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Treatment of cardiogenic shock

1) Make sure of the absence of hypovolemia (absolute or relative). In order to do this, administer intravenously quickly 250-500 ml of liquid under CVP and AP control.

If CVP index increases and AP remains low, it is necessary to start infusion of vasopressors:

a) AP_syst lower than 70 mm Hg — norepinefrine intravenously drop-by-drop 0.5-30 jug/kg per min.;

b) AP_syst from 70 to 100 mm Hg — change over to dopamin infusion at the rate of 2.5-20/<g/kg per min. In absence of dopamin effect one should add a dobutamin introduction. If it needs to administer dopamin at the rate of more than 20/zg/kg/min to maintain AP, norepinefrine should be added.

It is necessary to try to retain AP at the level of 100-110 mm Hg.

2) In CS certain measures are carried out on correction of myocardial
contractility disorders:

— correction of VCB and heart rate;

— elimination of hypoxia, hypoglycemia;

— decrease of pre- and postload (arterial vasodilatators, diuretics et al.);

— thrombolytic therapy, but more advantageous in case of CS are invasive methods of revascularization (angioplasty, aortocoronary shunting).

In CS as a result of the right heart infarction with a decrease of AP, CVP in absence of congestion in the lungs, a preparation of choice is dobutamin. Vasodilators must be excluded, apply infusions of physiologic solution strictly to the dosage. Eliminate paroxysms of ciliary arrhythmia, and in case of complete A-V block perform a cardiostimulation.

Glucocorticoids are of little effect in CS.

3) Myocardial rupture. If it did not lead to an immediate death, the only measure to save the patient's life is an urgent operative intervention.

4) Arrhythmias. Ventricular extrasystoles and short paroxysms of ventricular tachycardia do not require a special treatment. Long paroxysms are eliminated with lidocaine (a preparation of choice) 120-150 mg as a stream, and then 2-4 mg drop-by-drop in the same dosage (up to 2 g/hour). In arrhythmias it is important to determine electrolytes in plasma and to carry on K⁺ correction, since not a single of the antiarrhythmic agents is effective in hypokalemia. Acidosis also needs to be corrected.

In paroxysms of ciliary arrhythmia (its tachysystolic form) digoxin, isoptin, novocainamidum are indicated.

Defibrillation is carried out only by life indications.

In bradycardia atropine and blockers (alupent, ephedrine) are applied.

In complete A-V block (Morgagni-Adams-Stokes syndrome) — cardiostimulation, if it is of no effect atropine is introduced. In so doing one must avoid placing endocardial electrode through subclavian vein (prescription of TLT, heparin).

Regimen. It is recommended to keep to bed regmen in uncomplicated AMI for 12-24 hours. A prolongation of bed regimen in the patients with stable hemodynamics for more than 24 hours is not recommended. Diet must be poor

in cellulose, daily enemas allow to avoid making supreme efforts during the act of defecation.

THROMBOEMBOLISM OF PULMONARY ARTERY (TEPA)

It is a grave complication of a number of diseases both surgical and therapeutic profile. A probability of TEPA development is particularly great in certain groups of patients: postoperative, with prolonged immoblization, in old age, with circulatory failure, thrombosis of deep veins of the lower extremities, obesity, pregnancy, with infarction or insult in anamnesis. The most often (in 75% of cases) the emboli are brought in from the veins of pelvis and extremities.

Clinical forms of TEPA:

Circulatory form (cardiogenic syndrome) — pulmonary heart and decompensation of blood circulation by the right ventricular type acutely develop. Clinical picture: a pain behind the breast bone, sense of discomfort, swelling of cervical veins, cyanosis, increased cardiac beat, second sound accent on a. pulmonalis, murmurs in the heart. In this form of TEPA a circulatory decompensation acutely develops with high lethality.

Respiratory form is distinguished by a slower development. Here, dyspnea with pains in the chest and bloody expectoration are observed.

Diagnosis of TEPA:

— dyspnea is a constant sign as a result of MVC and ventilation-perfusion ratios in the lungs;

— pains in the chest are often, but not constantly; more often in the lower sections of the chest, but they may be behind the breast bone, sometimes in the abdomen (edema of the liver);

— cough in 60% of patients;

— bloody expectoration — in 1/3 of patients;

— tachycardia > 100 per min;

— cyanosis;

— hypoxic encephalopathy associated with hypoxia;

— increased sweating in half of the patients;

— hyperthermia in 40-50% of patients;

— on X-ray film of the chest — there are dilatation of the heart in transverse dimension, more at the expense of the right heart, dilatation, deformation and induration of roots of the lungs on the affected side. Pulmonary infarction is determined in 2-5 days in the form of clinoid shadows, elevation of diaphragm is also typical. Multifocal shadows are observed in thromboembolism of small branches of pulmonary artery.

ECG is nonspecific for TEPA. Namely, S wave depression and ST drop are determined in leads I—II, T is negative in leads III and V,-V₃. S wave is deep in thoracic leads.

Scanning of the lungs — if a normal pulmonary perfusion is determined here, then TEPA is not present. And, on the contrary, disturbance of pulmonary perfusion and their normal X-ray pattern is the evidence of TEPA.

Angiopneumography — filling defects of vessels.

AP elevates in pulmonary arteries.

On autopsy TEPA is found only in 3.5-14% of all the patients with this diagnosis.

Virchov's triad is typical for TEPA:

— a slowing down of blood flow;

— increase of coagulative properties of blood;

— a local lesion of vascular wall.

Heparin and fibrinolysin are produced in pulmonary artery and pulmonary tissue that contributes to lysis of thrombi. Lysis starts in 3 hours. A thrombus comes off in the elevation of blood flow velocity and CVP that is observed in physical exercise.

Most often emboli are located in the lower lobes of the lungs, particularly on the right.

Embolisms are divided into 3 groups:

1) massive (truncal);

2) submassive (lobar and segmental vessels);

3) lobar, segmental and smaller vessels causing a lesion in the volume of whole lung.

In TEPA the following effects are distinguished:

1) Mechanical effect is manifested when the vessel is occluded by 30% and blood flow along a pulmonary artery decreases. A right ventricular failure advances at the expense of difficulty with blood outflow from the heart and the left ventricular one — at the expense of blood inflow to the heart. Myocardial hypoxia develops;

2) Reflex-humoral effect — spasm of pulmonary vessels may produce 3 groups of reflexes:

— Pulmo-pulmonary reflexes (vaso-vasal). Stimulation leads to a gene­ralized spasm of all branches of pulmonary artery that causes an elevation of pressure in the pulmonary artery leading to the overextension of the right ventricle and fibrillation;

— Pulmocoronary reactions with immediate circulatory arrest;

— Pulmobronchial reflex that causes a reflex spasm of bronchi
(bronchiolospasm);

3) Humoral effect as a result of histamine release from the cells, as well as
serotonin and other BAS intensifying spasm.

The following forms of TEPA are distinguished:

— instant — a death comes at once;

— acute — in 30% of cases TEPA develops in the course of 10 minutes;

— subacute — in 35-45% of cases TEPA develops for a few hours or days;

— recurrent — (15-20% of cases) — TEPA is more often diagnosed as chronic pneumonia.

In thromboembolism of the main trunk and large branches of a. pulmonalis the death advances fast — from a few minutes to several hours. Precursors of thromboembolism are:

— pain syndrome (in the chest, epigastrium);

— loss of consciousness;

— attack of asphyxia;

— cyanosis, more often of the upper part of the trunk as a result of diffuse bronchiolospasm;

— collapse;

— swelling of external jugular veins and enlargement of the liver (at:he expense of disturbance of blood outflow from periphery to the heart), a clockwise heart rotation (its electrical axis is turned to the right).

Thromboembolism of small branches is not diagnosed in 60-90%. Clinical picture: pains in the chest, elevation of the body temperatur e. moist rales, bloody expectoration. The pain is of pleurogenic genesis.

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