B.42 Pulmonary Embolism

Question 1

B.42 Pulmonary Embolism

define

Answer 1

luminal obstruction of one or more pulmonary arteries, typically due to blood thrombi from deep vein thrombosis (DVT)

Question 2

B.42 Pulmonary Embolism

Epidemiology

Answer 2

Incidence :
- ∼ 1–2 venous thromboembolism per 1,000 in the United States per year
- Rises with age

Sex: overall ♂ > ♀ but women have a slight increase during the reproductive years

Mortality: Venous thromboembolism accounts for ∼ 100,000 deaths in the US per year.

Question 3

B.42 Pulmonary Embolism

Etiology

Answer 3

Most common: Deep vein thrombosis

Causes of nonthrombotic embolism:
Fat embolism
Air embolism
Amniotic fluid embolism
Others: bacterial embolism, pulmonary tumor embolism, pulmonary cement embolism

PE is FATAL: PE caused by Fat, Air, Thrombus, Amniotic fluid, and Less common, i.e., bacterial, tumor, and cement.

Question 4

B.42 Pulmonary Embolism

Pathophys

Answer 4

thrombus formation (see “Virchow’s triad.”) → deep vein thrombosis in the legs or pelvis (most commonly iliac vein) → embolization to pulmonary arteries via inferior vena cava → partial or complete obstruction of pulmonary arteries

Question 5

B.42 Pulmonary Embolism

Pathophysiologic response of the lung to arterial obstruction

Answer 5

Infarction and inflammation of the lungs and pleura
- Causes pleuritic chest pain and hemoptysis
- Leads to surfactant dysfunction → atelectasis → ↓ PaO2
- Triggers respiratory drive → hyperventilation and tachypnea → respiratory alkalosis with hypocapnia (↓ PaCO2)

Impaired gas exchange
- Mechanical vessel obstruction → ventilation-perfusion mismatch → arterial hypoxemia (↓ PaO2) and elevated A-a gradient

Cardiac compromise
- Elevated pulmonary artery pressure (PAP) due to blockage → right ventricular pressure overload → forward failure with decreased cardiac output → hypotension and tachycardi

Question 6

B.42 Pulmonary Embolism

pathophys of Pulmonary vasoconstriction

Answer 6

thromboxane A2, prostaglandins, adenosine, thrombin, and serotonin secreted by activated platelet and the thrombus → pulmonary vasoconstriction and bronchospasm

Question 7

B.42 Pulmonary Embolism

pathophys of Saddle Thrombus

Answer 7

A blood clot (e.g., from deep vein thrombosis) that lodges at the bifurcation of the pulmonary trunk as it splits into the right and left pulmonary arteries.

Can obstruct blood flow through the pulmonary arteries and lead to right heart strain, hemodynamic instability, and/or death.

Question 8

B.42 Pulmonary Embolism

clinical

Answer 8

Acute onset of symptoms
- Dyspnea (> 75% of cases) [5]
- Tachycardia and tachypnea (up to 50% of cases)
- Sudden pleuritic chest pain (∼ 20% of cases)
- Cough and hemoptysis
- Associated features of DVT: e.g., unilaterally painful leg swelling

Less common features of PE [5]
- Decreased breath sounds
- Dullness to percussion
- Split S2
- Low-grade fever
- Rarely, upper abdominal pain

Features of massive PE (e.g., due to a saddle thrombus)
- Presyncope or syncope
- Jugular venous distension and Kussmaul sign
- Hypotension and obstructive shock
- Circulatory collapse

Question 9

B.42 Pulmonary Embolism

Wells Criteria

Answer 9

The Wells score is a diagnostic algorithm for assessing the probability of PE and has been validated in inpatient and outpatient settings

Criteria:
Clinical symptoms of DVT
PE more likely than other diagnoses
Previous PE/DVT
Tachycardia (heart rate > 100/min)
Surgery or immobilization in the past 4 weeks
Hemoptysis
Malignancy

Total score 0–1: low probability of PE (6%)
Total score 2–6: intermediate probability of PE (23%)
Total score ≥ 7: high probability of PE (49%)

Question 10

B.42 Pulmonary Embolism

DX in Hemodynamically Unstable Pt

Answer 10

Assess for signs of RV dysfunction.
- Obtain an ECG.
- Perform a bedside echocardiogram or focused cardiac ultrasound (FoCUS)

Consider adding DVT point-of-care ultrasound (POCUS).

Obtain confirmatory imaging (CTPA or V/Q scan) when stable enough for transport.

Question 11

B.42 Pulmonary Embolism

DX

Answer 11

D-dimer - Normal levels: < 500 ng/mL

ABG:
↑ Alveolar-arterial gradient
Hypoxemia (e.g., ↓ SaO2, PaO2 < 80 mm Hg)
Respiratory alkalosis

CBC: may show leukocytosis

BMP: used to assess renal function

Cardiac biomarkers: e.g., troponin, BNP, NT-proBNP

Question 12

B.42 Pulmonary Embolism

CXR Findings

Answer 12

Hampton hump: a wedge-shaped opacity in the peripheral lung with its base at the thoracic wall; caused by pulmonary infarction and not specific for PE

Westermark sign: an area of lung parenchyma lucency caused by oligemia secondary to occlusion of blood flow

Fleischner sign: a prominent pulmonary artery caused by vessel distention due to a large pulmonary embolus (common in massive PE)

Question 13

B.42 Pulmonary Embolism

ECG Findings

Answer 13

Most common findings
- T-wave inversions or flattening
- Sinus tachycardia
- Normal ECG

Signs of right heart strain
- SIQIIITIII-pattern
- New right bundle branch block

Question 14

B.42 Pulmonary Embolism

CT pulmonary angiography (CTPA)

Answer 14

CTPA is the preferred test for the diagnosis of acute PE.

Technique: CT chest with bolus IV contrast enhancement of the pulmonary arteries

Indications:
- All patients with a high PTP of PE
- Elevated D-dimer in patients with a low or intermediate PTP of PE

Contraindications
- Renal insufficiency
-Contrast allergy

Findings
- Direct finding of PE: intraluminal filling defects of pulmonary arteries
- Pulmonary infarct: opacity with consolidated border; may be accompanied by pleural effusion
- Evidence of RV dysfunction

Question 15

B.42 Pulmonary Embolism

Ventilation/perfusion scintigraphy (V/Q scan)

Answer 15

Technique: comparison of perfusion and ventilation scintigraphy to identify ventilation-perfusion mismatch

Indication: alternative to CTPA in patients with contraindications for iodinated IV contrast

Findings
- The absence of perfusion in normally ventilated areas of the lung (mismatch) suggests PE.
- Discordance between V/Q scan results and the clinical PTP necessitates further evaluation.

Question 16

B.42 Pulmonary Embolism

General Treatment

Answer 16

• Manage unstable patients using the ABCDE approach
• Provide oxygen therapy for hypoxic patients.
• Treat PE based on severity and bleeding risk; start empiric anticoagulation for PE if indicated.
• Provide analgesia; avoid NSAIDs if possible.

Question 17

B.42 Pulmonary Embolism

Empiric anticoagulation for PE

Answer 17

Stable patients: low molecular weight heparin (LMWH)

Unstable patients or patients with renal insufficiency: unfractionated heparin

Question 18

B.42 Pulmonary Embolism

Tx Protocol

Answer 18

Treatment Protocol:

1. Initial Management:
   - Administer O2, IV saline, vasopressors, and morphine.
   - Initiate anticoagulation (contraindicated in high bleeding risk).
2. Anticoagulation Strategy:

• For stable patients: use Low Molecular Weight Heparin (LMWH).
• For unstable patients: follow the Unstable Pulmonary Hypertension (UFH) protocol.
• Long-term: Warfarin therapy for 3 weeks to 6 months.

3. Thrombolytic Therapy:
   - Administer tPA, streptokinase, or urokinase (e.g., streptokinase infusion for 24 hours with hydrocortisone to mitigate side effects).

• Consider for massive pulmonary embolism causing right heart failure (RHF).

1. Embolectomy:
   - Reserved as a last resort when thrombolysis is contraindicated.