She Clutched Her Chest in Horror.

"I... Can't... Breathe...Help!" The woman stared up in horror as she clutched her chest.

This was a pulmonary embolism. I knew it right away. She screamed PE from the doorway - Sudden onset dyspnea, pleuritic chest pain, cough, her swollen right leg - It wasn't hard to figure out. It was like she took a page out of a textbook.

She and her family, however, had no idea what was going on. They just knew she couldn't breathe.

"Help her! Help her!" the patient's inconsolable daughter screamed as she was being dragged away by her boyfriend after trying to assault my partner for not taking a BP fast enough.

We had already placed the patient on O2 - her sat was 86% - and began working on a plan to extricate her from the tiny third-floor apartment.

A pulmonary embolism, or PE, is an obstruction of the pulmonary artery (or one of its branches) by material - usually from a thrombus - that originated from somewhere else in the body. Usually, this was from a deep vein thrombus (DVT) of the lower legs. DVT and PE together comprise the spectrum of diseases termed venous thromboembolism (VTE).

These emboli can be anywhere in the lungs, really, and can affect one or both of them. A commonly thrown-around term is a "saddle PE" which is one that lodges at the bifurcation of the main pulmonary artery. Interestingly, these are often thought of as "massive PEs" due to their location and obstruction of both lung highways, however, the vast majority of saddle PEs are actually hemodynamically stable.

In fact, the term "massive PE" has absolutely nothing to do with the physical size of the clot and relates instead to hemodynamic changes. The American Heart Association (AHA) breaks PE down into three categories based on presentation, hemodynamic instability, and treatment pathways: Nonmassive PE (low-risk PE), submassive PE, and massive PE.

Massive PE is the worst case, obviously. In massive PE there is both hypotension (defined as a SBP <90 or a drop in BP >40 from baseline) and evidence of right heart strain on imaging or sometimes ECG. An example being that whole s1q3t3 thing you here about - which is actually not present in the vast majority of massive PEs. Now, this is usually caused by a big clot, sure, but it doesn't have to be - more on that later. Submassive PE also results in right heart strain but without the hemodynamic hit of the massive PE. Nonmassive PE has no hemodynamic compromise and does not show evidence of right heart strain.

Notice none of these definitions mention hypoxia... That's because hypoxia, while often present in massive PE, isn't actually the primary issue at hand. It's all about the right heart in PE.

So let's talk about the pathophysiology real quick, because I think this concept confuses a lot of people.

As I said, the vast majority of PE results from DVTs. Basically, it starts with the formation of the thrombus in the deep veins of the lower legs, it breaks off and gets lodged in the pulmonary vasculature. These clots can form due to things like venous stasis from a long trip to endothelial injury from a recent surgery and really, anything in between.

When this clot gets stuck in the pulmonary arteries, what happens? Well obviously there is a mechanical obstruction of blood flow from the clot burden itself, sure, but that's actually not the biggest issue... Yes, that increases pulmonary vascular resistance, but there is usually more to it. The bigger jam tends to be vasoconstriction. The body doesn't like that there is this big clot in the way of the right heart doing its thing... So all these vasoactive substances are released. That, combined with some hypoxia end up clamping down a lot of the pulmonary vasculature - not just the area with the clot itself.

When you block forward flow you get a traffic jam. Here, the jam is in the lungs and the blood then backs up into the right heart. The right heart, unlike the strong, steadfast left heart, is comparatively weak. It doesn't have to pump blood all around the body - just the lungs. So it doesn't have to work very hard. But in PE it does, and it doesn't like it - So it quits. Turns out when the right heart quits and stops pushing blood into the left heart, the left heart doesn't have anything to pump out to the body... The cardiac output drops and thus the perfusion and BP, etc. THIS is the main pathophysiology behind the death of PE patients: Obstructive shock. These patients die from right heart failure.

With all that said, these patients can also become quite hypoxic too. There is definitely an impaired gas exchange component to this. PE, especially massive PE, can cause a big V/Q mismatch. Initially, this is a pulmonary dead space issue - you have blocked perfusion leading to a useless alveoli. But, eventually becomes a shunt issue too due to atelectasis and/or pulmonary hemorrhage, etc. So really, there are a few mechanisms of hypoxia that can be seen - it's just generally not what kills the patient.

So, let's jump back into the scenario for a minute:

"Hey man, her pressure sucks. 82/46."

I didn't think it would be stellar... "I figured, let's go."

We extricated the patient and loaded her in the ambulance. There we got a full set of vitals, placed her on the monitor, and got an IV.

"Want a litre?" My partner was pointed to the fluid cabinet.

"No, all set, let's just go." And off we went to the big, University hospital in our area.

You don't want to give lots of fluid to massive PE patients... I'm really leerious about it. The issue here is RV backup, right? We don't want to make that worse. This isn't like an inferior MI for example, where you want to give a bolus. There you have a wounded RV, not an obstruction. Here you have an obstruction to forward flow. Fluids, especially an excessive amount of fluid, can worsen RV distension, RV ischemia, and, thus, RV failure.

So, what is the treatment for massive PE?

Really, it is supportive care until we can get the patient to a hospital where they can get blood thinners, thrombolytics, or mechanical thrombectomy.

In this case, I gave this patient 100% O2 via a non-rebreather. We have 2 issues here, hypoxia and pulmonary vasoconstriction. We need to manage those aggressively and that includes O2. O2 can actually reduce pulmonary artery pressure and improve CO in some patients with pulmonary hypertension (which PE causes).

Another key A&B move is avoiding intubation at all costs - which we did here. Intubation causes a CO hit in sick patients, both from the meds and the positive pressure itself. You want to avoid intubating PE patients as long as you can. RSI is a REALLY quick and efficient way to murder these folks.

From a C perspective, we want to limit IV fluid, right? But she was hypotensive... True. To be fair, small alequotes of fluid at a time is probably fine. 250 mL at a time kinda thing. You just need to be very careful. But what if that doesn't help, or worse, the patient further decompensates after you give fluid, now what?

One word: Pressors. Give vasopressors. There are reasonable arguments on both sides when it comes to epi vs. norepi as first-line in PE. Norepi comes with less tachycardia but is associated with increased pulmonary vascular constriction and doesn't do a lot to help that RV out. Epi on the other hand is a better inotrope, but you trade off a risk of worsening tachycardia. Ultimately, there really isn't a strong consensus here to push one or the other - so dealers choice. I started her on epi - I didn't have norepi at the time anyway.

I also gave her a bit of fentanyl for analgesia... She appreciated it. You just need to be careful.

So from us: We recognized PE, ruled out STEMI as a cause of her issues by getting an ECG, started her on O2, got a line, and gave 250 mL of fluid while starting an epi infusion and avoiding intubation.

When we arrived at the ED the patient underwent a CT. They found a big 'ol PE and started thrombolytics. She spent a few days in the ICU post-tPA and was discharged home on blood thinners.

If you have any questions, comment below! Have you treated a massive PE patient yet? How'd it go?

Until next week - Thanks for reading!

-Dean Stockley