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Summary Table

Category	Details
Risk Factors	Virchow triad: stasis (immobilization, long flights, post-surgery), endothelial injury (trauma, surgery, central lines), hypercoagulability (Factor V Leiden, antiphospholipid syndrome, malignancy, OCPs, pregnancy, nephrotic syndrome). Recent orthopedic surgery (hip/knee replacement) is the highest-risk surgical scenario.
Etiology	Thrombus originating from deep veins of the lower extremities (iliac, femoral, popliteal) that embolizes to the pulmonary vasculature. Less commonly: fat emboli (long bone fracture), amniotic fluid emboli (peripartum), air emboli (central line placement), septic emboli (endocarditis in IV drug users).
Patient Presentation	Acute-onset dyspnea, pleuritic chest pain, tachycardia, tachypnea. May present with syncope or sudden cardiovascular collapse in large clot burden. Hemoptysis occurs in pulmonary infarction. Can be asymptomatic.
Classic Physical Exam	Tachycardia, tachypnea, hypoxia. Unilateral leg swelling suggesting concurrent DVT. Loud P2 (pulmonic component of S2), right ventricular heave, JVD, and hypotension in hemodynamically significant PE. Low-grade fever may be present.
Key Diagnostic Results	ABG: respiratory alkalosis with hypoxemia, elevated $A\text{-}a\ gradient$. D-dimer elevated (sensitive but not confirmatory). CT pulmonary angiography (CTPA) shows filling defect in pulmonary arteries. ECG may show sinus tachycardia, S1Q3T3 pattern, right heart strain, or new right bundle branch block.
Management	Anticoagulation is the cornerstone: heparin (unfractionated or LMWH) bridged to warfarin, or direct oral anticoagulants (DOACs). Thrombolytics (alteplase) reserved for hemodynamically unstable (massive) PE. IVC filter for patients who cannot receive anticoagulation.
Keywords	"Sudden dyspnea post-surgery," "pleuritic chest pain with tachycardia," "immobilization," "unilateral leg swelling," "wedge-shaped opacity," "saddle embolus," "S1Q3T3"

1. Pathophysiology

Pulmonary embolism results from obstruction of the pulmonary arterial vasculature, most commonly by a thrombus that has migrated from the deep venous system of the lower extremities. Understanding the mechanism begins with Virchow triad: venous stasis, endothelial injury, and hypercoagulability. Any clinical condition that promotes one or more of these elements increases thrombus formation risk.

Once a thrombus dislodges and travels to the pulmonary vasculature, it causes mechanical obstruction of blood flow. This obstruction increases pulmonary vascular resistance (PVR), which directly raises right ventricular (RV) afterload. The RV is a thin-walled, compliant chamber not designed to pump against high pressures. When afterload rises acutely, the RV dilates and eventually fails. This explains why patients with large clot burden present with hypotension, syncope, or cardiac arrest: the RV cannot generate enough output to fill the left ventricle, leading to decreased systemic cardiac output.

The ventilation-perfusion (V/Q) mismatch is the central gas exchange abnormality. Areas of the lung that are ventilated but not perfused (dead space ventilation) cannot participate in gas exchange. The result is hypoxemia and a compensatory increase in respiratory rate, producing hypocapnia and respiratory alkalosis on ABG. The $A\text{-}a\ gradient$ is elevated because the problem is at the level of the lung, not the respiratory drive. This is a critical distinction: a patient hyperventilating from anxiety will also have respiratory alkalosis and hypocapnia, but the $A\text{-}a\ gradient$ will be normal because the lungs themselves are functioning properly.

Pulmonary infarction occurs in a minority of cases (roughly 10%) because the lung has a dual blood supply from the pulmonary arteries and the bronchial arteries. When infarction does occur, it presents as pleuritic chest pain and hemoptysis, and imaging may reveal a wedge-shaped, pleural-based opacity (Hampton hump) on chest X-ray.

Release of platelet-derived mediators (serotonin, thromboxane A2) from the clot causes local bronchoconstriction and vasoconstriction, worsening the V/Q mismatch beyond what would be expected from mechanical obstruction alone.

2. Classification and Clinical Manifestation

Classification	Hemodynamics	RV Dysfunction	Troponin/BNP	Clinical Features
Low-risk (small PE)	Stable (SBP > 90 mmHg)	Absent	Normal	Dyspnea, pleuritic chest pain, tachycardia. May be asymptomatic.
Submassive PE	Stable (SBP > 90 mmHg)	Present (RV dilation on echo or CT)	Elevated	Dyspnea, tachycardia, possible syncope. Evidence of RV strain on ECG or imaging without frank shock.
Massive PE	Unstable (SBP < 90 mmHg or requiring vasopressors)	Present	Elevated	Hypotension, syncope, cardiovascular collapse, obstructive shock, possible cardiac arrest. Saddle embolus commonly responsible.
Chronic thromboembolic PE	Variable; may be stable initially	Progressive RV failure over time	May be elevated late	Progressive exertional dyspnea over weeks to months. Develops chronic thromboembolic pulmonary hypertension (CTEPH).

The distinction between submassive and massive PE is hemodynamic stability. Both show RV dysfunction, but only massive PE has sustained hypotension. This classification directly dictates whether thrombolytics are indicated.

Additional Clinical Patterns:

Variant	Mechanism	Distinguishing Feature
Fat embolism syndrome	Fat globules from bone marrow after long bone fractures	Triad: hypoxia + petechial rash (axillae, chest) + neurologic changes. Onset 24 to 72 hours post-fracture.
Amniotic fluid embolism	Amniotic fluid entering maternal circulation during labor or C-section	Sudden cardiovascular collapse during or immediately after delivery, followed by DIC.
Air embolism	Air entering venous circulation (central line insertion/removal, neurosurgery in sitting position)	Sudden cardiovascular collapse during procedure. "Mill-wheel" murmur on auscultation.
Septic embolism	Infected thrombi from right-sided endocarditis	Multiple peripheral nodular infiltrates on chest X-ray, IV drug use history, fever, positive blood cultures.

3. Diagnostic Workup

Test	Role	Key Findings
Clinical probability scoring (Wells score / Geneva score)	Pre-test probability assessment	Determines whether D-dimer testing or direct imaging is appropriate
D-dimer	Screening / rule-out test (high sensitivity, low specificity)	Elevated (> 500 ng/mL). Useful only in low-probability patients. Normal D-dimer effectively rules out PE in low-risk patients.
CT Pulmonary Angiography (CTPA)	Best initial imaging test and confirmatory in most settings	Intraluminal filling defect in pulmonary arteries
V/Q scan	Alternative when CTPA is contraindicated (contrast allergy, renal insufficiency, pregnancy consideration)	High-probability scan: perfusion defects with normal ventilation (mismatch)
Pulmonary angiography	Historical gold standard (rarely performed now)	Direct visualization of filling defect
Lower extremity duplex ultrasound	Adjunct; identifies source DVT	Non-compressible vein segment
Echocardiography	Bedside assessment of RV function; critical in unstable patients	RV dilation, hypokinesis, McConnell sign (RV free wall hypokinesis with apical sparing), D-shaped septum (interventricular septum bowing into LV)
ECG	Supportive, not diagnostic	Sinus tachycardia (most common). S1Q3T3 pattern, right axis deviation, new RBBB, T-wave inversions in V1 to V4 (RV strain pattern)
ABG	Supportive	Respiratory alkalosis, hypoxemia, elevated $A\text{-}a\ gradient$
Chest X-ray	Primarily to exclude other diagnoses	Often normal. May show Hampton hump (wedge-shaped opacity), Westermark sign (oligemia distal to embolus), or Palla sign (enlarged right descending pulmonary artery).
Troponin / BNP	Prognostic stratification (not diagnostic)	Elevated values indicate RV strain and classify submassive PE

The diagnostic approach to PE is probability-driven, not reflex-driven. The first step is always to estimate clinical probability using a validated scoring system, most commonly the Wells criteria.

Wells Score components: clinical signs of DVT (+3), PE is the most likely diagnosis (+3), heart rate > 100 (+1.5), immobilization or surgery within 4 weeks (+1.5), previous DVT/PE (+1.5), hemoptysis (+1), active malignancy (+1). A score of 4 or less is "PE unlikely," while a score above 4 is "PE likely."

In low-probability patients (Wells score 4 or less): obtain a D-dimer first. D-dimer is a fibrin degradation product with high sensitivity (> 95%) but poor specificity. A negative D-dimer in a low-probability patient effectively rules out PE, and no further imaging is needed. However, D-dimer is elevated in many conditions: infection, malignancy, pregnancy, recent surgery, trauma, DIC. Therefore, a positive D-dimer does not confirm PE; it simply mandates further imaging.

In high-probability patients (Wells score > 4): skip D-dimer entirely and proceed directly to CTPA. Ordering D-dimer in a high-probability patient wastes time, because even a negative D-dimer cannot safely exclude PE when pre-test probability is high.

CTPA is the imaging modality of choice. It provides direct visualization of filling defects within the pulmonary arterial tree, can identify alternative diagnoses (aortic dissection, pneumonia, pericardial effusion), and can assess RV size to help with prognostic stratification.

V/Q scintigraphy is the alternative when CTPA cannot be performed. A normal V/Q scan rules out PE. A high-probability V/Q scan (segmental perfusion defects with normal ventilation) strongly supports PE. The problem with V/Q scanning is the intermediate or indeterminate result, which is non-diagnostic and requires further testing.

In the hemodynamically unstable patient who cannot be transported to CT: bedside echocardiography showing RV dilation and dysfunction is sufficient to justify empiric thrombolysis. Do not delay treatment to obtain a CTPA in a patient who is in obstructive shock.

Chest X-ray is not diagnostic for PE but is useful to exclude pneumothorax, pneumonia, or heart failure as causes of dyspnea. Classic findings (Hampton hump, Westermark sign) are insensitive and appear in the minority of cases.

4. Management and Treatment

Clinical Scenario	Treatment	Details
Hemodynamically stable PE (low-risk)	Anticoagulation	LMWH, UFH, fondaparinux, or DOAC. Transition to long-term oral anticoagulation.
Submassive PE	Anticoagulation + close monitoring	Consider thrombolytics if clinical deterioration occurs. ICU-level care recommended.
Massive PE (hemodynamically unstable)	Systemic thrombolysis + anticoagulation	Alteplase 100 mg IV over 2 hours. Surgical embolectomy or catheter-directed therapy if thrombolytics fail or are contraindicated.
Contraindication to anticoagulation	IVC filter	Placed to prevent further embolization. Does not treat existing clot. Anticoagulation should be started as soon as the contraindication resolves.
PE in pregnancy	LMWH (enoxaparin)	Warfarin is teratogenic (category X). DOACs are contraindicated in pregnancy. UFH is an alternative near delivery due to shorter half-life.
Cancer-associated PE	LMWH or DOAC	LMWH (historically preferred); recent evidence supports edoxaban and rivaroxaban, though DOACs carry higher GI bleeding risk in GI malignancies.
Chronic thromboembolic pulmonary hypertension (CTEPH)	Pulmonary thromboendarterectomy (PTE)	Surgical removal of organized thrombus. Riociguat (soluble guanylate cyclase stimulator) for inoperable cases.

Acute stabilization in any suspected PE begins with supportive care: supplemental oxygen to maintain $SpO_2$ above 90%, IV fluid resuscitation (use cautiously, as volume overload worsens RV failure), and vasopressors (norepinephrine preferred) if hypotensive.

Anticoagulation is the foundation of PE treatment and should be initiated as soon as the diagnosis is confirmed, or even before confirmation if clinical suspicion is high. The goal is to prevent clot propagation and allow the body's fibrinolytic system to dissolve the existing thrombus.

Initial anticoagulation options:

Unfractionated heparin (UFH): 80 units/kg IV bolus, then 18 units/kg/hr continuous infusion, titrated to aPTT 1.5 to 2.5 times control. Preferred in patients who may need thrombolysis or surgery (short half-life, reversible with protamine).
Low-molecular-weight heparin (LMWH): Enoxaparin 1 mg/kg subcutaneously every 12 hours (or 1.5 mg/kg once daily). Preferred for stable outpatient management. Avoid in severe renal impairment ($CrCl$ < 30 mL/min); use UFH instead.
Fondaparinux: 5 mg (< 50 kg), 7.5 mg (50 to 100 kg), or 10 mg (> 100 kg) subcutaneously once daily. Cannot be reversed; avoid in renal failure.
Rivaroxaban or apixaban (DOACs): Can be used as initial monotherapy without heparin bridging. Rivaroxaban: 15 mg twice daily for 21 days, then 20 mg once daily. Apixaban: 10 mg twice daily for 7 days, then 5 mg twice daily.

Transition to long-term anticoagulation:

Warfarin: Start on day 1 of heparin. Continue heparin until INR is 2.0 to 3.0 for at least 24 hours (overlap period of at least 5 days). Target INR: 2.0 to 3.0.
DOACs (rivaroxaban, apixaban, edoxaban, dabigatran): Rivaroxaban and apixaban can be used from the start without bridging. Edoxaban and dabigatran require 5 to 10 days of initial parenteral anticoagulation before switching.

Duration of anticoagulation:

Provoked PE (identifiable transient risk factor such as surgery or immobilization): 3 months
Unprovoked PE (no identifiable risk factor): minimum 3 months, then reassess for indefinite anticoagulation based on bleeding risk
Recurrent PE or persistent risk factor (active cancer, thrombophilia): indefinite anticoagulation

Thrombolysis is indicated only in massive PE with hemodynamic instability. The standard regimen is alteplase (tPA) 100 mg IV over 2 hours. Absolute contraindications include active internal bleeding, recent hemorrhagic stroke, intracranial neoplasm, and recent intracranial surgery. In massive PE, the mortality benefit of thrombolysis outweighs the bleeding risk.

For submassive PE, thrombolysis is not routinely recommended. However, if a patient with submassive PE deteriorates hemodynamically despite anticoagulation, escalation to thrombolysis or catheter-directed therapy is appropriate.

Surgical embolectomy is a last-resort option for massive PE when thrombolytics are contraindicated or have failed. Catheter-directed therapy (fragmentation, aspiration, or catheter-directed thrombolysis) is an evolving alternative.

IVC filter is placed when anticoagulation is absolutely contraindicated (e.g., active hemorrhage, recent brain surgery) or when recurrent PE occurs despite adequate anticoagulation. Retrievable filters are preferred and should be removed once anticoagulation can be safely resumed.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Acute coronary syndrome (ACS)	Chest pain, tachycardia, dyspnea, troponin elevation	ACS presents with substernal pressure radiating to the arm/jaw, ST changes in a coronary territory. PE chest pain is pleuritic (sharp, worse with inspiration). PE troponin elevation reflects RV strain, not coronary ischemia.
Pneumothorax	Sudden dyspnea, pleuritic chest pain, tachycardia, hypoxia	Unilateral absent breath sounds, hyperresonance on percussion, visible pneumothorax on chest X-ray. No filling defect on CTPA.
Pneumonia	Dyspnea, tachycardia, hypoxia, possible pleuritic chest pain	Productive cough, fever, consolidation on chest X-ray, elevated WBC with left shift. No risk factors for thromboembolism.
Acute pericarditis	Pleuritic chest pain, dyspnea	Pain relieved by sitting forward, diffuse ST elevation on ECG (not in a coronary or RV strain pattern), pericardial friction rub on auscultation.
Aortic dissection	Sudden chest pain, hypotension, tachycardia	"Tearing" pain radiating to the back, blood pressure differential between arms, mediastinal widening on chest X-ray.
Heart failure exacerbation	Dyspnea, tachycardia, elevated BNP, bilateral leg edema	Bilateral (not unilateral) lower extremity edema, orthopnea, PND, pulmonary crackles, cardiomegaly, and pulmonary vascular congestion on chest X-ray.
COPD exacerbation	Dyspnea, hypoxia, tachycardia	History of chronic smoking, wheezing, prolonged expiratory phase, hyperinflation on chest X-ray. ABG may show chronic respiratory acidosis with metabolic compensation.
Anxiety/Panic attack	Dyspnea, tachycardia, tachypnea, respiratory alkalosis on ABG	Normal $A\text{-}a\ gradient$. No hypoxemia. No risk factors for VTE. Diagnosis of exclusion.

6. Traps and High-Yield Pearls

The single most common way students lose points on PE questions is by ordering D-dimer in a high-probability patient. When the clinical picture strongly suggests PE (post-surgical patient with acute dyspnea and unilateral leg swelling), the correct next step is CTPA, not D-dimer. D-dimer is a rule-out test for low-probability scenarios only. This is the most tested decision point.

The second major trap involves the unstable patient. When a question describes a post-operative patient with sudden hypotension, tachycardia, and hypoxia where PE is the leading diagnosis but the patient is too unstable to transport for CT, students often freeze. The answer is bedside echocardiography to look for RV strain, followed by empiric thrombolysis if findings are consistent. Do not delay treatment to get a confirmatory CTPA in a crashing patient.

Another frequently tested concept is the $A\text{-}a\ gradient$. Students confuse PE with hyperventilation from anxiety. Both produce tachypnea, hypocapnia, and respiratory alkalosis. The differentiator is the $A\text{-}a\ gradient$: it is elevated in PE (because the lung itself has impaired gas exchange) and normal in anxiety (because the lungs are functioning normally and the patient is simply breathing faster).

Watch for the S1Q3T3 pattern on ECG. While it is neither sensitive nor common, it appears frequently in exam vignettes as a clue pointing toward right heart strain. More commonly, PE produces sinus tachycardia and nonspecific ST-T wave changes, but vignette writers favor S1Q3T3 because it is recognizable and distinct.

Do not forget that warfarin is contraindicated in pregnancy. Any PE question set during pregnancy should trigger immediate recognition that the answer is LMWH (enoxaparin), not warfarin and not DOACs.

Finally, remember the distinction between provoked and unprovoked PE for treatment duration. A PE following knee replacement surgery (clear provoking factor) requires only 3 months of anticoagulation, while an unprovoked PE warrants evaluation for indefinite therapy. Test questions commonly present a follow-up scenario asking about duration of treatment, and students who do not distinguish provoked from unprovoked will select the wrong timeframe.

The core competency being tested across PE questions is clinical decision-making under uncertainty: knowing which test to order based on pre-test probability, recognizing when to escalate from anticoagulation to thrombolysis based on hemodynamic status, and understanding that the workup algorithm changes depending on the patient's stability.

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