Thomas Muders

Electrical impedance tomography compared with thoracic computed tomography during a slow inflation maneuver in experimental models of lung injury

Objective: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. Design:Randomized prospective experimental study. Setting:Academic research laboratory. Subjects:Sixteen anesthetized, tracheotomized, and mechanically ventilated pigs. Interventions: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. Measurements and Main Results: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. Conclusions: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.

The impact of spontaneous breathing during mechanical ventilation.

Purpose of reviewIn 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. Recent findingsThe 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 patients 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. SummaryIn 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.

Spontaneous breathing with airway pressure release ventilation favors ventilation in dependent lung regions and counters cyclic alveolar collapse in oleic-acid-induced lung injury: a randomized controlled computed tomography trial

IntroductionExperimental and clinical studies have shown a reduction in intrapulmonary shunt with spontaneous breathing during airway pressure release ventilation (APRV) in acute lung injury. This reduction was related to reduced atelectasis and increased aeration. We hypothesized that spontaneous breathing will result in better ventilation and aeration of dependent lung areas and in less cyclic collapse during the tidal breath.MethodsIn this randomized controlled experimental trial, 22 pigs with oleic-acid-induced lung injury were randomly assigned to receive APRV with or without spontaneous breathing at comparable airway pressures. Four hours after randomization, dynamic computed tomography scans of the lung were obtained in an apical slice and in a juxtadiaphragmatic transverse slice. Analyses of regional attenuation were performed separately in nondependent and dependent halves of the lungs on end-expiratory scans and end-inspiratory scans. Tidal changes were assessed as differences between inspiration and expiration of the mechanical breaths.ResultsWhereas no differences were observed in the apical slices, spontaneous breathing resulted in improved tidal ventilation of dependent lung regions (P < 0.05) and less cyclic collapse (P < 0.05) in the juxtadiaphragmatic slices. In addition, with spontaneous breathing, the end-expiratory aeration increased and nonaerated tissue decreased in dependent lung regions close to the diaphragm (P < 0.05 for the interaction ventilator mode and lung region).ConclusionSpontaneous breathing during APRV redistributes ventilation and aeration to dependent, usually well-perfused, lung regions close to the diaphragm, and may thereby contribute to improved arterial oxygenation. Spontaneous breathing also counters cyclic collapse, which is a risk factor for ventilation-associated lung injury.

Tidal recruitment assessed by electrical impedance tomography and computed tomography in a porcine model of lung injury

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.

Impedance tomography as a new monitoring technique.

Purpose of reviewElectrical impedance tomography (EIT) noninvasively creates images of the local ventilation and arguably lung perfusion distribution at bedside. Methodological and clinical aspects of EIT when used as a monitoring tool in the intensive care unit are reviewed and discussed. Recent findingsWhereas former investigations addressed the issue of validating EIT to measure regional ventilation, current studies focus on clinical applications such as detection of pneumothorax. Furthermore, EIT has been used to quantify lung collapse and tidal recruitment in order to titrate positive end-expiratory pressure. Indicator-free EIT measurements might be sufficient for the continuous measurement of cardiac stroke volume, but assessment of regional lung perfusion presumably requires the use of a contrast agent such as hypertonic saline. SummaryGrowing evidence suggests that EIT may play an important role in individually optimizing ventilator settings in critically ill patients.

Effects of spontaneous breathing during airway pressure release ventilation on cerebral and spinal cord perfusion in experimental acute lung injury.

Background Systemic-blood flow, cerebral-blood flow, and spinal cord blood flow can be affected by mechanical ventilation. We investigated the effect of spontaneous breathing on cerebral and spinal blood flow during airway pressure release ventilation (APRV) with and without spontaneous breathing. Methods Twelve pigs with oleic-acid-induced lung injury were ventilated with APRV with or without spontaneous breathing in random order. Without spontaneous breathing, either the upper airway pressure limit of mechanical ventilation or the ventilator rate was increased to maintain pH and PaCO2 constant. Systemic hemodynamic parameters were determined by the double indicator dilution method, cerebral and spinal cord blood flow was measured with colored microspheres. Statistics: ANOVA+Newmann-Keuls-test. Results As compared with APRV without spontaneous breathing and high tidal volume (VT) spontaneous breathing during APRV showed higher systemic blood flow and perfusion of the basal ganglia, frontal lobe, hippocampus, brain stem, temporal lobe, thalamus (all P<0.001), cerebellum, spinal cord (all P<0.01), and the central cortical region (P<0.05). During APRV without spontaneous breathing and low VT blood flow was lower in the basal ganglia, frontal lobe, hippocampus (all P<0.01), and temporal lobe (P<0.05) whereas perfusion of the thalamus, central cortical region, brain stem, cerebellum, and spinal cord were not different compared with APRV with spontaneous breathing. Conclusions In parallel with higher systemic blood flow regional cerebral and spinal cord blood flow were also higher when spontaneous breathing was maintained during APRV. The higher regional blood flow by maintaining spontaneous breathing was more pronounced when compared with full ventilatory support using high VT.

Cardiorespiratory effects of spontaneous breathing in two different models of experimental lung injury : a randomized controlled trial

IntroductionAcute lung injury (ALI) can result from various insults to the pulmonary tissue. Experimental and clinical data suggest that spontaneous breathing (SB) during pressure-controlled ventilation (PCV) in ALI results in better lung aeration and improved oxygenation. Our objective was to evaluate whether the addition of SB has different effects in two different models of ALI.MethodsForty-four pigs were randomly assigned to ALI resulting either from hydrochloric acid aspiration (HCl-ALI) or from increased intra-abdominal pressure plus intravenous oleic acid injections (OA-ALI) and were ventilated in PCV mode either with SB (PCV + SB) or without SB (PCV – SB). Cardiorespiratory variables were measured at baseline after induction of ALI and after 4 hours of treatment (PCV + SB or PCV – SB). Finally, density distributions and end-expiratory lung volume (EELV) were assessed by thoracic spiral computed tomography.ResultsPCV + SB improved arterial partial pressure of oxygen/inspiratory fraction of oxygen (PaO2/FiO2) by a reduction in intrapulmonary shunt fraction in HCl-ALI from 27% ± 6% to 23% ± 13% and in OA-ALI from 33% ± 19% to 26% ± 18%, whereas during PCV – SB PaO2/FiO2 deteriorated and shunt fraction increased in the HCl group from 28% ± 8% to 37% ± 17% and in the OA group from 32% ± 12% to 47% ± 17% (P < 0.05 for interaction time and treatment, but not ALI type). PCV + SB also resulted in higher EELV (HCl-ALI: 606 ± 171 mL, OA-ALI: 439 ± 90 mL) as compared with PCV – SB (HCl-ALI: 372 ± 130 mL, OA-ALI: 192 ± 51 mL, with P < 0.05 for interaction of time, treatment, and ALI type).ConclusionsSB improves oxygenation, reduces shunt fraction, and increases EELV in both models of ALI.

[Lung protective ventilation - protective effect of adequate supported spontaneous breathing].

Based on available data, it can be suggested that spontaneous breathing during ventilator support has not to be suppressed even in patients with severe pulmonary dysfunction if no contraindications are present. Experimental data do not support the contention that spontaneous breathing aggravates ventilator-induced lung injury. During spontaneous breathing increase in PTP is maximal in the depended lung areas in adjunct to the diaphragm and causes recruitment of initially atelectatic lung areas thereby avoiding cyclic alveolar collapse and reopening. This should result in a lung protective effect of adequate supported spontaneous breathing. Clinical data supported this belief demonstrating improvement in pulmonary gas exchange, systemic blood flow, and oxygen supply to the tissue and a decrease in days on ventilator support and duration of stay in the intensive care unit.

The effect of pumpless extracorporeal CO2 removal on regional perfusion of the brain in experimental acute lung injury.

Background: Lung-protective mechanical ventilation with low tidal volumes (VT) is often associated with hypercapnia (HC), which may be unacceptable in patients with brain injury. CO2 removal using a percutaneous extracorporeal lung assist (pECLA) enables normocapnia despite low VT, but its effects on regional cerebral blood flow (rCBF) remain ambiguous. We hypothesized that reversal of HC by pECLA impairs rCBF in a porcine lung injury model. Methods: Lung injury was induced in 9 anesthetized pigs by hydrochloric acid aspiration. rCBF and systemic hemodynamics were measured by colored microsphere technique and transpulmonary-thermodilution during a randomized sequence of 4 experimental situations: pECLA shunt-on (1) with HC and (2) without HC, pECLA shunt-off (3) with HC and (4) without HC. Results: HC increased rCBF (P<0.05). CO2 removal with pECLA resulting in normocapnia, decreased rCBF to levels comparable to those without pECLA and normocapnia. HC resulted in increased cardiac output (+25.5%). Cardiac output was highest during HC with pECLA shunt (+44.9%). During pECLA with CO2 removal, cardiac output (+38.1%) decreased compared with pECLA without CO2 removal, but stayed higher than during normocapnia/no pECLA shunt (P<0.05). Conclusions: In this animal model, mechanical ventilation with low VT was associated with HC and increased rCBF. CO2 removal by pECLA restored normocapnia, reduced rCBF to levels of normocapnia, but required a higher systemic blood flow for the perfusion of the pECLA device. If these results could be transferred to patients, extracorporeal CO2 removal might be an option for treatment of combined lung and brain injury in condition of a sufficient cardiac flow reserve.

Hemorrhage under veno-venous extracorporeal membrane oxygenation in acute respiratory distress syndrome patients: a retrospective data analysis

Background Despite being still invasive and challenging, technical improvement has resulted in broader and more frequent application of extracorporeal membrane oxygenation (ECMO), to prevent hypoxemia and to reduce invasiveness of mechanical ventilation (MV). Heparin-coated ECMO-circuits are currently standard of care, in addition to heparin based anticoagulation (AC) regimen guided by activated clotting time (ACT) or activated partial thromboplastin time (aPTT). Despite these advances, a reliable prediction of hemorrhage is difficult and the risk of hemorrhagic complication remains unfortunately high. We hypothesized, that there are coagulation parameters that are indices for a higher risk of hemorrhage under veno-venous (VV)-ECMO therapy. Methods Data from 36 patients with severe respiratory failure treated with VV-ECMO at a University Hospital intensive care unit (ICU) were analyzed retrospectively. Patients were separated into two groups based on severity of hemorrhagic complications and transfusion requirements. The following data were collected: demographics, hemodynamic data, coagulation samples, transfusion requirements, change of ECMO-circuit during treatment and adverse effects, including hemorrhage and thrombosis. Results In this study 74 hemorrhagic events were observed, one third of which were severe. Patients suffering from severe hemorrhage had a lower survival rate on VV-ECMO (43% vs. 91%; P=0.002) and in ICU (36% vs. 86%; P=0.002). SAPS II, factor VII and X were different between mild and severe hemorrhage group. Conclusions Severe hemorrhage under VV-ECMO is associated with higher mortality. Only factor VII and X differed between groups. Further clinical studies are required to determine the timing of initiation and targets for AC therapies during VV-ECMO.