A hypertensive emergency is severe hypertension (often defined as systolic blood pressure (BP) ≥ 180 mm Hg and/or diastolic blood pressure ≥ 120 mm Hg) with signs of damage to target organs (primarily the brain, cardiovascular system, and kidneys). Diagnosis is by BP measurement, ECG, urinalysis, and serum electrolyte and creatinine measurements. Treatment is immediate BP reduction with IV antihypertensives.
(See also Hypertension.)
Signs of target-organ damage include
Hypertensive encephalopathy
Acute left ventricular failure with pulmonary edema
Acute aortic dissection
Damage is rapidly progressive and sometimes fatal.
Hypertensive encephalopathy may involve a failure of cerebral autoregulation of blood flow. Normally, as blood pressure increases, cerebral vessels constrict to maintain constant cerebral perfusion. Above a mean arterial pressure (MAP) of about 160 mm Hg (lower for people who are normotensive whose BP suddenly increases), the cerebral vessels begin to dilate rather than remain constricted. As a result, the very high BP is transmitted directly to the capillary bed with transudation and exudation of plasma into the brain, causing cerebral edema, including papilledema.
Although many patients with stroke and intracranial hemorrhage present with elevated BP, elevated BP is often a consequence rather than a cause of the condition. Whether rapidly lowering BP is beneficial in these conditions is unclear; it may even be harmful.
Невідкладні стани при гіпертензії
Severe hypertension (eg, systolic pressure > 180 mm Hg) without target-organ damage (except perhaps grades 1 to 2 retinopathy) may be considered a hypertensive urgency. Although BP at these very high levels often concerns clinicians, acute complications are unlikely, so immediate BP reduction is not required.
Anxiety is by far the most common cause of hypertensive urgency. Treating the anxiety by counseling and/or use of anxiety-alleviating medications is often helpful in reducing BP (1) and thus reducing the incidence of hypertensive urgencies. If elevated blood pressure persists, patients should be started on medications, such as combination therapy with 2 oral antihypertensives (for severe hypertension), and closely evaluated for treatment efficacy on an outpatient basis.
Довідковий матеріал щодо невідкладних станів при гіпертензії
1. Williams B, Mancia G, Spiering W, et al: 2018 Practice Guidelines for the management of arterial hypertension of the European Society of Hypertension and the European Society of Cardiology: ESH/ESC Task Force for the Management of Arterial Hypertension [published correction appears in J Hypertens 2019 Feb;37(2):456]. J Hypertens 2018;36(12):2284-2309. doi:10.1097/HJH.0000000000001961
Symptoms and Signs of Hypertensive Emergencies
Blood pressure is elevated, often markedly (systolic pressure > 180 mm Hg and/or diastolic pressure ≥ 120 mm Hg). Central nervous system symptoms include rapidly changing neurologic abnormalities (eg, confusion, transient cortical blindness, hemiparesis, hemisensory defects, seizures). Cardiovascular symptoms include chest pain and dyspnea. Renal involvement may be asymptomatic, although severe azotemia due to advanced renal failure may cause lethargy or nausea.
Physical examination focuses on target organs, with neurologic examination, funduscopy, and cardiovascular examination. Global cerebral deficits (eg, confusion, obtundation, coma), with or without focal deficits, suggest encephalopathy; normal mental status with focal deficits suggests stroke.
Severe retinopathy (sclerosis, cotton-wool spots, arteriolar narrowing, hemorrhage, papilledema) is usually present with hypertensive encephalopathy, and some degree of retinopathy is present in many other hypertensive emergencies.
Jugular venous distention, basilar lung crackles, and a 3rd heart sound suggest pulmonary edema.
Asymmetry of pulses between arms suggests aortic dissection.
Diagnosis of Hypertensive Emergencies
Systolic blood pressure > 180 mm Hg
Testing to identify target-organ involvement: ECG, urinalysis, serum electrolytes, and creatinine; if neurologic findings, head CT
Testing typically includes ECG, urinalysis, and serum electrolytes, and creatinine.
Patients with neurologic findings require head CT to diagnose intracranial bleeding, edema, or infarction.
Patients with chest pain or dyspnea require and ECG and chest x-ray. ECG abnormalities suggesting acute target-organ damage include acute ischemic changes.
Urinalysis abnormalities typical of renal involvement include red blood cells (RBCs), RBC casts, and proteinuria.
Diagnosis is based on the presence of a very high BP and findings of target-organ involvement.
Treatment of Hypertensive Emergencies
Initiate short-acting IV medication (eg, labetalol, clevidipine, esmolol) in the emergency department
Admit to intensive care unit (ICU)
Goal: 20 to 25% reduction MAP in 1 to 2 hours
Hypertensive emergencies are treated in an ICU; blood pressure is progressively (although not abruptly) reduced using a short-acting, titratable IV medication. Choice of medication and speed and degree of reduction vary somewhat with the target organ involved, but generally a 20 to 25% reduction in MAP over about an hour or two is appropriate, with further titration based on symptoms. Achieving “normal” BP urgently is not necessary. Typical first-line medications include nitroprusside, fenoldopam, nicardipine, and labetalol (see table Parenteral Medications for Hypertensive Emergencies). Nitroglycerin alone is less potent.
Oral medications are not indicated because onset is variable and the medications are difficult to titrate. Although short-acting oral nifedipine reduces blood pressure rapidly, it may lead to acute hypotension, which may lead to cardiovascular and cerebrovascular ischemic events (sometimes fatal) and is therefore not recommended.
Clevidipine is an ultra-short-acting (within 1 to 2 minutes), 3rd-generation calcium channel blocker that reduces peripheral resistance without affecting venous vascular tone and cardiac filling pressures. Clevidipine is rapidly hydrolyzed by blood esterases and, thus, its metabolism is not affected by renal or hepatic function. It has been shown to be effective and safe in the control of perioperative hypertension and hypertensive emergencies and was associated with lower mortality than nitroprusside (1). Clevidipine may thus be preferred over nitroprusside for most hypertensive emergencies, although it should be used with caution in acute heart failure with reduced ejection fraction as it may have negative inotropic effects. If clevidipine is not available, then fenoldopam, nitroglycerin, or nicardipine are reasonable alternatives.
Fenoldopam is a peripheral dopamine-1 agonist that causes systemic and renal vasodilation and natriuresis. Onset is rapid and half-life is brief, making it an effective alternative to nitroprusside, with the added benefit that it does not cross the blood-brain barrier.
Labetalol is a beta-blocker with some alpha-1-blocking effects, thus causing vasodilation without the typical accompanying reflex tachycardia. It can be given as a constant infusion or as frequent boluses; use of boluses has not been shown to cause significant hypotension. Labetalol is used during pregnancy, for intracranial disorders requiring BP control, and after myocardial infarction. Adverse effects are minimal, but because of its beta -blocking activity, labetalol should not be used for hypertensive emergencies in patients with asthma. Low doses may be used for left ventricular failure if nitroglycerin is given simultaneously.
Nitroprusside is a venous and arterial dilator, reducing preload and afterload; thus, its use is mostly limited to patients with acute decompensated heart failure who are hypertensive. It is also used for hypertensive encephalopathy and, with beta-blockers, for aortic dissection.The medication is rapidly broken down into cyanide and nitric oxide (the active moiety). Cyanide is detoxified to thiocyanate. However, administration of > 2 mcg/kg/minute can lead to cyanide accumulation with toxicity to the central nervous system and heart; manifestations include agitation, seizures, cardiac instability, and an anion gap metabolic acidosis.
Prolonged administration of nitroprusside (> 1 week or, in patients with renal insufficiency, 3 to 6 days) leads to accumulation of thiocyanate, which can result in lethargy, tremor, abdominal pain, and vomiting. Other adverse effects include transitory elevation of hair follicles (cutis anserina) if BP is reduced too rapidly. Thiocyanate levels should be monitored daily after 3 consecutive days of therapy, and the medication should be stopped if the serum thiocyanate level is > 12 mg/dL (> 2 mmol/L). Because nitroprusside is broken down by ultraviolet light, the IV bag and tubing are wrapped in an opaque covering. Given data showing increased mortality with nitroprusside compared to clevidipine, nitroglycerin, and nicardipine, nitroprusside should not be used when other alternatives are available.
Nitroglycerin is a vasodilator that affects veins more than arterioles. It can be used to manage hypertension during and after coronary artery bypass graft surgery, acute myocardial infarction, unstable angina pectoris, and acute pulmonary edema. IV nitroglycerin is preferable to nitroprusside for patients with severe coronary artery disease because nitroglycerin increases coronary flow, whereas nitroprusside tends to decrease coronary flow to ischemic areas, possibly because of a “steal” mechanism.
For long-term BP control, nitroglycerin must be used with other medications. The most common adverse effect is headache, occurring in the majority of patients (2); others include tachycardia, nausea, vomiting, apprehension, restlessness, muscular twitching, and palpitations.
Nicardipine, a dihydropyridine calcium channel blocker with less negative inotropic effects than nifedipine, acts primarily as a vasodilator. It is most often used for postoperative hypertension and during pregnancy. It may cause flushing, headache, and tachycardia; it can decrease glomerular filtration rate (GFR) in patients with renal insufficiency.
Довідкові матеріали щодо лікування
1. Aronson S, Dyke CM, Stierer KA, et al. The ECLIPSE trials: comparative studies of clevidipine to nitroglycerin, sodium nitroprusside, and nicardipine for acute hypertension treatment in cardiac surgery patients. Anesth Analg 107(4):1110-1121, 2008. doi:10.1213/ane.0b013e31818240db
2. Tfelt-Hansen PC, Tfelt-Hansen J. Nitroglycerin headache and nitroglycerin-induced primary headaches from 1846 and onwards: a historical overview and an update. Headache 49(3):445-456, 2009. doi:10.1111/j.1526-4610.2009.01342.x
Ключові моменти
A hypertensive emergency is significantly elevated blood pressure (eg, systolic blood pressure > 180 mm Hg and/or diastolic pressure ≥ 120 mm Hg) that causes target-organ damage; it requires intravenous therapy and hospitalization.
Target-organ damage includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure.
Do ECG and urinalysis, measure serum electrolytes and creatinine, and, for patients with neurologic symptoms or signs, obtain head CT.
Reduce mean arterial pressure by about 20 to 25% over the first hour using a short-acting, titratable IV medication such as clevidipine, nitroglycerin, fenoldopam, nicardipine, or labetalol.
It is not necessary to achieve “normal” blood pressure urgently (especially true in acute stroke).
Додаткова інформація
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