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3 thoughts on “Venous Congestion: A Reader’s Questions. #FOAMed, #FOAMcc, #FOAMus

  1. I agree with Phil’s response to your first question. If there is increased IAP, I would say that there could be a small IVC, but I don’t think you’d find it very collapsible with respiratory or ventilator breath variation. These would be a pretty small minority of cases though.

    One thing about POCUS is that in many (most) cases, a finding must be taken in context to what else is going on. For example, portal HTN is caused by either pre-hepatic, intra-hepatic, or post-hepatic causes, so if you find it, you have to consider where the cause is. So, if you happen to notice Doppler evidence of portal HTN, a small IVC, and a liver that on 2-D is hyper-echoic relative to the kidney, and nodular, cirrhosis should be considered as the likely cause, rather than congestion.

    To look at another organ were you could have local edema largely unrelated to elevated RAP, consider a kidney you have been doing serial Doppler exams on during a case of sepsis that has been getting generous crystalloid volume resuscitation and is third spacing. When you Doppler this kidney, over time you might see an increase in the renal resistive index (RRI) with a flatter looking IVC (providing the third spacing was outpacing the venous congestion, or some time had elapsed since the last fluid had been given). Also, the intra-renal venous pattern wouldn’t have much of a congested Doppler pattern either. BUT, you have to again be careful, because the RRI is also increased in cases where the pulse pressure and cardiac output is elevated–your septic patient will most likely have these findings as well. This increase in the RRI is due to an increase in the systolic component of the RRI, where as the renal edema effects the RRI more via decreasing the diastolic portion of the RRI. If, however, you noticed the patient’s CO had dropped and the pulse pressure had declined as the SVR increased after a norepinephrine infusion, then this would learn towards (but not prove) renosarca as the cause of the increasing RRI.

    So again, this is POCUS telling you a story, and you have to hear enough of the rest of the story (more POCUS, physical, history, time course, etc.) in order to act wisely in your next step in management.

  2. Thanks Philippe and Korbin for the explanation and illustrative examples which have given me more insights into this subject. I haven’t done a lot of RRI so far as I don’t feel knowing enough of it and am often perplexed by its findings. Your example has elegantly highlighted some important physiology it displays. It is interesting to see how much the relationship between RRI & CO/SVR mirrors that of cerebral & carotid arteries i.e. Lindegaard.

  3. and I’d like to ask a quick follow up question. I know some discussions on this blog & twitter are on similar subjects but not quite exactly on this situation: a conundrum which isn’t all that uncommon.




    I’ll illustrate my point with the following scenario:







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