Effects of maternal hyperoxia with and without normocapnia in uteroplacental and fetal Doppler studies.

OBJECTIVE: One hundred percent oxygen is given in pregnancy to improve fetal oxygenation, yet has been shown in both animal and human studies ex utero to increase cerebral vascular resistance. Adjusting end-tidal pCO2 (ET-pCO2) levels to normocapnic levels during hyperoxygenation offsets this effect in non-pregnant individuals. We aimed to evaluate the effect of maternal hyperoxygenation with and without maintaining normocapnia on the fetal and uteroplacental circulations in healthy near-term human pregnancies. METHODS: Eight healthy pregnant women, serving as their own controls, sequentially breathed room air, breathed 100% oxygen, and underwent normocapnic hyperoxygenation (NH) in a three-phase experiment involving a tight-fitting facemask. Each phase lasted 10-15 min. After steady state had been reached, peak velocities and pulsatility index (PI) values were obtained from the uterine, umbilical and fetal middle cerebral arteries (MCA) by color/pulsed Doppler. In addition, maternal ventilation and ET-pCO2 were monitored. RESULTS: One hundred percent oxygen induced maternal hyperventilation and hypocapnea. Uterine artery PI and peak systolic velocities were stable during 100% oxygen. In contrast, during NH uterine artery PI values decreased by 21% (P=0.04). Umbilical artery PI and peak velocities were stable during 100% oxygen; PI increased by 16% during NH (P=0.056), with no change in peak velocities. Peak MCA velocities decreased by 8% during 100% oxygen, and by 9.6% during NH, while MCA-PI decreased by 13% during 100% oxygen and by 21% during NH (P=0.06). CONCLUSIONS: Maternal and fetal circulations exhibit divergent responses to 100% oxygen and NH. While no change is observed in the uteroplacental circulation on 100% oxygen, decreased resistance and increased flow velocity are evident during NH. Increased umbilical artery PI during NH with no change in absolute velocities may suggest a reduction in fetoplacental blood flow. Maintaining normocapnia during hyperoxygenation does not appear to beneficially influence the circulation of the near-term human fetus as it does in non-pregnant individuals.

A simple apparatus for accelerating recovery from inhaled volatile anesthetics.

UNLABELLED: Hyperpnea increases anesthetic elimination but is difficult to implement with current anesthetic circuits without decreasing arterial PCO2. To circumvent this, we modified a standard resuscitation bag to maintain isocapnia during hyperpnea without rebreathing by passively matching inspired PCO2 to minute ventilation. We evaluated the feasibility of using this apparatus to accelerate recovery from anesthesia in a pilot study in four isoflurane-anesthetized dogs. The apparatus was easy to use, and all dogs tolerated being ventilated with it. Under our experimental conditions, isocapnic hyperpnea reduced the time to extubation by 62%, from an average of 17.5 to 6.6 min (P = 0.012), but not time from extubation to standing unaided. This apparatus may provide a practical means of applying isocapnic hyperpnea to shorten recovery time from volatile anesthetics. IMPLICATIONS: A simple modification to a standard resuscitation bag allows one to increase ventilation without decreasing blood carbon dioxide levels. In dogs, we confirmed that this circuit can be used to accelerate the elimination of and recovery from volatile anesthetics.

MRI mapping of cerebrovascular reactivity using square wave changes in end-tidal PCO2.

Cerebrovascular reactivity can be quantified by correlating blood oxygen level dependent (BOLD) signal intensity with changes in end-tidal partial pressure of carbon dioxide (PCO2). Four 3-min cycles of high and low PCO2 were induced in three subjects, each cycle containing a steady PCO2 level lasting at least 60 sec. The BOLD signal closely followed the end-tidal PCO2. The mean MRI signal intensity difference between high and low PCO2 (i.e., cerebrovascular reactivity) was 4.0 +/- 3.4% for gray matter and 0.0 +/- 2.0% for white matter. This is the first demonstration of the application of a controlled reproducible physiologic stimulus, i.e., alternating steady state levels of PCO2, to the quantification of cerebrovascular reactivity.

A simple "new" method to accelerate clearance of carbon monoxide.

The currently recommended prehospital treatment for carbon monoxide (CO) poisoning is administration of 100% O(2). We have shown in dogs that normocapnic hyperpnea with O(2) further accelerates CO elimination. The purpose of this study was to examine the relation between minute ventilation (V E) and the rate of elimination of CO in humans. Seven healthy male volunteers were exposed to CO (400 to 1,000 ppm) in air until their carboxyhemoglobin (COHb) levels reached 10 to 12%. They then breathed either 100% O(2) at resting V E (4.3 to 9.0 L min) for 60 min or O(2) containing 4.5 to 4.8% CO(2) (to maintain normocapnia) at two to six times resting V E for 90 min. The half-time of the decrease in COHb fell from 78 +/- 24 min (mean +/- SD) during resting V E with 100% O(2) to 31 +/- 6 min (p < 0. 001) during normocapnic hyperpnea with O(2). The relation between V E and the half-time of COHb reduction approximated a rectangular hyperbola. Because both the method and circuit are simple, this approach may enhance the first-aid treatment of CO poisoning.