The Vitals: Lactic Acidosis

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Picture of Obiajulu Anozie
Obiajulu Anozie
Critical Care Physician trained at Cooper University Hospital. Special interests include: Physiology, Ultrasonography, Echocardiography....and Video Games.

The Pre-brief

This discussion will focus on the interpretation of critical labs.

Whether in the Emergency Room, Medical Wards, or Intensive Care Unit, the interpretation of critical lab results has become a routine aspect of our daily workflow. As such, it is paramount to adopt a physiological approach that also integrates the presenting history to not only yield an accurate interpretation, but to also avoid “knee-jerk” reactions such as the universal administration of fluid challenges each time we are faced with an elevated lactate.

Consider the following two patients

Patient 1: 67 y/o F with an unremarkable history presenting with profuse vomiting, diarrhea, and weakness after having returned from a cruise ship tour.
Vitals: Hr: 120 bpm, BP: 70/50 mmHg, SpO2: 99% on room air
Remarkable Labs: BUN/Cr: 80/3.3, Urine Na+ < 10,  Lactate: 7 mmol/L

Patient 2: 67 y/o F with a hx of Heart Failure presenting with altered mental status, decreased responsiveness, and shortness of breath. Distal extremities are cool to the touch.
Vitals: Hr: 120 bpm, BP: 70/50 mmHg, SpO2: 93% on 4 L Nasal Cannula
Chest X-ray: Perihilar infiltrates and pulmonary vascular congestion
Remarkable Labs: BUN/Cr: 80/3.3, Urine Na+ < 10, Lactate: 7 mmol/L, ProBNP: 48922

In the above two case scenarios, the onset of lactic acidosis is a critical lab finding that may signify the development of severe illness and mark the pathophysiological transition from aerobic to anaerobic metabolism and activation of the adrenergic system. In the setting of critical illness, this may have serious implications regarding morbidity and mortality prompting the need for dire intervention. However, to intervene we must first interpret; to interpret we must first understand how to classify:

The Physiological Approach

Lactic acidosis in the above patients correlates best with tissue hypoxia (Type A). Hypoxia results from impaired oxygen delivery and/or utilization by the tissues. To understand and address this, familiarizing ourselves with the oxygen delivery equation (DO2) along with its various components will not only allow us to determine where the link in the chain was broken, but also provide some insight as to which intervention is needed to appropriately address it. For a more in-depth review of the oxygen delivery equation and how to use it at the bedside, please refer to THIS POST.

Patient 1:

This patient’s presenting history is highly suggestive of viral gastroenteritis (i.e. Norovirus). Her remarkably low blood pressure and recent history of profuse vomiting and diarrhea point towards a state of hypovolemia due to extensive volume loss from the GI tract. This is supported by lab findings suggestive of pre-renal failure (BUN/Cr > 20:1) and low urine sodium; however, volume status would, ultimately, be best confirmed via point of care bedside echocardiography (i.e. Cardiac filling pressures, IVC, VTI). Recall, stroke volume is a major determinant of overall cardiac output and is preload-dependent. Hypovolemia reduces stroke volume by decreasing preload, thereby preventing the ventricles from taking advantage of Frank-Starling mechanisms whereby optimal myocyte stretch generates more forceful contractions. Volume resuscitation with fluid challenges is, thus, likely to be highly beneficial for this patient. As a side note, it may be best to avoid Normal Saline in favor of more balanced crystalloids such as Lactated Ringer’s or Plasmalyte. Normal saline has the potential to exacerbate renal failure which could prove catastrophic in similar patient scenarios.

Patient 2: 

The patient’s history of heart failure combined with her presentation, exam findings, significantly elevated proBNP and edema on chest -x-ray, raises concern for decompensated heart failure with progression into cardiogenic shock. Despite these findings, this is a diagnosis that can be best confirmed through point of care bedside echocardiography (i.e. Cardiac filling pressures, VTI). In cardiogenic shock, stroke volume is diminished by inherently poor contractility and overall cardiac output is reduced. Her mental state is likely the result of diminished cerebral perfusion from her low output state. Similarly, her labs and urine studies are analogous to a state of hypovolemic hypoperfusion as in both conditions, there is diminished effective circulating blood flow to all organs.  Administration of a fluid challenge in this clinical scenario is unlikely to yield any benefit, in fact, it may prove disastrous. Given her poor cardiac performance, there exists the possibility of ventricular dilation well past the optimal point on the Frank-Starling curve. Causing further increments in myocyte stretching with fluid challenges may paradoxically worsen cardiac function and result in increased morbidity and mortality. To improve stroke volume, efforts should be focused on augmenting contractility using inotropes (i.e. Epinephrine, Dobutamine, Milrinone) with consideration for mechanical assistance (Balloon Pump, Impella, V-A ECMO) if inotropes alone are inadequate.

The Debrief

  • Critical lab findings are the result of significant, pathophysiological perturbations that demand an equally physiological approach to properly address.

References

  1. Marik, P. iSepsis – The Lactate Myths. EMCrit.org 2018.
  2. Semler MW, Self WH, Wanderer JP,  et al. Balanced Crystalloids versus Saline in Critically Ill Adults. N Engl J Med. 2018 Mar 1;378(9):829-839. doi: 10.1056/NEJMoa1711584. Epub 2018 Feb 27. PMID: 29485925; PMCID: PMC5846085.(this is the SALT-ED trial)
  3. Adeva-Andany M, Lopez-Ojen M, Funcasta-Calderon R, et. al.: Comprehensive review on lactate metabolism in human health. Mitochondrion 2014; 17: pp. 76-100
  4. Nichol A, Ahmed B: Shock: causes, initial assessment and investigations. Anaesth Intensive Care Med 2014; 15: pp. 64-67.
  5. Levy B: Lactate and shock state: the metabolic view. Curr Opin Crit Care 2006; 12: pp. 315-321.
  6. Topalian S, Ginsberg F, Parrillo JE: Cardiogenic shock. Crit Care Med 2008; 36: pp. S66-S74.

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