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A 32-year-old woman, in the 22nd week of pregnancy, underwent emergency coronary artery bypass grafting to the left anterior descending artery (LAD). She had suffered an acute myocardial infarction 10 days previously, and continued to suffer from intractable angina pectoris afterwards. Cardiac catheterization revealed spontaneous dissection of the LAD. The left internal mammary artery was used to bypass the LAD, and the operation was performed on a beating heart without the use of cardiopulmonary bypass. The patient's recovery was uneventful, and ultrasound examination and pulse monitoring of the fetus were both normal. She subsequently gave birth to a healthy term baby. To our knowledge this is the second report of coronary artery bypass surgery performed successfully in a pregnant woman. We believe the unique surgical approach avoided the risk of cardiopulmonary bypass to the fetus and placenta.

The authors studied the effect of changes in arterial carbon dioxide tension on plasma lidocaine concentrations during a constant lidocaine infusion in eight healthy volunteers. With a PaCO2 of 41.4 +/- 0.9 mmHg (mean +/- SE), total plasma lidocaine concentrations were 3.97 +/- 0.20 microgram X ml-1. There was no significant change associated with hypercarbia (PaCO2 = 55.7 +/- 1.5 mmHg, lidocaine = 3.93 +/- 0.18 microgram X ml-1) or hypocarbia (PaCO2 = 19.5 +/- 1.4 mmHg, lidocaine = 4.29 +/- 0.25 microgram X ml-1), despite the known effects of changes in CO2 tension on hepatic blood flow and lidocaine protein binding. During hypercarbia, plasma lidocaine binding decreases while total plasma lidocaine remains essentially constant; therefore, increased CO2 tensions could cause toxicity if total lidocaine concentrations were in the high therapeutic range (5 micrograms X ml-1). Four subjects experienced transient symptoms of mild lidocaine toxicity during acute increases in carbon dioxide tension.

The authors determined the accuracy of the Ohmeda 3700 (version J) pulse oximeter in healthy volunteers rendered hypoxic (SaO2 from 60-98%) by breathing mixtures of O2 in N2. When equipped with an ear probe, the pulse oximeter reading (y) reliably predicted arterial saturation (x) under steady-state conditions (y = 1.05x - 4.66, r = 0.98) as well as when oxygen saturation was rapidly decreasing (y = 1.05x - 6.38, r = 0.96). Conversely, when equipped with a finger probe, the oximeter tended to significantly underestimate steady-state arterial saturation (y = 1.21x - 19.1, r = 0.98, P less than 0.001). In response to this information, the manufacturer modified the oximeter's software (version XJ1), resulting in improved agreement between oximeter readings and arterial values (y = 0.96x + 4.59, r = 0.99). Despite the close correlation between steady-state oximeter readings and arterial saturation, the 99% prediction limits for both the ear and finger probes (version XJ1) were +/- 8%. Finger probe readings did not reliably reflect radial arterial oxygenation during rapid desaturation (y = 0.55x + 45.2, r = 0.78). This may be related to the time required to "arterialize" the blood in the finger; during acute resaturation, we found that the ear- to finger-probe delay was 24.0 +/- 2.3 s (means +/- SE, P less than 0.001).