4.5 - Pulmonary Embolism Flashcards
What is a pulmonary embolism (PE)?
Clot either thromboembolus or other undissolved solid, liquid or gaseous material that has traveled to the lung by the venous system. It becomes lodged in the pulmonary arterial circulation causing a cessation or obstruction of blood flow. Acute PE is a form of venous thromboembolism (VTE) that is common and sometimes fatal.
How is the extent of lung tissue injury determined for a PE?
It is determined by the size of the embolus which is considered massive if more than 50% of the blood flow is obstructed
What is a hemodynamically unstable PE?
It is a PE that results in Hypotension:
- SBP <90 mmHg or a drop in SBP of > 40 mmHg from baseline for a period of > 15 minutes OR
- Hypotension that requires vasopressors or inotropic support and the change in BP cannot be explained by sepsis, arrhythmia, left ventricular dysfunction from MI or infarction or hypovolemia
You would expect to see this with a massive PE but can also be caused by a smaller PE if there is underlying cardiopulmonary disease
What is a hemodynamically stable PE and why is the distinction important?
- Hemodynamically stable PE is defined as a PE that does not include hypotension
- The distinction between unstable and unstable PE is important to determine risk of death. Death can occur as quickly as 2 hours after the event but remains for approximately 72 hours.
What are the risk factors associated with PE development?
Factors that predispose patients for thrombotic emboli (Virchow triad) such as:
1. Venous stasis: DVT in LE and pelvis leads to 70% of PE
- Prolonged immobility or surgery involving general anesthesia longer than 30 minutes
- Congestive heart failure
- Dehydration
- Obesity
- Advanced age
2. Endothelial injury, Vessel wall injury (surgery, fractured hip and/or pelvis)
3. Hypercoagulability (estrogen, malignancy)
4. Genetic predisposition
5. Other:
- Fat embolism, orthopedic trauma especially through marrow containing bone
- Air embolism
- Tumor fragments
- Pregnancy -Amniotic fluid embolism
Septic debris from indwelling venous devices
What are the signs and symptoms associated with a PE?
Patients with PE can present acutely, sub acutely or chronically. The following list describes acute and sub acute symptoms with the difference being the time of presentation. Acute = S & S appear immediately after obstruction of the pulmonary vessels. Sub acute = within days or weeks after the initial event. Chronic = develop pulmonary HTN over many years. This is presented in a different module (pulmonary HTN)
- Dyspnea, insidious or acute onset is the most common symptom
- Apprehension, anxiety and perception of “impending doom”
- Chest pain, dull, central and pleuritic with pulmonary infarction
- Substernal discomfort
- Pleuritic pain with PE with infarction
- Hemoptysis with pulmonary infarction
- Syncope
What are the physical exam findings associated with a PE?
- Tachycardia
- Tachypnea and dyspnea – most common presenting symptom
- Initially elevated BP
- Diaphoresis
- Decreased cardiac output
-
Cardiovascular compromise with hypotension and shock
- Hypotension from PE is from diminished stroke volume and cardiac output. The pulmonary vascular resistance is increased impeding right ventricular outflow diminishing flow from the right side of the heart. This in turn decreases the left ventricular preload and decreases left heart cardiac output
-
Signs of right ventricular overload
- Jugular venous distention
- Increased intensity of the second heart sound
- Peripheral phlebitis
-
Signs of fat embolization
- Sudden, marked dyspnea in a susceptible patient
- Altered consciousness
- Body temperature elevation higher than 102 F
- Petechiae over the thorax, shoulder and axillae
What 8 diagnostic/laboratory tests are used to diagnose a PE?
1. ABG – impaired gas exchange from PE is due to mechanical and functional obstruction of the vascular bed altering the ventilation to perfusion ratio and also due to inflammation resulting in surfactant dysfunction and atelectasis resulting in intrapulmonary shunting
- Acute respiratory alkalosis
- Variable degrees of hypoxemia
2. D dimer – is usually obtained if DVT and PE are suspected. This is not a diagnostic test that can stand alone.
- It indicates there is formation and/or breakdown of a clot. A negative D dimer can indicate a clot is unlikely. A positive D dimer indicates the need for further testing to determine the location of the clot.
3. EKG – Rule out possible cardiac causes for presentation
- Nonspecific changes
- Sinus tachycardia or atrial fibrillation is possible
4. Chest X-ray – would likely be normal or with small infiltrates and/or effusion
5. Contrast enhanced spiral (helical) chest CT
- PE protocol chest CT requires IV administration of iodinated contrast
- Contraindications to spiral CT include renal dysfunction and dye allergy
- Used according to standardized protocols in conjunction with expert interpretation, this test has good accuracy for detection of large (proximal) PEs but it has a lower sensitivity for detecting small (distal) emboli
- The sensitivity of CT for PE improves by combining the CT pulmonary angiography results with objective grading of clinical suspicion
6. Ventilation perfusion scan
- Require administration of radioactive material (via inhaled and IV routes)
- VQ scans are most useful in a patient with a normal chest x-ray
- VQ scans may be classified as normal, non-diagnostic or high probability
- If read as high probability for PE, treat with anticoagulation
- If read as indeterminate or low probability for PE, consider pulmonary angiography if clinical suspicion remains high
- If CXR is abnormal or if COPD is present, lung scanning may lead to an erroneous interpretation. Consider CT angiogram
7. Pulmonary angiography remains the gold standard for diagnosis of PE. Anatomic locations can be confirmed (saddle, lobar, segmental, sub-segmental.
- Saddle – lodges at the bifurcation of the main pulmonary artery (PA) and often extends into the R and L main pulmonary arteries
- Most PEs move beyond this bifurcation and lodge distally in the main lobar, segmental and sub segmental branches of the PA.
- PE can be bilateral or unilateral.
- Smaller thrombi that end up in the peripheral segmental or sub segmental branches are more likely to cause pulmonary infarctiion and pleuritic
8. Venous Doppler studies of the LE – may reveal DVT that requires anticoagulation, in part obviating the need for evaluation of PE
What are the goals of treatment for a patient with a PE?
When a patient presents with suspected acute pulmonary embolism:
1. Initial resuscitative therapy should focus on oxygenating and stabilizing the patient.
- Resuscitative therapy can range from supplemental oxygen to ventilator support and hemodynamic support.
- Supplemental oxygen is indicated to keep oxygen saturation above 90%
- Hemodynamic support may be needed for massive emboli with hypotension
- Surgical embolectomy is reserved for those patients with massive emboli in the central pulmonary arteries and the clot is causing hypotension and shock
- Inferior vena cave interruption (“umbrella” device; Greenfield filter) is indicated when the risk of further emboli is perceived to be high or when there is an absolute contraindication to anticoagulation
3. Then begin the mainstay of therapy which is anticoagulation.
What medications are used in the long term treatment of a PE?
Fondaparinus (Arixa)
- 5 mg SQ once daily for patients < 50 kg
- 7.5 mg SQ once daily for patients 50-100 kg
- 10 mg SQ once daily for patients > 100 kg
Argatroban
- Use weight based dosing to achieve a partial thromboplastin time of 1.5 – 3 times baseline
What anticoagulation medications are used in the treatment of a PE?
1. Heparin may be started while confirmatory tests are being conducted
- Weight based dosing includes an initial bolus of 80 units/kg followed by a continuous infusion of 18 units/kg
- Dosage should be sufficient to maintain a PTT at 2-2.5 times control
- Some hospitals use a heparin protocol with PTT checks every 6 hours to guide the heparin therapy
2. Low molecular weight heparin (enoxaparin/Lovenox) 1 mg/kg SQ every 12 hours
- Lower risk of bleeding
- No extensive monitoring is needed
3. Warfarin (Coumadin)
- Begin at the time of diagnosis of PE, first dose is 5-10 mg PO
- Heparin should be continued until the therapeutic range is achieved with warfarin
- Monitor the international normalized ratio (INR) after initial daily doses of Coumadin. Adequate** **oral anticoagulation effect is 2-2.5 for at least 2-3 days
- Length of treatment is 3-6 months for the initial episode of PE. For recurrent episodes, treat longer for 6-12 months. Consider placement of an indwelling vena cava filter to protect against massive embolization in patients with ongoing risks
What is Wegener granulomatosis?
- Necrotizing granulomas of the respiratory tract, both upper and lower, pulmonary microangiitis and glomerulonephritis
- Associated with the following:
- Hemoptysis
- Dyspnea
- Cough
- Pulmonary infiltrates
