The Possible Influence of Pulmonary Arterio-Venous Shunt and Hypoxic Pulmonary Vasoconstriction on Arterial Sevoflurane Concentration During One-Lung Ventilation

Abstract

Sevoflurane is widely used for its rapid onset and offset due to a lower blood/gas coefficient. However, involuntary movements, tachycardia, and hypertension have been observed in some patients despite a continuing constantly delivered concentration of sevoflurane during 1-lung ventilation (OLV), indicating the possibility of insufficient depth of anesthesia. We observed a temporary but obvious decrease in arterial sevoflurane concentration and pulse oximeter readings in a patient during OLV. This may have resulted in the depth of inhaled anesthesia being insufficient during OLV because the arterial sevoflurane concentration was lower than expected in spite of constantly delivered and inspiratory/expiratory sevoflurane concentrations.

Anesthetic Management of Pleurectomy/Decortication Under Differential Lung Ventilation

“…In the current case, no major changes in the inspiratory or expiratory desflurane concentration of the healthy lung were observed when bilateral ventilation was switched to DLV. It has been reported that when switching from bilateral ventilation to one-lung ventilation, an uneven balance of ventilation-perfusion between the two lungs can reduce the concentration of inhaled anesthetic in arterial blood [2], indicating that there is a risk of the depth of anesthesia being insufficient, even if the inspiratory and expiratory anesthetic concentrations remain stable. Although a postoperative interview with the patient did not indicate that any intraoperative awakening had occurred, it might be preferable to control intravenous anesthesia with a bispectral index monitor instead of an inhalational anesthetic to avoid intraoperative awakening.…”

Inhibitory effects of sevoflurane on pacemaking activity of sinoatrial node cells in guinea‐pig heart

“…One minimum alveolar concentration (MAC) of sevoflurane is approximately 2% in humans (Frink et al ., 1992), and in the clinical settings, sevoflurane is usually administered at concentrations of above 0.8 MAC to maintain anaesthesia and to prevent awareness during anaesthesia (Ghoneim, 2000; Avidan et al ., 2008). It has been reported that the blood concentration of sevoflurane ranges between approximately 0.29 and 0.65 mM in patients during inhalation of sevoflurane at concentrations of ≥2% (Frink et al ., 1992; Matsuse et al ., 2011). The present experiments examined the electrophysiological effects of sevoflurane at concentrations ranging between 0.12 and 0.71 mM, which is relevant to the clinically used concentrations.…”

“…The mM concentrations of sevoflurane in bath solutions were measured to be 0.12, 0.32, 0.44, 0.58 and 0.71 mM by gas chromatography, when delivered via vaporizer at volume percentages of 1, 2, 3, 4 and 5% of sevoflurane respectively (Kojima et al ., 2011). These ranges in mM concentrations of sevoflurane are equivalent to the blood concentrations reported in patients during sevoflurane anaesthesia (Frink et al ., 1992; Matsuse et al ., 2011; refer to Discussion). In the present experiments, sevoflurane concentration is expressed as mM concentrations throughout, except for the experiments of sevoflurane inhalation in vivo where sevoflurane concentration is expressed as volume percentage.…”

Quantitative analysis of changes in blood concentrations and ‘presumed effect‐site concentration’ of sevoflurane during one‐lung ventilation

“…Prospective power analysis was based on potential differences in the arterial blood concentration of sevoflurane, as in our previous report [2]. The primary end‐point was the detection of a difference of > 20% in the presumed effect‐site concentration of sevoflurane between the groups.…”

“…It is considered an appropriate target for anaesthetic concentration when using a balanced‐anaesthesia regimen that incorporates regional or local anaesthesia supplemented with opioids for analgesia and with neuromuscular blocking agents for immobilisation, provided that the concentration of inhaled anaesthetic is constant. However, in a recent report of a single case we noted that during one‐lung ventilation (OLV), ventilation‐perfusion mismatch caused a decrease in the arterial anaesthetic concentration as a result of the gap it created between the arterial and venous anaesthetic concentrations [2]. This alerted us to the need for a quantitative analysis of changes in the depth of inhalation anaesthesia during OLV.…”