Lecture No. 6. Emergency conditions in cardiology

1. Myocardial infarction

Myocardial infarction is a discrepancy between myocardial oxygen demand and its delivery, resulting in limited necrosis of the heart muscle. The most common cause is a thrombus, less often an embolus, less often a spasm of the coronary arteries. Thrombosis is most often observed against the background of atherosclerotic damage to the coronary arteries. In the presence of atheromatous plaques, a swirling of the blood flow occurs. Atherosclerotic lesions develop as a result of impaired lipid metabolism, blood clotting increases, which is associated with a decrease in the activity of mast cells that produce heparin. Increased blood clotting and turbulence contribute to the formation of blood clots. Disintegration of atheromatous plaques, hemorrhages in them can lead to the formation of blood clots. Predisposing factors are male gender, age over 50, obesity, heredity, psycho-emotional stress, hard work.

Clinic and diagnostics

Classically, myocardial infarction begins with increasing pain behind the sternum, which is burning and pressing in nature. Characterized by extensive irradiation of pain in the arms (more often in the left), back, abdomen, head, under the left shoulder blade, in the left lower jaw, etc. Patients are restless, anxious, sometimes they note a feeling of fear of death. There are signs of heart and vascular insufficiency - cold extremities, clammy sweat, etc. The pain syndrome is prolonged, and is not relieved by nitroglycerin for 30 minutes or more. There are various disorders of the heart rhythm, a drop in blood pressure or its rise. Patients subjectively note the feeling of lack of air. The above signs are typical for period I - painful or ischemic, the duration of which ranges from several hours to 2 days. Objectively, an increase in blood pressure (then a decrease); increased heart rate or rhythm disturbance; on auscultation, an abnormal IV tone is heard; heart sounds are muffled; on the aorta accent II tone; there are practically no biochemical changes in the blood, characteristic signs on the ECG.

The second period is acute (feverish, inflammatory), characterized by the occurrence of necrosis of the heart muscle at the site of ischemia. The pain usually goes away.

The duration of the acute period is up to 2 weeks. The patient's state of health gradually improves, but general weakness, malaise, and tachycardia persist. Heart sounds are muffled. An increase in body temperature due to the inflammatory process in the myocardium, usually small, up to 38 ° C, usually appears on the 3rd day of the disease. By the end of the first week, the temperature usually returns to normal. When examining blood, they find: leukocytosis, moderate, neutrophilic (10-15 thousand) with a shift to rods: eosinophils are absent or eosinopenia; gradual acceleration of ESR; C-reactive protein appears; increased transaminase activity; increased activity of lactate dehydrogenase, creatine phosphokinase and other markers of infarction. Cardiospecific are CPK-MB fraction and cardiac troponin.

The third period (subacute, or scarring) lasts 4-6 weeks.

Characteristic for it is the normalization of blood parameters (enzymes), body temperature normalizes, all other signs of an acute process disappear: the ECG changes, a connective tissue scar develops at the site of necrosis.

The fourth period (rehabilitation period, recovery) lasts from 6 months to 1 year. There are no clinical signs. During this period, compensatory hypertrophy of intact myocardial muscle fibers occurs, and other compensatory mechanisms develop. There is a gradual restoration of myocardial function. But the pathological Q wave persists on the ECG.

But we should not forget about the presence of atypical forms of myocardial infarction, which are often found in clinical practice. These include the following.

1. The abdominal form proceeds according to the type of pathology of the gastrointestinal tract with pain in the epigastric region, under the xiphoid process, in the abdomen, accompanied by nausea, vomiting. More often this form (abdominal) of myocardial infarction occurs with infarction of the posterior wall of the left ventricle. In general, the option is rare. ECG leads II, III, and VL.

2. The asthmatic form is characterized by signs of cardiac asthma and provokes pulmonary edema as an outcome. Pain may be absent. The asthmatic form occurs more often in older people with cardiosclerosis or in recurrent infarction, or in very large infarcts. There is shortness of breath, suffocation, cough. Auscultatory in the lungs - moist fine bubbling rales.

3. Brain form, or cerebral. At the same time, in the foreground, symptoms of cerebrovascular accident by the type of stroke with loss of consciousness are more common in older people with cerebral vascular sclerosis. There is dizziness, nausea, vomiting, focal neurological symptoms.

4. Silent, or painless, form is an accidental finding during medical examination. Of the clinical manifestations: suddenly it became "ill", there was a sharp weakness, sticky sweat, then everything, except for weakness, disappears. This situation is typical for a heart attack in old age and with repeated myocardial infarctions. An unmotivated decrease in exercise tolerance develops.

5. Arrhythmic form: the main symptom is paroxysmal - tachycardia, pain may be absent. It begins with a sign of ventricular or supraventricular tachycardia, AV block II-III degree, acute blockade of the legs of the atrioventricular bundle. Morgagni-Adams-Stokes attacks often occur in the debut. In most cases, cardiac arrhythmias are complicated by hypotension, arrhythmogenic shock, and acute heart failure.

Signs of myocardial infarction on the ECG are as follows:

1) with penetrating myocardial infarction or transmural (i.e., the necrosis zone extends from the pericardium to the endocardium): displacement of the ST segment above the isoline, the shape is convex upward - like a “cat’s back”; fusion of the T wave with the ST segments on days 1-3; deep and wide Q wave is the main sign; decrease in the size of the R wave, sometimes QS form; characteristic discordant changes - opposite shifts of ST and T (for example, in the 1st and 2nd standard leads compared to the 3rd standard lead); on average, from the 3rd day, a characteristic reverse dynamics of ECG changes is observed: the ST segment approaches the isoline, a uniform deep T appears. The Q wave also undergoes reverse dynamics, but the altered Q and deep T can persist for life;

2) with intramural or non-transmural myocardial infarction: there is no deep Q wave, the ST segment displacement can be not only up, but also down.

The main criteria for the diagnosis of myocardial infarction:

1) clinical signs;

2) electrocardiographic signs;

3) biochemical signs.

Complications: cardiac arrhythmias, atrioventricular conduction disturbances, acute left ventricular failure: pulmonary edema, cardiac asthma, cardiogenic shock, gastrointestinal disorders (paresis of the stomach and intestines, gastric bleeding), pericarditis, parietal thromboendocarditis, myocardial ruptures, acute and chronic heart aneurysm, syndrome Dressler, thromboembolic complications, postinfarction angina pectoris.

Treatment

Treatment is aimed at preventing complications, limiting the infarct zone, pain relief and correction of hypoxia.

Removal of a pain syndrome: begin with reception of nitrates. With severe hypotension, neuroleptanalgesia is performed - fentanyl 1-2 ml intravenously on glucose, droperidol 0,25% 2 ml per 40 ml 5% glucose solution. With an incomplete effect, morphine 1% 1,0 is re-introduced after an hour subcutaneously or intravenously by stream; omnopon 2% - 1,0 subcutaneously or intravenously; promedol 1% - 1,0 subcutaneously.

To enhance the analgesic effect, relieve anxiety, anxiety, arousal, apply: analgin 50% - 2,0 intramuscularly or intravenously; diphenhydramine 1% - 1,0 intramuscularly (sedative effect) + chlorpromazine 2,5% - 1,0 intramuscularly, intravenously (drug potentiation).

To limit the zone of necrosis, anticoagulants are used (heparin 5 thousand units - 1 ml bolus followed by intravenous administration of an infusion pump 1 thousand units per hour), thrombolytics (fibrinolysin 6 thousand units intravenously drip; streptase 250 thousand in saline intravenously drip) and antiplatelet agents (aspirin, cardiomagnyl, thrombo-ACS, Plavix).

Prevention and treatment of arrhythmias.

1. Polarizing mixture, which promotes the penetration of potassium into the cells.

2. Lidocaine is the drug of choice, more effective for ventricular arrhythmias 80-100 mg bolus.

3. Cordarone or amiodarone 450 mg intravenously in saline.

Given that the pumping function of the heart suffers, the appointment of b-blockers (egilok 12,5-25 mg) is indicated to enhance myocardial contractility. In the presence of edema in the lower extremities or moist rales in the lungs, diuretics are used (Lasix at a dose of 40-80 mg).

Great emphasis falls on blood pressure, which must either be increased with hypotension (dopamine) or reduced (isoket intravenous drip, antihypertensive drugs - enalapril). To eliminate hypoxia, oxygen therapy is carried out using humidified oxygen through a mask or nasal catheters.

2. Cardiogenic shock

Cardiogenic shock is a critical circulatory disorder with arterial hypotension and signs of acute deterioration of blood circulation in organs and tissues.

Clinic and diagnostics

The main diagnostic sign is a significant decrease in systolic blood pressure, which is below 90 mm Hg. Art. The difference between systolic and diastolic pressure (pulse pressure) is 20 mm Hg. Art. or getting even smaller. In addition, a clinic of a sharp deterioration in the perfusion of organs and tissues is developing:

1) impaired consciousness from mild lethargy to psychosis or coma, focal neurological symptoms may appear;

2) diuresis less than 20 ml/h.

Symptoms of deterioration of peripheral circulation: pale cyanotic, marbled, brick, moist skin; collapsed peripheral veins, a sharp decrease in the temperature of the skin of the hands and feet; decrease in blood flow.

The value of the CVP can be different. Normal indicators of CVP are 5-8 cm of water. Art.; indicator below 5 cm of water. Art. indicates hypovolemia and low blood pressure, and above 8 cm of water. Art. indicates right ventricular failure.

Diagnosis of cardiogenic shock is usually not difficult. It is more difficult to determine its type and leading pathophysiological mechanisms. First of all, it is necessary to distinguish true (contractile) cardiogenic shock from arrhythmic, reflex (painful), medical shock due to right ventricular failure or slowly ongoing myocardial rupture. When conducting intensive care for a patient with shock, it is important to exclude causes of low blood pressure, such as hypovolemia, cardiac tamponade, tension pneumothorax, thromboembolic complications, and not to miss internal bleeding, for example, with stress erosions or ulcers of the gastrointestinal tract.

Treatment

Oxygen therapy with humidified oxygen through a mask or nasal catheters is indicated. Anticoagulants are administered as a bolus at a dose of 10 IU, followed by intravenous administration of an infusion pump at 000 IU per hour. It is necessary to administer analgesics: morphine 1000% 1 ml subcutaneously or intravenously by bolus; analgin 1,0% 50 ml intramuscularly, intravenously.

Vascular tonics: Cordiamin 1-4 ml intravenously; mezaton 1% 1,0 g subcutaneously, intravenously, in saline; norepinephrine 0,2% 1,0 intravenously. True cardiogenic shock is treated as follows.

To increase the contractile activity of the myocardium, the following is used: strophanthin 0,05% 0,5-0,75 g intravenously slowly per 20,0 isotonic solution, korglukon 0,01 g intravenously, also in an isotonic solution or in a polarizing mixture, glucagon 2- 4 mg intravenously drip on a polarizing solution.

Normalization of blood pressure: norepinephrine 0,2% 2-4 ml per 1 liter of 5% glucose solution or isotonic solution. BP is maintained at 100 mm Hg. Art., mezaton 1% 1,0 g intravenously; cordiamine 2-4 ml, dopamine 200 mg in 400 ml of rheopolyglucin or 5% glucose. With an unstable effect from the above drugs, hydrocortisone 200 mg, prednisolone 90-120 mg are used.

Normalization of the rheological properties of blood (since microvascular thrombi are necessarily formed, microcirculation is disturbed). Elimination of hypovolemia, as there is sweating of the liquid part of the blood: reopoliglyukin, polyglukin - in a volume of up to 100 ml at a rate of 50,0 ml per minute.

Correction of acid-base balance (fight against acidosis): sodium bicarbonate 5% to 200,0 ml. Re-introduction of painkillers. Restoration of rhythm and conduction disturbances. But it is always necessary to control the CVP, which allows the resuscitator to determine the acceptable infusion therapy. Patients with cardiogenic shock should not be loaded with water. The higher the CVP, the less infusion therapy.

3. Hypertensive crisis

A hypertensive crisis is a sudden increase in blood pressure to a level that is usually not characteristic of this patient, leading to acute regional circulatory disorders and damage to target organs (heart, brain, kidneys, intestines). External factors provoking a crisis can be:

1) psycho-emotional stress;

2) meteorological influences;

3) excessive consumption of table salt.

In spring and autumn, crises occur more often than in winter and summer. Crises can also occur against the background of an exacerbation of a number of chronic diseases. MS Kushakovsky (1982) distinguishes the following variants of hypertensive crises: neurovegetative, water-salt, convulsive (encephalopathy).

Clinic

The clinical symptoms of the crisis are manifested by tinnitus, flashing flies before the eyes, bursting headache in the occipital region, aggravated by bending over, straining, coughing, nausea, vomiting, and heart rhythm disturbances. During a crisis, dangerous violations of the cerebral coronary, less often renal and abdominal circulation occur, which leads to stroke, myocardial infarction and other serious complications. ECG reveals left ventricular hypertrophy. Chest x-ray shows an enlarged heart, aortic deformity in the form of the number "3", usury of the ribs as a result of increased collateral blood flow through the intercostal arteries. Aortography confirms the diagnosis.

The neurovegetative form of the crisis is characterized by a sudden onset, excitation, hyperemia and moisture of the skin, tachycardia, frequent profuse urination, a predominant increase in systolic pressure with an increase in pulse amplitude. Such crises are otherwise called adrenal, or type I crises. Type I crises usually have a relatively benign course, although they can lead to paroxysmal arrhythmias or angina pectoris, and in severe cases, myocardial infarction.

With the water-salt form of the crisis, the condition worsens gradually, drowsiness, weakness, lethargy, disorientation, pallor and puffiness of the face, and swelling are noted. Systolic and diastolic pressure increase evenly or with a predominance of the latter and a decrease in pulse pressure. Such crises are called type II crises. Crises of type II, as a rule, are severe and can be complicated by myocardial infarction, stroke, acute left ventricular failure.

It is necessary to highlight hypertensive crises that develop as a result of an abrupt cessation of permanent antihypertensive therapy, in particular, taking b-blockers, nifedipine, sympatholytics, and especially clonidine.

Treatment

Treatment of a hypertensive crisis consists in an urgent decrease in blood pressure to a normal level, necessary to prevent or limit damage to target organs in hypertension, to prevent complications up to death in the most severe cases, or permanent disability in the development of stroke, myocardial infarction.

In the neurovegetative form of the crisis, intravenous jet, slow administration of 0,1 mg of clonidine or repeated intravenous infusions of 50 mg of labetalol are usually used. The hypotensive effect of clonidine can be enhanced by sublingual administration of 10 mg of nifedipine. In extremely severe cases, sodium nitroprusside is injected intravenously, and in its absence, intravenous drip or very slowly fractionally - up to 50 mg of pentamine.

The main dangers and complications of antihypertensive therapy:

1) arterial hypotension;

2) violation of cerebral circulation (hemorrhagic or ischemic stroke, encephalopathy);

3) pulmonary edema;

4) angina pectoris, myocardial infarction;

5) tachycardia.

Life-threatening hypertensive crises are grounds for immediate intensive care.

Types of hypertensive crises.

1. Convulsive form of hypertensive crisis (acute severe hypertensive encephalopathy).

2. Crisis with pheochromocytoma.

3. Acute arterial hypertension in life-threatening diseases and conditions (acute coronary syndrome, acute myocardial infarction, dissecting aortic aneurysm, internal bleeding).

4. Hypertensive crisis complicated by pulmonary edema or hemorrhagic stroke.

A convulsive form of a hypertensive crisis (acute severe hypertensive encephalopathy) develops in a malignant form of hypertension or secondary arterial hypertension, for example, in late toxicosis of pregnant women or acute glomerulonephritis. Crises begin with a severe throbbing, arching headache, psychomotor agitation, repeated vomiting that does not bring relief, visual disturbances; loss of consciousness quickly occurs and clonic-tonic convulsions appear. In patients with recent arterial hypertension (with acute glomerulonephritis, toxicosis of pregnant women), a convulsive hypertensive crisis may develop with a relatively small increase in blood pressure.

In the convulsive form of the crisis, emergency care is aimed at eliminating the convulsive syndrome and an emergency lowering of blood pressure. The convulsive syndrome is eliminated by intravenous administration of diazepam. Additionally, 10 ml of a 25% solution of magnesium sulfate can be administered intravenously by drip or slow stream, or intramuscularly. Sodium nitroprusside, labetalol, diazoxide are used to urgently lower blood pressure. To combat cerebral edema, intravenous jet administration of lasix is ​​indicated.

With eclampsia, especially with intravenous administration, magnesium sulfate is still widely used, which is administered at a dose of 4 g per 100 ml of a 5% glucose solution. Then, if necessary, a drip injection of the drug is carried out, or instead of the subsequent drip injection of magnesium sulfate, 20 ml of a 25% solution of magnesium sulfate can be injected deep intramuscularly. Intravenous magnesium sulfate should be avoided if the pregnant woman is being treated with calcium antagonists (a sharp drop in blood pressure is dangerous). Perhaps with eclampsia and intravenous administration of chlorpromazine (100-250 mg), diazoxide (300 mg). Seduxen (diazepam) is administered intravenously slowly (20-30 mg), and then drip (300 mg in 500 ml of 5% glucose solution).

A crisis in pheochromocytoma is manifested by a sudden, very rapid and sharp increase in blood pressure, mainly systolic, and an increase in pulse pressure, accompanied by pale skin, cold sweat, palpitations, pain in the heart and epigastric region, nausea, vomiting, throbbing headache, dizziness. During a crisis, an increase in body temperature, visual and hearing disorders are possible. Characterized by a decrease in blood pressure after the transition to a vertical position.

Emergency care in cases of crisis with pheochromocytoma begins with raising the head end of the bed to an angle of 45 °, which causes a decrease in blood pressure. For emergency antihypertensive therapy, the drug of choice is phentolamine, which is administered intravenously in a stream of 5 ml every 5 minutes. For the same purpose, intravenous injection of labetalol 50 ml every 5 minutes or drip infusion of 30 ml of sodium nitroprusside in 300 ml of 5% glucose solution is used. As an additional drug, droperidol (5-10 ml IV) may be useful. To suppress tachycardia, propranolol is prescribed at a dose of 20-40 mg.

In acute myocardial infarction (especially often noted in its anterior localization), when during a crisis the load on the myocardium increases, myocardial oxygen demand increases, it is first necessary to stop a severe pain attack with the help of modern painkillers (including narcotic analgesics) and administer sedatives which can significantly lower blood pressure. If significant hypertension persists and at the same time the tone of the sympathetic nervous system is increased, then b-blockers (propranolol, metoprolol, esmolol) are administered intravenously, which, along with the hypotensive effect, can limit the area of ​​peri-infarction myocardial ischemia. Often resort to intravenous administration of nitroglycerin to cause a decrease in pre- and afterload. This allows you to control the level of blood pressure. However, the appointment of sodium nitroprusside should be avoided, which in these cases can increase myocardial ischemia, apparently due to the phenomenon of "coronary steal" (reduction of coronary collateral blood flow to the ischemic zone). If hypertension persists after the acute stage of myocardial infarction, treatment with the main antihypertensive agents is started, taking into account indications and contraindications. However, in recent years, in connection with data on secondary prevention, b-blockers and ACE inhibitors are most often preferred, which, in the absence of contraindications, are tried to be prescribed from an early period.

With the development of acute heart failure, the hypertensive crisis is stopped by intravenous administration of nitroglycerin (contraindicated in severe mitral stenosis); prescribe vasodilators (although tolerance often develops to them), IFKA.

With persistent hypertension in cases of severe heart failure, a combination with diuretics is resorted to, and even small doses of a thiazide diuretic together with a potassium-sparing diuretic (triamterene or amiloride) can not only normalize blood pressure, but also prevent the occurrence of arrhythmias caused by potassium and magnesium deficiency in such patients. (Metelitsa V.I., 1996).

In hemorrhagic stroke or subarachnoid hemorrhage, blood pressure should be reduced especially carefully, with the help of drugs, the hypotensive effect of which can be easily controlled (sodium nitroprusside), and to a level higher than usual (working). Any decrease in blood pressure, accompanied by a deterioration in neurological status, should be considered excessive.

In case of pulmonary edema, nitroglycerin or sodium nitroprusside or pentamine, as well as lasix, are prescribed intravenously to urgently lower blood pressure.

With a dissecting aortic aneurysm or rupture, the following drugs are used intravenously to regulate blood pressure and prepare for surgical treatment: sodium nitroprusside, loop diuretics (furosemide), nifedipine, propranolol (along with sodium nitroprusside), methyldopa, reserpine (as an additional agent).

In crises caused by an increase in cardiac output, tachycardia and a predominant increase in systolic and pulse pressure are often observed, a good effect in these cases is the intravenous administration of anaprilin, and then, if necessary, furosemide.

4. Life-threatening arrhythmias

Arrhythmia

An arrhythmia is a heart rhythm other than sinus.

A normal heart rhythm has the following characteristics:

1) heart rate from 60 to 120 per minute;

2) the pacemaker is the sinus node, evidence of which is a positive P wave preceding the QRS complex in standard lead II and negative in AVR;

3) RR intervals differ by no more than 0,01 s;

4) the actual indicators, reflecting the size of the intervals and teeth in the norm.

All changes on the ECG are carried out in the II standard lead.

Arrhythmia classification

1. Violation of the formation of impulses:

1) in the sinus node:

a) sinus tachycardia;

b) sinus bradycardia;

c) sinus arrhythmia;

d) sick sinus syndrome (SSS);

2) ectopic arrhythmias:

a) extrasystole;

b) paroxysmal tachycardia;

c) atrial fibrillation and flutter;

d) flicker and flutter of the ventricles.

2. Violation of impulse conduction:

1) additional pathways (Kent bundles);

2) heart block:

a) atrial (intra-atrial);

b) atrioventricular;

c) intraventricular.

Mechanisms of arrhythmias

A decrease in the resting potential, the excitability threshold occurs only on the basis of a deficiency of cellular potassium, the ratio "plasma - cell" (normally 80 meq of potassium is in the cell and 5 meq in plasma).

Asymmetry of the electrophysiological-metabolic focus of the myocardium due to ischemia, inflammation, reperfusion during thrombolysis. Electrophysiological weakness of the superior pacemaker. Congenital accessory conduction pathways.

Paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia is a sudden attack of heartbeat with a frequency of 150-250 beats per minute. There are 3 forms:

1) atrial;

2) nodal;

3) ventricular.

The etiology of supraventricular paroxysmal tachycardia is more often associated with an increase in the activity of the sympathetic nervous system. It is clinically manifested by a sudden attack of the heartbeat, the vessels of the neck pulsate, cardiac activity switches to a different rhythm. The duration of the attack is from several minutes to several days. The number of heartbeats in the ventricular form is usually in the range of 150-180 beats per minute, with supraventricular forms - 180-240 beats per minute.

During an attack, a pendulum-like rhythm is characteristic auscultatory, there is no difference between I and II tone. It increases myocardial oxygen demand and can provoke an attack of acute coronary insufficiency.

ECG signs

1. QRS complexes are not changed.

2. In the supraventricular form, the P wave merges with T.

Treatment begins with intravenous administration of cordarone at a dose of 300 mg or novocainamide up to 1 g, and then adenosine 1 ml - 1% (10 mg) bolus. Calcium antagonists verapamil (Isoptin) are used intravenously as a bolus at a dose of 2,5-5 mg over 2-4 minutes. But it is used for narrow QRS complexes, and for wide ones it can fibrillate. It is possible to take b-blockers (propranolol 20-40 mg sublingually).

Paroxysm of atrial fibrillation

Paroxysm of atrial fibrillation is characterized by the absence of atrial complexes, and instead of an isoline, sawtooth waves of atrial flutter are detected, which are most distinct in leads II, III, and VF with a frequency of 250-400 beats per minute. Or there are no atrial complexes, flicker waves, large- or small-wave oscillations of the isoline are detected, the frequency of atrial waves is 350-600 beats per minute.

Clinic. The pulse is arrhythmic with waves of different filling, the presence of a pulse deficit (the difference between heart rate and pulse); different intervals and different volume of heart sounds during auscultation.

Treatment. In case of paroxysm, it begins with the introduction of digoxin 0,25 mg (1 ml of 0,025%) per 20 ml of physiological saline as an intravenous bolus. To achieve the desired effect of saturation with glycosides, a dose of 1,5 mg of digoxin per day or 3 days is recommended.

With uncomplicated paroxysm, the drug of choice is novocainamide, administered intravenously slowly at a dose of up to 2000 ml over 30 minutes (10 ml of a 10% solution) with constant monitoring of blood pressure, heart rate, ECG. Atrial flutter is treated with electrical impulse therapy.

Paroxysmal ventricular tachycardia

Paroxysmal ventricular tachycardia is characterized by the detection of 3 or more consecutive wide (more than 0,12 s) QRS complexes with a frequency of 100-250 beats per minute with a discordant shift of the ST segment and the T wave in the direction opposite to the main wave of the QRS complex.

Pirouette, or bidirectional, fusiform ventricular tachycardia occurs when the QT interval is lengthened. In this case, an irregular rhythm is recorded with a heart rate of 150-250 beats per 1 min with wide polymorphic deformed QRS complexes.

Treatment. In conditions of hypodynamia of blood circulation, electrical impulse therapy is required, after which maintenance therapy is carried out with lidocaine drip. In conditions of stable hemodynamics, the drug of choice is lidocaine, intravenous bolus 1-2 mg/kg (80-100 mg) for 3-5 minutes, followed by drip infusion during the day at 4 mg/min.

Ventricular extrasystole

Ventricular extrasystole is the occurrence of an extraordinary wide deformed QRS complex, discordant ST and T shift, a complete compensatory pause (the interval between the pre- and post-extrasystolic P wave is equal to twice the normal RR interval). The drug of choice is lidocaine, which is administered according to the above scheme. Perhaps the use of cordarone at a dose of 300-450 mg intravenously drip.

Violation of AV conduction with the development of syncope (Morgagni-Adams-Stokes syndrome)

When conduction is disturbed, various types of heart blocks occur, there is a slowdown or complete cessation of the conduction of the impulse through the conduction system of the heart. Sinoauricular blockade is characterized by dysfunction of T cells and impaired conduction of impulses from the sinus node to the atria.

There are 3 degrees.

I degree - slowing down the impulse. On the ECG - prolongation of the PQ interval for more than 0,20 s. Prolapse of the QRS complex. The RR interval is stable.

II degree - loss of part of the impulses, incomplete conduction. Mobitz type I - as the impulses are carried out, the PQ interval gradually lengthens until the complete loss of the pulse wave. QRS is not changed. At the site of the QRS prolapse, the greatest distance is RR. Prognostically, this type is relatively favorable.

Mobitz type II with a constant PQ interval and an unchanged QRS complex. At the same time, not all impulses reach the ventricles - in some cases, every second impulse is carried out, in others - every third, etc., i.e., there is a periodic prolapse of the QRS complex 3: 2, 4: 3, 5: 6, etc. d.

III degree - complete blockade of conduction. At the same time, the conduction of impulses to the ventricles is completely stopped, and a heterotopic focus of idioventricular rhythm is born in the ventricles, and the lower the automatism, the more difficult the clinic. Complete dissociation is observed: the atrial rhythm is close to normal, and the ventricles have their own frequency - 40 beats per minute or less. The latter depends on the level of damage: if the AV node suffers, 40-50 beats per 1 minute, if the leg of the bundle of His - 20 beats per 1 minute or less.

The level of damage is also indicated by the degree of deformation of the QRS complex. The heart sounds are weakened, periodically there is a "cannon" I tone, when the systole of the atria and ventricles almost coincide in time. May be III additional tone. Systolic ejection murmurs may appear at the base of the heart. Often a pulsation of the veins associated with atrial contraction is found, especially distinct with Strazhesko's cannon tone.

Clinic. Failing of the heart, if one impulse falls out. Vertigo if several impulses fall out. Morgagni-Adams-Stokes syndrome (loss of consciousness), if 6-8 complexes fall out.

Treatment. To restore an adequate rhythm, atropine is administered at a dose of 0,5-1 mg to 3 mg. Every 3 minutes, 1 mg to a total dose of 0,4 mg/kg. Calcium antagonists - isoptin 0,04 mg/kg. With frequent loss of consciousness, the patient is transferred to permanent electropulse therapy. But more often pacing has to be done "on demand".

Author: Kolesnikova M.A.

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Random news from the Archive The brain predicts the future 12.12.2018 We constantly predict the future, and there is no mysticism here. For example, a driver, seeing how a red traffic light has changed from yellow, to get ready to take off - he knows that there will be a green signal soon. Or when we just tap out the rhythm to the sound of music - our finger begins to move in advance to get into the rhythm beat. In this sense, predicting the future is indeed commonplace; moreover, without such a skill, our life would be much more difficult. But it's easy to see that the example of the driver is not like the example of tapping the rhythm. In the first case, the brain guesses the future based on past experience: we know that after a yellow signal, green always lights up. In the second case, the brain feels the rhythm, and even if we have not heard this music before, we can still follow the rhythmic pattern. Researchers from the University of California at Berkeley found that different areas of the brain are responsible for both types of predictions. Patients with Parkinson's syndrome and cerebellar degeneration participated in the experiments: they were shown multi-colored squares replacing each other on the screen - red, white and green, with white after red and green after white. It was necessary to predict the appearance of green by pressing a special button. But in one case, the squares appeared with a constant rhythm, and in the other case, the time between red and green was constantly changing. That is, the appearance of green could be predicted either by rhythm or by focusing on the white square. Squares with a constant rhythm felt worse in patients with Parkinson's syndrome, and where there was no clear rhythm and it was necessary to focus on the previous white, big problems arose in patients with cerebellar degeneration. Parkinson's disease affects the so-called basal ganglia, which have quite a few different functions. Obviously, among other things, they control "rhythmic predictions". The cerebellum, apparently, controls the ability to guess events by their sequence, when we know that one must necessarily be followed by something else. It used to be believed that both types of "guessing the future" are regulated by the same system of nerve centers. Perhaps now that we know that there are actually two of these systems, we can better understand the nature of some neuropsychiatric disorders accompanied by impairments to speech, attention, and other higher cognitive functions.

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