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

Quadriceps femoris muscle needle biopsies were performed in ten patients with chronic obstructive pulmonary disease and acute respiratory failure and in ten age- and sex-matched healthy control subjects. The main indices of skeletal muscle cell energy metabolism, intracellular acid-base equilibrium and lactate metabolism were evaluated. Reduced ATP and phosphocreatine content, intracellular acidosis related to hypercapnia, increased muscle lactate without alterations of the muscle lactate concentration gradient were observed in the skeletal muscle of the hypercapnic-hypoxemic COPD patients studied, in which group no correlation was found between hypoxia and energy or lactate metabolism parameters. These results suggest that an overall derangement of cell energy metabolism and acid-base equilibrium is present in severely hypercapnic-hypoxemic chronic obstructive pulmonary disease and that in this condition skeletal muscle seems to metabolize anaerobically-even though, in addition to hypoxia, other factors interfering with both cell energy and lactate metabolism are likely to be present.
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PMID:Skeletal muscle energetics, acid-base equilibrium and lactate metabolism in patients with severe hypercapnia and hypoxemia. 366 4

Although abnormal blood gases are unusual in status asthmaticus, hypercapnia indicates a considerable increase in bronchial resistance. The authors report their experience of 106 personal cases of acute severe asthma. Emergency management of acute respiratory failure consisted in symptomatic therapy (low rate oxygen or mechanical ventilation after nasal intubation). Corticosteroids, rehydration, antibiotics and beta-2 adrenergic agents were associated. Mechanical ventilation was necessary in patients who developed alterations of consciousness or PaCO2 above 60 mm Hg (8 kPa). In respirator-patients, sedative drugs were needed. Terbutaline and salbutamol were occasionally beneficial but epinephrine remains the drug of choice. In our series of 106 cases (79 with hypercapnia) the overall mortality was 3.8 p. 100. Of the 33 cases who underwent mechanical ventilation, there were 4 deaths (12 p. 100). A review of the literature showed a much higher mortality in other series.
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PMID:[Treatment of severe acute asthma in adults]. 370 59

We studied eleven patients during 14 attempts at weaning from mechanical ventilation to determine whether central ventilatory drive, measured as airway occlusion pressure 0.1 s after onset of inspiration (P 0.1), during spontaneous breathing before and during a brief hypercapnic challenge, could accurately predict the success or failure of the attempt. All patients were recovering from acute respiratory failure and could breathe spontaneously for 20 minutes on a T-piece but were judged clinically to be marginal weaning candidates. Minute ventilation (VI) and P 0.1 were measured while breathing spontaneously and were repeated during a hypercapnic challenge that raised end-tidal PCO2 approximately 10 mm Hg. Seven of the 14 weaning attempts were unsuccessful, requiring reinstitution of mechanical ventilation. Although the failure group had lower mean maximum inspiratory force and higher spontaneous respiratory rate, no threshold value separated the failure from the success group. Ventilation increased more during hypercapnic challenge in those patients whose weaning attempt was successful, but overlap of results between the two groups rendered this test inaccurate for predicting weaning success. In contrast, successfully weaned patients had greater augmentation of P 0.1 during hypercapnia, expressed as the ratio of P 0.1 during CO2-stimulated to P 0.1 during baseline values, than did those who failed weaning (p less than 0.005). This ratio succeeded, and was thus both specific and sensitive as a predictor of successful weaning from mechanical ventilation in these patients.
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PMID:Prediction of successful ventilator weaning using airway occlusion pressure and hypercapnic challenge. 382 40

Blood gas measurements obtained during 35 episodes of acute, severe asthma in 19 children were analysed. Arterial carbon dioxide tension (PaCO2) was mean (SD) 5.7 (1.2) kPa and the arterial oxygen tension (PaO2) was 7.7 (1.1)kPa. Hypoxaemia was severe (PaO2 less than or equal to 7.9 kPa) on 19 occasions, was present alone (type I) on eight of these, and was associated with hypercapnia (type II) on 11. The PaO2 was similar in both the type I and type II subgroups, but PaCO2 was significantly higher in the type II and the alveolar-arterial oxygen tension difference was significantly higher in the type I subgroup. Classification of acute respiratory failure into these two types proved useful in understanding the pathophysiology of acute, severe asthma. Type I failure, conventionally regarded as a precursor of type II, itself caused severe, critical hypoxaemia.
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PMID:Pathophysiological analysis of hypoxaemia during acute severe asthma. 392 52

Acute respiratory failure is a common life-threatening process with myriad causes. It is characterized by a failure of oxygenation or ventilation, or both. Hypoxemia is common to all causes of respiratory failure, whereas PaCO2 may be normal, decreased, or elevated. These abnormalities result from several pathophysiologic processes, including intrapulmonary venoarterial shunt, alveolar hypoventilation, diffusion impairment, and ventilation-perfusion mismatch. Type I failure results from processes that lead to hypocapnia or normocapnia; type II failure is distinguished by the presence of hypercapnia. The clinical manifestations of acute respiratory failure are nonspecific; for this reason, a high index of suspicion and early examination of arterial blood gases are essential to successful management.
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PMID:Acute respiratory failure. Pathophysiology, causes, and clinical manifestations. 394 15

This study describes the case of a 58 year old man who presented with an episode of acute respiratory failure and right heart decompensation. After recovery from the acute illness, hypoxaemia, hypercapnia and pulmonary arterial hypertension remained, the causes of which were not known. There was no airway obstruction, only a moderate restrictive ventilatory defect, a little weight increase and a unilateral diaphragmatic paralysis. Obstructive sleep apnoea was finally suspected and confirmed by sleep recording. The obstructive sleep apnoea probably explained the respiratory insufficiency and the pulmonary hypertension. Loss of weight was associated with the disappearance of hypercapnia and pulmonary hypertension. As a result of this study, the value of sleep recording is emphasized. When respiratory failure or pulmonary hypertension seem unexplained, think of obstructive sleep apnoea.
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PMID:[Value of sleep polygraph examination in the etiological diagnosis of apparently inexplicable respiratory insufficiency]. 404 63

Six patients with acute carbon dioxide narcosis following nebulised salbutamol therapy were described. They had chronic obstructive airflow disease and were admitted in acute respiratory failure. The patients were treated with aerosolized salbutamol delivered from oxygen powered nebulizers. They developed severe acute hypercapnia. Five of the six patients died. The hazards of indiscriminate oxygen use in this clinical situation was discussed.
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PMID:Acute carbon dioxide narcosis during inhalational therapy with oxygen powered nebulizers in patients with chronic airflow limitation. 407 10

The effect of profound hypercapnia on acute hypoxic respiratory failure is evaluated. Eight dogs were subjected to oleic acid-induced acute respiratory failure. Four dogs were ventilated normally, and four dogs were made hypercapneic by rebreathing exhaled CO2. In the hypercapneic animals, heart rate and alveolar-arterial oxygen difference were significantly lower than in normocapneic animals, while mixed venous O2 cardiac index, oxygen delivery index, stroke volume index, and left ventricular stroke work were significantly higher. Mean arterial pressure was maintained at preinjury levels. Pulmonary and systemic vascular resistance increased in both experimental groups. There was no significant difference between groups for gravimetric determination of lung water. Cardiopulmonary performance in acute respiratory failure is improved with hypercapnia. This may be related to CO2-induced catecholamine release.
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PMID:The hemodynamic effect of profound hypercapnia on acute hypoxic respiratory failure. 665 77

A study on two groups of patients in acute respiratory failure with hypercapnia (18 subjects) and in hypercapnic coma (18 subjects) has been carried out to determine the related changes in sodium ion, potassium ion, chloride ion, urea and osmolality in blood and cerebrospinal fluid. There were significant differences between the two pathological states and particularly in coma, changes in transmembrane active transport of electrolytes are significantly related to high concentrations of CO2 in the brain.
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PMID:Changes in plasma and cerebrospinal fluid electrolytes in hypercapnia. 678 28

Acute respiratory failure developed in three patients needing ventilatory support within hours after total parenteral nutrition was started. We postulate that the high carbohydrate load provided in the parenteral solution resulted in the use of glucose as the primary energy source, with the development of substantial increases in the carbon dioxide production and the respiratory quotient. Because these patients had a relatively fixed ventilatory response, hypercapnia ensued. Excessive carbohydrate loading may precipitate respiratory acidosis in patients unable to adequately improve their alveolar ventilation when compensating for increased carbon dioxide production.
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PMID:Respiratory failure precipitated by high carbohydrate loads. 679 9


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