So Rory (@EMnerd) is in the process of working on a fluid resus protocol for Shock-Trauma, and asked me if we could have a chat about it, which I feel very honored for – and had a brief impostor syndrome crisis – but it’s always great to chat with people who are really bright, really physiological and after the same goal, to make patients better. Always a pleasure to chat with Rory, so here it is.
I really can’t wait to see their protocol, because I think this is a huge and complex endeavor, but has to be done. I will try to put pen to paper (probably really pixels to a screen but that doesn’t sound as good) and put what I try to do for fluid resus on a diagram of sorts.
Love to hear comments and questions.
PS please skip the first 30 seconds which are a technical blank… Ièm not tech saavy so can’t trim it!
cheers!
Philippe
A great comment by Dr. Korbin Haycock
One issue to consider is the degree of pulmonary vascular leakage. If, as in the case of sepsis, the pulmonary vasculature is more prone to the development of lung interstitial edema, lower LVEDP’s possibly will still result in as much lung wetness as higher LVEDP’s. Therefore, reliance of E/e’ ratios may not be the best measure of a fluid resuscitative endpoint in sepsis (and aren’t we really talking about sepsis resuscitation here?). I believe that it’s relatively clear that EVLW will adversely affect outcomes, but pushing for every bit of increased stroke volume/fluid responsiveness is less clear to be beneficial, even if it makes sense from a DO2/VO2 perspective (which may not be the real issue in sepsis anyway, as mitochondrial utilization of the DO2 provided may be the real problem, rather than DO2/VO2 balance). If the assumption is that the kidneys and lungs are the most delicate organs and most at risk to over aggressive fluid administration, and will impact mortality/LOS in the ICU, perhaps a combined strategy of attention to E/e’ ratios, development of B-lines, or the renal resistive index increasing would be a signal for a different strategy rather than fluids to increase venous return (i.e. switching from crystalloids to norepinephrine or vasopressin if the CO is elevated and will tolerate a minor ding from the increase in SVR). If any of those three variables indicate a problem, stop the fluids, switch to a vasopressor. If the issue is the CO rather than the SVR, use an inotrope instead. Of course RV/LV interactions as mentioned in the comments above must be considered. No point in giving fluids to an empty LV if the RV is failing–you’ll just congest the kidneys.
thinking critical care 
Thanks Phillipe and Rory. Great listening. Two questions.
1. Is the portal vein pulsatility thing something you could measure as a resistive index?
2. Do you ever use the doppler on the mitral inflow and increase fluids until the E wave is up around the same height as A?(something I have heard Mike Mallon, and seen Greg Comadeiras do)
Thanks for listening!
1. I’m not sure, will check.
2. in isolation, that would assume fluids are going to get from right to left, an assumption I am not comfortable with, because in cases where RV failure will result in a small, underfilled LV, the LV would be volume responsive, but the RV not. So unless one was able to selectively volume load the LV alone, volume may worsen the RV status, septal shift, etc… However as a measure of LV fluid tolerance, it’s probably as good as anything else…
On top of IVC and LV EF, I’m starting to use estimates of LAP and LVEDP to help estimate fluid status. These pressures can be estimated by measuring E and e’ (diastology pressures); these numbers have been shown to correlate with Pwedge pressure, and may be helpful here.
Here, E/e’ would be 129/9.25 = 13.5, which correlates with a wedge pressure of just under 19. This confirmed my clinical impression of congestive heart failure in this particular patient. The numbers only take a minute or two to measure.
Thanks,
Sameer
>
There is certainly use to these measures, but the only issue I have is relating to a pressure, which to me is pertinent in fluid tolerance, but less so in responsiveness, and can change with ventricular compliance regardless of volume status…
One issue to consider is the degree of pulmonary vascular leakage. If, as in the case of sepsis, the pulmonary vasculature is more prone to the development of lung interstitial edema, lower LVEDP’s possibly will still result in as much lung wetness as higher LVEDP’s. Therefore, reliance of E/e’ ratios may not be the best measure of a fluid resuscitative endpoint in sepsis (and aren’t we really talking about sepsis resuscitation here?). I believe that it’s relatively clear that EVLW will adversely affect outcomes, but pushing for every bit of increased stroke volume/fluid responsiveness is less clear to be beneficial, even if it makes sense from a DO2/VO2 perspective (which may not be the real issue in sepsis anyway, as mitochondrial utilization of the DO2 provided may be the real problem, rather than DO2/VO2 balance). If the assumption is that the kidneys and lungs are the most delicate organs and most at risk to over aggressive fluid administration, and will impact mortality/LOS in the ICU, perhaps a combined strategy of attention to E/e’ ratios, development of B-lines, or the renal resistive index increasing would be a signal for a different strategy rather than fluids to increase venous return (i.e. switching from crystalloids to norepinephrine or vasopressin if the CO is elevated and will tolerate a minor ding from the increase in SVR). If any of those three variables indicate a problem, stop the fluids, switch to a vasopressor. If the issue is the CO rather than the SVR, use an inotrope instead. Of course RV/LV interactions as mentioned in the comments above must be considered. No point in giving fluids to an empty LV if the RV is failing–you’ll just congest the kidneys.
P.S. I couldn’t figure out how to listen to the audio, so apologies if my comments were already discussed.
fixed the audio, do give it a try!
Korbin,
Can’t agree more! I would love to work w EVLW myself. Thanks for contributing!