PART 1: The Bicarbonate Debate
Theory: Three mechanisms whereby bicarbonate could decrease serum potassium
Mechanism #2: Renal Excretion Acute metabolic acidosis impairs potassium excretion by the kidney, whereas metabolic alkalosis facilitates potassium excretion. This is largely due to regulation of potassium channels in the distal nephron, which are down-regulated by acidosis and up-regulated by alkalosis. Metabolic alkalosis additionally inhibits proximal tubule reabsorption of sodium bicarbonate, which facilitates potassium excretion by increasing distal sodium concentration and flow rate (Aronson 2011):
Hypertonic bicarbonate appears ineffective
Bicarbonate appears ineffective in the absence of acidosis
Isotonic bicarbonate may be effective in patients with metabolic acidosis
Conclusions about bicarbonate?
Ultimately the literature regarding bicarbonate remains unsatisfying. All studies above, aside from Fraley 1977, investigated patients with chronic end-stage renal disease and moderate hyperkalemia attending routine hemodialysis. Results from this patient population may not be generalizable to patients presenting with acute life-threatening hyperkalemia who often have more severe acidosis and acute renal failure. For example, it is possible that patients undergoing chronic hemodialysis could have chronically elevated intracellular potassium levels, and thus be less able to shift additional potassium intracellularly. Indeed, end-stage renal disease is known to impair extra-renal potassium metabolism in numerous ways, including impaired function of Na-K channels (Ahmed 2001).
Overall it is impossible to reach any definite conclusion based on existing evidence. Theoretical and experimental evidence suggest that isotonic bicarbonate may be beneficial among patients with metabolic acidosis. Potassium might decrease by roughly 0.15 mM for every 1 mM increase in bicarbonate, suggesting that a large volume of isotonic bicarbonate may be required (e.g., a sufficient volume to increase serum bicarbonate levels by 5-10 mM, roughly 1-2 liters)(1). This cannot be done in a patient with volume overload. The ideal candidate for bicarbonate therapy would be a patient with volume depletion, hyperkalemia, and metabolic acidosis, because isotonic bicarbonate may improve all three of these problems simultaneously.
PART 2: Avoid normal saline
PART 3: Diuresis vs. Dialysis
Most diuretics cause potassium loss in the urine. A loop diuretic (e.g., furosemide) is the most potent agent, and is generally used as the backbone of the diuretic regimen. For patients with life-threatening hyperkalemia and renal insufficiency, it may be reasonable to use multiple diuretics, as these will operate in a synergistic fashion by blocking potassium reabsorption at different sites in the nephron (figure above). The combination of a loop diuretic and thiazide is commonly used in diuretic-resistant patients, with increased efficacy and potassium loss (Jentzer 2010). Acetazolamide may be especially kaliuretic because it increases bicarbonate delivery to the distal nephron (Weisberg 2008, Goodman & Gillman 12e Chapter 25).
- Neither Kayexalate nor hypertonic bicarbonate (i.e., ampules of 8.4% bicarbonate) are effective for emergent treatment of hyperkalemia.
- Isotonic bicarbonate may be effective for patients with metabolic acidosis. Unfortunately this requires a large volume of fluid, and cannot be used in patients with volume overload.
- Normal saline is proven to worsen hyperkalemia and should be avoided. For a hypovolemic patient without metabolic acidosis, lactated ringers is a reasonable fluid choice.
- Kaliuresis (facilitating urinary potassium excretion with diuretics) may be quite effective in patients with residual renal function. Otherwise, emergent dialysis is generally needed.
- Podcast by Scott Weingart about treatment of severe hyperkalemia from 2010.
- Review article by Weisberg regarding the management of severe hyperkalemia. Although this article is now seven years old, it remains one of the best reviews out there.
- Is Kayexalate effective? This has been discussed in EMLyceum, EMCrit, Precious Bodily Fluids, and Kamel 2012. There's not much I can add to this discussion that hasn't already been said, so if you're interested in the Kayexalate issue please see these sources.
- Prior post on pH-guided resuscitation describes the rationale for choosing different fluids during resuscitation in order to optimize the final acid-base status.
- The effects of pH on renal handling of potassium is reviewed by Aronson 2011. This is a very detailed article with lots of information about various potassium channels.
(3) I'm not aware of any direct evidence upon which to base this selection. Theoretically, acetazolamide may be expected to be more kaliuretic than a thiazide diuretic. However, acetazolamide overall may be a less powerful agent, and less effective at eliciting diuresis in a patient with renal dysfunction. A common practice of nephrologists and intensivists at Genius General Hospital has been to combine intravenous furosemide and chlorothiazide, and this seems to be effective.
Diagram of nephron: http://www.boomer.org/c/p2/Exam/Exam9905/Exam9905-1.html