Model-based stability assessment of ventilatory control in overweight adolescents with obstructive sleep apnea during NREM sleep.

Obstructive sleep apnea (OSA) involves the interplay of several different factors such as an unfavorable upper airway anatomy, deficiencies in pharyngeal muscle responsiveness, a low arousal threshold, and ventilatory control instability. Although the stability of ventilatory control has been extensively studied in adults, little is known about its characteristics in the pediatric population. In this study, we developed a novel experimental setup that allowed us to perturb the respiratory system during natural non-rapid eye movement (NREM) sleep conditions by manipulating the inspiratory pressure, provided by a bilevel pressure ventilator, to induce sighs after upper airway stabilization. Furthermore, we present a modeling framework that utilizes the noninvasively measured ventilatory responses to the induced sighs and spontaneous breathing data to obtain representations of the processes involved in the chemical regulation of respiration and extract their stability characteristics. After validation with simulated data, the modeling technique was applied to data collected experimentally from 11 OSA and 15 non-OSA overweight adolescents. Statistical analysis of the model-derived stability parameters revealed a significantly higher plant gain and lower controller gain in the OSA group (P = 0.046 and P = 0.007, respectively); however, no differences were found in loop gain (LG) and circulatory time delay between the groups. OSA severity and LG, within the 0.03-0.04-Hz frequency band, were significantly negatively associated (r = -0.434, P = 0.026). Contrary to what has been found in adults, our results suggest that in overweight adolescents, OSA is unlikely to be initiated through ventilatory instability resulting from elevated chemical loop gain.

Autonomic and metabolic effects of OSA in childhood obesity.

This study investigates the effects of exposure to intermittent hypoxia on cardiovascular autonomic control and metabolic function in obese children with obstructive sleep apnea (OSA). Each subject underwent: (1) a polysomnography; (2) morning fasting blood samples and a subsequent FSIVGTT; (3) noninvasive measurement of respiration, arterial blood pressure, and heart rate during supine and standing postures. Assessment of adiposity was performed using a DEXA scan. From these measurements, we deduced the pertinent sleep parameters, Bergman minimal model parameters and the parameters characterizing a minimal model of cardiovascular variability. Results suggest that intermittent hypoxia in OSA contributes independently to insulin resistance and autonomic dysfunction in overweight children.

Time-varying closed-loop modeling of autonomic control in pediatric obstructive sleep apnea syndrome during cold face stimulation.

Adults with obstructive sleep apnea syndrome (OSAS) are known to have impaired autonomic function but the corresponding effects in children appear to be more subtle. Model-based analysis of the cardiovascular response to cold face test (CFT) was used to quantify daytime autonomic dysfunction. The increase in transfer gain between respiration and RRI was not different between controls and OSAS. However, the transfer gain between "surrogate cardiac output" (pulse pressure+R-R interval) and systolic blood pressure (SBP) and the transfer gain between cardiac output and SBP both increased significantly in controls but not in OSAS during CFT. These findings suggest that the parasympathetic function remains relatively normal in pediatric OSAS, but cardiovascular sympathetic reactivity is impaired.

Hypoxia reveals posterior thalamic, cerebellar, midbrain, and limbic deficits in congenital central hypoventilation syndrome.

Congenital central hypoventilation syndrome (CCHS) patients show deficient respiratory and cardiac responses to hypoxia and hypercapnia, despite apparently intact arousal responses to hypercapnia and adequate respiratory motor mechanisms, thus providing a model to evaluate functioning of particular brain mechanisms underlying breathing. We used functional magnetic resonance imaging to assess blood oxygen level-dependent signals, corrected for global signal changes, and evaluated them with cluster and volume-of-interest procedures, during a baseline and 2-min hypoxic (15% O(2), 85% N(2)) challenge in 14 CCHS and 14 age- and gender-matched control subjects. Hypoxia elicited significant (P < 0.05) differences in magnitude and timing of responses between groups in cerebellar cortex and deep nuclei, posterior thalamic structures, limbic areas (including the insula, amygdala, ventral anterior thalamus, and right hippocampus), dorsal and ventral midbrain, caudate, claustrum, and putamen. Deficient responses to hypoxia included no, or late, changes in CCHS patients with declining signals in control subjects, a falling signal in CCHS patients with no change in controls, or absent early transient responses in CCHS. Hypoxia resulted in signal declines but no group differences in hypothalamic and dorsal medullary areas, the latter being a target for PHOX2B, mutations of which occur in the syndrome. The findings extend previously identified posterior thalamic, midbrain, and cerebellar roles for normal mediation of hypoxia found in animal fetal and adult preparations and suggest significant participation of limbic structures in responding to hypoxic challenges, which likely include cardiovascular and air-hunger components. Failing structures in CCHS include areas additional to those associated with PHOX2B expression and chemoreceptor sites.

Hypercapnic exposure in congenital central hypoventilation syndrome reveals CNS respiratory control mechanisms.

Congenital central hypoventilation syndrome (CCHS) patients show impaired ventilatory responses and loss of breathlessness to hypercapnia, yet arouse from sleep to high CO2, suggesting intact chemoreceptor afferents. The syndrome provides a means to differentiate brain areas controlling aspects of breathing. We used functional magnetic resonance imaging to determine brain structures responding to inspired 5% CO2-95% O2 in 14 CCHS patients and 14 controls. Global signal changes induced by the challenge were removed on a voxel-by-voxel basis. A priori-defined volume-of-interest time trends (assessed with repeated measures ANOVA) and cluster analysis based on modeling each subject to a step function (individual model parameter estimates evaluated with t-test, corrected for multiple comparisons) revealed three large response clusters to hypercapnia distinguishing the two groups, extending from the 1) posterior thalamus through the medial midbrain to the dorsolateral pons, 2) right caudate nucleus, ventrolaterally through the putamen and ventral insula to the mid-hippocampus, and 3) deep cerebellar nuclei to the dorsolateral cerebellar cortex bilaterally. Smaller clusters and defined areas of group signal differences in the midline dorsal medulla, amygdala bilaterally, right dorsal-posterior temporal cortex, and left anterior insula also emerged. In most sites, early transient or sustained responses developed in controls, with little, or inverse change in CCHS subjects. Limbic and medullary structures regulating responses to hypercapnia differed from those previously shown to mediate loaded breathing ventilatory response processing. The findings show the significant roles of cerebellar and basal ganglia sites in responding to hypercapnia and the thalamic and midbrain participation in breathing control.

fMRI signal changes in response to forced expiratory loading in congenital central hypoventilation syndrome.

Congenital central hypoventilation syndrome (CCHS) patients show impaired ventilatory responses to CO2 and hypoxia and reduced drive to breathe during sleep but retain appropriate breathing patterns in response to volition or increased exercise. Breath-by-breath influences on heart rate are also deficient. Using functional magnetic resonance imaging techniques, we examined responses over the brain to voluntary forced expiratory loading, a task that CCHS patients can perform but that results in impaired rapid heart rate variation patterns normally associated with the loading challenge. Increased signals emerged in control (n = 14) over CCHS (n = 13; ventilator dependent during sleep but not waking) subjects in the cingulate and right parietal cortex, cerebellar cortex and fastigial nucleus, and basal ganglia, whereas anterior cerebellar cortical sites and deep nuclei, dorsal midbrain, and dorsal pons showed increased signals in the patient group. The dorsal and ventral medulla showed delayed responses in CCHS patients. Primary motor and sensory areas bordering the central sulcus showed comparable responses in both groups. The delayed responses in medullary sensory and output regions and the aberrant reactions in cerebellar and pontine sensorimotor coordination areas suggest that rapid cardiorespiratory integration deficits in CCHS may stem from defects in these sites. Additional autonomic and perceptual motor deficits may derive from cingulate and parietal cortex aberrations.

Noninvasive assessment of cardiovascular autonomic control in congenital central hypoventilation syndrome.

The goal of this study was to quantify autonomic system dysfunction, as manifested by cardiovascular and respiratory response abnormalities, in patients with congenital central hypoventilation syndrome (CCHS). During wakefulness, we continuously measured the ECG, arterial blood pressure (ABP), airflow, end-tidal CO2 partial pressure (PETCO2), and arterial oxygen saturation (SatO2) in each subject. These measurements were made during spontaneous breathing in supine, sitting and standing postures, and also when each subject tracked his/her prior spontaneous breathing pattern while supine. We also performed the cold face test, hyperoxic hypercapnic rebreathing and the isocapnic hypoxic rebreathing challenges. Using spectral analysis and modeling techniques, we sought to computationally delineate the physiological mechanisms that mediate these abnormalities, as well as to determine the extent to which these abnormalities are related to peripheral or central chemoreflex dysfunction. Our preliminary results support the notion that sympathetic tone is markedly elevated in CCHS, and that differences in autonomic control from normal controls can be delineated by observing the responses to different stressors.

Cardiorespiratory events recorded on home monitors: Comparison of healthy infants with those at increased risk for SIDS.

CONTEXT: Home monitors designed to identify cardiorespiratory events are frequently used in infants at increased risk for sudden infant death syndrome (SIDS), but the efficacy of such devices for this use is unproven. OBJECTIVE: To test the hypothesis that preterm infants, siblings of infants who died of SIDS, and infants who have experienced an idiopathic, apparent life-threatening event have a greater risk of cardiorespiratory events than healthy term infants. DESIGN: Longitudinal cohort study conducted from May 1994 through February 1998. SETTING: Five metropolitan medical centers in the United States. PARTICIPANTS: A total of 1079 infants (classified as healthy term infants and 6 groups of those at risk for SIDS) who, during the first 6 months after birth, were observed with home cardiorespiratory monitors using respiratory inductance plethysmography to detect apnea and obstructed breathing. MAIN OUTCOME MEASURES: Occurrence of cardiorespiratory events that exceeded predefined conventional and extreme thresholds as recorded by the monitors. RESULTS: During 718 358 hours of home monitoring, 6993 events exceeding conventional alarm thresholds occurred in 445 infants (41%). Of these, 653 were extreme events in 116 infants (10%), and of those events with apnea, 70% included at least 3 obstructed breaths. The frequency of at least 1 extreme event was similar in term infants in all groups, but preterm infants were at increased risk of extreme events until 43 weeks' postconceptional age. CONCLUSIONS: In this study, conventional events are quite common, even in healthy term infants. Extreme events were common only in preterm infants, and their timing suggests that they are not likely to be immediate precursors to SIDS. The high frequency of obstructed breathing in study participants would likely preclude detection of many events by conventional techniques. These data should be important for designing future monitors and determining if an infant is likely to be at risk for a cardiorespiratory event.

Bronchoscopic instillation of surfactant in acute respiratory distress syndrome.

Abnormalities of surfactant action in acute respiratory distress syndrome (ARDS) result in decreased lung compliance and significant hypoxemia. Several case reports and small studies suggest that there is an improvement in patients with ARDS following the administration of surfactant. However, there is no clear-cut ideal method for surfactant administration. The bronchoscopic administration of surfactant may represent an effective method of surfactant delivery in ARDS. Bronchoscopic instillation offers the theoretical advantages that the surfactant may be distributed directly to the desired regions of the lung, a more economical use of surfactant, and the opportunity to lavage leaked serum proteins prior to instillation. Surfactant has been administered in adults with success. We present a case of initial improvement in oxygenation index, ventilation index, and mechanical ventilatory support in a pediatric patient with ARDS following the bronchoscopic administration of surfactant.

Home ventilator low-pressure alarms fail to detect accidental decannulation with pediatric tracheostomy tubes.

BACKGROUND: Positive-pressure ventilators are equipped with low-inspiratory-pressure alarms to protect patients from hypoventilation. Small uncuffed tracheostomy tubes have a high resistance, and may not trigger these alarms during decannulation. STUDY OBJECTIVE: To determine whether ventilator low-inspiratory-pressure alarms are effective in detecting tracheostomy decannulation. DESIGN: We connected tracheostomy tubes of varying inner diameters (3.0 to 6.0 mm) to a home ventilator and simulated decannulation using low (tidal volume [VT], 600 mL; peak inspiratory pressure [PIP], 25 cm H(2)O), medium (VT, 800 mL; PIP, 30 cm H(2)O), and high (VT, 1,000 mL; PIP, 35 cm H(2)O) ventilator settings. RESULTS: When the ventilator low-inspiratory-pressure alarm was set at 4 cm H(2)O below the desired PIP, it failed to alarm for simulated decannulation of tracheostomy tubes < 4.5 mm on low and medium settings, and < 4.0 mm on high settings. When the ventilator low-inspiratory-pressure alarm was set at 10 cm H(2)O below the desired PIP, it failed to alarm with tracheostomy tubes < 6.0 mm. CONCLUSION: We conclude that ventilator low-inspiratory-pressure alarms fail to alarm during simulated decannulation with small tracheostomy tubes commonly used in children. We speculate that low-inspiratory-pressure alarms set at 4 cm H(2)O below the desired PIP will detect more decannulation than when set at 10 cm H(2)O below the desired PIP.

Latex allergy in children on home mechanical ventilation.

STUDY OBJECTIVE: Determining the incidence of latex allergy in children receiving home mechanical ventilation. BACKGROUND: The prevalence of latex allergy in the general population ranges from 0.1 to 1.0%. However, in patients with spina bifida and other chronic medical conditions associated with repeated exposure to latex, the prevalence may be as high as 60%. Children receiving home mechanical ventilation are frequently exposed to latex products. Therefore, we hypothesized that these children would be at increased risk for latex allergy. DESIGN: Fifty-seven children receiving home mechanical ventilation (31 boys, 26 girls; mean [+/- SD] age, 7.8+/-6.6 years; range, 0.3 to 23.2 years) were enrolled. A radioallergosorbent test (RAST) for latex was administered and serum IgE levels were obtained in all patients. RESULTS: Seventeen patients (29.8%) were found to have a positive RAST for latex. Patients with latex allergy had required mechanical ventilation for an average of 6.1+/-4.1 years vs. 5.5+/-5.4 years (p = 0.69; not significant) in those without latex allergy. Eleven of 17 patients (64.7%) had elevated serum IgE levels in the group with latex allergy vs only 14 of 40 patients (35.0%) in the group with a negative latex RAST (p = 0.04; odds ratio, 3.4). CONCLUSION: We conclude that there is a high incidence of latex allergy in children requiring home mechanical ventilation. We speculate that screening all children receiving home mechanical ventilation may lead to the identification of patients with previously undiagnosed latex allergy and the prevention of untoward reactions from exposure to latex.

Respiratory failure in postpneumonectomy syndrome complicated by thoracic lordoscoliosis: treatment with prosthetic implants, partial vertebrectomies, and spinal fusion.

STUDY DESIGN: This study investigated the case of a 17-year-old girl with postpneumonectomy syndrome, complicated by a thoracic lordoscoliosis, who was successfully treated with prosthetic implants, partial vertebrectomies, and anteroposterior spinal fusion. OBJECTIVE: To report a unique case and describe the authors' method of treatment. SUMMARY OF BACKGROUND DATA: Postpneumonectomy syndrome is an uncommon complication of pneumonectomy. Many case reports describe successful treatment with insertion of prosthetic implants into the empty hemithorax to shift the mediastinum to its original position. Thoracic lordoscoliosis reportedly has contributed to pulmonary compromise, but no cases have shown its occurrence in the setting of postpneumonectomy syndrome. METHODS: The patient was observed at the National Children's Hospital in Tokyo, referred to Children's Hospital in Los Angeles, California for surgical correction, and followed in Tokyo for the next year. RESULTS: Two prosthetic implants with an injection port for further expansion were positioned in the right hemithorax to restore the mediastinum to its normal position. Anterior discectomies, partial vertebrectomies, and fusion of T5-T10 was performed concurrently. Then 5 days later, posterior spinal fusion of T1-T12 with instrumentation and bone graft were performed to correct the thoracic lordoscoliosis and increase the chest cavity space. At 1 month after the surgery, the patient was extubated after being ventilator dependent for 5 months. At the time of operation, the girl was ventilator dependent and nonambulatory, but 1 year later could participate in all activities of daily living without any oxygen supplementation. CONCLUSIONS: Postpneumonectomy syndrome can be treated successfully with prosthetic implants to restore the normal position of the mediastinum. Thoracic lordoscoliosis can complicate the syndrome and may be corrected to help restore normal pulmonary function.

Should children with suspected obstructive sleep apnea syndrome and normal nap sleep studies have overnight sleep studies?

STUDY OBJECTIVES: Overnight polysomnography (ONP) is the "gold standard" for the diagnosis of sleep-disordered breathing, but it is expensive and time-consuming. Thus, daytime nap studies have been used as screening tests. If the findings of a nap study are normal or mildly abnormal, should ONP be performed? Do specific abnormalities in nap studies predict abnormal findings in ONP? To answer these questions, we conducted this study. DESIGN: Retrospective chart review. SETTING: Children's hospital. PARTICIPANTS: One hundred forty-three children with suspected obstructive sleep apnea syndrome secondary to isolated adenotonsillar hypertrophy, who had normal or mildly abnormal nap studies, and underwent ONP. MEASUREMENTS AND RESULTS: We compared daytime nap and overnight polysomnograms in 143 children (52 girls; mean [+/- SD] age, 5.6 +/- 3.1 years). Total sleep time was 1 h in daytime nap, and 5.1 +/- 1.3 h in ONP. The interval between the two studies was 5.9 +/- 4.8 months. The findings of 59% of the nap studies were mildly abnormal, while 66% of overnight studies were abnormal. No individual nap study parameter (including short obstructive apneas, hypopneas, hypoxemia, hypoventilation, snoring, paradoxical breathing, gasping, retractions) had good sensitivity at predicting abnormal overnight polysomnograms, but most had good specificity and positive predictive value. CONCLUSIONS: We conclude that individual nap study parameters are not very sensitive in predicting abnormal ONP findings. However, when nap study parameters are abnormal, the chance of obstructive sleep apnea syndrome is high.

Longitudinal assessment of hemoglobin oxygen saturation in healthy infants during the first 6 months of age. Collaborative Home Infant Monitoring Evaluation (CHIME) Study Group.

Limitations in home monitoring technology have precluded longitudinal studies of hemoglobin oxygen saturation during unperturbed sleep. The memory monitor used in the Collaborative Home Infant Monitoring Evaluation addresses these limitations. We studied 64 healthy term infants at 2 to 25 weeks of age. We analyzed hemoglobin oxygen saturation by pulse oximetry (SpO(2)), respiratory inductance plethysmography, heart rate, and sleep position during 35, 127 epochs automatically recorded during the first 3 minutes of each hour. For each epoch baseline SpO(2) was determined during >/=10 s of quiet breathing. Acute decreases of at least 10 saturation points and <90% for >/=5 s were identified, and the lowest SpO(2) was noted. The median baseline SpO(2) was 97.9% and did not change with age or sleep position. The baseline SpO(2) was <90% in at least 1 epoch in 59% of infants and in 0.51% of all epochs. Acute decreases in SpO(2) occurred in 59% of infants; among these, the median number of episodes was 4. The median lowest SpO(2) during an acute decrease was 83% (10th, 90th percentiles 78%, 87%); 79% of acute decreases were associated with periodic breathing, and >/=16% were associated with isolated apnea. With the use of multivariate analyses, the odds of having an acute decrease increased as the number of epochs with periodic breathing increased, and they lessened significantly with age. We conclude that healthy infants generally have baseline SpO(2) levels >95%. The transient acute decreases are correlated with younger age, periodic breathing, and apnea and appear to be part of normal breathing and oxygenation behavior.

Prognosis in pediatric idiopathic pulmonary hemosiderosis.

STUDY OBJECTIVES: Previously, IPH patients have been reported to have an average survival of 2.5 years. However, at our institution, many IPH patients have survived longer than that. Therefore, we conducted this study to determine the clinical course and current mortality of pediatric IPH patients treated with immunosuppressants. DESIGN: Retrospective chart review. SETTING: Children's hospital. PARTICIPANTS: Seventeen patients in whom IPH was diagnosed between 1972 and 1998. MEASUREMENTS AND RESULTS: Mean age at diagnosis was 4.5 +/- 3.5 years, and 12 patients were female. At diagnosis, all patients had anemia and pulmonary infiltrates; 85% had hypoxemia, 65% had hemoptysis, and 70% had fever. The diagnosis was made by open lung biopsy in 13 patients (76%), hemosiderin-laden macrophages in BAL fluid in 1 patient (6%), hemosiderin-laden macrophages in gastric aspirate in 2 patients (12%), or by clinical presentation alone in 1 patient (6%). The mean duration of follow-up for all patients was 3.6 +/- 3.4 years (range, 0.7 to 10.2). Initial treatment consisted of prednisone only in 14 patients (82%), and prednisone and hydroxychloroquine in two patients (12%). Thirteen patients (76%) required long-term corticosteroids because of recurrent hemoptysis. Eight patients (47%) required other immunosuppressants (hydroxychloroquine or azathioprine) in addition to prednisone to control their hemoptysis. One patient who was not treated with prednisone remained asymptomatic for 1.8 years. Three patients (17%) died of acute massive pulmonary hemorrhage (4.1 +/- 5.0 years postdiagnosis). CONCLUSION: Five-year survival for IPH patients in our study was 86% (by Kaplan-Meier method). We conclude that these IPH patients who received long-term treatment had a better outcome than those previously reported who were not treated with extended courses of immunosuppressive therapy. We speculate that long-term immunosuppression therapy may improve the prognosis in IPH.

Frequency, causes, and outcome of home ventilator failure.

STUDY OBJECTIVES: The safety of home ventilators has been questioned. We collected data to study the following: frequency of home ventilator failure, apparent causes for the failure or malfunction, and adverse consequences following the failure. STUDY DESIGN: Information on all requests to correct home ventilator failures reported to a home respiratory equipment vendor was collected prospectively between November 1991, and November 1992. PATIENTS: There were 150 ventilator-assisted patients aged 2 to 77 years; 44 were < or = 18 years. They received 841,234 h of home mechanical ventilation (average, 15.4 h/d per ventilator-assisted patient). RESULTS: There were 189 reports of home ventilator failure. Defective equipment or mechanical failure was found in only 39% (73 reports), equivalent to one home ventilator failure for every 1.25 years of continuous use. Other causes of ventilator failure included the following: improper care, damage, or tampering with the ventilator by caregivers (13%), functional equipment improperly used by caregivers (30%), and equipment functional but the patient's condition changed, mimicking ventilator failure (3%). No problem could be identified in 16%. The following actions were required: ventilator replacement (44%), repair of a defective part (6%), replacement of a functioning ventilator for psychological comfort (14%), ventilator adjustments made (21%), caregiver reeducation (7%), caregiver anxiety or distress reduced (3%), and no action required (4%). Hospitalization was required only in two cases (1%). No adverse outcomes, deaths, or serious injuries were associated with home ventilator failure. CONCLUSIONS: We conclude that in 150 patients requiring home mechanical ventilation, ventilator failure occurred relatively infrequently, and there were no adverse outcomes as a result of equipment failure at home. We speculate that equipment failure is not a frequent or serious problem for ventilator-assisted patients treated at home.

Factors associated with the transition to nonprone sleep positions of infants in the United States: the National Infant Sleep Position Study.

CONTEXT: Studies have demonstrated strong associations between the prone sleep position (on the stomach) and sudden infant death syndrome (SIDS). In 1992, the American Academy of Pediatrics recommended that infants be placed to sleep laterally (on their side) or supine (on their back) to reduce SIDS risk, and in 1994, the national public education campaign "Back to Sleep" was launched. OBJECTIVE: To determine the typical sleep position of infants younger than 8 months in the United States, the changes that occurred after these recommendations, and the factors associated with the placement of infants prone or supine. DESIGN: Annual nationally representative telephone surveys. SETTING: The 48 contiguous states of the United States. PARTICIPANTS: Nighttime caregivers of infants born within the last 7 months between 1992 and 1996. Approximately 1000 interviews were conducted per year. MAIN OUTCOME MEASURES: The position the infant was usually placed in for sleep, and the position the infant was most commonly found in when checked during the night's sleep. RESULTS: Ninety-seven percent of respondents in each wave of the survey usually placed their infant to sleep in a specific position. Infants were placed in the prone position by 70% of caregivers in 1992, prior to the campaign, but only 24% in 1996. Supine and lateral placements increased during this time period, from 13% in 1992 to 35% in 1996 and from 15% in 1992 to 39% in 1996, respectively. Significant predictors of prone placement included maternal race reported as black (odds ratio [OR], 2.34; 95% confidence interval [CI], 1.68-3.26), mother's age 20 to 29 years (OR, 1.28; 95% CI, 1.09-1.50), region reported as the mid-Atlantic (OR, 1.41; 95% CI, 1.12-1.78) or southern states (OR, 1.47; 95% CI, 1.22-1.70), mothers with a previous child (OR, 1.68; 95% CI, 1.43-1.97), and infants younger than 8 weeks (OR, 0.63; 95% CI, 0.46-0.85). Infants aged 8 to 15 weeks were significantly more likely to be placed nonprone over time compared with the other age groups. Most of the risk factors for prone were significantly related in the opposite direction to supine placement. CONCLUSIONS: The prevalence of infants placed in the prone sleep position declined by 66% between 1992 and 1996. Although causality cannot be proved, SIDS rates declined approximately 38% during this period. To achieve further reduction in prone sleeping, efforts to promote the supine sleep position should be aimed at groups at high risk for prone placement.

Determinants of aerobic and anaerobic exercise performance in cystic fibrosis.

We examined aerobic and anaerobic exercise performance in 17 subjects with cystic fibrosis (CF) (age 25+/-10 [SD] yr; 47% females; FEV1 62+/-21% pred) and 17 age- and sex-matched control subjects (age 25+/-8 [SD] yr; 41% females; FEV1 112+/-15% pred) in relation to pulmonary function and nutritional status. Aerobic capacity was determined as maximal oxygen consumption (VO2max) (ml/kg/min) and anaerobic threshold (AT; ml VO2/kg/min) from a graded exercise stress test on an electronically braked bicycle ergometer. Anaerobic performance was assessed from the average work of two bouts of pedaling to exhaustion at a load corresponding to 130% Vo2max from graded exercise. Both aerobic and anaerobic performances were decreased in subjects with CF (p < 0.001). The duration of anaerobic exercise in subjects with CF was similar to control subjects. In control subjects, pulmonary function did not correlate to aerobic or anaerobic exercise. In subjects with CF significant relationships between FEV1, vital capacity, and FEF25-75% to AT were found, suggesting the pulmonary limitation to aerobic capacity. In both patients with CF and control subjects, lean body mass and arm muscle area significantly correlated with anaerobic performance but not with VO2max or AT. We conclude that nutritional status, rather than pulmonary function, is the major determinant of anaerobic exercise capacity in CF. The preserved duration of anaerobic exercise at equivalent workloads (corresponding to 130% of VO2max from graded exercise) suggests that readily available energy stores in muscle may be similar in CF and normal individuals.