Acid base teaching – Case 6

An elderly man was admitted as an emergency after collapsing in the street, was deeply comatose. A clinical examination showed that he had a ruptured aortic aneurysm leading to shock and circulatory failure.

Her results were:

[H+] = 30 nmol/L   PH = 7.52
PaCO2 = 6.5 kPa
[HCO3] = 37 mmol/L
[Na+] = 148 mmol/L
[K+] = 2.8 mmol/L

Question 1

What is his acid base disturbance in this case? (Choose one of these and then click to see if you are correct)

FALSE – Metabolic acidaemia presents with high [H+], significantly low [HCO3-] and low PaCO2

TRUE – He has a metabolic alkalaemia due to loss of [H+] in the vomit.

TRUE – He has a metabolic alkalaemia due to loss of [H+] in the vomit with a small compensatory raise in PCO2.

FALSE – Respiratory alkalaemia usually occurs due to hyperventilation of the lungs and results in significant low PaCO2 and a fall in [H+]

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

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.

Circulatory failure and shock (following a ruptured aortic aneurysm, in this case) result in metabolic (= lactic) acidaemia. He is hypoventilating as a consequence of his comatose state, causing the respiratory acidaemia. These sorts of results are commonly seen in patients with cardiorespiratory arrest.