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At least 307 records · Page 17Linked to original sources
PubMed1978

Case report: severe respiratory alkalosis--unusual manifestation of viral hepatitis.

A middle-aged man who had been in good general health presented with marked hyperventilation and severe respiratory alkalosis. Typical signs and symptoms of viral hepatitis subsequently developed. Investigation showed that he and 32 other patients with hepatitis had all eaten at the same restaurant prior to illness. Because of his distressing constitutional symptoms and markedly elevated hepatic enzyme levels, corticosteroid therapy was begun. The symptoms and hyperventilation improved dramatically. Although respiratory alkalosis has been observed during the course of other infectious diseases, to our knowledge it has not previously been reported in association with hepatitis A infection.

Alkalosis, Respiratory↗
PubMed1977

Oxygen uptake of canine whole body and hind limb with hypocapnic alkalosis.

The effect of hypocapnic alkalosis induced by hyperventilation on whole-body and hind-limb oxygen uptake (VO2) was studied in dogs anesthetized with pentobarbital. In the intact dog with a self-perfused hind limb, increasing pHa from 7.41 to 7.58 increased whole-body VO2 8% and decreased hind-limb VO2 6%. Isolated hind limbs perfused with heparinized whole blood had similar decreases in VO2 with increases in arterial blood pH (pHa). However, isolated hind limbs perfused with whole blood containing citrate, phosphate, and dextrose (CPD) showed muscle twitches, had larger VO2 values at identical pHa's, and had an increase in VO2 with increase in pHa. These changes with a CPD perfusate were associated with low levels of ionized calcium (less than 0.5 mEq/1), disappeared when calcium ion spontaneously increased to 1.0 mEq/1, and could be prevented or abolished by the addition of calcium chloride, dantrolene, d-tubocurarine, or succinylcholine. These results are in accord with the findings of others regarding an increase in whole-body VO2 with hypocapnic alkalosis, but do not support a contributory role of skeletal muscle to the overall increase.

Alkalosis↗
PubMed1998

Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease.

BACKGROUND: Variation of the arterial carbon dioxide partial pressure (PaCO2) is not uncommon in anesthetic practice. However, little is known about the myocardial consequences of respiratory alkalosis and acidosis, particularly in patients with coronary artery disease. The aim of the current study was to investigate the effects of variation in PaCO2 on myocardial blood flow (MBF), metabolism, and systemic hemodynamics in patients before elective coronary artery bypass graft surgery. METHODS: In 10 male anesthetized patients, measurements of MBF, myocardial contractility, metabolism, and systemic hemodynamics were made in a randomized sequence at PaCO2 levels of 30, 40, and 50 mmHg, respectively. The MBF was measured using the Kety-Schmidt technique with argon as a tracer. End-diastolic left ventricular pressure and the maximal increase of left ventricular pressure were assessed using a manometer-tipped catheter. RESULTS: The cardiac index significantly changed with varying PaCO2 levels (hypocapnia, - 9%; hypercapnia, 13%). This reaction was associated with inverse changes in systemic vascular resistance index levels. The MBF significantly increased by 15% during hypercapnia, whereas no change was found during hypocapnia. Myocardial oxygen and glucose uptake and the maximal increase of left ventricular pressure were not affected by varying PaCO2 levels. CONCLUSIONS: In anesthetized patients with coronary artery disease, short-term variations in PaCO2 have significant effects on MBF but do not influence global myocardial oxygen and glucose uptake. Changes in systemic hemodynamics associated with respiratory alkalosis and acidosis are caused by changes in systemic vascular resistance rather than by alterations in myocardial contractility.

Acidosis, Respiratory↗
PubMed1974

Ulcer disease, metabolic alkalosis and hyperparathyroidism: A mechanism of interrelationship?

In both normal volunteers and in patients with primary hyperparathyroidism, the induction of a metabolic alkalosis by infusion of sodium bicarbonate results in a decrease in serum calcium ion and in an increase of circulating parathyroid hormone concentrations. Bicarbonate infusion may serve in man as a new provocative test for release of parathyroid hormone. Furthermore, we speculate that the metabolic alkalosis which is found at times in patients with the Zollinger-Ellison syndrome and severe peptic ulcer disease may result in parathyroid gland stimulation.

Adult↗
PubMed1985

Hydrochloric acid infusion for treatment of metabolic alkalosis: effects on acid-base balance and oxygenation.

The effects of hydrochloric acid (HCl) administration were studied in 15 critically ill patients whose metabolic alkalosis caused a significant alkalemia (pH 7.50 to 7.58) unresponsive to sodium and potassium chloride administration. Arterial pH and bicarbonate and chloride concentrations normalized after a 6- to 12-h mean infusion of 200 +/- 54 mmol of .25 N HCl. There were no deleterious vascular, hematologic, or metabolic side-effects. HCl administration was associated with an increase in mean PaO2 from 94 +/- 21 to 121 +/- 31 torr (p less than .001). This increase was comparable in patients breathing spontaneously and those treated with controlled mechanical ventilation, and was attributed at least in part to a decrease in pulmonary shunt. These results indicate that .25 N HCl, infused at the rate of 100 ml/h into the superior vena cava, can correct metabolic alkalosis safely and rapidly. The persistence of the beneficial effects of this treatment on arterial oxygenation remains to be confirmed.

Acid-Base Equilibrium↗
PubMed1999

Single versus multiple doses of acetazolamide for metabolic alkalosis in critically ill medical patients: a randomized, double-blind trial.

OBJECTIVE: To compare two dosing regimens of acetazolamide for the reversal of metabolic alkalosis in mechanically ventilated patients with asthma or chronic obstructive pulmonary disease. DESIGN: A randomized, double-blind, placebo-controlled trial. SETTING: A 35-bed medical intensive care unit in a tertiary care teaching hospital. PATIENTS: Forty mechanically ventilated patients with a metabolic alkalosis (arterial pH > or = 7.48 and serum bicarbonate concentration > or = 26 mEq/L) resistant to fluid or potassium therapy (serum potassium concentration, > or = 4 mEq/L) not receiving acetazolamide or sodium bicarbonate in the previous 72 hrs. INTERVENTIONS: Stratified by previous diuretic use and randomized to receive intravenous administration of acetazolamide, one dose of 500 mg or 250 mg every 6 hrs for a total of four doses. MEASUREMENTS AND MAIN RESULTS: Serum bicarbonate and potassium concentrations were drawn every 6 hrs for 72 hrs, arterial blood gases were drawn every 12 hrs for 72 hrs, and both urine chloride and pH were drawn at hours 0, 6, 12, 18, 24, 48, and 72. By using generalized estimating equation techniques, no difference was found between the two dosing regimens at any point over the study period for serum bicarbonate, serum potassium, or urine chloride end points. Results did not differ between diuretic- and nondiuretic-treated patients. Serum bicarbonate concentrations remained significantly decreased in both treatment groups 72 hrs after administration of the first acetazolamide dose (31.8 +/- 4.9-25.3 +/- 3.8 mEq/L, p < .0001 [250 mg x 4]; 31.9 +/- 25.4-25.4 +/- 3.6 mEq/L, p < .0001 [500 mg x 1]). CONCLUSIONS: We conclude that a single 500-mg dose of acetazolamide reverses nonchloride responsive metabolic alkaloses in medical intensive care unit patients as effectively as multiple doses of 250 mg. Studies to examine the prolonged duration of action of acetazolamide observed in this study as well as the effect of acetazolamide on clinical end points, such as duration of mechanical ventilation, are warranted.

Acetazolamide↗
PubMed1995

Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty.

PURPOSE: To help determine the etiology and most appropriate treatment regimen for hypergastrinemia, dysuria-hematuria and metabolic alkalosis following augmentation gastrocystoplasty. MATERIALS AND METHODS: Two patients who presented with refractory metabolic alkalosis (1 with dysuria-hematuria) underwent extensive laboratory evaluation, complete upper gastrointestinal evaluation and intravesical pH probe placement. RESULTS: Both patients eventually required high dose oral potassium chloride supplementation. Bladder mucosal pH was not reflected by buffered urinary pH. Both patients demonstrated significant gastroesophageal reflux and diminished overall gastric acid output. CONCLUSIONS: Outpatient maintenance on potassium chloride supplementation may be warranted in select patients and appears to be preferable to histamine blockade or omeprazole. Postoperative screening esophagogastroscopy and an additional surgical maneuver might be indicated to prevent possible adverse sequelae of reflux esophagitis. Gastrocystoplasty may be an inappropriate operation in children with renal insufficiency who have not had metabolic acidosis.

Alkalosis↗
PubMed1994

Severe metabolic alkalosis.

Our patient's acid-base disturbance may be among the highest recorded in nonfatal cases of metabolic alkalosis. This case also shows that life-threatening alkalemia can be safely and effectively treated by defining and removing the causes of alkalosis and applying aggressive supportive therapy with fluid repletion and potassium and electrolyte replacement. The need for potentially dangerous therapy such as exogenous acid administration, dialysis, or forced mechanical depression of respiration should not routinely be used on the basis of blood pH alone, and it should never replace thoughtful, organized supportive care.

Alkalosis↗
PubMed2006

Baking soda pica: a case of hypokalemic metabolic alkalosis and rhabdomyolysis in pregnancy.

BACKGROUND: We report a case of baking soda pica in a woman at 31 weeks of pregnancy causing severe hypokalemic metabolic alkalosis and rhabdomyolysis. CASE: A multigravida at 31 weeks of gestation presented with weakness and muscle pain. She was found to have severe hypokalemic metabolic alkalosis and rhabdomyolysis, with elevation in serum transaminases and hypertension. We initially thought the patient had an atypical presentation of preeclampsia until it was realized that she was ingesting 1 full box of baking soda (454 g sodium bicarbonate) per day. Symptoms and abnormal laboratory findings resolved with discontinuation of the patient's pica practices. CONCLUSION: Pica is a common but often overlooked practice that can potentially lead to life-threatening disorders. A thorough evaluation of a patient's dietary intake is extremely important, especially in the setting of atypical presentations of disease in pregnancy.

Adult↗
PubMed2005

Chest wall necrosis and death secondary to hydrochloric acid infusion for metabolic alkalosis.

Central line complications are common, and extravasation injuries related to infusion of caustic substances have been previously described. Although hydrochloric acid has been used for many years to treat metabolic alkalosis, there have been no reported fatal complications. We report the case of a 53-year-old female who received a fatal chemical burn due to extravasation from a subclavian central venous catheter of hydrochloric acid infused to correct severe metabolic alkalosis. This case illustrates the hazards of the infusion of caustic substances through central lines and underscores the importance of constant vigilance regarding line positioning and changes to the surrounding tissues when infusing these substances.

Alkalosis↗
PubMed1991

Chloride-depletion metabolic alkalosis induces ECF volume depletion via internal fluid shifts in nephrectomized dogs.

We recently reported that chloride-depletion metabolic alkalosis (CDMA) results in renal losses of Na, K, and water. In these studies we investigated whether CDMA (induced using a new model that avoids external changes in Na and water balance) was also associated with internal Na and water shifts out of the ECF. CDMA was induced using haemofiltration in functionally nephrectomized dogs. Plasma ultrafiltrate was substituted quantitatively with a solution duplicating each dog's plasma electrolyte composition in control animals, and with a solution containing HCO3 as the sole anion in CDMA animals. ECF volume was estimated as the space of distribution of [3H]-mannitol. Plasma composition and [3H]-mannitol distribution space were unchanged in control dogs. In CDMA dogs metabolic alkalosis developed; despite the absence of external changes in Na and water balance, the space of distribution of [3H]-mannitol decreased by 335 +/- 46 ml (equivalent to 8% of baseline ECF volume), calculated chloride space fell by 304 +/- 50 ml, and haematocrit increased from 45.6 to 48.5 vol%. We conclude that CDMA causes an internal shift of fluid out of the ECF. The resulting ECF volume contraction appears to be an inherent feature of CDMA.

Alkalosis↗
PubMedDate not supplied

Effects of acidosis or alkalosis on the actions of nifedipine on excitation-contraction coupling in the rat tail artery.

1. The clinical success of calcium channel blockers in the management of organ ischaemia is less than theoretically anticipated. Blood gas/pH changes are associated with organ ischaemia; therefore, we studied the possibility that pH changes could alter the pharmacological effects of the calcium channel blocker nifedipine on rat tail artery contracted by either noradrenaline (NA) or potassium. 2. Segments (2-2.5 cm) of the proximal third of the male Sprague-Dawley rat tail ventral artery were initially bathed and perfused with a physiological salt solution (PSS; pH 7.48) for 25-30 min, after which time bathing/perfusion was continued with a nominally calcium-free PSS made acidotic (pH 7.20), alkalotic (pH 7.67) or unaltered (control). After equilibration, the perfusion pressure (PP) responses to increasing concentrations of calcium in the presence of NA (3.0 mumol/L) or potassium (100 mmol/L) with nifedipine or its vehicle were recorded. 3. The calcium sensitivity of potassium- or NA-stimulated rat tail arteries was reduced during acidosis, as was the maximum PP in potassium- but not NA-stimulated tissues. Alkalosis reduced the calcium sensitivity in potassium- but not NA-stimulated contraction and had no effect on maximum PP. 4. The inhibitory effect of nifedipine (0.6 mumol/L) on contraction was enhanced during acidosis in either NA- or potassium-stimulated arteries and also during alkalosis in NA-treated arteries, although it had little effect during normal conditions. 5. The results indicate that changes in pH alter the vascular contractility profile in a manner dependent on the excitation-contraction coupling mode. The calcium antagonistic effect of nifedipine is pH dependent and it is suggested that pH changes associated with ischaemic conditions may alter the therapeutic profile of nifedipine.

Acidosis↗
PubMed2005

Clinical presentation of metabolic alkalosis in an adult patient with cystic fibrosis.

In subtropical and tropical climates, dehydration is common in cystic fibrosis patients with respiratory exacerbations. This may lead to a clinical presentation of metabolic alkalosis with associated hyponatraemia and hypochloraemia. An adult cystic fibrosis patient who presented with a severe respiratory exacerbation accompanied by metabolic alkalosis is presented and the effects of volume correction are reported.

Acidosis↗
PubMed2002

Bicarbonate-induced alkalosis augments cellular acetyl group availability and isometric force during the rest-to-work transition in canine skeletal muscle.

Increasing blood bicarbonate content has long been cited as a potential mechanism to improve contractile function. We investigated whether sodium bicarbonate-induced metabolic alkalosis could positively affect force development during the rest-to-work transition in ischaemic skeletal muscle. Secondly, assuming it could, we investigated whether bicarbonate could augment acetyl group availability through the same equilibrium reaction as sodium acetate pre-treatment and whether this underpins, at least in part, its ergogenic effect. Multiple biopsy samples were obtained from the canine gracilis muscle during 5 min of electrically evoked ischaemic contraction, which enabled the determination of the time course of acetyl group accumulation, substrate utilisation, pyruvate dehydrogenase complex activation and tension development in animals treated with saline (control; n = 6) or sodium bicarbonate (n = 5). Treatment with bicarbonate elevated acetylcarnitine content above the control level at rest (P < 0.05), but at no time point during subsequent contraction. The pyruvate dehydrogenase complex was activated following 40 s of contraction in both groups, with no differences existing between treatments at any time point. The requirement for ATP re-synthesis from non-oxygen-dependent routes was no different between groups at any time point during contraction. No difference in peak twitch force production existed between groups. However, at 3 min of stimulation, tension development was better maintained in the bicarbonate group (P < 0.05), being approximately 20% greater than control following 5 min of contraction (P < 0.05). The results demonstrate, for the first time, that bicarbonate can augment acetyl group availability prior to contraction, independent of pyruvate dehydrogenase complex activation, but cannot influence the requirement for non-oxidative ATP re-synthesis during subsequent contraction. It would appear, therefore, that the bicarbonate-induced improvement in muscle tension development was probably mediated through the metabolic alkalosis and not via the increased availability of acetyl groups within the cell.

Acetylcarnitine↗
PubMed1987

Metabolic alkalosis following administration of an organophosphorus compound, O,S,S-trimethyl phosphorodithioate.

The oral administration of a single dose of O,S,S-trimethyl phosphorodithioate (OSSMe) to rats was found to result, 24 hours after treatment, in a dose-related metabolic alkalosis. Non-invasive indices of kidney damage revealed that during the first 4 hours after OSSMe administration there was a fourfold increase in urine flow with increases in albumin, beta 2-microglobulin and N-acetyl-glucosaminidase excretion. These results suggest that OSSMe-induced metabolic alkalosis may result from early renal functional disturbances.

Acetylcholinesterase↗
PubMed1976

Effects of respiratory alkalosis and acidosis on myocardial excitation.

In anesthetized dogs electrocardiogram and monophasic action potentials (MAPs) were recorded from the right atrium and the right ventricle by intracardiac suction electrode technique. The animals were subjected, by means of ventilation with CO2 and hyperventilation, to periods of respiratory acidosis and respiratory alkalosis, respectively. Pronounced respiratory acidosis induced an increased sympathetic activity followed by a decrease in heart rate and prolongation of the A-V conduction time whereas the shape and duration of the atrial and ventricular MAPs remained unaltered. Arterial hypoxia in combination with pronounced respiratory acidosis did not influence the MAP durations. Respiratory alkalosis resulted in an increased sympathetic influence on the heart activity whereas the shape and duration of the atrial and the ventricular MAPs remained unaffected. During pronounced hyperventilation with increasing central venous pressure an increased parasympathetic influence on the heart activity with decrease in the heart rate, prolongation of the A-V conduction time and shortening of the atrial MAP duration was recorded.

Acidosis, Respiratory↗