- Pulmonary embolism (PE) is a blockage in the lung's arteries caused by blood clots that travel from deep veins, most often in the legs. - Risk factors include recent surgery or trauma, cancer, older age, and genetic predispositions. Symptoms can range from mild to life-threatening depending on the size and location of the clots. - Diagnosis involves blood tests, imaging like CT scans, ventilation-perfusion scans, or angiography. Treatment focuses on anticoagulation with blood thinners to prevent further clotting as well as supporting heart and lung function. For some patients, more aggressive options like thrombolysis or surgery may be considered.

1. Pulmonary Embolism

2. Introduction
• Venous thromboembolism (VTE) encompasses
deep vein thrombosis(DVT) and pulmonary
embolism (PE).
• It is the third most frequent cardiovascular
disease with an overall annual incidence of 100–
200 per 100 000 inhabitants.
• The epidemiology of PE is difficult to determine
because it may remain asymptomatic, or its
diagnosis may be an incidental finding.
• in some cases, the first presentation of PE may be
sudden death

3. Predisposing factors
• VTE is considered to be ‘provoked’ in the
presence of a temporary or reversible risk
factor (such as surgery, trauma,
immobilization, pregnancy, oral contraceptive
use or hormone replacement therapy)within
the last 6 weeks to 3 months before diagnosis,
and ‘unprovoked’ in the absence thereof.

4. Modifiable Risk Factors
• Obesity
• Metabolic syndrome
• Cigarette smoking
• Hypertension
• Abnormal lipid profile
• High consumption of red meat
• low consumption of fish, fruits, and
vegetables

5. Not Readily Modifiable
• Advancing age
• Arterial disease, including carotid
and coronary disease
• Personal or family history of
venous thromboembolism
• Recent surgery, trauma, or
immobility, including stroke
• Congestive heart failure
• Chronic obstructive pulmonary
disease
• Acute infection
• Air pollution
• Long-haul air travel
• Pregnancy, OC pills, or
postmenopausal hormone
replacement therapy
• Pacemaker, implantable cardiac
defibrillator leads, or indwelling
central venous catheter
• Hypercoagulable states
• Factor V Leiden resulting in
activated protein C resistance
• Prothrombin gene mutation
20210
• Antithrombin deficiency
• Protein C deficiency
• Protein S deficiency
• Antiphospholipid antibody
syndrome

6. • Massive PE accounts for 5-10% of cases, and 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.
• Submassive 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.
• Low-risk PE constitutes about 70-75% of cases. These patients
have an excellent prognosls.

7. Pathophysiology
• Acute PE interferes with both the circulation and gas
exchange.
• Right ventricular (RV) failure due to pressure overload is
considered the primary cause of death in severe PE.
• PA pressure increases only if more than 30–50% of the
total cross-sectional area of the pulmonary arterial bed
is occluded by thromboemboli.
• PE-induced vasoconstriction, mediated by the release
of thromboxane A2 and serotonin, contributes to the
initial increase in pulmonary vascular resistance after
PE, an effect that can be reversed by vasodilators

8. Key factors contributing to haemodynamic collapse in acute pulmonary
embolism

9. Pathophysiology of right ventricular dysfunction.
LV = left ventricular; PA = pulmonary artery; RV = right ventricular.

10. Initial risk stratification of acute PE.

11. Most Common Symptoms and Signs of
Pulmonary Embolism
• Symptoms
• Otherwise unexplained
dyspnea
• Chest pain, either
pleuritic or “atypical”
• Anxiety
• Cough
• Syncope
• Signs
• Tachypnea
• Tachycardia
• Low-grade fever
• Left parasternal lift
• Tricuspid regurgitant
murmur
• Accentuated P2
• Hemoptysis
• Leg edema, erythema,
tenderness

12. Diagnosis
• Laboratory
• Leucocytosis
• Increased ESR
• Increased LDH
• ABG- Hypoxemia, hypocapnia, respiratory
alkalosis.
- Massive PE with hypotension can cause
hypercapnia and combined respiratory and
metabolic acidosis(due to lactic acidosis)

13. Elevated BNP
-Insensitive, nonspecific
- level >600pg/ml
-BNP had 60% sensitivity and 62%specificity
-BNP may have prognostic role in PE
Elevated TROPONIN
-30-50% of mod to large PE
-Due to acute right heart overload
-Resolve within 40hrs ( more prolonged after acute MI)
Heart-type fatty acid-binding protein (H-FABP)
-levels ≥6 ng/mL had sensitivity 28% , specificity 99% for an
adverse 30-day outcome

14. ECG
• Sinus tachycardia
• Incomplete or complete right bundle branch block
• Right-axis deviation
• T wave inversions in leads III and aVF or in leads V1-V4
• S wave in lead I and a Q wave and T wave inversion in
lead III (S1Q3T3)
• QRS axis greater than 90 degrees or an indeterminate
axis
• Atrial fibrillation or atrial flutter

15. heart rate of 90/min, S1Q3T3, and incomplete right bundle branch block,
with inverted or flattened T waves in leads V1 through V4.

16. Chest X-ray

17. D-dimer
• D-dimer levels are elevated in plasma in the presence of
acute thrombosis because of simultaneous activation of
coagulation and fibrinolysis.
• >500ng/ml is considered as abnormal.
• diagnostic sensitivity of 95%
• The negative predictive value of D-dimer testing is high and
a normal D-dimer level renders acute PE or DVT unlikely.
• Also raised in cancer, inflammation, necrosis, bleeding,
trauma, surgery , pregnancy, eclampsia, DIC, MI, severe
liver disease, renal failure, stroke.
• three-month thromboembolic risk was 1.5% in PE-unlikely
patients with a negative D-dimer.

18. Wells rule

19. Revised Geneva rule

20. Computed tomographic pulmonary
angiography
• method of choice for imaging the pulmonary
vasculature in patients with suspected PE.
• sensitivity of 83% and a specificity of 96%.
• three-month thromboembolic risk would have
been 1.5%

21. Lung scintigraphy (V/Q scan)
• Ventilation–perfusion scintigraphy (V/Q scan).
• Intravenous injection of technetium (Tc)-99m-
labelled macroaggregated albumin particles,
which block a small fraction of the pulmonary
capillaries and thereby enable scintigraphic
assessment of lung perfusion.
• Perfusion scans are combined with ventilation
studies, for which multiple tracers such as xenon-
133 gas, Tc-99m-labelled aerosols, or Tc-99m-
labelled carbon microparticles (Technegas) can
be used.

22. • Radiation exposure from a lung scan is 1.1
mSv for an average sized adult, and thus is
significantly lower than that of CT angiography
(2–6 mSv).
• Applied in young (particularly female)
patients, in pregnancy, h/o contrast medium-
induced anaphylaxis and strong allergic
history, in severe renal failure, and myeloma
and paraproteinaemia

25. Pulmonary angiography
• ‘gold standard’ for the diagnosis or exclusion
of PE.
• Pulmonary angiography is more often used to
guide percutaneous catheter-directed
treatment of acute PE.

26. Magnetic resonance angiography MRA
• low sensitivity,
• high proportion of inconclusive MRA scans,
• low availability in most emergency settings.

27. Echocardiography
• Right ventricular enlargement or hypokinesis, especially free wall
hypokinesis, with sparing of the apex (the McConnell sign)
• Interventricular septal flattening and paradoxical motion toward the left
ventricle, resulting in a D-shaped left ventricle in cross section
• Tricuspid regurgitation
• Pulmonary hypertension with a tricuspid regurgitant jet velocity >2.6
m/sec
• Loss of respiratory-phasic collapse of the inferior vena cava with
inspiration
• Dilated inferior vena cava without physiologic inspiratory collapse
• Direct visualization of thrombus (more likely with transesophageal
echocardiography)

28. Compression venous ultrasonography
• DVT was found in 30-50% of patients with
proven PE.
• sensitivity 90% and a specificity 95% for
symptomatic DVT

29. Diagnostic strategies
• Suspected pulmonary embolism with shock or
hypotension.

32. Prognostic assessment
• pulmonary embolism severity index (PESI)
• PESI performed better than the older Geneva
prognostic score for identification of patients
with an adverse 30-day outcome.

33. Original and simplified PESI

34. Classification of patients with acute PE based on early mortality risk

35. Treatment in the acute phase
Haemodynamic and respiratory support
• Aggressive volume expansion is of no benefit and may
even worsen RV function by causing mechanical
overstretch, or by reflex mechanisms that depress
contractility.
• Modest (500 mL) fluid challenge may help to increase
cardiac index in patients with PE, low cardiac index,
and normal BP.
• Norepinephrine appears to improve RV function via a
direct positive inotropic effect, while also improving RV
coronary perfusion by peripheral vascular alpha-
receptor stimulation and the increase in systemic BP.

36. • Epinephrine combines the beneficial properties of
norepinephrine and dobutamine, without the systemic
vasodilatory effects of the latter.
• Vasodilators decrease pulmonary arterial pressure and
pulmonary vascular resistance, but the main concern is the
lack of specificity of these drugs for the pulmonary
vasculature after systemic (intravenous)administration.
• Inhalation of nitric oxide may improve the haemodynamic
status and gas exchange of patients with PE.
• levosimendan may restore right ventricular–pulmonary
arterial coupling in acute PE by combining pulmonary
vasodilation with an increase in RV contractility

37. • Hypoxaemia and hypocapnia
• patent foramen ovale may aggravate
hypoxaemia due to Right to left shunting .
• Mechanical ventilation is required.
• Low tidal volumes (approximately 6 mL/kg
lean body weight) should be used in an
attempt to keep the end-inspiratory plateau
pressure,30 cm H2O.

38. Anticoagulation
• acute-phase treatment consists of administering
parenteral anticoagulation [unfractionated heparin
(UFH), low molecular weight heparin(LMWH), or
fondaparinux] over the first 5–10 days.
• Parenteral heparin should overlap with the initiation of
a vitamin K antagonist (VKA); alternatively, it can be
followed by administration of one of the new oral
anticoagulants: dabigatran or edoxaban.
• If rivaroxaban or apixaban is given instead, oral
treatment with one of these agents should be started
directly or after a 1–2 day administration of UFH,
LMWH or fondaparinux.

39. Parenteral anticoagulation
• UNFRACTIONATED HEPARIN
• Heparin is the cornerstone for treatment of acute
PE. For patients with average bleeding risk, begin
with an intravenous UFH bolus of 80 units/kg,
followed by a continuous infusion at 18 units/kg
per hour.
• Target the aPTT between 1.5 and 2.5 times the
control value.
• Commonly, the therapeutic range is 60 to 80
seconds.

40. Adjustment of unfractionated heparin dosage
based on the aPTT
aPTT : activated partial thromboplastin time; U : units.

41. • LMWH or fondaparinux are preferred over
UFH for initial anticoagulation in PE, as they
carry a lower risk of inducing major bleeding
and heparin-induced thrombocytopenia (HIT).
• UFH is recommended in serious renal
impairment (creatinine clearance,30 mL/min),
or severe obesity.
• dosing of UFH is adjusted, based on the
activated partial thromboplastin time (aPTT)

42. LMWH and pentasaccharide (fondaparinux) approved for them
treatment of pulmonary embolism

43. • Subcutaneous fondaparinux is contraindicated in
severe renal insufficiency (creatinine clearance -
30 mL/min).
• Moderate renal insufficiency (clearance 30–50
mL/min) - dose should be reduced by 50%.
• Anticoagulation with UFH, LMWH, or
fondaparinux should be continued for at least 5
days and until the international normalized ratio
(INR) has been 2.0–3.0 for two consecutive days.

44. Oral anticoagulation
Vitamin K antagonists
• Warfarin is a vitamin K antagonist that prevents
gammacarboxylation activation of coagulation factors
II, VII, IX, and X.
• The full anticoagulant effect of warfarin may not be
apparent for 5 to 7days, even if the prothrombin time,
used to monitor warfarin’s effect, becomes elevated
more rapidly
• Oral anticoagulants should be initiated as soon as
possible, and preferably on the same day as the
parenteral anticoagulant.
• The daily dose is adjusted according to the INR over
the next 5–7 days, aiming for an INR level of 2.0–3.0.

45. New oral anticoagulants (NOACs)
• immediate onset of action
• half-life is short.
• administration in fixed doses without routine
laboratory coagulation monitoring.
• few drug-drug or drug-food interactions, more
“user friendly” than warfarin for patients and
for health care providers.

47. Optimal Duration of Anticoagulation

48. Thrombolytic treatment
• Unfractionated heparin infusion should be
stopped during administration of streptokinase or
urokinase; it can be continued during rtPA
infusion.
• In patients receiving LMWH or fondaparinux at
the time that thrombolysis is initiated, infusion of
UFH should be delayed until 12 hours after the
last LMWH injection (given twice daily), or until
24 hours after the last LMWH or fondaparinux
injection (given once daily).

49. • Greatest benefit is observed when treatment
is initiated within 48 hours of symptom onset.
• Thrombolysis can still be useful in patients
who have had symptoms for 6–14days.

50. Approved thrombolytic regimens for pulmonary embolism
IU : international units; rtPA : recombinant tissue plasminogen activator.

51. Contraindications to thrombolytic therapy

52. Surgical embolectomy
• The first successful surgical pulmonary
embolectomy was performed in 1924.
• Transportable extracorporeal assistance systems
with percutaneous femoral cannulation can be
helpful in critical situations, ensuring circulation
and oxygenation until definitive diagnosis.
• With bilateral PA incisions, clots can be removed
from both pulmonary arteries down to the
segmental level under direct vision.

53. Percutaneous catheter-directed treatment
• objective of interventional treatment is the removal of
obstructing thrombi from the main pulmonary arteries to
facilitate RV recovery and improve symptoms and
survival.
• For patients with absolute contraindications to
thrombolysis, interventional options include
• (i) thrombus fragmentation with pigtail or balloon
catheter,
• (ii) rheolytic thrombectomy with hydrodynamic catheter
devices,
• (iii) suction thrombectomy with aspiration catheters and
• (iv) rotational thrombectomy.

54. Techniques and devices for percutaneous catheter-
directed treatment of pulmonary embolism

56. Venous filters
• Venous filters are usually placed in the infrarenal
portion of the inferior vena cava (IVC).
• acute PE who have absolute contraindications to
anticoagulant drugs.
• Non-permanent IVC filters are classified as
temporary or retrievable devices.
• late complication rate of at least 10%; this
includes filter migration, tilting or deformation,
penetration of the cava wall by filter limbs,
fracturing of the filter and embolization of
fragments, and thrombosis of the device.

58. • Thank you