The use of noninvasive mechanical ventilation in COPD with severe hypercapnic acidosis.
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STUDY OBJECTIVES: To compare the effect of noninvasive mechanical ventilation (NIV) in severely acidotic with mildly acidotic patients with acute hypercapnic chronic obstructive lung disease (COPD). DESIGN: Comparison of NIV in consecutively enrolled patients with acute hypercapnic COPD with mild (pH 7.25-7.35) or severe (pH<7.25) acidosis on time to normalise pH and improve PaCO(2), duration of NIV treatment, length of stay in hospital and survival. Results (meadian (IQR)): Twenty-nine patients had 36 episodes of acute hypercapnic respiratory failure: Seventeen with pH<7.25 and 19 with pH 7.25-7.34. Compared with the mildly acidotic group, the severely acidotic group took a similar length of time for pH to normalise and PaCO(2) improve (12 (6-34) vs 12 (4-28)h, respectively, P=0.42), with similar duration of NIV treatment (60 (35-96) vs 68 (36-48)h, respectively, P=0.25) and hospital length of stay (8 (7-18) vs 9 (5-17) days, respectively, P=0.61). Overall survival was 89%, with 95% in the mild and 82% in the severely acidotic groups. CONCLUSIONS: Noninvasive ventilation is effective in the treatment of patients with severe acidosis due to acute hypercapnic COPD. (+info)
End-tidal carbon dioxide as a measure of acidosis among children with gastroenteritis.
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OBJECTIVES: We aimed to determine the correlation between end-tidal carbon dioxide levels and serum bicarbonate concentrations among patients with gastroenteritis, to compare the end-tidal carbon dioxide with other clinical parameters that might also be associated with the degree of acidosis, and to examine the relationship between end-tidal carbon dioxide levels and return visits. METHODS: Our prospective sample included patients presenting to the emergency department with a chief complaint of vomiting and/or diarrhea. The association between end-tidal carbon dioxides and serum bicarbonate concentrations was determined with simple linear-regression analysis. Receiver operating characteristic curves were computed to determine the predictive ability of the end-tidal carbon dioxide to detect metabolic acidosis. RESULTS: One hundred thirty of 146 subjects who were approached were included in the final analysis. For those for whom laboratory studies were performed, the mean serum bicarbonate concentration was 17.3 +/- 4.3 mmol/L and the mean end-tidal carbon dioxide level was 34.2 +/- 5.2 mm Hg. End-tidal carbon dioxide levels and serum bicarbonate concentrations were correlated linearly in bivariate analysis. Receiver operating characteristic curves were calculated for end-tidal carbon dioxide as a predictor of serum bicarbonate concentrations of < or = 13, < or = 15, and < or = 17 mmol/L, with areas under the curves of 0.94, 0.95, and 0.90, respectively. The relationship between end-tidal carbon dioxide levels and serum bicarbonate concentrations was independent of other potential predictors of acidosis in multivariable analysis. The mean end-tidal carbon dioxide level for patients who required an unanticipated return visit (33.0 +/- 4.0 mm Hg) was lower than the level for those who did not seek reevaluation (36.6 +/- 3.6 mm Hg). CONCLUSIONS: End-tidal carbon dioxide levels were correlated with serum bicarbonate concentrations among children with vomiting and diarrhea, independent of other clinical parameters. Capnography offers an objective noninvasive measure of the severity of acidosis among patients with gastroenteritis. (+info)
Oxygen alert cards and controlled oxygen: preventing emergency admissions at risk of hypercapnic acidosis receiving high inspired oxygen concentrations in ambulances and A&E departments.
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BACKGROUND: Appropriate resuscitation of hypoxic patients is fundamental in emergency admissions. To achieve this, it is standard practice of ambulance staff to administer high concentrations of oxygen to patients who may be in respiratory distress. A proportion of patients with chronic respiratory disease will become hypercapnic on this. OBJECTIVES AND METHODS: A scheme was agreed between the authors' hospital and the local ambulance service, whereby patients with a history of previous hypercapnic acidosis with a Pao2 >10.0 kPa--indicating that oxygen may have worsened the hypercapnia--are issued with "O2 Alert" cards and a 24% Venturi mask. The patients are instructed to show these to ambulance and A&E staff who will then use the mask to avoid excessive oxygenation. The scheme was launched in 2001 and this paper present the results of an audit of the scheme in 2004. RESULTS: A total of 18 patients were issued with cards, and 14 were readmitted on 69 occasions. Sufficient documentation for auditing purposes was available for 52 of the 69 episodes. Of these audited admissions, 63% were managed in the ambulance, in line with card-holder protocol. This figure rose to 94% in the accident and emergency department. CONCLUSION: These data support the usability of such a scheme to prevent iatrogenic hypercapnia in emergency admissions. (+info)
Nerve excitability changes in critical illness polyneuropathy.
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Patients in intensive care units frequently suffer muscle weakness and atrophy due to critical illness polyneuropathy (CIP), an axonal neuropathy associated with systemic inflammatory response syndrome and multiple organ failure. CIP is a frequent and serious complication of intensive care that delays weaning from mechanical ventilation and increases mortality. The pathogenesis of CIP is not well understood and no specific therapy is available. The aim of this project was to use nerve excitability testing to investigate the changes in axonal membrane properties occurring in CIP. Ten patients (aged 37-76 years; 7 males, 3 females) were studied with electrophysiologically proven CIP. The median nerve was stimulated at the wrist and compound action potentials were recorded from abductor pollicis brevis muscle. Strength-duration time constant, threshold electrotonus, current-threshold relationship and recovery cycle (refractoriness, superexcitability and late subexcitability) were recorded using a recently described protocol. In eight patients a follow-up investigation was performed. All patients underwent clinical examination and laboratory investigations. Compared with age-matched normal controls (20 subjects; aged 38-79 years; 7 males, 13 females), CIP patients exhibited reduced superexcitability at 7 ms, from -22.3 +/- 1.6% to -7.6 +/- 3.1% (mean +/- SE, P approximately 0.0001) and increased accommodation to depolarizing (P < 0.01) and hyperpolarizing currents (P < 0.01), indicating membrane depolarization. Superexcitability was reduced both in patients with renal failure and without renal failure. In the former, superexcitability correlated with serum potassium (R = 0.88), and late subexcitability was also reduced (as also occurs owing to hyperkalaemia in patients with chronic renal failure). In patients without renal failure, late subexcitability was normal, and the signs of membrane depolarization correlated with raised serum bicarbonate and base excess, indicating compensated respiratory acidosis. It is inferred that motor axons in these CIP patients are depolarized, in part because of raised extracellular potassium, and in part because of hypoperfusion. The chronic membrane depolarization may contribute to the development of neuropathy. (+info)
Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule.
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The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either hypercapnia and hypoxia [8% CO(2) and 13% O(2) (hypercapnic, n = 6) or normal air (controls, n = 6)] in an environmental chamber for 10 days and were killed under the same atmosphere. In hypercapnic rats, arterial pH was lower than controls (7.31 +/- 0.01 vs. 7.39 +/- 0.01, P = 0.03), blood HCO(3)(-) concentration was increased (42 +/- 0.9 vs. 32 +/- 0.24 mM, P < 0.001), arterial Pco(2) was increased (10.76 +/- 0.4 vs. 7.20 +/- 0.4 kPa, P < 0.001), and plasma chloride concentration was decreased (92.2 +/- 0.7 vs. 97.2 +/- 0.5 mM, P < 0.001). Plasma aldosterone levels were unchanged. In the proximal tubule, immunoblotting showed an increased expression of sodium/bicarbonate exchanger protein (188 +/- 22 vs. 100 +/- 11%, P = 0.005), confirmed by immunohistochemistry. Total Na/H exchanger protein expression in the cortex was unchanged by immunoblotting (119 +/- 10 vs. 100 +/- 11%, P = 0.27) and immunohistochemistry. In the cortex, the abundance of pendrin was decreased (51 +/- 9 vs. 100 +/- 7%, P = 0.003) by immunoblotting. Immunohistochemistry revealed that this decrease was clear in both cortical collecting ducts (CCDs) and connecting tubules (CNTs). This demonstrates that pendrin expression can be regulated in acidotic animals with no changes in aldosterone levels and no external chloride load. This reduction of pendrin expression may help in redirecting the CNT and CCD toward chloride excretion and bicarbonate reabsorption, contributing to the increased plasma bicarbonate and decreased plasma chloride of chronic respiratory acidosis. (+info)
Chronic ethanol increases fetal cerebral blood flow specific to the ethanol-sensitive cerebellum under normoxaemic, hypercapnic and acidaemic conditions: ovine model.
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Cerebral hypoxia has been proposed as a mechanism by which prenatal ethanol exposure causes fetal alcohol spectrum disorder (FASD) in children, but no study had tested this hypothesis using a chronic exposure model that mimicks a common human exposure pattern. Pregnant sheep were exposed to ethanol, 0.75 or 1.75 g kg(-1) (to create blood ethanol concentrations of 85 and 185 mg dl(-1), respectively), or saline 3 days per week in succession (a 'binge drinking' model) from gestational day (GD) 109 until GD 132. Fetuses were instrumented on GD 119-120 and studied on GD 132. The 1.75 g kg(-1) dose resulted in a significant increase in fetal biventricular output (measured by radiolabelled microsphere technique) and heart rate, and a reduction of mean arterial pressure and total peripheral resistance at 1 h, the end of ethanol infusion. The arterial partial pressure of CO(2) was increased, arterial pH was decreased and arterial partial pressure of O(2) did not change. Fetal whole-brain blood flow increased by 37% compared with the control group at 1 h, resulting in increased cerebral oxygen delivery. The elevation in brain blood flow was region specific, occurring preferentially in the ethanol-sensitive cerebellum, increasing by 44% compared with the control group at 1 h. There were no changes in the lower dose group. Assessment of regional differences in the teratogenic effects of ethanol by stereological cell-counting technique showed a reduced number of cerebellar Purkinje cells in response to the 1.75 g kg(-1) dose compared with the control brains. However, no such differences in neuronal numbers were observed in the hippocampus or the olfactory bulb. We conclude that repeated exposure to moderate doses of ethanol during the third trimester alters fetal cerebral vascular function and increases blood flow in brain regions that are vulnerable to ethanol in the presence of acidaemia and hypercapnia, and in the absence of hypoxia. (+info)
Reperfusion accelerates acute neuronal death induced by simulated ischemia.
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Observations in real time can provide insights into the timing of injury and the mechanisms of damage in neural ischemia-reperfusion. Continuous digital imaging of morphology and cell viability was applied in a novel model of simulated ischemia-reperfusion in cultured cortical neurons, consisting of exposure to severe hypoxia combined with glucose deprivation, mild acidosis, hypercapnia, and elevated potassium, followed by return of oxygenated, glucose-containing physiological saline. Substantial acute injury resulted following 1 h of simulated ischemia, with 36+/-8% neurons dying within 2 h of reperfusion. Inclusion of moderate glutamate elevation (30 microM) in the simulation of ischemia increased the acute neuronal death to 51+/-6% at 2 h of reperfusion. While some swelling and neuritic breakdown occurred during ischemia, particularly with inclusion of glutamate, neuronal death, as marked by loss of somatic membrane integrity, was entirely restricted to the reperfusion phase. Morphological and cytoskeletal changes suggested a predominance of necrotic death in the acute phase of reperfusion, with more complete delayed death accompanied by some apoptotic features occurring over subsequent days. Prolonged simulated ischemia, without reperfusion, did not induce significant acute neuronal death even when extended to 3 h. We conclude that while morphological changes suggesting initiation of neuronal injury appear during severe simulated ischemia, the irreversible injury signaled by membrane breakdown is accelerated by the events of reperfusion itself. (+info)
Expression of rat renal Na/H antiporter mRNA levels in response to respiratory and metabolic acidosis.
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The mammalian proximal tubule is an important mediator of the renal adaptive response to systemic acidosis. In chronic metabolic and respiratory acidosis the bicarbonate reabsorptive (or proton secretory) capacity is increased. This increase is mediated, at least in part, by an increase in Vmax of the luminal Na/H antiporter. To determine whether this adaptation involves increased mRNA expression, Na/H antiporter mRNA levels were measured by Northern analysis in renal cortex of rats with metabolic (6 mmol/kg body wt NH4Cl for 2 or 5 d) and respiratory (10% CO2/air balanced for 2 or 5 d) acidosis and of normal, pair-fed rats. Na/H antiporter mRNA levels were unchanged after 2 d of both metabolic and respiratory acidosis. After 5 d, however, Na/H antiporter mRNA expression was increased 1.76 +/- 0.12-fold in response to metabolic acidosis (P less than 0.005, n = 8), but was not different from normal in response to respiratory acidosis: 1.1 +/- 0.2 (NS, n = 8). Thus, the renal adaptive response to metabolic acidosis involves increased cortical Na/H antiporter mRNA levels. In contrast, the enhanced proximal tubule Na/H antiporter activity and bicarbonate reabsorption in respiratory acidosis seem to involve mechanisms other than increased Na/H antiporter gene expression. (+info)