Author: Bryan Boling

I'm a critical care nurse practitioner and co-director of the Critical Care APP Fellowship Program at the University of Kentucky. I split my clinical time between the Neurocritical Care Service, the Surgical Critical Care Service, and the ECMO Service. I'm also an Adjunct Faculty Member in the Acute Care Nurse Practitioner Program at Georgetown University. I have a passion for education and #FOAM.

Fluid Boluses

We frequently give fluid boluses to patients in the ICU. And a not infrequent question I’ll get from the nurses is, “do you want that on the pump or on a pressure bag?” Does it matter? My usual response is, “whatever,” unless the patient is crashing in which case I opt for the pressure bag. Why? Because they need fluid faster than 999ml/h (which is as fast as the IV pump will go). 999ml/h sounds like a lot until you think about it. That would take an entire hour for a liter bolus to go in. In urgent resuscitation, that’s too long. You can see from this chart that the flow rate of even a 20g IV is a lot more than that.

But, Dr. Eddy Joe Gutierrez makes a pretty solid argument that even if it’s not an urgent situation where we all assume the fluid needs to get in fast, we should be using pressure bags. It has to do with the fact that not all of that fluid ends up in the vascular space. And over time, more and more of it with extravasate out. So, when a liter of crystalloid given over 1 hour, only 200ml will end up staying in the vessel. Hardly enough to raise the SV and thus the MAP. So, maybe we should always be using pressure bags for fluid boluses? His Instagram post below summarizes it nicely, but you should definitely give the entire post a read here.

“What would you like us to do?”

This is probably the best question that can be asked surrounding a new consult. I’ve been asked it when calling consults and I’ve asked it myself when receiving consult requests. It sometimes sounds aggressive and even jerky, but it’s not. It’s seeking a moment of clarification. Looking to define why exactly the consult is needed.

Consults are not benign. Like everything else we do, there are consequences as well as benefits to asking for a consult. You’re adding to someone’s workload, however large or small the request. We often think, “it’s a minor issue, won’t be any trouble for them.” But even a “minor” issue requires a consultant to review a patient’s record, see the patient, make recommendations, write a note. There’s really no such thing as an inconsequential consult.

In addition to the effect on the consultant, there’s the added burden on the patient. “How could a consult burden or be detrimental to the patient?” you may ask. “Too many cooks…” is the phrase that comes to mind. The more teams that are involved, the more complicated things become. Again, there’s really no such thing as an inconsequential consult.

All of these downsides are perfectly acceptable if the consult is needed. But often, it isn’t. We often consult a specialist for something that we don’t really need a specialist for. Sometimes it’s a knee jerk reaction to a problem. “New AKI, consult renal.” “New afib? Better call cards.” But the fact is, many times the primary team, especially an ICU team, is perfectly capable of handling these issues.

I know an attending who likes to break her specialty into “101” and “401.” The basics and the upper level stuff. 101 is the bread and butter that an ICU team should be able to manage. 401 is the higher level stuff where you need a consultant.

“What do you want us to do?” is the question that clarifies that. It prevents the knee jerk reaction and forces you to stop and think, “do I really need this consult?” If the answer is “yes,” by all means, call it. Because the flip side of that coin is just as bad (if not worse).

Waiting until it’s too late for the consultant to be of any help is bad for the patient and the consultant. This is my approach to, “should I transfer a patient to the ICU?” If there’s any doubt, call. I’d rather go look at a dozen patients who are safe to stay on the ward than have to admit a patient who is crashing and likely beyond saving because the service was afraid to call.

So, I guess what I’m saying is, err on the side of caution, but always ask yourself, “what would I like for them to do?”

Ventilator Dyssynchrony

Dyssynchrony with the mechanical ventilator is a common problem in the ICU. Often, we treat this with increased sedation, but that’s not always what is needed. In fact, it’s usually not what’s needed. Matt Siuba has a nice summary of common dyssynchronies on Instagram. Take a look at them to better understand why patients are dyssynchronous and what to do about them. We did an episode of the Critical Care Scenarios podcast covering this as well. Give it a listen here.

Reading EEG (Reports)

OK, so we’re not quite getting into the nuts and bolts of reading EEGs (although, I think we will attack that in a future post, at least a little). But, even the terminology on the EEG report can be confusing. with terms like “epileptiform discharges,” that sound like seizures but aren’t, and “generalized slowing,” how do you make sense out of all that?

Maybe you’re saying, “I don’t need an EEG. I don’t work in a neuro-ICU.” Or, “I can recognize seizures when I see them.” Well, firstly, if you work in a neuro-ICU, you probably have a lot more experience with EEGs and already understand how to read them (or at least the reports). Secondly, if working in neurocritical care has taught me one thing, it’s that almost ANYTHING can be a seizure. Seizures are often tonic-clonic and large muscle twitching, but just as often (probably more often), they look like anything but seizures. So, EEG is super helpful in any kind of encephalopathy or altered mental status that can’t be readily explained.

“When do I order a routine (spot) EEG and when do I want continuous/video EEG?” Well, that’s tricky and, like a lot in critical care, is somewhat institution dependent. Continuous EEG is probably better, it’s like just getting a 12-lead for a patient with arrhythmias but not putting them on some sort of continuous ECG. You may see some stuff, but you may miss some stuff. But, continuous is cost and labor intensive and lots of places have protocols for who needs the longer studies and when you can get away with a 1h.

This post from Casey Albin and Neha Dangayach over at EMCrit have written this great post on the basics of EEG and how to read the report. They go over when to order EEGs, when to do routine vs continuous, some of the basic terminology, and what they call the “not quite seizures.” So, check it out and hopefully it will help you make sense of the next EEG report you get.

One day soon, we’ll do a post on how to read (at least on a kindergarten level) the EEG yourself. Just so you can make sense of the squiggly lines before the epileptologist gets back with you. For now, I’ll leave you with what I was taught when I first started in neurocritical care. EEGs should be the opposite of ECGs. Rhythmic stuff is bad. You want the squiggly lines to be random-ish. Also, flat lines are bad (unless you’re trying to burst suppress someone). In that respect, I guess they’re exactly like ECGs.

One-Handed Knots

I’ve been doing a lot of procedures lately and I’ve been thinking about how we tie knots. Strange thing to think about, but we do it a lot. Most of the procedures that we do in the ICU require some suturing (chest tubes, arterial lines, central lines) and suture needs to be tied.

Now, most ICU providers who aren’t surgeons probably use an instrument tie for this. And it works fine. But I did a few surgical rotations in school and first assisted on lots of different cases. So the surgeons and surgical PAs taught me their ways. So the one that I use most often is the one-handed knot.

Once you get facile with it, it’s faster than an instrument tie. It also allows you to have a hand (somewhat) free for other things. I particularly like it when I’m putting in a line that I’d like to keep a finger on until that suture is good and secured. And – I think – it makes you look like you have some special skill.

There are lots of good instructional videos out there, but I really like this one from Rishi Kumar. He’s an intensivist (and a good follow in general, BTW) so he approaches this from that perspective. In this video, he walks you through the technique and explains why, as an intensivist, he uses the one-handed knot. (We have mostly the same reasons, so that probably biases me a little as well, haha!) Like him, I also prefer to tie left-handed, even though I’m right-handed. I don’t really know why, I guess that’s how I learned and it’s all muscle memory at this point. It probably is worth practicing with both hands and being ambidextrous with the technique.

You can get a knot tying board like he uses, or just get some extra suture (or regular old thread) and practice on anything. I like his steering wheel suggestion. I used to practice by sewing up rips and tears in my kids’ stuffed animals. Now that we have a puppy, there is ample opportunity to practice on her toys when she loves them too much! I also recommend wearing gloves when you practice because the feel is slightly different. But, please don’t wet your hand (like he suggests) if you’re practicing on your steering wheel in traffic!

Bivalirudin vs Heparin for ECMO

ECMO is a therapy that’s becoming more and more common, particularly during the COVID-19 pandemic, as it’s often the only support therapy that will get some of these patients through when all conventional ARDS treatments have failed. ECMO involves the use of lots of plastic, catheters, pumps, oxygenators, etc. Blood traditionally doesn’t really like plastic, it often forms clots. So, typically, ECMO patients require some sort of systemic anticoagulation while they’re on the circuit.*

Unfractionated heparin as a continuous infusion has long been the mainstay of ECMO anticoagulation, but there are other options, including bivalirudin. Bivalirudin is a direct thrombin inhibitor (similar to dabigatran) that works by preventing the conversion of fibrinogen to fibrin (you knew that, I’m sure you have the clotting cascade memorized still, right?). It has a rapid plasma clearance, small volume of distribution, and elimination half-life of about 30 mins. All that means that it’s easy to titrate and you can usually just shut it off if there are bleeding problems. Also, it can’t cause heparin induced thrombocytopenia (HIT).

So, should we be using bivalirudin to anticoagulate all our ECMO patients? Well, in the interest of full disclosure, I’m a little biased. We use bivalirudin on all ECMO patients in our center.** We made that decision based on the overall safety of bivalirudin as compared to heparin, but another factor influenced that decision as well, COVID (doesn’t everything seem to come back to COVID these days?). In this case, our average ECMO run for patients who are COVID + is over 30 days. That amount of time presents lots of opportunities for bleeding issues and lots of opportunities for clotting issues (especially given the hypercoagulability of COVID patients). Ordinarily, if an ECMO patient develops clots in their circuit or oxygenator, while not ideal, it’s not the end of the world. You simply cut out the section of clotted circuit or exchange the oxygenator. However, with most patients with COVID, even a 30 second oxygenator exchange can see rapid desaturation, bradycardia, and peri-arrest (or actual arrest). So, it is a good idea to minimize the need for those. Additionally, the long ECMO runs require a lot of exposure to heparin, which increases the risk of developing HIT. HIT isn’t necessarily common, even in ECMO patients, but again, when it happens, it’s BAD.

The podcast ED ECMO, recently discussed this controversy with Ryan Rivosecchi, a pharmacist at University of Pittsburgh and lead author of a new study comparing heparin to bivalirudin. (You can read the original study here) They found a significant decrease in ECMO circuit events as well as decreased incidence of major bleeding in ECMO patients on bivalirudin as compared to heparin. They also discuss the potential cost differences in bivalirudin vs heparin, and, like lots of these things, it’s not as straightforward are the cost of one drug vs the other.

*Not all ECMO patients technically require systemic anticoagulation. Theoretically, if your flow rate is >5lpm on VV ECMO, the risk of significant clotting is low. At our center, we used to run VV ECMO quite frequently with no systemic anticoagulation. Also, shorter runs typically can avoid anticoagulation. VA ECMO can avoid this as well, but the stakes are higher. If a clot forms on VV and it embolizes, it’s going to get caught in the lungs, and well, you’re already on ECMO. But if a clot embolizes on VA, that’s a stroke. That’s bad. In the ED ECMO podcast linked above, Rivosecchi discusses this concept of “dry” ECMO and mentions an upcoming study at University Health Network in Toronto examining the feasibility of an “anticoagulation-free strategy” for VV ECMO.

**Again, not ALL. We have done a few short runs of ECMO with no anticoagulation even recently. However, these were done in patients without COVID and the associated hypercoagulability and in patients for whom systemic anticoagulation was contraindicated for some other reason.

CT Abdomen and Pelvis Anatomy

I love a good visual guide to anatomy. As someone who looks at more than a few CTs of the belly, this is super helpful in making sense of what I’m seeing. Also, as someone who does a fair amount of POCUS exams of the abdomen, it’s also super helpful.

The Rule of 15

I tweeted about this yesterday but wanted to do a whole post on it, because I think it’s a great tip! ABGs and acid-base disturbances are difficult topics to grasp. There are lots of great ways to remember how to interpret these, and we’ll cover them in time. But one of the hardest parts, especially for learners, seems to be the concept of proper compensation. How do I know if this primary problem is all that’s going on or if there is more? With anion gap metabolic acidoses, we teach students to use Winter’s Formula to calculate the expected pCO2 and thereby determine if you’re dealing with a purely metabolic problem, or if there is a concomitant respiratory derangement as well.

Of course, you can always use your handy ABG analyzer app (ABG Eval is my personal favorite), but what if you just want to know quickly? You can use the Rule of 15. Dr Jeremy Faust (@jeremyfaust on Twitter) mentioned this in a thread I was reading yesterday and it sparked my interest. I retweeted his tweet, but wanted to know more. I found a very quick video that he does along with Dr Corey Slovis on Academic Life in Emergency Medicine (ALiEM, another great resource for critical care education!). Basically, take the bicarb and add 15. That should give you roughly the expected pCO2 and if you throw a “7.” in front of it, roughly the expected pH. Watch the video here for more!

Pacemakers

Before I became an NP, I worked for a lot of years as a nurse in a cardiac surgical ICU. So, I became pretty acquainted with external pacemakers. Essentially, all the heart surgery patients came out with epicardial pacing wires attached to an external pacemaker. Because the CTICU I was working in was also the CCU, I got a fair amount of experience with transvenous pacemakers as well. But, unless you’ve worked in those specialized environments (and really just due to the volume, the CTICU is the place you really get to know these devices), you probably have a limited exposure to external pacing. At least outside of the transcutaneous pacing learned in ACLS.

Two great resources for you today on this topic (well, more really because one of these has some other really good links in it as well). Scott Weingart over at EMCrit just did a really great episode of his podcast dealing with transvenous pacemakers. He covers insertion – which is a really pretty specialized skill, but one that you should have if you practice in a setting where cardiology isn’t always readily available – as well as the box itself and some troubleshooting. The same principles (other than insertion, of course) apply to epicardial pacing if you should find yourself in a CTICU and need some help with this complex topic. He covers modes and sensitivity as well. He does a good job of explaining sensitivity, which is probably the most confusing part of pacemakers. The wall analogy that he uses is pretty similar to the “see over the fence” analogy that I use when I teach this concept, so I won’t belabor it here. He also mentions a great talk that Dr Sarah Wesley gives on the subject at the Bedside Critical Care conference. He links to it in his post, or you can go directly there.

Finally, a great new site that I just discovered, ICU One Pager, has a phenomenal resource on emergency pacing that covers everything you need to know on one page. Shown below, or you can download it as a PDF from their site.

Hampton’s Hump

We all know that CTA is the way to diagnose PE in a patient, but this requires a trip to CT and a large dose of IV contrast. So, there are ways to narrow things down in patients for whom PE is suspected. Most of us are familiar with evaluating right heart strain on bedside echo, and lots of us know that you can identify certain characteristic ECG changes. But, somewhat less well known is the radiographic sign known as Hampton’s Hump. This is a dome-shaped opacification that is most commonly associated with PE, but also can be a sign of pulmonary infarction due to other causes, such as angioinvasive aspergillosis. PE causes a wedge shaped infarct with sparing of the apex due to collateral circulation in the bronchial arteries. This leads to the characteristic rounded shape.

New England Journal of Medicine’s Images in Clinical Medicine series recently featured a nice example of this. This requires a free NEJM Online account to view the entire post (but the free account is well worth your time).