A B S T R A C TWith advances in mechanical circulation, venoarterial extracorporeal membrane oxygenation has become an established technique to provide cardiopulmonary support for patients with cardiovascular collapse. This article reviews the physiological principles of such extracorporeal technique and its interaction with the native heart. Practical aspects including equipment, patient selection, and common complications with their prevention and specific management are summarised. The strategy for weaning from venoarterial extracorporeal membrane oxygenation is also discussed.

Extracorporeal membrane oxygenation has been used clinically for more than 40 years. The technique provides respiratory and/or circulatory support via venovenous and veno-arterial configurations, respectively. We review the basic physiological principles of extracorporeal membrane oxygenation systems in venovenous extracorporeal membrane oxygenation. Clinical aspects including patient selection, equipment, setup, and specific patient management are outlined. Pros and cons of the use of extracorporeal membrane oxygenation in respiratory failure are discussed.

Simultaneous 22-h measurements of intra-oesophageal and intragastric pH were made in 22 patients with symptoms of gastro-oesophageal reflux (7 with peptic oesophagitis, 8 with peptic oesophageal stricture, and 7 with peptic oesophagitis and previous partial gastrectomy) to determine whether alkaline intra-oesophageal pH is a consequence of alkaline gastro-oesophageal reflux. In the three groups of patients intra-oesophageal pH was greater than 7 for 16.9 +/- 4.8%, 27.5 +/- 7.6%, and 21.0 +/- 7.7%, respectively, of total recording time (p = NS). Intragastric pH greater than 7 was recorded only in the patients with partial gastrectomy (10.3 +/- 5.3% of recording time; p less than 0.01 in comparison with the other groups). Elevations of intra-oesophageal pH to greater than 7 never occurred during episodes of alkalinization of intragastric pH. These results suggest that refluxed fluids are unlikely to be the cause of alkaline intra-oesophageal pH in patients with peptic oesophagitis.

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