Effects of Anesthetics, Sedatives, and Opioids on Ventilatory Control

Stuth, Eckehard A. E.; Stucke, Astrid G.; Zuperku, Edward J.

doi:10.1002/cphy.c100061

Cited by 15 publications

(12 citation statements)

References 773 publications

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“…Conditions in which neural circuits controlling breathing are disturbed (recently reviewed in Feldman et al 2013), e.g. in single gene disorders (Amir et al 1999;Amiel et al 2003;Weese-Mayer et al 2003;Gallego, 2012), with sleep apnoea (Javaheri & Dempsey, 2013), following opiate intoxication (Stuth et al 2012), or in sudden infant death syndrome (Lavezzi & Matturri, 2008;Weese-Mayer et al 2008) have severe consequences for human health. Despite the development of rodent models for these conditions (Dubreuil et al 2008;Calfa et al 2011;Davis & O'Donnell, 2013), our current understanding of such disturbances of respiratory behaviour is insufficient for developing effective therapies or treatments and will depend on a better grasp of basic mechanisms underlying the neural control of breathing, including respiratory rhythmogenesis.…”

Section: Why Breathing?mentioning

confidence: 99%

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Facing the challenge of mammalian neural microcircuits: taking a few breaths may help

Feldman

Kam

2014

The Journal of Physiology

124

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Breathing in mammals is a seemingly straightforward behaviour controlled by the brain. A brainstem nucleus called the preBötzinger Complex sits at the core of the neural circuit generating respiratory rhythm. Despite the discovery of this microcircuit almost 25 years ago, the mechanisms controlling breathing remain elusive. Given the apparent simplicity and well-defined nature of regulatory breathing behaviour, the identification of much of the circuitry, and the ability to study breathing in vitro as well as in vivo, many neuroscientists and physiologists are surprised that respiratory rhythm generation is still not well understood. Our view is that conventional rhythmogenic mechanisms involving pacemakers, inhibition or bursting are problematic and that simplifying assumptions commonly made for many vertebrate neural circuits ignore consequential detail. We propose that novel emergent mechanisms govern the generation of respiratory rhythm. That a mammalian function as basic as rhythm generation arises from complex and dynamic molecular, synaptic and neuronal interactions within a diverse neural microcircuit highlights the challenges in understanding neural control of mammalian behaviours, many (considerably) more elaborate than breathing. We suggest that the neural circuit controlling breathing is inimitably tractable and may inspire general strategies for elucidating other neural microcircuits.

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Section: Why Breathing?mentioning

confidence: 99%

“…; Gallego, ), with sleep apnoea (Javaheri & Dempsey, ), following opiate intoxication (Stuth et al . ), or in sudden infant death syndrome (Lavezzi & Matturri, ; Weese‐Mayer et al . ) have severe consequences for human health.…”

Section: Introductionmentioning

confidence: 99%

Facing the challenge of mammalian neural microcircuits: taking a few breaths may help

Feldman

Kam

2014

The Journal of Physiology

124

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“…Anesthesia for cataract surgery often includes sedatives and hypnotics (such as propofol, ketamine, or midazolam) with or without opioids, along with topical analgesia or peribulbar block. Propofol and benzodiazepines may induce persistent sedation and respiratory depression, particularly when they are administered in combination with opioids in elderly patients [4]. Opioids may also lead to nausea, vomiting, and perioperative neurocognitive disorders [5].…”

Section: Introductionmentioning

confidence: 99%

Perioperative Dexmedetomidine for outpatient cataract surgery: a systematic review

Jones

Aldwinckle

2020

BMC Anesthesiol

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Background: Cataract surgery is one of the most common procedures performed worldwide in the elderly. Various medications can provide effective anesthesia and analgesia for cataract surgery, but undesirable side effects limit the utility of each medication or combination of medications. Dexmedetomidine may serve as an anesthesia adjunct for outpatient cataract surgery in the elderly. Methods: Searches were conducted in Cochrane, Embase, and PubMed for randomized clinical trials investigating the use of dexmedetomidine in adult patients undergoing outpatient, or ambulatory, cataract surgery with sedation and topical or peribulbar block. Ninety-nine publications were identified, of which 15 trials satisfied the inclusion criteria. A total of 914 patients were included in this review. The following data were collected: American Society of Anesthesiologists' (ASA) physical status and age of study patients; method of blinding and randomization; medication doses and routes of administration; and intraoperative levels of sedation. We also recorded statistically significant differences between dexmedetomidine and other study medications or placebo with respect to the following outcomes: hemodynamic and respiratory parameters; pain; sedation; post-operative nausea and vomiting (PONV); discharge from post-anesthesia care unit (PACU) or recovery times; patient satisfaction; surgeon satisfaction; and effects on intraocular pressure (IOP). Results: Hypotension with or without bradycardia was reported following bolus doses of dexmedetomidine ranging from 0.5-1.0 mcg/kg with or without a continuous dexmedetomidine infusion. Delayed PACU discharge times were associated with the use of dexmedetomidine, but no clear association was identified between delayed recovery and higher levels of intraoperative sedation. Better analgesia and higher patient satisfaction were commonly reported with dexmedetomidine as well as reductions in IOP. Conclusions: Overall, this review demonstrates better analgesia, higher patient satisfaction, and reduced IOP with dexmedetomidine for outpatient cataract surgery when compared to traditional sedatives, hypnotics, and opioids. These benefits of dexmedetomidine, however, must be weighed against relative cardiovascular depression and delayed PACU discharge or recovery times. Therefore, the utility of dexmedetomidine for outpatient cataract surgery should be considered on a patient-by-patient basis.

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“…Although this latter group of patients represents a minority among OSA populations [ 32 ▪ ], they might be at a greater risk for opioid-related respiratory events in the postoperative period because they rely heavily on arousal to restore adequate airflow and oxygenation. Opioids, by inhibiting chemical, behavioral, and motor control of respiration [ 17 , 33 ], could further raise arousal thresholds, prolong airway obstruction, and precipitate hypoxemia. The observation that fatal outcomes were more likely to occur during night-time in patients who were difficult to arouse [ 11 ], although not indicating a direct association with OSA, reinforces the belief that OSA patients with high arousal thresholds, longer obstructive events, and potentially larger arterial desaturations may demonstrate a lower reserve to withstand a serious respiratory event in the postoperative period than patients with a different disease phenotype.…”

Section: Apnea Mechanisms and Opioid Effects In Obstructive Sleep Apnmentioning

confidence: 99%

Obstructive sleep apnea, pain, and opioids

Lam

Kunder

Wong

et al. 2016

Current Opinion in Anaesthesiology

122

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Purpose of reviewPerioperative opioid-based pain management of patients suffering from obstructive sleep apnea (OSA) may present challenges because of concerns over severe ventilatory compromise. The interaction between intermittent hypoxia, sleep fragmentation, pain, and opioid responses in OSA, is complex and warrants a special focus of perioperative outcomes research.Recent findingsLife-threatening opioid-related respiratory events are rare. Epidemiologic evidence suggests that OSA together with other serious renal and heart disease, is among those conditions predisposing patients for opioid-induced ventilatory impairment (OIVI) in the postoperative period. Both intermittent hypoxia and sleep fragmentation, two distinct components of OSA, enhance pain. Intermittent hypoxia may also potentiate opioid analgesic effects. Activation of major inflammatory pathways may be responsible for the effects of sleep disruption and intermittent hypoxia on pain and opioid analgesia. Recent experimental evidence supports that these, seemingly contrasting, phenotypes of pain-increasing and opioid-enhancing effects of intermittent hypoxia, are not mutually exclusive. Although the effect of intermittent hypoxia on OIVI has not been elucidated, opioids worsen postoperative sleep-disordered breathing in OSA patients. A subset of these patients, characterized by decreased chemoreflex responsiveness and high arousal thresholds, might be at higher risk for OIVI.SummaryOSA may complicate opioid-based perioperative management of pain by altering both pain processing and sensitivity to opioid effect.

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Effects of Anesthetics, Sedatives, and Opioids on Ventilatory Control

Cited by 15 publications

References 773 publications

Facing the challenge of mammalian neural microcircuits: taking a few breaths may help

Facing the challenge of mammalian neural microcircuits: taking a few breaths may help

Perioperative Dexmedetomidine for outpatient cataract surgery: a systematic review

Obstructive sleep apnea, pain, and opioids

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