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

A relation was found between persistent stridor and gastroesophageal reflux in seven infants, aged 6 weeks to 6 months. Stridor began at 11 days to 2 months of age, and four of the seven infants had transient hypercarbia on at least one occasion before study. Only one had a history of frequent vomiting; three had recurrent pneumonia. Midesophageal pH, chest and abdominal movement, exhaled carbon dioxide partial pressure, and heart rate of six of the infants were recorded for 4 to 12 hours as they slept. Esophageal pH of the seventh infant was recorded for 24 hours. In the six completely studied infants, there were persistent increases of greater than 10 mm Hg in exhaled carbon dioxide level (three infants), of greater than 10 breaths per minute in respiratory rate (four infants), and in retractions and stridor (six infants) 5 to 20 minutes after onset of reflux. Stridor improved with medical management in 48 hours (five of five infants) and disappeared in 3 weeks (three of five infants) to 2 months (one of five infants). One of these medically treated infants subsequently was treated by Nissen gastric fundoplication because of a recurrence of persistent and severe stridor. Three infants had antireflux surgery, and in two of these stridor disappeared in 48 hours. In the third infant stridor disappeared 3 weeks after surgery. Based on this experience, reflux occasionally causes stridor, probably because of acute inflammation of the upper airway. If structural anomalies are ruled out, infants with severe stridor should be examined for gastroesophageal reflux.
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PMID:Stridor and gastroesophageal reflux in infants. 233 26

The present study compared the responses of rib cage and abdominal expiratory muscles to chemical and mechanical stimuli. In pentobarbital-anesthetized spontaneously breathing dogs, electromyograms (EMG) were recorded from the triangularis sterni (TS) and transverse abdominis (TA) muscles using bipolar intramuscular wire electrodes. During resting oxygen breathing, both muscles were electrically active during expiration. Progressive hyperoxic hypercapnia significantly augmented the expiratory activity of both the TA and the TS. However, the mean percent increases in electrical activity in response to CO2 were substantially greater for the TA than for the TS at all PCO2 levels greater than 50 Torr (P less than 0.01). Occlusion of the airway at end inspiration significantly delayed the onset of TS EMG (from 0.35 +/- 0.07 to 3.35 +/- 0.67 sec; P less than 0.002) and decreased TS EMG rate of rise (P less than 0.002), but did not significantly alter these parameters for the TA. Esophageal distension increased TS EMG in all dogs (by mean of 220 +/- 64%; P less than 0.01), but in contrast decreased TA EMG in all dogs (by a mean of 63 +/- 12%; P less than 0.001). The response to esophageal distention occurred in a graded manner and appeared to be mediated predominantly via vagal afferents. We concluded that expiratory muscles of the rib cage and abdomen manifest substantial differences in their electrical responses to chemoreceptor, pulmonary stretch receptor, and esophageal mechanoreceptor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rib cage and abdominal expiratory muscle responses to CO2 and esophageal distension. 296 76

Chest wall compartment kinematics and respiratory muscle coordinate activity, during either hypercapnia or hypoxia, have not been comparatively assessed in healthy humans. We assessed the displacement volume of the chest wall (Vcw) in 5 normal subjects during hypoxic-normocapnic and hypercapnic-hyperoxic rebreathing by using linearized magnetometers. Vcw was divided into displacement volumes of the rib cage (Vrc) and the abdomen (Vab). Esophageal (Pes) and gastric (Pga) pressures were simultaneously recorded and transdiaphragmatic pressure (Pdi) was calculated by subtracting Pes from Pga. Pressure swings (sw) from end expiration (EE) to end inspiration (EI) were also calculated. During both hypoxia and hypercapnia, from quiet breathing to 40 L/min VE, Vrc,EI increased consistently but Vrc,EE, and Vab,EI did not. Moreover, Vab,EE decreased significantly during hypercapnia and remained unchanged during hypoxia. PesEI decreased (more negative values) and PesEE increased (less negative values) during either stimulus, while PgaEE increased with hypercapnia. Pdisw, calculated as the difference between PdiEE and PdiEI, increased significantly with both hypercapnia and hypoxia ( p = 0.002 for both). On the plot of Pes vs Pga, the slope of a line from end expiratory to end inspiratory lung volume between 20 and 40 L/min VE progressively increased during hypercapnia indicating increasing rib cage muscle (RCM) contribution to inspiratory pressure swings relative to the diaphragm. From these results we conclude that in healthy man: (i) with both chemical stimuli RCM contribution accounts for increase in Vrc displacement; (ii) with hypercapnia, the decrease in Vab,EE displacement indicates abdominal muscle (ABM) contribution to tidal volume; (iii) RCM and ABM assist the diaphragmatic function during hypercapnic stimulation.
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PMID:Chest wall kinematics during chemically stimulated breathing in healthy man. 1264 36

We designed a new servoventilator that proportionally adjusts airway pressure to transdiaphragmatic pressure (Pdi) generated by the subject during inspiration. Each cycle is triggered by either a preset Pdi increase or a preset inspiratory flow value (whichever is reached first), whereas cycling-off is flow-dependent. We evaluated the servoventilator in seven healthy subjects at normocapnia and three levels of hypercapnia (normocapnia + 3, + 6, and + 9 mm Hg) comparatively with spontaneous breathing. Triggering was by Pdi in six subjects and flow in one. At all end-tidal carbon dioxide pressure levels, time from onset of diaphragm electromyographic activity to inspiratory flow was similar with and without the servoventilator. Airway pressure increased proportionally to Pdi variation during servoventilator breathing. Flow, tidal volume, respiratory rate, intrinsic positive end-expiratory pressure, and esophageal and transdiaphragmatic pressure-time products increased significantly with hypercapnia with and without the servoventilator. Breathing pattern parameters were similar in the two breathing modes, and no differences were found for intrinsic positive end-expiratory pressure or gastric pressure variation during exhalation. Esophageal and transdiaphragmatic pressure-time products were lower with than without the servoventilator. The Pdi-driven servoventilator was well synchronized to the subjects effort, delivering a pressure proportional to Pdi and reducing respiratory effort at normocapnia and hypercapnia.
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PMID:Transdiaphragmatic pressure control of airway pressure support in healthy subjects. 1452 8

The muscular-hydrostat model of tongue function proposes a constant interaction of extrinsic (external bony attachment, insertion into base of tongue) and intrinsic (origin and insertion within the tongue) tongue muscles in all tongue movements (Kier WM and Smith KK. Zool J Linn Soc 83: 207-324, 1985). Yet, research that examines the respiratory-related effects of tongue function in mammals continues to focus almost exclusively on the respiratory control and function of the extrinsic tongue protrusor muscle, the genioglossus muscle. The respiratory control and function of the intrinsic tongue muscles are unknown. Our purpose was to determine whether intrinsic tongue muscles have a respiration-related activity pattern and whether intrinsic tongue muscles are coactivated with extrinsic tongue muscles in response to respiratory-related sensory stimuli. Esophageal pressure and electromyographic (EMG) activity of an extrinsic tongue muscle (hyoglossus), an intrinsic tongue muscle (superior longitudinal), and an external intercostal muscle were studied in anesthetized, tracheotomized, spontaneously breathing rats. Mean inspiratory EMG activity was compared at five levels of inspired CO2. Intrinsic tongue muscles were often quiescent during eupnea but active during hypercapnia, whereas extrinsic tongue muscles were active in both eupnea and hypercapnia. During hypercapnia, the activities of the airway muscles were largely coincident, although the onset of extrinsic muscle activity generally preceded the onset of intrinsic muscle activation. Our findings provide evidence, in an in vivo rodent preparation, of respiratory modulation of motoneurons supplying intrinsic tongue muscles. Distinctions noted between intrinsic and extrinsic activities could be due to differences in motoneuron properties or the central, respiration-related control of each motoneuron population.
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PMID:Coordination of intrinsic and extrinsic tongue muscles during spontaneous breathing in the rat. 1471 75

The present study was designed to verify whether during hypercapnic stimulation, as we had previously found during exercise or walking, the partitioning of the respiratory motor output is equally distributed to the muscles of chest wall compartments to assist diaphragm function. We studied chest wall kinematics and respiratory muscle recruitment in seven healthy men during rebreathing of a hypercapnic-hyperoxic gas mixture (CO(2) RT). Data were compared with those previously obtained during either cycling exercise or walking. The chest wall volume ( Vcw), assessed by optoelectronic plethysmography (OEP), was modeled as the sum of the volumes of the lung-apposed rib cage ( Vrc,p), diaphragm-apposed rib cage ( Vrc,a) and abdomen ( Vab). Esophageal ( Pes), gastric ( Pga) and transdiaphragmatic ( Pdi= Pga- Pes) pressures were simultaneously recorded. Velocity of shortening ( V') and power ( W'= Px V') of the diaphragm ( W'di), rib cage muscles ( W'rcm) and abdominal muscles ( W'abm) were also calculated. During CO(2) RT the progressive increase in end-inspiratory Vcw resulted from an increase in both end-inspiratory Vrc,p and Vrc,a, while the progressive decrease in end-expiratory Vcw was entirely due to the decrease in end-expiratory Vab. The increase in Vrc,p was proportionally slightly greater than that in Vrc,a. The end-inspiratory increase and end-expiratory decrease in Vcw were accounted for by inspiratory rib cage (RCM,i) and abdominal (ABM) muscle recruitment, respectively. W'di, W'rcm and W'abm progressively increased. However, while most of W'di was expressed in terms of velocity of shortening, most of W'rcm and W'abm was expressed as force or pressure. A comparison of CO(2) results with data obtained during exercise revealed: (1). a gradual vs. an immediate response, (2). a similar decrease in Vab,e and Pabm, (3). an apparent lack of any difference in ABM recruitment, (4). less gradual ABM relaxation, (5). no drop in Pdi but a similar Wdi change and decrease in pressure-to-velocity ratio of the diaphragm. We have found that in healthy humans: (1). the increased motor output with hypercapnia is equally distributed between RCM and ABM to minimize transdiaphragmatic pressure and (2). data on chest wall kinematics and respiratory muscle recruitment are only partly in line with those obtained during walking or cycling exercise.
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PMID:Chest wall kinematics and respiratory muscle coordinated action during hypercapnia in healthy males. 1473 63

The assessment of the work of breathing (WOB) of patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) is difficult, particularly when the patient first presents with acute hypercapnia and respiratory acidosis. Acute exacerbations of COPD patients are in significant respiratory distress and noninvasive measurements of WOB are easier for the patient to tolerate. Given the interest in using alternative therapies to noninvasive ventilation, such as high flow nasal oxygen therapy or extracorporeal carbon dioxide removal, understanding the physiological changes are key and this includes assessment of WOB. This narrative review considers the role of three different methods of assessing WOB in patients with acute exacerbations of COPD. Esophageal pressure is a very well validated measure of WOB, however the ability of patients with acute exacerbations of COPD to tolerate esophageal tubes is poor. Noninvasive alternative measurements include parasternal electromyography (EMG) and electrical impedance tomography (EIT). EMG is easily applied and is a well validated measure of neural drive but is more likely to be degraded by the electrical environment in intensive care or high dependency. EIT is less well validated as a tool for WOB in COPD but extremely well tolerated by patients. Each of the different methods assess WOB in a different way and have different advantages and disadvantages. For research into therapies treating acute exacerbations of COPD, combinations of EIT, EMG and esophageal pressure are likely to be better than only one of these.
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PMID:Assessment of Work of Breathing in Patients with Acute Exacerbations of Chronic Obstructive Pulmonary Disease. 3169 6

We present a case of a young boy who sustained a traumatic brain injury (TBI) complicated by intractable intracranial hypertension and severe acute respiratory distress syndrome (ARDS) with hypercapnia. The coexisting pulmonary pathology significantly impacted intracranial pressure management. Oesophageal pressure manometry was used to guide ventilator and airway pressure management, allowing the team to optimise ARDS care while mitigating the risk of elevated intracranial pressure. While the literature describing the use of oesophageal pressure-guided ARDS management continues to evolve, there are no reported cases demonstrating use in patients with ARDS and intractable intracranial hypertension due to TBI.
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PMID:Oesophageal pressure-guided management of severe acute respiratory distress syndrome in a patient with intractable intracranial hypertension. 3178 Jun 14