Normal P waves are:

• Positive in lead II
• Negative in aVR
• Biphasic in V1
• < 120 msec wide
• < 2.5mm tall ( < 1.5mm in chest leads)

Tall P waves are >2.5mm tall (1.5mm in chest leads). They can suggest right atrial enlargement. Tall peaked P waves are also known as P pulmonale because of their association with pulmonary disease.

Wide P waves are >120msec wide (3 small squares). They can suggest left atrial enlargement. Wide bifid P waves with two peaks are also known as P mitrale because they are associated with mitral valve disease.

Inverted P waves are negative in leads where they should normally be positive. They suggest that the rhythm is not sinus and as such depolarisation did not spread through the ventricles in a normal direction.

Electrode misplacement can also mimic inverted P waves.

Variable P waves have different shapes within the one lead. Causes include ectopic (extra) beats or arrhythmias.

If there are 3 or more different shapes within the one lead, the rhythm may be a wandering atrial pacemaker, which is also called multifocal atrial tachycardia if fast.

P waves that appear to be missing may be actually absent, or hidden within the T wave or QRS complex. They can be very hard to see if small, or if the rhythm is fast. They may be easier to see after adenosine or with special Lewis Leads.

If the P waves are truly absent, there may be an arrhythmia such as Atrial Fibrillation. If they are intermittently absent, there may be ectopic (extra) beats or sinus node conduction blocks.

If the P waves are hidden in the QRS they may be retrograde P waves

U waves are often mistaken for P waves, so take care!

A normal PR interval is 120-200 msec (3-5 small squares).

A short PR interval is <120 msec. It takes less time than usual for depolarisation to reach the ventricles either because the rhythm originates closer to the AV node than normal (e.g. atrial tachycardia), or there is an abnormal accessory pathway providing a shortcut through to the ventricles (e.g. Wolff Parkinson White syndrome).

A long PR interval is >200msec. It is caused by a conduction block at the AV node, which can be called a first degree AV block if the PR is consistently long and always followed by a QRS complex.

A variable PR interval can be caused by a higher degree of AV block, e.g. second or third degree block. A special type of a variable PR interval is a lengthening PR interval. It gets longer each beat until it is so long that the QRS complex is dropped (missing), before the cycle resets again for the next beat. A lengthening PR interval is classically caused by a second degree AV block called Wenckebach.

The PR segment is the brief gap between the end of the P wave and the start of the QRS complex. It is usually flat, but can be abnormal with atrial ischaemia or pericarditis.

PR depression can be caused by ischemia or pericarditis. In the setting of MI, significant PR depression is > 1.5 mm in chest leads, or 1.2mm in leads I-III.

PR elevation may occur in association with reciprocal PR depression in atrial ischemia or infarction. it is > 0.5mm in V5-6 (with PRD in V1-2) or lead I (with PRD in II-III).

A normal QRS complex is narrow (< 100 msec or 2.5 small squares). This occurs when the rhythm originates above the ventricles (supraventricular), which allows the impulse to speed down through the ventricles on the normal conduction highways.

Wide QRS complexes are >100 msec. They can occur if the rhythm originates from within the ventricles, or if it is supraventricular with a conduction problem (aberrancy). It is wide because conduction spreads more slowly through the ventricles.

QRS height can be normal, short or tall.

A short QRS is < 5 mm in all of the limb leads or < 10 mm in all of the chest leads. It is also known as low voltage QRS. It can be caused by an increased barrier between the heart and the surface electrodes (e.g. pericardial effusion, pleural effusion, obesity, pneumothorax), or reduced myocardial signal (e.g. massive MI, cardioyopathy, myxoedema or infiltrative cardiac disease). A massive pericardial effusion with tamponade is the most important diagnosis to exclude urgently.

A tall QRS is surprisingly hard to define. It can be caused by ventricular hypertrophy, but athletes and people who are slim may also have tall QRS complexes. The Sokolov-Lyon criteria defines a tall QRS as the height of S in V1 + the tallest R in V5 or V6 > 35mm, but it is not enough on its own to diagnose left ventricular hypertrophy.

The QRS height can also be alternating, known as QRS alternans. This can be caused by swinging movement of the heart (e.g. a large pericardial effusion or hypertrophic cardiomyopathy), or alternating cardiac conduction alone (e.g. atrial fibrillation, AVRT, MI, myocardial contusion, LV dysfunction, pulmonary embolism).

A twisting QRS suggests a particular type of VT called Torsades de Pointes.The QRS height changes gradually, so that the trace looks like it is being twisted around a rope.

Normally the QRS complex is negative in V1, positive in V6, and gradually transitions from negative to positive between these leads. The lead(s) where the QRS is isoelectric is known as the transition point, which is normally lead V3 or V4.

Late QRS transition occurs when the R in V3 is ≤ 3 mm. This can be a normal variant, or can suggest left ventricular hypertrophy, previous MI or electrode misplacement. It is also known as poor R wave progression.

Disrupted QRS transition can occur with electrode misplacement.

If there is no QRS progression, all of the QRS complexes in V1-V6 may be negative. Absent QRS transition is classically associated with dextrocardia.

Pathological Q waves are > 40msec wide (1 small square), >2mm deep or >25% of the QRS height. They can suggest a myocardial infarction, or sometimes a cardiomyopathy or an electrode misplacement.

Normal Q waves can occur in most leads except V 1-3. They should be present in V5-6.

Extra waves adjacent to the QRS complex can occur with several distinct syndromes.

A Delta wave occurs at the start of the QRS complex, as a slurred upstroke. It is caused by pre-excitation of the ventricles, e.g. Wolff Parkinson White syndrome.

An Epsilon wave occurs at the end of the QRS complex, as a subtle positive wave in V 1-4. It is caused by delayed depolarisation of some areas of the right ventricle. It is associated with arrhythmogenic right ventricular dysplasia.

A J wave occurs at the end of the QRS, as a positive wave where the ST segment begins. It is also known as an Osborn wave and is classically associated with hypothermia, but can also be caused by hypercalcemia, intracranial problems, ischemia, cardiomyopathy, or a normal variant. In the setting of Benign Early Repolarisation, a notched J point is known as a fishhook pattern.

Subtle QRS changes can be useful for rhythm and ischemia interpretation.

Extra waves within a wide QRS complex can be caused by conduction delays. The presence of a delayed second R wave within the complex can be called a RSR' complex. More specifically it can be called rSR' if the first R is smaller, or RSr' if the second R is smaller. A rSR' complex in V1 is classically associated with a right bundle branch block, whereas a RSr' complex is associated with VT.

A QRS complex that is narrow but has multiple extra waves can be called a fragmented QRS. It suggests the presence of an old infarction scar causing areas of the myocardium to have altered depolarisation. A delayed activation wave may also be associated with ischemia.

Another subtle QRS sign is prolonged R wave Peak time, which is measured from the start of the QRS to the peak of the R wave and is long if ≥ 50 msec. It is associated with a left bundle branch or fascicular block, ventricular tachycardia or left ventricular hypertrophy.

Subtle notching of the QRS complex can help with rhythm analysis in wide complex tachycardia. A notched S wave nadir in V1 is also known as Josephson sign, and it is a specific sign for VT. A notched R wave downslope in V1 is like a subtle RSr' complex and also suggests VT.

ST elevation (STE) can be described as concave, straight (or oblique) or convex.

Convex or straight ST elevation is classically associated with myocardial infarction, though MI can present with any shape of ST segments. The severe convex ST elevation of a massive anterior MI is also known as tombstone ST elevation. Massive MI can also form a Shark Fin pattern. Coved ST elevation is classically associated with Brugada syndrome.

The concave ST elevation of pericarditis is often described as saddleback.

A rare but critical ST elevation pattern is the Spiked Helmet sign, where ST elevation appears to begin before the QRS complex. It is associated with critical illness and risk of death.

ST depression (STD) can be described as horizontal, downsloping or upsloping.

Horizontal or downsloping ST depression is classically associated with myocardial ischemia. In leads V1-3, horizontal ST depression can be caused by acute posterior MI. Downsloping ST depression that appears sagging is associated with digoxin use. Other causes include hypokalemia, right ventricular hypertrophy and right bundle branch block.

Upsloping ST depression that occurs with large (hyperacute) T waves is known as a De Winter sign due to an acute anterior MI.

In the presence of an abnormally wide QRS rhythm, ST segments often have elevation or depression without any ischemia or infarction. These changes are known as secondary changes because they occur secondary to the rhythm problems. Shapes that help to determine whether the ST changes are primary or secondary include concordance and discordance.

Concordant ST changes occur in the same direction as the QRS complex. They include concordant ST elevation with a positive QRS complex, or concordant ST depression with a negative QRS complex. Concordant ST elevation, or concordant ST depression in V1-3, are part of the Sgarbossa criteria for diagnosing MI in the presence of a left bundle branch block.

Discordant ST changes occur in the opposite direction to the QRS complex. They include ST elevation with a negative QRS complex, or ST depression with a positive QRS complex. This is often normal, but can still indicate ischemia or infarction if the changes are excessive, i.e. ≥ 25% of the S wave height.

Tall T waves are difficult to define, but in general should be > 5mm in limb leads or > 10mm in chest leads. They should also be subjectively assessed in proportion to the size of the QRS complex.

• Peaked T waves have a sharp point and a narrow base. They are classically associated with hyperkalemia.
• Hyperacute T waves have a broader base and are 'fatter' so that there is more area under the curve. They are associated with MI.

Flattened or inverted T waves can also suggest ischemia or electrolyte problems. Ischemia is more likely if the findings are dynamic.

T waves are normally inverted in V1, and sometimes in III. Children normally have inverted T waves in V1-3, and this juvenile T wave pattern sometimes persists into adulthood.

Other causes of inverted T waves include secondary changes following an abnormal QRS (e.g. ventricular hypertrophy, bundle branch block), raised intracranial pressure or pulmnary embolism causing right heart strain.

Biphasic T waves have both positive and negative elements. They can be caused by ischemia or electrolyte problems.

• Up-Down T waves are associated with ischemia. When they occur in a patient who had chest pain but is now pain free they can suggest a Wellens syndrome with a critical LAD stenosis.
• Down-Up T waves are associated with hypokalemia.

U waves are small mysterious extra waves that sometimes appear after the T wave. They normally have the same positivity as the T wave. Their origin is unclear, but there are several theories. They are more likely to be visible with bradycardia or hypokalemia.

Tall U waves are >1-2mm or 25% of the T wave height. They are associated with bradycardia and severe hypokalemia, also hypocalcaemia, hypomagnesaemia or hypothermia.

Inverted U waves are associated with heart disease, and may be the earliest marker of ischemia.

Camel hump T waves have two peaks, which can either be caused by a combined T+U wave, or a hidden P wave within the T.

The QT interval can be normal, short or long.

A normal QT depends on the heart rate and gender of the patient. At a heart rate of 60 bpm, the QT is normal if 350-440 msec in men, or 350-460msec in women. A corrected QT (QTc) is calculated to allow QT comparisons at different heart rates using the same ranges.

A long QTc is > 440 msec in men or 460msec in women, but is particularly significant if >500 msec as this increases the risk of Torsades de Pointes.

A short QTc is <350 msec. It can be caused by hypercalcemia, digoxin or a congenital short QT syndrome.