To determine the validity of functional electric impedance tomography to monitor regional ventilation distribution in experimental acute lung injury, and to develop a simple electric impedance tomography index detecting alveolar recruitment. Randomized prospective experimental study. Academic research laboratory. Sixteen anesthetized, tracheotomized, and mechanically ventilated pigs. Acute lung injury was induced either by acid aspiration (direct acute lung injury) or by abdominal hypertension plus oleic acid injection (indirect acute lung injury) in ten pigs. Six pigs with normal lungs were studied as a control group and with endotracheal suction-related atelectasis. After 4 hrs of mechanical ventilation, a slow inflation was performed. During slow inflation, simultaneous measurements of regional ventilation by electric impedance tomography and dynamic computed tomography were highly correlated in quadrants of a transversal thoracic plane (r2 = .63-.88, p < .0001, bias <5%) in both direct and indirect acute lung injury. Variability between methods was lower in direct than indirect acute lung injury (11 +/- 2% vs. 18 +/- 3%, respectively, p < .05). Electric impedance tomography indexes to detect alveolar recruitment were determined by mathematical curve analysis of regional impedance time curves. Empirical tests of different methods revealed that regional ventilation delay, that is, time delay of regional impedance time curve to reach a threshold, correlated well with recruited volume as measured by CT (r2 = .63). Correlation coefficients in subgroups were r2 = .71 and r2 = .48 in pigs with normal lungs with and without closed suction related atelectasis and r2 = .79 in pigs subject to indirect acute lung injury, respectively, whereas no significant correlation was found in pigs undergoing direct acute lung injury. Electric impedance tomography allows assessment of regional ventilation distribution and recruitment in experimental models of direct and indirect acute lung injury as well as normal lungs. Except for pigs with direct acute lung injury, regional ventilation delay determined during a slow inflation from impedance time curves appears to be a simple index for clinical monitoring of alveolar recruitment.

Objectives: To determine the validity of electrical impedance tomography to detect and quantify the amount of tidal recruitment caused by different positive end-expiratory pressure levels in a porcine acute lung injury model. Design: Randomized, controlled, prospective experimental study. Setting: Academic research laboratory. Subjects: Twelve anesthetized and mechanically ventilated pigs. Interventions: Acute lung injury was induced by central venous oleic acid injection and abdominal hypertension in seven animals. Five healthy pigs served as control group. Animals were ventilated with positive end-expiratory pressure of 0, 5, 10, 15, 20, and 25 cm H₂O, respectively, in a randomized order. Measurements and Main Results: At any positive end-expiratory pressure level, electrical impedance tomography was obtained during a slow inflation of 12 mL/kg of body weight. Regional-ventilation-delay indices quantifying the time until a lung region reaches a certain amount of impedance change were calculated for lung quadrants and for every single electrical impedance tomography pixel, respectively. Pixel-wise calculated regional-ventilation-delay indices were plotted in a color-coded regional-ventilation-delay map. Regional-ventilation-delay inhomogeneity that quantifies heterogeneity of ventilation time courses was evaluated by calculating the scatter of all pixel-wise calculated regional-ventilation-delay indices. End-expiratory and end-inspiratory computed tomography scans were performed at each positive end-expiratory pressure level to quantify tidal recruitment of the lung. Tidal recruitment showed a moderate inter-individual (r = .54; p < .05) and intra-individual linear correlation (r = .46 up to r = .73 and p < .05, respectively) with regional-ventilation-delay obtained from lung quadrants. Regional-ventilation-delay inhomogeneity was excellently correlated with tidal recruitment intra- (r = .90 up to r = .99 and p < .05, respectively) and inter-individually (r = .90; p < .001). Conclusions: Regional-ventilation-delay can be noninvasively measured by electrical impedance tomography during a slow inflation of 12 mL/kg of body weight and visualized using ventilation delay maps. Our experimental data suggest that the impedance tomography-based analysis of regional-ventilation-delay inhomogeneity provides a good estimate of the amount of tidal recruitment and may be useful to individualize ventilatory settings.

Electrical impedance tomography (EIT) is a bedside monitoring tool that noninvasively visualizes local ventilation and arguably lung perfusion distribution. This article reviews and discusses both methodological and clinical aspects of thoracic EIT. Initially, investigators addressed the validation of EIT to measure regional ventilation. Current studies focus mainly on its clinical applications to quantify lung collapse, tidal recruitment, and lung overdistension to titrate positive end-expiratory pressure (PEEP) and tidal volume. In addition, EIT may help to detect pneumothorax. Recent studies evaluated EIT as a tool to measure regional lung perfusion. Indicator-free EIT measurements might be sufficient to continuously measure cardiac stroke volume. The use of a contrast agent such as saline might be required to assess regional lung perfusion. As a result, EIT-based monitoring of regional ventilation and lung perfusion may visualize local ventilation and perfusion matching, which can be helpful in the treatment of patients with acute respiratory distress syndrome (ARDS).

We observed opioid-related respiratory depression in a patient receiving tramadol via patient-controlled analgesia. Predisposing factors were the patient's genetic background and renal impairment. Complete recovery occurred after naloxone administration, thus confirming opioid intoxication. Analysis of the patient's genotype revealed a CYP2D6 gene duplication resulting in ultra-rapid metabolism of tramadol to its active metabolite (+)O-desmethyltramadol. Concomitant renal impairment resulting in decreased metabolite clearance enhanced opioid toxicity. This genetic CYP2D6 variant is particularly common in specific ethnic populations and should be a future diagnostic target whenever administration of tramadol or codeine is anticipated, as both drugs are subject to a comparable CYP2D6-dependent metabolism.

In patients with acute respiratory distress syndrome, controlled mechanical ventilation is generally used in the initial phase to ensure adequate alveolar ventilation, arterial oxygenation, and to reduce work of breathing without causing further damage to the lungs. Although introduced as weaning techniques, partial ventilator support modes have become standard techniques for primary mechanical ventilator support. This review evaluates the physiological and clinical effects of persisting spontaneous breathing during ventilator support in patients with acute respiratory distress syndrome. The improvements in pulmonary gas exchange, systemic blood flow and oxygen supply to the tissue which have been observed when spontaneous breathing has been maintained during mechanical ventilation are reflected in the clinical improvement in the patient's condition. Computer tomography observations demonstrated that spontaneous breathing improves gas exchange by redistribution of ventilation and end-expiratory gas to dependent, juxtadiaphragmatic lung regions and thereby promotes alveolar recruitment. Thus, spontaneous breathing during ventilator support counters the undesirable cyclic alveolar collapse in dependent lung regions. In addition, spontaneous breathing during ventilator support may prevent increase in sedation beyond a level of comfort to adapt the patient to mechanical ventilation which decreases duration of mechanical ventilator support, length of stay in the intensive care unit, and overall costs of care giving. In view of the recently available data, it can be concluded that maintained spontaneous breathing during mechanical ventilation should not be suppressed even in patients with severe pulmonary functional disorders.