Pulse oximetry vs. PaO2 metrics in mechanically ventilated children: Berlin definition of ARDS and mortality risk. (Singh)

Khemani RG, Rubin S, Belani S, et al. Pulse oximetry vs. PaO2 metrics in mechanically ventilated children: Berlin definition of ARDS and mortality risk. Intensive Care Med. 2015 Jan;41(1):94-102.

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PURPOSE: Requiring PaO2/FiO2 ratio (PF) to define ARDS may bias towards children with cardiovascular dysfunction and hypoxemia. We sought to evaluate (1) the Berlin definition of ARDS in children using PF; (2) the effect of substituting SpO2/FiO2(SF) ratio; (3) differences between patients with and without arterial blood gases; and (4) the ability of SpO2 and PaO2 indices to discriminate ICU mortality.

METHODS: Single center retrospective review (3/2009-4/2013) of mechanically ventilated (MV) children. Initial values for PF, SF, oxygenation index (OI), and oxygen saturation index (OSI) after intubation and average values on day 1 of MV were analyzed against ICU mortality, subgrouped by Berlin severity categories.

RESULTS: Of the 1,833 children included, 129 met Berlin PF ARDS criteria (33 % mortality); 312 met Berlin SF ARDS criteria (22 % mortality). Children with a PaO2 on day 1 of MV had higher mortality and severity of illness, were older, and had more vasoactive-inotropic infusions (p < 0.001). SF could be calculated for 1,201 children (AUC for ICU mortality 0.821), OSI for 1,034 (0.793), PF for 695 (0.706), and OI for 673 (0.739). Average SF on day 1 discriminated mortality better than PF (p = 0.003).

CONCLUSIONS: Berlin PF criteria for ARDS identified less than half of the children with ARDS, favoring those with cardiovascular dysfunction. SF or OSI discriminate ICU mortality as well as PF and OI, double the number of children available for risk stratification, and should be considered for severity of illness scores and included in a pediatric-specific definition of ARDS. Multicenter validation is required.

Mechanical ventilation-induced intrathoracic pressure distribution and heart-lung interactions. (Dugan)

Lansdorp B, Hofhuizen C, van Lavieren M, van Swieten H, Lemson J, van Putten MJ, van der Hoeven JG, Pickkers P. Mechanical ventilation-induced intrathoracic pressure distribution and heart-lung interactions*. Crit Care Med. 2014 Sep;42(9):1983-90.

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OBJECTIVE: Mechanical ventilation causes cyclic changes in the heart’s preload and afterload, thereby influencing the circulation. However, our understanding of the exact physiology of this cardiopulmonary interaction is limited. We aimed to thoroughly determine airway pressure distribution, how this is influenced by tidal volume and chest compliance, and its interaction with the circulation in humans during mechanical ventilation.

DESIGN: Intervention study.

SETTING: ICU of a university hospital.

PATIENTS: Twenty mechanically ventilated patients following coronary artery bypass grafting surgery.

INTERVENTION: Patients were monitored during controlled mechanical ventilation at tidal volumes of 4, 6, 8, and 10 mL/kg with normal and decreased chest compliance (by elastic binding of the thorax).

MEASUREMENTS AND MAIN RESULTS: Central venous pressure, airway pressure, pericardial pressure, and pleural pressure; pulse pressure variations, systolic pressure variations, and stroke volume variations; and cardiac output were obtained during controlled mechanical ventilation at tidal volume of 4, 6, 8, and 10 mL/kg with normal and decreased chest compliance. With increasing tidal volume (4, 6, 8, and 10 mL/kg), the change in intrathoracic pressures increased linearly with 0.9 ± 0.2, 0.5 ± 0.3, 0.3 ± 0.1, and 0.3 ± 0.1 mm Hg/mL/kg for airway pressure, pleural pressure, pericardial pressure, and central venous pressure, respectively. At 8 mL/kg, a decrease in chest compliance (from 0.12 ± 0.07 to 0.09 ± 0.03 L/cm H2O) resulted in an increase in change in airway pressure, change in pleural pressure, change in pericardial pressure, and change in central venous pressure of 1.1 ± 0.7, 1.1 ± 0.8, 0.7 ± 0.4, and 0.8 ± 0.4 mm Hg, respectively. Furthermore, increased tidal volume and decreased chest compliance decreased stroke volume and increased arterial pressure variations. Transmural pressure of the superior vena cava decreased during inspiration, whereas the transmural pressure of the right atrium did not change.

CONCLUSIONS: Increased tidal volume and decreased chest wall compliance both increase the change in intrathoracic pressures and the value of the dynamic indices during mechanical ventilation. Additionally, the transmural pressure of the vena cava is decreased, whereas the transmural pressure of the right atrium is not changed.

 

The effect of the pressure-volume curve for positive end-expiratory pressure titration on clinical outcomes in acute respiratory distress syndrome: a systematic review. (Stockwell)

Hata JS, Togashi K, Kumar AB, Hodges LD, Kaiser EF, Tessmann PB, Faust CA, Sessler DI. The Effect of the Pressure-Volume Curve for Positive End-Expiratory Pressure Titration on Clinical Outcomes in Acute Respiratory Distress Syndrome: A Systematic Review. J Intensive Care Med. 2013 Jul 11. [Epub ahead of print]

PURPOSE Methods to optimize positive end-expiratory pressure (PEEP) in acute respiratory distress syndrome (ARDS) remain controversial despite decades of research. The pressure-volume curve (PVC), a graphical ventilator relationship, has been proposed for prescription of PEEP in ARDS. Whether the use of PVC’s improves survival remains unclear.

METHODS In this systematic review, we assessed randomized controlled trials (RCTs) comparing PVC-guided treatment with conventional PEEP management on survival in ARDS based on the search of the National Library of Medicine from January 1, 1960, to January 1, 2010, and the Cochrane Central Register of Controlled Trials. Three RCTs were identified with a total of 185 patients, 97 with PVC-guided treatment and 88 with conventional PEEP management.

RESULTS The PVC-guided PEEP was associated with an increased probability of 28-day or hospital survival (odds ratio [OR] 2.7, 95% confidence interval [CI] 1.5, 4.9) using a random-effects model without significant heterogeneity (I 2 test: P = .75). The PVC-guided ventilator support was associated with reduced cumulative risk of mortality (-0.24 (95% CI -0.38, -0.11). The PVC-managed patients received greater PEEP (standardized mean difference [SMD] 5.7 cm H2O, 95% CI 2.4, 9.0) and lower plateau pressures (SMD -1.2 cm H2O, 95% CI -2.2, -0.2), albeit with greater hypercapnia with increased arterial pCO2 (SMD 8 mm Hg, 95% CI 2, 14). Weight-adjusted tidal volumes were significantly lower in PVC-guided than conventional ventilator management (SMD 2.6 mL/kg, 95% CI -3.3, -2.0).

CONCLUSION This analysis supports an association that ventilator management guided by the PVC for PEEP management may augment survival in ARDS. Nonetheless, only 3 randomized trials have addressed the question, and the total number of patients remains low. Further outcomes studies appear required for the validation of this methodology.

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Early acute lung injury: criteria for identifying lung injury prior to the need for positive pressure ventilation. (Ruth)

Crit Care Med. 2013 Aug;41(8):1929-37. PMID: 23782966

OBJECTIVE: Mortality associated with acute lung injury remains high. Early identification of acute lung injury prior to onset of respiratory failure may provide a therapeutic window to target in future clinical trials. The recently validated Lung Injury Prediction Score identifies patients at risk for acute lung injury but may be limited for routine clinical use. We sought to empirically derive clinical criteria for a pragmatic definition of early acute lung injury to identify patients with lung injury prior to the need for positive pressure ventilation.

DESIGN: Prospective observational cohort study.

SETTING: Stanford University Hospital.

PATIENTS: We prospectively evaluated 256 patients admitted to Stanford University Hospital with bilateral opacities on chest radiograph without isolated left atrial hypertension.

INTERVENTIONS: None.

MEASUREMENTS AND MAIN RESULTS: Of the 256 patients enrolled, 62 patients (25%) progressed to acute lung injury requiring positive pressure ventilation. Clinical variables (through first 72 hr or up to 6 hr prior to acute lung injury) associated with progression to acute lung injury were analyzed by backward regression. Oxygen requirement, maximal respiratory rate, and baseline immune suppression were independent predictors of progression to acute lung injury. A simple three-component early acute lung injury score (1 point for oxygen requirement > 2-6 L/min or 2 points for > 6 L/min; 1 point each for a respiratory rate ≥ 30 and immune suppression) accurately identified patients who progressed to acute lung injury requiring positive pressure ventilation (area under the receiver-operator characteristic curve, 0.86) and performed similarly to the Lung Injury Prediction Score. An early acute lung injury score greater than or equal to 2 identified patients who progressed to acute lung injury with 89% sensitivity and 75% specificity. Median time of progression from early acute lung injury criteria to acute lung injury requiring positive pressure ventilation was 20 hours.

CONCLUSIONS: This pragmatic definition of early acute lung injury accurately identified patients who progressed to acute lung injury prior to requiring positive pressure ventilation. Pending further validation, these criteria could be useful for future clinical trials targeting early treatment of acute lung injury.

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