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Heart rate

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Spark

The conduction system and the waves it writes

Each heartbeat starts as an impulse in the sinoatrial node and spreads through the atria, the atrioventricular node, the His–Purkinje system and the ventricles. The ECG records the sum of these currents at the body surface over time.

Sinoatrial node and the P wave

The sinoatrial (SA) node lies high in the right atrium, near the entry of the superior vena cava. It depolarizes spontaneously, at 60–100 times per minute at rest in adults. The impulse spreads through the right atrium and then, mainly through Bachmann's bundle, to the left atrium.

Atrial depolarization writes the P wave. The impulse travels leftward and downward, so a sinus P wave is upright in lead II and negative in aVR. A normal P wave lasts less than 120 ms.

Atrioventricular node and the PR interval

The atrioventricular (AV) node is the only normal electrical connection between the atria and the ventricles. Conduction slows there, which lets the atria finish emptying into the ventricles before the ventricles contract. The PR interval runs from the start of the P wave to the start of the QRS complex. It includes atrial depolarization, the AV nodal delay and conduction through the His–Purkinje system. It is normally 120–200 ms.

His–Purkinje system and the QRS complex

The His bundle divides into the right and left bundle branches, which end in the Purkinje fibers under the endocardium. Conduction through this system is very fast, so the large ventricular mass depolarizes almost at once. The result is a narrow QRS complex, normally under 120 ms.

The septum depolarizes first, from left to right. This small rightward force makes the narrow septal q waves in leads I, aVL, V5 and V6, and the small r wave in V1.

ST segment and T wave

During the plateau of the ventricular action potential, the whole ventricle is depolarized and no current flows between regions, so the ST segment is flat, at the baseline. Ventricular repolarization writes the T wave. Repolarization runs from epicardium to endocardium, opposite in direction to depolarization, so in most leads the T wave points the same way as the QRS complex.

Atrial repolarization is small and happens during the QRS complex, so it is normally not seen.

Key points

P wave = atrial depolarization; QRS = ventricular depolarization; T wave = ventricular repolarization.
The PR interval is mostly the AV nodal delay, and is normally 120–200 ms.
Fast His–Purkinje conduction keeps the QRS narrow (< 120 ms). A wide QRS means slow conduction through the ventricular muscle.

Heart rate

Rate method

Paper

Calibration and heart rate

ECG paper is a graph of voltage against time. At the standard paper speed of 25 mm/s and gain of 10 mm/mV, one small box is 40 ms by 0.1 mV, and one large box is 200 ms by 0.5 mV.

Check the calibration first

Every tracing starts with a calibration pulse. At standard gain, the 1 mV pulse is 10 mm (two large boxes) tall. If the voltages are very large, the machine may record at half gain (5 mm/mV), and every amplitude must then be doubled before you apply voltage criteria. Check the paper speed too. At 50 mm/s every interval looks twice as long.

1 small box = 0.04 s · 0.1 mV · 1 large box = 0.20 s · 0.5 mV · 5 large boxes = 1 s

Three ways to measure the rate

300 ÷ large boxes: Find an R wave on a heavy line and count the large boxes to the next R wave. Rate = 300 ÷ boxes. With practice you can recite the sequence 300, 150, 100, 75, 60, 50 line by line. This method is fast, but rough at high rates.
1500 ÷ small boxes: Count the small boxes between two R waves. Rate = 1500 ÷ small boxes. This is the most precise method for a regular rhythm.
6-second count: Count the QRS complexes in 6 seconds (30 large boxes) and multiply by 10. A standard 12-lead rhythm strip is 10 s long, so you can also count every complex on it and multiply by 6. Use this method when the rhythm is irregular, as in atrial fibrillation.

A normal resting rate in adults is 60–100 per minute. Below 60 is bradycardia and above 100 is tachycardia.

Key points

Confirm 25 mm/s and 10 mm/mV before you measure anything.
Regular rhythm: 300 ÷ large boxes for speed, 1500 ÷ small boxes for precision.
Irregular rhythm: count the complexes over 6 or 10 seconds.

Plane

Direction of depolarization

Leads

Twelve views of one heartbeat

A 12-lead ECG records the same electrical activity from twelve directions. Depolarization that travels toward a lead's positive pole makes an upright deflection, and depolarization that travels away makes a negative one. Depolarization at right angles to the lead makes a small or equiphasic deflection.

Limb leads: the frontal plane

The six limb leads look at the heart in the frontal plane. Leads I, II and III are bipolar and compare pairs of limbs. The augmented leads aVR, aVL and aVF compare one limb with the average of the other two. Together they form the hexaxial reference system. Angles are measured from lead I at 0°, and are positive in the clockwise (inferior) direction:

I 0° · II +60° · aVF +90° · III +120° · aVL −30° · aVR −150°

Chest leads: the transverse plane

The six precordial leads look at the heart in the transverse plane. V1 and V2 face the right ventricle and septum from the front. V5 and V6 face the lateral wall of the left ventricle.

V1: 4th intercostal space, right sternal border. V2: 4th intercostal space, left sternal border.
V3: halfway between V2 and V4. V4: 5th intercostal space, midclavicular line.
V5: anterior axillary line, level with V4. V6: midaxillary line, level with V4.

Normally the QRS changes from a small r and deep S in V1 to a tall R and small s in V6. The lead where R and S are about equal, the transition zone, is usually V3 or V4.

Contiguous leads and territories

Inferior: II, III, aVF
Lateral: I, aVL, V5, V6
Septal: V1, V2 · Anterior: V3, V4

Electrode position matters. A chest electrode placed one intercostal space too high or too low can change the R-wave progression enough to mimic an infarct.

Key points

Depolarization toward a lead gives an upright deflection; away from it, a negative one; at right angles, an equiphasic one.
aVR looks at the heart from the upper right, so in sinus rhythm everything is negative in aVR.
R waves normally grow from V1 to V5, with the transition at V3–V4.

QRS axis

Practice

Axis

The mean direction of ventricular depolarization

The QRS axis is the average direction of ventricular depolarization in the frontal plane. In adults the normal axis lies between −30° and +90°.

The two-lead method

Look at the net QRS deflection (R minus S) in lead I and in aVF.

I positive, aVF positive: normal axis (0° to +90°).
I positive, aVF negative: the axis is between 0° and −90°. Check lead II. If II is positive, the axis is still normal (0° to −30°). If II is negative, there is left axis deviation.
I negative, aVF positive: right axis deviation (+90° to +180°).
I negative, aVF negative: extreme axis (−90° to ±180°).

Refining with the isoelectric lead

Find the limb lead where the QRS is most equiphasic. The axis is at right angles to that lead, on the side of whichever perpendicular lead is positive. For example, if aVL is equiphasic and II is positive, the axis is about +60°.

Common causes

Left axis deviation (−30° to −90°): Left anterior fascicular block, inferior myocardial infarction, left ventricular hypertrophy, left bundle branch block, ventricular pre-excitation and ventricular rhythms.
Right axis deviation (+90° to +180°): Right ventricular hypertrophy or strain (including acute pulmonary embolism), left posterior fascicular block, lateral myocardial infarction, dextrocardia and reversed arm electrodes. A rightward axis can be normal in children and in tall, thin adults.
Extreme axis (−90° to ±180°): Ventricular rhythms, severe hyperkalemia and lead misplacement.

Key points

Normal axis is −30° to +90°.
Leads I and aVF give the quadrant; lead II separates a normal axis of 0° to −30° from left axis deviation.
Before you diagnose right axis deviation, make sure the arm electrodes are not reversed. Reversal also makes lead I and its P wave negative.

Examples

Heart rate

PR interval

QRS duration

QT interval

Intervals

PR, QRS and QT

Intervals measure how long each part of conduction takes. A long PR points to the AV node, a wide QRS to the ventricular conduction system, and a long QT to repolarization.

PR interval: 120–200 ms

Measure from the start of the P wave to the start of the QRS complex.

Longer than 200 ms: first-degree AV block. Every P wave is still conducted, only slowly.
Shorter than 120 ms: think of ventricular pre-excitation (Wolff–Parkinson–White, with a delta wave and a wide QRS) or a low atrial or junctional rhythm.

QRS duration: under 120 ms

Measure from the first to the last deflection of the QRS, in the lead where it is widest.

110–119 ms: incomplete bundle branch block or a nonspecific intraventricular conduction delay.
120 ms or longer: complete right or left bundle branch block, a ventricular rhythm, pre-excitation, a paced rhythm, hyperkalemia or a sodium-channel-blocking drug.

QT interval and rate correction

Measure from the start of the QRS to the end of the T wave, in the lead with the longest QT (often II or V5). The QT shortens as the heart rate rises, so it is corrected to a rate of 60/min:

Bazett: QTc = QT ÷ √RR · Fridericia: QTc = QT ÷ ∛RR (RR in seconds)

Bazett's formula overcorrects at fast heart rates and undercorrects at slow ones. Fridericia's formula is more accurate away from 60/min. A QTc above 450 ms in men or above 460 ms in women is prolonged. A QTc above 500 ms carries a substantially higher risk of torsades de pointes. A QT of 390 ms or less is short.

Key points

PR 120–200 ms · QRS < 120 ms · QTc < 450 ms (men) or < 460 ms (women).
Always correct the QT for heart rate, and know which formula your ECG machine uses.
A QTc above 500 ms: review the medications and check potassium and magnesium.

Rhythm

Practice

Ladder diagram

Rhythm

Rate, regularity, P waves and QRS width

Rhythm analysis comes down to four questions. What is the rate? Is it regular? Is there a P wave before every QRS, and a QRS after every P wave? Is the QRS narrow or wide? The ladder diagram under the strip shows the answer to the third question.

A systematic approach

Rate: atrial and ventricular. They are different whenever some P waves are not conducted.
Regularity: regular, regularly irregular (a repeating pattern) or irregularly irregular.
P waves: present? Upright in II? One before every QRS? Is the PR constant?
QRS: narrow (supraventricular origin) or wide (aberrant conduction or ventricular origin)?

AV block

First degree: PR longer than 200 ms, with every P wave conducted.
Second degree, Mobitz I (Wenckebach): The PR lengthens beat by beat until one P wave is not conducted. The block is usually in the AV node and is usually benign.
Second degree, Mobitz II: The PR stays constant until a P wave is suddenly not conducted. The block is usually below the AV node, often with a wide QRS, and may progress to complete block. It usually needs a pacemaker.
Third degree (complete): No P wave is conducted. The atria and ventricles beat independently (AV dissociation), and the ventricular rate is set by a junctional or ventricular escape rhythm.

Tachyarrhythmias

Atrial fibrillation: No organized P waves, a fibrillatory baseline and an irregularly irregular ventricular rhythm.
Atrial flutter: Sawtooth flutter waves at about 300/min, negative in II, III and aVF in typical flutter. With 2:1 conduction the ventricular rate is about 150/min. Consider flutter for any regular narrow-complex tachycardia at 150/min.
Ventricular tachycardia: Three or more consecutive wide ventricular beats at more than 100/min. AV dissociation, with P waves marching through at their own rate, strongly supports VT. Treat any wide-complex tachycardia as VT until proven otherwise.

Key points

Measure the atrial and ventricular rates separately.
Wenckebach: progressive PR prolongation. Mobitz II: a constant PR, then a dropped beat.
A wide-complex tachycardia is VT until proven otherwise.

Injured territory

Severity of injury

Show

Highlight the leads

Injury

ST elevation and the culprit artery

Acute transmural ischemia raises the ST segment in the leads that face the injured wall and depresses it, reciprocally, in leads that look from the opposite side. Which leads are involved points to the culprit artery.

ST-elevation criteria

The Fourth Universal Definition of Myocardial Infarction (2018) defines significant ST elevation as new elevation at the J point in at least two contiguous leads of:

≥ 1 mm in all leads other than V2–V3;
in V2–V3: ≥ 2 mm in men aged 40 or older, ≥ 2.5 mm in men under 40, and ≥ 1.5 mm in women.

This figure uses the simpler 1 mm / 2 mm thresholds. ST depression of 0.5 mm or more is marked as reciprocal.

Territories

Anterior (left anterior descending artery): ST elevation in V1–V4. Elevation that also involves I, aVL, V5 and V6 suggests a proximal occlusion and a large territory.
Inferior (right coronary artery, or a dominant circumflex): ST elevation in II, III and aVF, with reciprocal depression in aVL, often the earliest sign. If ST elevation is greater in III than in II, the right coronary artery is more likely. Record right-sided leads (V4R) to look for right ventricular infarction.
Lateral (circumflex or a diagonal branch): ST elevation in I, aVL, V5 and V6, with reciprocal depression in the inferior leads.
Posterior: ST depression in V1–V3, often with tall R waves there, is the mirror image of posterior injury. Record V7–V9.

Mimics

Not every ST elevation is an infarct. Consider pericarditis (diffuse elevation with PR depression), early repolarization, left ventricular hypertrophy, left bundle branch block, ventricular pacing, Brugada pattern and left ventricular aneurysm. Reciprocal depression and a pattern that fits one coronary territory both favor acute occlusion.

The tracings here come from a simplified teaching model. Real ECGs of acute infarction also show hyperacute T waves, evolving Q waves and T-wave inversion. In practice, compare with earlier tracings, repeat the ECG and follow your institution's protocol for reperfusion.

Key points

ST elevation in two contiguous leads, with reciprocal depression, is acute injury until proven otherwise.
V1–V4 → LAD · II, III, aVF → RCA (or circumflex) · I, aVL, V5–V6 → circumflex or diagonal.
ST depression in V1–V3 may be posterior infarction. Record V7–V9.

Conduction

Blocks

Bundle branch and fascicular blocks

When a bundle branch fails, the ventricle on that side is activated late, through slow muscle-to-muscle conduction. The QRS widens to 120 ms or more, and its late part points toward the ventricle that is activated last.

Right bundle branch block

QRS ≥ 120 ms.
rsr′, rsR′ or rSR′ in V1 or V2. The R′ is usually taller than the initial r.
A wide S wave in I and V6, longer than the R wave or over 40 ms.

The septum and left ventricle depolarize normally, so the first 60 ms look normal and infarct Q waves stay visible. RBBB can be seen in healthy people, and it also occurs with right ventricular strain, pulmonary embolism, congenital heart disease and conduction-system disease. The inverted T waves in V1–V3 are secondary and expected.

Left bundle branch block

QRS ≥ 120 ms.
A broad, notched or slurred R wave in I, aVL, V5 and V6, with no septal q wave in those leads.
R-peak time over 60 ms in V5–V6.
ST segments and T waves usually point opposite the QRS (appropriate discordance).

The septum is activated from the right, so the normal septal q waves disappear. LBBB almost always means heart disease (hypertension, cardiomyopathy, coronary or valve disease) and should prompt an echocardiogram. It also hides ischemia: the Sgarbossa criteria (concordant ST elevation ≥ 1 mm, concordant ST depression ≥ 1 mm in V1–V3, or excessively discordant ST elevation) help identify acute occlusion.

Fascicular blocks

Left anterior fascicular block: Axis −45° to −90°, qR in aVL with an R-peak time ≥ 45 ms, rS in II, III and aVF, and a QRS under 120 ms. It is the most common cause of marked left axis deviation.
Left posterior fascicular block: Axis +90° to +180°, rS in I and aVL, qR in III and aVF, and a QRS under 120 ms. It is rare, and is diagnosed only after right ventricular hypertrophy, lateral infarction and a vertical heart are excluded.
Bifascicular block: RBBB with either fascicular block. Add a long PR and some call it “trifascicular”, although the PR often reflects AV nodal delay. Bifascicular block with unexplained syncope needs evaluation for intermittent high-grade AV block.

Key points

RBBB: rsR′ in V1, wide S in I and V6. LBBB: broad R without q in I and V6, QS or rS in V1.
Fascicular blocks shift the axis without widening the QRS: LAFB to the left, LPFB to the right.
New LBBB is a marker of heart disease. Use the Sgarbossa criteria when you suspect infarction.

Pattern

Hypertrophy

Chamber enlargement and voltage

A thicker ventricle produces larger voltages, and an enlarged atrium changes the size and timing of the P wave. The ECG criteria are specific but miss many cases, so echocardiography remains the reference.

Left ventricular hypertrophy

Sokolow–Lyon: S in V1 + R in V5 or V6 ≥ 35 mm · Cornell: R in aVL + S in V3 > 28 mm (men), > 20 mm (women)

Supporting findings include left atrial enlargement, left axis deviation, a slightly wider QRS and an R-peak time over 50 ms in V5–V6. Young, thin people and athletes often exceed the voltage criteria without hypertrophy, while obesity, emphysema and effusions reduce the voltage.

Strain pattern

Downsloping ST depression with asymmetric T-wave inversion in the lateral leads (I, aVL, V5, V6) is a repolarization change caused by hypertrophy. It marks more severe hypertrophy and a worse prognosis, and it can mimic or hide ischemia.

Right ventricular hypertrophy

Right axis deviation (≥ +110° in adults).
A dominant R in V1: R/S > 1 or R ≥ 7 mm.
A deep S wave in V5–V6 (R/S < 1).
Often right atrial enlargement and T-wave inversion in V1–V3.

Causes include pulmonary hypertension, chronic lung disease, pulmonary stenosis and congenital heart disease. Other causes of a tall R in V1 are posterior infarction, RBBB, WPW with a left-sided pathway, and dextrocardia or lead misplacement.

Atrial enlargement

Left atrial enlargement (“P mitrale”): P duration ≥ 120 ms, often notched in II, and a negative terminal P in V1 at least 1 mm deep and 40 ms wide.
Right atrial enlargement (“P pulmonale”): P amplitude > 2.5 mm in II, III or aVF, or an initial positive P > 1.5 mm in V1.

Key points

LVH: Sokolow–Lyon ≥ 35 mm or Cornell > 28 mm (men) / > 20 mm (women). Lateral strain makes it more likely and more serious.
RVH: right axis, tall R in V1, deep S in V6.
Broad notched P plus a deep terminal P in V1 means a large left atrium; a tall peaked P in II means a large right atrium.

Potassium

Calcium (total)

Electrolytes

Potassium and calcium

Potassium sets the resting membrane potential and the speed of repolarization; calcium sets the length of the plateau. Their changes are among the few ECG findings that can be lethal within minutes and are quickly reversible.

Hyperkalemia

The changes progress roughly in this order as potassium rises, but the correlation with the serum level is loose. Some patients go straight from a near-normal ECG to an arrhythmia.

Tall, narrow, peaked T waves with a narrow base, best seen in V2–V4.
A longer PR, then flattening and loss of the P wave.
Widening of the QRS, bizarre bundle-branch-like shapes, bradycardia and junctional rhythms.
A sine-wave pattern as the QRS merges with the T, then ventricular fibrillation or asystole.

Hyperkalemic ECG changes are an emergency: give intravenous calcium to stabilize the membrane, then insulin with glucose and other measures to shift and remove potassium.

Hypokalemia

T waves flatten, the ST segment sags, and a U wave appears after the T wave, best seen in V2–V3. As the T and U merge, the apparent QT (really a QU interval) lengthens, which raises the risk of torsades de pointes, especially with QT-prolonging drugs or low magnesium.

Calcium

Hypocalcemia: The ST segment lengthens, so the QT is long but the T wave itself keeps its normal shape and width.
Hypercalcemia: The ST segment shortens or disappears, so the T wave seems to start right after the QRS and the QT is short. Very high levels can cause J (Osborn) waves and bradyarrhythmias.

The tracing shows the typical progression for teaching. Real patients vary widely, and a normal ECG does not exclude dangerous hyperkalemia.

Key points

Hyperkalemia: peaked T → long PR and flat P → wide QRS → sine wave.
Hypokalemia: flat T, ST depression, prominent U wave, long QU.
Calcium changes the ST segment: long with hypocalcemia, short with hypercalcemia.

Accessory pathway

Degree of pre-excitation

Pre-excitation

Wolff–Parkinson–White

An accessory pathway is a strand of muscle that bypasses the AV node. It conducts without the nodal delay, so part of the ventricle is activated early: the PR shortens and the QRS starts with a slurred delta wave.

The WPW pattern

Short PR, under 120 ms.
A delta wave: a slurred, slow upstroke at the start of the QRS.
A wide QRS (often 110–140 ms), because each beat is a fusion of pathway and normal conduction.
Secondary ST–T changes that point opposite the delta wave.

How much pre-excitation shows depends on how fast each route conducts. Vagal tone, a slow AV node or a pathway close to the sinus node increase it; a far left-lateral pathway may show little.

Locating the pathway

The delta wave points away from the pathway. A positive delta wave in V1 (“type A”) means a left-sided pathway; a negative one (“type B”) means a right-sided pathway. Negative delta waves can mimic infarct Q waves: in the lateral leads with left-lateral pathways, and in the inferior leads with posteroseptal pathways.

Pattern versus syndrome

The WPW pattern is the ECG alone. WPW syndrome adds tachyarrhythmias:

Orthodromic AVRT: Down the AV node and up the pathway: a regular narrow-complex tachycardia, and the most common arrhythmia in WPW.
Antidromic AVRT: Down the pathway and up the node: a regular, fully pre-excited wide-complex tachycardia that looks like VT.
Pre-excited atrial fibrillation: Irregular, very fast, wide complexes of varying shape. It can degenerate into ventricular fibrillation. Do not give AV nodal blockers (adenosine, beta-blockers, calcium channel blockers, digoxin), which can speed conduction down the pathway. Cardiovert if unstable; otherwise procainamide or ibutilide.

Symptomatic patients, and those with high-risk pathway features, are usually referred for catheter ablation.

Key points

Short PR + delta wave + wide QRS = pre-excitation.
A positive delta wave in V1 means a left-sided pathway, a negative one a right-sided pathway.
Pre-excited AF: irregular, wide and very fast. Avoid AV nodal blockers.

Case

Practice

Brugada algorithm

VT vs SVT

The wide-complex tachycardia

A regular tachycardia with a QRS of 120 ms or more is either ventricular tachycardia or a supraventricular rhythm conducted with a bundle branch block (aberrancy). Most are VT, especially in patients with structural heart disease, and mistaking VT for SVT can be fatal.

Before the ECG

History is powerful. In a patient with a prior myocardial infarction, heart failure or a cardiomyopathy, a wide-complex tachycardia is VT in the large majority of cases. Hemodynamic stability does not help: VT can be well tolerated.

The Brugada algorithm (1991)

Answer four questions in order. The first “yes” diagnoses VT. If all four are “no”, the rhythm is SVT with aberrancy.

No RS complex in any chest lead? All QRS complexes in V1–V6 are entirely positive or entirely negative (concordance). → VT
RS interval > 100 ms in any chest lead? Measured from QRS onset to the deepest point of the S wave. → VT
AV dissociation? P waves unrelated to the QRS, or capture and fusion beats. → VT
Morphology criteria for VT in V1–V2 and V6?
- Right bundle shape (V1 ends positive): monophasic R, qR or Rs in V1; R/S < 1 or QS in V6.
- Left bundle shape (V1 ends negative): initial r > 30 ms, notched S downstroke, or > 60 ms to the S nadir in V1–V2; any Q wave in V6.

Other clues to VT

Capture beats (a narrow, early beat) and fusion beats.
An extreme (“northwest”) axis, between −90° and ±180°.
A very wide QRS: > 140 ms with a right bundle shape, > 160 ms with a left bundle shape.
An initial R wave in aVR, or a slow initial part of the QRS (the Vereckei aVR algorithm).

Management

An unstable patient needs synchronized cardioversion, whatever the mechanism. A stable regular wide-complex tachycardia of uncertain origin is treated as VT. Adenosine may be considered only if the rhythm is regular and monomorphic. Avoid verapamil and diltiazem, which can cause collapse in VT.

The cases are model tracings designed to show each step. Real tracings are harder: criteria overlap, and pre-existing bundle branch block, drugs and pre-excitation (antidromic AVRT) can all make SVT look like VT.

Key points

A wide-complex tachycardia is VT until proven otherwise, especially after an MI.
Brugada: no RS → RS > 100 ms → AV dissociation → morphology. The first yes is VT.
When in doubt, treat as VT. Never give verapamil to an undiagnosed wide-complex tachycardia.

Measure	Adult normal	Outside the range
Heart rate	60–100 /min	< 60 bradycardia · > 100 tachycardia
P wave	< 120 ms	Upright in II, negative in aVR in sinus rhythm
PR interval	120–200 ms	> 200 first-degree AV block · < 120 pre-excitation or junctional
QRS duration	< 120 ms	110–119 incomplete block · ≥ 120 complete bundle branch block or ventricular origin
QRS axis	−30° to +90°	< −30° left · > +90° right
QTc	≤ 450 ms (men), ≤ 460 ms (women)	> 500 ms high risk of torsades · ≤ 390 ms short QT
R-wave transition	V3–V4	Early (V1–V2) or late (V5–V6) transition
P amplitude (II)	≤ 2.5 mm	> 2.5 mm right atrial enlargement
LVH voltage	Sokolow–Lyon < 35 mm	Cornell > 28 mm (men), > 20 mm (women)
Potassium	3.5–5.0 mmol/L	Peaked T above; flat T and U waves below
Septal q wave	< 40 ms	Wider or deeper Q waves suggest infarction