Question 16#

An 8-week-old boy is brought to the ED with a 3-day history of vomiting. His venous blood gas shows:

• pH 7.55 (7.35–7.45)
• HCO₃ − 40 mmol/L (22–24)
• PCO₂ 48 mmol/L (35–45)
• K⁺ 2.8 mmol/L (3.5–5.0)
• Na⁺ 135 mmol/L (135–145)
• Cl⁻ 85 mmol/L (95–105)

His gas improves with normal saline therapy.

Which ONE of the following conditions is the MOST likely cause of his blood gas result?

A. Sepsis

Answer: D: The venous blood gas shows an alkalaemia (pH > 7.45). A high bicarbonate level and high carbon dioxide level indicates a metabolic alkalosis. The expected carbon dioxide level as calculated from the compensation rule (0.7 x HCO₃ + 20) would be 48, which is appropriate indicating no secondary respiratory acid–base disorder. The hypochloraemia and hypokalaemia are consistent with a metabolic alkalosis. The most common cause of a hypochloraemic hypokalaemic metabolic alkalosis that responds to saline, is protracted vomiting or diuretic use. In this age group, vomiting due to sepsis or gastrointestinal obstruction (pyloric stenosis in this age group) needs to be excluded. Sepsis, however, will typically cause a metabolic acidosis. Surgery is performed to correct the pyloric stenosis after the acid–base and electrolyte abnormalities are corrected with normal saline replenishment.

Reference:

1. Murray L, Daly F, Little M, et al. Acid–base disorders. In: Murray L, Daly F, Little M, editors. Toxicology handbook. 2nd ed. Sydney: Churchill Livingston Elsevier; 2011. p. 109–13.

Question 17#

A 78-year-old man is brought in from home after a 3-day history of diarrhoea. His venous blood gas shows:

• pH 7.27 (7.35–7.45)
• HCO₃ − 14 mmol/L (22–24)
• PCO₂ 28 mmol/L (35–45)
• K⁺ 2.6 mmol/L (3.5–5.0)
• Na⁺ 134 mmol/L (135–145)
• Cl⁻ 113 mmol/L (95–105)
• Ur 14 mmol/L (2–7)
• Cr 320 mmol/L (50–100)
• lactate 1.5 mmol/L (<2.2)

Which ONE of the following options would BEST explain the clinical scenario?

A. High AG metabolic acidosis secondary to renal failure

Answer: C: The venous blood gas shows an acidaemia (pH < 7.35). The low bicarbonate level indicates a metabolic acidosis. The expected carbon dioxide if appropriately compensated can be calculated by the formula [CO₂ = 1.5 x HCO₃ − + 8] (± 2). In this scenario, the expected carbon dioxide would be 29 (±2) indicating a single acid–base disturbance of a metabolic acidosis. The AG is calculated to be [Na⁺ ] – {[HCO₃ ⁻ + Cl⁻ ]} = 7.

Therefore, there is a normal AG metabolic acidosis. Renal failure can cause a high AG metabolic acidosis. However, in this case the degree of renal failure present has not been sufficient enough to elevate the AG indicating that there is not significant retention of acid anions. Furthermore, tissue perfusion is still adequate to prevent lactic acidosis.

Diarrhoea causes a normal AG metabolic acidosis due to loss of bicarbonate from the gastrointestinal system. To maintain electrical neutrality, chloride ions are retained hence the hyperchloraemia. Additionally, hypovolaemia caused by profuse diarrhoea stimulates aldosterone production, which increases sodium reabsorption and increases potassium excretion contributing to the hypokalaemia. In severe profuse diarrhoea, however, the acid–base disturbance can progress to a high AG metabolic acidosis secondary to the severe dehydration, lactic acidosis and renal failure.

References:

1. Nicolaou D, Kelen G. Acid–base disorders. In: Tintinalli J, Stapczynski J, Ma O, et al, editors. Tintinalli’s emergency medicine: a comprehensive study guide. 7th ed. NewYork: McGraw Hill Medical; 2011. p. 102–12.
2. Murray L, Daly F, Little M, et al. Acid–base disorders. In: Murray L, Daly F, Little M, editors. Toxicology handbook. 2nd ed. Sydney: Churchill Livingston Elsevier; 2011. p. 109–13.
3. Brandis K. Acid–base physiology. Online. Available: http:// www.anaesthesiaMCQ.com.

Question 18#

Which ONE of the following blood gas pictures would you expect to see in a 6-year-old boy being treated for acute life-threatening asthma?

A. pH 7.21, CO₂ = 76, HCO₃ = 27, K⁺ 3.3

Answer: A: In acute asthma, there is an initial increase in respiratory rate and work of breathing, leading to an initial respiratory alkalosis. However, in severe or life-threatening asthma as patients tire and their work of breathing falls, carbon dioxide can be retained secondary to hypoventilation. Additionally, as the disease progresses and mucous plugging and V/Q mismatch occurs, gas exchange is impaired further increasing retention of carbon dioxide.

Salbutamol is the first-line pharmacological therapy used in the treatment of acute asthma. It causes a shift of potassium into cells thereby reducing the extracellular concentration of potassium. Total body potassium, however, is unchanged and is usually normal. Used in excess, it can also cause a salbutamol lactic acidosis toxicity and V/Q mismatch in the lungs.

Keeping this in mind, working through each of the above blood gas pictures:

A. Acidaemia with a respiratory acidosis. Expected HCO₃ can be calculated to be HCO₃ = 24 +{[CO₂] – 40}/10 i.e. ~27, therefore single acid–base disturbance. Hypokalaemia as expected, hence answer A is correct.

B. Acidaemia with respiratory acidosis. Expected HCO₃ calculated as 27. Hyperkalaemia however, is not typically expected, hence answer B is incorrect.

C. Alkalaemia with respiratory alkalosis. Expected HCO₃ can be calculated to be HCO₃ = 24 – {40 – [CO₂ ]}/10 i.e. ~ 22. However, in life-threatening asthma you would expect carbon dioxide levels to be elevated with an associated respiratory acidosis following an initial respiratory alkalosis. Additionally, hyperkalaemia is not generally expected from treatment with continuous nebulised or intravenous salbutamol.

D. Alkalaemia with respiratory alkalosis. Expected HCO₃ calculated as 22. Again, however, in life-threatening asthma you would typically expect carbon dioxide levels to be elevated with an associated respiratory acidosis following the initial respiratory alkalosis. 

References:

1. Murray L, Daly F, Little M, et al. Acid–base disorders. In: Murray L, Daly F, Little M, editors. Toxicology handbook. 2nd ed. Sydney: Churchill Livingston Elsevier; 2011. p. 109–13.
2. Brookes J, Dunn R. Respiratory. In: Dunn R, Brookes J, Leach D, editors. The emergency medicine manual. 4th ed. Adelaide: Venom Publishing; 2006. p. 765–810.

Question 19#

A 48-year-old man presents to the ED with a right middle lobe pneumonia. His arterial blood gas on room air taken on arrival is as follows:

• pH 7.55 (7.35–7.45)
• PCO₂ 18 mmol/L (35–45)
• PO₂ 70 mmol/L (80–100)
• HCO₃ − 18 mmol/L (22–24)

Which ONE of the following is his A-a gradient?

A. 127 mmHg

Answer: C: The A-a gradient is the difference between the alveolar (PAO2 ) and arterial (PaO₂ ) oxygen pressures and is a measure of how well the lungs are functioning. The PaO₂ is measured from arterial blood samples and the PAO₂ can be calculated using the alveolar gas equation. The A-a gradient is essentially [PAO₂ – PaO₂ ] . . A normal A-a gradient is <10 mmHg or corrected for age [10 + (age/10)]. There are multiple causes of an elevated A-a gradient including ventilation perfusion mismatch, intracardiac shunts and causes of diffusion abnormalities.

In this scenario, using the alveolar gas equation, the PAO2 would be: 

• PAO₂ = FIO2 [760–47] – [PaCO₂ /0.8 (respiratory quotient)]
• PAO₂ = 150 – 22.5 = 127.5
• A-a gradient = 127 – 70 = 57

References:

1. Dunn R. Investigations. In: Dunn R, Brookes J, Leach D, editors. The emergency medicine manual. 4 ed. Adelaide: Venom Publishing; 2006. p. 471–508.
2. Slesinger T. Blood gases: pathophysiology and interpretation. In: Tintinalli J, Stapczynski J, Ma O, et al, editors. Tintinalli’s emergency medicine: a comprehensive study guide. 7th ed. NewYork: McGraw Hill Medical; 2011. p. 112–7.

Question 20#

The concentration of sodium ions in a 1 L bag of normal saline is:

A. 115 mmol/L

Answer: C: A 1 L bag of normal saline has equal concentrations of sodium and chloride at 154 mmol/L of each. The osmolality of the same bag is 300 mmol/L. Hartmann’s solution contains 130 mmol/L of sodium and 109 mmol/L of chloride, that is, values almost equal to normal serum electrolyte concentrations.

Reference:

1. Kelen G, Hsu E. Fluids and electrolytes. In: Tintinalli J, Stapczynski J, Ma O, et al, editors. Tintinalli’s emergency medicine: a comprehensive study guide. 7th ed. NewYork: McGraw Hill Medical; 2011. p. 117–29.