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

A 63-year-old man with obstructive pulmonary disease developed severe metablic alkalosis and coma while receiving steroid therapy and nasogastric suction. Treatment, which included the acute induction of hypercarbia and the simultaneous administration of acetazolamide and saline, restored acid-base balance within 24 hours. This combined approach eliminated the need to infuse hydrochloric acid.
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PMID:Life-threatening metabolic alkalosis in a comatose patient. 47 5

Friedreich's Ataxia (F.A.) is a degenerative disease which commonly leads to premature death of cardiorespiratory origin. To explain the early death of these patients, previous investigations have established the existence of 1) a cardiomyopathy in nearly 100% of cases, 2) a restrictive pulmonary syndrome of scoliotic origin and 3) a mild hypoxemia associated with slight respiratory alkalosis and a normal oxyhemoglobin dissociation curve. To further assess the cause of early death in patients with such neuromyopathy, we evaluated, in eleven F.A. patients, the sensitivity of the respiratory centers to hypercapnia, hypoxia, and hyperoxia. Ventilatory (VE, VT, F, VT/Ti) and occlusion pressure (P0.1) responses were taken as indices of the respiratory centers output during progressive hypercapnia (Read's method) and isocarbic hypoxia (Weil's method). We studied 11 Friedreich's Ataxia patients and 11 age, sex, and armspan matched controls. The responses of patients to hypercapnia were significantly greater than controls but their responses to hypoxia were similar to controls. Our study establishes that the respiratory centers are functioning adequately in early Friedreich's Ataxia and do not contribute to cardio-respiratory insufficiency in such neuromyopathy.
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PMID:Regulation of respiration in Friedreich's ataxia. 48 4

Changes in acid-base equilibrium and blood lactate and pyruvate concentrations were studied during recovery (breathing room air) after three days hypercapnia (FICO2 = 0.10) in awake dogs. Fast return to FICO2 = 0 produced a slight alkalosis in arterial blood and an increase in lactate and pyruvate concentrations which seemed to be maximum at the 15th minute. These changes were inhibited by previous injection of acetazolamide (50 mg/kg body weight). During progressive return to FICO2 = 0, over 1 hour, the peak value of blood lactate and pyruvate was delayed until the end of that hour, at the same time as a slight blood alkalosis appeared. These phenomen are most probably explained by a stimulation, due to alkalosis, of glycolysis at the level of phosphofructokinase.
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PMID:Post-hypercapnia recovery in the dog: arterial blood acid-base equilibrium and glycolysis. 60 52

We tested the hypothesis that increased pressures within the lung vessels would inhibit hypoxic pulmonary vasoconstriction at all levels of alveolar CO2 tension. Selective hypoxia of the left lower lobe of the lung in open chested dogs caused the electromagnetically measured blood flow to the lobe to decrease 51 plus or minus 4 (SE) percent and its vascular resistance to increase 132 plus or minus 13 percent. Pressure and blood flow in the main pulmonary artery and left atrial pressure did not change during the hypoxic response. Stepwise increments in left artrial and pulmonary arterial pressures induced either by inflating a left atrial balloon or infusing dextran, progressively diminished the vasoconstrictive response to hypoxia. The response was usually abolished when left atrial pressure reached 25 mmHg. For all vascular pressures, hypoxic vasoconstriction was blunted by hypocapnic alkalosis but not enhanced by hypercapnia. We conclude that the redistribution of blood flow away from an hypoxic lobe of the lung to lobes with high Po2 was greatly attenuated by increasing pressures within lung vessels or by inducing respiratory alkalosis.
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PMID:Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures. 112 94

In 11 normally oxygenated, normotensive mongrel dogs, blood flow and oxidative metabolism of the brain was studied during normocapnia and during respiratory alkalosis and respiratory acidosis. During respiratory alkalosis (mean PaCO2 17.8 mm Hg) CBF decreased significantly from 61.0 to 33.9 ml/100 g/min (44%) while arteriovenous-substrate differences increased and the rates of oxygen and glucose metabolism remained constant. Cerebral venous-arterial difference of lactate was increased significantly as compared with the resting state. During hypercapnia CBF increased significantly from 61.0 (resting state) to 115.7 ml/100 g/min (89%) (mean PaCO2 64.7 mm Hg). The arteriovenous-substrate differences decreased while the cerebral metabolic rates remained constant. The data show that the relationship between PaCO2 and CBF in the range 20-65 mm Hg PaCO2 is expressed by a linear relationship: y = 2.88 + 1.69x; in this range, the oxidative metabolism of the brain is unchanged and the increased cerebral lactate production in respiratory alkalosis is not necessarily linked to tissue hypoxia.
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PMID:The effect of carbon dioxide on cerebral blood flow and cerebral metabolism in dogs. 119 82

Disturbance in acid-base balance is commonly observed in patients with heart failure. The most common disturbance is metabolic alkalosis combined with hypokalemia, as a result of the excessive use of loop diuretics. Occasionary, hypoxia due to pulmonary edema stimulates ventilation, resulting in respiratory alkalosis. When pulmonary edema develops, carbon dioxide retention occurs, resulting in respiratory acidosis. Decreased tissue oxygen delivery may also produce lethal lactic acidosis. Compensatory mechanisms, coexistence of independent acid-base disorders and changes in electrolytes complicate acid-base balance in the individual patients. As acid-base disturbances have harmful effects on the cardiovascular system, precise diagnosis and proper treatment are highly important.
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PMID:[Acid-base disturbances in heart failure]. 143 8

In 20 patients with chronic renal failure on a hemodialysis with acetate-containing dialysing fluid gasometric, ventilation and breathing patterns disturbances were determined. The loss of CO2 in the dialysate is attributed the major cause of hypoxemia due to alveolar hypoventilation. Hemodialysis with bicarbonate-containing dialysate can be performed in the absence of any change in ventilation and PaO2 despite a systemic alkalosis. Hyperventilation during HD with high concentration of bicarbonate indicate that changes in CO2 tension in the pulmonary circulation can lead to a change in minute ventilation due to the presence of slowly adapting pulmonary chemoreceptors. In patients with low respiratory response, respiratory muscle weakness intensified additionally by hypercapnia may explain this phenomenon.
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PMID:[Effect of carbon dioxide (CO2) pressure on minute ventilation, parameters of gas exchange and blood gases during hemodialysis using fluid containing acetate and bicarbonate buffers]. 143 19

Unanaesthetized rats whose arterial chemoreceptors were stimulated by an one hour acute exposition to hypoxic gaseous mixtures with various carbon dioxide concentrations, presented depletion of the catecholamines content of their adrenal glands only when hypocapnia or increased pH was present (non compensated hypoxia). Moreover, exposition to simultaneous hypoxia and hypercapnia increased the epinephrine stock of the adrenal glands. No changes were found in the myocardium amine content in the same conditions. When anaesthetized rats were treated by iv injection of almitrine bismesylate, a peripheral chemoreceptors stimulating drug, adrenal catecholamines content was insignificantly reduced. In the myocardium, the amines remained at control levels. The most powerful factor related to catecholamines depletion in the adrenals seems to be the hypocapnia or the alkalosis induced by the hyperventilation provoked by glomic stimulation. No indication has been found in favor of an effective adrenergic stimulation caused directly by chemoreceptors stimulation.
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PMID:[Chemostimulation and catecholamine content of the rat adrenal medulla]. 171 97

The CO2 rebreathing method can be very useful to test the hypercapnic ventilatory response in patients, including those with chronic acid-base changes (e.g. chronic metabolic acidosis due to renal failure). The ventilatory response to hypercapnia (CO2-R) was measured in 4 normal men by the rebreathing method under control conditions (CaCO3: 0.1 g.kg-1.day-1) and with induced metabolic acidosis (NH4Cl: 0.3 g.kg-1.day-1) and alkalosis (NaHCO3: 0.7 g.kg-1.day-1). The slope of the CO2-R did not change as a result of the acid-base alterations, but was shifted to the left of normal by metabolic acidosis, and to the right by metabolic alkalosis. These results compare favorably with previous reports on the CO2-R as measured by the steady-state technique, and validate the rebreathing method as a reliable and useful technique for evaluating CO2-R in man with altered acid-base states.
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PMID:Effects of chronic acid-base changes on the rebreathing hypercapnic ventilatory response in man. 174 52

Physiological characteristics of dorsal root ganglia microvessels have not been reported in detail. In this study we examined local blood flow and oxygen tension in the L4 dorsal root ganglion (DRG) of the rat. Under normal physiological conditions, local DRG blood flow measured 36.1 +/- 2.7 ml/100 g/min, over twice that within the endoneurium of the sciatic nerve. DRG blood flow was better maintained during hypotension than endoneurial blood flow suggesting partial autoregulation. Unlike endoneurium, there was relative constancy of flow between mean arterial pressures of 60 and 120 mm Hg. Hypercarbia with acidosis, and hypocarbia with alkalosis did not influence blood flow. The histogram of oxygen tensions within the dorsal root ganglion resembled that in brain but included more values at lower tensions than observed in published endoneurial histograms. Theses findings suggest that the DRG differ from endoneurium in ways that reflect the higher metabolic requirements of neural soma.
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PMID:Unique microvascular characteristics of the dorsal root ganglion in the rat. 178 62


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