Pulmonary Embolism Flashcards
What is a venous thromboembolism
either a pulmonary or deep vein thrombosis
Define submassive PE
A PE associated with evidence of right ventricular dysfunction and/or biomarkers of myocardial injury without systemic hypotension (systolic blood pressure < 90 mmHg).
Define massive PE
A PE associated with persistent systemic hypotension (systolic blood pressure < 90 mmHg) or hemodynamic collapse
What is Virchows triad?
The pathophysiologic factors contributing to development of PE:
- Vascular injury
- Coagulation alteration
- Venous stasis
• Immobility (paralysis, prolonged travel, critical illness)
• Casting
• Congestive heart failure
• Obesity
• Age > 60
These are all risk factors for what aspect of Virchow’s triad?
venous stasis
• Hereditary thrombophilias
• Heparin-induced thrombocytopenia
• Antiphospholipid antibody syndrome
• Nephrotic syndrome (loss of anti-thrombin III)
• Estrogen therapy
• Malignancy
These are all risk factors for what aspect of Virchow’s triad?
altered coagulation
• Surgery • Trauma • Post-partum • Indwelling vascular access • History of VTE These are all risk factors for what aspect of Virchow's triad?
vascular injury
What are the 3 most common hereditary thrombophilias?
The three most common hereditary thrombophilias are factor V Leiden deficiency (the most common), prothrombin G20210A, and hyperhomocysteinemia.
When is screening for hereditary thrombophilias such as factor V leiden defciency recommended?
a strong family history of VTE
an unprovoked VTE at a young age
recurrent VTE in the absence of other risk factors
thrombosis at an unusual vascular site (i.e., not a deep vein in the leg or upper extremities)
What is the most common cause of a PE? (be specific)
proximal lower extremity DVT
Why are upper extremity DVT’s an increasingly common cause of PE?
increased use of PICC lines
How do you define a proximal lower extremity DVT?
above the knee
What is a saddle PE?
When thrombus lodges in the main pulmonary artery trunk
How does the body compensate for the dead space created by a PE?
Most patients are able to respond to this increased dead space by increasing minute ventilation and often hyperventilating so that an elevated PaCO2 is an uncommon finding in PE. However, in patients unable to augment minute ventilation (e.g., deeply sedated patients on a ventilator), a sudden increase in PaCO2 that occurs absent a change in minute ventilation may signal the development of a VTE.
What is the main cause of hypoxemia in patients with PE
dysregulated V/Q matching
In patients with a massive PE, what contributes to hypoxemia?
decreased mixed venous oxyhemoglobin saturation
What causes death in PE, usually?
cardiovascular collapse
How can relatively healthy patients with a PE maintain CO?
recruitment of pulmonary vessels and increased right ventricular (RV) stroke volume even when 40% of their pulmonary vasculature is obstructed.
In patients with limited CV reserve or when vascular obstruction exceeds 50%, shock and hemodynamic collapse rapidly develop through 2 major pathways.
At what point does vascular obstruction prevent compensation of CO in health patients?
when obstruction is > 50%
How does a PE affect the heart acutely?
increases RV afterload, which leads to fatigue and dilation
How is CO affected in a PE by RV afterload increases?
RV dilation pushes the septum to the side, which impacts LV preload and decreases CO
Why is the drop in CO a problem during a PE?
it worsens the O2 mismatch in the RV, leading to ischemia, progressive dilation and eventually cardiac arrest
What is a chest xray good for in working someone up for a PE?
identifying other causes of symptoms (i.e. ruling in, not out)
a normal CXR should RAISE suspicion of a PE!!!
Why are pulmonary and venography angiography not ideal, despite being the previous gold standard for PE?
these exams are invasive (they require intravenous cannulation of a proximal deep vein), require specialized expertise to perform, are subject to significant interrater reliability especially for smaller thrombi, and require injection of intravenous contrast putting patients at risk for allergic reactions and kidney injury.
venography has been replaced with ultrasound
Does lower extremity ultrasound have good or bad sensitivity for PE?
poor sensitivity - it is good for above the knee DVT in the setting of PE, but not good for PE in isolation
In theory, what should a PE do to the V/Q mismatch scan results?
a PE should produce mismatched segmental-sized ventilation and perfusion defects.
However, 80% of scans are non specific
What is the most frequent diagnostic scan for a PE?
the PE-CT/CTPA
What are two drawbacks of the CTPA?
A CTPA does require exposure to ionizing radiation which is especially a concern for younger and/or pregnant patients and requires intravenous contrast which (as with invasive angiography) puts patients at risk for allergic reactions and kidney injury.
What should diagnostic testing for a suspected VTE be guided by?
an assessment of the patients pre test probability!!
i.e. validated risk score
What is a PE likely Wells score?
> 4
What is a PE unlikely Wells score?
< 4
What does a D dimer assay measure?
product of fibrin degradation
Are D dimer assays sensitive or specific for VTEs?
sensitive (good screen) but not specific - they are used to rule out a PE but not to rule in
What can cause an elevated D dimer? what is the level? What does this mean for assessment of VTE?
advanced age, inflammation, trauma, pregnancy, malignancy, VTE
> 500
Does not rule-in PE, only a low level can rule out VTE
If someone has a Wells score of less than 4, what should you do next to evaluated for VTE?
D dimer testing
If someone has a Wells score over 4, what should you do next to evaluate for a VTE?
CTPA
What are the two options for acute VTE therapy?
- An infusion of unfractionated heparin (UFH). Dosing typically follows a weight-based dosing nomogram with an 80 U/kg bolus followed by an 18 U/kg/hour infusion. Activated partial thromboplastin times (aPTTs) are monitored every 6 hours to ensure sufficient and safe levels of anticoagulation.
- Subcutaneous injections of low-molecular-weight heparin (LMWH). Examples include enoxaparin or dalteparin.
How do you monitor unfractionated heparin anticoagulation in a VTE patient?
aPTT’s every 6 hours
What are drawbacks to the use of LMWH in acute VTE therapy?
- dosing can be difficult in patients at the extremes of body weight and in those with renal insufficiency. In these scenarios, monitoring anti-Xa levels is usually required. 2. LMWHs are not as immediately reversible as UFH which has a readily available antidote – protamine. This can be problematic in cases of severe bleeding.
When should you start anticoagulant therapy in a patient with a high pre test probability of PE?
immediately, while waiting for diagnostic testing
If someone has an absolute contraindication to anticoagulation (i.e. active bleeding) what should you do in the treatment of a PE?
Placement of an inferior vena cava filter to prevent further embolization
In patients with a persistent systemic hypotension, hemodynamic collapse, and a PE (massive), what is indicated as treatment?
systemic fibrinolytic therapy
Does the term “massive PE” refer to the size of the thrombus, the degree of hemodynamic collapse, or both?
only to hemodynamic alterations
What does the American college of chest physicians recommend for the treatment of submassive PE?
The American College of Chest Physicians (ACCP) recommends against routine use of systemic fibrinolytic therapy for patients with submassive PE. Patients with submassive PE (especially those with multiple high-risk features) are best managed as part of a multidisciplinary PE team (as is done here at Northwestern).
What is the most common long term therapy for VTE?
Vitamin K antagonists (VKAs): VKAs (most commonly warfarin) remain one of the most common anticoagulants used for the treatment of VTE. Advantages includes their low cost, reversibility, and safety in patients with renal impairment. The major disadvantage is the need for life-long periodic laboratory monitoring to ensure safe and sufficient levels of anticoagulation.
What is the preferred long term therapy for cancer associated VTE?
LMWH
What does the ACCP recommend for long term therapy of non-cancer associated VTE? What are the cons of this?
novel oral anticoagluants like apixaban or edoxaban, NOT warfarin.
Advantages include their rapid onset and predictable pharmacokinetic profiles (obviating the need for laboratory monitoring). Disadvantages include cost, variable insurance coverage, and limited or no options for immediate drug reversal in the setting of bleeding.
What is the minimum length of long term therapy for a VTE, regardless of the type?
3 months
If a patient has an unprovoked VTE and low to moderate bleeding risk how long should anticoagulant long term therapy be continued?
3 months - infinity
What is the most severe complication of a PE?
the development of chronic thromboembolic pulmonary hypertension (CTEPH) which occurs in ≈ 1-4% of patients with a PE.
When is anticoagulant prophylaxis recommended in the setting of increased VTE risk?
For patients with at least one risk factor for VTE, prophylactic doses of anticoagulantion are recommended to help prevent the development of VTE. Options include subcutaneous heparin and LMWH. The intensity of dosing is adjusted based on a patient’s risk profile. For patients with a contraindication to pharmacologic thromboprophylaxis, intermittent pneumatic calf compression devices are recommended.
A 65-year-old male with stage IIIB lung adenocarcinoma presents to the emergency department with pleuritic chest pain and shortness of breath. He undergoes computed tomography pulmonary angiography and is found to have an acute PE in a segmental branch of his right pulmonary artery. He is started on an infusion of unfractionated heparin (UFH) and transferred to an inpatient medicine floor as he is hemodynamically stable without evidence of right heart strain or myocardial injury. He tolerates anticoagulation without complication and has no clear contraindications to long-term therapy. Your team begins planning for discharge in the coming days. Which anticoagulation regimen would you recommend?
a. Warfarin (a vitamin K antagonist) for 6 months
b. Enoxaparin (a low-molecular-weight heparin) for 3 months
c. Warfarin for 3 months followed by consideration of an inferior vena cava filter given his risk profile.
d. Extended-duration (12 months or greater) of enoxaparin
D. This patient has a malignancy-associated PE without clear contraindications to anticoagulation or a high risk of bleeding. The ACCP recommends LMWH over VKA therapy for patients with malignancy-associated VTE. For patients with active cancer, consideration should be given to extending anticoagulation indefinitely if the patient is not at high risk of bleeding.
A 75-year-old female presents to urgent care clinic with dyspnea. She has a history of a provoked right femoral DVT 10 years ago treated following a cholecystectomy for which she was treated with 3 months of warfarin. Her heart rate is 110 and she is tachypneic but her blood pressure is normal. A basic metabolic panel and complete blood count are unrevealing. What is the most appropriate next step?
a. Obtain a D-dimer level
b. Obtain a CTPA
c. Administer systemic fibrinolytic therapy
d. Administer unfractionated heparin before pursuing additional testing
D. This patient has a Wells score of 6 and is at very high risk of having a PE. In patients with a very high pre-test probability of having a PE, anticoagulation therapy should be promptly initiated while pursuing additional testing as long as there are no clear contraindications to anticoagulation.
What are the major disadvantages of computed tomography pulmonary angiography?
Major disadvantages of CTPA include exposure to ionization radiation, risk of allergic reaction and/or kidney injury with intravenous contrast administration, and low interrater reliability for small sub-segmental thrombi.
