Pulmonary embolism is a common and potentially lethal condition.

Most patients who succumb

to pulmonary embolism do so within the first few hours of the event. Despite diagnostic
advances, delays in pulmonary embolism diagnosis are common and represent an important
issue. As a cause of sudden death, massive pulmonary embolism is second only to sudden
cardiac death.

DEFINITION

Pulmonary embolism (PE) is an acute and potentially fatal condition in which embolic
material, usually a thrombus originating from one of the deep veins of the legs or pelvis,
blocks one or more pulmonary arteries, causing impaired blood flow and increased
pressure to the right cardiac ventricle

Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the
lower extremities; however, they rarely also originate in the pelvic, renal, upper extremity
veins, or the right heart chambers. After traveling to the lung, large thrombi can lodge at the
bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic
compromise.

Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of

underlying venous thrombosis.

When a pulmonary embolism is identified, it is characterized as acute or chronic.

Acute Pulmonary embolism- - In terms of pathologic diagnosis, an embolus is acute if it is

situated centrally within the vascular lumen or if it occludes a vessel (vessel cutoff sign) Acute
pulmonary embolism commonly causes distention of the involved vessel.

Chronic Pulmonary embolism- An embolus is chronic if it is eccentric and contiguous with

the vessel wall, it reduces the arterial diameter by more than 50%, evidence of recanalization
within the thrombus is present, and an arterial web is present.

A pulmonary embolism is also characterized as central or peripheral, depending on the location

or the arterial branch involved.

Central pulmonary embolism -Central vascular zones include the main pulmonary artery, the
left and right main pulmonary arteries, the anterior trunk, the right and left interlobar arteries,
the left upper lobe trunk, the right middle lobe artery, and the right and left lower lobe arteries.
A pulmonary embolus is characterized as massive when it involves both pulmonary arteries or
when it results in hemodynamic compromise

Peripheral pulmonary embolism Peripheral vascular zones include the segmental and
subsegmental arteries of the right upper lobe, the right middle lobe, the right lower lobe, the
left upper lobe, the lingula, and the left lower lobe.

Three primary influences predispose a patient to thrombus formation; these form the so-
called Virchow triad, which consists of the following [8, 9, 10] :
 Endothelial injury
 Stasis or turbulence of blood flow
 Blood hypercoagulability

Venous stasis-

 Venous stasis leads to accumulation of platelets and thrombin in veins. Increased

viscosity may occur due to polycythemia and dehydration, immobility, raised venous
pressure in cardiac failure, or compression of a vein by a tumor.

Hypercoagulable states-

 The complex and delicate balance between coagulation and anticoagulation is altered
by many diseases, by obesity, or by trauma. It can also occur after surgery.
 Concomitant hypercoagulability may be present in disease states where prolonged
venous stasis or injury to veins occurs. Hypercoagulable states may be acquired or
congenital. Factor V Leiden mutation causing resistance to activated protein C is the
most common risk factor.
 Primary or acquired deficiencies in protein C, protein S, and antithrombin III are other
risk factors. The deficiency of these natural anticoagulants is responsible for 10% of
venous thrombosis in younger people.

Immobilization-

Immobilization leads to local venous stasis by accumulation of clotting factors and fibrin,
resulting in thrombus formation. The risk of pulmonary embolism increases with prolonged
bed rest or immobilization of a limb in a cast.
Surgery and trauma

A prospective study by Geerts and colleagues indicated that major trauma was associated
with a 58% incidence of DVT in the lower extremities and an 18% incidence in proximal
veins.
Leg amputations and hip, pelvic, and spinal surgery are associated with the highest risk.
Fractures of the femur and tibia are associated with the highest risk of fracture-related
pulmonary embolism, followed by pelvic, spinal, and other fractures. Severe burns also carry
a high risk of DVT or pulmonary embolism.

Pregnancy-

The incidence of thromboembolic disease in pregnancy has been reported to range from 1
case in 200 deliveries to 1 case in 1400 deliveries Fatal events are rare, with 1-2 cases
occurring per 100,000 pregnancies.

Oral contraceptives and estrogen replacement-

Estrogen-containing birth control pills have increased the occurrence of venous

thromboembolism in healthy women. The risk is proportional to the estrogen content and is
increased in postmenopausal women on hormonal replacement therapy. The relative risk is 3-
fold, but the absolute risk is 20-30 cases per 100,000 persons per year.

Malignancy -

Malignancy has been identified in 17% of patients with venous thromboembolism. Pulmonary
emboli have been reported to occur in association with solid tumors, leukemias, and
lymphomas.

Hereditary factors

Hereditary factors associated with the development of pulmonary embolism include the
following:
 Antithrombin III deficiency
 Protein C deficiency
 Protein S deficiency
 Factor V Leiden (most common genetic risk factor for thrombophilia)
 Plasminogen abnormality
 Plasminogen activator abnormality
  Fibrinogen abnormality
 Resistance to activated protein C

Acute medical illness

Acute medical illnesses associated with the development of pulmonary embolism include the
following:
 AIDS (lupus anticoagulant)
 Congestive heart failure (CHF)
 Myocardial infarction
 Polycythemia
 Systemic lupus erythematosus
 Ulcerative colitis
In the PIOPED II study, 94% of patients with pulmonary embolism had 1 or more of the
following risk factors
 Immobilization
 Travel of 4 hours or more in the past month
 Surgery within the last 3 months
 Malignancy, especially lung cancer
 Current or past history of thrombophlebitis
 Trauma to the lower extremities and pelvis during the past 3 months
 Smoking
 Central venous instrumentation within the past 3 months
 Stroke, paresis, or paralysis
 Prior pulmonary embolism
 Heart failure
 Chronic obstructive pulmonary disease
Symptoms
 Dyspnea
 Chest pain (pleuritic)
 Apprehension
 Cough
 Hemoptysis
 Syncope
 Palpitations
 Wheezing
 Leg pain
 Leg swelling
Signs
 Tachycardia
 Tachypnea
 hypoxemia
 Accentuated S2
 Fever
 Diaphoresis
 Signs of DVT
 Cardiac murmur
 Jugular venous distention
 Cyanosis
 Hypotension
The incidence of pulmonary embolism may differ substantially from country to country;
observed variation is likely due to differences in the accuracy of diagnosis rather than in the
actual incidence. death rates from pulmonary embolism were 20-30% higher among men than
among women. [20] The incidence of venous thromboembolic events in the older population is
greater among men than women. In patients younger than 55 years, the incidence of
pulmonary is higher in females. The overall age- and sex-adjusted annual incidence of venous
thromboembolism is reported to be 117 cases per 100,000 people (DVT, 48 cases per
100,000; pulmonary embolism, 69 cases per 100,000)
DIAGNOSIS-
Clinical Scoring Systems
Evidence-based literature supports the practice of determining the clinical probability of
pulmonary embolism before proceeding with testing. One study assessed the performance of
four4 clinical decision rules in addition to D-dimer testing to exclude acute PE. All four4
rules, Wells rule, simplified Wells rule, revised Geneva score, and simplified revised Geneva
score, showed similar performance for excluding acute PE when combined with a normal D-
dimer result
Modified Wells Scoring System
The AAFP/ACP guideline advocates use of the Modified Wells prediction rule for the above-
specified estimation and interpretation requirements. However, the guideline notes that the
Wells rule performs better in younger patients without comorbidities or a history of venous
thromboembolism. Current evidence also suggests this tool is effective in pregnant patient

D-Dimer, a degradation product produced by plasmin-mediated proteases of cross-linked

fibrin, is measured by a variety of assay types, including quantitative, semiquantitative, and
qualitative rapid enzyme-linked immunosorbent assays (ELISAs); quantitative and
semiquantitative latex; and whole-blood assays.

White Blood Cell Count

The white blood cell (WBC) count may be normal or elevated in patients with pulmonary
embolism, with a WBC count as high as 20,000 being not uncommon in patients with this
condition.
Arterial Blood Gases
Arterial blood gas determinations characteristically reveal hypoxemia, hypocapnia, and
respiratory alkalosis; however, the predictive value of hypoxemia is quite low.
Troponin levels
Serum troponin levels can be elevated in up to 50% of patients with a moderate to large
pulmonary embolism, presumptively due to acute right ventricular myocardial stretch.
V/Q lung scan - Ventilation (V) Perfusion (Q) lung scanning is based on the flawed
expectation that regions of the lung excluded from perfusion by emboli maintain normal
ventilation, thus giving rise to V/Q mismatch (it is performed by IV injection of particles of
human serum albumin labeled with iodine 131 or technetium. These particals are trapped in
the pulmonary microvasculature and distributed acc to pulmonary flow. Both lung are
scanned and amount of radioactivity counted gives an indication of obstruction to flow

Chest radiograph- Chest radiographs are abnormal in most cases of pulmonary embolism, but
the findings are nonspecific. Common radiographic abnormalities include atelectasis, pleural
effusion, parenchymal opacities, and elevation of a hemidiaphragm. The classic radiographic
findings of pulmonary infarction include a wedge-shaped, pleura-based triangular opacity with
an apex pointing toward the hilus (Hampton hump) or decreased vascularity (Westermark
sign). These findings are suggestive of pulmonary embolism but are infrequently observed

Pulmonary angiography radiopaque material is injected into right arterium and pulmonary
artery via catheter through peripheral vein and visualization of filling defects done by
radiographs.

Computed tomographic angiography (CTA)- outlines thrombi in the pulmonary arteries

with intravenous contrast medium, has become the most widely used technique for the
diagnosis or exclusion of PE.

MEDICAL MANAGEMENT

GOAL-stabilize cardio pulmonary system and reduce threat of further PE with anticoagulant
therapy and fibrinolytic therapy.

 Stabilizing cardio pulmonary system .It is first priority.

 Hypoxemia, respiratory distress, can be reversed with low flow O2 by nasal cannula.
 Client may require endotracheal intubation to maintain PO2 greater than 60 mm of hg
  Hypotension treated with iv fluids(if not raised then inotropic agents-dobutamine,
dopamine may be used)
 Acidosis-corrected with bicarbonate

Anticoagulant Therapy

 Initially Heparin sodium based LMWH( decrease risk of further clots and prevent is
extension as well) initial target of which is INR 2.5-3
 Sodium warfarin administration begun about 3-5 days before heparin stopped to
provide a transition to oral anticoagulation ,because the half life of warfarin is long
about 2-3 days is required to achieve normal coagulation. Clients are maintained on it
for 3-6 months..
 Side effects-bleeding ,anaphylactic reaction - shock and death

FIBRINOLYTIC (thrombolytic) THERAPY

 It is useful in hemodynamically unstable clients.

 Thrombolytic agents lyse the clot and restore right sided heart function. Thrombolytic
therapy usually followed with heparin and warfarin treatment to prevent additional
thrombus formation.
 . Streptokinase (Streptase) is given in a 250,000-IU loading dose, followed by
100,000 IU per hour for 24 hours. Delivery of thrombolytics directly into the
thrombus by catheter has been described but has not been shown to be superior to
peripheral infusion
 Systemic thrombolytic therapy is most commonly used, typically as 100 mg of tissue
plasminogen activator given as a two hour infusion .Eg- urokinase ,streptokinase
 Side effect-bleeding

ANALGESICS-MORPHINE

Diuretics: lasix if right ventricular failure develops.

Long-term secondary prophylaxis and prevention of recurrence- For intermediate and

low risk patients with PE, international guidelines recommend to start administration of
vitamin K antagonists (such as warfarin) as early as the first or second day; LMWH or
fondaparinux therapy should be continued in conjunction for at least five days and stopped
when the international normalized ratio is in the therapeutic range (2.0 to 3.0) for at least a
day.

SURGICAL MANAGEMENT

 Vena cava interruption with insertion of a

filter: The Greenfield filter which looks like
umbrella is most commonly used,it is inserted by
threading it up the veins of leg or neck until it
reaches vena cava at level of renal arteries,which
allow blood flow while trapping emboli.it may
lead to DVT

 Pulmonary embolectomy-It is surgical removal of emboli either by thoracotomy or an

embolectomy cather . it is USED in clients with unstable circulation and contraindication
to thrombolytic therapy.

NURSING MANAGEMENT

Nursing Assessment

 Take nursing history with emphasis on onset and severity of dyspnea and nature of
chest pain.

 Examine the patient's legs carefully.

 Assess for swelling of leg, duskiness, warmth, pain on pressure over gastrocnemius
muscle, pain on dorsiflexion of the foot (positive Homans' sign), which indicate
thrombophlebitis as source

 Monitor respiratory rate may be accelerated out of proportion to degree of fever and
tachycardia.

 Observe rate of inspiration to expiration.

 Percussion for resonance, dullness, and flatness.

 Auscultate for friction rub, crackles, rhonchi, and wheezing.

  Auscultate heart; listen for splitting of second heart sound.

 Evaluate results of PT/PTT tests for patients on anticoagulants

 Nursing diagnosis

 INEFFECTIVE BREATHING PATTERN/IMPAIRED GAS EXCHANGE

RELATED TO ACUTE INCREASE IN ALVEOLAR DEAD AIR SPACE AND
POSSIBLE CHANGES IN LUNG MECHANICS FROM EMBOLISM
 Monitor respiratory rate, depth, breath sound
 Raise head of bed (Keep the patient with fowler position to enhance ventilation)
 Manage o2 therapy
 ASSESS –hypoxemia and pulse oximetry
 Assist in deep breathing exercises and incentive spirometry
 Assist with turning, coughing, and deep breathing to mobilize secretions and clear
airway
 Nebulizer therapy ,percussion and postural drainage

Bed rest with active and passive range of motion..

 INEFFECTIVE TISSUE PERFUSION RELATED TO DECREASED BLOOD

CIRCULATION
 Elevate lower extremities of patient and assess peripheral pulses
 ABGs monitoring to evaluate the need for mechanical ventilation
 – Administer O2 to enhance oxygenation

 ANXIETY RELATED TO DYSPNEA AND SERIOUSNESS OF CONDITION

 Correct dyspnea and relieve physical discomfort.
 Explain diagnostic procedures and the patient's role; correct misconceptions.
 Listen to the patient's concerns; attentive listening relieves anxiety and reduces
emotional distress.
 Speak calmly and slowly.
 Do everything possible to enhance the patient's sense of control.
 Acute PAIN RELATED TO DISEASE CONDITION
 Watch patient for signs of discomfort and pain.
 Ascertain if pain worsens with deep breathing and coughing; auscultate for
friction rub.
 Give prescribed morphine, and monitor for pain relief and signs of respiratory
depression.
 Position with head of bed slightly elevated (unless contraindicated by shock)
and with chest splinted for deep breathing and coughing.
 Nurse offers support and make patient comfortable
 Teaches patient relaxation techniques
 Encourage patient to verbalize fear and concerns
 RISK FOR INJURY RELATED TO ALTERED HEMODYNAMIC
FACTORS AND ANTICOAGULANT THERAPY

 PREVENTING THORMBUS FORMATION-

 encourage early ambulation
 Active and passive leg exercises
 Avoid-prolonge sitting ,standing and constrictive clothing ,crossing legs
 Avoid leaving IV catheters in veins for long times

 MONITOR ANTICOAGULENT AND THORMBOLYTIC THERAPY

 Monitor vitals every 2 hrly
 Advise bed rest ,limit invasive procedures
 Measure INR,PTT every 3-4 hrly after thrombolytic infusion started to
confirm activation of fibrinolytic system
 Perform essential ABG ,apply compression for atleast 30 min after
 MINIMIZING CHEST PAIN
 Administer analgesics
 Position-semi fowlers

 MONITOR FOR COMPLICATIONS

 RT. VENTRICULAR FAILURE
 CARDIOGENIC SHOCK
 POSTOPERATIVE NURSING CARE CARE
 MEASURE Pulmonary arterial pressure and urinary output
 Encourage isometric exercises ,anti embolism stockings
 Discourage-sitting (hip flexion compress large veins in legs)