Category: Shock/Resuscitation

Tracheoinnominate Fistulas

There are a number of potentially scary complications from tracheostomies, particularly early on in the post-procedure period. Although accidental decannulation and loss of airway is probably the most common, Brandon Oto describes the management of a much scarier complication in the latest in our TIRBO series on the Critical Care Scenarios podcast.

I’ve never experienced one of these (thank goodness), but I have had to rush to the OR with a bleeding ENT patient and they’re some of the scariest scenarios that we encounter in the ICU. I think Brandon is right on when he says that just because the incidence of these types of things is low and the mortality is high doesn’t mean that we should be fatalistic and use that as an excuse not to be prepared for these.

Best Vasopressor in TBI?

What vasopressor do you routinely use in the management of traumatic brain injury patients? Admittedly, in my neurocritical care practice, I don’t manage a lot of true TBI patients. In our system, the only neurotrauma patients that come to the neuro ICU are isolated neurotrauma (brain and/or spine without other major trauma). Polytrauma patients go to the trauma service and are comanaged in the TICU along with neurosurgery.

But, in my limited experience, I typically use norepinephrine. I might have formerly said phenylephrine, as that used to be the vasopressor of choice in the neuro ICU. This was mostly due to the fact that at one point, we were mostly using vasopressors to augment BP in order to increase perfusion to the brain or spine, a practice that has largely fallen out of favor. In these cases, the patients often just needed short runs of low dose pressor and so phenylephrine was considered safer to run without a central line, making it appealing in this subset.

But, in the past few years, we’ve gradually shifted away from this to favoring norepinephrine. I think this is largely because we’ve seen a steady increase in the overall acuity of the patients and now those who need pressors typically need them for actual shock, not just to drive MAPs. In that case, central access is typically needed anyway, eliminating the one benefit of phenylephrine.

In this episode of the Elective Rotation podcast, Pharmacy Joe covers a recent study in Anesthesia and Analgesia that seems to favor the use of phenylephrine as the first line vasopressor in TBI patients. It was a rather large retrospective study that showed a statistically significant increase in in-hospital mortality in patients who received norepinephrine as compared to those who received phenylephrine. The study found that norepinephrine was much more common in sicker patients (higher ISS, use of ICP monitoring, comorbidities, etc.), but the authors used propensity-matching statistical analysis to account for this.

Overall, it is an interesting study but there are number of issues including incomplete data regarding shock states. Despite the propensity-matching analysis, I think it’s reasonable to assume that there is probably some bias with patients receiving norepinephrine instead of phenylephrine being sicker at baseline which may account for the difference to a greater degree than is appreciated.

What about you? What is your practice regarding vasopressors in TBI? After reading this study and/or listening to the podcast episode, will you change your practice?

When to Scope in GI Bleeds

I ran across a great video on Instagram yesterday by one of my favorite GI docs, @docschmidtig. If you’re not already following him, you should, his videos are great! This particular one was funny, but also dealt with an interesting point, why do GI docs wait so long to scope someone with a GI bleed? I liked the video on my IG account, but this morning thought it merited a quick post of its own.

This is something I sometimes get frustrated by (or did until Elliot Tapper set me straight). I’ve got a patient with an obvious GI bleed. I call GI, expecting them to scope and fix the problem. And then it feels like they drag their feet over it. In this video clip, Schmidt explains why.

If you want to delve more into the management of GI bleeding. The aforementioned, always informative Elliot Tapper did an episode of our Critical Care Scenarios podcast not long ago on the subject. Listen here.

PS: If you’re a fan of the TV show M*A*S*H, in episode 4 of season 1, Chief Surgeon Who?, Hawkeye explains a similar rationale to Frank regarding why he’s waiting to operate on the patient in obvious shock.

Low-Concentration Peripheral Norepinephrine

We’ve talked before about norepinephrine as a powerful and commonly used vasopressor in the ICU. This is often my go-to pressor for all types of shock, unless it’s cardiogenic shock or I’ve got reason to suspect that contractility is part of the problem. But, historically it has to be infused through a central venous catheter because of the potential risks of infiltration.

It used to be my practice to use phenylephrine when I needed a little bit of vasopressor but wanted to avoid a central line or the need for pressors was too urgent to wait for central line placement. This might be in the face of rapidly progressing, life-threatening shock when even the few minutes it would take to place a central line would be an unacceptable delay in pressor administration. Or, maybe the patient just needs a time-limited run of pressors, while recovering from anesthesia/procedural sedation, for example.

But, while phenylephrine is generally thought of as safe for peripheral administration, it’s really not the optimal vasopressor. I do use push doses of phenylephrine for transient hypotension associated with endotracheal intubation, for example. But, a phenylephrine drip is almost never what I want. If my patient needs a drip, they probably need norepinephrine.

In this episode of the Elective Rotation, Pharmacy Joe discusses the safety and efficacy of using low-concentration norepinephrine through peripheral venous access. Low-concentration norepinephrine has decreased risks in cases of infiltration as compared to standard-dose. Additionally, Tyler Jones has a great post over at Critical Care now discussing more broad use of peripheral vasopressors.

Either way, I think if a patient is sick enough to require norepinephrine at higher doses and/or longer periods of time, the risk of peripheral administration outweighs the risks associated with central venous access. So, put in the central line.

Ultrasound Case: PE

Bedside echo can be very helpful in the diagnosis of pulmonary embolism. There are a number of things to look for including septal bowing, right-heart strain in the form of increased RV size and decreased RV function, McConnell’s sign, and the always exciting clot in transit. Sarah Wolochatiuk is a PGY-4 in Emergency Medicine at the University of Cincinnati just up the road from me. She has a great case presentation on the UC EM blog Taming of the SRU that covers all of this with some great echo images as well.

Estimating Cardiac Output with POCUS

I always love learning new things to do with POCUS and learning new POCUS skills. Pulse wave Doppler is not a mode that I use often and it is on my list of things to practice with. I think there are a lot of really nice benefits of it in the management of critical illness and shock. Now, at first you may have looked at the title of this post and thought, “I know how to do this, EPSS or fractional shortening. But those don’t use PWD? What gives?” Well, E-point Septal Separation (EPSS) and fractional shortening don’t use pulse wave Doppler, they use simple M-Mode. But, they also don’t measure cardiac output, they measure left ventricular ejection fraction (LVEF), and those 2 aren’t the same.

Matt Siuba explains why we want to measure CO as opposed to being content with LVEF in this video from the Zentensivist YouTube Channel. He also explains everything you need to know about pulse wave Doppler (or at least everything you need to know right now) and how to use it to measure the CO. Don’t worry, there is nothing wrong with your ears, the audio is sped up to 1.25x in order to reduce the time of the video to 14 minutes (this is critical care, time is brain! and heart! and…you know, we’re busy!).

Lactate “Clearance”

We often trend lactate in critical illness. We use it as a marker of hypoperfusion in shock and as a guide to fluid volume resuscitation. But, why does it matter (or does it matter)? It’s pretty clear that elevated lactate in critical illness is not a great sign. But what does it mean and do we need to trend it? @eddyjoemd goes through the evidence for us, showing us why elevated lactate is bad and why we should trend it (or maybe why there really is a better trend we should be using instead).

Update: There is a great episode of his Saving Lives podcast on this as well. Just listened to it on my morning walk! Listen here.

Waveform Capnography

While we’ve used colorimetric capnography for years to confirm ETT placement, not all ICU providers are as familiar with waveform capnography. It offers significant benefits to the intubated and non-intubated patient alike.

Using waveform capnography to confirm ETT placement offers a benefit over colorimetric confirmation. during the peri-intubation period, while the patient is being ventilated via BVM, there can be an accumulation of CO2 in the stomach so that it is possible to get color change on an esophageal intubation. The use of waveform capnography prevents this. As carbon dioxide is not manufactured in the stomach, eventually the levels will fall. So, by trending the waveform over a few breaths, you should see a steady decrease in end-tidal CO2 over the course of a few breaths.

In addition to ETT positioning, ETCO2 has a number of other benefits including detecting displaced ETTs, monitoring effectiveness of ventilation in non-intubated patients, assessing ROSC during CPR, and much more. But essential to its use is understanding how to interpret the waveform and not just read the number. In this video, Obiajulu Anozie (@icuexplained) does a great job of explaining what the waveform means and how to use it in the ICU.

Sinus Tachycardia

We see lots of arrhythmias in the ICU, but one that often comes up that isn’t really an arrhythmia is sinus tachycardia. Sinus tach often makes us nervous, and not without good reason, as this echo from Dr Obiajulu Anozie demonstrates. As the heart rate goes up, stroke volume may decrease. Likewise, tachycardia may often be in response to decreased stroke volume as the body attempts to compensate and maintain adequate cardiac output. Sinus tach can often be in response to pain or agitation as well. What do we do about sinus tach? Well, start off by treating potential causes. Pain. Agitation. Hypovolemia. But we very rarely need to treat tachycardia itself. There are cases (as with patients on VV ECMO) where beta blockade is indicated to reduce heart rate, but typically once the potential causes are addressed, nothing else needs to be done. In some cases (as demonstrated below), the tachycardia may in fact be compensatory and by slowing it down, we actually cause harm.

Norepinephrine

Earlier, we discussed epinephrine. Now, Rishi Kumar has another great post about another vasopressor, norepinephrine. When I was first starting out as a nurse, norepi had quite the reputation, and not in a good way. Known by the brand name Levophed, it was often called “Leave-em-dead.” These days, norepi is the go-to pressor for just about any type of shock except cardiogenic. It’s a good all around drug, causing mainly vasoconstriction, but also having some positive inotropic/chronotropic effects as well.