Acid base teaching – Case 1

Case 1

A road traffic accident victim had been trapped under a car for several hours. After admission his urinary output was low, despite an apparently adequate fluid intake.

These results were obtained three days after admission:

  • [H+] = 50 nmol/L  pH = 7.3
  • PaCO2 = 3.2 kPa
  • [HCO3] = 12 mmol/L

Question 1

The patient has? (Choose one of these then –  click to see if your correct)

Metabolic acidaemia


This is metabolic acidaemia with partial respiratory compensation. The metabolic acidaemia is due to renal failure.

Metabolic alkalaemia


Typical metabolic alkaleamia presents with increased HCO3- followed by a small compensatory PCO2 increase.

Respiratory acidaemia


Typical respiratory acidaemia presents with increased PaCO2 and compensatory increased [HCO3-].

Respiratory alkalaemia


The PaCO2 is low,
which occurs in respiratory acidaemia,
but in this case the low PaCO2 is due to a compensatory response to metabolic acidaemia.

Mixture of metabolic alkalaemia and respiratory acidaemia


Consider the clinical circumstances. [HCO3-] is lowered which indicates acidaemia but the drop in PaCO2 is a compensatory effect due to hyperventilation.

Question 2

What is the cause of his acid disturbance? (Choose one of these – then click to see if your correct)

Acute renal failure


Myoglobin is less soluble in more acidic conditions and precipitates in renal tubules causing renal failure.

Crush injury - rhabdomyolysis


In rhabdomyolysis muscle cells are damaged with the release of their content.

Decreased respiratory efficiency


This would cause respiratory acidaemia.




General feedback on these answers

In crush injuries, muscle cells become “leaky” (“rhabdomyolysis”), releasing their contents, including myoglobin and creatine kinase. Myoglobin is relatively soluble at normal physiological [H+], but less so under the more acidic conditions found in the renal tubules. It therefore precipitates, causing renal failure. Rhabdomyolysis can be diagnosed by detecting high plasma creatine kinase levels, or by finding myoglobin in the urine (“myoglobinuria”).

Once the condition is established myoglobin will no longer be detectable in the urine since it cannot get through the nephron. Treatment in the early stages is to give large volumes of intravenous fluids to try to flush the myoglobin through the nephron,
and sometimes bicarbonate is given to try to alkalinise the urine to prevent precipitation. However, once renal failure has occurred, as here, fluids must be given cautiously. The metabolic acidaemia is caused by a combination of the failure to excrete non-volatile acids, possible increased production of non-volatile acids as the patient enters a catabolic state, and the failure of renal tubular mechanisms for reabsorbing/regenerating bicarbonate.