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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study examined the possibility that mechanoreceptors in the chest wall structures (rib cage and diaphragm) contribute to the increase in the neuromuscular drive to breathe (occlusion pressure) when the load on the respiratory muscles is increased in conscious animals and humans. Studies were carried out in 4 awake dogs in which external resistive loads (12 cmH2O/L/s) were applied during inspiration to increase the load on the respiratory muscles. Loads were applied via a tracheostomy during complete vagal blockade performed by cooling exteriorized cervical vagal loops. The ventilatory and occlusion pressure responses to the load were compared over the same range of chemical drive by applying loads during CO2 rebreathing. During vagal blockade, inspiratory resistive loads had no consistent effect on the duration of inspiration or expiration and decreased the ventilatory response to hypercapnia by decreasing average inspiratory flow rate. In all animals, however, inspiratory loading increased the occlusion pressure (P100) response to hypercapnia. The P100 at PCO2 = 55 mmHg increased during flow loading in all 4 animals, and the slope of the change in P100 produced for a given change in PCO2 (delta P100/delta PCO2) increased in 3 of the 4. Flow loading had no effect on end-expiratory lung volume at rest and did not influence the decrease in lung volume observed during hypercapnia. The present study indicated that the neuromuscular drive to breathe, as assessed from the occlusion pressure, is increased in conscious animals subjected to ventilatory loads during vagal blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory responses to external resistive loads during vagal blockade in awake dogs. 672 Dec 79

Twelve patients exhibiting difficulties during discontinuation of artificial ventilation permitted us to investigate physical examination techniques used in diagnosing inspiratory muscle fatigue. Diaphragmatic and intercostal electromyographic tracings, arterial blood gases, rate and depth of ventilation, and thoracoabdominal motion were monitored during spontaneous breathing. Six patients showed electromyographic evidence of inspiratory muscle fatigue. A sequence of events leading to respiratory acidemia emerged--namely electromyographic evidence of fatigue, accompanied or followed by an increased respiratory rate, in turn followed by alternation between abdominal and rib cage breathing (respiratory alternans), paradoxical inward abdominal motion during inspiration (abdominal paradox), and finally an increase in PaCO2 associated with a fall in minute ventilation and respiratory rate, and worsening of respiratory acidemia. The abnormalities of respiratory movements may be reliable clinical signs of inspiratory muscle fatigue, particularly when accompanied by tachypnea and hypercapnia.
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PMID:Clinical manifestations of inspiratory muscle fatigue. 681 17

This report describes a patient with primary alveolar hypoventilation who, after 2 yr of successful treatment with nocturnal oxygen, developed severe hypoxemia and hypercapnia during sleep, morning headaches, and daytime fatigue. Sleep studies demonstrated prolonged periods of hypoventilation and apnea without evidence of upper airway occlusion. Therefore, a phrenic nerve stimulator was implanted to allow pacing of the diaphragm during sleep. However, diaphragm pacing was accompanied by paradoxical movement of the rib cage and upper airway occlusion during sleep, and was unsuccessful in maintaining adequate ventilation. Therefore, the patient underwent a tracheostomy after which diaphragm pacing maintained adequate nocturnal ventilation; however, paradoxical movement of the rib cage persisted. The induction of upper airway occlusion as a result of diaphragm pacing, in contrast to the absence of occlusion during spontaneous breathing, highlights the importance of the normal temporal coordination of inspiratory activation of the upper airway muscles and diaphragm. The findings have important implications for the pathogenesis of obstructive sleep apneas in general.
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PMID:Upper airway occlusion induced by diaphragm pacing for primary alveolar hypoventilation: implications for the pathogenesis of obstructive sleep apnea. 697 4

Studies were performed to examine the decrease in ventilatory response to hypoxia and hypercapnia in the elderly and to explore its etiology. For this purpose, matched groups of normal elderly (65 to 79 yr of age) and young subjects were used. Standard pulmonary function tests were supplemented in both groups by determination of total respiratory compliance and the ventilatory responses to hyperoxic hypercapnia and isocapnic hypoxia using rebreathing methods. While testing the ventilatory responses, we recorded minute ventilation and its components, as well as mouth occlusion pressures, and rib cage and abdominal-diaphragmatic compartmental ventilation (magnetometry). We found that ventilatory responses to both hypercapnia and hypoxia were reduced in the elderly by approximately 50%. These reductions were not related to any change in control of respiratory timing, but to a large reduction in mean inspiratory airflow. The reduced airflow could not be attributed to alterations in pulmonary mechanics since the differences in mechanics between the groups were small. Instead, since the occlusion pressure responses to hypercapnia and hypoxia were reduced in the elderly proportionately to the ventilatory responses, reduction in neuromuscular inspiratory output was likely to be the major factor.
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PMID:Effects of aging on ventilatory and occlusion pressure responses to hypoxia and hypercapnia. 729 1

Weaning patients from mechanical ventilation constitutes a major portion of the workload in an intensive care unit, as over 40% of total ventilator time is consumed by the weaning process. Several pathophysiological mechanisms may be responsible for weaning failure, but the precise role of each is incompletely understood. Patients who fail a weaning trial commonly develop hypercapnia, which appears to be due to decreased tidal volume rather than a primary decrease in respiratory drive. Respiratory muscle performance is impaired as a result of dynamic hyperinflation and paradoxic motion of the rib cage and abdomen. Worsening of pulmonary mechanics will cause further embarrassment of the respiratory muscles. However, the clinical importance of respiratory muscle fatigue remains unclear. Afferent stimuli arising in the lung parenchyma, respiratory muscles, or as a consequence of impaired gas exchange will be transmitted to the respiratory control centers and result in severe dyspnea in patients who fail a weaning trial.
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PMID:Pathophysiology of failure to wean from mechanical ventilation. 799 29

Pregnancy often poses a risk to patients with neuromuscular and skeletal disorders when these affect the respiratory muscles or the rib cage. The outlook is determined both by the severity of the underlying condition and the physiological changes during pregnancy. Patients with a vital capacity of less than 1 to 1.5 litres, hypercapnia, severe scoliosis, diaphragm weakness or pulmonary hypertension before pregnancy are particularly at risk. Pregnancy may adversely affect the conducting airways, respiratory pump and gas exchange in the lungs. Close monitoring of high risk patients during pregnancy is required and either a termination of pregnancy or mechanical respiratory support may be indicated if ventilatory or cardiac failure develops.
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PMID:Pregnancy in neuromuscular and skeletal disorders. 808 20

We compared maturation of the responses of the rib cage [triangularis sterni (TS)] and abdominal [transversus abdominis (TA)] expiratory muscles with each other and with the responses of the diaphragm (DIA) during hypercarbic and hypoxic stimulation. Studies were performed in anesthetized (urethan and chloralose) piglets of two age groups (< 6 days, n = 10; 14-21 days, n = 11) before and after bilateral cervical vagotomy. Hypercarbia (7% CO2-93% O2) was associated with comparable sustained increases in the minute electromyograms (EMGs) of both TS and TA, which were closely coupled to the DIA responses in both age groups. Hypoxia (12% O2-88% N2) caused a biphasic response of the minute EMG of both expiratory muscles and DIA; these biphasic responses were less prominent at 14-21 days than at < 6 days. Vagotomy caused an increase in the amplitude of both TS and TA (38 +/- 30 and 27 +/- 21%, respectively) as well as the DIA (45 +/- 16%) but did not affect their relative responses to chemostimulation. We conclude that during postnatal development 1) the rib cage and abdominal expiratory muscle responses to chemostimulation are coupled to each other and parallel those of the DIA and 2) the presence of vagal afferents attenuates the drive to both inspiratory and expiratory motoneurons under the current experimental conditions but does not influence the relative responses of expiratory muscles and DIA to hypercarbia or hypoxia. We speculate that comparable activation of inspiratory and expiratory pumping muscles serves to stabilize respiratory control in the face of altered chemosensory or vagal inputs during early postnatal life.
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PMID:Regulation of expiratory muscles during postnatal development in anesthetized piglets. 836 65

A 48-year-old man was referred to our hospital because of hypoxemia (PaO2 = 43 mmHg), hypercapnia (PaCO2 = 70 mmHg), complete atrio-ventricular block, and heart failure. He also had limitation of spine flexion, scoliosis, deformity of the rib cage, and constriction of the ankle joints, complicated by cor pulmonale. These findings were compatible with rigid spine syndrome. To avoid progressive pulmonary hypertension and hypoxemia, nasal BiPAP and home oxygen therapy (0.5 liters/minute) were begun. Rigid spine syndrome is clinically characterized by limitation of spine flexion, and the limitation of thoracic movement often causes severe constrictive respiratory dysfunction. This syndrome should be considered when evaluating patients who have both thoracic deformity, especially scoliosis, and respiratory failure.
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PMID:[Rigid spine syndrome associated with marked hypoxemia and hypercapnia]. 875 23

Sleep has a physiological influence on respiration, which can have major adverse effects on gas exchange in patients with respiratory insufficiency. These effects relate largely to a reduction in various stimulant inputs to the brainstem respiratory centre. Conditions that may be associated with sleep-related respiratory insufficiency range from pulmonary disorders (such as chronic obstructive pulmonary disease (COPD)), to central respiratory insufficiency (such as central alveolar hypoventilation), neurological and neuromuscular disorders (such as polio and muscular dystrophy), and thoracic cage disorders (such as kyphoscoliosis). All these conditions have in common the finding of hypoxaemia and hypercapnia, which become more pronounced during sleep. The relative hypoventilation, which is common to each condition, is due to varying combinations of an inadequate respiratory drive and an increase in the work of breathing. Management of respiratory insufficiency during sleep should be directed first at optimizing the underlying disorder, then at correcting hypoxaemia with controlled low-flow supplemental oxygen. Pharmacological therapy may be effective in some instances, but the choice of agent varies with the underlying disorder. Assisted ventilation is an important part of the management of advanced cases, and the recent development of intermittent positive pressure ventilation by nasal mask (NIPPV) has been an important advance in this area. Use of NIPPV during the night is associated with beneficial effects during the day, particularly improved awake gas exchange and respiratory muscle strength, in addition to less dyspnoea and improved quality of life. Electrophrenic pacing of the diaphragm is helpful in highly selected cases, particularly patients with central respiratory insufficiency and high quadriplegia, but is frequently complicated by the development of obstructive sleep apnoea.
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PMID:Impact of sleep in respiratory failure. 915 Mar 36

The aim of this experiment was to determine whether ventilatory measurements in adult restrained mice provide a valid assessment of chemosensitivity. We used whole-body plethysmography to compare breathing patterns in eight restrained and eight unrestrained outbred Swiss mice during air breathing, hypercapnia, and hypoxia. The mice in the restrained group were each placed in a loosely restraining wire-mesh cage. The unrestrained mice could move freely inside the plethysmograph. All the mice received three hypercapnic stimuli (8.5% CO2) and three hypoxic isocapnic stimuli (10% O2, 3.5% CO2). As compared to unrestrained mice, restrained mice had significantly lower breath durations (TT, 445+/-110 ms vs. 323+/-32 ms) and higher ventilation (VE) levels (15.7+/-2.6 microl/(sec x g) vs. 22.2+/-4.5 microl/(sec x g)), whereas no difference was observed for tidal volume (VT). The increases in frequency and ventilation from baseline to hypercapnia were not significantly different in restrained and unrestrained mice. The VE response to hypoxia was marginally higher in restrained mice. We conclude that chemosensitivity to hypercapnia, and to a lesser extent to hypoxia, can be measured in restrained adult mice, but that the baseline breathing pattern cannot.
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PMID:The effects of restraint on ventilatory responses to hypercapnia and hypoxia in adult mice. 971 5


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