THE ROLE OF HYPOVOLEMIA AND HEMOREOLOGICAL CHANGES IN THE PATHOGENESIS OF SYSTEMIC CIRCULATION DISEASES IN THE POSTRESUSCITATION PERIOD OF ACUTE MYOCARDIAL INFARCTION

Aim. To determine the role of volume imbalance and alterations in the rheological properties of blood in the pathogenesis of postresuscitation hemocirculatory disorders in dogs after clinical death due to acute myocardial infarction.

Methods. Changes in systemic hemodynamics, volume and dynamic viscosity of circulating blood within a 5-minute period after clinical death due to myocardial infarction were evaluated in a dog model. 152 dogs received pentobarbital anesthesia.

Results. In the early postresuscitation period after myocardial infarction dogs developed phase changes in systemic hemodynamics, volume and dynamic viscosity of circulating blood with an increase in the target indicators, followed by their decrease and final normalization as compared to the baseline. The development of postresuscitation systemic hyperperperfusion (1–3 min) was associated with significantly increased blood volume and its components. The subsequently decreased perfusion volume (5–30 min) was caused by depressed contractile function of the heart. The further progression (1–9 hours) of the hypoperfusion syndrome was mainly attributed to hypovolemia, increased dynamic viscosity of the blood and the viscoelastic properties of the red blood cells. The contribution of heart rhythm disturbances (polytopic ventricular extrasystoles) to the development of circulatory failure 4–5 hours after the successful resuscitation was determined. The subsequent hemodynamic improvements were associated with the normalization of the circulating plasma volume and hemorheological properties of the blood.

Conclusion. Staged disorders of the systemic circulation formed in the recovery period after clinical death following acute myocardial infarction. They were accompanied by the alterations in the volume and dynamic viscosity of the circulating blood. Immediately after the revival, elevated values of the hemodynamic parameters were attributed to the increased blood flow as well as to the increased in plasma and globular components. The initial (5–30 min) decrease in the cardiac output was caused by impaired myocardial contractility. After a recovery period of 1–9 hours, a progressive decrease in the perfusion volume demonstrated a direct linear relationship with a deficit of blood flow and its plasma component. Heart rhythm disturbances contributed to the development of insufficient blood circulation in the 4–5-hour recovery period. Thus, hypovolemia and the hyperviscous syndrome associated with it significantly contributed to the development of insufficient systemic circulation within the 1–9-hour recovery period after clinical death provoked by myocardial infarction.

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