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Biomedical subjects

B Lachmann

Publications and source records attributed to B Lachmann.

At least 217 records · Page 12Linked to original sources
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Treatment and prevention of acute respiratory failure: physiological basis.

Acute respiratory failure is caused by many factors and remains one of the most common reasons for admission to the intensive care unit (ICU). In all cases of acute respiratory failure, there is a shortage of surfactant at the alveolar level. This deficit of surfactant leads to an increase in alveolar surface tension that increases the retraction forces of the lung, leading to end-expiratory alveolar collapse, finally resulting in respiratory dysfunction, which includes hypoxemia, low lung compliance, increase of intrapulmonary shunts, low functional residual capacity, atelectasis, and pulmonary edema. The goal of the treatment and prevention of acute respiratory failure is therefore based on the following three main items: re-opening the collapsed alveolar units; preserving the active surfactant component in the remaining functional alveolar units, and preventing end-expiratory collapse. The following strategies can be used to prevent and/or treat acute respiratory failure: counterbalancing the retraction forces of the lung by applying sufficiently high external pressures; and/or decreasing the surface tension at the air-liquid interface by means of exogenous surfactant, and/or eliminating the air-liquid interface by filling the lung with perfluorocarbons. By applying these therapeutic strategies in routine clinical practice, we should achieve a reduction in the mortality rate of patients suffering from acute respiratory failure.

Acute Disease↗
PubMedDate not supplied

Respiratory inductive plethysmography accuracy at varying PEEP levels and degrees of acute lung injury.

BACKGROUND AND OBJECTIVE: This study was performed to assess the accuracy of respiratory inductive plethysmographic (RIP) estimated lung volume changes at varying positive end-expiratory pressures (PEEP) during different degrees of acute respiratory failure. METHODS: Measurements of inspiratory tidal volume were validated in eight piglets during constant volume ventilation at incremental and decremental PEEP levels and with increasing severity of pulmonary injury. RIP accuracy was assessed with calibration from the healthy state, from the disease state as the measurement error was assessed, and at various PEEP levels. RESULTS: Best results (bias 3%, precision 7%) were obtained in healthy animals. RIP accuracy decreased with progressing degrees of acute respiratory failure and was PEEP dependent, unless RIP was calibrated again. When calibration was performed in the disease state as the measurement error was assessed, bias was reduced but precision did not improve (bias -2%, precision 9%). CONCLUSIONS: RIP accuracy is within the accuracy range found in monitoring devices currently in clinical use. Most reliable results with RIP are obtained when measurements are preceded by calibration in pulmonary conditions that are comparable to the measurement period. When RIP calibration is not possible, fixed weighting of the RIP signals with species and subject size adequate factors is an alternative. Measurement errors should be taken into account with interpretation of small volume changes.

Acute Disease↗
PubMedDate not supplied

Lung protective ventilation in ARDS: role of mediators, PEEP and surfactant.

Lung protective ventilation such as the ARDSnet low tidal volumes strategy can reduce mortality in ARDS patients. The knowledge that an essential therapy such as mechanical ventilation on the intensive care influences patient outcome has given rise to the re-evaluation of current ventilation practices. This review addresses the current state of lung protective strategies and their physiological rationale. Latest knowledge on the instigation and progression of lung injury by mechanical ventilation is explored, particularly the interaction between ventilation and the inflammatory response occurring in an ARDS lung. Furthermore, the role of tidal volume, PEEP, recruitment manoeuvres and surfactant on lung injury is discussed. Finally, we discuss results from clinical studies on mechanical ventilation and elucidate these results with data acquired in experimental studies. Guidelines for future strategies and/or investigations are presented.

Cytokines↗