Hypertensive emergencies

1. How does a “hypertensive emergency” differ from “hypertensive urgency”?

A “hypertensive emergency” is a clinical situation in which severely elevated blood pressure is associated with acute, progressive target-organ damage that needs to be treated immediately with a safe and controlled reduction of blood pressure. “Hypertensive urgencies” (if they truly exist; see Question 15 below) are characterized by elevated blood pressures in a patient who has no acute, progressive target-organ damage; these are typically treated with oral antihypertensive medications and close follow-up thereafter. Typical scenarios that are hypertensive emergencies include the following:

  • Hypertensive encephalopathy: typically a diagnosis of exclusion (see later)

  • Acute left ventricular failure and/or pulmonary edema (see later)

  • Subarachnoid or intracerebral hemorrhage

  • Acute aortic dissection: Target blood pressure is <120/70 mm Hg, within 20 minutes (see later).

  • Acute myocardial infarction or acute coronary syndrome

  • Adrenergic crisis: for example, pheochromocytoma, phencyclidine, or cocaine overdose (see later)

  • Glomerulonephritis or acute kidney injury

  • Epistaxis, gross hematuria, or threatened suture lines after vascular surgery

  • Eclampsia (some authorities would include preeclampsia here, but most obstetricians hasten to deliver the baby and lower blood pressure BEFORE a seizure occurs)

The absolute level of blood pressure does not distinguish between emergencies and urgencies. Patients who were previously normotensive can develop a hypertensive emergency with a blood pressure that is only 30 to 50 mm Hg higher than their usual and customary blood pressure (e.g., 160/100 in a woman with preeclampsia). Conversely, some patients with chronic hypertension remain asymptomatic and might qualify as only hypertensive urgencies, even with a blood pressure of 250/150 mm Hg. Seldom, if ever, does such a high blood pressure require hospitalization if there is no acute target-organ damage.

2. What is “malignant hypertension,” and how does it differ from “accelerated hypertension”?

Malignant hypertension is the term historically given when severely elevated blood pressure was accompanied by retinal hemorrhages, exudates, and originally papilledema. The term arose in the 1920s when no effective treatment was available, and the prognosis of patients with this condition was similar to cancer. Now that treatment is available and effective, the term is used predominantly by hospital-based coders. In the last millennium, “accelerated hypertension” was severely elevated blood pressure without papilledema; this term is now only rarely used outside its historical context.

3. What are the epidemiologic characteristics of patients who present with a hypertensive emergency?

Most such patients have a history of stage 2 hypertension that has not been adequately treated. The most common cause of this is nonadherence to prescribed medication. In the last millennium, patients presenting with “malignant hypertension” typically had very high blood pressures (before treatment) and were often cigarette smokers. Secondary hypertension, especially renovascular hypertension, was often found in patients with Keith-Wagener-Barker Grade III (hemorrhages/exudates) or IV (frank papilledema) retinopathy; chronic kidney disease was also very common in such patients in the 1970s.

4. What is the pathophysiology of “malignant hypertension”?

A rapid and sustained rise in blood pressure causes endothelial dysfunction and then frank arteritis, leading to platelet and fibrin deposition within the vessel and eventually fibrinoid necrosis. The juxtaglomerular apparatus of the kidney releases renin when it senses relative ischemia, which increases circulating angiotensin II levels and causes severe vasoconstriction. The kidney responds to the elevated blood pressure with natriuresis, causing relative volume depletion and further activating the renin-angiotensin-aldosterone system. These events typically reinforce each other and lead to the “vicious cycle” of increasing blood pressure and worsening vascular function.

5. What were the typical pathologic findings in “malignant hypertension?”

The patient’s blood vessels undergo myointimal proliferation (and medial thickening, leading to the “onion-skin” appearance) and fibrinoid necrosis. If the process is chronic, vascular smooth muscle hypertrophy occurs and collagen deposits in the small vessels and arterioles.

6. Historically, what were the common clinical features of “malignant hypertension”?

Typically the blood pressure was very high (often diastolic >140 mm Hg). The optic fundi showed bilateral papilledema, often with hemorrhages and exudates in the periphery. Hypertensive encephalopathy was common, usually preceded by headache, somnolence, visual changes, and confusion. Microangiopathic hemolytic anemia, with schistocytes and helmet cells on peripheral smear, and increased serum lactate dehydrogenase often were associated with fibrinoid necrosis of arterioles. Normal kidney function was distinctly unusual; most patients had oliguria, azotemia, proteinuria, and (usually microscopic) hematuria. The major reason malignant hypertension is uncommon today is that, in early studies, even a single antihypertensive drug reduced the risk of malignant hypertension by more than 90%.

7. How does one diagnose hypertensive encephalopathy?

Such patients typically present with very high blood pressures and altered mental status. Optic fundi may show Grade III (hemorrhages/exudates) or IV (papilledema) retinopathy. Usually other evidence of hypertensive target-organ damage is present, such as hematuria, elevated serum creatinine, or left ventricular hypertrophy. Although the differential diagnosis in such a patient is long and complex, consideration can be given to starting a short-acting, easily titratable, intravenous antihypertensive agent while transporting the patient to the computed tomographic scanner. It is rewarding to see an improvement in central nervous system function after the blood pressure is reduced even by 10%. However, other causes of stupor and coma have to be considered, appropriately evaluated, and eliminated before one can make the diagnosis of hypertensive encephalopathy.

8. What are the major principles of treating a patient with a hypertensive emergency?

Normal autoregulation of vascular beds allows a tissue to receive relatively constant perfusion across a wide range of blood pressures. In hypertensive emergencies, the autoregulatory capacity of many vascular beds is reset, so that the autoregulatory zone is optimized for the much higher blood pressure in the days to weeks before the medical encounter. This allowed the vessels, over time, to constrict and continue to deliver an appropriate (if not quite normal) flow of blood and oxygen, despite the very high blood pressures. A primary treatment goal is to gradually reduce the blood pressure over a short but sufficient amount of time to allow vascular beds to adjust to the “new, lower” pressure without causing ischemia. A corollary is that lowering blood pressure into the “normal” range should be avoided, because prior to the patient’s presentation, the threshold for ischemia has also been shifted to the right.

Most authorities recommend admission to an intensive care unit, although a method to monitor blood pressure (intraarterial line versus automated oscillometric device), an intravenous line to deliver the antihypertensive agent, and an attentive physician can begin treatment in the emergency department.

No trials have been done to establish a blood pressure target ( Table 68.1 ), but most authorities recommend a decrease in mean arterial pressure by about 10% in the first hour and no more than 25% during the first 2 hours. Most patients tolerate a blood pressure of about 160 to 180/100 mm Hg well after the first 2 hours or so, but the antihypertensive medication dose should be individualized and should be reduced if deterioration occurs when the blood pressure is decreased “too fast” or “too far.” After the blood pressure has been stabilized (usually for 6 to 24 hours) and after oral treatment is administered, intravenous antihypertensive therapy can be withdrawn.

Table 68.1.

Types of Hypertensive Emergencies, With Suggested Drug Therapy and Blood Pressure Targets

Modified from Elliott, W. J. (2003). Management of hypertensive emergencies. Current Hypertension Reports, 5 , 486–492.

Aortic dissection Beta blocker + nitroprusside a 120 mm Hg systolic in 20 min (if possible)
Ischemia/infarction Nitroglycerin, nitroprusside, nicardipine, or clevidipine Cessation of ischemia
Heart failure (or pulmonary edema) Nitroprusside a and/or nitroglycerin Improvement in failure (typically only a 10%–15% decrease is required)
Epistaxis, gross hematuria, or threatened suture lines Any (perhaps with anxiolytic agent) To decrease bleeding rate (typically only 10%–15% reduction over 1–2 h is required)
Eclampsia or preeclampsia MgSO 4 , hydralazine, methyldopa Typically <90 mm Hg diastolic, but often lower
Catecholamine Excess States
Pheochromocytoma Phentolamine To control paroxysms
Drug withdrawal Drug withdrawn Typically only one dose necessary
Cocaine (and similar drugs) Phentolamine Typically only 10%–15% reduction over 1–2 h
Major hematuria or acute renal impairment Fenoldopam 0%–25% reduction in mean arterial pressure over 1–12 h
Hypertensive encephalopathy Nitroprusside a 25% reduction over 2–3 h
Acute head injury/trauma Nitroprusside a 0%–25% reduction over 2–3 h (controversial)

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Jul 23, 2019 | Posted by in NEPHROLOGY | Comments Off on Hypertensive emergencies

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