The Vitals: IV Fluids – Lactated Ringers (Part 2)

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Jon Pickos
Jon Pickos

Emergency Medicine Resident at Detroit Receiving Hospital, pursuing a critical care fellowship. Budding and developing passions include balanced fluid resuscitation, palliative care, and all things critical care. Outside of work, craft beer, sporadic ice hockey, learning how to brew coffee different ways, and spending time with my fiance and nearly 5 year old black lab/border collie, Maya.

Sam Epstein • Illustrator
Sam Epstein • Illustrator

Aspiring Medical Student and current Critical Care RN. Enjoys everything outdoors but can also be found inside nerding out on her medical education artwork.

The Pre-brief

We discussed one misconception, the effect of Lactated Ringers (LR) on potassium levels, in a previous post. Another common misconception with LR is the effect it has on lactic acidosis and whether it increases the lactic acid level. It is easy to suspect LR of raising the lactic acid; it has lactate in the name right? However, many don’t consider the different types of “lactate” that exist, how they are metabolized in the body, and the overall effect they have on human physiology. In this post, we are going to review this common misconception associated with LR, the data behind it, and how to address it in clinical practice.

Lactated Ringers in “Lactic Acidosis”

To begin, we need to rename some common terminology in what is typically known as “lactic acidosis”. The entity, lactic acid, does not exist in large quantities in the human body despite the concept being perpetuated for decades. Per Robergs et al and Gladden, the primary form of existence in the body is lactate, with an estimated greater than 99% of lactic acid (H+ + Lactate) existing as lactate with the hydrogen ion dissociated at physiologic pH. In critical illness, sepsis, hypoxia, or otherwise, mitochondrial metabolism is altered by a variety of factors. The decrease in oxygen delivery causes cellular signaling that leads to an increased reliance on glycolytic pathways and byproducts, one of which is lactate. Therefore, our patients do not have a lactic acidosis, but instead have hyperlactatemia and may or may not have an associated metabolic acidosis from decreased bicarbonate levels. This represents a minute change in terminology; however, it is an important distinction to make as more of the beneficial effects of lactate are elucidated, a few of which we will touch on here.

Briefly, lactate is primarily the end product of glycolysis and is commonly associated with hypoxic conditions, poor perfusion, and anaerobic metabolism. All of these associations are typically viewed as markers of worsening clinical condition or shock. However, more and more research suggests that although increased lactate production is associated with hypoxia and perfusion abnormalities, it may also be a normal response by the body under stress to maintain adequate energy sources.

Sun and Li outlined mechanisms by which lactate supports energy production in working skeletal muscle, helps regulate and increase cerebral blood flow, and contributes to anti-inflammatory effects through signaling. Furthermore, lactate appears to have neuroprotective qualities and promotes wound healing. 

In a pig model, Duburq et al found that, after induction of shock with endotoxin infusion, infusion of hyperosmolar sodium lactate improved hemodynamic and microvascular reactivity and was associated with a negative fluid balance and improved oxygenation. 

In humans, Mustafa and Leverve found that, while not significant, infusion of hypertonic sodium lactate was associated with increased cardiac index and oxygen delivery and an increase in pH. Later, Nalos et al infused half molar sodium lactate into patients diagnosed with acute heart failure and requiring inotropes or vasopressors and found the infusion improved cardiac function. However, there were no significant differences in the need for vasoactive therapy, respiratory support, duration of ICU and hospital stay, or 28- and 90-day mortality. 

Why all the harping on sodium lactate? Because that is the form present in LR, at 28mEq, and it has taken the brunt of plenty of negative discussion on LR, while the rest has focused on potassium.

So the question is, does LR raise serum lactate? Zitek et al found that serum lactate levels increased similarly after either LR or NS infusions in healthy volunteers. With lactate rising similarly regardless of type of fluid administration, the issue of increasing lactate levels with LR administration appears to be insignificant. Most importantly, evidence continuing to accumulate suggests lactate may have overall multiple physiologic benefits (increased pH, bicarbonate buffering, energy substrate) and clinically beneficial effects (improved hemodynamic stability, increased cardiac index, increased oxygen delivery).

Now, when you are in your next resuscitation of a critically ill patient pondering the best fluid to use between LR and NS, remember all of the benefits covered here and the misconceptions often attributed to LR. All that little bit of sodium lactate is trying to provide some extra energy, buffer your patients pH, and just help out in general.

The Debrief

  • LR contains sodium lactate, not lactic acid, and as evidenced by prior studies, does not significantly raise lactate levels, a lab typically monitored in critically ill patients
  • Lactate can be utilized as an energy source by the body in critical illness and rising levels are likely the body trying to provide increased substrates for energy.
  • Sodium lactate is associated with multiple potential benefits including cerebral blood flow circulation, healing, energy production, and improved hemodynamics through better cardiac function.
  • Additionally, the sodium lactate in LR provides an additional source of bicarbonate, a much needed component of the buffer system in the body, especially in shock states.
  • The lactate in LR is not to be feared, but embraced, and provides added support for the use of LR as the primary fluid for balanced and pH guided resuscitation in critically ill patients.

References

  1. Foucher CD, Tubben RE. Lactic Acidosis. [Updated 2020 Nov 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470202/
  2. Nalos et al. Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: a pilot randomised controlled clinical trial. Critical Care. 2014;18:R48.
  3. Robergs RA, McNulty CR, Minett GM, Holland J, Trajano G. Lactate, not Lactic Acid, is Produced by Cellular Cytosolic Energy Catabolism. Physiology. 2018;33:10-12.
  4. Sun S, Li H, Chen J, Qian Q. Lactic Acid: No Longer an Inert and End-Product of Glycolysis. Physiology. 2017;32:453-463. doi:10.1152/physiol.00016.2017.
  5. Fontaine et al.: Hyperosmolar sodium-lactate in the ICU: vascular filling and cellular feeding. Critical Care 2014 18:599.
  6. Mustafa I, Leverve XM: Metabolic and hemodynamic effects of hypertonic solutions: sodium-lactate versus sodium chloride infusion in postoperative patients. Shock 2002, 18:306–310.
  7. Garcia-Alvarez et al. Sepsis-associated hyperlactatemia. Critical Care. 2014;18:503. 
  8. Dennis SC et al. Protons in Ischemia: Where Do They Come From; Where Do They Go To?. J Mol Cell Cardiol. 1991;23:1077-1086.
  9. Singh S, Kerndt CC, Davis D. Ringer’s Lactate. [Updated 2021 Apr 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK500033/
  10. Brinkman JE, Dorius B, Sharma S. Physiology, Body Fluids. [Updated 2020 May 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482447/. 
  11. Gladden LB. Lactate metabolism: a new paradigm for the third millennium. J Physiol. 2004;558(Pt 1):5-30. doi:10.1113/jphysiol.2003.058701

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