All of the following are true statements regarding acid base balance except
|A||Diarrhoea is associated with normal anion gap|
|B||Respiratory acidosis is associated with increased PaCO2|
|C||Lactic acidosis can produce an increase in anion gap|
|D||Hyperkalemia is associated with metabolic alkalosis|
a. Hyperkalemia is defined as a serum potassium concentration above the normal range of 3.5 to 5.0 mEq/L.
b. Increased intake can be either from oral or intravenous supplementation, as well as from blood transfusions.
c. Cell destruction or breakdown can release potassium in association with hemolysis, rhabdomyolysis, crush injuries, and gastrointestinal hemorrhage.
d. Acidosis and a rapid increase of extracellular osmolality (hyperglycemia or mannitol administration) can raise serum potassium levels by causing a shift of potassium ions to the extracellular compartment.
e. The kidney will also increase secretion of hydrogen and thus increase urinary excretion of NH4+ (H++ NH3+ = NH4+). In evaluating a patient with a low serum bicarbonate level and metabolic acidosis, first measure the anion gap (AG), an index of unmeasured anions.
-Hydroxybutyrate and acetoacetate in ketoacidosis
-Lactate in lactic acidosis
-Organic acids in renal insufficiency
a. Metabolic acidosis with a normal anion gap results from either acid administration (HCl or NH4+) or a loss of bicarbonate from gastrointestinal sources such as diarrhea, fistulas (enteric, pancreatic, or biliary), ureterosigmoidostomy, or from renal loss. The bicarbonate loss is accompanied by a gain of chloride, thus the AG remains unchanged.
b. To determine if the loss of bicarbonate is renal in etiology, the urinary [NH4+] can be measured. A low urinary [NH4+] in the face of hyperchloremic acidosis would indicate the kidney as the site of loss, and evaluation for renal tubular acidosis should be undertaken.