Accuracy of plateau pressure and stress index to identify injurious ventilation in patients with acute respiratory distress syndrome.

BACKGROUND: Guidelines suggest a plateau pressure (PPLAT) of 30 cm H(2)O or less for patients with acute respiratory distress syndrome, but ventilation may still be injurious despite adhering to this guideline. The shape of the curve plotting airway pressure versus time (STRESS INDEX) may identify injurious ventilation. The authors assessed accuracy of PPLAT and STRESS INDEX to identify morphological indexes of injurious ventilation. METHODS: Indexes of lung aeration (computerized tomography) associated with injurious ventilation were used as a "reference standard." Threshold values of PPLAT and STRESS INDEX were determined assessing the receiver-operating characteristics ("training set," N = 30). Accuracy of these values was assessed in a second group of patients ("validation set," N = 20). PPLAT and STRESS INDEX were partitioned between respiratory system (Pplat,Rs and STRESS INDEX,RS) and lung (PPLAT,L and STRESS INDEX,L; esophageal pressure; "physiological set," N = 50). RESULTS: Sensitivity and specificity of PPLAT of greater than 30 cm H(2)O were 0.06 (95% CI, 0.002-0.30) and 1.0 (95% CI, 0.87-1.00). PPLAT of greater than 25 cm H(2)O and a STRESS INDEX of greater than 1.05 best identified morphological markers of injurious ventilation. Sensitivity and specificity of these values were 0.75 (95% CI, 0.35-0.97) and 0.75 (95% CI, 0.43-0.95) for PPLAT greater than 25 cm H(2)O versus 0.88 (95% CI, 0.47-1.00) and 0.50 (95% CI, 0.21-0.79) for STRESS INDEX greater than 1.05. Pplat,Rs did not correlate with PPLAT,L (R(2) = 0.0099); STRESS INDEX,RS and STRESS INDEX,L were correlated (R(2) = 0.762). CONCLUSIONS: The best threshold values for discriminating morphological indexes associated with injurious ventilation were Pplat,Rs greater than 25 cm H(2)O and STRESS INDEX,RS greater than 1.05. Although a substantial discrepancy between Pplat,Rs and PPLAT,L occurs, STRESS INDEX,RS reflects STRESS INDEX,L.

Tidal volume lower than 6 ml/kg enhances lung protection: role of extracorporeal carbon dioxide removal.

BACKGROUND: Tidal hyperinflation may occur in patients with acute respiratory distress syndrome who are ventilated with a tidal volume (VT) of 6 ml/kg of predicted body weight develop a plateau pressure (PPLAT) of 28 < or = PPLAT < or = 30 cm H2O. The authors verified whether VT lower than 6 ml/kg may enhance lung protection and that consequent respiratory acidosis may be managed by extracorporeal carbon dioxide removal. METHODS: PPLAT, lung morphology computed tomography, and pulmonary inflammatory cytokines (bronchoalveolar lavage) were assessed in 32 patients ventilated with a VT of 6 ml/kg. Data are provided as mean +/- SD or median and interquartile (25th and 75th percentile) range. In patients with 28 < or = PPLAT < or = 30 cm H2O (n = 10), VT was reduced from 6.3 +/- 0.2 to 4.2 +/- 0.3 ml/kg, and PPLAT decreased from 29.1 +/- 1.2 to 25.0 +/- 1.2 cm H2O (P < 0.001); consequent respiratory acidosis (Paco2 from 48.4 +/- 8.7 to 73.6 +/- 11.1 mmHg and pH from 7.36 +/- 0.03 to 7.20 +/- 0.02; P < 0.001) was managed by extracorporeal carbon dioxide removal. Lung function, morphology, and pulmonary inflammatory cytokines were also assessed after 72 h. RESULTS: Extracorporeal assist normalized Paco2 (50.4 +/- 8.2 mmHg) and pH (7.32 +/- 0.03) and allowed use of VT lower than 6 ml/kg for 144 (84-168) h. The improvement of morphological markers of lung protection and the reduction of pulmonary cytokines concentration (P < 0.01) were observed after 72 h of ventilation with VT lower than 6 ml/kg. No patient-related complications were observed. CONCLUSIONS: VT lower than 6 ml/Kg enhanced lung protection. Respiratory acidosis consequent to low VT ventilation was safely and efficiently managed by extracorporeal carbon dioxide removal.

ECMO criteria for influenza A (H1N1)-associated ARDS: role of transpulmonary pressure.

PURPOSE: To assess whether partitioning the elastance of the respiratory system (E (RS)) between lung (E (L)) and chest wall (E (CW)) elastance in order to target values of end-inspiratory transpulmonary pressure (PPLAT(L)) close to its upper physiological limit (25 cmH(2)O) may optimize oxygenation allowing conventional treatment in patients with influenza A (H1N1)-associated ARDS referred for extracorporeal membrane oxygenation (ECMO). METHODS: Prospective data collection of patients with influenza A (H1N1)-associated ARDS referred for ECMO (October 2009-January 2010). Esophageal pressure was used to (a) partition respiratory mechanics between lung and chest wall, (b) titrate positive end-expiratory pressure (PEEP) to target the upper physiological limit of PPLAT(L) (25 cmH(2)O). RESULTS: Fourteen patients were referred for ECMO. In seven patients PPLAT(L) was 27.2 ± 1.2 cmH(2)O; all these patients underwent ECMO. In the other seven patients, PPLAT(L) was 16.6 ± 2.9 cmH(2)O. Raising PEEP (from 17.9 ± 1.2 to 22.3 ± 1.4 cmH(2)O, P = 0.0001) to approach the upper physiological limit of transpulmonary pressure (PPLAT(L) = 25.3 ± 1.7 cm H(2)O) improved oxygenation index (from 37.4 ± 3.7 to 16.5 ± 1.4, P = 0.0001) allowing patients to be treated with conventional ventilation. CONCLUSIONS: Abnormalities of chest wall mechanics may be present in some patients with influenza A (H1N1)-associated ARDS. These abnormalities may not be inferred from measurements of end-inspiratory plateau pressure of the respiratory system (PPLAT(RS)). In these patients, titrating PEEP to PPLAT(RS) may overestimate the incidence of hypoxemia refractory to conventional ventilation leading to inappropriate use of ECMO.

Extracorporeal CO2 removal.

The extracorporeal carbon dioxide removal (ECCO(2)R) concept, used as an integrated tool with conventional ventilation, plays a role in adjusting respiratory acidosis consequent to tidal volume (Vt) reduction in a protective ventilation setting. This concept arises from the extracorporeal membrane oxygenation (ECMO) experience. Kolobow and Gattinoni were the first to introduce extracorporeal support, with the intent to separate carbon dioxide removal from oxygen uptake; they hypothesized that to allow the lung to 'rest' oxygenation via mechanical ventilation could be dissociated from decarboxylation via extracorporeal carbon dioxide removal. Carbon dioxide is removed by a pump-driven modified ECMO machine with veno-venous bypass, while oxygenation is accomplished by high levels of positive end-expiratory pressure, with a respiratory rate of 3-5 breaths/min. The focus was that, in case of acute respiratory failure, CO(2) extraction facilitates a reduction in ventilatory support and oxygenation is maintained by simple diffusion across the patient's alveoli, called 'apneic oxygenation'. Concerns have been raised regarding the standard use of extracorporeal support because of the high incidence of serious complications: hemorrhage; hemolysis, and neurological impairments. Due to the negative results of a clinical trial, the extensive resources required and the high incidence of side effects, low frequency positive pressure ventilation ECCO(2)R was restricted to a 'rescue' therapy for the most severe case of acute respiratory distress syndrome (ARDS). Technological improvement led to the implementation of two different CO(2) removal approaches: the iLA called 'pumpless arteriovenous ECMO' and the veno-venous ECCO(2)R. They enable consideration of extracorporeal support as something more than mere rescue therapy; both of them are indicated in more protective ventilation settings in case of severe ARDS, and as a support to the spontaneous breathing/lung function in bridge to lung transplant. The future development of more and more efficient devices capable of removing a substantial amount of carbon dioxide production (30-100%) with blood flows of 250-500 ml/min is foreseeable. Moreover, in the future ARDS management should include a minimally invasive ECCO(2)R circuit associated with noninvasive ventilation. This would embody the modern mechanical ventilation philosophy: avoid tracheal tubes; minimize sedation, and prevent ventilator-induced acute lung injury and nosocomial infections.