Venous Congestion: A Reader’s Questions. #FOAMed, #FOAMcc, #FOAMus

I’m always glad for questions, because I think that it’s what forces everyone’s thinking to progress. So yesterday a couple of really good ones from Jonathan Cheung:

My 1st question: I am just curious if it is possible for a collapsible IVC and PW findings suggestive of venous congestion to coexist, say, for example, if the congestion actually leads to increased IAP (perhaps not to the extent of intra-abdominal hypertension) or even 3rd spacing to form ascites in a leaky patient.
This is a question that has come up a couple of times. My physiological answer would be that, in primary systemic congestion, the start point is the increased CVP, which leads to IVC distension, then hepatic vein distension, whose pressure transmits thru the hepatic to the portal circulation, and then pulsatility develops. So in these cases a plethoric IVC is an inherent part.
On the other hand, local phenomena, such as cirrhosis, organ-specific edema (ischemic bowel, renal capsular hematoma, etc) can lead to edema and congestive signs in the local circulation without central venous congestion.
This is an important delineation, because the therapy for localized inflammation and edema is not likely the same as for central venous hypertension.
My 2nd question is: does the physiological changes by pronation (e.g. variable change in transpulmonary pressure, slight “off loading” of the abdomen etc.) cause an observable change to the spectral findings? I often have this question in mind when I want to assess fluid status in a prone patient on whom doing an echo isn’t always possible.
First I would argue that the only trouble with prone and POCUS is for cardiac views – hence TEE. But for venous doppler, the kidneys are perfect, the PV and IVC are totally accessible laterally and the IVC even posteriorly.
Secondly, I think it’s important to remember that physiologically, venous congestion is venous congestion, no matter the cause, and that end organs can suffer similar consequences. At least initially, proning should drop the PAP and unload the RV, but this will likely change over a variable amount of time. Very tough to properly assess the physiology in my opinion.
I’ll try to get Korbin, Rory and Jon-Emile to chime in!
Click here to come meet this interesting bunch of docs!

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.

    Most people would probably agree that florid congestive signs on POCUS means the RV is unable to pass any more extra volume to the left heart; whilst the absence of those signs mean that the patient may be able to cope with some additional volume without immediately engorging the vital organs.

    And my question is: what about those in between? i.e. the patients who start to develop some mild congestive features on POCUS.

    For those who are on the verge of congestion, diuresis would push the RV to the left (i.e. steep part) of Starling curve resulting in significant CO drop; conversely, extra volume pushes the RV to the right (i.e. flat part) leading to congestion or even D-shape LV, directly hindering CO as well. This margin becomes even smaller in patients whose RV starts to fail (i.e. entire Starling curve shifted downwards)

    I’ll illustrate my point with the following scenario:

    for previously healthy middle aged patients intubated and admitted to the ICU for ARDS from severe pneumonia, they quite often develop some acute cor pulmonale after mechanically ventilated for several days even if the PEEP/driving pressure isn’t exceptionally high; and they usually have resp failure and shock to start with.

    Given that they don’t have pre-existing heart disease, the only signs suggesting the emergence of cor pulmonale could be subtle, without structural changes like dilated RV (RVEDD at most at upper normal range) nor abnormal septal movements. You may see TAPSE dropping to marginal level and portal vein PW signal may become a bit more pulsatile. IVC looks full and RVSP usually rises but not skyrocket. The MV inflow pattern & E/E’ suggest rather normal LA filling pressure, not surprising from a previously healthy heart.

    In this case, it isn’t the LV diastolic dysfunction that overly afterloads the RV; and it isn’t the RV dilation that impairs the (D-shape) LV from ventricular interdependence. Therefore I’d consider the right heart circulation & left heart circulation running purely in series, whereby limiting the RV preload could reduce the LV CO.

    Now, if this patient goes into shock, would you consider fluid challenge or diuretics? Everyone probably would also get other therapies on board, e.g pressor, inotrope, source control etc. But when the patient’s BP is 80/40mmHg, I am more prone to giving some fluid as I believe that reducing preload in a septic patient can precipitate arrest; and that RV only directly impairs LV CO once the IVS starts to shift, which should take more time and thereby easier to monitor.

    I fully appreciate how ambiguous this situation is and that in reality the only way to find out the treatment that works is often by trial and error. Serial assessment by POCUS is definitely needed and one may even put the entire fluid thing aside and focus on other treatments. But just want to know your take and the reasons behind.

    Thanks again for all your work and these thought provoking posts; and my apologies for the supposedly quick question ending up being not so quick. It took me some effort to clearly delineate my question in mind.

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