Hypertension ecg. ECG criteria for hypertensive heart

Rice. 105. Scheme of ECG changes in case of disturbances of electrolytes in the blood serum.

Patients with circulatory failure and kidney disease often use diuretics. If they take diuretics systematically and in high doses, the body loses electrolytes, especially sodium and potassium. They experience disturbances in the levels of electrolytes in the blood serum.

With edema, such disorders are also common. Pay attention to the content of electrolytes in the blood: potassium, sodium, calcium, and less often magnesium. Changes in the ECG occur with hypokalemia, hyperkalemia. In case of loss potassium ion the ECG lengthens P-Q interval, there is an elongation QT interval, the appearance of a U wave.

Changes occur with hypoparathyroidism (there are disturbances in potassium, calcium, and phosphorus metabolism). Hypocalcemia leads to tetany.

At increased potassium in the blood, the T wave becomes high, pointed, and the Q-T interval shortens. Hyperkalemia is observed in parathyroid adenomas and acute renal failure. Patients also experience hypercalcemia and severe weakness.

Electrolyte imbalances occur in patients with acute or chronic enteritis, with pyloric stenosis and repeated vomiting, in patients with malabsorption syndrome (malabsorption).

Deep violations electrolyte metabolism lead to comatose state, To serious violations heart functions. Changes in the ECG are sometimes the first signs of such disorders. In acute renal failure, hyperkalemia is important sign for the use of hemodialysis.

Rice. 106. ECG in case of disturbance of potassium metabolism in the body: 1) with hyperkalemia (due to renal failure), 2) with hypokalemia (after intensive treatment with diuretics).

ECG for arterial hypertension (AH).

Hypertension is a heterogeneous group of diseases with different causes and pathogenetic mechanisms. During the course of hypertension and arterial hypertension, some common pathogenetic mechanisms and signs. These include increased blood pressure, the development of myocardial hypertrophy, cardiac changes and electrical axis to the left. These heart changes are detected on an ECG. There are changes depending on the level of increase in blood pressure (degree of hypertension).

There are several degrees of change: normal blood pressure, increased rate(borderline state), hypertension of the 1st, 2nd and 3rd degrees.

At first degree hypertension Blood pressure ranges from 140/90 – 159/99 mm Hg. Art., which corresponds to the initial stage of hypertension. In the majority of patients, only a slight deviation of the electrical axis of the heart to the left is detected. S-T intervals do not change or decrease slightly; T wave voltage may decrease.

In the second degree of hypertension(moderate arterial hypertension) is characterized by the fact that during an arterial crisis, blood pressure increases within the range of 160-179/100-109 mm Hg. An ECG recorded in this condition shows signs of left ventricular myocardial overload - the S-T interval decreases, and T wave inversion is noted in the left leads. Some patients develop “coronary” T waves.

Third degree AH increased blood pressure (severe hypertension) - blood pressure above 180/110 mm Hg. It should be noted that in healthy person during physical exertion or during a stress reaction arterial pressure may rise to

significant numbers. In older people, some authors believe normal indicators Blood pressure is about 160/90 mm Hg. Art. ECGs in patients with hypertension take on a fairly typical shape and reflect the rotation of the heart and the degree of hypertrophy of the left ventricular myocardium.

Rice. 107 ECG in a patient with stage I hypertension. (BP 160/90 mm Hg). An increase in the R wave in lead V 6 was noted.

Rice. 108. ECG of a patient with stage II hypertension. Blood pressure 170/100 mm Hg. Art. High R waves in the left leads, decreased S-T intervals and inversion of T waves were noted. Waves RV6> RV5> RV4.

Rice. 109. ECG in a patient of stage III. Tall and wide R waves in the left leads, the QRS complex is widened. S-T interval reduced and T negative. Left bundle branch block.

Rice. 110. ECG in a patient with stage II hypertension with sharp increase Blood pressure (210/120 mm Hg), S-T interval is slightly lowered, high R wave in the left leads.

Rice. 111 GB Stage III. Condition after hypertensive crisis. Myocardial infarction in the anterior apical zone of hypertrophied myocardium. Blood pressure 110/70 mm Hg. Art. Fourth day of complications.

Rice. 112. Hypertension with signs of hypertrophic cardiomyopathy (left ventricular myocardial thickness 21 mm). Chronic pyelonephritis and chronic renal failure Stage II. Arterial hypertension (BP 210/110 mm Hg).

Rice. 113. 1. ECG of a patient during a hypertensive crisis (BP 180/115 mm Hg) and (2) after (BP 130/80) treatment of the crisis.

Rice. 114. ECG in a patient with arterial hypertension and long QT interval syndrome. An attack of ventricular tachycardia that lasted about 10 seconds.

Group A.

1 deviation of the electrical axis of the heart to the left;

2 R 1 > 10 mm;

3 S(Q)aVR > 14 mm;

4 RV5 - V6 > 16 mm;

5 RaVL > 7 mm;

6 TV5, V6 = 1 mm with RV5, V6 > 10 mm and no signs of coronary insufficiency;

7 TV1 > TV6 when TV1 > 1.5 mm.

Group B:

1 RI + SIII > 20 mm,

2 Reduction of the S-TI interval down > 0.5 mm at RI > SI;

3 SV1 >12 mm;

4 SV1 + RV5 (V6) > 28 mm in persons over 30 years of age or SV3 + RV5 (V6) > 30 mm in persons under 30 years of age;

5 RaVF > 20 mm;

6 RII > 20 mm. (Adapted from Orlov’s book with some abbreviation).

According to ultrasound diagnostics the thickness of the left ventricular myocardium is not more than 11 mm. An increase in the thickness of the left ventricular myocardium is observed with myocardial hypertrophy, which occurs as a result of hypertension, aortic and mitral-aortic defects, obesity, and hypertrophic cardiomyopathy.

The ultrasound method of measuring the thickness of the myocardium of the left and right ventricles, especially the septum, impresses with its reliability and simplicity, but does not cancel ECG study.

Rice. 115. ECG of a patient with hypertension and left ventricular myocardial hypertrophy. A turn of the EOS to the left and signs of left ventricular myocardial hypertrophy are detected (ST interval is lowered in leads I, aVL, V 5-6).

ECG for heart defects.

With heart defects, disturbances in intracardiac hemodynamics occur. With stenosis of the orifices, increased resistance to blood flow occurs. In case of valve insufficiency, part of the blood is discharged back into the cavity of the ventricle or atrium. These changes constitute an additional load on the myocardium of the ventricles or atria. Changes in the size of the heart and changes in the direction of the electrical axis of the heart occur.

Long-term resistance to blood flow occurs with mitral stenosis. The myocardium of the left atrium is hypertrophied. Later, as a result of a compensatory reaction and an increase in pressure in the vessels of the pulmonary circulation, hypertrophy of the myocardium of the right ventricle and atrium develops. In case of insufficiency bicuspid valve the myocardium of the left ventricle and left atrium changes, and the myocardium of the right heart changes to a lesser extent.

In the case of aortic disease, especially aortic valve stenosis, overload of the left ventricular myocardium is formed under the influence of increased resistance to blood flow.

In case of aortic valve insufficiency, part of the blood is discharged from the aorta into the left ventricle. Left ventricular myocardial hypertrophy gradually increases. Such loads cause powerful myocardial hypertrophy, rotation of the heart to the left and dilatation of the cavities with increasing decompensation.

With an abnormal development of the heart, changes in intracardiac hemodynamics and overload of the ventricular or atrium myocardium exist from the birth of the child. With age, their influence increases and leads to heart failure. The most common defect is bicuspid valve insufficiency. It is formed during rheumatism. During atrial systole, blood flows into the left ventricle in increased quantities. The myocardium of the left atrium and left ventricle undergoes hypertrophy. The ECG shows signs of myocardial hypertrophy in the left parts of the heart (P1, R1, V 6) and rotation of the EOS to the left.

Mitral stenosis is common. In this case, a presystolic murmur is heard at the apex of the heart and at the fifth point, hypertrophies and dilates left atrium. The plethora of blood vessels in the lungs and pressure in the system increases pulmonary artery.

The myocardium of the right ventricle and atrium hypertrophies. EOS turns right. There are signs of atrial hypertrophy (high P 1 waves, it is cardiac), hypertrophy of the right ventricular myocardium (EOS reveals a right gram, RIII, V1 - rR, RR or R, in V 5, 6 - S). There may be signs of right bundle branch block. Rice. 114, 2).

Rice. 116. ECG in patients with heart defects: 1) with mitral insufficiency. 2) in a patient with mitral stenosis. 3) in a patient with aortic disease. 4) in a patient with mitral-aortic disease (with hypertrophy of both ventricles), 5) in a patient with mitral-tricuspid disease

In patients with aortic heart defects (aortic insufficiency or aortic stenosis) severe hypertrophy of the left ventricular myocardium develops. If the vice exists long time, myocardial hypertrophy is pronounced (myocardial thickness can reach 15-25 mm), and with increasing dilatation of the left ventricle, the EOS turns to the left (left-gram). The ECG shows a high wave R 1, RV 5-6. In V 1-2, an S wave is observed. Signs of blockade of the branches of the left bundle branch may occur.

With a tricuspid defect, hypertrophy of the myocardium of the right ventricle and right atrium occurs. The changes are usually weakly expressed. The defect is revealed clinical methods bad, better when examined by ultrasound.

Isolated heart defects (stenosis or valve insufficiency) are less common than combined (stenosis and insufficiency) or combined (mitral-aortic, aortic-tricuspid defects).

Heart change when congenital defects . Such defects are determined mainly by clinical and ultrasonic methods. They are often detected by clinical methods with great difficulty, especially if they are complicated by infective endocarditis. Electrocardiographic and ultrasonography significantly improved the diagnosis of such diseases. The main criteria for the disease are the appearance of signs of myocardial hypertrophy of the left or right ventricles, atria, and signs of blockade. A comprehensive study (ECG, ultrasound, radiographic methods with contrast of the heart and blood vessels) facilitated the diagnosis of congenital defects.

Heart in respiratory diseases.

Inflammatory disease respiratory organs in case of the most mild course causes a number of changes in cardiovascular system. Tachycardia often occurs. Toxic effects on the myocardium are noted.

Rice. 117 ECG in a patient with chronic obstructive bronchitis and pneumosclerosis. Pulmonary heart. Respiratory failure Stage III. Heart failure stage II.

Heart changes are observed in chronic lung diseases, pneumosclerosis (for example, silicosis), especially in chronic obstructive bronchitis (bronchiectasis, lung abscesses), malignant tumors.

Rice. 118. ECG in a patient with chronic obstructive bronchitis during an exacerbation of the inflammatory process and in the presence of pneumonia. Widening of the R wave (sign incomplete blockade right bundle branch).

Rice. 120. ECG in a patient with bronchial asthma during an attack of suffocation. Atrial tachycardia. A sharp turn of the EOS to the right due to overload of the right ventricle. The frequency of ventricular contractions is about 200 per minute.

Rice. 121. ECG in a patient with bronchial asthma. High tooth RIII and R V 1. Legal form. QRS 0.10 s is a sign of right ventricular myocardial hypertrophy.

Rice. 122 ECG in a patient with bronchial asthma during remission. Legal form. P pulmonary. QRS = 0.12 s Right bundle branch block.

Heart in chronic bronchitis. The inflamed and swollen bronchial mucosa creates resistance to air flow. Arises spastic reaction bronchi, difficulty in exhaling. Pulmonary emphysema increases. The resistance to blood flow increases in compressed arterioles and capillaries in the interalveolar space. The pressure in the pulmonary artery and its branches increases.

The myocardium of the right ventricle is hypertrophied. The electrical axis of the heart deviates to the right. Signs of right ventricular myocardial hypertrophy appear: a high R wave in the right leads (III, V 1-2, aVR), the S-T interval is reduced, the T wave is inverted, blockade of the right bundle branch.

The pressure in the pulmonary artery of a healthy person is about 20 mm Hg. It increases during the period of bronchial obstruction and decreases during the period of remission. The electrocardiographic method provides a certain opportunity to observe this process. So, at a pressure of about 30 mm Hg. Art. a distinct turn of the EOS to the right appears, with an increase in pressure in the range of 50-80 mm Hg. Art. There is a decrease in the S-T interval in the right leads and the formation of a negative T wave in lead III. In some patients, the pressure in the pulmonary artery rises to 300 mm Hg. There is an increase in signs of cardiosclerosis of the right ventricle and the appearance of right bundle branch block.

ECG for bronchial asthma. Changes in the heart muscle during bronchial asthma resemble changes that develop in patients with chronic obstructive bronchitis. Let's repeat the main points: turning the EOS to the right, the right-hand diagram, high R waves in the right leads, signs of overload of the right ventricle (the S-T interval is lowered, the T wave is negative). During an attack of suffocation, tachycardia develops. The more severe the attack of suffocation, the more changes on the ECG (extrasystoles, paroxysms of atrial tachycardia, attacks of atrial fibrillation). Patients with bronchial asthma receive glucocorticosteroid drugs sometimes large doses, which may affect the state of electrolyte metabolism in the myocardium. Some patients show signs of the influence of such electrolyte disturbances on the heart.

ECG in patients with pneumonia and exudative pleurisy. Pneumonia is an infectious bacterial or viral process. A patient with pneumonia exhibits signs of intoxication - fever, tachycardia, cardiac arrhythmias, decreased contractility heart and signs of heart failure.

With pneumonia, part of the lungs is switched off from the respiratory process. Gas exchange disturbance occurs. Compensatory stretching of the healthy part of the lung (emphysema) increases. Resistance to blood flow in the lungs may increase, which leads to overload of the right ventricular myocardium. The changes are more pronounced in lobar (lobar) pneumonia, small-focal diffuse processes, and with a large accumulation of effusion in the pleural cavity.

Infectious process may not be limited to lung damage. The heart muscle may contain necrobiotic or inflammatory process. Pericarditis with pneumonia is rare.

ECG for primary pulmonary hypertension. Primary pulmonary hypertension– a disease of the vessels of the pulmonary circulation, in which fibrosing processes, lipid deposits, and the formation of blood clots progress in the vascular wall. The disease is genetic in nature, sometimes complicated by vasculitis, more often by thrombus formation. Such changes in the pulmonary artery lead to increased pressure in the vessel, overload and hypertrophy of the right ventricular myocardium.

Ayersa syndrome. The cause of the disease has not been established. Morphological changes: a pronounced sclerotic process in the vessels of the lungs, and in some patients around the bronchi. Mostly small vessels and bronchi are affected.

Rice. 123. ECG in a patient with thrombotic embolism of a large branch of the pulmonary artery: 1 – rise in the S-T interval in leads III and V1, “pulmonary” R. Pravogramma. 2. 2 months after treatment.

The disease has been discovered in humans different ages. There is an increase in weakness. The cyanosis can be pronounced. Blood polycytosis develops, increasing its viscosity. The ECG shows pronounced signs of overload and hypertrophy of the myocardium of the right heart (high R wave, decreased S-T interval and T wave inversion).

Thrombotic pulmonary embolism.

The reason is the introduction of emboli from the veins or cavities of the heart into the branches of the pulmonary artery. Blood clots in the veins occur with phlebitis of the veins lower limbs And abdominal cavity after surgical interventions. They arise in the cavity of the right heart when infective endocarditis, myocarditis.

Emboli from the left side of the heart are carried into the branches of the arteries, most often into the vessels of the limbs, kidneys, and brain.

Very large venous thrombi get stuck in the area of ​​the pulmonary artery fork, causing overload of the right heart, oxygen starvation And fatal outcome process.

Small blood clots cause obstruction small vessels. Clinical signs resemble focal pneumonia. Repeated emboli with small blood clots lead to pneumosclerosis. Some patients develop pulmonary hypertension and cor pulmonale.

TREATMENT OF HEART RHYTHM DISORDERS

Antiarrhythmic drugs.

Drug treatment for heart rhythm disturbances. Heart rhythm disturbances are secondary. Treatment of the underlying disease becomes the main thing in the treatment of arrhythmia. It is also noted that the use of a number of antiarrhythmic drugs has a beneficial effect on the course of diseases such as ischemic heart disease, cardiosclerosis, and circulatory failure. Anti-arrhythmic drugs are used most often for paroxysmal tachycardia - flutter, atrial fibrillation, paroxysmal ventricular arrhythmias. In such cases, cardiac glycosides, beta-blockers, and calcium channel blockers are effective.

Antiarrhythmic drugs are currently divided into a number of groups according to V. Williams. This classification is of relative practical importance. Group 1 - membrane stabilizing drugs, II - β-adrenergic blocking drugs, III - drugs that increase the duration of the action potential, Group IV - drugs that block calcium channels. The classification is based on the effect of drugs on certain mechanisms of formation of excitation of myocardial cells.

I class drugs - drugs that block fast sodium channels cell membrane, inhibit the rate of initial depolarization with a rapid electrical response. They inhibit myocardial excitability and suppress ectopic foci of excitation.

Pyromecaine suppresses ectopic foci of excitability during intoxication with glycosides and when using constant electrical stimulation (used intramuscularly and intravenously, 5–10 ml). Gilurhythmal, for example, slows down atrioventricular impulse conduction, suppresses automaticity sinus node. All drugs have a stabilizing effect on cell membranes (Table 2).

The ECG has long been a reliable assistant in the study and treatment of hypertension. This instrumental diagnostic method, required for every patient with hypertension, identifies interruptions in the functioning of the heart, determines the presence of angina, provides data on the condition of the myocardium, cardiac hypertrophy, and displacement of its electrical axis.

To decipher an electrocardiogram means to evaluate the efficiency of the heart muscle and its potential. This allows the doctor to detect rhythm disturbances, ischemia and other abnormalities.

A more detailed picture of heart deformations in hypertension is demonstrated by echocardiography. With its help, you can see hypertrophy plus measure the thickness of the ventricular wall, which tends to increase with increasing vascular resistance.

ECG interpretation

Decoding the cardiographic pattern involves measuring the length, area of ​​the segments and amplitude of vibration of the teeth.

The rhythm of contractions of the heart muscle is calculated by the duration of the intervals. If their duration is the same or varies by no more than 10%, the indicators are normal; with other data, the possibility of rhythm disturbance is possible. But an objective diagnosis can only be made by the attending doctor.

The most obvious indicators of hypertension on the electrocardiogram are:

• Overload or hypertrophy of the left ventricle;
• Indirect symptoms of coronary heart disease or ischemia of myocardial areas.

Diagnosis and ECG indications for hypertension according to the stages of disease progression

Stage I

The onset of hypertension is accompanied by a small number of unstable symptoms that arise quickly and also disappear suddenly.

High blood pressure is sometimes detected by chance. Blood pressure tends to jump sometimes due to physical or emotional stress.

At this stage of the disease there is no target organ damage. Accordingly, the electrocardiogram, echocardiogram and radiograph do not demonstrate pathological metamorphoses.

Diagnosis at stage 1 is limited to measuring pressure.

Stage II

For the next period hypertension A certain set of its manifestations is characteristic; patients sometimes experience.

The ECG shows changes characteristic of left ventricular hypertrophy. They are also visible on X-ray and echocardiographic examination. Later, the ECG for stage 2 hypertension will reflect data on rhythm disturbances and conduction of the heart, as well as coronary circulation.

At the second stage of hypertension, diagnosis is still simple: recording the increase in blood pressure, ECG for left ventricular hypertrophy and identifying unwanted transformations in the fundus.

Stage III

The highest stage of hypertension is determined by constant high blood pressure, plus :

• Brain: hemorrhage in the area of ​​the cerebral cortex or cerebellum;
• Fundus: retinal hemorrhage;
• Heart: left ventricular failure, myocardial infarction;
• Kidney: renal failure.

An ECG reveals damage to the coronary circulation and manifestations of left ventricular hypertrophy.

At stage III of the disease, the examination includes recording high pressure, severe damage internal organs, including hearts.

It is possible to avoid the progression of hypertension if you follow the recommendations:

• Be sure to do it daily physical exercise in order to keep blood vessels elastic;
• It is necessary to maintain optimal weight, because excess weight tends to provoke both hypertension and ischemic disease hearts;
• It is important to avoid smoking, including passive smoking, since exposure to nicotine leads to blockage of blood vessels;
• Mandatory proper rest with alternating intellectual and physical activity is required;
• It is necessary to do tests for sugar from time to time;
• Important at regular intervals

Sokolov-Lyon index(SV1+ RV5/RV6 >35 mm)

>45 mm in persons under 45 years of age

Cornell Voltage Index:

RAVL+ SV3> 28 mm for men

> 20 mm in women.

Echocardiography. Criteria for left ventricular hypertrophy:

LVTS > 1.2 cm; TMZH > 1.2 cm

LVMI is calculated using the formula Devereux, Reicher (1977) = 1.04 [(TMZHP 3 + TZSLZH 3 + EDR 3) - EDR 3 ] 3 -13.6 (g)

LVMI in men >134 g/m2

LVMI in women > 110 g/m2

Laboratory data for hypertension.

If hypertension is more than 2 years old, moderate hyperproteinemia and hyperlipidemia.

Magnetic resonance imaging of the heart.

Cardiac magnetic resonance imaging (MRI) may be considered for assessing left ventricular size and mass when echocardiography is not technically feasible and when delayed-enhanced imaging will provide information relevant to treatment decisions.

Myocardial ischemia.

There are special procedures in reserve for diagnosing myocardial ischemia in patients with hypertension and LVH. This diagnosis is particularly difficult because hypertension reduces the specificity of stress echocardiography and perfusion scintigraphy. If ECG results with exercise are positive or cannot be interpreted (ambiguous), then a reliable diagnosis of myocardial ischemia requires a technique that allows visualization of the appearance of ischemia, for example, cardiac stress MRI, perfusion scintigraphy or stress echocardiography.

Carotid arteries.

Ultrasonography carotid arteries with measurement of intima-media thickness (IMT) and assessment of the presence of plaques allows predicting both stroke and myocardial infarction, independent of traditional cardiovascular risk factors. This is true for both the IMT thickness value at the level of the carotid bifurcation (which reflects mainly atherosclerosis) and the IMT value at the level of the common carotid artery (which mainly reflects vascular hypertrophy).

Pulse wave speed.

It has been established that the phenomenon of large artery stiffness and pulse wave reflection are the most important pathophysiological determinants of ISAH and the increase in pulse pressure with aging. Carotid-femoral pulse wave velocity (CPW) is the “gold standard” measurement of aortic stiffness. In a recent consensus statement, this threshold was adjusted to 10 m/s, taking into account the immediate distance from carotid to femoral arteries and taking into account the 20% shorter true anatomical distance traveled by the pressure wave (i.e., 0.8 x 12 m/sec or 10 m/sec).

Ankle-brachial index.

The ankle-brachial index (ABI) can be measured either automatically using instruments or using a continuous wave Doppler meter and a sphygmomanometer to measure blood pressure. Low ABI (<0,9) указывает на поражение периферических артерий и на выраженный атеросклероз в целом, является предиктором сердечно-сосудистых событий и ассоциирован примерно с двукратным увеличением сердечно-сосудистой смертности и частоты основных коронарных событий, по сравнению с общими показателями в каждой фремингемской категории риска.

Taking an electrocardiogram is necessary to make a diagnosis of diseases of the cardiovascular system. Since arterial hypertension syndrome is the main symptom of this type of pathology, an ECG may also be prescribed to clarify the causes of increased pressure.

Carrying out the procedure

Accurate diagnosis requires certain preparation from the patient. On the eve of the test it is prohibited:

• be very overtired;
• find yourself in stressful situations;
• eat before bed;
• drink plenty of fluids in the morning before going to the doctor;
• drink coffee during the day before the ECG;
• In the morning, take a shower with hygiene products: gels or soap, since the thin oil film that forms on the skin will delay the electrical impulse, distorting the test results.

A feature of the ECG for hypertensive patients is greater attention to deciphering the analysis. First of all, the task of the health worker is to identify coronary artery disease, heart attack, and heart rhythm disturbances.

The difficulty is that the pressure can increase for a short period of time, so ideally testing should be carried out during the next hypertensive attack. Causes of future, possibly serious pathology may not appear constantly, alternating with periods of normal health.

Stages of hypertension on an ECG image

The main sign of hypertension on the ECG is the hypertrophied state of the left ventricular myocardium. Pathology manifests itself:

• deviation to the left side of the electrical axis of the heart muscle;
• the formation of high R-teeth in leads V4-V6 of the chest;
• increased muscle mass of the left myocardium.

Deformations in the shape of the heart will allow it to move large volumes of blood per unit of time, and this is an increase in blood pressure.

An ECG examination clearly shows the stages of hypertension.

1. At the first stage, decoding the image does not show any signs of pathological changes. Therefore, the diagnosis is made by a doctor based on the patient’s complaints about periods of increased pressure.
2. The second stage is already manifested on the ECG in the form of left ventricular hypertrophy, decreased cardiac conduction and blood circulation in the myocardium.
3. The main signs of the third form are a persistent overload of the left ventricle, leading to its hypertrophy, as well as a significant failure of the coronary circulation.

The more severe the disease, the more additional tests may be required to diagnose the patient.

Signs of a hypertensive crisis according to the cardiogram

This condition is dangerous due to its suddenness. In the initial stages of a crisis, the patient may experience harmless symptoms:

• slight dizziness;
• slight pain in the head area;
• skin redness.

Then the patient's condition rapidly deteriorates.

• there is a throbbing pain in the head;
• flies may flash before your eyes;
• very sick;
• convulsions are possible;
• heart pain occurs;
• blood pressure rapidly increases to 210/120 mm Hg. Art.;
• After overcoming the crisis, spontaneous urination is possible.

If during an attack the patient arrives in a medical facility in a timely manner and is given a cardiogram, the following results will appear on the image:

• decrease in the S-T segment;
• failure in the repolarization phase in the form of flattening of the T-wave in the area of ​​the left chest leads;
• reduction in conduction inside the ventricles of the heart.

An electrocardiogram allows you to quickly recognize hypertension and begin maintenance therapy or treatment of the disease. Persons suffering from arterial hypertension should undergo regular hardware examinations, including during periods of improvement for the purpose of prevention.

– a condition accompanied by a sudden critical increase in blood pressure, against the background of which neurovegetative disorders, disturbances of cerebral hemodynamics, and the development of acute heart failure are possible. A hypertensive crisis occurs with headaches, noise in the ears and head, nausea and vomiting, visual disturbances, sweating, lethargy, sensitivity and thermoregulation disorders, tachycardia, heart failure, etc. Diagnosis of a hypertensive crisis is based on blood pressure indicators, clinical manifestations , auscultation data, ECG. Measures to relieve a hypertensive crisis include bed rest, a gradual controlled decrease in blood pressure using medications (calcium antagonists, ACE inhibitors, vasodilators, diuretics, etc.).

General information

A hypertensive crisis is regarded in cardiology as an emergency condition that occurs with a sudden, individually excessive jump in blood pressure (systolic and diastolic). Hypertensive crisis develops in approximately 1% of patients with arterial hypertension. A hypertensive crisis can last from several hours to several days and lead not only to the occurrence of transient neurovegetative disorders, but also to disorders of cerebral, coronary and renal blood flow.

During a hypertensive crisis, the risk of severe life-threatening complications (stroke, subarachnoid hemorrhage, myocardial infarction, ruptured aortic aneurysm, pulmonary edema, acute renal failure, etc.) increases significantly. In this case, damage to target organs can develop both at the height of a hypertensive crisis and with a rapid decrease in blood pressure.

Causes

Typically, a hypertensive crisis develops against the background of diseases occurring with arterial hypertension, but it can also occur without a previous persistent increase in blood pressure.

Hypertensive crises occur in approximately 30% of patients with hypertension. They are most common in women experiencing menopause. Often, a hypertensive crisis complicates the course of atherosclerotic lesions of the aorta and its branches, kidney diseases (glomerulonephritis, pyelonephritis, nephroptosis), diabetic nephropathy, periarteritis nodosa, systemic lupus erythematosus, nephropathy of pregnancy. A crisis course of arterial hypertension can be observed with pheochromocytoma, Itsenko-Cushing's disease, and primary hyperaldosteronism. A fairly common cause of hypertensive crisis is the so-called “withdrawal syndrome” - rapid cessation of taking antihypertensive drugs.

In the presence of the above conditions, the development of a hypertensive crisis can be provoked by emotional arousal, meteorological factors, hypothermia, physical activity, alcohol abuse, excess consumption of table salt, electrolyte imbalance (hypokalemia, hypernatremia).

Pathogenesis

The mechanism of development of hypertensive crises in various pathological conditions is not the same. The basis of a hypertensive crisis in hypertension is a violation of neurohumoral control of changes in vascular tone and activation of the sympathetic influence on the circulatory system. A sharp increase in arteriolar tone contributes to a pathological increase in blood pressure, which creates additional stress on the mechanisms of regulation of peripheral blood flow.

Hypertensive crisis with pheochromocytoma is caused by an increase in the level of catecholamines in the blood. In acute glomerulonephritis, we should talk about renal (decreased renal filtration) and extrarenal factors (hypervolemia) that determine the development of the crisis. In the case of primary hyperaldosteronism, increased secretion of aldosterone is accompanied by a redistribution of electrolytes in the body: increased excretion of potassium in the urine and hypernatremia, which ultimately leads to an increase in peripheral vascular resistance, etc.

Thus, despite the various reasons, common points in the mechanism of development of various variants of hypertensive crises are arterial hypertension and dysregulation of vascular tone.

Classification

Hypertensive crises are classified according to several principles. Taking into account the mechanisms of increased blood pressure, hyperkinetic, hypokinetic and eukinetic types of hypertensive crisis are distinguished. Hyperkinetic crises are characterized by an increase in cardiac output with normal or decreased peripheral vascular tone - in this case, an increase in systolic pressure occurs. The mechanism of development of a hypokinetic crisis is associated with a decrease in cardiac output and a sharp increase in peripheral vascular resistance, which leads to a predominant increase in diastolic pressure. Eukinetic hypertensive crises develop with normal cardiac output and increased peripheral vascular tone, which entails a sharp jump in both systolic and diastolic pressure.

Based on the reversibility of symptoms, an uncomplicated and a complicated version of a hypertensive crisis are distinguished. The latter is said in cases where a hypertensive crisis is accompanied by damage to target organs and is the cause of hemorrhagic or ischemic stroke, encephalopathy, cerebral edema, acute coronary syndrome, heart failure, dissection of aortic aneurysm, acute myocardial infarction, eclampsia, retinopathy, hematuria, etc. e. Depending on the location of complications that developed against the background of a hypertensive crisis, the latter are divided into cardiac, cerebral, ophthalmological, renal and vascular.

Taking into account the prevailing clinical syndrome, neuro-vegetative, edematous and convulsive forms of hypertensive crises are distinguished.

Symptoms of hypertensive crisis

A hypertensive crisis with a predominance of neuro-vegetative syndrome is associated with a sharp, significant release of adrenaline and usually develops as a result of a stressful situation. A neurovegetative crisis is characterized by excited, restless, nervous behavior of patients. Increased sweating, flushing of the skin of the face and neck, dry mouth, and hand tremors are noted. The course of this form of hypertensive crisis is accompanied by pronounced cerebral symptoms: intense headaches (spread out or localized in the occipital or temporal region), a feeling of noise in the head, dizziness, nausea and vomiting, blurred vision (“veil”, “flickering of flies” before the eyes) . In the neurovegetative form of a hypertensive crisis, tachycardia, a predominant increase in systolic blood pressure, and an increase in pulse pressure are detected. During the period of resolution of the hypertensive crisis, frequent urination is observed, during which an increased volume of light urine is released. The duration of a hypertensive crisis ranges from 1 to 5 hours; There is usually no threat to the patient's life.

The edematous or water-salt form of hypertensive crisis is more common in overweight women. The crisis is based on an imbalance of the renin-angiotensin-aldosterone system, which regulates systemic and renal blood flow, the constancy of blood volume and water-salt metabolism. Patients with the edematous form of hypertensive crisis are depressed, apathetic, drowsy, and poorly oriented in the environment and in time. During an external examination, attention is drawn to pallor of the skin, puffiness of the face, swelling of the eyelids and fingers. Typically, a hypertensive crisis is preceded by a decrease in diuresis, muscle weakness, and interruptions in heart function (extrasystoles). In the edematous form of a hypertensive crisis, there is a uniform increase in systolic and diastolic pressure or a decrease in pulse pressure due to a large increase in diastolic pressure. A water-salt hypertensive crisis can last from several hours to a day and also has a relatively favorable course.

Neuro-vegetative and edematous forms of hypertensive crisis are sometimes accompanied by numbness, a burning sensation and tightening of the skin, a decrease in tactile and pain sensitivity; in severe cases - transient hemiparesis, diplopia, amaurosis.

The most severe course is characteristic of the convulsive form of hypertensive crisis (acute hypertensive encephalopathy), which develops when the regulation of the tone of cerebral arterioles is disturbed in response to a sharp increase in systemic blood pressure. The resulting cerebral edema can last up to 2-3 days. At the height of a hypertensive crisis, patients experience clonic and tonic convulsions and loss of consciousness. For some time after the end of the attack, patients may remain unconscious or disoriented; amnesia and transient amaurosis persist. The convulsive form of a hypertensive crisis can be complicated by subarachnoid or intracerebral hemorrhage, paresis, coma and death.

Diagnosis of hypertensive crisis

One should think about a hypertensive crisis when blood pressure rises above individually tolerable values, relatively sudden development, and the presence of symptoms of a cardiac, cerebral and vegetative nature. An objective examination may reveal tachycardia or bradycardia, rhythm disturbances (usually extrasystole), percussion expansion of the boundaries of relative dullness of the heart to the left, auscultatory phenomena (gallop rhythm, accent or splitting of the second sound over the aorta, moist rales in the lungs, hard breathing, etc.).

Blood pressure can increase to varying degrees; as a rule, during a hypertensive crisis it is above 170/110-220/120 mm Hg. Art. Blood pressure is measured every 15 minutes: initially on both arms, then on the arm where it is higher. When registering an ECG, the presence of disturbances in heart rhythm and conduction, left ventricular hypertrophy, and focal changes is assessed.

To carry out differential diagnosis and assess the severity of a hypertensive crisis, specialists may be involved in examining the patient: cardiologist, ophthalmologist, neurologist. The scope and feasibility of additional diagnostic studies (EchoCG, REG, EEG, 24-hour blood pressure monitoring) is determined individually.

Treatment of hypertensive crisis

Hypertensive crises of various types and genesis require differentiated treatment tactics. Indications for hospitalization in a hospital include intractable hypertensive crises, repeated crises, and the need for additional research aimed at clarifying the nature of arterial hypertension.

When blood pressure rises critically, the patient is provided with complete rest, bed rest, and a special diet. The leading place in stopping a hypertensive crisis belongs to emergency drug therapy aimed at lowering blood pressure, stabilizing the vascular system, and protecting target organs.

To lower blood pressure values ​​during an uncomplicated hypertensive crisis, calcium channel blockers (nifedipine), vasodilators (sodium nitroprusside, diazoxide), ACE inhibitors (captopril, enalapril), ß-blockers (labetalol), imidazoline receptor agonists (clonidine) and other groups of drugs are used . It is extremely important to ensure a smooth, gradual decrease in blood pressure: by approximately 20-25% of initial values ​​during the first hour, over the next 2-6 hours - to 160/100 mm Hg. Art. Otherwise, with an excessively rapid decrease, the development of acute vascular accidents can be provoked.

Symptomatic treatment of a hypertensive crisis includes oxygen therapy, administration of cardiac glycosides, diuretics, antianginal, antiarrhythmic, antiemetic, sedatives, analgesics, and anticonvulsants. It is advisable to conduct hirudotherapy sessions and distraction procedures (hot foot baths, heating pads on the feet, mustard plasters).

Possible outcomes of treatment of hypertensive crisis are:

• improvement of condition (70%) – characterized by a decrease in blood pressure by 15-30% of the critical level; a decrease in the severity of clinical manifestations. There is no need for hospitalization; selection of adequate antihypertensive therapy on an outpatient basis is required.
• progression of hypertensive crisis (15%) – manifested by an increase in symptoms and the addition of complications. Requires hospitalization in a hospital.
• lack of effect from treatment - there is no dynamics of reduction in blood pressure levels, clinical manifestations do not increase, but do not stop. A change in medication or hospitalization is necessary.
• complications of an iatrogenic nature (10-20%) – occur with a sharp or excessive decrease in blood pressure (hypotension, collapse), side effects from medications (bronchospasm, bradycardia, etc.). Hospitalization is indicated for the purpose of dynamic observation or intensive care.

Prognosis and prevention

If timely and adequate medical care is provided, the prognosis for a hypertensive crisis is conditionally favorable. Cases of death are associated with complications arising from a sharp rise in blood pressure (stroke, pulmonary edema, heart failure, myocardial infarction, etc.).

To prevent hypertensive crises, one should adhere to the recommended antihypertensive therapy, regularly monitor blood pressure, limit the amount of salt and fatty foods consumed, monitor body weight, avoid drinking alcohol and smoking, avoid stressful situations, and increase physical activity.

In case of symptomatic arterial hypertension, consultations with specialized specialists - a neurologist,