Thromboembolic Disease

Pulmonary embolism above all: why the patient is tachycardic and hypoxic with a clear chest, the massive PE that arrests, and why fluids can make it worse.

CEN Content Outline, Cardiovascular Emergencies J. A clot forms, usually in a deep vein of the leg or pelvis, breaks off and lodges in the pulmonary circulation. Everything that follows comes from one fact: the right ventricle is suddenly working against a much higher resistance, and it is not built for it.

How It Presents

• Sudden dyspnea, often with pleuritic chest pain. • Tachycardia and tachypnea — the two most consistent findings. • Hypoxia with a chest that sounds clear and a chest X-ray that looks normal. That mismatch is the signature. • Cough, sometimes haemoptysis. • Syncope, which suggests a large clot. • Leg swelling in a minority; most patients have no leg findings at all. Risk factors are Virchow triad again: recent surgery or immobility, long travel, malignancy, pregnancy and the postpartum period, oestrogen-containing contraception, previous venous thromboembolism, inherited thrombophilia, obesity, smoking.

The Workup

• ECG: sinus tachycardia is the commonest finding by far. S1Q3T3 is classic, quoted constantly, and rarely present. New right bundle branch block or right axis deviation suggests strain. • D-dimer: useful only to rule out in a low-probability patient. Above the cut-off, usually 500 ng/mL, it means a scan, not a diagnosis. • CT pulmonary angiogram is the usual diagnostic study. Check renal function and contrast allergy. • A V/Q scan is the alternative when contrast cannot be given, including in pregnancy. • Bedside echo: a dilated, strained right ventricle in a hypotensive patient is enough to act on. • Troponin and BNP rise with right ventricular strain and predict a worse course.

Severity Decides Treatment

• Low risk: haemodynamically stable, no right ventricular strain. Anticoagulation. • Submassive (intermediate): stable pressure but right ventricular strain on echo or raised troponin. Anticoagulation, close monitoring, and thrombolysis considered if they deteriorate. • Massive: sustained hypotension, or arrest. Systemic thrombolysis, catheter-directed therapy or embolectomy.

Treatment

• Anticoagulation — heparin infusion, low molecular weight heparin, or a direct oral anticoagulant depending on the patient and the plan. • Thrombolytics for massive PE, with the bleeding contraindications weighed. • An inferior vena cava filter where anticoagulation is contraindicated.

The Haemodynamics, and the Trap

A hypotensive PE patient looks like they need fluid. Be careful. The right ventricle is already dilated and failing; overfilling it pushes the septum into the left ventricle and reduces left-sided output further. A modest fluid challenge — around 500 mL — is reasonable, and if the pressure does not respond, the next step is a vasopressor such as norepinephrine, not more litres. Intubating a massive PE patient is dangerous for the same reason as tamponade: the sedatives drop the pressure, and positive pressure reduces venous return to a ventricle that depends on it. Arrest on induction is a recognised event. If it must be done, have a vasopressor running first.

Nursing Priorities

• Tachycardia and hypoxia with a clear chest is the pattern to hold in your head. It is the one that gets sent home as anxiety. • Ask directly about travel, surgery, immobility, contraception and pregnancy — the history makes the diagnosis more often than any test. • On a heparin infusion: baseline PTT or anti-Xa, Hgb and Hct and coagulation studies, then repeat on schedule, and check for bleeding — gums, urine, stool, neurological change. • Continuous monitoring. A submassive PE can become a massive one on the way to the scanner. Topic list from the CEN Examination Content Outline effective July 2026 (BCEN, public document). This chapter was written for this app as study material and is not from any BCEN course.

Thromboembolic Disease