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

Marked variability in resting steady-state arterial PCO2 (PaCO2) values are observed among patients with chronic obstructive pulmonary disease (COPD), independent of severity of their obstructive airways defect. The reasons for the development of hypercapnia in some but not in the others remain unclear. One hypothesis states that the level of morbid resting PaCO2 may be related to the premorbid hypercapnic ventilatory response (HCVR); accordingly, subjects who were relatively insensitive to CO2 breathing (low responders) develop CO2 retention in the face of lung disease. The present study investigated this hypothesis in the hamster model of elastase-induced emphysema. After obtaining steady-state HCVR in 19 unanesthetized unrestrained hamsters, emphysema was induced by intratracheal instillation of pancreatic elastase. Forty-five days later, minute ventilation and PaCO2 measurements were done, and lung function tests were obtained. The slopes of HCVR and morbid PaCO2 values varied from -0.09 to 2.36 ml/min/mmHg inspired PCO2 and 48.7 to 63.1 mmHg, respectively. There were no significant correlations between morbid PaCO2 values and premorbid HCVR or lung function test abnormalities caused by emphysema. These animal model studies do not support the hypothesis that the level of PaCO2 in patients with COPD is related to their premorbid HCVR.
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PMID:Premorbid ventilatory response to hypercapnia is not related to resting arterial carbon dioxide tension in hamsters with elastase-induced emphysema. 393 90

The value and risk of transbronchial biopsy (TBB) was assessed in 15 cases requiring mechanical ventilation for progressive pulmonary infiltrates. TBB was diagnostic in five patients, and in two additional cases a diagnosis was made from the accompanying bronchial secretions. TBB results significantly altered the therapeutic management in seven cases. The alveolar-arterial gradient P(A-a)O2, widened by a mean of 110 mm Hg in nine patients; however, this change was transient and clinically insignificant. Three instances of reversible hypercapnia (mean of 15 mm Hg) occurred. Complications included self-limited bleeding in three cases and one tension pneumothorax. No fatalities were attributable to TBB. In these hemodynamically stable patients requiring mechanical ventilation for diffuse lung disease, TBB was performed safely and provided important data.
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PMID:Transbronchial biopsy during mechanical ventilation. 394 76

To assess clinical significance of breath-by-breath variation of tidal volume and its distribution pattern displayed as a histogram, continuous measurement of tidal volume was made with electrical impedance pneumography for about 60 minutes. Subjects were composed of 26 normal male and 46 patients including 17 patients with restrictive lung disease and 29 patients with obstructive lung disease. To evaluate variation of tidal volume quantitatively, coefficient of variance (C.V.) was used. In comparison to the normal pattern of distribution (C.V. = 26.0 +/- 7.5%, mean +/- S.D.), patients with restrictive lung disease showed extremely narrow pattern of the distribution and significantly smaller C.V. (17.5 +/- 4.6% in old pulmonary tuberculosis, P less than 0.005 and 18.9 +/- 9.3% in pneumonitis, P less than 0.025). Whereas, patients with obstructive lung disease showed widespread pattern of the distribution and significantly greater C.V. (43.2 +/- 13.0% in pulmonary emphysema with hypercapnia, 33.0 +/- 7.5% in normocapnia and 35.8 +/- 9.4% in asthmatic attack, P less than 0.005). In all the patients with bronchial asthma after the treatment, the extremely widespread pattern of histogram was returned toward the normal one and the C.V. was decreased (22.4 +/- 6.4%). It was suggested that the distribution pattern of tidal volume was affected by the change of clinical condition, and was well correlated to the pathophysiological process related to restrictive or obstructive lung disease. We conclude that analysis of tidal volume distribution by the histogram is one of the useful approach to manage patients with respiratory diseases.
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PMID:Variability of breath-by-breath tidal volume and its characteristics in normal and diseased subjects. Ventilatory monitoring with electrical impedance pneumography. 402 Dec 11

From January 1983 to September 1984 our neonatal ICU (NICU) treated eight endotracheally intubated infants who had suspected airway obstruction characterized by hypercarbia dissonant with severity of lung disease and difficulty in ventilation with lack of chest movement, both on conventional intermittent mandatory ventilation and high-frequency oscillation. Bronchoscopic removal of necrotic tissue was possible in six infants, two of whom survived. Bronchoscopy showed desquamation of epithelial surfaces, leaving encrusted exudations considered to be characteristic of necrotizing tracheobronchitis (NTB). The four nonsurvivors of bronchoscopy and one of the infants not submitted to bronchoscopy had NTB confirmed at autopsy. NTB was not associated with any specific lung disease, humidifier, or ventilator. The autopsy frequency of NTB during this period was 5 per 160 NICU admissions. A separate chart review of unselected autopsied cases in 1981 and 1982 showed that 12 of 284 neonates admitted to the NICU had NTB. NTB appears to be a rediscovered condition related to endotracheal intubation and mechanical ventilation using high mean airway pressures.
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PMID:Diagnosis and therapy of necrotizing tracheobronchitis in ventilated neonates. 402 49

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

Ventilatory responses to carbon dioxide (Sco2) were measured in 15 asymptomatic asthmatic patients in whom CO2 retention had been documented during a previous attack of acute asthma. At the time when Sco2 was measured, the patients had normal or only mildly impaired ventilatory function (vital capacity (VC) 3,5 +/- 0,19 I, 98,7 +/- 4% of predicted (mean +/- SE); forced expiratory volume in 1 second (FEV1) 2,37 +/- 0,161, 83,8 +/- 5,2% of predicted; and FEV1/VC 68 +/- 2,5%). Fifteen control subjects without lung disease were also studied (VC 4,38 +/- 0,28 I, 103 +/- 2,6% of predicted; FEV1 3,76 +/- 0,23 I, 112 +/- 4,4% of predicted; FEV1/VC 86 +/- 7,8%). Sco2 in the patients (1,21 +/- 0,14 l/min/mmHg, range 0,62 - 2,81) was significantly different (P less than 0,001) from that in controls (2,13 +/- 0,17 l/min/mmHg, range 1,13 - 3,17). Sco2 in a subgroup of 5 patients with normal pulmonary function was also significantly different from that in controls. Correction for lung size (Sco2/VC) did not detract from the significance of the difference between patients and controls, suggesting that inherently low respiratory centre sensitivities to CO2 may have played a role in the development of hypercapnia during severe asthma in these patients.
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PMID:Ventilatory responses to carbon dioxide in asthmatics with previous carbon dioxide retention during severe asthma. 640 23

We studied 53 patients with proximal myopathy to determine at what level of muscle weakness hypercapnic respiratory failure is likely, and which tests of pulmonary function or respiratory muscle strength would best suggest this development. Respiratory muscle strength was determined from maximal static efforts and in half the patients, both inspiratory and expiratory muscle strengths were less than 50% of normal. In the 37 patients without lung disease respiratory muscle weakness was accompanied by significant decreases in vital capacity, total lung capacity, and maximum voluntary ventilation; by significant increases in residual volume and arterial carbon dioxide tension (PaCO2); and greater likelihood of dependence on ventilators, atelectasis, and pneumonia. Hypercapnia was particularly likely when respiratory muscle strength was less than 30% of normal in uncomplicated myopathy, and when vital capacity was less than 55% of the predicted value in any patient.
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PMID:Respiratory muscle and pulmonary function in polymyositis and other proximal myopathies. 641 85

Rats were subjected to chronic hypoxia (10% O2) or hypoxia and hypercapnia (10% O2 + 4% CO2) for 3-4 weeks and their carotid bodies (twenty-three from twenty rats) were compared with those of litter-mate controls. Both chronic exposures, which simulated high altitude or chronic lung disease, caused a 4-10-fold increase in carotid body volume. The larger increases were attributed to higher fixation-perfusion pressures. The organs were fixed by perfusion with glutaraldehyde. Semi-thin (1 micron) sections for light microscopy and ultra-thin sections for electron microscopy were cut at regular intervals and were examined by stereological techniques to determine the nature of the enlargement. The proportion occupied by blood vessels was much increased in both chronic hypoxia and hypoxia plus hypercapnia; the endothelium appeared stretched with conspicuous fenestrations. There were increased numbers of endothelial cells which suggested new growth as well as stretching of endothelium and the mean transectional area of the vessels was increased. The mean surface area of blood vessels per unit area of carotid body was unaltered but the total surface area of blood vessels in the whole carotid body was greatly increased. Both the Type 1 cell nucleus and cytoplasm were increased in size. The proportion nucleus/cytoplasm was unaltered in hypoxia but reduced in hypoxia plus hypercapnia. There were fewer Type 1 cell nuclei per unit area but the estimated total number of Type 1 cell nuclei per carotid body was increased 2-4-fold; this was interpreted as Type 1 cell hyperplasia. Some of the dense-cored vesicles in Type 1 cells were enlarged with eccentric dense cores but their number per unit area of cytoplasm was decreased. Their mean size was not significantly altered. However, the total number of vesicles per carotid body was presumed to be increased because their decreased density in the cell was offset by a greater increase in total Type 1 cell volume. The harmonic and arithmetic mean distances between endothelium and the boundary of glomus tissue were significantly reduced. The harmonic mean distance is an indication of the diffusion distance for gases to and from blood and glomus tissue. The arithmetic mean distance is a measure of the amount of tissue in between. The significance of the vascular enlargement and hyperplasia and the Type 1 cell hyperplasia cannot be assessed at present. We do not know if enlargement is associated with the same, greater, or lesser activity of the organ for a given stimulus.
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PMID:The enlarged carotid body of the chronically hypoxic and chronically hypoxic and hypercapnic rat: a morphometric analysis. 672 19

Hypoxemia, hypercarbia, and cor pulmonale ultimately occur in most patients with chronic lung disease. Although oxygen therapy may reduce or delay the development of pulmonary hypertension and myocardial failure in these patients, its use is thought to lead to CO2 narcosis and apnea. The effect of O2 administration during sleep has been examined in 12 patients (seven with cystic fibrosis, three with bronchopulmonary dysplasia, one with bronchiolitis obliterans, and one with severe hypersensitivity pneumonitis) using skin surface O2 (Roche) and CO2 (Radiometer) electrodes. Both electrodes were calibrated over wet gas and applied at 44 C. Ten patients had chronic hypercarbia (PaCO2 62 +/- 19 torr; range 46 to 103 torr) when awake. Humidified oxygen was administered by nasal cannula, Venturi mask, or head hood. Oxygen flow was increased every 20 minutes from 80 minutes or until the patient awoke. In eight of ten patients with hypercarbia and in the two normocarbic patients, skin surface carbon dioxide tension (PsCO2) increased by 10% or less as the skin surface oxygen tension (PsO2) was increased. In the remaining two patients with hypercarbia (both had cystic fibrosis) PsCO2 increased 18% and 24% as PsO2 was increased. These last two patients with depressed responsiveness to CO2 could not be separated from the other patients by clinical or laboratory criteria. It is concluded that the skin surface blood gas tensions are a simple and reproducible method for adjusting oxygen therapy in patients with chronic lung disease, and although the response to oxygen varies from patient to patient, most patients with chronic hypercarbia retain their central responsiveness to CO2 during sleep and for them O2 therapy is probably safe.
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PMID:Effect of oxygen administration during sleep on skin surface oxygen and carbon dioxide tensions in patients with chronic lung disease. 678 98

During an 18-month period, 11 preterm infants with birthweights between 700 and 1560 g (mean 1.2 kg) developed excessive tracheobronchial secretions during intensive care. No single obstetric factor was incriminated. Copious, viscous, tracheobronchial secretions were noted at about 5 days during mechanical ventilation via endotracheal tube causing recurrent segmental collapse, hypoxia, and hypercapnia (median peak PCO2 13.5 kPa). All infants were treated with frequent bronchial lavages and continued intermittent positive pressure ventilation, together with high concentrations of oxygen. No infant died, but morbidity was high. Tracheostomy was performed on 2 infants (one at age 3 months, because of severe croup) and 2 others had clinical or physiological evidence of upper airways narrowing. Follow-up studies showed that this group had more problems of airways obstruction throughout the first year of life as well as increased lung stiffness. The hypersecretion group showed a higher incidence of chronic lung disease. Likely aetiological factors were sought. Contamination of the mechanical ventilation equipment by detergent and activated glutaraldehyde was found; this could have been a contributory factor.
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PMID:Bronchial hypersecretion in preterm neonates. 706 6


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