What does a notched Q (q wave) on an electrocardiogram (ECG) indicate and how is it managed?

Notched Q Wave on ECG

A notched Q wave represents fragmented ventricular depolarization, most commonly indicating myocardial scarring from prior infarction, though it has superior sensitivity for detecting myocardial damage compared to traditional pathologic Q waves and requires systematic evaluation to distinguish from normal variants and non-ischemic causes.

Definition and Recognition

A notched Q wave is part of the broader category of fragmented QRS complexes (fQRS), which includes various RSR' patterns, notching in the nadir of the S wave, or multiple R' waves within a QRS duration <120 ms in two contiguous leads corresponding to a major coronary artery territory 1. This differs from traditional pathologic Q waves, which are defined by duration ≥0.03 seconds and depth ≥0.1 mV in two contiguous leads 2.

Clinical Significance

Superior Diagnostic Performance

• Fragmented QRS (including notched Q waves) demonstrates 85.6% sensitivity for detecting myocardial scar compared to only 36.3% for traditional Q waves alone 1
• The negative predictive value is 92.7% for fQRS versus 70.8% for Q waves, making notched Q waves a more reliable marker for excluding prior myocardial infarction 1
• When combined, Q waves and/or fQRS achieve 91.4% sensitivity for detecting myocardial scar 1

Pathophysiologic Implications

• Notched Q waves indicate altered ventricular depolarization from myocardial scarring, representing areas of non-uniform electrical activation 1
• They can indicate transmural myocardial infarction with necrosis, typically associated with infarct size >6.2% of left ventricular mass 2
• Pathologic Q waves (including notched variants) are associated with increased mortality risk, even in "silent" Q-wave MIs 2

Systematic Evaluation Algorithm

Step 1: Verify Technical Factors

• Check lead placement first to avoid pseudo-septal infarct patterns, as Q waves in V1-V2 commonly result from high lead placement 3
• Obtain prior ECGs for comparison, as this dramatically improves diagnostic accuracy 3

Step 2: Distinguish Normal from Pathologic

Normal variants that should NOT be considered pathologic:

• Small septal Q waves <0.03 sec and <25% of R-wave amplitude in leads I, aVL, aVF, and V4-V6 2, 3
• QS complex in lead V1 2, 3
• Q wave in lead III <0.03 sec and <25% of R wave amplitude when frontal QRS axis is between 30° and 0° 2, 3
• Isolated Q waves in lead III without repolarization abnormalities in other inferior leads 3

Step 3: Check for QRS Confounders

These conditions invalidate Q wave interpretation:

• Left bundle branch block 3
• Pre-excitation syndromes (WPW) 2
• Left ventricular hypertrophy 2
• Hypertrophic cardiomyopathy 3

Step 4: Assess Acuity

Acute versus chronic changes:

• Q waves with ST-segment elevation ≥0.2 mV in V1-V3 or ≥0.1 mV in other leads suggest acute or evolving infarction 3
• Measure cardiac biomarkers (troponin) to distinguish acute from chronic changes 3
• Up to 25% of NSTEMI patients with elevated CK-MB develop Q waves during hospital stay 3
• Transient Q waves during acute MI may represent severely ischemic but salvageable myocardium, not irreversible damage 4, 5

Step 5: Evaluate for Non-Ischemic Causes

Important differential diagnoses:

• Hypertrophic cardiomyopathy 3
• Arrhythmogenic right ventricular cardiomyopathy 3
• Cardiac amyloidosis 2
• Infiltrative myocardial diseases 3
• Myocardial fibrosis without coronary artery disease 2

Management Approach

Immediate Actions

• Measure cardiac biomarkers (troponin) immediately to determine if this represents acute coronary syndrome 3
• Perform echocardiography as minimum evaluation to exclude cardiomyopathy and assess wall motion abnormalities 3
• If acute MI suspected with new Q waves at presentation, recognize this independently predicts increased cardiac mortality (17% vs 7% at long-term follow-up) and warrants aggressive management 6

Risk Stratification

• New Q waves on presenting ECG independently predict worse outcomes with lower ejection fraction (51% vs 61%), larger end-systolic volume, and increased 30-day cardiac mortality (7% vs 2%) 6
• Serial ECG monitoring is essential, as when three or more ECGs are obtained, at least two consecutive ECGs should demonstrate the abnormality to confirm evolution 3

Therapeutic Considerations

• In evolving Q-wave MI, early coronary reperfusion (thrombolysis, angioplasty) may reverse new Q waves if perfusion is restored very early, suggesting myocardial salvage 4, 5
• Q waves that disappear following thrombolysis represent stunned but viable myocardium rather than irreversibly damaged tissue 4

Critical Pitfalls to Avoid

• Do not assume all Q waves represent irreversible necrosis - transient Q waves can represent severe ischemia with potentially salvageable myocardium, particularly in the acute setting 5
• Combining Q waves with other ECG findings (ST-T changes) increases diagnostic accuracy rather than relying on Q waves alone 2
• Fragmented QRS patterns have substantially higher sensitivity than traditional Q wave criteria and should not be dismissed as insignificant 1
• Age, new Q waves at presentation, and history of angina are independent predictors of cardiac mortality on multivariate analysis 6