ECG after cardiac surgery

What it looks like on ECG

After cardiac surgery, the ECG almost never returns to an ideal "normal" immediately — there are expected changes and warning signs.

Expected (non-specific changes / reactive pericarditis): in the first few days, non-specific ST-T changes unrelated to ischemia frequently appear. Diffuse, non-territory-specific ST-segment elevation, predominantly concave, sparing aVR and often V1, combined with PR-segment depression in most leads (reciprocally — ST depression and PR elevation in aVR) supports the diagnosis of postoperative pericarditis only in the appropriate clinical context (pain, pericardial friction rub, dynamics). The absence of reciprocal ST depression in opposite coronary territories increases the probability of pericarditis (ST depression in aVR and sometimes V1 is physiological here), but does not rule out myocardial infarction — the absence of reciprocal changes does not rule out ischemia and should not delay serial evaluation, echocardiography, and emergency coronary management in the appropriate clinical setting. The shape of the elevation (concave or convex) is not a reliable differentiator on its own, especially postoperatively, so differentiation is based on dynamics, symptoms, troponin, echocardiography, and, if necessary, coronary angiography.

Frequently encountered:

• Atrial fibrillation or atrial flutter — peak on days 2–4.
• Sinus tachycardia as a reaction to pain, hypovolemia, inflammation, inotropic support.
• Transient conduction abnormalities: first-degree AV block, new bundle branch block (especially after aortic valve surgery — due to the proximity of the AV conduction system and left bundle branch to this area).
• Low QRS voltage and electrical alternans — suspect pericardial effusion.

Requires immediate evaluation:

• Localized ST elevation in a single artery territory, de novo pathological Q wave, Sgarbossa criteria or modified Smith criteria in the presence of left bundle branch block — suspicion of acute coronary occlusion (perioperative infarction, thrombosis, or graft kinking), requiring immediate clinical, biochemical, echocardiographic, and, where indicated, angiographic verification.
• Progressive QRS widening, complete AV block — injury to the conduction system, often requiring temporary or permanent pacing.
• Progressive tachycardia with low voltage and alternans — tamponade.

Mechanism

Surgical trauma, periotomy, and contact with blood cause aseptic pericarditis and non-specific repolarization changes — hence diffuse ST-PR shifts mimicking acute pericarditis. Sutures, atrial cannulation, incisions near the sinus and AV nodes, as well as tissue edema and inflammation temporarily alter conduction, resulting in blocks and atrial arrhythmias. Electrolyte shifts (hypokalemia, hypomagnesemia following diuresis and cardiopulmonary bypass), sympathetic activation, pain, and hypovolemia create a substrate for AF and ventricular ectopy. The aortic region is surgically very close to the AV conduction system and the left bundle branch, which is why interventions on the aortic valve and interventricular septum more frequently cause conduction blocks; in mitral and congenital surgeries, the risk of conduction disorders depends on the specific suture area and reconstruction.

Causes

• Non-specific postoperative ST-T changes / reactive pericardial inflammation
• Hypovolemia, blood loss, anemia
• Electrolyte disturbances (potassium, magnesium) secondary to diuretics and cardiopulmonary bypass
• Surgical trauma to the conduction system (valve replacement, congenital defect correction)
• Perioperative ischemia, graft thrombosis, or spasm during CABG
• Inflammatory response to cardiopulmonary bypass
• Pericardial effusion up to tamponade
• Postpericardiotomy syndrome (delayed pericarditis, usually 1–6 weeks)

Differential diagnosis

• STEMI — focality of ST elevation in a single coronary territory and reciprocal depression in the opposite wall increase the probability of MI, but their absence does not rule out MI — postoperative changes and baseline repolarization abnormalities reduce ECG specificity, so serial evaluation, echocardiography, and, when indicated, emergency coronary management are required in the appropriate clinical setting; ST morphology (concave/convex) is not used as an independent criterion.
• Sgarbossa/Smith criteria in left bundle branch block — to be applied when acute occlusion is suspected in a patient with a new or known LBBB postoperatively; a positive result requires urgent clinical-biochemical and, where indicated, angiographic verification.
• Tamponade — low voltage and alternans combined with hypotension and tachycardia, rather than isolated ST-PR changes.
• AF with pre-existing WPW or other features — check pre-operative ECG for baseline rhythm and conduction.
• Normal postoperative tachycardia secondary to pain and inotropes — differs from pathological tachycardia by context and dynamics, not by the ECG itself.

Clinical significance and management

Any new ECG finding after cardiac surgery requires comparison with the baseline tracing and clinical evaluation. Diffuse ST elevation with PR depression, lacking reciprocal depression in coronary territories and typical ischemic pain, combined with clinical signs of pericarditis (pain, pericardial friction rub), warrants assessment of pain, inflammatory markers, troponin, and indicated echocardiography to rule out effusion. In clinically significant postpericardiotomy syndrome, management is chosen jointly with the cardiac surgeon: acetylsalicylic acid and/or colchicine are generally preferred in the absence of contraindications, while other NSAIDs in the early period after CABG are typically avoided due to an increased risk of cardiovascular events, bleeding, and impaired sternal healing; isolated ECG ST-PR changes without the clinical syndrome are not an indication for anti-inflammatory therapy. For new AF: assess hemodynamics, rate or rhythm control, and anticoagulation based on stroke risk while accounting for surgical bleeding. For a new bundle branch block or AV block: repeat serial ECGs; upon progression to complete or high-grade AV block, temporary pacing and monitoring for recovery of AV conduction are indicated; the need for a permanent pacemaker is considered if high-grade or complete AV block persists after a monitoring period (typically about 5–7 days), tailored to the type of surgery and likelihood of recovery. Localized ischemic changes in a single coronary territory require emergency evaluation (serial high-sensitivity troponin, echocardiography, repeat ECG, and angiography if indicated). By current definitions, the diagnosis of perioperative myocardial infarction (Type 5) is not made solely based on the ECG: within the first 48 hours after CABG, it requires a cardiac troponin elevation greater than 10 times the 99th percentile of the upper reference limit, combined with at least one objective sign of ischemia—new pathological Q waves, new LBBB, angiographically confirmed graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality; after 48 hours, general myocardial infarction criteria apply, taking into account troponin kinetics and clinical/instrumental signs of ischemia. If graft thrombosis is suspected, discuss emergency revascularization with the cardiac surgeon. Progressive tachycardia with low voltage and electrical alternans warrants emergency echocardiography and, in cases of tamponade, pericardiocentesis.

Common interpretation errors

• Mistaking diffuse reactive ST-PR changes for STEMI and referring for unnecessary emergency angiography without evaluating clinical presentation and dynamics.
• Diagnosing pericarditis solely based on the shape and magnitude of ST elevation without clinical correlation.
• Failing to compare the current ECG with the pre-operative and previous day's ECGs, missing dynamic changes.
• Ignoring a new bundle branch block or PR prolongation as an "incidental finding" without monitoring for progression to complete AV block.
• Diagnosing perioperative myocardial infarction based solely on ECG without serial troponin levels (including the threshold >10× the 99th percentile in the first 48 hours after CABG) and other objective criteria.
• Failing to associate low voltage and alternans with potential pericardial effusion.

Frequently asked questions

Related terms

More in the section "Pericardium, Lungs, Brain and Others"

Entire section

Sources

• Goldberger's Clinical Electrocardiography, latest edition
• Hampton. The ECG in Practice
• Surawicz, Knilans. Chou's Electrocardiography in Clinical Practice
• Orlov V.N. Guide to Electrocardiography

Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.