Pulmonary embolism

1. History

• Onset and character of dyspnea: sudden vs. progressive, at rest vs. exertional — dyspnea is present in ~80% of cases [4]
• Chest pain: pleuritic in nature (60–70%), distinguish from pressure-type ACS pain [4]
• Hemoptysis (5–13%), syncope/presyncope, cough [1][4]
• Timing: acute onset is classic; ask about symptom duration and progression
• Triggers: recent travel (>4 hrs), surgery, immobilization, hospitalization, trauma
• Provoked vs. unprovoked: critical for long-term anticoagulation decisions
• Important negatives: absence of leg swelling/pain, no prior VTE, no recent immobilization, no estrogen use, no malignancy [1]

2. Alarm Features

• Hemodynamic instability: SBP <90 mmHg, persistent hypotension, cardiogenic shock [2-3]
• Syncope — may indicate massive PE with transient cardiac output failure
• Severe hypoxemia refractory to supplemental O₂
• Altered mental status, signs of end-organ hypoperfusion (elevated lactate, oliguria) [2-3]
• Cardiac arrest — PE is a common cause of PEA arrest
• Normotensive shock (AHA/ACC Category D): normal BP but elevated lactate, AKI, reduced cardiac index [2-3]
• The first 24–72 hours are the critical window for hemodynamic collapse in intermediate-high risk PE [2]

3. Medications

4. Diet

• No specific dietary triggers for PE
• Patients on warfarin require consistent vitamin K intake; DOACs have fewer dietary interactions [2]
• Rivaroxaban (15 mg and 20 mg doses) should be taken with the largest meal of the day to promote absorption [7]
• Adequate hydration during travel and immobilization periods for VTE prevention

5. Review of Systems

• Pulmonary: dyspnea, pleuritic chest pain, cough, hemoptysis
• Cardiovascular: palpitations, syncope, presyncope, exertional intolerance
• Lower extremity: unilateral leg swelling, pain, warmth, erythema (concurrent DVT in ~40% of PE patients) [4]
• Neurologic: lightheadedness, confusion (suggests hemodynamic compromise)
• Constitutional: anxiety, sense of impending doom
• GI: abdominal pain (rare, may indicate hepatic congestion from RV failure)

6. Collateral History and Family History

• Prior VTE in patient or first-degree relatives — strongest historical predictor
• Known thrombophilia: Factor V Leiden, prothrombin G20210A mutation, protein C/S deficiency, antithrombin deficiency, antiphospholipid syndrome [8]
• Active malignancy or recent cancer treatment [2-3]
• Recent hospitalization, surgery, or immobilization — collateral from family/caregivers may be essential in obtunded patients
• Medication history: estrogen use, anticoagulant compliance

7. Risk Factors

• Major transient: surgery (especially orthopedic), hospitalization, immobilization ≥3 days, major trauma [2-3]
• Minor transient: long-haul travel, oral contraceptives, pregnancy/postpartum, minor injury
• Persistent: active cancer, inflammatory disorders (IBD, SLE), chronic venous disease, inherited thrombophilia
• Patient-related: age, obesity (BMI ≥30 synergistically increases risk with OCP use — OR ~23.8), prior VTE, heart failure, COPD [5]
• Obesity + OCP is a particularly high-risk combination [5]

8. Differential Diagnosis

• Acute coronary syndrome — pressure-type chest pain, ST changes, troponin elevation (can also occur in PE)
• Pneumonia — fever, productive cough, focal consolidation
• Pneumothorax — sudden pleuritic pain, absent breath sounds, hyperresonance
• Acute heart failure/pulmonary edema — bilateral crackles, BNP elevation, cardiomegaly
• Pericarditis/tamponade — diffuse ST elevation, friction rub, Beck's triad
• Aortic dissection — tearing pain, pulse differential, widened mediastinum
• COPD/asthma exacerbation — wheezing, known history [9]
• Pleural effusion, musculoskeletal chest pain, anxiety/panic attack
• Cannot-miss mimics: PE can present identically to STEMI (ST elevation on ECG from RV strain) [10]

9. Past Medical History

• Prior VTE (DVT or PE) — strongest individual risk factor
• Malignancy — active or treated within 6 months
• Thrombophilia — inherited or acquired (antiphospholipid syndrome)
• Heart failure, COPD — increase PESI score and mortality risk
• Recent surgery — especially hip/knee replacement, abdominal/pelvic surgery
• Chronic kidney disease — affects anticoagulant choice and dosing
• Liver disease — affects anticoagulant metabolism and bleeding risk

10. Physical Exam

11. Lab Studies

• D-dimer: 97–100% NPV at threshold of 500 ng/mL; use only in low/intermediate pretest probability patients [1]
  • Age-adjusted cutoff (age × 10 μg/L for patients >50 years) safely reduces imaging [2]
  • YEARS algorithm: D-dimer threshold of 1000 μg/L if no YEARS criteria present [2]
  • D-dimer has limited utility in cancer patients [7]
• Troponin I/T: elevated in RV strain; prognostic, not diagnostic [3][7]
• NT-proBNP/BNP: marker of RV dysfunction and adverse outcomes [7]
• CBC, BMP, PT/aPTT: baseline before anticoagulation [7]
• Lactate: elevated suggests tissue hypoperfusion (normotensive shock) [2]
• ABG: hypoxemia with respiratory alkalosis (classic but nonspecific); A-a gradient often elevated

12. Imaging

• CT Pulmonary Angiography (CTPA): gold standard — wide availability, excellent diagnostic performance, also assesses RV size and identifies alternative diagnoses [3][12]
  • [3]
• V/Q scan: appropriate when CTPA is contraindicated (contrast allergy, severe renal insufficiency); best combined with SPECT [3]
• Echocardiography: not diagnostic for PE but critical for RV function assessment — look for RV dilation, McConnell's sign, TAPSE reduction, septal bowing, elevated RVSP [3]
• Lower extremity venous duplex ultrasound: useful if DVT suspected; positive DVT in setting of PE symptoms may obviate CTPA in select cases [3]
• Chest X-ray: often normal or nonspecific; useful to exclude pneumothorax, pneumonia, effusion. Classic findings (Hampton's hump, Westermark's sign) are uncommon
• Imaging is unnecessary if PERC-negative in low-probability patients or if D-dimer is negative in low/intermediate probability [1][13]

13. Special Tests

14. ECG

ECG is insensitive for PE but may raise suspicion and help with risk stratification: [15-16]

• Sinus tachycardia: most common finding (~31%) [17]
• S1Q3T3 pattern: classic but present in only ~15% of cases [17]
• T-wave inversion in V1–V3: best ECG predictor of RV dysfunction and massive/submassive PE (18% prevalence) [17-18]
• Right bundle branch block (new or incomplete): ~14% [17]
• Right axis deviation, clockwise rotation (transition zone shift)
• P pulmonale (right atrial enlargement): rare
• ST elevation in right precordial leads: can mimic STEMI [10]
• Normal ECG in 20–25% of confirmed PE, including large clot burden [11]
• Classical ECG findings have minimal independent diagnostic accuracy and should not be used alone to rule in or rule out PE [16]

15. Assessment

The 2026 AHA/ACC guideline introduces 5 clinical categories (A–E) for severity stratification: [2-3]

• Category A: Asymptomatic/incidental PE — safe for ED discharge
• Category B: Symptomatic, low-risk (sPESI <1, Hestia <1) — early discharge candidates
• Category C: Symptomatic, elevated severity score (sPESI ≥1) ± biomarker/RV dysfunction
• Category D: Pre-cardiopulmonary failure (normotensive shock, transient hypotension, approaching ventilatory support)
• Category E: Cardiopulmonary failure — persistent hypotension, cardiogenic shock, cardiac arrest

A respiratory modifier (R) is added when significant hypoxemia, tachypnea, or supplemental O₂ requirement is present. [2-3]

16. Treatment Plan

17. Disposition

Per the 2026 AHA/ACC guidelines: [2-3]

• ED discharge (outpatient management):
  • Category A (asymptomatic/incidental PE)
  • Category B (symptomatic, low-risk: sPESI <1, Hestia 0) — if adequate outpatient follow-up, medication access, and stable home circumstances [2][14][22]
• Admit to floor/telemetry:
• Admit to step-down/ICU:
  • Category C3 (elevated troponin AND RV dysfunction) — close monitoring for first 24–72 hours [2]
  • Category D (pre-cardiopulmonary failure)
• ICU admission:
• Transfer to higher-level center if advanced therapies (catheter intervention, surgical embolectomy, ECMO) are needed but unavailable locally [3]

Specialist consultation triggers: PERT activation for Category C3 and above; hematology for thrombophilia workup; oncology if cancer-associated PE

18. Follow-Up / Return Precautions

• Initial follow-up within 48 hours to 7 days after diagnosis — focus on medication adherence, patient education, and barrier assessment [2-3]
• Dedicated visit at ~3 months: discuss anticoagulation duration, assess for ongoing symptoms, evaluate for thrombophilia/cancer screening if indicated [2-3]
• Screen for CTEPD at every visit for at least 1 year — one-third to one-half of PE patients report persistent dyspnea; CTEPD with PH complicates 2.3–4% of acute PEs [2-3]
• Anticoagulation duration: [2-3][12]
  • Provoked by major transient risk factor: 3 months, then stop
  • Unprovoked or persistent risk factor: extended/indefinite anticoagulation recommended
  • After 3–6 months of full-dose therapy, consider reduced-dose apixaban (2.5 mg BID) or rivaroxaban (10 mg daily) for extended phase [12]

Return precautions — counsel patients to return immediately for:

• New or worsening shortness of breath
• Chest pain, hemoptysis
• Lightheadedness, syncope, or near-syncope
• Unilateral leg swelling or pain (recurrent DVT)
• Signs of bleeding: blood in urine/stool, unusual bruising, prolonged bleeding from cuts
• Expected recovery: symptoms typically improve over days to weeks; persistent dyspnea beyond 3 months warrants further evaluation for CTEPD [2-3]