Bicarbonate metabolic acidosis

Advanced stages Increased potassium, phosphorus, and magnesium decreased bicarbonate (metabolic acidosis) calcium levels are generally low in earlier stages of CKD and may be elevated in stage 5 CKD, secondary to the use of calcium-containing phosphate binders. 

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. 

Metabolic Effects. Severe metabolic acidosis with high anion gap and hyperglycemia was reported in humans after acute poisoning with endosulfan (Blanco-Coronado et al. 1992 Lo et al. 1995). In five of the six cases reported by Blanco-Coronado et al. (1992), the metabolic acidosis was corrected with gastric lavage with activated charcoal and intravenous sodium bicarbonate and diazepam. No further information regarding metabolic effects in humans after exposure to endosulfan was located. 

Hyperchloremic (nonanion gap) metabolic acidosis ° Consumption/loss of bicarbonate... 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Studies have demonstrated that reversal of metabolic acidosis can improve bone disease associated with CKD.38 Serum bicarbonate levels should be maintained at 22 mEq/L (22 mmol/L) in patients with bone disease associated with CKD.39 The treatment of metabolic acidosis is described below. 

As kidney function declines, bicarbonate reabsorption is maintained, but hydrogen excretion is decreased because the ability of the kidney to generate ammonia is impaired. The positive hydrogen balance leads to metabolic acidosis, which is characterized by a serum bicarbonate level of 15 to 20 mEq/L (15 to 20 mmol/L). This picture is generally seen when the GFR declines below 20 to 30 mL/minute.38... 

Treatment of metabolic acidosis in CKD requires pharmacologic therapy. Other disorders that may contribute to metabolic acidosis should also be addressed. Altering bicarbonate levels in the dialysate fluid in patients receiving dialysis may assist with the treatment of metabolic acidosis, although pharmacologic therapy may still be required. 

Electrolytes Daily doses based on daily maintenance requirements, renal function, gastrointestinal losses, acid-base status, concomitant drug therapy, nutritional and anabolic status Pa lion I has hyponatremia, hypokalemia, hypomagnesemia, and hypophosphatemia, also has low serum bicarbonate concentration, could be component of metabolic acidosis due to sepsis... 

Acid-base disturbances associated with PN usually are related to the patient s underlying condition(s). However, acid-base abnormalities may develop as a result of changes in chloride or acetate concentrations in PN admixtures. Because acetate is converted to bicarbonate in the body, excessive acetate salts in PN can lead to metabolic alkalosis excessive chloride salts in PN can lead to metabolic acidosis. PN should not be used to... 

Metabolic acidosis An acid-base disorder caused by overproduction or accumulation of acid (often lactic acid see lactic acidosis) or a deficit of base (i.e., bicarbonate). 

The answer is c. (Hardman, pp 6917 693 J Acetazolamide is a carbonic anhydrase inhibitor with its primary site of action at the proximal tubule of the nephron. Acetazolamide promotes a urinary excretion of Na, K, and bicarbonate There is a decrease in loss of Cl ions The increased excretion of bicarbonate makes the urine alkaline and may produce metabolic acidosis as a consequence of the loss of bicarbonate from the blood. None of the other diuretic drugs promote a reduction in the excretion of the Cl ion... 

Sodium bicarbonate administration for cardiac arrest is controversial because there are few clinical data supporting its use, and it may have some detrimental effects. Sodium bicarbonate can be used in special circumstances (i.e., underlying metabolic acidosis, hyperkalemia, salicylate overdose, or tricyclic antidepressant overdose). The dosage should be guided by laboratory analysis if possible. 

Metabolic and/or respiratory acidosis should be assessed by ABG measurements to determine pH, Pa02, PaC02, and HC03. If pH is less than 7.2, secondary to metabolic acidosis, sodium bicarbonate should be given. 

Metabolic acidosis is characterized by decreased plasma bicarbonate concentrations (HC03 ), whereas metabolic alkalosis is characterized by increased HC03T... 

Alkali therapy can be used to treat patients with acute severe metabolic acidosis due to hyperchloremic acidosis, but its role is controversial in patients with lactic acidosis. Therapeutic options include sodium bicarbonate and tromethamine. 

Metabolic acidosis in patients undergoing dialysis can often be managed by using higher concentrations of bicarbonate or acetate in the dialysate. 

Metabolic acidosis may result when pC02 reads higher than 44 mm Hg or bicarbonate levels fall below 20 mEq/L, resulting in a pH lower than 7.35. A rise of 5 mEq/L of bicarbonate for every 10 mm Hg maybe necessary to normalize the pH. 

Calculation of the amount of bicarbonate in terms of milliequivalents needed in the treatment of metabolic acidosis is as follows ... 

Metabolic acidosis and hyperchioremia Potassium depletion is rarely associated with metabolic acidosis and hyperchloremia. Replace with potassium bicarbonate, citrate, acetate, or gluconate. 

Metabolic acidosis In severe renal disease uncontrolled diabetes circulatory insufficiency due to shock, anoxia, or severe dehydration extracorporeal circulation of blood cardiac arrest and severe primary lactic acidosis where a rapid increase in plasma total CO2 content is crucial. Treat metabolic acidosis in addition to measures designed to control the cause of the acidosis. Because an appreciable time interval may elapse before all ancillary effects occur, bicarbonate therapy is indicated to minimize risks inherent to acidosis itself. 

Less urgent forms of metabolic acidosis - Sodium bicarbonate injection may be added to other IV fluids. The amount of bicarbonate to be given to older children and adults over a 4- to 8-hour period is approximately 2 to 5 mEq/kg, depending on the severity of the acidosis as judged by the lowering of total CO2 content, blood pH, and clinical condition. Initially, an infusion of 2 to 5 mEq/kg over 4 to 8 hours will produce improvement in the acid-base status of the blood. 

Metabolic acidosis Hyperchloremic, nonanion gap, metabolic acidosis is associated with topiramate treatment. This metabolic acidosis is caused by renal bicarbonate loss because of the inhibitory effect of topiramate on carbonic anhydrase. Generally, topiramate-induced metabolic acidosis occurs early in treatment, although cases can occur at any time during treatment. Bicarbonate decrements usually are mild to moderate rarely, patients can experience severe decrements to values below 10 mEq/L. Conditions or therapies that predispose to acidosis may be additive to the bicarbonate lowering effects of topiramate. If metabolic acidosis develops and persists, consider reducing the dose or discontinuing topiramate. 

The answer is C. Ingestion of an acid or excess production by the body, such as in diabetic ketoacidosis, may induce metabolic acidosis, a condition in which both pH and HCOj become depressed. In response to this condition, the carbonic acid-bicarbonate system is capable of disposing of the excess acid in the form of CO2. The equilibrium between bicarbonate and carbonic acid shifts toward formation of carbonic acid, which is converted to COj and HjO in the RBC catalyzed by carbonic anhydrase, an enzyme found mainly in the RBC. The excess CO2 is then expired by the lungs as a result of respiratory compensation for the acidosis (Figure 1-2). The main role of the kidneys in managing acidosis is through excretion of H" rather than CO2. 

Management of methanol and ethylene glycol poisoning is similar. Symptomatic support of respiration and circulation is augmented by correction of metabolic acidosis with intravenous bicarbonate infusion, and control of seizures with diazepam. Ethanol inhibits the metabolism of methanol and ethylene glycol to the toxic metabolites, and can give time for further treatment. The goal is to maintain blood ethanol concentrations between 100 and 150 mg per decilitre, sufficient to saturate alcohol... 

Acidosis and alkalosis are infrequent. Metabolic acidosis is a side effect of acetazolamide therapy and is due to bicarbonate loss in the PCT. All the K+-sparing diuretics can cause metabolic acidosis by H+ retention in the cells of the collecting duct. Metabolic alkalosis is associated with the loop and thiazide drugs. Reflex responses to volume depletion cause reabsorption of HCO-3 in the PCT and H+ secretion in the collecting tubule. 

It is critical that the blood methanol level be determined as soon as possible if the diagnosis is suspected. Methanol concentrations higher than 50 mg/dL are thought to be an absolute indication for hemodialysis and treatment with fomepizole or ethanol, although formate blood levels are a better indication of clinical pathology. Additional laboratory evidence includes metabolic acidosis with an elevated anion gap and osmolar gap (see Chapter 59). A decrease in serum bicarbonate is a uniform feature of severe methanol poisoning. 

Metabolic acidosis follows, and an increased anion gap results from accumulation of lactate as well as excretion of bicarbonate by the kidney to compensate for respiratory alkalosis. Arterial blood gas testing often reveals this mixed respiratory alkalosis and metabolic acidosis. Body temperature may be elevated owing to uncoupling of oxidative phosphorylation. Severe hyperthermia may occur in serious cases. Vomiting and hyperpnea as well as hyperthermia contribute to fluid loss and dehydration. With very severe poisoning, profound metabolic acidosis, seizures, coma. 

The blood pH may return to normal in adults with mild overdoses. However, the blood pH can drop too far in children or more severely poisoned adults, resulting in metabolic acidosis. A lower buffering capacity or plasma protein-binding capacity may underlie the increased susceptibility to acidosis in children. Excretion of bicarbonate also means the bicarbonate in the blood is lower, and hence, there is an increased likelihood of metabolic acidosis. 

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