1. Pulmonary Embolism /Pulmonary hypertension
Khaled Al Oweidat, MD

2. PE Introduction Source of emboli Pathogenesis & Risk factors S&S
Management approach:
- Assess clinical probability
-Assess risk of mortality
-Investigation
* Diagnostic
*Non diagnostic ( helpful test)
-Treatment (medications and duration of treatment)

3. Introduction
Partial or complete occlusion of a pulmonary arterial branch by blood clot(thrombus or multiple thrombi).
Deep vein thrombosis and PE are different presentations of the same underlying pathophysiological event, venous thromboembolism (VTE).
The annual incidence rate of VTE ranges between 75 and 269
cases per 100,000 persons (North America ,Western Europe)

4. VTE is the third most common cardiovascular condition after ACS and stroke
lack of public awareness *(not like stroke and ACS)
PE is a major cause of death in the United States, with estimated annual incidence of VTE about one episode per 1000 patients.
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.

5. Source of emboli Thrombotic
Most cases (80–95 percent) as a result of thrombus originating in the lower extremity
Most thrombi originate in the deep veins of the calf and propagate proximally to the popliteal and femoral veins.
Calf-limited thrombi pose a minimal embolic risk
Emboli may also originate from upper-extremity thrombosis associated with central venous catheters or intravascular cardiac 2*devices, or may be associated with thoracic outlet obstruction or effort thrombosis

6. Non thrombotic

10. Once detached from their point of origin, emboli travel via the systemic venous system, through the right chambers of the heart, and eventually reach the pulmonary arterial system.
Physiologic effects and clinical consequences of pulmonary thromboembolism vary widely, ranging from asymptomatic disease to hemodynamic collapse and death

11. Major factors that determine the outcome include:
(1) size and location of emboli
(2) coexisting cardiopulmonary diseases
(3) secondary humoral mediator release and vascular hypoxic responses
(4) the rate of resolution of emboli.

12. Hemodynamic consequences

13. Gas exchange abnormality
Gas exchange abnormalities
Right to left shunt
Leads to…
Hypoxemia
Increased A–a gradient.
V/Q mismatch.
Increased dead space
Respiratory alkalosis from hyperventilation
Often a sign of increased dead space and impaired minute ventilation
may suggest massive PE
Gas exchange abnormality

14. S&S

16. Management approach Assess clinical probability
Assess risk of mortality
Investigation
Diagnostic
Non diagnostic ( helpful test)
Treatment (medications and duration of treatment)

19. Assess risk of mortality
High Risk:
- Hemodynamically Unstable with SBP<90 mmHg or drop in SBP>45mmHg IN 15 minutes.
- Early mortality is 15%.
Non High Risk ( According to RVD and Myocardial injury)
- Intermediate Risk
- Low Risk
Assess risk of mortality

25. Diagnostic investigation
D-dimer
- Non specific measure of fibrinolysis
High sensitivity (positive in presence of dx)
High negative predictive value (dx is absent when test is negative) in the outpatient setting
-Useful in outpatient setting/emergency room, not an inpatient test for ruling out PE

26. V/Q scan Currently reserved for Renal impairment IV contrast allergies
Pregnancy
Hospital resources

28. CT with PE protocol Spiral CT Larger dose of Contrast
Rapid rate of contrast
Effective dose at pulmonary CT angiography, without significant loss of objective or subjective image quality.

31. Electrocardiogram demonstrating findings consistent with embolism including sinus tachycardia, incomplete right bundle branch block, S1Q3T3 pattern, and inverted precordial T waves.(minority of patients)

32. Others CXR: Most patients with pulmonary embolism have abnormal
but nonspecific chest radiographic findings
Echocardiogram:
Suspected massive pulmonary embolism who are too ill for transportation or
have an absolute contraindication to the administration of a contrast agent.
Troponin :
Increase in right heart strain .

33. Treatment
New oral anticoagulants(NOACs) were recommended in the 2014 ESC Guidelines as an alternative to the standard heparin/VKA(warfarian) treatment.
But on most recent 2016 ATS guidelines NOACs become the recommended treatment and alternative is VKAs.

35. CKD with Ccl less than 30 ml/min (apixaban & edoxaban can be used Ccl bet ml/min with reduced dose )
Moderate to severe hepatic impairment
Pregnancy and lactation:
Still the use of LMWH is the standard of care in pregnant lady and VKAs can be used in lactating women
PE with cancer :
LMWH
Antiphospholipid syndrome :
not proved yet
NOACs are not used

36. Duration of treatment

38. Pulmonary hypertension

42. Evaluation of patients with pulmonary hypertension

45. Thank you