Influence of Gas Composition on Recurrence of Atelectasis after a Reexpansion Maneuver during General Anesthesia

Background: Atelectasis, an important cause of impaired gas exchange during general anesthesia, may be eliminated by a vital capacity maneuver. However, it is not clear whether such a maneuver will have a sustained effect. The aim of this study was to determine the impact of gas composition on reappearance of atelectasis and impairment of gas exchange after a vital capacity maneuver.

Methods: A consecutive sample of 12 adults with healthy lungs who were scheduled for elective surgery were studied. Thirty minutes after induction of anesthesia with fentanyl and propofol, the lungs were hyperinflated manually up to an airway pressure of 40 cmH2 O. FI sub O2 was either kept at 0.4 (group 1, n = 6) or changed to 1.0 (group 2, n = 6) during the recruitment maneuver. Atelectasis was assessed by computed tomography. The amount of dense areas was measured at end-expiration in a transverse plane at the base of the lungs. The ventilation-perfusion distributions (V with dot A/Q with dot) were estimated with the multiple inert gas elimination technique. The static compliance of the total respiratory system (Crs) was measured with the flow interruption technique.

Results: In group 1 (FIO2 = 0.4), the recruitment maneuver virtually eliminated atelectasis for at least 40 min, reduced shunt (V with dot A/Q with dot < 0.005), and increased at the same time the relative perfusion to poorly ventilated lung units (0.005 < V with dot A/Q with dot < 0.1; mean values are given). The arterial oxygen tension (PaO2) increased from 137 mmHg (18.3 kPa) to 163 mmHg (21.7 kPa; before and 40 min after recruitment, respectively; P = 0.028). In contrast to these findings, atelectasis recurred within 5 min after recruitment in group 2 (FIO2 = 1.0). Comparing the values before and 40 min after recruitment, all parameters of V with dot A/Q with dot were unchanged. In both groups, Crs increased from 57.1/55.0 ml *symbol* cmH2 O sup -1 (group 1/group 2) before to 70.1/67.4 ml *symbol* cmH2 O sup -1 after the recruitment maneuver. Crs showed as low decrease thereafter (40 min after recruitment: 61.4/60.0 ml *symbol* cmH2 O sup -1), with no difference between the two groups.     

Extended NO analysis in health and disease

Extended NO analysis is a promising tool in different diseases where NO metabolism is altered. One single exhalation cannot give insight to the NO production in the respiratory system; rather the use of multiple exhalation flows can give the alveolar levels (C(A)NO), airway wall concentration (C(aw)NO) and the diffusion rate of NO (D(aw)NO). Increased values of C(A)NO are shown in COPD, systemic sclerosis, hepatopulmonary syndrome and in severe asthma. In asthma the C(aw)NO and D(aw)NO are increased leading to an increase in bronchial NO flux (J'(aw)NO). Low levels of J'(aw)NO are seen in cystic fibrosis, primary ciliary dyskinesia and in smoking subjects. More studies are needed to evaluate the clinical usefulness of the extended NO analysis, similar to what has been done in systemic sclerosis where a cut-off value has been identified predicting pulmonary function deterioration.     

Elemental composition of airway surface liquid in the pig determined by x-ray microanalysis

The ionic composition of the airway surface liquid (ASL) is of importance in cystic fibrosis and exercise-induced asthma. However, literature data on the composition of the ASL vary markedly. The aim of the study was to determine the composition of the ASL, using two different methods involving minimal manipulation. In one method, the composition of the ASL was measured by X-ray microanalysis of frozen-hydrated samples. In the second method, small dextran beads were equilibrated with the ASL in a moisture chamber, isolated, dried, and analyzed. Plasma or serum from the same pigs was also analyzed. Both methods showed that the Na and Cl concentrations in the ASL are close to the concentrations of these ions in plasma. X-ray microanalysis of frozen-hydrated ASL showed significantly higher K, P, and S because here the upper layer (containing cell debris and secreted mucus) is sampled, whereas the bead method samples the watery component of the ASL. Ultrastructural analysis of the epithelium at various osmotic values showed evident damage at concentrations of 50 mM or less. These data support the notion that the physiologically important watery component of the pig ASL has an ionic composition close to that of plasma.     

Guidance for a personal target value of FeNO in allergic asthma: Case report and theoretical example

Abstract

In clinically stable asthma the exhaled NO values (F_ENO) are generally higher than in control subjects. Therefore, reference values are of limited importance in clinical practice. This is demonstrated in this case report, but it is also shown that NO parameters from non-linear modelling do have a clinical value. A subject with asthma was treated with inhaled corticosteroids for 1 week. The non-linear NO model was used to measure the response to treatment. The NO parameters from subjects with atopic rhinitis and asthma were fed into a computer program to generate theoretical F_ENO_0.05 values, i.e. target values. There was a dramatic decrease in F_ENO_0.05 due to treatment, from 82 to 34 ppb, but it remained higher than in healthy controls. This is due to the elevated diffusion rate of NO, unchanged by treatment. When the NO parameters are known, a personal best value of F_ENO_0.05 (fractional concentration of exhaled NO in the gas phase, 0.05 L/s) can be calculated, which can be the target value when only F_ENO_0.05 can be monitored. In conclusion, reference values for NO parameters are shown to be clinically useful. It is essential that every patient receives his/her target value of F_ENO_0.05, when only a single NO measurement is available. In our opinion, this is the reason why there are few successful studies of trying to target the NO value with inhaled corticosteroids.     

Side effects of endotracheal suction in pressure- and volume-controlled ventilation

STUDY OBJECTIVES: To investigate the effects of endotracheal suction in volume-controlled ventilation (VCV) and pressure-controlled ventilation (PCV) with an open suction system (OSS) or a closed suction system (CSS). DESIGN: Randomized comparison. SETTING: Animal research laboratory. PATIENTS: Twelve healthy anesthetized pigs. INTERVENTIONS: The effects of endotracheal suction during VCV and PCV with tidal volume (VT) of 14 mL/kg were compared. A 60-mm inner-diameter endotracheal tube was used. Ten-second suction was performed using OSS and CSS with 12F and 14F catheters connected to - 14 kPa vacuum. MEASUREMENTS AND RESULTS: Thirty minutes after suction in PCV, VT was still decreased by 27% (p < 0.001), compliance (Crs) by 28% (p < 0.001), and PaO(2) by 26% (p < 0.001); PaCO(2) was increased by 42% (p < 0.0001) and venous admixture by 158% (p = 0.003). Suction in VCV affected only Crs (decreased by 23%, p < 0.001) and plateau pressure (increased by 24%, p < 0.001). The initial impairment of gas exchange following suction in VCV was no longer statistically significant after 30 min. CONCLUSIONS: In conclusion, endotracheal suction causes lung collapse leading to impaired gas exchange, an effect that is more severe and persistent in PCV than in VCV.     

Extended NO analysis in a healthy subgroup of a random sample from a Swedish population

INTRODUCTION: There is an interest in modelling exhaled nitric oxide (NO). Studies have shown that flow-independent NO parameters i.e. NO of the alveolar region (C(A)NO), airway wall (C(aw)NO), diffusing capacity (D(aw)NO) and flux (J(aw)NO), are altered in several disease states such as asthma, cystic fibrosis, alveolitis and chronic obsmuctive pulmonary disease (COPD). However, values from a healthy population are missing. OBJECTIVES: To calculate NO parameters in a healthy population by collecting NO values at different exhalation flow rates. METHODS: A random sample from the ECRHS II study was investigated. Among the 281 subjects that had performed a bronchial hyperreactivity (BHR)-test, FEV(1.0), IgE and NO-analyses 89 were found to be healthy. RESULTS: There were no differences in F(E)NO(0.05) or NO parameters between men and women. There were weak correlations between height and both F(E)NO(0.05) (r = 0.23, P = 0.03) and C(aw)NO (r = 0.22, P = 0.04). There was also a correlation between age and C(A)NO (r = 0.28, P = 0.007). When controlled for gender, this correlation was more powerful in women (r = 0.51, P = 0.001) but did not remain for male subjects. CONCLUSION: Extended NO analysis is a simple non-invasive tool that gives by far more information than F(E)NO(0.05). Based on our results, we suggest that the values for healthy subjects should be considered to fall between the following ranges: F(E)NO(0.05), 10-30 ppb; C(aw)NO, 50-250 ppb; D(aw)NO, 5-15 ml s(-1); J(aw)NO, 0.8-1.6 nl s(-1); and C(A)NO, 0-4 ppb. Values outside these intervals indicate the need for further investigation to exclude a state of disease.     

How anaesthesiologists understand difficult airway guidelines—an interview study

Background: In the practice of anaesthesia, clinical guidelines that aim to improve the safety of airway procedures have been developed. The aim of this study was to explore how anaesthesiologists understand or conceive of difficult airway management algorithms.

Methods: A qualitative phenomenographic design was chosen to explore anaesthesiologists’ views on airway algorithms. Anaesthesiologists working in three hospitals were included. Individual face-to-face interviews were conducted.

Results: Four different ways of understanding were identified, describing airway algorithms as: (A) a law-like rule for how to act in difficult airway situations; (B) a cognitive aid, an action plan for difficult airway situations; (C) a basis for developing flexible, personal action plans for the difficult airway; and (D) the experts’ consensus, a set of scientifically based guidelines for handling the difficult airway.

Conclusions: The interviewed anaesthesiologists understood difficult airway management guidelines/algorithms very differently.     

Ceramide potentiates, but sphingomyelin inhibits, vitamin D-induced keratinocyte differentiation: comparison between keratinocytes and HL-60 cells

Abstract Differentiation of epidermal keratinocytes and leukemia HL-60 cells induced by 1,25-dihydroxyvitamin D [1,25(OH)₂D] has been reported to be mediated, at least in part, by increases in cellular ceramide levels. Ceramides produced by 1,25(OH)₂D-induced sphingomyelin (SM) hydrolysis also contribute to the permeability barrier lipids in keratinocytes. Exogenously supplied SM is taken up by mammalian cells, including keratinocytes, and is incorporated into cellular pools. However, the effects of exogenously added SM on keratinocyte differentiation have not been studied. Therefore, in this study, we compared exogenously added SM with a cell-permeable ceramide for their ability to stimulate keratinocyte differentiation induced by 1,25(OH)₂D. Both short-chain ceramide (C2-cer) and SM stimulated the differentiation and inhibited the proliferation of HL-60 cells. As expected, this effect was potentiated by 1,25(OH)₂D. However, SM inhibited the differentiation and stimulated the proliferation of keratinocytes. While C2-cer potentiated the effects of 1,25(OH)₂D, SM reversed the effects of 1,25(OH)₂D on keratinocytes. The ratio of SM to ceramide was significantly different between keratinocytes and HL-60 cells. While the SM level of HL-60 cells were twice that of keratinocytes, keratinocytes contained ten times more ceramides than HL-60 cells, resulting in a ceramide/SM ratio 17 times higher in keratinocytes. Thus, we identified similarities and significant differences in the sphingolipid-mediated cell signaling pathway between keratinocytes and HL-60 cells. While SM stimulated HL-60 cell differentiation, presumably by incorporation into SMase-accessible membrane pools, it inhibited keratinocyte differentiation. In keratinocytes, SM was possibly incorporated into a different cellular pool (barrier lipid pool) or altered membrane phospholipid metabolism and membrane fluidity. Received: 12 August 1998 / Received after revision: 5 November 1998 / Accepted: 6 November 1998