Pulmonary Embolism

Pulmonary embolism (PE) is a potentially life-threatening condition that occurs when a blood clot blocks one or more arteries in the lungs. Most commonly, these clots originate in the deep veins of the legs (deep vein thrombosis) and travel through the bloodstream to the lungs. PE can range from small, asymptomatic clots to massive blockages that cause sudden death. Prompt recognition and treatment are essential, as untreated PE has a mortality rate of up to 30%, while appropriate treatment reduces this to 2-8%.

Medical Disclaimer: This information is for educational purposes only and should not replace professional medical advice. If you suspect you have a pulmonary embolism, seek emergency medical attention immediately. PE is a medical emergency that requires immediate treatment.

Overview

Pulmonary embolism occurs when material, most commonly a blood clot, becomes lodged in a pulmonary artery, blocking blood flow to lung tissue. This blockage prevents oxygen from reaching the affected lung tissue and increases pressure on the right side of the heart, potentially leading to heart failure. The severity of PE depends on the size and number of clots, the patient's underlying cardiopulmonary status, and how quickly treatment is initiated.

PE is part of a disease spectrum called venous thromboembolism (VTE), which also includes deep vein thrombosis (DVT). Together, VTE affects approximately 900,000 Americans annually and causes an estimated 60,000-100,000 deaths. PE is the third most common cause of cardiovascular death after heart attack and stroke. The incidence increases dramatically with age, doubling with each decade after age 40.

The pathophysiology of PE involves both respiratory and hemodynamic consequences. The blockage of pulmonary arteries leads to increased dead space ventilation, impaired gas exchange, and potential lung infarction. Hemodynamically, the obstruction increases right ventricular afterload, which can lead to right heart strain and failure. Additionally, the release of vasoactive mediators can cause pulmonary vasoconstriction, further compromising cardiopulmonary function. Understanding these mechanisms is crucial for appropriate risk stratification and treatment selection.

Symptoms

The symptoms of pulmonary embolism can vary widely, from no symptoms at all to sudden catastrophic cardiovascular collapse. The classic triad of dyspnea, chest pain, and hemoptysis occurs in less than 20% of patients, making clinical diagnosis challenging. Symptoms depend on the clot burden, rate of development, and the patient's cardiopulmonary reserve.

Common Respiratory Symptoms

  • Shortness of breath - most common symptom, often sudden onset
  • Difficulty breathing - worsens with exertion
  • Cough - dry or productive, sometimes with blood
  • Hemoptysis - coughing up blood, indicates lung infarction
  • Rapid breathing (tachypnea) - compensatory response
  • Wheezing or decreased breath sounds

Chest and Cardiac Symptoms

  • Sharp chest pain - pleuritic, worsens with breathing
  • Chest tightness - feeling of pressure or constriction
  • Side pain - often indicates peripheral emboli
  • Rapid heart rate (tachycardia) - compensatory mechanism
  • Irregular heartbeat or palpitations
  • Chest wall tenderness in some cases

Associated DVT Symptoms

  • Leg pain - often in calf, may precede PE
  • Leg swelling - unilateral, indicates DVT source
  • Leg warmth and redness
  • Visible surface veins
  • Cord-like feeling in leg

Systemic Symptoms

  • Weakness - generalized fatigue and malaise
  • Sweating - often profuse, cold sweats
  • Anxiety or feeling of impending doom
  • Lightheadedness or dizziness
  • Syncope (fainting) - indicates massive PE
  • Low-grade fever

Signs of Massive PE

  • Severe hypotension or shock
  • Cyanosis (blue discoloration of skin)
  • Jugular venous distension
  • Right ventricular heave
  • Loud P2 heart sound
  • Cardiac arrest

Causes

Pulmonary embolism occurs when material blocks the pulmonary arteries. While blood clots are the most common cause, understanding the various sources and mechanisms helps in prevention and treatment. The underlying pathophysiology involves Virchow's triad: venous stasis, endothelial injury, and hypercoagulability.

Blood Clots (Thrombotic PE)

The vast majority (>90%) of PE cases result from blood clots:

  • Deep vein thrombosis (DVT):
    • Lower extremity DVT - most common source (90%)
    • Upper extremity DVT - often catheter-related
    • Pelvic vein thrombosis - pregnancy, malignancy
    • Inferior vena cava thrombosis
  • Right heart thrombi:
    • Atrial fibrillation with right atrial clot
    • Right ventricular thrombus
    • Catheter-associated thrombus
    • Pacemaker lead thrombus

Non-thrombotic Causes

  • Fat embolism:
    • Long bone fractures
    • Orthopedic procedures
    • Liposuction
    • Bone marrow transplant
  • Air embolism:
    • Central venous catheter manipulation
    • Trauma with vascular injury
    • Barotrauma (diving accidents)
    • Surgical procedures
  • Amniotic fluid embolism:
    • Obstetric complication
    • During or after delivery
    • Abortion or amniocentesis
  • Tumor embolism:
    • Renal cell carcinoma
    • Hepatocellular carcinoma
    • Choriocarcinoma
    • Right atrial myxoma

Other Embolic Materials

  • Septic emboli: Infected vegetation from endocarditis
  • Foreign bodies: Broken catheter fragments, talc (IV drug use)
  • Cement emboli: Vertebroplasty or kyphoplasty
  • Parasitic emboli: Schistosomiasis, echinococcosis

Pathophysiologic Mechanisms

  • Venous stasis:
    • Immobilization
    • Heart failure
    • Obesity
    • Pregnancy
  • Endothelial injury:
    • Surgery or trauma
    • Central venous catheters
    • Previous DVT
    • Vasculitis
  • Hypercoagulability:
    • Inherited thrombophilias
    • Acquired conditions
    • Medications
    • Malignancy

Risk Factors

Understanding risk factors for pulmonary embolism is crucial for prevention, early detection, and determining the need for prophylaxis. Risk factors can be classified as strong, moderate, or weak based on their association with VTE development.

Strong Risk Factors (Odds Ratio >10)

  • Major surgery:
    • Hip or knee replacement
    • Major abdominal or pelvic surgery
    • Neurosurgery
    • Multiple trauma surgery
  • Major trauma:
    • Spinal cord injury
    • Multiple long bone fractures
    • Pelvic fractures
  • Previous VTE: Highest risk factor for recurrence
  • Active cancer: Especially with metastases or chemotherapy

Moderate Risk Factors (Odds Ratio 2-9)

  • Immobilization:
    • Hospitalization >3 days
    • Bed rest with bathroom privileges
    • Long-distance travel (>4 hours)
    • Plaster cast immobilization
  • Female-specific factors:
    • Pregnancy and postpartum period
    • Oral contraceptives
    • Hormone replacement therapy
    • Assisted reproductive therapy
  • Medical conditions:
    • Heart failure (NYHA III/IV)
    • Acute myocardial infarction
    • Acute respiratory failure
    • Inflammatory bowel disease
    • Nephrotic syndrome

Weak Risk Factors (Odds Ratio <2)

  • Age: Risk doubles each decade after 40
  • Obesity: BMI >30 kg/m²
  • Varicose veins: Mild increased risk
  • Smoking: Especially with other risk factors
  • Hypertension: Modest association

Inherited Thrombophilias

  • Factor V Leiden: Most common, 3-8 fold increased risk
  • Prothrombin G20210A mutation: 2-3 fold increased risk
  • Protein C deficiency: 10-15 fold increased risk
  • Protein S deficiency: 10 fold increased risk
  • Antithrombin deficiency: Highest risk, 20-40 fold increase

Acquired Thrombophilias

  • Antiphospholipid syndrome: Lupus anticoagulant, anticardiolipin antibodies
  • Heparin-induced thrombocytopenia: Paradoxical thrombosis
  • Myeloproliferative disorders: Polycythemia vera, essential thrombocythemia
  • Paroxysmal nocturnal hemoglobinuria: Rare but high risk

Diagnosis

Diagnosing pulmonary embolism requires a systematic approach combining clinical assessment, laboratory tests, and imaging studies. The challenge lies in the nonspecific nature of symptoms and the potentially fatal consequences of missed diagnosis. Modern diagnostic strategies use validated clinical prediction rules to guide testing.

Clinical Assessment

Wells Score for PE

Points assigned for clinical features (score >4 = PE likely):

  • Clinical signs of DVT: 3 points
  • PE as likely as alternative diagnosis: 3 points
  • Heart rate >100: 1.5 points
  • Immobilization/surgery in past 4 weeks: 1.5 points
  • Previous DVT/PE: 1.5 points
  • Hemoptysis: 1 point
  • Malignancy: 1 point

Revised Geneva Score

Alternative scoring system based on objective criteria

Laboratory Tests

D-dimer

  • High sensitivity (>95%) but low specificity
  • Useful for ruling out PE in low-risk patients
  • Age-adjusted cutoffs improve specificity
  • Elevated in many conditions (pregnancy, cancer, infection)
  • Not useful if high pretest probability

Arterial Blood Gas

  • Hypoxemia with increased A-a gradient
  • Respiratory alkalosis from hyperventilation
  • Normal ABG does not exclude PE

Cardiac Biomarkers

  • Troponin: Elevated in RV strain
  • BNP/NT-proBNP: Indicates RV dysfunction
  • Used for risk stratification, not diagnosis

Imaging Studies

CT Pulmonary Angiography (CTPA)

  • Gold standard for PE diagnosis
  • Sensitivity >95%, specificity >95%
  • Visualizes clots to subsegmental level
  • Provides alternative diagnoses
  • Assesses RV strain (RV/LV ratio)
  • Contraindicated in severe renal impairment

Ventilation-Perfusion (V/Q) Scan

  • Alternative when CTPA contraindicated
  • High probability scan + high clinical suspicion = PE
  • Normal scan essentially rules out PE
  • Many indeterminate results
  • Preferred in pregnancy (lower radiation)

Echocardiography

  • Bedside assessment for unstable patients
  • Shows RV dysfunction and dilation
  • McConnell's sign: RV free wall hypokinesis
  • Cannot definitively diagnose PE
  • Useful for risk stratification

Additional Diagnostic Tools

Chest X-ray

  • Usually normal or nonspecific
  • Hampton's hump: peripheral wedge opacity
  • Westermark's sign: focal oligemia
  • Mainly to exclude other diagnoses

Lower Extremity Ultrasound

  • If positive for DVT, supports PE diagnosis
  • Negative ultrasound doesn't exclude PE
  • Useful when chest imaging contraindicated

Pulmonary Angiography

  • Historical gold standard, rarely used now
  • Reserved for catheter-directed therapy
  • Invasive with risk of complications

Treatment Options

Treatment of pulmonary embolism aims to prevent clot extension, promote resolution, prevent recurrence, and manage complications. The approach depends on hemodynamic stability, clot burden, bleeding risk, and patient factors. Risk stratification is crucial for selecting appropriate therapy.

Risk Stratification

  • Low risk: Hemodynamically stable, no RV dysfunction
  • Intermediate-low risk: RV dysfunction by imaging or biomarkers
  • Intermediate-high risk: RV dysfunction + elevated biomarkers
  • High risk (massive PE): Hemodynamic instability

Anticoagulation Therapy

The cornerstone of PE treatment for all risk groups:

Initial Anticoagulation

  • Low molecular weight heparin (LMWH):
    • Enoxaparin 1 mg/kg twice daily or 1.5 mg/kg daily
    • Dalteparin 200 units/kg daily
    • Preferred in cancer patients
    • No monitoring required in most cases
  • Unfractionated heparin (UFH):
    • Bolus 80 units/kg then 18 units/kg/hr infusion
    • Preferred if thrombolysis anticipated
    • Requires aPTT monitoring
    • Reversible with protamine
  • Direct oral anticoagulants (DOACs):
    • Rivaroxaban 15 mg twice daily x 21 days
    • Apixaban 10 mg twice daily x 7 days
    • Can be used for initial treatment

Long-term Anticoagulation

  • Warfarin: INR target 2-3, requires bridging
  • DOACs: Fixed dosing, no monitoring
    • Rivaroxaban 20 mg daily
    • Apixaban 5 mg twice daily
    • Dabigatran 150 mg twice daily
    • Edoxaban 60 mg daily
  • Duration:
    • Provoked PE: 3 months minimum
    • Unprovoked PE: Consider indefinite
    • Cancer-associated: While cancer active
    • Recurrent VTE: Indefinite

Thrombolytic Therapy

For massive PE or selected intermediate-high risk patients:

  • Systemic thrombolysis:
    • Alteplase 100 mg IV over 2 hours
    • Reduces mortality in massive PE
    • Major bleeding risk 9-20%
    • Intracranial hemorrhage 1.5-3%
  • Catheter-directed thrombolysis:
    • Lower dose thrombolytics directly to clot
    • May reduce bleeding risk
    • Combined with mechanical fragmentation
    • Requires expertise and resources
  • Contraindications:
    • Recent major surgery or trauma
    • Active bleeding
    • Recent stroke
    • Intracranial pathology

Embolectomy

  • Surgical embolectomy:
    • Reserved for massive PE with contraindication to thrombolysis
    • Failed thrombolysis
    • Requires cardiopulmonary bypass
    • Mortality 20-30% in experienced centers
  • Catheter-based embolectomy:
    • Mechanical clot removal
    • Various devices available
    • Less invasive than surgery
    • Growing evidence base

Inferior Vena Cava (IVC) Filters

  • Indications:
    • Absolute contraindication to anticoagulation
    • Recurrent PE despite adequate anticoagulation
    • Massive PE with poor cardiopulmonary reserve
  • Considerations:
    • Does not treat existing PE
    • Retrievable filters preferred
    • Complications include filter migration, fracture
    • Remove when anticoagulation possible

Supportive Care

  • Oxygen therapy: Maintain SpO2 >90%
  • Mechanical ventilation: If respiratory failure
  • Hemodynamic support:
    • IV fluids cautiously (avoid RV overload)
    • Vasopressors if hypotensive
    • Consider ECMO in extreme cases
  • Pain management: Opioids for pleuritic pain

Prevention

Prevention of pulmonary embolism focuses on preventing deep vein thrombosis and reducing risk factors. Prophylaxis strategies are tailored to individual risk levels and clinical settings. Both mechanical and pharmacological methods are employed, often in combination for high-risk patients.

Risk Assessment

All hospitalized patients should undergo VTE risk assessment:

  • Validated risk assessment models:
    • Caprini score for surgical patients
    • Padua score for medical patients
    • Assess bleeding risk concurrently
    • Reassess risk with clinical changes

Mechanical Prophylaxis

  • Early mobilization:
    • Most effective prevention strategy
    • Progressive ambulation protocols
    • Physical therapy involvement
    • Avoid prolonged bed rest
  • Compression devices:
    • Graduated compression stockings (GCS)
    • Intermittent pneumatic compression (IPC)
    • Use when pharmacologic prophylaxis contraindicated
    • Continue until fully ambulatory

Pharmacological Prophylaxis

Medical Patients

  • Low-risk: Early ambulation only
  • Moderate to high-risk:
    • LMWH: Enoxaparin 40 mg daily
    • UFH: 5000 units subcutaneous 2-3 times daily
    • Fondaparinux: 2.5 mg daily
    • Continue throughout hospitalization

Surgical Patients

  • General surgery: Risk-stratified approach
  • Orthopedic surgery:
    • Hip/knee replacement: Extended prophylaxis 10-35 days
    • Hip fracture: Continue 28-35 days
    • DOACs increasingly used
  • Neurosurgery: Mechanical methods initially
  • Trauma: LMWH when bleeding risk acceptable

Special Populations

  • Pregnancy:
    • LMWH throughout pregnancy if prior VTE
    • Continue 6 weeks postpartum
    • Mechanical prophylaxis during delivery
  • Cancer patients:
    • Hospitalized: Routine prophylaxis
    • Ambulatory high-risk: Consider prophylaxis
    • LMWH preferred over warfarin
  • Travel:
    • Frequent ambulation during long flights
    • Compression stockings for high-risk
    • Consider prophylactic LMWH if very high risk

Lifestyle Modifications

  • Weight management: Reduce obesity-related risk
  • Smoking cessation: Eliminate prothrombotic effects
  • Regular exercise: Improve venous return
  • Hydration: Prevent hemoconcentration
  • Leg elevation: When sitting for prolonged periods

Secondary Prevention

For patients with previous VTE:

  • Complete anticoagulation course: Reduce recurrence risk
  • Address reversible risk factors:
    • Discontinue estrogen therapy if possible
    • Treat underlying conditions
    • Weight loss if obese
  • Consider extended anticoagulation:
    • Assess bleeding vs. clotting risk
    • Low-dose DOACs for extended therapy
    • Regular reassessment of need
  • Prophylaxis during high-risk periods:
    • Surgery
    • Hospitalization
    • Immobilization
    • Pregnancy

When to See a Doctor

Call 911 or seek emergency care immediately for:

Seek urgent medical attention for:

Contact your doctor if you have:

  • Risk factors for PE and develop any concerning symptoms
  • Questions about VTE prevention before surgery or travel
  • Family history of blood clots
  • Concerns about anticoagulation therapy
  • Previous VTE and planning pregnancy

Related Conditions

References

  1. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543-603.
  2. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report. Chest. 2016;149(2):315-352.
  3. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension. Circulation. 2011;123(16):1788-1830.
  4. Stevens SM, Woller SC, Kreuziger LB, et al. Antithrombotic Therapy for VTE Disease: Second Update of the CHEST Guideline and Expert Panel Report. Chest. 2021;160(6):e545-e608.
  5. Righini M, Robert-Ebadi H, Le Gal G. Diagnosis of acute pulmonary embolism. J Thromb Haemost. 2023;21(7):1592-1603.