Influence of respiratory rate on gas trapping during low volume ventilation of patients with acute lung injury.

OBJECTIVE: Reduction in tidal volume (Vt) associated with increase in respiratory rate to limit hypercapnia is now proposed in patients with acute lung injury (ALI). The aim of this study was to test whether a high respiratory rate induces significant intrinsic positive end-expiratory pressure (PEEPi) in these patients. DESIGN: Prospective crossover study. SETTING: A medical intensive care unit. INTERVENTIONS AND MEASUREMENTS: Ten consecutive patients fulfilling criteria for severe ALI were ventilated with a 6 ml/kg Vt, a total PEEP level at 13+/-3 cmH(2)O and a plateau pressure kept at 23+/-4 cmH(2)O. The respiratory rate was randomly set below 20 breaths/min (17+/-3 breaths/min) and increased to 30 breaths/min (30+/-3 breaths/min) to compensate for hypercapnia. External PEEP was adjusted to keep the total PEEP and the plateau pressure constant. PEEPi was computed as the difference between total PEEP and external PEEP. The lung volume retained by PEEPi was then measured. RESULTS: Increase in respiratory rate resulted in significantly higher PEEPi (1.3+/-0.4 versus 3.9+/-1.1 cmH(2)O, p<0.01) and trapped volume (70+/-43 versus 244+/-127 ml, p<0.01). External PEEP needed to be reduced from 11.9+/-3.4 to 9.7+/-2.9 cmH(2)O ( p<0.01). PaO(2) was not affected but the alveolar-arterial oxygen tension difference slightly worsened with the high respiratory rate (p<0.05). CONCLUSIONS: An increase in respiratory rate used to avoid Vt reduction-induced hypercapnia may induce substantial gas trapping and PEEPi in patients with ALI.

Mechanical effects of airway humidification devices in difficult to wean patients.

OBJECTIVE: To evaluate the influence of airway humidification devices on the efficacy of ventilation in difficult to wean patients. DESIGN: A prospective, randomized, controlled physiologic study. SETTING: A 22-bed medical intensive care unit in a university hospital. PATIENTS: Chronic respiratory failure patients. INTERVENTIONS: Performances of a heated humidifier and a heat and moisture exchanger were evaluated on diaphragmatic muscle activity, breathing pattern, gas exchange, and respiratory comfort during weaning from mechanical ventilation by using pressure support ventilation. Eleven patients with chronic respiratory failure were submitted to four pressure support ventilation sequences by using the heated humidifier and the heat and moisture exchanger at two different levels of pressure support ventilation (7 and 15 cm H(2)O). MEASUREMENT AND MAIN RESULTS: Compared with the heated humidifier and regardless of the pressure support ventilation level used, the heat and moisture exchanger significantly increased all of the inspiratory effort variables (inspiratory work of breathing expressed in J/L and J/min, pressure time product, changes in esophageal pressure, and transdiaphragmatic pressure; p <.05) and dynamic intrinsic positive end-expiratory pressure (p <.05). Similarly, the heat and moisture exchanger produced a significant increase in Paco(2) (p <.01) responsible for severe respiratory acidosis (p <.05), which was insufficiently compensated for despite a significant increase in minute ventilation (p <.05). This resulted in respiratory discomfort for all patients with the heat and moisture exchanger (p <.01). Adverse effects were partially counterbalanced by increasing the pressure support ventilation level with the heat and moisture exchanger by >or=8 cm H(2)O. CONCLUSIONS: The type of airway humidification device used may negatively influence the mechanical efficacy of ventilation and, unless the pressure support ventilation level is considerably increased, the use of a heat and moisture exchanger should not be recommended in difficult or potentially difficult to wean patients with chronic respiratory failure.

Respective effects of end-expiratory and end-inspiratory pressures on alveolar recruitment in acute lung injury.

OBJECTIVE: A low tidal volume can induce alveolar derecruitment in patients with acute lung injury. This study was undertaken to evaluate whether this resulted mainly from the decrease in tidal volume or from the reduction in end-inspiratory plateau pressure and whether there is any benefit in raising the level of positive end-expiratory pressure (PEEP) while plateau pressure is kept constant. DESIGN: Prospective crossover study. SETTING: Medical intensive care unit of a university teaching hospital. PATIENTS: Fifteen adult patients ventilated for acute lung injury (PaO2/FiO2, 158 +/- 34 mm Hg; lung injury score, 2.7 +/- 0.6). INTERVENTIONS: Three combinations were tested: PEEP at the lower inflection point with 6 mL/kg tidal volume, PEEP at the lower inflection point with 10 mL/kg tidal volume, and high PEEP with tidal volume at 6 mL/kg, keeping the plateau pressure similar to the preceding condition. MEASUREMENTS AND MAIN RESULTS: Pressure-volume curves at zero PEEP and at set PEEP were recorded, and recruitment was calculated as the volume difference between both curves for pressures ranging from 15 to 30 cm H2O. Arterial blood gases were measured for all patients. For a similar PEEP at the lower inflection point (10 +/- 3 cm H2O), tidal volume reduction (10 to 6 mL/kg) led to a significant derecruitment. A low tidal volume (6 mL/kg) with high PEEP (14 +/- 3 cm H2O), however, induced a significantly greater recruitment and a higher Pao than the two other strategies. CONCLUSION: At a given plateau pressure (i.e., similar end-inspiratory distension), lowering tidal volume and increasing PEEP increase recruitment and PaO2.