Metabolic alkalosis

Mixed acid-base disorder More than one of the following disorders occurring simultaneously acidosis (metabolic or respiratory) and alkalosis (metabolic or respiratory). 

Losing chloride by vomiting or from continuous Gl suction receiving diuretics known to produce a hypochloremic alkalosis metabolic and respiratory alkalosis hypocalcemia in which alkalosis may produce tetany, hypertension, convulsions, or congestive heart failure (CHF) when sodium use could be clinically detrimental. 

Adults who have taken a single large quantity usually develop a respiratory alkalosis. Metabolic acidosis suggests severe poisoning. Often, a mixed picture is seen clinically. In children imder 4 years, severe metabolic acidosis is more likely than respiratory alkalosis, especially if the drug has been ingested over many hours (mistaken for sweets). 

Hypoventilation causes retention of C02 by the lungs, which can lead to a respiratory acidosis. Hyperventilation can cause a respiratory alkalosis. Metabolic acidosis can result from accumulation of metabolic acids (lactic acid or the ketone bodies p-hydroxybutyric acid and acetoacetic acid), or ingestion of acids or compounds that are metabolized to acids (methanol, ethylene glycol). Metabolic alkalosis is due to increased HC03, which is accompanied by an increased pH. Acid-base disturbances lead to compensatory responses that attempt to restore normal pH. For example, a metabolic acidosis causes hyperventilation and the release of C02, which tends to lower the pH. During metabolic acidosis, the kidneys excrete NH4+, which contains H+ buffered by ammonia. 

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. 

The primary acid-base disturbance observed with salicylate overdosage depends on age and severity of intoxication. Respiratory alkalosis predominates in children over age 4 and in adults, except in very severe cases that may progress through a mixed respiratory alkalosis-metabolic acidosis to metabolic acidosis. In 97 adult patients who had plasma salicylate concentrations greater than 700mg/L, 19% were found to have respiratory alkalosis, 61% had combined res-... 

Tizianello A, Deferraii G, Gurreri G Acquarone N. (1977). Effects of metabolic alkalosis, metabolic acidosis and uraemia on whole-body intracellular pH in man. Chn Sci Mol Med (Oxford) 52, 125-135. 

The use of CA inhibitors as diuretics is limited by their propensity to cause metabolic acidosis and hypokalemia. Their use can be indicated in patients with metabolic alkalosis and secondary hyperaldosteronism resulting for example from aggressive use of loop diuretics. Furthermore, CA inhibitors are effective dtugs to produce a relatively alkaline urine for the treatment of cysteine and uric acid stones as well as for the accelerated excretion of salicylates. Perhaps the most common use of CA inhibitors is in the treatment of glaucoma. 

Liddle s syndrome is an autosomal dominant disorder that is caused by persistent hyperactivity of the epithelial Na channel. Its symptoms mimic aldosterone excess, but plasma aldosterone levels are actually reduced (pseudoaldosteronism). The disease is characterized by early onset arterial hypertension, hypokalemia, and metabolic alkalosis. 

Calcium-containing antacids—rebound hyperacidity, metabolic alkalosis, hypercalcemia, vomiting, confusion, headache, renal calculi, and neurologic impairment... 

Administration of protein substrates (amino acids) may result in nausea, fever, flushing of the skin, metabolic acidosis or alkalosis, and decreased phosphorus and calcium blood levels. 

Metabolic alkalosis is the increase in pH resulting from illness or chemical ingestion. Repeated vomiting or the overuse of diuretics can cause metabolic alkalosis. Once again the body compensates, this time by decreasing the rate of respiration. 

Excretion into urine of ammonia produced by renal mbu-lar cells facilitates cation conservation and regulation of acid-base balance. Ammonia production from intracellular renal amino acids, especially glutamine, increases in metabolic acidosis and decreases in metabolic alkalosis. 

Metabolic alkalosis (citrate hepatically metabolized to bicarbonate)... 

These goals may minimize an overshoot metabolic alkalosis = Remember that ketoacids and lactic acid are metabolized to bicarbonate... 

Low serum chloride and elevated serum bicarbonate levels indicate metabolic alkalosis. 

Arterial blood gases with a normal or elevated pH indicates metabolic alkalosis that may or may not be compensated. 

Monitor serum electrolytes and arterial blood gases regularly. Correct metabolic acidosis slowly to prevent the development of metabolic alkalosis or other electrolyte abnormalities. 

This isotonic volume expander contains sodium, potassium, chloride, and lactate that approximates the fluid and electrolyte composition of the blood. Ringer s lactate (also known as lactated Ringer s or LR) provides ECF replacement and is most often used in the perioperative setting, and for patients with lower GI fluid losses, burns, or dehydration. The lactate component of LR works as a buffer to increase the pH. Large volumes of LR may cause metabolic alkalosis. Because patients with significant liver disease are unable to metabolize lactate sufficiently, Ringer s lactate administration in this population may lead to accumulation of lactate with iatrogenic lactic acidosis. The lactate is not metabolized to bicarbonate in the presence of liver disease and lactic acid can result. 

The findings of hypomagnesemia include muscle weakness, cramps, agitation, confusion, tremor, seizures, ECG changes (increased PR interval, prolonged QRS complex, and increased QT interval), findings of hypocalcemia (see above), refractory hypokalemia (see above), metabolic alkalosis, and digoxin toxicity.42,47,48... 

Respiratory acidosis and alkalosis result from primary disturbances in the arterial carbon dioxide (C02) levels. Metabolic compensation of respiratory disturbances is a slow process, often requiring days for the serum HC03 to reach the steady state. 

Metabolic alkalosis is characterized by an increase in serum HC03A This disorder requires loss of fluid that is low in HC03 from the body or addition of HC03 to the body. The compensation for metabolic alkalosis is a decrease in ventilation with an increase in arterial C02. 

Metabolic alkalosis t Increased6 PaC02 = (0.9 x HCO3-) + 15 Increased3... 

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