Pulmonary Embolism

Clinical Orientation

A 45-year-old woman 1 week post-cesarean section suddenly develops pleuritic chest pain, dyspnea, and tachypnea. Her SpO2 is 89%. She is tachycardic at 118. CT pulmonary angiogram shows bilateral pulmonary emboli. This chapter answers: What mechanism links PE to bedside findings, tests, red flags, and nursing priorities?

What Goes Wrong?

PE = thrombus (usually from DVT) travels to the pulmonary arteries → obstructs pulmonary blood flow.

The consequences depend on clot size and cardiopulmonary reserve:

Respiratory effects:

• High V/Q (dead space): Ventilated alveoli are not perfused → ventilation wasted. CO2 elimination impaired if dead space is large.
• Hypoxemia: V/Q mismatch, right-to-left shunting through a patent foramen ovale, low mixed venous O2 from low CO.

Hemodynamic effects:

• Obstruction → increased pulmonary vascular resistance (PVR) → increased RV afterload.
• Small PE: RV compensates. Large PE (>30-50% of pulmonary circulation): RV fails → RV dilation → intraventricular septum bows into LV → LV filling impaired → reduced CO → hypotension → obstructive shock.
• Acute RV failure is the cause of death in massive PE.

What the Nurse May See

Classic triad (present in minority): Pleuritic chest pain, dyspnea, hemoptysis (pulmonary infarction).

More common: Sudden dyspnea, tachypnea, tachycardia. May have low-grade fever. Syncope (massive PE).

Massive PE: Hypotension (SBP <90 for >15 min or requiring vasopressors), syncope, JVD, RV heave, loud P2. Obstructive shock pattern.

Submassive PE: Normotensive but RV dysfunction on echo or elevated troponin/BNP — these are the patients at risk for deterioration.

Tests and Monitoring

• CT pulmonary angiography (CTPA): Gold standard. Filling defects in pulmonary arteries.
• V/Q scan: Alternative if CT contrast contraindicated (renal failure, allergy).
• D-dimer: High sensitivity, low specificity. Negative D-dimer effectively rules out PE in low/moderate-risk patients. Positive D-dimer requires imaging. Do NOT check D-dimer in high-risk patients — go straight to imaging.
• Echocardiogram: RV dilation, RV dysfunction, McConnell's sign. Used for risk stratification, not diagnosis.
• Troponin, BNP: Elevated = myocardial strain/injury → higher risk.
• Lower extremity duplex: Find the source DVT.

Nursing Priorities

1. ABC assessment: High-flow oxygen. If hypotensive — massive PE → prepare for thrombolysis or embolectomy.

1. Anticoagulation: Start immediately once PE is suspected (unless contraindicated). LMWH, fondaparinux, or unfractionated heparin. This prevents further clot propagation while the body's fibrinolytic system dissolves the existing clot.

1. Thrombolysis (massive PE with hypotension): tPA — dissolves the clot rapidly. Risk: major bleeding (especially intracranial). Reserved for massive PE with persistent hypotension.

1. Hemodynamic monitoring: BP, HR, SpO2, urine output, mental status. Trend is crucial.

1. Avoid Valsalva: Prevent straining with bowel movements — increases intrathoracic pressure → decreased venous return. Stool softeners.

Red Flags