pulmonary venous embolism Flashcards
- Obstruction of the pulmonary
artery or one of its branches by
material (thrombus, tumor, air,
or fat) that originated elsewhere
in the body
pulmonary venous thromboembolism (PE)
- Thromboembolism (most common)
- Septic embolism
- Venous air embolism (aka non-thrombotic pulmonary embolism)
- Central line removal
- Fat embolism (large fractures like femur)
- Amniotic fluid embolism
- Tumor embolism
- Foreign material embolism (e.g. silicone, broken catheters, guide wires, vena cava filters,
embolization coils, and endovascular stent components)
types of emboli
VIRCHOW’S TRIAD
- Venous stasis increases with immobility
- Obesity
- Stroke
- Bed rest (esp. post-op)
- Injury to vessels
- Trauma
- Orthopedic surgery
- Hypercoagulability
- Medications – oral contraceptives, hormonal replacement therapy (HRT)
- Diseases – malignancy, surgery
- Inherited gene defects – factor V Leiden, prothrombin mutation
- Acquired thrombophilia – protein C and S deficiency, antithrombin deficiency, antiphospholipid antibodies
PE risk factors
- Inherited
- 20-30 genetic risk factors for VTE have been identified
- Includes factor V Leiden and the prothrombin gene mutation
- Acquired (this distinction will matter for length of anticoagulation)
- Provoking
- Recent surgery
- Trauma
- Immobilization
- Initiation of hormone therapy
- Active cancer
- Non-provoking
- Obesity
- Heavy cigarette smoking
what is the source of PE
- Most emboli arise from lower extremity proximal veins (iliac, femoral, popliteal)
- Calf vein DVT rarely embolizes to the lung
- 2/3 of calf vein thrombi resolve spontaneously after detection
- If untreated, 1/3 of calf vein DVT eventually extend into the proximal veins where they have greater
potential to embolize - PE can also arise from DVT in non-lower-extremity veins (renal and upper extremity veins)
- Embolization from these veins is less common, but possible
- More likely if patient has a port, PICC line, central line, or other venous device
- Most thrombi develop at sites of decreased flow in the lower extremity veins, such as valve
cusps or bifurcations
pathophysiologic response to PE
lung infarction:
More likely to have pleuritic chest pain and hemoptysis due to an intense inflammatory response in the lung and adjacent
visceral and parietal pleur
abnormal gas exchange:
hypocapnia and respiratory alkalosis
* Hypercapnia and acidosis are unusual in PE unless shock is pres
cardiovascular compromise:
Pulmonary vascular resistance (PVR) is increased due to physical obstruction of the vascular bed with thrombus and hypoxic
vasoconstriction within the pulmonary arterial syste
- Dyspnea
- Cough (hemoptysis uncommonly)
- Tachycardia/complaint of palpitations
- Altered mental status
- Pleuritic chest pain
- Bronchospasm/wheezing
- Syncope or pre-syncope
- DVT symptoms possible (muscle cramping, pain, redness, swelling) but may be absent
signs and symptoms of PE
pulmonary embolism physical exam
- Usually unremarkable aside from dyspnea/tachypnea and tachycardia; possible fever
- Occasionally find bronchospasm and wheezing (mediator induced)
- Cardiac Exam (possible, may be absent):
- Precordial heave from right heart strain
- Loud pulmonary second sound or a gallop
- Wells score is MC used and quantifies clinical risk assessment, allowing separation of patients into low,
intermediate, or high probability groups; or PE-likely vs. PE-unlikely groups - Pulmonary Embolism Rule-out Criteria (PERC) may be used to identify patients for whom no further
testing is indicated
PERC rule
- If patients meet NONE of the criteria to the left, PE can be ruled out
- <2% chance of PE
- No further work-up needed if clinician deeps pt low risk
- If meet minimum of 1 criteria obtain D-Dimer
- If D-Dimer negative and pre-test probability of PE
per provider is low (<15% chance of having PE): No further work-up - Positive D-Dimer Proceed with CT PE
PE diagnostics
- D-Dimer
- EKG
- CXR
- CT PE (test of choice)
PE ekg
S1Q3T3 and wedge shaped infarcts
profound hypoxia with normal CXR is highly suspicious of what?
PE
diagnostic for PE
CT scan with PE protocol
Criteria
* Sustained hypotension
* Systolic blood pressure < 90 mm Hg or drops by >40 mm Hg below baseline for ≥ 15 minutes, requiring a vasopressor, or causing cardiac arrest
* Not due to a cause other than PE (arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction)
* Persistent profound bradycardia (heart rate < 40 beats per minute with signs or symptoms of shock)
* Pulselessness
Outcomes
* Death from hemodynamically unstable PE often occurs within the first two hours
* Risk remains elevated for up to 72 hours after presentation
MASSIVE OR HIGH-RISK PE
HEMODYNAMICALLY UNSTABLE
next step after PE diagnosis
risk stratification
* After PE diagnosis is made risk stratification is next step (guides management)
* Three categories based on morality data:
* High-risk PE (massive PE)
* Intermediate-risk PE (submassive PE)
* Low-risk PE
Submassive or Intermediate-Risk PE
* Acute PE without systemic hypotension BUT with either right ventricular (RV) dysfunction or myocardial necrosis
Low-Risk PE
* Acute PE without clinical markers of adverse prognosis that define massive or submassive PE
SUBMASSIVE PE AND LOW-RISK PE
HEMODYNAMICALLY STABLE
Associated with high mortality (up to 40%
Clot that is “in transit” through the heart
- Lodges at the bifurcation of the main pulmonary artery, often extending into the right and left main pulmonary
arteries - Makes up 3-6% of patients with PE
- Traditionally thought to be associated with hemodynamic instability and death, however only 22% are
hemodynamically unstable - 5% mortality
saddle PE
- Most PE move beyond the bifurcation of the main pulmonary artery to these locations
- Smaller thrombi that are located in the peripheral segmental or subsegmental branches are more likely to cause pulmonary infarction and pleuritis
Lobar, segmental, subsegmental branches of pulmonary artery
PE treatement
- Stabilization
- Oxygen
- Endotracheal intubation and mechanical ventilation may be necessary
- IV fluids/vasopressors for hypotension
Anticoagulation!!!!
* Heparin drip – start immediately then switch to DOAC
minimum of 3 months*
PE treatment if anticoagulation is contraindicated or whom risk of bleeding is very high
IVC filter
Exceptions to duration of anticoagulation rules
- Cancer, pregnant women, or patients in whom indefinite anticoagulation should be considered
duration of anticoagulation
1st episode of VTE (provoked or unprovoked) anticoagulation for a minimum of 3 months
- Extended anticoagulation beyond 3 months is NOT routinely considered in patients who have a provoked episode
of VTE with the following: - Transient risk factors, assuming the risk factor is no longer present (surgery, cessation of hormones)
- Isolated distal DVT
- Subsegmental or incidental PE
- Risk of bleeding is considered to be high
- In select populations, anticoagulation is extended to 6 to 12 months although the benefits of this are unproven
VTE prophylaxis
- Nearly all hospitalized patients qualify for chemical VTE prophylaxis with Lovenox or heparin
- Post-operative VTE prophylaxis (particularly following high-risk orthopedic surgeries (hip) is
well defined as occurring for a minimum of 35 days post-op - Lovenox
- Xarelto
- Eliquis
- Hospitals lose Medicare stars and reimbursement for every VTE that was not properly prevented
