8.3: Infusion of Hydrochloric Acid

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Page ID: 11267

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At first this seems like a silly thing to do, but intravenous infusions of hydrochloric acid are sometimes used in Intensive Care Units in patients with chronic respiratory acidosis and high plasma bicarbonate levels as a way to more rapidly return the bicarbonate towards normal levels.

As an example, consider the infusion via a central line of 100 mls of 1N hydrochloric acid solution in a healthy adult. This represents an acute acid load of 100 mmols of H⁺ which is sufficient to cause a metabolic acidosis. The defence against changes in [H⁺] involves buffering, compensation and correction.

Buffering

Buffering is a rapid physicochemical process that involves titration of the acid by the body's extracellular buffers (predominantly bicarbonate). Assuming a [HCO₃^-] of 24 mmols/l and an extracellular volume of 19 liters, this represents a bicarbonate pool in ECF of about 450 mmols. An acid load of 100 mmols of [H⁺] will titrate the bicarbonate buffer to about 18.7 mmol/l (ie \( \frac {350} {450} \times 24 \) ) assuming all the buffering is by bicarbonate.

Compensation

The metabolic acidosis will stimulate the peripheral chemoreceptors resulting in an increase in ventilation. The resultant hypocapnia is the physiological compensatory response which returns pH towards normal. This response starts early but can take 12 to 24 hours to reach its maximum value. Compensation will not return pH completely to normal. The expected pCO₂ at maximum compensation is:

\( \text {Expected } pCO_{2} = 1.5 \times [HCO_{3}^{-}] + 8 \)

where pCO₂ is arterial pCO₂ in mmHg and [HCO₃^-] is arterial bicarbonate (in mmol/l) calculated from arterial blood gases.

Correction

The kidney will excrete the excess acid anion (Cl^-) and this is equivalent to reabsorption of bicarbonate & excretion of acid. Normal acid-base status will be restored.

Other Physiological Effects.

These include:

The oxygen dissociation curve will be shifted to the right by the acidosis. This decrease in oxygen affinity will assist peripheral oxygen unloading. Subsequently, the acidosis causes a decrease in 2,3 DPG synthesis and the ODC moves leftward
Anion gap will be unchanged and the acidosis will tend to be a hyperchloraemic metabolic acidosis
Metabolic acids do NOT cross the blood-brain barrier so direct effects on the brain are not significant. (As mentioned above, the respiratory centre will be stimulated secondary to stimulation of the peripheral chemoreceptors)
Hyperkalaemia occurs due to H⁺-K⁺ exchange across cell membranes and urinary K⁺ losses are increased. (Hyperkalaemia is less common when the metabolic acid involves organic anions -eg lactate- as the anion tends to cross cell membranes with the H⁺ and the net cellular exchange with K⁺ is less).