Formation of atelectasis is one mechanism of impaired gas exchange during general anaesthesia. We have studied manoeuvres to re-expand such atelectasis in 16 consecutive, anaesthetized adults with healthy lungs. In group 1 (10 patients), the lungs were inflated stepwise to an airway pressure (Paw) of 10, 20, 30 and 40 cm H2O. In group 2 (six patients), three repeated inflations up to Paw = 30 cm H2O were followed by one inflation to 40 cm H2O. Atelectasis was assessed by analysis of computed x-ray tomography (CT). In group 1 the mean area of atelectasis in the CT scan at the level of the right diaphragm was 6.4 cm2 at Paw = 0 cm H2O, 5.9 cm2 at 20 cm H2O, 3.5 cm2 at 30 cm H2O and 0.8 cm2 at 40 cm H2O. A Paw of 20 cm H2O corresponds approximately to inflation with twice the tidal volume. In group 2 the mean area of atelectasis was 9.0 cm2 at Paw = 0 cm H2O and 4.2 cm2 after the first inflation to 30 cm H2O. Repeated inflations did not add to re-expansion of atelectasis. The final inflation (Paw = 40 cm H2O) virtually eliminated the atelectasis. We conclude that, after induction of anaesthesia, the amount of atelectasis was not reduced by inflation of the lungs with a conventional tidal volume or with a double tidal volume ("sigg"). An inflation to vital capacity (Paw = 40 cm H2O), however, re-expanded virtually all atelectatic lung tissue.
The aim of the study was to investigate the distribution of lactate in plasma, whole blood, erythrocytes, and capillary finger blood, before and during submaximal exercise. Ten healthy male subjects performed submaximal graded cycle ergometer exercise for 20-25 min. Venous blood samples and capillary finger blood samples were taken before exercise and every 5th min during exercise for lactate determination. The plasma lactate concentration was significantly higher (P less than 0.001, approximately 50%) than in the erythrocytes. This difference was not altered by the venous blood lactate concentration or exercise intensity. A significant difference (P less than 0.01) in lactate concentration was also found between capillary whole blood and venous whole blood. It was concluded that direct comparisons between lactate in capillary finger blood, venous whole blood and plasma could not be made.
More than any other chronic respiratory disease, asthma is characterized by functional and clinical variability: expiratory flow obstruction, dyspnoea and wheezing may be absent, mild, or severe. Moreover, pulmonary gas exchange often does not closely relate to measured airway obstruction. Accordingly, the correlation between arterial oxygen tension and airflow (Pa,O 2 ) rate indices of obstruction is poor, both in a single patient over time, and within groups of clinically similar patients. Here, these concepts are extended by examining relationships between airflow obstruction and gas exchange across the clinical spectrum of asthma (from asymptomatic to acute severe).Six individual studies encompassing 86 patients are analysed together, focusing on: 1) airways obstruction; 2) arterial blood gas data; and 3) the distribution of alveolar ventilation/perfusion (V'A/Q') ratios, measured by the multiple inert gas elimination technique.V'A/Q' mismatching was greater than normal even when forced expiratory volume in one second (FEV1) was normal, but with increasing severity of airways obstruction there was essentially no further deterioration in gas exchange until FEV1 reached about 40% of predicted normal values. Then, with little further airways obstruction, gas exchange rapidly worsened, Pa,O 2 falling to about 50 torr.This study emphasizes that what has been observed in individual patients and within clinically similar patient groups can be extended across the spectrum of asthma severity: airways obstruction and gas exchange are poorly correlated. Furthermore, these results suggest that spirometric data alone may not adequately define remission, nor clearly identify those patients liable to serious gas exchange deterioration.
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