POCUS to Assess for Venous Congestion: Part I

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Korbin Haycock
Korbin Haycock
VExUS. Echocardiography in resuscitation. Likes to Doppler stuff.

The Pre-brief

The venous side of the body’s circulation has long been overlooked and under-appreciated. Most clinicians focus on the hemodynamic components of mean arterial pressure, cardiac output, systemic vascular resistance, and central venous pressure (CVP).  However, CVP is often considered in the context of optimizing ventricular preload–and thus increasing cardiac output–rather than as a marker of right ventricular dysfunction or volume overload when it is elevated.  This approach to CVP has only become more prevalent since the publication of the early goal-directed therapy for sepsis study and the ensuing surviving sepsis campaign.  

Even within the more advanced realm of the POCUS in critical care, much recent attention has been given to concepts of volume responsiveness (as often investigated by Doppler evaluation of the left ventricular outflow tract’s velocity time integral) leading to the quest to extinguish volume responsiveness in the hope of optimizing oxygen delivery to tissues supposedly suffering from tissue hypoxia due to lack of cardiac output (which is frequently already supranormal in distributive shock states).  

But while we strive to push cardiac output to its limit, we fail to consider that venous side congestion results, as we approach the flat part of the Frank-Starling curve, and that elevated CVP actually can decrease flow to the tissues, as it is the downstream pressure with which upstream pressures must overcome in order to drive flow across the capillaries.  

Impedance to capillary flow aside, there is increasing evidence that the effects of venous congestion on the various organs has other serious deleterious effects.  Portal hypertension has been linked to gut bacterial translocation, inflammatory cytokines, and ICU delirium, amongst other undesirable outcomes.  Both chronic renal dysfunction and acute kidney injury due to venous congestion has been shown to affect mortality and morbidity.  Interstitial edema increases diffusion distances from the capillary exchange interface to the cells we are trying to perfuse and an elevated CVP inhibits lymphatic return of capillary filtrate, only leading to a feedback loop of a bad situation made terribly worse.  Even the integrity of the glycocalyx–critical for capillary endothelial function–has been shown to be compromised by excess venous congestion.  “You have to swell to get well” is now unquestionably an irresponsible paradigm and reckless approach to resuscitation and critical care.

Venous congestion is an entity to be considered and respected across the continuum of caring for the sickest patients–from the emergency department to the ICU.  The temptation to injudiciously give fluids up front needs to be tempered by the understanding that short-term gains may not equate to long-term success.  Later, when the patient is out of the wards or ED and in the ICU, the astute clinician will understand the best strategy for resuscitation, what has already been given, and be on guard not to cause further iatrogenic harm.  There are also many important angles to venous congestion that apply to non-critically ill patients, but this is a critical care website, so I will leave these discussions alone. 

So having hopefully made my point, this brings us to VExUS (or the Venous Excess with UltraSound).  VExUS uses a venous Doppler exam of three different veins to quantify the degree of venous congestion.  As a prerequisite, the inferior vena cava (IVC) should be plethoric (greater than 2 cm), otherwise, in most situations, we need not waste time looking further for congestion.  Once an abnormal IVC has been identified, the three vessels to be interrogated are a hepatic vein, the portal vein, and an intrarenal vein.  Each vein, depending on the Doppler pattern, is assigned a level of venous congestion–none, mild congestion, or severe congestion.  VExUS score is then based on the absence or how many severe congestive findings are found in the three veins.  A VExUS grade of 0 is given when the IVC is less than 2 cm.  If only mild abnormalities are found in all the three veins, then the VExUS is grade 1.  If one severe finding is found, the VExUS is grade 2.  Two or more severe findings in the three vessels evaluated gets us to VExUS grade 3, indicating severe venous congestion.  Here is a summary of the Doppler waveforms and VExUS grading system:

In future posts, we will look at each of the three-vessel waveforms and discuss how to obtain the Doppler traces as well as to what contributes to each abnormality as we progress from normal to severe congestion.  For now, it should be said that each of the three vessels was originally chosen to both mitigate each vessels’ inherent pitfalls and also obtain a global view of the systemic venous congestion both near to the right ventricle, where the venous pulsations are generated, and far from the heart, where the peripheral veins can be assessed for reaching the limits of their compliance. The hepatic vein, being close to the right ventricle, will mimic the famous jugular venous pulsations we were all taught in physiology class.  Therefore this vein will give us valuable information on how the right atrium and ventricle are dealing with the venous return and loading conditions they are faced with.  The portal vein, being deeper inside the liver, will give us information on how the venous system there is reaching the limits of its compliance with progressive venous congestion. With little congestion, the portal vein will absorb pressure waves transmitted to it from the heart, but as the vein is more and more distended, we can see the pressure affects the forward flow because of backpressure waves transmitted in a retrograde direction.  Finally, the intra-renal veins are a kind of hybrid between the two other veins we look at.  

The Debrief

  • Venous congestion is often not considered but is actually an important factor for organ perfusion and other deleterious clinical conditions.
  • With the use of VExUS, venous congestion can be assessed.
  • By investigating different vessels with Doppler, we can assess the effects of venous return on the right atrium and ventricle, and also view venous congestion’s effect on more peripheral organs.
  • By investigating the different vessels as a whole, we also can take advantage of eliminating the various pitfalls inherent in looking at only one area affected by venous congestion. 

References

  1. Rivers, E., et al. (2001). “Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock.” New England Journal of Medicine 345(19): 1368-1377.
  2. Benkreira, A., et al. (2019). “Portal Hypertension Is Associated With Congestive Encephalopathy and Delirium After Cardiac Surgery.” Can J Cardiol 35(9): 1134-1141.
  3. Sandek, A., et al. (2014). “Intestinal blood flow in patients with chronic heart failure: a link with bacterial growth, gastrointestinal symptoms, and cachexia.” J Am Coll Cardiol 64(11): 1092-1102.
  4. Sundaram, V. and J. C. Fang (2016). “Gastrointestinal and Liver Issues in Heart Failure.” Circulation 133(17): 1696-1703.
  5. Valentova, M., et al. (2016). “Intestinal congestion and right ventricular dysfunction: a link with appetite loss, inflammation, and cachexia in chronic heart failure.” Eur Heart J 37(21): 1684-1691.
  6. Bhardwaj, V., et al. (2020). “Combination of Inferior Vena Cava Diameter, Hepatic Venous Flow, and Portal Vein Pulsatility Index: Venous Excess Ultrasound Score (VEXUS Score) in Predicting Acute Kidney Injury in Patients with Cardiorenal Syndrome: A Prospective Cohort Study.” Indian J Crit Care Med 24(9): 783-789.
  7. Iida, N., et al. (2016). “Clinical Implications of Intrarenal Hemodynamic Evaluation by Doppler Ultrasonography in Heart Failure.” JACC Heart Fail 4(8): 674-682.
  8. Bouchard, J. and R. L. Mehta (2009). “Fluid accumulation and acute kidney injury: consequence or cause.” Curr Opin Crit Care 15(6): 509-513.
  9. Gambardella, I., et al. (2016). “Congestive kidney failure in cardiac surgery: the relationship between central venous pressure and acute kidney injury.” Interact Cardiovasc Thorac Surg 23(5): 800-805.
  10. Maxwell, M. H., et al. (1950). “Renal Venous Pressure in Chronic Congestive Heart Failure.” J Clin Invest 29(3): 342-348.
  11. Nijst, P., et al. (2017). “Intrarenal Flow Alterations During Transition From Euvolemia to Intravascular Volume Expansion in Heart Failure Patients.” JACC Heart Fail 5(9): 672-681.
  12. Nijst, P., et al. (2017). “Renal response to intravascular volume expansion in euvolemic heart failure patients with reduced ejection fraction: Mechanistic insights and clinical implications.” Int J Cardiol 243: 318-325.
  13. Woodward, C. W., et al. (2019). “Fluid Overload Associates With Major Adverse Kidney Events in Critically Ill Patients With Acute Kidney Injury Requiring Continuous Renal Replacement Therapy.” Crit Care Med 47(9): e753-e760.
  14. Zhang, L., et al. (2015). “Associations of fluid overload with mortality and kidney recovery in patients with acute kidney injury: A systematic review and meta-analysis.” J Crit Care 30(4): 860 e867-813.
  15. Chappell et.al., Hypervolemia increases release of atrial natriuretic peptide and shedding of the endothelial glycocalyx. Critical Care 2014, 18:538
  16. Beaubien-Souligny, W., et al. (2020). “Quantifying systemic congestion with Point-Of-Care ultrasound: development of the venous excess ultrasound grading system.” Ultrasound J 12(1): 16.

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