Quest: ECG Basics

To begin, it’s useful to describe ECG deflections as positive, negative, or biphasic. Think of the baseline (the isoelectric line) as sea level: crests rise above it, troughs fall below it.

Positive waves rise above the baseline. They occur when the net activation vector (e.g., during depolarisation) is directed toward the lead’s positive electrode (i.e., aligned with the lead axis). Repolarisation produces the opposite polarity for the same vector orientation.

Negative waves fall below the baseline. They occur when the net activation vector is directed away from the lead’s positive electrode (i.e., toward the negative pole or opposite the lead axis). Again, note that repolarisation in the same direction generates the opposite polarity to depolarisation.

Biphasic waves have both positive and negative components within a single deflection - often when the activation vector is roughly perpendicular to the lead axis or changes direction as it passes the recording electrode. When the upstroke and downstroke are of similar size, the wave may be described as equiphasic.

ECG waves are conventionally labelled using letters of the alphabet.

The first deflection of each beat is the P wave, which represents atrial depolarisation. It is usually small and may be subtle or difficult to identify.

The atrial activity is followed by the QRS complex, which represents ventricular depolarisation. This complex consists of one or more sharp deflections:

A Q wave is the first negative deflection of the complex. Q waves are always negative. An R wave is a positive deflection within the complex and is often tall and sharp. An S wave is a negative deflection that follows an R wave. By convention, Q and S waves are always negative, while R waves are positive.

Following ventricular depolarisation, the T wave appears. It reflects ventricular repolarisation and is usually broad and rounded compared to the sharper deflections of the QRS complex.

An ECG complex refers to a closely grouped series of deflections that represent a coordinated cardiac event.

The principal complex is the QRS complex, which reflects ventricular depolarisation. It is named according to the specific waves that are present. Not every complex contains all three deflections:

If the complex has a Q and R wave but no S wave, it is described as a QR complex. If there is no R wave and only a negative deflection is seen, it can described as a QS complex. Variations in morphology occur depending on the direction of the electrical vector relative to the recording lead.

Just like individual waves, QRS complexes can be described as positive, negative, or equiphasic. This convention is particularly useful when determining the cardiac axis later in interpretation.

A positive complex has a greater overall deflection above the baseline than below it.

A negative complex has a greater overall deflection below the baseline than above it.

If the positive and negative deflections are approximately equal, the complex is described as isoelectric or equiphasic.

ECG segments are the flat portions of the tracing that lie between two waves. They are usually named according to the waves that bound them.

The PR segment extends from the end of the P wave to the beginning of the QRS complex. It represents conduction through the atrioventricular node, His bundle, and Purkinje system before ventricular depolarisation begins.

The ST segment extends from the end of the QRS complex to the beginning of the T wave. It corresponds to the plateau phase of ventricular repolarisation and is clinically important when assessing for ischaemia or infarction.

The TP segment extends from the end of the T wave to the beginning of the next P wave. It represents the period when the heart is electrically at rest and is often used as the reference baseline for measuring deviations such as ST elevation or depression.

Clinical relevance: The ST segment is the most clinically important segment, as its elevation or depression is a hallmark of myocardial ischaemia or infarction. The PR segment may also show subtle shifts in conditions such as pericarditis.

ECG intervals are measured periods of time that include at least one wave and one segment. They are usually named according to the waves that define their boundaries.

The PR interval extends from the beginning of the P wave to the beginning of the QRS complex. It represents atrial depolarisation and conduction through the atrioventricular node up to the onset of ventricular depolarisation.

The QT interval extends from the beginning of the QRS complex to the end of the T wave. It reflects the total duration of ventricular depolarisation and repolarisation, and its correction for heart rate (QTc) is clinically important in assessing risk of arrhythmia.

The RR interval extends from one R wave to the next R wave. It represents a full cardiac cycle and is used to calculate the heart rate and assess rhythm regularity.

Clinical relevance: Interval measurements are central to rhythm analysis. A prolonged PR interval defines first-degree AV block, a widened QRS suggests bundle branch block or ventricular origin, and prolonged QT increases the risk of torsades de pointes and sudden cardiac death.

Each ECG wave, segment, and interval reflects a different stage of the cardiac conduction cycle. In the normal heart, each beat begins in the sinoatrial (SA) node, a cluster of specialised cells in the right atrium that spontaneously depolarises at a rate of 60–100 beats per minute. The SA node itself is too small to generate a visible deflection on the ECG. Instead, as the impulse spreads through the atria, it produces the P wave, which represents atrial depolarisation.

The impulse then reaches the atrioventricular (AV) node, located in the interatrial septum. Here conduction slows briefly, allowing atrial contraction to complete before ventricular activation begins. This delay is recorded on the ECG as the PR segment, while the total conduction time from the start of atrial depolarisation to the start of ventricular depolarisation is measured as the PR interval. The AV node also serves as the only normal electrical bridge between atria and ventricles, since the atrial and ventricular muscle are otherwise electrically insulated.

From the AV node, the impulse enters the Bundle of His, the short conduction pathway that delivers the signal into the ventricles. It then divides into the right and left bundle branches; the left further divides into anterior and posterior fascicles. The specialised Purkinje fibres rapidly distribute depolarisation throughout the ventricular myocardium, ensuring a coordinated contraction. This entire process is recorded on the ECG as the QRS complex, which represents ventricular depolarisation.

Once depolarisation is complete, the ventricles contract mechanically and then reset electrically in preparation for the next beat. This recovery is seen as the ST segment followed by the T wave, reflecting ventricular repolarisation. The total duration of ventricular depolarisation and repolarisation is measured as the QT interval.

ECG interpretation becomes easier when the principles behind common variations in waves, segments, and intervals are understood. These variations often reflect differences in cardiac muscle mass, conduction speed, or the electrical environment between the heart and the surface electrodes.

Tall depolarisation waves may indicate larger amounts of myocardium to depolarise, such as in atrial or ventricular hypertrophy. They can also appear when there is less tissue between the heart and the electrodes, for example in slender patients.

Short depolarisation waves may indicate reduced myocardial mass or the presence of a barrier between the heart and the electrodes, such as a pericardial effusion.

Narrow waves suggest rapid conduction via the normal His–Purkinje pathways. In the ventricles, a narrow QRS complex usually indicates a supraventricular origin, as the impulse is conducted efficiently through the established conduction system.

Wide waves suggest slower conduction. A wide QRS complex may occur when the rhythm originates within the ventricles, or when supraventricular impulses encounter a conduction block, such as a bundle branch block.

Segments may be described as isoelectric (flat), elevated, or depressed. Elevation or depression is measured relative to the baseline, usually the TP segment.

Intervals can be normal, short, or prolonged. Short intervals may reflect conduction shortcuts such as accessory pathways or ion channel disorders. Prolonged intervals suggest conduction delay, which may occur in nodal disease, drug effects, or metabolic disturbances.Prolonged QT intervals are an important risk factor for arrhythmia.

ECG electrodes must be positioned in precise locations on the skin to ensure accurate recordings.

The first four electrodes are placed on the limbs. They are named according to their location: Right Arm (RA), Left Arm (LA), Right Leg (RL), and Left Leg (LL). The right leg electrode usually serves as the electrical ground.

The remaining six electrodes are placed across the anterior chest wall (the precordium) and are labelled V1–V6:

• V1: 4th intercostal space, right sternal border.
• V2: 4th intercostal space, left sternal border.
• V4: 5th intercostal space, mid-clavicular line.
• V3: midway between V2 and V4.
• V5: same horizontal level as V4, at the anterior axillary line.
• V6: same horizontal level as V4, at the mid-axillary line.

In practice, V4 is often placed before V3 to help accurately locate the position for V3.

Clinical relevance: Accurate electrode placement is essential for correct interpretation. Misplaced precordial leads can mimic or obscure pathology, for example suggesting anterior myocardial infarction, right bundle branch block, or ventricular hypertrophy when none is present.

The four limb electrodes are used to generate six limb leads on the standard 12-lead ECG. These leads provide different views of the heart in the frontal plane.

The first three limb leads are bipolar leads, meaning they record the potential difference between two electrodes:

• Lead I: compares RA (–) to LA (+). It views the heart from right to left across the horizontal axis.
• Lead II: compares RA (–) to LL (+). It views the heart diagonally from the right shoulder to the left foot.
• Lead III: compares LA (–) to LL (+). It views the heart diagonally from the left shoulder to the left foot.

The next three are augmented unipolar leads. Each uses a single positive electrode, with the negative reference being a combination of the other limb electrodes. They are mathematically amplified to make their signals large enough for interpretation:

• aVR: views the heart toward the right shoulder.
• aVL: views the heart toward the left shoulder.
• aVF: views the heart toward the feet (inferiorly).

Together, these six limb leads provide complementary perspectives on atrial and ventricular activity when viewed in the frontal plane, forming the basis for axis determination and localisation of pathology.

Clinical relevance: The limb leads are especially useful for assessing the cardiac axis and for identifying regional abnormalities. For example, leads II, III, and aVF highlight inferior wall pathology, while lead aVL is often a reciprocal lead in inferior myocardial infarction.

Chest leads (precordial leads) provide views of the heart in the horizontal plane. They are unipolar leads, using the average of all limb electrodes as the negative (–) reference. Each chest lead records electrical activity directed outward from the centre of the heart toward a single positive electrode.

• V1: views the heart from the right sternal border. It is particularly useful for assessing the right ventricle and interventricular septum.
• V2: placed at the left sternal border at the same level as V1. Like V1, it emphasises right ventricular and septal activity.
• V3: positioned midway between V2 and V4. It provides an anterior view of the left ventricle.
• V4: located at the mid-clavicular line in the 5th intercostal space. It is also an anterior lead, highlighting left ventricular activity.
• V5: aligned horizontally with V4 at the anterior axillary line. It reflects the lateral wall of the left ventricle.
• V6: aligned horizontally with V4 at the mid-axillary line. It also reflects the lateral left ventricle.

Together, the chest leads provide a sequential view across the anterior and lateral surfaces of the heart, from right to left.

Clinical relevance: The precordial leads are key for localising pathology. For example, ST elevation in V1–V2 can suggest septal infarction, V3–V4 can indicate anterior infarction, and V5–V6 can indicate lateral infarction. V1 is also important for detecting right bundle branch block and arrhythmias originating in the right ventricle.

When interpreting an ECG, specific groups of leads correspond to different regions of the heart. This localisation helps to identify the site of myocardial infarction and can also be linked to the usual coronary artery supply.

Right-sided leads can be used to identify right ventricular infarction. They are obtained by placing one or more of the precordial electrodes in the same positions on the right side of the chest. The most useful is V4R, which is placed opposite the usual V4 position.

Posterior leads are used to detect posterior infarction. They are recorded by moving chest electrodes to the same horizontal level as V6, but around the posterior thorax: V7 at the posterior axillary line, V8 at the mid-scapular line, and V9 at the paraspinal region.

Clinical relevance: Extension of a standard 12-lead ECG with right-sided or posterior leads is important when inferior infarction is suspected, as right ventricular or posterior involvement may be missed without them. Recognition of the affected coronary territory helps guide acute management and prognostication.

Most 12-lead ECGs are printed in a fairly standard format, although there are variations. Knowing how to orient yourself on the page is an important part of ECG interpretation.

Typical layout:

• 12 leads: The top rows usually display the six limb leads (I, II, III, aVR, aVL, aVF) and the six chest leads (V1–V6).
• Rhythm strip: At the bottom, there is often a longer recording of one lead (the rhythm strip) to make rate and rhythm easier to assess.
• Lead II: is the most common rhythm strip, but some machines use other leads (e.g. V1 or V5). Occasionally there may be multiple rhythm strips.

Variations:

• Right-sided leads: Sometimes right-sided chest leads (e.g. V4R) are recorded instead of V4, V5, or V6. These are often written or crossed out manually on the page.
• Posterior leads: Leads V4–V6 may be relabelled as V7–V9 when electrodes are placed on the posterior chest wall. This is useful for detecting posterior infarction.
• Cabrera format: In some European centres, the limb leads are printed in Cabrera sequence (I, II, aVR, aVL, aVF, III) instead of the usual order. This can be disorienting at first glance.
• Synchronous vs sequential recording: Many modern machines record all 12 leads simultaneously, but some still use sequential recording. This means that leads may represent activity at slightly different times.

Practical tip: Always check the labels carefully, especially for rhythm strips and for any manually added right-sided or posterior leads. If the format looks unusual (e.g. Cabrera order), take a moment to re-orient before starting your systematic interpretation.

ECGs are recorded on grid paper that provides a standardised scale for measuring time and voltage. This standardisation ensures that tracings can be compared across different patients and machines.

The usual calibration settings are a paper speed of 25 mm per second and an amplitude of 10 mm per millivolt (mV). At this speed, the grid squares represent consistent time intervals:

• Large squares (5 mm wide) represent 0.20 seconds each. There are 5 large squares per second, or 300 per minute.
• Small squares (1 mm wide) represent 0.04 seconds each. There are 25 small squares per second.

Clinical relevance: Understanding the timing represented by each square allows accurate calculation of heart rate, intervals, and conduction delays. For example, the width of the QRS complex or the length of the PR interval is measured directly in milliseconds using these grid values.

One of the quickest ways to estimate heart rate on an ECG is to use the large square method. At a standard recording speed of 25 mm/s, there are 300 large grid squares per minute. By counting the number of large squares between two adjacent QRS complexes and dividing 300 by this number, an approximate heart rate can be calculated.

For greater precision, the small square method can be used. Each small square represents 0.04 seconds, and there are 1500 small squares per minute. Dividing 1500 by the number of small squares between two QRS complexes gives the exact rate.

A useful shortcut for regular rhythms is the 300/150/100 method. At standard speed, if the next QRS complex is one large square away the rate is about 300 bpm; two squares away is 150 bpm; three squares is 100 bpm; four squares is 75 bpm; five squares is 60 bpm; and six squares is 50 bpm. This method works by memorising the sequence 300–150–100–75–60–50, which corresponds to 300 divided by the number of large squares between QRS complexes.

Caution: These methods assume a regular rhythm. They may be misleading in irregular rhythms, where alternative approaches are required.

The heart rate can also be calculated using a longer recording, such as a rhythm strip. A standard rhythm strip is usually 10 seconds long. By counting the number of QRS complexes on this strip and multiplying by 6, the average rate in beats per minute can be obtained (10 seconds × 6 = 60 seconds). For shorter strips, the calculation can be adjusted, for example: count the number of QRS complexes in a 6-second strip and multiply by 10.

This method is particularly useful for irregular rhythms, such as atrial fibrillation or rhythms with frequent ectopic beats, where single beat-to-beat measurements are unreliable. In these cases, the rate may also be described as a range, for example “atrial fibrillation at 120 - 160 bpm.”

Clinical relevance: The average rate method provides a reliable estimate of ventricular response in irregular rhythms, guiding decisions about rate control. It avoids the pitfalls of instantaneous calculations, which can under- or overestimate the true rate.

Regularity describes how consistently the QRS complexes are spaced across the ECG.

If the rhythm is regular, the QRS complexes are evenly spaced with consistent RR intervals.

If the rhythm is grouped, there are repeating clusters of beats separated by pauses or gaps of different lengths. This pattern is often seen with conduction blocks (e.g. Wenckebach phenomenon) or with grouped ectopy.

If the rhythm is interrupted, the QRS complexes are mostly regular but occasionally broken by an early or late beat, producing a pause in the pattern. This may occur with premature atrial or ventricular contractions, or with sinus pauses.

If the rhythm is irregular, the QRS complexes are unevenly spaced with no repeating pattern. Atrial fibrillation is the classic example.

Terminology note: It is common to hear rhythms described as “regularly irregular” or “irregularly irregular.” While this language is traditional, it is often confusing and adds little value. A clearer approach is to describe rhythms as regular, grouped, interrupted, or irregular. This provides a more precise description of the pattern observed.

Clinical relevance: At first glance, many irregular rhythms resemble atrial fibrillation. Careful inspection, however, often reveals a grouped or interrupted pattern, pointing instead to phenomena such as Wenckebach block or frequent ectopy. Recognising these patterns helps avoid overdiagnosis of atrial fibrillation and narrows the differential diagnosis of arrhythmia.

A key feature of ECG rhythms is whether the QRS complexes are narrow or wide.

A narrow complex rhythm has QRS complexes less than 100 ms in duration (2.5 small squares at standard settings). Narrow complexes indicate that ventricular depolarisation is occurring normally via the His–Purkinje system. These rhythms therefore originate above the ventricles and include normal sinus rhythm, sinus tachycardia, atrial fibrillation, and atrial flutter.

A wide complex rhythm has QRS complexes greater than 100 ms in duration (more than 2.5 small squares). Wide complexes arise either because the rhythm originates within the ventricles (e.g. ventricular tachycardia), or because a supraventricular impulse is conducted abnormally due to a block in the His–Purkinje system (e.g. supraventricular tachycardia with aberrancy, or bundle branch block).

Clinical relevance: QRS width is a fundamental discriminator in rhythm analysis. A narrow complex tachycardia is almost always supraventricular, while a wide complex tachycardia should be considered ventricular in origin until proven otherwise, as mistaking ventricular tachycardia for SVT with aberrancy can lead to inappropriate management.

Two common arrhythmia mechanisms are fibrillation and flutter.

Fibrillation is completely disorganised electrical activity, where many sites within the myocardium attempt to depolarise simultaneously. This produces chaotic, ineffective contraction of the affected chamber.

• Atrial fibrillation (AF): the most common sustained arrhythmia. It is characterised by an irregularly irregular rhythm with absent P waves, replaced by a chaotic baseline.
• Ventricular fibrillation (VF): a totally chaotic rhythm with no organised QRS complexes, resulting in loss of cardiac output. This is a medical emergency requiring immediate defibrillation.

Flutter is more organised than fibrillation. It arises from a re-entrant circuit that produces rapid, regular atrial depolarisations, typically at around 300 beats per minute. The baseline shows characteristic flutter waves, often described as a “sawtooth” pattern.

• Atrial flutter: regular flutter waves replace P waves, giving the sawtooth baseline. Because the AV node cannot usually conduct at 300 bpm, it allows only some impulses through, commonly in ratios such as 2:1 or 3:1 conduction, producing ventricular rates of 150 or 100 bpm.

Clinical relevance: Atrial fibrillation and atrial flutter both predispose to thromboembolism and stroke, requiring consideration of anticoagulation. Ventricular fibrillation is a form of cardiac arrest and is universally fatal without immediate defibrillation.

Tachycardia refers to any rhythm with a rate greater than 100 beats per minute. Tachycardias can arise from different parts of the conduction system, and their classification is usually based on the origin of the rhythm and the QRS width.

Sinus tachycardia originates from the sinoatrial (SA) node. It shows a regular rhythm with normal P waves before each QRS complex and is usually a physiological response to stressors such as exercise, fever, hypovolaemia, pain, or anxiety. Treatment is directed at the underlying cause rather than the rhythm itself.

Supraventricular tachycardia (SVT) is a broad term for rapid rhythms that originate above the ventricles and conduct through the His–Purkinje system, producing narrow QRS complexes. Common mechanisms include atrioventricular nodal re-entry tachycardia (AVNRT) and atrioventricular re-entrant tachycardia (AVRT). These typically present with abrupt onset and termination.

Ventricular tachycardia (VT) originates within the ventricles, producing wide QRS complexes. It may be monomorphic (uniform QRS appearance) or polymorphic (variable QRS appearance). VT is a potentially life-threatening arrhythmia and must be distinguished from SVT with aberrant conduction, as management differs significantly.

Clinical relevance: Narrow-complex tachycardias are usually supraventricular, while wide-complex tachycardias should be assumed to be ventricular until proven otherwise. Identifying the type of tachycardia is critical for selecting the correct acute management strategy.

Bradycardia refers to any rhythm with a rate less than 60 beats per minute. Bradycardias may be physiological, particularly in athletes or during sleep, or pathological when caused by conduction system disease, drugs, or metabolic disturbance.

Sinus bradycardia originates from the sinoatrial (SA) node. It shows normal P waves before each QRS complex, but at a slower rate. It can be normal in young, fit individuals, or occur as a response to increased vagal tone, beta-blockers, or hypothyroidism.

Junctional escape rhythms arise from the atrioventricular (AV) node or junction when the SA node fails or conduction is impaired. They are typically slow (40–60 bpm), may lack visible P waves, or may show inverted P waves due to retrograde atrial activation.

Ventricular escape rhythms occur when both the SA node and AV node fail to generate impulses. These rhythms originate in the ventricles at rates of 20–40 bpm and present as wide-complex bradycardias. They represent a protective mechanism to maintain minimal cardiac output.

Sometimes the rate is slow because of a conduction block, even though the rhythm is generated at the correct site (for example, the SA node). In these cases, the problem lies in delayed or failed conduction through the AV node or bundle branches. These types of block will be discussed in more detail in later sections.

Clinical relevance: Bradycardias can be well tolerated in healthy individuals but may cause syncope, hypotension, or cardiac arrest in compromised patients. Identifying whether the slow rate is due to reduced impulse generation (sinus or escape rhythms) or impaired conduction (blocks) is essential for management and for determining whether pacing is required.

One situation where rapid and reliable rhythm interpretation is essential is during cardiac arrest. The arrest algorithms are based on quickly identifying which rhythm is present, as this determines the immediate management strategy.

There are four critical arrest rhythms in which there may be no palpable pulse:

• Ventricular tachycardia (VT): a fast rhythm with wide QRS complexes. In the arrest setting, any wide-complex tachycardia should be assumed to be VT until proven otherwise, as misclassification may delay defibrillation.
• Ventricular fibrillation (VF): a chaotic, disorganised rhythm with no identifiable QRS complexes, resulting in no cardiac output.
• Pulseless electrical activity (PEA): organised electrical activity is seen on the ECG but it fails to produce effective mechanical contraction, resulting in the absence of a pulse. PEA can occur with a variety of underlying rhythms.
• Asystole: a flat line with no discernible electrical activity.

Shockable vs non-shockable rhythms: Of these, only the ventricular rhythms (VT and VF) are shockable. PEA and asystole are non-shockable rhythms and are treated with high-quality CPR, adrenaline, and correction of reversible causes rather than defibrillation.

Clinical relevance: Correct identification of an arrest rhythm guides immediate life-saving management. Wide-complex tachycardia in an arrest should be treated as VT, VF requires prompt defibrillation, and PEA/asystole require urgent resuscitation with a focus on identifying reversible causes (the “4 Hs and 4 Ts”).

Learning to interpret the cardiac axis is often one of the more intimidating steps in ECG interpretation. Many students find it abstract and difficult to grasp at first. To reduce that barrier, we start with a simple shortcut method that gives a quick answer and builds confidence. Once this feels less daunting, we will later work through the mechanisms and logical reasoning that explain why the axis shifts in different conditions.

A practical shortcut is the thumbs method. In this version, we use leads I and II as our reference points. Visualise lead I as the left thumb and lead II as the right thumb:

• If the QRS complexes in both leads I and II are predominantly positive (two thumbs up), the axis is normal.
• If lead I is positive but lead II is negative, the thumbs have left each other, and this suggests left axis deviation
• If lead I is negative but lead II is positive, the thumbs are heading right for each other, and this suggests right axis deviation.
• If both are negative, the axis is either into the farthest reaches of right axis deviation or extreme deviation (“northwest axis”), but this is uncommon.

Some textbooks and teachers use leads I and aVF instead of leads I and II. Both approaches work for most situations, but I and II are conveniently located and accomodate a more precise definition of a normal axis range. For teaching and clinical practice, the important point is to be consistent with whichever version you choose.

Clinical relevance: The thumbs method is especially useful in emergencies and rhythm analysis. Left axis deviation is often seen with left anterior fascicular block or inferior myocardial infarction, right axis deviation with right ventricular strain or pulmonary embolism, and extreme axis deviation with ventricular rhythms.

The hexaxial reference system is a model that maps the orientation of the six limb leads onto a circle, allowing the cardiac axis to be calculated more precisely. “Hexa” refers to the six limb leads, each of which views the heart from a different angle in the frontal plane.

The circle is divided into degrees, measured clockwise from a horizontal line pointing left (lead I):

• Lead I: 0° (looks directly left, across the chest)
• Lead II: +60° (diagonal down to the left foot)
• Lead III: +120° (diagonal down to the right foot)
• Lead aVR: –150° (up towards the right shoulder)
• Lead aVL: –30° (up towards the left shoulder)
• Lead aVF: +90° (straight down to the feet)

Using these directions, the axis can be described within specific ranges:

• Normal axis: –30° to +90°
• Left axis deviation: –30° to –90°
• Right axis deviation: +90° to +180°
• Extreme axis deviation: –90° to –180° (“northwest axis”)

Clinical relevance: The hexaxial reference system provides the foundation for more accurate axis determination. While the thumbs method is a quick shortcut, the hexaxial system explains the underlying geometry and is especially useful when the axis lies close to the borderline between categories.

The quadrants method is a simple way to calculate the cardiac axis using leads I and aVF as reference points. These leads form convenient horizontal (I) and vertical (aVF) axes in the hexaxial system. Because the “normal” range is slightly larger than one quadrant, lead II is sometimes used to refine the result.

The method is based on two rules:

• The axis points towards a lead with a positive QRS.
• The axis points away from a lead with a negative QRS.

How to use the quadrants method:

1. Draw the axes: Imagine lead I running horizontally (0°) and lead aVF running vertically downwards (+90°).
2. Check lead I:
   • If QRS is positive, the axis must lie on the left side of the circle (towards I).
   • If QRS is negative, the axis must lie on the right side (away from I).

   Tip: Cross out the half of the circle that does not apply - this leaves only the possible side where the axis can be.

3. Check lead aVF:
   • If QRS is positive, the axis must lie in the lower half (towards aVF).
   • If QRS is negative, the axis must lie in the upper half (away from aVF).

   Tip: Again, cross out the half of the circle that does not apply. Now you should be left with only one quadrant.

4. Find the quadrant: This quadrant represents the overall axis: normal, left, right, or extreme axis deviation.
5. Refine with lead II: If the axis falls in the upper-left quadrant (between –30° and –90°), check lead II:
   • If lead II is positive, the axis is directed towards +60° and is therefore normal.
   • If lead II is negative, the axis is directed away from +60° and is therefore left axis deviation.

Clinical relevance: The quadrants method is widely taught because it is systematic and reliable. By progressively crossing out the halves that do not apply, you narrow down to one quadrant. Adding lead II then helps distinguish borderline cases between normal and left axis deviation.

The isoelectric method is another quick way to determine the cardiac axis. It relies on finding a limb lead where the QRS complex is isoelectric — that is, the positive and negative deflections are roughly equal in size. The overall axis must lie at right angles (90°) to this lead.

How to use the isoelectric method:

1. Draw the axes: Visualise all six limb lead directions on the hexaxial reference circle.
2. Find the isoelectric lead: Identify the limb lead in which the QRS is equally positive and negative.
3. Determine the perpendicular: The axis lies 90° from the isoelectric lead, either clockwise or counter-clockwise.
4. Check the perpendicular lead:
   • If the perpendicular lead’s QRS is positive, the axis points directly towards it.
   • If the perpendicular lead’s QRS is negative, the axis points directly opposite.

Learning note: In practice, QRS complexes are rarely perfectly isoelectric. Instead, look for the lead that is most nearly isoelectric - the one where the positive and negative deflections are closest in size. This shortcut makes the method less intimidating and more practical at the bedside.

Clinical relevance: The isoelectric method is often faster than the quadrants method and can be particularly useful when the axis is borderline. It is also a good way to double-check your result, since many ECGs will have one limb lead that is nearly isoelectric.

ECGs can only be compared reliably if they are recorded at the same calibration settings. The most common standard settings are a paper speed of 25 mm/sec and an amplitude of 10 mm/mV. These values may be printed on the edge of the page, or shown by a calibration signal at the start of the trace. This signal is usually a rectangle 5 mm wide and 10 mm tall, although some ECG machines use a narrower signal and instead print the speed and gain (e.g. “25 mm/sec”) in text on the page.

Non-standard calibration settings can make the ECG appear misleading if they are not recognised:

• Double speed (50 mm/sec): the complexes appear twice as spread out as normal. Rate calculations must be adjusted because there are now 600 large squares per minute instead of 300. This setting is sometimes used to make subtle features easier to see, and it is more common in some European countries where 50 mm/sec may be the default.
• Half height (5 mm/mV): used when the complexes are very tall (e.g. left ventricular hypertrophy) and risk overlapping. This reduces the amplitude but does not change the paper speed, so the overall rate calculation is unaffected.

Practical tip: Always check the calibration box at the start of an ECG before interpreting. A normal rhythm recorded at double speed or half height may otherwise be mistaken for tachycardia, left ventricular hypertrophy, or other pathology.

Baseline wander is a low-frequency artefact where the ECG baseline drifts slowly up and down. Unlike fast interference from tremor or electrical devices, baseline wander gives the tracing a “floating” or “wobbling” appearance. The QRS complexes and waves are usually preserved, but they ride on a shifting baseline.

Common causes include:

• Respiration: chest wall movement with breathing can shift electrodes.
• Patient movement or position: rolling, shifting, or fidgeting during the recording.
• Poor skin–electrode contact: sweat, hair, oily skin, or dried-out electrodes.
• Loose electrodes or cables: mechanical drift of the leads during the trace.

ECG appearance: baseline wander is seen as the whole trace drifting or sloping up and down together. This can mimic ST elevation or depression if not recognised, or make it difficult to measure intervals accurately.

Troubleshooting:

• Ask the patient to remain still and breathe gently.
• Re-clean the skin and replace electrodes if needed; shave hair or remove sweat/oil.
• Check lead placement and ensure they are well-secured.
• If persistent, note “baseline wander” on the ECG report so it is not mistaken for pathology.

Clinical relevance: Baseline wander can obscure subtle ischaemic changes or prolong interval measurements. Recognising it prevents false alarms and unnecessary investigations.

Artefacts are changes on the ECG that are caused by anything other than the heart’s electrical activity. Recognising them is critical, as they can mimic serious pathology or obscure the true rhythm.

Common causes include:

• Movement artefacts: patient shivering, muscle tremor, or deliberate tapping of an electrode.
• External electrical devices: interference from nerve stimulators, infusion pumps, or electrically powered beds.
• Poor electrode contact: loose or dried electrodes, or electrodes placed on sweaty or oily skin.

One of the most important artefacts to recognise is the chest compression artefact. During CPR, chest compressions generate large deflections that can resemble a very wide complex rhythm. In reality, this artefact completely obscures the underlying rhythm and prevents meaningful rhythm analysis until compressions are paused.

Practical tip: A key clue to artefact is whether the abnormality is present in all leads simultaneously. A true rhythm change should affect every lead recorded at the same time. If an apparent abnormality is only visible in some leads, it is more likely to be an artefact. For example, asystole cannot selectively affect a few leads - if it appears in only part of the tracing, it is more likely that an electrode has fallen off.

Clinical relevance: Artefacts are a frequent source of misinterpretation. Awareness of their patterns prevents unnecessary alarms, false diagnoses, or inappropriate interventions, especially during resuscitation.

Automated ECG interpretation can be a helpful starting point, but it is frequently inaccurate and should never be relied on in isolation. These algorithms lack clinical context and are especially prone to errors in rhythm and ischaemia interpretation. The safest approach is to treat the computer print-out with extreme caution or disregard it altogether.

Common errors include:

• Rate errors: miscounting tall T waves as extra QRS complexes, or failing to count ectopic beats.
• Rhythm errors: overcalling atrial fibrillation (“not all that is irregular is AF”), missing pacemaker spikes, mistaking artefacts for ventricular tachycardia or fibrillation, or misinterpreting lead disconnection as asystole.
• Interval errors: inaccurate QT measurement, particularly in the presence of baseline artefact or prominent U waves.
• Baseline artefact: any interpretation becomes unreliable when the baseline is unstable.
• Ischaemia errors: missing subtle changes of myocardial infarction or ischaemia, or mislabelling secondary ST/T changes as primary infarction.

In general, the computer is better at: calculating rate, intervals, and axis. It is worse at: rhythm interpretation, recognising pacemaker activity, and identifying ischaemia.

Clinical relevance: Automated ECG reports may be used as a prompt, but they must never replace clinician review. A correct ECG interpretation always depends on correlating the trace with the clinical context — something no algorithm can currently achieve.

ECGs can be recorded and displayed in different formats depending on the setting. A standard 12-lead ECG has traditionally been printed on paper, while bedside monitors and defibrillators often display a limited number of leads on a screen. These differences can sometimes cause confusion.

Paper ECGs:

• Usually show all 12 leads in a standard format with a rhythm strip.
• Printed at standard calibration (25 mm/s, 10 mm/mV), which makes them reliable for measuring intervals and amplitudes.
• Provide a permanent record that can be compared with previous ECGs.

Screen ECGs:

• Most bedside monitors only display 1–3 leads at a time (often lead II and V5).
• These leads may look slightly different from the paper ECG because some monitors apply filtering or smoothing to reduce artefacts. This can alter ST segments, T waves, or pacemaker spikes.
• Not all screen displays use standard calibration, so careful measurement is more difficult.
• Some machines record leads sequentially rather than simultaneously, which can cause subtle differences in wave timing.

Practical tip: Always confirm important findings (especially ST changes, QT measurement, or pacemaker activity) on a full 12-lead ECG rather than relying only on the screen display. Use the monitor for rhythm and trend recognition, but the full 12-lead ECG for accurate measurement and diagnosis.

Clinical relevance: Screen ECGs are invaluable for real-time monitoring, but they are not a substitute for a properly calibrated 12-lead ECG when making diagnostic or treatment decisions.

One of the most helpful ways to approach ECG interpretation is to use a systematic checklist. This prevents important features from being overlooked and provides a structure that can be repeated every time.

A simple ECG interpretation checklist:

1. Quality check: Confirm patient identity and calibration, check for artefacts and electrode misplacement.
2. Rate: Calculate the heart rate (average and beat-to-beat if needed).
3. Rhythm: Describe the rhythm by its rate, regularity, and QRS width. Name the rhythm if you can.
4. Axis: Estimate the cardiac axis (thumbs, quadrants, or isoelectric method).
5. Waves (overview only): Make a mental note of P waves, QRS complexes and T waves.
   We will explore the shapes, relationships, durations, and morphologies of these waves as well as several other wave types in detail in the next quest.
6. Intervals and segments: Identify the PR interval, QT interval, ST segment, and TP segment.
7. Comparison: Compare to any previous ECGs for changes over time.
8. Clinical context: Always interpret the ECG in light of the patient’s symptoms, history, and current presentation.