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Biomedical subjects

M Kryger

Publications and source records attributed to M Kryger.

At least 19 recordsLinked to original sources
PubMed1992

The effect of short-term nasal CPAP on Cheyne-Stokes respiration in congestive heart failure.

We studied male patients (BMI = 27.6 +/- 3.4, mean +/- SD), mean age 54.1 +/- 8.9 years, with stable NYHA class 3-4 congestive heart failure (CHF) (LVEF = 24.3 +/- 11.5 percent) and normal daytime arterial blood gas values. These patients underwent three consecutive nights of full polysomnography; adaptation, control, and treatment with nasal CPAP. Each night's study was followed during the day by cognitive testing and multiple sleep latency tests (MSLT). The purpose of the study was to document the effect of nasal CPAP on these variables. The main findings of the study showed no significant differences between control and treatment nights with respect to the amount of Cheyne-Stokes respiration (CSR) observed, the nocturnal oxygenation, or sleep quality. Both subjective and objective measures of sleep quality showed no change from night to night. In addition, the degree of cognitive functioning and daytime sleepiness (as measured by MSLT) showed no significant differences between control and treatment nights. We conclude that short-term treatment with nasal CPAP in patients with CHF does not improve either CSR, nocturnal oxygenation, or sleep quality. Furthermore, most of our patients did not tolerate nasal CPAP therapy.

Adult↗
PubMed1992

The importance of nasal resistance in obstructive sleep apnea syndrome.

The importance of nasal airflow resistance in the pathogenesis of obstructive sleep apnea syndrome (OSAS) remains contentious. We performed formal nocturnal polysomnography (PSG) on OSAS patients under conditions of baseline and reduced nasal resistance to answer two main questions. First, to what degree does baseline nasal airflow resistance influence upper airway collapse in OSAS patients? Second, in what proportion of the OSAS population is baseline nasal resistance contributing to the pathogenesis of upper airway collapse? Our study group consisted of 10 patients with a wide range of OSAS severity. Six of these patients had symptoms and clinical evidence of chronic nasal obstruction which, in some, was associated with markedly elevated nasal resistance. A placebo (normal saline) was instilled in the nose of each patient on the night of baseline data collection. On the treatment night of the study, nasal resistance was reduced by application of topical vasoconstrictor and insertion of vestibular stents designed to dilate the area of the nasal valve. Posterior rhinomanometry was used to measure resistance to nasal airflow immediately before and after each PSG study. Although treatment was associated with a subjective improvement in sleep quality and mean drop in nasal resistance of 73% (P less than 0.001), there was no significant improvement in sleep architecture, nocturnal oxygenation, or the amount of apnea experienced by patients. The most significant improvement was a reduced number of arousals/hour from 52.4 +/- 12.4 on placebo to 43.7 +/- 10.2 on treatment (P less than 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Sleep quality in children with asthma treated with theophylline or cromolyn sodium.

The effect of theophylline and cromolyn sodium on sleep was studied in 10 children with asthma who were 10 to 17 years of age (mean 13.5 +/- 2.4 years). Theophylline or cromolyn sodium was taken for 14 days in a double-blind, crossover, placebo-controlled trial. Theophylline blood levels before sleep were 10.2 +/- 4 micrograms/ml during the theophylline period. There was no difference in pulmonary function between the two periods. Theophylline did not disrupt sleep as measured by sleep latency, total sleep time, sleep efficiency, movement time, microarousals, and arousals. Apneic episodes (greater than or equal to 10 seconds) were of central origin and less frequent during the theophylline period (p less than 0.05). Arterial oxygen desaturation (greater than 5% decrease from baseline saturation when awake) was less frequent during the theophylline treatment (p less than 0.05). We conclude that theophylline treatment of the children's asthma did not disrupt sleep and appeared to have a protective effect in regard to apnea, hypopnea, and arterial oxygen saturation.

Adolescent↗
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↗
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↗
PubMed1977

Case report.

Explore the source record for details and available documents.

Adenoma↗