MLT GlobeChemistry: Acid-base & blood gases – page 3
63 Chemistry MCQs on Acid-base & blood gases with answers and explanations.
Type B lactic acidosis, occurring without tissue hypoxia, is associated with:
Type B lactic acidosis arises from impaired metabolism without poor perfusion, e.g. metformin, liver failure, thiamine deficiency or malignancy. Shock states cause type A (hypoxic) lactic acidosis.
Base excess is best defined as:
Base excess reflects the metabolic (non-respiratory) component of acid–base status. A negative value (base deficit) indicates metabolic acidosis.
How long does full renal compensation for a primary respiratory acid-base disorder usually take?
Kidneys adjust H+ excretion and bicarbonate reabsorption slowly, reaching full compensation over several days. Respiratory compensation for metabolic disorders begins within minutes to hours.
A patient with metabolic alkalosis has urine chloride of 8 mmol/L. Which cause is most likely?
Low urine chloride (below about 20 mmol/L) shows chloride and volume depletion, as in vomiting; this alkalosis corrects with saline. Mineralocorticoid excess and Bartter syndrome give high urine chloride.
An arterial sample in a plastic syringe will be analysed within 20 minutes. Why is placing it in ice water not recommended?
Current guidance is to keep plastic syringes at room temperature and analyse within 30 minutes. Cooling increases gas diffusion through plastic, allowing oxygen entry and falsely high pO2. Cold slows, not increases, glycolysis.
A 40-year-old woman with normal anion gap metabolic acidosis, K 2.8 mmol/L and nephrocalcinosis cannot lower her urine pH below 6.0. The most likely diagnosis is:
Distal RTA is a failure to secrete H+ in the collecting duct, so urine pH stays above 5.5 despite acidosis, with hypokalemia and calcium stones. Type 4 RTA causes hyperkalemia.
A healthy woman in the third trimester of pregnancy has a blood gas. Which finding is normal for this state?
Progesterone stimulates breathing, lowering pCO2 to about 30 mmHg; the kidneys compensate by lowering HCO3−, so pH is near normal or slightly high. Respiratory acidosis is not normal in pregnancy.
Before capillary blood gas collection from a newborn's heel, the skin is warmed mainly to:
Warming the heel (to no more than about 42 °C) dilates vessels and "arterializes" the capillary blood. It does not replace antiseptic cleaning or anticoagulant in the tube.
Standard bicarbonate is defined as the plasma bicarbonate concentration:
Standard bicarbonate removes the respiratory influence by equilibrating blood to pCO2 40 mmHg at 37 °C, so a change reflects the metabolic component. Actual bicarbonate is at the patient's own pCO2.
In what form is most carbon dioxide transported in the blood?
About 70% of CO2 is carried as bicarbonate formed in RBCs by carbonic anhydrase; about 20–25% is bound to hemoglobin as carbamino compounds and 5–10% is dissolved.
What is the hydrogen ion concentration of plasma with a pH of 7.00?
pH = −log[H+]; pH 7.00 means [H+] = 10^−7 mol/L = 100 nmol/L. The normal value at pH 7.40 is about 40 nmol/L, so pH 7.00 means [H+] has more than doubled.
Early in an acute asthma attack, a patient breathes rapidly. Which acid-base disorder is most likely at this stage?
Rapid breathing early in an asthma attack blows off CO2, lowering pCO2 and raising pH. A normal or rising pCO2 later signals tiring and impending respiratory failure.
A patient with advanced chronic kidney failure is most likely to have which acid-base disorder?
Failing kidneys cannot excrete daily acid or regenerate bicarbonate, so bicarbonate falls and metabolic acidosis develops.
A patient has been taking large amounts of sodium bicarbonate antacid. Which acid-base disorder is expected?
Ingesting excess bicarbonate raises plasma bicarbonate and pH, causing metabolic alkalosis.
Acetic acid has a pKa of 4.76. What is the approximate pH of a 0.1 mol/L acetic acid solution?
For a weak acid, pH ≈ ½(pKa − log C) = ½(4.76 + 1) = 2.88. pH equals pKa (4.76) only when acid and conjugate base are equal, as in a buffer.
In metabolic acidosis, Winter's formula predicts expected pCO2 = 1.5 × HCO3− + 8 (±2). A patient has HCO3− 12 mmol/L and pCO2 32 mmHg. This indicates:
Expected pCO2 = 1.5 × 12 + 8 = 26 (24–28) mmHg. The measured 32 mmHg is higher than expected, so ventilation is inadequate, meaning an additional respiratory acidosis.
Why is a sample from a patient with extreme leukocytosis at risk of 'leukocyte larceny'?
Very high white cell or platelet counts consume oxygen rapidly after collection, causing spurious hypoxemia. Immediate analysis (or chilling if a delay is unavoidable) and comparison with pulse oximetry help identify it.
Most enzymatic lactate methods and sensors measure:
Lactate oxidase and lactate dehydrogenase methods are specific for L-lactate. D-lactic acidosis (e.g. short bowel syndrome) needs a D-lactate-specific assay.
Which is the main effect of temperature correction if a hypothermic patient's blood gas is analysed at 37 °C?
Gas solubility increases as blood cools, so at 37 °C the analyser reports higher partial pressures than exist in the cold patient, and a lower pH.
A patient has acute respiratory failure with pCO2 70 mmHg. Baseline HCO3− was 24 mmol/L. If the disorder is purely acute with expected compensation (1 mmol/L per 10 mmHg), HCO3− should be about:
pCO2 rose by 30 mmHg, so acute buffering raises HCO3− by about 3 mmol/L, giving 27 mmol/L. About 35 mmol/L would fit chronic compensation (3.5 per 10 mmHg).