Biomedical subjects

K J Omlin

Publications and source records attributed to K J Omlin.

8 recordsLinked to original sources

PubMed1995

Ventilatory response to consecutive short hypercapnic challenges in children with obstructive sleep apnea.

In healthy adults, a ventilatory pattern characterized by progressively increased tidal volume (VT), and decreased respiratory rate (RR) accompany repeated short hypercapnic ventilatory challenges, while minute ventilation (VE) remains constant. We hypothesized that the peculiar ventilatory pattern seen in adults would be blunted in children with obstructive sleep apnea syndrome (OSAS) who undergo comparable intermittent or chronic alveolar PCO2 elevation. We measured ventilatory responses to five challenges of 2-min duration (C1-C5) with 5% CO2 in O2, separated by 5-min room-air breathing intervals (R1-R4), in nine children with OSAS and in eight age-, sex-, and body mass index-matched controls. In all children, CO2 significantly increased VE when compared with baseline conditions (22.3 +/- 2.2 vs. 9.5 +/- 0.9 (SE) l/min; P < 0.001). In control subjects, progressive VT increases from 0.67 +/- 0.10 liter in C1 to 0.92 +/- 0.13 liter in C5 occurred (P < 0.01), whereas RR decreased from 33.9 +/- 5.1 breaths/min in C1 to 27.8 +/- 3.7 breaths/min in C5 (P < 0.02), resulting in VE increases across CO2 challenges (22.3 +/- 4.9 l/min in C1 vs. 25.1 +/- 5.0 l/min in C5; P < 0.005). The RR decrease was primarily related to progressive prolongation of expiratory time (TE) (1.1 +/- 0.1 s in C1 to 1.5 +/- 0.2 s in C5; P < 0.002). In contrast, VT, RR, and TE did not change in a consistent fashion in OSAS patients with repeated CO2 challenges (OSAS vs. control: P < 0.0001). Furthermore, in OSAS, VE was similar with repeated challenges (22.4 +/- 2.2 1/min in C1 vs. 23.9 +/- 1.9 l/min; P = not significant), such that changes in VE over time significantly differed in OSAS and controls (P < 0.001). We conclude that healthy children modify their ventilatory strategy to repeated hypercapnia. We speculate that in OSAS these mechanisms are already fully implemented because of recurrent alveolar hypoventilation accompanying increased upper airway resistance, leading to blunted temporal trends of ventilatory response.

Adolescent↗

PubMed1995

Peripheral chemoreceptor function in children with myelomeningocele and Arnold-Chiari malformation type 2.

Blunted rebreathing hyperoxic hypercapnic ventilatory and arousal responses are frequent in older children with myelomeningocele (MMC) and Arnold-Chiari malformation type 2 (ACM). In contrast, isocapnic hypoxic rebreathing ventilatory responses are only occasionally affected. Thus, regions mediating the hypoxic ventilatory response appear usually preserved in children with MMC and ACM. Peripheral chemoreceptor function (PCR), however, has not been critically assessed in these children. To study this, PCR was measured in ten children and adolescents with MMC and ACM with normal alveolar ventilation during wakefulness, and in ten sex- and age-matched controls by measuring the ventilatory responses induced by 100% O2 breathing, five tidal breaths of 100% N2, and vital capacity breaths of 15% CO2 in O2. In general, tidal breathing of 100% O2 resulted in smaller decreases in minute ventilation (VE) responses in patients with MMC, although absent VE responses to hyperoxia were found in four patients. Vital capacity breaths of 15% CO2 elicited similar increases in VE in five patients and in ten controls, but no changes in VE were found in the remaining five patients (p < 0.02). Acute hypoxia induced by N2 tidal breathing resulted in significant linear regression correlations between VE and SpO2 in five patients with MMC, while absent responses were measured in those same five patients with absent hypercapnic responses. We conclude that PCR, when assessed by acute hypoxia, hyperoxia, or hypercapnia is abnormal in some children with MMC and ACM, particularly in those demonstrating abnormal ventilation during sleep. We postulate that the large interindividual variability of PCR is dependent on the severity of brainstem involvement of PCR afferents or central respiratory integration sites.

Adolescent↗

PubMed1994

Maturational differences in step vs. ramp hypoxic and hypercapnic ventilatory responses.

The influence of the speed of stimulus presentation on hypoxic and hypercapnic ventilatory responses (step vs. ramp) is not known. Furthermore, it is unclear whether children and adults respond similarly. We tested ramp ventilatory responses to hypercapnia and hypoxia with use of rebreathing in 8 prepubertal children and 11 adults. We tested step ventilatory responses to hypercapnia with single vital capacity breaths of 15% CO2 in O2 and to hypoxia with five tidal breaths of 100% N2. For children, slopes of step hypercapnic ventilatory responses were always greater than those of ramp responses (0.85 +/- 0.07 vs. 0.71 +/- 0.07 l.min-1.Torr end-tidal PCO2-1; P < 0.0005). Conversely, for adults, step responses were always less than ramp responses (0.88 +/- 0.19 vs. 2.10 +/- 0.29 l.min-1.Torr end-tidal PCO2-1; P < 0.0007). Similarly, for children, the slopes of step hypoxic ventilatory responses were always greater than those of ramp responses (-0.71 +/- 0.09 vs. -0.45 +/- 0.04 l.min-1.Torr O2 saturation-1; P < 0.02), and for adults, step responses were always less than ramp responses (-0.68 +/- 0.14 vs. -1.85 +/- 0.46 l.min-1.Torr O2 saturation-1; P < 0.04). We conclude that ventilatory responses vary depending on step vs. ramp presentation of hypercapnia or hypoxia and that the ratio of these responses is reversed in children compared with adults. We speculate that the responsiveness of peripheral chemoreceptors is increased in children compared with adults and that it may play a role in the mechanisms leading to increased ventilatory responses observed during childhood.

Adult↗

PubMed1994

Hypoxic and hypercapnic ventilatory responses in Prader-Willi syndrome.

Abnormalities of ventilatory control may play a significant role in the pathophysiology of sleep-disordered breathing in patients with the Prader-Willi syndrome (PWS). We measured rebreathing hypercapnic and hypoxic ventilatory responses (HCVR and HPVR, respectively) during wakefulness in 8 nonobese PWS (NOB-PWS) and 9 obese PWS (OB-PWS) patients and compared their results with those from 24 healthy nonobese control (NOB-CON) and 10 obese control (OB-CON) subjects. The slope of HCVR was similar in NOB-PWS patients and NOB-CON subjects (NS). However, HCVR was significantly lower in OB-PWS patients than in OB-CON subjects (P < 0.02). In PWS patients, the mean point of origin of the positive slope of HCVR occurred at a significantly higher end-tidal PCO2 than in either control group. During isocapnic hypoxic challenges, six PWS patients had no significant HPVR. In the remainder, mean slopes of HPVR were -0.80 +/- 0.06 l.min-1.%arterial O2 saturation-1 in five NOB-PWS patients and -0.68 +/- 0.15 l.min-1.%arterial O2 saturation-1 in six OB-PWS patients. These responses were significantly decreased compared with those in the control groups (P < 0.006). We conclude that NOB-PWS patients have normal HCVR, which is blunted in OB-PWS patients. Furthermore, isocapnic HPVR is either absent or markedly reduced in PWS patients. The severity of abnormality of the HPVR is independent of the degree of obesity. We postulate that the primary abnormality of ventilatory control in PWS affects peripheral chemoreceptor pathways.

Adult↗

PubMed1994

Absent peripheral chemosensitivity in Prader-Willi syndrome.

Abnormalities in ventilatory control during wakefulness and sleep have been observed in patients with Prader-Willi syndrome (PWS). The role of peripheral chemoreceptors in the pathophysiology of abnormal ventilatory responses in PWS is unknown. We studied peripheral chemoreceptor function during wakefulness in 17 genetically confirmed PWS patients [age 27.0 +/- 2.5 (SE) yr; 7 males, 10 females; body mass index 31.1 +/- 1.4 kg/m2] and compared their responses with 17 control subjects matched for age, sex, and body mass index. All PWS and control subjects had normal resting end-tidal PCO2 and arterial O2 saturation while awake. Peripheral chemoreceptor function was assessed by the ventilatory responses to 100% O2 breathing, five tidal breaths of 100% N2, and vital capacity breaths of 15% CO2 in O2. Control subjects decreased minute ventilation (VE) by 15.5 +/- 3.6% during hyperoxia. However, PWS patients increased VE by 17.6 +/- 3.3%, indicating a paradoxical response to hyperoxia (P < 0.00001). After CO2 vital capacity breaths, PWS patients showed no significant change and control subjects showed a marked increase (P < 0.0001) in VE. During N2 breathing, again PWS patients showed no change and control subjects exhibited a marked increase (P < 0.00005) in VE. We conclude that PWS patients have absent peripheral chemoreceptor ventilatory responses. We speculate that the lack of ventilatory responses is due to primary peripheral chemoreceptor dysfunction and/or defective afferent pathways to central controllers.

Adult↗

PubMed1994

Ventilatory responses during wakefulness in children with obstructive sleep apnea.

The pathophysiology of the obstructive sleep apnea syndrome (OSAS) is not fully understood. In children, airway obstruction secondary to tonsilloadenoidal hypertrophy is the leading cause of OSAS. However, not all children with tonsilloadenoidal hypertrophy develop OSAS. Thus, other factors, including abnormalities in ventilatory control, may contribute to the etiology of OSAS. To test this, we performed polysomnography and hypercapnic and hypoxic ventilatory response testing in 20 children and adolescents with OSAS (mean age, 8 +/- 3 [SD] yr) and 19 control subjects. Only two children with OSAS were obese. Children with OSAS had an apnea index of 16 +/- 20, peak PETCO2 of 54 +/- 5 mm Hg, and SaO2 nadir of 84 +/- 13% during polysomnography. Ventilatory responses were performed by rebreathing techniques. The slope of the hypercapnic ventilatory responses, corrected for body surface area, was 1.74 +/- 0.79 L/min/m2/mm Hg PETCO2 in children with OSAS and 1.45 +/- 0.58 L/min/m2/mmHg PETCO2 in control subjects (NS). Hypoxic ventilatory responses, corrected for body surface area, were -0.94 +/- 0.49 L/min/m2/% SaO2 in children with OSAS and -0.95 +/- 0.45 L/min/m2/% SaO2 in control subjects (NS); however, the sample size was small. There was a weak inverse correlation between the slope of the hypercapnic ventilatory response and the duration of hypoventilation during polysomnography (r = -0.44, p < 0.05). We conclude that children with OSAS have normal ventilatory responses to hypercapnia, and they may have normal ventilatory responses to hypoxia. We speculate that abnormal central ventilatory drive plays little if any role in the pathogenesis of pediatric OSAS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoids↗

PubMed1994

Comparison of high frequency chest compression and conventional chest physiotherapy in hospitalized patients with cystic fibrosis.

Clearance of bronchial secretions is essential in the management of cystic fibrosis (CF) patients admitted for acute pulmonary exacerbation. Conventional physiotherapy (CPT) is labor-intensive, time-consuming, expensive, and may not be available as frequently as desired during hospitalization. High frequency chest compression (HFCC), which uses an inflatable vest linked to an air-pulse delivery system, may offer an attractive alternative. To study this, we prospectively studied 50 CF patients admitted for acute pulmonary exacerbation who were randomly allocated to receive either HFCC or CPT three times a day. On admission, clinical status and pulmonary function tests (PFT) in the HFCC group were not significantly different from those measured in the CPT group. Significant improvements in clinical status and PFT were observed after 7 and 14 d of treatment, and were similar in the two study groups, leading to patient discharge after similar periods of hospitalization. We conclude that HFCC and CPT are equally safe and effective when used during acute pulmonary exacerbations in CF patients. We speculate that HFCC may provide an adequate alternative in management of CF patients in a hospital setting.

Acute Disease↗

PubMed1992

Normal polysomnographic values for children and adolescents.

Although polysomnography is routinely performed to evaluate children and adolescents with sleep-disordered breathing, normal polysomnographic values for the pediatric age group have not yet been established. We therefore performed overnight polysomnography in 50 normal children and adolescents (mean age 9.7 +/- 4.6 SD yr, range 1.1 to 17.4 yr). Of the children 56% were male. Chest wall motion, ECG, oronasal airflow, end-tidal PCO2 (PETCO2), arterial oxygen saturation (SaO2), and electrooculogram were monitored. Children had 0.1 +/- 0.5 (range 0 to 3.1) obstructive apneas per hour of total sleep time, with only 18% of children having any obstructive apneas. No child had obstructive apneas > 10 s in duration. Of the children 30% had central apneas > or = 10 s in duration, and one child had a central apnea associated with SaO2 < 90%. Peak PETCO2 was 46 +/- 4 mm Hg (range 38 to 53 mm Hg), and hypoventilation (PETCO2 > 45 mm Hg) occurred for 7 +/- 19% total sleep time (range 0 to 91%). The SaO2 nadir was 96 +/- 2% (range 89 to 98%), with only one child desaturating below 90% in association with a central apnea. We conclude that polysomnographic results in the pediatric age group differ from those in adults. Recommendations for normal polysomnographic criteria are given.

Adolescent↗