naloxone and Airway-Obstruction

Pulmonary edema is a generalized descriptive term for the accumulation of fluid within the interstitium and/or the alveolar spaces of the lungs. This accumulation of fluid has a cause that may be termed cardiogenic or noncardiogenic. Pulmonary edema of cardiogenic origin is usually due to failure of the left side of the heart, but it also can be attributed to the right side of the heart. Noncardiogenic pulmonary edema (NCPE) usually is attributable to certain lung injuries or disease states, but it also can be neurogenic in origin. Some occurrences of NCPE can be traced directly to the administration of anesthesia. For example, NCPE can result from upper airway obstruction or the administration of naloxone.

Topics: Airway Obstruction; Anesthesia; Capillary Permeability; Capillary Resistance; Humans; Laryngismus; Naloxone; Narcotic Antagonists; Osmotic Pressure; Pressure; Pulmonary Edema; Risk Factors

Opioids increase abdominal muscle activity during anaesthesia. We proposed that opioid activity during anaesthesia would change chest wall size and movement, and contribute to ventilation. Using an optical system to measure chest wall volume, we studied 10 patients during isoflurane anaesthesia, first under the influence of an opioid and then after reversal with naloxone. Measurements were made during quiet breathing and with carbon dioxide stimulation. Airway occlusion pressure was measured to assess inspiratory and expiratory muscle activity. Chest wall volume decreased with the onset of spontaneous breathing, and decreased further when breathing was stimulated by carbon dioxide. Reversal of opioid activity increased chest wall volume. Breathing movements were predominantly abdominal. Opioid action affected the timing and amplitude of breathing but the pattern of abdominal movement was not affected. Since opioids augment abdominal muscle action during expiration, the unchanged pattern of movement can be attributed to both diaphragm and abdominal activity displacing the abdominal wall reciprocally, in the inspiratory and expiratory phases of the respiratory cycle, respectively.

Topics: Abdominal Muscles; Adult; Airway Obstruction; Airway Resistance; Analgesics, Opioid; Anesthetics, Inhalation; Drug Interactions; Exhalation; Female; Humans; Isoflurane; Male; Middle Aged; Models, Biological; Naloxone; Narcotic Antagonists; Pulmonary Gas Exchange; Respiration, Artificial; Respiratory Mechanics; Respiratory Muscles; Thoracic Wall; Tidal Volume

A case of pulmonary edema after the administration of naloxone for laparoscopic splenectomy is reported. Previous reports of naloxone-induced pulmonary edema are listed and reviewed. The clinical course is compared to other forms of non-cardiogenic pulmonary edema. Uncertainty remains about the underlying pathophysiological process and the true impact of naloxone on the development of pulmonary edema.

Topics: Adolescent; Airway Obstruction; Analgesics, Opioid; Drug Overdose; Echocardiography; Fluid Therapy; Humans; Laparoscopy; Male; Naloxone; Narcotic Antagonists; Oxygen; Platelet Count; Positive-Pressure Respiration; Pulmonary Edema; Purpura, Thrombocytopenic, Idiopathic; Radiography; Respiration, Artificial; Respiratory Function Tests; Splenectomy

Expiratory muscle action is prominent during anaesthesia and can impair lung function. This activity is exaggerated by the use of opioids. Airway pressure during occlusion of expiration would be a valuable measure in the study of expiratory muscle activation. However, this would only be valid if the imposed occlusion did not itself alter muscle activation. This possibility can be checked by directly assessing muscle activity by electromyography; varying arterial carbon dioxide tensions and opioid action should be considered.. We studied seven spontaneously breathing patients, anaesthetized with nitrous oxide and isoflurane, in four conditions: during an infusion of fentanyl and after naloxone, breathing normally and with breathing stimulated with CO(2). We compared diaphragm and external oblique abdominal electromyogram (EMG) signals during normal and occluded breaths. We also measured chest wall volume and compared airway occlusion pressure, during inspiration and expiration, with the EMG results.. Inspiratory occlusion increased the duration of inspiration during hypercapnia by 20%, but not the rate of electrical activation of the diaphragm, indicating that occlusion does not cause a reflex increase in diaphragm contraction. In contrast, expiratory occlusion did not affect either the duration of expiration or the electrical activity of the external oblique muscles.. In these conditions, except for a change in inspiratory duration, respiratory muscle activity is unaffected by airway occlusion. Airway occlusion will permit valid measures of muscle activity in inspiration and expiration and provide simple measurements of respiratory muscle function during anaesthesia.

Topics: Abdominal Muscles; Adult; Aged; Airway Obstruction; Analgesics, Opioid; Anesthetics, Inhalation; Carbon Dioxide; Child; Electromyography; Female; Fentanyl; Humans; Hypercapnia; Isoflurane; Male; Middle Aged; Naloxone; Nitrous Oxide; Respiratory Muscles

Topics: Airway Obstruction; Anesthetics, Intravenous; Bradycardia; Cardiotonic Agents; Cholangiopancreatography, Endoscopic Retrograde; Choledocholithiasis; Decerebrate State; Flumazenil; GABA Agonists; Humans; Hypnotics and Sedatives; Hypoxia; Intraoperative Complications; Intubation, Intratracheal; Male; Midazolam; Middle Aged; Naloxone; Piperidines; Propofol; Remifentanil; Sleep Apnea, Obstructive

Several procedures performed in the electrophysiology laboratory (EP lab) require surgical manipulation and are lengthy. Patients undergoing such procedures usually receive general anesthesia or deep sedation administered by an anesthesiologist. In 536 consecutive procedures performed in the EP lab, we assessed the safety and efficacy of deep sedation administered under the direction of an electrophysiologist and in the absence of an anesthetist. Patients were monitored with pulse oximetry, noninvasive blood pressure recordings, and continuous ECGs. The level of consciousness and vital signs were evaluated at 5-minute intervals. Deep sedation was induced in 260 patients using midazolam, phenergan, and meperidine, then maintained with intermittent dosing of meperidine at the following mean doses: midazolam 0.031 +/- 0.024 mg/kg; phenergan 0.314 +/- 0.179 mg/kg; and meperidine 0.391 +/- 0.167 mg/kg per hour. In the remaining 276 patients, deep sedation was induced with midazolam and fentanyl and maintained with a continuous infusion of fentanyl at a mean dose of 2.054 +/- 1.43 micrograms/kg per hour. Fourteen patients experienced a transient reduction in oxygen saturation that was readily reversed following administration of naloxone. An additional 11 patients desaturated secondary to partial airway obstruction, which resolved after repositioning the head and neck. Fourteen patients experienced hypotension with fentanyl. All but one returned to baseline blood pressures following an infusion of normal saline. No patient required intubation and no death occurred. Only three patients had recollection of periprocedure events. No patient remembered experiencing pain with the procedure. Hospital stays were not prolonged as a result of the sedation used.. (1) deep sedation during EP procedures can be administered safely under the guidance of the electrophysiologist without an anesthetist present; (2) the drugs used should be readily reversible in case of respiratory depression; and (3) this approach may reduce the overall cost of the procedures in the EP lab, maintaining adequate patient comfort.

Topics: Adjuvants, Anesthesia; Airway Obstruction; Anesthesia, Intravenous; Anesthesiology; Anesthetics, Intravenous; Blood Pressure; Consciousness; Cost Control; Electrocardiography; Electrophysiology; Evaluation Studies as Topic; Female; Fentanyl; Heart Rate; Humans; Hypnotics and Sedatives; Hypotension; Laboratories; Length of Stay; Male; Memory; Meperidine; Midazolam; Middle Aged; Monitoring, Physiologic; Naloxone; Narcotic Antagonists; Oximetry; Oxygen; Promethazine; Safety

Acute resistive loading of the airway has been shown to activate the endogenous opioid system, with subsequent depression of ventilation. The present investigation was designed to assess the effect of chronic airway loading on ventilation and CO2 sensitivity, and to determine whether the endogenous opioid system contributes to long-term modulation of ventilatory control in this setting. A flow-resistive ventilatory load was imposed in 2-mo-old rats by surgical implantation of a circumferential tracheal band that approximately tripled tracheal resistance. Respiration and CO2 sensitivity were serially and noninvasively assessed by barometric plethysmography over a period of 21 wk. Ventilatory output was assessed as minute inspiratory effort, which was defined as the product of plethysmograph signal amplitude, inspiratory time, and respiratory rate (RR). CO2 sensitivity was calculated as the percent change in minute inspiratory effort from room air to CO2 exposure. The effect of naloxone administration on these parameters was also determine. Arterial blood gases demonstrated hypercapnia with maintenance of normoxia in loaded rats; these findings persisted for the duration of the study. Two days after surgery, rats with tracheal obstruction demonstrated a lower RR than controls during room air breathing and during CO2 stimulation. CO2 sensitivity was significantly depressed in obstructed animals at this time. Escape from suppression of RR and CO2 sensitivity was evident by 14 to 21 d after obstruction; however, suppression of these parameters reappeared and was maintained from 56 to 147 d after obstruction. Naloxone augmented minute inspiratory effort during CO2 stimulation at 2 d after obstruction but not thereafter; naloxone had no effect in control rats. These data indicate that chronic airway loading suppresses RR and CO2 sensitivity in a triphasic manner. The early suppression is partially reversible by naloxone; late-appearing suppression is unaffected by naloxone and is presumably mediated by mechanisms that do not involve endogenous opioids.

Topics: Airway Obstruction; Airway Resistance; Animals; Carbon Dioxide; Chronic Disease; Disease Models, Animal; Eating; Hypercapnia; Inhalation; Male; Naloxone; Opioid Peptides; Oxygen; Oxygen Consumption; Plethysmography; Pulmonary Ventilation; Rats; Rats, Sprague-Dawley; Respiration; Tracheal Diseases