Patients with relatively normal pulmonary function at the time of brain death may have declines in functioning, and only 15% to 20% of these patients' lungs are subsequently suitable for transplantation.^1-3 This may result from the pulmonary damage associated with brain injury⁴ or the iatrogenic effects of mechanical ventilation.^5,6

Objectives: The value of visual inspection of ventilator waveforms in detecting patient–ventilator asynchronies in the intensive care unit has never been systematically evaluated. This study aims to assess intensive care unit physicians' ability to identify patient–ventilator asynchronies through ventilator waveforms. Design: Prospective observational study. Setting: Intensive care unit of a University Hospital. Patients: Twenty-four patients receiving mechanical ventilation for acute respiratory failure. Intervention: Forty-three 5-min reports displaying flow-time and airway pressure-time tracings were evaluated by 10 expert and 10 nonexpert, i.e., residents, intensive care unit physicians. The asynchronies identified by experts and nonexperts were compared with those ascertained by three independent examiners who evaluated the same reports displaying, additionally, tracings of diaphragm electrical activity. Measurements and Main Results: Data were examined according to both breath-by-breath analysis and overall report analysis. Sensitivity, specificity, and positive and negative predictive values were determined. Sensitivity and positive predictive value were very low with breath-by-breath analysis (22% and 32%, respectively) and fairly increased with report analysis (55% and 44%, respectively). Conversely, specificity and negative predictive value were high with breath-by-breath analysis (91% and 86%, respectively) and slightly lower with report analysis (76% and 82%, respectively). Sensitivity was significantly higher for experts than for nonexperts for breath-by-breath analysis (28% vs. 16%, p < .05), but not for report analysis (63% vs. 46%, p = .15). The prevalence of asynchronies increased at higher ventilator assistance and tidal volumes (p < .001 for both), whereas it decreased at higher respiratory rates and diaphragm electrical activity (p < .001 for both). At higher prevalence, sensitivity decreased significantly (p < .001). Conclusions: The ability of intensive care unit physicians to recognize patient–ventilator asynchronies was overall quite low and decreased at higher prevalence; expertise significantly increased sensitivity for breath-by-breath analysis, whereas it only produced a trend toward improvement for report analysis.

Positive end-expiratory pressure (PEEP) can be effective in improving oxygenation, but it may worsen or induce intracranial hypertension. The authors hypothesized that the intracranial effects of PEEP could be related to the changes in respiratory system compliance (Crs). A prospective study investigated 21 comatose patients with severe head injury or subarachnoid hemorrhage receiving intracranial pressure (ICP) monitoring who required mechanical ventilation and PEEP. The 13 patients with normal Crs were analyzed as group A and the 8 patients with low Crs as group B. During the study, 0, 5, 8, and 12 cm H2O of PEEP were applied in a random sequence. Jugular pressure, central venous pressure (CVP), cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral compliance, mean velocity of the middle cerebral arteries, and jugular oxygen saturation were evaluated simultaneously. In the group A patients, the PEEP increase from 0 to 12 cm H2O significantly increased CVP (from 10.6 ± 3.3 to 13.8 ± 3.3 mm Hg; p < 0.001) and jugular pressure (from 16.6 ± 3.1 to 18.8 ± 3.2 mm Hg; p < 0.001), but reduced mean arterial pressure (from 96.3 ± 6.7 to 91.3 ± 6.5 mm Hg; p < 0.01), CPP (from 82.2 ± 6.9 to 77.0 ± 6.2 mm Hg; p < 0.01), and mean velocity of the middle cerebral arteries (from 73.1 ± 27.9 to 67.4 ± 27.1 cm/sec; F = 7.15; p < 0.001). No significant variation in these parameters was observed in group B patients. After the PEEP increase, ICP and cerebral compliance did not change in either group. Although jugular oxygen saturation decreased slightly, it in no case dropped below 50%. In patients with low Crs, PEEP has no significant effect on cerebral and systemic hemodynamics. Monitoring of Crs may be useful for avoiding deleterious effects of PEEP on the intracranial system of patients with normal Crs.

Evaluating the physiologic effects of varying depths of propofol sedation on patient-ventilator interaction and synchrony during pressure support ventilation and neurally adjusted ventilatory assist. Prospective crossover randomized controlled trial. University hospital ICU. Fourteen intubated patients mechanically ventilated for acute respiratory failure. Six 25-minute trials randomly performed applying both pressure support ventilation and neurally adjusted ventilatory assist during wakefulness and with two doses of propofol, administered by Target Control Infusion, determining light (1.26 ± 0.35 μg/mL) and deep (2.52 ± 0.71 μg/mL) sedation, as defined by the bispectral index and Ramsay Sedation Scale. We measured electrical activity of the diaphragm to assess neural drive and calculated its integral over time during 1 minute (∫electrical activity of the diaphragm/min) to estimate diaphragm energy expenditure (effort), arterial blood gases, airway pressure, tidal volume and its coefficient of variation, respiratory rate, neural timing components, and calculated the ineffective triggering index. Increasing the depth of sedation did not cause significant modifications of respiratory timing, while determined a progressive significant decrease in neural drive (with both modes) and effort (in pressure support ventilation only). In pressure support ventilation, the difference in ineffective triggering index between wakefulness and light sedation was negligible (from 5.9% to 7.6%, p = 0.97); with deep sedation, however, ineffective triggering index increased up to 21.8% (p < 0.0001, compared to both wakefulness and light sedation). With neurally adjusted ventilatory assist, ineffective triggering index fell to 0%, regardless of the depth of sedation. With both modes, deep sedation caused a significant increase in PaCO2, which resulted, however, from different breathing patterns and patient-ventilator interactions. In pressure support ventilation, deep propofol sedation increased asynchronies, while light sedation did not. Propofol reduced the respiratory drive, while breathing timing was not significantly affected. Gas exchange and breathing pattern were also influenced by propofol infusion to an extent that varied with the depth of sedation and the mode of ventilation.

We investigated whether intervention with antioxidant vitamins C and E in enteral feeding influenced oxidative stress and clinical outcome in critically ill patients. Two-hundred-sixteen patients expected to require at least 10 days of enteral feeding completed the study. One-hundred-five patients received enteral feeding supplemented with antioxidants, and 111 control patients received an isocaloric formula. Plasma lipoperoxidation (by thiobarbituric acid reactive substances [TBARS] and prostaglandin F(2alpha) isoprostane levels), low-density lipoprotein (LDL) oxidizability, and LDL tocopherol content were determined at baseline and at the end of the 10-day period. The clinical 28-day outcome was also assessed. Plasma TBARS and isoprostanes were 5.33 +/- 1.26 nM/mL and 312 +/- 68 pg/mL, respectively, before treatment and 2.42 +/- 0.61 nM/mL and 198 +/- 42 pg/mL after intervention (P < 0.01 for both comparisons). Antioxidants improved LDL resistance to oxidative stress by approximately 30% (the lag time before treatment was 87 +/- 23 min and was 118 +/- 20 min after treatment; P < 0.04). There was a significantly reduced 28-day mortality after antioxidant intervention (45.7% in the antioxidant group and 67.5% in the regular-feeding group; P < 0.05). Isoprostanes may provide a sensitive biochemical marker for dose selection in studies involving antioxidants.