Pulmonary Embolism

Pulmonary Embolism (PE)

Etiology and Pathophysiology

  • Blockage of pulmonary arteries by thrombus, fat, air embolus, or tumor tissue.

    • Leads to lung tissue death.

    • Most often affects lower lobes due to them being smaller.

    • Commonly originates from DVT (VTE = spectrum from DVT to PE).

      • Most Common Causes: deep veins of legs, femoral or iliac veins, right side of heart (Afib causes risk of PE or stroke due to vascular stasis), and pelvic veins (especially after surgery or childbirth).

        • Superficial doesn’t normally become a PE → they don’t break off as often as a DVT does.

      • Less Common Causes: Central venous catheter or arterial lines (breaks off and causes PE from blood clotting around it and breaking off), fat (fractured long bones with more yellow marrow and breaks off), air (IV → air embolus from too much air), vegetation on heart valves, amniotic fluid, cancer (tumor tissue growing in lungs and blocking off vasculature).

Risk Factors

  • Include immobility

  • History of VTE

  • Recent surgery within 3 months (especially pelvic and lower extremity)

    • Likelihood of developing blood clot is about 60% for patients that have a total knee replacement.

  • Cancer

  • Obesity

  • Hormonal therapies

  • Smoking

  • Heart failure

  • Pregnancy

  • Clotting disorders

Clinical Manifestations

  • Depends on type, size, and extent of emboli.

    • Larger Emboli: Sudden onset

    • Smaller Emboli: Gradual onset

  • Dyspnea most common

  • Mild-moderate hypoxemia

    • Determined by ABGs → SPO2 in blood.

  • Other: Tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope (not perfusing brain/lacking blood flow to brain), pulmonic heart sounds.

    • Symptoms caused by decreased perfusion

  • Massive PE: Altered mental status (deoxygenation), hypotension, impending doom, cardiorespiratory arrest/death.

Complications

  • Pulmonary Infarction: Death of lung tissue.

    • PE decreases blood flow to lung tissues and causes alveolar lung necrosis and hemorrhage.

  • Pulmonary Hypertension: Increased pressure in pulmonary artery.

    • Commonly due to back up of blood from a large PE and/or multiple PEs.

    • Scarring after multiple prior PEs

      • Ex. If someone has a DVT that’s slowly breaking off it can lead to scar tissue.

    • Right ventricular hypertrophy (Cor pulmonale)

      • Cor pulmonale (right sided HF) symptoms: Dependent pitting edema → weeping edema if it worsens.

        • Pt already has respiratory symptoms like dyspnea since it started as a PE, but Cor pulmonale develops into the “rest of the body” HF symptoms.

Diagnostic Studies for PE (3)

  • D-Dimer: Indicates fibrin degradation, often elevated.

    • Also performed for normal VTE or DVT.

  • CT Angiography (CTA): Looks at vasculature through chest cavity/lungs. Requires IV contrast. GOLD STANDARD.

    • Worried About: Kidney failure patients & shellfish allergy.

  • Ventilation-Perfusion (V/Q) Scan: Assess ventilation and perfusion.

    • Perfusion Scanning → radioscopic injection; looks at pulmonary circulation (not nephrotoxic, it takes a chest scan and looks at where vasculature goes).

    • Ventilation Scanning → Pt breathes in radioactive gas to visualize air distribution.

    • Intubated and sedated patients unable to participate.

Important but Non-Diagnostic Studies

  • ECG (nonspecific ST segment and T wave changes)

    • Hypoxia → Depressed ST segment

  • Chest x-ray (atelectasis or pleural effusion from immune system activation to break down PE by sending more WBCs and fluid to that area)

  • Lactic acid if worried about alveolar necrosis.

  • H&H if worried about hemorrhage.

    • Platelets generally low in patients who are bleeding.

  • Troponin levels usually high

    • Levels increase when there’s cardiac ischemia (not enough oxygen to heart muscle)

  • BNP

    • Determines if there’s stretch from potential fluid volume overload

Interprofessional Care for PE

Immediate Management

  • Start anticoagulation immediately (prevents clot from getting bigger and decrease risk of emboli)

    • 3 Phases (dependent on cause):

      • Initial: First 7 days

      • Longer: Up to 6 weeks

      • Extended: 6 months and beyond

  • Support cardiorespiratory status (varies by size and location of PE).

    • Oxygen → ABG tells provider what type of oxygen is needed.

      • Mild Hypoxemia: nasal cannula or face mask.

      • Extreme Hypoxemia: Mechanical ventilation or hiflow

    • Pulmonary hygiene (IS, ambulation, position into semi-high fowlers)

    • Obstructive Shock: IV fluids (not for HF patients nor elevated BNP), vasopressors (helps perfuse major organs)

    • HF: Diuretics

      • Check BNP and see if patient has peripheral edema

    • Pain: Opioids

      • Make sure respiratory rate (O2) is good

      • Respiratory acidosis risk

  • Monitor coagulation levels closely and adjust treatment accordingly.

Surgical and Med Therapy

  • Anticoagulant Medication (immediate):

    • LMWH (Lovenox): Weight based

      • Molecules are all the same size (more predictable, no lab monitoring)

    • Unfractionated IV Heparin:

    • Warfarin (Coumadin):

      • Takes several days to reach therapeutic levels.

      • Admission 3 months or longer.

  • Fibrinolytic Agents (dissolves clot): High risk for bleeding

    • Tissue Plasminogen Activator (tPA)

    • Alteplase (Activase)

  • Pulmonary embolectomy for massive PE (removes PE)

    • For hemodynamically unstable patients (not well perfused → present with altered mentation and cyanosis, monitor vital signs)

    • Contraindicated: thrombolytic therapy.

  • Inferior vena cava filter to prevent migration of clots in pulmonary system

    • Used if they deliver a PE related to a DVT

    • It can get full especially in patients where a lot of clots are breaking off and may end up needing an embolectomy or tPA.

    • Medications: Antiplatelet and anticoagulants (dual)

      • IVC introduces something new to body that body will try to fight off = need antiplatelets.

  • Percutaneous Catheter Embolectomy:

Patient Education and Follow-Up

  • Prevention #1:

    • Intermittent pneumatic compression devices (SCDs)

    • Early ambulation

    • Anticoagulation

      • High risk pts also encouraged to take antiplatelets like low-dose baby aspirin (81mg).

  • Immediate Treatment:

    • Bed rest in semi-fowler’s position to bring more oxygen

    • Assess cardiopulmonary status

      • Listen to lungs and heart, check cap refill, check for edema, cyanosis.

    • Administer: Oxygen, IV fluids and medications (question these orders as needed, ex. HF pts → fluid restriction).

    • Monitor For:

      • Coagulation (specific to medication)

        • Warfarin → Check INR

        • Heparin → aPTT or factor Xa

        • Anticoagulants → Kidney function

      • Complications

        • Heparin-Induced Thrombocytopenia (HIT)

        • Generalized bleeding (from the gums, ears, eyes, nose)

        • Hemorrhagic stroke (from anticoagulants)

          • Monitor neurologic function & pupil response.

  • Nursing Management:

    • Fall precautions once out of bed (bleeding risk = immediate fall risk)

    • Patient emotional support

    • Patient Education: Long-term anticoagulant therapy (3+ months), importance of follow-up exams, VTE prevention.