PubMed Health⌕ Search

Biomedical subjects

M H Kryger

Publications and source records attributed to M H Kryger.

At least 73 records · Page 4Linked to original sources
PubMed1987

The effect of excessive ethanol ingestion on sleep in severe chronic obstructive pulmonary disease.

The effect of a moderately intoxicating dose of ethanol on sleep was evaluated in five patients with severe emphysematous chronic obstructive pulmonary disease (COPD) (mean FEV1 0.83 L, PaO2 75 mm Hg). Mean serum ethanol before sleep was 129 mg/dl. With alcohol, total sleep time per night decreased from a mean of 293 to 238 min. Relative sleep time per stage also changed; NREM time increased, and REM time decreased greater than 50%. Alcohol caused significant O2 desaturation; group mean sleep arterial oxygen saturation (SaO2) decreased from 90.6 to 87.7% with alcohol. Although the decrease in SaO2 was not uniform across all sleep stages, no individual sleep stage accounted for the desaturation. The fall in SaO2 with alcohol was not explained by increasing apneas or hypopneas. Mean heart rate increased significantly from 71.8 to 77.1 with alcohol, with premature ventricular contractions increasing in two subjects. Excessive alcohol ingestion in severe COPD alters total sleep time and stage distribution, decreases SaO2 without significant change in apneas, and increases heart rate. Prior to sleep, patients with severe COPD should strictly limit ingestion of alcohol.

Aged↗
PubMed1987

Oxygenation and breathing pattern during phasic and tonic REM in patients with chronic obstructive pulmonary disease.

Oxygen desaturation in chronic obstructive pulmonary disease (COPD) occurs during sleep and is most marked in REM sleep. REM is not a homogeneous state, consisting of phasic REM (PREM) (REMs, myoclonic twitches) and tonic REM (TREM) (muscle atonia, desynchronized electroencephalogram). In normals, onset of PREM produces transient changes in breathing pattern with a decrease in respiratory amplitude and an increase in frequency, which produce reductions in oxygen saturation (SaO2). Because it is reasonable to expect such breathing pattern changes to cause more desaturation in COPD, and because systematic all-night studies of PREM and TREM have not been reported, we studied 18 patients with severe COPD [Forced expiratory volume in one second (FEV1) = 25.7 +/- 3.5 (SEM) % predicted] during sleep and monitored SaO2 and breathing pattern in PREM and TREM. PREM made up 19.7% of total REM (4.6% total sleep time) but was associated with 81.7% of the total REM desaturations of greater than 5% (57.9% of all sleep desaturations of greater than 5%). With PREM onset, breathing pattern changed 72.5% of the time, most often with a transient decrease in amplitude and increase in frequency. Even though 27.5% of PREM was not associated with changes in breathing pattern and many PREM segments were very short, we were still able to show highly significant SaO2 differences between PREM and TREM. Mean TREM SaO2 was 88.0 +/- 1.2%; mean PREM SaO2 was 86.6 +/- 1.4%, with mean nadir SaO2 for individual PREM segments falling to 84.8 +/- 1.5%. Mean awake SaO2 was 89.7 +/- 0.8%. We conclude that in COPD the transition from TREM to PREM is associated with breathing pattern changes and oxygen desaturation. Differences in breathing pattern with PREM onset may be related to different effects of PREM processes on respiratory neurons and diaphragm motor neurons.

Aged↗
PubMed1987

Dynamic in vivo response characteristics of three oximeters: Hewlett-Packard 47201A, Biox III, and Nellcor N-100.

Pulse oximeters (Biox III, Nellcor N-100) and a transmittance oximeter [Hewlett-Packard 47201A (HP)] were compared for SaO2 measurement and responsiveness during dynamic changes in arterial oxygen saturation and heart rate. Five sleep apnea syndrome patients were studied because they had large oscillations in SaO2 and heart rate in sleep. During sleep, each patient exhibited a series of rapid (18.0 +/- 8.3 s, mean +/- SD) oscillations in oxygen saturation (92.1 +/- 2.6% to 74.2 +/- 7.7%). Oxygen saturation measurements were sampled simultaneously from each oximeter by computer (at 2 Hz). Accuracy was assessed by comparing pulse and transmittance oxygen saturation measurements at the peak and trough of each apnea-related oscillation. Oximeter response was defined in terms of the "delay" or absolute time difference between the pulse oximeters and the transmittance oximeter for the determination of the peak and trough saturations. Linear regression analysis was used to establish accuracy and response relationships between pulse oximeter sensors (reusable ear, reusable digit, disposable digit, and disposable nasal sensors) and the transmittance oximeter sensor (reusable ear sensor). Pulse oximeter response delay was highly correlated with heart rate. Pulse oximeter SaO2 measurement and response characteristics varied considerably with sensor type (disposable, reusable) and sensor location (ear, nose, and digit). One must be aware of these differences in clinical and research application.

Adult↗
PubMed1987

Sleep in restrictive lung disease.

Restrictive lung disease patients exhibit a wide range of breathing and oxygenation abnormalities during sleep. The combination of degree of restriction, whether it is intrapulmonary or extrapulmonary, and confounding factors, such as obesity, age, and sex, will ultimately determine the degree of disturbed nocturnal physiology. The sleep literature is still sparse in most restrictive diseases. For patients with interstitial lung disease, the role of nocturnal oxygen in chronic established fibrosis, and also in acute alveolitis (e.g., farmer's lung, bird fancier's lung, etc.), has not been addressed. As fibrotic lung disease progresses, the degree of nocturnal desaturation and breathing dysrhythmias will progress. Changes in sleep architecture are likely related to the progression of the disease, but this is not known with certainty. Long-term evaluation of sleep and breathing in interstitial lung disease will give further insight into whether or not sleep changes are primary or secondary events. For kyphoscoliosis patients, again, we need more information on sleep as the thoracic deformity changes. In addition, the use of drugs (acetazolomide, medroxyprogesterone, and almitrine) and/or nasal CPAP to treat nocturnal desaturation needs to be assessed in a controlled fashion. In neuromuscular disease, the dynamics of gas exchange and sleep structure need to be defined in a larger group of patients. Factors such as degree of muscle weakness, degree of underlying lung diseases, and medications must be taken into consideration. Nocturnal hypoxemia may cause muscle weakness and fatigue, which in time, could cause more nocturnal hypoventilation and further hypoxemia. Supplemental nocturnal oxygen should be evaluated in this population.

Female↗
PubMed1987

Perfluorochemical artificial blood as a volume expander in hypoxemic respiratory failure in dogs.

The perfluorochemical O2-transport fluid, Fluosol-DA 20 percent (PFC), is being clinically evaluated as a volume expander in patients who are unable to receive blood products. Since patients treated with Fluosol-DA may be at risk of developing adult respiratory distress syndrome (ARDS) as a complication of the original disorder for which they were transfused, we examined central hemodynamics and gas exchange in anesthetized O2-ventilated dogs with oleic-acid induced pulmonary edema before and after transfusion with 400 ml of either PFC (n = 5) or whole blood (n = 5). Transfusion produced similar increases in cardiac output, pulmonary and systemic vascular pressures and intrapulmonary shunt in the two groups. Arterial O2 tension, however, fell from 209 +/- 117 to 172 +/- 81 mmHg in the blood transfused group but increased from 219 +/- 145 to 302 +/- 138 mmHg in the PFC group. Arterial O2 content, on the other hand, increased in the blood transfused group due to an increase in hematocrit, but fell with PFC because of hemodilution. This lower total arterial O2 content in the PFC group was, however, compensated for by more efficient O2 transport by the PFC in that the PFC arteriovenous O2 content difference accounted for 26 percent of the total arteriovenous O2 content difference, making it about four times as efficient as hemoglobin in tissue O2 delivery. Fluosol DA, 20 percent, is an effective volume expander in this model of hypoxemic respiratory failure, and it can transport significant amounts of O2 even in the presence of a substantial intrapulmonary shunt.

Animals↗
PubMed1986

Breathing during sleep in normal pregnant women.

Physiologic changes during the last trimester of pregnancy include reduced functional residual capacity and residual volume, increased alveolar-arterial difference for oxygen, and in the supine position reduced cardiac output. In conjunction with sleep-related apnea or hypoventilation, these could lead to maternal oxygen desaturation during sleep. Because we could not find detailed respiratory sleep studies in late pregnancy, we performed complete polysomnography on 6 pregnant women at 36 wk gestation and again postpartum. Contrary to what we expected, oxygenation was well maintained, with neither mean nor minimal arterial oxygen saturation significantly different during pregnancy. Frequency of apnea and hypopnea and total apnea and hypopnea time were significantly reduced during pregnancy. This finding may be due to increased levels of progesterone during pregnancy and may contribute to preservation of maternal oxygenation during late pregnancy.

Apnea↗
PubMed1986

Alteration in breathing pattern with progression of chronic obstructive pulmonary disease.

We examined the relationship between breathing pattern and severity of disease in patients with chronic obstructive pulmonary disease (COPD). Resting breathing pattern was recorded for 45 min using the respiratory inductance plethysmograph (RIP) in 22 patients with stable COPD. Six subjects (moderate group) had FEV1 25 to 50% predicted, 8 subjects (severe group) had FEV1 less than 25% predicted, and 8 subjects (respiratory failure group) had FEV1 less than 25% predicted and were hypoxemic. Seven of the subjects with respiratory failure were also hypercapnic. Subjects with respiratory failure were studied with and without supplemental O2. All subjects were studied in the seated position. There were no significant differences in breathing pattern between the moderate and severe groups. Tidal volume (VT) was 120 ml lower in the severe group, but breathing frequency (f) was slightly elevated, allowing minute ventilation (VI) to be maintained. The respiratory failure group demonstrated a significant decrease in VT compared with that in the moderate group and a significant decrease in VT/TI as compared with both moderate and severe groups; TI was unchanged in subjects with respiratory failure, and, as f did not increase significantly, VI was decreased. Acute relief of hypoxemia had no effect on breathing pattern in respiratory failure. Variability was assessed by comparing the coefficients of variation for each timing component. There was no difference in intraindividual variability of breathing pattern between all groups. These results suggest that changes in ventilatory control as reflected by breathing pattern are to some extent independent of mechanical abnormalities.

Forced Expiratory Volume↗
PubMed1985

Breathing during sleep in patients with interstitial lung disease.

Patients with interstitial lung disease (ILD) have a rapid shallow breathing pattern while awake that is thought to be due to activation of lung reflexes. We wondered whether sleep would result in changes in respiratory control and thus cause hypoxemia and poor sleep quality. Eleven patients with ILD (5 men and 6 women) and 11 age- and sex-matched control subjects were studied during sleep. Sleep quality was worse in patients with ILD, with more time in Stage 1 (33.7% of total sleep time (TST) versus 13.5%) and less time in REM sleep (11.8 versus 19.9% TST) than found in control subjects, and more fragmentation of sleep (13.7 +/- 3.1 arousals/h and 24.3 +/- 6.0 sleep stage changes/h versus 6.9 +/- 1.0 and 12.7 +/- 1.4, respectively). Patients with ILD with awake SaO2 less than 90% had greater abnormalities in sleep structure than did those with SaO2 greater than 90%. The incidence of apneas and hypopnea periods in patients with ILD was low (apnea plus hypoventilation index of 1.3 +/- 0.45 versus 2.9 +/- 0.82 in control subjects, p = NS). Oxygen saturation dropped during REM sleep in patients, especially in those with more severe awake hypoxemia. Expiratory time (Te), inspiratory time (Ti), and their sum (Ttot) were shorter in the patients, whereas Ti/Ttot was the same as in control subjects. No systematic changes during sleep were seen in these variables. The variability of inspiratory volume index, Ti, Te, and Ti/Ttot was similar to that in control subjects, and was lowest during NREM sleep. The incidence of snoring was comparable in patients and control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Sleep and control of heart rate.

The heart rate in normal humans is determined by many factors. Assuming a normal hemoglobin concentration, left ventricular function, and metabolic rate, respiration, and its effects, along with autonomic nervous activity, appear to influence heart rate the most. Hypoxia and hypercapnia both increase heart rate during wakefulness and probably do the same during sleep. The hypoxic response is dependent on information from lung inflation and the carotid bodies. Respiratory rate, within limits, will determine the amplitude of the well-known (respiratory) sinus arrhythmia. During sleep, a distinct pattern of heart rate response and its respiratory arrhythmia are seen for each stage of sleep and are related to the level of autonomic nervous system activity during wakefulness. Blood pressure follows the same trend as heart rate during sleep, and changes in cardiac output and total peripheral vascular resistance are variable during sleep, but there is no consensus of opinion about the direction of these changes. Rhythm disturbances are predominantly those of bradyarrhythmias, exaggerated sinus arrhythmias, and transient AV block, which are probably occurring in REM sleep.

Arousal↗
PubMed1985

Sleep in restrictive lung disorders.

Abnormalities in sleep occur in patients with both extrapulmonary restriction and intrapulmonary restriction. Patients with extrapulmonary restriction such as kyphoscoliosis may develop severe apneas during sleep, particularly during the REM stage. Patients with interstitial lung disease continue to have a rapid shallow breathing pattern during sleep, but may also develop abnormalities in the breathing pattern. During periods of snoring patients with interstitial lung disease may develop further hypoxemia.

Arousal↗
PubMed1985

Sleep and respiration: a postscript.

The recent advances in our understanding of breathing in sleep include an evolution in the selection and surgical therapy of patients with the sleep apnea syndrome. Recent work suggests that shorter polysomnographic studies may be adequate for diagnostic purposes in many sleep apnea patients. It is now clear that central apnea may occur, paradoxically, in patients with either very blunted chemical drives to breathe or increased drives to breathe.

Acetazolamide↗
PubMed1985

Fat, sleep, and Charles Dickens: literary and medical contributions to the understanding of sleep apnea.

Although the relationship between breathing and sleep has only recently been "discovered" by the medical community, excellent literary descriptions of what we know to be the sleep apnea syndrome were made long ago. Although ancient Greek writings described probable sleep apnea, the most important literary contributions in this area are by Charles Dickens. His description of Joe the fat boy in the Pickwick Papers is an example of his brilliant skills of observation and description. It was not until about 140 years after Pickwick Papers was published that we understood what he was describing.

Drama↗
PubMed1985

Sleep and respiration: terminology and methodology.

Sleep and respiratory recording techniques and the methods of interpretation employed in a clinical setting are reviewed. Sleep organization and the rules by which sleep state is classified are discussed, as well as the theory of operation pertaining to respiratory instrumentation.

Adult↗
PubMed1984

Breathing patterns in patients with chronic obstructive pulmonary disease.

The respiratory inductance plethysmograph (RIP) was used to record resting breathing for 45 min in 12 patients with stable chronic obstructive pulmonary disease (COPD) and 8 age- and sex-matched control subjects. The COPD group had mean FEV1.0 of 31% predicted (range: 15 to 49%), mean PaO2 of 70 mmHg (56 to 83 mmHg), and mean PaCO2 of 37 mmHg (31 to 47 mmHg). All subjects were studied in the sitting position, and the rib cage (RC) and abdomen (ABD) RIP signals were simultaneously recorded on a polygraph and sampled at 20 Hz by a microcomputer. The summed RC and ABD signals were processed to create a spirogram from which the timing components of the respiratory cycle were subsequently analyzed. The mean number of breaths analyzed per subject was 702 +/- 213 (SD). Mean tidal volumes were identical in both groups. Inspiratory and expiratory times were significantly less (p less than 0.01), and mean inspiratory flow was significantly greater (p less than 0.01) in the COPD group. Frequency and minute ventilation also were significantly greater in the COPD group (p less than 0.005). Variability of breathing pattern, assessed in terms of coefficients of variation, was significantly less for TI, TI/Ttot, and VI in COPD patients than in normal subjects, even after sighs had been excluded from the analysis. We suggest that alterations in breathing pattern and its variability reflect changes in neural control of breathing consequent to disease.

Female↗
PubMed1983

Sleep apnea. From the needles of Dionysius to continuous positive airway pressure.

It is generally believed that the first description of the sleep apnea syndrome was made by Charles Dickens in the Pickwick Papers and that the first medical description was published in 1956. In fact, some of the features of the sleep apnea syndrome were described in antiquity and brief medical reports were published prior to the Pickwick Papers. This article traces the literary and medical contributions to our understanding of sleep apnea.

History, 18th Century↗
PubMed1983

Sighs during sleep in adult humans.

We analyzed sighs (breaths with a tidal volume at least twice that of baseline breaths) during sleep in 12 normal adults. We found a total of 124 sighs in the group, with an average of 1.66 sighs/h of sleep, but with great intersubject variation (range: 1-25 sighs/night). There were sighs in all sleep stages, but there were more per hour in stage 1. 64.4% of the sighs were associated with an increase in EMG activity or EEG frequency, starting either before or immediately after the sigh. The remainder of the sighs were not associated with any arousal or sleep stage changes. The normal variability of heart rate with breathing is exaggerated during sighs, probably because of the greater inflation and the associated arousal. Sighs have larger mean inspiratory flows (Vt/Ti), expiratory flows (Vt/Te), and a larger fraction of respiratory cycle spent in inspiration (Ti/Ttot) than the previous breaths, all evidence of a change in respiratory control. Sighs during sleep may occasionally be followed by central apneas, hypoventilation, or considerable slowing of respiratory rate. Although it has been shown that a sigh renders the respiratory centers refractory to another sigh, we found that sighs sometimes occur in pairs.

Adult↗