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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In four awake dogs we measured EMG activity of three inspiratory and four expiratory muscles during sustained central chemoreceptor stimulation (CO2 inhalation), and peripheral chemoreceptor stimulation (intravenous infusion of almitrine bismesylate (almitrine)). By using this selective pharmacological stimulation of the peripheral chemoreceptors and reversibly cold-blocking pulmonary stretch receptors, we were able to determine the effects of each type of stimulation on respiratory muscle recruitment in the absence of such complicating influences as pulmonary stretch receptor feedback, cerebral hypoxia or hypocapnia, and differences in breathing pattern. 2. During 10 min of steady-state hyperpnoea (minute ventilation VI, approximately twice eupnoea) caused by either hypercapnia or isocapnic stimulation of the carotid bodies with almitrine, all three inspiratory and all four expiratory muscles demonstrated significant and sustained elevations in EMG activity. 3. With both types of chemoreceptor stimulation, as tidal volume, VT, increased, so did the mean electrical activities of the crural diaphragm (r = 0.88), costal diaphragm (r = 0.93), parasternals (r = 0.82), triangularis sterni (r = 0.74), transversus abdominis (r = 0.77), external obliques (r = 0.68) and internal intercostals (r = 0.75). 4. In each dog, the response of ventilation and of the diaphragmatic EMG to a given level of central or peripheral chemoreceptor stimulation is highly reproducible from one test day to the next. On the other hand, accessory inspiratory and expiratory abdominal and rib cage muscles in two of the four dogs showed highly significant changes from day to day in the amount of their EMG activity at any given VT. 5. During steady-state ventilatory stimulation, 2 min intervals were chosen during which the two types of chemoreceptor stimulation had caused hyperpnoeas with similar values for VT, total time per breath (TTOT) and inspiratory time divided by the total time (TI/TTOT). Comparison of EMG activities during these matched hyperpnoeas revealed that there were no differences in the activities of any of the muscles between the two forms of stimulation. We conclude that peripheral chemoreceptor stimulation causes significant and sustained recruitment of expiratory muscles even in the absence of pulmonary feedback and that both expiratory and inspiratory muscles are recruited to the same extent during peripheral chemoreceptor stimulation as they are during an identical hyperpnoea caused by central chemoreceptor stimulation.
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PMID:Respiratory muscle recruitment during selective central and peripheral chemoreceptor stimulation in awake dogs. 159 81

We assessed respiratory muscle response patterns to chemoreceptor stimuli (hypercapnia, hypoxia, normocapnic hypoxia, almitrine, and almitrine + CO2) in six awake dogs. Mean electromyogram (EMG) activities were measured in the crural (CR) diaphragm, triangularis sterni (TS), and transversus abdominis (TA). Hypercapnia and normocapnic hypoxia caused mild to marked hyperpnea [2-5 times control inspiratory flow (VI)] and increased activity in CR diaphragm, TS, and TA. When hypocapnia was permitted to develop during hypoxia and almitrine-induced moderate hyperpnea, CR diaphragm activity increased, whereas TS and TA activities usually did not change or were reduced below control. Over time in hypercapnia, CR diaphragm, TS, and TA were augmented and maintained at these levels over many minutes; with hypoxic hyperventilation CR diaphragm, TS, and TA were first augmented but then CR diaphragm remained augmented while TS and, less consistently, TA were inhibited over time. Marked hyperpnea (4-5 times control) due to carotid body stimulation increased TA and TS EMG activity despite an accompanying hypocapnia. We conclude that in the intact awake dog 1) carotid body stimulation augments the activity of both inspiratory and expiratory muscles; 2) hypocapnia overrides the augmenting effect of carotid body stimulation on expiratory muscles during moderate hyperpnea, usually resulting in either no change or inhibition; 3) at higher levels of hyperpnea both chemoreceptor stimulation and stimulatory effects secondary to a high ventilatory output favor expiratory muscle activation; these effects override any inhibitory effects of a coincident hypocapnia; and 4) expiratory muscles of the rib cage/abdomen may be augmented/inhibited independently of one another.
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PMID:Differential responses of expiratory muscles to chemical stimuli in awake dogs. 249 85

Using 6 chronically-instrumented awake dogs, we characterized the response of the respiratory muscles to mild and moderate treadmill exercise in terms of (1) the magnitude and timing of the EMGs of the costal and crural diaphragm, triangularis sterni and transverse abdominal muscles, and (2) the concomitant changes in esophageal (PE) and gastric (PG) pressures during treadmill exercise. Dogs wore a bivalved breathing mask which constrained breathing frequency and prevented some of the exercise-induced hypocapnia. Inspiratory and chest expiratory muscle EMGs increased linearly with a 1.5-fold tidal volume (VT) change during exercise. Abdominal muscle recruitment occurred during most exercise levels and exhibited (1) phasic activity coincident with footplant and (2) tonic activation evidenced by a baseline shift in PG and EMG activities. During control, inspiratory and expiratory flow preceded the onset of respiratory muscle EMG activity, but during exercise, electrical activation of these muscles coincided with the onset of mechanical flow. We conclude that phasic and tonic activation of expiratory muscles during exercise in the dog is significantly influenced by both respiratory and locomotory requirements. These patterns of expiratory muscle recruitment may assist inspiration by lengthening inspiratory muscles through decrements in end-expiratory lung volume and by passive recoil of the rib cage and abdominal compartments.
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PMID:The effects of locomotion on respiratory muscle activity in the awake dog. 260 25

The order of recruitment of single-motor units in parasternal intercostal muscles during inspiration was studied in normal human subjects during quiet breathing and voluntary hyperventilation. Electromyograms were recorded from the second and third intercostal spaces by means of bipolar fine wire electrodes. Flow at the mouth, volume, end-expired CO2, and rib cage and abdominal anterior-posterior diameters were monitored. Single-motor units were identified using criteria of amplitude and shape, and the time of first appearance of each unit in each inspiration was noted. Hyperventilation was performed with visual feedback of the display of rib cage and abdomen excursions, keeping the ratio of rib cage to abdominal expansion. Subjects were normocapnic in quiet breathing and developed hypocapnia during hyperventilation. Recruitment order was stable in quiet breathing, but in some cases was altered during voluntary hyperventilation. Some low threshold units that fired early in the breath in quiet breathing fired earlier at the beginning of a period of voluntary hyperventilation but progressively later in the breath as hyperventilation went on, whereas later firing units moved progressively toward the early part of inspiration. This suggests that different groups of motoneurons in the pool supplying parasternal intercostal muscles receive different patterns of synaptic input.
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PMID:Voluntary hyperventilation changes recruitment order of parasternal intercostal motor units. 355 79

Dysfunctional breathing is a term describing breathing disorders where chronic changes in breathing pattern result in dyspnoea and other symptoms in the absence or in excess of the magnitude of physiological respiratory or cardiac disease. We reviewed the literature and propose a classification system for the common dysfunctional breathing patterns described. The literature was searched using the terms: dysfunctional breathing, hyperventilation, Nijmegen questionnaire and thoraco-abdominal asynchrony. We have summarised the presentation, assessment and treatment of dysfunctional breathing, and propose that the following system be used for classification. 1) Hyperventilation syndrome: associated with symptoms both related to respiratory alkalosis and independent of hypocapnia. 2) Periodic deep sighing: frequent sighing with an irregular breathing pattern. 3) Thoracic dominant breathing: can often manifest in somatic disease, if occurring without disease it may be considered dysfunctional and results in dyspnoea. 4) Forced abdominal expiration: these patients utilise inappropriate and excessive abdominal muscle contraction to aid expiration. 5) Thoraco-abdominal asynchrony: where there is delay between rib cage and abdominal contraction resulting in ineffective breathing mechanics.This review highlights the common abnormalities, current diagnostic methods and therapeutic implications in dysfunctional breathing. Future work should aim to further investigate the prevalence, clinical associations and treatment of these presentations.
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PMID:Dysfunctional breathing: a review of the literature and proposal for classification. 2758 28