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Showing papers on "Hypoventilation published in 1985"


Journal ArticleDOI
TL;DR: Patients with idiopathic Parkinson's disease showed significantly reduced REM sleep, and more frequent and prolonged waking throughout the night, and respiration was disorganised with frequent central and obstructive apnoeas in the autonomic disturbance group.
Abstract: Sleep and respiration during sleep were studied in patients with idiopathic Parkinson's disease, patients with Parkinsonism with autonomic disturbance, and normal age and sex matched controls. Patients with idiopathic Parkinson's disease showed significantly reduced REM sleep, and more frequent and prolonged waking throughout the night. Hypoventilation and sleep apnoea did not occur in the idiopathic Parkinson's disease or normal groups, but respiration was disorganised with frequent central and obstructive apnoeas in the autonomic disturbance group. Respiratory rate during non rapid eye movement sleep was similar in the idiopathic Parkinson's disease and normal groups, but patients with idiopathic Parkinson's disease showed tachypnoea awake and during REM sleep.

129 citations


Journal ArticleDOI
TL;DR: It is suggested that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation duringREM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.
Abstract: In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.

92 citations


Journal ArticleDOI
TL;DR: The involvement of brain stem respiratory centers in subjects with chronic hypoventilation may suggest a failure of neural respiratory control that further compromises respiratory function.
Abstract: Chronic hypoventilation is important in the pathogenesis of congenital hypoventilation syndromes and sudden infant death syndrome. Cases of hypoventilation can be divided clinically into those with a defective respiratory drive and those with mechanical impairment of either the lungs or the chest wall. To determine the relationship between chronic hypoventilation and brain stem gliosis, the development of astrocytes in the brain stem of normal and abnormal cases with either type of chronic hypoventilation was studied morphometrically. The glial fibrillary acidic protein immunoperoxidase method of staining astrocytes showed a transient increase of astrocytes in some parts of the brain stem during early infancy in thirty-five normal cases. The astrocytosis was even greater in both types of chronic hypoventilation including subjects with myopathy, Ondine's curse, and sudden infant death syndrome. Gliosis in these subjects may have resulted from "asphyxia" of the brain stem, as seen in cases with myopathies involving respiratory muscles. However, the involvement of brain stem respiratory centers may suggest a failure of neural respiratory control that further compromises respiratory function.

65 citations


Journal ArticleDOI
TL;DR: Important apnea syndromes include apnea of prematurity, "narrow upper airway syndrome," congenital hypoventilation syndrome, breath-holding spells, and "near-miss" sudden infant death syndrome.

54 citations


Journal ArticleDOI
TL;DR: It is suggested that their finding of sleep-onset rapid-eye movement periods (SOREMPs) in the nocturnal sleep in five of nine patients with Prader-Willi syndrome (PWS) was due to hypothalamic dysfunction, and a shortened REM sleep latency could result from chronic REM sleep deprivation due to REM sleep-related hypoventilation.
Abstract: To the Editor. —Dr Vela-Bueno and colleagues 1 suggest that their finding of sleep-onset rapid-eye movement periods (SOREMPs) in the nocturnal sleep in five of nine patients with Prader-Willi syndrome (PWS) was due to hypothalamic dysfunction. They failed to mention that a shortened REM sleep latency could result from chronic REM sleep deprivation due to REM sleep-related hypoventilation. If episodes of hypoventilation are more frequent or more severe in REM sleep, then the associated arousals will interrupt and reduce the amount of REM sleep. An SOREMP is one typical effect of REM sleep deprivation. We have previously reported a case in which hypoventilation did not result in apneic events but did produce severe oxygen desaturation associated with the hypoventilation during REM sleep. 2 This patient had SOREMPs (REM latencies of one and 11 minutes) on each of two nocturnal sleep recordings. Dr Vela-Bueno and associates' finding of severe hypoventilation and hypoxic

51 citations


Journal ArticleDOI
TL;DR: Routine ENT evaluation should be a regular part of the workup of infants under one year who suffer from failure to thrive, and Adenoidectomy and tonsillectomy at 9 1/2 months of age completely reversed the patient's hypoventilation and growth pattern.

41 citations


Journal ArticleDOI
TL;DR: Obesity should be viewed as a medical problem deserving medical attention and long-term medical follow-up and weight reduction and weight maintenance, while difficult, are essential in patients with obesity, obesity and obstructive sleep apnea, and the hypoventilation syndrome.

40 citations


Journal ArticleDOI
TL;DR: The data suggest that both delta- and mu-agonists induce alveolar hypoventilation despite a decrease in VO2, and that endorphins do not modulate ventilation and metabolic rate tonically, but it is speculated that they may do so in response to stressful stimulation.
Abstract: To study the effect of endorphins on metabolic rate and on the relationship between O2 consumption (VO2) and ventilation, we administered enkephalin analogues (relatively selective delta-receptor agonists) and a morphiceptin analogue (a highly selective mu-receptor agonist) intracisternally in nine unanesthetized chronically instrumented adult dogs. Both delta- and mu-agonists decreased VO2 by 40-60%. delta-Agonists induced a dose-dependent decrease in mean instantaneous minute ventilation (VT/TT) associated with periodic breathing. The decrease in VT/TT started and resolved prior to the decrease and returned to baseline of VO2, respectively. In contrast, the mu-agonists induced an increase in VT/TT associated with rapid shallow breathing. Arterial PCO2 increased and arterial PO2 decreased after both delta- and mu-agonists. Low doses of intracisternal naloxone (0.002-2.0 micrograms/kg) reversed the opioid effect on VT/TT but not on VO2; higher doses of naloxone (5-25 micrograms/kg) reversed both. Naloxone administered alone had no effect on VT/TT or VO2. These data suggest that 1) both delta- and mu-agonists induce alveolar hypoventilation despite a decrease in VO2, 2) this hypoventilation results from a decrease in VT/TT after delta-agonists but an increase in dead space ventilation after mu-agonists, and 3) endorphins do not modulate ventilation and metabolic rate tonically, but we speculate that they may do so in response to stressful stimulation.

21 citations


Journal ArticleDOI
TL;DR: The data imply that an overactivity of central adenosine mechanisms may have a pathophysiological significance for the irregular breathing or apnea of prematurity sometimes seen in the human neonate.
Abstract: The respiratory performance was studied after intraperitoneal administration of the adenosine agonists N6-phenyl-isopropyl-adenosine (PIA) and adenosine-5-ethylcarboxamide to preterm (gestational age 29-30 days) newborn halothane-anesthetized rabbits. Both agonists induced marked hypoventilation and irregular breathing by decreases in the breathing frequency as well as the tidal volume. Expiratory time was markedly prolonged, resulting in a decrease in the respiratory duty cycle (inspiratory time/total cycle duration). Analysis using the occluded-breath technique revealed that the adenosine analogues altered the time setting of the expiratory (inspiratory) neuronal circuits and lowered the inspiratory off-switch level, while inspiratory drive and the bulbopontine setting of the inspiratory phase were unaltered. The ventilatory response to CO2 was blunted after both adenosine analogues studied. Theophylline almost completely reversed the hypoventilation and irregular breathing seen after PIA injection. It is concluded that activation of central nervous adenosine receptors induced a marked respiratory depression in the preterm rabbit. Furthermore, our data imply that an overactivity of central adenosine mechanisms may have a pathophysiological significance for the irregular breathing or apnea of prematurity sometimes seen in the human neonate.

21 citations



Journal ArticleDOI
TL;DR: Finally, sleep, and REM sleep in particular, significantly aggravates hypoventilation in patients with chronic obstructive pulmonary disease (COPD), kyphoscoliosis or chest musculoskeletal disorders.
Abstract: Neurologists are becoming increasingly aware of the frequency and clinical importance of sleep-related respiratory impairment. Sleep-induced narrowing of the upper airways underlies the widespread and supposedly trivial complaint of snoring, which may not only constitute a risk factor for the cardiocirculatory system, but in predisposed individuals, may lead to a sleep apnea syndrome, with its array of serious disturbances, including hypersomnia, systemic and pulmonary hypertension and ultimately heart failure. Idiopathic chronic alveolar hypoventilation, or Ondine's curse, is a fairly stereotyped clinical syndrome: sleep-related respiratory insufficiency in the absence of airways stenosis. Finally, sleep, and REM sleep in particular, significantly aggravates hypoventilation in patients with chronic obstructive pulmonary disease (COPD), kyphoscoliosis or chest musculoskeletal disorders.

Journal ArticleDOI
TL;DR: The data indicate that the ventilatory pattern can be decisive for the vasoconstrictor response during experimental stress and suggest that remote neurogenic mechanisms account for the increased responsiveness during hyperventilation and the decreased responsiveness during hypoventilation.
Abstract: The combined effects of defined changes in ventilation and stress-induced vasoconstriction were studied in the intestinal vascular bed in cats (n = 20) anaesthetized with fentanyl, nitrous oxide and diazepam. Intestinal reflex vasoconstriction was induced by stimulation either of the hypothalamic defence-alarm area or of somatic and visceral pain afferents. The volume-controlled ventilation was changed by altering the tidal volume, and stimulations were performed during either control conditions (Paco2 4.5-5.0 kPa), hyperventilation (Paco2 3.0-3.5 kPa) or hypoventilation (Paco2 6.5-7.5 kPa). The increase in intestinal vascular resistance (IVR) elicited by defence-alarm area stimulation was potentiated during hyperventilation (306 +/- 83% vs 198 +/- 62%; P less than 0.01) and attenuated during hypoventilation (176 +/- 62% vs 240 +/- 44%; P less than 0.05). The increase in IVR elicited by pain fibre stimulation was potentiated during hyperventilation (73 +/- 21% vs 54 +/- 19%; P less than 0.01), but not significantly changed during hypoventilation (47 +/- 19% vs 68 +/- 34% during control ventilation). Our data indicate that the ventilatory pattern can be decisive for the vasoconstrictor response during experimental stress. We suggest that remote neurogenic mechanisms account for the increased responsiveness during hyperventilation. The decreased responsiveness during hypoventilation, on the other hand, seems to correlate with the local vasodilator effects of carbon dioxide.

Journal ArticleDOI
TL;DR: It is suggested that the compensatory cardiovascular reflexes may be impaired during hypoventilation, and the blood pressure and pulse rate in response to adrenaline and acetylcholine were significantly reduced.
Abstract: Blood pressure and pulse rate in reponse to administered adrenaline and acetylcholine during hypoventilation were studied in urethane-anaesthetized rats. Hypoventilation was induced by decreasing the

Journal ArticleDOI
TL;DR: The findings indicate that the increase of left to right shunt flow in respiratory acidosis might be one of the risk factors of congestive heart failure for the patients with ventricular septal defect.
Abstract: The effects of respiratory acidosis on ventricular shunt flow and hemodynamics were studied in 20 anesthetized dogs with a ventricular septal defect and a normal pulmonary vascular bed. The interventricular shunt flow was measured directly by using a specially designed electromagnetic flow probe. Respiratory acidosis was produced by hypoventilation and tachypnea with constant minute volume. Hypoxemia was also induced by hypoventilation, but not by tachypnea with constant minute volume. Systemic vascular resistance was increased in severe hypoventilation at 100 and 50 ml of tidal volume, and tachypnea at 100 ml of tidal volume. However the increase of pulmonary vascular resistance was observed in only severe hypoventilation: arterial pH 6.9, PaO2 24 mmHg, and PaCO2 88 mmHg. Left to right ventricular shunt flow and pulmonary blood flow were increased significantly with no change of systemic blood flow in both conditions of respiratory acidosis. The diastolic fraction of shunt flow was increased significantly. These findings indicate that the increase of left to right shunt flow in respiratory acidosis might be one of the risk factors of congestive heart failure for the patients with ventricular septal defect.


Journal ArticleDOI
01 Oct 1985
TL;DR: In this article, the authors proposed the use of CPAP + IM V for patients with acute respiratory failure to produce the best outcome with the least complications and distress to the patient.
Abstract: It should be the aim of clinicians caring for patients with acute respiratory failure to produce the best outcome with the least complications and distress to the patient. Most patients with acute respiratory failure can contribute significantly to their own respiratory homeostasis with carefully applied airway pressure therapy, with the likelihood of reduced barotrauma and improved cardiovascular function. At present, the technique of CPAP + IM V is the method most suited to the above goals and allows independent treatment of the two forms of respiratory failure - hypoxaemia and hypoventilation. It offers flexibility in management of a wide range of conditions. Severe ARDS can be managed using high levels of CPAP, often with little or no mechanical ventilation, and invasive haemodynamic monitoring is frequently unnecessary. CPAP delivered by nasal prongs in adults is a useful new technique.

Book ChapterDOI
01 Jan 1985
TL;DR: From inspection of breathing patterns recorded for 12 hours at monthly intervals on 100 infants, it was determined that the longest episode of normal apnea, almost invariably following a sigh, was 14 sec. or greater.
Abstract: From inspection of breathing patterns recorded for 12 hours at monthly intervals on 100 infants, we determined that the longest episode of normal apnea, almost invariably following a sigh, was 14 sec. Therefore, we define abnormal apnea as an episode of 15 sec. or greater.

Journal ArticleDOI
TL;DR: There was no evidence that a SOREMP, which was present in five of the patients, resulted from chronic REM sleep deprivation due to REMrelated hypoventilation, and in the one patient whose oxygen saturation was monitored, the desaturation observed continued during REM sleep for ten to 15 minutes without an arousal.
Abstract: In Reply. —The patient described by Thorpy et al 1 is clearly different from any of the patients with Prader-Willi syndrome in our study. Their patient with adult-onset muscular atrophy was unable to sustain the supine position "for more than a few minutes because of dyspnea." For this patient "the maximum duration of sleep without an arousal was two minutes," resulting in a sleep efficiency of only 44%. In contrast, we did not observe any relationship between any type of breathing difficulty and arousal. 2 In fact, in the one patient whose oxygen saturation was monitored, the desaturation observed continued during REM sleep for ten to 15 minutes without an arousal. During this time the oxygen saturation levels were maintained below 50%. Also, there was no evidence that a SOREMP, which was present in five of our patients, resulted from chronic REM sleep deprivation due to REMrelated hypoventilation. The overall disturbance of