The Pharmacist's Guide to Pulmonary Embolisms (PE)
(Image)
Steph’s Note: After our last post’s financial chat, we’re returning this week to the hard-hitting clinical info. Happily, here to make this info easy to digest is our favorite critical care expert, Joe Nissan. I don’t know about you, but I always get excited when I see a new Joe post because I know I’m about to get knowledge-bombed in a concise, memorable manner. Take it away, Joe!
We’ve all seen this plenty of times before. Someone comes into your emergency department complaining of The Infamous Chest Pain. Would you believe me if I told you that only about 5.5% of emergency room visits for chest pain results in a diagnosis of a serious heart-related issue? So statistically speaking, your patient is probably going to be okay and is likely experiencing acid reflux, costochondritis, anxiety, or some other non-life threatening condition.
Despite the statistics, we should never take chest pain complaints lightly! We should always assume the worst until we’ve ruled out all the life-threatening differentials. Specifically, myocardial infarction (heart attack) and pulmonary embolism should be on the top of your list.
What happens when that chest pain complaint is actually something serious? What if your patient is diagnosed with a massive pulmonary embolism and is on the verge of coding? Are you comfortable being called to the bedside to assist with medication recommendations and preparation? If not, then keep reading because this article is for you.
Blood Flow through the Heart
Before we deep dive into the specifics of pulmonary embolism, let’s take a step back and revisit our pathophysiology course in pharmacy school. Remember that picture in your textbook that explained how blood flows through the heart? It showed where oxygenation happens and where it gets pumped to the rest of the body-does that ring a bell? It looked a little something like this:
(Image)
Hear me out. It looks overwhelming, I know. But let’s walk through it. It really isn’t that bad. To make it a little more simple, here is a little diagram I made for you to make the blood flow easier to follow. Everything in blue is deoxygenated, while everything in red is oxygenated. It all starts with the inferior and superior vena cava:
Does it make sense? Great. So why are going over the heart when we’re talking about a pulmonary problem? Great question!
Pathophysiology/Etiology of Pulmonary Embolism
Pulmonary embolism (PE) is really just a fancy way to say “lung clot.” So, as the name clearly suggests, PE is a condition in which one or more arteries in the lungs becomes blocked by a blood clot. Where does the clot actually happen though?
In the pulmonary arteries.
Scroll back up to the picture above, and you’ll see I highlighted the exact location in orange (my favorite color). Why are PEs so dangerous? Because if left untreated, PEs can lead to impaired gas exchange due to obstruction of the pulmonary vascular bed, leading to a mismatch in the ventilation-to-perfusion ratio. This can lead to hypoxemia, increased pulmonary artery pressure, and reduced cardiac output. (More on the reduced cardiac output portion later.)
So what causes a PE? A lot. However, the majority of PEs originate as lower extremity DVTs (deep vein thromboses). Wait, I want to go on a side quest really quickly!
There is always confusion amongst the medical terminology of venous thromboembolism (VTE), pulmonary embolism (PE), and deep vein thrombosis (DVT). People use them interchangeably all the time, and that’s just flat out wrong. PEs and DVTs are both types of VTE. An untreated DVT can dislodge from the lower extremities and travel to the lungs, causing a PE. But not the other way around. To better understand it, here is a little diagram that I made to help summarize:
Anyway, now that we’ve had that terminology moment, back to what we were discussing. Most PEs originate as lower extremity DVTs (e.g., a blood clot in the leg). Therefore, PE risk factors are the same as for DVTs: the Virchow triad of hypercoagulability, venous stasis, and endothelial injury. Risk factors can further be classified as genetic and acquired. Here are some examples of both:
Diagnosis of Pulmonary Embolism
As pharmacists, we aren’t trained to diagnose anything. (Let’s raise a toast to our physician and mid-level partners!) So here at tl;dr pharmacy, we try to keep this section pretty brief. I won’t go into too much detail, but I want to give you some general basic information to get you by. So the first thing we should discuss is the Wells score.
The Wells score is a clinical prediction rule used to classify patients suspected of having pulmonary embolism into risk groups by quantifying the pre-test probability. What that means is that we can calculate the Wells score to give us a better idea of who is at high risk for developing a PE.
So, what criteria goes into the Wells score calculation?
Using the three-tier model, risk of a pulmonary embolism is as follows:
Low-risk score (0-1): 1.3% prevalence
Moderate-risk score (2-6): 16.2% prevalence
High-risk score (>6): 37.5% prevalence
Patients with moderate to high risk for PE according to the Wells score should undergo further testing to confirm potential diagnosis. While there are many tests that can be used to help guide a PE diagnosis (such as D-dimer, V/Q scan, etc), true confirmation should be achieved with a computed tomography pulmonary angiography (CTPA). CTPA uses contrast dye to create detailed images of the lung blood vessels, allowing providers to identify blood clots in the lungs.
Classification of Pulmonary Embolisms
Once a pulmonary embolism diagnosis is confirmed with a CTPA, it’s time to classify the type of PE. PEs can be classified as massive, sub-massive, and low risk. As the name suggests, massive PEs have the highest risk of mortality, followed by sub-massive, then low risk. How do we differentiate these types of PEs?
Remember earlier when we went over how blood flows through the heart? We did that for a reason. As you can see, massive and sub-massive PEs have higher mortality rates and are considered life-threatening. Why? Because they can cause cardiac compromise and lead to decreased cardiac output and cardiogenic shock. Now how does a clot in the lungs affect the heart?
Remember when we said that a PE occurs in the pulmonary arteries. Well, when a clot is large enough, it can block blood flow between the right ventricle and lungs. That pressure/fluid has to go somewhere. As a result, you get back up into the right ventricle, leading to right ventricular distention and dysfunction. Kind of like a traffic jam.
To simplify things, let’s say you have a water pump (right ventricle), a water hose (pulmonary artery), and a bucket (lungs). You turn that faucet on, and water will flow from the water pump, through the hose, and into the bucket. Now let’s say there’s a large rock (blood clot) that gets stuck in the hose. If that rock is large enough (massive/submassive PE), it can prevent water (blood) from getting through the hose (pulmonary artery) and into the bucket (lungs). Eventually the water will back up. As enough time goes on, the water will collect in the water pump (heart) until it no longer can function (heart failure). Does that make a little more sense now?
(Image)
If not, here’s a picture explaining why right ventricular strain occurs in massive/sub-massive PEs:
Treatment of Pulmonary Embolism
Treatment is heavily dependent on the type of PE that a patient presents with. Obviously patients with massive PEs require more aggressive/invasive treatment to achieve immediate fibrinolysis, while low-risk PEs require less aggressive treatment.
However, regardless of the type, supportive therapy should be provided to all patients with a PE. These supportive measures include oxygen supplementation (noninvasive or invasive) in patients with oxygen saturation <90% and vasopressors for patients with hemodynamic instability.
Surgical interventions for reperfusion may be utilized for massive/submassive PEs and may include catheter-directed treatment, surgical embolectomy, and vena cava filters.
And now, we talk about medications :). The best and most important part to us pharmacy nerds. Let’s start with the higher risk PEs and then move on to the low-risk PE treatment.
A few points to discuss. When using thrombolytic therapy, there is a long list of contraindications. They’re the same contraindications for when we use thrombolytic therapy for stroke. There are a ton of them. And in case you forgot them, I will list them here for you:
Also, this is a common question that always freaks people out. Let’s say you have a patient with a massive PE, and your team gave 100 mg of alteplase over 2 hours. Their next question to you will almost always be this: when do we start the heparin drip? It’s not as bad as you might think.
At the conclusion of the infusion of alteplase, an aPTT should be obtained. If the aPTT is <80 seconds, intravenous heparin should be restarted/started as a continuous infusion without a bolus. In the rare instances when the aPTT exceeds 80 seconds after fibrinolysis, heparin should be withheld, and the aPTT should be rechecked in 4 hours.
Now let’s move on to the not-so-critical low-risk PEs.
If you need more help with warfarin, check out this post!
Obviously there are more anticoagulants that could be used to treat low-risk PEs such as fondaparinux, edoxaban, dabigatran, and so on. But I mean, who really uses those anyway? A lot of factors can go into play when deciding which anticoagulant to start a patient on…things like clinical stability, inpatient vs outpatient treatment, renal function, pricing, access, etc. It is important you take these into consideration before recommending which anticoagulant to start a patient on. If you need a refresher check out our anticoagulant post here.
Well folks, that’s really all we have to discuss. I hope this article gave you a good overview of what a pulmonary embolism is, how to classify, and how to treat them. And remember, pathophysiology is always key! As long as you understand the pathophysiology, you never have to rely on memorization again.