Portal Vein Pulsatility Index to Differentiate Hypervolemic and Hypovolemic Hyponatremia

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Picture of Sharad Patel
Sharad Patel
Professional Intensivist/Nephrologist/Dad, and very amateur surfer and coder.
Picture of 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

Hypotonic hyponatremia is a common electrolyte disorder defined by a blood serum sodium value of less than 136 meq/L. Hyponatremia usually occurs in the state of a pathologic reduction in free water clearance. Reductions in free water clearance can occur in situations with either inappropriate antidiuretic hormone (ADH) excess or neurohormonal activation in a low-effective circulating volume state. Hypotonic hyponatremia can be further broken down by extracellular volume such as hypovolemic, euvolemic, and hypervolemic states (Figure 1). Precision in the diagnosis of volume status is notoriously low when dependent on the traditional examination findings of pitting edema and diagnostic studies such as chest x-ray, leading to inappropriate interventions. Urine electrolytes can be helpful, but analogous neurohormonal activation in hypovolemic and hypervolemic hyponatremia will exhibit similar urine sodium values, hence the diagnostic conundrum. Euvolemic hyponatremia will display high urine electrolyte values. Now, the terms hypovolemic and hypervolemic may be reductionist and not entirely accurate, but we will use these terms for the sake of discussion. Hypervolemic pathologic states include congestive heart failure, nephrotic syndrome, and cirrhosis. In contrast, hypovolemic pathologic conditions include prolonged dehydration in the context of severe malnutrition (aka “tea and toast” diet), excessive diuretic use… The focus of this post will be venous congestion related to congestive heart failure. How can we differentiate hypervolemic and hypovolemic hyponatremia; I propose the use of portal vein pulsatility.


As Figure 3 describes, it is commonly understood that hyponatremia can progress to acute kidney injury in the setting of low effective circulating volume (includes hyper and hypovolemia). As the Renin-Angiotensin-Aldosterone System (RAAS) activates to preserve systemic perfusion, elevated levels of Angiotensin II force the proximal tubules to retain sodium (and therefore free water). Since RASS only reacts to the “effective” circulating volume, the resulting hyponatremia (and subsequently low sodium levels in the urine) can occur in either volume up or down states. What’s needed is a tie-breaker that helps us discern venous congestion; contrast with euvolemic hyponatremia which exhibits elevated urine electrolytes. Several studies have shown the predictive association between pulse-wave doppler pulsatility in the portal vein (PV) and AKI in critically ill post-surgical patients (1,2). Under normal circumstances, flow is relatively uniform through the PV. In congested/ hypervolemic states, pulsatility increases as estimated via the pulsatility index (Figure 2), with >50% being highly suggestive of venous congestion and hypervolemia (1, 2). Furthermore, a small case series have demonstrated portal vein pulsatility to predict better characterize hyponatremia(5).

Figure 1 - Hyponatremia etiologies classified using volume status. Demonstration of common physiology of RAAS activation for both hypovolemia and hypervolemia, hence the low urine sodium in both.
Figure 2 - Pulse Wave doppler of the Portal vein can be quantified using the Pulsatility Index. Pulsatility Index > 50% may indicate marked venous congestion (thin patients may exhibit pulsatility in health).
Figure 3 - RAAS activation in the physiology of Hyponatremia and AKI. RAAS stimulates proximal tubule sodium retention, loss of free water clearance, and reduced renal blood. Consequences of persistent RAAS activation are hyponatremia, volume overload, and AKI.


A 95-year-old male with a history of HfpEF, atrial fibrillation, and hypothyroidism presented to the hospital with increased dyspnea, which prompted noninvasive positive pressure ventilation. Laboratory values were remarkable for serum sodium of 120 meq/L, serum creatinine of 1.91 mg/dl. Echocardiography was difficult due to poor windows. Bedside portal vein assessment showed a biphasic portal vein pattern consistent with venous congestion (Figure 4). Diuresis with IV furosemide and PO metolazone was initiated, leading to a net negative fluid balance of 3.5 L in the next 48 hours. Significant improvement in symptoms, serum sodium levels (120 to 136 meq/L), and a decrease in the portal vein pulsatility fraction (Figure 5) was seen. The patient was discharged home on day 5.

Figure 4 - PW doppler of portal vein with biphasic (pulsatility index greater than 100%) pattern. The portal vein doppler can be performed using a phased array probe. The probe should be oriented in a right posterior-axillary coronal view in the 9th to 11th intercostal spaces to identify the portal vein. Color doppler scale should be reduced to 20 to 30 cm/s, which can help identify the low-velocity portal vein flow. The portal vein is determined by its position in the caudal part of the liver, and color doppler, which will usually be red (flow coming towards the probe, except biphasic flow, which will have red and blue appearance). PW gate should be placed on the portal vein with an angle parallel to the vein as possible.
Figure 5 - Portal vein doppler with minimal pulsatility.


A simple protocol for the differentiation of hyponatremia is given in (Figure 6). The first step is to evaluate urine sodium (or Fractional Excretion of Sodium/FENA). The reduced urine Na and FENA demonstrate high RAAS activation (angiotensin II stimulates proximal tubule sodium retention). As discussed before, the low urine Na does not help distinguish the hyponatremia subtypes (Anecdotally, I have observed that low urine sodium may demonstrate possible reversibility as there is still enough tubular function to retain sodium avidly). Urea’s fractional excretion can be considered for patients on loop diuretics with a cutoff of less than 35%(6). The next step is to perform portal vein doppler evaluation. High portal vein pulsatility suggests hypervolemic hyponatremia, which should warrant diuretics (or volume reduction) for treatment. A non-pulsatile portal vein may be evidence for hypovolemic hyponatremia which would warrant volume expansion.

Figure 6 - Protocol to distinguish hypervolemic and hypovolemic hyponatremia using portal vein pulsatility.

The Debrief

  • Hypervolemic and hypovolemic hyponatremia can be difficult to distinguish; therefore, treatment can often be inappropriate.
  • Portal vein pulsatility can indicate venous congestion. Venous congestion can lead to high neurohormonal and RAAS activation, predisposing to hyponatremia and
  • Portal vein pulsatility index may be a good marker to distinguish hypervolemic and hypovolemic hyponatremia when the physical examination is inconclusive/difficult, but further studies are warranted.


  1. Beaubien-Souligny W, Benkreira A, Robillard P, et al. Alterations in Portal Vein Flow and Intrarenal Venous Flow Are Associated With Acute Kidney Injury After Cardiac Surgery: A Prospective Observational Cohort Study. J Am Heart Assoc. Oct 2 2018;7(19):e009961. doi:10.1161/jaha.118.009961
  2. Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with Point-Of-Care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J. Apr 9 2020;12(1):16. doi:10.1186/s13089-020-00163-w
  3. Rangaswami J, Bhalla V, Blair JEA, et al. Cardiorenal Syndrome: Classification, Pathophysiology, Diagnosis, and Treatment Strategies: A Scientific Statement From the American Heart Association. Circulation. 2019-04-16 2019;139(16)doi:10.1161/cir.0000000000000664
  4. Filippatos TD, Elisaf MS. Hyponatremia in patients with heart failure. World J Cardiol. Sep 26 2013;5(9):317-28. doi:10.4330/wjc.v5.i9.317
  5. Singh, G., Rachoin, J. S., Chien, C., & Patel, S. (2019). The Use of Portal Vein Pulsatility to Differentiate Hypervolemic and Hypovolemic Hyponatremia. Case reports in critical care, 2019, 9591823. https://doi.org/10.1155/2019/9591823
  6. Kaplan AA, Kohn OF. Fractional excretion of urea as a guide to renal dysfunction. Am J Nephrol. 1992;12(1-2):49-54. doi: 10.1159/000168417. PMID: 1415365.


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