sodium-bicarbonate and Water-Electrolyte-Imbalance

Acute kidney injury (AKI) is a common sequela of critical illness. Clinical manifestation of AKI varies and can include electrolyte abnormalities, anion gap, or non-anion-gap metabolic acidosis. Treatment strategies require careful identification of the cause of the AKI, relying on both clinical history and laboratory data. Once the cause has been identified, treatment can then target the underlying cause and avoid further insults. Conservative management should first be attempted for patients with AKI. If conservative management fails, renal replacement therapy or hemodialysis can be used.

Topics: Acute Kidney Injury; Critical Illness; Diuretics; Emergency Medicine; Emergency Service, Hospital; Fluid Therapy; Humans; Renal Replacement Therapy; Sodium Bicarbonate; Vasoconstrictor Agents; Water-Electrolyte Imbalance

A number of feeding and management practices, dietary electrolyte supplements, and medications may affect fluid and electrolyte status in resting and exercising horses. The contents of the gastrointestinal tract of the equine athlete, unlike its human counterpart, are responsible for more than 10% of body weight. Although ingesta traditionally has been considered dead weight for the sprinting horse, it is a valuable reservoir of fluid and electrolytes that may be used during endurance exercise. Numerous strategies for hyperhydration of the equine athlete and for replacement of fluid and electrolytes lost via sweating were developed in preparation for competing in the hot and humid climate of the 1996 Olympic Games in Atlanta. These strategies have implications for all equine athletes. Medications, including sodium bicarbonate, furosemide, and acetazolamide commonly are used to enhance performance by either buffering alterations in fluid and electrolyte homeostasis or by ameliorating the effects of other conditions that may limit performance.

Topics: Acetazolamide; Animals; Carbonic Anhydrase Inhibitors; Diuretics; Fluid Therapy; Furosemide; Horse Diseases; Horses; Humans; Physical Conditioning, Animal; Sodium Bicarbonate; Water-Electrolyte Imbalance

We have previously investigated the fate of administered bicarbonate infused as a hypertonic solution in animals with each of the 4 chronic acid-base disorders. Those studies did not address the fate of sodium, the coadministered cation.. We examined baseline total body water (TBW), Na+ space, HCO3- space, and urinary sodium and bicarbonate excretion after acute hypertonic NaHCO3 infusion (1-N solution, 5 mmol/kg body weight) in dogs with each of the 4 chronic acid-base disorders. Observations were made at 30, 60, and 90 min postinfusion. Retained sodium that remains osmotically active distributes in an apparent space that approximates TBW. Na+ space that exceeds TBW uncovers nonosmotic sodium storage.. Na+ space approximated TBW at all times in normal and hyperbicarbonatemic animals (metabolic alkalosis and respiratory acidosis), but exceeded TBW by ~30% in hypobicarbonatemic animals (metabolic acidosis and respiratory alkalosis). Such osmotic inactivation was detected at 30 min and remained stable. The pooled data revealed that Na+ space corrected for TBW was independent of the initial blood pH but correlated with initial extracellular bicarbonate concentration (y = -0.01x + 1.4, p= 0.002). The fate of administered sodium and bicarbonate (internal distribution and urinary excretion) was closely linked.. This study demonstrates that hypobicarbonatemic animals have a Na+ space that exceeds TBW after an acute infusion of hypertonic NaHCO3 indicating osmotic inactivation of a fraction of retained sodium. In addition to an expanded Na+ space, these animals have a larger HCO3- space compared with hyperbicarbonatemic animals. Both phenomena appear to reflect the wider range of titration of nonbicarbonate buffers (Δ pH) occurring during NaHCO3- loading whenever initial [HCO3-]e is low. The data indicate that the fate of administered bicarbonate drives the internal distribution and the external disposal of sodium, the co-administered cation, and is responsible for the early, but non-progressive, osmotic inactivation of a fraction of the retained sodium.

Topics: Animals; Cations, Monovalent; Disease Models, Animal; Dogs; Female; Humans; Hydrogen-Ion Concentration; Hypertonic Solutions; Infusions, Intravenous; Kidney; Renal Elimination; Sodium; Sodium Bicarbonate; Tissue Distribution; Water-Electrolyte Imbalance

The Edelman equation has long guided the expected response of plasma [Na+] to changes in sodium, potassium, and water balance, but recent short-term studies challenged its validity. Plasma [Na+] following hypertonic NaCl infusion in individuals on low-sodium diet fell short of the Edelman predictions supposedly because sodium restriction caused progressive osmotic inactivation of 50% of retained sodium. Here, we examine the validity of this challenge.. We evaluated baseline total body water (TBW) and Na+ space following acute hypertonic NaHCO3 infusion in dogs with variable sodium and potassium stores, including normal stores, moderate depletion (chronic HCl feeding), or severe depletion (diuretics and dietary NaCl deprivation).. TBW (percentage body weight) averaged 65.9 in normals, 62.6 in HCl-induced metabolic acidosis and moderate sodium and potassium depletion, and 57.6 in diuretic-induced metabolic alkalosis and severe sodium and potassium depletion (p < 0.02). Na+ space (percentage body weight) at 30, 60, and 90 min postinfusion averaged 61.1, 59.8, and 56.1, respectively, in normals (p = 0.49); 70.0, 74.4, and 72.1, respectively, in acidotic animals (p = 0.21); and 56.4, 55.1, and 54.2, respectively, in alkalotic animals (p = 0.41). Absence of progressive expansion of Na+ space in each group disproves progressive osmotic inactivation of retained sodium. Na+ space at each time point was not significantly different from baseline TBW in normal and alkalotic animals indicating that retained sodium remained osmotically active in its entirety. However, Na+ space in acidotic animals at all times exceeded by ∼16% baseline TBW (p < 0.01) signifying an early, but nonprogressive, osmotic inactivation of retained sodium, which we link to baseline bone-sodium depletion incurred during acid buffering.. Our investigation affirms the validity of the Edelman construct in normal dogs and dogs with variable sodium and potassium depletion and, consequently, refutes the recent observations in human volunteers subjected to dietary NaCl restriction.

Topics: Animals; Body Water; Diet, Sodium-Restricted; Disease Models, Animal; Dogs; Female; Humans; Hypertonic Solutions; Infusions, Intravenous; Potassium; Sodium Bicarbonate; Water-Electrolyte Imbalance

Metabolic acidosis (MAC) is a constant symptom of chronic kidney disease (CKD) in advanced stages. However, its onset and degree do not depend only on the decrease of glomerular filtration but also on tubular functions. Therefore, in patients with predominant tubulointerstitial involvement it may already appear in earlier stages of CKD, usually as MAC with normal anion gap. The progressive decrease of glomerular filtration leads to acid retention that develops in a MAC with an increased anion gap. MAC has many adverse clinical impacts, including the progression of the underlying CKD. The development and degree of MAC in CKD is usually influenced by a combination of several pathophysiological mechanisms and a number of external factors, the most important of them being the diet - the intake and type of proteins - and hydration status. A correct identification of the factors contributing to MAC determines the therapeutic possibilities of its correction. However, optimal serum concentrations of bicarbonate in conservatively treated patients are still subject to debate. Opinions are even more divided on the question of optimal serum concentration of bicarbonate before and after dialysis, in particular due to the risk of post-dialysis meta-bolic alkalosis.Key words: dialysate bicarbonate - chronic kidney disease - metabolic acidosis - sodium bicarbonate - sodium-chloride difference.

Topics: Acidosis; Bicarbonates; Disease Progression; Humans; Renal Dialysis; Renal Insufficiency, Chronic; Sodium Bicarbonate; Water-Electrolyte Imbalance

A 32-year old male, with a history of depression and previous suicide attempts, was brought to hospital comatose after ingestion of brake fluid. He developed severe metabolic acidosis with an increased anion gap, hypotension, seizures and mild renal impairment. He required intensive care treatment for ventilatory and inotropic support. The clinical features, diagnosis and treatment of this unusual poison are discussed.

Topics: Acid-Base Equilibrium; Acidosis; Adult; Ethylene Glycol; Humans; Male; Sodium Bicarbonate; Suicide, Attempted; Water-Electrolyte Imbalance

We experienced two Duchenne muscular dystrophy patients with advanced congestive heart failure, who showed abrupt severe hyponatremia, hyperkalemia and metabolic acidosis. Two patients received respiratory management, parenteral nutrition, and drugs including angiotensin converting enzyme inhibitors (ACEI). The patient 1 who was 19 years old showed abdominal pain, hematuria, diarrhea and disorientation. Laboratory findings were as follows; Na 120 mEq/L, K 7.3 mEq/L, BUN > 140 mg/dl (scale over), ACTH 20.2 pg/ml, cortisol 25 micrograms/dl, renin 40.7 ng/ml/hr and aldosterone 203 ng/dl. Arterial blood gas analysis (ABG) showed metabolic acidosis (pH 7.232). Combination therapy with hydrocortisone, glucose-insulin therapy (GIT) and NaHCO3 successfully rescued this patient. The patient 2 (28 years of age) was admitted to our hospital because of congestive heart failure. Laboratory findings were as follows; Na 129 mEq/L, K 5.5 mEq/L, BUN 60 mg/dl, cortisol 21 micrograms/dl, renin 36 ng/ml/hr and aldosterone 47 ng/dl. He complained abdominal discomforts from the next day of admission. Ten days after the admission Na, K and BUN were 111 mEq/L, 6.2 mEq/L and 154 mg/dl, respectively. ABG showed compensated metabolic acidosis. He fell into shock during GIT therapy. Laboratory findings at that time were as follows; Na 108 mEq/L, K 3.2 mEq/L, ACTH 77.6 pg/ml, cortisol 24 micrograms/dl, renin 58 ng/ml/hr and aldosterone 24 ng/dl. Although hydrocortisone was introduced, he could not recover and died. There are some reports about life-threatening electrolyte abnormalities and metabolic acidosis in the patients receiving ACEI. These phenomena were more frequent in patients with renal dysfunction and/or congestive heart failure. Hyponatremia, hypovolemia, combination therapy with nonsteroidal anti-inflammatory drugs (NSAID) and/or potassium sparing diuretics were reported as risk factors. We could not prove the correlation between the acute changes in our cases and ACEI. However ACEI is suspicious, because many of these risk factors were observed in our cases. Aldosterone was extremely elevated in the patient 1 when potassium was severely elevated. On the other hand, the patient 2 showed lower aldosterone level after correction of potassium than that on admission. Potassium is regarded as a major secretion factor of aldosterone for patients receiving ACEI. The fact the patient 2 fell into shock during GIT, tells us that we should use steroid simultaneously when we try to

Topics: Acidosis; Adult; Angiotensin-Converting Enzyme Inhibitors; Anti-Inflammatory Agents, Non-Steroidal; Diuretics; Glucose; Heart Failure; Humans; Hydrocortisone; Hyponatremia; Insulin; Male; Muscular Dystrophy, Duchenne; Risk Factors; Sodium Bicarbonate; Treatment Outcome; Water-Electrolyte Imbalance

Topics: Humans; Kidney Failure, Chronic; Pica; Sodium Bicarbonate; Water-Electrolyte Imbalance

Toxicity and hazards of sodium hydrocarbonate (SH) and potassium carbonate (PC) were experimentally assessed. Both substances caused impairments of electrolytic equilibrium, protein metabolism, changes of functional and biochemical indicators of the cardiovascular system, etc. LD50 of SH for white rats constituted 9940 +/- 350 mg/kg, for mice 3360 +/- 210 mg/kg and of PC 2980 +/- 142 and 2570 +/- 142 mg/kg, respectively. The authors failed to define mean lethal concentrations of both substances. The following threshold values Limac were established at 74 mg/m3 for SH and at 54 mg/m3 for PC. Limch was respectively 14.9 and 4.7 mg/m3. MAC for SH was established at 5 mg/m3 and for PC at 2 mg/m3.

Topics: Air Pollutants, Occupational; Animals; Bicarbonates; Carbonates; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Maximum Allowable Concentration; Potassium; Rats; Sodium; Sodium Bicarbonate; Water-Electrolyte Imbalance

The purpose of this study was to determine which urine electrolytes should be measured to confirm that the extracellular fluid (ECF) volume is depleted. ECF volume contraction was induced by furosemide administration to rats consuming an electrolyte-free diet. An external potassium balance was achieved by replacing potassium losses with KHCO3 and KCl so that the sodium and chloride deficits were comparable (equivalent to a 30% reduction in ECF volume). As expected, the urine sodium and chloride concentrations fell to 2 +/- 0.3 mmol/l and 3 +/- 0.3 mmol/l, respectively. Rats were then randomized to receive 50-75% of their sodium or chloride deficit as either: NaCl (control group), NH4Cl or NaHCO3 to mimic clinical situations associated with ECF volume contraction. In the NaCl group, the urine sodium and chloride concentrations remained low (6 +/- 2 mmol/l and 7 +/- 2 mmol/l), consistent with persistent ECF volume contraction. Although the NH4Cl group continued to have a low urine sodium concentration (2 +/- 0.2 mmol/l), there was now a marked increase in the urine chloride concentration (51 +/- 7 mmol/l; p less than 0.01 vs. NaCl group). In contrast, although the NaHCO3 group continued to have a low urine chloride concentration (2 +/- 1 mmol/l), there was a significant increase in the urine sodium concentration (19 +/- 3 mmol/l; p less than 0.01 vs. NaCl group). We conclude that the clinical assessment of ECF volume by urine electrolytes requires an evaluation of both the urine sodium and chloride concentrations.

Topics: Ammonium Chloride; Animals; Bicarbonates; Electrolytes; Furosemide; Male; Potassium Chloride; Random Allocation; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Sodium Chloride; Vomiting; Water-Electrolyte Imbalance

Topics: Alkalosis; Aluminum Hydroxide; Antacids; Bicarbonates; Brain Diseases; Calcium; Constipation; Diarrhea; Drug Interactions; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Kidney Calculi; Magnesium Hydroxide; Osteomalacia; Phosphates; Sodium; Sodium Bicarbonate; Urine; Water-Electrolyte Imbalance

Early-lactation Holstein cows fed a corn silage-based diet low in chloride and supplemented with sodium bicarbonate were observed for clinical, metabolic, and production alterations over the course of 8 to 11 weeks. In 3 of the more severely affected cows, metabolic derangements included a rapidly developing primary hypochloremic, secondary hypokalemic and hyponatremic metabolic alkalosis, and hemoconcentration. Clinical signs included severe hypophagia, weight loss, muscle weakness, hypogalactia, dehydration, constipation, cardiopulmonary depression, and a depraved appetite. It was concluded that the rapid progression of these derangements, apart from any anatomic abnormalities or infectious causes, emphasizes the need for rapid assessment and therapeutic intervention in primary imbalance associated with body chloride depletion and metabolic alkalosis.

Topics: Alkalosis; Animals; Bicarbonates; Carbon Dioxide; Cattle; Cattle Diseases; Chlorides; Diet; Electrolytes; Female; Lactation; Pregnancy; Sodium Bicarbonate; Water-Electrolyte Imbalance

Acute renal failure (ARF) implies a sudden decrease in glomerular filtration rate with consequent retention of nitrogen waste products, water and electrolytes normally excreted by the kidney. The causes of ARF fall into three main groups: prerenal, intrinsic, and postrenal. Prerenal or functional failure can usually be controlled by simple therapeutic measures. If unrelieved, it leads to the development of renal parenchymal damage. Early biochemical indices are useful in distinguishing prerenal from intrinsic renal failure. Potentially reversible obstruction must be searched for by ultrasonographic and radiological procedures, and rapidly relieved. Symptoms of ARF result from disturbance of physiological regulatory functions. Prerenal failure requires urgent vascular expansion and careful monitoring of fluid and electrolyte replacement. Established renal failure demands careful management of electrolyte and water overload, metabolic acidosis, anemia, hypertension, infections and nutrition. Peritoneal dialysis or hemodialysis should be prepared for whenever severe hypertension, pulmonary edema or worsening biochemistry occur. Acute renal failure has a generally good prognosis if properly treated.

Topics: Acute Kidney Injury; Bicarbonates; Calcium Gluconate; Child; Fluid Therapy; Humans; Ion Exchange Resins; Peritoneal Dialysis; Sodium Bicarbonate; Water-Electrolyte Imbalance

The true incidence of malignant hyperthermia is unknown, but the frequency has been estimated as high as 1/14,000 anesthetic events. Review of the literature reports mortality rates up to 70%. Without prompt medical intervention, it is a uniformly fatal disease. Thus, it behooves the physician to have an awareness of the syndrome and its features, so that early recognition and adequate treatment take place. This paper presents a review of the literature on the occurrence, pathology, symptoms and treatment of malignant hyperthermia.

Topics: Acidosis; Bicarbonates; Calcium; Creatine Kinase; Dantrolene; Diuretics; Fever; Humans; Malignant Hyperthermia; Muscle Rigidity; Muscle Tonus; Sarcoplasmic Reticulum; Sodium Bicarbonate; Succinylcholine; Water-Electrolyte Imbalance

Topics: Administration, Oral; Animals; Bicarbonates; Fluid Therapy; Glucose; Iatrogenic Disease; Infusions, Parenteral; Injections, Subcutaneous; Sodium; Sodium Bicarbonate; Water-Electrolyte Imbalance