The ECG in pulmonary embolism, hypothermia and digoxin effect

What it is

These three patterns are classic exam tracings because each has a sign worth recognising and a trap. In acute pulmonary embolism the ECG is neither sensitive nor specific: it is often normal or shows only sinus tachycardia, the most common finding. When the right ventricle is under acute pressure load, signs of right heart strain appear: T-wave inversion in V1–V4 and III, a new complete or incomplete right bundle branch block, right axis deviation, a deep S in I with a Q wave and inverted T in III (S1Q3T3), atrial arrhythmias and sometimes ST elevation in aVR or V1. These signs point to a larger clot and a worse prognosis, but their absence never rules out embolism. In hypothermia the conduction system slows: sinus bradycardia, then prolonged PR, QRS and QT, often with shivering artefact; the hallmark is the Osborn or J wave, a positive hump at the junction of the QRS and ST segment, best seen in the inferior and lateral precordial leads, which grows as the core temperature falls. Atrial fibrillation with a slow ventricular rate is common, and below about 30 °C the risk of VF and asystole rises sharply. Digoxin effect is the expected change of a therapeutic level: a sagging, scooped ST depression (the «reverse tick»), flattened or inverted T waves, a short QT and sometimes prominent U waves. It is not toxicity. Digoxin toxicity shows as arrhythmias from increased automaticity together with slowed AV conduction: frequent ventricular ectopics or bigeminy, atrial tachycardia with block, junctional rhythms, AV block, regularised slow atrial fibrillation and, rarely but characteristically, bidirectional VT.

How to recognise it

• PE: sinus tachycardia >100 bpm; T inversion in right precordial (V1–V4) and inferior (III, aVF) leads; complete or incomplete RBBB; axis shifting rightwards; S in I, Q and inverted T in III; new atrial fibrillation or flutter; P pulmonale.
• Hypothermia: sinus bradycardia; PR, QRS and QTc prolong progressively; Osborn wave = positive deflection at the J point, upright in leads with an upright QRS, biggest in V2–V5 and inferior leads.
• Hypothermia rhythms as the core temperature falls: sinus bradycardia, then atrial fibrillation with slow ventricular rate, junctional rhythm, ventricular ectopics, VF and asystole.
• Digoxin effect: down-sloping, scooped ST depression most visible in leads with tall R waves (lateral), T flattening or inversion, QT shortening, mild PR prolongation, prominent U waves.
• Digoxin toxicity: ventricular bigeminy or multifocal ectopics, atrial tachycardia with 2:1 block, accelerated junctional rhythm, regularised slow AF (complete heart block under the AF), Mobitz I, bidirectional VT.
• Hypokalaemia, hypomagnesaemia, hypercalcaemia, renal impairment and interacting drugs make digoxin toxicity more likely; acute overdose may cause hyperkalaemia.

Why it happens

• PE: a sudden rise in pulmonary pressure dilates and stretches the right ventricle, which slows right bundle conduction, rotates the axis to the right and causes right ventricular ischaemia (T inversion in the right-facing leads).
• Hypothermia: cold slows ion channel kinetics in every cell, so all intervals lengthen; the Osborn wave reflects a larger transient outward current in the epicardium than in the endocardium at the start of repolarisation.
• Digoxin blocks the sodium-potassium pump, raising intracellular calcium (more automaticity and delayed afterdepolarisations), and increases vagal tone at the AV node (slower conduction); the ST scoop reflects a shorter action potential.

Step by step

1. Start with rate and rhythm — tachycardia suggests PE, bradycardia suggests hypothermia or digoxin, and ectopy with block suggests digoxin toxicity.
2. Look at V1–V4 and III for T inversion and at V1 for a new RBBB — the right heart strain signs of PE.
3. Work out the axis and check lead I for a deep S and III for Q and an inverted T — a rightward shift fits acute right ventricular load.
4. Look at the J point in V2–V5 and inferior leads for a positive hump — the Osborn wave; then measure PR, QRS and QTc.
5. Look at the ST shape in the lateral leads — a scooped sag with a short QT is digoxin effect.
6. If on digoxin, look hard for AV block with ectopy or an atrial tachycardia with block — the combination points to toxicity.
7. Match the tracing to the patient: oxygen, temperature, drug list, potassium and kidney function — each pattern has a clinical twin.

Three patterns side by side

Differential and pitfalls

• PE differentials of right precordial T inversion: anterior ischaemia (Wellens pattern), RVH, ARVC, normal in children; T inversion in both V1–V4 and III favours PE.
• S1Q3T3 is neither sensitive nor specific; it also appears in acute bronchospasm, pneumothorax and other causes of right heart strain.
• Osborn waves also occur with hypercalcaemia, brain injury and early repolarisation; shivering artefact can be mistaken for an arrhythmia.
• Pitfall: a slow pulse in hypothermia may be appropriate; handle the patient gently, because movement can trigger VF, and confirm cardiac arrest carefully.
• Digoxin effect alone does not need a dose change; the scooped ST depression makes an exercise ECG uninterpretable for ischaemia.
• Pitfall: relying on the digoxin level alone; toxicity is a clinical and ECG diagnosis (nausea, visual change, confusion with an arrhythmia), and levels taken too soon after a dose mislead.

Next step

• Suspected PE: estimate the clinical probability, then D-dimer or CT pulmonary angiography; in a shocked patient, bedside echo for right ventricular dilatation and call a senior now.
• Confirmed PE: anticoagulation (heparin) is the basis; thrombolysis (alteplase) is a senior decision for high-risk, haemodynamically unstable embolism.
• Hypothermia: measure the core temperature, rewarm actively, monitor continuously and follow the local hypothermia and cardiac arrest protocol; the ECG should normalise as temperature rises.
• Suspected digoxin toxicity: stop digoxin, check potassium, magnesium, creatinine and a timed digoxin level, monitor the rhythm, and discuss digoxin immune Fab with a senior or poison centre for serious arrhythmias.
• Record a follow-up ECG after treatment in all three to document resolution.

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Elsewhere in DurgiPedia

• ECG basics: waves, intervals and leads
• The cardiac electrical axis
• The ECG in potassium and calcium disorders
• Hypothermia and cold injury

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Educational content; it does not replace supervised hands-on training, your institution's protocols or a prescriber's order. A procedure is learnt with a teacher and done only once you are trained to do it.

Sources: Acute Pulmonary Embolism (StatPearls (NCBI Bookshelf), 2024); Hypothermia (StatPearls (NCBI Bookshelf), 2026); Cardiac Glycoside and Digoxin Toxicity (StatPearls (NCBI Bookshelf), 2025).

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