The influence of different anesthetics on the oxygen delivery to and consumption of the heart.
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Biomedical subjects
Publications and source records attributed to B Lachmann.
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This paper presents the rationale for surfactant replacement therapy. In 6 animal models in which respiratory failure was induced by damaging the bronchial surfactant, surfactant depletion by lung lavage, by free oxygen radicals, by influenza virus and by anti-lung serum, it is demonstrated that surfactant instillation always led to an improvement in gas exchange and lung mechanics. A first clinical trials shows that surfactant instillation also improved lung function in a patient with severe respiratory failure. It is speculated that surfactant replacement therapy will become an acceptable therapeutic measure for treating lung failure in patients suffering with ARDS.
The effects of high frequency jet ventilation (HFJV) at 2 and 15 Hz on the pulmonary clearance of technetium 99m diethylene triamine pentaacetate (99mTc-DTPA) were compared with conventional volume-controlled (VC) ventilation with positive end-expiratory pressure (PEEP), in a model of respiratory failure induced by two lung lavages in adult rabbits. In group 1 the lungs were ventilated with HFJV at 2 Hz, and in group 2 ventilation was with HFJV at 15 Hz; group 3 underwent conventional VC ventilation. Group 4 also had conventional ventilation, but without previous lung lavage and functioned as a control group. In all groups, mean airway pressure was maintained at a value to ensure PaO2 greater than 25 kPa. The measured half-life time (T1/2) of the 99mTc-DTPA (mean (SD] was: group 1, 28 (7.8) min; group 2, 73.5 (7.9) min; group 3, 56.5 (12.4) min and group 4, 92.6 (13.2) min. Assuming that conventional VC with PEEP ventilation causes no additional harm to surfactant depleted lungs, it is concluded that HFJV at 2 Hz leads to further damage of the lungs, whereas HFJV at 15 Hz improves reparative processes, by keeping the lungs constantly inflated.
High-frequency jet ventilation (HFJV) is used in respiratory distress syndrome (RDS) to avoid high airway pressures and barotrauma. This study was designed to find rational strategies to regulate oxygenation and alveolar ventilation at HFJV and to determine appropriate monitoring methods. Seven dogs were subjected to total lung lavage with saline to induce RDS. PEEP was increased at conventional intermittent positive-pressure ventilation until re-expansion was indicated by a PaO2 of 300 torr at an FIO2 of 1.0 HFJV at 4 and 15 Hz was each tried at 0 and 10 cm H2O PEEP. Intermittent low-frequency inflations were also added to HFJV at 0 PEEP. Lung expansion was maintained without circulatory depression by adjustment of minute ventilation (VE) delivered by the HFJ ventilator; external PEEP was a useful complement. PaCO2 was controlled by frequency adjustment. HFJV at 4 Hz resulted in hypocapnia; intermittent low-frequency inflations had no effect. VE monitoring, CO2 elimination monitoring, and PEEP adjustment was done with a standard ventilator during HFJV. This study illustrates that HFJV is efficient in RDS; VE and external PEEP strongly influence oxygenation and may be used to regulate this factor, and frequency affects CO2 elimination, thus suggesting a method of PaCO2 control.
In the healthy and surfactant-depleted lungs of five pigs the influence of different forms of high frequency ventilation superimposed on conventional mechanical ventilation during the expiratory phase of the ventilatory cycle (SHFVE) on gas exchange and cardiocirculatory parameters was investigated. Subsequently the effects of end-expiratory flushing (EF), i.e. cleaning the large airways and connecting tubes from the ventilator free from end-expiratory CO2, with a volume greater than the dead space of the large airways and connecting tubes was investigated. SHFVE and EF resulted in a significant improvement in CO2 elimination in both healthy and surfactant-depleted lungs. Furthermore, in stiff lungs, at a certain level of oxygenation and CO2 elimination, SHFVE produced the lowest peak and mean airway pressure without any additional depression of cardiocirculatory parameters.
Non-biological descriptors such as jet feeding pressure and oscillator stroke volume are often used to describe HFV. This results in confusion and hinders acceptance of HFV. The goal of this paper is to show how physiological parameters which are valid during HFV can be monitored. Airway pressure measured in narrow tubes with high linear flow rates is underestimated. A relevant airway pressure must be measured well below the tracheal tube. Pressure measured higher up should be validated against peripheral pressure measurements. Minute ventilation and expired CO2 concentration can be determined with a ServoVentilator and a CO2 analyzer arranged at its exit port. Minute ventilation and CO2 elimination can thereby be continuously monitored during high frequency jet ventilation or so-called "combined high frequency jet ventilation" to prevent undetected disturbance of ventilation and perfusion. Physiological dead space can be studied for optimization of ventilatory pattern. The principle of gas analysis at the exit port of the ventilator may be used for FRC determinations with sulfur-hexafluoride.
Before using surfactant preparations in animal experiments or in clinical trials, it is necessary that they fulfil specific in vivo requirements. But conclusive criteria for the effectiveness of a surfactant have not yet been defined. Thus, some standard levels for improvement of lung function, or threshold levels, must be established in standardized animal models with surfactant deficiency. The respiratory distress syndrome model of premature rabbit fetuses is the most sensitive model, followed by the surfactant deficiency model by lung lavage, while the model of viral pneumonia is the least sensitive when testing exogenous surfactant. With a less-effective exogenous surfactat, a small improvement in lung function in the rabbit fetus model and the lung lavage model can be observed, while in the viral pneumonia model almost no improvement occurred. Only a functional effective surfactant fulfilled all our criteria for functional improvement in lung function.
This brief review describes the pathogenesis of the adult respiratory distress syndrome (ARDS) and the rationale for surfactant replacement therapy. In four animal models in which respiratory failure was induced by: 1) lung lavage leading to surfactant depletion; 2) free oxygen radicals; 3) anti-lung serum; or 4) influenza virus, surfactant instillation consistently led to an improvement in gas exchange and lung mechanics. Data from a first clinical trial show that surfactant instillation also improved lung function in a 4 year old patient with severe respiratory failure. It is speculated that surfactant replacement therapy may soon become accepted as a therapeutic measure in ARDS.
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Administration of physiological saline or drugs together with saline into the airways is becoming common clinical practice. However, there are few studies on possible side effects. We have studied the effects of saline, saline plus xanthine oxidase, and saline plus xanthine oxidase plus superoxidase dismutase on lung-thorax compliance and on arterial blood gases in anesthetized, paralyzed guinea pigs, ventilated for 2.5 h. Saline bolus (2-3 ml isotonic saline/kg body weight) into the airways reduced the compliance within 20 min to a mean of 39% of the pretreatment levels, and necessitated as increase in the respirator pressure. Saline plus xanthine oxidase decreased the compliance to 16% of the pretreatment levels. The xanthine oxidase-induced (but not saline-induced) decrease in lung compliance was relieved by superoxide dismutase. According to the present results xanthine oxidase induces a lung injury possible by production of free oxygen radicals. Superoxide dismutase can be valuable in prevention of free oxygen radical-mediated lung damage. Saline alone can be harmful when applied to the airways. This should be considered in clinical trials and in clinical practice.
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