PE AH4 WK2

Pulmonary Embolism (PE)

is particulate matter — solid, liquid, or air — that enters venous circulation and lodges in the pulmonary vessels, obstructing blood flow.

Most begin as a DVT -

1. A clot forms in a deep vein, usually in the leg. A DVT raises PE risk by 50%.

2. Clot breaks free - travels through the bloodstream to the right side of the heart

3. Lodges in the Lung - Clot obstructs the pulmonary artery or its branches - DVT + PE = VTE

How a PE Impairs Gas Exchange

1. Obstruction - Clot blocks alveolar perfusion and outflow in the affected vessel

2. V/Q Mismatch - Alveolar dead space increases - alveoli are ventilated but not perfused

3. Vasoconstriction - Platelets collect on the embolus triggering widespread pulmonary vessel constriction

4. Hypertension - Pulmonary vessel constriction leads to pulmonary hypertension, impairing gas exchange further

5. Hypoxemia - deoxygenated blood shunts into arterial circulation - leading to low oxygen levels in arterial blood flow

Not all patients with PE are hypoxemic. Some patients with a small embolus have normal oxygen levels — don't rule out PE based on a normal SpO₂ alone.

Virchow Triad (PE Risk Factors)

Venous Stasis - Abnormal, sluggish blood flow often due to prolonged immobility, long travel, bed rest.

Vessel Wall Injury - Damage to the vein lining e.g. to surgery, trauma, central venous catheters

Hypercoagulability - increased tendency to clot e.g. genetic conditions, cancer, pregnancy, estrogen therapy.

Additional PE Risk Factors

Prolong Immobility

Central Venous Catheters

Surgery in last 3 months

Pregnancy to 3 months postpartum

Obesity

Advanced Age

History of thromboembolism

COVID -19 infection

Cancer - especially lung, gastric, brain, pancreatic, hematologic

Hip/knee replacements

Older Adult Health VTE Risk

60% of all VTE’s occur in adults older than 70 years of age

Common factors -

• Nonadherence - complex regimens and polypharmacy make to take anticoagulants consistently

• Fall risk - falls carry much higher bleeding risk in anticoagulated patients

• Chronic Kidney Disease - impaired renal clearance affects dosing of many anticoagulants

• Polypharmacy - multiple drugs and food interactions raise risk of dosing errors

Fat Emboli

Occur with femur fractures; injure pulmonary vessels and can cause ARDS rather than direct blockage. ~10% mortality.

Oil Emboli

Can occur following certain diagnostic procedures; also carry roughly a 10% mortality rate.

Amniotic Fluid / Fetal Debris

A rare but life-threatening obstetric emergency involving amniotic fluid entering circulation.

Septic Clots

Develop from a pelvic abscess, infected IV catheter, or injection of illegal drugs.

Mobility & Positioning (VTE Prevention)

Start Passive/Active ROM for immobilized Patients

Ambulate as soon as possible after surgery

Reposition every 2 hours: avoid crossing legs

Never Massage leg muscles

Mechanical & Drug Prophylaxis (VTE Prevention)

Apply compression devices as ordered

Give prophylactic low-dose anticoagulants post op

Avoid tight garters, girdles, constricting clothing

No pillow under the knee - avoid popliteal pressure

Assessment & Lifestyle (VTE Prevention)

Assess peripheral circulation at least once per shift

Elevate affected Limb above or equal to 20 degrees above heart level

Encourage Smoking Cessation

Teach hydration + positioning changes on long trips

PE S/S

Many patients with PE do NOT have the “classic” presentation — this is why PE is so often overlooked.

• Sudden Onset of Dyspnea

• Feeling of Impending Doom

• Extreme anxiety and fear

• Diaphoresis - tachypnea

• Low-grade fever

• Sharp, stabbing chest pain

• light-headedness

• Crackles - pleural friction rub

• Petechiae over chest/axillae (fat embolism)

• Apprehension, restlessness

• Cough, hemoptysis

• Tachycardia - S3 or S4 sounds

• Distended Neck Veins

• Syncope

• Systemic Hypotension

• Abnormal ECG- T-wave/ST changes, axis deviation, arrythmias

• Right ventricular failure, cardiac arrest, obstructive shock

• Hypoxemia

PE Lab Testing

No single lab test can diagnose a PE — imaging is required for confirmation.

• D-dimer - rises with fibrinolysis: a normal/low result can rule OUT a PE

• Troponin and BNP - Elevated associate with greater severity and death risk

• ABG - Early respiratory alkalosis (Low PaCO2), later, respiratory then metabolic acidosis

PE Imaging Studies

CTPA (Diagnostic Standard) - Computed tomography pulmonary angiography also reveals other lung abnormalities causing symptoms.

V/Q Scan (Lung Scintigraphy) - Used if CTPA contraindicated (pregnancy, renal disease, contrast allergy. Reports probability only - not confirmatory)

MRA - Used in place of CTPA in some settings

Doppler Ultrasound - documents presence of DVT

TTE (Echocardiography)

Supports Diagnosis via clot in right/ right heart strain - not definitive alone.

PE 3 priority Problems

Hypoxemia - from mismatch of lung perfusion and alveolar gas exchange

Hypotension - due to right ventricular failure

Potential for Bleeding - due to anticoagulation or fibrinolytic therapy

PE Priority Actions

• Activate rapid response team

• Apply Oxygen: keep SpO2 above 90

• Place patient in High-Fowlers position

• Reassure patient; stay and speak calmly

• Obtain venous access

• Apply Telemetry

• Continuous Pulse Ox and VS

• Prepare for ABG and 12-lead ECG

Massive PE (Symptoms and Management)

Symptoms - Severe hypotension, cardiac arrest, shock, RV dysfunction, severe respiratory distress

Management - CPR · vasopressors · systemic thrombolysis · catheter-directed tx · surgical embolectomy

Submassive PE (Symptoms and Management)

Symptoms - Normotension with RV dysfunction/dilation, elevated BNP or troponin

Management - Anticoagulation · weigh thrombolytics vs. bleed risk · possible vena cava filter

Non massive PE (Symptoms and Management

Symptoms - Normotension, no RV dysfunction, normal BNP/troponin

Management - LMWH · DOAC · warfarin · inpatient stay not usually required

PE (Drug Therapy)

Initial Therapy - Unfractionated heparin, LMWH, or fondaparinux — LMWH/fondaparinux preferred (less bleeding/HIT risk)

Transition - Oral anticoagulant (e.g., warfarin) started day 1–2; overlap with heparin until INR 2.0–3.0

Fibrinolytics - e.g., alteplase — for shock, hemodynamic collapse/instability; high bleed risk, requires ICU monitoring

Heparin & fibrinolytics are both HIGH-ALERT drugs — verify dose and concentration per NPSG.

Heparin Reversal Agent

Protamine sulfate (partial for LMWH)

Warfarin Reversal Agent

Vitamin K1 ± FFP / clotting factors

Dabigatran Reversal Agent

Idarucizumab

Factor Xa inhibitors Reversal Agent

Andexanet alfa

Fibrinolytics

Clotting factors, FFP, antifibrinolytics

Minimizing Bleeding — Nursing Priorities

Assess puncture sites, gums, stools, urine, and emesis for occult blood · monitor platelets & coagulation daily · handle patient gently · institute Bleeding Precautions

Home Care & Self-Management Teaching

• Discharge occurs once hypoxemia/instability resolve and anticoagulation is adequate — therapy continues at home

• Teach Bleeding Precautions and VTE recurrence-reduction activities

• Warfarin patients need frequent lab monitoring (clinic or home care nurse)

• DOACs (dabigatran, rivaroxaban, apixaban) don't require lab monitoring

• Coordinate home O₂ and respiratory therapy for patients with severe dyspnea

• Modify living space to limit stair climbing if activity intolerance persists

Evaluate Outcomes — The Patient:

• Attains and maintains adequate gas exchange and oxygenation

• Does not experience hypovolemia and shock

• Remains free from bleeding episodes

• Shows understanding of drug therapy plan, timing, dose, and adverse effects

• Verbalizes symptoms to report to the primary health care provider

• Demonstrates adherence to Bleeding Precautions and VTE prevention