No abstract

Using adult guinea-pigs, we have developed an experimental model in which alveolar surfactant phospholipids are removed by repeated lung lavage in vivo, and in which the short-term survival of the animals is ensured by artificial ventilation. Blood gases, parameters of lung mechanics, and histologic and electron microscopic findings indicate that the lavage procedure induces a condition similar to the adult respiratory distress syndrome. We propose that our technique might be used for evaluation of pharmacological agents and various forms of artificial ventilation which have been suggested for treatment of this disease.

Based on a literature search, an overview is presented of the pathophysiology of venous and arterial gas embolism in the experimental and clinical environment, as well as the relevance and aims of diagnostics and treatment of gas embolism. The review starts with a few historical observations and then addresses venous air embolism by discussing pulmonary vascular filtration, entrapment, and the clinical occurrence of venous air emboli. The section on arterial gas embolism deals with the main mechanisms involved, coronary and cerebral air embolism (CAE), and the effects of bubbles on the blood-brain barrier. The diagnosis of CAE uses various techniques including ultrasound, perioperative monitoring, computed tomography, brain magnetic resonance imaging and other modalities. The section on therapy starts by addressing the primary treatment goals and the roles of adequate oxygenation and ventilation. Then the rationale for hyperbaric oxygen as a therapy for CAE based on its physiological mode of action is discussed, as well as some aspects of adjuvant drug therapy. A few animal studies are presented, which emphasize the importance of the timing of therapy, and the outcome of patients with air embolism (including clinical patients, divers and submariners) is described.

Frequency of atelectasis was much less following the alveolar recruitment strategy, compared with children who did not have the maneuver performed. The mere application of 5 cm H2O of CPAP without a prior recruitment did not show the same treatment effect and showed no difference compared to the control group without PEEP.

The analgesic efficacy and safety of tramadol and morphine were compared in a double-blind, randomized study of 150 female patients after gynecologic surgery. As required, patients could receive up to three intravenous doses of either 50 mg of tramadol or 5 mg of morphine within a period of 6 h. Pain intensity (verbal response score) was recorded before injection and at 0.5, 1, 2, 3, 5, and 6 h after the initial dose; at these times, pain relief was also assessed. Oxygen saturation was monitored continuously by pulse oximetry for at least 30 min after each injection. In 13.3% of the morphine group (but in none of the tramadol group) transcutaneous pulse oxygen saturation decreased to less than 86%; in 50% of these patients the decrease occurred after only the first 5 mg of morphine. Both drugs produced acceptable analgesia, and there were no clinically significant adverse events. In demonstrating the absence of clinically relevant respiratory depression with tramadol, we underline its safety for postoperative pain relief.

This review summarizes the state-of-the-art in electrical impedance tomography (EIT) for ventilation and perfusion imaging. EIT is a relatively new technology used to image regional impedance distributions in a cross-sectional area of the body. After the introduction, a brief overview of the recent history is provided followed by a review of the literature on regional ventilation monitoring using EIT. Several recently presented indices that are useful to extract information from EIT image streams are described. Selected experimental and clinical findings are discussed with respect to future routine applications in intensive care. Finally, past and ongoing research activities aimed at obtaining cardiac output and regional perfusion information from EIT image streams are summarized.

Ventilation strategies which are known to induce ventilation-induced lung injury (VILI) disturb the compartmentalization of the early cytokines response in the lung and systemically. Furthermore, the loss of compartmentalization is a two-way disturbance, with cytokines shifting from the vascular side to the alveolar side and vice versa. A ventilation strategy (PEEP level of 10 cmH2O) which prevents VILI significantly diminished this shift in cytokines.

No abstract