pulmonary embolism
Overview of Pulmonary Embolisms (PE)
Discussion Topic: Focus on Pulmonary Embolisms (PE) and Aneurysms
This week will cover cardiovascular topics including PEs.
A case study on a PE patient is planned for the end of the session.
Multimedia Resources
Speaker mentions several videos related to PE treatment procedures but did not post them in advance.
Thrombolectomy and other treatments are highlighted in short videos.
Resources are selected to be concise and relevant.
Additional video available for review of pulmonary circulation, which is assumed to be prior knowledge from Anatomy and Physiology courses.
Anatomy & Physiology Recap
Basic Recap of the Circulatory System:
Right side of the heart receives deoxygenated blood from the body.
Blood is then pumped into the pulmonary circuit via the pulmonary artery for oxygenation in the lungs.
Oxygenated blood is returned to the left side of the heart through the pulmonary veins for circulation to the body.
Etiology of Pulmonary Embolism
Definition: A pulmonary embolism is an obstruction of the pulmonary vasculature.
Most often caused by:
Thrombotic obstructions: Blood clots that originate in the peripheral circulation (commonly from the lower extremities).
Clots travel through the bloodstream and get lodged in the pulmonary arteries.
Non-thrombotic causes (less common):
Fat embolism (from large bone fractures, e.g. femur)
Air embolism (from invasive procedures, central line access)
Foreign body embolism (e.g. amniotic fluid during childbirth, catheter-related materials like balloon fragments)
Most pulmonary embolisms originate in the lower half of the body.
Risk Factors for PE
General risk factors for PE correlate with those for DVT (Deep Vein Thrombosis).
High risk factors also include:
Atrial fibrillation and atrial flutter: Increased risk of clot formation, particularly in the right atrium, leading to potential PE.
Immobility: Previous history of spinal cord injury or severe immobilization due to illness.
Virchow's Triad: Factors leading to thrombosis that also apply to PE risks:
Endothelial damage: Trauma, catheter placement, smoking.
Hemostasis: Conditions leading to abnormal clotting.
Hypercoagulability: Genetic factors including deficiencies in proteins C and S, and certain gene mutations.
Pathophysiology of PE
Overview of hemodynamics when a PE occurs:
Clots lead to obstruction of blood flow in the pulmonary arterial system.
Increased resistance in pulmonary vessels leads to elevated pressure (pulmonary artery pressure).
Right ventricular afterload increases substantially, impacting right ventricular function and potentially leading to dilation and decreased output.
If blood flow is not restored, decreased stroke volume and diminished left-sided cardiac output occurs, leading to hypotension.
Pulmonary Component: Clots prevent gas exchange by obstructing capillary beds surrounding alveoli:
Result is alveolar dead space where no gas exchange occurs, leading to hypoxemia and potentially progressing to hypoxia if not corrected.
Severity of PE (Grades)
Massive PE: High risk; can lead to acute respiratory failure, requiring interventions like intubation and mechanical ventilation.
Characterized by significant obstruction of blood flow (40% or more) leading to severe hypotension and possible coding of the patient.
Submassive PE: Patients present with signs of right ventricular dysfunction but may maintain reasonable blood pressure.
Low-risk PE: Symptoms may be present but without hemodynamic instability; often admitted to medical/surgical units for management.
Signs and Symptoms of PE
Pleuritic chest pain: Sharp, tearing, or stabbing pain.
Dyspnea: Shortness of breath is a common report.
Hemoptysis: Coughing up blood due to vascular pressure.
Tachypnea: Increased respiratory rate.
Crackles and bronchial sounds: Associated with turbulent airflow.
Tachycardia: Compensatory mechanism for decreased oxygenation.
Hypotension: May develop in severe cases.
Anxiety and restlessness: Often concomitant with respiratory distress.
Loud S2 heart sounds: Indicates increased pressure in the pulmonary circulation.
Diagnosis of PE
Laboratory Tests:
D-dimer: Elevated levels suggest clot presence but not specific to PE.
ABGs: Assess gas exchange; hypoxemia is expected.
Imaging: Spiral CT scan is preferred for confirmation; VQ scan may also be performed.
Chest ultrasound: Often used to evaluate for DVT.
Treatment of PE
General Nursing Management:
Ensure oxygenation and cardiac monitoring.
Maintain IV access for fluids and medications.
Monitor anticoagulation therapy closely.
Anticoagulation:
Commonly managed with Heparin: Requires monitoring for therapeutic levels (APTT).
Transition to Warfarin for long-term management upon discharge after achieving stable coagulation levels.
Fibrinolytic therapy: Used for massive PEs under high-acuity care settings to dissolve clots rapidly.
Surgical interventions:
Thrombectomy: Suction removal of clot material, typically done under specialty care.
Embolectomy: Rare surgical removal of emboli when other treatments are contraindicated.
Complications of PE and Treatment Considerations
Risk of hemorrhage with thrombolytic therapy.
Potential for cardiogenic shock due to right ventricular dysfunction.
Development of pulmonary hypertension due to increased afterload from the obstruction.
Comorbidities can complicate the clinical picture (e.g., COPD).
IVC Filter Placement: Used in recurrent DVT/PE cases to prevent further embolization from lower extremity clots. However, complications may arise from their presence.
Patient Education: Necessary to understand anticoagulation management and the signs of potential complications.
Prevention Strategies for PE
Emphasis on DVT prophylaxis, particularly in surgical settings.
Measures include early mobilization, mechanical devices (e.g., sequential compression devices), and anticoagulation prophylaxis.
Low-risk vs High-risk: Interventions vary based on patient risk profile for DVT and subsequently PE.