Chapter 45. Hypertensive Emergencies & Urgencies

• Emergency: Very elevated blood pressure with acute, ongoing target-organ damage that should be lowered within minutes.
• Urgency: Very elevated blood pressure without acute, ongoing target-organ damage that should be lowered within hours (controversial).

Many patients present to emergency departments or physician offices with very elevated BPs, but few of these involve either hypertensive emergencies or urgencies. True hypertensive emergencies occur in only one to two people per 100,000 population per year in developed countries, but may be up to four times more common in developing nations, minority populations, economically challenged individuals, and those who are nonadherent to prescribed antihypertensive drugs. To triage such patients appropriately it is important to identify symptoms or signs indicating acute, ongoing target-organ damage. This can take several forms, but usually involves the central nervous system (including the optic fundi), cardiovascular system, kidneys, and/or uterus (see the first three columns of Table 45–1). Patients with acute, ongoing target-organ damage are at very high risk of cardiovascular events and generally should be treated within minutes in a heavily monitored setting with a short-acting intravenously delivered antihypertensive agent (typically sodium nitroprusside). Individuals who do not have acute, ongoing target-organ damage may be referred to a source of ongoing care for hypertension (if at low risk), or treated with orally administered antihypertensive agents (if at moderate risk) and the BP response observed.

Examples of hypertensive urgencies that would usually be treated in a hospital include patients with very elevated BPs in the perioperative period, organ transplant recipients (especially if the transplant was recent), and patients with severe burns. Most other hypertensive urgencies are treated in the outpatient department; whether such treatment is beneficial in the emergency department is controversial and depends on traditions local to the specific jurisdiction.

The key pathophysiologic feature in understanding hypertensive emergencies is that the normal blood pressure–blood flow curve in most vascular beds is shifted to the right in patients who develop hypertensive emergencies. Over time, their arteries adapt to the very high BPs in order to maintain organ perfusion, a process called “autoregulation.” If the BP is lowered too quickly or if the BP is too low to maintain autoregulation, blood flow to important organs will be compromised and ischemia (to the brain, heart, or kidneys) may result.

See the first three columns of Table 45–1.

Neurologic subtypes of hypertensive emergencies are the most difficult to distinguish from each other. The distinction is very important, since drug therapy to lower BP is usually withheld in the setting of an ischemic stroke in evolution, whereas it is not only beneficial, but often diagnostic in hypertensive encephalopathy. The results of CT or MRI scans are often helpful.

Many other syndromes include acute, ongoing target-organ damage (eg, papilledema) that could be (but is not) directly related to hypertension (eg, hematuria from glomerulonephritis, acute elevation in serum creatinine from toxic nephropathy), but these generally lack the very elevated BP that is characteristic of the hypertensive emergency.

Because of the extreme BP level and the existence of acute, ongoing target-organ damage, patients with hypertensive emergencies are at very high short-term risk for cardiovascular and renal complications if left untreated. Treatment, however, can lead to an even greater risk if carried out improperly. The most feared complication of treatment for a hypertensive emergency is reduction of the BP too quickly or to a too low level for autoregulation to be maintained. This results in reduced blood flow to important organs and is ischemic in cardiac, neurologic, renal, or peripheral beds. The major reason for not using quick-acting oral hypotensive drugs is that they can precipitously lower BP and lead to major complications (myocardial infarction, stroke, acute renal failure).

Patients with hypertensive urgencies are at much lower cardiovascular risk than patients with hypertensive emergencies. There are currently no data to indicate that such patients benefit from acute treatment of their hypertension, but they certainly can be harmed if treatment is too aggressive (eg, oral nifedipine capsules).

Patients with hypertensive emergencies are best treated in a closely monitored environment (eg, intensive care unit) with a short-acting, quickly reversible intravenously administered drug (see the last two columns of Table 45–1). Sodium nitroprusside is the drug with the longest track record and is very inexpensive, but it carries the risk of cyanide and thiocyanate toxicity with prolonged use or at high doses. After the BP is maintained at the target range for several (typically 6–12) hours, oral therapy (typically with an intermediate-acting calcium antagonist) can be given, and the intravenously administered drug can be tapered and discontinued.

Left untreated, patients with hypertensive emergencies have a dismal prognosis (typically a 5-month mean survival); in 1928 (when the term was introduced), “malignant hypertension” reflected a prognosis that was as poor as patients with cancer. Since the introduction of effective antihypertensive drug therapy, the prognosis depends more on the level of renal, cardiac, and neurologic function at presentation than on the initial level of BP. Sufficient kidney function sometimes returns to allow stopping of dialysis, if it is required acutely for a hypertensive emergency, particularly if the BP is well controlled during follow-up.