Effects of I.V. Midazolam on Upper Airway Resistance

Anesthesiology, 2002

Background Traditional methods of assessing ventilatory effects of sedative agents do not measure their propensity to cause upper airway obstruction (UAO). The primary objective of this study was to develop a method, using dynamic negative airway pressure (DNAP), for replicating UAO during deep sedation. Methods A state of deep sedation (defined as an Observer Assessment of Alertness and Sedation score of 3 and a bispectral index < 80) was attained in 10 healthy volunteers, aged 19-41, using midazolam. Volunteers breathed through a chamber connected to a regulated source of negative pressure that was gradually adjusted downward to produce UAO based on maximal inspiratory flow. The study consisted of three phases: A control phase while awake, a study phase during midazolam deep sedation, and a recovery phase after flumazenil administration. Results During the control phase no subject demonstrated airway obstruction at negative pressures to -30-cm H2O. All subjects exhibited comple...

Journal of Chittagong Medical College Teachers' Association

Background: The most vital element in providing functional respiration is the airway and the major responsibility of the anesthetist is to provide respiration for the patient through a patent airway and adequate ventilation. The use of Laryngeal Mask Airway (LMA) is well established in anesthetic practice. The LMA is an innovative airway management device intended as an alternative airway to face mask use and being used in millions of patients for routine and emergency procedures. LMA obviates the need for tracheal intubation during anesthesia. The efficacy of thiopentone can be altered by midazolam or succinylcholine in combination. We used thiopentone sodium (5mg/kg) and midazolam (0.05mg/kg) as induction agent in group A (Control group) and thiopentone sodium (5mg/kg) and succinylcholine (0.25mg/kg) in group B for LMA. This randomized trial was conducted to compare the effectiveness of midazolam and succinylcholine added with thiopentone in smooth insertion of LMA. Materials and ...

Canadian Journal of Anesthesia/Journal canadien d'anesthésie, 2006

INTRODUCTION: Laryngoscopy and tracheal intubation produce stress response in the form of tachycardia, hypertens ion and increased levels of catecholamines.1,2, As the control of blood pressure and heart rate is of utmost importance to prevent the detrimental effects; there is a need for a safe and effective drug to attenuate the cardiovascular response to laryngoscopy and intubation. Nalbuphine and midazolam are inexpensive and most commonly used in our community as a premedicant. Our aim was to compare the effects of nalbuphine and midazolam on haemodymanic responses to endotracheal intubation to help the selection of a better drug in this respect. METHOD: After approval from the hospital committee a study was carried out on ninety adult male patients of ASA I or II status, undergoing general surgery under standard general anaesthesia. After informed consent, three groups of 30 patients each were made by random allocation. On arrival in the theatre, E.C.G monitor, pulse oximeter and Noninvasive blood pressure monitor were applied. After 3 minutes of preoxygenation, all groups were induced with thiopentone 4mg/kg and suxamathonium 1mg/kg. Group I was control in which 3ml of saline was given. Group II received nalbuphine 75ug/kg and Group III received midazolam 30ug/kg before the induction agents. Following intubation, anaesthesia was maintained with O2+N2O+halothane (0.8%). Heart rate, systolic blood pressure, diastolic blood pressure and mean arterial pressure were recorded before induction, at laryngoscopy and intubation and after intubation every minute for three minutes. Concluding parameters were analysed statistically by ANOVA. p<0.05 was taken as significant. RESULTS: Demographic data showed similarity in age and weight between groups. Baseline values did not differ significantly between groups. A decrease in HR ,SBP, DBP, MAP was seen in Group II and III but the decrease was more pronounced in Group II.(p<0.05) DISCUSSION: The haemodynamic observations were noteworthy in our study. Significant attenuation of cardiovascular response to laryngoscopy and tracheal intubation was seen with nalbuphine and midazolam as compared to the control group. Analysis of haemodynamic response showed better suppression with nalbuphine than midazolam. The results of our study were consistent with previous study showing reduction in heart rate and systolic arterial pressure with nalbuphine as compared to other drugs.4 CONCLUSION: Our study results suggest that nalbuphine when used as premedicant, in dose of 75ug/kg is more effective than midazolam in blunting the stress response to laryngoscopy and intubation. We recommend its use in our settings before induction of anaesthesia. REFERENCES:

Clinical Therapeutics, 2011

Background: Intranasal (IN) midazolam is a potential alternative to rectal diazepam for the acute treatment of epileptic seizures.

Anesthesia & Analgesia, 2009

Background-Upper airway patency may be compromised during sleep and anesthesia due to either anatomical alterations (mechanical properties) or disturbances in the neural control (compensatory neuromuscular responses). The pathophysiology of upper airway obstruction during anesthesia may differ between men and women. Recently, we reported that the upper airway mechanical properties were comparable to those found during natural non-rapid eye movement sleep, as evaluated by measurements of passive critical closing pressure (P CRIT ) and upstream resistance (R US ) during midazolam sedation. In this study, we compared the effects of gender on compensatory neuromuscular responses to upper airway obstruction during midazolam general anesthesia.

Journal of Applied Physiology, 2011

The critical closing pressure (Pcrit) is the airway pressure at which the airway collapses and reflects the anatomical contribution to the genesis of obstructive sleep apnea. Pcrit is usually determined during non-rapid eye movement sleep at night, but has been determined under midazolam sedation during the day in the absence of sleep stage monitoring. Indeed, little is known about the effects of midazolam on sleep architecture. Moreover, deeper sedation with midazolam can decrease upper airway muscle activity and increase collapsibility compared with natural sleep. Pcrit under sedation has not been systematically compared with the usual method performed during natural sleep. Therefore, this study aimed to test the hypothesis that Pcrit following low doses of midazolam during the day would be comparable to Pcrit measured during natural sleep in the same patient. Fifteen men (age 54 ± 10 yr, body mass index 30 ± 4 kg/m2) with obstructive sleep apnea underwent a baseline standard over...

Journal of Anesthesia, 2010

Purpose We examined the hypothesis that remifentanil decreases the bispectral index (BIS) as well as blunts cardiovascular responses to tracheal intubation during anesthesia with midazolam. Methods Sixty patients were randomly allocated to three groups according to the dose of remifentanil-0.1 (S), 0.2 (M), or 0.5 (L) lg kg-1 min-1 , respectively. Infusion of remifentanil was started 5 min before the induction of general anesthesia with midazolam 0.2 mg/kg in all groups. Following the administration of vecuronium 0.1 mg/kg, the trachea was intubated 5 min after induction, and the infusion rate of remifentanil was then reduced to 0.05 lg kg-1 min-1 in all groups. Mean arterial blood pressure (MAP), heart rate (HR), BIS, and 95% spectral edge frequency (SEF95) were measured until 10 min after tracheal intubation. Results Infusion of remifentanil alone before the induction of anesthesia did not affect the hemodynamic or electroencephalographic parameters. MAP was significantly decreased after induction in all groups of patients (P \ 0.01), with no differences among the three groups, while it was significantly increased after tracheal intubation in the patients of groups S and M, but not in those of group L. The HR did not change after induction in any of the groups, but it was also significantly increased after tracheal intubation of group S and M patients, although not in those of group L. The BIS decreased after induction, and both the BIS and SEF95 were significantly lower in group L patients than in those of group S (P \ 0.01). All patients were unconscious after induction, and none complained of intraoperative awareness. Conclusion In our patient cohort, remifentanil 0.5 lg kg-1 min-1 effectively decreased the BIS after the induction of general anesthesia with midazolam 0.2 mg/kg and suppressed the increase of MAP and HR in response to subsequent laryngoscopy and tracheal intubation.

British Journal of Anaesthesia, 1996

We have examined the effects of sedation with midazolam 0.1 mg kg 91 and reversal with flumazenil 0.5 mg on beat-to-beat heart rate (HR) variability (HRV), systolic arterial pressure (SAP), finger photoplethysmograph amplitude (PLA) and impedence pneumography in eight volunteers. With the onset of sedation there was a small decrease in SAP and increase in HR (ns). Spectral analysis of the HR time series showed reductions in the proportion of power in the high (90.15 Hz) frequency "ventilatory" band consistent with midazolam causing vagolysis. During sedation, low frequency (:0.05 Hz) oscillations of PLA, HR, SAP and ventilation were observed. These were thought to be secondary to activity of coupled cardiorespiratory neurones within the brain stem and the ventilatory periodicity appeared similar to that observed during the early stages of sleep. The diminished high frequency and increased low frequency oscillations induced by midazolam sedation were reversed by administration of flumazenil.

Respiratory Physiology & Neurobiology, 2013

Understanding the inter-relationship between pharmacological agents, ventilatory control, upper airway physiology and their consequent effects on sleep-disordered breathing may provide new directions for targeted drug therapy. Where available, this review focuses on human studies that contain both drug effects on sleep-disordered breathing and measures of ventilatory control or upper airway physiology. Many of the existing studies are limited in sample size or comprehensive methodology. At times, the presence of paradoxical findings highlights the complexity of drug therapy for OSA. The existing studies also highlight the importance of considering inter-individual pharmacokinetics and underlying causes of sleep apnea in interpreting drug effects on sleep-disordered breathing. Practical ways to assess an individual's ventilatory control and how it interacts with upper airway physiology is required for future targeted pharmacotherapy in sleep apnea.

Survey of Anesthesiology, 1997

and the Zablocki Veterans Administration Medical Center, Milwaukee, Wisconsin