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Background: This study was undertaken to investigate the effect of a small dose of perfluorocarbon on the recruitment pressure needed to open atelectatic lung areas., Methods: In 12 Yorkshire pigs (body weight, 9 kg), lung injury was induced by whole lung lavage. After 1 h of conventional ventilation, an open lung maneuver was performed to obtain PaO2 values equal to the pre-lavage PaO2 values (+/-10%). After 1 h of ventilation at the lowest possible airway pressure that stabilized the recruited lung volume, the animals were disconnected from the ventilator to allow the lung to collapse. Six animals received a 5 ml/kg intratracheal dose of perfluorocarbon and a second open lung maneuver was performed. Six animals served as controls and received no perfluorocarbon but also underwent a second open lung maneuver., Results: In both groups, an open lung maneuver resulted in a significant increase in oxygenation. The peak pressures needed to open the lung after 1 h of mechanical ventilation in the perfluorocarbon and control groups were 43.8 +/- 8.4 cmH2O and 46.6 +/- 4 cmH2O, respectively. The addition of perfluorocarbon significantly reduced the opening pressure to 34.5 +/- 6.3 cmH2O (P < 0.01), whereas the opening pressure in the control group, 45.0 +/- 0.2 cmH2O, did not change., Conclusion: The instillation of a small amount of perfluorocarbon significantly reduces the opening pressures needed to recruit atelectatic lung areas.

Severe pulmonary oxygenation impairment resulting from peripheral lung atelectasis occurred in some patients with pleurotomy during the harvest of the internal mammary artery graft followed by coronary artery bypass grafting (CABG). We studied the efficacy of intraoperative positive end-expiratory airway pressure (PEEP) therapy for the prevention of postoperative pulmonary oxygenation impairment. A total of 66 patients with solitary CABG procedure were included in this study. The pleural cavity was intraoperatively opened in 44 patients and not opened in 22. PEEP therapy was not used in any patient before May 1996 (referred to herein as the former period) and was used more recently in eight patients with pleurotopmy (referred to herein as the latter period). PEEP was initiated immediately after pleurotomy during the harvest of the internal mammary artery graft. Without PEEP therapy, values of PaO2, A-aDO2, and respiratory index (RI) were worse in patients with pleurotomy than in those without pleurotomy. Meanwhile, there were no major differences in these values between patients with or without pleurotomy after the induction of PEEP therapy. Respiratory insufficiency (A-aDO2 > 400 mmHg and RI > 1.5) was detected in six patients with pleurotomy in the former period. Three of these six patients required over 1 week of long-term mechanical respiratory support. No respiratory insufficiency occurred in patients of the latter period. In conclusion, PEEP therapy, which is initiated just after pleurotomy, may prevent oxygen impairment and pulmonary atelectasis after extracorporeal circulation (ECC) and is recommended for patients with pleurotomy, especially for patients with preoperative low respiratory function.

Pulmonary atelectasis, as found during general anaesthesia, may be reexpanded by hyper-inflation of the lungs. The purpose of this study was to determine whether such a recruitment is maintained and whether this is accompanied by an improved gas exchange. We studied a consecutive sample of twelve lung healthy adults, scheduled for elective surgery. After induction of intravenous anaesthesia, the lungs were hyperinflated manually. The ventilationperfusion relationship (VA/Q) was estimated with the multiple inert gas method, and in six patients atelectasis was assessed by computed x-ray tomography. The mean pulmonary shunt was 7.5% of cardiac output after induction of anaesthesia and this decreased to 1.0% and 2.8% at 20 and 40 min after the recruitment manoeuvre. Perfusion of poorly ventilated lung regions (low VA/Q), however, increased from 3.7% to 10.6% and 7.8% at 20 and 40 min after the recruitment, respectively. The mean alveolar-arterial oxygen tension difference (PA-aO2) was 14.3 kPa after induction of anaesthesia and 11.1 kPa immediately after recruitment. Forty minutes later PA-aO2 was still 2.0 kPa lower than after induction of anaesthesia (95% confidence interval [CI] 0.3 to 3.8 kPa). PA-aO2 decreased more in obese patients. The mean area of atelectasis decreased from 9.0 cm2 after induction of anaesthesia to 0.1 cm2 immediately after recruitment, and there was a slow increase to 1.9 cm2 (95% CI 0.0 to 3.9 cm2) 40 min later. During general anaesthesia in lung healthy patients, most of the reexpanded atelectatic lung tissue remains inflated for at least 40 min. The recruitment manoeuvre decreases pulmonary shunt, but increases low VA/Q. The net effect on gas exchange is a small reduction of PA-aO2.

Acute ipsilateral pulmonary oedema is a well documented complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion and atelectasis. We present a case of bilateral re-expansion pulmonary oedema following removal of an intrathoracic haematoma. High protein concentration of the oedema fluid suggests increased pulmonary vascular permeability as a cause of this pulmonary oedema.

A frequent dilemma facing the anaesthetist is the child with respiratory tract symptoms. The risks of anaesthesia and surgery in these patients have not been clearly established. We present three cases which illustrate a potentially serious complication which may arise. Our patients each had symptoms of cough, but were systemically healthy. Two of the children had absent clinical signs, whilst the third had a normal chest X ray. However, during surgery and anaesthesia each child developed significant pulmonary collapse, associated with desaturation on oximetry.

We developed a technique for blind bronchial suction using a curved-tip catheter with a guide mark, for the treatment of atelectasis of the lower and middle lobes of the lung. Suction of the upper lobe bronchi could not be performed because of the combination of the peculiar anatomy of the upper lobe bronchi with catheter design. We treated successfully two cases of atelectasis of the right upper lobes using a Rusch Metras bronchography catheter with a guide mark which is not readily available. Therefore we devised a J-shape tipped catheter with a guide mark. We have successfully treated 13 episodes of atelectasis of the right upper lobe in 10 patients and one episode in the left upper lobe in one patient with this new catheter.

Three cases are described of complete collapse of a lung in the absence of bronchial obstruction. The condition was treated by the application of a sustained high pressure (6 kPa) to the affected lung through one limb of a double lumen bronchial tube whilst intermittent positive pressure ventilation was continued through the other limb.

A technique of selective intubation is described for infants who have recurrent or persistent atelectasis. The technique is safe and straightforward.