Oh bicarbonate… how you’ve become the drug which elicits the majority of my soap box lessons on ICU rounds and in the operating room. Truth to be told, it’s a medication which remains controversial among intensivists, nephrologists, and overall physiologists.
Bicarbonate (HCO3) comes as sodium bicarbonate (NaHCO3), and at that, a highly concentrated solution! An 8.4% sodium bicarbonate solution is a molar solution with an osmolality of ~ 2,000 mOsm/kg – roughly 7 times that of human plasma! This hypertonic solution confers a significant sodium load (primarily an extracellular ion) causing intracellular fluid to shift outward thereby expanding the extracellular fluid compartment. This can lead to a hyperosmolar (hypernatremic) state acutely!
Next, bicarbonate’s ability to help improve pH is contingent on the patient’s ability to eliminate carbon dioxide (CO2) because of this incredibly important physiologic buffer.
HCO3 + H+ ⇆ H2CO3 ⇆ H2O + CO2
Le Chatelier’s principle states that a dynamic equilibrium will shift to offset a stress. In this case, the “stress” of additional HCO3 will generate more CO2. Next time you push bicarbonate into a patient with end-tidal CO2 monitoring, watch how quickly it rises. Before you’ve even finished pushing the 50 cc syringe, you’ll see how real hypercarbia can be if you don’t adequately ventilate the patient. In general, if your patient has a respiratory acidosis, increasing your patient’s minute ventilation is the key to treatment (NOT bicarbonate). However, hypoventilation in the face of bicarbonate can potentially make your acidosis worse. Also, ever wonder why NaHCO3 comes in glass syringes? Over time, CO2 can diffuse through more conventional storage causing the HCO3 concentration to change,
Now what if you overshoot with bicarbonate therapy and hyperventilation leading to alkalosis? This can cause decreased ionized calcium (more calcium can bind albumin) and a leftward shift of the O2 dissociation curve resulting in tissue hypoxia from decreased unloading of oxygen from oxyhemoglobin.
Before I come across as anti-bicarbonate, there are plenty of instances in which I use this wonderful medication: hyperosmolar therapy in patients with increased intracranial pressure (ICP), salicylate toxicity (weak acids which are more ionized with bicarbonate leading to less penetration into the central nervous system and less reuptake from the renal tubules), treating hyperkalemia (although this remains controversial) and SID/non-SID (strong ion difference) metabolic acidosis. In cases of refractory acidosis where renal replacement therapy (RRT) is indicated, I’ll often start patients on an isotonic bicarbonate drip (3 amps of 8.4% NaHCO3 in a liter of D5W or sterile water). This is a poor man’s RRT. 😀 Oh, and I don’t use bicarbonate to prevent contrast-induced acute kidney injury. 😛
So how much bicarbonate do I give? I calculate a patient’s overall bicarbonate deficit as: weight (in kg) x 0.3 x [24 – serum bicarb]. For example, in a 70 kg trauma patient coming in with a bicarb of 16, their overall deficit is roughly 170 mEq. I’ll give about half of that deficit up front (especially if the pH is < 7.10) and then rely on correcting the underlying problem (hypovolemic shock, ischemic bowel, etc.) with frequent assessment of my hemodynamics, response to medications, and blood gases to guide further therapy.
Although there is some literature showing increased mortality with bicarbonate administration in severe acidosis, once a patient’s arterial pH falls below ~7.10, many of our resuscitative measures (namely vasoactive agents) fail in the face of worsening acidemia. While we attempt to correct the underlying etiology of acidosis, sometimes it becomes necessary to simply treat a number (the pH) to buy valuable time for other interventions to kick in.