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

A prospective evaluation of the prevalence of CO2 retention and its relationship to lung mechanics and inspiratory muscle strength was carried out in 311 clinically stable patients with chronic obstructive pulmonary disease (COPD). Of these patients 32.8% had hypercapnia (PaCO2 greater than or equal to 43 mm Hg). PaCO2 was directly related to lung resistance (RL; r = 0.53) and inversely related to FEV1 (r = 0.53) and to an expression of the dead space/tidal volume ratio (1 - VD/VT) (r = 0.48). RL was found to be a major determinant of the mean intrathoracic pressure swing developed during inspiration (PI) at rest (r = 0.85). Maximal inspiratory pressure (PImax) was found to improve the predictive value for PaCO2 of several mechanical loads, with RL/PImax the best predictor (r = 0.57). The prevalence of hypercapnia increased from virtually 0 to 100% with increases in the RL/PImax value and was higher in the obese subjects at intermediate RL/PImax values, probably because of the burden placed on the respiratory muscles by chest wall mass loading. Our results show that chronic alveolar hypoventilation is likely to develop in COPD patients who have a combination of high inspiratory loads and inspiratory muscle weakness. hypercapnia may be one strategy available to avoid overloading of the inspiratory muscles leading to fatigue and possible irreversible failure.
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PMID:Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. 202 40

The percentage of the patients with PaCO2 more than 60 Torr and PaO2 more than 50 Torr were 13% in the patients with tuberculosis sequela (N = 502) and 4% in the patients with chronic obstructive lung disease (COLD, N = 727), who were treated with home oxygen therapy in the western region of Japan. Patients with chronic respiratory failure caused by tuberculosis sequela have higher PaCO2 than patients with COLD. Although the prognosis of patients with hypercapnia and moderate hypoxemia is not necessarily poor, some patients may need treatment for severe hypoventilation to prevent respiratory muscle fatigue and abnormal breathing during sleep. In this study, nine patients with hypercapnic chronic respiratory failure caused by tuberculosis sequela were ventilated by Chest Negative Pressure Ventilation (CNPV). The patients were monitored as in polysomnography by transcutaneous PCO2 (PtcCO2) electrode and Respiratory Inductance Plethysmography (RIP). Tidal volume induced by CNPV was larger during mouth breathing (504 +/- 128 ml, mean +/- s.d.) than during nose breathing (438 +/- 109 ml) calculated from RIP in awake state (N = 7). Oxygen saturation measured by ear oximeter and PtcCO2 were 94.4 +/- 2.9% and 57.8 +/- 12.2 Torr in awake state. Following CNPV SaO2 and PtcCO2 were 95.7 +/- 3.0%, 42.7 +/- 12.1 Torr in awake state (N = 9) and 93.0 +/- 4.4%, 57.0 +/- 15.7 Torr in Non-REM sleep (N = 5), respectively. CNPV is effective in these patients in awake state. During Non-REM sleep, CNPV maintains the PtcCO2 level only in awake state.
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PMID:[Tuberculosis sequelae: pathophysiological aspect (ventilation)]. 207 61

We studied the relationship between contractile function and intracellular pH (pHi) in the isolated rat diaphragm when superfusate PCO2 was changed during hyperoxia or hypoxia. Superfused diaphragm strips were field stimulated at 0.5 Herz, and twitch tension (TT) was recorded. The pHi was calculated from the volume distribution of a weak acid, dimethyl-oxazolidinedione. In hyperoxia, hypercapnic acidosis (pH 7.06-6.63) depressed diaphragm pHi and TT, whereas hypocapnic alkalosis (pH 7.82-8.15) increased pHi but did not significantly affect TT. TT was maximum at physiological pHi (7.06), but in hyperoxic hypercapnic muscles substantial force was still generated at pHi values as low as 6.44. Hypoxia (PO2 30-38 mm Hg) markedly reduced TT; this effect was slightly exacerbated by hypercapnia and attenuated by hypocapnia. Hypoxia lowered pHi by about 0.2 units, which was insufficient to account for the hypoxic contractile failure. Knowledge of the hyperoxic muscle TT/pHi relationship suggests that, in other contexts, caution should be exercised in attributing severe muscle fatigue or force loss to modest falls in pHi.
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PMID:The effect of pH and hypoxia on function and intracellular pH of the rat diaphragm. 210 18

In 15 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) divided into two groups, one with normocapnia (A) and one with chronic hypercapnia (B), we evaluated the maximal voluntary inspiratory muscle strength (MIP), the pattern of breathing, the mouth occlusion pressure (Po.1), the neural respiratory drive (NRD), assessed by surface electromyographic (EMG) activity of the diaphragm (EMGd) and EMG activity of intercostal muscles (EMGint), and the chest wall neuromuscular coupling, assessed in terms of Po.1/EMGd ratio. Compared with an age-matched normal control group, both A and B groups exhibited lower MIP, significantly greater EMGd and EMGint, and lower Po.1/EMGd ratio. However, a similar pattern, along with a rapid and shallow breathing, differentiated group B from group A. In group B we found a significant direct relationship between Po.1/EMGd ratio and MIP, and an inverse relationship between PaCO2 and Po.1/EMGd ratio. These data seem to indicate the following: (1) EMG is a more precise method than Po.1 in assessing the magnitude of the NRD; (2) NRD is increased in these patients; and (3) clinical manifestations probably associated with inspiratory muscle fatigue (marked decrease in muscle strength, rapid and shallow breathing, and alveolar hypoventilation) may be accompanied by a greater NRD and a more marked derangement in chest wall neuromuscular coupling in COPD.
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PMID:Neural respiratory drive and neuromuscular coupling in patients with chronic obstructive pulmonary disease (COPD). 222 64

The effect of acute hypercapnia on skeletal muscle contractility and relaxation rate was investigated. The contractile force of fresh and fatigued quadriceps femoris (QF) and adductor pollicis (AP) was studied in normal humans by use of electrical stimulation. Maximum relaxation rate from stimulated contractions was measured for both muscles. Acute hypercapnia led to a rapid substantial reduction of contraction force. The respiratory acidosis after 9% CO2 was breathed for 20 min [mean venous blood pH 7.26 and end-tidal PCO2 (PETCO2) 65.1 Torr] reduced 20- and 100-Hz stimulated contractions of QF to 72.8 +/- 4.4 and 80.0 +/- 5.1% of control values, respectively. After 8 and 9% CO2 were breathed for 12 min, AP forces at 20- and 50-Hz stimulation were also reduced. Twitch tension of AP was reduced by a mean of 25.5% when subjects breathed 9% CO2 for 12 min [mean arterialized venous blood pH (pHav) 7.25 and PETCO2 66 Torr]. Over the range of 5% (pHav 7.38 and PETCO2 47 Torr) to 9% CO2, there was a linear relationship between twitch tension loss and pHav, arterialized venous blood PCO2, and PETCO2. Acute respiratory acidosis (mean PETCO2 61 Torr) increased the severity of low-frequency fatigue after intermittent voluntary contractions of AP. At 20 min of recovery, twitch tension was 63.2 +/- 13.4 and 46.8 +/- 16.4% of control value after exercise breathing air and 8% CO2, respectively. Acute hypercapnia (mean PETCO2 65.1 and 60.5 Torr) did not alter the maximum relaxation rate from tetanic contractions of fresh QF and from twitch tensions of AP.
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PMID:Effect of acute hypercapnia on limb muscle contractility in humans. 226 73

We studied the effect of aminophylline on twitch tension (TT) and intracellular pH (pHi) in isolated rat diaphragm strips that were fatigued, hypercapnic, or hypoxic. Superfused muscles were directly stimulated at 0.5 Hz. The pHi was measured from distribution volumes of dimethyl-oxazolidinedione. Fatigue was induced by intermittent tetanic stimulation. Hypercapnia and hypoxia were produced by altering superfusate carbon dioxide tension (PCO2) or oxygen tension (PO2). Aminophylline (1.0 mmol.l-1) reversed the twitch decay seen during fatigue or hypercapnic acidosis, and caused partial recovery of twitch depression during hypoxia. Muscle fatigue was not due to an intracellular acidosis. Both hypercapnia and hypoxia lowered pHi. Aminophylline did not alter pHi in unstimulated muscles, but caused a significant fall in pHi in stimulated muscles that were fatigued or hypoxic. High dose aminophylline improved twitch tension in diaphragm strips that were fatigued, acidotic, or hypoxic. Twitch potentiation was not due to an intracellular alkalosis. Aminophylline lowered pHi in stimulated muscle, and thus, theoretically, could sometimes be harmful in the treatment of muscle fatigue.
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PMID:The effect of aminophylline on function and intracellular pH of the rat diaphragm. 228 69

Patients with severe COPD may be in a state of ventilatory muscle (VM) fatigue. In these patients, rapid and shallow breathing has been hypothesized to be a compensatory mechanism that prevents more severe fatigue from taking place. To test these hypotheses, we studied the effects of VM resting in a group of patients with severe COPD. Eleven clinically stable patients with COPD and chronic hypercapnia were studied. Six of them (group A) had a seven-day period of negative pressure-assisted ventilation (NPV), and five (group B) with similar functional characteristics served as a control group. Compared with a normal age-matched control group, both A and B groups exhibited significantly lower tidal volume (VT), inspiratory time (TI), total time of the respiratory cycle (Ttot) and Ti/Ttot ratio, decrease in muscle strength, and greater electromyographic activity of diaphragm (EMGd) and parasternal muscles, but similar ventilation and VT/TI. After the study period, group A exhibited significant increase in VT, Ti, and TI/Ttot (p less than 0.05), and decrease in PaCO2 (p less than 0.05), EMGd, and EMGint (p less than 0.05 for both), and a slight but significant increase in maximal inspiratory pressure (MIP) (p less than 0.05). These data suggest that NPV rests VM, increases their strength, and reduces hypercapnia in patients with severe COPD.
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PMID:Changes in ventilatory muscle function with negative pressure ventilation in patients with severe COPD. 229 58

Respiratory arrests occur in the clinical setting of respiratory failure, but the mechanism is unclear. We used a dog model with increased inspiratory resistance and hypoxemia to explore the cause. We hypothesized that respiratory muscle fatigue (RMF) played a role in these respiratory arrests, and that the combination of hypoxia and resistive loading would produce respiratory arrest by the mechanism of RMF. Our preparation had transdiaphragmatic pressures that were 40% of maximum (Pdimax = 46.3 +/- 10.0 cm H2O) and progressive hypoxia resulting in a final arterial PO2 of 38 +/- 9 mm Hg and a phrenic vein O2 content of 1.8 +/- 1.1 mg/dl. Instead of failure associated with carbon dioxide retention and RMF, we saw a rapid decrease in tidal volume and respiratory rate, leading to apnea over 30 to 60 s while the diaphragm still responded with significant pressure generation when externally stimulated. These results suggest that respiratory muscle fatigue may not be a major factor in respiratory arrests associated with inspiratory loading and hypoxia, but that suppression of central drive, induced by the combination of inspiratory loading and hypoxemia, may be important.
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PMID:The mechanism of respiratory arrest in inspiratory loading and hypoxemia. 232 56

Hypoxia and hypercapnic acidosis have been shown to have a negative inotropic effect on diaphragmatic contractility. The effect of combined hypercapnia and hypoxia was studied in vitro using hamster diaphragm strips. A 12% CO2, 21% O2, and 67% N2 gas mixture was used to produce hypoxic, hypercapnic acidosis. Force-frequency curves were generated using twitches and maximal tetanic contractions produced by stimulating with 0.2-ms pulses at 10 to 120 Hz for 300 to 500 ms. Moderate fatigue was then induced by repeated submaximal contractions (25 Hz, 160 ms, at the rate of 1/s for 45 contractions). Muscle strips exposed to hypoxic, hypercapnic acidosis had a decreased force response at all frequencies. The decrease in force was not different from that seen with hypoxia alone but was significantly worse than with hypercapnia alone. In the combined hypercapnic, hypoxia solution, tension produced by stimulating at 25 Hz for 160 ms was decreased to 52 +/- 11% of control (p less than 0.001). For these submaximal contractions, hypercapnic acidosis had a greater negative inotropic effect than did hypoxia alone. With repeated contractions, tension declined at a faster rate than in control, hypoxia alone, or hypercapnia alone. In the combined hypoxic, hypercapnic solution, the time constant of relaxation (tau) was increased prior to the start of the fatigue run compared to the control (tau = 35 +/- 6 versus 45 +/- 5 ms; p less than 0.001), and the tau increased at a faster rate than in control. These studies suggest that hypoxic, hypercapnic acidosis has a greater detrimental effect on the muscle than either abnormality alone and makes the muscle more susceptible to fatigue.
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PMID:Hypoxic, hypercapnic acidosis decreases tension and increases fatigue in hamster diaphragm muscle in vitro. 265 1

The presence of a peripheral myopathy in hypothyroidism has been well recognized. Involvement of the diaphragm has been suggested recently but the clinical spectrum never clearly defined. We studied three patients with hypothyroidism presenting with fatigue, dyspnea, exercise limitation, and in two, chronic alveolar hypoventilation (PaCO2 of 51 and 75 mm Hg) before and after thyroid hormone replacement. In all patients diaphragmatic strength as determined by the maximal transdiaphragmatic pressure was low (2, 13, and 64 cm H2O) and improved with therapy (86, 84, and 90 cm H2O). Similarly, all patients manifested a fatiguing breathing pattern, as determined by the diaphragmatic tension time index. These values (0.22, 0.55, and 0.36) decreased after hormone replacement (0.16, 0.20, and 0.15). These changes were associated with the correction of hypercarbia in the two patients with hypoventilation and an improvement in lung volumes and exercise endurance in all patients. This study confirms that in patients with hypothyroidism diaphragmatic dysfunction occurs more frequently than has been suspected and might be of varying severity. This dysfunction reverses with adequate hormone replacement.
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PMID:Hypothyroidism. A reversible cause of diaphragmatic dysfunction. 280 37


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