2. INTRODUCTION
A pulmonary embolism (PE) is a potential
cardiovascular emergency where a blood clot
develops in a blood vessel elsewhere in the body
(most commonly from the leg), travels to an artery
in the lung, and forms an occlusion (blockage) of the
artery.
3. DEFINITION
PE refers to the obstruction of the pulmonary artery or
one of its branches by a thrombus (or thrombi) that
originates somewhere in the venous system or in the
right side of the heart.
4. INCIDENCE
Approximately 15% patients died, causing, contributing or
accompanying in hospital related to pulmonary embolism
for the past 40 years.
Recent large, contemporary observational studies of PE
have reported an overall 3 months mortality of 17% and
an hospital mortality of 31% when PE associated with
hypotension.
6. TYPES
Their are two types:-
1. Thrombotic
2. Non-thrombotic : Fat, Air, Tumor, Amniotic fluid.
7. Thrombotic
Even when a blood vessel is not injured, blood clots
may form in the body under certain conditions. A clot,
or a piece of the clot, that breaks free and begins to
travel around the body is known as an embolus.
Thrombosis may occur in veins (venous
thrombosis) or in arteries.
11. 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.
The arterioles constrict because of platelet
degranulation, accompanied by a release of histamine,
serotonin, catecholamine's and prostaglandins.
13. These chemical agents result in bronchial and
pulmonary artery constriction.
• vasoconstriction
• pulmonary embolism
15. SIGNS AND SYMPTOMS
Dyspnea
Tachypnea
Syncope,
Hypotension,
Cyanosis
Pleuritic pain,
Cough,
Haemoptysis often suggests a
small embolism located
distally near the pleura.
16. Cont…
Anxiety, Apprehension, Fever, Tachycardia, Cough,
Diaphoresis, Hemoptysis, Shock, and sudden death
may occur.
Clinical picture may mimic that of bronchopneumonia
or HF.
In atypical instances, PE causes few signs and
symptoms, whereas in other instances it mimics
various other cardiopulmonary disorders.
17. LABORATORY TESTS
1. D-dimer blood test. This test detects the presence of
a protein produced when a blood clot breaks down
somewhere in the body. A negative result is a good
indicator that a clot is not present. A positive result
suggests that clots may be present, but more testing
is needed to confirm.
2. Arterial blood gas analysis. A sudden drop in the
blood oxygen level may suggest a pulmonary
embolism.
18. Cont…
3. Coagulation Profile. Additional blood work should
include coagulation studies to evaluate for a hyper-
coagulable state, if clinically indicated. A prolonged
prothrombin time or activated partial thromboplastin
time does not imply a lower risk of new thrombosis.
Progression of DVT and PE can occur despite full
therapeutic anticoagulation in 13% of patients.
19. INVESTIGATIONS
History and physical examination
Venous studies
Chest X-ray
Continuous ECG monitoring
ABGs
CBC count with WBC differential
D –dimer level
Lung scan(ventilation and perfusion)
Pulmonary angiography
CT scan
20. Lung Scan.
This test, called a ventilation perfusion scan , uses small
amounts of radioactive material to study airflow (ventilation)
and blood flow (perfusion) in the lungs. First, pt. inhale a small
amount of radioactive material while a special camera designed
to detect radioactive substances records air movement in lungs.
Then a small amount of radioactive material is injected into a
vein via arm. Images taken after the injection show whether pt.
have a normal or diminished flow of blood to the lungs.
21. Pulmonary Angiogram
During this test, a flexible tube (catheter) is inserted
into a large vein — usually in femoral vein — and
threaded through the heart's right atrium and ventricle
and then into the pulmonary arteries. A special dye is
injected into the catheter, and X-rays are taken as the
dye travels along the arteries in the lungs.
Pulmonary angiogio-graphy also can measure the
pressure in the right side of the heart..
22. Ultrasound
A noninvasive sonar test known as duplex venous
ultra-sonography (sometimes called duplex scan or
compression ultra-sonography) uses high-frequency
sound waves to check for blood clots in the lower
limb veins. (thighs)
23. Magnetic Resonance Imaging
(MRI)
MRI scans use radio waves and a powerful magnetic
field to produce detailed images of internal structures.
24. D-Dimer
D-dimer test is a blood test that measures the
presence of an inappropriate blood clot (thrombus).
Some of the conditions that the D-dimer test is used
to rule out include: disseminated intravascular
coagulation (DIC) , Deep Vein Thrombosis (DVT),
Pulmonary Embolism (PE).
25. Arterial Blood Gases
•Blood gases may increase the suspicion and
contribute to the clinical assessment, but they are
insufficient to permit proof or exclusion of PE.
26. ECG
In minor pulmonary embolism, the only finding is
sinus tachycardia.
In massive pulmonary embolism, evidence of right
heart strain may be seen (rightward shift of the QRS
axis, transient RBBB, T-wave inversion), but these
signs are non-specific. The main value of ECG is
exclusion other diagnoses, such as MI or Peri-carditis.
28. Chest x-ray
Signs with relative high specificity but low sensitivity
for acute pulmonary embolism:
Decreased vascularity in the peripheral lung (Westermark
sign).
Enlargement of the central pulmonary artery (Fleischner
sign).
Pleural based areas of increased opacity (Hampton hump).
Hemidiaphragm elevation
31. Vena Cava Filter or IVC
An inferior vena cava filter or IVC filter is a small
cone-shaped device that is implanted in the inferior
vena cava just below the kidneys.
The filter is designed to capture an embolism, a
blood clot
33. Heparin
The initial treatment of PE is LMWH or UFH (Unfractionated
Heparin )for at least 5 days, followed by warfarin.
Dose of UFH: 80 IU/kg/h bolus followed by18 IU/kg.
Monitoring by APTT(1.5-3)times normal. (Activated Partial
Thromboplastin Time)
It binds to endogenous anti-thrombin, This heparin – anti-
thrombin complex catalyzes the inactivation of factor Xa
(trypsin) and IIa (thrombin).
34. Oral Anticoagulant
Warfarin inhibits gamma-carboxylation of the vitamin
K-dependent coagulation factors II, VII, IX, and X.
Warfarin and heparin can be started on the same day,
but colleteral administration of these drugs for 4 or 5
days is recommended.
35. Thrombolytic Therapy
Tissue plasminogen activator is a protein involved in
the breakdown of blood clots. It is a serine protease
found on endothelial cells, the cells that line the blood
vessels.
Tissue plasminogen activator (tPA) has a short
infusion time and has been recommended as the best
agent for this reason.
37. Pulmonary Embolectomy
Embolectomy is the emergency surgical removal of
emboli which are blocking blood circulation. It
usually involves removal of thrombi (blood clots), and
is then referred to as thrombectomy.
39. Catheter-Based Thrombus
Removal
for the Initial Treatment of Patients With PE if
appropriate expertise and resources are available, we
suggest catheter-assisted thrombus removal over no
such intervention
40. 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.
43. Cont…
Monitor respiratory rate may be accelerated out of proportion
to degree of fever and tachycardia.
Observe rate of inspiration to expiration.
Percuss 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
44. Nursing Diagnosis
1. Ineffective Breathing Pattern related to acute increase in alveolar
dead air space and possible changes in lung mechanics from
embolism
2. Ineffective Tissue Perfusion (Pulmonary) related to decreased
blood circulation
3. Acute Pain (pleuritic) related to congestion, possible pleural
effusion, possible lung infarction
4. Anxiety related to dyspnea, pain, and seriousness of condition
5. Risk for Injury related to altered hemodynamic factors and
anticoagulant therapy
45. Nursing Interventions
Correcting Breathing Pattern
1. Assess for hypoxia, headache, restlessness, apprehension,
pallor, cyanosis, behavioral changes.
2. Monitor vital signs, ECG, oximetry, and ABG levels for
adequacy of oxygenation.
3. Monitor patient's response to I.V. fluids/vasopressors.
4. Monitor oxygen therapy used to relieve hypoxemia.
5. Prepare patient for assisted ventilation when hypoxemia is
due to local areas of pneumo-constriction and abnormalities
of [V with dot above]/[Q with dot above] ratios.
46. Improving Tissue Perfusion
1. Closely monitor for shock decreasing blood pressure,
tachycardia, cool, clammy skin.
2. Monitor prescribed medications given to preserve right
ventricular filling pressure and increase blood pressure.
3. Maintain patient on bed rest to reduce oxygen demands and
risk of bleeding.
4. Monitor urinary output hourly, because there may be reduced
renal perfusion and decreased glomerular filtration.
47. Relieving Pain
1. Watch patient for signs of discomfort and pain.
2. Ascertain if pain worsens with deep breathing and
coughing; auscultate for friction rub.
3. Give prescribed morphine, and monitor for pain relief
and signs of respiratory depression.
4. Position with head of bed slightly elevated (unless
contraindicated by shock) and with chest splinted for
deep breathing and coughing.
48. Cont…
5. Evaluate patient for signs of hypoxia thoroughly when
anxiety, restlessness, and agitation of new onset are
noted, before administering as needed sedatives.
6. Consider physician evaluation when these signs are
present, especially if accompanied by cyanotic nail beds,
circumoral pallor, and increased respiratory rate.
49. Reducing Anxiety
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.
51. 1. Cardiac arrest (a sudden, sometimes temporary, cessation of
function of the heart. ) and sudden death
2. Shock
3. Abnormal heart rhythms
4. Death of part of the lung, called pulmonary infarction
5. A buildup of fluid (pleural effusion) between the outside
lining of the lungs and the inner lining of the chest cavity
6. Paradoxical embolism
7. Pulmonary hypertension
52. Paradoxical Embolism
It is a kind of stroke or other form of arterial thrombosis
caused by embolism of a thrombus (blood clot), air,
tumor, fat, or amniotic fluid of venous origin, which
travels to the arterial side through a lateral opening in the
heart,
53. Cont…
Pulmonary hypertension is a rare lung disorder in
which the arteries that carry blood from the heart to
the lungs become narrowed, making it difficult for
blood to flow through the vessels. As a result, the
blood pressure in these arteries -- called pulmonary
arteries -- rises far above normal levels.
54. Intervening for Complications
Be alert for shock from low cardiac output secondary to
resistance to right ventricular outflow or to myocardial
dysfunction due to ischemia.
Assess for skin colour changes, particularly nail beds, lips,
ear lobes, and mucous membranes.
Monitor blood pressure.
Measure urine output.
Monitor I.V. infusion of vasopressor or other prescribed
agents.
55. Bleeding Related To Anticoagulant
Or Thrombolytic Therapy
Assess patient for bleeding; major bleeding may occur from GI tract,
brain, lungs, nose, and genitourinary (GU) tract.
Perform stool test to detect occult blood loss.
Monitor platelet count to detect heparin-induced thrombocytopenia.
Minimize risk of bleeding by performing essential ABG analysis on upper
extremities; apply digital compression at puncture site for 30 minutes;
apply pressure dressing to previously involved sites; check site for oozing.
Maintain patient on strict bed rest during thrombolytic therapy; avoid
unnecessary handling.
56. Cont..
Discontinue infusion in the event of uncontrolled bleeding.
Notify health care provider on call immediately for change
in LOC, ability to follow commands, sensation, ability to
move limbs, and respond to questions with clear
articulation. Intracranial bleed may necessitate
discontinuation of anticoagulation promptly to avert massive
neurologic catastrophe
57. Patient Education and Health
Maintenance
Advise patient of the possible need to continue taking
anticoagulant therapy for 6 weeks up to an indefinite period.
Teach about signs of bleeding, especially of gums, nose,
bruising, blood in urine and stools.
For patients on anticoagulants, instruct to use soft toothbrush,
avoid shaving with blade razor (use electric razor instead), and
avoid aspirin-containing products. Notify health care provider
of bleeding or increased bruising
58. Warn against taking medications unless approved by health
care provider, because many drugs interact with anticoagulants.
Instruct patient to tell dentist about taking an anticoagulant.
Warn against inactivity for prolonged periods or sitting with
legs crossed to prevent recurrence.
Warn against sports/activities that may cause injury to legs and
predispose to a thrombus.
Encourage wearing a Medic Alert bracelet identifying patient
as anticoagulant user.
59. Prognosis
depends on the amount of lung that is affected and on the co-
existence of other medical conditions; chronic embolisation to the
lung can lead to pulmonary hypertension.
In massive PE, the embolus must be resolved somehow if the patient
is to survive.
In thrombotic PE, the blood clot may be broken down by
fibrinolysis, or it may be organized and recanalized so that a new
channel forms through the clot.
Once anticoagulation is stopped, the risk of a fatal pulmonary
embolism is 0.5% per year.