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

Acute respiratory failure can be diagnosed using clinical judgment and simple bedside measurement of physiologic function. Respiratory support is based on the pathophysiology of the disorder. Initial therapy is directed at correcting life-threatening hypercapnia, hypoxia, and acidosis. The final outcome is positively influenced by skillful intensive care and a team approach.
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PMID:Acute respiratory failure: an approach to diagnosis and management. 25 27

A survey has been conducted among French chest physicians and physicians involved in intensive care. 296 physicians have prescribed IPPB at home to 3 778 patients with chronic respiratory insufficiency between 1960 and 1977. Acute respiratory failure was the first criteria considered in the indications (57% of the patients); hypercapnia, hypoxemia and right heart failure episode frequency were the other criteria of severity the most often taken into account. Since 1960, the indications among those with airflow obstruction have decreased, whereas they have increased for those with restrictive insufficiencies, expressing the questions raised about the efficacy of IPPB in these two types. 18% of the patients have had IPPB through tracheostomy canula. 70% of the patients have used a pressure cycling respirator and 30% a volume or flow cycling respiratory. This second type was quite always used in the case of IPPB through canula. Oxygen was added for half of the patients. The physicians have regularly followed the patients. Great importance was accorded to home care surveillance.
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PMID:[IPPB therapy at home in chronic respiratory insufficiency in France. II. Indications. Technics and surveillance (author's transl)]. 39 55

The bronchodilator effects of aminophylline have been well documented but its effect on ventilatory drives has not been systematically evaluated. Accordingly, the ventilatory responses to hypoxia and to hypercapnia were measured before and after the intravenous administration of 5 mg of aminophylline per kg of body weight to 6 normal subjects. Hypoxic ventilatory response, as measured by an index of the relation between ventilation and hypoxia (parameter A) increased from a mean +/- SE control value of 146 +/- 25 to 254 +/- 35 75 min after the infusion (P less than 0.05). Significant increases in A were also noticed immediately after and 35 and 50 min after the aminophylline infusion. Oxygen consumption increased from a control value of 235 +/- 21 to 263 +/- 21 ml per min STPD (P less than 0.03), and CO2 production increased from 184 +/- 12 to 202 +/- 13 ml per min STPD (P less than 0.01) after aminophylline. Hypercapnic ventilatory response, measured as the slope of the ventilatory response to hypercapnia, was not altered after the aminophylline. Thus, in addition to bronchodilation, the augmentation of the ventilatory response to hypoxia may be a useful factor when this drug is used in acute respiratory failure secondary to airway obstruction.
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PMID:Effect of aminophylline on ventilatory responses in normal man. 61 22

24 subjects with chronic obstructive pulmonary disease were investigated in the course of acute respiratory failure defined by hypoxaemia, hypercapnia and respiratory acidosis. Haemodynamic data of right heart catheterization and coagulation tests were particularly studied. 12 of these subjects had right heart failure defined by a rise of right ventricular end-diastolic pressure above 10 Torr. Coagulation tests brought evidence of consumption coagulopathy in 8 patients, 7 of whom had right heart failure. Data suggest a significant correlation between right heart failure and coagulation disorders in patients with acute exacerbation of chronic obstructive pulmonary disease. These disturbances, accompanied by reduction of pulmonary vascular area, could be in part related to the presence of microthrombi in pulmonary arterial vessels.
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PMID:[Haemodynamic data, blood gas measurements and coagulation disorders in acute respiratory failure of patients with chronic lung disease (author's transl)]. 67 57

Controlled oxygen therapy may aggravate carbon dioxide retention during acute exacerbations of chronic obstructive pulmonary disease (COPD). Of 50 consecutive patients with COPD and acute respiratory failure, 13 required intubation because of carbon dioxide narcosis. With discriminant analysis of their arterial oxygen tension (PaO2) and pH on admission, a diagram separated patients into those at high risk and those at low risk for carbon dioxide narcosis. This diagram was then used to predict carbon dioxide narcosis in 73 patients with COPD and acute respiratory failure who were treated with controlled oxygen. In 16 of these patients carbon dioxide narcosis developed. Thirteen (81 per cent) were predicted by the diagram to be at high risk for this complication. Only two (4 per cent) patients judged by the diagram to be at low risk for carbon dioxide narcosis required mechanical ventilation. Utilizing an oxygen tension (PO2), carbon dioxide tension (PCO2) diagram a patient's ventilatory response was compared to that of ambulatory patients with COPD. These data suggest that hypoxemia and acidosis are more discriminatory for "carbon dioxide narcosis" than hypercapnia.
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PMID:Controlled oxygen administration in acute respiratory failure in chronic obstructive pulmonary disease: a reappraisal. 74 28

Thirty-two patients were evaluated within 24 hours of admission for 36 episodes of acute respiratory failure (arterial oxygen pressure less than or equal to 50 mm Hg). Clinical data, spirometric determinations, blood gas analysis, and synchronization of chest (rib cage) and abdominal (diaphragmatic) breathing movements were studied. All patients were initially treated with controlled oxygen therapy. In 25 episodes the patients recovered without intubation (successes). In nine episodes the patients required intubation and assisted ventilation; two of these patients died. Two patients died without intubation. The 25 successful episodes were compared with the 11 requiring intubation or associated with death (failures). The breathing pattern proved to be the best single factor for predicting success or failure (77 percent correct prediction). The breathing pattern plus the arterial carbon dioxide tension on admission was the best two-factor guide (86 percent correct prediction). Patients with asynchronous breathing and severe hypercapnia are so unlikely to do well with a program of controlled oxygen therapy that preparations for intubation and assisted ventilation should be made on admission and such measures should be instituted at the first sign of deterioration.
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PMID:Prospective study of controlled oxygen therapy. Poor prognosis of patients with asynchronous breathing. 85 43

1. The concentration of metabolites in intercostal and quadriceps muscle, and pulmonary function, were studied in twelve patients with chronic obstructive lung disease and acute respiratory failure before, during and after standardized treatment at an intensive care unit. The findings were compared with those obtained in hospitalized patients of comparable age with non-pulmonary diseases. 2. On admission, when the patients had marked hypoxaemia, hypercapnia and acidosis, the concentrations of ATP and creatine phosphate were low in both intercostal and quadriceps muscle, particularly the latter. The lactate concentration was increased in relation to control values but glycogen did not differ significantly. 3. In response to therapy, the Pa,CO2 and the patient's acidosis decreased, the vital capacity increased and lung mechanics improved along with the clinical condition. At the same time there were significant increases in the concentrations of ATP, creatine phosphate and glycogen in intercostal and quadriceps muscles, to values similar to, and for glycogen in excess of, those found in control subjects. Lactate concentration fell significantly during treatment. 4. In view of the low initial muscle concentrations of ATP and creatine phosphate in the patients, it is suggested that dysfunction of the respiratory muscles may be an important component of respiratory failure. Moreover, the concentration of energy-rich compounds in muscle rose significantly as the patients responded to treatment, which emphasizes the importance of adequate nutritional therapy in this disorder.
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PMID:Muscle metabolism in patients with chronic obstructive lung disease and acute respiratory failure. 86 35

Adrenocortical function and plasma growth hormone pattern were investigated in 15 patients with chronic obstructive lung disease, in a period of acute respiratory failure and again after recovery. During the acute period, secretion rate and plasma concentrations of cortisol were markedly enhanced; urinary excretion of cortisol metabolites was only slightly increased, suggesting an alteration of the catabolism of cortisol under these conditions; adrenocortical sensitivity to corticotropin and capacity of maximal adrenal secretion were normal. The increase of cortisol secretion was probably due to hypoxemia and/or hypercapnia acting through the hypothalamo-pituitary axis. During the chronic phase of respiratory insufficiency, adrenocortical secretion and responsiveness were within the normal range. Finally, respiratory failure did not stimulate the secretion of growth hormone.
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PMID:Adrenocortical and somatotrophic secretions in acute and chronic respiratory insufficiency. 114 86

A 21-year old women with rhizomelic muscular deficit and signs of hypercapnia developed acute respiratory failure. Laboratory tests revealed high creatine kinase activity, and electromyograms showed myogenic patterns with a few myotonic discharges. Biopsy of the quadriceps muscle elicited major vacuolar myopathy with glycogen overload. Acid maltase activity was undetectable in muscular tissue. After 7 months on high-protein diet (1540 calories, 37% proteins) there was no clinical or biochemical improvement. The other published cases of acid maltase deficiency treated with high-protein diet are discussed.
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PMID:[Myopathy in adults caused by acid maltase deficiency. A trial of treatment with high protein diet]. 141 Aug 90

Respiratory muscle fatigue is induced experimentally by adding high external resistances to breathing. The role played by respiratory muscle fatigue in exercise limitation and in acute respiratory failure is still unclear. The electromyogram often reflects contractions beyond the fatigue threshold, but overt force failure has been only rarely demonstrated under these circumstances. Hypercapnic ventilatory failure may possibly not result from fatigue, but rather from an adaptation of the respiratory system for avoiding fatigue. The treatment of fatigue comprises respiratory muscle support by adequate nutrition and oxygen delivery, and if needed respiratory muscle rest by mechanical ventilation.
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PMID:[Fatigue of the respiratory muscles]. 154 80


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