This document discusses pulmonary embolism (PE), including its risk factors, pathophysiology, diagnosis, and management. It notes that PE is a leading cause of cardiovascular death and hospital mortality. Rudolf Virchow identified three main factors that contribute to venous thrombosis and PE: venous stasis, hypercoagulability of blood, and endothelial injury. The pathophysiology of PE involves increased pulmonary vascular resistance and right heart strain or failure. Diagnosis involves assessing clinical risk factors, biomarkers like troponin and BNP, imaging tests like CTPA, and echocardiography. PE is classified as massive, submassive, or low-risk depending on the presence of hypotension and right heart dysfunction. Management involves he

1. PULMONARY EMBOLISM

2. • Pulmonary embolism is the third leading cause of cardiovascular death
• Most common preventable cause of death in hospitalized patients
• Daily concern in ICU patients, who typically have one or more risk factors for venous
thrombosis-the precursor of pulmonary embolism
• Thrombus , air, fat, infected clots, amniotic fluid, tumor, and inorganic substances
• VTE - most common pulmonary embolic condition encountered.
• Prevention of venous thrombosis is the single most important measure for prevention
of pulmonary embolism

3. RISK FACTORS

4. PATHOPHYSIOLOGY
Rudolf Virchow described 3 factors that are critically important in the development of
venous thrombosis:
• VENOUS STASIS
• HYPERCOAGULABILITY OF BLOOD
• ENDOTHELIAL DAMAGE

5. VENOUS STASIS/ABNORMAL BLOOD FLOW:
• Major factor in development of venous thrombi
• It allows platelets and leucocytes to come in contact with endothelium
• Stasis and turbulence promote endothelial cell activation and procoagulant activity
• Slows the wash out of activated clotting factors
ENDOTHELIAL INJURY:
• Trigger thrombosis by exposing VWF and tissue factor
• Endothelium becomes prothrombotic
• Caused by venous stasis, physical injury , infectious agents , inflammatory mediators ,
metabolic abnormalities , toxins
• Activated endothelial cells secrete plasminogen activator inhibitor which limit
fibrinolysis

6. HYPERCAOGULABILITY:
• Abnormally high tendency of blood to clot
• Caused by alterations in coagulation factors
Egs: APLA
Deficiencies of antithrombin
protein C, protein S
high levels of homocysteine

7. • Arterial hypoxemia
• Alveolar ventilation – perfusion mismatch
• Increased P (A-a )O2 gradient
• Alveolar dead space increases
• Increased pulmonary vascular resistance
• Impaired gas exchange
• Decreased pulmonary compliance
PULMONARY CONSEQUENCES

8. CARDIAC CONSEQUENCES
• Pulmonary artery obstruction
• Rise in pulmonary arterial pressure & Pulmonary vascular resistance
• RV wall tension increases  compress Rt coronary A. RV microinfarction 
release of troponin
• RV dilation & dysfunction
• Release of BNP – abnormal RV stretch
• Interventricular septum bulges into & compresses an intrinsically normal LV
• Diastolic LV dysfunction – impaired LV filling  fall in cardiac output

10. CLINICAL FEATURES

11. History
Age, cancer, heart and lung disease,
dyspnoea, shock, mental confusion
Physical examination
Heart rate
Elevated jugular venous pressure
Sao2
Respiratory rate
Hypotension
Sustained hypotension (or need for
inotropic/vasopressor support)
denotes high-risk PE
Laboratory testing
NT-BNP
Troponin
Serum lactate
Imaging
RV dilatation
RV dysfunction
RISK STRATIFICATION IN PE

12. REVISED GENEVA SCORE

13. MODIFIED WELLS SCORE

14. simplified Pulmonary Index Scoring System (sPESI)

15. The most commonly used schemes for the classification of PE severity are those
proposed by the American Heart Association (AHA) and the European Society of
Cardiology (ESC). These 2 schemes, which have much in common, divide PE severity
into 3 main categories.
Massive (AHA) or high risk (ESC):
• Hypotension, defined as a systolic blood pressure <90 mm Hg, a drop of >40 mm Hg
for at least 15 min or need for vasopressor support.
• have an average mortality of ≈30% within 1 month.
CLASSIFICATION

16. •Sub massive (AHA) or intermediate risk (ESC):
•The AHA criterion for sub massive PE is RV strain without hypotension.
• The ESC criteria for intermediate-risk PE are broader and include patients who have
a sPESI >1 regardless of whether there is RV strain.
• The ESC then subdivides intermediate-risk patients into 2 subgroups according to
whether patients have both RV dysfunction and RV injury (intermediate risk–high) or
only one or neither of these findings (intermediate risk–low).
•higher mortality rates in this population, with the range being 3% to 15% over a
period of 7 to 90 days.

17. •RV strain includes RV dysfunction on computed tomography pulmonary angiography or
echocardiography (RV/left ventricular [LV] ratio >0.9) or RV injury and pressure overload
detected by an increase in cardiac biomarkers such as troponins or brain natriuretic
hormone.
Low risk (ESC and AHA):
These patients do not meet criteria for submassive (AHA) or intermediate-risk (ESC) PE.
They account for 40% to 60% of hospitalized patients with PE and have an average
mortality of ≈1% within 1 month.

18. AHA Classification

19. DIAGNOSIS

20. • Rises in DVT or PE due to break down of fibrin by plasmin
• Sensitive , not specific
• High negative predictive value
• Levels rise in MI , pneumonia , sepsis , cancer , post operative state & 2nd or 3rd
trimester of pregnancy
D- DIMER
S. Troponin – RV microinfarction
NT –pro – BNP : myocardial stretch
CARDIAC BIOMARKERS

21. The S1Q3T3 sign (prominent S wave in lead I, Q wave and inverted T
wave in lead III)
• Sinus tachycardia
• S1Q3T3 sign – non specific, insensitive
• Features of RV strain- RBBB , T inversion in V1 to V4 – MC abnormality
ECG

22. COMPRESSION ULTRASONOGRAPHY
Acute DVT – loss of vein compressibility
98 to 100 % sensitivity & specificity for proximal DVT

23. • usually normal
• Focal oligemia –
Westermark sign
• Peripheral wedge
shaped density at
pleural base –
Hampton’s hump
• Enlarged Right
descending pulmonary
artery – Palla’s sign
CHEST XRAY

24. • RV dilatation and hypokinesis
• Mc Connell‘s sign – hypokinesis of RV free wall with normal or hyperkinetic motion
of the RV apex
• Ventricular septal flattening or deviation towards LV
• Paradoxical septal motion
• Mobile thrombi in Right heart chambers
ECHOCARDIOGRAPHY

25. CT PULMONARY ANGIOGRAPHY
• To visualize pulmonary artery
• Alternative diagnosis can be established
• Negative predictive value of 99%
• Highest sensitivity
• Shows filling defects

26. MANAGEMENT

29. If hypotension(+) , initially restore perfusion IV fluid resuscitation/
vasopressor support
Aggressive fluid administration can further worsen RV failure
ESC guidelines : norepinephrine in hypotensive patients

30. • Only recommended indication is massive PE – hemodynamically unstable patients
• Alteplase(tPA) 100 mg IV infused over 2 hours
• Continuous infusion of heparin used in conjunction
• For accelerated clot lysis : 0.6mg/kg infused over 15 min
• Current guidelines discourage thrombolytic therapy in intermediate risk PE
If patient deteriorates thrombolysis can be considered.
THROMBOLYTIC THERAPY

31. • Streptokinase 2.5L U IV loading dose followed by 1L U/hr for 24 hr
• Urokinase
• Watch for bleeding manifestations and monitor vitals during thrombolysis

32. Risk Factors for Bleeding and Contraindications to Use of Thrombolytic Therapy
Major contraindications
Structural intracranial disease
Previous ICH
Ischemic stroke within 3 mo
Active bleeding
Recent brain or spinal surgery
Recent head trauma with fracture or brain injury
Bleeding diathesis
Relative contraindications
Systolic blood pressure >180 mm Hg
Diastolic blood pressure >110 mm Hg
Recent bleeding (non intracranial)
Recent surgery
Recent invasive procedure
Ischemic stroke >3 mo previously
Anticoagulated (eg, VKA therapy)
Traumatic cardiopulmonary resuscitation
Pericarditis or pericardial fluid
Diabetic retinopathy
Pregnancy
Age >65 y and particularly >75 y
Low body weight (eg, <60 kg)
Female

33. • 5000 U bolus f/b 1000 U/h infusion) or adjusted doses using a weight-based nomogram
OR
Initial bolus 80 U/kg , followed by infusion rate of 18 U/kg /hour
• Target APTT is 1.5 to 2.5 times normal ( 46 to 70 sec )
UNFRACTIONATED HEPARIN

34. Fragments of UFH
Greater bioavailability
LMWH is equivalent to LDUH for most conditions
The incidence of heparin induced thrombocytopenia with LMWH is less than LDUH
Enoxaparin 1 mg/kg S/C BD
Reduce dose to 0.5 mg/kg if CrCl < 30 ml/min
LOW MOLECULAR WEIGHT HEPARIN

35. WARFARIN
• Started overlapping with heparin
• 5-10 mg daily with a target INR of 2-3
• When INR reaches therapeutic range; heparin can be discontinued

36. FONDAPARINUX
• Weight < 50kg – 5mg s/c once a day
• Weight 50 to 100 kg – 7.5 mg s/c OD
• Weight > 100 kg – 10 mg s/c OD

44. THROMBOPROPHYLAXIS
ENOXAPARIN(LMWH):
Usual dose – 40mg sc OD
Obesity – 0.5mg/kg sc OD (BMI>40)
Renal failure – 30mg OD
UNFRACTIONATED HEPARIN:
5000 units sc every 12 hrs
obesity – 5000 units sc every 8 hrs
MECHANICAL THROMBOPROPHYLAXIS
External compression of lower extremities can be used to promote venous outflow
from legs
Graded compression stockings/TED stockings
Intermittent pneumatic compression

45. THANK YOU