Acid-Base Physiology

Case 12 : A weak patient after a week of diarrhoea

History

A 68 year old woman was admitted with a one week history of severe diarrhoea. She was now weak and clinically dehydrated. Blood pressure was 100/60 (lying) and 70/40 (sitting). She was admitted and treated with IV fluids and potassium supplementation to repair her volume and electrolyte deficits. Urine output improved with fluid repletion. Electrolytes and arterial blood gases were collected on admission and the next day.

Case 12 - Arterial Blood Gas & Electrolyte Results
	On Admission	Next Day
Na+	137	137
K⁺	2.5	4.2
Cl-	118	114
HCO3-	5	15
Creatinine	0.31
Anion gap	10	8
pH	7.11	7.49
pCO2	16	20
HCO3	4.9	14.7

Assessment

Firstly: Initial clinical assessment

A week of diarrhoea would certainly be enough to cause a hyperchloraemic (or normal anion gap) metabolic acidosis. A possible complicating factor is hypovolaemia with poor perfusion and a lactic acidosis. Hypokalaemia is also likely with severe diarrhoea.

Secondly: The acid-base diagnosis

pH: A severe acidaemia means a severe acidosis is present
Pattern: The bicarbonate is very low so a metabolic acidosis must be present. The pattern of low bicarbonate and a low pCO2 (compensatory hyperventilation) confirms this diagnosis
Clues: The anion gap is not elevated so a normal anion gap acidosis is present. An elevated chloride is present as expected. The creatinine is elevated to about the level at which impairment of excretion of acid-anions would occur. The delta ratio is low (< 0.4) as expected in a pure hyperchloraemic acidosis
Compensation: The expected pCO2 (15.5mmHg) by rule 5 matches the actual pCO2 (16mmHg) so no respiratory disorder is present. Sufficient time has elapsed to expect that compensation should have reached its maximum value
Formulation: Hyperchloraemic (or normal anion gap) metabolic acidosis with appropriate respiratory compensation
Confirmation: No further investigations are necessary for confirmation. A lactate level would be useful to check in view of the clinical hypovolaemia (postural hypotension & oliguria) but would not be expected to be particularly elevated in view of the normal anion gap

Finally: The Clinical Diagnosis

The diagnosis is a severe diarrhoea causing a severe hyperchloraemic metabolic acidosis and hypokalaemia. Diarrhoea is the most common cause of this type of acidosis.

The hypokalaemia should be treated urgently and IV potassium is indicated in view of:

the potential life-threatening hypokalaemia
the continuing losses (diarrhoea)
the probable worsening of the hypokalaemia as the acidosis improves and K⁺ moves intracellularly

Comments

The pattern the next day is interesting. The metabolic acidosis is being corrected (increased bicarbonate) but the actual pCO2 is much lower (20 mmHg) than that predicted (30.5 = 1.5 x 15 + 8) resulting in an alkalaemia! This situation is common especially if intravenous NaHCO3 has been given. The cause in this case is probably the slowness of the reversal (lag) of the central chemoreceptor mediated component of the compensatory hyperventilation as the metabolic acidosis is corrected.

The hyperventilation in systemic metabolic acidosis occurs because of stimulation of both peripheral and central chemoreceptors. The drop in pCO2 inhibits the central chemoreceptors and this slows the development of the full increase in ventilation. Bicarbonate will slowly enter the brain ISF over about a 12 to 24 hour period and the central chemoreceptor inhibition will be progressively eliminated. During the recovery phase, the situation occurs in reverse. The recovery of pCO2 to normal lags behind the rise in the bicarbonate.

A similar process is responsible for limiting the hyperventilatory response to the hypoxaemia at high altitude. The hypoxic drive is mediated by peripheral chemoreceptor stimulation. The drop in the pCO2 is sensed by the central chemoreceptors and ventilation is inhibited until bicarbonate slowly equilibrates across the blood-brain barrier.

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