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

In anaesthetized dogs, a mixed acid-base disturbance was induced by adding a pronounced metabolic alkaline to an established respiratory acidosis or alkalosis. Cerebral blood flow (CBF) was measured by the radioisotope washout method. In the hypocapnic dogs, the addition of metabolic alkalosis did not significantly change cerebral blood flow. In the hypercapnic dogs, the intravenous infusion of alkali led to a substantial reduction of cerebral blood flow, parallelled by a reduction of cerebrovenous oxygen tension. Acid-base analysis of cerebrospinal fluid (CSF) indicated an increased bicarbonate concentration. Hypercapnia is suggested to facilitate the passage of bicarbonate over the blood-brain barrier, leading to cerebral vasoconstriction by means of increased extravascular pH.
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PMID:Influence on cerebral blood flow of infusion of sodium bicarbonate during respiratory acidosis and alkalosis in the dog. 627 52

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
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PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76

Acetazolamide, an inhibitor of carbonic anhydrase, which catalyzes hydration/dehydration of carbon dioxide, has been used for correction of metabolic alkalosis in patients with chronic obstructive pulmonary disease (COPD). Animal experiments have shown that the gradient between tissue and the alveolar CO2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO2. In order to determine the true degree of carbon dioxide retention after total inhibition of carbonic anhydrase, 10 patients with COPD and pronounced metabolic alkalosis (base excess above 6) under controlled mechanical ventilation were studied. The study showed that there was a statistically significant increase in tissue PCO2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that PaO2 and PVO2 increased significantly after inhibition of carbonic anhydrase, which could, at least partly, explain the improvement seen in patients with COPD and metabolic alkalosis after treatment with acetazolamide.
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PMID:Carbon dioxide elimination after acetazolamide in patients with chronic obstructive pulmonary disease and metabolic alkalosis. 641 Jun 68

Previous studies from this laboratory have characterized the "whole-body" response to acute hypercapnia in normal dog and humans. A more recent investigation has demonstrated that this response is markedly altered by graded degrees of chronic respiratory acidosis. The present studies were carried out to assess the influence, if any, of chronic metabolic acid-base disturbances on the acute CO2 titration curve in the dog. To this purpose we first produced a broad range of chronic plasma bicarbonate concentration of metabolic nature. Metabolic acidosis (n = 14) was produced by prolonged HCl-feeding and metabolic alkalosis (n = 11) by diuretics and a chloride-free diet. Animals with normal acid-base status (n = 4) were also studied. After the establishment of a chronic steady state of acid-base equilibrium, we then performed an acute CO2 titration of the unanesthetized dogs within a large environmental chamber. Three levels of inspired CO2 fraction (FICO2) were employed ranging from 4 to 15%. The results indicate that chronic metabolic acid-base disturbances exert a dramatic influence on the whole-body response to acute hypercapnia. The acute change in plasma bicarbonate for a given change in partial pressure of CO2 in arterial blood (PaCO2) or plasma pH decreases as a function of the chronic level of plasma bicarbonate concentration. Yet the ability of the organism to defend plasma hydrogen ion concentration is progressively strengthened as the chronic level of plasma bicarbonate increases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of chronic metabolic acid-base disorders on the acute CO2 titration curve. 641 15

Experimental uremia created by obstructing the urethra of 7 cross-bred bulls was associated with significant (P less than 0.05) increases in PCV, blood urea nitrogen concentration, arterial and venous pH and PCO2, arterial bicarbonate, and base excess. Total serum protein concentration decreased nonsignificantly. Arterial PO2 reduced significantly during later stages of uremia. Arterial and venous oxygen saturation, arteriovenous oxygen difference, oxygen extraction ratio, and arteriovenous pH difference were not affected significantly. Uremia was characterized by progressive metabolic alkalosis with, as a compensation, hypercapnia, and arterial hypoxemia. There was no evidence of systemic shunting of blood except in 1 animal.
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PMID:Acid-base status and blood gas alterations following experimental uremia in cattle. 678 24

The responses of the same aortic chemoreceptor afferents to steady-state isocapnic hypoxia and to hypercapnia on hyperoxia, before and after the induction of metabolic alkalosis, were investigated in 12 anesthetized cats. Metabolic alkalosis was achieved by intravenous administration of sodium bicarbonate in the average dose of 7 mmol . kg-1. On the average, arterial pH (pHa) increased from 7.383 to 7.650 at an arterial CO2 partial pressure (PaCO2) of 30 Torr. The increase in pHa resulted in a decrease in chemoreceptor activity, the effect being greater at a lower arterial O2 partial pressure. Increases in PaCO2 during hyperoxia resulted in an increased activity of the chemoreceptors both before and after NaHCO3 injection. The stimulatory effect of hypercapnia, however, was attenuated by metabolic alkalosis. At a constant PaCO2, decreases in arterial [H+] by the NaHCO3 administration caused an approximately linear decrease in the chemoreceptor activity. At a constant arterial [H+], higher PaCO2 was associated with a slightly greater activity of the chemoreceptors. These results indicate that the major effect of CO2 is mediated by [H+], but there appears to be another mechanism, albeit small, for the effect of CO2.
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PMID:Inhibition of aortic chemoreceptor responses by metabolic alkalosis in the cat. 681 27

In patients with metabolic alkalosis, compensatory alveolar hypoventilation may induce hypercapnia and hypoxemia. In edematous or normally-hydrated patients without electrolyte deficiencies, acetazolamide--a carbonic anhydrase inhibitor--has been advocated to correct the primary acid-base disturbance, thereby preventing hypoxemia. The hemodynamic consequences and the effect on oxyhemoglobin dissociation of acetazolamide, were studied. Twelve critically ill patients with metabolic alkalosis were given 15 mg/kg body wt. acetazolamide intravenously. Cardiovascular performance was completely unchanged. The P50 was 26.6 mm Hg at the beginning and the end of the study, indicating that hemoglobin-oxygen affinity is unaffected by acetazolamide. In six patients, investigated after open-heart surgery, the arterial oxygen tension increased by 10-45%. This was probably related to the combined effects of slight reductions in total body oxygen consumption or shunting of venous blood through the lungs. Eight of the 12 patients were on controlled ventilation. After acetazolamide there was a mean increase in mixed venous carbon dioxide tension (PvCO2) of 4.5 mm Hg, with no increase in arterial carbon dioxide tension (PaCO2), indicating only a limited interference with carbon dioxide uptake and release of the carbonic anhydrase inhibition. No other adverse reactions were observed.
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PMID:Cardiovascular performance and oxyhemoglobin dissociation after acetazolamide in metabolic alkalosis. 681 46

The use of acetazolamide, a carbonic anhydrase inhibitor, in chronic obstructive pulmonary disease (COPD) remains controversial. A substantial improvement in blood gas values has been documented, with correction of metabolic alkalosis in COPD, in hypoxemic sleep apnea at high altitudes and in acute mountain sickness. This randomized, double-blind study examined the short and long term effects of acetazolamide (2 X 250 mg) on 14 patients with hypoxemia, hypercapnia and metabolic alkalosis (paO2 49 +/- 5.2 mm Hg, paCO2 50 +/- 3.6 mm Hg, base excess + 5.7 +/- 2.3). A crossover between acetazolamide and placebo occurred on days 3, 6 and 9. On day 12 the patients were again randomized and one group further treated with acetazolamide for 4 1/2 (1-7) months. During the short term phase, a significant rise in paO2 to 58 +/- 6.6 mm Hg with acetazolamide was noted, followed by a drop to 53 +/- 5.7 mm Hg with placebo. The paO2 of the five patients on long-term acetazolamide therapy remained unchanged (59 +/- 2.5 mm Hg) while the untreated patients showed a significant drop in paO2 to 46 +/- 8.2 mm Hg. No side effects and no severe metabolic acidosis were noted during acute or long term treatment. Acetazolamide appears to improve hypoxemic and hypercapnic COPD patients with metabolic alkalosis on short and long term therapy.
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PMID:[Acetazolamide in hypercapnic chronic obstructive lung disease--a renaissance?]. 682 42

It is well known that the incidence of cardiac arrhythmia is particularly high in patients with chronic respiratory insufficiency (CRI). This study examines the prevalence, incidence and prognostic clinical importance of arrhythmia occurring during the course of CRI on the basis of data taken from the literature and the authors' personal experience using dynamic electrocardiographic diagnosis (24-hour Holter monitoring). The majority of arrhythmias observed in these patients appeared to take the form of premature ventricular and/or supraventricular beats and less frequently of atrial fibrillation and/or attacks of supraventricular paroxysmal tachycardia. Cardiac rhythm alterations were observed using Holter monitoring in 70-90% of patients. No cardiac rhythm disorder is specific to this pathological condition. The aim of this study was to formulate, as far as was possible, a rational therapeutic approach which took account of the electrogenesis of arrhythmic phenomena, variations in the type of arrhythmia and the hemodynamic conditions under which they occur. The etiopathogenesis of arrhythmias within the framework of CRI is relatively complex and probably multifactorial since there are a number of concomitant pathological conditions able to trigger off arrhythmogenic processes both inducing the onset of reflux circuits and enhancing cardiac automatism centres. Many studies correlate the presence of arrhythmia with hypoxemia, hypercapnia and both respiratory and metabolic alkalosis. Even the combined effect of hypoxia with respiratory acidosis and the integrity or otherwise of cardiac function (chronic pulmonary heart, right ventricular hypertrophy, ischemic cardiopathy) have a notable pro-arrhythmic effect. Hypokalemia induced by both respiratory alkalosis and by drugs used during the course of CRI (eg diuretics and/or steroids) may induce a marked dispersion of refractory periods of the various fibrocells thus encouraging the onset of arrhythmia. With regard to drugs, it has been observed that both digitalis and theophylline and beta-2 stimulants if frequently used during the course of CRI may possibly induce arrhythmia. It is therefore important to underline that they should be used with particular caution. As far as concerns the use of beta-2 adrenergic compounds, it is advised that they be administered using an aerosol rather than systemic route. Digitalis has limited indications; the molecules of the methylxanthine classes require careful pharmacological dose monitoring. Arrhythmic therapy should also be seen in terms of prophylaxis and the correction of predisposing and decisive factors such as hypoxemia, hypercapnia, hemoglobin and electrolyte levels, and alterations in blood pH following the obstruction of small airways.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Respiratory insufficiency and cardiac arrhythmia: the rationale of treatment]. 833 38

In this article, we review how the knowledge of the pathophysiology of panic disorder has expanded, with special emphasis on laboratory models using lactate and carbon dioxide challenges. Experiments in the late 1960s revealed that lactate infusion can induce panic attacks. A prominent feature of these attacks is hyperventilation. Because lactate infusion induces a metabolic alkalosis, one would rather expect a compensatory hypoventilation. For years hyperventilation was thought to be causally linked to panic, but it has since been proven to be a symptom rather than a cause of panic attacks. Similarly, it is not hypocapnia but hypercapnia that has proven to be capable of provoking panic attacks. Carbon dioxide challenges are comparable to lactate infusion in the degree to which they meet the criteria for an ideal model of panic disorder. Experiments with carbon dioxide in first-degree relatives of panic disorder patients and in monozygotic twins support the idea of a constitutional predisposition to panic disorder. Of the various other agents that have been used to trigger panic attacks, cholecystokinin seems particularly promising as a valid laboratory model of panic disorder and may provide valuable data regarding the mechanism of panic attacks. The false suffocation alarm theory, proposed by Klein, is an integrative hypothesis that may account for a large number of the laboratory as well as clinical observations.
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PMID:Experimental pathophysiology of panic. 985 52


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