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Biomedical subjects

M H Kryger

Publications and source records attributed to M H Kryger.

At least 91 records · Page 5Linked to original sources
PubMed1983

Single-position calibration of the respiratory inductance plethysmograph.

Since we intended to use the respiratory inductance plethysmograph (RIP) to study breathing patterns in a single body position, we developed a method to calibrate the RIP in one position (seated) and verified the stability of this calibration procedure during a 60-min period. The subject breathed spontaneously through a pneumotachograph for 1 min during all calibration and verification runs. All inspiratory data from the abdomen and rib cage RIP transducers was analyzed using multiple linear regression analysis to calculate calibration factors for the transducers. Eight normal subjects were studied, and the stability of calibration at 20, 40, and 60 min was determined. The correlation coefficients were all greater than 0.94. The mean slope and mean intercept describing the relationship of the RIP volume to the pneumotachograph volume for all calibration and verification runs were 0.995 +/- 0.074 and 0.012 +/- 0.018 liter, respectively. This calibration method allows a spirogram to be generated from the RIP signals. Therefore, this technique may be valuable in further investigating resting breathing patterns in humans.

Adult↗
PubMed1982

Protriptyline in obstructive sleep apnea: a double-blind trial.

We evaluated protriptyline, a nonsedating tricyclic antidepressant, as a treatment for obstructive sleep apnea in a double-blind crossover study of five men. After two weeks of treatment, with no change in body weight, daytime somnolence was markedly reduced and nocturnal oxygenation was improved, although apnea duration and frequency were not significantly decreased. Rapid-eye-movement (REM) stage time as a fraction of the total sleep time was reduced during treatment from 0.231 +/- 0.031 to 0.107 +/- 0.013 (mean +/- S.E.M.) (P less than 0.05). REM apnea time as a fraction of total sleep time was reduced from 0.145 +/- 0.022 to 0.054 +/- 0.006 (P less than 0.05). REM reduction during treatment with protriptyline can account for decreased REM apnea time. Similar decreases in REM stage time and REM apnea duration and similar improvement in oxygenation continued after six months of treatment. In addition, body weight, apnea, and arousal frequency were decreased at this time. Although the obstructive sleep apnea was not resolved, it was reduced. Protriptyline can be effective in patients with sleep apnea when the disorder is not life-threatening.

Adult↗
PubMed1982

Breathing during sleep in parents of sudden infant death syndrome victims.

Some children with "aborted" sudden infant death syndrome (SIDS) and parents of SIDS victims have abnormal control of ventilation. Because apnea during sleep occurs in some children who go on to die of SIDS, and because the abnormality in ventilatory control may be familial, we examined breathing during sleep in parents of SIDS victims to determine whether breathing pattern abnormalities were common in them. We studied 12 patients (6 couples) of SIDS victims and 12 age-matched control parents with healthy children. We failed to demonstrate significant differences in the incidence of apneas or breathing pattern irregularities between the SIDS and control parents. However, 2 SIDS parents, 1 male and 1 female, had 44 and 31 apneic episodes, respectively, exceeding the number conventionally used to document excessive apneic episodes during sleep. Neither of these parents had the hundreds of apneic episodes usually seen in the sleep apnea syndrome. Although these 2 SIDS parents support the notion that a sleep breathing abnormality may exist in SIDS parents, most of the SIDS parents had normal breathing during sleep. Because the abnormalities in the two SIDS parents were minor, and because the remainder of the subjects were normal, we conclude that polysomnographic recordings fail to reveal a "marker" that might identify potential SIDS parents.

Adult↗
PubMed1982

Diagnosis of sleep breathing disorders in a general hospital. Experience and recommendations.

In the 24 months after a sleep breathing laboratory opened in a general hospital, 48 patients thought to have a primary sleep breathing disorder were referred for study. Evaluation of breathing during sleep was most useful in those having excessive daytime sleepiness or unexplained polycythemia. The sleep apnea syndrome was documented in 19 of 24 patients with excessive daytime sleepiness. Of 15 patients with unexplained polycythemia, ten were found to have severe hypoxemia during sleep. This experience suggests that facilities for evaluation of sleep breathing disorders should be available in larger medical centers.

Electrocardiography↗
PubMed1982

Central apnea.

Explore the source record for details and available documents.

Acetazolamide↗
PubMed1981

Sleep disorders in chronic airflow obstruction.

Sleep is the period of greatest physiologic disturbance in chronic airflow obstruction and so is likely the time of greatest danger to these patients. Sleep in these patients aggravates gas exchange abnormalities resulting in secondary pulmonary hypertension and cardiac arrhythmias. The mechanism of these disturbances is not fully explained, but patients with chronic airflow obstruction do not characteristically have the sleep apnea syndrome. Patients with chronic airflow obstruction sleep badly, with less rapid eye movement sleep and increased sleep stage changes. Nocturnal oxygen therapy helps relieve pulmonary hypertension and may decrease cardiac arrhythmia, but has no effect on sleep profile.

Airway Obstruction↗
PubMed1980

Sleep apnea in acromegaly.

In patients with acromegaly obstruction of the upper airway may develop due to enlargement of the tongue and thickening of the tissues of the larynx. The sleep apnea syndrome may develop in patients with upper airway obstruction from other causes. We studied a somnolent patient with acromegaly in whom we documented the sleep apnea syndrome. Endoscopy, while the patient was sleeping, revealed that periodic obstruction during sleep occurred because the large tongue bulged into the pharynx and obliterated the pharyngeal airway. Tracheostomy was followed by the disappearance of the somnolence. The upper airway obstruction in acromegaly may result in severe hypoxemia and disruption of normal sleep.

Acromegaly↗
PubMed1980

Chemical control of ventilation and sleep arterial oxygen desaturation in patients with COPD.

In 41 patients with hypoxemic COPD, nocturnal changes in arterial O2 saturation were compared with measurements of hypoxic and hypercapnic ventilatory control, which were carried out during wakefulness. In 24 patients, sleep was judged visually, whereas in 17, sleep was staged by electroencephalogram (EEG). There were no differences between the 2 groups in terms of lung function, blood gases, or sleep desaturation. All patients desaturated during sleep, with maximal desaturation occurring during rapid eye movement (REM) sleep. The maximal nocturnal change in O2 saturation observed in each patient was negatively correlated with the patient's ventilatory sensitivity to hypercapnia; this relationship was independent of sleep stage. Both maximal and mean nocturnal changes in O2 saturation were negatively correlated with O2 saturation during wakefulness. Hypoxic ventilatory response was not related to nocturnal desaturation. Patients who are sensitive to hypercapnia are unlikely to show major sleep desaturation, whereas those who are insensitive to CO2 may do so, particularly if they have low O2 saturations while awake.

Aged↗
PubMed1980

The effect of low flow oxygen therapy on the chemical control of ventilation in patients with hypoxemic COPD.

To determine whether the decreased hypoxic responses present in patients with hypoxemic chronic obstructive pulmonary disease (COPD) were reversible with correction of their hypoxemia, we measured ventilatory and P0.1 responses to CO2 and hypoxia in 30 such patients. These patients were then randomly allocated to either 24-h continuous oxygen or 12-h nocturnal oxygen therapy. Responses to CO2 and hypoxia were then remeasured in all patients after 6 months of oxygen therapy, and in 13 patients after 1 yr of oxygen therapy. The blunt hypoxic responses showed no increase after either regimen of oxygen therapy and were further reduced after 6 months of 12-h nocturnal oxygen. The decreased hypoxic response in patients with hypoxemic COPD appears nonreversible with the relief of the hypoxemia. Responses to CO2 were depressed after 6 months of 24-h oxygen therapy and associated with a significant increase in PaCO2. The change in PaCO2 after oxygen therapy was nonpredictable in terms of the initial responses to hypoxia or CO2. Minute ventilation (VE) and mean inspiratory flow during resting breathing at an arterial O2 saturation of 95% decreased after 6 months of 24-h oxygen therapy, indicating a reduction in central ventilatory drive.

Carbon Dioxide↗
PubMed1978

Familial aspects of decreased hypoxic drive in endurance athletes.

One difference between endurance athletes and nonathletes is decreased ventilatory responsiveness to hypoxia and hypercapnia. It has never been clear whether these decreased responses are a consequence of conditioning or precede participation in endurance athletics. Recent studies demonstrating clusters of decreased ventilatory responses to hypoxia in families of patients with unexplained respiratory failure suggest that decreased responses in endurance athletes might be familial. To investigate this possibility, ventilatory response to hypoxia and hypercapnia were measured in 16 nonathletic, healthy parents and siblings of five successful long-distance runners. Response were compared to 34 nonathletic controls. As measured by the shape parameter A, hypoxic response was decreased to a similar extent in runners 74 +/- 6.4 (mean +/- SE) (P less than 0.05) and their relatives 69 +/- 15.2 (P less than 0.01) compared to control 128 +/- 11.3. Hypercapnic responses were slightly, but not significantly, decreased in runners and their families. We conclude familial influences made a major contribution to the decreased hypoxic ventilatory response seen in long-distance runners.

Adolescent↗
PubMed1976

Depression of hypoxic ventilatory response by nitrous oxide.

Ventilatory responses to CO2 and hypoxia were measured in four normal volunteers breathing 30-50 per cent N2O with and without added inspiratory resistance. CO2 response was measured by a steady-state technique, hypoxic response by a non-steady-state progressive technique. Added inspiratory resistance depressed ventilatory responses to both CO2 and hypoxia. N2O had no effect on CO2 response either with or without resistance. N2O depressed the ventilatory response to hypoxia without added resistance and further depressed the response measured with added resistance. It is thought that this was probably the result of selective depression of peripheral chemoceptor function by N2O.

Adult↗
PubMed1976

Effect of meperidine on occlusion pressure responses to hypercapnia and hypoxia with and without external inspiratory resistance.

In 5 normal subjects we measured ventilation and P0.1, the pressure generated by the first 0.1 sec of inspiratory effort against a closed airway, in response to hypercapnia and hypoxia with and without added inspiratory resistance before and after oral meperidine (1.1 to 1.3 mg per kg). CO2 responses were studied in the steady state, whereas progressive hypoxia was used to elicit hypoxic responses. In general, resistance decreased ventilatory responses to hypercapnia but increased P0.1 responses to both hypoxia and hypercapnia. Meperidine depressed both ventilatory and P0.1 responses, more so in hypoxia than in hypercapnia. The combination of resistance and merperidine was additive in depressing responses to hypercapnia but in hypoxia produced little more depression than did meperidine alone. In both hypercapnia and hypoxia, meperidine decreased the augmentation of P0.1 that was associated with increased resistance. Normal subjects responded to acute increases of inspiratory resistance by increasing inspiratory motor output; this increase was distinctly blunted by meperidine.

Adult↗