Isoflurane Inhalation Enhances Increased Physiologic Deadspace Volume Associated with Positive Pressure Ventilation and Compromises Arterial Oxygenation

Praetel, Claudia; Banner, Michael J.; Monk, Terri G.; Gabrielli, A.

doi:10.1213/01.ane.0000131727.52766.f7

Cited by 10 publications

(7 citation statements)

References 25 publications

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“…The minute ventilation was calculated as the expiratory tidal volume multiplied by the respiratory rate. The minute alveolar ventilation (MAV) was derived from the minute ventilation, as described in previous publications (11,12). …”

Section: Methodsmentioning

confidence: 99%

Hyperventilation accelerates the rise of arterial blood concentrations of desflurane in gynecologic patients

Lu¹,

Lin²,

Hsu³

et al. 2012

Clinics

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OBJECTIVES:Under a constant inspired concentration, the uptake of a volatile anesthetic into the arterial blood should mainly be governed by alveolar ventilation, according to the assumption that the patient's cardiac output remains stable during anesthesia. We investigated whether ventilation volume affects the rate of desflurane uptake by examining arterial blood concentrations.METHOD:Thirty female patients were randomly allocated into the following three groups: hyperventilation, normal ventilation and hypoventilation. Hemodynamic variables were measured using a Finometer, inspiratory and end-tidal concentrations of desflurane were measured by infrared analysis, and the desflurane concentration in the arterial blood (Ades) was analyzed by gas chromatography.RESULTS:During the first 10 minutes after the administration of desflurane, the Ades was highest in the hyperventilation group, and this value was significantly different from those obtained for the normal and hypoventilation groups. In addition, hyperventilation significantly increased the slope of Ades-over-time during the first 5 minutes compared with patients experiencing normal ventilation and hypoventilation, but there were no differences in these slopes during the periods from 5-10, 10-20 and 20-40 minutes after the administration of desflurane. This finding indicates that there were no differences in desflurane uptake between the three groups after the first 5 minutes within desflurane administration.CONCLUSIONS:Hyperventilation accelerated the rate of the rise in Ades following desflurane administration, which was time-dependent with respect to different alveolar ventilations levels.

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Section: Methodsmentioning

confidence: 99%

Hyperventilation accelerates the rise of arterial blood concentrations of desflurane in gynecologic patients

Lu¹,

Lin²,

Hsu³

et al. 2012

Clinics

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“…Isoflurane increases VD alv more than propofol under positive pressure ventilation. 23 Although sevoflurane we used may have the same mode of action as isoflurane, its concentration was kept constant throughout this study. Ventilation-perfusion relationships during epidural analgesia show no significant changes when compared with the control state.…”

Section: Figmentioning

confidence: 99%

Dependence of the gradient between arterial and end-tidal PCO on the fraction of inspired oxygen

Yamauchi

Ito

Sasano

et al. 2011

British Journal of Anaesthesia

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“…Minute ventilation was calculated as expiratory tidal volume multiplied by respiratory rate. Minute alveolar ventilation was derived from minute ventilation as described in a previous publication [8,9] .…”

Section: Determination Of Cardiac Index and Minute Alveolarmentioning

confidence: 99%

Effects of Changes in Alveolar Ventilation on Isoflurane Arterial Blood Concentration and Its Uptake into the Human Body

Lu¹,

Lin²,

et al. 2009

Pharmacology

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We investigated whether minute alveolar ventilation affects isoflurane concentration in arterial blood and uptake of isoflurane into the body. Thirty female patients scheduled to undergo elective gynecological surgery were randomly assigned to one of three groups: i.e. hyperventilation, normal ventilation and hypoventilation. Inspiratory (CIiso) and end-tidal (CEiso) concentrations of isoflurane were measured by infrared analysis, and arterial blood isoflurane concentration (Aiso) was analyzed by gas chromatography. Cardiac index was measured by Doppler ultrasonography. The body uptake of isoflurane was determined by multiplying alveolar ventilation by the gradient of CIiso–CEiso. Aiso was highest in the hyperventilation group (significant), followed by the normal ventilation and hypoventilation groups, during the 40-min study. During the first 10 min of the study, the slope of the Aiso-over-time curve was highest in the hyperventilation group, followed by the normal ventilation group and the hypoventilation group. During the second half of the study (20–40 min), the slope Aiso-over-time curve did not differ among the three groups. Changes in ventilation affected the concentration of isoflurane in arterial blood but did not significantly alter the uptake of it during the last 20 min of the study. The change of alveolar ventilation altered the speed of functional residual capacity wash-in by isoflurane, which was the integral factor influencing Aiso and body uptake of isoflurane.

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Isoflurane Inhalation Enhances Increased Physiologic Deadspace Volume Associated with Positive Pressure Ventilation and Compromises Arterial Oxygenation

Cited by 10 publications

References 25 publications

Hyperventilation accelerates the rise of arterial blood concentrations of desflurane in gynecologic patients

Hyperventilation accelerates the rise of arterial blood concentrations of desflurane in gynecologic patients

Dependence of the gradient between arterial and end-tidal PCO on the fraction of inspired oxygen

Effects of Changes in Alveolar Ventilation on Isoflurane Arterial Blood Concentration and Its Uptake into the Human Body

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