Influence of tidal volume on pulse pressure variation and stroke volume variation during experimental intra-abdominal hypertension.

BACKGROUND: Pulse pressure variation (PPV) and stroke volume variation (SVV) are frequently used to assess fluid responsiveness in critically ill patients on mechanical ventilation (MV). There are many factors, in addition to preload that influence the magnitude of these cyclic variations. We sought to investigate the effect of tidal volume (V(T)) on PPV and SVV, and prediction of fluid responsiveness in a model of intra-abdominal hypertension (IAH).

METHODS: Twelve anesthetized and mechanically ventilated piglets on continuous pulse contour cardiac output monitoring. Hypovolemia was ruled out with 2 consecutive fluid boluses after instrumentation. IAH was induced by intraperitoneal instillation of colloid solution with a goal of reducing respiratory system compliance by 50 %. Subjects were classified as fluid responders if stroke volume increased >15 % after each fluid challenge. SVV and PPV were recorded with tidal volumes (VT) of 6, 12 and 18 ml/kg before IAH after IAH induction and after a fluid challenge during IAH.

RESULTS: V(T) influenced PPV and SVV at baseline and during IAH, being significantly larger with higher V(T). These differences were attenuated after fluid administration in both conditions. After IAH induction, there was a significant increase in SVV with the three-tested V(T), but the magnitude of that change was larger with high V(T): with 6 ml/kg from 3 % (3, 4) to 5 % (4, 6.25) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 11 % (8.75, 17) (p = 0.02) and 18 ml/kg from 5 % (4,7.5) to 15 % (8.75, 19.5) (p = 0.02). Similarly, PPV increased with all the tested VT after IAH induction, being this increase larger with high VT: with 6 ml/kg from 3 % (2, 4.25) to 6 % (4.75, 7) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 13.5 % (10.25, 15.5) (p = 0.02) and 18 ml/kg from 7 % (5.5, 8.5) to 24 % (13.5, 30.25) (p = 0.02). One third of subjects responded to fluid administration after IAH, but neither SVV nor PPV were able to identify the fluid responders with the tested V(T).

CONCLUSION: IAH induction in non-hypovolemic subjects significantly increased SVV and PPV with the three tested V(T), but the magnitude of that change was higher with larger V(T). This observation reveals the dependence of functional hemodynamic markers on intrathoracic as well intra-abdominal pressures, in addition to volemic status. Also, PPV and SVV were unable to predict fluid responsiveness after IAH induction. Future studies should take into consideration these findings when exploring relationships between dynamic preload indicators and fluid responsiveness during IAH.