PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cheyne-Stokes Respiration”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1992

Evidence that circulatory oscillations accompany ventilatory oscillations during exercise in patients with heart failure.

Periodic breathing (PB) during exercise in patients with congestive heart failure (CHF) is associated with prominent oscillations (OSC) of O2 uptake (VO2). We hypothesized that the VO2 OSC represent OSC in true O2 exchange, resulting from concomitant cardiac output fluctuations and are not merely due to OSC of lung O2 stores. We compared the amplitude of the OSC of VO2, ventilation (VE), and end-expiratory lung volume (EELV) in 17 patients with CHF and PB and in seven healthy control subjects who volitionally simulated PB. Subjects underwent an incremental and/or a constant work-rate exercise test. VE and VO2 were measured breath by breath. EELV change was estimated by summing the difference between inspiratory and expiratory tidal volumes for each breath. The amplitude of the OSC, delta, is expressed as the ratio of the difference between the peak and nadir of the oscillating variable divided by its mean [delta = (peak - nadir)/mean]. In CHF, during incremental testing, the amplitude of the VE OSC was smaller than that of the VO2 OSC (delta VE = 49 +/- 15% [SD], delta VO2 = 63 +/- 25%, p less than 0.01). In contrast, during volitional PB in the control subjects, VE OSC were larger than VO2 OSC (delta VE = 48 +/- 12%, delta VO2 = 25 +/- 11%, p less than 0.01). This suggests that changing VE itself cannot account for the marked VO2 OSC seen in CHF. In the patients, EELV showed no systematic OSC, did not correlate with delta VO2, and was not significantly different from zero.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Periodic breathing imitating hyperventilation syndrome.

We report a male patient who developed an unusual periodic breathing. At presentation, the differential diagnosis at bedside between Cheyne-Stokes and primary hyperventilation syndrome was laborious, and the final verification was based on the result of capnography.

Cheyne-Stokes Respiration↗
PubMed1976

Changes in local cerebral blood flow following profound systemic hypotension.

The authors studied local cerebral blood flow in monkeys rendered hypotensive by infusion of a ganglionic blocking agent. Application of the 14C-antipyrine method demonstrated that the blood flow: 1) normally varies reproducibly from one structure to another within the brain; 2) appears at its lowest level in all structures during the early minutes of a rapid-onset hypotension; 3) maintains the same general rank order of blood flow rate during hypotension as was present during normotension; and 4) returns to supranormal levels immediately following the rapid restoration of blood pressure. The values for local cerebral blood flow remain close-to-normal in some animals and diminish significantly in others during late recovery from hypotension. The close-to-normal values accompany uncomplicated recoveries while the diminished values appear in those animals which became neurologically depressed. Areas of the brain considered predisposed to hypotensive injury did not exhibit depressions in blood flow rate during hypotension more markedly than did other brain areas. The present results are interpreted as strong evidence against the "border zone" hypothesis.

Animals↗
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↗
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↗