Skip to content

Episode Notes

Source / episode info

  • Episode: 339
  • Title: Divine Intervention Episode 339 – The HY Pulmonary Embolism Podcast
  • Published: 2021-09-08
  • Source: Episode page

One-liner

This episode provides a comprehensive review of Pulmonary Embolism (PE), covering its pathophysiology via Virchow's Triad, the diagnostic algorithm using D-dimer and CT angiography, management with anticoagulants (LMWH vs. UFH), and specific considerations for special populations like pregnancy.

High-yield summary

  • Virchow's Triad: The three components of VTE risk are stasis (e.g., long immobility, bedrest), hypercoagulability (e.g., Factor V Leiden, Antithrombin III deficiency), and endothelial injury (e.g., surgery, trauma).
  • PE Presentation: PE is an acute event; the most common EKG finding is sinus tachycardia. The associated pleural effusion is typically exudative (E in PE -> Exudative).
  • Diagnostic Algorithm: For low clinical probability, a normal D-dimer can rule out PE. For high clinical probability, proceed directly to CT Pulmonary Angiogram (CTPA), regardless of the D-dimer result.
  • Anticoagulation Choice: Standard therapy is Low Molecular Weight Heparin (LMWH). Use Unfractionated Heparin (UFH) specifically in patients with renal dysfunction.
  • Thrombolytics (TPA): Reserved for life-threatening PE, specifically when the patient is hemodynamically unstable or shows definitive signs of right ventricular failure.
  • Special Populations: In pregnant women and those on Combined Oral Contraceptives (COC Ps), prophylactic anticoagulation with Heparin (LMWH/UFH) is mandatory.

Learning objectives

  • Describe the pathophysiology of PE using Virchow's Triad (stasis, hypercoagulability, endothelial injury).
  • Differentiate between low-risk and high-risk patients for PE to guide diagnostic testing (D-dimer vs. CTPA).
  • Select the appropriate anticoagulant based on renal function (LMWH vs. UFH) and patient status (pregnancy/COC Ps).
  • Recognize the clinical signs of massive PE, including hemodynamic instability and right ventricular failure.
  • Classify pleural effusions associated with PE as exudative rather than transudative.

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
PEAcute onset dyspnea/tachycardiaDVT -> Pulmonary Artery OcclusionRemember the E in PE stands for Exudative effusion.
Virchow's TriadStasis, Hypercoagulability, Endothelial InjuryImmobility, Factor V Leiden, TraumaAlways think of these three components when asked about DVT/PE risk factors.
D-dimerElevated levels (high sensitivity)Low clinical probability PE workupOnly use D-dimer in low-risk patients; a negative result is highly reassuring.
LMWH vs UFHLMWH for normal renal function; UFH for renal dysfunctionRenal clearance of drug metabolitesThis is a classic trap question: always check the patient's creatinine/eGFR first.

Rapid review table

TopicKey PointContextExam Relevance
PE DiagnosisCT Pulmonary Angiogram (CTPA)Preferred imaging modality for high suspicion PEGold standard is pulmonary angiogram, but it's too toxic/invasive for routine use.
D-dimer TestHigh Negative Predictive Value (NPV)Used to rule out PE in low-risk patientsIf D-dimer is negative AND the patient is low risk, PE can be excluded.
AnticoagulationLMWH vs UFH selectionRenal function status of the patientUse UFH if renal failure is present; use LMWH otherwise (unless contraindicated).
TPA IndicationsHemodynamic instability or RV failure signsMassive PE managementTPA is a reperfusion therapy, reserved for life-threatening situations.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A patient presents with acute shortness of breath and tachycardia, having recently undergone orthopedic surgery following a long period of immobility.Pulmonary Embolism (PE)Surgery/immobility causes endothelial injury and stasis, fulfilling Virchow's Triad components for VTE formation.
A patient has known DVT in the iliac veins and subsequently develops acute respiratory distress with hypoxemia.PE secondary to DVTThe most common source of PE is a thrombus that dislodges from a deep vein (DVT) and travels through the inferior vena cava into the pulmonary circulation.
A patient presents with signs of severe right heart strain, including elevated jugular venous pressure and hypotension, following suspected PE.Massive/High-Risk PE requiring ThrombolysisHemodynamic instability or clear evidence of RV failure mandates immediate reperfusion therapy (TPA) because the risk outweighs bleeding risk.
A patient is found to have a pleural effusion associated with acute respiratory distress due to suspected PE.Exudative Pleural EffusionInflammation from pulmonary vascular occlusion and subsequent inflammatory cascade increases capillary permeability, leading to an exudate.
In a stable patient with confirmed DVT who has renal impairment, the preferred initial anticoagulant is...Unfractionated Heparin (UFH)LMWH is cleared renally; therefore, UFH must be used in patients with compromised kidney function.
A pregnant woman requires prophylactic anticoagulation due to increased risk of VTE.Anticoagulation: Heparin-basedWarfarin and DOA Cs are generally avoided in pregnancy due to teratogenicity or altered metabolism; heparin is the preferred agent.

Differential diagnosis / distinguishing features

PE vs. Acute Heart Failure

Key FeaturesDistinguishing FindingsNext Step
Dyspnea, orthopnea, peripheral edema; often associated with elevated BNP.PE: Tachycardia is usually sinus tachycardia; physical exam may reveal signs of RV strain (e.g., JVD); EKG findings are more suggestive of acute pulmonary pressure changes. HF: Often has bilateral crackles/rales and S3 gallop.Measure BNP levels; assess for signs of right heart failure (JVD, peripheral edema) to differentiate primary cause.

Management pearls

  • Initial PE Management: Start with IV anticoagulation ( LMWH or UFH) immediately upon suspicion, even before definitive imaging results are available if the patient is unstable.
  • DVT -> PE Pathway: If a DVT is found in conjunction with suspected PE, treat both conditions aggressively with anticoagulants and consider an IVC filter if anticoagulation is contraindicated.
  • TPA Use Criteria (The "Two Ways"): Only administer thrombolytics if the patient is hemodynamically unstable OR has clear evidence of right ventricular failure .
  • Long-Term Therapy: All patients with confirmed PE require long-term anticoagulation for at least 3 months to prevent recurrence.

Don't miss

🚨
D-dimer Limitation: Never use D-dimer as the sole diagnostic tool in a high-probability patient; proceed directly to CTPA.
🚨
LMWH/UFH Rule: Always adjust anticoagulant choice based on renal function: LMWH -> normal kidney; UFH -> renal impairment.
🚨
Pregnancy Anticoagulation: Heparin (LMWH or UFH) is the only safe class of anticoagulants during pregnancy.
🚨
PE Effusion Type: PE causes an exudative pleural effusion due to increased vascular permeability, not a transudative one.

Integration & clinical reasoning

  • VTE and Cardiac Risk: Chronic PE can lead to sustained pulmonary hypertension, which may progress to Chronic Thromboembolic Pulmonary Hypertension ( CTEPH ), requiring specialized management (e.g., lung transplant evaluation).
  • DVT/PE Cascade: The formation of a DVT in the lower extremity is often the source material for a subsequent PE event; thus, treating the underlying venous thrombosis is critical to preventing pulmonary complications.
  • Hypercoagulability Syndromes: Genetic conditions like Factor V Leiden or Antithrombin III deficiency significantly increase baseline risk and require lifelong prophylactic anticoagulation measures.

OMM / COMLEX integration

🦴
For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Acute/Unstable Pathology: In any scenario involving suspected massive PE or hemodynamic instability, standard emergency management (IV fluids, vasopressors, immediate anticoagulation, and potential TPA) takes absolute priority over OMT considerations.
  • Bleeding Risk: The primary contraindication to both LMWH and UFH is active bleeding. If the patient has recent surgery or major trauma, caution must be exercised regarding thrombolytics (TPA).

Concept connections / cross-references

  • For detailed information on deep vein thrombosis (DVT) pathophysiology and initial management, review [ Episode 309 ].
  • Understanding the general principles of coagulation cascade disorders is covered in [ Episode 285 ] (Coagulation).

High-yield association table

ConditionAssociationMechanismClinical Significance
PEExudative Pleural EffusionIncreased vascular permeability due to inflammatory mediators.Helps distinguish PE from other causes of pleural effusion; meeting one Light's criterion is sufficient.
DVT -> PEThromboembolismClot dislodgement (embolization) into the pulmonary circulation.The most common source of PE; risk factors for DVT are also risk factors for PE.
LMWH/UFHRenal Function StatusLMWH is cleared renally; UFH clearance is less dependent on renal function.Critical decision point in management: always check the patient's eGFR before choosing an anticoagulant.
Pregnancy/COC PsIncreased VTE RiskHormonal changes and physical compression of veins (pelvic congestion).Requires mandatory prophylactic anticoagulation with Heparin-based agents.

Key terms glossary

TermDefinitionContextExample
DVTDeep Vein Thrombosis; clot formation in deep leg veins.Primary source material for PE.A patient who is bedridden develops a DVT in the popliteal space.
CTPAComputed Tomography Pulmonary Angiogram.Gold standard imaging test for diagnosing PE.Used when clinical suspicion remains high despite negative D-dimer results.
LMWHLow Molecular Weight Heparin (e.g., enoxaparin).Preferred anticoagulant in most stable patients.Given to a patient with confirmed PE who has normal renal function.
UFHUnfractionated Heparin.Anticoagulant preferred when the patient has significant renal impairment.Used for anticoagulation in a patient with acute kidney injury (AKI).

Study optimization

TopicStudy ApproachPriorityResources
PE Workup AlgorithmFlowchart approach: Risk -> D-dimer -> Imaging/Treatment.HighPractice questions focusing on low vs. high probability stratification.
Anticoagulation ChoiceDecision tree: Renal function, Pregnancy status, Contraindications (Bleeding).CriticalMemorize the LMWH/UFH rule and the Heparin-only rule for pregnancy.
VTE Risk FactorsRecall Virchow's Triad components.MediumLink immobility to stasis; hormonal changes to hypercoagulability.

Question pattern recognition

  • Clinical Clue: Acute dyspnea, tachycardia, and history of recent surgery/immobility -> Suspect PE (High suspicion).
  • Lab Finding: Negative D-dimer in a low-risk patient -> Rule out PE; no further testing needed.
  • Management Trap: Patient with renal failure + suspected PE -> Use UFH, NOT LMWH.

Test yourself

Common mistakes to avoid

🚫
Mistake 1: Assuming all PE effusions are transudative. Correction: Due to the inflammatory cascade, PE causes an exudative effusion (violates one or more Light's criteria).
🚫
Mistake 2: Using D-dimer in high-risk patients. Correction: High risk means skipping D-dimer and proceeding directly to CTPA. The test is only useful for ruling out PE in low-risk individuals.
🚫
Mistake 3: Confusing the indications for TPA. Correction: TPA is reserved for life-threatening instability or clear signs of RV failure, not just any suspected PE.

Common traps

⚠️
Trap 1 (DVT vs. PE): The question asks about DVT management but implies a need for anticoagulation in the setting of potential PE; always treat both underlying conditions aggressively.
⚠️
Trap 2 (Anticoagulant Choice): Presenting a patient with renal failure and offering LMWH as an option is a common trap designed to test knowledge of drug clearance pathways.
⚠️
Trap 3 (PE vs. Heart Failure): The student may confuse the signs of PE (RV strain, JVD) with classic heart failure findings (rales, S3 gallop). Always look for evidence of acute pulmonary vascular compromise.

Original transcript with highlights

Original transcript with highlights

Okay, welcome. This is episode 309 of the Divine Intervention Podcasts. In this podcast, I'm going to be talking about Pomonarium Balli and the USMLA exams. We know P Es are a very high-altopic and they are just certain classic things that they love to test on these exams. So first things first, what's a Pomonarium Balli? Well, we know Pomonarium Balli is something that happens and you have occlusion of a Pomonarium artery. Anytime that occlusion of the Pomonarium artery happens in a person that has had a DVT. Right, to remember, most times a DVT is when you have a blood clot that forms in your lower extrudic veins. Anytime it's going to be like the iliac veins, again like a deep vein, that's what's called DVT, deep vein, osterombosis. You have a clot or a thrombus that forms in a deep vein of the leg and then it travels all the way through your inferior vein achiva. And then it's mixed with to your Pomonarium arteries. And obviously when your Pomonarium arteries are obstructed, that becomes a problem. Because your right heart cannot drain properly. The presence right heart will ultimately begin to fail. In fact, there are some Pomonarium physiological consequences to a Pomonarium Balli. So what are those things? The first thing is we know that as your Pomonarium arteries are obstructed, then the presence right ventricle cannot drain properly. And if your right ventricle cannot drain properly, you'll start having some element of shock.

Again, depending on how big the Pomonarium Balli is. And also if you think about it, because your Pomonarium is obstructed, yes, there is adequate ventilation for the lungs, but there is not adequate perfusion. So you have a VQ Mage. In that case, you're EE Gridient or Rice, because again, if you think about it, oxygen is able to get to the LV Lage just fine, right? So your PBG AO2 is okay. But, perfusion cannot come to a Pomonarium coupler very well because of that obstruction, right? So ventilation is okay. Profusion is not there. So because perfusion is not there, your VQ Mage. So your blood is not getting to your lungs to get oxygen either, basically, even if the oxygen is there. So your PBG AO2 is fine for the most part, but your P little AO2 goes lower, right? So that's why your EE Gridient expands. And if you also think about this, these people, because they become hypoxic, their body starts saying, whoo, whoo, whoo, they start trying to breathe and breathe really hard. If you're breathing really hard, you're going to start hyperventilating. You're going to be blowing off a lot of P, you're going to be blowing off a lot of CO2, right? So those people, they develop a respiratory alkalosis, right? So because as your blowing off CO2, your CO2 goes down, right? You're blowing off that CO2, your CO2 goes down. Since your CO2 is down, you're going to develop a respiratory alkalosis, right? So that's something that's very high yield, high yield to no. Right?

So now, what are the risk factors for a pulmonary embolus? On an in-beaming example, the key thing I want to remember is vercolstriode, right? And vercolstriode of hyperquagulability, right? So there's steases. Many people remember it with the term she, right? Right? SHE. So the S stands for steases. The H stands for hyperquagulability, right? And then the E stands for endothelial dysfunction, right? So steases can arise from any different reasons, right? For example, if a person is bedbound, right? When a person is bedbound, then they have blood steases. That's why many times in hospitals, they put these things on your legs to just keep the blood and your lower extremities are contracting. And that's why they like after surgery. They like you to ambolitas quickly as possible. They do all these things to reduce your risk of having a PE. Right? So steases, if you think about it, right? Like for example, a man that is pregnant, right? Again, a man that is pregnant just is not moving around very much, right? All those things can ultimately cause cause problems, right? Or if you think about it, a person that goes on a long plane ride or a long train ride or something like that, right? Again, since you're staining a one place, your blood is not moving as a short, right? And the thing is, I just kind of think of it this way. When you're stoking one place doing nothing, you start doing like strange things, right?

So your blood, when it's just kind of stuck, you kind of start getting in trouble, right? Or like say, for example, a person gets a, a person again, get like, you know, gets drunk and then the, the leon the ground or something for many, many hours. Again, that blood is not really moving anywhere, right? That can cause problems, right? And they hypercogulability, right? There are just many things that can set up a person for hypercogulability, right? So if you have like, for example, factor five lighting, right? With factor five lighting, your factor five is, is almost as like a longer half life than you should, right? So because of that, you're going to have like that person being hypercogulable. If a person has antithrom in three deficiency, right? Because remember normally, antithrom in three, in he beats factors 10 and factor two, right? So people can have that as a genetic disease or they can get an acquired cause of it in the setting of people to have an euphrodix syndrome. Remember one of the proteins you, you pee out in the euphrodix syndrome because your kidney is a leaky, is antithrom in three. So factor two, factor 10, basically those things are no longer being inhibited, right? So you're going to have a high risk of problems, right? And then in the philial dysfunction, right? Again, whenever you have surgery or you have injury or you're in an accident, right? You're pretty much puncture like a blood vessel or something, right?

Again, by doing that, you're pretty much triggering the coagulation cascade, right? So those are all things that can put a person in a pretty bad spot or pretty supposed to get an pulmonary embolite in the first place, right? But again, if they ask you what is the biggest risk factor for a PE, once you pick an azure that says DVT, those people that have a PE, they get it because they had a DVT that arose initially. And remember, there are many other things that can include the pulmonary artery besides just like, you know, like a clot, right? People can have like fat, embolite. Remember, they are going to test that in the context of like a person having like a recent fracture, right? Or like an orthopedic procedure because again, remember the, your bone contains bone marrow. And as you get older, your red marrow shifts towards yellow marrow, right? That yellow marrow is fat, right? So if you have a fracture orthopedic surgical procedure and you have manipulating your bones, that can release some of that yellow marrow. And then that can travel in the bloodstream and look, you know, clota blood vessels, right? And then an air embolite, many times they put it in the context of a pressing getting like a vascular procedure, right? So it can be like, either they got like a central line, please, or something like that, right? And then don't forget, I'm not afraid of embolite.

You'll put a temporal association with the one being like in a third trimester, and maybe having had an abortion or intrauterine fetal demise. And you just see a DIC picture in the setting of a pregnancy. So those are all things, right? That can guide the person towards having a, towards having a, those are all things that kind of essentially include the pulmonary arteries, right? And one thing I just want to say is that these people that have P Es, right? What kind of plural effusion could they have? The thing is usually they will have an exudative plural effusion. Again, many people have this misconception that P Es are associated with transudative effusions. Even when I had that misconception back in the day, it's actually not true, right? So it's very high up to know that P Es only cause exudative effusions, just remember the E in PE for exudative, right? Because the thing is whenever you have a conclusion of a pulmonary artery, there's an inflammatory cascade that gets kick-started, right? And that inflammatory cascade, right? Ultimately leads to the production of many of these inflammatory markers. And those inflammatory markers, one thing they do is they can increase vascular permeability, and that can make your lungs litty, okay? So in general, people that have pulmonary embolite tend to have exudative plural effusions, right? So they're not going to meet with all three of those, basically they're going to violate one or more of our lights, right?

So that's very high up to know. Now, one thing I want to say is how do you know that you're dealing with PE? Well, the big thing is, time frame helps a lot on endemic exams, right? People that have P Es, their condition is acute, right? So it will be highly unlikely for a person to have had a situation for like two to three months, and then you notice that, oh, she all of a sudden is a PE, no, right? A PE is usually going to be an acute event on endemic exams. Although, one thing I would say to watch out for is, let's say a person has had a PE or they've had recurrent P Es, and then you start noticing, you start seeing them having signs and symptoms of like, right, heart dysfunction, like months, years later, right? I want you to think of pulmonary hypertension. Those people have, there's a kind of pulmonary hypertension I believe that's known as CTF, CTEPH, right? Basically, those people would have pulmonary hypertension because they've had like recurrent pulmonary embolite, right? But again, the big thing about PE is the way we'll present on exams, it'll be acute onset, the person will be very short of breath, the person will be hyperventilating, right? Many times, those people are going to be a tacky cardiac, right? Remember, the most common EKG anomaly in a person that has a pulmonary embolite embolose is sinus tacky cardiac, right? I know many people are like, ooh, S1, Q3, T3, to be honest with you, I would not even worry about that for your exam, right?

For the most part, if a person has a PE, they're going to have sinus tacky cardiac, right? The EKG is likely going to be normal, they're just going to be, the heart is just going to be slogging along very quickly, right? The heart is going to be slogging along very quickly. So now, the thing is, when you suspect the PE, what are you supposed to do? So the thing is, there's all these criteria that exist, right? But the thing is, again, the most of these criteria help you answer questions correctly on your exams? No, right? So let me just tell you what you're supposed to do on your exams. The first thing you ask yourself is, is this person low-risk or high-risk? And again, it'll be plenty obvious from the question. So say, for example, if a person is over the age of 35, they smoke, right? And they will know CP's. That person very likely has a PE, that's a high-risk person, right? Now, contrast this with the college athlete that is very active, doesn't use any drugs, has a normal BMI, is not hypoxic or anything like that on labs, right? If you see all those things, that person is low-risk, that's pretty much it, right? The thing is, if you, again, I feel like many people, the thing that kind of crushes them on these USMLA exams, is just pervasive over thinking. You don't have to be an over thinker on these exams. So what I would just encourage you to do is just ask yourself, okay, let me just break things down to the bare bones, bare bones, right?

So breaking things down to the bare bones, are you low-risk or high-risk? If you are low-risk, the first thing I'm supposed to do for those people is to get a D-dimer, right? Get a D-dimer. If the D-dimer is elevated, then you can proceed to a more invasive test, like you can do like a CT and geogram of the chest, that's it, right? But if a person is low probability and you get that D-dimer, and the D-dimer is normal, right? Then you've pretty much crossed out PE, you can go ahead and stop your diagnostic testing at that point. Now, if a person is high-risk, though, like the person I mentioned, you're not going to be messing around with D-dimer, right? You're going to just go straight to the CT and geogram of the chest, right? Those people are very, very high-risk, so in those circumstances, you're just going to go ahead and proceed to CT and geogram of the chest. Now, the thing is, in pregnant women, you have some other considerations. In general, for pregnant women, on in-beaming exams, you really want to try a VQ scan first, right? You try a VQ scan, right? So if VQ scan shows you a high probability for PE, that's all you're done with that, right? That tells you, okay, this pregnant woman likely has a PE. Let's go ahead and start treating her, right? But in a pregnant woman, if you get like any other kind of result from a VQ scan, you need to proceed to a CT and geogram of the chest, right?

Now, one thing I'll go ahead and say is, there are actually certain situations that are not even related to these classic things I mentioned, where you don't do a CT and geogram of the chest, right? So say, for example, a person has like kidney damage, right? A person has like renal dysfunction. That's just like a contraindication to those people getting a CT chest and geogram. But for the most part, I will just say this, if you kind of parse people out as being lures versus high risk, you're pretty much going to be set on end-game exams. And one thing I will say is, sometimes you may see this in error on a test, when you give you a question about a person that is high risk, and they check the D-dimer, and the D-dimer is normal. And then you'll see, what is the next best step? Your next best step, again, is to still get that CT and geogram. Once you're a high risk person for PE, you need to get that CT and geogram, regardless of what the D-dimer shows, okay? Regardless of what the D-dimer shows, that's very important, right? In general, D-dimer should only be administered to people that are low risk, okay? D-dimer should only be administered to people that are low risk. Yes, the D-dimer test is very sensitive, has a very high negative predictive value. But again, it's something you should, on exams, only be administering people that are low risk for PE, right?

Now, one thing I want to go ahead and then say is, what do we usually, like, what's the whole business with a VQ scan? Because that's one thing that people usually confuse. But again, it's actually a pretty simple concept, right? It's a VQ scan, V ventilation, Q, profusion, right? So basically, it's a scan, it's a new clear medicine test, believe it or not, where they will check the ventilation of the lungs and then they will check the profusion of the lungs. And then it's basically like a two-part test, right? They check the ventilation first and then they check the profusion. If you have ventilation, if you notice that, wow! I look at this person as an entire lung and bone. The ventilation graph looks perfectly fine, right? I look at the person's lungs on imaging. The ventilation looks great. Well, then I notice that, wow! The ventilation does it much or perfectly with the profusion in a certain area, right? Then that person likely has some kind of PE. And again, there are many different permutations you have to consider in calling these VQ scans, but that's well beyond the scope of the USM Ls. So we're going to go ahead and skip that, right? Now, one thing I will just see, sometimes in terms of workup, the medication that you give you some questions where, you may notice that doing a CT angiogram is not the right answer or anything like that, but you may not even supply CT angiogram or VQ scan, right? Or even D-dimer as an answer. Let me just see this.

If, for example, they give you a question about like a person that you suspect has a PE. And for some reason, you don't see CT angiogram as an answer, you don't see VQ scan as an answer, you don't see D-dimer as an answer. And they put an answer choice that says to do a duplex ultrasound of the lower extremities. Go ahead and pick that answer. Again, it's just the thing that has the closest relationship to PE in those circumstances. Again, this is just GIMS MANSHAPE for, for exams. But that's one thing, occasionally we see throning on NB exams. And obviously, the gold standard test for diagnosing a PE is a pulmonary angiogram, right? So again, remember, a CT angiogram is not the same thing as a pulmonary angiogram, right? A CT angiogram you inject contrasts into a person's vein, right? And then take pictures of their lungs. A pulmonary angiogram is almost like you're thinking of catheter and dip in contrast in the pulmonary arteries. It's super sensitive, it's super specific, but it's super toxic, right? So, basically you should essentially never perform a pulmonary angiogram on your USMID exams. That's pretty much the way you work up P Es. So now let's talk about what you're supposed to do for P Es, right? For pressing as a PE, what are you supposed to do? Well, you're supposed to treat those people with IV heparin. That's very high up to no. You're supposed to treat those people with IV heparin, IV heparin, right? And the thing is, there are two kinds of heparins in general.

You know, there is low molecular weight heparin and there is unfroxinated heparin. Let me tell you this. The only people that you should really be using on fraction-eat-head heparin are people that have renal dysfunction. For pressing has renal dysfunction, use unfroxinated heparin in those people. Well, for pretty much every other case you see on your exam, use low molecular weight heparin, right? Many times the NBM is not tacky like that, where they would put low molecular weight heparin as an answer or unfroxinated heparin as an answer. If they do both, they're basically trying to get you to distinguish between a person that has renal dysfunction. In that case, you're going to use unfroxinated heparin. Versus a person that doesn't have renal dysfunction. In that case, you're going to use low molecular weight heparin, right? That's the primary treatment for PE, because most times, it will help the body have enough time to take care of the clot and deal with the issue at hand. But to be honest with you, I wouldn't go... I wouldn't say, oh, you know what, for every PE question, pick TPA, pick TPA, pick TPA, pick TPA. There are very few situations where you should pick TPA on your exams, right? And one thing I will say is, the only time you should pick TPA is when a person that has a PE and they fall into one of two categories. One is they're hemodynamically unstable. You notice the person going into shock in those circumstances. You should be giving those people TPA.

That's one. Now, the second circumstance where you should be giving TPA is where they give you clear definitive signs in the question of the person's right ventricle beginning to fail. What do I mean by that? So they will give you signs in the question like they may say that. Or an echocardiography. The person's right ventricle pressures are found to be elevated or the right ventricle is beginning to descend. In those circumstances, you need to go gangbusters and do TPA. Now, obviously there are some people that cannot even get hair printing in the first place or even TPA. And again, who are those people? The big, big thing I want you to remember are people that have had a recent surgery. A person has had a recent surgery or a person has like bleeding, right? Or they've had like a neurosurgical procedure. In those circumstances, you really should not be giving those people hair print or giving those people TPA, right? In those circumstances, especially when they have like a very bad like massive PE where they are hypotensive, they are right ventricle is failing. Really, the only thing you can do for those people is embolectomy, right? You can perform embolectomy, you can perform embolectomy. And then one other case, you may notice that today I'm just giving a lot of scenarios because that's the reason I'm giving a lot of scenarios is this is the way you really test this thing, right? One of the scenarios they can give you is they can give you a person that has a DVT, right?

And again, the person has one of these contraindications like recent because usually the prematurement of a DVT is with hair print, right? But when a person has a DVT, right? Unless they have a history of bleeding or less they have like recent neurosurgical procedure or again they've had recent surgery. In those circumstances again, you really should not be giving those people hair print for their DVT. The primary trippend of DVT in those people is to place an IVC filter, okay? It's to place an IVC filter and in fear of an akeva filter, right? Again, that's very, very, very, very high autonome, right? Very, very high autonome on, on exams. And the thing is, after a person has been treated for, for PE, do they need any further therapy like long term? Yes, the answer to that is yes, absolutely, right? Those people need to be placed on anti-qualgulation for, you know, at least three months. I'll say at the very least, after they've had that problem, they should be treated for like three months with an anti-qualgulant. And really to be honest with you, the anti-qualgulants you should use use your doox, right? Use your oral anti-qualgulants like your factor 10 inhibitors or your factor 2 inhibitors. Remember, your factor 10 inhibitors have X in their name, a pixaban, river oxaban, a doxaban, right? Your factor 2 inhibitors are things like bivaleridine, dhabigatran, agatroban, right? Those are all drugs you can use, right?

I mean, in certain circumstances, you can use warframe, right? But use warframe if those other things are not options, right? But in pretty much every other case, you should go ahead and use a user. Use these doox, right? As I call them again, they are basically factor 2 and factor 10 inhibitors. Now, one thing I would say though is, if a person is a concert patient or a person is pregnant, the only thing you should be using in those people is hairpric. That's it, right? If a person is a concert patient or the person is pregnant, the only thing you should be using in those people is hairpric. We're pretty much everyone else. You can go ahead and use those oral anti-qualgulants. So, I think those are kind of like the big things I want to talk about from the setting of a bone armbolus. Again, if you know these things I've talked about, you should be able to pretty much answer all the questions you see on your exam, or at least most of them. So, thank you for listening to me. Again, as I do at the end of a very podcast, I actually have a step 2, see case step 3 course. One is ongoing now, but obviously probably can join me anymore. But I have one in October. The one in October is going to be a test-ticking strategy course. It's pretty much going to be happening. I believe between the 4th and the 8th of October. Just email me and you'll get specific details on that. What is going to be basically the first 3 days in October is like leading to a weekend.

But that first full week of October is where we're going to have it. On the Monday of that week, we're going to have the NV Me test-ticking strategy course. And then from Tuesday to Friday, we're going to be having the review course. For step 2, see case step 3, come Lex. If you're interested, just shoot me an email. And I also do offer one on one Twitter info all the USMID exams. Step 1, step 2, see case step 3. Pretty clean cool med school exams, 30-ish off exams. And I also help with your applications and things of that nature. Again, I've worked with tons of people that I've had a lot of really good benefit from it. So if you're interested, just shoot me an email. And then I have all these podcasts on all the podcast apps. I have a website, divininginterventionpodcast.com. If you subscribe to that, whenever I make a new podcast, you get an email notification. And then I also have a You Tube channel, diviningintervention.usmilypodcasts and videos. That's where I post the videos that I make. And then finally, I have this new website called our diviningintervention, Life Lessons.com. Many people have emailed me that, oh, divining, I love your life lessons. So I kind of decided to start a website where like every week I put like two lessons, like like Life Lessons, they're kind of Bible based. And they're all less than 10 minutes long. And we just discussed a Life Lesson that I know is particularly important for people in this day and age that we live in.

So thank you for listening to me. I'll see you next time. God bless you. Thank you.

Practice questions — USMLE style

Question 1 — Diagnosis/Workup

A 45-year-old male presents to the emergency department with acute onset shortness of breath and a history of recent long-haul air travel. He has no signs of distress, normal vital signs, and is deemed low clinical probability for pulmonary embolism (PE). The physician orders a D-dimer test. If the patient's initial assessment places him in the low-risk category, what is the most appropriate next step if the D-dimer result is negative?

  • A) Proceed immediately to a CT angiogram of the chest due to high clinical suspicion.
  • B) Administer IV heparin and monitor for signs of worsening respiratory status.
  • C) Discharge the patient with no further diagnostic testing required, as the PE risk is effectively ruled out.
  • D) Perform an immediate V/Q scan before considering any advanced imaging.

Answer: C. The D-dimer test has a very high negative predictive value (NPV). In a low-risk patient where the initial clinical probability is low and the D-dimer result is negative, further diagnostic testing for PE can be safely discontinued. High-risk patients require immediate advanced imaging regardless of the D-dimer status.

Question 2 — Management/Thrombolysis

A 68-year-old woman with a history of immobility and known deep vein thrombosis (DVT) presents with signs of acute respiratory distress. Physical examination reveals tachycardia, tachypnea, and evidence of right ventricular strain. An echocardiogram confirms elevated right ventricular pressures and suggests impending right heart failure. Given these findings, what is the most appropriate initial treatment?

  • A) Low molecular weight heparin (LMWH) alone for anticoagulation.
  • B) Immediate administration of thrombolytic therapy (e.g., tPA).
  • C) Placement of an Inferior Vena Cava (IVC) filter and observation.
  • D) Oxygen supplementation and serial monitoring without pharmacological intervention.

Answer: B. Thrombolytics (tPA) are indicated in patients with PE who present with signs of hemodynamic instability or clear evidence of right ventricular failure/strain, as these conditions suggest a massive or submassive PE requiring aggressive reperfusion therapy. LMWH is the standard initial treatment for stable PE but is insufficient when RV failure is evident.

Question 3 — Pathophysiology/Complications

A patient suffers from a large pulmonary embolism (PE). Upon admission, the patient develops a pleural effusion. Based on the underlying pathophysiology of PE, what type of pleural effusion is most commonly expected?

  • A) Transudative, due to increased hydrostatic pressure in the pulmonary capillaries.
  • B) Exudative, resulting from an inflammatory cascade and increased vascular permeability.
  • C) Serous, caused by local irritation leading to fluid accumulation.
  • D) Empyema, secondary to underlying infection exacerbated by PE.

Answer: B. Pulmonary emboli trigger a significant inflammatory cascade within the pulmonary vasculature. This inflammation increases vascular permeability, which is characteristic of an exudative effusion (fluid containing high concentrations of protein and inflammatory markers). It is crucial to remember that P Es are associated with exudative, not transudative, effusions.

Question 4 — Pharmacology/Anticoagulation

A 75-year-old man presents with a confirmed DVT and PE. He has a history of chronic kidney disease (CKD) requiring careful medication selection. Which anticoagulant agent should be prioritized for his initial anticoagulation therapy?

  • A) Low molecular weight heparin (LMWH).
  • B) Warfarin, due to its long half-life allowing time for INR stabilization.
  • C) Unfractionated heparin (UFH).
  • D) Direct oral anticoagulants (DOA Cs), such as rivaroxaban.

Answer: C. In patients with renal dysfunction or CKD, LMWH and many DOA Cs are contraindicated or require significant dose adjustment due to impaired clearance. While DOA Cs are preferred for long-term management in non-renal failure states, Unfractionated Heparin (UFH) is the safest choice for acute anticoagulation in a patient with renal impairment because its metabolism is primarily via protein binding and has minimal renal excretion compared to other agents.

Quick fire review

What are the three components of Virchow's Triad?

Stasis (blood not moving), Hypercoagulability (increased clotting tendency), and Endothelial Dysfunction (damage to vessel lining).

If a patient is low-risk for PE, what is the initial diagnostic test recommended?

D-dimer. A normal result effectively rules out PE.

What type of pleural effusion is classically associated with pulmonary embolism?

Exudative effusion (due to inflammation and increased vascular permeability).

When should TPA be administered for a suspected PE?

Only in cases of hemodynamic instability (shock) or definitive signs of right ventricular failure.

What is the primary alternative treatment for DVT/PE when the patient has recent surgery, bleeding, or neurosurgical history?

Placement of an IVC filter.

For long-term anticoagulation management after a PE, what class of drugs should be preferred over Warfarin?

DOA Cs (Direct Oral Anticoagulants), specifically Factor X inhibitors (e.g., Rivaroxaban) or Factor II inhibitors (e.g., Dabigatran).

What is the primary indication for using Unfractionated Heparin (UFH)?

Patients with renal dysfunction, as UFH clearance is less dependent on kidney function than LMWH.

Name two specific situations where TPA should be administered for PE.

1) Hemodynamic instability/shock, or 2) Clear signs of right ventricular failure (e.g., elevated RV pressures).

What is the recommended duration for long-term anticoagulation following a PE?

At least three months.

Which type of effusion is associated with PE, and why?

Exudative; due to an inflammatory cascade that increases vascular permeability.

If a patient has DVT but contraindications to thrombolytics (e.g., recent surgery), what device should be placed?

IVC filter.

What is the general rule for using D-dimer testing on USMLE exams?

Only administer D-dimer to patients who are low clinical probability/low risk for PE.

Quick recall / Anki-style questions

What is the primary indication for using Unfractionated Heparin (UFH)?

Patients with renal dysfunction, as UFH clearance is less dependent on kidney function than LMWH.

Name two specific situations where TPA should be administered for PE.

1) Hemodynamic instability/shock, or 2) Clear signs of right ventricular failure (e.g., elevated RV pressures).

What is the recommended duration for long-term anticoagulation following a PE?

At least three months.

Which type of effusion is associated with PE, and why?

Exudative; due to an inflammatory cascade that increases vascular permeability.

If a patient has DVT but contraindications to thrombolytics (e.g., recent surgery), what device should be placed?

IVC filter.

What is the general rule for using D-dimer testing on USMLE exams?

Only administer D-dimer to patients who are low clinical probability/low risk for PE.