Mouth-opening increases upper-airway collapsibility without changing resistance during midazolam sedation.

Sedative doses of anesthetic agents affect upper-airway function. Oral-maxillofacial surgery is frequently performed on sedated patients whose mouths must be as open as possible if the procedures are to be accomplished successfully. We examined upper-airway pressure-flow relationships in closed mouths, mouths opened moderately, and mouths opened maximally to test the hypothesis that mouth-opening compromises upper-airway patency during midazolam sedation. From these relationships, upper-airway critical pressure (Pcrit) and upstream resistance (Rua) were derived. Maximal mouth-opening increased Pcrit to -3.6 +/- 2.9 cm H2O compared with -8.7 +/- 2.8 (p = 0.002) for closed mouths and -7.2 +/- 4.1 (p = 0.038) for mouths opened moderately. In contrast, Rua was similar in all three conditions (18.4 +/- 6.6 vs. 17.7 +/- 7.6 vs. 21.5 +/- 11.6 cm H2O/L/sec). Moreover, maximum mouth-opening produced an inspiratory airflow limitation at atmosphere that was eliminated when nasal pressure was adjusted to 4.3 +/- 2.7 cm H2O. We conclude that maximal mouth-opening increases upper-airway collapsibility, which contributes to upper-airway obstruction at atmosphere during midazolam sedation.

Therapeutic electrical stimulation of the hypoglossal nerve in obstructive sleep apnea.

BACKGROUND: Hypoglossal nerve stimulation has been demonstrated to relieve upper airway obstruction acutely, but its effect on obstructive sleep apnea is not known. OBJECTIVE: To determine the response in obstructive sleep apnea to electrical stimulation of the hypoglossal nerve. METHODS: Eight patients with obstructive sleep apnea were implanted with a device that stimulated the hypoglossal nerve unilaterally during inspiration. Sleep and breathing patterns were examined at baseline before implantation and after implantation at 1, 3, and 6 months and last follow-up. RESULTS: Unilateral hypoglossal nerve stimulation decreased the severity of obstructive sleep apnea throughout the entire study period. Specifically, stimulation significantly reduced the mean apnea-hypopnea indices in non-rapid eye movement (mean +/- SD episodes per hour, 52.0 +/- 20.4 for baseline nights and 22.6 +/- 12.1 for stimulation nights; P<.001) and rapid eye movement (48.2 +/- 30.5 and 16.6 +/- 17.1, respectively; P<.001) sleep and reduced the severity of oxyhemoglobin desaturations. With improvement in sleep apnea, a trend toward deeper stages of non-rapid eye movement sleep was observed. Moreover, all patients tolerated long-term stimulation at night and did not experience any adverse effects from stimulation. Even after completing the study protocol, the 3 patients who remained free from stimulator malfunction continued to use this device as primary treatment. CONCLUSION: The findings demonstrate the feasibility and therapeutic potential for hypoglossal nerve stimulation in obstructive sleep apnea.

Effects of arousal and sleep state on systemic and pulmonary hemodynamics in obstructive apnea.

During obstructive sleep apnea (OSA), systemic (Psa) and pulmonary (Ppa) arterial pressures acutely increase after apnea termination, whereas left and right ventricular stroke volumes (SV) reach a nadir. In a canine model (n = 6), we examined the effects of arousal, parasympathetic blockade (atropine 1 mg/kg iv), and sleep state on cardiovascular responses to OSA. In the absence of arousal, SV remained constant after apnea termination, compared with a 4.4 +/- 1.7% decrease after apnea with arousal (P < 0.025). The rise in transmural Ppa was independent of arousal (4.5 +/- 1.0 vs. 4.1 +/- 1.2 mmHg with and without arousal, respectively), whereas Psa increased more after apnea termination in apneas with arousal compared with apneas without arousal. Parasympathetic blockade abolished the arousal-induced increase in Psa, indicating that arousal is associated with a vagal withdrawal of the parasympathetic tone to the heart. Rapid-eye-movement (REM) sleep blunted the increase in Psa (pre- to end-apnea: 5.6 +/- 2.3 mmHg vs. 10.3 +/- 1.6 mmHg, REM vs. non-REM, respectively, P < 0.025), but not transmural Ppa, during an obstructive apnea. We conclude that arousal and sleep state both have differential effects on the systemic and pulmonary circulation in OSA, indicating that, in patients with underlying cardiovascular disease, the hemodynamic consequences of OSA may be different for the right or the left side of the circulation.

Neural and local effects of hypoxia on cardiovascular responses to obstructive apnea.

Obstructive sleep apnea (OSA) acutely increases systemic (Psa) and pulmonary (Ppa) arterial pressures and decreases ventricular stroke volume (SV). In this study, we used a canine model of OSA (n = 6) to examine the role of hypoxia and the autonomic nervous system (ANS) in mediating these cardiovascular responses. Hyperoxia (40% oxygen) completely blocked any increase in Ppa in response to obstructive apnea but only attenuated the increase in Psa. In contrast, after blockade of the ANS (20 mg/kg iv hexamethonium), obstructive apnea produced a decrease in Psa (-5.9 mmHg; P < 0.05) but no change in Ppa, and the fall in SV was abolished. Both the fall in Psa and the rise in Ppa that persisted after ANS blockade were abolished when apneas were induced during hyperoxia. We conclude that 1) hypoxia can account for all of the Ppa and the majority of the Psa response to obstructive apnea, 2) the ANS increases Psa but not Ppa in obstructive apnea, 3) the local effects of hypoxia associated with obstructive apnea cause vasodilation in the systemic vasculature and vasoconstriction in the pulmonary vasculature, and 4) a rise in Psa acts as an afterload to the heart and decreases SV over the course of the apnea.

The effect of tensor veli palatini stimulation on upper airway patency.

OBJECTIVE: To evaluate the effect of selective electrical stimulation of the tensor veli palatini muscle on upper airway patency. METHODS: Pressure-flow relationships were evaluated, in a feline isolated upper airway preparation, to determine the role of the soft palate musculature on airflow dynamics. The tensor veli palatini muscles were selectively stimulated while monitoring upper airway collapsibility (critical pressure), maximal inspiratory airflow, and the nasal resistance upstream to the flow-limiting site. RESULTS: Tensor veli palatini stimulation resulted (mean +/- SEM) in an increase in maximal inspiratory airflow from 74 +/- 13 mL/s to 93 +/- 18 mL/s (P= .04). The increase in maximal inspiratory airflow was associated with a decrease in critical pressure from -2.3 +/- 1.7 cm H2O to -4.7 +/- 2.7 cm H2O (P= .01) and an increase in nasal resistance from 32.4 +/- 24.3 cm H2O x L(-1) s(-1) to 50.8 +/- 29.7 cm H2O x L(-1) s(-1) (P= .02). CONCLUSIONS: Tensor veli palatini stimulation decreases upper airway collapsibility and is likely an integral component in maintaining airway patency. However, the effects of the isolated tensor veli palatini muscles are less significant than those seen previously with physiologic stimuli such as hypercapnia. These findings suggest that upper airway patency, although contributed to by the tensor veli palatini, requires the coordinated activation of palatopharyngeal muscles to adequately influence upper airway collapsibility.

Evaluation of patients with sleep apnea after tracheotomy.

OBJECTIVE: To determine the effect of tracheotomy on polysomnographic and arterial blood gas data in patients with obstructive sleep apnea (OSA). DESIGN: A retrospective study of all patients who underwent tracheotomy and were studied polysomnographically at the Johns Hopkins Sleep Disorders Center, Baltimore, Md, since 1981. SETTING: A regional sleep disorders center. PATIENTS: Twenty-eight patients (8 women and 20 men), aged 22 through 77 years. Patients were categorized into 2 groups on the basis of whether they had already undergone tracheotomy before polysomnography. Group 1 patients all had a polysomnographic diagnosis of OSA before tracheotomy. They were further subdivided on the basis of whether cardiopulmonary decompensation had been absent (group 1a, n=10) or present (group 1b, n=13). Group 2 patients (n=5) had undergone tracheotomy to treat upper airway obstruction that developed after non-apnea-related upper aerodigestive tract surgeries. INTERVENTION: Tracheotomy. MAIN OUTCOME MEASURES: Nocturnal non-rapid eye movement, apnea-hypopnea index, percentage oxyhemoglobin saturation, and arterial blood gas data. RESULTS: Patients with OSA underwent tracheotomy as definitive treatment for the apnea (n=15), to prevent postoperative upper airway compromise after uvulopalatopharyngoplasty (n=7), and to treat upper airway compromise after non-apnea-related upper aerodigestive tract surgeries (n=6). Tracheotomy alleviated apnea in all 10 patients with uncomplicated sleep apnea (group 1a). For patients with OSA complicated by cardiopulmonary decompensation (group 1b), tracheotomy improved but did not eliminate sleep apnea in 7 of the 13 patients, despite overall improvement in arterial blood gas values. For patients whose sleep apnea had not been diagnosed polysomnographically before tracheotomy (group 2), tracheotomy was still required to treat OSA that had previously not been recognized. CONCLUSIONS: Tracheotomy effectively treated patients with uncomplicated OSA, but was much less effective in treating patients with OSA and cardiopulmonary decompensation. In patients who underwent tracheotomy in conjunction with other upper aerodigestive tract surgeries, concomitant obstructive sleep apnea often required continued use of a tracheotomy to maintain upper airway patency.

Direct hypoglossal nerve stimulation in obstructive sleep apnea.

OBJECTIVES: To determine the motor responses resulting from direct electrical stimulation of the hypoglossal (HG) nerve and to correlate these responses to changes in upper airway patency during sleep. DESIGN: The motor effects of direct electrical stimulation of the main trunk of the HG nerve and the branch that supplies the genioglossus muscle during anesthesia and wakefulness were assessed visually. Responses in airflow during sleep to HG nerve stimulation were assessed with standard polysomnographic techniques. SETTING: University medical center. PATIENTS: Fifteen patients undergoing a surgical procedure that involved the neck that exposed the HG nerve and 5 volunteer patients with obstructive sleep apnea constituted the study population. INTERVENTIONS: The main trunk (n = 3) and genioglossus branch (n = 2) of the HG nerve were stimulated electrically with a half-cuff tripolar electrode. RESULTS: Stimulation of the branch of the HG nerve that innervates the genioglossus muscle caused protrusion and contralateral deviation of the tongue. Stimulation of the main trunk of the HG nerve caused slight ipsilateral deviation and retrusion of the tongue. The arousal threshold for stimulation exceeded the motor recruitment threshold by 0.8 +/- 0.4 V. Inspiratory airflow increased in all patients by 184.5 +/- 61.7 mL/s (mean +/- SD; P = .02, analysis of variance) with stimulation. CONCLUSION: Direct HG nerve stimulation below the arousal threshold can improve airflow in patients with obstructive sleep apnea.

The effects of selective nerve stimulation on upper airway airflow mechanics.

OBJECTIVE: To evaluate the effect of electrical stimulation of hypoglossal nerve branches and ansa cervicalis nerve branches on upper airway patency. DESIGN: Pressure-flow relationships obtained during supramaximal stimulation of hypoglossal nerve branches and ansa cervicalis nerve branches were analyzed in the isolated feline upper airway to determine the maximum inspiratory airflow as well as to determine pharyngeal collapsibility (upper airway critical pressure) and nasal resistance upstream from the site of pharyngeal collapse. Comparisons were performed between baseline and stimulation conditions with paired two-tailed t tests. RESULTS: Stimulation of the proximal hypoglossal nerve trunk, distal medial hypoglossal nerve branch, nerve branches to the suprahyoid muscles, the infrahyoid muscles, and the suprahyoid and infrahyoid muscles simultaneously increased maximum inspiratory airflow significantly by decreasing airway collapsibility. A greater reduction in airway collapsibility was observed with stimulation of the tongue muscles compared with stimulation of the strap muscles. CONCLUSIONS: Stimulation of specific hypoglossal and ansa cervicalis nerve branches consistently increased maximum inspiratory airflow by decreasing airway collapsibility. The major decrease in airway collapsibility from hypoglossal nerve stimulation is dependent on the action of the genioglossus muscle.

Diagnosis and treatment of obstructive sleep apnea of the larynx.

To determine the mechanism for obstructive sleep apnea in two patients with clinical abnormalities of laryngeal function, airflow dynamics during sleep were analyzed. The site of airway obstruction was assessed by examining pressure gradients across specific airway segments. The relation between maximal inspiratory airflow and nasal pressure was analyzed to determine (1) the critical pressure, a measure of the collapsibility of the laryngeal airway, and (2) the effect of nasal continuous positive airway pressure on airflow during sleep. Large inspiratory pressure gradients developed during sleep between the supraglottic and pleural spaces, indicating that collapse had occurred in the larynx. Elevated critical pressures of -6.4 and +1.2 cm H2O, respectively, occurred in the two patients. When the nasal pressure was raised to 10 cm H2O, normal levels of tidal airflow occurred, and obstructive apneas were eliminated. These findings indicate that sleep apnea was caused by laryngeal airflow obstruction that resulted from elevations in the collapsibility of the larynx. The response to nasal continuous positive airway pressure suggested that laryngeal sleep apnea was similar to pharyngeal sleep apnea in pathophysiologic characteristic and response to treatment.

Upper airway collapsibility in children with obstructive sleep apnea syndrome.

In adults, the critical nasal pressure (Pcrit) at which the upper airway collapses is higher in patients with the obstructive sleep apnea syndrome (OSAS) than in those with primary snoring. Pediatric OSAS differs clinically from adult OSAS. We therefore compared Pcrit between prepubertal children with OSAS and primary snoring. Pcrit was determined by correlating the maximal inspiratory airflow with the level of positive or negative nasal pressure applied via a nasal mask. As in adults, we found that the maximal inspiratory airflow varied in proportion to the upstream (nasal) rather than the downstream (esophageal) pressure changes. Pcrit was 1 +/- 3 cmH2O in OSAS compared with -20 +/- 9 cmH2O in primary snorers (P < 0.002). In three OSAS patients reevaluated after tonsillectomy and adenoidectomy, Pcrit declined to -7.2 +/- 4.0 cmH2O. We conclude that the pediatric airway behaved as predicted by the Starling resistor model and that Pcrit, a measure of airway collapsibility, correlated with the degree of upper airway obstruction and was reduced postoperatively, consistent with increased upper airway stability.

Effect of uvulopalatopharyngoplasty on upper airway collapsibility in obstructive sleep apnea.

Previous investigators have demonstrated variable responses to uvulopalatopharyngoplasty (UPP) in patients with obstructive sleep apnea. We hypothesized that this variability is due to either (1) differences in baseline pharyngeal collapsibility preoperatively or (2) differences in magnitude of the decrease in pharyngeal collapsibility resulting from surgery. To determine the relationship between changes in collapsibility and the response to UPP surgery, we measured the upper airway critical pressure (Pcrit) before and after UPP in 13 patients with obstructive sleep apnea. During non-REM sleep, maximal inspiratory airflow (VImax) was quantitated by varying the level of nasal pressure (PN), and Pcrit was determined by the level of PN below which VImax ceased. A positive response to UPP was defined by a greater than or equal to 50% fall in non-REM disordered breathing rate (DBR). In the entire group, UPP resulted in significant decreases in DBR from 71.1 +/- 22.4 to 44.7 +/- 38.4 episodes/h (p = 0.025) and in Pcrit from 0.2 +/- 2.4 to -3.1 +/- 5.4 cm H2O (p = 0.016). Moreover, the percent change in DBR was correlated significantly with the change in Pcrit (p = 0.001). Subgroup analysis of responders and nonresponders demonstrated that significant differences in Pcrit were confined to the responders. Specifically, responders demonstrated a significant fall in Pcrit from -0.8 +/- 3.0 to -7.3 +/- 4.9 cm H2O (p = 0.01), whereas no significant change in Pcrit was detected in the nonresponders (1.1 +/- 1.6 versus 0.6 +/- 2.0 cm H2O. No clinical, polysomnographic, or physiologic predictors of a favorable response were found preoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Recognition of diabetes insipidus in postpartum hypopituitarism.

The association of diabetes insipidus with postpartum hypopituitarism is unusual. This report presents a patient with both conditions. Evidence pointing to the pathogenesis of the diabetes insipidus is discussed. This case and selected others illustrate the wide spectrum in the severity of diabetes insipidus encountered in postpartum hypopituitarism, as well as the masking of symptoms caused by concomitant glucocorticoid insufficiency. Histopathologic and experimental evidence suggests that patients with hypopituitarism occurring postpartum might also display mild diabetes insipidus if challenged with antidiuretic stimuli. Diabetes insipidus may be a feature of postpartum hypopituitarism that is infrequently recognized.