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

The act of breathing diminishes the discomfort associated with hypercapnia and breath-holding. To investigate the mechanisms involved in this effect, we studied the effect of tidal volume (VT) on CO2-evoked air hunger in 5 high-level quadriplegic subjects whose ventilatory capacity was negligible, and who lacked sensory information from the chest wall. Subjects were ventilated at constant frequency with a hyperoxic gas mixture, and end-tidal PCO2 was maintained at a constant but elevated level. VT was varied between the subjects' normal VT and a smaller VT. Subjects used a category scale to rate their respiratory discomfort or 'air hunger' at 30-40 sec intervals. In 4 of 5 subjects there was a strong inverse relationship between breath size and air hunger ratings. The quality of the sensation associated with reduced VT was nearly identical to that previously experienced with CO2 alone. We conclude that afferent information from the lungs and upper airways is sufficient to modify the sensation of air hunger.
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PMID:Reduced tidal volume increases 'air hunger' at fixed PCO2 in ventilated quadriplegics. 145 95

We reviewed the Mayo Clinic experience with nocturnal nasal ventilation (NNV) and retrospectively assessed the clinical benefits, patient compliance, and complications. NNV had been instituted in 26 patients with daytime hypercapnia and nocturnal hypoventilation due to neuromuscular diseases or chronic obstructive pulmonary disease. After initiation of NNV, 21 of 26 patients continued to use this treatment regularly (81% compliance rate) and considered their life-style improved. In this subset of patients, the arterial partial pressure of carbon dioxide during unassisted breathing decreased from 64 +/- 13 to 51 +/- 7 mm Hg, and the arterial partial pressure of oxygen increased from 58 +/- 12 to 68 +/- 8 mm Hg. No significant change was noted in the forced vital capacity or maximal respiratory pressures. Four of the five patients in whom NNV had been discontinued cited discomfort related to the mask or severity and poor prognosis of the underlying illness as reasons for cessation of treatment. We conclude that NNV is well tolerated by most patients and may improve alveolar ventilation and arterial oxygenation in patients with chronic respiratory failure.
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PMID:Nocturnal nasal ventilation for treatment of patients with hypercapnic respiratory failure. 192 93

The tolerance of totally curarized subjects for prolonged breath hold is viewed by many as evidence that respiratory muscle contraction is essential to generate the sensation of breathlessness. Although conflicting evidence exists, none of it was obtained during total neuromuscular block. We completely paralyzed four normal, unsedated subjects with vecuronium (a non-depolarizing neuromuscular blocker). Subjects were mechanically ventilated with hyperoxic gas mixtures at fixed rate and tidal volume. End-expiratory PCO2 (PETCO2) was varied surreptitiously by changing inspired PCO2. Subjects rated their respiratory discomfort or 'air hunger' every 45 sec. At low PETCO2 (median 35 Torr) they felt little or no air hunger. When PETCO2 was raised (median 44 Torr) all subjects reported severe air hunger. They had reported the same degree of air hunger at essentially the same PETCO2 before paralysis. When questioned afterwards all subjects said the sensation could be described by the terms 'air hunger', 'urge to breathe', and 'shortness of breath', and that is was like breath holding. They reported no fundamental difference in the sensation before and after paralysis. We conclude that respiratory muscle contraction is not important in the genesis of air hunger evoked by hypercapnia.
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PMID:'Air hunger' from increased PCO2 persists after complete neuromuscular block in humans. 212 Jul 57

Breathing during hypercapnia is determined by reflex mechanisms but may also be influenced by respiratory sensations. The present study examined the effects of voluntary changes in level and pattern of breathing on the sensation of dyspnea at a constant level of chemical drive. Studies were carried out in 15 normal male subjects during steady-state hypercapnia at an end-tidal PCO2 of 50 Torr. The intensity of dyspnea was rated on a Borg category scale. In one experiment (n = 8), the level of ventilation was increased or decreased from the spontaneously adopted level (Vspont). In another experiment (n = 9), the minute ventilation was maintained at the level spontaneously adopted at PCO2 of 50 Torr and breathing frequency was increased or decreased from the spontaneously adopted level (fspont) with reciprocal changes in tidal volume. The intensity of dyspnea (expressed as percentage of the spontaneous breathing level) correlated with ventilation (% Vspont) negatively at levels below Vspont (r = -0.70, P less than 0.001) and positively above Vspont (r = 0.80, P less than 0.001). At a constant level of ventilation, the intensity of dyspnea correlated with breathing frequency (% fspont) negatively at levels below fspont (r = -0.69, P less than 0.001) and positively at levels above fspont (r = 0.75, P less than 0.001). These results indicate that dyspnea intensifies when the level or pattern of breathing is voluntarily changed from the spontaneously adopted level. This is consistent with the possibility that ventilatory responses to changes in chemical drive may be regulated in part to minimize the sensations of respiratory effort and discomfort.
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PMID:Effects of changes in level and pattern of breathing on the sensation of dyspnea. 226 46

A number of investigators have proposed that the sense of respiratory discomfort accompanying hypercapnia depends on respiratory mechanoreceptors which inform the sensory cortex of reflex increases in breathing. To test this hypothesis, we studied subjects whose respiratory muscles were paralyzed, and who were thus unable to increase breathing in response to hypercapnia. We gradually elevated inspired PCO2 in four tracheostomized quadriplegic subjects supported by constant mechanical ventilation. These subjects reported sensations of 'air hunger' (e.g., "short of breath", "air-starved") when end-tidal PCO2 increased 10 Torr (mean) above their resting levels. In a second experiment we used the forced-choice technique to determine the ability of three of these subjects to detect repeated changes of end-tidal PCO2. Two detected 7 Torr changes, the third detected 11 Torr changes. These data suggest that changes in breathing are not necessary to evoke the sense of 'air hunger'. We conclude that the likely mechanisms are (1) projection of chemoreceptor afferent traffic to the sensory cortex, and (2) projection of corollary discharge from brainstem respiratory centers to the sensory cortex.
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PMID:'Air hunger' arising from increased PCO2 in mechanically ventilated quadriplegics. 249 25

Congenital central hypoventilation syndrome (CCHS) has been thought to be a disorder of central chemoreceptor responsiveness. Previous studies in CCHS have shown decreased or absent ventilatory responsiveness to both hypercarbia and hypoxia. However, hypoxic responsiveness during wakefulness has not been systematically studied. We studied hypoxic and hypercapnic ventilatory responses during wakefulness in five children with CCHS (6 to 11 yr of age). To measure the hypercapnic response, the children rebreathed a hyperoxic hypercapnic mixture until PaCO2 reached 56 to 69 mm Hg. For the hypoxic response, the children rebreathed a hypoxic gas mixture, at mixed venous PCO2, until SaO2 had fallen to less than 78%. We found that the ventilatory responses to hypercapnia and hypoxia were very variable (linear correlation coefficients ranging from -0.44 to +0.63 for hypercapnic responses and from -0.15 to +0.77 for hypoxic responses), with no significant change from baseline in response to either stimulus. There was no evidence of progressive ventilatory stimulation despite increasing stimulus. Additionally, these children had no subjective sensation of dyspnea or discomfort. This establishes that hypoxic and hypercapnic ventilatory control is absent during wakefulness. Chemoreceptor control (peripheral and central) is, therefore, defective in all states in children with CCHS. We speculate that the defect in CCHS lies in central integration of the central and peripheral chemoreceptor signals.
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PMID:Hypoxic and hypercapnic ventilatory responses in awake children with congenital central hypoventilation syndrome. 276 73

A model of the respiratory control system incorporating both chemical and respiratory neuromechanical feedbacks is proposed to describe the steady-state ventilatory responses to CO2 inhalation and exercise. It is postulated that ventilatory output (VE) is set by the respiratory center to minimize a net operating cost representing the conflicting challenges of arterial chemical imbalance and respiratory-mechanical discomfort (intolerance of effort), given, respectively, by a quadratic function of arterial PCO2 and a logarithmic function of VE. In addition, the system is assumed to be mechanically limited at maximum VE (Vmax). The predicted responses in VE during moderate hypercapnia, exercise, and ventilatory loading closely mimic those normally observed, even though no separate signal unique to exercise is assumed. As a quantitative validation, the model yielded good fits to ventilatory response data obtained in eight healthy subjects during eucapnic and hypercapnic exercise; the predicted Vmax averaged approximately 77% of the maximum voluntary ventilation in all subjects. The results demonstrate the plausibility of the proposed optimization mechanism and suggest an important role for respiratory-mechanical factors in the control of VE.
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PMID:Ventilatory control in hypercapnia and exercise: optimization hypothesis. 311 8

A method for measuring human nasal airflow resistance (Rnaw) is described. Air flows at constant pressure through both nasal cavities via a face mask and out through the mouth. Airflow is inversely related to Rnaw. The method has several advantages over many other methods for measuring Rnaw, in particular allowing aerodynamic separation of nose and lungs, and frequent measurements over long periods without discomfort to or intervention with subjects or patients. We have used this method to obtain standard values of Rnaw in healthy subjects and in patients with asthma and/or rhinitis. Age has a negative correlation with Rnaw but no sexual difference was seen. Cigarette smoking increases Rnaw especially in young adults. Patients with rhinopathy have much higher resistances than healthy subjects, but those with asthma alone do not. Rnaw is sensitive to changes in ventilation and lung volumes; deep inspiration and oral hyperventilation decrease Rnaw, while deep expiration, nasal hyperventilation and breath-holding increase it. Hypoxia and hypercapnia locally applied in the nose increase Rnaw. It is suggested that these changes are predominantly due to changes in control of the nasal vascular bed.
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PMID:Measurement and regulation of nasal airflow resistance in man. 373 73

Adenosine infusion (100 micrograms X kg-1 X min-1) in humans stimulates ventilation but also causes abdominal and chest discomfort. To exclude the effects of symptoms and to differentiate between a central and peripheral site of action, we measured the effect of adenosine infused at a level (70-80 micrograms X kg-1 X min-1) below the threshold for symptoms. Resting ventilation (VE) and progressive ventilatory responses to isocapnic hypoxia and hyperoxic hypercapnia were measured in six normal men. Compared with a control saline infusion given single blind on the same day, adenosine stimulated VE [mean increase: 1.3 +/- 0.8 (SD) l/min; P less than 0.02], lowered resting end-tidal PCO2 (PETCO2) (mean fall: -3.9 +/- 0.9 Torr), and increased heart rate (mean increase: 16.1 +/- 8.1 beats/min) without changing systemic blood pressure. Adenosine increased the hypoxic ventilatory response (control: -0.68 +/- 0.4 l X min-1 X %SaO2-1, where %SaO2 is percent of arterial O2 saturation; adenosine: -2.40 +/- 1.2 l X min-1 X %SaO2-1; P less than 0.01) measured at a mean PETCO2 of 38.3 +/- 0.6 Torr but did not alter the hypercapnic response. This differential effect suggests that adenosine may stimulate ventilation by a peripheral rather than a central action and therefore may be involved in the mechanism of peripheral chemoreception.
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PMID:Effects of adenosine on ventilatory responses to hypoxia and hypercapnia in humans. 378 85

A therapeutic regimen is described for sedative, analgesic, and anti-emetic effect in patients receiving intra-arterial carmustine (BCNU) for malignant gliomas. This regimen consists of nalbuphine, 30 mg, i.v., and droperidol, 2.5 mg, i.v., given immediately prior to intra-carotid BCNU infusion. Droperidol, 2.5 mg, i.v., is then administered on four hour intervals for sixteen hours post-procedure. This combination provided excellent effect in nine patients treated for twelve intra-carotid infusions. None of the nine patients experienced vomiting, one experienced mild nausea several hours post-infusion, and non complained of severe pain or discomfort. Thirteen additional patients received diazepam, 10 mg, P.O., prior to the intra-carotid BCNU infusion, with fentanyl, 100 mcg, i.v., and prochlorperazine, 10 mg, i.m. at the onset of infusion. All thirteen patients suffered from severe nausea, vomiting, and orbital pain. The nalbuphine/droperidol combination is thought to provide a superior alternative to the traditional narcotic/pheonothiazine/benzodiazepine combination for carotid BCNU infusion. This combination has theoretical advantages for the patient with intracranial mass lesions by providing analgesia and sedation with minimal potential for respiratory depression and carbon dioxide retention.
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PMID:Nalbuphine and droperidol in combination for sedation and prevention of nausea and vomiting during intra-carotid BCNU infusion. 395 77


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