So a few nights ago I got pulled out of slumber to rush to the ER for an elderly patient who had arrested in hospital shortly after having been brought in for chest pain. The sharp ER doc had diagnosed a tamponade on a presumed aortic dissection, managed to get a needle in, aspirated some fluid and managed to get ROSC.
So when I got there we had a patient post-ROSC in rapid atrial fibrillation with a thready but palpable pulse. POCUS showed a large pericardial effusion with minimal LV filling. So here is what we did:
With the catheter in, we were able to drain. Note a couple of POCUS teaching points, always make sure to (1) visualize your guidewire in the right space, and (2) second, when using a dilator, you can note the disappearance of the proximal part of the guidewire as it is covered by the dilator. This tells you you have adequately dilated into the target structure – pericardium in this case, because it is possible (personal experience) to advance a dilator fairly deep, but not go through a perhaps fibrotic pericardium, and then result in pigtail mis-placement just outside of the target.
In part 2 you can also see the aspiration of the effusion and improved LV filling. The patient’s BP instantly rose to 140’s systolic.
More case details and POCUS teaching points to come in part 2.
ps – a sterile probe cover was unavailable immediately in the ER. By the time it showed up the pigtail was in. We didn’t feel we could wait. We doused it in alcohol.
I’ll let your imaginations tell you where it would be most useful.
But think, no leads getting in the way or falling off. Think of the time saved in echo labs and clinics.
What does it give you?
leads for a monitored bed (ED, ICU, CCU, stepdown, etc).
a continuous 9-lead ECG. Sure, “it’s not a 12 lead,” but it doesn’t stop you from ordering one. And from my understanding of ECGs (let’s check with Steve Smith maybe?), I think that if you are isoelectric (ST-wise) in 9 leads, the chances of missing a STEMI are…somewhere between slim and none.
no problem with a gown, extra adipose tissue or sweat – those help if anything.
yes, the patient can be on his or her side, no problem.
infection control? they’re gonna love it.
eco-conscious – just wipe and reuse!
Yes. For those who don’t realize that an electrical signal is an electrical signal and that the challenge is to obtain it, two studies are underway to compare it to the current gold standard traditional ECG.
First deliveries anticipated mid-2018.
We’re looking at about $5K apiece. Final price TBA and will vary with bulk orders. Expected to last years – so actually cheaper than all the leads we throw away.
The first run will be limited.
When it’s officially available for pre-order, how many do you think you would want? 😉
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!
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.