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MEDICAL SURGICAL NURSING (CRITICAL CARE NURSING)
TOPIC :- PULMONARY EMBOLISM
PRESENTED BY,
Ms. YAGNIKA DAMOR
PULMONARY EMBOLISM
INTRODUCTION
• Pulmonary embolism (PE) is a life-threatening
condition characterized by the blockage of arteries in the
lungs, often caused by blood clots traveling from
elsewhere in the body.
 With an annual incidence rate of approximately 60-70
cases per 100,000 individuals, PE poses a significant
public health concern worldwide.
 Approximately 10% of patients with massive PE die
within the first hour.
 Treatment with anticoagulants significantly reduces
mortality.
 Pulmonary embolism refers to the obstruction of
the pulmonary artery or one of its branches by a
thrombus (or thrombi) originating somewhere in
the venous system or the right side of the heart.
 In other words, pulmonary embolism (PE) is the
blockage of one or more Pulmonary arteries by a
thrombus, fat or air embolus, or tumor.
DEFINITION
Deep vein thrombosis a related condition, refers to thrombus formation in
the deep veins usually in the calf or thigh, but sometimes in the arm,
especially in patients with peripherally inserted central catheters. VTE is a
term that includes both DVT and PE.
 Other sites of origin of PE
include femoral or iliac
veins, right side of the heart
(atrial fibrillation), and
pelvic veins (especially after
surgery or childbirth).
 Upper extremity DVT
occasionally occurs in the
presence of central venous
catheters or arterial lines.
 These cases may be resolved
with the removal of the
catheter.
RISK FACTORS
SMOKING
BEING
OVERWEIGHT
Supplementalestrogen
PREGNANCY
RISK FACTORS
Virchow's triad or the triad of
Virchow's describes the three broad
categories of factors that are thought
to contribute to thrombosis.
RUDOLF VIRCHOW
CAUSES
 Prolonged immobilization
(especially postoperative)
 Prolonged periods of
sitting/traveling
 Varicose vein
 Spinal cord injury
 VENOUS STASIS  HYPERCOAGULABILITY
 Injury
 Tumor (pancreatic, GI,
breast, lung)
 Increased platelet count
(splenectomy)
 VENOUS ENDOTHELIAL DISEASE
-Thrombophlebitis
-Vascular disease
-Foreign bodies (IV/central venous
catheters)
 CERTAIN DISEASE STATES (combination
of stasis, coagulation alterations, and venous injury)
OTHER PREDISPOSING CONDITIONS
-Advanced age
-Constrictive clothing
-History of previous thrombophlebitis,
pulmonary embolism
-Heart disease (especially heart
failure)
-Trauma (especially fracture of
hip, pelvis, vertebra, lower
extremities)
-Postoperative state/postpartum
period
-Diabetes mellitus
-Chronic obstructive pulmonary
disease
PATHOPHYSIOLOGY
_____________________________________________
Pulmonary Embolism
Hypoxemia/Clot obstruction
Increased PA pressure
Increased right ventricular (RV) afterload
RV dysfunction
Decreased RV output Displacement of IVS towards
LV
Decreased Left ventricular preload
Decreased cardiac output Hypotension
Decreased Systemic perfusion
Predisposing factors
CLINICAL MANIFESTATION
 Dyspnea is the most common presenting symptom, occurring in 85% of patients with
PE.
 Hypoxemia
 Tachypnea, Tachycardia
 Crackles or a friction rub on auscultation
 Wheezing
 Fever
 Syncope
 Cough
 Chest pain
 Hemoptysis
ASSESSMENT AND DIAGNOSTIC FINDINGS
HISTORY COLLECTION
PHYSICAL EXAMINATION
Physical signs of pulmonary embolism include the following:
1. Tachypnea (respiratory rate >16/min)
2. Rales
3. Tachycardia (heart rate >100/min)
4. Fever (temperature >37.8 C)
5. Diaphoresis
6. S3 or S4 gallop
7. Clinical signs and symptoms suggesting thrombophlebitis
8. Lower extremity edema
9. Cardiac murmur
10. Cyanosis
Computed tomography angiography (CTA)/CT angiography
Pulmonary angiography
Chest radiography
V/Q scanning
ECG
Echocardiography
Venography
Doppler ultrasonography
1. D-dimer testing
2. Arterial blood gases
3. CBC
4. Coagulation studies
4. Brain natriuretic peptide
LAB INVESTIGATION
PREVENTION
 For patients at risk for PE, the most effective approach is prevention.
 Leg elevation
 Compression stockings
 Physical activity
 Pneumatic compression
 Your provider might suggest the following to help prevent blood clots during travel
• Drink plenty of fluids
• Take a break from sitting
• Move in your seat
• Wear support stockings
SUPPORTIVE THERAPY
 O2 can be given via mask or cannula, and the concentration of FIO2 is determined by
ABG analysis, in some situations, endotracheal intubation, and mechanical
ventilation are necessary to maintain adequate oxygenation.
 Respiratory measures such as turning, coughing deep breathing, and incentive
spirometry are important to help prevent or treat atelectasis.
 If manifestations of shock are present, IV fluids are administered followed by
vasopressor agents as needed to support perfusion.
 If heart failure is present, diuretics are used.
 Pain resulting from pleural irritation or reduced coronary blood flow is
treated with opioids.
MANAGEMENT
OF
PULMONARY EMBOLISM
EMERGENCY MANAGEMENT
 Nasal oxygen is given immediately to relieve hypoxemia, respiratory distress, and central cyanosis; severe
hypoxemia may necessitate emergent endotracheal intubation and mechanical ventilatory support.
 IV infusion lines are inserted to establish routes for medications or fluids that will be needed.
 For hypotension that does not resolve with IV fluids prompt initiation of vasopressor therapy is recommended with
agents that may include dobutamine, dopamine, or norepinephrine.
 Hemodynamic measurements and evaluation for hypoxemia (pulse oximetry or arterial blood gas) are performed. If
available, MDCTA will be performed.
 The ECG is monitored continuously for dysrhythmias and right ventricular failure, which may occur suddenly.
 An indwelling urinary catheter is inserted to monitor urinary output.
 Small doses of IV morphine or sedatives are given to relieve patient anxiety,
 to alleviate chest discomfort,
 to improve tolerance of the endotracheal tube,
 and to ease adaptation to the mechanical ventilator, if necessary.
PHARMACOLOGICAL THERAPY
 ANTICOAGULATION THERAPY
 Immediate anticoagulation is required for patients with PE. Subcutaneous administration of low-
molecular-weight heparin (LMWH) (e.g., enoxaparin) or fondaparinux is safer and more effective
than unfractionated heparin. It is the recommended treatment for patients with acute PE,
administered once daily.
 Warfarin (Coumadin), an oral anticoagulant, should also be initiated at the time of diagnosis.
Warfarin should be administered for at least 3 months and then reevaluated. Anticoagulant therapy
may be contraindicated if the patient has complicating factors such as blood dyscrasias, hepatic
dysfunction causing alterations in the clotting, overt bleeding, a history of hemorrhagic stroke, or
heparin-induced thrombocytopenia (HIT).
THROMBOLYTIC THERAPY
 Thrombolytic therapy (urokinase, streptokinase, alteplase, anistreplase, reteplase)
also, may be used in treating PE,
 particularly in patients who are severely compromised (eg, those who are hypotensive
and have significant hypoxemia despite oxygen supplementation).
 Thrombolytic therapy resolves the thrombi or emboli quickly and restores more normal hemodynamic
functioning of the pulmonary circulation, thereby reducing pulmonary hypertension and improving
perfusion, oxygenation, and cardiac output.
 Before thrombolytic therapy is started, INR, partial thromboplastin time (PTT) and platelet counts
obtained. An anticoagulant is stopped prior to administration of a thrombolytic agent. During therapy, all
but essential invasive procedures are avoided because of potential bleeding.
SURGICAL MANAGEMENT
 A surgical embolectomy is rarely performed but may be indicated if the patient has a massive
PE or hemodynamic instability or if there are contraindications to thrombolytic (fibrinolytic)
therapy. Embolectomy can be performed using catheters or surgically. Surgical removal must be
performed by a cardiovascular surgical team with the patient on cardiopulmonary bypass.
 An inferior vena cava (IVC) filter may be inserted. IVC filters are not recommended for the initial
treatment of patients with PE and should not be used in patients receiving anticoagulants. The IVC filter
provides a screen in the IVC, allowing blood to pass through while large emboli from the pelvis or lower
extremities are blocked or fragmented before reaching the lung. Numerous catheters have been developed
since the introduction of the original Greenfield filter.
 Vein ligation to prevent the embolus from traveling to heart.
NURSING MANAGEMENT
1. Impaired Gas Exchange related to decreased perfusion of lung tissue
2. Ineffective Tissue Perfusion related to obstruction of pulmonary blood flow
3. Acute Pain related to pleural irritation and chest discomfort
4. Anxiety related to dyspnea, fear of death, or uncertainty about the condition
5. Risk for Impaired Skin Integrity related to immobility or prolonged bed rest
6. Knowledge Deficit related to lack of information about the condition, treatment, and
prevention strategies
COMPLICATIONS
1. Pulmonary infarction
2. Chronic thromboembolic pulmonary
3. Right ventricular dysfunction
4. Pleural effusion
5. Recurrent embolism
6. Death
"Pulmonary Embolism Demystified: An Essential Primer for Nursing Education"

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"Pulmonary Embolism Demystified: An Essential Primer for Nursing Education"

  • 1. MEDICAL SURGICAL NURSING (CRITICAL CARE NURSING) TOPIC :- PULMONARY EMBOLISM PRESENTED BY, Ms. YAGNIKA DAMOR
  • 2. PULMONARY EMBOLISM INTRODUCTION • Pulmonary embolism (PE) is a life-threatening condition characterized by the blockage of arteries in the lungs, often caused by blood clots traveling from elsewhere in the body.  With an annual incidence rate of approximately 60-70 cases per 100,000 individuals, PE poses a significant public health concern worldwide.  Approximately 10% of patients with massive PE die within the first hour.  Treatment with anticoagulants significantly reduces mortality.
  • 3.  Pulmonary embolism refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) originating somewhere in the venous system or the right side of the heart.  In other words, pulmonary embolism (PE) is the blockage of one or more Pulmonary arteries by a thrombus, fat or air embolus, or tumor. DEFINITION
  • 4. Deep vein thrombosis a related condition, refers to thrombus formation in the deep veins usually in the calf or thigh, but sometimes in the arm, especially in patients with peripherally inserted central catheters. VTE is a term that includes both DVT and PE.
  • 5.  Other sites of origin of PE include femoral or iliac veins, right side of the heart (atrial fibrillation), and pelvic veins (especially after surgery or childbirth).  Upper extremity DVT occasionally occurs in the presence of central venous catheters or arterial lines.  These cases may be resolved with the removal of the catheter.
  • 7. RISK FACTORS Virchow's triad or the triad of Virchow's describes the three broad categories of factors that are thought to contribute to thrombosis. RUDOLF VIRCHOW
  • 8. CAUSES  Prolonged immobilization (especially postoperative)  Prolonged periods of sitting/traveling  Varicose vein  Spinal cord injury  VENOUS STASIS  HYPERCOAGULABILITY  Injury  Tumor (pancreatic, GI, breast, lung)  Increased platelet count (splenectomy)
  • 9.  VENOUS ENDOTHELIAL DISEASE -Thrombophlebitis -Vascular disease -Foreign bodies (IV/central venous catheters)  CERTAIN DISEASE STATES (combination of stasis, coagulation alterations, and venous injury) OTHER PREDISPOSING CONDITIONS -Advanced age -Constrictive clothing -History of previous thrombophlebitis, pulmonary embolism -Heart disease (especially heart failure) -Trauma (especially fracture of hip, pelvis, vertebra, lower extremities) -Postoperative state/postpartum period -Diabetes mellitus -Chronic obstructive pulmonary disease
  • 10. PATHOPHYSIOLOGY _____________________________________________ Pulmonary Embolism Hypoxemia/Clot obstruction Increased PA pressure Increased right ventricular (RV) afterload RV dysfunction Decreased RV output Displacement of IVS towards LV Decreased Left ventricular preload Decreased cardiac output Hypotension Decreased Systemic perfusion Predisposing factors
  • 11. CLINICAL MANIFESTATION  Dyspnea is the most common presenting symptom, occurring in 85% of patients with PE.  Hypoxemia  Tachypnea, Tachycardia  Crackles or a friction rub on auscultation  Wheezing  Fever  Syncope  Cough  Chest pain  Hemoptysis
  • 12. ASSESSMENT AND DIAGNOSTIC FINDINGS HISTORY COLLECTION PHYSICAL EXAMINATION Physical signs of pulmonary embolism include the following: 1. Tachypnea (respiratory rate >16/min) 2. Rales 3. Tachycardia (heart rate >100/min) 4. Fever (temperature >37.8 C) 5. Diaphoresis 6. S3 or S4 gallop
  • 13. 7. Clinical signs and symptoms suggesting thrombophlebitis 8. Lower extremity edema 9. Cardiac murmur 10. Cyanosis Computed tomography angiography (CTA)/CT angiography Pulmonary angiography Chest radiography V/Q scanning ECG Echocardiography Venography Doppler ultrasonography
  • 14. 1. D-dimer testing 2. Arterial blood gases 3. CBC 4. Coagulation studies 4. Brain natriuretic peptide LAB INVESTIGATION
  • 15. PREVENTION  For patients at risk for PE, the most effective approach is prevention.  Leg elevation  Compression stockings  Physical activity  Pneumatic compression  Your provider might suggest the following to help prevent blood clots during travel • Drink plenty of fluids • Take a break from sitting • Move in your seat • Wear support stockings
  • 16. SUPPORTIVE THERAPY  O2 can be given via mask or cannula, and the concentration of FIO2 is determined by ABG analysis, in some situations, endotracheal intubation, and mechanical ventilation are necessary to maintain adequate oxygenation.  Respiratory measures such as turning, coughing deep breathing, and incentive spirometry are important to help prevent or treat atelectasis.  If manifestations of shock are present, IV fluids are administered followed by vasopressor agents as needed to support perfusion.  If heart failure is present, diuretics are used.  Pain resulting from pleural irritation or reduced coronary blood flow is treated with opioids.
  • 18. EMERGENCY MANAGEMENT  Nasal oxygen is given immediately to relieve hypoxemia, respiratory distress, and central cyanosis; severe hypoxemia may necessitate emergent endotracheal intubation and mechanical ventilatory support.  IV infusion lines are inserted to establish routes for medications or fluids that will be needed.  For hypotension that does not resolve with IV fluids prompt initiation of vasopressor therapy is recommended with agents that may include dobutamine, dopamine, or norepinephrine.  Hemodynamic measurements and evaluation for hypoxemia (pulse oximetry or arterial blood gas) are performed. If available, MDCTA will be performed.  The ECG is monitored continuously for dysrhythmias and right ventricular failure, which may occur suddenly.  An indwelling urinary catheter is inserted to monitor urinary output.  Small doses of IV morphine or sedatives are given to relieve patient anxiety,  to alleviate chest discomfort,  to improve tolerance of the endotracheal tube,  and to ease adaptation to the mechanical ventilator, if necessary.
  • 19. PHARMACOLOGICAL THERAPY  ANTICOAGULATION THERAPY  Immediate anticoagulation is required for patients with PE. Subcutaneous administration of low- molecular-weight heparin (LMWH) (e.g., enoxaparin) or fondaparinux is safer and more effective than unfractionated heparin. It is the recommended treatment for patients with acute PE, administered once daily.  Warfarin (Coumadin), an oral anticoagulant, should also be initiated at the time of diagnosis. Warfarin should be administered for at least 3 months and then reevaluated. Anticoagulant therapy may be contraindicated if the patient has complicating factors such as blood dyscrasias, hepatic dysfunction causing alterations in the clotting, overt bleeding, a history of hemorrhagic stroke, or heparin-induced thrombocytopenia (HIT).
  • 20. THROMBOLYTIC THERAPY  Thrombolytic therapy (urokinase, streptokinase, alteplase, anistreplase, reteplase) also, may be used in treating PE,  particularly in patients who are severely compromised (eg, those who are hypotensive and have significant hypoxemia despite oxygen supplementation).  Thrombolytic therapy resolves the thrombi or emboli quickly and restores more normal hemodynamic functioning of the pulmonary circulation, thereby reducing pulmonary hypertension and improving perfusion, oxygenation, and cardiac output.  Before thrombolytic therapy is started, INR, partial thromboplastin time (PTT) and platelet counts obtained. An anticoagulant is stopped prior to administration of a thrombolytic agent. During therapy, all but essential invasive procedures are avoided because of potential bleeding.
  • 21. SURGICAL MANAGEMENT  A surgical embolectomy is rarely performed but may be indicated if the patient has a massive PE or hemodynamic instability or if there are contraindications to thrombolytic (fibrinolytic) therapy. Embolectomy can be performed using catheters or surgically. Surgical removal must be performed by a cardiovascular surgical team with the patient on cardiopulmonary bypass.  An inferior vena cava (IVC) filter may be inserted. IVC filters are not recommended for the initial treatment of patients with PE and should not be used in patients receiving anticoagulants. The IVC filter provides a screen in the IVC, allowing blood to pass through while large emboli from the pelvis or lower extremities are blocked or fragmented before reaching the lung. Numerous catheters have been developed since the introduction of the original Greenfield filter.  Vein ligation to prevent the embolus from traveling to heart.
  • 22. NURSING MANAGEMENT 1. Impaired Gas Exchange related to decreased perfusion of lung tissue 2. Ineffective Tissue Perfusion related to obstruction of pulmonary blood flow 3. Acute Pain related to pleural irritation and chest discomfort 4. Anxiety related to dyspnea, fear of death, or uncertainty about the condition 5. Risk for Impaired Skin Integrity related to immobility or prolonged bed rest 6. Knowledge Deficit related to lack of information about the condition, treatment, and prevention strategies
  • 23. COMPLICATIONS 1. Pulmonary infarction 2. Chronic thromboembolic pulmonary 3. Right ventricular dysfunction 4. Pleural effusion 5. Recurrent embolism 6. Death