Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is reported of acute respiratory failure occurring during upper abdominal surgery in a patient not previously known to have chronic respiratory failure. Preoperatively, this 68 year old patient presented with mild obesity, slight effort dyspnoea and paralysis of the right hemidiaphragm, a sequela of polytrauma she suffered the year before. Respiratory tests were not considered useful with regard to the results of clinical examination. Moreover, she had already several previous general anaesthetics without any problems. A thoracic epidural anaesthesia was performed with a mixture of 150 mg lidocaine, 37.5 mg bupivacaine with adrenaline and 100 micrograms fentanyl, injected in the T8-T9 epidural space via a catheter. Ten minutes after the starting of surgery, the patient became agitated and complained of difficulty in breathing. Blood gas analysis showed hypercapnia, with respiratory acidosis (Pao2: 28.19 kPa; Paco2: 9.2 kPa; pH 7.273). Clinical examination revealed a bilateral Horner syndrome (T1-T4 sympathetic blockade). The patient was intubated and ventilated after adequate sedation. She was extubated 3 h 30 min after the initial epidural injection. Epidural analgesia was maintained during 72 h, with 0.1% bupivacaine, with no recurrence of respiratory failure.
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PMID:[Transient acute respiratory failure and thoracic epidural anesthesia]. 273 73

In order to assess the mechanisms of gas exchange disturbances (i.e. to what extent shunting and diffusion impairment contribute to hypoxemia) in chronic obstructive pulmonary disease (COPD) and respiratory failure, ventilation-perfusion relationships (V/Q) by the multiple inert gas elimination technique were obtained in 16 patients with respiratory failure breakthrough. In 6 instances the study was repeated after long-term treatment with the aim to analyze V/Q changes after therapy. Initially, patients showed severe hypoxemia and hypercapnia and they presented signs of marked bronchoconstriction. A great dispersion of V and Q distribution was present as indicated by the marked increase of the second moment of V and Q distributions. Interestingly, few patients presented a unimodal distribution of both V and Q, whereas most-patients had bimodal distributions where the ventilation was distributed in a mode such that high V/Q areas were present between 10 and 100 of V/Q ratio and blood flow was displaced leftward or toward lower V/Q values. No correlations were found between V and Q distribution and clinical types A or B of COPD. Significant relationships were found between measured and calculated arterial PO2 (r = 0.90, p less than 0.001) and between measured PO2 and the sum of the fractional perfusion to regions with V/Q ratio less than 0.1, suggesting that V/Q inequality and shunting, instead of the impairment of diffusion equilibration, can account for all the hypoxemia. Finally, the reduced inhomogeneity of ventilation after treatment, especially in the fraction located in high V/Q regions is mostly related to some functional and reversible damages in COPD.
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PMID:[Changes in pulmonary gas exchange in chronic obstructive bronchopneumopathies and their modifications induced by therapy]. 273 33

Sarcoidosis very rarely progresses towards severe subacute respiratory failure. We report three observations of recent atypical cases of pulmonary sarcoidosis which were proven by open lung biopsy and developed severe diffuse pulmonary granulomatosis in a few weeks with an associated interstitial fibrosis. In these patients there were diffuse crepitant rales, a dramatic reduction in lung function of 30-60% of lung volumes and diffusion capacity accompanied by major hypoxemia (m +/- DS: 63.3 +/- 4.0 mmHg) without hypercapnia. Bronchoalveolar lavage showed an alveolar neutrophil leucocytosis (7.3 +/- 5.5%) without a lymphocytosis (4.3 +/- 11.5%). In the three cases under study, the clinical picture, the radiological and lung function studies, as well as the data from the bronchoalveolar lavage, were more suggestive of an acute diffuse interstitial fibrosis than of sarcoidosis.
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PMID:[Pulmonary sarcoidosis simulating primary acute interstitial fibrosis at presentation. Clinical, radiologic, functional and bronchoalveolar cytologic study in 3 cases]. 274 May 89

A previously unrecognized, striking movement disorder has been observed in 10 premature infants with severe bronchopulmonary dysplasia. Chronic hypoxemia, hypercarbia, bronchospasm, and inadequate nutrition were present in all. The movement disorder developed from approximately the third postnatal month. The dominant movements involve the limbs, neck, trunk, and oral-buccal-lingual structures. The limb movements were most prominent distally and consisted of rapid, random, jerky movements (similar to chorea) and "restless" movements (similar to akathisia). Similar movements of the neck and face were observed; tongue movements had a "darting" quality. The oral-buccal-lingual movements were similar to the dyskinesia of older patients. Movements were exacerbated during episodes of respiratory failure and attenuated during sleep. All infants exhibited feeding disorders, largely due to tongue movements. In 3 infants treated with clonazepam, there was striking improvement in motor function, including feeding. The natural history was partial or complete resolution or a static course. Thus, of the 7 surviving infants, the movements were absent (without therapy) at 15, 18, and 30 months of age. In the remaining 4 infants (3 of whom receive clonazepam), the movements, though attenuated, persisted at 6, 12, 15 and 21 months of age, respectively. Neuropathologically, 1 infant showed neuronal loss with astrocytosis in caudate, putamen, globus pallidus, and thalamus. These data defined a previously unrecognized extrapyramidal movement disorder of infants with severe bronchopulmonary dysplasia; pathogenesis may be related to chronic hypoxemia.
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PMID:Movement disorder of premature infants with severe bronchopulmonary dysplasia: a new syndrome. 237 Nov 10

Noninvasive face mask ventilation has been used successfully in patients with paralytic respiratory failure. This study evaluated whether noninvasive face mask ventilation can be used for patients with acute respiratory failure due to intrinsic lung disease. Six patients with hypercapnia and four with hypoxemic acute respiratory failure met clinical and objective criteria for mechanical ventilation, which was delivered with pressure control and pressure support via a tightly strapped, clear face mask. No patient terminated the study because of inability to deliver adequate ventilation or to improve oxygen exchange; three eventually required endotracheal intubation. The mask was generally well tolerated. All patients had a nasogastric tube placed on suction, and none vomited or aspirated. The mean duration of treatment was 33 h (range, 3 to 88). The physiologic response was considered similar to that which would have been achieved with conventionally delivered ventilation. Noninvasive face mask ventilation may have a role in managing respiratory failure.
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PMID:Noninvasive face mask ventilation in patients with acute respiratory failure. 292 16

In December 1986 a 30-month-old female child with morbid obesity and respiratory failure was admitted to the Izaak Walton Killam Hospital for Children in Halifax. The etiology of the obesity was found to be dietary in origin after ruling out genetic, neurological and metabolic causes. This patient exhibited somnolence and cyanosis in association with hypercapnia and right ventricular overload. Her respiratory failure in the presence of a normal upper airway required ventilatory support, first with nasal endotracheal intubation, and then, tracheotomy. Weight reduction normalized her capillary blood gases and her somnolence disappeared. Subglottic stenosis hampered removal of the tracheotomy tube until 9 months after admission. The pathogenesis and management of obese hypoventilation syndrome are reviewed by the authors.
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PMID:Obese hypoventilation syndrome of early childhood requiring ventilatory support. 306 Apr 36

It has been hypothesized that naloxone may alter the ventilation-perfusion relationship in patients with chronic obstructive pulmonary disease (COPD) with associated respiratory failure, through the release of hypoxic pulmonary vasoconstriction. To investigate the effects of naloxone on gas exchange, seven clinically stable patients with severe COPD (type B) (forced expiratory volume in one second/forced vital capacity (FEV1/FVC) 38.3 +/- 4.0%) with hypoxaemia and hypercapnia (PaO2 7.6 +/- 0.4 kPa; PaCO2 6.4 +/- 0.3; pH 7.37 +/- 0.02), aged 59.0 +/- 4.6 yr, were studied. Breathing patterns, haemodynamic and conventional and inert gas exchange measurements were made while breathing room air before, during and 60 min after i.v. naloxone infusion. Naloxone and catecholamine plasma levels were also determined. In three subjects (protocol A), measurements were made using increasing concentrations of naloxone (cumulative dose: 54 mg), while the remaining four patients were studied (protocol B) at a fixed concentration of naloxone (cumulative dose: 38 mg). Despite high levels of naloxone (up to 150 ng.ml-1), no significant differences from baseline were observed in any of the measurements, during or after infusion. It is concluded that i.v. naloxone given as described has no effects on pulmonary gas exchange in clinically stable COPD patients with chronic respiratory failure.
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PMID:Gas exchange response to naloxone in chronic obstructive pulmonary disease with hypercapnic respiratory failure. 311 49

Excessive rates of carbohydrate infusion during total parenteral nutrition (TPN) have been reported to cause hypercapnia leading to respiratory failure or inability to wean from a ventilator. This case history illustrates the hitherto unreported syndrome of cyclic hypercapnia resulting from high rates of carbohydrate infusion during peak TPN flow rates when TPN was provided in a cyclic fashion. The patient was given TPN daily over an 18 1/2-h period followed by 5 1/2 h without nutritional support. Elevated CO2 production, increased respiratory quotient, hypercapnia, and inability to wean from a ventilator occurred during peak cycle TPN flow rates. When the same carbohydrate load was infused continuously over a 24-h period, CO2 production, respiratory quotient and PaCO2 were reduced. The patient was then able to tolerate periods of unassisted ventilation.
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PMID:Total parenteral nutrition-induced cyclic hypercapnia. 313 Oct 69

Hypercapnia is common in chronic respiratory failure (IRCO), and may be further increased in a significant way by oxygen therapy, used for severe hypoxaemia in acute exacerbations. The determinants of PaCO2 are metabolic (hence importance of alkalosis) and ventilatory. In chronic airflow obstruction, CO2 production and ventilation are normal; thus the factor responsible for hypercapnia is essentially the fraction of total ventilation lost in the anatomical and alveolar (VD/VT ratio) dead space, whose effect on PaCO2 is all the more marked on account of the high starting point. From the time of administering pure oxygen hypercapnia is only weakly linked to changes in total ventilation (which, after a few minutes returns to its initial level) and only slightly to the correction of hypoxaemia and desaturation (Haldane effect). On the other hand, the ventilation-perfusion ratios are altered, as evidenced by increased VD/VT ratios. The exact mechanisms are ill understood, but one could consider the worsening venous admixture effect by the reduction of hypoxic vasoconstriction and micro-atelectasis in the poorly ventilated zones, as well as the rise in the anatomical dead space (broncho-dilatation) and alveolar dead space (redistribution of ventilation to poorly perfused zones). In comparison with standard ideas, the genesis of hypercapnia from oxygen therapy depends more on an AIR/BLOOD mis-match, than on the suppression of the hypoxic ventilatory stimulus.
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PMID:[Relationship between hypercapnia and hypoxemia in chronic obstructive respiratory insufficiency]. 314 Mar 17

During a seven-year interval, 78 children had documented episodes of respiratory failure from asthma, defined as arterial hypoxemia, hypercapnia, or use of mechanical ventilatory support or intravenous isoproterenol hydrochloride. During 407 patient-years of follow-up (5.2 years per patient), these 78 children had 227 episodes of respiratory failure (2.9 episodes per patient). Fifty-three patients (68%) have had two or more of such episodes. Second episodes usually followed the initial episodes within two years, but some were delayed for over six years. Seven of the 78 children died, and two others have incurred hypoxic brain damage, compared with two deaths among 2892 children with asthma--seen at this hospital during that interval--but without a documented previous episode of respiratory failure. We conclude that children whose asthma has caused even one episode of respiratory failure constitute a special group of asthmatic patients, members of which are at high risk for repeated episodes of respiratory failure and its catastrophic complications. This recognition allows special attention to be focused on them in designing both clinical and research strategies.
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PMID:Respiratory failure from asthma. A marker for children with high morbidity and mortality. 317 98


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