PULMONARY EMBOLISM, CAUSES, CLINICAL FEATURES, DIAGNOSTIC TESTS, MANAGEMENT

1. • PULMONARY EMBOLISM

2. DEFINITION
• Pulmonary embolism is the blockage of pulmonary
arteries by thrombus, fat or air emboli and tumour tissue.
• It is the most common complication in hospitalised
patients.
• An embolus is a clot or plug that is carried by the
bloodstream from its point of origin to a smaller blood
vessel, where it obstructs circulation.

3. INCIDENCE
• Actual incidence of mortality and morbidity from
pulmonary embolism is unknown.
• It is estimated that nearly 50,000 people die of
pulmonary disease each year in the United states
and another 650,000 have non fatal pulmonary
embolism.

4. ETIOLOGY AND RISK FACTORS
• Virtually all pulmonary embolisms develop
from thrombi(clots),most of which originate
in the deep calf, femoral, popliteal, or iliac
veins.
• Other sources of emboli include tumours,
fat, air, bone marrow, amniotic fluid, septic
thrombi, and vegetations on heart valves
that develop with endocarditis.

5. • Major operations ,especially hip, knee, abdominal
and extensive pelvic procedures predispose the
client to thrombus formation because of reduced flow
of blood through pelvis.
• Travelling in for a long time or sitting for long periods
is also associated with stasis and clotting of blood.

6. • The most common sources of embolism are proximal
leg deep venous thrombosis (DVTs) or pelvic vein
thromboses.
• Any risk factor for DVT also increases the risk that
the venous clot will dislodge and migrate to the lung
circulation, which may happen in as many as 15% of
all DVTs.

7. • The conditions are generally regarded as a
continuum termed venous thromboembolism (VTE).
• The development of thrombosis is classically due to
a group of causes named Virchow's triad (alterations
in blood flow, factors in the vessel wall and factors
affecting the properties of the blood).
• Often, more than one risk factor is present.

8. CLINICAL FEATURES:
• Severity of clinical manifestations of pulmonary
embolism depends on the size of the emboli and the
size and number of blood vessels occluded. Most
common manifestations are,
 Anxiety
 Sudden onset of unexplained dyspnea
 Tachypnea or tachycardia
 Cough
 Pleuritic chest pain
 Hemoptysis
 Crackles

9. Fever
Accentuation of the pulmonic heart sound
Sudden change in mental status as a result of hypoxemia
•In massive emboli,
Shock
Pallor
Severe dyspnea
Crushing chest pain
Pulse is rapid and weak
Bp is low
ECG indicates right ventricular strain

10. •In medium sized emboli,
Pleuritic chest pain
Dyspnea
Slight fever
Productive cough with blood streaked sputum
•In small emboli,
Pulmonary hypertension
ECG and chest X-ray indicates right ventricular hypertrophy

11. PATHOPHYSIOLOGY
• When emboli travel to the lungs, they lodge in the
pulmonary vasculature .
• The size and number of emboli determine the
location.
• Blood flow is obstructed ,leading to decreased
perfusion of the section of the lung supplied by the
vessel.
• The client continues to ventilate the lung portion ,but
because the tissue is not perfused, resulting in
hypoxemia.

12. •If an embolus lodges in a large pulmonary vessel, it
increases proximal pulmonary vascular resistance, causes
atelectasis, and eventually reduces cardiac output.
•If the embolus is in a smaller vessel, less dramatic clinical
manifestations follow but perfusion is still altered.
•The arterioles constrict because of platelet degranulation,
accompanied by a release of histamine, serotonin,
catecholamines and prostaglandins.
•These chemical agents result in bronchial and pulmonary
artery constriction.
•This vasoconstriction probably plays a major role in the
hemodynamic instability that follows pulmonary embolism.

13. •Pulmonary embolism can lead to right sided heart failure.
•Once the clot lodges, affected blood vessels in the lung
collapse.
•This collapse increases the pressure in the pulmonary
vasculature.
•The increased pressure increases the work load of the right
side of the heart, leading to failure.
•Massive pulmonary embolism of the pulmonary artery can also
result in cardiopulmonary collapse from lack of perfusion and
resulting hypoxia and acidosis.

15. DIAGNOSTIC STUDIES
 History and physical examination
 Venous studies
 Chest X-ray
 Continous ECG monitoring
 ABGs
 CBC count with WBC differential

16.  D –dimer level(D-dimer test is a blood test that
checks for blood-clotting problems. It
measures the amount of D-dimer, a protein our
body makes to break down blood clots)
 Lung scan(ventilation and perfusion)
 Pulmonary angiography
 Spiral CT scan(A spiral CT scan, also known as a
helical CT scan, is a type of computed
tomography (CT) scan where the X-ray
machine scans the body in a continuous spiral
path. This allows for more images to be taken
in a shorter time than older CT methods,
creating detailed 3D images. )

17. MEDICAL MANAGEMENT
• The objectives of treatment are,
 Prevent further growth or multiplication of thrombi in
the lower extremities
 Prevent embolization from the upper or lower
extremities to the pulmonary vascular system.
 Provide cardiopulmonary support if indicated.

18. CONSERVATIVE THERAPY
• The administration of O2 by mask or nasal cannula
may be adequate for some patients.O2 is given in a
concentration determined by ABG analysis.
• In some situations, endotracheal intubation and
mechanical ventilation may be needed to maintain
adequate oxygenation.
• Respiratory measures such as turning, coughing and
deep breathing are necessary to prevent or treat
atelectasis.

19. •If shock is present, vasopressor agents may be
necessary to support systemic circulation .If
heart failure is present, digitalis and diuretics
are used.
•Pain resulting from pleural irritation or reduced
coronary blood flow is treated with narcotics,
usually morphine.

20. DRUG THERAPY
• Anticoagulant therapy-Properly managed anticoagulant
therapy is effective in the treatment of many patients with
pulmonary embolism.
• Heparin and Warfarin are the anticoagulant drugs of
choice.
• Unless contraindicated, heparin should be started
immediately and is continued while oral anticoagulants
are initiated.
• The dosage of heparin is adjusted according to PTT and
warfarin dose is determined by International normalized
ratio.

21. •Fibrinolytic therapy-The effectiveness of fibrinolytic
therapy in the management of a massive
pulmonary embolism is not clear, but it may be
useful in clients who are hemodynamically unstable.
•Thrombolytic agents breaks the clots and restore
right-sided heart function.

22. SURGICAL MANAGEMENT
• Surgical interventions that may be used in the
treatment of pulmonary embolism include,
 Vena caval interruption with the insertion of a filter
and
 Pulmonary embolectomy
• The Greenfield filter, a basket like cone of wires bent
to look like an umbrella ,is the most commonly used
filter.

24. •The filter is inserted by threading it up the veins in the leg
or neck until it reaches the venacava at the level of renal
arteries.
•The filter allows blood flow while trapping emboli, however
venacava filters are less effective than coagulation and may
lead to deep vein thrombosis and so these are generally are
used only when anticoagulants are contraindicated or
ineffective.

25. •Embolectomy is used in clients with significant
hemodynamic instability caused by the embolus,especially
those with unstable circulation and contraindications to
thrombolytic therapy.
•An embolectomy involves surgical removal of emboli from
the pulmonary arteries by either thoracotomy or an
embolectomy catheter.

26. NURSING DIAGNOSIS:
 Impaired gas exchange related to decreased lung
perfusion.
 Ineffective breathing pattern related to chest pain ,
hypoxia.
 Deficient knowledge related to medical condition and
new treatment
 Risk for bleeding related to abnormal blood profiles,
anticoagulant or fibrinolytic therapy.