Clinical Scenario:
You are working in the emergency department when an elderly male is brought in by EMS after being found unresponsive at home with an
unknown downtime. The paramedics report a possible seizure. His finger stick glucose registers as critical high. Post-intubation for poor GCS, his initial labs reveal an ABG of 6.8/20/90 and a lactate of 18. As you are signing out the patient to the ICU, the ICU team requests a sodium bicarbonate infusion.
Physiology & Literature Review:
Other than well-defined indications for sodium bicarbonate administration (such as treatment of Na-channel blockade in TCA overdose or to induce alkalinization in salicylate toxicity), one should be skeptical about administering sodium bicarbonate simply for acidosis. On the one hand if a patient is acidotic, it makes intuitive sense that you should try to alkalinize them, which is why sodium bicarbonate has been used so often in the past. On the other hand, there is evidence to show that administration of sodium bicarbonate shifts the oxygen dissociation curve, increasing hemoglobin affinity to oxygen, and resulting in paradoxical tissue hypoxia and causes an increase in lactate production. In addition, it causes an intracellular acidosis. Despite this, because it tends to be part of the "code cocktail", it is often administered anyway.
Other than well-defined indications for sodium bicarbonate administration (such as treatment of Na-channel blockade in TCA overdose or to induce alkalinization in salicylate toxicity), one should be skeptical about administering sodium bicarbonate simply for acidosis. On the one hand if a patient is acidotic, it makes intuitive sense that you should try to alkalinize them, which is why sodium bicarbonate has been used so often in the past. On the other hand, there is evidence to show that administration of sodium bicarbonate shifts the oxygen dissociation curve, increasing hemoglobin affinity to oxygen, and resulting in paradoxical tissue hypoxia and causes an increase in lactate production. In addition, it causes an intracellular acidosis. Despite this, because it tends to be part of the "code cocktail", it is often administered anyway.
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| Rise in EtC02 after bicarb (Dr. Sacchetti video) |
The effect of administration of Sodium bicarbonate on the end-tidal CO2 in an intubated patient with severe metabolic acidosis is well demonstrated by this video by
Dr. Alfred Sacchetti. While we disagree in giving a bicarb drip as
mentioned in the video, it does demonstrate the acid-base physiology in
real time.
A small randomized-controlled trial published in Critical Care Medicine more than 20 years ago gave either a blinded bolus of saline or sodium bicarbonate to patients with lactic acidosis vasopressor support [1]. They then checked ABGs one hour later. While sodium bicarbonate did increase the venous bicarb level, improved pH, it did not improve
hemodynamics.
