Case Studies

Case 10

In your morning clinic you see two patients, Ron and Jim. Ron is a 55-year-old chef who has had severe diarrhoea over the last couple of days, and has laboured breathing. Jim is a 65-year-old builder, who has been on thiazide diuretics to treat his heart failure for 4 months, but has now been diagnosed with lobar pneumonia. He has rapid, shallow breathing, and feels weak. You receive the following blood analyses:

After taking a look, you ask that the ABGs (arterial blood gases) for Jim are performed again; you are happy with his second set of results (Jim 2). After reviewing the patients and their history you initiate treatment for the most urgent concern highlighted by the blood results, and then consider their acid–base status in more detail.

• 1. Why did you ask that Jim’s ABG’s were done again, but not Ron’s?

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  Correct answer:
  You should always check to make sure the ABG results are internally consistent. The pH, P_aCO₂ and [^HCO₃–] (the latter generally calculated by the blood gas analyzer) should follow the Henderson–Hasselbalch equation (Chapter 10). A quick and easy way of doing this (now that [H⁺] is commonly reported) is to use a simple derived calculation; so from:
  

  pH = 6.1 + log(

  [^HCO₃–] / P_aCO₂ × s

  )

  (s = solubility of CO₂, 0.23 mmol/L per kPa), we can derive:

  [H⁺]=183 ×

  P_aCO₂ / [^HCO₃–]

  ([H⁺] in nmol/L, PCO₂ in kPa), as s and 6.1 are constants at 37C. So for the first set of Jim’s results the calculated [H⁺] is 183 × 6/22 = 50 nmol/L (pH 7.31), clearly way off the reported value of 24 nmol/L (pH 7.62), so something was wrong with the measurement or reporting. Ron’s results, and the second set of Jim’s, showed no significant deviation, so can be regarded as at least internally consistent.

• 2. What needs to be dealt with immediately?

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  Correct answer:
  Jim has quite severe hypokalaemia, which can cause muscle weakness (so may impair breathing), but also cardiac dysfunction and arrhythmias (a potentially major risk as arrhythmias are a major cause of sudden death in patients with heart failure). Immediate steps to correct the hypokalaemia should be taken. Note that alkalaemia commonly causes hypokalaemia due to the way H⁺ and K⁺ are handled by the kidney. Jim would also be prescribed initial antibiotic therapy for his pneumonia (Chapter 38). Ron has a mild hypokalaemia, most probably due to loss of K⁺ in diarrhoea (his pH is normal). Part of his treatment may include giving appropriate fluids to correct his fluid and electrolyte loss, which would also correct the hypokalaemia.

• 3. Ron has a normal arterial pH, but is his acid–base status normal?

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  Correct answer:
  Though Ron has a normal pH, his P_aCO₂ and [^HCO₃–] are clearly not normal, so he must have an acid–base disorder. This is an important point – a normal pH does NOT mean the patient has a normal acid–base balance.

• 4. What is your diagnosis concerning the acid–base status of these two patients?

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  Correct answer:
  There are a number of guidelines for evaluating acid–base status which differ according to local schools of thought. They are mostly based on a step approach, a set of empirical rules and the anion gap (Chapter 11), although base excess may be used to a provide an initial indication of a non–respiratory component as this can be obtained quickly. A basic step approach for aiding diagnosis of acid–base disorders is provided after Case 11. Refer to this when a Step is mentioned below.
  

  Ron: His pH is normal, but the P_aCO₂ and [^HCO₃–] are both low, implying respiratory compensation of metabolic acidosis, and as reflected by his laboured breathing. His diarrhoea would lead to loss of and thus the low [^HCO₃–], but also loss of water and other ions, so he may be hypovolumic. Unusually, there is apparently complete compensation of his pH (it is not normally complete), which might suggest an additional metabolic alkalosis related to hypovolaemia. However, applying Step 4 suggests his P_aCO₂ is within the range for normal compensation of a metabolic acidosis. You have not been provided with the data needed to calculate his anion gap, but you already have sufficient information to make a fairly firm diagnosis. Note however that acid–base disorders can be multifactorial in origin and therefore complex.
  Diagnosis: Compensated non-anion gap metabolic acidosis due to severe diarrhoea.

  
  

  Jim: This is more complicated. He has alkalaemia, hypocapnia, hypoxaemia and a high [^HCO₃–]. The alkalaemia means there must be an alkalosis (Step 2), and as his pH is high and P_aCO₂ low this is probably a respiratory alkalosis (Step 3) caused by hyperventilation. The latter is most likely related to his rapid, shallow breathing as a result of increased lung stiffness (due to the pneumonia) rather than his relatively mild hypoxaemia (see Chapter 12). However, his P_aCO₂ and [^HCO₃–] have changed in opposite directions, indicating a mixed disorder. This is confirmed by Step 4, as his predicted [^HCO₃–] for a simple respiratory alkalosis, even if it had been present for some time, is less than 28 mmol/L, whereas his actual [^HCO₃–] is 32 mmol/L. This implies a co-existent metabolic alkalosis, most likely due to the thiazide diuretic he takes for heart failure, which increases renal [H⁺] excretion and also contributes to the hypokalaemia.
  Diagnosis: Respiratory alkalosis due to pneumonia–associated hyperventilation plus a metabolic alkalosis related to diuretic therapy, with associated hypokalaemia.

See “An example of a step approach to diagnosing acid–base disorders” at the end of Case 11.