Hypertonic crisis

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Last reviewed: 11.04.2020

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

The diagnosis is determined by measuring blood pressure, ECG, urinalysis and the study of urea and creatinine in the blood. Treatment of hypertensive crisis suggests immediate reduction in blood pressure by intravenous administration of drugs (for example, sodium nitroprusside, b-adrenoblockers, hydralazine).

The defeat of target organs includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection and renal insufficiency. Defeats quickly progress and often lead to death.

Hypertensive encephalopathy can include violations of central regulation of blood circulation. Normally, if blood pressure rises, the cerebral vessels narrow to maintain a constant blood supply to the brain. At a level above the significant BP, which is approximately 160 mm Hg. Art. (and lower in patients with normal normal BP when it suddenly increases), the brain vessels begin to expand. As a result, a very high blood pressure spreads directly to the capillaries, there is a transudation and exudation of plasma in the brain, which leads to brain edema, including edema of the optic nerve.

Despite the fact that many patients with stroke or intracranial hemorrhage have a high blood pressure, an increase in blood pressure can often be the result of development, rather than the cause of these conditions. It is not clear whether a rapid decrease in blood pressure is advisable under such conditions; in some cases it can be harmful.

Very high blood pressure (for example, diastolic> 120-130 mm Hg) without lesion of target organs (with the exception of I-III stages of retinopathy) can be regarded as a hypertensive crisis. BP of this level usually worries the doctor, but acute complications are rare, so there is no urgent need for a rapid decline in blood pressure. At the same time, patients need a combination of two drugs taken internally? And careful monitoring (to determine the effectiveness of treatment) is necessary, continuing on an outpatient basis.

trusted-source[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]

Symptoms of hypertensive crisis

BP is increased, often significantly (diastolic> 120 mm Hg). Symptoms of CNS involvement include rapidly changing neurological symptoms (eg, impaired consciousness, transient blindness, hemiparesis, hemiplegia, seizures). Signs of cardiovascular damage include chest pain and shortness of breath. Kidney damage can be asymptomatic, but severe azotemia due to the development of renal failure can lead to retardation and nausea.

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Diagnosis of hypertensive crisis

In the physical examination, special attention is paid to the target organs (investigate the nervous, cardiovascular systems, conduct ophthalmoscopy). Common brain symptoms (including disorders of consciousness, sopor, coma) with or without local manifestations indicate encephalopathy; normal mental status with local symptoms is a symptom of a stroke. Severe retinopathy (sclerosis, narrowing of arterioles, hemorrhages, edema of the nipple of the optic nerve) is often present in hypertensive encephalopathy, and some degree of retinopathy is possible in many other types of crises. The tension of the jugular veins, wheezing in the basal parts of the lungs and the third heart tone indicate pulmonary edema. Asymmetry of the pulse on the hands can be a sign of aortic dissection.

The examination usually includes an ECG, urinalysis, determination of serum urea and creatinine. Patients with neurological symptoms need CT of the head to exclude intracranial hemorrhage, edema or cerebral infarction. Patients with chest pain and shortness of breath need radiography of the chest. ECG findings with lesions of target organs include signs of left ventricular hypertrophy or acute ischemia. Changes in urine tests are typical for involvement in the kidney process and include hematuria and proteinuria.

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

trusted-source[11], [12], [13], [14], [15], [16], [17], [18]

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Treatment of hypertensive crisis

Patients with hypertensive crisis are treated in intensive care units. BP gradually (but not sharply) reduced by the appointment of intravenous short-acting drugs. The choice of the drug and the rate of BP reduction can be different and depend on which target organ is affected. More often, the rate of decline is 20-25% per hour until a significant BP is achieved; further treatment depends on the symptomatology. In a very rapid achievement of "normal" blood pressure is not necessary. Usually the drugs of the first line are sodium nitroprusside, phenoldopam, nicardipine and labetalol. Nitroglycerin as a monotherapy is not so effective.

Medicines for hypertensive crisis

Medicinal forms for oral administration are not prescribed, because hypertensive crises are different, and such drugs are difficult to dose. Oral nifedipine short-acting, despite the fact that it quickly reduces blood pressure, can lead to acute cardiovascular and cerebral events (sometimes fatal) and is therefore not recommended.

Sodium nitroprusside is a venous and arterial vasodilator that reduces pre- and postnagruzka, and is therefore most indicated for patients with heart failure. It is also used in hypertensive encephalopathy and together with b-adrenoblockers with aortic dissection. The initial dose is 0.25-1.0 μg / kg per minute, then add 0.5 μg / kg to a maximum of 8-10 μg / kg per minute. The maximum dose is prescribed for no more than 10 min to prevent the risk of cyanide toxicity. The drug quickly decomposes into cyanide and nitric oxide (the active substance). Cyanide is converted into thiocyanate. Nevertheless, the appointment of more than 2 μg / kg per minute can lead to the accumulation of cyanide and toxic effects on the central nervous system and heart; manifestations include anxiety, convulsions, cardiac instability, and anionic metabolic acidosis. Long-term use (more than 1 week or 3-6 days - in patients with renal insufficiency) leads to the accumulation of thiocyanate, which causes retardation, tremor, abdominal pain and nausea. Other side effects include transient hair loss, "goosebumps", if blood pressure drops too quickly. The content of thiocyanate should be monitored daily after three consecutive days of use; the drug is canceled if the concentration of thiocyanate in the serum becomes> 2 mmol / l (> 12 mg / dL). Since the drug is destroyed by exposure to ultraviolet light, the container for the intravenous preparation and the tubes must be closed with a special package.

Parenteral drugs for the treatment of hypertensive crises

A drug


Side effects*

Special indications

Sodium nitroprusside

0.25-10 μg / kg per minute for intravenous infusion (maximum dose, the effect persists for 10 minutes)

Nausea, vomiting, agitation, muscle twitching, sweating (with a rapid decrease in blood pressure), toxicity, a mechanism similar to the toxicity of thiocyanates and cyanides

Most hypertensive crises; with caution appoint to patients with high intracranial pressure or azotemia


5-15 mg / h intravenously

Tachycardia, headache, hyperemia of the face, local phlebitis

Most hypertensive crises, with the exception of heart failure; with caution appoint patients with myocardial ischemia


0.1-0.3 μg / kg per minute for intravenous administration; the maximum dose of 1.6 mcg / kg per minute

Tachycardia, headache, nausea, hyperemia of the face, hypokalemia, increased intraocular pressure in patients with glaucoma

Most hypertensive crises; with caution appoint patients with myocardial ischemia


5-100 μg / min, intravenous infusion

Headache, tachycardia, nausea, vomiting, a sense of fear, tension, muscle twitching, palpitations, methemoglobinemia, tolerance with prolonged use

Myocardial ischemia, heart failure


0.625-5 mg intravenously every 6 hours

It provokes a sharp drop in blood pressure in patients with a high level of renin, a different sensitivity

Acute left ventricular failure, it is necessary to avoid the use of acute myocardial infarction


10-40 mg intravenously; 10-20 mg intramuscularly

Tachycardia, hyperemia of the face, headache, nausea, exacerbation of angina



20 mg bolus intravenously for 2 minutes; then continue 40 mg every 10 minutes, then up to 3 doses of 80 mg; or 0.5-2 mg / min intravenously as an infusion

Nausea, tenderness of the scalp, sore throat, dizziness, nausea, heart block, orthostatic hypotension

Most hypertensive crises, except acute left ventricular failure; It is necessary to avoid prescribing bronchial asthma


250-500 μg / kg per minute for 1 minute, then 50-100 μg / kg per minute for 4 minutes; can be repeated in the future

Arterial hypotension, nausea

Perioperatively with aortic dissection

* Arterial hypotension can develop when using any medication.

+ Requires special devices for administration (eg, infusomat for sodium nitroprusside, for nitroglycerin).

Phenol-dopam is a peripheral agonist of dopamine 1, which leads to systemic and renal vasodilation and sodium nares. The effect occurs quickly, and the half-life is short, which makes it an effective alternative to sodium nitroprusside, with an additional positive effect, as it does not penetrate the blood-brain barrier. The initial dose is 0.1 μg / kg per minute as an intravenous infusion, then add 0.1 μg / kg every 15 minutes to a maximum dose of 1.6 μg / kg per minute.

Nitroglycerin is a vasodilator that acts more on veins than on arterioles. It can be used to control arterial hypertension during and after coronary artery bypass, acute myocardial infarction, unstable angina, and acute pulmonary edema. Intravenous nitroglycerin is preferable to sodium nitroprusside for patients with severe coronary artery disease, since nitroglycerin increases coronary blood flow, while sodium nitroprusside reduces it in areas of affected arteries, possibly due to the syndrome of "stealing." The initial dose is 10-20 μg / min, then add 10 μg / min every 5 minutes until the maximum hypotensive effect is achieved. For long-term monitoring of blood pressure, nitroglycerin can be used together with other medicines. The most common side effect is headache (approximately 2% of cases), in addition, there are tachycardia, nausea, vomiting, anxiety, fatigue, muscle twitching and palpitations.

Nicardipine is a dihydropyridine calcium channel blocker with a less pronounced negative inotropic effect than nifedipine; has an effect 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. Nicaradipine can lead to reddening of the face, headache and tachycardia; it can inhibit the filtration function of the kidneys in patients with renal insufficiency.

Labetalol is an adrenoblocker with some a 1- blocking properties, which leads to vasodilation without a typical reflex tachycardia. Can be given as a permanent infusion or frequent boluses; The use of boluses did not demonstrate a significant reduction in blood pressure. Labetalol is used during pregnancy, with intracranial pathology requiring control of blood pressure, and after MI. Infusion is administered 0.5-2 mg / min, increasing the dose to a maximum of 4-5 mg / min. The bolus is started 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 for left ventricular failure simultaneously with the administration of nitroglycerin.

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