Pulmonary Embolism

A DVT patient who suddenly becomes tachycardic, hypoxic, and short of breath may have minutes — not hours. Recognizing PE fast changes survival.

A pulmonary embolism occurs when a thrombus — most often originating from a deep leg vein — lodges in the pulmonary vasculature, creating a ventilation-perfusion (V/Q) mismatch: the lung is ventilated but not perfused. The hallmark triad is sudden-onset dyspnea, tachypnea, and pleuritic chest pain, but tachycardia is often the earliest detectable sign. Hypoxemia develops rapidly, and SpO2 may drop despite supplemental oxygen. A massive PE can cause right ventricular failure, hemodynamic collapse, and cardiac arrest. CT pulmonary angiography (CTPA) is the gold-standard diagnostic. D-dimer is a sensitive but nonspecific screening tool — a negative D-dimer helps rule out PE, but a positive result does not confirm it. Nursing priorities include high-flow oxygen, continuous pulse oximetry and cardiac monitoring, IV access, and positioning the client in high Fowler's. Anticoagulation with IV unfractionated heparin is the first-line treatment; monitor aPTT (therapeutic goal 1.5–2.5× control). For massive PE with hemodynamic instability, thrombolytics (e.g., alteplase) may be administered — monitor closely for bleeding. Virchow's triad (stasis, endothelial injury, hypercoagulability) underpins risk, but DVT is the sibling atom — PE teaching focuses on what happens after the clot migrates.

Key Distinctions

Don't confuse PE chest pain (sudden, pleuritic, worse with breathing) with MI chest pain (crushing, substernal, radiating). A negative D-dimer is clinically useful to exclude PE; a positive D-dimer is not diagnostic — students frequently reverse this logic. PE causes right-sided heart strain (distended neck veins, right axis deviation on ECG), not left-sided failure signs like pulmonary crackles.

Clinical Pearl

Sudden dyspnea + tachycardia + clear lung sounds = think PE. Crackles point elsewhere. Clear lungs in a hypoxic patient should alarm you.