Mr. J’s BP clearly needs to be lowered, and the primary question is how quickly this needs to be accomplished. In other words, is this a hypertensive emergency or hypertensive urgency? These syndromes are defined by the degree of BP elevation and whether there is acute end organ damage.
A hypertensive emergency exists when there is severe BP elevation and acute target organ involvement: acute neurologic syndromes (encephalopathy, cerebrovascular accident, intracerebral or subarachnoid hemorrhage), acute aortic dissection, acute coronary syndrome, acute pulmonary edema, acute kidney injury, severe preeclampsia/eclampsia, microangiopathic hemolytic anemia, or acute postoperative hypertension.
In hypertensive urgency, there is severe BP elevation without any acute TOD. The exact definition of “severe BP elevation” has not been established, but many experts use a cutoff of > 180/110–120 mm Hg. Common causes of hypertensive urgency and emergency include medication nonadherence, abrupt cessation of clonidine, CKD, renovascular disease, drugs (cocaine, PCP), systemic lupus erythematosus, eclampsia, and postoperative state; Cushing disease and pheochromocytoma are less common causes.
A hypertensive emergency is defined by the presence of TOD, not by the degree of BP elevation.
To some extent, the degree of the acute TOD in patients with very elevated BP depends on the time course of the BP elevation. For example, normotensive women in whom acute hypertension develops from eclampsia can have significant TOD at pressures of 160/100 mm Hg, whereas patients with chronic hypertension can be asymptomatic at much higher pressures. So, despite his very elevated BP, it is quite likely that Mr. J falls into the “hypertensive urgency” rather than the “hypertensive emergency” category. Nevertheless, hypertensive emergency is always the “must not miss” diagnosis in such patients (Table 23-10).
You tell the nurse to put Mr. J in an exam room. On further history, he has no shortness of breath, chest pain, edema, abdominal pain, feelings of confusion, vomiting, or focal weakness or numbness. He generally appears well and is clearly happy to have a new job. Physical exam confirms BP of 220/112 mm Hg, pulse of 84 bpm, and RR of 16 breaths per minute. There is no papilledema. Lungs are clear, jugular venous pressure is not elevated, there is an S4 and a 2/6 systolic ejection murmur without an S3, abdomen is nontender, there is no peripheral edema, and neurologic exam is normal.
Is the clinical information sufficient to make a diagnosis? If not, what other information do you need?
Table 23-10.Diagnostic hypotheses for Mr. J. ||Download (.pdf) Table 23-10. Diagnostic hypotheses for Mr. J.
|Diagnostic Hypotheses ||Demographics, Risk Factors, Symptoms and Signs ||Important Tests |
|Leading Hypothesis |
|Hypertensive urgency ||Absence of hypertensive emergency syndromes || |
|Active Alternative—Must Not Miss |
|Hypertensive emergencies Acute coronary syndrome ||Chest pain || |
|Aortic dissection || |
Chest, back pain
|Pulmonary edema || |
|Chest radiograph |
|Hypertensive encephalopathy || |
|Acute kidney injury || |
|Serum creatinine |
Leading Hypothesis: Hypertensive Urgency
A patient with chronic hypertension has extremely high BP; by definition, patients have no symptoms or signs of acute TOD.
Hypertensive urgency or emergency occurs in about 1% of adults with hypertension; with urgency occurring in three-quarters of these patients.
The most common presenting symptoms are headache (22%), epistaxis (17%), faintness (10%), psychomotor agitation (10%), chest pain (9%), and dyspnea (9%).
Must rule out acute TOD through history, physical, and selected laboratory tests.
BP should be measured in both arms, and pulses palpated in both the upper and lower extremities; all patients should have a complete cardiovascular and neurologic exam, including fundoscopic exam.
All patients should have a serum creatinine and urinalysis performed.
Patients with symptoms suggestive of myocardial ischemia or pulmonary edema should have an ECG, chest radiograph, and cardiac enzymes.
Patients with neurologic signs or symptoms need a head CT scan and sometimes a brain MRI.
In stable outpatients with chronically elevated BP, there is NOT an urgent need to reduce the BP, and it is fine if it takes several days for the BP to be reduced.
There are several ways to approach treatment, depending on the overall condition of the patient, whether the patient has been treated previously, and the ability of the patient to return for follow-up.
In patients who have stopped their medications, it is usually sufficient just to restart them.
In previously untreated patients, options include
Starting 2 long-acting agents, such as a diuretic and either a calcium channel blocker or ACE inhibitor
Beginning treatment with more rapid-acting agents, such as oral labetalol or clonidine, and then transitioning to longer acting agents; patients can be observed for several hours to assess their response to the short-acting agents.
Too rapid reduction of BP can lead to hypotension and cerebral hypoperfusion with stroke.
IV and sublingual medications can have unpredictable effects on BP and should be avoided in asymptomatic patients.
IV hydralazine causes a progressive and sometimes precipitous fall in BP 5–15 minutes after administration.
Although the circulating half-life of hydralazine is only 3 hours, the half time of its effect on BP is 10 hours.
Sublingual nifedipine causes completely unpredictable lowering of BP and should never be used.
Do not be in a hurry to normalize BP in patients without acute TOD!