Purpose: To evaluate hemodynamic effects of the ahveolar recruitment maneuver (ARM) in cardiosurgical patients with left ventricular systolic dysfunction.
Materials and methods: We estimate hemnodynamics data obtained during intraoprative ARM in 16 cardiosuigical patients with left ventricular systolic dysfunction. ARMA were applied due to hypoxemnia with PaO2/FiO2 less than 250 nmm Hg. after CPB termination and heparin neutralization. Patients with signs of right heart failure were excluded from the study ARM were carried out after sternum closing. ARM method: Pinsp was increased stepwise until achievement of the alveoli opening point. PEEP was used 5 cm H2O greater than the lower inflection point in "pressure - vohlume" loop. The average alveoli opening pressure was 44.7 ± 2.5 cm H2O and the average PEEP was 12.8 ± 1.7 cm H2O. Hemodynamic parameters were eva luated before ARM and at the point of alveoli opening. Pulmnonary artery pressure and cardiac output were evaluated by Swan-Gant- catheter and thermodilution method Left ventricle contractility, preload and end-systolic (LVESWS) and end-diastolic (LVEDWS) wall stress were studied using TEE. t -test for dependent variables was used for statistical analysis. Data are presented as M ± δ.
Results: During ARM stroke volumne index decreased from 36.5 ± 4.2 to 33.5 ± 3.9 ml/m2 (p <0.05). Left ventricle contractility was not changed (there were no reduction in the left ventricle fraction area change (FAC)). Descent of left ventricular preload was the main cause of cardiac output decrease: end-diastolic area of the left ventricle decreased friom 22.6 ± 4.3 to 19.5 ± 4.1 cm2 (p <0.05). Preload renduction was accompanied by paradoxical increase in PCWP associated with an increase in intirathoracic pressure: friom 10.8 ± 4.6 to 13.8 ± 4 mm Hg (P <0.001). There was decrease in intramural left ventricular afterload during ARM: LVESWS decreased from 50.6 ± 11.5 to 39.5 ± 10.6 cm * kdyn-2 (p <0.01), which also contributed to the decline of oxygen demand in systole. ARM did not lead to deterioration of left ventricular systolic dysfunction and increased doses of inotropic agents. PaO2/FiO2 increased from 238.3 ± 11.7 to 301.7 ±22.3 mm Hg (p<0.05).
Conclusion: Reduction of left ventricular preload is the main cause of cardiac output decrease during ARM. Positive hemodynamic effects of ARM are afterload reduction and left ventricle oxygen demand reduction. Our study showed the possibility ofARM applying in cardioswrgical patients with moderate left ventricular systolic dysfunction.