PE
PULMONARY EMBOLISM
PULMONARY CIRCULATION
ETIOLOGY
Obstruction of the pulmonary artery or its branches by a thrombus:
Originates from the venous system or the right side of the heart.
Thrombotic:
Most common type of pulmonary embolism (PE).
Frequently arises from lower extremities, such as Deep Vein Thrombosis (DVT).
Non-Thrombotic:
Fat emboli.
Gas (air) emboli.
Foreign body emboli (e.g., amniotic fluid).
GENERAL RISK FACTORS FOR PE
High Risk:
Atrial fibrillation/flutter
Cardiac disease
Bed rest exceeding 3 days
Myocardial Infarction (MI) in the last 3 months
History of stroke
Moderate Risk:
Long flight or road trip
Joint replacement surgery
Joint surgery (knee)
Hypertension (HTN)
Diabetes Mellitus (DM)
Lower extremity fracture
Hormone Replacement Therapy (HRT)
Advanced age
History of Venous Thromboembolism (VTE)
Oral contraceptives
Pregnancy
Spinal cord injury
Cancer
Obesity
VIRCHOW’S TRIAD
Components:
Endothelial Damage:
Causes: Surgery, catheter placement, trauma, smoking, hypertension, hereditary coagulopathies.
Hypercoagulability:
Factors include cancer and chemotherapy, HRT/oral contraceptives, pregnancy, obesity, immobilization, polycythemia, dehydration, varicose veins, and heart/kidney disease.
Venous Stasis:
Conditions that hinder normal blood flow can result in pooling and increase clot formation risk.
INHERITED CLOT RISK FACTORS
Each factor influences different clotting aspects, raising the risk for clot formation:
Protein C and S deficiency
Prothrombin gene mutation
Factor V Leiden
Antithrombin III deficiency
PULMONARY EMBOLUS
PATHOPHYSIOLOGY: HEMODYNAMIC EFFECTS
Pulmonary Artery Obstruction:
Causes increase in Pulmonary Artery (PA) Pressure.
Leads to increased Right Ventricular (RV) Afterload.
Results in RV Dilation.
Septal displacement into the Left Ventricle (LV).
Affected by:
Decrease in RV output.
Decrease in LV Preload.
Decrease in overall cardiac output, leading to tissue edema and hypotension.
Consequences include strain on the right side of the heart, back-up of blood, and lung tissue without blood supply from the embolus.
PATHOPHYSIOLOGY: PULMONARY EFFECTS
Decreased Blood Flow:
Causes alveolar deadspace (ventilation without perfusion).
Leads to lack of gas exchange in affected areas, resulting in pulmonary shunting and hypoxemia.
PATHOPHYSIOLOGY: MASSIVE PE (SADDLE)
Clinical Presentation:
Severe dyspnea.
Cyanosis.
Sustained hypotension (SBP < 90 mmHg for 15 minutes).
RV dysfunction.
Potential for pulselessness and shock, occurring in 5-10% of PE cases.
PATHOPHYSIOLOGY: SUB-MASSIVE PE
Details:
Acute presentation without sustained hypotension.
RV dysfunction with preserved blood pressure.
Accounts for 20-25% of PE cases.
PATHOPHYSIOLOGY: LOW-RISK PE
Characteristics:
Lacks major clinical presentation typical of massive/sub-massive PE.
RV is not dysfunctional.
Represents 70-75% of PE cases.
SIGNS AND SYMPTOMS
Anxious and restless demeanor.
Hemoptysis (coughing up blood).
Rales (crackles in lung sounds).
Loud S2 heart sound.
Several unspecified symptoms may exist.
DIAGNOSIS
D-dimer:
A protein byproduct resulting from clot breakdown.
Levels greater than 500 ng/mL indicate high suspicion for PE.
Arterial Blood Gas (ABG):
Measures gas exchange efficiency.
Spiral CT and V/Q Scan:
Advanced imaging techniques for diagnosis.
Pulmonary Angiogram:
Gold standard for visualizing pulmonary arteries.
Ultrasound for DVT Detection:
To find deep vein thrombosis as a source.
TREATMENT: NURSING MANAGEMENT
Administration of Oxygen.
Cardiac monitoring to assess heart function.
Maintaining IV access and active fluid administration.
Close monitoring of anticoagulation therapy.
Pain management strategies as needed.
TREATMENT: ANTICOAGULATION
General Notes:
Anticoagulation therapy is essential before invasive procedures unless the patient is hemodynamically unstable.
Heparin:
Monitor activated Partial Thromboplastin Time (aPTT).
Warfarin:
Monitor International Normalized Ratio (INR); therapeutic range is specified.
Overlap therapy with Heparin for 4 days.
Direct Oral Anticoagulants (DOACs):
Examples include Apixaban (Eliquis) and Rivaroxaban (Xarelto).
Fibrinolytic Therapy:
Administered for massive PE using tPA and Heparin.
QUESTION:
Antidotes for Anticoagulants:
Heparin: [specific antidote information].
Warfarin: [specific antidote information].
DOACs: Idarucizumab, Andexanet alfa, and Ciraparantag.
Fibrinolytics: Aminocaproic acid (Amicar) and Tranexamic acid (TXA).
Importance of Knowing Antidotes:
Essential for emergency reversal of anticoagulation.
Context of Use:
Understanding when a nurse might need to use them.
TREATMENT: POST-SURGICAL MANAGEMENT
Risk Level Management:
Low Risk:
Minor surgery, under 40 years.
No DVT risk factors present.
Strategies: Early mobilization and mechanical aids.
Moderate Risk:
Major surgery, over 40 years with no DVT risk factors.
Strategies: Early mobilization, mechanical aid, and possible Heparin or Enoxaparin use.
High Risk:
Major surgery, over 40 years with DVT risk factors.
Necessitates mechanical aid and anticoagulation (Heparin/Enoxaparin).
High-risk surgeries such as hip or knee arthroplasty should involve mechanical aids and anticoagulation management.
TREATMENT: THROMBECTOMY INTERVENTIONS
Thrombectomy:
Catheter aspiration thrombectomy: removal of blood clots using suction.
Mechanical thrombectomy: breaking blood clots into smaller pieces for removal.
TREATMENT: EMBOLECTOMY
Indications:
For massive PE with hemodynamic instability.
When thrombolytic therapy is contraindicated.
Surgical removal of the clot is warranted in such scenarios.
TREATMENT: INFERIOR VENA CAVA FILTER (IVC)
Indications:
For patients at high risk for recurrent PE.
Situations where chronic anticoagulation is contraindicated.
This approach reduces but does not fully eliminate PE risk.
Risks associated with IVC filters: [not specified in the transcript].
TREATMENT: PREVENTION
Best Management Practices:
Key strategy is preventing PE occurrence.
Avoid prolonged placement of IV catheters.
Use Low Molecular Weight Heparin (LMWH) for prevention.
Education:
Importance of ambulation and early mobilization for patients.
Use Sequential Compression Devices (SCDs) for non-ambulatory patients.
Encouragement for passive leg exercises.
Recommendations for leg positioning (feet resting on the floor).
In cases with known genetic factors, chronic, lifelong oral anticoagulation is advised.
COMPLICATIONS OF PE
Possible complications resulting from thrombolytic therapy include:
Pain.
Cardiogenic shock.
Chronic pulmonary hypertension.
Respiratory failure.
Potential for death as a critically severe outcome.
NURSING CONSIDERATIONS
[contents not specified in the transcript]