Acid-Base Disorders MCQs

Explanation: This patient's labs show acidemia (pH 7.3), low bicarbonate (16), and a normal PCO2 (44), suggesting that the primary abnormality is metabolic acidosis (not compensated by respiratory alkalosis/hyperventilation). The anion gap is: Na+ - (Cl- + HCO3-) = 130 - (84 + 16) = 130 - 100 = 30 This is a high-anion-gap metabolic acidosis. The findings are consistent with acute severe tissue hypoperfusion (due to shock or trauma), leading to lactic acidosis. Explanation of Incorrect Options: Partially compensated respiratory acidosis with an anion gap of 12 (Option A): PCO2 is not elevated, and the anion gap is much higher than 12. Chronic respiratory acidosis with anion gap 30 (Option B): The primary problem is metabolic, not respiratory, as PCO2 is not high but HCO3- is low. Acute metabolic acidosis with anion gap 16 (Option D): The actual anion gap is 30, not 16.

Acid-base imbalance can be confirmed by pH arterial blood, pH venous blood, CO2 venous blood. Alternatives to ABG include VBG, end tidal carbon dioxide, transcutaneous carbon dioxide.

Metabolic alkalosis is established by an elevated arterial pH, an increase in the serum [HCO3 -], and an increase in Paco2 as a result of compensatory alveolar hypoventilation. It is often accompanied by hypochloremia and hypokalemia . The arterial pH establishes the diagnosis, because it is increased in metabolic alkalosis and decreased in respiratory acidosis. Metabolic alkalosis frequently occurs as a mixed acid base disorder in association with either respiratory acidosis, respiratory alkalosis, or metabolic acidosis Reference: Harrison's Principles Of Internal Medicine, 21 st Ed, Ch: 55, Pg: 359

The anion gap is calculated with the formula (Na + K)-(Cl+HCO3). Normally itself, there is an anion excess in our body. Anion gap signifies the unmeasured anions in the plasma, which includes, albumin, phosphate, sulfate and organic anions. Anion gap = Unmeasured anions - unmeasured cations A decrease in the AG can be due to an increase in unmeasured cations the addition to the blood of abnormal cations, such as lithium (lithium intoxication) or cationic immunoglobulins (plasma cell dyscrasias) a reduction in the plasma anion albumin concentration (nephrotic syndrome, liver disease, or malabsorption) hyperviscosity and severe hyperlipidemia, which can lead to an underestimation of sodium and chloride concentrations. Reference: Harrison's Principles of Internal Medicine 21st ed, Chap 55, Pg. 360

Because of the association of metabolic acidosis in advanced CKD with muscle catabolism, bone disease and more rapid progression of CKD, both the 'uremic acidosis' of ESRD and the non-AG metabolic acidosis of stages 3 and 4 CKD require oral alkali replacement to maintain the [HCO3 −] to approximately the normal value (25 mmol/L). This can be accomplished with relatively modest amounts of alkali (1.0-1.5 mmol/kg body weight per day). Either NaHCO3 tablets (650-mg tablets contain 7.8 meq) or sodium citrate (Shohl's solution) is effective. Reference: Harrisons Principles of Internal Medicine, 21 st Ed, Ch:55 Pg: 365

Early renal failure is associated with hyperchloremic acidosis . But in late CKD, there is no further decrease in HCO3. DKA, salicylate poisoning and lactic acidosis cause high anion gap acidosis . Late uremia also causes high anion gap acidosis. So the possible option is B

A non-anion gap metabolic acidosis can result from either renal or extrarenal causes. Renal causes of metabolic acidosis occur when renal bicarbonate generation, which results from net acid excretion, does not balance the loss of bicarbonate and other alkali buffers consumed in the buffering of normal endogenous acid production. This failure of net acid excretion is termed renal tubular acidosis (RTA). Extrarenal causes occur when exogenous acid loads, endogenous acid production, or endogenous bicarbonate losses are elevated and exceed renal net acid excretion. The most common extrarenal cause of non-anion gap metabolic acidosis is chronic diarrhea. Reference: Harrison's Principles Of Internal Medicine, 21 st Ed, Ch: 55, Pg: 364