Basic ECG Information

ECG Leads and Placement

A standard ECG records the heart’s electrical activity from 12 leads (angles), giving a 3D view:

• 6 limb leads (I, II, III, aVR, aVL, aVF) → looks at the frontal plane
• 6 chest (precordial) leads (V1-V6) → looks at the horizontal plane

However, only 10 physical electrodes are attached to the patient, the ECG machine then uses these 10 electrodes to mathematically derive 12 leads of the heart.

Limb Leads Placement

Mnemonic for limb lead electrode placement: Ride Your Green Bike (in clockwise order, starting from the right arm)

The black electrode on the right leg is a neutral / ground electrode that does not trace any electrical activity.

Chest Leads Placement

ECG Paper Basics

An ECG trace is a graph of voltage (Y-axis) against time (X-axis).

Understanding the ECG paper scale allows you to accurately measure ECG rate, intervals, and amplitudes.

Paper Speed and Calibration

X and Y Axis Interpretation

The X (horizontal) axis on the ECG paper represents time.

The Y (vertical) axis on the ECG paper represents voltage.

ECG Paper Layout

Standard 12-lead ECG has 12 simultaneous views:

• Each lead is recorded for ~2.5 sec
• Most ECGs also show a rhythm strip (usually lead II) along the bottom for ~10 sec

Assessing an ECG

When assessing an ECG, always compare it with any previous ECGs, especially when there are abnormal changes.

The following is a stepwise approach to ECG interpretation

1. Rhythm

Assess the rhythm by looking at the distance between R-R intervals:

• If the spacing is consistent, the rhythm is regular
• If the spacing varies, the rhythm is irregular

There are 3 types of rhythm patterns:

• Regular rhythm: R-R intervals are equal throughout

• Irregular rhythm can be sub-classified as following:
  • Irregularly irregular: R-R intervals vary unpredictably
  • Regularly irregular: R-R intervals vary, but in a predictable pattern

2. Heart Rate

Rate category:

• <60 bpm: bradycardia
• >100 bpm: tachycardia

There are 3 methods to calculate the heart rate from an ECG strip:

3. Waveforms, Segments, and Intervals

This illustration nicely outlines and summarises the various waveforms, segments and intervals:

This table only included the clinically and exam-important information (e.g. extra information like normal amplitude of the waves is omitted):

4. Axis

The cardiac axis describes the overall direction of ventricular depolarisation

• In simple terms, it tells you which way the electrical current in the heart is predominantly moving

Normal axis and axis deviations:

The 4-quadrant helps visualise the axis deviation and how it corresponds with the limb leads.

Non-Arrhythmic ECG Abnormalities

Abnormal Wave / Interval / Segment

Abnormal ECG Waves

P Wave Abnormalities

There are 3 main P wave abnormalities:

ECG Example – Absent P Wave in Atrial Fibrillation

ECG Example – P Mitrale

ECG Example – P Pulmonale

QRS Abnormalities

Key QRS abnormalities:

ECG Example – Wide QRS

This left bundle branch block ECG demonstrates globally widened QRS complexes.

ECG Example – Pathological Q Wave

This ECG demonstrates pathological Q waves in leads V1-V4 (most prominent in V1-V3), due to anterior myocardial infarction.

T wave Abnormalities

ECG Example – Tall tented T wave

This ECG demonstrates tall tented T waves (most prominent in the precordial leads), secondary to hyperkalaemia.

ECG Example – Hyperacute T wave

This ECG demonstrates hyperacute T waves, secondary to an anterior STEMI, concurrent ST elevation is also visible.

ECG Example – Flat / Invisible T wave

This ECG demonstrates flat / invisible T waves globally, secondary to hypokalaemia.

ECG Example – Inverted T wave

This ECG demonstrates inverted T waves in the precordial leads, secondary to anterior NSTEMI, pathological Q waves are also visible in leads V1-V4.

Additional Waves

The following waves are not usually seen on a normal ECG:

ECG Example – U Wave

Note that there is a positive deflection (arrowed) after the T wave, and before the next P wave, that is the U wave.

ECG Example – J Wave (Osborne Wave)

A narrow notch can be seen at the J point (junction between the end of QRS and ST segment), that is the J wave. This ECG is secondary to hypothermia.

Abnormal Intervals

Main abnormal intervals to be aware of:

ECG Example – PR Prolongation

This ECG demonstrates PR prolongation (PR interval is roughly 9 small boxes / 360ms), secondary to 1st degree heart block.

ECG Example – PR Shortening

This ECG demonstrates PR shortening (PR interval is roughly 2.5 small boxes / 100ms), secondary to Wolff-Parkinson-White syndrome. Concurrent delta wave (the slurred upstroke R wave) is also visible.

ECG Example – QTc Prolongation

This ECG demonstrates QTc prolongation (on the rhythm strip, one can appreciate that the end of the T wave is immediately right behind the start of the P wave). The QTc is 510ms, secondary to hypomagnesaemia.

ECG Example – QTc Shortening

This ECG demonstrates QTc shortening (one can appreciate that the T wave began immediately after the QRS, and the T wave duration remains unaltered). The QTc is 260ms, secondary to hypercalcaemia.

Axis Deviation

Causes

Main causes of left axis deviation:

Main causes of right axis deviation:

 ECG Examples

This ECG shows left axis deviation. Applying the thumb rule: lead I is up (+ve) and lead aVF is down (-ve). The left axis deviation is secondary to left ventricular hypertrophy.

This ECG shows right axis deviation. Applying the thumb rule: lead I is down (-ve) and lead aVF is up (+ve). The right axis deviation is secondary to right ventricular hypertrophy (from cor pulmonale).

Tachyarrhythmias

For the management of tachyarrhythmias, see this article.

Tachyarrhythmias can be broadly categorised into atrial and ventricular arrhythmia (by the anatomical origin of electrical impulses).

Atrial Arrhythmias

Atrial Fibrillation (AF)

AF is one of the most commonly encountered arrhythmias in both clinical practice and exams. See this article for information beyond ECG features.

Atrial fibrillation is characterised by:

• Rapid, disorganised electrical activity in the atria from multiple foci
• → Irregularly ventricular contraction

Key ECG features of AF:

• Invisible P waves
• Irregularly irregular rhythm
• Narrow QRS (unless aberrancy is present)
• Heart rate can vary
  • Untreated AF often presents as fast AF (rate >100 bpm)
  • However, it is common for AF to have a normal heart rate, esp. if on treatment
  • Slow AF (rate <100 bpm) is less common

This is an ECG of atrial fibrillation. Note the irregularly irregular rhythm in the rhythm strip, no discrete P waves are seen before each QRS.

Atrial Flutter

Atrial flutter is caused by a single macro re-entry circuit within the right atrium → regular, rapid ventricular contraction

Key ECG features of atrial flutter:

• Regular, narrow complex tachycardia
• Flutter waves are visible instead of normal P waves → classic sawtooth pattern of flutter waves (best seen in inferior leads)
• Heart rate is very rapid and predictable (R-R intervals are multiples of P-P interval)
  • Most common: 2:1 atrial flutter (only 1 in every 2 atrial impulses is conducted to the ventricles) → ~150bpm
  • 1:1 atrial flutter → ~300bpm (rare)
  • 3:1 → ~100 bpm
  • 4:1 → ~75 bpm

However, atrial flutter can have variable blocks (unpredictable conduction of atrial impulses to the ventricles), giving an irregular narrow complex tachycardia. This is mentioned for completeness’s sake and is unlikely to be examined

This is an ECG of atrial flutter with 2:1 block. Note the regular narrow complex tachycardia and heart rate of 150bpm. Flutter waves are highly visible in the inferior leads (II, III, aVF).

Supraventricular Tachycardia (SVT)

The term and concept of SVT often create a lot of confusion:

• Anatomically speaking, SVT refers broadly to any arrhythmia originating above the ventricles (including AF and atrial flutter)
• However, clinically, SVT is used to describe a specific group or regular, narrow complex tachycardia
  • Atrioventricular nodal re-entrant tachycardia (AVNRT) – most common
  • Atrioventricular re-entrant tachycardia (AVRT)
  • Atrial tachycardia

Pathophysiology of he 3 main SVTs:

*The electrophysiology of AVNRT goes beyond what is described (e.g. subtypes of AVNRT and AVRT depending on the direction of the circuit). This information is omitted as it is very advanced knowledge and will almost certainly not be examined in the UKMLA.

SVTs have similar ECG features:

• Regular, narrow complex tachycardia
• Heart rate is usually 150-250 bpm

This is an ECG of SVT (specifically AVNRT). Note that regular, narrow complex tachycardia. Heart rate is roughly ~220 bpm. There are no signs of atrial fibrillation or atrial flutter, therefore it’s safe to consider this as SVT.

Wolf-Parkinson-White Syndrome (WPW syndrome)

WPW syndrome is a congenital conduction disorder characterised by the presence of an accessory pathway (bundle of Kent) that directly connects the atria to the ventricles, bypassing the normal AV node and bundle of His conduction system

• The accessory pathway allows pre-excitation of the ventricles, meaning that part of the ventricular myocardium is activated earlier than usual because the electrical impulse bypasses the AV node and travels down this accessory pathway
• ​​​​WPW syndrome is technically not a tachyarrhythmia itself, but if the accessory pathway participates in a reentrant circuit, it can cause atrioventricular re-entrant tachycardia (AVRT)

ECG features:

• Short PR interval (<3 small boxes) – due to early conduction of the electrical impulse from the atria to the ventricles via the accessory pathway
• Delta wave (a slurred, slow initial upstroke of the R wave) – due to the pre-excitation of the ventricles
• Wide QRS interval (>3 small boxes) – due to fusion of pre-excitation and normal conduction

1st line definitive management: catheter ablation of the accessory pathway

• A very dangerous complication is if a patient with WPW develops atrial fibrillation
• The accessory pathway in WPW can conduct the very rapid atrial impulses directly to the ventricles without the usual AV node delay, significantly increasing the risk of ventricular fibrillation

This is an ECG of WPW syndrome. The above-described ECG changes can be seen clearly in lead II.

Ventricular Arrhythmias

Premature Ventricular Complex (PVCs) / Ventricular Ectopics / Ventricular extrasystoles

PVCs arise when a ventricular focus becomes electrically active earlier than the sinus node, leading to an ectopic ventricular beat that occurs independently of the normal electrical conduction system.

• Since the impulse is generated by a ventricular focus and NOT conducted via the normal bundle of His conduction system, it gives an abnormal ECG morphology compared to the “normal” QRS complexes

ECG features:

• Broad QRS (>3 small boxes)
• Premature (the beat occurs earlier than would be expected for the next sinus impulse)
• Abnormal morphology
  • Unusual overall shape that differs from the normal QRS complexes (the shape depends on the origin)
  • Discordant ST-segment and T-wave changes

• PVCs can be classified based on their repeating pattern
  • Bigeminy: every other beat is a PVC
  • Trigeminy: every third beat is a PVC
  • Quadrigeminy: every fourth beat is a PVC
  • Couplet: two consecutive PVCs
  • Non-sustained ventricular tachycardia: 3-30 consecutive PVCs (lasting <30 sec)

This is an ECG of bigeminy PVCs. Each normal beat is followed by a PVC.

This is an ECG of PVC couplets. The PVCs come in pairs (2 conductive ones).

This is an ECG of non-sustained ventricular tachycardia. There are 4 consecutive PVCs, then 3 consecutive PVCs.

Ventricular Tachycardia (VT)

VT is a tachyarrhythmia that originates from the ventricles, defined by ≥3 consecutive PVCs at a rate of >100 bpm

• VT occurs when abnormal electrical impulses arise from ventricular tissue, either due to reentry, abnormal automaticity, or triggered activity
• The classic cause is a re-entrant circuit that forms around scarred myocardium (e.g. in MI), leading to rapid activation of the ventricles

Classification of VTs:

• Sustained vs non-sustained
  • Sustained VT: lasts >30 sec
  • Non-sustained VT: lasts <30 sec (3-30 consecutive PVCs)

• Monomorphic vs polymorphic
  • Monomorphic VT: all QRS have the same shape (as they originate from the same ventricular focus / circuit)
  • Polymorphic VT: there are >1 QRS shapes (as they originate from different ventricular foci / circuits)

Torsade de pointes (TdP) is a specific type of polymorphic VT that occurs in the context of QTc prolongation​​​​​​.

ECG features:

• Regular, broad complex tachycardia is VT until proven otherwise (at least for medical students and non-specialists…)
• There are specific ECG features that suggest VT over other causes, but they are of excessive detail
• TdP has a varying QRS morphology and the QRS complexes appear to be “twisting” around the isoelectric line

This is an ECG of monomorphic VT. Note the very regular, broad complex tachycardia and the same QRS morphology throughout.

This is an ECG of polymorphic VT (specifically, Torsades de Pointes – a type of polymorphic VT). The varying QRS morphology can be appreciated, with the characteristic morphology of QRS complexes “twisting” around the isoelectric line.

Ventricular Fibrillation

VF is characterised by the ventricles quivering in a rapid, irregular, and disorganised manner instead of contracting effectively.

ECG features:

• Chaotic irregular deflections of varying amplitude
• No identifiable P / QRS / T waves

This is an ECG of VF. Note that it looks very chaotic, and no waveforms or patterns can be identified.

Bradyarrhythmias

Heart Blocks / AV Blocks

Heart block occurs when electrical conduction from the atria to the ventricles is delayed or completely blocked.

There are 3 different types of heart block.

1st Degree Heart Block

ECG feature:

• PR interval consistently prolonged (>5 small squares)
• Each P wave is always followed by a QRS

This is an ECG of 1st degree heart block. In lead II, the PR interval is consistently prolonged (~7 small boxes / 280ms). Each P wave is followed by a QRS complex.

2nd Degree Heart Block

There are 2 subtypes of 2nd degree heart block:

This is an ECG of a 2nd degree, Mobitz I heart block. Appreciate the progressive PR prolongation (marked by the arrow), then a non-conducted P wave (dropped QRS). Afterwards, the same cycle begins with progressive PR prolongation, until a non-conducted P wave.

This is an ECG of 2nd degree, Mobitz II heart block. The vertical arrows indicate the non-conducted P wave (dropped QRS), and note the constant PR interval throughout.

Image source: LITFL ECG Library – Mobitz II (Hay) Second-Degree AV Block. https://litfl.com/second-degree-heart-block-mobitz-ii-ecg-library/ © Life in the Fast Lane. Licensed under CC BY-NC 4.0

3rd Degree / Complete Heart Block

ECG features:

• AV dissociation
  • Atrial activity (i.e. P wave) and ventricular activity (i.e. QRS) are independently regular, but there are no association between P wave and QRS (normally, each P wave is followed by QRS)
• Severe bradycardia (the ventricles have a slow intrinsic pacing rate)

This is an ECG of a 3rd-degree / complete heart block. Note the lack of association between the P waves (marked by upward-pointing arrow) and QRS (marked by downward-pointing arrow). While atrial activity (P waves) is occurring regularly, and ventricular activity (QRS) is occurring regularly.

Junctional Rhythm

Junctional rhythm is characterised by a rhythm that originates near or within the AV node
ECG features:

• Narrow QRS (as the rhythm originates from above the ventricles, and is conducted through the normal His-Purkinje system)
• Absence / inverted P waves
• Heart rate varies depending on the origin of the impulse
  • Junctional bradycardia <40 bpm
  • Junctional escape rhythm 40-60 bpm
  • Accelerated junctional rhythm 60-100 bpm
  • Junctional tachycardia >100 bpm

This is an ECG of an accelerated junctional rhythm. One can appreciate the narrow QRS and inverted P waves. Heart rate is ~120bpm.

Bundle Branch Blocks (BBBs)

Apart from LBBB and RBBB, there are also other types of BBBs (e.g. left anterior fascicular block, left posterior fascicular block, bifascicular block, trifascicular block), but they are very unlikely to be examined in the UKMLA.

LBBB is by far the most important one to recognise.

Left Bundle Branch Block (LBBB)

ECG features:

• Wide QRS (>3 small boxes)
• -ve QRS in V1 (dominant S wave)
• +ve QRS in V6, classically notched like an M (dominant R wave)
• Discordant ST-segment and T-wave changes

This is an ECG of LBBB. First, note the widened QRS complex across all leads. Second, a deep S wave is seen in V1 along with a dominant R wave in V6. Third, discordant changes are best seen in V1, where there is ST elevation and upright T wave while the QRS is -ve (dominant S wave).

Right Bundle Branch Block (RBBB)

ECG features:

• Wide QRS (>3 small boxes)
• +ve QRS in V1, classically notched like an M (dominant R wave)
• Wide slurred S wave in V6
• Discordant ST-segment and T-wave changes

This is an EGG of RBBB. First, note the widened QRS complex across all leads. Second, an M-shaped +ve QRS in V1 along with a wide slurred S wave in V6. Third, discordant changes are best seen in V1, where there is T wave inversion while the QRS is +ve (dominant R wave).

Myocardial Infarction

ECG Leads and Corresponding Myocardial Territory

This mapping allows localising specific areas of myocardial ischemia or infarction based on the changes in corresponding ECG leads.

*Some sources make the distinguishment between V1-V2 (septal wall) and V3-V4 (anterior wall), however they are both supplied by the LAD, such distinguishment does not make a huge clinical difference.

ECG Examples

Antero-lateral STEMI

ST elevation can be clearly seen in V2-V4 and V5, V6, I, and aVL. This corresponds to the myocardial territory of the anterior and lateral wall.

Inferior STEMI

ST elevation can be clearly seen in leads II, III, aVF. This corresponds to the myocardial territory of the inferior wall.

Other ECG Changes

Acute Pericarditis

See this article for more details.

ECG features:

• Diffuse concave ST elevation
• Global PR depression
• Reciprocal changes in aVR and V1 (ST depression and PR elevation)
• Spodick’s sign (downsloping TP segment)

This is an ECG of acute pericarditis, widespread concave ST elevation can be seen (most obvious in precordial leads, I, II, and aVL). PR depression can also be seen (most obvious in lead I, V2, V3).

Pulmonary Embolism (PE)

ECG features:

• Sinus tachycardia – the most common abnormality
• Right axis deviation
• Right ventricular strain pattern
  • T wave inversion in V1-V4 (right precordial leads) +/- II, III, aVF (inferior leads)

The classic textbook S1Q3T3 pattern (deep S wave in lead 1, Q wave in lead III, and inverted T wave in lead III) is only seen in 20% cases of PE and is neither sensitive nor specific for PE.

This ECG shows features suggestive of PE. Sinus tachycardia is present (rate 100 bpm). There is clear T wave inversion in right precordial leads (V1-V4) and in inferior leads (II, III, aVF). S1Q3T3 pattern is also present.

Cardiac Pacing (Pacemakers)

The key ECG feature is the presence of pacing spikes (sharp, narrow vertical lines) before P wave and/or QRS complexes

• The exact ECG finding in those with pacemakers may vary depending on whether intrinsic electrical activity is sensed or not, and the type of pacemaker, but this level of detail would not be necessary for the UKMLA.

This is an ECG of dual-chamber pacing. Pacing spikes can be seen consistently before both P waves (which are tiny) and QRS.

Left Ventricular Hypertrophy (LVH)

ECG feature:

• Deep S wave in V1 + tall R wave in V5 / V6 (cut-off shuod be >35 mm / 7 large boxes)
• Left axis deviation

At a glance, the QRS in LVH has very high voltages, often overlapping across leads.

This is an ECG of LVH. Very deep S waves can be seen in V1-V3, with very tall R waves in V4-V6.

Electrolyte Imbalance

Be aware that sodium disturbances (both hyponatraemia and hypernatraemia do not cause specific ECG changes, unlike other electrolyte imbalances (potassium, calcium, magnesium)

Hyperkalaemia

It is very important to recognise ECG changes in hyperkalaemia, see this article for more details.

Progressive ECG changes seen in hyperkalaemia:

This ECG shows hyperkalaemia. Tall, tented T waves are best seen in V2-V5. There are no identifiable P waves and the QRS is starting to widen.

This ECG shows very severe hyperkalaemia, with tall, tented T waves, and severe QRS widening, resembling a sine wave.

Hypos (Hypokalaemia, Hypocalcaemia, Hypomagnesaemia)

Hypokalaemia, hypocalcaemia and hypomagnesaemia all cause QTc prolongation.

Additional changes for hypokalaemia:

• Tall P waves
• PR prolongation
• U waves (can be hard to spot)
• ST depression and T wave flattening / inversion
• QTc prolongation

Drug Toxicity

There are 2 main drug toxicity-related ECG changes one should be aware of.

Tricyclic Antidepressant (TCA) Toxicity

ECG features:

• QRS widening (>3 small boxes)
• QTc prolongation

Note that TCA toxicity lacks the tall, tented T waves in hyperkalaemia (as it can be easy to be mixed up with hyperkalaemia).

Digoxin Toxicity

ECG features:

• Downsloping ST depression with a characteristic “reverse tick” appearance
• Flattened / inverted / biphasic T waves
• QTc shortening

The reverse tick downsloping ST depression is most prominent at lead II.