Acute pulmonary embolism is a form of venous thromboembolism that occurs when a blood clot breaks off and lodges in the pulmonary arteries of the lungs. The clinical presentation of PE can be variable and non-specific, making diagnosis challenging. It is important to efficiently evaluate patients suspected of having a PE to diagnose and treat it quickly in order to reduce morbidity and mortality. Treatment involves hemodynamic and respiratory support, initial anticoagulation with drugs like heparin, and potentially reperfusion therapies for more severe cases including thrombolysis or embolectomy.

1. Acute Pulmonary
Embolism

2. INTRODUCTION
ACUTE PULMONARY EMBOLISM (PE) IS A FORM OF VENOUS
THROMBOEMBOLISM (VTE) THAT IS COMMON AND SOMETIMES
FATAL. THE CLINICAL PRESENTATION OF PE IS VARIABLE AND
OFTEN NONSPECIFIC MAKING THE DIAGNOSIS CHALLENGING. THE
EVALUATION OF PATIENTS WITH SUSPECTED PE SHOULD BE
EFFICIENT SO THAT PATIENTS CAN BE DIAGNOSED AND THERAPY
ADMINISTERED QUICKLY TO REDUCE THE ASSOCIATED MORBIDITY
AND MORTALITY.

3. INTRODUCTION
• Definition — Pulmonary embolus (PE) refers to
obstruction of the pulmonary artery or one of its
branches by material (eg, thrombus, tumor, air, or
fat) that originated elsewhere in the body. This
topic review focuses upon PE due to thrombus.
• PE most commonly results from deep vein
thrombosis (a blood clot in the deep veins of the
legs or pelvis) that breaks off and migrates to the
lung, a process termed venous thromboembolism
(VTE).

4. Why is it important?
 PE is the most common preventable cause of death in
hospitalized patients
 Untreated mortality - 30%
 80% of pulmonary emboli occur without prior
warning signs or symptoms
 Diagnosis can be difficult
 Early treatment is highly effective

5. PATHOGENESIS: THE PATHOGENESIS OF PULMONARY EMBOLISM
(PE) IS SIMILAR TO THAT WHICH UNDERLIES THE GENERATION OF
THROMBUS (IE, VIRCHOW'S TRIAD). VIRCHOW'S TRIAD CONSISTS OF
VENOUS STASIS, ENDOTHELIAL INJURY, AND A HYPERCOAGULABLE
STATE

6. Stasis
 Immobility/cast/travel
 Advanced age
 Acute medical illness
 Major surgery
 Spinal cord injury
 Obesity
Endothelial
• Damage
• Major surgery
• Trauma
• Central venous
• Catheterization
Hypercoagulability
Hereditary Deficiencies:
• Antithrombin deficiency
• Protein C deficiency
• Protein S deficiency
• Factor V Leiden
• Prothrombin gene mutation
Dysfibrinogenemia
Acquired:
• Cancer
• Pregnancy & postpartum
period
• Oral contraceptives
• Hormone replacement
therapy
• Polycythemia rubravera
• Smoking
• Anti phospholipid syndrome
• Chemotherapy

7. PREDISPOSING FACTORS
Threre is an extensive collection of predisposing environmental and genetic
factors for VTE
Strong risk factors Moderate risk factors Weak risk factors
•Fracture of lower limb
•Hospitalization for heart
failure or atrial
fibrillation/flutter (within
previous 3 months)
•Hip or knee replacement
•Major trauma
•Myocardial infarction
(within previous 3
months)
•Previous VTE
•Spinal cord injury
•Arthroscopic knee surgery
•Autoimmune diseases
•Blood transfusion
•Central venous lines
•Intravenous catheters and
leads
•Chemotherapy
•Congestive heart failure or
respiratory failure
•Erythropoiesis-stimulating
agents
•Hormone replacement
therapy (depends on
formulation)
•In vitro fertilization
•Oral contraceptive therapy
•Bed rest >3 days
•Diabetes mellitus
•Arterial hypertension
•Immobility due to sitting
(e.g. prolonged car or air
travel)
•Increasing age
•Laparoscopic surgery
(e.g. cholecystectomy)
•Obesity
•Pregnancy
•Varicose veins
Predisposing factors for venous thromboembolism

8. Pathophysiology
The pathophysiology of pulmonary embolism: Although pulmonary embolism
can arise from anywhere in the body, most commonly it arises from the calf
veins. The venous thrombi predominately originate in venous valve pockets
(inset) and at other sites of presumed venous stasis. To reach the lungs,
thromboemboli travel through the right side of the heart.

9. Pathophysiology

10. THE TEMPORAL PATTERN OF PRESENTATION (ACUTE,
SUBACUTE, OR CHRONIC) – PATIENTS WITH PE CAN
PRESENT ACUTELY, SUBACUTELY, OR CHRONICALLY:
• ACUTE – PATIENTS WITH ACUTE PE TYPICALLY
DEVELOP SYMPTOMS AND SIGNS IMMEDIATELY AFTER
OBSTRUCTION OF PULMONARY VESSELS.
• SUBACUTE – SOME PATIENTS WITH PE MAY ALSO
PRESENT SUBACUTELY WITHIN DAYS OR WEEKS
FOLLOWING THE INITIAL EVENT.
• CHRONIC – PATIENTS WITH CHRONIC PE SLOWLY
DEVELOP SYMPTOMS OF PULMONARY HYPERTENSION
OVER MANY YEARS (IE, CHRONIC THROMBOEMBOLIC
PULMONARY HYPERTENSION; CTEPH).
CLASSIFICATION OF PULMONARY EMBOLISM

11. THE PRESENCE OR ABSENCE OF HEMODYNAMIC STABILITY
(HEMODYNAMICALLY UNSTABLE OR STABLE)
• HEMODYNAMICALLY UNSTABLE PE IS ALSO CALLED "MASSIVE" OR
"HIGH-RISK" PE.
• HEMODYNAMICALLY STABLE PE IS CALLED
"SUBMASSIVE" OR "INTERMEDIATE-RISK" PE IF THERE IS
ASSOCIATED RIGHT VENTRICULAR STRAIN
• "LOW-RISK" PE IF THERE IS NO EVIDENCE OF RIGHT VENTRICULAR
STRAIN.
CLASSIFICATION OF PULMONARY EMBOLISM

12. Hemodynamically stable and unstable PE are defined as the following:
 Hemodynamically unstable PE is that which results in hypotension.
Hypotension is defined as a systolic blood pressure <90 mmHg or a
drop in systolic blood pressure of ≥40 mmHg from baseline for a
period >15 minutes or hypotension that requires vasopressors or
inotropic support and is not explained by other causes such as
sepsis, arrhythmia, left ventricular dysfunction from acute
myocardial ischemia or infarction, or hypovolemia.
 Although hemodynamically unstable PE is often caused by large
(ie, massive) PE, it can sometimes be due to small PE in patients
with underlying cardiopulmonary disease. Thus, the term "massive"
PE does not necessarily describe the size of the PE as much as its
hemodynamic effect.
CLASSIFICATION OF PULMONARY EMBOLISM

13. • HEMODYNAMICALLY STABLE PE IS DEFINED AS PE THAT
DOES NOT MEET THE DEFINITION OF HEMODYNAMICALLY
UNSTABLE PE. THERE IS A SPECTRUM OF SEVERITY WITHIN
THIS POPULATION RANGING FROM PATIENTS WHO
PRESENT WITH SMALL, MILDLY SYMPTOMATIC OR
ASYMPTOMATIC PE (ALSO KNOWN AS "LOW-RISK PE") TO
THOSE WHO PRESENT WITH MILD OR BORDERLINE
HYPOTENSION THAT STABILIZES IN RESPONSE TO FLUID
THERAPY, OR THOSE WHO PRESENT WITH RIGHT
VENTRICLE DYSFUNCTION (ALSO KNOWN AS "SUBMASSIVE"
OR "INTERMEDIATE-RISK" PE).
CLASSIFICATION OF PULMONARY EMBOLISM

14. Diagnosis

15. • PULMONARY EMBOLISM (PE) HAS A WIDE VARIETY OF PRESENTING
FEATURES, RANGING FROM NO SYMPTOMS TO SHOCK OR SUDDEN
DEATH. THE MOST COMMON PRESENTING SYMPTOM IS DYSPNEA
FOLLOWED BY CHEST PAIN (CLASSICALLY PLEURITIC IN NATURE),
COUGH, AND SYMPTOMS OF DEEP VENOUS THROMBOSIS.
• HEMOPTYSIS IS AN UNUSUAL PRESENTING SYMPTOM.
• RARELY DO PATIENTS PRESENT WITH SHOCK, ARRHYTHMIA, OR
SYNCOPE.
• MANY PATIENTS, INCLUDING SOME WITH LARGE PE, ARE ASYMPTOMATIC
OR HAVE MILD OR NONSPECIFIC SYMPTOMS. THUS, IT IS CRITICAL THAT
A HIGH LEVEL OF SUSPICION BE MAINTAINED SUCH THAT CLINICALLY
RELEVANT CASES ARE NOT MISSED. THE SIGNS AND SYMPTOMS OF PE
ARE DISCUSSED IN DETAIL SEPARATELY.
Clinical presentation

16. Symptom Frequency
Dyspnea 73 percent
Pleuritic chest pain 66 percent
Cough 37 percent
Hemoptysis 13 percent
Sign
Tachypnea 70 percent
Rales 51 percent
Tachycardia 30 percent
Fourth heart sound 24 percent
Accentuated pulmonic component
second heart sound
23 percent
Circulatory collapse 8 percent
Clinical presentation

17. Assessment of clinical (pre-test) probability
Of these, the most frequently used prediction rules are
the revised Geneva rule (Table 5) and the Wells rule.
Both prediction rules have been simplified in an attempt
to increase their adoption into clinical practice; the
simplified versions have been externally validated.

18. The revised Geneva clinical
prediction rule for
pulmonary embolism

19. The Wells clinical prediction rule for pulmonary embolism

20. Laboratory tests and
biomarkers
 D-dimer testing
 White blood cell count
 Arterial blood gases
 Markers of myocardial injury - serum troponin
 Markers of right ventricular dysfunction - brain
natriuretic peptide

21. D-Dimer
 Fibrin degradation product.
 Non specific (~40%): cancer, sepsis, severe infection or inflammation
disease increase D-dimer levels.
Negative D dimer with Low clinical Probability is sufficient to exclude PE :
92% sensitive.
Raised D- dimer does not imply VTE ( negative predictive value )
D dimer should not be done if clinical probability is high
Laboratory tests and
biomarkers

22.  Markers of right ventricular dysfunction
In normotensive patients with PE, the positive predictive value of elevated
BNP or NT-proBNP concentrations for early mortality is low.
Haemodynamically stable patients with low NT-proBNP levels may be
candidates for early discharge and outpatient treatment
 Markers of myocardial injury
Elevated plasma troponin concentrations on admission have been reported
in connection with PE and were associated with worse prognosis (troponin
T concentrations >14pg/mL). Elevated serum creatinine levels and a
decreased (calculated) glomerular filtration rate are related to 30-day-all-
cause mortality in acute PE.
Laboratory tests and biomarkers

23. Imaging studies that aid in the
diagnosis of pulmonary
embolism

24. Chest radiograph
 Nonspecific abnormalities on chest radiography are
common (eg, atelectasis, effusion) in PE, but a normal
chest radiograph can be seen in 12 to 22 percent of
patients.
 A Hampton's hump and Westermark's sign are rare
but, when present, should raise the suspicion for PE

25. Hampton's hump
 Hampton's hump is a shallow, hump-shaped opacity in the periphery of
the lung, with its base against the pleural surface and hump towards the
hilum

26. Westermark's sign
The sign results from a combination of:
 The dilation of the pulmonary arteries proximal to the embolus and
 The collapse of the distal vasculature creating the appearance of a
sharp cut off on chest radiography.
Has a low sensitivity (11%) and
high specificity (92%) for the
diagnosis of pulmonary embolism.

27. Computed tomographic pulmonary angiography
 Sensitivity of 83% and a specificity of
96% for CTPA in PE diagnosis.
 In patients with a low or intermediate
clinical probability of PE, a negative
CTPA had a high negative predictive
value for PE (96 and 89%,
respectively). But its negative
predictive value was only 60% if the
pre-test probability was high.
 Conversely, the positive predictive
value of a positive CTPA was high (92-
96%) in patients with an intermediate
or high clinical probability, but much
lower (58%) in patients with a low pre-
test likelihood of PE.

28. Lung scintigraphy
With multiple tracers such as xenon-133 gas, Tc-
99m-labelled aerosols, or Tc-99m-labelled
carbon microparticles
The high-probability criteria are as follows:
 Two large (>75% of a segment) segmental
perfusion defects without corresponding
ventilation or chest radiographic abnormalities
 One large segmental perfusion defect and 2
moderate (25-75% of a segment) segmental
perfusion defects without corresponding
ventilation or radiographic abnormalities
 Four moderate segmental perfusion defects
without corresponding ventilation or chest
radiographic abnormalities

29. Pulmonary angiography
 For several decades, pulmonary angiography was the ‘gold standard’
for the diagnosis or exclusion of acute PE, but it is now rarely
performed as less-invasive CTPA offers similar diagnostic accuracy.
 The diagnosis of acute PE is based on direct evidence of a thrombus
in two projections, either as a filling defect or as amputation of a
pulmonary arterial branch.

30. Magnetic resonance
angiography
 А large pulmonary
embolus in the left
main branch of the
pulmonary artery

31. Echocardiography

32. PULMONARY EMBOLISM: ECG

33. PULMONARY EMBOLISM: differential
diagnoses

34. Diagnostic strategies

36. Treatment
TREATMENT IN THE ACUTE PHASE
1. HAEMODYNAMIC AND RESPIRATORY SUPPORT:
• OXYGEN THERAPY AND VENTILATION.
• PHARMACOLOGICAL TREATMENT OF ACUTE RIGHT VENTRICULAR FAILURE
• MECHANICAL CIRCULATORY SUPPORT AND OXYGENATION
2. INITIAL ANTICOAGULATION
• PARENTERAL ANTICOAGULATION
• NON-VITAMIN K ANTAGONIST ORAL ANTICOAGULANTS
• VITAMIN K ANTAGONISTS
3. REPERFUSION TREATMENT
• SYSTEMIC THROMBOLYSIS
• PERCUTANEOUS CATHETER-DIRECTED TREATMENT
• SURGICAL EMBOLECTOMY

37. Treatment in the acute phase
Haemodynamic and respiratory support:
 Hypoxaemia is one of the features of severe PE, and is mostly due to
the mismatch between ventilation and perfusion. Administration of
supplemental oxygen is indicated in patients with PE and SaO2 <90%.
 Further oxygenation techniques should also be considered, including
high-flow oxygen (i.e. a high-flow nasal cannula) and mechanical
ventilation (non-invasive or invasive) in cases of extreme instability
(i.e. cardiac arrest)

38. Pharmacological treatment of acute right
ventricular failure

39. Mechanical circulatory support and
oxygenation
 The temporary use of mechanical cardiopulmonary
support, mostly with veno–arterial extracorporeal
membrane oxygenation (ECMO), may be helpful in
patients with high-risk PE, and circulatory collapse or
cardiac arrest

40. Parenteral anticoagulation
 In patients with high or intermediate clinical probability of PE,
anticoagulation should be initiated while awaiting the results of
diagnostic tests.

41. Vitamin K antagonists
 When VKAs are used, anticoagulation with UFH, LMWH, or
fondaparinux should be continued in parallel with the oral
anticoagulant for ≥5 days and until the international normalized ratio
(INR) value has been 2.0–3.0 for 2 consecutive days.

42. Systemic thrombolysis
 Accelerated i.v. administration of recombinant tissue-type plasminogen
activator (rtPA; 100 mg over 2 h) is preferable to prolonged infusions of
first-generation thrombolytic agents (streptokinase and urokinase).

43. Systemic thrombolysis

44. Percutaneous catheter-directed treatment
 For patients contraindications with to absolute thrombolysis
Surgical embolectomy
• Aortic cross-clamping and cardioplegic
cardiac arrest should be avoided.
• With bilateral PA incisions, clots can be
removed from both pulmonary arteries down
to the segmental level under direct vision.

45. Recommendations for
acute-phase treatment
of high-risk
pulmonary embolism

46. Recommendations for
acute-phase treatment
of intermediate- or
low-risk pulmonary
embolism

47. Chronic treatment and
prevention of recurrence
• THE AIM OF ANTICOAGULATION AFTER ACUTE PE IS TO
COMPLETE THE TREATMENT OF THE ACUTE EPISODE AND
PREVENT RECURRENCE OF VTE OVER THE LONG-TERM.
• ORAL ANTICOAGULANTS ARE HIGHLY EFFECTIVE IN
PREVENTING RECURRENT VTE DURING TREATMENT, BUT
THEY DO NOT ELIMINATE THE RISK OF SUBSEQUENT
RECURRENCE AFTER THE DISCONTINUATION OF TREATMENT.

49. References:
1. Harrison's Manual of Medicine
2. Bates' Guide to Physical Examination and History Taking:
https://booksdoctor.blogspot.com/2019/12/bates-guide-to-physical-
examination-and-history-taking-pdf-download.html
3. Davidson's Principles And Practics Of Medicine:
https://www.elsevier.com/books/davidsons-principles-and-practice-of-
medicine/ralston/978-0-7020-7028-0
4. Treatment, prognosis, and follow-up of acute pulmonary embolism in
adults: https://www.uptodate.com/contents/treatment-prognosis-and-
follow-up-of-acute-pulmonary-embolism-in-adults