The Vitals: Lactic Acidosis

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.