Suzanne Karan

Differences between midazolam and propofol sedation on upper airway collapsibility using dynamic negative airway pressure.

Background:Upper airway obstruction (UAO) during sedation can often cause clinically significant adverse events. Direct comparison of different drugs’ propensities for UAO may improve selection of appropriate sedating agents. The authors used the application of negative airway pressure to determine the pressure that causes UAO in healthy subjects sedated with midazolam or propofol infusions. Methods:Twenty subjects (12 male and 8 female) completed the study. After achieving equivalent levels of sedation, the subjects’ ventilation, end-tidal gases, respiratory inductance plethysmographic signals, and Bispectral Index values were monitored for 5 min. Negative airway pressure was then applied via a facemask in steps of 3 cm H2O from −3 to −18 cm H2O. UAO was assessed by cessation of inspiratory airflow and asynchrony between abdomen and chest respiratory inductance plethysmographic signals. Results:Equivalent levels of sedation were achieved with both drugs with average (± SD) Bispectral Index levels of 75 ± 5. Resting ventilation was mildly reduced without any changes in end-tidal pressure of carbon dioxide. There was no difference between the drugs in the negative pressure resulting in UAO. Five female subjects and one male subject with midazolam and four female subjects and one male subject with propofol did not show any UAO even at −18 cm H2O. Compared with males, female subjects required more negative pressures to cause UAO with midazolam (P = 0.02) but not with propofol (P = 0.1). Conclusions:At the mild to moderate level of sedation studied, midazolam and propofol sedation resulted in the same propensity for UAO. In this homogeneous group of healthy subjects, there was a considerable range of negative pressures required to cause UAO. The specific factors responsible for the maintenance of the upper airway during sedation remain to be elucidated.

The effects of hypo- and hyperglycaemia on the hypoxic ventilatory response in humans

Animal and tissue studies have indicated that the carotid bodies are sensitive to glucose concentrations within the physiological range. This glucose sensitivity may modulate the ventilatory response to hypoxia, with hyperglycaemia suppressing the hypoxic response and hypoglycaemia stimulating it. This study was designed to determine whether hypo‐ and hyperglycaemia modulate the hypoxic ventilatory response in humans. In 11 normal research participants, glucose levels were clamped at 2.8 and 11.2 mmol l−1 for 30 min. At the start and end of each clamp, blood was drawn for hormone measurement and the isocapnic hypoxic ventilatory response was measured. Because generation of reactive oxygen species may be a common pathway for the interaction between glucose and oxygen levels, the experiments were repeated with and without pretreatment for 1 week with vitamins C and E. Hypoglycaemia caused an increase in the counter‐regulatory hormones, a 54% increase in isocapnic ventilation, and a 108% increase in the hypoxic ventilatory response. By contrast, hyperglycaemia resulted in small but significant increases in both ventilation and the hypoxic ventilatory response. Antioxidant vitamin pretreatment altered neither response. In conclusion, the stimulant effect of hypoglycaemia on the hypoxic ventilatory response is consistent with a direct effect on the carotid body, but an indirect effect through the activation of the counter‐regulatory response cannot be excluded. The mechanisms behind the mild stimulating effect of hyperglycaemia remain to be elucidated.

Risk factors for opioid-induced excessive respiratory depression.

Opioid use has increased significantly over the past ten years and so has the incidence of reportable adverse events, such as respiratory depression and/or arrest. It is important for nurses to understand and know how to assess patients for risk factors for respiratory depression secondary to opioid therapy. This paper presents the pharmacodynamics of opioids, the risk factors for excessive respiratory depression, recommendations for identifying patients at high risk, and interventions to prevent adverse effects. After reading this paper, nurses will have the knowledge to provide safe administration of opioid medications for the management of acute pain.

Hypoxia: developments in basic science, physiology and clinical studies.

Airway management is primarily designed to avoid hypoxia, yet hypoxia remains the main ultimate cause of anaesthetic‐related death and morbidity. Understanding some of the physiology of hypoxia is therefore essential as part of a ‘holistic’ approach to airway management. Furthermore, it is strategically important that national specialist societies dedicated to airway management do not only focus upon the technical aspects of airway management, but also embrace some of the relevant scientific questions. There has been a great deal of research into causation of hypoxia and the body’s natural protective mechanisms and responses to it. This enables us to think of ways in which we might manipulate the cellular and molecular responses to confer greater protection against hypoxia‐induced tissue injury. This article reviews some of those aspects.

Effects of Pain and Audiovisual Stimulation on the Opioid-induced Depression of the Hypoxic Ventilatory Response

Background:Normoxic and hypoxic ventilation are influenced by chemoreceptor and nonchemoreceptor drives. Although inhalational anesthetics blunt hypoxic ventilation, this effect is reversed by audiovisual stimulation but not by pain. Opioids reduce both normoxic and hypoxic ventilation, but their interaction with pain and audiovisual stimulation has not been fully reported. Methods:Isocapnic, acute hypoxic ventilatory responses (AHRs) were measured in 11 volunteers. AHR and normoxic ventilation were measured under the following conditions: (1) eyes closed, no audio stimulation (low wakefulness); (2) low wakefulness conditions plus painful thermal stimulation; and (3) playing a computer game (high wakefulness), each with and without remifentanil infusion. Results:The average (± sd) remifentanil dose was 0.035 ± 0.012 μg · kg−1 · min−1. Both normoxic and hypoxic ventilation were significantly reduced by the remifentanil infusion under all three conditions. The AHR values under low wakefulness conditions were 0.33 ± 0.19 and 0.89 ± 0.49 l · min−1 · sat−1 with and without remifentanil, respectively (P < 0.05). High wakefulness significantly increased AHR with and without remifentanil, whereas low wakefulness with pain did not. However, high wakefulness with remifentanil did not increase the AHR back to what was observed during low wakefulness without remifentanil. Conclusions:The computer game was a more potent stimulus than pain in countering the depressant effect of remifentanil on AHR. Although the effect of high wakefulness was more attenuated than was previously observed with respect to inhalational anesthetics, the significance of these findings is underlined by the more clinically relevant scenario of what is experienced in the face of opioid administration.

Effects of pain and arousal on the control of breathing

The control of breathing is a complex physiological process that results from the integration of multiple dynamic inputs. The perioperative period represents a particularly dynamic situation, requiring adjustment of the level of ventilation on a moment-to-moment basis as the result of multiple conflicting requirements. The autonomic or metabolic controller adjusts ventilation depending on the level of arterial pH, Pao2, and Paco2, and has been extensively studied and reviewed [2–4]. The stimulation of the central chemoreceptors in the medulla with carbon dioxide or the stimulation of the peripheral chemoreceptors in the carotid bodies with hypoxemia (or also with hypercapnia or acidemia) results in a relatively prompt increase in ventilation (over seconds to minutes). Ventilation increases linearly with hypercapnia and desaturation. However, the relative magnitude of the contribution of these chemoreflexes in determining ventilation is uncertain under many circumstances, and it would appear that only under (deep) anesthesia or nonrapid eye movement (NREM) sleep [5] are the chemoreflexes the sole determinants of ventilation. However, even with most levels of anesthesia (e.g., supra minimum alveolar concentration [MAC] concentrations of inhalational anesthetics), painful surgical stimuli that do not elicit a purposeful movement will elicit a change in ventilation. The role of chemoreflexes in determining resting ventilation in awake subjects is subject to some controversy [6,7] and it may be that a “wakefulness drive”, as proposed by Fink [8], plays a major part, possibly accounting for the often irregular breathing that is observed at rest. There are many other factors arising from peripheral (nociceptors, lung receptors, muscle stretch receptors, etc.) or central (cortical, limbic, hypothalamic, etc.) structures that normally affect ventilation and, under certain circumstances, can completely override the autonomic controller (e.g., speech, vomiting, voluntary breath holding, yawning, sighing, etc.), at least for some period of time. The autonomic system does ultimately prevail, as seen by the involuntary termination of voluntary breath holding. Figure 1 illustrates some of the complex interconnections between the metabolic and nonmetabolic ventilatory control pathways. This brief review will focus on the ventilatory effects of pain and arousal, two stimuli that are important during the perioperative period, and how the effects of these stimuli are modified by pharmacological agents used in anesthesiology.

Perioperative Implementation of Continuous Positive Airway Pressure: A Review of the Considerations

OSA patients present unique challenges in the peri-operative period. They routinely require more monitoring, oxygen therapy, unplanned ICU admissions, longer hospital stays, and have more adverse events than healthy counter- parts. Some data suggest that perioperative CPAP use is associated with reduced morbidity and mortality of patients with OSA, and yet its application remains inconsistent. This review aims to summarize existing literature on the peri-operative use of CPAP, identify barriers to its implementation, and begin defining an algorithm for the practical application of peri-operative CPAP.

Enhancing Feedback on Professionalism and Communication Skills in Anesthesia Residency Programs

BACKGROUND: Despite its importance, training faculty to provide feedback to residents remains challenging. We hypothesized that, overall, at 4 institutions, a faculty development program on providing feedback on professionalism and communication skills would lead to (1) an improvement in the quantity, quality, and utility of feedback and (2) an increase in feedback containing negative/constructive feedback and pertaining to professionalism/communication. As secondary analyses, we explored these outcomes at the individual institutions. METHODS: In this prospective cohort study (October 2013 to July 2014), we implemented a video-based educational program on feedback at 4 institutions. Feedback records from 3 months before to 3 months after the intervention were rated for quality (0–5), utility (0–5), and whether they had negative/constructive feedback and/or were related to professionalism/communication. Feedback records during the preintervention, intervention, and postintervention periods were compared using the Kruskal-Wallis and &khgr;2 tests. Data are reported as median (interquartile range) or proportion/percentage. RESULTS: A total of 1926 feedback records were rated. The institutions overall did not have a significant difference in feedback quantity (preintervention: 855/3046 [28.1%]; postintervention: 896/3327 [26.9%]; odds ratio: 1.06; 95% confidence interval, 0.95–1.18; P = .31), feedback quality (preintervention: 2 [1–4]; intervention: 2 [1–4]; postintervention: 2 [1–4]; P = .90), feedback utility (preintervention: 1 [1–3]; intervention: 2 [1–3]; postintervention: 1 [1–2]; P = .61), or percentage of feedback records containing negative/constructive feedback (preintervention: 27%; intervention: 32%; postintervention: 25%; P = .12) or related to professionalism/communication (preintervention: 23%; intervention: 33%; postintervention: 24%; P = .03). Institution 1 had a significant difference in feedback quality (preintervention: 2 [1–3]; intervention: 3 [2–4]; postintervention: 3 [2–4]; P = .001) and utility (preintervention: 1 [1–3]; intervention: 2 [1–3]; postintervention: 2 [1–4]; P = .008). Institution 3 had a significant difference in the percentage of feedback records containing negative/constructive feedback (preintervention: 16%; intervention: 28%; postintervention: 17%; P = .02). Institution 2 had a significant difference in the percentage of feedback records related to professionalism/communication (preintervention: 26%; intervention: 57%; postintervention: 31%; P < .001). CONCLUSIONS: We detected no overall changes but did detect different changes at each institution despite the identical intervention. The intervention may be more effective with new faculty and/or smaller discussion sessions. Future steps include refining the rating system, exploring ways to sustain changes, and investigating other factors contributing to feedback quality and utility.

Gestational sleep apnea: have we been caught napping?

Obstructive sleep apnea (OSA) is a modern epidemic whose historical chronology has paralleled the development of the obesity epidemic. Despite the publication of guidelines regarding the perioperative management of patients with OSA, the formation of protocols by hospitals and the adoption of these practices by individual practitioners are typically inadequate. This may be even more manifest for OSA in pregnancy. In this issue of the International Journal of Obstetric Anesthesia, Dominguez et al. present a survey of members of the Society for Obstetric Anesthesia and Perinatology (SOAP) which focused on OSA-awareness in pregnancy. While most respondents accepted that OSA in pregnancy is a potential problem that can affect maternal and fetal well-being, the vast majority never screen their patients for OSA, and work in hospitals where there is no departmental policy for screening or management of OSA during pregnancy. In the few (<10%) respondents who did screen for OSA, most used the STOP-Bang screening tool, which may have limited utility during pregnancy. It is likely that this study was in a non-representative sample, as reflected in a very low response rate with a high predisposition towards academic practice. Nevertheless, it is unlikely that the situation among non-responders or in private practice is better and may well be worse. In this editorial, we briefly review what we know about OSA in pregnancy, as compared to the non-pregnant population, and comment on the disparities between what we can do and what we actually do in this cohort. We ask why we are not doing more and conclude with the suggestion that there is need for a new diagnosis, ‘‘gestational sleep apnea”, to parallel other established transient diagnoses of pregnancy, like gestational hypertension and gestational diabetes mellitus. Obstructive sleep apnea is defined as recurrent episodic cessation or limitation of normal breathing during sleep mainly due to exaggerated depression of pharyngeal muscle tone. Sleep-disordered breathing (SDB) is the term used to capture the spectrum of the condition whereby OSA is a manifestation of its severity. The syndrome of OSA arises from increased sympathetic output from intermittent asphyxia and repeated nocturnal arousal. This results in increased arterial stiffness and endothelial dysfunction, which may lead to pulmonary hypertension and cor pulmonale. The etiology of pregnancy-related SDB is multifactorial due in part to generalized hyperemia (with nasal congestion and airway edema) along with decreased functional residual capacity. This may be partially offset by a progesterone-mediated ventilatory stimulation and a preference for lateral sleep posture in pregnancy. Recently, OSA has been more widely appreciated as endemic in the general female population, particularly during pregnancy and especially in the presence of comorbidities. Surveys and home monitoring devices have documented the prevalence of OSA during pregnancy but few studies have quantified pregnancyassociated OSA with overnight in-lab polysomnography (PSG), which is the gold standard of diagnosis. Based on currently available evidence, SDB seems to occur with a prevalence of 15% in healthy obese pregnant women and 50% in high-risk pregnancies. Pregnancy-related morbidity related to OSA has been well established. Maternal adverse effects include a more than five-fold increase in in-hospital mortality due to multiple diagnoses including cardiomyopathy and pulmonary embolism. The occurrence of SDB during pregnancy has been shown to be an independent risk factor for gestational hypertension and diabetes, even after adjusting for multiple confounding variables. Indeed, some have suggested PSG referral for all pregnant women with fetal growth restriction and preeclampsia with snoring or obesity. Certainly, poor fetal outcomes including fetal growth restriction and preterm delivery have been reported to be associated with SDB during pregnancy. Although there is evidence of OSA abatement after pregnancy, the immediate postpartum period still presents a risk for increased respiratory-related maternal morbidity. A state-wide study of anesthesia-related maternal deaths over a 15-year period demonstrated that unrecognized hypoventilation or obstruction was associated with both OSA/SDB and obesity. In addition, the administration of postpartum opioids has been shown to be significantly correlated with increased apnea-hypopnea index (AHI) in the supine position. Nevertheless, it has not been possible to find an association between the use of neuraxial opioids in surgical patients with OSA and adverse respiratory outcomes and neuraxial opioids are probably safer than systemic opioids in these patients. In the non-pregnant adult population with OSA, local and national protocols have been proposed for International Journal of Obstetric Anesthesia (2016) 26, 1–3 0959-289X/

A Randomized, Prospective, Double-Blinded Study of Physostigmine to Prevent Sedation-Induced Ventilatory Arrhythmias.

see front matter ! 2016 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijoa.2016.03.001