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PubMed1975

[Combined effects of hypoxia and hypercapnia on the functional state of the respiratory center].

Experiments were conducted on cats under nembutal anesthesia; a study was made of pulse activity of bulbar respiratory neurons, electrical activity of the diaphragm and of the intercostal muscles; pO2, pCO2, pH, arterial blood oxygen saturation were determined in combined action of hypoxia and hypercapnia. When hypoxic gaseous mixture was given for respiration the developing hypocapnia disturbed the discharge rhythmic activity of the respiratory neurons, the respiration acquiring a pathological character of the Cheyne--Stokes type. After addition to the hypoxic gaseous mixture of 2% CO2 the gaseous composition of the arterial blood approached the initial values; this addition prevented the development of hypercapnia and disturbances of rhythmic discharge activity of the respiratory neurons. Addition of 5% CO2 to the hypoxic gaseous mixture produced a negative effect: at first it intensified and then depressed the pulse activity of the respiratory neurons, caused metabolic and respiratory acidosis, and promoted asphyxia.

Animals↗
PubMed1979

Monitoring as anesthesia draws to a close.

The closing phase of anesthesia is defined. Some of the hazards of this period are reported and illustrated by capnograms. It is claimed that the dangers arising at the end of anesthesia are insufficiently appreciated.

Anesthesia↗
PubMed1992

[Fulminant meningoencephalitis due to Listeria monocytogenes].

We present a case of meningoencephalitis due to Listeria monocytogenes type IV in a patient in which the diagnosis of small-cells malignant diffuse non-Hodgkin's lymphoma had been established. He was hospitalized with vague clinical manifestations and without showing any neurological focus. Hours later, he presented clinical brain stem semiology. Within a 24-hour period, Listeria monocytogenes was isolated from blood and cephalorhachidian fluid (being the first time that this microorganism had been isolated for the past 20 years in our laboratory). The patient evolved to a state of coma, with Cheyne-Stokes's respiration, abolition of pupillary reflexes, decerebration position and exitus laetalis. The affection of the central nervous system has been fully documented. However, its fulminant presentation, as in the case that we present here, is less frequent, although it has been described in the literature by other authors, like Finegold et al., with cases in which the interval between the onset of the neurological focality and death ranged from 8 to 16 hours. The antibiogram showed a wide sensibility to several groups of drugs, despite the fast evolution of the disease that prevented the modification of the initial antibiotherapy (Vancomicine and imipenem).

Acute Disease↗
PubMed1992

Right and left ventricular functional impairment and sleep apnea.

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.

Cheyne-Stokes Respiration↗
PubMed1991

[Oxygen saturation and sleep structure in patients with dilated cardiomyopathy].

It is known that patients suffering from severe cardiomyopathy may develop cyclic changes in breathing (Cheyne-Stokes-breathing) (2, 3). Coughing and dyspnea may be linked to periodic breathing. Specific detailed polysomnographic studies of sleep architecture and oxygen saturation have not been published. Eight patients suffering from dilatative cardiomyopathy (NYHA III-IV) were studied by pulse oximetry and polysomnography. Six of eight patients had severe breathing irregularities. These disturbances became manifest partially as Cheyne-Stokes breathing, partially as central sleep apnea. During these periods, oxygen saturation dropped as far as to 65 per cent of the original level.

Adult↗
PubMed1977

Hypersomnia and periodic breathing. Report of a case and review of the literature.

A patient with hypersomnia and periodic breathing has been studied. Both airflow obstruction and an abnormally of the respiratory control mechanism were implicated in the pathogenesis of the ventilatory arrhythmia. It is suggested that the older terms "Pickwick" syndrome and primary alveolar hypoventilation are abandoned for more descriptive terms, e.g. "hypersomnia with periodic breathing".

Adult↗
PubMed1978

The definition of "Cheyne-Stokes rhythms".

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.

Animals↗
PubMed1978

Variability of the respiratory phase, respiratory pause, and numbers and durations of respirations during periodic breathing.

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.

Brain Diseases↗
PubMed1979

Experimentally induced Cheyne-Stokes breathing.

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.

Animals↗
PubMed1990

Stability analysis of CO2 control of ventilation.

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).

Carbon Dioxide↗
PubMed1978

Respiratory oscillations of the arterial PO2 and their effects on the ventilatory controlling system in the cat.

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.

Animals↗