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

To determine the clinical features and outcome of patients with hypercapnia from acute asthma, we examined 229 (62 men, 167 women) consecutive episodes of acute asthma over a 6-yr period. Sixty-one episodes were associated with hypercapnia at presentation (PaCO2 greater than 38 mm Hg). Men more commonly presented with hypercapnia: 31 of 62 (50%) men with acute asthma had hypercapnia compared with only 30 of 167 (18%) women (p less than 0.001). Patients with hypercapnia had a longer duration of chronic asthma and were more likely to be steroid-dependent. Hypercapnic patients had greater airway obstruction, respiratory rate, and pulsus paradoxus than did nonhypercapnic patients. Findings of a quiet chest on auscultation, inability to talk, and cyanosis also suggested the presence of hypercapnia. Five hypercapnic patients required mechanical ventilation, but hypercapnia did not prolong hospitalization. In nonventilated patients, hypercapnia resolved in a mean time of 5.9 h; 50% of hypercapnic episodes resolved by 4 h, and all resolved by 16 h. No patient presenting with normocapnia progressed to hypercapnia with therapy, and there were no deaths in either the hypercapnic group or the nonhypercapnic group. In patients with more than one admission, the PaCO2 of one episode correlated with the PaCO2 on a subsequent admission, suggesting a role for individual variation in ventilatory control. With appropriate medical therapy, most patients with hypercapnia from acute asthma have rapid reversibility, and mechanical ventilation usually can be avoided. However, these patients require close inhospital observation until it is certain that the acute asthmatic episode has resolved.
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PMID:Clinical features and outcome in patients with acute asthma presenting with hypercapnia. 320 9

The optimal management of asthma during pregnancy and lactation requires a cooperative approach between the physician managing asthma, the obstetrician-gynecologist, and the patient. Goals of therapy include: 1) avoidance of repeated episodes of asthma, 2) avoidance of emergency room visits, 3) avoidance of status asthmaticus, 4) prevention of death in the mother, 5) use of minimal medications in the gravida, and 6) avoidance of maternal medication use with uncertain or deleterious effects on the fetus. Because acute severe asthma may have it onset during pregnancy, the physician must be prepared to diagnose and treat the gravida to avoid or reduce episodes of maternal hypoxemia, hypocarbia or hypercarbia. Status asthmaticus has been associated with maternal and fetal deaths as well as intrauterine growth retardation. Although it is logical to assume that prevention of repeated episodes of asthma would be associated with a more favorable outcome in pregnancy, only recently was this actually documented. The purpose of this manuscript is to review issues in diagnosis and management of asthma during pregnancy and lactation.
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PMID:The management of asthma during pregnancy and lactation. 331 23

In three consecutive patients suffering from life-threatening asthma in a comatose state (mean age: 37 +/- 4 yr; Glasgow coma score: 3; bilateral mydriasis), intracranial pressure was monitored with an extradural transducer set-up a mean of 2 h after the onset of the coma. The aims were to detect intracranial hypertension and to improve its therapy. Basal therapy associated: 1) mechanical ventilation; 2) theophylline 1.5 g X 24 h-1, salbutamol 30 mg X 24 h-1, hydrocortisone 2 g X 24 h-1, pancuronium 0.5 mg X kg-1 X 24 h-1; 3) pentobarbitone 35 mg X kg-1 X 24 h-1, normal hydration, normothermia and 30 degrees head-up tilt. If the intracranial pressure rose above 15 mmHg, an i.v. bolus of pentobarbitone (5 mg X kg-1) was given if the barbiturate blood level was equal or below 100 micrograms X l-1. In case of failure, a dose of mannitol (20 mg) completed the therapy if blood therapy was equal or below 320 mosm X l-1. All patients developed intracranial hypertension (21, 53 and 23 mmHg, respectively). The intracranial hypertension followed the bronchospasm and disappeared with it. Hypoxaemia, hypercapnia and high peak airway pressures could explain the intracranial hypertension. All patients recovered without sequelae. This data should make us use with great care all treatments likely to increase the intracranial pressure during life-threatening asthma.
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PMID:[Intracranial hypertension during status asthmaticus]. 357 44

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

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

Hydropneumothorax is an uncommon but potentially fatal complication for a patient undergoing positive pressure ventilation. The case of a 23-year-old woman with severe asthma requiring lung lavage is described. Twenty minutes after an uneventful left lung lavage, the patient experienced increased peak airway pressure, decreased oxygen saturation and hypercarbia, despite ventilation with 90 per cent oxygen. A chest x-ray revealed mediastinal shift and a left sided pneumothorax. Drainage was carried out, revealing air and clear fluid in the pleural space. The importance of technical problems such as patient and endotracheal tube positioning, elimination of cross-spilling and cardiopulmonary effects of lavage are discussed.
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PMID:Hydropneumothorax--an unusual complication of lung lavage. 376 71

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

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

Studies of the arterial blood gas tensions and pH in 21 children during 24 acute attacks of asthma showed that all were hypoxic on admission to hospital, and in 10 there was evidence of carbon dioxide retention. Cyanosis, invariably present when the So(2) was below 85%, and restlessness in patients breathing air were the most reliable indices of the severity of hypoxia. There were no reliable clinical guides to the Pco(2) level. Conventional oxygen therapy in tents (25-40%) did not always relieve hypoxia, and in three cases the administration of oxygen at a concentration of 40% or over failed to produce a normal arterial oxygen tension. Uncontrolled oxygen therapy may aggravate respiratory acidosis, and three of our patients developed carbon dioxide narcosis while breathing oxygen. The necessity for blood gas measurements in the management of severe acute asthma in childhood is emphasized.
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PMID:Arterial blood gas tensions and pH in acute asthma in childhood. 566 2

Pretreatment and posttreatment arterial blood gas and pulmonary function testing measurements were prospectively compared as to their ability to assess asthma severity accurately and, thus, predict the outcome in 102 episodes of acute bronchial asthma initially seen in the emergency department. The Pao2, Paco2, or pH was unable to separate these patients requiring admission from those that could be confidently discharged, while the 1-s forced expiratory volume (FEV1) and peak expiratory flow rate (PEFR) did so both before and after treatment. Furthermore, virtually all patients with hypercarbia (Paco2 greater than 42 mm Hg) and/or severe hypoxemia (Pao2 less than 60 mm Hg) had a PEFR below 200 L/min, or an FEV1 below 1.0 L. Thus, selective use of arterial blood gas analysis should substantially decrease both diagnostic cost and patient discomfort without jeopardizing health care.
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PMID:Arterial blood gases and pulmonary function testing in acute bronchial asthma. Predicting patient outcomes. 640 19


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