Gastric alkalosis

Sodium bicarbonate is a gastric antacid that may cause systemic alkalosis on overdose and may contribute to edema owing to sodium retention. It is useful for systemic acidosis because both deficient ions are present in the same molecule, and it can be used topically as a moist paste or in solution as an antipmritic. Sodium bicarbonate also is an ingredient of many effervescent mixtures, alkaline solutions, etc. One gram of NaHCO neutralizes 115 mL 0.1 NHCl. 

In some instances, excessive oral use may produce nausea and vomiting. Some individuals may use sodium bicarbonate (baking soda) for the relief of gastric disturbances, such as pain, discomfort, symptoms of indigestion, and gas. Prolonged use of oral sodium bicarbonate or excessive doses of IV sodium bicarbonate may result in systemic alkalosis. 

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

No unique signs or symptoms are associated with mild to moderate metabolic alkalosis. Some patients complain of symptoms related to the underlying disorder (e.g., muscle weakness with hypokalemia or postural dizziness with volume depletion) or have a history of vomiting, gastric drainage, or diuretic use. 

Because acid-pepsin disease rarely occurs in the absence of gastric acid and pepsin, antacids are highly effective in its overall management. Antacids consist of a mixture of magnesium, aluminum, and calcium compounds. Their efficacy is based on their inherent ability to react with and neutralize gastric acid. Sodium bicarbonate, which may leave the stomach rapidly, can cause alkalosis and sodium retention. Calcium salts may produce hypercalcemia, which can be detrimental in patients with impaired renal function. Aluminum salts may decrease the absorption of tetracyclines and anticholinergic drugs. 

Sodium bicarbonate (eg, baking soda, Alka Seltzer) reacts rapidly with HC1 to produce carbon dioxide and NaCl. Formation of carbon dioxide results in gastric distention and belching. Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to patients with renal insufficiency. Sodium chloride absorption may exacerbate fluid retention in patients with heart failure, hypertension, and renal insufficiency. 

Metabolic alkalosis can occur when there is excessive H+ loss from the body, via loss of gastric contents in vomiting, or when a patient takes excessive quantities of antacid medication. 

Hjqiochloremia is common in gastrointestinal disease (Svendsen et al 1979), because of the loss of gastric hydrochloric acid in high volume reflux from the stomach (in proximal enteritis and grass sickness) and the secretion and/or lack of absorption of chloride in severe colitis. It may also occur in exhausted horse syndrome, chronic compensated respiratory acidosis and following furosemide (frusemide) administration. Hypochloremia in the absence of hyponatremia results in a metabolic alkalosis (Corley Marr 1998). The alkalosis associated with hypochloremia may also result in increased cellular uptake of potassium, leading to hypokalemia (Schaer 1999). 

Animals may manifest toxicity to salicylates with signs and symptoms similar to those seen in humans. These may include fever, hyperpnea, seizures, respiratory alkalosis, metabolic acidosis, gastric hemorrhage, and kidney damage. Methemoglobinemia has also been seen in animals following salicylate toxicity. Activated charcoal has been used in animals. Methylene blue or ascorbic acid may be utilized for the treatment of methemoglobinemia. 

Loss of gastric acid from vomiting or nasogastric suction- ing is often responsible for the development of a metabolic alkalosis, characterized by hypochloremia and hyperbicar-bonatemia. 

Metabolic alkalosis Gastric losses Treat underlying cause, increase Cl and decrease acetate in PN solution... 

A patient who has had prolonged nasogastric. suction following surgery will lo.se gastric lliiid in large quantities and may develop a metabolic alkalosis. 

Altered gastric pH An acidic drug may be incompletely absorbed if gastric pH is increased. This may occur through the use of antacids, H,-receptor antagonists, or the use of proton pump inhibitors, or in conditions where vomiting is present. This may result in systemic alkalosis, which further lowers drug potency. 

Systemic alkalosis caused by an excessive decrease in gastric acid production is unlikely, because the drug must be activated by an acid environment within the parietal cell. Thus, the conversion of the drug to the active form is related to the amount of carbonic acid available. 

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