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Showing papers on "Hypoventilation published in 1992"


Journal ArticleDOI
TL;DR: Data support a diffuse central nervous system process, the specific cause and the mode of inheritance remain unclear, and with early diagnosis and careful ventilatory management, the sequelae of hypoxia and morbidity should be minimized and long-term outcome improved.

188 citations


Journal ArticleDOI
TL;DR: Respiratory instability during sleep onset was found to be a result of two factors, a between-state effect in which transitions from alpha to theta were associated with falls, and from theta to alpha with increases, in ventilation and a within-stateeffect in which ventilation fell during consecutive alpha breaths and increased during consecutive theta breaths.
Abstract: It has been hypothesized that regulatory control in the respiratory system is state dependent. According to this view respiratory instability during sleep onset is a consequence of repeated fluctuations in arousal state. However, these speculations are based primarily on measurements during stable sleep, not during sleep onset itself. The aim of the present study was to assess changes in ventilation and gas tensions during sleep onset as a function of arousal state. Twenty-one subjects (12 males and 9 females, mean age 20 yr) were assessed over an average of 11.3 sleep onsets. The subject's state was classified as alpha, theta, body movement, or stage 2 sleep, and expiratory tidal volume, minute ventilation, respiratory rate, and end-tidal CO2 and O2 were measured by means of a face mask, valve, and pneumotachograph on a breath-by-breath basis. Respiratory instability during sleep onset was found to be a result of two factors. The first factor was a between-state effect in which transitions from alpha to theta were associated with falls, and from theta to alpha with increases, in ventilation. The magnitude of the change was a positive function of metabolic drive at the time of the state change (as indicated by alveolar PCO2 and PO2 levels). The second was a within-state effect in which ventilation fell during consecutive alpha breaths and increased during consecutive theta breaths. These changes were due to the influence of the relative hyperventilation of the alpha state and the relative hypoventilation of the theta state on metabolic drive.

154 citations


Journal ArticleDOI
01 Sep 1992-Chest
TL;DR: It is believed nIPPV offers an effective therapeutic approach for patients with end-stage CF in hypercapnic respiratory failure and may be particularly advantageous for those awaiting heart-lung transplant.

136 citations


Journal ArticleDOI
TL;DR: A measure of pulmonary hyperinflation was used to assess the degree of airflow obstruction and to guide the extent and duration of hypoventilation in patients with severe asthma.
Abstract: Mechanical ventilation causes significant morbidity and mortality in patients with severe asthma. Hypoventilation may reduce this morbidity and mortality, but indicators to guide the degree of hypoventilation are unclear. We used a measure of pulmonary hyperinflation to assess the degree of airflow obstruction and to guide the extent and duration of hypoventilation. Ten patients who required mechanical ventilation for acute severe asthma were studied. All were sedated, paralyzed, and given an initial minute ventilation (e) of 200 ml/kg/min. End-inspiratory lung volume (Vei) above FRC was measured from the total exhaled gas volume during 40 to 60 s of apnea. Vei was used to regulate e to a safe level (esafe), irrespective of PaCO2, by reducing the rate when Vei was > 20 ml/kg and increasing it when Vei was < 20 ml/kg. Each patient was weaned when esafe resulted in PaCO2 ⩽ 40 mm Hg (the weaning point). FRC was measured by computer analysis of anterior and lateral chest radiographs taken at the end of apnea....

116 citations


Journal ArticleDOI
TL;DR: Treatment of idiopathic CSA is a relatively benign condition in which cardiorespiratory failure is not a feature, but the use of nocturnal nasal CPAP appears to be quite effective.

114 citations


Journal ArticleDOI
TL;DR: Patients with neuromuscular and chest wall disorders are vulnerable at night when alterations in ventilatory mechanics and control associated with their disease are imposed on the changes in mechanics and Control associated with sleep.

27 citations


Journal ArticleDOI
01 Jun 1992-Chest
TL;DR: It is concluded that children receiving volume controlled mechanical ventilation via uncuffed tracheostomy tubes can exhibit hypoventilation due to uncompensated air leak.

24 citations



Journal ArticleDOI
TL;DR: It is concluded that stimulation of respiration by CO2 or by acetazolamide appears to recruit chest wall muscles and promote upper airway patency in Arnold‐Chiari malformation and a treatment trial with acetazlamide seems justifiable in these infants when respiratory problems are present.
Abstract: We studied respiratory patterns and transcutaneous gas pressures in two infants with Arnold-Chiari type II malformation referred to us due to repeated episodes of stridor and cyanosis. During both active and quiet sleep, respiration was irregular and absent or inverse thoracic breathing movements and frequent decreases in oxygen saturation to below 80% were observed. When breathing air with 2% CO2 or when given acetazolamide 10 mg/kg, chest wall movements normalized and oxygenation increased to near normal levels. After three months of treatment with acetazolamide 20 mg/kg/24 h no further episodes of hypoventilation or hypoxemia were observed and further treatment could be discontinued. We conclude that stimulation of respiration by CO2 or by acetazolamide appears to recruit chest wall muscles and promote upper airway patency in Arnold-Chiari malformation. A treatment trial with acetazolamide seems justifiable in these infants when respiratory problems are present.

19 citations


Journal ArticleDOI
01 Jul 1992-Chest
TL;DR: In younger patients without complicating disease, long-term survival was achieved with LTO, but with time, an increasing proportion of the patients changed to AVH, with or without LTO.

14 citations


Journal Article
TL;DR: It is concluded that manifest hypoventilation is rare in this unselected material of post-polio patients and that a vital capacity below 45-50% of predicted normal and the presence of frequent headaches indicate an increased risk to develop hypovENTilation.
Abstract: Post-polio patients sometimes complain about the occurrence of breathing difficulties decades after the polio infection. We have examined 40 post-polio patients who have had respiratory or non-respiratory poliomyelitis for at least 30 years in an attempt to elucidate whether hypoventilation is common and to what extent certain symptoms and simple lung function tests are related to hypoventilation or incipient hypoventilation. We measured arterial blood gases, vital capacity (VC), maximal expiratory and inspiratory pressures (MEP, MIP) and CO2 rebreathing response. Symptoms were assessed by a yes/no questionnaire. Six patients required respiratory assistance at the onset of the disease. At present, two require nocturnal assisted ventilation. Two patients showed manifest hypoventilation; one of which required night-time ventilator, whereas the other patient had not required ventilatory assistance even at the onset of the disease. Significant correlation (p less than 0.05) was found between arterial carbon dioxide tension (a-PCO2) and VC, MEP and ventilation increase during CO2 rebreathing. A significantly higher a-PCO2 was found among those who required respiratory assistance at the onset of the disease, who admitted headache and who felt the cough ineffective. Low VC and low ventilatory increase during CO2 rebreathing and the presence of headache explained 45% of the variation in a-PCO2 in a multiple regression analysis. We conclude that manifest hypoventilation is rare in this unselected material of post-polio patients and that a vital capacity below 45-50% of predicted normal and the presence of frequent headaches indicate an increased risk to develop hypoventilation.

Journal Article
TL;DR: Results of observations made during sequential immobilizations suggest that young giraffes tend to hypo ven tilate during anesthesia, resulting in significant respiratory acidosis, and Pulse oximetry and end tidal C02 measurements are recommended as adjunct monitoring techniques for routine chemical restraint in the giraffe.
Abstract: A 1-mo-old reticulated giraffe (Giraffa camelopardalis) received repeated immobili zations for treatment of a fractured left metatarsus. Etorphine and xylazine or etorphine and iso flurane adjunct anesthesia were used for immobilization. During immobilizations, pulse oximetry and end tidal C02 measurements were made and correlated with arterial blood gas values. Results of observations made during sequential immobilizations suggest that young giraffes tend to hypo ven tilate during anesthesia, resulting in significant respiratory acidosis. By monitoring pulse oximetry and end tidal C02, periods of hypo ventilation and subsequent respiratory acidosis in this case were detected and overcome. Pulse oximetry and end tidal C02 measurements are recommended as adjunct monitoring techniques for routine chemical restraint in the giraffe. In addition, reversing or avoiding hypoventilation and respiratory acidosis in young giraffes can be best accomplished through routine trach?al intubation and assisted ventilation.

Journal ArticleDOI
TL;DR: Quality of life can be significantly improved and life itself can be prolonged for some ventilator users by maintaining effective communication and good nutrition and using noninvasive expiratory muscle aids to eliminate aspirated food and airway secretions.
Abstract: Many individuals with progressive neuromuscular conditions, including post-poliomyelitis, develop severe bulbar dysfunction, which adversely affects quality of life and can indirectly exacerbate cardiopulmonary insufficiency. The incidence of dysarthria and dysphagia appears to increase as patients advance to the point of requiring ventilatory assistance. In a study of post-poliomyelitis ventilator users, the incidence of dysphagia was found to be 50 percent by contrast to approximately 21 percent in non-ventilator users. The incidence of dysarthria and dysphagia is even higher for patients with some advanced neuromuscular conditions. Various therapeutic interventions, including prevention of the fatigue and hypoventilation associated with inspiratory muscle insufficiency, can improve communication, swallowing, and nutrition. The use of noninvasive expiratory muscle aids can eliminate aspirated food and airway secretions. Quality of life can be significantly improved and life itself can be prolonged for s...

Journal Article
TL;DR: It is suggested that central apnea occurs not infrequently in the cases of Wallenberg's syndrome.
Abstract: We reported here a 64-year-old man with a central apnea resulted from unilateral medullary infarction. He was admitted because of cerebellar ataxia, dysarthria and dysphasia of abrupt onset. After the injection of diazepam for alcohol forbidden syndrome, he induced complete apnea and required the endotracheal intubation. At the spontaneous respiration under room air, his arterial blood gas showed hypercapnea without hypoxemia, and he fell into severe hypoventilation when hypnotic drug was injected. Respisomnogram revealed the frequent presence of central apnea both while he was awake and asleep. MRI demonstrated an abnormal high intensity area on T2 weighted image at the right lateral medulla just below the ponto-medullary junction. At autopsy, areas of the infarction were limited within the right lateral medulla, including lateral portion of the medullary reticular formation, the ambigual nucleus, one part of the solitary nuclear complex, the inferior cerebellar peduncle and the spinal trigeminal nucleus. However, the dorsomotor nucleus of vagus was completely free from the infarct lesion. There was no other lesion within central nervous system. Such a distribution seemed the minimal extent of the lesion responsible for central, apnea compared to the previous reports. We suggest that central apnea occurs not infrequently in the cases of Wallenberg's syndrome.

Journal ArticleDOI
TL;DR: Opioids produce unpredictable anesthesia that is associated with poor muscle relaxation, prolonged onset, and relatively difficult intubation, making postoperative assessment of the patient's condition difficult.
Abstract: Opioids produce unpredictable anesthesia that is associated with poor muscle relaxation, prolonged onset, and relatively difficult intubation. They often induce bradycardia, which must be countered with atropine or glycopyrrolate, and hypoventilation, which requires ventilatory support. Return to consciousness is often delayed, making postoperative assessment of the patient's condition difficult. Finally opioid induction is relatively expensive compared with other anesthetic induction regimens.

Journal Article
TL;DR: The results indicate that both the central and peripheral mechanisms contribute to hypoventilation in anaesthetized rats with denervated diaphragm.
Abstract: The aim of this study was to explore the mechanism resulting in hypoventilation in rats with denervated diaphragm. Bilateral cervical phrenicotomy (PX) was performed in 15 male rats anaesthetized with urethane (1.3 g/kg i.p.); other 8 rats were sham operated (SX). Ventilation, PaCO2 and the integrated EMG of the external intercostal muscles (iEMG) were measured before and after the surgery, at regular intervals, up to 4 hours postoperatively. During the 4 hours after PX there was a progressive decrease in minute ventilation and an increase in PaCO2 compared with the control values and with that in the SX rats. The increase in PaCO2 was accompanied by an increase in the peak amplitude of the iEMG to 155 +/- 18% of control values after PX and to 228 +/- 33% 4 hours later. Despite the augmented EMG activity tidal volume gradually decreased. The iEMG of the intercostal muscles, however, did not reach a maximum because the shortlasting stimulation of breathing by acute hypercapnia and hypoxia as the result of added dead space (0.5 ml) increased the iEMG still further. These results indicate that both the central and peripheral mechanisms contribute to hypoventilation in anaesthetized rats with denervated diaphragm.

Journal ArticleDOI
TL;DR: Anesthetic management of patients with head injury must include intravenous induction with barbiturates or narcotics, smooth endotracheal intubation, controlled ventilation with oxygen, and minimal amounts of inhalational agents.
Abstract: Patients undergoing anesthesia soon after head trauma are at great risk for further neural damage during the anesthetic, especially if the head injury is severe or the anesthetic technique is suboptimal. Secondary complications of the anesthetic that are often lethal include hypoventilation, increases in ICP, airway obstruction, and brain-stem herniation. Anesthetic management of patients with head injury must include intravenous induction with barbiturates or narcotics, smooth endotracheal intubation, controlled ventilation with oxygen, and minimal amounts of inhalational agents. It is important to position the patient so that jugular veins are not occluded, in about 10 degrees head up position, and to avoid inducing patient coughing and straining. Recovery from anesthesia should be quiet and rapid, with the maintenance of a clear airway and the use of as little depressant medication post-operatively as possible. Oxygen should be provided.

Journal Article
TL;DR: The results suggest that during high spinal anesthesia severe hypotension causes hypoventilation and if not treated respiratory arrest ensues, and hyperventilation tended to occur in patients with high spinalesthesia unless hypotension was severe enough.
Abstract: The ventilatory changes during the course of high spinal anesthesia and the effect of hypotension on ventilation during high spinal anesthesia were studied. Spinal anesthesia with hyperbaric tetracaine was applied to 30 patients scheduled for elective surgery. Patients breathed by mask for ten minutes at rest before and after receiving spinal anesthesia. Respiratory parameters were measured in supine position during (1) pre-anesthetic period under resting condition, (2) anesthetic period when analgesia with pin prick extended to T4 level and (3) anesthetic period when analgesia extended to T1 level. The patients were divided into two groups; those with and without hypotension. In hypotension group, tidal volume and minute ventilation decreased significantly for 30% compared with the control values after spinal anesthesia. PaO2 decreased and PaCO2 increased. In non-hypotension group, tidal volume and minute ventilation after spinal anesthesia increased for 10% compared with the control values. In conclusion, hyperventilation tended to occur in patients with high spinal anesthesia unless hypotension was severe enough. Once severe hypotension had occurred, obvious hypoventilation and respiratory irregularity were observed. Decrease of tidal volume and minute ventilation, hypoxia, hypercarbia and increase in VD/VT were significant during hypotension. The results suggest that during high spinal anesthesia severe hypotension causes hypoventilation and if not treated respiratory arrest ensues.

Journal ArticleDOI
TL;DR: It appears that vertical banded gastroplasty is efficacious in the treatment of morbid obesity with sleep apnea and hypoventilation.
Abstract: We report a case of morbid obesity accompanied by obstructive sleep apnea syndrome (SAS) and obesity hypoventilation syndrome (OHS). Satisfactory weight control was obtained without significant surgical complications after vertical banded gastroplasty. With the reduction in weight, the symptoms of SAS and OHS, as well as several other complications caused by the severe obesity, disappeared. Quality of life also improved remarkably, as exhibited by improved activity performance and disappearance of irritability at waking. Thus, it appears that vertical banded gastroplasty is efficacious in the treatment of morbid obesity with sleep apnea and hypoventilation.

Journal ArticleDOI
TL;DR: It is speculated that halothane anesthesia and/ or loss of consciousness impair transmission of afferent information from the lung and/or chest wall musculature and may be responsible for the depression of load compensatory mechanism during anesthesia.
Abstract: Mechanical influences independent of chemoreceptor function on ventilatory control were studied in halothane-anesthetized, artificially ventilated patients using the technique reported by Altose et al. (Respir Physiol 66: 171–180, 1986). Contribution of mechanical factor was indirectly assessed by comparing the values of arterial carbon dioxide tension at which the subjects started breathing efforts during CO2 loading induced by the following two methods. 1) Partial rebreathing of expired gas and 2) Mechanical hypoventilation (successive decrease in inflation volume). These two maneuvers resulted in a similar rate of increase in end-expiratory carbon dioxide tension. However, contrary to the observation made by Altose et al. in awake volunteers, we found comparable values of ventilatory recruitment threshold for PaCO 2. Thus, we speculate that halothane anesthesia and/or loss of consciousness impair transmission of afferent information from the lung and/or chest wall musculature. Such effects may be responsible for the depression of load compensatory mechanism during anesthesia.

Journal Article
TL;DR: O2 inhalation in patients receiving home oxygen therapy was effective in terms of the endurance time and ventilatory pattern analyzed by the Konno-Mead (K-M) diagram during exercise.
Abstract: The purpose of respiratory muscle training for patients with chronic respiratory failure is to improve exercise performance during daily life. Firstly, to confirm the clinical effect on respiratory muscle training, the abdominal pad method for inspiratory muscle training and abdominal pad method with expiratory resistor for both inspiratory and expiratory muscle training were simultaneously performed. Both methods were clinically useful to increase respiratory muscle power and to subjectively decrease dyspnea. Ventilatory pattern analyzed by the Konno-Mead (K-M) diagram during exercise also showed their effectiveness. Secondly, the influence of hypoxemia and hypophosphatemia, which are important factors producing respiratory muscle fatigue, was investigated in a patient with respiratory failure. (1) O2 inhalation in patients receiving home oxygen therapy was effective in terms of the endurance time and ventilatory pattern analyzed by the K-M diagram during exercise. (2) A case of hypercapnea due to hypoventilation caused by respiratory muscle fatigue developed reduced PaCO2 following correction of serum phosphate level, suggesting that hypophosphatemia is an important clinical factor producing respiratory muscle fatigue.

Book ChapterDOI
01 Jan 1992
TL;DR: This discussion includes a review of physiology and pharmacology of the normal and abnormal regulation of breathing as it relates to both anesthesia and high altitude and offers new insight into the mechanism of CO2 and pH detection as a transmembrane pH gradient change.
Abstract: This discussion includes a review of physiology and pharmacology of the normal and abnormal regulation of breathing as it relates to both anesthesia (1) and high altitude (2,3), and discusses several recent relevant advances in understanding. During days to weeks of hypoxia the ventilation is gradually stimulated not only by a fall of CSF Hco- 3 but also by a rise in hypoxic drive, probably due to a greater carotid body sensitivity. The central CO2 chemoreceptor neurons have been histologically identified in rats by c-fos staining after hypercapnia. They apparently generate acid in hypoxia which may be detected on the local surface in ECF. This presumed intracellular lactic acidosis may underlie hypoxic ventilatory depression, which occurs after 5–20 minutes of hypoxia. This complicates understanding of altitude acclimatization while offering new insight into the mechanism of CO2 and pH detection as a transmembrane pH gradient change. The effects of anesthesia on hypoxic response is in part due to the raising of PCO2 threshold by both the anesthetic and hypoxia and the flattening of CO2 response which hypoxia multiplies. After anesthesia, respiration may be compromised by interactions between the effects of residual depressant drugs, lack of lung-pump strength and airway patency, and hypoventilation at normal PCO2 due to repaying a deficit of body CO2 stores.

Book ChapterDOI
01 Jan 1992
TL;DR: In order to investigate the influence of altitude acclimatization on chemoresponsiveness, consecutively examined hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses in 7 lowlanders during sojourn in Lhasa (3700m), China.
Abstract: Increased ventilation is important for persons going to high altitude and this is attributable to hypoxic stimulation of the peripheral chemoreceptors. However, the hypocapnia induced by hyperventilation and central hypoxic ventilatory depression substantailly attenuate the initial ventilatory response to hypoxia. Huang et al. (5) demonstrated that the combination of hypocapnia and sustained hypoxia might have blunted the ventilatory response on the first day after arrival on Pikes Peak (4300 m). Acute mountain sickness (AMS) occurs as acommon feature of ascent to high altitude usually within a few hours of ascent and lasting a few days. It has been recognized that ventilation is depressed in persons with symptoms of AMS (4). The reason for the hypoventilation in symptomatic persons is unknown. Moore et al. (8) suggest that hypoventilation in symptomatic compared to asymptomatic subjects is responsible for attenuated ventilatory response to acute hypoxia. In order to investigate the influence of altitude acclimatization on chemoresponsiveness, we consecutively examined hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses in 7 lowlanders during sojourn in Lhasa (3700m), China.

Book ChapterDOI
01 Jan 1992
TL;DR: The hyperventilatory response to continuous hypoxic exposure in adult animals typically comprises an initial sharp rise of ventilation, a following precipitous fall to a lower level of hyperventilation, and finally a gradual re-rising of ventilatory acclimatization.
Abstract: The hyperventilatory response to continuous hypoxic exposure in adult animals typically comprises an initial sharp rise of ventilation, a following precipitous fall to a lower level of hyperventilation (so-called “ventilatory depression”), and finally a gradual re-rising of ventilatory acclimatization. In contrast, the hypoxic ventilatory response in newborn animals and infants1, 2, 3 is predominantly hypoventilation instead of hyperventilation although an initial brief sharp rise of ventilation does appear as a rule.