Time Course of Ventilatory Depression Following Induction Doses of Propofol and Thiopental

Blouin, Robert T.; Conard, Pattilyn F.; Gross, Jeffrey B.

doi:10.1097/00000542-199112000-00003

Cited by 48 publications

(16 citation statements)

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“…6) following the observation that propofol alters the slope of the ventilation response to rising arterial CO 2 (Blouin et al, 1991). Subsequently, we incorporated propofol effects through the modulator compartment as inhibition of K mod :…”

Section: Methodsmentioning

confidence: 99%

Modeling Respiratory Depression Induced by Remifentanil and Propofol during Sedation and Analgesia Using a Continuous Noninvasive Measurement of pCO2

Hannam

Borrat

Trocóniz

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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Respiratory depression is a common adverse effect of propofol and remifentanil. We aimed to develop a model for respiratory depressant effects of propofol with remifentanil in patients undergoing endoscopy with sedation. Data were available for 136 patients undergoing endoscopy with sedation. Participants randomly received infusions of propofol and remifentanil. Predicted plasma concentrations, outputted by infusion pumps, were available. Transcutaneous arterial pressure of carbon dioxide (pCO 2 ) was measured. Data were analyzed using nonlinear mixed-effects modeling methods. Covariate relationships were investigated for age, noxious stimuli (endoscopy tube insertion), and A118G genotype for the m-opioid receptor (OPRM1). Participants had a median ( An indirect-effect model with a "modulator" compartment best described pCO 2 data (P , 0.001) over a direct-effect model. Remifentanil inhibited pCO 2 removal with an IC 50 of 1.13 ng/ml and first-order rate constant (k e0 ) of 0.28 minute 21. Propofol affected the modulator compartment with an IC 50 of 4.97 mg/ml (no effect-site compartment). Propofol IC 50 and remifentanil k e0 were reduced with increasing age. Noxious stimuli and genotype were not significant covariates. An indirect-effect model with a rebound mechanism can describe remifentanil-and propofolinduced changes in pCO 2 in patients undergoing noxious procedures. The model may be useful for identifying optimal dosing schedules for these drugs in a combination that provides adequate sedation but avoids respiratory depression.

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Section: Methodsmentioning

confidence: 99%

Modeling Respiratory Depression Induced by Remifentanil and Propofol during Sedation and Analgesia Using a Continuous Noninvasive Measurement of pCO2

Hannam

Borrat

Trocóniz

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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“…Blouin et al [67] demonstrated that the slope of the CO 2 response curve decreases by 56 % after a 2.5 mg kg -1 bolus of propofol. Importantly, the slope remains depressed up to 20 min after the propofol bolus, despite patients being fully awake at that time, suggesting that the ventilatory effects of propofol may outlast its sedative properties.…”

Section: Propofolmentioning

confidence: 99%

Sources of Inspiration: A Neurophysiologic Framework for Understanding Anesthetic Effects on Ventilatory Control

Czick

Waldman

Gross

2013

Curr Anesthesiol Rep

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Almost every medication that is presently available to provide sedation, analgesia, or general anesthesia significantly depresses one or more ventilatory control mechanisms. This places patients at risk of developing hypoventilation and hypoxemia during moderate or deep sedation as well as general anesthesia. As the neurophysiologic processes underlying normal ventilatory drive are discovered, new insights into the influence of anesthetics on ventilation have been recognized. More importantly, research into ways to circumvent these effects is underway. For example, drugs such as serotonin agonists and ampakines have been shown to counteract opioidinduced ventilatory depression without reversing the analgesic effect. On the other hand, efforts to identify agents that reverse the respiratory depression associated with propofol and the inhalation anesthetics have been less promising. Until reliable means for reversing drug-induced ventilatory depression are developed, prompt recognition of ventilatory insufficiency and initiation of resuscitative measures remain the keys to patient safety.

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“…A small (4 mg/kg) intravenous induction dose caused unconsciousness and peak respiratory depression within one arm-to-brain circulation time at which time the ventilatory response slope to CO 2 was maximally depressed by about 50% with recovery over several minutes (55). Knill et al showed that thiopental caused only minimal depression of the ventilatory response to CO 2 in humans during sedation but the slope of the ventilatory response to CO 2 was depressed by 65% at anesthetic levels (340).…”

Section: Barbituratesmentioning

confidence: 99%

Effects of Anesthetics, Sedatives, and Opioids on Ventilatory Control

Stuth

Stucke

Zuperku

2012

Comprehensive Physiology

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This article provides a comprehensive, up to date summary of the effects of volatile, gaseous, and intravenous anesthetics and opioid agonists on ventilatory control. Emphasis is placed on data from human studies. Further mechanistic insights are provided by in vivo and in vitro data from other mammalian species. The focus is on the effects of clinically relevant agonist concentrations and studies using pharmacological, that is, supraclinical agonist concentrations are de-emphasized or excluded.

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Time Course of Ventilatory Depression Following Induction Doses of Propofol and Thiopental

Cited by 48 publications

References 0 publications

Modeling Respiratory Depression Induced by Remifentanil and Propofol during Sedation and Analgesia Using a Continuous Noninvasive Measurement of pCO2

Modeling Respiratory Depression Induced by Remifentanil and Propofol during Sedation and Analgesia Using a Continuous Noninvasive Measurement of pCO2

Sources of Inspiration: A Neurophysiologic Framework for Understanding Anesthetic Effects on Ventilatory Control

Effects of Anesthetics, Sedatives, and Opioids on Ventilatory Control

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