What do you want to learn today?

Pulmonary Embolism: A Nurse's Reference Guide

William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
14 min read

A pulmonary embolism (PE) is a blood clot that lodges in the pulmonary vasculature of the lungs. Sometimes it's asymptomatic, often it causes mild-to-moderate symptoms, and other times patients go straight into cardiac or respiratory arrest.

No matter the presentation, pulmonary embolisms can be deadly. This guide walks through the causes, assessment, diagnosis, treatment, and monitoring you need to know to care for these patients at the bedside.

What Is a Pulmonary Embolism?

A pulmonary embolism is a blood clot that lodges within the lungs. They can be large or small, single or many at once. The larger and more numerous the clots, the more dangerous — a PE can put significant strain on the heart and even cause cardiac arrest.

Hs & Ts. Remember that a Thrombus is one of the Hs and Ts to think about when a patient is coding. PEs are also highly associated with deep vein thrombosis (DVT) — and VTE (venous thromboembolism) is the umbrella term for any clot, including DVTs and PEs.

Causes of a PE: Virchow's Triad

Many things can cause a PE, but it all traces back to Virchow's Triad — for a clot to form, at least one of three conditions must be present. The more a patient has, the higher their risk (though a small percentage clot with none of these).

Stasis of blood
Stasis of Blood
Anything that makes blood "sit still": immobility, hospitalization, varicose veins, atrial fibrillation, heart failure, or elderly age (>65).
Endothelial injury
Endothelial Injury
Damage to vessels: recent surgery (especially orthopedic), trauma, chemotherapy, implanted devices, central lines, inflammation, or sepsis.
Hypercoagulable state
Hypercoagulable State
Increased clotting tendency: malignancy, estrogen (birth control), pregnancy, inherited mutations (Factor V Leiden), severe liver disease, smoking, or obesity.
Virchow's triad: stasis, endothelial injury, and hypercoagulable state
Virchow's Triad — the three drivers of clot formation.

Nursing Assessment

Patients with a PE usually present with shortness of breath. An area of the lung can still take in oxygen but can't exchange it for carbon dioxide at the clot site, creating a ventilation-perfusion (V/Q) mismatch.

Symptoms
Dyspnea
Dyspnea
Shortness of breath — with exertion or at rest. The most common symptom.
Chest pain
Chest Pain
Usually pleuritic — worse with deep breaths or coughing.
Cough
Cough
Usually non-productive, but may have pink frothy or bloody sputum.
Syncope
Syncope
Syncope with chest pain and SOB is suspicious for PE.
Signs of DVT
Signs of DVT
Extremity erythema, edema, or pain — clues to the clot's origin.

Hemoptysis Is Overrated

Coughing up blood (hemoptysis) is not nearly as common a PE symptom as your nursing textbook may have suggested. Many patients are asymptomatic or have vague symptoms — and some go straight into cardiac arrest, especially with very large PEs.

Physical exam
Inspection
Inspection
Respiratory distress — tachypnea, increased work of breathing, accessory muscle use — plus cough, pallor, and diaphoresis. Tachypnea is usually the first thing you'll notice.
Vital signs
Vital Signs
Temp may be low-grade; BP normal, high (pain), or low (severe); HR tachycardic (>100); RR increased; SpO₂ normal or low.
Auscultation
Auscultation
Lungs often normal, may be diminished; crackles if pulmonary infarct or acute CHF; possible pleural friction rub. Heart tachycardic.
Pleuritic pain pattern
Pleuritic Breathing
Pleuritic chest pain limits full breaths, so patients compensate with frequent shallow breathing — driving the respiratory rate up.
Quick tip: if a patient has chest pain or SOB and recently had surgery or is pregnant, always think PE. Very large PEs can cause hemodynamic compromise including hypotension and shock.

Nursing Interventions

1
Cardiac Monitoring

Place all chest-pain/SOB patients on a monitor. PEs often cause sinus tachycardia that doesn't fully resolve with fluids, plus arrhythmias like atrial fibrillation, bradycardia, RBBB, PVCs, and VTach/VFib.

2
STAT EKG

Obtain an EKG within 10 minutes of arrival — primarily to rule out STEMI/ischemia. Large PEs can cause right heart strain; in <10% of patients you may see a right heart strain pattern or the classic S1Q3T3.

3
Oxygen Support

If hypoxic or tachypneic, apply 2–4 L/min NC; titrate to SpO₂ >90%. Escalate to a non-rebreather, then BiPAP or intubation if needed.

4
IV Access & Labs

Start a large-bore peripheral IV (18–20g) in the AC — these patients will likely need a CTA, and high-pressure dye requires a big line. Draw a blue top (D-dimer, PT/INR) while you're in there.

S1Q3T3 pattern of right heart strain on EKG
The S1Q3T3 pattern — a classic (if uncommon) sign of right heart strain.

Diagnosis of a PE

Wells' criteria
Wells' Criteriaclinical risk stratification
A clinical tool that assigns points to estimate PE risk:
  • Signs of DVT — 3 points
  • PE the #1 likely diagnosis — 3 points
  • HR >100 bpm — 1.5 points
  • Immobilization ×3 days — 1.5 points
  • Surgery within 4 weeks — 1.5 points
  • Previous PE/DVT — 1.5 points
  • Hemoptysis — 1 point
  • Malignancy (treated within 6 mo or palliative) — 1 point
Low risk: 0–1 · Moderate: 2–6 · High: >6. A score of ≤4 with a negative D-dimer can effectively rule out a PE.
D-dimer
D-Dimersensitive, not specific
A byproduct of fibrin that rises whenever there's a clot — useful to minimize radiation in low-to-moderate suspicion. A negative D-dimer (below threshold, ~230 depending on the lab) reliably rules out a clot when suspicion is low to moderate. But it's not specific: bruising, pregnancy, heart disease, and infection all raise it, so a positive result usually forces a CTA. In high-likelihood patients, a D-dimer can miss a PE up to 15% of the time.
Other lab work
Other Lab Worktroponin, BNP, renal, coags
Order a troponin for chest pain/SOB (may be mildly elevated, or high if the PE causes an MI). A BNP if heart-failure signs are present. Check renal function before a CTA — a GFR >30 is usually adequate for dye. Coagulation studies may be done inpatient to find genetic clotting predispositions.
ABG
ABGif significant distress
Obtained if the patient is in significant respiratory distress or has AMS. A PE causing distress typically shows: PaO₂ low (<80), PCO₂ low (<35), pH alkalotic (>7.45), and HCO₃ possibly low (<22) — see ABG interpretation.
Chest X-ray
Chest X-rayrules out mimics
Almost always ordered — it rules out pneumothorax or pneumonia, but won't show the PE itself. It may reveal nonspecific atelectasis or effusions, or be completely normal.
CT pulmonary angiography
CTA (CT Pulmonary Angiography)the definitive test
Radiopaque dye is injected to visualize the pulmonary vasculature on CT, letting the radiologist directly see the embolism. Avoid contrast if GFR <30 (facility-dependent). If dye can't be given (low GFR or anaphylaxis), the alternative is a V/Q scan.
CT pulmonary angiography showing pulmonary emboli
CT pulmonary angiography directly visualizes the clot.
V/Q scan
V/Q Scannuclear medicine alternative
Uses radioisotopes with X-rays to detect ventilation/perfusion mismatches. Less definitive than a CTA — it gives probabilities (e.g., "very low probability"). The CXR should be clear, since significant consolidation or effusions make the scan unreliable.

Treatment of a PE

For a hemodynamically stable patient, treatment is admission, parenteral anticoagulation, then transition to oral anticoagulation. Patients with significant hemodynamic compromise may need reperfusion therapy.

Parenteral anticoagulation
Parenteral Anticoagulationheparin drip
Usually IV unfractionated heparin as a titratable drip guided by PTT (checked ~every 6 hours per protocol): a bolus IV, then a slow drip. SQ Lovenox 1 mg/kg BID is an alternative. Anticoagulants don't dissolve the existing clot — they prevent new clots and stabilize the existing one from breaking off and embolizing further.

Why Heparin Over Lovenox?

IV heparin is often preferred because it's more easily titrated and stopped quickly — useful if bleeding occurs or a procedure is needed while inpatient.

Oral anticoagulation
Oral Anticoagulationlong-term therapy
Stable patients may start directly on an oral agent (Eliquis, Coumadin) and go home, depending on the provider. Most need at least 3 months of therapy (the clot typically reabsorbs in ~6 weeks). Some need lifelong anticoagulation (genetic clotting disorders, atrial fibrillation). Not started in very recent surgery, hemorrhagic stroke, or active bleeding.
IVC filter
IVC Filtercatches clots
An inferior vena cava filter "catches" clots before they reach the right atrium. Used for patients who can't be anticoagulated or who get repeat PEs despite therapy. Can be temporary or permanent.
Thrombolytics
Thrombolyticsfor unstable patients
In hemodynamically unstable patients, thrombolytics dissolve the clot — like TPA in a stroke, but for a PE. There are many contraindications and a real bleeding risk.
Procedural removal
Procedural Removalembolectomy
An embolectomy can be performed when thrombolytics fail or are contraindicated, if the facility is capable. Options include ultrasound-assisted thrombolysis, rheolytic/rotational/suction embolectomy, thrombus fragmentation, and surgical embolectomy. Most facilities have thrombolytics but not all of these.

Saddle PE

A saddle PE is a very large clot at the bifurcation of the main pulmonary artery. Rare, but likely to cause significant hemodynamic compromise and cardiopulmonary arrest.

Patient Monitoring

Monitoring mainly consists of watching vital signs and supporting the patient through treatment.

Cardiac rhythm
Cardiac Rhythm
Continuous monitoring for tachycardia and arrhythmias — sinus tach that doesn't fully resolve with fluids is common.
Oxygenation
Oxygenation
Track SpO₂ and work of breathing; escalate support (NC → NRB → BiPAP → intubation) as needed.
Anticoagulation labs
Anticoagulation Labs
On a heparin drip, follow PTT (usually every 6 hours per protocol) and titrate accordingly.
Hemodynamics
Hemodynamics
Watch for hypotension and shock — signs a large PE is straining the right heart.
Bottom line: pulmonary embolisms are serious and potentially deadly. Knowing how to assess, anticoagulate, and monitor these patients — and when to escalate to reperfusion therapy — is essential bedside care.

Clinical Pearls

1
Surgery or pregnancy + chest pain/SOB = think PE. These are major Virchow's Triad red flags; a high index of suspicion saves lives.
2
Place a large-bore AC IV early. A CTA needs high-pressure dye injection, so an 18–20g AC line saves time when the patient heads to CT.
3
D-dimer rules out, it doesn't rule in. Use it for low-to-moderate suspicion; a positive result usually means a CTA is coming.
4
Anticoagulation stabilizes, it doesn't dissolve. Heparin prevents new and propagating clots — thrombolytics are what actually break down the clot in unstable patients.

References

Clinical Databases & Guidelines
  1. Thompson BT, Kabrhel C. Overview of acute pulmonary embolism in adults. UpToDate.
  2. Thompson BT, Kabrhel C, Pena C. Clinical presentation, evaluation, and diagnosis of suspected acute PE. UpToDate.
  3. Tapson VF, Weinberg AS. Treatment, prognosis, and follow-up of acute PE in adults. UpToDate.
  4. Haag A, et al. Pulmonary embolism. WikEM.
  5. Sharma R. Pulmonary embolism. Radiopaedia.org.
4.4 9 votes
Article Rating
14
0
Would love your thoughts, please comment.x
()
x