Important for medical students

1. Pulmonary Embolism
Dr. Habib Shafi Niazi

2. Definition
 A pulmonary embolism (PE) is a sudden blockage in a lung artery. It usually
happens when a blood clot breaks loose and travels through the bloodstream
to the lungs

3. EPIDEMIOLOGY
Venous thromboembolism (VTE) encompasses deep venous thrombosis
(DVT) and pulmonary embolism (PE) and causes cardiovascular
death and disability. PE is the most common preventable cause of death
among hospitalized patients.

4. Nonthrombotic PE etiologies
 fat embolism after pelvic or long bone fracture
 tumor embolism
 bone marrow
 air embolism
 Cement embolism and bony fragment embolism can occur after total hip or
knee replacement
 Intravenous drug users may inject themselves with a wide array of
substances that can embolize such as hair, talc, and cotton
 . Amniotic fluid embolism occurs when fetal membranes leak or tear at the
placental margin.

5. PATHOPHYSIOLOGY
Virchow’s triad :
 Venus stasis
 endothelial injury
 Hypercoagulability:
The two most common autosomal dominant genetic mutations are factor V
Leiden, which causes resistance to the endogenous anticoagulant, activated
protein C (which inactivates clotting factors V and VIII)
the prothrombin gene mutation, which increases the plasma prothrombin
concentration

6. Other common predisposing factors include
 Cancer
 obesity
 cigarette smoking
 systemic arterial hypertension,
 chronic obstructive pulmonary disease,
 chronic kidney disease,
 blood transfusion,
 long-haul air travel, air pollution,
 oral contraceptives,
 pregnancy,
 postmenopausal hormone replacement,
 surgery, and trauma.

7. Embolization
When deep venous thrombi detach from their site of formation, they
embolize to the vena cava, right atrium, and right ventricle, and lodge in
the pulmonary arterial circulation, thereby causing acute PE.
Paradoxically, these thrombi occasionally embolize to the arterial
circulation through a patent foramen ovale or atrial septal defect. Many
patients with PE have no evidence of DVT because the clot has already
embolized to the lungs.

8. Pulmonary artery obstruction causes a rise in
pulmonary artery pressure and in pulmonary
vascular resistance.
 Pulmonary Hypertension
 Right Ventricular (RV) Dysfunction
 RV Microinfarction
 Diastolic LV dysfunction reduces LV distensibility and impairs LV filling.
 Underfilling of the LV may lead to a fall in LV cardiac output and systemic arterial pressure, with
consequent circulatory collapse and death.( obstructive shock)

9. CLASSIFICATION OF PULMONARY EMBOLISM
 Massive PE
 Sub massive PE
 Low-risk PE

10. Massive PE
is characterized by extensive thrombosis affecting at least
half of the
pulmonary vasculature. Dyspnea, syncope, hypotension,
and cyanosis
are hallmarks of massive PE. Patients with massive PE may
present
in cardiogenic shock and can die from multisystem organ
failure.

11. Sub massive PE
 accounts for 20–25% of patients, and is characterized by :
 RV dysfunction despite normal systemic arterial pressure. The
 combination of right heart failure and release of cardiac biomarkers indicates
an increased likelihood of clinical deterioration.

12. Low-risk PE
 constitutes about 70–75% of cases. These patients have an excellent
prognosis

13. Diagnosis of PE
 History
 Physical examination
 Laboratory examination
 Elevated cardiac biomarkers
 Electrocardiogram
 Noninvasive Imaging Modalities
 Chest roentgenography
 Chest CT
 Lung scanning
 Magnetic resonance (MR) (contrast-enhanced) imaging
 Echocardiography
 Invasive Diagnostic Modalities • Pulmonary angiography
 Use wells Clinical prediction rule for pulmonary embolism (PE).

14. Clinical sign and symptoms
 The clinical diagnosis of PE is difficult for two reasons
First, the clinical findings depend on both the size of the embolus and the
patient’s preexisting cardiopulmonary status
Second, common symptoms and signs of pulmonary emboli are not specific to
this disorder
 Some findings are fairly sensitive: dyspnea and pain on inspiration occur in
75–85% and 65–75% of patients, respectively. Tachypnea is the only sign
reliably found in more than half of patients
 Use wells Clinical prediction rule for pulmonary embolism (PE).

15. wells Clinical prediction rule for pulmonary
embolism (PE).
 Signs and symptoms of DVT……………………………………………….3.0
 Alternative diagnosis less likely than PE…………………………..3.0
 Heart rate >100/min …………………………………………………………1.5
 Immobilization >3 days; surgery within 4 weeks …….……….1.5
 Prior PE or DVT…………………………………………………………….…….1.5
 Hemoptysis……………………………………………………………..………… 1.0
 Cancer…………………………………………………………………..…………… 1.0
 High Clinical Likelihood of PE if Point Score Exceeds 4

18. Symptoms
 Dyspnea
 Respirophasic chest pain
 Cough
 Leg pain
 Hemoptysis
 Palpitations
 Wheezing
 Anginal pain

19. Signs
 Respiratory rate ≥ 16 UPET, ≥ 20 PIOPED I
 Crackles (rales)
 Heart rate ≥ 100/min
 Fourth heart sound (S4)
 Accentuated pulmonary component of second heart sound (S2P)
 T ≥ 37.5°C UPET, ≥ 38.5°C PIOPED
 Homans sign
 Pleural friction rub
 Third heart sound (S3)
 Cyanosis

20. Pulmonary embolism rule-out criteria (PERC)
for low-risk patients.
For patients with a Modified Wells Score ≤ 4 who meet ALL of the following criteria,
PE is excluded, follow off anticoagulation, and search for alternative diagnoses.
 Age < 50 years
 Heart rate < 100 bpm
 Oxyhemoglobin saturation on room air ≥ 95%
 No prior history of venous thromboembolism
 No recent (within 4 weeks) trauma or surgery requiring hospitalization
 No presenting hemoptysis
 No estrogen therapy
 No unilateral leg swelling

22. blood exam
 Elevated cardiac biomarkers
 Serum troponin and plasma heart-type fatty acid–binding protein levels increase because of RV
microinfarction.
 Myocardial stretch causes release of BNP or NT-pro-BNP
 Elevated of D-dimer
 breakdown of fibrin by plasmin.
 Elevation of d-dimer indicates endogenous although often clinically ineffective thrombolysis
 ABG
 acute respiratory alkalosis due to hyperventilation.

23. Electrocardiogram
 sinus tachycardia:
 S1Q3T3
 right ventricular hypertrophy
 RV strain and ischemia
 T-wave inversion in leads V1 to V4.
 P pulmonale
 right axis deviation
 and right bundle branch block.

25. Chest roentgenography
A normal or nearly normal chest x-ray often occurs in PE
Westermark’s sign: focal oligemia
Hampton’s hump: a peripheral wedged-shaped density above the diaphragman
Palla’s sign :enlarged right descending pulmonary artery

27. Echocardiography
McConnell’s sign: hypo kinesis of the RV free wall with normal
or hyperkinetic motion of the RV apex. One should consider transesophageal.

28. Differential Diagnosis
 Pneumonia, asthma, chronic obstructive pulmonary disease
 Congestive heart failure
 Pericarditis
 Pleurisy: “viral syndrome,” costochondritis, musculoskeletal discomfort
 Rib fracture, pneumothorax
 Acute coronary syndrome
 Anxiety

29. Treatment
 Anticoagulation
 Thrombolytic Therapy
 Inferior vena cava filters

31. Immediate Anticoagulation
 Unfractionated heparin, bolus and continuous infusion, to achieve aPTT
2–3 times the upper limit of the laboratory normal, or
 Enoxaparin 1 mg/kg twice daily with normal renal function, or
 Dalteparin 200 U/kg once daily or 100 U/kg twice daily, with normal renal
function, or
 Tinzaparin 175 U/kg once daily with normal renal function, or
 Fondaparinux weight-based once daily; adjust for impaired renal function
 Direct thrombin inhibitors: argatroban or bivalirudin
 Rivaroxaban 15 mg twice daily for 3 weeks, followed by 20 mg once daily
with the dinner meal thereafter
 Apixaban (not yet licensed)
 Edoxaban (not yet licensed)
 Dabigatran (not yet licensed)

32. Warfarin Anticoagulation
 Requires 5–10 days of administration to achieve effectiveness as monotherapy
(Unfractionated heparin, low-molecular-weight heparin, and fondaparinux
are the usual immediately effective “bridging agents” used when initiating
warfarin)
 Usual start dose is 5 mg
 Titrate to INR, target 2.0–3.0
 Continue parenteral anticoagulation for a minimum of 5 days and until two
sequential INR values, at least 1 day apart, achieve the target INR range

33. Thrombolytic Therapy
 Guidelines support systemic thromb liysis for high-risk or massive PE
(hemodynamically unstable) with low risk of bleeding.
 Streptokinase
 Urokinase
 Alteplase; recombinant tissue plasminogen activator
increase plasmin levels and thereby directly lyse intravascular thrombi.

34. Inferior vena cava filters
 patients with a major contraindication to anticoagulation who have or are at
high risk for development of proximal DVT or PE. Placement of an inferior
vena cava filter is also recommended OR recurrent cases

35. duration of anticoagulation therapy
those with major transient/reversible risk faotors (such as fractureof lower limb;
hip or knee surgery; or hospitalization for heart failure, atrial fibrillation, or
myocardial infarctton) may be considered for discontinuation of anticuagulatinn
after 3 months.

36. Thanks for attention