Elimination of central sleep apnoea by mitral valvuloplasty: the role of feedback delay in periodic breathing.

Central sleep apnoea is a form of periodic breathing which resembles Cheyne-Stokes respiration but occurs only during sleep. One mechanism in the pathogenesis is a delay in chemical feedback from the lungs to the medullary respiratory centre. We explored the relationship between circulatory feedback delay in a patient with central sleep apnoea and Cheyne-Stokes respiration before and after mitral valve repair. Preoperatively the patient had severe central sleep apnoea and an increased circulation time. Following mitral valvuloplasty the circulation time was decreased with resolution of central sleep apnoea. This case demonstrates the role of feedback delay in central sleep apnoea and suggests that similar haemodynamic mechanisms may lead to central sleep apnoea and Cheyne-Stokes respiration.

Effect of alae nasi activation on maximal nasal inspiratory airflow in humans.

The upper airway is a complicated structure that is usually widely patent during inspiration. However, on inspiration during certain physiological and pathophysiological states, the nares, pharynx, and larynx may collapse. Collapse at these locations occurs when the transmural pressure (Ptm) at a flow-limiting site (FLS) falls below a critical level (Ptm'). On airway collapse, inspiratory airflow is limited to a maximal level (VImax) determined by (-Ptm')/Rus, where Rus is the resistance upstream to the FLS. The airflow dynamics of the upper airway are affected by the activity of its associated muscles. In this study, we examine the modulation of VImax by muscle activity in the nasal airway under conditions of inspiratory airflow limitation. Each of six subjects performed sniffs through one patent nostril (pretreated with an alpha agonist) while flaring the nostril at varying levels of dilator muscle (alae nasi) EMG activity (EMGan). For each sniff, we located the nasal FLS with an airway catheter and determined VImax, Ptm', and Rus. Activation of the alae nasi from the lowest to the highest values of EMGan increased VImax from 422 +/- 156 to 753 +/- 291 ml/s (P < 0.01) and decreased Ptm' from -3.6 +/- 3.0 to -6.0 +/- 4.7 cmH2O (P < 0.05). Activation of the alae nasi had no consistent effect on Rus. VImax was positively correlated with EMGan, and Ptm' was negatively correlated with EMGan in all subjects. Our findings demonstrate that alae nasi activation increases VImax through the nasal airway by decreasing airway collapsibility.

The study of maximal nasal inspiratory flow in humans.

During inspiration through one nostril, airflow becomes limited to a maximal level (VImax) when the transmural pressure (Ptm) at a flow-limiting site (FLS) falls below a critical level (Ptm'). We compared two methods for measuring the Ptm' of the nasal FLS. Each of six subjects (four normal and two with allergic rhinitis out of season) performed multiple inspirations through one nostril as we varied the resistance at the nasal opening. Studies were performed after application of a topical decongestant without activation of the alae nasi. We determined Ptm' by regressing the resulting values of VImax on the corresponding transnasal pressure gradients (Regression Method). We also measured Ptm' directly using pressure catheters to measure the pressure surrounding the FLS and the lateral pressure near the FLS at VImax (Catheter Method). The mean value of Ptm' by the Regression Method was -3.8 +/- 3.2 (SD) cmH2O. The value by the Catheter Method with the catheter just downstream from the nasal FLS was -3.5 +/- 2.9 cmH2O, which correlated closely with the Ptm by the Regression Method (r = 0.98). Our findings suggest that the Ptm' of the nasal airway can be determined by either method. The Catheter Method, however, requires only one inspiratory effort for each determination and simultaneously localizes the nasal FLS.

Pulmonary function and respiratory chemosensitivity in moderately obese patients with sleep apnea.

To determine whether moderately obese, normocapnic, sleep apnea patients are distinguished from normal obese individuals by differences in waking pulmonary function and respiratory chemosensitivity, we compared the waking pulmonary function, hypercapnic, and hypoxic ventilatory responses of 35 nonhypercapnic sleep apnea patients (32 men and 3 women) with those of 17 age-, sex-, weight-, and obesity-matched nonapneic control subjects (16 men and 1 woman). The waking ventilatory response to hypercapnia was lower among sleep apnea patients (mean +/- SD, 2.05 +/- 1.29 L/min/mm Hg) than control subjects (3.02 +/- 2.05 L/min/mm Hg, p < 0.05). Patients with sleep apnea demonstrated a higher waking PaCO2 (40.4 +/- 2.9 vs 37.0 +/- 2.7 mm Hg, p < 0.001), and a lower waking PaO2 (81.4 +/- 11.7 vs 89.7 +/- 10.4 mm Hg, p < 0.03). The waking hypoxic ventilatory response, however, was not significantly different between the groups. Moreover, control subjects had a higher total lung capacity than sleep apnea patients (6.99 +/- 1.12 L and 6.27 +/- 1.09 L, respectively, p < 0.05). The lower hypercapnic ventilatory response, higher waking PaCO2, and lower total lung capacity in the sleep apnea patients resemble the pattern observed in patients with pickwickian syndrome. This suggests that disturbances in pulmonary function and ventilatory control in moderately obese sleep apnea patients are intermediate along a continuum from normal obesity to the pickwickian syndrome.

Premises liability.

Like other health care providers, optometrists have a duty to maintain offices and equipment in a safe condition. Failure to meet this duty results in premises liability. This article discusses premises liability with particular emphasis on pupillary dilation as a causative factor for patient injuries.

Effect of weight loss on upper airway collapsibility in obstructive sleep apnea.

Previous investigators have demonstrated in patients with obstructive sleep apnea that weight reduction results in a decrease in apnea severity. Although the mechanism for this decrease is not clear, we hypothesize that decreases in upper airway collapsibility account for decreases in apnea severity with weight loss. To determine whether weight loss causes decreases in collapsibility, we measured the upper airway critical pressure (Pcrit) before and after a 17.4 +/- 3.4% (mean +/- SD) reduction in body mass index in 13 patients with obstructive sleep apnea. Thirteen weight-stable control subjects matched for age, body mass index, gender (all men), and non-REM disordered breathing rate (DBR) also were studied before and after usual care intervention. During non-REM sleep, maximal inspiratory airflow was measured by varying the level of nasal pressure and Pcrit was determined by the level of nasal pressure below which maximal inspiratory airflow ceased. In the weight loss group, a significant decrease in DBR from 83.3 +/- 31.0 to 32.5 +/- 35.9 episodes/h and in Pcrit from 3.1 +/- 4.2 to -2.4 +/- 4.4 cm H2O (p less than 0.00001) was demonstrated. Moreover, decreases in Pcrit were associated with nearly complete elimination of apnea in each patient whose Pcrit fell below -4 cm H2O. In contrast, no significant change in DBR and a minimal reduction in Pcrit from 5.2 +/- 2.3 to 4.2 +/- 1.8 cm H2O (p = 0.031) was observed in the "usual care" group. We conclude that (1) weight loss is associated with decreases in upper airway collapsibility in obstructive sleep apnea, and that (2) the resolution of sleep apnea depends on the absolute level to which Pcrit falls.

A review of five recent cases of significance for optometrists.

The standard of care expected of optometrists continues to be defined by the courts. Misdiagnosis of ocular disease and liability for injuries caused by ophthalmic products remain the leading causes of litigation. Documentation of findings, warnings, and key management decisions is an essential aspect of clinical practice and must not be neglected by clinicians.

Induction of upper airway occlusion in sleeping individuals with subatmospheric nasal pressure.

In collapsible biologic conduits, occlusion and cessation of flow occur when upstream pressure falls below a critical pressure (Pcrit). To examine the relationship between Pcrit and the development of upper airway occlusion, we examined the relationship between maximal inspiratory airflow and nasal pressure in seven normal subjects during sleep. At varying levels of subatmospheric pressure applied to a nasal mask during non-rapid-eye-movement (NREM) sleep, maximal inspiratory airflow decreased in proportion to the level of nasal pressure. When nasal pressure fell below a Pcrit, subjects demonstrated upper airway occlusions terminated by arousals. In these normal subjects, the upper airway Pcrit was found to be -13.3 +/- 3.2 (SD) cmH2O. In four subjects who sustained sleep while nasal pressure remained below the Pcrit, recurrent occlusive apneas were demonstrated. The relationship between maximal inspiratory airflow and nasal pressure in each subject was fit by linear regression and demonstrated upper airway Pcrit at the zero-flow intercept that were not significantly different from those observed experimentally. These data demonstrate that the normal human upper airway during sleep is characterized by a negative Pcrit and that occlusion may be induced when nasal pressure is decreased below this Pcrit.

Upper airway pressure-flow relationships in obstructive sleep apnea.

We examined the pressure-flow relationships in patients with obstructive sleep apnea utilizing the concepts of a Starling resistor. In six patients with obstructive sleep apnea, we applied incremental levels of positive pressure through a nasal mask during non-rapid-eye-movement sleep. A positive critical opening pressure (Pcrit) of 3.3 +/- 3.3 (SD) cmH2O was demonstrated. As nasal pressure was raised above Pcrit, inspiratory airflow increased in proportion to the level of positive pressure applied until apneas were abolished (P less than 0.01). However, at pressures greater than Pcrit, esophageal pressures either did not correlate or correlated inversely with inspiratory airflow provided that esophageal pressure was less than Pcrit. When pressure was applied to a full face mask, inspiratory airflow did not occur and Pcrit could not be obtained at pressures well above Pcrit demonstrated with the nasal mask. These results are consistent with the view that the upper airway functions as a Starling resistor with a collapsible segment in the oropharynx. These findings offer a unifying construct for the association of sleep apnea, periodic hypopnea, and snoring.

Malpractice reform.

The continuing debate over malpractice claims against physicians has led to widespread efforts to reform state laws affecting these claims. The most common changes have been: limitations on size of awards; shortening the statute of limitations; abolition of the collateral source rule; proscription of ad damnum clauses for damages; limitation of contingency fees; the establishment of screening panels; and the use of arbitration. Inevitably, optometrists and other health care practitioners have also benefitted from these changes, which serve to lessen the likelihood of malpractice claims or to limit their effects. Optometrists continue to be among the least-sued practitioners in health care.

The effect of chronic nocturnal oxygen administration upon sleep apnea.

Administration of nocturnal oxygen for 1 night to patients with obstructive sleep apnea (OSA) causes a moderate reduction in apnea frequency without improving hypersomnolence. Therefore, we administered oxygen chronically to patients with OSA to determine: whether apnea frequency would be further reduced, whether the effect of oxygen upon apnea frequency is correlated with an increased ventilatory response to hypoxia and hypercapnia, and whether hypersomnolence improves with more prolonged oxygen administration. In a single-blinded, nonrandomized trial, we compared the effects of 1 month of oxygen (4 L/min by nasal cannula) with room air (4 L/min by nasal cannula) placebo during sleep in 7 men and 1 woman with obstructive sleep apnea. During non-REM sleep, acute oxygen administration elevated the average low oxy-hemoglobin saturation during apneic events and decreased apnea frequency. These acute effects persisted during chronic oxygen administration but reverted to the preoxygen effects immediately upon discontinuing oxygen. One month of oxygen did not affect the waking ventilatory response to hypoxia or hypercapnia; however, waking PaCO2 increased from 40 +/- 1 mm Hg (mean +/- SE) after placebo to 43 +/- 1 mm Hg after oxygen (p less than 0.01). Neither subjective nor objective hypersomnolence consistently improved after 1 month of oxygen administration. We conclude that: first, oxygen has no effect upon apnea frequency beyond the period of administration, and the reduction of apnea frequency is not correlated with an increased sensitivity to chemical ventilatory stimuli. The reduced apnea frequency may be related to an increased PaCO2 stimulating ventilation during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Weight loss in mildly to moderately obese patients with obstructive sleep apnea.

The therapeutic effects of weight loss were evaluated in 15 hypersomnolent patients with moderately severe obstructive sleep apnea. As patients decreased their body weight from 106.2 +/- 7.3 kg (mean +/- SE) to 96.6 +/- 5.9 kg, apnea frequency fell from 55.0 +/- 7.5 to 29.2 +/- 7.1 episodes/h (p less than 0.01) in non-rapid-eye-movement sleep with an associated significant decline in the mean oxyhemoglobin saturation during the remaining episodes of sleep apnea from 11.9 +/- 2.4% to 7.9 +/- 1.9% (p less than 0.02). Sleep patterns also improved, with a reduction in stage I sleep from 40.2 +/- 7.3% to 23.5 +/- 4.8% (p less than 0.01), and a rise in stage II sleep from 37.3 +/- 7.0% to 49.4 +/- 4.6% (p less than 0.03). In the 9 patients with the most marked fall in apnea frequency, the tendency toward daytime hypersomnolence was decreased (p less than 0.05). No significant changes in sleep patterns occurred in 8 age- and weight-matched control patients who did not lose weight. Moderate weight loss alone can alleviate sleep apnea, improve sleep architecture, and decrease daytime hypersomnolence.

A shift from central and mixed sleep apnea to obstructive sleep apnea resulting from low-flow oxygen.

Low-flow oxygen decreases the frequency of the 3 types of apnea (central, mixed, and obstructive) in patients with predominantly obstructive sleep apnea. The decrease in frequency appears to be accompanied by a shift in apnea distribution, consisting of a decrease in the proportion of central and mixed apneas and an increase in that of obstructive apneas. To determine whether this shift represents a greater inhibitory effect on central and mixed apneas or an increased tendency toward obstructive apneas, we administered low-flow oxygen during sleep to 9 patients who demonstrated predominantly central and mixed sleep apnea (51 +/- 33% and 33 +/- 21% of apneic events, respectively, mean +/- SD) and had resting, room air, oxygen tensions of 83 +/- 11 mmHg. During non-REM sleep, oxygen increased the baseline oxyhemoglobin saturation while reducing the average peak fall in oxyhemoglobin saturation during each apneic event. Oxygen reduced the overall apnea frequency from 66 +/- 7.8 (mean +/- SE) to 43.0 +/- 10.7 episodes per hour (p less than 0.02). Central and mixed apneas decreased markedly from 31.4 +/- 0.6 to 6.4 +/- 4.3 episodes per hour (p less than 0.02) and from 20.9 +/- 5.0 to 4.9 +/- 1.5 episodes per hour (p less than 0.02), respectively. However, obstructive apnea frequency more than doubled from 13.9 +/- 7.0 to 32.1 +/- 9.2 episodes per hour (p less than 0.02). We conclude that in these patients oxygen tension altered both the frequency and distribution of sleep-induced apnea, with a lower oxygen tension increasing the frequency of central and mixed apneas and a higher oxygen tension increasing the frequency of obstructive apneas.(ABSTRACT TRUNCATED AT 250 WORDS)

Rise in female-initiated sexual activity at ovulation and its suppression by oral contraceptives.

This study was designed to test the hypothesis that women exhibit peaks of sexual activity at ovulation, as would be predicted from estrous effects in animals. Married women who used contraceptive devices other than oral contraceptives experienced a significant increase in their sexual behavior at the time of ovulation. This peak was statistically significant for all female-initiated behavior, including both autosexual and female-initiated heterosexual behavior, but was not present for male-initiated behavior except under certain conditions of contraceptive use. Previous failures to find an ovulatory peak may be due to use of measures of sexual behavior that are primarily determined by initiation of the male partner. Women using oral contraceptives did not show a rise in female-initiated sexual activity at the corresponding time in their menstrual cycles, probably owing to the suppression of ovulatory increases in hormone secretion by the oral contraceptives.

Reexamining barriers to women's career development.

This paper reviews recent literature concerned with beliefs and values relevant to women's careers. Changes in sex-role stereotyping, potential problems relating to affirmative action programs, and the conflict between "counter-culture" values and values of the women's liberation movement are discussed.