A Compendium of Electrocardiographic (ECG) Diagnostic Criteria
Ischaemic Changes
ST-Segment Elevation
Diagnostic Criteria
New ST-segment elevation at the J-point in at least two contiguous leads is required, meeting the following voltage thresholds, as defined by the Fourth Universal Definition of Myocardial Infarction (9):
In all leads other than V2–V3: ≥0.1 mV (1 mm).
In leads V2–V3 (sex- and age-specific):
In men aged 40 years and older: ≥0.2 mV (2 mm).
In men younger than 40 years: ≥0.25 mV (2.5 mm).
In women (any age): ≥0.15 mV (1.5 mm).
Clinical Interpretation and Notes
ST-segment elevation (STE) is the electrocardiographic hallmark of acute, full-thickness (transmural) myocardial ischaemia, resulting from the complete occlusion of a coronary artery. This finding is the primary trigger for emergent reperfusion therapy (e.g., percutaneous coronary intervention or thrombolysis) in patients with ST-Elevation Myocardial Infarction (STEMI) (1, 11). The concept of contiguous leads is crucial as it localizes the ischaemia to a specific myocardial territory supplied by a particular coronary artery (e.g., leads II, III, and aVF for an inferior wall MI, typically due to Right Coronary Artery occlusion).
It is critical to expand the standard view by considering leads I and aVL as contiguous for the high lateral wall (often supplied by the Left Circumflex artery) and recognizing that posterior and right ventricular infarctions require additional leads for diagnosis. A true posterior MI may not show STE in the standard 12-lead ECG; instead, it classically presents with ST-segment depression ≥0.5 mm in leads V1-V3. In this context, obtaining posterior leads (V7-V9) is essential, where STE of ≥0.5 mm is diagnostic. Similarly, in an inferior STEMI, routine placement of a right-sided lead V4R is mandatory to assess for right ventricular infarction, which is diagnosed by STE ≥1 mm in this lead.
ST-Segment Depression and T-Wave Inversion
Diagnostic Criteria
These findings are characteristic of non-ST-elevation acute coronary syndromes (NSTE-ACS), which include unstable angina and NSTEMI. They typically indicate subendocardial ischaemia, where the ischaemia is limited to the inner layer of the myocardium (5, 11).
ST-Segment Depression: New horizontal or down-sloping ST-segment depression ≥0.05 mV (0.5 mm) in two or more contiguous leads.
T-Wave Inversion: New, symmetrical T-wave inversion ≥0.1 mV (1 mm) in two or more contiguous leads that have a prominent R-wave or an R/S ratio >1.
Clinical Interpretation and Notes
The morphology of the ST segment and T-wave provides vital prognostic information. Down-sloping or horizontal ST depression is highly specific for myocardial ischaemia, while up-sloping depression is a non-specific finding. A pattern of widespread ST depression, especially when most prominent in leads V4-V6 and I, II, aVL, accompanied by ST elevation in lead aVR (≥1 mm), is a high-risk finding. This pattern suggests severe, diffuse subendocardial ischaemia, often resulting from significant left main coronary artery stenosis or severe three-vessel disease, and requires urgent invasive evaluation (11).
Similarly, deep, symmetrical T-wave inversions in the precordial leads can signify critical stenosis of the left anterior descending (LAD) artery, a pattern known as Wellens' syndrome. Recognizing these high-risk patterns is crucial for timely intervention to prevent progression to a large anterior wall STEMI.
Hyperacute T-Waves
Diagnostic Criteria
Characterized by tall, prominent, broad-based, and symmetrical T-waves in at least two contiguous leads.
There are no absolute voltage criteria. The diagnosis is made by comparing to a prior ECG or by identifying T-waves that appear disproportionately large relative to the amplitude of the corresponding QRS complex. They are often described as "too tall for the QRS."
Clinical Interpretation and Notes
Hyperacute T-waves are often the earliest electrocardiographic sign of acute myocardial infarction, typically appearing within the first 30 minutes of coronary artery occlusion and often preceding the development of ST-segment elevation (8). They are caused by an efflux of potassium from ischaemic myocardial cells, which accelerates repolarization. This finding is often transient, highlighting the importance of serial ECGs in patients with suspected ACS. It is crucial to differentiate hyperacute T-waves from the tall, narrow, "tented" T-waves of hyperkalaemia, which are typically more symmetrical and have a sharper peak.
Pathological Q-Waves
Diagnostic Criteria
The presence of any of the following in at least two contiguous leads is evidence of a pathological Q-wave, indicating prior myocardial infarction and myocardial necrosis (9):
Any Q-wave in leads V2–V3 with a duration ≥0.02 seconds (20 ms), or a QS complex in V2 and V3.
A Q-wave with a duration ≥0.03 seconds (30 ms) and a depth >0.1 mV (1 mm), or a QS complex in leads I, II, aVL, aVF, or V4–V6.
An R-wave with a duration ≥0.04 seconds (40 ms) in leads V1–V2 and an R/S ratio ≥1 with a concordant positive T-wave (in the absence of a conduction defect). This is an equivalent for a posterior wall MI.
Clinical Interpretation and Notes
Pathological Q-waves represent dead myocardial tissue that is no longer electrically active. This creates an "electrical window" through which the exploring electrode "sees" the negative potential from the opposite side of the heart, resulting in a negative deflection (Q-wave). They typically appear hours to days after the onset of an infarction and often persist indefinitely as a permanent marker of necrosis. It is important not to apply these criteria in the presence of LBBB or ventricular pacing, as these conditions can produce Q-wave patterns that mimic infarction.
Occlusion MI in the Presence of Left Bundle Branch Block (LBBB)
Diagnostic Criteria
In a patient with symptoms of acute myocardial ischaemia and LBBB, the Modified Sgarbossa Criteria are used to diagnose an underlying occlusion MI. The presence of any one of the following is considered diagnostic, as they represent changes that are not expected from LBBB alone:
Concordant ST-segment elevation ≥1 mm in any lead (i.e., ST elevation in a lead with a positive QRS).
Concordant ST-segment depression ≥1 mm in any of leads V1-V3 (i.e., ST depression in a lead with a negative QRS).
Excessively discordant ST elevation where the ST elevation at the J-point is ≥25% of the amplitude of the preceding S-wave in any lead.
Clinical Interpretation and Notes
Historically, a new or presumed new LBBB was considered a STEMI equivalent. This is no longer the case due to low specificity. LBBB fundamentally alters the QRS and ST-T segments, creating "appropriate discordance" (ST depression in leads with a positive QRS, and vice versa), which masks the typical signs of MI. The Sgarbossa criteria (and particularly the modified version, which is more specific) are designed to identify changes that go against this expected pattern. Concordant changes are highly specific for MI because they defy the underlying LBBB pattern. Excessively discordant STE is also a strong indicator of underlying occlusion.
Arrhythmias
Atrial Fibrillation (AF)
Diagnostic Criteria
According to the 2020 ESC Guidelines, a diagnosis of clinical AF is made from a standard 12-lead ECG or a single-lead tracing of at least 30 seconds showing (14):
Irregularly irregular R-R intervals.
Absence of discernible, repeating P-waves.
Chaotic, irregular atrial activations (fibrillatory or 'f' waves), which may be coarse or fine.
Clinical Interpretation and Notes
Atrial fibrillation is the most common sustained arrhythmia and is a major risk factor for thromboembolic stroke. The chaotic atrial activity prevents effective atrial contraction, leading to blood stasis, particularly in the left atrial appendage, which promotes clot formation. The ventricular response is also critical; if it is excessively fast (e.g., >100 bpm), it is termed "AF with a rapid ventricular response (RVR)," which can lead to symptoms of palpitations, shortness of breath, and may precipitate heart failure.
Atrial Flutter
Diagnostic Criteria
Rapid, regular atrial activity, typically at a rate of 250–350 bpm.
Characteristic "sawtooth" flutter waves, most prominent in the inferior leads (II, III, aVF) and lead V1.
The ventricular response is often regular due to a fixed atrioventricular (AV) block (e.g., a 2:1 block resulting in a ventricular rate of ~150 bpm). A variable block will produce an irregular ventricular response.
Clinical Interpretation and Notes
Atrial flutter is a macro-reentrant tachycardia, most commonly involving a large circuit in the right atrium that rotates around the tricuspid annulus. The classic "sawtooth" pattern is produced by constant, organized atrial depolarization. A ventricular rate of exactly 150 bpm in an adult should always raise suspicion for atrial flutter with a 2:1 block, a common and easily missed presentation.
Supraventricular Tachycardia (SVT)
Diagnostic Criteria
A regular tachycardia with a rate typically ranging from 150 to 250 bpm.
Narrow QRS complex (<120 ms), unless a bundle branch block is present.
P-waves are often difficult to identify. They may be absent (buried in the QRS), distort the end of the QRS (pseudo R' in V1), or appear after the QRS as retrograde P-waves (15).
Clinical Interpretation and Notes
SVT is an umbrella term for tachycardias originating above the ventricles. The most common type is AV Nodal Re-entrant Tachycardia (AVNRT), which involves a small re-entry circuit within the AV node itself. This near-simultaneous activation of the atria and ventricles is why P-waves are often buried within the QRS. The second most common is AV Re-entrant Tachycardia (AVRT), which involves an accessory pathway (as in WPW syndrome). Vagal maneuvers (e.g., Valsalva, carotid sinus massage) can often terminate AVNRT by temporarily blocking the AV node and should be the first-line intervention in a stable patient.
Ventricular Tachycardia (VT)
Diagnostic Criteria
A rhythm of three or more consecutive ventricular beats (19).
A rate of greater than 100 bpm.
Wide QRS complex (≥120 ms) with an abnormal, bizarre morphology.
Clinical Interpretation and Notes
Differentiating VT from SVT with aberrant conduction is a critical and often difficult clinical challenge, but VT is far more dangerous and should be assumed in any wide complex tachycardia until proven otherwise. The following features are highly specific for VT as they are signs of AV dissociation (21):
AV Dissociation: P-waves and QRS complexes are independent of each other, with P-waves "marching through" the QRS complexes at a slower rate.
Capture Beats: An occasional supraventricular impulse is conducted to the ventricles, producing a normal, narrow QRS complex amidst the tachycardia. This proves the existence of an independent atrial rhythm.
Fusion Beats: A supraventricular impulse and a ventricular impulse simultaneously activate the ventricles, resulting in a QRS complex with a hybrid morphology. This is pathognomonic for VT.
Sinus Bradycardia
Diagnostic Criteria
A sinus rhythm (normal P-wave axis, 1:1 AV conduction) with a heart rate less than 50 bpm (24).
Note: This reflects an update from the traditional definition of <60 bpm, as rates between 50-60 bpm are often benign.
Clinical Interpretation and Notes
Sinus bradycardia can be physiological, as seen in well-trained athletes or during sleep. However, it can also be pathological, caused by medications (e.g., beta-blockers, calcium channel blockers), or underlying cardiac disease such as sick sinus syndrome or ischaemia affecting the SA node. The clinical significance is determined entirely by the patient's symptoms. If the patient is asymptomatic with adequate blood pressure, it is often benign. If it causes syncope, dizziness, or signs of hypoperfusion, it requires urgent management.
First-Degree AV Block
Diagnostic Criteria
Every P-wave is followed by a QRS complex (1:1 AV conduction).
The PR interval is constant but prolonged >200 ms (24).
Clinical Interpretation and Notes
First-degree AV block represents a delay in conduction, usually within the AV node itself. In most cases, it is a benign finding, especially in athletes or as a result of medications that slow AV conduction. It is typically asymptomatic and does not require treatment. However, a markedly prolonged PR interval can cause symptoms if the atrial contraction occurs too close to the previous ventricular contraction, impairing diastolic filling (pseudo-pacemaker syndrome).
Second-Degree AV Block, Mobitz I (Wenckebach)
Diagnostic Criteria
Progressive prolongation of the PR interval over consecutive beats.
This culminates in a single non-conducted P-wave (a "dropped" QRS).
The cycle then repeats, and the R-R interval progressively shortens before the dropped beat (24).
Clinical Interpretation and Notes
This rhythm is caused by a progressive "fatiguing" of the AV nodal cells. The block is almost always located at the level of the AV node, which is why it is generally considered benign. It can be seen in athletes, during sleep, or due to medications. It rarely causes symptoms and has a very low risk of progression to complete heart block.
Second-Degree AV Block, Mobitz II
Diagnostic Criteria
The PR interval is constant in all conducted beats.
There are intermittent, unexpected non-conducted P-waves (dropped QRS complexes).
The block often occurs in a fixed ratio (e.g., 2:1, 3:1).
Clinical Interpretation and Notes
Mobitz II is a much more dangerous rhythm than Mobitz I. The block is located distal to the AV node, within the His-Purkinje system. This indicates more extensive and severe conduction system disease. There is a high risk of sudden progression to complete heart block, which can cause asystole. For this reason, Mobitz II is a primary indication for permanent pacemaker implantation, even in asymptomatic patients (24).
Third-Degree (Complete) AV Block
Diagnostic Criteria
Complete failure of conduction between the atria and ventricles.
The ECG shows no relationship between P-waves and QRS complexes (AV dissociation).
The atrial rhythm (P-waves) and ventricular rhythm (QRS complexes) are independent, each firing at its own intrinsic rate (24).
Clinical Interpretation and Notes
In complete heart block, the ventricles are driven by a subsidiary escape pacemaker. The location of this pacemaker determines the QRS morphology and rate, and thus the patient's stability. If the escape rhythm is junctional, it originates near the AV node, producing a narrow QRS complex at a rate of 40-60 bpm. If the escape rhythm is ventricular, it originates from within the ventricles, producing a wide, bizarre QRS at a slow and unreliable rate of 20-40 bpm. A ventricular escape rhythm is a sign of a very distal block and is associated with a high risk of syncope and sudden death.
Bundle Branch Blocks
Right Bundle Branch Block (RBBB)
Diagnostic Criteria
QRS duration ≥120 ms.
An rsr', rsR', or rSR' pattern in leads V1 or V2 (the "rabbit ears").
A wide, slurred S-wave in the lateral leads (I, aVL, V5, V6) (22).
Clinical Interpretation and Notes
RBBB is caused by a block in the right bundle branch, leading to delayed activation of the right ventricle. The left ventricle depolarizes normally first (producing the 'r' and 'S' waves), followed by the delayed depolarization of the right ventricle, which produces the secondary R' wave. In isolation, RBBB is a common and often benign finding in the general population.
Left Bundle Branch Block (LBBB)
Diagnostic Criteria
QRS duration ≥120 ms.
A broad, notched, or slurred R-wave in the lateral leads (I, aVL, V5, V6).
Absence of septal Q-waves in the lateral leads.
ST-segments and T-waves are typically discordant (directed opposite to the main QRS vector) (24).
Clinical Interpretation and Notes
LBBB is caused by a block in the left bundle branch. This fundamentally alters the sequence of ventricular activation. Normally, the septum depolarizes from left to right, creating small Q-waves in the lateral leads. In LBBB, this is reversed; the septum depolarizes from right to left, which abolishes the lateral Q-waves and produces the tall R-waves. New-onset LBBB is almost always pathological and is a marker of underlying heart disease (e.g., ischaemia, hypertension, cardiomyopathy).
Left Ventricular Hypertrophy (LVH)
Diagnostic Criteria
The diagnosis is supported by one or more voltage criteria. While many exist, the most common are:
Sokolow-Lyon Index: S wave in V1 + R wave in V5 or V6 > 35 mm.
Cornell Voltage Index: R wave in aVL + S wave in V3 > 28 mm (men) or > 20 mm (women).
Clinical Interpretation and Notes
LVH refers to an increase in the muscle mass of the left ventricle, typically due to pressure overload (e.g., from hypertension or aortic stenosis). While ECG has low sensitivity for LVH, it is quite specific, meaning a positive result is clinically significant. A key supporting finding is the presence of secondary ST-T abnormalities (the "strain" pattern), which includes downsloping ST depression and T-wave inversion in the lateral leads (I, aVL, V5, V6). This pattern is thought to reflect relative subendocardial ischaemia due to the increased muscle mass outstripping its blood supply. Its presence with high voltage significantly increases the diagnostic certainty and indicates more advanced, and often symptomatic, LVH (30).
Right Ventricular Hypertrophy (RVH)
Diagnostic Criteria
ECG diagnosis is often challenging due to the dominance of the left ventricle. However, the following criteria are highly suggestive:
Right axis deviation (≥ +90°).
A dominant R-wave in lead V1 (R/S ratio > 1 or R wave > 7 mm).
A dominant S-wave in lead V5 or V6 (S wave > 7 mm or R/S ratio < 1).
Secondary ST-T abnormalities (ST depression/T-wave inversion) in right-sided leads (V1-V3) and inferior leads (30).
Clinical Interpretation and Notes
RVH develops in response to pressure overload of the right ventricle, most commonly from pulmonary hypertension (e.g., due to COPD, pulmonary embolism, or congenital heart disease). The ECG changes reflect the shift of electrical forces towards the thickened right ventricle. The presence of a "strain" pattern in the right-sided leads indicates significant RVH and is associated with a poorer prognosis.
Electrolyte Imbalances
Hyperkalaemia
Diagnostic Criteria
ECG changes progress in a predictable sequence as the serum potassium level rises (31):
Early (K+ > 5.5 mEq/L): Tall, peaked, narrow-based T-waves are the first sign.
Moderate (K+ > 6.5 mEq/L): PR interval prolongation, decreased P-wave amplitude (P-wave flattening), and widening of the QRS complex.
Severe (K+ > 8.0 mEq/L): The P-wave may disappear entirely, and the QRS complex continues to widen, eventually merging with the T-wave to form a sinusoidal pattern ("sine wave"). This pattern immediately precedes ventricular fibrillation or asystole and is a medical emergency.
Clinical Interpretation and Notes
Potassium is a critical determinant of the cardiac resting membrane potential. High potassium levels partially depolarize the cell membrane, which inactivates sodium channels and slows conduction (widening the QRS) while also speeding up repolarization (peaking the T-waves). These ECG changes are a more reliable indicator of cardiac toxicity than the absolute potassium level itself. The presence of any change beyond peaked T-waves warrants immediate intervention to stabilize the cardiac membrane (with calcium gluconate) and lower the serum potassium.
Hypokalaemia
Diagnostic Criteria
Characteristic findings include (31):
ST-segment depression.
Decreased T-wave amplitude (flattening).
Appearance of a prominent U-wave, which is best seen in the mid-precordial leads (V2-V4).
Apparent QT prolongation (actually QU prolongation as the T-wave and U-wave merge).
Clinical Interpretation and Notes
Low potassium levels hyperpolarize the resting membrane potential, leading to delayed ventricular repolarization. This manifests as T-wave flattening and the appearance of U-waves (thought to represent repolarization of the Purkinje fibers). The main danger of severe hypokalaemia is the increased risk of life-threatening ventricular arrhythmias, particularly Torsades de Pointes, especially in patients who are also taking QT-prolonging drugs.
Wolff-Parkinson-White (WPW) Syndrome
Diagnostic Criteria
The characteristic triad of the WPW pattern on a resting ECG is due to ventricular pre-excitation via an accessory pathway (the Bundle of Kent) (42):
Short PR interval (<120 ms): Resulting from rapid conduction down the accessory pathway, bypassing the normal AV nodal delay.
Delta Wave (δ): A slurring of the initial portion of the QRS complex, representing the early, slow muscle-to-muscle activation of the ventricle via the accessory pathway.
Wide QRS complex (>120 ms): The QRS is widened because it is a fusion beat, resulting from ventricular activation via both the accessory pathway and the normal His-Purkinje system.
Clinical Interpretation and Notes
The term WPW Syndrome is reserved for individuals who have the WPW pattern on their ECG and have also experienced documented tachyarrhythmias. The presence of an accessory pathway creates a substrate for re-entrant tachycardias, most commonly Orthodromic AVRT (where the impulse travels down the normal pathway and back up the accessory pathway, creating a narrow complex tachycardia). Less commonly, but more dangerously, patients can develop pre-excited AF, where rapid atrial impulses conduct down the fast accessory pathway, leading to an extremely rapid, irregular wide complex tachycardia that can degenerate into ventricular fibrillation.
Brugada Pattern
Diagnostic Criteria
The Type 1 (coved type) Brugada pattern is the only pattern considered diagnostic of this high-risk channelopathy. It is characterized by (43):
A coved ST-segment elevation with an amplitude of ≥2 mm (0.2 mV) at its peak.
This must be present in one or more right precordial leads (V1, V2), which may need to be positioned in higher intercostal spaces (3rd or 2nd) to be unmasked.
The elevated ST segment descends into a negative, symmetrical T-wave.
Clinical Interpretation and Notes
A diagnosis of Brugada Syndrome is made when a patient with a spontaneous or drug-induced Type 1 pattern also has symptoms like arrhythmic syncope, documented ventricular arrhythmia, or a family history of sudden cardiac death at a young age (<45 years). The underlying cause is a genetic mutation in cardiac sodium channels (most commonly SCN5A) that creates a voltage gradient in the right ventricular outflow tract, predisposing to polymorphic VT and sudden death. The Type 2 ("saddle-back") pattern is considered suspicious but is not diagnostic on its own and may require a pharmacological challenge (e.g., with flecainide) to see if it converts to the diagnostic Type 1 pattern.
