Large volume N 2 O uptake alone does not explain the second gas effect of N 2 O on sevoflurane during constant inspired ventilation †

Hendrickx, Jan F. A.; Carette, Rik; Lemmens, Hendrikus J. M.; Wolf, André M. De

doi:10.1093/bja/ael008

Cited by 24 publications

(23 citation statements)

References 13 publications

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“…This is consistent with most previous clinical and theoretical studies, including those of Peyton et al , who measured the second gas effect on arterial sevoflurane and oxygen partial pressures in anesthetized patients. 5,10 The augmentation to blood desflurane partial pressures at 20 to 30 min predicted by the model is in the order of 10 to 15% with moderate degrees of V̇/Q̇ scatter. This compares to a mean 12% increase in arterial sevoflurane partial pressures at this time point in ventilated patients measured by Peyton et al 10 The lesser augmentation in gas phase desflurane concentrations predicted here is also broadly consistent with the findings of Taheri and Eger, and those of Hendrickx et al for end-expired sevoflurane concentrations, in anesthetized patients.…”

Section: Discussionmentioning

confidence: 93%

“…This compares to a mean 12% increase in arterial sevoflurane partial pressures at this time point in ventilated patients measured by Peyton et al 10 The lesser augmentation in gas phase desflurane concentrations predicted here is also broadly consistent with the findings of Taheri and Eger, and those of Hendrickx et al for end-expired sevoflurane concentrations, in anesthetized patients. 4,5 …”

Section: Discussionmentioning

confidence: 99%

“…4,5 However, in a clinical study prompted by results of computer modeling of gas-exchange in the lung, 6–8 Peyton et al found that the magnitude of the second gas effect is considerably greater where the effect on arterial blood partial pressures is measured instead. 9 They explained this by the effect of inhomogeneity or scatter of ventilation and blood flow ratios (ventilation-perfusion [V̇/Q̇] ratios) on the distribution of perfusion-driven nitrous oxide uptake throughout the lung, with more powerful concentrating effects generated in lung compartments with higher blood flow and low V̇/Q̇.…”

mentioning

confidence: 99%

“…They suggested furthermore that this could produce a significant second gas effect on blood partial pressures of oxygen and volatile agent even at relatively low “maintenance phase” rates of nitrous oxide uptake, 10 a suggestion that has been questioned, 11 but is supported by clinical studies. 5,9 …”

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Can Mathematical Modeling Explain the Measured Magnitude of the Second Gas Effect?

2018

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Background Recent clinical studies suggest that the magnitude of the second gas effect is considerably greater on arterial blood partial pressures of volatile agents than on end-expired partial pressures, and a significant second gas effect on blood partial pressures of oxygen and volatile agents occurs even at relatively low rates of nitrous oxide uptake. We set out to further investigate the mechanism of this phenomenon with the help of mathematical modeling. Methods Log-normal distributions of ventilation and blood flow were generated representing the range of ventilation-perfusion scatter seen in patients during general anesthesia. Mixtures of nominal delivered concentrations of volatile agents (desflurane, isoflurane and diethyl ether) with and without 70% nitrous oxide were mathematically modeled using steady state mass-balance principles, and the magnitude of the second gas effect calculated as an augmentation ratio for the volatile agent, defined as the partial pressure in the presence to that in the absence of nitrous oxide. Results Increasing the degree of mismatch increased the second gas effect in blood. Simultaneously, the second gas effect decreased in the gas phase. The increase in blood was greatest for the least soluble gas, desflurane, and least for the most soluble gas, diethyl ether, while opposite results applied in the gas phase. Conclusions Modeling of ventilation-perfusion inhomogeneity confirms that the second gas effect is greater in blood than in expired gas. Gas-based minimum alveolar concentration readings may therefore underestimate the depth of anesthesia during nitrous oxide anesthesia with volatile agents. The effect on minimum alveolar concentration is likely to be most pronounced for the less soluble volatile agents in current use.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Can Mathematical Modeling Explain the Measured Magnitude of the Second Gas Effect?

2018

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“…NUMBER of studies [1][2][3] have shown that the rapid uptake of high concentrations of nitrous oxide at induction of inhalational anesthesia produces an increase in alveolar concentrations of oxygen and the accompanying volatile anesthetic agent. This process is known as the second gas effect.…”

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confidence: 99%

Nitrous Oxide Diffusion and the Second Gas Effect on Emergence from Anesthesia

et al. 2011

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Background: Rapid elimination of nitrous oxide from the lungs at the end of inhalational anesthesia dilutes alveolar oxygen, producing "diffusion hypoxia." A similar dilutional effect on accompanying volatile anesthetic agent has not been evaluated and may impact the speed of emergence. Methods: Twenty patients undergoing surgery were randomly assigned to receive an anesthetic maintenance gas mixture of sevoflurane adjusted to bispectral index, in airoxygen (control group) versus a 2:1 mixture of nitrous oxideoxygen (nitrous oxide group). After surgery, baseline arterial and tidal gas samples were taken. Patients were ventilated with oxygen, and arterial and tidal gas sampling was repeated at 2 and 5 min. Arterial sampling was repeated 30 min after surgery. Sevoflurane partial pressure was measured in blood by the double headspace equilibration technique and in tidal gas using a calibrated infrared gas analyzer. Time to eye opening and time extubation were recorded. The primary endpoint was the reduction in sevoflurane partial pressures in blood at 2 and 5 min. Results: Relative to baseline, arterial sevoflurane partial pressure was 39% higher at 5 min in the control group (P Ͻ 0.04) versus the nitrous oxide group. At 30 min the difference was not statistically significant. Time to eye opening (8.7 vs. 10.1 min) and time to extubation (11.0 vs.13.2 min) were shorter in the nitrous oxide group versus the control group (P Ͻ 0.04). Conclusions: Elimination of nitrous oxide at the end of anesthesia produces a clinically significant acceleration in the

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Special Aspects of Pharmacokinetics of Inhalation Anesthesia

Hendrickx¹,

Wolf²

2008

Handbook of Experimental Pharmacology

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Recent interest in the use of low-flow or closed circuit anesthesia has rekindled interest in the pharmacokinetics of inhaled anesthetics. The kinetic properties of inhaled anesthetics are most often modeled by physiologic models because of the abundant information that is available on tissue solubilities and organ perfusion. These models are intuitively attractive because they can be easily understood in terms of the underlying anatomy and physiology. The use of classical compartment modeling, on the other hand, allows modeling of data that are routinely available to the anesthesiologist, and eliminates the need to account for every possible confounding factor at each step of the partial pressure cascade of potent inhaled agents. Concepts used to describe IV kinetics can readily be applied to inhaled agents (e.g., context-sensitive half-time and effect site concentrations). The interpretation of the F(A)/F(I) vs time curve is expanded by reintroducing the concept of the general anesthetic equation-the focus is shifted from "how F(A) approaches F(I)" to "what combination of delivered concentration and fresh gas flow (FGF) can be used to attain the desired F(A)." When the desired F(A) is maintained with a FGF that is lower than minute ventilation, rebreathing causes a discrepancy between the concentration delivered by the anesthesia machine (=selected by the anesthesiologist on the vaporizer, F(D)) and that inspired by the patient. This F(D)-F(I) discrepancy may be perceived as "lack of control" and has been the rationale to use a high FGF to ensure the delivered matched the inspired concentration. Also, with low FGF there is larger variability in F(D) because of interpatient variability in uptake. The F(D)-F(I) discrepancy increases with lower FGF because of more rebreathing, and as a consequence the uptake pattern seems to be more reflected in the F(D) required to keep F(A) constant. The clinical implication for the anesthesiologist is that with high FGF few F(D) adjustments have to be made, while with a low FGF F(D) has to be adjusted according to a pattern that follows the decreasing uptake pattern in the body. The ability to model and predict the uptake pattern of the individual patient and the resulting kinetics in a circle system could therefore help guide the anesthesiologist in the use of low-flow anesthesia with conventional anesthesia machines. Several authors have developed model-based low FGF administration schedules, but biologic variability limits the performance of any model, and therefore end-expired gas analysis is obligatory. Because some fine-tuning based on end-expired gas analysis will always be needed, some clinicians may not be inclined to use very low FGF in a busy operating room, considering the perceived increase in complexity. This practice may be facilitated by the development of anesthesia machines that use closed circuit anesthesia (CCA) with end-expired feedback control--they "black box" these issues (see Chapter 21). In this chapter, we first explore how and why the kinetic propert...

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Large volume N 2 O uptake alone does not explain the second gas effect of N 2 O on sevoflurane during constant inspired ventilation †

Cited by 24 publications

References 13 publications

Can Mathematical Modeling Explain the Measured Magnitude of the Second Gas Effect?

Can Mathematical Modeling Explain the Measured Magnitude of the Second Gas Effect?

Nitrous Oxide Diffusion and the Second Gas Effect on Emergence from Anesthesia

Special Aspects of Pharmacokinetics of Inhalation Anesthesia

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