Effects of perfluorohexane vapor in the treatment of experimental lung injury.

RATIONALE: We investigated the effects of vaporized perfluorohexane (PFH) on pulmonary vascular tone, pulmonary vascular resistance and peak inspiratory pressure as well as lipid mediator formation in the treatment of calcium ionophore induced lung injury in a model of the isolated perfused and ventilated rabbit lungs. METHODS: Lung injury was induced in isolated perfused and ventilated rabbit lungs by calcium ionophore A23187. Lungs were treated with either 4.5 vol.% (4.5 vol.% PFH; n = 6) or 18 vol.% (18 vol.% PFH; n = 6) PFH. Six lungs remained untreated (Control). In addition 5 lungs (PFH-sham) remained uninjured receiving 18 vol.% PFH only. Mean pulmonary artery pressure (mPAP), peak inspiratory pressure (P(max)), and lung weight (weight) were monitored for 120 min. Experiments were terminated before when the increase in lung weight exceeded 40 g. Perfusate samples were taken at regular intervals for analysis of TXB(2), 6-keto-PGF(1) and LTB(4). RESULTS: Controls reached the study end point significantly earlier than both PFH groups. Significant differences were found for a weight gain of 10 g and 20 g between the control and the 4.5 vol.% PFH and the 18 vol.% PFH. Differences in mPAP were more pronounced in the 4.5 vol.% PFH. However increases in P(max) were more marked in 4.5 vol.% PFH. TXA(2)-, PGI(2)-, and LTB(4)-levels were significantly lower in PFH groups. Uninjured lungs remained unaffected by the presence of 18 vol.% PFH. CONCLUSION: Inflammatory lung injury was attenuated by the treatment with 4.5 vol.% PFH and 18 vol.% PFH vapor in the isolated perfused rabbit lung. Therapeutic effects were more pronounced with a concentration of 4.5 vol.% PFH.

Pilot study of vaporization of perfluorohexane during high-frequency oscillatory ventilation in experimental acute lung injury.

Inhalation of perfluorohexane vapor (PFH) and high-frequency oscillatory ventilation (HFOV) both have been shown to improve lung function in acute lung injury (ALI). Their combination implies synergistic action. The authors investigated technical aspects of PFH vaporization during HFOV and effects on gas exchange in a pilot study of experimental ALI. Eighteen anesthetized sheep were randomly assigned to HFOV or HFOV with PFH inhalation after oleic acid-induced ALI. HFOV was set to a continuous distending pressure of 25 cm H2O, and an oscillation of 80 to 100 cm H2O at a frequency of 5 Hz. PFH vapor was delivered by means of bypassed high-flow oxygen through a thin endotracheal tube. PFH concentration was measured by infrared absorption. Blood gases and hemodynamic data were taken. PaO2 significantly increased from 9.1 ± 0.9 to 32.7 ± 9.5 kPa (mean ± SEM) in the HFOV group and from 12.5 ± 1.1 to 27.0 ± 6.8 kPa in the HFOV PFH group. PaCO2 significantly decreased from 6.3 ± 0.3 to 5.5 ± 0.5 kPa in the HFOV group and from 5.7 ± 0.4 to 4.9 ± 0.5 kPa in the HFOV PFH group. Changes in gas exchange were not different between groups. These results show that the inhalation of PFH during HFOV is technically feasible, but did not enhance gas exchange in a 210-minute observation period of experimental ALI.

Pretreatment with perfluorohexane vapor attenuates fMLP-induced lung injury in isolated perfused rabbit lungs.

The authors investigated the protective effects and dose dependency of perfluorohexane (PFH) vapor on leukocyte-mediated lung injury in isolated, perfused, and ventilated rabbit lungs. Lungs received either 18 vol.% (n = 7), 9 vol.% (n = 7), or 4.5 vol.% (n = 7) PFH. Fifteen minutes after beginning of PFH application, lung injury was induced with formyl-Met-Leu-Phe (fMLP). Control lungs (n = 7) received fMLP only. In addition 5 lungs (PFH-sham) remained uninjured receiving 18 vol.% PFH only. Pulmonary artery pressure (mPAP), peak inspiratory pressure (P(max)), and lung weight were monitored for 90 minutes. Perfusate samples were taken at regular intervals for analysis and representative lungs were fixed for histological analysis. In the control, fMLP application led to a significant increase of mPAP, P(max), lung weight, and lipid mediators. Pretreatment with PFH attenuated the rise in these parameters. This was accompanied by preservation of the structural integrity of the alveolar architecture and air-blood barrier. In uninjured lungs, mPAP, P(max), lung weight, and lipid mediator formation remained uneffected in the presence of PFH. The authors concluded that pretreatment with PFH vapor leads to an attenuation of leukocyte-mediated lung injury. Vaporization of perfluorocarbons (PFCs) offers new therapeutic options, making use of their protective and anti-inflammatory properties in prophylaxis or in early treatment of acute lung injury.

[Standard operating procedures and operating room management: Improvement of patient safety and the efficiency of processes]. / Standard operating procedures und OP-Management zur Steigerung der Patientensicherheit und der Effizienz von Prozessabläufen.

Financial pressures have led the way more efficiency in health care management. To decrease hospital costs a more proficient use of personal resources is required. The drive to increase efficiency with the concomitant increase in workload can cause a reduction in quality of patient care and of patient security. A professional operating room (OR) management and the introduction of standard operating procedures (SOP) have helped to optimise workflow in and around the OR. OR management can control an efficient workflow and generate data concerning performance, costs and quality. SOPs lead to a standardisation of workflow in the OR and in patient treatment modalities. This guaranties a high quality in patient care and more safety despite an increase in work-load.

Perfluorohexane vapor has only minor effects on spatial pulmonary blood flow distribution in isolated rabbit lungs.

We tested the hypothesis that administration of perfluorohexane (PFH) vapor does not significantly affect the relative pulmonary blood flow (Qrel) distribution in isolated rabbit lungs. Fourteen isolated rabbit lungs were perfused with a Krebs-Henseleit buffer solution (flow 150 mL/min). Pulmonary afterload was set to 3 mm Hg. The lungs were ventilated with 4% CO(2) in room air using a small animal ventilator (respiratory rate, 30 breaths/min; tidal volume, 12 mL/kg body weight; positive end-expiratory pressure, 2 cm H(2)O). After a steady-state period, 18 vol. % of PFH vapor was administered to 9 lungs for 30 min. In a second set of experiments five lungs served as controls. Change in (Qrel) distribution was assessed using fluorescent-labeled microspheres. The unpaired Student's t-test was used to compare variables between groups. The paired Student's t-test, the one-sample Student's t-test, the Anderson-Hauck test of equivalence, and Pearson correlation were used to analyze changes within groups. The mean correlation coefficients of (Qrel) were 0.564 +/- 0.182 for the PFH group and 0.502 +/- 0.295 for the control group, respectively. No significant changes in (rel) distribution over time and between groups were found. However, in the PFH group a tendency towards redistribution of (Qrel) to more ventral lung areas was noted. Our results suggest that PFH vapor has no significant effects on redistribution of (Qrel) in isolated rabbit lungs.

Changes in pulmonary function and oxygenation during application of perfluorocarbon vapor in healthy and oleic acid-injured animals.

OBJECTIVES: To investigate the changes in pulmonary function and gas exchange during application of 18% perfluorohexane vapor in healthy and in oleic acid-injured animals and compare it with an injured control group. DESIGN: Prospective randomized controlled study. SETTING: Experimental research laboratory at a university medical center. SUBJECTS: Nineteen sheep weighing 31.4 +/- 4.1 kg. INTERVENTIONS: Lung injury was induced in 14 sheep by the intravenous injection of 0.1 mL/kg oleic acid. After establishment of lung injury (PaO(2)/F(IO(2)) ratio, <200; pulmonary artery occlusion pressure, <19 torr), seven animals were treated with 18% perfluorohexane vapor for 30 mins whereas seven animals served as controls. After the start of perfluorohexane treatment, blood gases and respiratory and hemodynamic data were collected in 10-min intervals throughout the study period of 1 hr. In addition, five healthy animals received perfluorohexane vapor for 30 mins and were followed up for 2 hrs to exclude delayed negative effects. MEASUREMENTS AND MAIN RESULTS: Treatment of healthy animals with 18% perfluorohexane vapor was not accompanied by any significant adverse effects. It was associated with a significant decrease of alveolar-arterial oxygen difference during perfluorohexane application (p <.05). In injured animals, 18% perfluorohexane led to a sustained improvement of peak inspiratory pressures within 10 mins of treatment (p <.001). The concomitant increase in compliance was equally significant (p <.001). Significant improvements in PaO(2) occurred despite a decrease in F(IO(2)) to 0.81 at the end of vaporization. CONCLUSION: Healthy animals tolerated perfluorohexane vapor well without significant changes in oxygenation and mechanical lung function for 2 hrs. In injured animals, application of perfluorohexane vapor primarily improved peak inspiratory pressure and compliance. The increase of oxygenation therefore could be secondary to an improvement in compliance.

Effects of perfluorohexane vapor on relative blood flow distribution in an animal model of surfactant-depleted lung injury.

OBJECTIVE: To test the hypothesis that treatment with vaporized perfluorocarbon affects the relative pulmonary blood flow distribution in an animal model of surfactant-depleted acute lung injury. DESIGN: Prospective, randomized, controlled trial. SETTING: A university research laboratory. SUBJECTS: Fourteen New Zealand White rabbits (weighing 3.0-4.5 kg). INTERVENTIONS: The animals were ventilated with an FIO(2) of 1.0 before induction of acute lung injury. Acute lung injury was induced by repeated saline lung lavages. Eight rabbits were randomized to 60 mins of treatment with an inspiratory perfluorohexane vapor concentration of 0.2 in oxygen. To compensate for the reduced FIO(2) during perfluorohexane treatment, FIO(2) was reduced to 0.8 in control animals. Change in relative pulmonary blood flow distribution was assessed by using fluorescent-labeled microspheres. MEASUREMENTS AND MAIN RESULTS: Microsphere data showed a redistribution of relative pulmonary blood flow attributable to depletion of surfactant. Relative pulmonary blood flow shifted from areas that were initially high-flow to areas that were initially low-flow. During the study period, relative pulmonary blood flow of high-flow areas decreased further in the control group, whereas it increased in the treatment group. This difference was statistically significant between the groups (p =.02) as well as in the treatment group compared with the initial injury (p =.03). Shunt increased in both groups over time (control group, 30% +/- 10% to 63% +/- 20%; treatment group, 37% +/- 20% to 49% +/- 23%), but the changes compared with injury were significantly less in the treatment group (p =.03). CONCLUSION: Short treatment with perfluorohexane vapor partially reversed the shift of relative pulmonary blood flow from high-flow to low-flow areas attributable to surfactant depletion.