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