improve organ perfusion and prevent an abrupt decrease in BP on initiation of antihypertensive agents.8 There is no consensus on which IV antihypertensive agent should be used in hypertensive emergencies. Hence, the choice of IV agent(s) should depend on the clinical presentation.9 Currently, the preferred parenteral agents are nicardipine, clevidipine, labetalol, and esmolol.2 Nifedipine, nitroglycerin, and hydralazine should no longer be considered as first-line drugs in the management of hypertensive emergencies because of their serious adverse effects and toxicities.
In conclusion, because hypertensive crises are commonly encountered by clinicians, the ability to recognize, evaluate, and treat these disorders appropriately is paramount to reducing existing high rates of morbidity.
See end of article for correct answers to questions.
CORRECT ANSWERS: 1. c. 2. b. 3. a. 4. b. 5. e