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

Direct assessment of tracheal circumference, which permits evaluation of constriction and dilatation in vivo, was made continuously in intact, pentobarbital-anesthetized, spontaneously breathing dogs. Immediate response to induction of hypercapnia included tracheal constriction and cessation of normal, vagus-dependent rhythmicity of airway tone. The characteristic constrictor response to acetylcholine was exaggerated significantly during hypercapnic acidosis and returned to normal when arterial pH, but not CSF pH, was corrected by NaHCO3 infusion. Epinephrine produced significant tracheal dilatation (infrequently followed by constriction) and isoproterenol produced only dilatation at normal pH. The catecholamine-induced dilatation was decreased significantly during hypercapnic acidosis, but improved after NaHCO3 infusion. Responses to acetylcholine and epinephrine were the the same as control during alkalemia, whereas the response to isoproterenol was unexplainedly diminished. Thus alkalemia may inhibit the action of isoproterenol; acidemia enhances parasympathomimetic constriction and reduces sympathomimetic dilatation; and correction of arterial pH returns these responses to normal, even if hypercapnia and CSF acidosis persist.
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PMID:Arterial pH, airway caliber and response to acetylcholine and catecholamines in vivo. 50 32

In anesthetized dogs, differences in the haemodynamic effects of propranolol and oxprenolol were observed during normoxia, hypercapnia and hypoxia. These differences are presumably due to the sympathomimetic activity of oxprenolol.
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PMID:[Proceedings: Experimental hemodynamic comparison of propranolol and oxprenolol]. 121 38

In dogs, plasma renin activity (PRA) was increased by anesthesia, by hypercapnia and by extreme hypoxia (paO2 47.6 mm Hg). Relatively moderate hypoxia (paO2 47.6 mm Hg) and artificial respiration had no appreciable influence on PRA. It appears that the sympathomimetic stimulus of CO2 has an important bearing on PRA.
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PMID:[Proceedings: Experimentally induced effects on the plasma renin activity]. 121 77

This paper reviews the principal aspects of the immediate management of patients suffering from spinal injury. An understanding of the pathophysiology of primary and secondary spinal cord injury enables appropriate initial care to be provided, thereby avoiding exacerbation and/or progressive deterioration of the lesion. It includes protective measures, restoration of vital functions to maintain adequate tissue perfusion and oxygenation, as well as pharmacological prevention of secondary injury. Protective measures include proper immobilisation of the spine with a semi-rigid collar and tape on a long backboard, or on vacuum mattress, taking great care to avoid deleterious in-line compression forces on the spinal column. The combination of cervical spine instability, a full stomach, unopposed vagal reflexes, hypoxia and hypercarbia makes airway management of these patients difficult. Tracheal intubation under fibroscopic control, with insertion of the tube only after topical anaesthesia of the airways under titrated intravenous sedation, offers safety and comfort to the patient. However, in cases of severe deterioration of vital functions, intubation must be performed without any delay at the site of the accident or in the emergency room. Three options are available: blind naso-tracheal intubation with spontaneous breathing, modified rapid sequence induction with orotracheal intubation under double protection, and immediate surgical airway if these techniques fail. Patients with cervical spine injury may demonstrate severe hypotension requiring sympathomimetic agents and careful fluid loading to avoid pulmonary oedema. To prevent aggravation of the spinal cord injury by systemic factors, the goal of initial resuscitation is to restore an adequate perfusion pressure of at least 60 mmHg, a PaO2 > 100 mmHg, and to keep PaCO2 below 45 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia of patients with injury to the cervical spine]. 130 64

Cardiac arrhythmias are common in patients with respiratory failure from chronic obstructive pulmonary disease (COPD). Several factors may be potentially arrhythmogenic in these patients, including hypoxemia and hypercapnia, acid-base disturbances, cor pulmonale and the use of digitalis, methylxanthines, and sympathomimetic drugs. The aim of this study was to examine the effect of hypoxemia and hypercapnia on QTc dispersion (QTcD) in COPD patients, and to evaluate the effect of a partial correction of one of these pro-arrhythmic factors, the hypoxemia, on Qtc dispersion, as QTcD has been proposed as a marker of heterogeneous repolarization and, hence of ventricular electrical instability. We showed that in 15 hypoxemic/hypercapnic COPD patients, compared to 20 controls, the QTcD was significantly higher (49.7 +/- 10.6 vs. 22.9 +/- 9.8 ms; P = 0.0001); furthermore, after only 24 h of oxygen therapy, and hence after a partial correction of hypoxemia, there was a significant reduction in QTcD in COPD patients (49.7 +/- 10.6 vs. 36.3 +/- 10.1 ms; P = 0.018). The data of the present study suggest that the increase in QTcD may be an early marker of a blood gas mediated electropathy in COPD patients.
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PMID:Effect of blood gas derangement on QTc dispersion in severe chronic obstructive pulmonary disease: evidence of an electropathy? 907 57