Clinical Application of PSV In Aliards

Recent data support the possibility of using PSV safely and effectively in the course of acute respiratory failure. Cereda et al. demonstrated that PSV could be used

Mechanical Ventilator Images

Fig. 2. Main ventilatory and gas exchange parameters during continuous positive pressure ventilation (CPPV) (white bars) and pressure support ventilation (PSV) (gray bars) in the PSV success (left histograms) and failure (right histograms) groups. PaO2/FiO2: oxygen arterial tension to inspiratory oxygen fraction ratio; PaCO2: carbon dioxide arterial tension; Ve: minute ventilation; RR: respiratory rate. * p<0.05 success vs failure for CPPV or PSV; § p<0.05 PSV vs CPPV in success or failure groups. Modified from [23].

Fig. 2. Main ventilatory and gas exchange parameters during continuous positive pressure ventilation (CPPV) (white bars) and pressure support ventilation (PSV) (gray bars) in the PSV success (left histograms) and failure (right histograms) groups. PaO2/FiO2: oxygen arterial tension to inspiratory oxygen fraction ratio; PaCO2: carbon dioxide arterial tension; Ve: minute ventilation; RR: respiratory rate. * p<0.05 success vs failure for CPPV or PSV; § p<0.05 PSV vs CPPV in success or failure groups. Modified from [23].

rather early in ALI/ARDS patients [23]. Forty-eight intubated, sedated and paralyzed patients were studied: all subjects had been receiving CPPV for at least 24 hours, and had PaO2 >80 mmHg, at any FiO2, with PEEP <15 cmH2O. Before switching the ventilator to PSV mode, muscle relaxants were withdrawn and sedative drugs reduced in order to obtain arousal on verbal command, while still relieving patients' pain and anxiety. The pressure support level was initially set to fully unload the patient respiratory muscles. The pressure support level was then adjusted to maintain RR and PaCO2 roughly constant. Switching to PSV was characterized by a decrease in PaCO2 (Fig. 2) with a corresponding increase inpH, with non-substantial changes in PaO2/FiO2 (Fig. 2), despite significantly lower FiO2 and mean airway pressure. Minute ventilation (Ve) and RR increased during PSV (Fig. 2), while Vt decreased. Ten patients (21%) failed the PSV trial, and CPPV was reinstituted. Return to CPPV was based on the occurrence of the following conditions: high RR in seven patients, increased PaCO2 in three, decreased PaO2 in one, and hemodynamic instability in three (Fig. 2). Patients who showed lower Crs, higher Ve, and longer time since intubation were more prone to fail the PSV trial.

Most ALI patients were successfully managed by means of PSV (79%), even if partial ventilatory support seemed more likely to fail in sicker patients.

A few aspects of this study require some comments. First, the authors may not have exploited all PSV features to full advantage, since the pressure support level was not targeted to enhance the patient's respiratory activity, but rather to maintain a constant PaCO2 level and RR. Second, prolonged use of CPPV might have caused respiratory muscle atrophy, and therefore some decrease in muscle function, particularly in the group of patient who failed the trial. Unfortunately, this issue was insufficiently investigated. Moreover, although a low Vt ventilation strategy actually represents a proven advantage in the management of ARDS patients, the collapse that may result from a strategy based on a low VT, both in assisted and controlled modes, could further impair gas exchange and respiratory mechanics, thus affecting PSV effectiveness [45].

Tejeda et al. compared PSV with assist-control ventilation in 45 patients with various causes of respiratory failure. PSV showed comparable efficacy to treat patients, with lower peak and mean airway pressure, in spite of a higher minute ventilation and dead space to tidal ventilation ratio [22].

Zeravik et al. investigated the effect of extravascular lung water (EVLW) on PSV efficacy [46]. PSV was successful in 29 of 32 patients with moderate acute respiratory failure. The effect of PSV on oxygenation was dependent on the EVLW: patients who failed the PSV trial showed higher basal levels of EVLW.

In a study by Putensen et al., PSV was compared with APRV with and without spontaneous breathing delivered at equal pressure limits (10 patients) or at equal minute ventilation (10 patients). The authors reported that in ARDS patients APRV with spontaneous breathing resulted in better cardiovascular function and V/Q distribution compared both to PSV and APRV alone. They could not demonstrate, however, any improvement with PSV compared to APRV alone [18]. The authors concluded that the spontaneous activity associated with PSV was not sufficient to reverse the V/Q mismatch caused by the alveolar collapse in ARDS patients. It is worth considering, however, whether the patients were somehow over-assisted during PSV; if this was the case then the patient's own contribution to inspiration was so limited to minimize the beneficial effects of PSV. Unfortunately, though Putensen et al. measured the esophageal pressure, no information about patient effort was reported. In COPD patients with ALI, in whom PSV and APRV were applied at equal pressure limits, APRV did not result in decreased WOB, or diaphragm electromyographic activity, while PSV determined a stable reduction of patient's effort [47]. This result suggested that the interface of spontaneous breathing during PSV and APRV is different and interpretation of results comparing these ventilatory modalities may be difficult.

Beside factors related to respiratory load (ventilatory needs and respiratory mechanics), another important aspect to consider during PSV is patient-ventilator interaction. An increased WOB, and a worse synchronization, likely associated to an increased respiratory drive, may more likely lead to PSV failure. We assessed the effects of short-term oxygenation changes on respiratory drive (P0.1, Ve and RR) on 12 ALI patients undergoing PSV [48]. We investigated three different levels of oxygenation (PaO2 was respectively 155±68,75± 12, and 55±6 mmHg) and found that decreased oxygenation level resulted in significant increases in Ve, RR, and

Physiology Mechanical Ventilator

Fig. 3. Oxygen arterial tension (PaO2), respiratory rate (RR), rapid shallow breathing index (SBI), and inspiratory occlusion pressure in the first 100 ms (P0.1), at different level of inspiratory oxygen fraction (FiO2): H1, high FiO2 (SatO2 > 95%); I, intermediate FiO2 (SatO2 between 90 and 95%); L, low FiO2 (SatO2 between 85 and 90%); H2, return to high FiO2 (SatO2 > 95%). *, ** p<0.05 or p<0.01 for the comparison I vs H1; § p<0.05 for the comparison of L vs H1+I. Modified from [48].

Fig. 3. Oxygen arterial tension (PaO2), respiratory rate (RR), rapid shallow breathing index (SBI), and inspiratory occlusion pressure in the first 100 ms (P0.1), at different level of inspiratory oxygen fraction (FiO2): H1, high FiO2 (SatO2 > 95%); I, intermediate FiO2 (SatO2 between 90 and 95%); L, low FiO2 (SatO2 between 85 and 90%); H2, return to high FiO2 (SatO2 > 95%). *, ** p<0.05 or p<0.01 for the comparison I vs H1; § p<0.05 for the comparison of L vs H1+I. Modified from [48].

P0.1 (Fig. 3). An important result of this study was that at PaO2 levels considered clinically adequate, patients still present an important residual hypoxic drive (Fig. 3). Since hypoxia is the main clinical feature of patients with ALI/ARDS, this suggests that acting on FiO2 to decrease respiratory drive and ventilatory needs (Ve and RR) may improve PSV tolerability and success.

Was this article helpful?

0 0

Post a comment