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At least 469 records · Page 26Linked to original sources
PubMed1989

Pulmonary artery catheter deterioration during hydrochloric acid infusion for the treatment of metabolic alkalosis.

Hydrochloric acid (HCl) infusions for the correction of metabolic alkalosis have been used for 20 yr. In the critical care setting, HCl is usually infused through a central venous or pulmonary artery (PA) catheter. In two patients receiving HCl infusions through a PA catheter, we observed and examined solid yellow particulate material in the aspirating syringe while testing the proximal lumen for patiency. We carried out in vitro investigation infusing PA catheters with 0.1, 0.2, 0.3, and 0.4 normal HCl at 20 degrees, 38 degrees, and 42 degrees C for 24 and 48 h. Although frank catheter deterioration could not be documented, the surface and interior of those catheters infused with greater than 0.1 normal HCl changed texture, indicating a change in catheter composition. Exceeding a concentration of 0.1 normal is not recommended when HCl is infused through PA catheters.

Alkalosis↗
PubMed1987

Hypernatremia and metabolic alkalosis as a consequence of the therapeutic misuse of baking soda.

When used appropriately, baking soda (sodium bicarbonate, USP) is a nontoxic, readily available, multipurpose product found in many households. We report an infant who presented with hypernatremia and metabolic alkalosis due to the addition of baking soda to her water. This case represents the possible dangerous use of a common household product in infants owing to the lack of proper warning labels.

Alkalosis↗
PubMed1989

Hypoelectrolytemia, hypovolemia, and alkalosis in cystic fibrosis with wood-burning stove in winter.

Hypoelectrolytemia, alkalosis, and shock were present in an infant subsequently diagnosed as having cystic fibrosis (CF). Environmental temperature control was poorly maintained by a wood-burning stove in winter and contributed to the process of fluid and electrolyte loss. Pediatricians must consider CF and other processes when electrolytes and fluid are lost during environmental heat excess.

Alkalosis↗
PubMed1979

Life-threatening metabolic alkalosis in a comatose patient.

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.

Acetazolamide↗
PubMedDate not supplied

Metformin-associated respiratory alkalosis.

We present an 84-year-old man with a history of chronic obstructive pulmonary disease, type 2 diabetes, hypertension, glaucoma, and bladder cancer who presented to the emergency department after the police found him disoriented and confused. Metformin therapy began 3 days before, and he denied any overdose or suicidal ideation. Other daily medications included glipizide, fluticasone, prednisone, aspirin, furosemide, insulin, and potassium supplements. In the emergency department, his vital signs were significant for hypertension (168/90), tachycardia (120 bpm), and Kussmaul respirations at 24 breaths per minute. Oxygen saturation was 99% on room air, and a fingerstick glucose was 307 mg/dL. He was disoriented to time and answered questions slowly. Metformin was discontinued, and by day 3, the patient's vital signs and laboratory test results normalized. He has been asymptomatic at subsequent follow-up visits. Metformin-associated lactic acidosis is a well-known phenomenon. Respiratory alkalosis may be an early adverse event induced by metformin prior to the development of lactic acidosis.

Aged↗
PubMed1995

Severe hyperventilation and respiratory alkalosis during pressure-support ventilation: report of a hazard.

A 53-year-old woman with a flaccid quadriparesis developed severe hyperventilation and respiratory alkalosis during pressure-support ventilation. A gas leak in the ventilator system caused a loss of positive end-expiratory pressure and autocycling of the ventilator. Large ventilator breaths were then delivered because a high level of pressure support was set in a patient with low respiratory impedance. The complication is rare and its occurrence requires a combination of patient and equipment factors. Awareness of the responsible factors will promote detection and prevention of the hazard.

Alkalosis, Respiratory↗
PubMed1986

Correction of metabolic alkalosis by HCl and acetazolamide: effects on extracellular and intracellular acid-base status in rats in vivo.

Extracellular plasma pH (pHe) of nephrectomized male or female Sprague-Dawley rats was changed by infusion of either sodium bicarbonate or HCl to predetermined values in the pH range of 7.53-7.14, and then held constant for 2 h. Intracellular pH (pHi) of the liver, heart, brain, and two skeletal muscle groups as calculated from the distribution of 14C-labelled DMO (5.5-dimethyl-2,4-oxazolidinedione) was compared to corresponding tissues of a control group and rats treated with the carbonic anhydrase inhibitor acetazolamide (Diamox). When compared to control, changes of the extracellular pH in male or female rats were followed by similar effects on pHi in the investigated tissues. At the same extracellular pH there were no statistical differences between pHi values of HCl or acetazolamide treated rats, though the arterial PCO2 following acetazolamide administration was significantly increased when compared to control or the corresponding HCl group. This study shows that administration of acetazolamide or HCl results in a dose-dependent decrease of plasma and tissue pH, and that both agents may be used as a logical and safe therapy during severe metabolic alkalosis in rats.

Acetazolamide↗
PubMed1995

Metabolic alkalosis due to the use of an oligoantigenic diet in infancy.

A 7-month-old boy on an oligoantigenic diet because of multiple food intolerances presented with anorexia, failure to gain weight and severe hypochloremic metabolic alkalosis with hyperreninemia. Clinical symptoms and biochemical abnormalities disappeared after adequate dietary supplementation with potassium and sodium chloride. This case emphasizes that minimal daily mineral requirements must be provided in infant diets, and highlights the risk of nutritional deficiencies inherent in the prolonged use of oligoantigenic diets not adequately supplemented.

Alkalosis↗
PubMed2005

Metabolic alkalosis reduces exercise-induced acidosis and potassium accumulation in human skeletal muscle interstitium.

Skeletal muscle releases potassium during activity. Interstitial potassium accumulation is important for muscle function and the development of fatigue resulting from exercise. In the present study we used sodium citrate ingestion as a tool to investigate the relationship between interstitial H+ concentration and K+ accumulation during exercise. Seven healthy subjects performed one-legged knee-extensor exercise on two separate days with and without sodium citrate ingestion. Interstitial H+ and K+ concentrations were measured with the microdialysis technique. Citrate ingestion reduced the plasma H+ concentration and increased the plasma HCO3- concentration. Citrate had no effect on interstitial H+ at rest. The increase in interstitial H+ concentration during intense exercise was significantly lower (P < 0.05) with citrate ingestion compared to control (peak interstitial H+ concentration 79 versus 131 nM). After 3 min of exercise interstitial K+ concentration was reduced (P < 0.05) in the citrate (alkalosis) compared to the control experiment (8.0 +/- 0.9 versus 11.0 +/- 2 mM) and interstitial K+ concentration remained lower during the rest of the exercise period. The present study demonstrated a link between interstitial H+ and K+ accumulation, which may be through the ATP-sensitive K+ channels (KATP channels), which are sensitive to changes in H+.

Acidosis↗
PubMed1971

Alkalosis in burns in children.

The acid-base changes in 14 children with severe burns were studied for varying periods after resuscitation. A long-continued metabolic alkalosis was found, which may be due to increased adrenocortical activity.

Adrenal Glands↗
PubMed1978

The use of dilute hydrochloric acid and cimetidine to reverse severe metabolic alkalosis.

Two cases of severe metabolic alkalosis associated with gastric hypersecretion were successfully treated with dilute hydrochloric acid and a histamine H2-receptor antagonist given by intravenous infusion. This combined therapy with electrolyte replacement and suppression of gastric secretion is valuable in the control of this serious metabolic abnormality when conventional treatment is unsuccessful or contraindicated.

Adult↗
PubMed1983

Extreme metabolic alkalosis with fludrocortisone therapy.

We present an unusual case of extreme metabolic alkalosis resulting from severe hypokalaemia caused by unmonitored fludrocortisone therapy. Biochemical aspects of the disorder are discussed, as is the successful treatment with diuretics and potassium replacement. Some dangers of this therapy and necessary precautions are emphasized.

Aged↗
PubMed2000

Effects of exercise and alkalosis on serum insulin-like growth factor I and IGF-binding protein-3.

This investigation examines the effects of orally induced alkalosis on serum IGF-I and IGFBP3 concentrations in response to an acute 90-s bout of high intensity cycle exercise. Ten healthy, active men, ages 24.60 +/- 4.90 years, participated in a randomized, double-blind, counterbalanced trial order with a cross-over design. Subjects ingested an experimental bicarbonate solution or a placebo solution. Blood was sampled at baseline; pre-exercise; and 0, 5, 10, and 30 min postexercise. The pH between groups for pre-exercise and postexercise time points differed significantly (p < or = .05) in the experimental condition (from 7.42 +/- 0.01 to 7.35 +/- 0.02) versus the placebo condition (from 7.36 +/- 0.01 to 7.25 +/- 0.03). Increases in IGF-I over resting conditions occurred with placebo conditions at 5 and 10 min postexercise and in the experimental condition at 5 min postexercise. Concentrations of IGFBP3 were elevated above baseline at IP in both experimental and placebo conditions.

Adolescent↗
PubMed2003

Polymodal regulation of hTREK1 by pH, arachidonic acid, and hypoxia: physiological impact in acidosis and alkalosis.

Expression of the human tandem P domain K+ channel, hTREK1, is limited almost exclusively to the central nervous system, where ambient Po2 can be as low as 20 Torr. We have previously shown that this level of hypoxia evokes a maximal inhibitory influence on recombinant hTREK1 and occludes the activation by arachidonic acid; this has cast doubt on the idea that TREK1 activation during brain ischemia could facilitate neuroprotection via hyperpolarizing neurons in which it is expressed. Using both whole cell and cell-attached patch-clamp configurations, we now show that the action of another potent TREK activator and ischemia-related event, intracellular acidification, is similarly without effect during compromised O2 availability. This occlusion is observed in either recording condition, and even the concerted actions of both arachidonic acid and intracellular acidosis are unable to activate hTREK1 during hypoxia. Conversely, intracellular alkalinization is a potent channel inhibitor, and hypoxia does not reverse this inhibition. However, increases in intracellular pH are unable to occlude either arachidonic acid activation or hypoxic inhibition. These data highlight two important points. First, during hypoxia, modulation of hTREK1 cannot be accomplished by parameters known to be perturbed in brain ischemia (increased extracellular fatty acids and intracellular acidification). Second, the mechanism of regulation by intracellular alkalinization is distinct from the overlapping structural requirements known to exist for regulation by arachidonic acid, membrane distortion, and acidosis. Thus it seems likely that hTREK1 regulation in the brain will be physiologically more relevant during alkalosis than during ischemia or acidosis.

Acidosis↗
PubMed1993

Relative roles of intracellular Ca2+ and pH in shaping myocardial contractile response to acute respiratory alkalosis.

During acute respiratory alkalosis, myocardial contractility initially increases but then declines toward control levels. To elucidate the mechanism of this response, two parallel strategies were adopted: isovolumic left ventricular developed pressure (DP) and intracellular pH (pHi) were measured in isolated ferret hearts using 31P-nuclear magnetic resonance spectroscopy, and isometric developed tension (DT) and intracellular Ca2+ concentration ([Ca2+]i) were measured in ferret papillary muscles using microinjected fura 2 salt. When hypocapnia was induced by sudden introduction of perfusate equilibrated with 2% CO2 (from 5% CO2 in control), DP increased to a maximum of 120 +/- 3% (SE; n = 7) of control within 40 s. Afterward, DP decreased toward control levels, reaching a new steady state in 2-3 min. In contrast, pHi increased from control (7.11 +/- 0.01) only after 30 s of hypocapnia and reached a peak of 7.25 +/- 0.02 between 80 and 100 s. Thus pHi lagged behind contractility. In contrast to pHi, [Ca2+]i changed in parallel with DT: when DT reached a maximum (251 +/- 63% of control; n = 5) during hypocapnia, the amplitude of [Ca2+]i transients also peaked (190 +/- 22% of control; n = 5). A simulation of contractile force based on our measurements of pHi and [Ca2+]i, along with published Ca(2+)-tension relations, described adequately the changes in developed force during hypocapnia. These results indicate that the biphasic changes in [Ca2+]i, coupled with an out-of-phase change in pHi, underlie the biphasic response of myocardial contractility to hypocapnia.

Adenosine Triphosphate↗