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The Second Gas Effect is Not Statistically Valid

Sun, Xing-Guo, MD; Lee, Chingmuh, MD

doi: 10.1097/00000539-200203000-00062
Letters To The Editor: Letters & Announcements
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Respiratory and Critical Care Physiology and Medicine

Department of Anesthesiology

Harbor-University of California Los Angeles Medical Center

Research and Education Institute

Torrance, CA

In Response:

We commend Drs. Uda et al. for their statistical re-analysis of the so-called “second gas effect” data (1) and appreciate the opportunity to comment on the theoretical aspects of this concept.

From a practical viewpoint, we (2) and others (3) have been unable to demonstrate the “second gas effect” that Taheri and Eger (4) found. Their differences in mean arterial pressure (MAP) (86 ± 15 mm Hg versus 76 ± 8 mm Hg) and heart rate (HR) (69 ± 16 bpm versus 76 ± 16 bpm) and broad range of Petco2 (33–37 mm Hg) suggest that differences in cardiac output and alveolar ventilation (𝑄̇A) (5), may explain their differences in the ratio of alveolar (end-tidal) concentration (FA) to inspired concentration (FI) (FA/FI) (4). Contrariwise, when we maintained a constant 𝑄̇A with stable MAP and HR, we found no significant differences in either arterial blood concentration or FA/FI of the second gas with or without 80% N2O (2).

From a theoretical viewpoint, to analyze the “second gas effect,” we conclude that a reasonable uptake of 200–400 mL/min in the early period of N2O anesthesia (unpublished data) (2,3,6,7) rather than value as a high as 1400–1500 mL/min (8,9) should be used.

Second, breath-by-breath analysis of “concentrating effect”(8) (with this reasonable N2O uptake and considering changes of O2 and CO2, and assuming the second gas zero uptake) (5,10) shows an increase of only relative 1.7% (absolute 0.01% in FA) in FA and FA/FI of the second gas. In fact, considering the uptake of the second gas minimizes any potential increase in FA and FA/FI.

Third, differences between inspired and expired gases in temperature and water vapor content would diminish the differences between inspired and expired volume (the theoretical basis for the “augmentation effect”).

Fourth, “concentration effect”(11) is different from “concentrating effect” and is not an explanation of “second gas effect.” Its mechanism is complex and will be discussed separately, but it can not be explained by either “concentrating effect” and/or “augmentation effect.”

Xing-Guo Sun, MD

Chingmuh Lee, MD

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References

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2. Sun X-G, Su F, Shi Y-Q, Lee C. The “second gas effect” is not a valid concept. Anesth Analg 1999; 88: 188–92.
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10. Sun XG, Hansen JE, Ting H, et al. Comparison of exercise cardiac output by the Fick principle using O2 and CO2. Chest 2000; 118: 631–40.
11. Eger EI II. The effect of inspired concentration on the rate of rise of alveolar concentration. Anesthesiology 1963; 24: 153–7.
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