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Biomedical subjects

M Kryger

Publications and source records attributed to M Kryger.

At least 37 records · Page 2Linked to original sources
PubMed1991

Effect of theophylline on lung function tests, sleep quality, and nighttime SaO2 in children with cystic fibrosis.

The effect of theophylline (T) was studied in 12 children with cystic fibrosis (CF) (seven males and five females) aged 7 to 17 yr (mean, 11.8 +/- 2.8). T or placebo (P) was taken for 10 days in a double-blind, crossover controlled trial. During Nights 9 and 10 of each study period, the subjects slept in a sleep laboratory, where complete polysomnographs were recorded. Patients were subdivided according to T blood levels above or below 10 micrograms/ml: five children had a mean serum T of 11.7 +/- 1.6 micrograms/ml (Group 1), and seven patients had serum T levels of 6.7 +/- 1.5 micrograms/ml (Group 2). There was no difference in pulmonary function between the two periods, but Group 2 had significantly better baseline lung function (p less than 0.01). During sleep while on T, Group 1 had a higher mean SaO2 (93.1 +/- 0.3% T versus 90.7 +/- 0.3% P; p less than 0.0001), less time with a decrease greater than 5% in SaO2 from baseline (43.7 +/- 7.9 min T versus 85.8 +/- 7.9 min P; p less than 0.01), and a lower heart rate (HR), (77.9 +/- 5.1 bpm T versus 86.1 +/- 4.2 bpm P; p less than 0.01). Group 2 did not show differences in these parameters. T significantly disrupted sleep as measured by sleep efficiency and total wake time independently of serum level (p less than 0.01). There was no significant effect of T on the incidence of apnea, hypopnea, or body movements during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1987

Hypercapnia and sleep O2 desaturation in chronic obstructive pulmonary disease.

There is a wide clinical spectrum in chronic obstructive pulmonary disease (COPD). The extremes of this spectrum, the "pink puffer" (PP) and "blue bloater" (BB) stereotypes differ in their degree of sleep hypoxemia and pulmonary hypertension. Most patients cannot be characterized as either PP or BB. The data amassed in the recent nocturnal oxygen therapy trial provide an opportunity to see to what extent differences in sleep oxygenation and hemodynamics in a large hypoxemic COPD population are related to awake hypoxemia and hypercapnia. From a large hypoxemic COPD population sleep SaO2 was examined in those with (PaCO2 greater than 44 mm Hg) and without (PaCO2 less than or equal to 44 mm Hg) hypercapnia. Hypercapnic patients (mean PaCO2 49.8 mm Hg) had the same PaO2 and degree of airflow obstruction as normocapnic patients (PaCO2 37.4 mm Hg) but had far greater sleep hypoxemia (measured by mean sleep SaO2, low sleep SaO2, and awake-low sleep SaO2, p less than 0.05). In addition, arterial blood gases of the large sleep O2 desaturaters were compared with those of the small desaturaters; PaO2 was similar in both groups, whereas PaCO2 was different (p less than 0.01). Two common subsets of hypoxemic patients were also compared; one was hypercapnic and overweight, the other normocapnic and hyperinflated. We found that patients in the hypercapnic group had far worse sleep hypoxemia, although they had better lung function. We conclude that hypercapnia is a marker for sleep O2 desaturation in hypoxemic COPD.

Aged↗
PubMed1987

Snoring in normal young adults: prevalence in sleep stages and associated changes in oxygen saturation, heart rate, and breathing pattern.

Six men and three women, asymptomatic light snorers ranging in age from 25-34 years, were studied during sleep to determine the prevalence of snoring in the different sleep stages, the associated changes in oxygen saturation (SaO2), heart rate (HR), and breathing frequency (f), and the associated breathing arrhythmias. Snoring was defined as a 1-minute epoch with more than 80% of the breaths associated with snores. Most of the snoring epochs as well as the apneas and hypopneas occurred during stage 2, mainly because it is the most prolonged sleep stage. The prevalence of snoring, however, normalized for differences in length of sleep stages, was highest in stages 3 and 4 but low in REM, whereas the converse was true for apneas and hypopneas. Snoring caused no change in the mean SaO2, mean HR, or f, as compared with nonsnoring periods in the same sleep stage. Continuous snoring in normal subjects can occur without significant O2 desaturation or breathing arrhythmia. Continuous snoring and breathing arrhythmia tended to occur together in a given subject but were unrelated in time, suggesting a different pathogenesis.

Adult↗
PubMed1986

Atypical manifestations of pulmonary adenoid cystic carcinoma.

Pulmonary adenoid cystic carcinoma (PACC) typically arises in large airways. A patient who presented with a peripheral lung mass due to PACC is reported. She was found to have multiple pulmonary nodules due to PACC 11 years after resection of the original tumour. We emphasize that 10-15% of patients with PACC present with peripheral tumours.

Carcinoma, Adenoid Cystic↗
PubMed1982

Sleep, arousals, and oxygen desaturation in chronic obstructive pulmonary disease. The effect of oxygen therapy.

In order to assess the role of hypoxemia in the sleep disruption of patients with COPD, we studied patients breathing air and oxygen during sleep. In 24 patients with COPD, we determined the 95% confidence bands for arterial O2 saturation (SaO2) in the various sleep stages. The lowest mean SaO2 was during REM sleep. Patients spent 22.4% of the night desaturated (SaO2 more than 5% below awake SaO2). Apneic episodes were uncommon and occurred in only 2 patients. When compared with established age-matched normal subjects from another center, poor sleep quality was indicated by reduced sleep time, increased sleep stage changes, and increased arousal frequency. Oxygen therapy had no apparent effect on sleep quality. Arousal frequency was independent of measurements of awake pulmonary function or chemical control of breathing. During room air breathing, arousals were strongly associated with periods of arterial oxygen desaturation. However, relief of the hypoxemia with supplemental oxygen had no effect on arousal frequency. This suggests that it is not hypoxemia per se, but an associated phenomenon such as hypercapnia that causes the arousals.

Aged↗
PubMed1980

Sleep breathing abnormalities in kyphoscoliosis.

Five patients with severe kyphoscoliosis were studied during sleep. A spectrum of breathing abnormalities was found ranging from no abnormalities to severe episodes of prolonged central apnea. Rapid-eye-movement (REM) sleep was the period of greatest physiologic disturbance in all the patients, being the time of greatest oxygen desaturation. Within this small group, those with the most clinical evidence of chronic hypoxemia, polycythemia, and cor pulmonale, had the most severe derangements during sleep. Derangements in breathing pattern and arterial oxygen saturation (SaO2) had no apparent relation to the degree of thoracic deformity, the results of pulmonary function tests, arterial PCO2, or the chemical drives to breathe.

Adult↗
PubMed1978

Impaired oxygenation during sleep in excessive polycythemia of high altitude: improvement with respiratory stimulation.

Although polycythemia of high altitude is usually due to excessive hypoxemia, in some patients the hematocrit is elevated out of proportion to the degree of hypoxemia measured awake. One possible explanation is that severe hypoxemia occurs during sleep in these subjects. We therefore monitored oxygen saturation (SaO2), breathing pattern, and electroencephalogram (EEG) during sleep in five normal high-altitude residents and in five patients with excessive polycythemia. The polycythemic patients were studied as part of a placebo--drug double-blind crossover trial of the respiratory stimulant drug medroxyprogesterone acetate (MPA). The polycythemic patients while taking placebo were much more hypoxemic during sleep than the normals (all-night mean SaO2: 79.4 +/- 1.7% versus 87.8 +/- 1.7%, p less than 0.01). Abnormalities in breathing patterns were observed in all the subjects, especially during REM stage sleep. In polycythemic subjects, this resulted in precipitous hypoxemia with SaO2 as low as 50%--70%. Severe hypoxemia was not observed in control subjects despite similar abnormalities in breathing. Significant improvement in nocturnal SaO2 occurred when the polycythemic patients were taking MPA, mean SaO2 rising from 79.4 +/- 1.7% to 83.7 +/- 0.7%, p less than 0.05. Of probably greater importance, MPA largely prevented the precipitous drops in SaO2, mean lowest SaO2 rising from 64.6 +/- 4.7% to 76.0 +/- 2.1% p less than 0.05. The severe decreases in SaO2 during sleep may explain elevations in hematocrit that are out of proportion to the awake SaO2 in man at high altitude. The therapeutic effect of MPA in this condition may be due to amelioration of sleep hypoxemia.

Adult↗
PubMed1978

Diagnosis of airflow obstruction at high altitude.

Using predicted sea level values for spirometry done at high altitude, underestimation of airway obstruction may result. We therefore established spirometric normal values for an altitude of 3,100 m for white men.

Adolescent↗
PubMed1978

Excessive polycythemia of high altitude: role of ventilatory drive and lung disease.

Persons residing at high altitude who develop excessive polycythemia are more hypoxemic than normal high-altitude residents. We investigated the causes of hypoxemia in 20 patients with excessive polycythemia residing at an altitude of 3,100 m. Lung disease evidenced by abnormal spirometric features and results of a respiratory questionnaire was present in 10 of 20 patients and resulted in increased alveolar-arterial difference for PO2 [(A-a)PO2]. The excessive hypoxemia in the patients with normal lungs was not due to increased (A-a)PO2. We measured ventilatory responses to hypoxia and to hypercapnia to determine whether blunting of these responses was a cause of this excessive hypoxemia. We found, however, that chemical drives to breathe, although blunted, were the same in patients with polycythemia as in high-altitude control subjects. However, an abnormal breathing pattern was observed; the polycythemic patients had a smaller tidal volume and a greater ratio of dead space to tidal volume than did the normal subjects. In addition, the polycythemic patients had increased minute ventilation on breathing 100 percent O2, whereas the normal subjects did not. Thus, hypoxic depression of ventilation may have been present. Our findings suggested that blunted chemical drives are not causative in this disease, and that some other cause of hypoxemia must be present.

Altitude↗