- Poster presentation
- Open Access
Influence of ventilatory settings on the value of static hemodynamic variables and pulse pressure variation
© BioMed Central Ltd 2006
- Published: 21 March 2006
- Ventilatory Setting
- Pulse Pressure Variation
- Hemodynamic Variable
- Pulmonary Artery Occlude Pressure
- Systolic Volume
Volume expansion is the first-line therapy proposed to improve hemodynamics. However, volemic evaluation remains a clinical problem mainly in mechanically ventilated patients. The cyclic change in the arterial pressure waveform during positive pressure mechanical ventilation as pulse pressure variation (dPP) has been proposed to identify responders to fluid administration. Despite this, there are no data about the performance of dynamic parameters during the use of different ventilatory settings in normovolemia and hypovolemia.
To evaluate the influence of positive end expiratory pressure (PEEP), tidal volume (VT) and inspiratory to expiratory ratio (I:E) on the value of hemodynamic variables, including dPP, during normovolemia and hypovolemia in pigs. To compare the ability of hemodynamic variables (right atrial pressure [RAP], pulmonary artery occluded pressure [PAOP], right ventricular end diastolic volume [RVEDV], mixed venous oxygen saturation [SVO2] and dPP) to identify hypovolemia during different ventilatory settings.
Ten anaesthetized pigs (67 ± 3.5 kg) were mechanically ventilated with VT 8 ml/kg, PEEP 5 cmH2O, I:E ratio 1:2 and monitored with a pulmonary artery catheter for continuous cardiac output, RVEDV and SVO2 measurement and a femoral artery catheter for systemic blood pressure and dPP recording. Animals were also ventilated in random order with VT 16 ml/kg, PEEP 15 cmH2O or I:E = 2:1 in normovolemia (PAOP 12–15 cmH2O), after withdraw of 20% of animal estimated volemia (hypovolemia) and after infusion of withdrawn blood (transfusion).
During normovolemia, use of PEEP 15 cmH2O decreased the systolic volume (SV) (77.6 ± 23.5 vs 64.5 ± 16.4 ml, P < 0.05) and SVO2 (78.8 ± 7.7 vs 67.4 ± 12.9%, P < 0.01), and increased the RAP (10.5 ± 2.1 vs 13.4 ± 2.1 mmHg), PAOP (14.6 ± 1.6 vs 17.4 ± 1.7 mmHg, P < 0.001) and dPP (15.8 ± 8.5 vs 25.3 ± 9.5%, P < 0.001). VT 16 ml/kg caused an increase in dPP (15.8 ± 8.5 vs 31.6 ± 10.4%, P < 0.001) and I:E = 2:1 did not affect hemodynamics. During hypovolemia, the high PEEP level affected significantly all studied variables except RVEDV but dPP was strongly influenced by high VT (40.5 ± 12.4% vs 84.2 ± 19.1%, P < 0.001). During the transfusion phase, SV and SVO2 (P <0.001) decreased with PEEP 15 cmH2O while RAP (P < 0,001), PAOP (P < 0.05) and dPP (P < 0.001) increased their values; VT 16 ml/kg caused further increase of dPP from 10.6 ± 5.6 to 32.4 ± 8.6% (P < 0.001). ROC curves analysis showed that dPP, SVO2 and RVEDV were better indicators of hypovolemia in all ventilatory settings with areas under the curve of 0.93, 0.91 and 0.87, respectively.
For the same volemic state, the results lead us to conclude that: use of a high PEEP level causes increase of filling pressures (RAP and PAOP), reduction of SVO2 and increase of dPP; VT causes a great influence on the dPP value; and RVEDV is the hemodynamic variable that is less influenced by ventilatory settings. The dPP, SVO2 and RVEDV are better indicators of hypovolemia than RAP and PAOP independently of the ventilatory settings.