A pulmonary embolism occurs when a blood clot forms in the deep veins of the legs or pelvis and travels through the bloodstream, lodging in the pulmonary arteries of the lungs. It can be difficult to diagnose and is a potentially life-threatening condition. Diagnostic tests may include a d-dimer blood test, CT scan, ventilation-perfusion scan, echocardiogram, and angiogram. Treatment involves anticoagulation medications to prevent further clotting and thrombolysis in some severe cases. Prevention by minimizing risk factors for deep vein thrombosis is important.

1. Pulmonary
Embolism

2.  Pulmonary embolism facts
 What is a pulmonary embolism?
 What are the causes and risk factors for pulmonary embolism?
 What are the signs and symptoms of pulmonary embolism?
 How is pulmonary embolism diagnosed?
 History and physical examination
 Basic testing (CBC, electrolytes, BUN, creatinine blood test,
chest x-ray, EKG)
 Pulmonary angiogram
 d-Dimer blood test
 CT Scan
 Ventilation-perfusion scans
 Venous Doppler study
 Echocardiography (EKG, ECG)
 What is the treatment for pulmonary embolism?
 Anticoagulation
 Thrombolytic therapy
 What is the prognosis for pulmonary embolism?

3. Pulmonary embolism facts
 Pulmonary embolism is a diagnosis that should
be considered in patients with chest
pain and/orshortness of breath, and is one of the
causes of sudden death.
 The diagnosis of pulmonary embolism may be
difficult to make, and is often missed. Diagnostic
strategies need to be individualized to each
patient and situation.

4.  Anticoagulation is the treatment of choice for
pulmonary embolism and the patient may be
required to continue treatment for months.
 Prevention is the best treatment for pulmonary
embolism, which can be accomplished by minimizing
the risk factors for deep vein thrombosis (DVT).

5. What is a pulmonary
embolism?
The lungs are primarily responsible for the
exchange of oxygen and carbon dioxide between
the air we breathe and blood.
If a blood clot (thrombus) forms in the one of the body's
veins (deep vein thrombosis or DVT), it has the
potential to break off and enter the circulatory system
and travel (or embolize) through the heart and
become lodged in the one of the branches of the
pulmonary artery of the lung.

6. A pulmonary embolus clogs the artery that provides
blood supply to part of the lung. The embolus not
only prevents the exchange of oxygen and carbon
dioxide, but it also decreases blood supply to the
lung tissue itself, potentially causing lung tissue to
die (infarct).
A pulmonary embolus is one of the life-threatening
causes of chest pain and should always be
considered when a patient presents to a healthcare
provider with complaints of chest pain and shortness
of breath.

7.  There are special types of pulmonary embolus that
are not due to blood clots, but instead are due to
other body materials.
These are rare occurrences and include:
 fat emboli from a broken femur,
 an amniotic fluid embolus in pregnancy, and
 in some cases, tumor tissue from cancer.
The signs and symptoms are the same as that of a
blood clot, and is caused by blockage of part of the
arterial tree of the lung, and prevents the bloods
ability to reach all parts of the lung tissue.

8. Picture of a blood clot is formed

9. What are the causes and risk
factors for pulmonary embolism?
Pulmonary embolus is the end result of a deep vein
thrombosis or blood clot elsewhere in the body.
Most commonly, the DVT begins in the leg, but they
also can occur in veins within the abdominal
cavity or in the arms.
The risk factors for a pulmonary embolism are the
same as the risk factors for deep vein thrombosis.

10. These are referred to as Virchow's triad and include:
 prolonged immobilization or alterations in normal
blood flow (stasis)
 increased clotting potential of the blood
(hypercoagulability)
 any damage to the walls of the veins.

11. Examples of these include the
following:
Prolonged immobilization
 Extended travel (sitting in a car, airplane, train,
etc.)
 Hospitalization or prolonged bed rest

12. Increased blood clotting
potential
 Medications: birth control pills, estrogen
 Smoking
 Genetic predisposition most commonly, Factor V
Leiden deficiency, Protein C or Protein S
deficiencies or anitithrobin III deficiency
 Polycythemia
 Cancer
 Pregnancy, including 6-8 weeks after delivery
 Surgery

13. Damage to vessel wall
 Prior deep venous thrombosis
 Trauma to the lower leg with or without surgery or
casting

14. Major acquired risk factors for
venous thromboembolism:
1- advancing age.
2- arterial disease including carotid & coronary disease.
3- obesity.
4- cigarette smoking.
5- C. O. P. D.
6- personal or family H.O. VTE
7- recent surgery, trauma, or immobility including stroke.
8- acute infection.
9- long-haul air travel.
10- cancer & cancer chemo therapy.
11- pregnancy, oral contraceptive pills, or H.R.T.
12- pace maker, implantable cardiac defibril. leads or indwelling
central venous catheters .

15. Major thrombophilias associated with
VTE:
i. Inherited:
- Factor V-leiden resulting in activated protein C
resistance.
- Prothrombin gene mutation 20210.
- Anti thrombin III deficiency.
- Protein C deficiency.
- Protein S deficiency.

16. ii. Acquired:
- Anti phospholipid anti-body syndrome.
- Hyperhomocysteinemia.

17. What are the signs and symptoms
of pulmonary embolism?
A pulmonary embolus may present with the sudden
onset of chest pain and shortness of breath.
The pain is classically sharp and worsens when
taking a deep breath, often called pleuritic pain
or pleurisy.
There may be cough that produces bloody sputum.

18. The patient may have stable vital signs (blood
pressure, heart rate, respiratory rate, and oxygen
saturation) but frequently presents with an elevated
heart rate.
If the blood clot is large enough, it can block blood
from leaving the right side of the heart thus
preventing blood from entering the lungs.
There is then no blood entering the left side of the
heart to pump to the rest of the body.
This can result in circulatory collapse (shock) and
death.

19. Often referred to as saddle embolus (named such as it
sits in the division between the left and right
pulmonary artery like a saddle).
Depending on the amount of blood clot (clot burden or
clot load), oxygen saturation can be variably affected
as can the blood pressure and heart rate.
Classic signs are such that the heart rate and
respiratory rate are elevated as the body tries to
compensate for less oxygen transfer capabilities in
the lung.

20. Oxygen saturation may be decreased.
Oxygen saturation in a healthy individual approaches
100% at sea level.
The patient may be cyanotic , lightheaded, and weak.
In some cases, pulmonary embolus will present with
sudden death.

21. Most common symptoms or signs of
P.E. :
Symptoms:
- Un explained dyspnea.
- Chest pain, either pleuritic or atypical.
Signs:
- Tachypnea.
- TachyCardia.
- Low-grade fever.
- Tri cuspid reg. murmur.
-Accentuated P2.

22. How is pulmonary embolism
diagnosed?
History and physical examination
There always needs to be a high a level of
suspicion that a pulmonary embolus may be the
cause of chest pain or shortness of breath.
The health care professional will take a history of
the chest pain, including its characteristics, its
onset, and any associated symptoms that may
direct the diagnosis to pulmonary embolism.
It may include asking about risk factors for deep
vein thrombosis.

23. Coughing up blood sputum may be a sign of
pulmonary embolism.
Physical examination will concentrate initially on the
heart and lungs, since chest pain and shortness of
breath may also be the presenting complaints
for heart attack,
pneumonia, pneumothorax (collapsed lung),
dissection of an aortic aneurysm, among others.

24. With pulmonary embolism, the chest examination is
often normal, but if there is some associated
inflammation on the surface of the lung , a rub may
be heard.
The surfaces of the lung and the inside of the chest
wall are covered by a membrane (the pleura) that is
full of nerve endings.
When the pleura becomes inflamed, as can occur in
pulmonary embolus, a sharp pain can result that is
worsened by breathing, so-called pleurisy or pleuritic
chest pain.

25. The physical examination may
include examining an
extremity, looking for signs
of a DVT, including warmth,
redness, tenderness, and
swelling.
It is important to note,
however, that the signs
associated with deep vein
thrombosis may be
completely absent even in
the presence of a clot.
Again, risk factors for
clotting must be taken into
consideration when making

26. Clinical decision rule:
> 4 score points = high probability
=/< 4 score points = non high probability
3DVT symptoms or signs
3An alternative diagnosis is
less likely P.E.
1.5HR > 100/min
1.5Immobilization or surgery
within 4 weeks
1Hemoptysis
1Cancer treated within 6/12 or
metastatic

27. D. D. of P.E.
1- anxiety, pleurisy, costochondritis.
2- Pneumonia, bronchitis.
3- MI.
4- Pericarditis.
5- Congestive Heart failure.
6- Idiopathic pulm. HTN.

28. Basic testing
Basic testing may include:
 CBC (complete blood count)
 Electrolytes,
 BUN (blood urea nitrogen),
 Creatinine blood test,
 Chest X-ray, and
 Electrocardiogram (EKG or ECG).

29. * Normal values of the alveolar-arterial Oxygen
grdient did not rule out the diagnosis of acute P.E.
So A.B.G. determination shouldn’t be part of the
routine diagnostic strategy.

30. The chest X-ray is often normal in
pulmonary embolism.
A Hampton hump in a person with a right lower
lobe pulmonary embolism

31. * A near-normal CXR in the setting of severe
respiratory compromise
is highly suggestive of massive P.E.
* CXR may show:-
focal oligmia (wester mark sign)
A peripheral wedge shaped density above the
diaphragm (Hampton hump) -> indicate pulm.
infarction

32. If there is significant
blockage in a
pulmonary artery, it
acts like a dam and
it is harder for the
right side of the
heart to push blood
past the
obstructing clot or
clots.
The EKG may be usually normal, but may demonstrate a
rapid heart rate, a sinus tachycardia (heart rate > 100
bpm).
The EKG can demonstrate a right heart strain.

33. Since the cost of missing the diagnosis of
pulmonary embolus can be death, the
health care professional has to consider the
diagnosis when caring for a patient
complaining of chest pain or shortness of
breath.

34. Pulmonary angiogram
In the past, the gold
standard for the
diagnosis of pulmonary
embolus is a
pulmonary angiogram.
Dye is injected and a clot
or clots can be
identified on imaging
studies.
This is considered an
invasive test and is

35. Pulm. Angio is required when:-
1- intervention are planned such as suction catheter
embolectomy.
2- mechanical clot fragmentation.
3- catheter directed thrombolysis.

36. d-Dimer blood test
If the healthcare provider's suspicion for pulmonary
embolism is low, a d-Dimer blood test can be used.
The d-Dimer blood test measures one of the
breakdown products of a blood clot.
If this test is normal, then the likelihood of a pulmonary
embolism is very low. Unfortunately, this test is not
specific for blood clots in the lung.
It can be positive for a variety of reasons including
pregnancy, injury, recent surgery, or infection. D-
dimer is not helpful if the potential risk for a blood
clot is high.

37. CT scan
If there is greater suspicion,
then computerized
tomography (CT scan) of
the chest with
angiography can be
done.
Contrast dye is injected into
an intravenous line in the
arm while the CT is being
taken, and the pulmonary
arteries can be
visualized.

38. There are some limitations of the test, especially if a
pulmonary embolism involves the smaller arteries in
the lung. However similar problems are seen with
the more invasive pulmonary angiogram.
As CT scan has become more and more sophisticated,
not identifying significant emboli is unusual.
There are risks with this test since some patients are
allergic to the dye, and the contrast dye can be
harsh on kidney function.

39. It may be wise to limit the patient's exposure to
radiation, especially in pregnant patients.
However, since pulmonary embolus can be fatal,
even in pregnancy this test can be performed,
preferably after the first trimester.
* CT scan can be used as a “one-stop shop” for
diagnosis or detection of source of thrombus &
prognosis.

40. Ventilation-perfusion scans
Ventilation-perfusion scans (VQ scans) use labeled
chemicals to identify inhaled air into the lungs and
match it with blood flow in the arteries.
If a mismatch occurs, meaning that there is lung tissue
that has good air entry but no blood flow, it may be
indicative of a pulmonary embolus.
These tests are read by a radiologist as having a low,
moderate, or high probability of having a pulmonary
embolism.
There are limitations to the test, since there may be a
5%-10% risk that a pulmonary embolism exists even
with a low probability V/Q result.

41. Venous Doppler study
Ultrasound of the legs, also known as venous
Doppler studies, may be used to look for blood
clots in the legs of a patient suspected of having
a pulmonary embolus.
If a deep vein thrombosis exists, it can be inferred
that chest pain and shortness of breath may be
due to a pulmonary embolism.
The treatment for deep vein thrombosis and
pulmonary embolus is generally the same.
The primary diagnostic criterion for DVT is loss of
vein compressibility.

42. Echocardiography (EKG, ECG)
Echocardiography or ultrasound of the heart may be
helpful if it shows that there is strain on the right side of
the heart.
RV enlargement or H.K. especially free wall H.K. must
sparing of the apex (the MC cannel sign)

43. If non-invasive tests are negative and the
healthcare provider still has significant concerns,
then the healthcare provider and the patient need
to discuss the benefits and risks of treatment
versus invasive testing like angiography.

44. Risk stratification:
* Clinical prediction of increased mortality:
1- S.B.P. =/< 100 mmHg
2- Age > 70 years
3- H.R. > 100 beat/min
4- C.H.F.
5- Ch. Lung disease
6- Cancer
* Cardiac biomarkers & imaging prediction of increased
mortality:
1- Elevated troponin I or T.
2- Elevated BNP or pre BNP.
3- R.V. - H.K. on Echo.
4- R.V. enlargement on chest C.T.

45. What is the treatment for
pulmonary embolism?
The best treatment for a pulmonary embolus is
prevention.
Minimizing the risk of deep vein thrombosis is key in
preventing a potentially fatal illness.
The initial decision is whether the patient requires
hospitalization.
Recent studies suggest that those patients with a small
pulmonary embolus, who are hemodynamically stable
(normal vital signs) may be treated at home with close
outpatient care.

46. Anticoagulation
The first step in stable patients with pulmonary embolism
is anticoagulation.
This is a two step process. Warfarin (Coumadin) is the
drug of choice for anti-coagulation.
It is taken by mouth beginning immediately upon the
diagnosis of pulmonary embolism, but may take up to
week for the blood to be appropriately thinned or
anticoagulated.
As an immediate solution and as a bridge until the
Coumadin becomes effective, low molecular weight
heparin (enoxaparin(Lovenox) or pentasaccharide
(Fondaparinux, Arixtra) is administered at the same
time.It thins the blood via a different mechanism.

47. For those patients who have contraindications to the
use of enoxaparin (Lovenox) (for example, kidney
failure does not allow the drug to be metabolized),
intravenous heparin can be used as the first step.
This requires admission to the hospital and careful
patient monitoring with blood tests.

48. Anticoagulation is usually suggested for a minimum of six
months, but each patient will have their treatment
regimen individualized.
The blood test utilized to monitor warfarin therapy is
referred to as the INR or international normalized ratio.
This test can be performed by finger stick or venous stick
depending on the laboratory procedures.
Essentially, this ratio is determined by measuring the
patients prothrombin time.
This value is divided by the lab standard normal value.
For patients with a pulmonary embolism, the warfarin
dosing will be titrated so that the INR value will be 2.0 –
3.0, basically the blood needs to be 2 to 3 times thinner
than the normal value.
It is very helpful for the patient to participate in their health
management by keeping a diary of their warfarin dose,
the date of testing, and their INR values.

49. Intravenous unfractionated Heparin
“Raschke Nomogram”
ActionVariable
80 U/kg bolus, then 18 U/kg/hrInitial heparin polus
80 U/kg bolus, then increase by 4
U/kg/hr
aPTT < 35 second (<1.2 * control)
40 U/kg bolus, then increase by 2
U/kg/hr
aPTT 35 to 45 second (1.2 to 1.5 *
control)
No changeaPTT 46 to 70 second (1.5 to 2.3 *
control)
Decrease infusion rate by 2 U/kg/hraPTT 71 to 90 second (2.3 to 3 *
control)
Hold infusion 1 hr, then decrease
infusion rate by 3 U/kg/hr
aPTT > 90 second ( >3 * control)

50. Fondaparinux dosing for patients
with Acute P.E. or DVT
>100 kg50 – 100 kg< 50 kgPatient
weight
10 mg7.5 mg5 mgDaily dose
of
Fondaparinu
x

51. Thrombolytic therapy
Pulmonary embolism can be fatal, especially if
involves a large amount of clot.
When the patient is unconscious, has low or no blood
pressure or are not breathing, clot busting or
thrombolytic therapy using medications like TPA
(tissue plasminogen activator) may be considered.
It is also often considered when signs of right heart
strain are present.
In certain centers, a special procedure can be
performed where is catherter is placed in the right
side of the heart and the clot is essentially vacuumed
out.

52. Inferior vena cava filter
Used inferior vena cava filter.
If anticoagulant therapy is contraindicated and/or
ineffective, or to prevent new emboli from
entering the pulmonary artery and combining with
an existing blockage, an inferior vena cava
filter may be implanted

53. Surgery
Surgical management of acute pulmonary
embolism (pulmonary thrombectomy) is
uncommon and has largely been abandoned
because of poor long-term outcomes. However,
recently, it came back again with the revision of
the surgical technique and is thought to benefit
certain people. Chronic pulmonary embolism
leading to pulmonary hypertension (known
as chronic thromboembolic hypertension) is
treated with a surgical procedure known as
a pulmonary thromboendarterectomy.

54. Optimal Duration of Anticoagulation
RecommendationClinical setting
6 moFirst provoked PE/proximal
leg DVT
3 moFirst provoked upper
extremity DVT or isolated
calf DVT
12 mo or indefinite durationSecond provoked VTE
Indefinite durationThird VTE
6 mo or indefinite durationCancer

55. What is the prognosis for
pulmonary embolism?
Patient survival depends upon:
 the underlying health of the patient,
 size of the pulmonary embolus,
 the cause of the pulmonary embolus, and
 the ability for a diagnosis to be made and treatment
initiated.
The diagnosis is often difficult, and it is estimated to
that there are up to 400,000 cases of pulmonary
embolus that are not diagnosed in the United States

56. In those patients where the diagnosis is made,
the mortality rate is less than 20% when
considering all patients.
Usually, however, the mortality risk is much
less in most patients.
The higher incidence of death occurs in
patients that are older, have other underlying
illnesses, or have a delay in diagnosis.
Racial differences may also exist, but probably
are due more to access to quality care than a
specific genetic difference.

57. How can pulmonary embolism be
prevented?
Minimizing the risk of deep vein thrombosis
minimizes the risk of pulmonary
embolism.
The embolism cannot occur without the
initial DVT.

58. In the hospital setting, the staff works hard to minimize
the potential for clot formation in immobilized
patients. Compression stockings are routinely used.
Surgery patients are out of bed walking (ambulatory)
earlier and low dose heparin or enoxaparin is being
used for deep vein thrombosis prophylaxis
(measures taken to prevent deep vein thrombosis).
For those who travel, it is recommended that they get
up and walk every couple of hours during a long trip.
Compression stockings may be helpful in preventing
future deep vein thrombus formation in patients with
a previous history of a clot.

59. Clinical syndrome of P.E.
TherapyPresentationClassificati
on
Thrombosis or
embolictomy or IVC
filter plus:- anti co-
ag.
Systemic B.P. < 90 mmHg
Or poor tissue perfusion
or multisystem organ faliure
Plus :- right or left main pulm, artery
thrombosis or high clot burden
Massive P.E.
Addition of
thrombolysis
emboletomy or
filter remains
controversal
Hemodynamically stable but moderate
or sever R.V. dysfunction or
enlargement.
Submassive
P.E.
Anti co-ag.Normal hemodynamic of normal R.V.
size & function.
Pulm. infarction.
Small to
moderate
P.E.
Anti co-agA sudden stroke & concomitant V.T.E.
DVT --> thrombus --> arterial system
through P.F.O.
Paradoxical
embolism

60. Thank You !