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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Animal experiments have shown that acute respiratory acidosis stimulates water, Na and Cl absorption and HCO3 secretion in the ileum. The aim of this study was to investigate whether the human ileum also responds to changes in systemic acid-base balance. Seven healthy volunteers (mean age 24, range 21-29 years) underwent segmental ileal perfusion using a multi-lumen tube assembly with a proximal occluding balloon. A 30 cm test segment was perfused under steady state conditions with a plasma-like electrolyte solution containing PEG as a non-absorbable volume marker. After a control period, respiratory acidosis (blood pCO2 56.2 mmHg, pH 7.29 and [HCO3] 26.4 mmol l-1) was induced by CO2-breathing over a period of 50 min. Acute respiratory acidosis stimulated net HCO3 secretion in patients secreting HCO3 and reduced absorption in patients exhibiting net HCO3 absorption. These changes were immediate and appeared to be at least partly reversible. Net water, Na, K and Cl movement were not affected. The data suggest that HCO3 transport in the human ileum responds to acute respiratory acidosis.
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PMID:Effects of acute respiratory acidosis on water and electrolyte transport in the human ileum. 850 May 12

The metabolic contributions to chronic acid-base changes were examined in the plasma of arterial blood in patients with chronic obstructive pulmonary disease (COPD) and chronic hypercapnia, by a quantitative physical-chemical analysis. Patients were stratified into three groups: group 1 (Paco2 less than 40 mmHg; 1 mmHg = 133.3 Pa), group 2 (Paco2 between 40 and 50 mmHg), and group 3 (Paco2 higher than 50 mmHg). With the development of hypercapnia (Paco2 from 38.2 +/- 1.6 to 53.8 +/- 0.6 mmHg) and hypoxemia (Pao2 from 73.6 +/- 2.5 to 62.1 +/- 2.1 mmHg), blood pH decreased slightly (from 7.405 +/- 0.007 to 7.372 +/- 0.009). The strong ion difference ([SID]) increased in the hypercapnic group (from 39.7 +/- 1.7 to 46.2 +/- 2.9 mequiv.L-1) parallel to the increase in [HCO3-] (from 23.8 +/- 0.5 to 30.8 +/- 0.8 mequiv.L-1). The change in [SID] was quantitatively similar to the [HCO3-] change, thus reflecting a metabolic compensation of chronic respiratory acidosis. [SID] increase was mainly accounted for by changes in the [Na+]/[Cl-] ratio due to a significant decrease in plasma [Cl-]. Other ions measured as well as the weak acid buffers ([ATOT]) remained constant. From the present results, we suggest the usefulness of the physical chemical approach in the characterization of acid-base disturbances due to chronic hypercapnia when water retention or protein depletion are expected further to hypochloremia, as can be the case in severe COPD patients.
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PMID:A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease. 902 82

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acid­base status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acid­base compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.
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PMID:Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout 932 95

The associated use of permissive hypercapnia (PHY) and high PEEP levels (PEEP(IDEAL)) has been recently indicated as part of a lung-protective-approach (LPA) in acute respiratory distress syndrome (ARDS). However, the net hemodynamic effect produced by this association is not known. We analyzed the temporal hemodynamic effects of this combined strategy in 48 patients (mean age 34 +/- 13 yr) with ARDS, focusing on its immediate (after 1 h), early (first 36 h), and late (2nd-7th d) consequences. Twenty-five patients were submitted to LPA--with the combined use of permissive hypercapnia (PHY), VT < 6 ml/kg, distending pressures above PEEP < 20 cm H2O, and PEEP 2 cm H2O above the lower inflection point on the static inspiratory P-V curve (P(FLEX))- and 23 control patients were submitted to conventional mechanical ventilation. LPA was initiated at once, resulting in an immediate increase in heart rate (p = 0.0002), cardiac output (p = 0.0002), oxygen delivery (DO2l, p = 0.0003), and mixed venous Po2 (p = 0.0006), with a maintained systemic oxygen consumption (p = 0.52). The mean pulmonary arterial pressure markedly increased (mean increment 8.8 mm Hg; p < 0.0001), but the pulmonary vascular resistance did not change (p = 0.32). Cardiac filling pressures increased (p < 0.001) and the systemic vascular resistance fell (p = 0.003). All these alterations were progressively attenuated in the course of the first 36 h, despite persisting hypercapnia. Plasma lactate suffered a progressive decrement along the early period in LPA but not in control patients (p < 0.0001). No hemodynamic consequences of LPA were noticed in the late period and renal function was preserved. A multivariate analysis suggested that these acute hyperdynamic effects were related to respiratory acidosis, with no depressant effects ascribed to high PEEP levels. In contrast, high plateau pressures were associated with cardiovascular depression. Thus, as long as sufficiently low distending pressures are concomitantly applied, the sudden installation of PHY plus PEEP(IDEAL) induces a transitory hyperdynamic state and pulmonary hypertension without harmful consequences to this young ARDS population.
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PMID:Temporal hemodynamic effects of permissive hypercapnia associated with ideal PEEP in ARDS. 937 61

Obstructive Sleep Apnea (OSA), Obesity-Linked Hypoventilation (OLH)--a hypoventilation which is independent of apneas and increased by sleep--, and COPD are mechanisms for respiratory failure in obese patients. We thought nasal bi-level positive airway pressure to be a suitable treatment: EPAP is useful to maintain upper airway patency and IPAP-EPAP difference to correct OLH and COPD hypoventilation. Our purpose is to report the results of such a therapeutic approach. We included 41 patients that we first treated by nasal bi-level positive airway pressure for a respiratory failure with an uncompensated respiratory acidosis. The initial setting was about 4 cm H2O for EPAP and 16 for IPAP. Under supervision of a real-time printed oximetry tracing, we furthermore increased EPAP until disappearance of repetitive dips in oxygen saturation (that we assimilated to obstructive events) and IPAP until obtaining an acceptable level of steady saturation (we assimilated a low level to a steady hypoventilation). Age (mean +/- SD) was 63 +/- 11 years, BMI 42 +/- 9 kg/m2, pH 7.32 +/- 0.04, PaCO2 71 +/- 13 mmHg, PaO2 45 +/- 7 mmHg. Thirty-nine out of 41 patients returned home without need for tracheal intubation. At 7 days of treatment, PaCO2 was 50 +/- 6 mmHg. Thus, nasal bi-level position airway pressure appears to be an efficient treatment in these patients.
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PMID:[Management of obesity and respiratory insufficiency. The value of dual-level pressure nasal ventilation]. 967 35

In order to evaluate the impact of water-borne copper on acid-base regulation in fresh water rainbow trout, chronically cannulated fish were exposed to copper (0.6 mg 1(-1)), hypercapnia (water PCO2 of 6 mmHg) or a combination of copper and hypercapnia, while a fourth untreated group served as the control. Blood samples obtained at 0 h, 4 h and 24 h were analysed for acid-base status, ion concentrations and respiratory parameters. Tissue samples from caudal skeletal muscle, liver and gill filaments were examined for intracellular acid-base status, ion- and water contents, and copper concentration. Exposure to copper alone elicited a small extracellular metabolic alkalosis, no changes in arterial PO2, and a minor decrease in plasma ion concentrations. Hypercapnia alone increased arterial PCO2 from approximately 2 mmHg to 7.2 mmHg, but the extracellular respiratory acidosis present at 4 h was almost completely compensated at 24 h due to an increase in plasma bicarbonate concentration [HCO3-] from 8.1 mM to 24.4 mM. Combined exposure to hypercapnia and copper resulted in a slightly larger acidosis at 4 h, and the fish failed to restore extracellular pH at 24 h, because plasma [HCO3-] only increased to 16.3 mM. Fish exposed to hypercapnia and copper also showed a delayed recovery of intracellular pH in skeletal muscle, compared to fish exposure to hypercapnia only. Thus, copper exposure impaired both extracellular and intracellular acid-base regulation during hypercapnia. When seen in connection with only minor effects of copper on osmoregulatory and respiratory parameters, the reduced ability to regulate acid-base suggests that acid-base regulation may be one of the most copper-sensitive branchial functions.
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PMID:Copper exposure impairs intra- and extracellular acid-base regulation during hypercapnia in the fresh water rainbow trout (Oncorhynchus mykiss). 987 43

The aim of this study was to compare three ventilatory techniques for reducing PaCO2 in patients with severe acute respiratory distress syndrome treated with permissive hypercapnia: (1) expiratory washout alone at a flow of 15 L/min, (2) optimized mechanical ventilation defined as an increase in the respiratory frequency to the maximal rate possible without development of intrinsic positive end- expiratory pressure (PEEP) combined with a reduction of the instrumental dead space, and (3) the combination of both methods. Tidal volume was set according to the pressure-volume curve in order to obtain an inspiratory plateau airway pressure equal to the upper inflection point minus 2 cm H2O after setting the PEEP at 2 cm H2O above the lower inflection point and was kept constant throughout the study. The three modalities were compared at the same inspiratory plateau airway pressure through an adjustment of the extrinsic PEEP. During conventional mechanical ventilation using a respiratory frequency of 18 breaths/min, respiratory acidosis (PaCO2 = 84 +/- 24 mm Hg and pH = 7.21 +/- 0.12) was observed. Expiratory washout and optimized mechanical ventilation (respiratory frequency of 30 +/- 4 breaths/min) had similar effects on CO2 elimination (DeltaPaCO2 = -28 +/- 11% versus -27 +/- 12%). A further decrease in PaCO2 was observed when both methods were combined (DeltaPaCO2 = -46 +/- 7%). Extrinsic PEEP had to be reduced by 5.3 +/- 2.1 cm H2O during expiratory washout and by 7.3 +/- 1.3 cm H2O during the combination of the two modes, whereas it remained unchanged during optimized mechanical ventilation alone. In conclusion, increasing respiratory rate and reducing instrumental dead space during conventional mechanical ventilation is as efficient as expiratory washout to reduce PaCO2 in patients with severe ARDS and permissive hypercapnia. When used in combination, both techniques have additive effects and result in PaCO2 levels close to normal values.
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PMID:Expiratory washout versus optimization of mechanical ventilation during permissive hypercapnia in patients with severe acute respiratory distress syndrome. 1039 Mar 83

Adult freshwater rainbow trout (Oncorhynchus mykiss) were exposed acutely (approximately 20 min) in a stepwise manner to increasing levels of environmental carbon dioxide ranging between 1.7 and 9.0 mmHg (0.23-1.2 kPa). Experiments were performed to examine, for the first time, the influence of hypercapnic acidosis on aspects of cardiovascular physiology including blood pressure, cardiac output and vascular resistance. Fish displayed dose (water CO(2) partial pressure) -dependent increases in ventral aortic (13-39 %) and dorsal aortic (17-54 %) blood pressures that reflected marked increases in systemic vascular resistance (16-78 %); branchial vascular resistance was unaffected by hypercapnia. At the highest level of hypercapnia (9.0 mmHg), central venous pressure was significantly elevated by 54 %. Although cardiac output remained constant, heart rate was significantly lowered by 4-7 beats min(-)(1) at the two highest levels of hypercapnia. To determine whether the cardiovascular responses to hypercapnia were being blunted by the stepwise increase in external P(CO2), a separate group of fish was exposed directly to a single step of hypercapnia (water P(CO2) 8.0 mmHg). The cardiovascular responses were similar to those exhibited by the more gradually exposed fish except that central venous pressure did not increase and the extent of the bradycardia was greater (13 beats min(-)(1)). After confirming the effectiveness of yohimbine in blocking the vasoconstrictory (&agr;)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (&agr;)-adrenoreceptor stimulation in promoting the cardiovascular responses during hypercapnia. Prior treatment of fish with yohimbine prevented the increased blood pressures and systemic vascular resistance during hypercapnia but did not influence the CO(2)-induced bradycardia. Plasma levels of catecholamines did not change during hypercapnia, and therefore the stimulation of the systemic (&agr;)-adrenoreceptors presumably reflected increased sympathetic nerve activity. To determine whether the cardiovascular changes elicited by hypercapnia were related to acidosis-induced hypoxaemia, fish were exposed to hypoxia in a stepwise manner (water P(O2) 65-151 mmHg). The cardiovascular responses to hypoxia were markedly different from those to hypercapnia and consisted of pronounced increases in systemic and branchial vascular resistance, but only at the most severe level of hypoxia; ventral and dorsal aortic pressures were unaffected. The differences between the responses to hypercapnia and hypoxia, coupled with the smaller reductions in blood oxygen content during hypercapnia, support the hypothesis that the cardiovascular responses to CO(2) are direct and are unrelated to hypoxaemia.
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PMID:The control of blood pressure during external hypercapnia in the rainbow trout (Oncorhynchus mykiss). 1040 89

Eastern painted turtles (Chrysemys picta picta) from Connecticut were submerged at 3 degrees C in normoxic and anoxic water to simulate potential respiratory environments within their hibernacula. Those in normoxic water could survive submergence for at least 150 d, while those in anoxic water could survive for a maximum of about 125 d. Turtles in normoxic water developed a slight metabolic acidosis as plasma lactate accumulated to about 50 mM in 150 d, while anoxic turtles developed a severe lactic acidosis as plasma lactate reached about 200 mM in 125 d; there was no respiratory acidosis in either group. Plasma [Na+] changed little in either group, [Cl-] fell by about one-third in both, and [K+] increased by about fourfold in anoxic turtles but only slightly in those in normoxic water. Total plasma magnesium and calcium increased profoundly in anoxic turtles but moderately in those in normoxic water. Consideration of charge balance indicates that all major ions were measured in both groups. Plasma glucose remained unchanged in anoxic turtles until after about 75 d of submergence, when it increased and continued to increase with the duration of anoxia, with much variation among individuals; glucose remained unchanged throughout in turtles in normoxic water. Hematocrit doubled in 150 d in turtles in normoxic water; in anoxic turtles, an initial increase was no longer significant by day 100. Plasma osmolality increased markedly in anoxic turtles, largely because of accumulation of lactate, but anoxic turtles only gained about half the mass of turtles in normoxic water, who showed no increase in osmolality. The higher weight gain in the latter group is attributed to selective perfusion and ventilation of extrapulmonary gas exchange surfaces, resulting in a greater osmotic influx of water. The physiologic responses to simulated hibernation of C. picta picta are intermediate between those of Chrysemys picta bellii and Chrysemys picta dorsalis, which correlates with the severity of the winter each subspecies would be expected to encounter.
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PMID:The physiology of hibernation among painted turtles: the Eastern painted turtle Chrysemys picta picta. 1043 85

Experiments were performed in vivo to elucidate the underlying mechanism(s) of apparent diffusion limitations for CO(2) excretion in rainbow trout (Oncorhynchus mykiss). Ligation of two gill arches and the associated expected reduction in gill surface area of 30% caused pronounced respiratory acidosis as indicated by elevated arterial blood P(CO(2)) (Pa(CO(2))) and reduced arterial blood pH. Under conditions of normoxia, arterial blood P(O(2)) (Pa(O(2))) was not significantly (statistically) reduced. However, during hypoxia (water P(O(2))=70-80 mmHg), the apparent trend for reduced Pa(O(2)) values became statistically significant in fish with 15% surface area reduction. To determine whether the elevated Pa(CO(2)) in fish with reduced surface area (30%) reflected true diffusion limitations or chemical equilibrium limitations imposed by the relatively slow rate of red blood cell Cl(-)/HCO(3)(-) exchange, fish were injected with carbonic anhydrase (CA) to permit catalysis of HCO(3)(-) dehydration within the plasma. Injection of CA caused a lowering of Pa(CO(2)) by 0.87+/-0.32 mmHg within 120 min and thus essentially eliminated the increase in Pa(CO(2)) (1.04+/-0.33 mmHg) that was caused by the reduction in surface area. These results clearly demonstrate that the elevation in Pa(CO(2)) evoked by gill surface area reduction is a consequence of chemical equilibrium limitations rather than true diffusion limitations, per se.
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PMID:Apparent diffusion limitations for CO(2) excretion in rainbow trout are relieved by injections of carbonic anhydrase. 1085 23


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