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

With the aim of testing a method that allows increasing concentrations of oxygen to be administered to patients with severe hypoxemia and hypercapnia while avoiding the risk of increasing respiratory acidosis, we studied 17 male patients with advanced chronic obstructive pulmonary disease (COPD) and severe hypercapnic respiratory failure. During 6 h and on one day only, all patients were given intermittent negative pressure ventilation (INPV) together with oxygenation starting at a concentration of 24 percent and increasing to 30 percent. Using this procedure, it was possible to raise arterial PaO2 to safe levels (from 47.2 +/- 3 mm Hg to 61.5 +/- 6 mm Hg, p less than 0.001) without increasing hypercapnia, and a significant drop in PaCO2 levels (from 74.4 +/- 9 mm Hg to 65.6 +/- 12 mm Hg, p less than 0.005) was even observed. One hour after INPV ended, the mean values of PaO2, PaCO2, oxygen saturation, and pH were also significantly better than prestudy values. We conclude that INPV and oxygen therapy with increasing oxygen flow could constitute an alternative option to intubation and mechanical ventilation in cases of severe hypercapnic respiratory failure due to advanced COPD.
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PMID:Intermittent short-term negative pressure ventilation and increased oxygenation in COPD patients with severe hypercapnic respiratory failure. 190 38

Deviations of the alveolar ventilation rate from normality induce respiratory acid-base disturbances. Alveolar hyperventilation leads to hypocapnia and thus respiratory alkalosis whereas alveolar hypoventilation induces hypercapnia leading to respiratory acidosis. The changes in CO2 induce compensatory alterations of renal bicarbonate transport: Hypercapnia stimulates renal reabsorption of bicarbonate whereas hypocapnia enhances urinary bicarbonates. The plasma bicarbonate concentration rises in response to hypercapnia and falls following hypocapnia. Renal regulation of plasma bicarbonate results in a characteristic dependence on systemic PCO2 permitting the formation of diagnostic criteria for respiratory imbalance of acid-base homeostasis. In chronic respiratory acidosis plasma bicarbonate should rise by 0.35 mmol/l per mmHg increase in PCO2. In chronic respiratory alkalosis, on the other hand, plasma bicarbonate should fall by 0.4 mmol/l for every mmHg decrease in PCO2. If the measured bicarbonate values do not fall into this expected range, acute respiratory or mixed (respiratory and metabolic) acid-base disturbances should be suspected. The clinical significance and application of these diagnostic criteria are illustrated by examples.
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PMID:[Hypo- and hyperventilation: consequences for acid-base balance]. 192 34

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.
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PMID:Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis. 199 47

Recent evidence indicates the existence of a protein related to the erythroid chloride-bicarbonate exchanger (band 3 protein) in the basolateral aspect of type A intercalated cells of the distal nephron. To probe the possible participation of this transporter in the renal adaptation to chronic hypercapnia, we examined the steady-state abundance of band 3 mRNA in the kidney during respiratory acidosis of variable duration. Total RNA was isolated from renal cortex and medulla of rats maintained in a 10% CO2 atmosphere for 2 or 5 days and from contemporaneous controls. The RNA was analyzed by Northern blot assay using cDNA probes for band 3 and beta-actin genes. Using a 3' cDNA probe encoding the membrane-associated domain of band 3 protein that is involved in anion exchange, we found a two- to threefold increase in steady-state mRNA levels (whether or not correction for the beta-actin signals was applied) in renal cortex and medulla at 5 days of hypercapnia. Similar, but less definitive, increases were observed at the 2-day time point. Using a 5' cDNA probe encoding an erythroid-protein segment absent from the kidney band 3 major transcript, we detected meager hybridization in renal tissue and no measurable variation during hypercapnia. Use of splenic RNA as a positive control for the 5' probe disclosed marked reduction of band 3 mRNA levels in hypercapnia, indicating organ specificity of band 3 gene expression. We conclude that steady-state levels of kidney band 3 mRNA increase in chronic respiratory acidosis as a result of transcriptional or posttranscriptional regulatory mechanisms. This adaptation might be involved in the augmentation of renal acidification characteristic of chronic hypercapnia.
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PMID:Rat kidney band 3 mRNA modulation in chronic respiratory acidosis. 199 72

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.
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PMID:Acid-base status affects gas exchange in canine oleic acid pulmonary edema. 201 14

To examine the effects of respiratory acidosis in vivo on the adaptation of acidification in the collecting tubule, New Zealand White rabbits were exposed to a 6.7% CO2-93.3% O2 gas mixture in an environmental chamber for 0, 6, 24, or 48 h before obtaining collecting tubules for in vitro study. These collecting tubules were then perfused and bathed in vitro in identical Krebs-Ringer bicarbonate solutions. After 1 h equilibration total CO2 flux (JtCO2) was measured. The urine pH of the rabbits fell, whereas the blood bicarbonate rose as CO2 exposure time increased. In cortical collecting tubules, JtCO2 in vitro correlated with length of animal exposure to hypercarbia (y = 1.14174 + 0.1437x, r = 0.57, P = 0.002), and with the blood bicarbonate of the animal (y = 26.8471 + 0.0858x, r = 0.59, P less than 0.05). In vitro JtCO2 in medullary collecting tubules from rabbits that had been in hypercarbic atmosphere for 48 h (23.2 +/- 4.9 pmol.mm-1.min-1) did not differ from JtCO2 in control tubules (25.0 +/- 3.2 pmol.mm-1.min-1, not significant). Thus the cortical collecting tubule exhibits an adaptive increase in JtCO2 in response to hypercarbia, whereas the medullary collecting tubule does not.
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PMID:Collecting tubule adaptation to respiratory acidosis induced in vivo. 210 60

We studied the relationship between contractile function and intracellular pH (pHi) in the isolated rat diaphragm when superfusate PCO2 was changed during hyperoxia or hypoxia. Superfused diaphragm strips were field stimulated at 0.5 Herz, and twitch tension (TT) was recorded. The pHi was calculated from the volume distribution of a weak acid, dimethyl-oxazolidinedione. In hyperoxia, hypercapnic acidosis (pH 7.06-6.63) depressed diaphragm pHi and TT, whereas hypocapnic alkalosis (pH 7.82-8.15) increased pHi but did not significantly affect TT. TT was maximum at physiological pHi (7.06), but in hyperoxic hypercapnic muscles substantial force was still generated at pHi values as low as 6.44. Hypoxia (PO2 30-38 mm Hg) markedly reduced TT; this effect was slightly exacerbated by hypercapnia and attenuated by hypocapnia. Hypoxia lowered pHi by about 0.2 units, which was insufficient to account for the hypoxic contractile failure. Knowledge of the hyperoxic muscle TT/pHi relationship suggests that, in other contexts, caution should be exercised in attributing severe muscle fatigue or force loss to modest falls in pHi.
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PMID:The effect of pH and hypoxia on function and intracellular pH of the rat diaphragm. 210 18

The explanation for the increased frequency of troubles with digoxin therapy in patients with chronic pulmonary diseases is debated. The reported effects of hypoxia in vivo on myocardial levels of digoxin are contradictory, and there have been few studies on the effects of hypercapnia. In the past, it has been shown in rat myocardial tissue at rest in vitro that hypoxia decreased and hypercapnic acidosis increased the digoxin uptake. We performed a new study in vitro in an isolated beating rat heart perfused at constant flow (37 degrees C) and stimulated at a constant frequency (6 Hz). The performances were recorded with an intraventricular balloon equipped with a tip-manometer catheter. The action of digoxin was studied by recording systolic pressure (PS) and diastolic pressure (PD), the left ventricular developed pressure (LVDP = PS - PD), the (dP/dt)max, and the ratio (dP/dt)max/PS. First, the heart was perfused for 30 min with a modified Tyrode's solution perfusate aerated with carbogen (pH = 7.40; PCO2 = 37 mmHg; PO2 = 530 mmHg) (1 mmHg = 133.32 Pa). Various parameters of contractions were recorded (initial control values). Then the heart was perfused for 15 min with Tyrode's solution aerated either with a hypoxic gas mixture (pH = 7.41; PCO2 = 36 mmHg; PO2 = 122 mmHg), a hypercapnic gas mixture (pH = 7.08; PCO2 75 mmHg; PO2 = 485 mmHg), or a hypoxic-hypercapnic gas mixture (pH = 7.09; PCO2 = 73 mmHg; PO2 = 124 mmHg). Control hearts were continuously perfused with Tyrode's solution aerated with carbogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The inotropic effect of digoxin on an isolated rat heart in hypercapnia and (or) hypoxia. 210 1

Neotenic larval Ambystoma tigrinum were subjected to hypercapnia (3% CO2, 22 Torr) for 24 h under different conditions: alpha-adrenergic blockade using phentolamine, beta-adrenergic blockade using propranolol, and sham treatments. The sham animals were able to carry out a partial extracellular pH compensation that consisted of an increase in extracellular [HCO3-]. Animals treated with catecholamine antagonists did not compensate to the same extent. Analysis of plasma samples by high-performance liquid chromatography with electrochemical detection revealed a significant increase in circulating norepinephrine, but not epinephrine, during the high-CO2 exposure. Measurements of cutaneous ion transport showed that beta-antagonists block the increased Na+ influx associated with hypercapnia, whereas alpha-antagonists inhibited the decrease in cutaneous Cl- influx that is also associated with respiratory acidosis. Additionally, both alpha- and beta-blockers inhibited the increase in transcutaneous potential difference that accompanied the respiratory acidosis. The results are consistent with a role for circulating catecholamines in compensatory ion transport responses to respiratory acidosis in this species.
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PMID:Acid-base-electrolyte balance responses to catecholamine antagonists in Ambystoma tigrinum. 211 75

Hypoxic vasoconstriction has been the subject of many studies, but little is known about the interaction of hypercapnia and the pulmonary circulation. We performed two haemodynamic studies on each of three patients with pulmonary vascular disease secondary to congenital heart disease. On the first occasion ventilation was inadequate due to technical problems, and the patients were therefore hypercapnic (arterial pCO2 greater than 5.3 kPa). On the second occasion, they were normocapnic. Pulmonary vascular resistance was measured on each occasion while the patients were breathing 100% oxygen (alveolar hyperoxia) and while epoprostenol (prostacyclin) was infused at doses of 5-20 ng/kg/min. Pulmonary vascular resistance was elevated in the presence of hypercapnia and, despite oxygen and epoprostenol, could not be reduced to the levels observed in the normocapnic study. We conclude that hypercapnia causes significant vasoconstriction in infants; and that epoprostenol is a relatively ineffective pulmonary vasodilator in infants who are hypercapnic due to inadequate ventilation. Where possible, respiratory acidosis should be corrected before using oxygen or epoprostenol as a pulmonary vasodilator.
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PMID:Interactions between alveolar hypercapnia and epoprostenol on the pulmonary circulation: clinical and pharmacological implications. 213 21


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