Various inciting events can cause hypertensive emergencies. The majority of hypertensive emergencies occur in patients already diagnosed with chronic hypertension. Noncompliance with antihypertensive medications and use of sympathomimetics are two of the more common causes. These leading to a rapid rise in blood pressure beyond the body's innate autoregulation capacity.
The levels of hypertension that constitute a hypertensive emergency, while often quoted, are not universally established and are arbitrary. The rate of rising above baseline is likely a more important contributor and explains why patients without chronic hypertension may show signs of hypertensive emergency at much lower levels, while patients with longstanding hypertension may tolerate exceedingly high blood pressure without developing acute organ dysfunction.
It is estimated that about 30% of adults in America have hypertension. Of these, 1% to 2% will have a hypertensive crisis, a term inclusive of hypertensive emergency and hypertensive urgency. Acute pulmonary edema, cardiac ischemia, and neurologic emergencies are the most common types of acute target organ dysfunction.
The pathophysiology resulting in end-organ dysfunction in hypertensive emergencies is not fully understood. However, the mechanical stress on vascular walls likely leads to endothelial damage and a pro-inflammatory response. This results increased vascular permeability, platelet, and coagulation cascade activation, and fibrin clot deposition leads to hypoperfusion at the level of the target organ tissue.
In patients who present with markedly elevated blood pressure, a careful history and exam are necessary to determine which of these patients is having a true hypertensive emergency. Symptoms such as a headache, dizziness, altered mental status, shortness of breath, chest pain, decreased urine output, vomiting, or changes in vision warrant further evaluation. The source of the abrupt onset of hypertension should also be investigated to direct treatment.
The expected exam findings vary depending on the specific target organ most affected. With cardiac dysfunction, rales may be heard on lung auscultation, jugular venous distention or peripheral edema may be noted, and extra heart sounds may be apparent. In the event of a very rapid onset of hypertension, often seen with sympathomimetic abuse, marked dyspnea in the absence of peripheral edema due to flash pulmonary edema may be encountered.
Neurologic dysfunction may result in altered mental status, blurry vision, ataxia or other cerebellar dysfunction, aphasia, or unilateral numbness or weakness. A careful neurologic exam that includes a cranial nerve exam, strength, and sensation testing, as well as cerebellar tests and gait testing should be done.
Acute renal failure may also result in signs of pulmonary edema or peripheral edema.
The evaluation for hypertensive emergencies also depends on the symptoms and signs present. Once it is determined that a true hypertensive emergency is present or likely, labs such as metabolic panels, urinalysis, B-natriuretic peptide, and cardiac enzymes may be useful. An ECG is recommended in any patient suspected of having cardiac ischemia. Head computed tomography (CT) is recommended in patients with acute neurologic complaints or signs on an exam. A chest x-ray may prove to be useful in patients with shortness of breath. A chest x-ray may also show widening of the mediastinum in the setting or aortic dissection, but this is a relatively insensitive marker, and CT angiography of the chest and abdomen should be obtained to rule out or confirm a dissection and to determine the extent of the intimal tear.
While the specific target organ that is affected may dictate some specifics of treatment, rapid lowering of blood pressure is the mainstay of therapy for hypertensive emergencies. The goal would be to lower the mean arterial pressure by 20% to 25% within the first 1 to 2 hours. Several agents can be used, but the unifying characteristics are that they are rapidly acting and easily titratable. For this reason, oral medications, such as clonidine and nifedipine, play no role in the immediate management of a hypertensive emergency. Intravenous vasoactive drips such as labetalol, esmolol, nicardipine, and nitroglycerin are typically effective options.
In the past, hypertensive emergencies were frequently associated with kidney impairment, myocardial infarction, stroke or death. With more awareness and better control of blood pressure, the mortality has decreased significantly in the past 3 decades. However, after the acute treatment righter control of blood pressure is vital if one wants to lower the morbidity and mortality.
Failure to make a diagnosis or treatment of a hypertensive emergency can lead to the following:
Until the blood pressure is controlled bed rest is recommended.
A low sodium diet and weight loss are recommended.
The best way to prevent a hypertensive emergency is to remain compliant with antihypertensive medications. While routine hypertension can be managed by the primary health care provider, consultation from a cardiologist is recommended when the patient is on more than 3 antihypertensives and the blood pressure still remains elevated.
Markedly elevated blood pressure is common with acute ischemic stroke and requires a specialized approach. Per AHA/ASA guidelines, patients eligible for thrombolysis should have blood pressure lowered to SBP lower than 185 mmHg and DBP lower than 110 mmHg and maintained at SBP lower than 180 mmHg and DBP lower than 105 mmHg for the first 24 hours. For those not receiving thrombolytics, only levels SBP higher than 220 mmHg or DBP higher than 120 mmHg should be lowered as hypertension in acute stroke is usually transient and may be protective. A reasonable goal is about 15% decrease in mean arterial pressure.
In an acute hemorrhagic stroke, reduction of SBP to lower than 140 mmHg may improve functional outcomes. This requires an aggressive approach with rapidly titrated intravenous antihypertensives, and extreme vigilance is necessary to prevent hypotension, which causes decreased cerebral perfusion pressure and adds to the ischemic insult. Easily titratable medications with rapid onset and short duration of action, such as nicardipine, are recommended.
Aortic dissection also deviates in the degree of blood pressure lowering that is recommended. Traditional teaching is to lower the blood pressure to as low as organs will allow, with close monitoring of the patient’s mental status as a guide. Intravenous beta-blockers, most commonly esmolol, are first-line treatments due to their ability to lower blood pressure while avoiding reflex tachycardia and increased shear stress to the aortic wall. Classically, nitroprusside has been used as an adjunct to beta-blockers in the treatment of aortic dissection, but this has become an infrequent practice due to its association with rapid and profound hypotension, tachyphylaxis, as well as the potential for cyanide toxicity. Nicardipine with the addition of a beta-blocker would also be a reasonable choice.
Preeclampsia is a particularly troubling and difficult to manage hypertensive emergency since there are two patients to consider. The first-line therapy is magnesium sulfate, administered as a 4 g to 6 g loading dose followed by 1 g to 2 g/hour infusion. Care must be taken to monitor for urine output, deep tendon reflexes, and respiratory status. If further antihypertensives are needed, beta-blockers can be used, but only to treat SBP higher than 160 mmHg. Hydralazine was once touted as the preferred agent in pregnant patients; however, its delayed onset of action, prolonged duration, and unpredictable hypotensive effects make it a less than ideal choice. Regardless of the agent, the patient is likely to need close monitoring in a critical care setting.
Hypertensive emergency is not an uncommon presentation to the ER. Despite awareness of its high morbidity and mortality, at least 50% of patients with hypertension do not remain compliant with their medications. The problem is exacerbated when the only access for these patients is the emergency room. There are countless guidelines by national agencies and organizations on blood pressure control, but the many patients do not seem to appreciate the seriousness of hypertension. An interprofessional approach to management of hypertension is recommended beginning with the primary caregiver. The treatment of hypertension is best done as an outpatient; the few minutes spent with a cardiologist in a hospital very rarely makes any difference.
The pharmacist, nurse, and the primary practitioner have a vital role to play in the education of patients with hypertension. The need to regularly measure the blood pressure and follow up with the healthcare provider cannot be overemphasized. Patients need to be told to change their lifestyle, eat healthy, exercise, discontinue smoking, and remain medication compliant. Sadly, evidence-based guidelines have not translated in reducing the number of people still presenting to the ER with hypertensive emergencies. (Level V)
There are many case series indicating that in the short term management of hypertensive emergency has good outcomes but the long-term results remain unknown. Part of the problem is that patients are lost to follow up, and the medication regimen is frequently changed. Many studies indicate that untreated hypertensive emergencies have a very high morbidity and mortality and unless healthcare providers make a determined effort to educate the patient on the seriousness of hypertension, this trend is likely to continue.  (Level V)