PE-2

Pulmonary Embolism — High-Yield Revision

Diagnosis → A–E severity → treatment → follow-up. All 61 original image references appear in collapsed, topic-matched figure galleries.

Clinical route

Suspect PE → assess shock → Wells/Geneva → PERC only if very low risk; otherwise D-dimer/YEARS if appropriate, or CTPA directly if high risk → A–E, RV, troponin/BNP → anticoagulation ± reperfusion. CTPA contraindicated → V/Q SPECT. No DVT signs ≠ no PE.

1. Mechanism, causes & presentation

Thrombus = stationary intravascular clot; embolus = dislodged traveling material. Usually leg/pelvic DVT → right heart → pulmonary arteries. Virchow triad: endothelial injury, stasis, hypercoagulability. Normal V/Q ≈1 permits O₂ entry/CO₂ exit. Occlusion creates ventilated/unperfused dead space (high V/Q); redirected blood produces low-V/Q units → hypoxemia. ↑PVR → RV dilation/failure → leftward septal bowing → ↓LV preload/output → hypotension → RV ischemia/arrest.

Reversible major	Reversible minor	Persistent
GA surgery >30 min; bedbound admission ≥72 h; cesarean; lower-limb fracture	GA surgery <30 min; hospital admission <72 h; bedbound at home ≥72 h; estrogen, peripartum, trauma with immobility ≥72 h	Active cancer; APS/SLE, thrombophilia; chronic immobility

Symptoms	Examination
Dyspnea (~70%; commonest); tachypnea; pleuritic pain (sharp on inspiration); cough/hemoptysis (infarction); syncope; DVT leg pain/swelling	HR >100, RR >20, hypoxemia; SBP <90 suggests danger; loud P2, RV heave, JVD; diminished breath sounds, rub, crackles; unilateral warm, tender, red swollen leg. Leg findings may be absent.

Figures: Pathophysiology (14)

2. Pretest probability & rule-out

Wells	Pts	Revised Geneva	Pts
DVT signs; PE most likely	3 each	Age >65; prior VTE	1; 3
HR >100; immobility ≥3 d or surgery <4 wk; past VTE	1.5 each	Surgery/fracture ≤1 mo; cancer	2 each
Hemoptysis; active cancer	1 each	Unilateral leg pain; hemoptysis	3; 2
—	—	HR 75–94 / ≥95	3 / 5
—	—	Leg tenderness + unilateral edema	4

Wells ≤4 → PE unlikely → D-dimer; >4 → PE likely → CTPA. Geneva 0–3 low; 4–10 intermediate; ≥11 high.

Rule	Exact application
PERC	Only gestalt <15%: age <50, HR <100, room-air SpO₂ ≥95%, no unilateral leg swelling, hemoptysis, surgery/trauma <4 wk, prior VTE, or oral estrogen. All 8 negative → no tests; otherwise evaluate further.
YEARS	Three items: DVT signs, hemoptysis, PE most likely. 0 → D-dimer <1,000 ng/mL FEU rules out; ≥1 → <500 ng/mL FEU rules out; otherwise imaging. Lecture: ~14% fewer CTPAs.
Age-adjusted D-dimer	If >50 years: age ×10 ng/mL FEU (same numeric value in μg/L FEU), in eligible low/intermediate-risk strategies; check assay units.
Probability pathway (2026)	<15%: PERC → D-dimer if failed; 15–50%: D-dimer strategy; >50%: image directly (do not exclude with D-dimer).

Figures: Algorithm (1)

3. Investigations: diagnosis vs prognosis

Investigation	What to remember
ECG	Sinus tachycardia = commonest; S1Q3T3 (McGinn–White) = deep S (I), Q + T inversion (III), classic but insensitive; T inversions V1–V4/III/aVF, right axis, RBBB, new AF → RV strain. Not diagnostic.
Labs	D-dimer often falsely raised: pregnancy, older age, cardiac disease, malignancy, trauma, infection. Troponin = RV injury; BNP/NT-proBNP = RV stretch (prognosis); ABG often hypoxemia/hypocapnia; normal results do not exclude PE.
CXR	Exclude pneumonia/pneumothorax, not PE. Westermark = focal oligemia (~10–15% sensitivity; lecture quiz ~92% specificity); Hampton hump = pleural wedge infarct (~20%); Fleischner = central PA enlargement (~20%); effusion ~35%.
CTPA	First-line confirmation, specificity ~96% (lecture). Central polo-mint filling defect, saddle clot at PA bifurcation. High suspicion + negative scan → consider further evaluation. Infarct: peripheral wedge/reversed-halo (atoll) ± effusion, especially small branches <3 mm → pleuritic pain/hemoptysis.
CT RV strain	RV/LV measured diameter ratio ≥1 (report numerically), RV enlargement, septal bowing, enlarged PA relative to aorta (figure: 28 vs 25 mm), IVC/hepatic contrast reflux → worse short-term prognosis.
Echo / triple POCUS	McConnell: RV free-wall hypokinesia, apical sparing. 60/60: PA acceleration <60 ms + TR gradient ≤60 mmHg. TAPSE <16 mm, RV>LV, flat septum, mobile clot-in-transit. Triple POCUS = heart + lung + leg veins (lecture ~90% sensitivity in studied settings; not definitive rule-out).
V/Q SPECT	Segmental perfusion defect with preserved ventilation (mismatch) → PE. Preferred to MRA if CTPA unsuitable (contrast allergy/severe kidney failure). Perfusion tracer ⁹⁹ᵐTc-macroaggregated albumin IV; ventilation inhaled aerosol/carbon tracer; 3-D reconstruction.
Pulmonary angiography	Historic invasive gold standard, now chiefly during catheter intervention.

Selective cause workup: thrombophilia: factor V Leiden, factor II mutation, homocysteine, protein C (chromogenic), protein S (activity), antithrombin III (factor Xa assay); APS: lupus anticoagulant, anticardiolipin, anti-β₂-glycoprotein-I; SLE: ANA, anti-dsDNA, anti-Sm; evaluate cancer when indicated. Not all tests are appropriate routinely or during acute anticoagulation.

Figures: Ecg (6)

Figures: Laboratory (1)

Figures: Cxr (4)

Figures: Ctpa (10)

Figures: Echo (2)

Figures: Vq (2)

4. Severity: 2011 → 2019 → 2026

2011 AHA: low / submassive / massive → 2019 ESC: low / intermediate-low / intermediate-high / high → 2026 AHA/ACC: A–E. Wells/Geneva/YEARS predict diagnosis; PESI/sPESI/Bova assess prognosis; Hestia evaluates outpatient suitability. PESI calculator.

PESI score: age in years; male +10, cancer +30, HF +10, lung disease +10, HR ≥110 +20, SBP <100 +30, RR >30 +20, T <36°C +20, altered consciousness +60, SaO₂ <90% +20. Class I ≤65 (0–1.6%); II 66–85 (1.7–3.5%); III 86–105 (3.2–7.1%); IV 106–125 (4–11.4%); V >125 (10–24.5% 30-day mortality, lecture cohorts).

sPESI: 1 point each for age >80, cancer, heart/lung disease, HR ≥110, SBP <100, SaO₂ <90%. 0 ≈1% vs ≥1 ≈10.9% 30-day mortality in cited cohort; only carefully selected low-risk patients qualify for home management.

Category	Distinguishing criteria
A	Incidental + asymptomatic (subclinical).
B	Symptomatic, PESI ≤85/sPESI 0 (lecture also Bova ≤4/Hestia 0); B1 single/multiple subsegmental, B2 non-subsegmental.
C	Symptomatic, PESI >85/sPESI ≥1 (lecture: Bova >4/Hestia ≥1); C1 RV and biomarkers normal; C2 one abnormal; C3 both RV + biomarker abnormal.
D	Impending cardiopulmonary failure: D1 transient hypotension; D2 normotensive shock (hypoperfusion despite preserved BP).
E	Failure: E1 recurrent/persistent hypotension with shock; E2 refractory shock or cardiac arrest.

Shock markers: arrest needing CPR; SBP <90 or drop ≥40 for >15 min (not arrhythmia/hypovolemia/sepsis); pressors despite adequate filling plus hypoperfusion (confusion, clammy skin, oliguria, lactate↑). R respiratory modifier: B/C SpO₂ <90%, RR ≥30 or supplemental O₂; D ≥6 L/min nasal cannula or non-rebreather mask (original lecture says >6 L); E hypoxemic/ventilatory failure. C–E: PERT assessment.

Figures: Classification (2)

5. Acute management

Low-risk: consider early discharge if safe. Intermediate-low: anticoagulate/admit; intermediate-high: monitor, rescue reperfusion if deterioration. AHA/ACC: C3 routine lysis benefit uncertain; D1–D2 advanced reperfusion may be considered; E1–E2 consider urgent systemic lysis when bleeding risk acceptable. O₂/support circulation (avoid RV-overloading fluids); anticoagulate promptly if safe. Parenteral LMWH preferred over UFH when suitable (fondaparinux also an option); DOACs over warfarin in eligible patients (less major bleeding; no INR checks).

Drug	Acute treatment → maintenance
Apixaban (Xa)	10 mg BID ×7 d → 5 mg BID; no heparin lead-in.
Rivaroxaban (Xa)	15 mg BID ×21 d → 20 mg daily; no heparin lead-in.
Dabigatran (thrombin)	≥5 d UFH/LMWH → 150 mg BID.
Edoxaban (Xa)	≥5 d UFH/LMWH → 60 mg daily; 30 mg if CrCl 15–50 mL/min, weight ≤60 kg or certain P-gp inhibitors (use CrCl, not eGFR alone).
Warfarin	Heparin overlap ≥5 d AND INR ≥2 for ≥24 h; target INR 2–3; e.g. APS/cost barriers.
Dalteparin (CLOT trial)	200 IU/kg daily ×1 mo (max 18,000 IU/d) → 150 IU/kg daily.

Systemic lysis: alteplase 100 mg IV over 2 h for appropriately selected high-risk/unstable PE. Lecture proposes 50 mg or 0.6 mg/kg to reduce bleeding with similar efficacy; evidence is less secure, so not routinely interchangeable with full dose. Other agents: streptokinase IV/24 h, urokinase IV/12 h (listed as PE-approved in lecture), tenecteplase single bolus, reteplase two boluses (last two not FDA-approved for PE, per lecture). Major danger: intracranial/retroperitoneal hemorrhage.

Systemic lysis contraindications in lecture	Examples
Absolute/major	Active bleeding, prior ICH, ischemic stroke <3 mo, brain/spinal surgery <1 mo, CNS tumor/vascular lesion, head trauma with skull fracture/brain injury, aortic dissection, abdominal surgery <7 d.
Relative	BP >180/110, recent bleeding, ischemic stroke >3 mo, current anticoagulant, recent non-CNS surgery/procedure, traumatic/prolonged CPR, pericarditis/effusion, retinopathy, pregnancy, age >75, weight <60 kg.

PERT (C–E/deterioration, shock, arrest) chooses anticoagulation, support, systemic lysis, catheter lysis, aspiration, surgery or VA-ECMO by instability/bleeding/anatomy/expertise. Catheter-directed lysis: consider with deterioration when systemic lysis is unsuitable (bleeding risk persists); 4–5 Fr PA catheter, lecture alteplase ~0.5–1 mg/h/catheter ×12–24 h. Mechanical aspiration: clot removal with little/no lytic → improves PA flow, RV/hemodynamics. Surgery: lysis contraindicated/failed; ECMO: bridge in refractory shock/arrest.

IVC filter: retrievable preferred if anticoagulation absolutely contraindicated (active bleeding); recurrent PE despite therapeutic anticoagulation is a contested exception (verify adherence/dose, consider changing agent first). Remove once anticoagulation resumes/risk subsides (lecture 29–54 d, not a universal deadline). Late risks: DVT, IVC occlusion, fracture, perforation, cardiac migration.

Figures: Treatment (8)

6. Duration, sequelae & special populations

• Major transient provocation: lecture 3–6 mo anticoagulation; commonly 3 mo. Unprovoked/persistent risk: consider extended therapy with periodic benefit–bleeding review.
• After ≥3 mo: post-PE dyspnea/functional limitation up to ~50%; RVO = persistent perfusion defect (~50%, often asymptomatic). CTED/CTEPD = symptomatic thromboembolic disease without resting PH; CTEPH = group 4 pulmonary hypertension. Persistent dyspnea warrants investigation.

Special case	Agent choice
Active cancer	DOAC or LMWH; usually continue while active.
Pregnancy	LMWH/UFH; avoid DOACs/warfarin.
Breastfeeding	LMWH/UFH/warfarin safe; avoid DOACs.
Obesity (BMI >30)	DOACs generally reasonable/preferred.
APS	Warfarin > DOACs, especially high-risk APS.
Brain tumors	Individualized DOAC vs LMWH balancing bleeding.
CKD stage 2–3	Suitable DOAC if renal dosing permits.
Child–Pugh C	Avoid DOACs.
HIT	Stop heparin; argatroban, bivalirudin, fondaparinux, or eligible DOAC.

7. Non-thrombotic pulmonary emboli

Gas, fat, amniotic fluid, septic, tumor emboli: non-biological material → chiefly mechanical blockage; biological emboli → inflammatory vascular/lung/RV injury. Management differs from thrombotic VTE.

Type	Sources → signature	Echo	Management
Air/gas	CVC/dialysis/cardiac line, laparoscopy, diving → sudden cardiopulmonary/neurologic deterioration; mill-wheel murmur	Air ± PFO	Stop source, 100% O₂, support, aspirate air if feasible, hyperbaric O₂ for severe neurologic events; lecture left lateral + Trendelenburg when appropriate.
Fat	Long-bone/pelvic fracture, orthopedics, liposuction, lipid infusion; latent 6–12 h, onset 24–72 h → respiratory distress + cerebral signs + petechiae	Nonspecific	O₂/ventilation, neuro monitoring ± ECMO; no proven drug.
Amniotic	Labor (~70% pre-delivery per lecture), C-section, abortion, amniocentesis → abrupt hypoxemia, collapse ± DIC, seizures/coma	↑PA pressure, RV failure, TR (TEE)	Resuscitate, correct coagulopathy (blood/FFP/platelets/cryo ± TXA), urgent delivery when indicated.
Septic	Tricuspid endocarditis, infected line, IV drugs, periodontal infection → fever, cough/hemoptysis, infection focus	Vegetation (TEE > TTE)	Broad-spectrum IV antibiotics + source control, remove infected line/drain abscess or empyema ± surgery.
Tumor	Hepatocellular, breast, renal, gastric, sarcoma, choriocarcinoma → subacute progressive dyspnea/cor pulmonale	Nonspecific	Treat cancer + pulmonary hypertension.

Figures: Ntpe (11)

Evidence/precision

Lecture-specific prevalence figures, assay cutoffs, doses and relative/absolute lysis restrictions are retained for exam revision; actual management depends on local protocol and the patient. V/Q mismatch = perfusion (not ventilation) defect; avoid combining different D-dimer adjustment rules without a validated pathway.