Pulmonary Embolism (PE) 

1. Epidemiology

ICU incidence

Higher due to:

  • Immobilization
  • Surgery/trauma
  • Malignancy
  • Sepsis
  • Central lines

Mortality

  • Untreated PE mortality: ≈30%
  • Treated PE mortality: 2–8%
  • Massive PE mortality: >25–50%

2. Source of Emboli

Source

Approx %

Lower limb proximal DVT

90%

Pelvic veins

5%

Upper limb DVT

<3%

Right heart thrombus

rare but high risk

3.Ventilation–Perfusion Mismatch

PE causes:

Mechanism

Result

Perfusion defect

V/Q mismatch

Dead space ventilation

PaCO₂ initially

Shunt physiology

Hypoxemia

Hypoxemia mechanisms:

  • V/Q mismatch
  • Atelectasis
  • Right-to-left shunt
  • Low cardiac output

4. Pathophysiology

PE causes three simultaneous processes:

  1. Mechanical obstruction
  2. Pulmonary vasoconstriction
  3. Right ventricular failure


 Mechanical Obstruction

Pulmonary vascular obstruction leads to:

  • Pulmonary vascular resistance (PVR)
  • Pulmonary blood flow
  • RV afterload

 Pulmonary Vasoconstriction

Mediators released:

  • Thromboxane A2
  • Serotonin
  • Histamine
  • Endothelin

Effects:

  • Additional increase in pulmonary vascular resistance
  • Worsening RV strain

 Right Ventricular Failure 

RV normally pumps against low pressure system.

PE causes:

RV afterload
RV dilation
RV ischemia
RV contractility

Consequences:

  1. Interventricular septal shift
  2. LV filling
  3. cardiac output
  4. Hypotension
  5. Cardiogenic shock

5. Virchow’s Triad (Risk Factors)

PE originates from Virchow’s triad.

Mechanism

Examples

Venous stasis

Immobilization, ICU stay

Hypercoagulability

Cancer, pregnancy

Endothelial injury

Surgery, trauma

6. Risk Factors

Major

  • Major surgery
  • Trauma
  • Malignancy
  • Prior VTE
  • Pregnancy/postpartum

Moderate

  • OCP use
  • Hormone therapy
  • Obesity
  • Heart failure
  • Stroke

ICU specific

  • Mechanical ventilation
  • Sepsis
  • Central venous catheter
  • Sedation/paralysis
  • ECMO

7. Clinical Presentation

Classic triad (rare)

  • Dyspnea
  • Chest pain
  • Hemoptysis

Common symptoms

Symptom

Frequency

Dyspnea

70–80%

Pleuritic chest pain

50%

Tachypnea

60%

Tachycardia

30–40%

Syncope

Massive PE


Massive PE symptoms

  • Hypotension
  • Shock
  • Syncope
  • Cardiac arrest

8. Classification of Pulmonary Embolism-2026

Category

Hemodynamic + RV + Biomarker + Clinical Profile

Management

 A (Low Risk)

Hemodynamically stable; No RV dysfunction; Normal troponin/BNP; Mild or no symptoms, minimal hypoxia

Anticoagulation only (DOAC preferred), early discharge

 B (Intermediate-Low)

Stable BP; Either RV dysfunction OR biomarker elevation (not both); Mild dyspnea, tachycardia

Anticoagulation + close monitoring

 C (Intermediate-High)

Stable BP; Both RV dysfunction + biomarkers; Tachycardia, hypoxia, early RV failure

ICU monitoring, anticoagulation, rescue thrombolysis if deterioration

 D (Impending Collapse)

Borderline/labile BP (SBP 90–100); Severe RV dysfunction + high biomarkers; Rising lactate, worsening hypoxia, pre-shock signs

Immediate thrombolysis ± catheter-directed therapy, vasopressors

 E (Massive PE)

Shock (SBP <90) or cardiac arrest; Severe RV failure; Markedly elevated biomarkers; PEA common

Thrombolysis (even during CPR), ECMO, surgical embolectomy

9. Clinical Prediction Scores

Used to estimate pre-test probability.


9.1 Wells Score

Variable

Points

Clinical DVT signs

3

PE more likely

3

HR >100

1.5

Recent surgery/immobilization

1.5

Previous VTE

1.5

Hemoptysis

1

Cancer

1

Interpretation:

Score

Probability

6

High

2–6

Moderate

<2

Low


Alternative:

Score

Interpretation

≤4

PE unlikely

4

PE likely

9.2 Geneva Score

Objective variables only:

  • Age
  • Previous VTE
  • Surgery
  • HR
  • Hemoptysis
  • DVT signs

9.3 PERC Rule

Used to rule out PE in low-risk patients.

Criteria:

  1. Age <50
  2. HR <100
  3. O2 sat >94%
  4. No hemoptysis
  5. No estrogen use
  6. No surgery/trauma
  7. No prior VTE
  8. No DVT signs

If all negative PE ruled out


10. Laboratory Tests

— D-dimer(High sensitivity)

Cutoff:

  • Standard: 500 ng/mL
  • Age-adjusted: age × 10 (if >50 yrs)

Use:Best for ruling out PE in low/moderate risk patients.

False positives in:

  • Sepsis
  • Trauma
  • Surgery
  • Cancer
  • ICU patients

 Cardiac Biomarkers

Troponin

Indicates RV myocardial injury.

Associated with:Worse prognosis

BNP / NT-proBNP

Reflects RV strain


11. Imaging for Pulmonary Embolism

11.1 CT Pulmonary Angiography (CTPA) — Gold Standard

Sensitivity: 83–100%
Specificity: 96–98%

Findings:

  • Intraluminal filling defect
  • Vessel cutoff
  • RV dilation

Secondary signs:

  • Pulmonary infarction
  • Pleural effusion
  • Atelectasis


11.2 Ventilation–Perfusion Scan (V/Q Scan)

Used when:

  • Contrast allergy
  • Renal failure
  • Pregnancy

Typical finding:

Mismatch defect

Normal ventilation + absent perfusion.


11.3 Echocardiography

Important in unstable patients.

Findings:

Sign

Meaning

RV dilation

RV strain

McConnell sign

RV free wall hypokinesia

Septal flattening

Pressure overload

Tricuspid regurgitation

RV dysfunction

McConnell Sign

  • Hypokinetic RV free wall
  • Normal RV apex

Highly suggestive of acute PE


11.4 Ultrasound for DVT

Compression ultrasound:

Positive proximal DVT treat as PE.

12. ECG Findings

Most common—Sinus tachycardia

Classic but rare:

Finding

Mechanism

S1Q3T3

Acute RV strain

Right axis deviation

RV overload

RBBB

RV dilation

T wave inversion V1–V4

RV ischemia

13. Chest X-ray Findings

Often normal.

Possible signs:

Sign

Description

Westermark sign

Focal oligemia

Hampton hump

Wedge infarct

Palla sign

Enlarged right pulmonary artery

 Acute Pulmonary Embolism – Diagnostic Algorithm

 STEP 1: Assess Hemodynamic Stability

Unstable patient? (Shock / SBP <90 / Cardiac arrest)

➡️ YES HIGH-RISK PE PATHWAY

  • Immediate bedside echo
  • If RV dysfunction present treat as PE
  • Start reperfusion (don’t delay for CT)
    • Systemic thrombolysis
  • If stable enough confirm with CTPA later

NO Hemodynamically stable

➡️ Proceed to Clinical Probability Assessment

 STEP 2: Clinical Pre-test Probability:

  • Wells Score for Pulmonary Embolism
  • Revised Geneva Score

Categorization:

  • Low probability
  • Intermediate probability
  • High probability


 STEP 3: Apply PERC (Low-risk patients only)

Use Pulmonary Embolism Rule-out Criteria (PERC)

If ALL PERC negative:➡️ PE ruled out NO further testing

If ANY positive:➡️ Go to D-dimer


 STEP 4: D-dimer Testing

When to use:Low or Intermediate probability

Interpretation:

  • Negative D-dimer PE ruled out
  • Positive Imaging required

 Age-adjusted D-dimer:

  • Age × 10 (if >50 years)

 STEP 5: Imaging

 Gold Standard CT Pulmonary Angiography (CTPA)

 If CTPA contraindicated:

  • Renal failure / contrast allergy / pregnancy

➡️ Use:Ventilation-Perfusion (V/Q) Scan