Inspiratory Airway Obstruction Research Articles

Effects of Opioids Given to Facilitate Mechanical Ventilation on Sleep Apnea After Extubation in the Intensive Care Unit.

Following extubation in the intensive care unit (ICU), upper airway (UA) edema and respiratory depressants may promote UA dysfunction. We tested the hypothesis that opioids increase the risk of sleep apnea early after extubation. Fifty-six ICU patients underwent polysomnography the night after extubation. Airflow limitation during wakefulness was identified using bedside spirometry. Correlation and ordinal regression analyses were used to quantify the effects of preextubation opioid dose on postextubation apnea-hypopnea index (AHI) and severity of sleep apnea and whether or not inspiratory airway obstruction (ratio of maximum expiratory and inspiratory airflows at 50% of vital capacity [MEF50/MIF50] ≥ 1) during wakefulness predicts airway obstruction during sleep. Data were adjusted for age, gender, body mass index, as well as a generalized propensity score balanced for APACHE II, score for preoperative prediction of obstructive sleep apnea, duration of mechanical ventilation, chronic obstructive pulmonary disease, and a procedural severity score for morbidity. Sleep apnea (AHI ≥ 5) was present in 40 (71%) of the 56 patients. Morphine equivalent dose given 24 hours prior extubation predicted obstructive respiratory events during sleep (r = 0.35, p = .01) and sleep apnea (odds ratio [OR] 1.17; 95% confidence interval [CI] 1.02-1.34). Signs of inspiratory UA obstruction (MEF50/MIF50 ≥ 1) assessed by bedside spirometry were strongly associated with sleep apnea (OR 5.93; 95% CI 1.16-30.33). High opioid dose given 24 hours prior to extubation increases the likelihood of postextubation sleep apnea in the ICU, particularly in patients with anatomical vulnerability following extubation.

Dyspnoea due to vocal fold abduction paresis in anti-MuSK myasthenia gravis

A 24-year-old female student who had inspiratory stridor and exertional dyspnoea for 2 years was seen in our neurology and otolaryngology outpatient department. The dyspnoea disabled her in walking stairs...

Needle cricothyroidotomy

Needle cricothyroidotomy

Cricothyroid Muscle Function and Vocal Fold Stability in Exercising Horses

To determine (1) if the cricothyroid muscle had respiratory-related electromyographic (EMG) activity that increased with respiratory effort and (2) if bilateral cricothyroid myotomy resulted in vocal fold instability and collapse in exercising horses. Experimental. Seven (3 EMG; 4 cricothyroid myotomy) Standardbred horses. Three horses exercised on a treadmill at speeds corresponding to the speed that produced maximum heart rate (HR(max)), 75% of maximum heart rate (HR(75%max)), and 50% of maximum heart rate (HR(50%max)) for 60 seconds at each speed while EMG activity of the cricothyroid muscle and nasopharyngeal pressures were measured. Another 4 normal horses were exercised on the treadmill at HR(max) and HR(75%max) for 60 seconds at each speed before and after bilateral cricothyroid myotomy. Upper airway pressures were measured and videoendoscopic examinations were performed and videotaped at each speed. Peak phasic EMBG activity of the cricothyroid muscle was coincident with inspiration and increased with treadmill speed. Bilateral cricothyroid myotomy resulted in vocal fold collapse in all horses. Mean peak inspiratory pressures were significantly more negative compared with control values at both HR(max) and HR(75%max). Cricothyroid muscle dysfunction may be implicated in vocal fold collapse and likely causes inspiratory airway obstruction in exercising horses. Conditions compromising cricothyroid muscle function or motor innervation could result in vocal fold collapse.

Bifid epiglottis: a case report

Bifid epiglottis is a rare congenital laryngeal anomaly, usually associated with multiple congenital anomalies which include digital anomalies and hypothalamic pituitary dysfunction manifesting as growth retardation. A case is presented of a 2-year-old child with this picture in whom the bifid epiglottis prolapsed over the laryngeal inlet to cause inspiratory airway obstruction. Corrective surgery was not successful and eventually a partial epiglottectomy was required.

Abnormal movement of the arytenoid region as a cause of upper airway obstruction.

A 75 year old woman presented with a three week history of severe dyspnoea and cough. Auscultation and spirometry suggested extrathoracic inspiratory airway obstruction, and bronchoscopy showed abnormal motion of the arytenoid region (supraglottic area), causing upper airway obstruction only during forced inspiratory efforts. Sedatives improved the symptoms within a week. It is suggested that reversible malfunction of the arytenoid region can be responsible for upper airway obstruction.

Functional Upper Airway Obstruction: Psychogenic Pharyngeal Constriction

A 15-year-old boy, known to have asthma, developed acute inspiratory airway obstruction with marked stridor. Spirometry indicated extrathoracic airway obstruction and a bronchofiberoptic examination disclosed narrowing in the hypopharynx. After administration of sedatives, the stridor suddenly disappeared. Psychotherapy decreased the frequency of subsequent stridor attacks. It is suggested that psychogenic pharyngeal constriction may have caused the upper airway obstruction with respiratory distress.

Chemosensitivity and the ventilatory response to airflow obstruction during sleep.

There is an accumulating body of evidence which suggests that chemical control of breathing can play a role in destabilizing respiratory rhythm during sleep. We hypothesized that the sleeping ventilatory response to hypercapnia (HCVR) and/or hypoxia (HVR) would predict respiratory events following release of inspiratory airway obstruction (IAO) in normal men during non-rapid-eye-movement (NREM) sleep. We therefore measured HCVR, HVR, and ventilation for three breaths preceding and eight breaths following three totally obstructed inspirations in eight normal subjects during NREM sleep. After IAO, we generally observed transient hyperventilation that resulted in hypocapnia and prolonged expiratory time. We found the initial increase in inspiratory minute ventilation (VI) following IAO to be correlated with HCVR (r = 0.72, P less than 0.05) but not HVR. In addition, the maximum decrease in PCO2 below base line was also related to HCVR (r = 0.83, P less than 0.05). This decrement in PCO2 predicted the subsequent prolongation in expiratory time (TE, r = 0.83, P less than 0.05) that was frequently observed. HCVR tended to predict the prolongation of TE, at the nadir of CO2 (r = 0.69, P = 0.057). In conjunction with this hypocapnia and prolongation of TE, hypoventilation with falling VI was often observed followed by periodic hyper- and hypoventilation. These results suggest that high HCVR may result in ventilatory overshoot following IAO and may contribute to ventilatory instability during sleep.

Inspiratory airway obstruction does not affect lung fluid balance in lambs. by hansen tn, gest al, and landers s. j appl physiol 1985; 58:1314–1318

Inspiratory airway obstruction does not affect lung fluid balance in lambs. by hansen tn, gest al, and landers s. j appl physiol 1985; 58:1314–1318

Inspiratory airway obstruction does not affect lung fluid balance in lambs.

The purpose of this study was to examine the effects of inspiratory airway obstruction on lung fluid balance in newborn lambs. We studied seven 2- to 4-wk-old lambs that were sedated with chloral hydrate and allowed to breathe 30-40% O2 spontaneously through an endotracheal tube. We measured lung lymph flow, lymph and plasma protein concentrations, pulmonary arterial and left atrial pressures, mean and phasic pleural pressures and airway pressures, and cardiac output during a 2-h base-line period and then during a 2- to 3-h period of inspiratory airway obstruction produced by partially occluding the inspiratory limb of a nonrebreathing valve attached to the endotracheal tube. During inspiratory airway obstruction, both pleural and airway pressures decreased 5 Torr, whereas pulmonary arterial and left atrial pressures each decreased 4 Torr. As a result, calculated filtration pressure remained unchanged. Inspiratory airway obstruction had no effect on steady-state lung lymph flow or the lymph protein concentration relative to that of plasma. We conclude that in the spontaneously breathing lamb, any decrease in interstitial pressure resulting from inspiratory airway obstruction is offset by a decrease in microvascular hydrostatic pressure so that net fluid filtration remains unchanged.

Subclinical reduction in airflows after Teflon injection of vocal cord.

Results of intracordal Teflon injection for symptoms of unilateral vocal cord paralysis have been excellent. There seems to be no significant long-term foreign body reaction or limitation to maximum airflows. However, acute inflammatory reactions and airflow obstruction have been reported. The objective of the present study was to evaluate the frequency, extent, and duration of airway obstruction following Teflon injection. Forced inspiratory and expiratory airflows were measured in seven consecutive patients before, 24 hours, and 10 days after Teflon injection. Significant variable upper airway obstruction, as demonstrated by an increase in the ratio of forced expiratory airflows at 50% Vital Capacity to the forced inspiratory airflows at the same lung volume (VE50/VI50), was found in each subject. At 24 hours after the injection this ratio increased from a baseline of .098 +/- 0.50 (mean +/- S.D.) to 1.41 +/- 0.67 (P less than 0.01), and returned to baseline values in 10 days (0.95 +/- 0.14). We conclude that Teflon injection into a paralyzed vocal cord creates a significant inspiratory airway obstruction that is reversible in 10 days.

1167 A NEUROMUSCULAR MECHANISM PREVENTING AIRWAY OBSTRUCTION

To function as a conduit for air, the extrathoracic airway (ETA) must resist closure when intraluminal pressure decreases during inspiration. Previous work (Fed. Proc., in press) suggested that a neuromuscular mechanism opposes ETA closure. Current experiments elucidate this mechanism. The ETA segment most vulnerable to passive closure was determined. Closing pressure (CP) was defined as that negative intraluminal pressure at which pressure changes are no longer transmitted across the ETA. In 5 rabbits, 30-32 days old, post mortem CP of the ETA was -6.0 ± 1.8 cm H2O; in each case, the nose and trachea remained open at -40 cm H2O, thus implicating the pharynx or larynx as the site of closure. In anesthetized rabbits, forward inspiratory movement of the hyoid bone and associated soft tissues was observed. Electromyography of muscles which pull the hyoid and tongue forward (mylohyoid, geniohyoid, genioglossus) demonstrated phasic inspiratory activity which increased during asphyxia from airway occlusion. Post mortem, the action of these muscles was simulated by traction on the hyoid. CP of the ETA with hyoid traction was -14.2 ± 3.1 cm H2O compared to -6.0 ± 1.8 cm H2O without traction (N=5, p <.01, paired t-test). This difference in CP with and without traction suggests that the mylohyoid, geniohyoid and genioglossus muscles function as accessory muscles of respiration to prevent inspiratory airway obstruction.