[Effects of PEEP on intrathoracic and extrathoracic blood volumes evaluated with the COLD system in patients with acute respiratory failure. Preliminary study]. / Effetti della PEEP sui volumi ematici intratoracico e totale valutai con sistema COLD in pazienti con insufficienza respiratoria acuta. Studio preliminare.

AIM OF THE STUDY: To evaluate the effects of positive end expiratory pressure (PEEP) on intrathoracic and extrathoracic blood volumes in patients with acute respiratory failure (ARF). METHODS: In 4 ARF patients, we have measured cardiac output (CI), intrathoracic blood volume (ITBVI), global end-diastolic ventricular volume (GEDVI), pulmonary (PBVI) and total (TBVI) blood volumes, during application of two PEEP levels (0 and 10 cm H2O). These measurements have been performed by PULSION COLD Z-021 system, using the double indicator dilution technique (thermal and dye dilution). RESULTS: PEEP application caused a significant reduction in CI (from 3.8 +/- 0.4 to 2.9 +/- 0.1 1/min/m2) and ITBVI (from 888 +/- 48 to 698 +/- 25 ml/m2). The reduction in intrathoracic blood volume was associated with a significant reduction in GEDVI and PBVI. After PEEP application, there was a significant reduction in TBVI (from 2437 +/- 135 to 1984 +/- 49 ml/m2). CONCLUSIONS: PEEP application decreases cardiac index, mainly through a preload reduction, as evidenced by the reduction in intrathoracic and end-diastolic ventricular blood volumes. The preload effect is due to an increase in intrathoracic pressure with reduction in total circulating blood volume. TBVI reduction is consistent with blood pooling in vascular compartments, e.g., splanchnic compartment, characterized by long vascular time constant.

Patient-ventilator interaction during acute hypercapnia: pressure-support vs. proportional-assist ventilation.

The objective of this study was to compare patient-ventilator interaction during pressure-support ventilation (PSV) and proportional-assist ventilation (PAV) in the course of increased ventilatory requirement obtained by adding a dead space in 12 patients on weaning from mechanical ventilation. With PSV, the level of unloading was provided by setting the inspiratory pressure at 20 and 10 cmH2O, whereas with PAV the level of unloading was at 80 and 40% of the elastic and resistive load. Hypercapnia increased (P < 0.001) tidal swing of esophageal pressure and pressure-time product per breath at both levels of PSV and PAV. During PSV, application of dead space increased ventilation (VE) during PSV (67 +/- 4 and 145 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001). This was due to a relevant increase in respiratory rate (48 +/- 4 and 103 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001), whereas the increase in tidal volume (VT) played a small role (13 +/- 1 and 21 +/- 2% during 20 and 10 cmH2O PSV, respectively, P < 0.001). With PAV, the increase in VE consequent to hypercapnia (27 +/- 3 and 64 +/- 4% during 80 and 40% PAV, respectively, P < 0.001) was related to the increase in VT (32 +/- 1 and 66 +/- 2% during 80 and 40% PAV, respectively, P < 0.001), respiratory rate remaining unchanged. The increase in pressure-time product per minute and per liter consequent to acute hypercapnia and the sense of breathlessness were significantly (P < 0.001) higher during PSV than during PAV. Our data show that, after hypercapnic stimulation of the respiratory drive, the capability to increase VE through changes in VT modulated by variations in inspiratory muscle effort is preserved only during PAV; the compensatory strategy used to increase VE during PSV requires greater muscle effort and causes more pronounced patient discomfort than during PAV.