shock cardiogenic

Cardiogenic shock develops with a lack of myocardial contractility.

Cause of the shock

    • Large focal MI
    • right ventricular MI
    • Acute myocarditis
    • Severe, acute aortic or mitral stenosis
    • Severe, acute aortic or mitral insufficiency
    • Rupture of the interventricular septum
    • Arrhythmias.


Compensatory mechanisms

    • Secretion of ADH
    • Release of aldosterone and renin
    • Secretion of catecholamines


Physiological reactions

    • Decreased urine output leading to hypervolemia
    • Vasoconstriction causing increased afterload
    • Tachycardia
    • Further inhibition of contractility and cardiac output (due to increased demands caused by the previous three changes).

Pathogenesis. In addition to the violation of the contractile function of the myocardium, the pain factor plays a role in the development of cardiogenic shock (with myocardial infarction and pulmonary embolism). Depending on the pathogenetic and clinical features, the following forms of cardiogenic shock are distinguished:

    • reflex shock. Violations of vascular tone caused by reflex reactions play a decisive role.
    • True cardiogenic shock is mainly due to impaired contractile function of the myocardium.
    • Arrhythmic shock is associated with the occurrence of cardiac arrhythmias
    • Areactive shock. The term is used in relation to cardiogenic shock, not amenable to drug therapy.

clinical picture. A sharp decrease in blood pressure against the background of symptoms characteristic of MI, acute myocarditis, ELA, etc. Patients are adynamic, complain of severe weakness. Their appearance: pointed features, pale cyanotic skin, sticky cold sweat. Breathing is rapid, shallow. The pulse is frequent, sometimes arrhythmic, weak filling. An important symptom is oliguria or anuria. In severe shock, loss of consciousness. Accession of pulmonary edema is possible. Treatment. Carry out therapy for the underlying disease that caused shock, incl. and surgical operations (drainage for pericardial tamponade, pulmonary embolectomy, coronary artery bypass grafting, etc.).

    • With reflex shock
    • Painkillers: promedol (1 ml 2% solution s / c or IV), analgin – (2 ml 50% solution IV) in combination with antihistamine products (diphenhydramine 1 ml 1% solution RA or diprazine 1 ml 2.5% solution IM or IV), anesthesia with nitrous oxide with oxygen, neuroleptanalgesia (thalamonal 2-4 ml IV).
    • Vasoconstrictors: mezaton (1 ml of 1% solution i / c or

i / m), noradrenaline (1-2 ml of 0.2% solution in 200 ml of 0.9% NaCl solution i.v. drip).

  • Fibrinolysin nbsp; – 60000 IU with 15000 IU of heparin IV drip,
  • Heparin nbsp; – 10,000 IU s / c or / in every 6 hours.
  • With true cardiogenic shock (except for the above drugs).
  • Strofantin 0.5-1 ml 0.05% solution in 20 ml 0.9% NaCl solution IV.
  • Potassium chloride (100 ml of 1% solution) or panangin (10-20 ml) in 100-150 ml of 5% glucose solution with 8-10 units of insulin intravenously.
  • Reopoliglyukin 400 ml IV drip.
  • Glucocorticoids: prednisolone up to 300 mg or hydrocortisone up to 500 mg IV.
  • To eliminate metabolic acidosis – infusion of 200 ml of 5% solution of sodium bicarbonate.
  • With arrhythmic shock
  • Lidocaine (0.1-0.2 g) or novocainamide (5-10 ml of 10% solution) IV.
  • Preparations containing potassium.
  • Electropulse therapy.
  • Electrical stimulation of the heart.
  • For areactive shock, see treatment of true cardiogenic shock and also counterpulsation. Counterpulsation is performed using a special balloon catheter inserted into the aorta. The catheter inflates rapidly during diastole and collapses during systole. The principle of the method is to remove a certain volume of blood from the arterial bed in systole and return it to diastole. Counterpulsation improves coronary blood flow and increases the ejection fraction of the left ventricle.

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