Chest
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Clinical Trial
Is tracheal gas insufflation an alternative to extrapulmonary gas exchangers in severe ARDS?
Tracheal gas insufflation (TGI) of pure oxygen combined with mechanical ventilation decreases dead space and increases CO2 clearance. In the present study, TGI was used in six patients with ARDS who met extracorporeal membrane oxygenation criteria and who were severely hypoxemic and hypercapnic despite optimal pressure-controlled ventilation. This open clinical study aimed to investigate the effects of 4 L/min continuous flow of oxygen given via an intratracheal catheter. ⋯ There was no change in airway pressures and hemodynamic variables. A slight increase in end-expiratory and end-inspiratory volumes with TGI possibly occurred, as seen on tracings from respiratory inductive plethysmography (Respitrace). We conclude that TGI improves tolerance of limited pressure ventilation by removing CO2, but it may induce changes in lung volumes that are not detected by ventilator measurements.
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To identify characteristics associated with mortality and the development of multiorgan dysfunction in patients who had undergone cardiac surgery and required prolonged mechanical ventilation, ie, > 48 h. ⋯ These data confirm that acquired multiorgan dysfunction is the best predictor of mortality in patients requiring prolonged mechanical ventilation following cardiac surgery. Additionally, they identify potential determinants of multiorgan dysfunction and suggest possible interventions for its reduction in this patient population.
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It is common practice to convert patients with acute respiratory insufficiency (ARI) from controlled mechanical ventilation to some form of assisted spontaneous breathing as early as possible. A widely used mode of assisted spontaneous breathing is patient-triggered inspiratory pressure support (IPS). We investigated 11 patients with ARI during weaning from mechanical ventilation using IPS and found that in 9 of these patients, desynchronization between patient and ventilator occurred, ie, that the ventilator did not detect and support all the patients' breathing efforts. ⋯ We present the analysis of gas flow, volume, esophageal pressure, airway pressure, and tracheal pressure of 1 patient with ARI displaying desynchronization under IPS. Our results imply that desynchronization can occur due to the following: (1) inspiratory response delays caused by the inspiratory triggering mechanisms and the demand flow characteristics of the ventilator; (2) a mismatch between the patient's completion of the inspiration effort and the ventilator's criterion for terminating pressure support; and (3) restriction of expiration due to resistance from patient's airways, endotracheal tube, and expiratory valve. From our analysis, we have made proposals for reducing desynchronization in clinical practice.
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To learn the value of bronchoscopy and biopsy in the early diagnosis of inhalation injury ARDS. ⋯ Bronchoscopy with biopsy is useful in predicting the development of ARDS in burn patients.
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We undertook the present study with the following objectives: (1) to compare the difference between the end-tidal and the arterial carbondioxide concentration (P[ETa] CO2) gradients at rest and during exercise in normal subjects and patients with COPD; and (2) to analyze the factors contributing to this gradient. We studied seven normal subjects and seven patients with COPD using a symptom-limited exercise test on a cycle ergometer. Our results show that the P(ET-a)CO2 increased progressively as the individuals went from rest to higher workloads in both the normal group and in the COPD group. ⋯ The PaCO2 in normal subjects and in the COPD group correlated significantly with the partial pressure of end-tidal carbon dioxide (PETCO2). Using multiple regression analysis, with the PaCO2 as the dependent variable and the PETCO2 (along with other physiologic measures) as the independent variables, we found that the standard error of the estimate was still above 2.1 mm Hg in normal subjects and in patients with COPD. We conclude that (1) during exercise, the P(ET-a)CO2 in normal subjects and in patients with COPD increases significantly, (2) the P(ET-a)CO2 gradient is more closely correlated with the VD/VT than any other physiologic variable, and (3) changes in the PETCO2 during exercise are not correlated closely with changes in the PaCO2.