[Influence of the pericardium in the pathophysiology of ventricular dysfunction in acute infarct of the right ventricle. Experimental study]

To obtain more information about the role of the pericardium in the setting of acute right ventricular infarction (ARVI) we studied the behaviour of the ventricular function curves (VFC) and the relationship of the ventricular end-diastolic pressures (R-VEDP-RV:LV) in two groups of dogs. Group A. (n = 12) Control (C), ARVI, Pericardiectomy (P). A parabolic behaviour of the C VFC was noted (r2 = 071) and it's flexion point (FP) was found in 13. +/- 2 mmHg. After the ARVI the right (R) VFC was shifted downwards and to the right and the FP was documented in 18 +/- 2 mmHg (p < 0.05) in relation to C VFC. After P the RVFC was displaced upwards and to the left in relation to ARVIC RVFC (p < 0.05). The C R-VEDP-RV:LV = 0.75 and only a trend to equalization after the ARVI and after P were noted (0.91, 0.84, respectively) (p = ns). Group B (n = 12). Control (C), P, ARVI. The RVFC after P was shifted up and to the left in relation to the C RVFC (p < 0.05) and the FP = 10 +/- 2 mmHg. After P in the setting of ARVI the RVFC was shifted downward and to the right in relation to P RVFC (p < 0.05). After P the R-VEDP-RV:LV = 0.45 and statistical significant equalized in the condition of ARVI without pericardium (0.95, p < 0.05).

Ours results support a partial restrictive role of the pericardium in the origin of the low cardiac output (LCO) in ARVI. Because, equalization of the R-VEDP-RV:LV is not only due to the restraining pericardial effect but is also due to right ventricular myocardial ischemia. The FP (18. +/- 2 mmHg) found seems to be the top value of RVEDP for volume infusion in experimental ARVI. Hemodynamic finding that could be useful in the preload volume management for humans with ARVI and LCO or systemic hypotension.