Hypertensive urgency is a marked elevation in blood pressure without evidence of target organ damage, such as pulmonary edema, cardiac ischemia, neurologic deficits, or acute renal failure. Specific cutoffs have been proposed, such as systolic blood pressure greater than 180 or diastolic blood pressure greater than 110, but these are arbitrarily derived numbers that have not been associated with short-term morbidity or mortality. Given this, some have proposed reserving the term hypertensive urgency for patients with severely elevated blood pressure and significant risk factors for progressive end-organ damage such as congestive heart failure or chronic kidney disease. However, hypertensive urgencies are associated with a higher incidence of adverse cardiovascular events over the long term and warrant a nuanced approach focused on ensuring better blood pressure control, reducing catalysts for marked elevations of blood pressure, and reliably following up with primary care.
The etiology of acute elevations is variable. Noncompliance with antihypertensive therapy, use of sympathomimetics, and thyroid dysfunction are among the many possible causes of hypertensive urgencies. Even anxiety and pain may cause acute elevations in blood pressure and require a different treatment strategy.
Pseudohypertension, a falsely elevated blood pressure reading due to sclerotic or calcified arteries that do not collapse during inflation of a blood pressure cuff, is another possible cause of elevated blood pressure readings. Pseudohypertension should be considered in patients presenting without symptoms suggestive of end-organ dysfunction but with markedly elevated blood pressure despite seemingly aggressive management.
About 30% of American adults have hypertension. Of those, about 1% to 2% will have a hypertensive crisis, a term that encompasses both hypertensive urgencies and emergencies. Studies on the epidemiology of acute hypertensive crises are limited, possibly due to difficulties in parsing out when a patient's symptoms are related to their blood pressure versus some other cause. Obesity, female gender, history of cardiovascular disease, diabetes, smoking, and most importantly, noncompliance with antihypertensive medications are some of the risk factors associated with acutely elevated blood pressure.
The pathophysiology of hypertension is complicated and not fully understood. At baseline, perfusion of cardiac, renal, and brain tissue is tightly autoregulated by varying mechanisms. With chronic hypertension, the cerebral perfusion curve shifts to the right, accommodating a higher baseline blood pressure while maintaining a steady cerebral perfusion pressure.
The rapidity of blood pressure elevation is presumed to be an important factor in causing end-organ damage. Severe acute elevations are likely related to an influx of humoral vasoconstrictors, resulting in elevated systemic vascular resistance. The increased vascular wall stress and associated endothelial injury results in increased vascular permeability, activation of coagulation factors and platelets, and fibrin deposition. Continued endothelial injury and fibrinoid necrosis result in ischemia, which then leads to further release of vasoactive mediators and further injury.
The history and physical exam for patients with markedly elevated blood pressure should focus on determining whether or not the patient has signs of target organ damage. Symptoms warranting further evaluation include a headache, dizziness, shortness of breath, chest pain, vomiting, or changes in vision.
The physical exam starts with an accurate blood pressure reading, with a properly-sized cuff placed on a bare upper arm. If a properly-sized cuff is not available due to large arm circumference, wrist measurement may be the most accurate but should be interpreted with some caution due to lack of data compared to invasive measurements.
Other physical exam signs should be carefully evaluated. Signs of heart failure such as elevated jugular venous distention, rales on lung auscultation, or a gallop on heart auscultation indicate that the patient may be actively experiencing a hypertensive emergency rather than urgency. A detailed neurologic exam including cerebellar testing is also important to rule out central nervous system impairment. Finally, fundoscopy showing papilledema may be a significant finding mandating more aggressive therapy.
No routine evaluation for hypertensive urgencies exists. The goal is to rule out target organ damage. If the history and physical suggest that this may be present, lab testing or imaging such as metabolic panels, urinalysis, electrocardiogram, chest X-ray, and brain computed tomography may be useful.
Patients at high risk for rapidly evolving target organ damage warrant particular caution, such as those with chronic congestive heart failure, chronic kidney disease, coronary artery disease, or history of stroke. While there is little data to guide specific evaluation in such patients, a lower threshold to obtain lab testing, electrocardiography, or imaging should be considered.
Pregnant patients with elevated blood pressure also require extra caution. In these patients, especially in the absence of preexisting hypertension, preeclampsia can ensue at blood pressure levels much lower than commonly seen in hypertensive emergencies. In the absence of a history of hypertension, especially if the patient complains of potentially worrisome symptoms such as a headache, vision changes, or abdominal pain, lab testing should be obtained, including complete blood count, hepatic function panel, and lactic dehydrogenase.
The treatment for hypertensive urgency is to ensure better long-term blood pressure control. Emphasizing the need for compliance with medications and close primary care follow up is paramount. Patients without symptoms or signs of target organ damage have not been shown to benefit from aggressive antihypertensive therapy in the acute setting. Rapid lowering of blood pressure in these patients offers no benefit and carries the theoretical risk of causing relative hypotension and end-organ hypoperfusion, especially in those individuals who have longstanding severely elevated blood pressure. However, it may be beneficial to start these patients on oral antihypertensives with the goal of lowering the blood pressure slowly over 24 to 48 hours. Little data directly address what specific agent is ideal in this situation. More importantly, close follow-up within a week with a primary care provider should be scheduled to ensure improved blood pressure control and to initiate or titrate medications as needed.
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