PE nursing and medical management

2. PULMONARY EMBOLISM
Moderator : Presenter
Mr. L Gopichandran Esther Mary Mathew
Lecturer, CON Msc. Nursing 2nd year

3. Pulmonary Embolism – The Killer Clot
in the Lungs
• Pulmonary embolism (PE) is a common and
potentially lethal condition.
• Most patients who succumb to PE do so within
the first few hours of the event.
•The most important conceptual advance regarding
PE is the realization that pulmonary embolism is
not a disease; rather, it is a complication of venous
thrombo-embolism (VTE), most commonly deep
venous thrombosis (DVT).

5. Definition
Pulmonary embolus (PE) refers to obstruction
of the pulmonary artery or one of its branches
by material (eg, thrombus, tumor, air, or fat)
that originated elsewhere in the body.
•Originate primarily from deep venous system
of lower extremities
•Ilio-femoral thrombi and pelvic veins appear to
be the most clinically recognized
•Air, amniotic fluid and fat emboli are rarer
causes.

6. Why care?
• PE is the most common preventable cause of death in
hospitalized patients. ~600,000 deaths/year
• 80% of pulmonary emboli occur without prior warning
signs or symptoms
• 2/3 of deaths due to pulmonary emboli occur within 30
minutes of embolization
• Death due to massive PE is often immediate

7. Incidence
• 2nd most common cause of unexpected death in
most age groups.
• Present in 60-80% of patients with DVT, more than
50 % them are asymptomatic
• Account for 15 % of all postoperative deaths
• It is estimated that in the USA .100 000 people die
each year of pulmonary embolism

8. Incidence
•A mortality rate up to 30% if untreated due to
recurrent embolization and 2-8 % mortality if well
treated.
•The overall incidence is higher in males compared
with females (56 versus 48 per 100,000,
respectively. However, the incidence rises with
increasing age, particularly in women after the age
of 75 years .

9. PE Indian Scenario : PGIMER,
Chandigarh study
An autopsy study on 1000 medical patients at the
Postgraduate Institute of Medical Education and
Research (PGIMER), Chandigarh revealed-
PE was present in 159 (16%) of 1000 patients who
died hospital —
1. It was a fatal embolus in 36
2. A major contributor to death in 90 patients
3. 30 patients, the embolus was an incidental
finding at autopsy as death occurred due to
some other cause.
THE NATIONALMEDICAL JOURNAL OF INDIA VOL. 23, NO.4, 2010

10. Normal anatomy of the lung and its
circulation

11. PE can arise from anywhere in the body, most commonly it
arises from the calf veins. The venous thrombi predominately
originate in venous valve pockets and at other sites of
presumed venous stasis.

12. Rudolf Virchow
Rudolf Virchow postulated more than a century ago
that a triad of factors predisposed to venous
thrombosis.
Rudolph Virchow, 1858
Triad:
Hypercoagulability
Stasis to flow
Vessel injury

15. RISK FACTORS
Modifiable Risk Factors for Venous
Thromboembolism
• Obesity
• Metabolic syndrome
• Cigarette smoking
• Hypertension
• Abnormal lipid profile
• High consumption of red meat and low
consumption of fish, fruits, and vegetables

16. RISK FACTORS
Non Modifiable :
Advancing age
Personal or family history of VTE
Congestive heart failure (So in AHF , prophylaxis is
indicated)
Chronic obstructive pulmonary disease
Acute infection, Air pollution
Postmenopausal hormone replacement therapy

17. Air travel and risk of PE
The risk of fatal PE in this setting is less than 1 in 1
million.
•Activation of the coagulation system during air
travel.
•For each 2-hour increase in travel duration, there
appears to be an 18% higher risk of VTE.

18. ETIOLOGY
•Nearly all PEs arise from thrombi in the lower
extremity or pelvic veins (deep venous thrombosis
[DVT]).
•Risk of embolization is higher with thrombi proximal
to the calf veins.
•Thromboemboli can also originate in upper
extremity veins

19. PATHOPHYSIOLOGY

21. Pathophysiology
There are both respiratory and hemodynamic
consequences associated with pulmonary
embolism.

22. Pathophysiology - Respiratory
consequences
It include the following:
•Increased alveolar dead space
•Hypoxemia
•Hyperventilation

23. •Vascular obstruction of pulmonary artery
•Ventilation without perfusion = increase alveolar
dead space = hypoxemia
•Bronchoconstriction and increase airway
resistance (due to secretion of vaso and broncho
active substances such as serotonin)
•Alveolar hyperventilation due to reflex stimulation
of irritant receptors = hypocapnia
Pathophysiology of PE

24. Hemodynamic Consequences
of PE

25. Hemodynamic consequences
complete or partial obstruction of a
pulmonary artery
alveolar dead space is increased
impaired or absent gas exchange
various substances are released from the
clot and surrounding area
causing regional blood vessels and
bronchioles to constrict

26. CONTD…
Increase in pulmonary vascular resistance
Increase in pulmonary arterial pressure
Increase in right ventricular work to
maintain pulmonary blood flow
Right ventricular failure
Decrease in cardiac output,systemic blood
pressure and the development of shock

27. PATHOPHYSIOLOGY
Pulmonary artery pressure increases only if more
than 30–50% of the total cross-sectional area of
the pulmonary arterial bed is occluded by
thrombo-emboli.
 PE-induced vasoconstriction, mediated by the
release of thromboxane A2 and serotonin,
contributes to the initial increase in pulmonary
vascular resistance after PE

28. PATHOPHYSIOLOGY
Anatomical obstruction and vasoconstriction lead to an
increase in pulmonary vascular resistance and a
proportional decrease in arterial compliance.
Increase in pulmonary vascular resistance results in
RV dilation, which alters the contractile properties of
the RV myocardium

29. The increase in RV pressure and volume leads to an
increase in wall tension and myocyte stretch.
RV contraction time is prolonged, while neuro-humoral
activation leads to inotropic and chronotropic stimulation.
Together with systemic vasoconstriction, these
compensatory mechanisms increase pulmonary artery
pressure, improving flow through the obstructed
pulmonary vascular bed, and thus temporarily stabilize
systemic blood pressure (BP).
PATHOPHYSIOLOGY

30. The extent of immediate adaptation is limited, since
a non-preconditioned, thin-walled right ventricle.
RV is unable to generate a mean pulmonary artery
pressure above 40 mm Hg. Result both of
abnormal RV wall tension and of circulatory shock
PATHOPHYSIOLOGY

31. PE - Types

33. 1. Air embolism
•An air embolism occurs when one or more air
bubbles enter a vein or artery and block it.
•Symptoms of a severe air embolism might include
low blood pressure or difficulty breathing.
•Arterial and venous air embolism
•Treatment for an air embolism has three goals:
•to stop the source of the air embolism
•to prevent the air embolism from damaging
•to resuscitate (hyperbaric oxygen therapy)

34. 2. Fat embolism
•Fat embolism is caused by introduction of fat or
bone marrow particles into the systemic venous
system and then into pulmonary arteries.
• Early splinting of fractures of long bones and
operative rather than external fixation are thought to
help prevent fat embolism.
•Maintenance of intravascular volume is important
because shock can exacerbate the lung injury

35. 3. Amniotic fluid embolism
An amniotic fluid embolism (AFE) is a rare
obstetric emergency in which amniotic fluid, fetal
cells, hair, or other debris enters the mother's blood
stream via the placental bed of the uterus and
triggers an allergic-like reaction.
There is no specific treatment for amniotic fluid
embolism, and initial emergency management is the
same as for any other cause of sudden maternal
collapse( with cardiovascular and respiratory
resuscitation and correction of the coagulopathy.)

36. 4. Septic embolism
•A septic embolism is a type of embolism that is
infected with bacteria, resulting in the formation of
pus that embolizes to the lung.
•Common microbes that can lead to widespread
dissemination of septic emboli is Fusobacterium
necrophorum, a Gram negative anaerobic bacillus.
•Treatment includes that of the underlying infection.

37. 5. Foreign body embolism
Foreign body embolism caused by introduction of
particulate matter into the pulmonary arterial
system, usually by IV injection of inorganic
substances.

38. 6.Tumor embolism
Tumor embolism is a rare complication of cancer
(usually adenocarcinoma) in which neoplastic cells
from an organ enter the systemic venous and
pulmonary arterial system, where they lodge,
proliferate, and obstruct flow

39. ACC/AHA Classification
Massive
Submassive
Low-Risk PE
Pulmonary infarction syndrome

40. Massive PE
Acute PE with sustained hypotension (systolic bp 90
mm Hg for at least 15 min. or requiring inotropic
support, not due to a cause other than PE, such as
•Arrhythmia
•Hypovolemia
•Sepsis
•Left ventricular (LV) dysfunction
•Persistent profound bradycardia (heart rate 40 bpm
with signs or symptoms of shock)

41. Saddle Embolus
• Clot occurs at the point of the pulmonary artery
branching.
•It can be fatal, due to the large amount of blood
flow is inhibited.

42. Submassive PE
Acute PE without systemic hypotension but with
either RV dysfunction or myocardial necrosis
Angiographically defined blockage of flow to an area
served by less than two lobar arteries. These
patients have acute or unexplained dyspnea with
exertion or at rest.

43. Sub massive PE
RV dysfunction means the presence of at least 1 of
the following
• RV dilation or RV systolic dysfunction on
echocardiography
• Elevation of BNP (90 pg/mL)
• Electrocardiographic changes (new complete
or incomplete RBBB, anteroseptal ST
elevation or depression, or anteroseptal T
wave inversion)

44. Low-Risk PE
Acute PE and the absence of the clinical markers
of adverse prognosis that define massive or
submassive PE

45. Pulmonary Infarction Syndrome
Caused by a tiny peripheral pulmonary embolism
• Pleuritic chest pain, often not responsive to
narcotics
• Low-grade fever
• Leukocytosis
• Pleural rub
• Occasional scant hemoptysis

46. Clinical Features
•Size of the embolus and blood vessel Occluded.
•State of the lung.
•Associated disease(s).

47. Presentation
•Dyspnea at rest (73 %)
•Pleuritic pain (44 %)
•Cough (34 %)
•Orthopnea (28 %)
•Calf or thigh pain (44 %)
•Wheezing (21 %)
Rapid onset of dyspnea
 Within seconds (46 %)
 within minutes (26 %)
• Tachypnea (54 %)
• Tachycardia (24 %)
• Rales (18 %),
• Decreased breath sounds (17 %)
• Jugular venous distension
(14%)
Most Common
Symptoms
Most Common Signs
The “classic” signs and
symptoms of pulmonary
embolism, namely dyspnea,
hemoptysis, and chest pain.

49. Differential Diagnosis

50. Diagnosis
Risk stratification
Clinical examination
Bed side tests (ECG, ABG, pulse oximetry)
Laboratory tests (D-dimer, Cardiac biomarkers)
Imaging techniques (Ultrasound/ Doppler scan,
CXR, CTPA, V/Q scan, Echocardiogram)

51. Risk stratification
• Wells score for PE
• Modified Geneva score for PE

52. Wells score
The most commonly used method to predict
clinical probability.
In 1995, Philip Steven Wells, developed , to
predict the likelihood of PE, based on clinical
criteria.
The prediction rule was revised in 1998, further
revised when simplified during a validation by
Wells et al. in 2000.

54. Simplified Geneva Score

55. Diagnosis…
Pulmonary Embolism Rule-out Criteria (PERC): Help
assess people in whom pulmonary embolism is
suspected. People in this low risk category without any
of these criteria may undergo no further diagnostic
testing for PE:
 Hypoxia
 SaO2 <95%
 Unilateral leg swelling
 Hemoptysis,
 Prior DVT/PE
 Recent surgery/trauma
Age >50
Hormone use
Tachycardia

56. Diagnostic Tests
Imaging Studies
– CXR
– V/Q Scans
– Spiral Chest CT
– Pulmonary Angiography
– Echocardiograpy
Laboratory Analysis
– CBC, ESR,
– D-Dimer
– ABG’s
Ancillary Testing
– ECG
– Pulse Oximetry

57. D-dimer Test
The D-dimer assay is a sensitive but nonspecific test
to detect the presence of venous thromboembolism.
•D-dimers are produced during the degradation of
fibrin clot by plasmin (Fibrin split product)
• Circulating half-life of 4-6 hours
• Quantitative test have 80-85% sensitivity
False Positives:
•Pregnant Patients
• Post-partum < 1week
•Malignancy
•Surgery within 1 week
•Sepsis
•Hemorrhage
•CVA
•Collagen Vascular Diseases
•Hepatic Impairment
•Advanced age > 80 years

58. D-dimer Test
False Negative D-Dimer
– Heparin
•A normal D-dimer result (< or = 500 ng/mL
Fibrinogen Equivalent Units{FEU}) has a negative
predictive value.
•If the D-dimer reads high, then further testing
(ultrasound of the leg veins or lung scintigraphy or
CT scanning) is required to confirm the presence
of thrombus.

59. BNP & pro-BNP
•Typically greater in patients with PE.
•Sensitivity of 60% and specificity of 62%.
•At a threshold of 500 pg/mL, the sensitivity of pro-
BNP for predicting adverse events was 95%, and
the specificity was 57%.

60. WBC
•Poor sensitivity and nonspecific
•Can be as high as 20,000 in some patients
Hb
•PE does not alter count but if extreme, consider
polycythemia, a known risk factor

61. Pulse oximetry & ABG
•Pulse oximetry provides a quick way to assess
oxygenation; hypoxemia is one sign of PE, and it
requires further evaluation.
•ABG measurement may show an increased
alveolar to arterial oxygen (A-a) gradient or
hypocapnia; one or both of these tests are
moderately sensitive for PE but are not specific.
Arterial blood gas analysis is not diagnostic for pulmonary
embolism but typically shows PaO2 less than 80 mm Hg and
PaCO2less than 36 mm Hg on room air. physiological dead
space and muscle fatigue then lead to respiratory acidosis.

62. Doppler ultrasound of leg veins
Principle - Veins are normally
compressible; Presence of DVT
renders veins non-compressible, 50%
of patients with PE have positive
ultrasound.
(95% of PE are due to leg DVT)

63. ECG
2 Most Common finding on ECG:
•Nonspecific ST-segment and T-wave changes
• Sinus Tachycardia
•S1Q3T3: Classic signs are a large S wave in lead I, a
large Q wave in lead III, and an inverted T wave in lead III
Acute cor pulmonale or right strain patterns
• Tall peaked T-waves in lead II (P pulmonale)
• Right axis deviation
• RBBB
• S1-Q3-T3 (occurs in only 20% of PE patients)

64. S wave in lead I, a Q wave in lead III, and a T-wave
inversion in lead III. This pattern only occurs in
about 10% of people with pulmonary embolisms

65. Echocardiography
This modality generally has limited accuracy in the
diagnosis.
•The overall sensitivity and specificity for diagnosis
of central and peripheral pulmonary embolism by
ECHO is 59% and 77%.
•It may allow diagnosis of other conditions that may
be confused with pulmonary embolism.

66. Echocardiography
Disturbed RV ejection pattern or on depressed
contractility of the RV free wall compared with the
RV apex (‘McConnell sign’)- Reported to retain a
high positive predictive value for PE, even in the
presence of pre-existing cardiorespiratory disease.
• Inter-ventricular septal flattening and paradoxical
motion toward the LV resulting in a “D-shaped” LV
in cross section.
•Tricuspid regurgitation

67. Echocardiography

68. Chest x-ray
A normal or nearly normal chest x-ray
Major chest radiographic abnormalities are
uncommon.

69. Radiographic signs of acute
pulmonary embolism
Signs with relative high specificity but low sensitivity for
acute pulmonary embolism:
•Decreased vascularity in the peripheral lung (Westermark
sign).
•Enlarged right descending pulmonary artery (Palla's sign)
• Pleural based areas of increased opacity (Hampton hump).
•Hemi-diaphragm elevation

70. Westermark’s sign
•Dilation of the pulmonary arteries proximal to the
embolus and the collapse of the distal vasculature.
• Represents a focus of oligemia (hypovolemia)

72. Hampton’s hump
shallow Dome-shaped opacity in the periphery of
the lung dur to pulmonary infraction

73. Spiral CT
•Major advantage of Spiral CT is speed:
•Often the patient can hold their breath for the entire
study, reducing motion artifacts.
•Spiral CT is quicker than the equivalent
conventional CT permitting the use of higher
resolution acquisitions in the same study time.
•Contraindicated in cases of renal disease.
•Sensitive for PE in the proximal pulmonary
arteries, but less so in the distal segments.

74. Computed tomographic pulmonary
angiography
Multi-detector computed tomographic (MDCT)
angiography with high spatial and temporal
resolution and quality of arterial opacification,
CT angiography has become the method of choice
for imaging the pulmonary vasculature in PE.
A negative MDCT is an adequate criterion for
excluding PE in patients with a non-high clinical
probability of PE.

75. Lung scintigraphy/
Ventilation/Perfusion Scan
- V/Q Scan”
Ventilation–perfusion scintigraphy (V/Q scan) is an
established diagnostic test for suspected PE.
Procedure:
- Ventilation scan with Xenon or technetium inhalation
-Perfusion scan with Tc99m labeled radioactive dye
infusion, IV injection of technetium (Tc)-99m-labelled
macro aggregated albumin particles which block a
small fraction of the pulmonary capillaries and
thereby enable scintigraphic assessment of lung
perfusion.

76. Ventilation/Perfusion Scan
- “V/Q Scan”
A common modality to image the lung.
• Relatively noninvasive.
• In many centers remains the initial test of choice
• Preferred test in pregnant and renal failure
patient
•breastfeeding should be discontinued for 24 hours
following use of radiocontrast
•
A normal ventilation/ perfusion ratio is reported as 0.8:1.

77. VQ scan Technique

78. Ventillation scan Perfusion scan
Normal Ventilation,
equally distributed
Left UL PE

79. Pulmonary Angiography

80. Pulmonary Angiography
 The “gold standard”
 DSA requires less contrast medium than
conventional cineangiography and has excellent
imaging quality for peripheral pulmonary vessels in
patients who can hold their breath;
 It is less useful for imaging of the main pulmonary
arteries, due to cardiac motion artefacts.

81. Pulmonary Angiography
Left-sided pulmonary
angiogram showing extensive
filling defects within the left
pulmonary artery and its
branches.

82. Imaging in Pregnancy
No validated clinical decision rules
No consensus in evidence for diagnostic imaging
algorithm
Balance- risk of radiation vs. risk of missed fatal
diagnosis or unnecessary anticoagulation
MDCT delivers higher radiation dose to mother
but lower dose to fetus than V/Q scanning
Consider low-dose CT-PA or reduced-dose
lung scintigraphy

83. Diagnostic Algorithm

84. Imaging – NUT SHELL
•Plain chest radiograph – Usually normal and
nonspecific signs.
•Radionuclide ventilation-perfusion lung scan –
Excellent negative predictive value.
•CT Angiography of the pulmonary arteries –Quickly
becoming method of choice.
•Pulmonary angiography – Gold standard but
Invasive

85. MANAGEMENT

86. 87
Emergency management.
–Nasal oxygen to relieve hypoxemia, respiratory distress, and
central cyanosis.
–Intravenous infusion lines to administer medications or fluids.
–Hypotension is treated by a slow infusion of dobutamine .
–The ECG is monitored continuously for dysrhythmias which
may occur suddenly.
– Intravenous diuretics, and antiarrhythmic agents may be
indicated.
–Blood is drawn for serum electrolytes and CBC
–Intubation and mechanical ventilation may be performed
based on clinical assessment and arterial blood gas analysis

87. Emergency management.
Aggressive volume expansion is of no benefit and may
even worsen RV function by causing mechanical
overstretch
Modest (500 mL) fluid challenge may help to increase
cardiac index in patients with PE, low cardiac index, and
normal BP.
vasopressors is often necessary, Norepinephrine appears
to improve RV function via a direct positive inotropic
effect. It also increases right coronary perfusion.

88. Emergency management.
•Dopamine and dobutamine are first-line inotropic
agents for the treatment of PE-related shock. Both
agents increase cardiac output.
•Norepinephrine increases both cardiac output and
systemic vascular resistance and may be
beneficial as monotherapy or in combination with
dopamine or dobutamine.

89. –.
As soon as massive PE is suspected, high-dose
unfractionated heparin should be administered in
larger-than-usual doses. Most patients should
receive at least a 10 000-U bolus of heparin,
followed by a continuous intravenous infusion of at
least 1250 U/h, with a target activated partial
thromboplastin time (aPTT) of at least 80 seconds
Emergency management.

90. Medical Management
•General measures to improve respiratory and
vascular status
• Anticoagulation therapy
• Thrombolytic therapy
• Surgical intervention

92. GENERAL MANAGEMENT
Oxygen therapy is administered to correct the
hypoxemia, relieve the pulmonary vascular
vasoconstriction, and reduce the pulmonary
hypertension.

93. Parenteral anticoagulation
Immediate anticoagulation can be achieved with IV
UFH, subcutaneous LMWH, or SC fondaparinux.
LMWH or fondaparinux are preferred over UFH for
initial anticoagulation in PE, as they have lower risk
of inducing major bleeding and heparin-induced
thrombocytopenia.
UFH is recommended for patients in whom primary
reperfusion is considered, as well as for those with
serious renal impairment (creatinine clearance,30
mL/min), or severe obesity.

94. Anticoagulant Therapy
Heparin
•Heparin augments the activity of antithrombin III and
prevents the conversion of fibrinogen to fibrin.
•5000-10000 Units IV Loading Dose, Then 1000
Units/hr IV infusion drip
• Duration: 7-10 days OR till clinical improvement
• Follow up by PTT (1.5-2.5)

95. LMWH
.
•It should be used whenever possible for the
initial inpatient treatment of DVT & PE.
Outpatient of DVT, and possibly PE ,is safe
and cost-effective for carefully selected
patients.

96. Fondaparinux
•Anticoagulant pentasaccharide that specifically
inhibits activated factor X
•By selectively binding to antithrombin, fondaparinux
potentiates (about 300 times) the neutralization of
factor Xa by antithrombin
•Fondaparinux does not cross-react with Heparin
induced antibodies
•FDA has approved fondaparinux for initial treatment
of acute PE and acute DVT as a bridge to oral
anticoagulation with warfarin

98. Vitamin K antagonists
Gold standard’ in oral anticoagulation.
•Warfarin prevents activation of factor II, VII, IX and
X.
•.
•Heparin is continued for 4–5 days to overlap with
warfarin therapy to counter paradoxical
hypercoagulability that occurs with warfarin
monotherapy.

99. Vitamin K antagonists
Anticoagulation with UFH, LMWH, or fondaparinux
should be continued for at least 5 days and until the
(INR) has been 2.0–3.0 for two consecutive day.
Warfarin can be started at a dose of 10 mg in
younger otherwise healthy outpatients, and at a dose
of 5 mg in older patients and in those who are
hospitalized.

100. Novel Anticoagulants
Promise immediate onset of action and
administration in fixed doses without routine
laboratory coagulation monitoring
•These drugs have few drug-drug or drug-food
interactions, making them more “user friendly”
•Dabigatran is a direct thrombin inhibitor
•Rivaroxaban is a factor Xa inhibitor
•Both are approved in Canada and Europe for VTE
prevention after knee or hip arthroplasty

101. Thrombolytic treatment
Thrombolytic treatment of acute PE restores
pulmonary perfusion more rapidly than
anticoagulation with UFH alone
Thrombolytic therapy has replaced surgical
embolectomy as the treatment for hemodynamically
unstable patients with massive pulmonary embolism
Accelerated regimens administered over 2 hours are
preferable to prolonged infusions of first-generation
thrombolytic agents over 12–24 hours.

102. Unfractionated heparin infusion should be stopped
during administration of streptokinase or
urokinase; it can be continued during rtPA
infusion.
In patients receiving LMWH or fondaparinux at the
time that thrombolysis is initiated, infusion of UFH
should be delayed until 12 hours after the last
LMWH injection (given twice daily), or until 24
hours after the last LMWH or fondaparinux
injection(given once daily).

103. Thrombolysis
Indications:
•Massive PE
•Sub-massive PE where risk of bleeding low (in
RVD)

104. THROMBOLYTIC THERAPY
Dose Schedules in PE
1. Streptokinase (STK)
• I V bolus 250,000 units over 30’ followed by
infusion of 100,000 units/hr for 12-24 hours
2.Recombinant tissue plasminogen activator (rtPA)
• IV bolus of 15 mg in 10’ followed by 85 mg in
next 2 hours (total =100 mg)
• To be followed by heparin infusion on
completion of TPA

105. THROMBOLYTIC THERAPY
Alteplase
•Indications:
•Documented PE with:
– Persistent hypotension
– Syncope with persistent hemodynamic
compromise
– Significant hypoxemia
– +/- patient with acute right heart strain
•Approved Alteplase regimen is 100mg as a
continuous IV infusion, in 2hr.

107. Before After

108. Potential benefits of TLT
•More rapid resolution of symptoms (eg, dyspnea,
Chest pain and psychological distress)
•Stabilization of respiratory and cardiovascular
function without need for mechanical ventilation or
vasopressor support
•Reduction of RV damage
•Improved exercise tolerance
•Prevention of PE recurrence
•Increased probability of survival

109. Potential harm
•Disabling or fatal hemorrhage including
intracerebral hemorrhage
•Increased risk of minor hemorrhage, resulting in
prolongation of hospitalization and need for blood
product replacement

110. Use of Heparin Before and After
Thrombolysis:

111. IVC filter
• Indications:
- DVT with massive pulmonary embolus
- Recurrent PE not treatable with anticoagulation
- Absolute contra-indications for anti-coagulation
- Chronic thromboembolic pulmonary hypertension
• Not used in:
- Patients with free-floating thrombi in the proximal
veins
- Patients scheduled for systemic thrombolysis,
surgical embolectomy

112. Complications associated with
IVC filter
Early complications
• Device malposition
(1.3%)
• Pneumothorax(0.02%),
• Hematoma (0.6%)
• Air embolism (0.2%)
• carotid artery puncture
(0.04%)
• Arteriovenous fistula
Late complications
• Recurrent DVT (21%)
• IVC thrombosis (2% to
10%),
• IVC penetration (0.3%)
• Filter migration (0.3%)
• Recurrent PE (2-5%)
•

113. Catheter Embolectomy
Interventional catheterization techniques
Another approach is mechanical clot
fragmentation and aspiration.
Pulmonary artery balloon dilation and stenting
Successful catheter embolectomy rapidly restores
normal blood pressure and decreases hypoxemia.

115. Surgical Embolectomy
 When contraindications preclude thrombolysis.
 Surgical excision of a right atrial thrombus.
 Rescue patients whose condition is refractory to
thrombolysis
 Older case series suggest a mortality rate
between 20% and 30%

117. Massive Pulmonary Embolism –
Management
•Begin bolus high-dose IV unfractionated heparin
as soon as massive PE is suspected.
• Begin continuous infusion of heparin to achieve a
target aPTT of at least 80 sec.
•Volume resuscitation with no more than 500 to
1000 mL of fluid.( Excessive volume resuscitation
will worsen right ventricular failure.
• Have a low threshold for administration of
vasopressors and inotropes.

118. Massive Pulmonary Embolism –
Management
• If thrombolysis is risky, consider placement of an
inferior vena caval filter, catheter embolectomy, or
surgical embolectomy.
•Do not use a combination of thrombolysis and vena
caval filter insertion. (The prongs of the filter insert
into the caval wall. Concomitant thrombolysis
predisposes to caval wall Hemorrhage.)
•Consider immediate referral to a tertiary care
hospital

121. Pulmonary Embolism in Pregnancy
Leading cause of death in pregnancy. DVT and PE
are common during all trimesters of pregnancy and
for 6-12 weeks after delivery.
Heparin and fibrinolysis are safe in pregnancy.
LMWH can be given throughout their pregnancy
Warfarin is contraindicated
Women experiencing a thromboembolic event during
pregnancy should receive therapeutic treatment with
UFH or LMWH during pregnancy,

122. Pregnancy & Postpartum
•Pregnant women who are in a hypercoagulable
state or who have had previous venous
thromboembolism should receive prophylactic
anticoagulation during pregnancy
•Anticoagulation may be restarted with UFH or
LMWH 4- 6 hours following vaginal delivery or 6-
12 hours following cesarean delivery.
•Anticoagulation continuing for 4-6 weeks
postpartum and for a total of at least 6 months.

123. Thrombolysis in pregnancy
Streptokinase (and probably other thrombolytic
drugs) does not cross the placenta because of its
high molecular weight.
•However in the mother, bleeding is the major side
effect, usually from the genital tract and often
severe. incidence of bleeding is about 8%.
• Because of the risk of bleeding, thrombolysis
should not be used routinely in pregnancy.
•Should not be used at the time of delivery unless it
appears that the patient is likely to die

124. Malignancy
•Four- to sevenfold higher risk of thrombosis
compared with patients without cancer.
•Caused by prothrombotic effects of the tumor and
also because of treatment, particularly with surgery,
use of a central venous catheter,and chemotherapy.
•~20% of patients presenting with VTE have active
cancer, associated with reduced survival.
•Initial treatment with heparin and warfarin is given in
the standard manner.

125. Complications
• Instant Death
• Chronic pulmonary hypertension
• Respiratory failure
• Congestive heart failure
• Recurrence

127. PREVENTION
BEFORE SURGERY
GENERAL SURGERY
• Unfractionated heparin 5000 units SC bid or tid or
•Enoxaparin 40 mg SC qd or
•Dalteparin 2500 or 5000 units SC qd
NEURO SURGERY
•Unfractionated heparin 5000 units SC bid or
•Enoxaparin 40 mg SC qd and
•Graduated compression stockings or intermittent
pneumatic compression

128. Prevention
Prevent deep venous thrombosis.
• Active leg exercises
•The intermittent pneumatic leg compression device
•Use of elastic compression stockings
•Anticoagulant therapy, Low molecular weight heparin
prophylaxis.
•Avoid oral contraceptive pill

129. Intermittent pneumatic
compression

130. Genetic Blood Tests
25-50% of patients with VTE have an inherited
disorder
There are genetic causes of metabolism which
may be tested for
Factor V Leiden – causes increased clotting as
variant cannot be inactivated
Factor Protein C Deficiency – results in normal
cleaving of Factor Va and Factor VIIIa

132. Prevention while traveling
•Drink plenty of fluids. Preven dehydration, which
can contribute to the development of blood clots..
•Take a break from sitting. Move around the
airplane cabin once an hour or so.,
•Fidget in your seat. Flex your ankles every 15 to 30
minutes.
•Wear support stockings.

134. Prognosis
•5 to 10% of symptomatic PEs are fatal within the
first hour of symptoms.
•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.
•Once anticoagulation is stopped, the risk of a fatal
pulmonary embolism is 0.5% per year

135. NURSING
MANAGEMENT

136. NURSING MANAGEMENT
Impaired gas exchange related to decreased
perfusion to lung tissues in pulmonary vascular
bed by embolus as manifested by dyspnea,
hypoxemia.

137. •Auscultate breath sounds, noting crackles,
wheezes.
•Administer supplemental oxygen as indicated.
•Look for indication of mechanical ventillator
•Treat underlying causes ( eg- respiratory acidosis)
•Monitor pulse oximetry and report O2 saturation
<92%.
•Encourage frequent position changes.
•Maintain chair or bed rest in semi-Fowler’s position.
Support arms with pillows.
Outcome-
Weaning from invasive to non invasive MV
Normal bilateral entry breath sound
Normal ABG findings.

138. Potential for decreased cardiac output
related to heart failure as evidenced by
increased CVP ,engorged neck veins,
pedal edema
•Auscultate apical pulse, assess heart rate, rhythm.
•Inspect skin for pallor, cyanosis.
•Monitor urine output, noting decreasing output and
concentrated urine.
•Note changes in sensorium: lethargy, confusion,
disorientation, anxiety, and depression.
•Encourage rest, semi recumbent in bed or chair.
•Elevate legs, avoiding pressure under knee.
Encourage active and passive exercises.
•Administer IV solutions, restricting total amount as
Outcome-
Vitals signs are within normal range
Intake output level maintained

139. Pain related to pulmonary embolism as
verbalized by the patient
•Asses the nature of the pain
•Asses related factors
•Provide comfortable position
•Relieve anxiety
•Provide psychological support
•Administer oxygen therapy
•Administer analgesics

140. Potential for impaired skin integrity
RT edema, immobility etc.
•Asses for the presence of related factor
•Observe condition of skin; pressure sore
•Implement pressure relieving mattresses
• Maintain functional body alignment
•Provide skin care
•Encourage adequate hydration and nutrition
•Encourage ambulation if patient is able

141. Potential for bleeding RT
anticoagulant/thrombolytic therapy
•Asses signs and symptoms of bleeding
•Asses patient for high risk for bleeding
condition like liver disease, kidney disease,
severe hypertension
•Monitor PT level
•Monitor IV dosage and delivery system to
minimize the risk of over coagulation / under
coagulation.
•Institute safety precautions- Pad the side rails
•Avoid IM inj.

142. Cont…
•Provide gentle oral care
•Avoid constipation
•Limit physical manipulation
•Compress IV sites for at least 10 min and
arterial sites for 30 min
•Draw all laboratory samples through existing
line
•Send specimens for cross matching
•Don’t give foods rich in vitamin K

143. Anxiety related to threat of death ,
change in health habits, increase in
respiratory difficulty
•Asses the level of anxiety.
•Encourage patient to ventilate feelings of
anxiety.
•Asses patient’s normal coping mechanisms
•Support previously effective coping
mechanisms - Be empathetic
•Provide adequate rest, Organize activities
•Decrease sensory stimulation

144. •The importance of continued warfarin administration
for 3 to 6 months to prevent further thrombus
development.
•Foods high in vitamin K, such as dark green
vegetables and apricots, must be limited during this
time period to prevent decreased warfarin action.
•Therapeutic INR value should be checked .
•Not to use warfarin with acetaminophen,
nonsteroidal anti-inflammatory drugs because such
combinations can quickly elevate the INR.
•To wear a Medic-Alert bracelet indicating her history
Knowledge deficit regarding
management of bleeding ,
embolism & homecare

145. Facilitate learning processes; inform patient and
significant others of the following
• Etiology
• Effects
• Common risk factors
• Inform patient and significant others about
medications, side effects, dosage, action etc.
• Discuss and give patient list of signs and
symptoms of excess of anticoagulation

146. Health Education
•Look for bleeding esp., with falls
•Avoid use of sharps
•Use soft tooth brush
•Don’t take aspirin and other O.T.C. drugs while
taking warfarin
•Avoid use of laxatives
•Report occurrence of dark /tarry stool to health
care provider immediately

147. Health Education
•Describe strategies to prevent recurrent DVT/PE
•Avoid sitting with legs crossed or sitting for
prolonged periods of time
•Follow the medication regimen
•When traveling change position regularly, walk
occasionally, do active movement of legs and ankles
while sitting
•Drink fluids esp. while traveling and in warm
weather, to avoid hemoconcentration due to fluid
deficit

148. Health Education
•Describe signs and symptoms of lower extremity
compromise; Homan’s sign, calf pain, edema,
increased local temperature etc.
•Describe how and when to contact the health care
provider if signs and symptoms of circulatory
compromise or pulmonary compromise are
identified.

149. Discharge and Home Care
Guidelines
Prevent recurrence. The nurse should instruct the
patient about preventing recurrence and reporting
signs and symptoms.
Adherence. The nurse should monitor the patient’s
adherence to the prescribed management plan
and enforces previous instructions.
Residual effects. The nurse should also monitor
for residual effects of the PE and recovery.
Follow-up checkups. Remind the patient about
follow-up appointments for coagulation tests.

150. References
•Harrison -18th edition
•ACCP guidelines
•Woods et al:``Cardiac Nursing’’LIPPINCOTT
•Brunner& Siddharth, Medical Surgical Nursing’’
•Meg Gulanick et al:Nursing Care Plan 200,204

151. THANK YOU