Pulmonary Embolism

Overview

Pulmonary embolism is the obstruction of one or more pulmonary arteries, most commonly by a thrombus that has embolized from a deep vein of the lower extremity or pelvis. PE and deep vein thrombosis (DVT) are considered manifestations of the same disease process—venous thromboembolism (VTE)—and share risk factors, workup principles, and anticoagulant treatment.

From a respiratory standpoint, the defining physiologic consequence is the creation of alveolar dead space: alveoli that are ventilated but no longer perfused. This wastes ventilation, widens the alveolar-arterial (A-a) gradient, and contributes to hypoxemia via V/Q mismatch. In large PE, the sudden rise in pulmonary vascular resistance (PVR) can precipitate acute right ventricular (RV) failure and obstructive shock—a life-threatening emergency requiring immediate intervention.

Key Concepts

Virchow’s Triad

Three conditions predispose to venous thrombosis: venous stasis (immobility, heart failure, long-haul travel), endothelial injury (trauma, surgery, indwelling catheters), and hypercoagulability (inherited thrombophilias, malignancy, estrogen use, pregnancy). Most patients with PE have more than one factor present.

Pathophysiology

• Dead space: The obstructed segment receives ventilation but no perfusion (V/Q approaches infinity). This wasted ventilation must be compensated by increased total minute ventilation or it accumulates as hypercapnia.
• Hypoxemia:Arises from three overlapping mechanisms—V/Q mismatch in the ischemic zone, low mixed-venous O₂ content (reduced cardiac output forces greater O₂ extraction by tissues), and true shunt (from atelectasis distal to the clot or from right-to-left shunting through a patent foramen ovale that opens when RV pressure rises).
• RV failure: Acute occlusion raises PVR abruptly. The thin-walled RV is not conditioned for high afterload and dilates rapidly, shifting the interventricular septum leftward, impairing LV filling, and reducing cardiac output. Massive PE can produce obstructive shock and cardiac arrest within minutes.

Capnography and Dead Space

End-tidal CO₂ (EtCO₂) reflects alveolar CO₂ from perfused lung units. When dead space increases—as in PE—the non-perfused alveoli dilute the exhaled CO₂, causing EtCO₂ to fall even though PaCO₂ remains normal or rises. The result is a widening PaCO₂–EtCO₂ gradient (normally <5 mmHg). A sudden, unexplained drop in EtCO₂ in a mechanically ventilated patient with unchanged ventilator settings should immediately raise suspicion for PE or a significant fall in cardiac output. Review capnography waveform patterns for additional context on dead-space monitoring.

Risk Stratification

• Massive (high-risk) PE:Sustained systolic BP <90 mmHg for ≥15 minutes, or vasopressor requirement, caused by the PE. Represents obstructive shock and is treated as a reperfusion emergency.
• Submassive (intermediate-risk) PE: Normotensive but with evidence of RV dysfunction on echocardiography or CT, or elevated cardiac biomarkers (troponin, BNP/NT-proBNP). Risk of deterioration is significant.
• Low-risk PE: Hemodynamically stable, no RV dysfunction, no biomarker elevation. Candidates for early discharge and outpatient anticoagulation in appropriately selected patients.

Assessment & Findings

Symptoms and Signs

The classic presentation is acute onset dyspnea, pleuritic chest pain (sharp, worsens with breathing—from pleural inflammation near a peripheral infarct), and tachycardia. Tachypnea is nearly universal. Hemoptysis, syncope, and unilateral leg swelling (suggesting DVT) are each present in a minority of patients but are clinically important when found. PE can also present silently, discovered incidentally on imaging performed for other reasons.

Pretest Probability: Wells Score and PERC Rule

Structured pretest probability assessment must precede any diagnostic test. The Wells score assigns points for clinical signs of DVT, alternative diagnosis being less likely than PE, heart rate >100, immobilization or surgery within the prior 4 weeks, prior DVT/PE, hemoptysis, and active malignancy. The total score stratifies patients into low, moderate, or high pretest probability, guiding the choice between D-dimer testing and direct imaging.

The PERC rule is a clinical tool for ruling out PE in patients already assessed as low pretest probability. All eight criteria must be absent:

• Age < 50 years
• Heart rate < 100 bpm
• SpO₂ ≥ 95%
• No hemoptysis
• No estrogen use
• No prior DVT or PE
• No unilateral leg swelling
• No surgery or trauma requiring hospitalization within the prior 4 weeks

If all eight criteria are negative in a low-risk patient, PE can be excluded without further testing. If even one is positive, further evaluation is required. PERC must never be applied to moderate- or high-pretest-probability patients.

D-Dimer

D-dimer is a highly sensitive but non-specific marker of fibrin degradation. A negative result effectively excludes PE in patients with low or intermediate pretest probability. A positive result requires imaging to confirm PE because D-dimer is elevated by many conditions (infection, malignancy, trauma, surgery, pregnancy). In patients older than 50 years, use the age-adjusted cutoff (age × 10 μg/L) rather than the fixed 500 μg/L threshold to reduce unnecessary CTPA in older adults. D-dimer adds no value—and should not be ordered—in high-pretest-probability patients, where imaging is required regardless of the result.

Confirmatory Imaging

• CT pulmonary angiography (CTPA): First-line in most patients. Rapid, widely available, high sensitivity and specificity, and also images the RV and pulmonary vasculature for risk stratification.
• V/Q scan: Preferred when CTPA contrast is contraindicated (renal insufficiency, contrast allergy, pregnancy). A high-probability scan in a patient with high pretest probability is diagnostic.
• Bedside echocardiography: Useful in the unstable patient who cannot be transported; RV dilation, septal flattening (D-sign), and McConnell’s sign suggest large PE and guide emergent treatment decisions.

ECG and ABG Findings

Sinus tachycardia is the most common ECG finding in PE. The S1Q3T3 pattern (deep S in lead I, Q wave and T-wave inversion in lead III) and right bundle branch block suggest RV strain and occur primarily in large PE—they are neither sensitive nor specific. ABG typically shows hypoxemia, hypocapnia (respiratory alkalosis from tachypnea), and a widened A-a gradient. However, a normal A-a gradient or normal SpO₂ does not exclude PE, particularly in younger patients with smaller clots. The A-a gradient calculator can help quantify the oxygenation defect when ABG results are available.

RT Priorities / Interventions

Oxygen and Ventilatory Support

Supplemental oxygen is the first-line intervention for hypoxemia. Target SpO₂ ≥ 94–95%. For patients with respiratory failure, high-flow nasal cannula (HFNC) or non-invasive ventilation (NIV) may bridge the need for intubation, but positive pressure ventilation carries important caveats in PE: increased intrathoracic pressure reduces venous return, further compromising RV preload and cardiac output in an already strained RV. Apply positive pressure cautiously and use the lowest effective PEEP. Intubation itself can precipitate cardiovascular collapse in massive PE—have vasopressors immediately available.

Capnography Monitoring

Continuously monitor EtCO₂ in ventilated patients at risk. A sudden, unexplained fall in EtCO₂ with an unchanged ventilator pattern should trigger immediate clinical reassessment, stat communication to the team, and consideration of emergent workup for PE or circulatory collapse. Do not dismiss this finding as a sampling artifact.

Anticoagulation (RT Awareness)

Anticoagulation is the cornerstone of PE treatment, preventing clot extension and recurrence. Options include unfractionated heparin (preferred in massive PE for rapid titration and reversibility), low-molecular-weight heparin (LMWH), fondaparinux, and direct oral anticoagulants (DOACs; rivaroxaban and apixaban are approved for acute PE). Respiratory therapists should be aware of anticoagulation status when planning invasive procedures and should report signs of bleeding complications.

Massive PE: Reperfusion and Hemodynamic Support

• Systemic thrombolysis (alteplase 100 mg IV over 2 hours) is first-line reperfusion therapy in massive PE without absolute contraindications. It rapidly reduces RV afterload and improves hemodynamics.
• Catheter-directed therapy (catheter-directed thrombolysis or mechanical thrombectomy) or surgical embolectomy are options when systemic thrombolysis is contraindicated or fails.
• Vasopressors (norepinephrine preferred) maintain systemic perfusion pressure and RV coronary perfusion while reperfusion is arranged.
• Avoid aggressive diuresis or volume depletion: RV failure in PE is preload-dependent. Excessive diuresis or high PEEP further drops RV preload and can worsen obstructive shock.

Common Pitfalls

• Relying on a normal SpO₂ or A-a gradient to exclude PE. Both can be normal in smaller PE. Clinical probability assessment and validated decision rules must drive the workup.
• Ordering a D-dimer in a high-pretest-probability patient.A negative D-dimer is not reassuring enough to stop the evaluation in high-risk patients—go directly to imaging.
• Forgetting the age-adjusted D-dimer cutoff.Using a fixed 500 μg/L threshold in patients older than 50 years leads to excessive CTPA in older adults, many of whom have modestly elevated D-dimer from age alone.
• Dismissing a sudden EtCO₂ drop.A new fall in EtCO₂ in a ventilated patient is a physiologic alarm that demands investigation, not reassurance that “the sensor is off.”
• Applying excessive positive pressure in massive PE. PEEP and positive-pressure ventilation reduce RV preload and can precipitate complete cardiovascular collapse when the RV is already failing under obstructive afterload.

Board Exam Pearls

• PE is the classic cause of increased alveolar dead space (high V/Q or V/Q = ∞)—ventilation without perfusion.
• EtCO₂ falls and the PaCO₂–EtCO₂ gradient widens as dead space increases; PaCO₂ may be normal or elevated.
• PERC rules OUT PE using 8 clinical criteria—applicable only in low pretest probability patients, and only when all 8 are negative.
• Massive PE = sustained hypotension caused by PE → treat with systemic thrombolysis (alteplase) unless contraindicated.
• Sinus tachycardia is the most common ECG finding in PE; S1Q3T3 is classically cited but is neither sensitive nor specific.
• Use the age-adjusted D-dimer cutoff (age × 10 μg/L) in patients older than 50 years to avoid over-imaging.
• A normal A-a gradient or normal SpO₂ does not exclude PE.

FAQ

Related Resources

Sources

1. Kacmarek RM, Stoller JK, Heuer AJ. Egan's Fundamentals of Respiratory Care. 12th ed. Elsevier; 2021.
2. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020;41(4):543-603.
3. Kline JA, Mitchell AM, Kabrhel C, Richman PB, Courtney DM. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost. 2004;2(8):1247-1255.