Pulmonary embolism (PE) is a common and potentially fatal cardiovascular condition caused by blood clots in the lungs. The document discusses the classification, pathophysiology, risk factors, clinical features, diagnostic testing and management of PE. Key points include that PE has a 15% fatality rate if untreated, but mortality decreases to around 10% with anticoagulation therapy. Rapid risk stratification and treatment of high-risk PE cases with thrombolysis, surgery or other interventions is important for reducing mortality.

1. PULMONARY EMBOLISM

2. THE GREAT MASQUERADER

3. INTRODUCTION
• One of “the big three” cardiovascular killers.
• Case fatality rate about 15%.
• Survivors with impaired quality of life.
• Common problem yet difficult to diagnose.
• No diagnostic test in utility unless PE is kept in D/D.
• Prevention is much easier than diagnosis and treatment.

4. CLASSIFICATION
 Clinical classification
 MASSIVE PE
 SUB MASSIVE PE
 SMALL TO MODERATE PE

5. CLASSIFICATION
 Temporal classification
 Acute
 Subacute
 Chronic
 Anatomical
 Saddle
 Lobar
 Segmental
 Subsegmental

6. PATHOPHYSIOLOGY

7. PATHOPHYSIOLOGY
• Modifiable risk factors:
• Obesity
• Metabolic syndrome
• Cigarette smoking
• Hypertension
• Abnormal lipid profile

8. PATHOPHYSIOLOGY
• Not readily modifiable risk factors
• Advancing age
• Arterial disease
• Personal or family history
• Recent surgery, trauma or immobility
• CCF
• COPD
• Air pollution
• Long haul air travel
• Pregnancy, OC pills
• Cardiac devices
• Hypercoagulable states
• Factor V Leiden
• Prothrombin gene mutation
• Antithrombin deficiency
• Protein C deficiency
• Protein S deficiency
• Antiphospholipid anti body syndrome

9. PATHOPHYSIOLOGY
 Relationship between DVT and PE :
 Thrombus forms in vein
 Via venacava to RA and RV
 Pulmonary arterial circulation
 Large embolus may lodge at bifurcation of pulmonary artery forming
saddle embolus.
 More commonly major pulmonary vessel is occluded.
 Usually in patients with PE, no doppler evidence of DVT.

10. PATHOPHYSIOLOGY

11. PATHOPHYSIOLOGY
• Pulmonary Infarction, atelectasis
• Increased pulmonary vascular resistance caused by vascular
obstruction, neurohormonal changes or baroreceptors
• Impaired gas exchange
• Alveolar hyperventilation due to reflex stimulation of irritant
receptors
• RV dysfunction and failure
• Myocardial ischemia and circulatory failure

12. CLINICAL FEATURES
 S/S nonspecific.
 Clinical suspicion is of paramount importance.
 SYMPTOMS
 Otherwise unexplained dyspnea
 Chest pain either pleuritic or atypical
 Anxiety
 Cough

13. CLINICAL FEATURES
 SIGNS
 Tachypnea
 Tachycardia
 Low grade fever
 Left parasternal lift
 TR murmur
 Loud P2
 Leg edema, erythema, tenderness

14. Pretest probability assessment
CLASSIC WELLS CRITERIA
SCORE POINTS
DVT symptoms or signs 3
An alternative diagnosis is less likely
than PE
3
Heart rate >100/min 1.5
Immobilization or surgery within 4
weeks
1.5
Prior DVT or PE 1.5
Hemoptysis 1
Cancer treated within 6 months or
metastatic
1

16. INVESTIGATIONS
 NONIMAGING METHODS
 CBC, RFT, BNP, Troponin
 Plasma D-dimer assay
 Highly sensitive but not specific.
 Other causes of elevations should be ruled out.
 ABG analysis
 Electrocardiogram
 Normal
 Sinus tachycardia
 Incomplete or complete RBBB
 RAD
 S1Q3T3 complex
 T wave inversion in leads III, aVf
 T wave inversion in leads V1-V4 – greatest accuracy for identification of right

17. INVESTIGATIONS

18. INVESTIGATIONS
 CHEST X-RAY
 Hampton’s Hump
 Westermark’s Sign
 Pallas Sign

19. INVESTIGATIONS

20. INVESTIGATIONS
 ECHOCARDIOGRAPHY
 Normal in about half of cases
 Not recommended for routine
diagnostic test
 SIGNS:
 RV enlargement or hypokinesis with
apical sparing( The McConnel Sign)
 IV septal flattening and paradoxical
motion toward left ventricle
 Tricuspid regurgitation
 Pulmonary hypertension
 Dilated IVC
 Direct visualization of thrombus

21. INVESTIGATIONS
 CHEST COMPUTED TOMOGRAPHY
 Has supplanted pulmonary radionuclide
perfusion scintigraphy
 Overall negative predictive value 99.4%
 Both diagnostic and prognostic test.
 One-stop shop.
 Also other lung diseases can be scanned
 RV enlargement protends a complicated
hospital course.

22. INVESTIGATIONS
 Lung Scanning
 Uses radio labelled aggregates of albumin or microspheres that lodge in pulmonary
microvasculature.
 Multiple perfusion defects.
 Ventilation perfusion mismatch.
 Magnetic resonance imaging
 Pulmonary angiography
 Formerly the reference standard
 Now, rarely performed.
 But is required when interventions are planned
 Doppler venous ultrasound

23. Diagnostic approach
 Pretest probability assessment
 D- Dimer testing
 Definitive diagnostic imaging

24. MANAGEMENT
 Initial management
 In Massive PE
 Circulatory support
 IV Fluids
 Vasopressors
 Respiratory support
 Supplemental oxygen
 Ventillatory support

25. MANAGEMENT
 ANTICOAGULATION
 Unfractionated heparin
 Starting bolus of 80 units/kg, followed by an infusion at 18 units/kg per hour
 Titrate the infusion rate every four to six hours to a goal activated partial
thromboplastin time (aPTT).
 Low molecular heparin
 Inj Enoxaparin 60 mg SC BD
 Inj Fondaparinux 5 mg SC OD

26. MANAGEMENT - THROMBOLYSIS
 In Massive PE
 Overall, 90% of patients with PE appear to respond favourably to
thrombolysis as indicated by clinical and echocardiographic improvement
within the first 36 h.
 The greatest benefit is observed when treatment is initiated within 48 h of
symptom onset, but thrombolysis can still be useful in patients who have had
symptoms for 6–14 days.

27. European Heart Journal (2012) 33, 3014–3022

29. SURGICAL OR INTERVENTIONAL
TREATMENT
 Pulmonary embolectomy
 Catheter directed thrombolysis
 Thrombus fragmenation
 Rheolytic thrombectomy
 Suction thrombectomy
 Rotational thrombectomy
 Pharmacomechanical thrombolysis

30. MANAGEMENT
 IVC filters
 Used as a means of primary or secondary PE prevention.
 Retrievable inferior venacava filters have a place mostly when
 anticoagulation is absolutely contraindicated, or
 in cases of recurrence despite therapeutic dosing of
anticoagulants

31. SECONDARY PROPHYLAXIS
 Warfarin
 Target INR 2-3.
 New oral anticoagulants
 Rivaroxaban
 Apixaban
 Dabigatran

32. SECONDARY PROPHYLAXIS
Optimal duration of antucoagulation
CLINICAL SETTINGS RECOMMENDATION
First provoked PE/proximal DVT 3 to 6 months
First provoked upper extremity DVT or
isolated calf DVT
3 months
Second provoked DVT Uncertain
Third VTE Indefinite duration
Cancer and VTE Indefinite duration or until cancer is
resolved
Unprovoked PE/proximal leg DVT Consider indefinite duration
First unprovoked calf DVT 3 months
Second unprovoked calf DVT Uncertian

33. DIFFERENTIAL DIAGNOSIS
 Anxiety, pleurisy, costocondritis
 Pneumonia, bronchitis
 Myocardial infarction
 Pericarditis
 Congestive cardiac failure
 Idiopathic pulmonary hypertension

34. PREVENTION
 Most preventable cause of inhospital death.
 Pharmacological prophylaxis measures.
 IV Heparin
 IV Enoxaparin
 New oral anticoagulants
 Mechanical measures:
 Intermittent pneumatic compression
 Graduated compression stockings

35. PROGNOSIS
 If Left untreated, 30% mortality. But decreases to around 10 % with
anticogulation.
 Death usually within first 7 days.
 Recurrence of PE. 25% at 5 years
 Chronic thromboembolic pulmonary hypertension(CTEPH)(1-4%)

36. TAKE HOME MESSAGE
 High Suspicion
 Rapid and accurate risk stratification into stable and
unstable PE.
 All patients should receive injectable anticoagulation.
 High risk PE should undergo immediate thrombolytic,
surgical or interventional therapy.
 Personalized assessment for optimal duration of
anticoagulation.
 Emerging management strategies may simplify secondary
prevention in future.