Hypertensive crisis

Hypertensive crisis is severe arterial hypertension with signs of damage to target organs (primarily the brain, cardiovascular system and kidneys).

The diagnosis is established by measuring blood pressure, ECG, urine analysis, and testing the urea and creatinine levels in the blood. Treatment of hypertensive crisis involves immediate reduction of blood pressure by intravenous administration of drugs (e.g., sodium nitroprusside, beta-blockers, hydralazine).

Target organ damage includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure. The lesions progress rapidly and are often fatal.

Hypertensive encephalopathy may involve disturbances in the central regulation of blood circulation. Normally, if blood pressure increases, cerebral vessels constrict to maintain a constant blood supply to the brain. When the blood pressure reaches a level above the significant blood pressure, which is approximately 160 mm Hg (and lower in patients with normally normal blood pressure if it increases suddenly), the brain vessels begin to dilate. As a result, very high blood pressure spreads directly to the capillaries, transudation and exudation of plasma into the brain occurs, which leads to cerebral edema, including papilledema.

Although many patients with stroke or intracranial hemorrhage have high blood pressure, the elevated blood pressure may often be a consequence of, rather than a cause of, these conditions. It is unclear whether rapid blood pressure reduction is beneficial in these conditions; in some cases, it may be harmful.

Very high BP (e.g. diastolic > 120-130 mmHg) without damage to target organs (except for stages I-III retinopathy) can be considered a hypertensive crisis. BP of this level usually worries the doctor, but acute complications are rare, so there is no urgent need to quickly reduce BP. At the same time, patients need a combination of two drugs taken orally? And careful monitoring (to determine the effectiveness of treatment), continuing in an outpatient setting, is necessary.

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Symptoms of hypertensive crisis

Blood pressure is elevated, often significantly (diastolic > 120 mm Hg). CNS symptoms include rapidly changing neurologic symptoms (eg, impaired consciousness, transient blindness, hemiparesis, hemiplegia, seizures). Cardiovascular symptoms include chest pain and dyspnea. Renal involvement may be asymptomatic, but severe azotemia due to renal failure may cause lethargy and nausea.

Diagnosis of hypertensive crisis

During physical examination, special attention is paid to target organs (the nervous and cardiovascular systems are examined, ophthalmoscopy is performed). General cerebral symptoms (including impaired consciousness, stupor, coma) with or without local manifestations indicate encephalopathy; normal mental status with local symptoms is a sign of stroke. Severe retinopathy (sclerosis, narrowing of arterioles, hemorrhages, edema of the papilla of the optic nerve) is often present in hypertensive encephalopathy, and some degree of retinopathy is possible in many other types of crises. Tension of the jugular veins, wheezing in the basal parts of the lungs and the third heart sound indicate pulmonary edema. Asymmetry of the pulse in the arms may be a sign of aortic dissection.

Evaluation typically includes an ECG, urinalysis, serum urea nitrogen, and creatinine. Patients with neurologic symptoms require a head CT scan to rule out intracranial hemorrhage, cerebral edema, or cerebral infarction. Patients with chest pain and dyspnea require a chest radiograph. ECG findings in the presence of target organ damage include left ventricular hypertrophy or acute ischemia. Urinalysis findings are typical of renal involvement and include hematuria and proteinuria.

The diagnosis is made on the basis of very high blood pressure figures and damage to target organs.

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Treatment of hypertensive crisis

Patients with hypertensive crisis are treated in intensive care units. BP is gradually (but not abruptly) reduced by intravenous short-acting drugs. The choice of drug and the rate of BP reduction may vary and depend on the target organ affected. Most often, a rate of reduction of 20-25% per hour is provided until significant BP is achieved; further treatment depends on the symptoms. There is no need to achieve “normal” BP very quickly. Sodium nitroprusside, fenoldopam, nicardipine, and labetalol are usually first-line drugs. Nitroglycerin as monotherapy is not as effective.

Medicines for hypertensive crisis

Oral dosage forms are not prescribed because hypertensive crises vary and such drugs are difficult to dose. Short-acting oral nifedipine, although it rapidly lowers blood pressure, can cause acute cardiovascular and cerebral events (sometimes fatal) and is therefore not recommended.

Sodium nitroprusside is a venous and arterial vasodilator that reduces pre- and afterload, making it most useful in patients with heart failure. It is also used in hypertensive encephalopathy and with beta-blockers in aortic dissection. The initial dose is 0.25-1.0 mcg/kg per minute, then 0.5 mcg/kg is added to a maximum of 8-10 mcg/kg per minute. The maximum dose is administered for no more than 10 minutes to prevent the risk of cyanide toxicity. The drug rapidly breaks down into cyanide and nitric oxide (the active substance). Cyanide is converted to thiocyanate. However, administration of more than 2 mcg/kg per minute may result in cyanide accumulation and CNS and cardiac toxicity; manifestations include agitation, seizures, cardiac instability, and anionic metabolic acidosis. Long-term use (more than 1 week or 3-6 days in patients with renal failure) leads to accumulation of thiocyanate, which causes lethargy, tremor, abdominal pain and nausea. Other side effects include transient hair loss, "goose bumps" if blood pressure decreases too rapidly. Thiocyanate levels should be monitored daily after three consecutive days of use; the drug should be discontinued if the serum thiocyanate concentration is > 2 mmol/L (> 12 mg/dL). Since the drug is destroyed by ultraviolet light, the intravenous container and tubing should be sealed with special packaging.

Parenteral drugs for the treatment of hypertensive crises

Preparation	Dose	Side effects*	Special indications
Sodium nitroprusside	0.25-10 mcg/kg per minute for intravenous infusion (maximum dose, effect lasts for 10 min)	Nausea, vomiting, agitation, muscle twitching, sweating (with rapid decrease in blood pressure), toxicity similar in mechanism to that of thiocyanates and cyanides	Most hypertensive crises; use with caution in patients with high intracranial pressure or azotemia
Nicardipine	5-15 mg/h intravenously	Tachycardia, headache, facial flushing, local phlebitis	Most hypertensive crises, with the exception of heart failure; use with caution in patients with myocardial ischemia
Fenoldopam	0.1-0.3 mcg/kg per minute for intravenous administration; maximum dose 1.6 mcg/kg per minute	Tachycardia, headache, nausea, facial flushing, hypokalemia, increased intraocular pressure in patients with glaucoma	Most hypertensive crises; use with caution in patients with myocardial ischemia
Nitroglycerine	5-100 mcg/min, intravenous infusion	Headache, tachycardia, nausea, vomiting, anxiety, tension, muscle twitching, palpitations, methemoglobinemia, tolerance with long-term use	Myocardial ischemia, heart failure
Enalaprilat	0.625-5 mg IV every 6 hours	Causes a sharp drop in blood pressure in patients with high renin levels, variable sensitivity	Acute left ventricular failure, avoid use in acute MI
Hydralazine	10-40 mg intravenously; 10-20 mg intramuscularly	Tachycardia, facial flushing, headache, nausea, increased angina	Eclampsia
Labetalol	20 mg IV bolus over 2 min; then continue with 40 mg every 10 min, then up to 3 doses of 80 mg; or 0.5-2 mg/min IV infusion	Nausea, scalp pain, sore throat, dizziness, nausea, heart block, orthostatic hypotension	Most hypertensive crises, except acute left ventricular failure; should be avoided in patients with bronchial asthma
Esmolol	250-500 mcg/kg per minute for 1 min, then 50-100 mcg/kg per minute for 4 min; may be repeated later	Arterial hypotension, nausea	Perioperatively for aortic dissection

*Arterial hypotension can develop with the use of any drug.

⁺ Requires special devices for administration (for example, an infusion pump for sodium nitroprusside, for nitroglycerin).

Fenoldopam is a peripheral dopamine 1 agonist that produces systemic and renal vasodilation and natriuresis. Its onset of action is rapid and its half-life is short, making it an effective alternative to sodium nitroprusside, with the additional benefit of not penetrating the blood-brain barrier. The initial dose is 0.1 mcg/kg per minute as an intravenous infusion, followed by 0.1 mcg/kg every 15 minutes to a maximum dose of 1.6 mcg/kg per minute.

Nitroglycerin is a vasodilator that acts more on veins than on arterioles. It can be used to control hypertension during and after coronary artery bypass grafting, acute myocardial infarction, unstable angina, and acute pulmonary edema. Intravenous nitroglycerin is preferable to sodium nitroprusside in patients with severe coronary artery disease because nitroglycerin increases coronary blood flow, whereas sodium nitroprusside decreases it in areas of diseased arteries, possibly due to a "steal" syndrome. The initial dose is 10-20 mcg/min, then 10 mcg/min is added every 5 minutes until the maximum hypotensive effect is achieved. For long-term control of blood pressure, nitroglycerin can be used together with other drugs. The most common side effect is headache (approximately 2% of cases), but tachycardia, nausea, vomiting, anxiety, fatigue, muscle twitching, and palpitations also occur.

Nicardipine is a dihydropyridine calcium channel blocker with a less pronounced negative inotropic effect than nifedipine; it acts primarily as a vasodilator. It is most often used in the postoperative period and during pregnancy. The initial dose is 5 mg/h intravenously, which is increased every 15 minutes to a maximum of 15 mg/h. Nicardipine can cause facial flushing, headache, and tachycardia; it can inhibit renal filtration function in patients with renal insufficiency.

Labetalol is an adrenergic blocker with some a ₁ -blocking properties, which leads to vasodilation without the typical reflex tachycardia. It can be administered as a continuous infusion or frequent boluses; the use of boluses has not demonstrated a significant decrease in blood pressure. Labetalol is used during pregnancy, in intracranial pathology requiring blood pressure control, and after MI. Infusion is administered at 0.5-2 mg / min, increasing the dose to a maximum of 4-5 mg / min. Bolus administration begins with 20 mg intravenously, continuing at 40 mg every 10 minutes, then 80 mg (up to 3 doses) to a maximum dose of 300 mg. Side effects are minimal, but due to the presence of b-blocking activity, labetalol should not be prescribed for hypertensive crises in patients with bronchial asthma. Small doses can be used in left ventricular failure simultaneously with the administration of nitroglycerin.