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Periodic bouts of laryngeal dyspnea in a 77-year-old man were observed early in the course of a syndrome due to bilateral opercular infarcts. Laryngoscopy showed alternate slow opening and closure of the glottis superimposed on respiratory vocal cord movements. The disorder could result from bilateral removal of cortical control of bulbar centers, its periodicity suggesting analogies with Cheyne-Stokes' dyspnea.
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To determine the incidence of periodic breathing (PB) episodes during sleep, 48 subsequent sudden infant death syndrome siblings and 48 control infants, matched by sex, gestational age, and chronologic age, were studied by home pneumogram technique. The sudden infant death syndrome siblings had a statistically significant increase in the percent of sleep time spent in PB, in the number of episodes/100 minutes of PB, in the longest episode PB, and in the average duration of all episodes of PB. We conclude that PB is present in a higher amount in sudden infant death syndrome siblings as compared to control infants.
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The review of the literature on Cheyne-Stokes respiratory periods reveals enormous variation of the opinions expressed. The original description concerned periodicity characterized by rhythmic changes of respiratory phases and respiratory pauses in a relation of 60 : 15 seconds. In the respiratory phase there were 30 respirations of increasing depths and frequency at the beginning of the phase and decreasing depths and frequency at the end of the phase. Literature data about Cheyne-Stokes respiration comprise a multiplicity of all rhythymic forms. The duration of respiratory cycles varies between 12 and 130 seconds. The relation of the respiratory phase and respiratory pause between 6 : 4 or 75 : 70 seconds, and the number of breaths between 3 and 30 during one respiratory phase. Cheyne-Stokes periods were observed in health subjects as well as in patients with neurological, neurosurgical, cardiac, pulmonary and paediatric diseases. Cheyne-Stokes periods were explained as sequel of prolongation of circulation time between pulmonary alveoli and respiratory centre, through increased sensitivity of the respiratory centre to CO2, diminished sensitivity of the respiratory centre to CO2 and O2-deficit, local blood flow disturbances, section of pathways in the brain stem with disinhibition of basic rhythms, brain immaturity, alterations of consciousness, and respiratory obstructions. Rhythmic changes of the heart beat, of excitability of the heart muscle, of blood pressure, of EEG and of neurological and mental signs were observed. In spite of numerous observations detailed analysis of the respiratory cycle was performed in only a few cases. Major studies are lacking.
The analysis of cycles of periodic breathing (Cheyne-Stokes rhythms) in 35 patients showed wide variability of mean values of respiratory phases. The respiratory pauses are usually shorter and the scatter of the mean values is smaller. Only in four cases were respiratory pauses longer than respiratory phases. The duration of the respiratory phase becomes extended through the increase of number of single respirations. The latter also shows a very small scatter. The respiratory rate in 32 out of 35 patients was higher than normal and is to be considered as tachypnoea.
A study was conducted in which two groups of female rats were exposed to vaporized MMA-m for a period of 20 minutes daily for 21 and 42 days, respectively. Systolic blood pressure, heart rate, respiration, and ECG were monitored for 5 minutes prior to MMA-m exposure and then during a 20-minute exposure to MMA-m. On the twenty-first and forty-second day, respectively, the aforementioned vectors were monitored again. During the first exposure 63% of the experimental animals displayed marked changes in respiration ranging from a modified Cheyne-Stokes type to periods of very shallow breathing followed by deep breathing. Thirty-eight percent showed ECG changes ranging from premature ventricular contractions and altered QRS complexes to markedly depressed T waves. Continued exposure resulted in an initial decrease followed by an increased systolic blood pressure with an increased respiratory and heart rate. At the final testing period all animals showed abnormal respiratory patterns and ECG changes and demonstrated a heart block pattern. In all animals systolic blood pressure increased the longer they were exposed to MMA-m.
We have studied the propensity for periodic breathing to occur in cats anaesthetized with pentobarbitone breathing either spontaneously or with the aid of a 'servo-respirator' governed continuously by the efferent phrenic nerve activity. Sustained periodic breathing could be induced increasing 'controller gain', either by increasing the gain of the respirator, or by lung deflation, which reflexly increased controller responses to both hypoxia and hypercapnia. Periodic breathing was potentiated both by hypoxia and by diminishing the central (CO2, H+)-drive by focal cooling at the ventral surface of the medulla, two procedures which increase the relative influence of hypoxic drive. Less hypoxia was needed to produce periodic breathing at high rather than low controller gains. Reducing controller gain to zero by constant artificial respiration always abolished periodic breathing. Periodic breathing was also eradicated when the relative importance of CO2 drive was enhanced by breathing the cats with CO2-enriched gas mixtures or with 100% O2. The results are consistent with theoretical predictions for the occurrence of oscillations in the mechanisms for the chemical control of breathing and indicate that increasing controller gas can produce periodic breathing. The results further emphasize the importance of the (CO2, H+)-drive in preserving ventilatory stability.
In the present study a mathematical model of the chemical control of respiration is described which attempts to simulate periodic breathing during sleep. The model is an extension of an earlier model which has been shown to successfully reproduce the transient effects of CO2 inhalation on breathing, controlled changes in ventilation on arterial gas tension, and Cheyne-Stokes breathing. Included in the extended model are the effects of chemical stimuli during sleep on both chest wall and upper airway muscle activity. Data is presented indicating that simulations from the model reproduce reasonably well the essential features of the results obtained in eight subjects with periodic respiration during sleep when breathing room air, O2, or low concentrations of CO2. Simulations from the model and the experimental data suggest that periodic breathing during sleep results from unstable operation in the respiratory control system analogous to that seen during instabilities in physical control systems. The model indicates that obstructive as well as central apneas can be produced by control system instability. Furthermore, central apneas increase the likelihood of obstructive apneas while obstructive apneas tend to aggravate the control instability. The model results predict that the characteristics of the periodic breathing seen during sleep, such as apnea length, will depend on circulation time and the sensitivity of both upper airway and chest wall muscles to hypercapnia and hypoxia.
A theoretical analysis of the CO2 control of the respiratory system is presented using both analytic and simulation techniques. A stability index (SI) is obtained by linearizing a dynamic first-order model with a time delay. Analytically, SI values greater than unity predict an unstable response to a disturbance. Because the first-order model is reduced from a higher-order physiological model, SI can be algebraically related to physiological parameters. This relationship shows that SI increases with a decrease in system tissue volume, metabolic rate, or inspired CO2 partial pressure; SI decreases with a decrease in time delay, cardiac output, controller gain, or controller intercept. Analytically, SI distinguishes stable from unstable domains. By simulations of the nonlinear first-order model, three domains are obtained: an unstable domain (sustained oscillations, SI greater than 1.1), an underdamped stable domain (transient oscillations, 0.3 less than SI less than 1.1), and an overdamped stable domain (no oscillations, 0 less than SI less than 0.3). With this classification, disturbances such as change of state (e.g., from awake to asleep) or sigh may produce transient oscillations if the system becomes underdamped even though stable. Potential applications of this work include quantitative distinction of the physiological factors in control disorders associated with short-term periodicities (e.g., Cheyne-Stokes breathing, sleep apnea, breathing at altitude).
The respiratory oscillations of the arterial PO2 were measured in paralyzed, artificially ventilated cats by a small (1.2 mm) fast-responding catheter oxygen electrode. The amplitude of these oscillations could be changed independently of the mean PA,O2n by a specially designed respirator circuit. deltaPaO2 was shown to increase with increasing tidal volume or decreasing frequency of the respirator, and with increasing mean PaO2. The amplitude of the oscillations was attenuated considerably from the left atrium to the aorta. No attenuation occurred from the aorta to the carotid artery, provided that the blood flow in the carotid artery was not impeded. The measured attenuation of the oscillations was compared to that calculated by Yokota and Kreuzer (1973) and found to be quite different. The output of the ventilatory controlling system of the cat was measured from the quantified phrenic nerve activity. When only deltaPaO2 was changed at a constant level mean PaO2, the quantified phrenic nerve activity did not change, indicating that the amplitude of the oscillations does not influence the ventilatory controlling system. In vagotomized animals, the periodicities of the oscillations and the phrenic nerve activity were completely dissociated. From the fact that no Cheyne-Stokes type of breathing occurred, it was concluded that the effect of timing is negligible.
A model of the human respiratory system is proposed which has a satisfactory performance under different physiological conditions. The model comprises a continuous plant and a discrete controller which generates and updates the drive signal to the plant at the end of every breath to represent the Hering-Breuer reflex. Arterial and central medullary sensors are included. The lung volume, dead space volume, cardiac output and cerebral blood flow are time varying. The respiratory work is minimized. The model is examined and simulation results of its performance in hypercapnia, hypoxia, periodic breathing and moderate exercise are presented. The responses presented include the relatively fast transients of Cheyne-Stokes breathing and the slower transients associated with carbon dioxide inhalation.
We describe a case of dirhythmic breathing in a 60-year-old man after neurosurgery. A large hemangioblastoma was removed from the cerebellum at the level of the fourth ventricle. The spirometric tracings showed two types of respiratory cycles: the rhythm. A was stable with a short inspiratory time; sometimes a second type of respiratory cycle, B, was present or erratically coupled with the A rhythm. It had very small tidal volume and mean inspiratory flow with phasic variations similar to those observed in Cheyne-Stokes breathing pattern.
The effect of theophylline on periodic breathing was measured by transcutaneous oxygen monitoring in 7 patients suffering from chronic congestive heart failure. Theophylline significantly decreased the frequency of Cheyne-Stokes breathing. Transcutaneous oxygen monitoring proved to be a useful method to follow changes in the breathing pattern. The suggested mechanism of action of theophylline in reducing the incidence of periodic breathing is blockade of adenosine receptors.
Of 22 patients investigated for sleep disorders, habitual snoring and/or daytime hypersomnolence, 12(10 men) had obstructive sleep apnea syndrome (OSAS). 3 OSAS were mild, 5 moderate and 4 severe. The leading symptoms were daytime hypersomnolence and habitual snoring. As risk factors we found retro-micrognathia in 2 patients, macroglossia secondary to acromegaly in 1, alcohol abuse in 7 and obesity in 6. Conservative measures improved the disorder subjectively in 6 patients. One patient had a relapse 6 months after uvulopalatopharyngoplasty. 4 patients were successfully treated by nasal CPAP. Other diagnoses were idiopathic alveolar hypoventilation (2), Cheyne-Stokes breathing secondary to low cardiac output (1), monosymptomatic narcolepsy (2), sleep disturbances secondary to depression (2), chronic benzodiazepine abuse (1) and chronic bronchitis without nocturnal hypoxemia (1). History, clinical observation and oxymetry make diagnosis possible in most cases of OSAS severe enough to require treatment. Polysomnography is time-consuming and should be reserved for selected cases.
The occurrence of breathing disorders and hypoxia during sleep was studied in 17 male patients with coronary artery disease, demonstrated by coronary angiography, who did not have symptomatic pulmonary disease. Thirteen patients (76 percent) experienced disordered breathing during sleep; of these, 11 had obstructive apnea and the other two had Cheyne-Stokes breathing. There was an average of 20 episodes of disordered breathing per hour during sleep among the 13 patients, with a mean duration of 24 seconds per episode; significant oxygen desaturation occurred in ten of these 13 patients. There was no episode of angina pectoris, myocardial infarction or sudden death. Although cardiac arrhythmias occurred in 12 patients, disordered breathing with hypoxia was not proven to be causative. Therefore, obstructive disordered breathing and nocturnal oxygen desaturation commonly occurred during sleep in patients with coronary artery disease. Although no immediate ill effects were noted, the longterm effects remain to be determined.