How to Read an ECG

From an electrical signal to a heartbeat

An ECG records small voltage differences between skin electrodes over time. It reflects the combined electrical activity of many heart cells; it does not directly measure contraction or how strongly the heart pumps. Reading it helps identify unusual rhythms or slowed conduction and guides assessment alongside the clinical context.

A change in a cell’s electrical state that activates it is called depolarization. In a sinus beat, a small group of cells in the right atrium generates the signal spontaneously: the sinus (SA) node. It spreads through the two upper chambers—the atria—and produces the P wave before they contract.

The atrioventricular (AV) node slows conduction between the atria and the two lower pumping chambers, the ventricles. This timing lets atrial contraction contribute to ventricular filling before the ventricles contract. The AV delay is only part of PR: the interval also includes atrial activation and conduction onward to the ventricles.

The signal then travels through the His bundle, its right and left branches and the Purkinje fibres. These pathways distribute activation rapidly through the ventricular muscle. This coordinated depolarization produces the QRS, followed by ventricular contraction.

The ventricles then recover electrically, or repolarize, producing the T wave. P, QRS and T describe electrical events. They are related to the mechanical heartbeat, but they are not recordings of movement.

Why the grid matters

The previous lesson showed what happens in the heart. Now we need to know how long those events take. A wide-looking wave is not enough: its duration depends on the recording scale. The ECG grid turns the picture into measurements we can compare.

Read from left to right: the horizontal axis is time. First check the recorded paper speed. At 25 mm/s, one millimetre—a small square—represents 0.04 seconds (40 ms). Five small squares form one large square: 0.20 seconds (200 ms).

Height measures voltage relative to the baseline, not the strength of contraction. At a gain of 10 mm/mV, one vertical small square represents 0.1 mV. The calibration pulse is 10 small squares high, corresponding to 1 mV.

Speed and gain can change. At 50 mm/s, a small square represents 20 ms; at a gain of 5 mm/mV, 1 mV is only 5 mm high. Check these settings before interpreting a width or height. On a resized screen image, count grid squares rather than using a physical ruler.

One heartbeat, several viewpoints

A standard ECG uses 10 skin electrodes to obtain 12 leads. Four electrodes go on the limbs and six on the chest. The machine combines their signals to create different voltage comparisons, rather than recording twelve separate heartbeats.

The limb leads—I, II, III, aVR, aVL and aVF—view electrical activity in the frontal plane. The chest leads V1–V6 view it in the horizontal plane. The right-leg electrode helps reduce interference; it does not create an additional diagnostic lead.

When the net direction of depolarization points toward a lead’s positive pole, it usually produces an upward deflection; pointing away usually produces a downward one. A nearly perpendicular direction can produce a small or biphasic waveform. That is why the same beat looks different in different leads.

Position the electrodes using anatomical landmarks. V1 and V2 lie in the fourth intercostal spaces beside the sternum; V4 is in the fifth, on the left midclavicular line. Place V3 between V2 and V4, then V5 and V6 at V4’s horizontal level. Misplacement can change the tracing and imitate disease.

A lead is a viewpoint of ongoing activity. On a printed ECG, different columns may show different time windows: they are not necessarily the same beat. Follow the lead labels and time markers, and use a continuous rhythm strip to assess spacing. Across V1–V6, the R wave usually becomes more prominent while S becomes smaller.

Finding P, QRS and T on the tracing

P reflects activation of the atria. QRS reflects activation of the ventricles. Because ventricular activation is rapid and coordinated, it usually produces a brief, sharper complex. Q, R and S name deflections within that complex; not every lead contains all three.

After activation, ventricular cells return toward their resting electrical state: repolarization. The T wave reflects this recovery across the ventricles. It is not a direct measurement of ventricular relaxation, and an upward T wave does not mean a second contraction.

A flat segment does not mean electrical inactivity. During the usual ST segment, much of the ventricular muscle is already depolarized, so there is little net voltage difference in that lead. The recovery of the atria is usually hidden by the larger QRS.

Within QRS, the first downward deflection before an upward one is Q; the first upward deflection is R; a downward deflection after R is S. An entirely negative complex is QS. These names describe the shape in a particular lead, not separate heartbeats.

Use this lead II example to learn the sequence, then compare the other leads. Shape, height and direction vary with the lead. Once you can locate P, QRS and the end of T, you have the landmarks needed to measure PR, QRS and QT.

Why measure the intervals?

You can now locate P, QRS and T. The next question is whether the electrical signal travels and recovers at the expected speed. Measuring an interval gives a duration rather than a visual impression. The three measurements below answer different questions; their meaning is shown when you select one.

PR runs from the start of P to the start of QRS: from the beginning of atrial activation to the beginning of ventricular activation. We measure it to assess atrioventricular conduction. A longer PR may indicate slower conduction; it is not a measurement of the AV node alone. The usual adult range is 120–200 ms.

QRS duration measures ventricular activation. It is commonly around 80–100 ms in adults; 120 ms or more is clearly wide. Intermediate values require attention to shape and context: “less than 120 ms” is a useful narrow-complex threshold, not a guarantee that conduction is normal. A wide QRS can have several causes.

QT runs from the start of QRS to the end of T and includes ventricular activation and electrical recovery. It changes with heart rate, so we also use a rate-corrected value, QTc. An excessively prolonged QTc can signal increased risk of certain ventricular arrhythmias; interpretation also requires the clinical context.

On a real 12-lead ECG, choose a lead with clear boundaries. Lead II is often useful for P and PR; for QT, lead II or V5/V6 may help when the end of T is clear. Compare other leads and several beats. Check speed and gain first, and do not measure across different leads or different beats as if they were one continuous waveform.

From one interval to beats per minute

You have measured time within one beat. The time between successive QRS complexes tells you how frequently the ventricles are activated. Use the same point on each QRS—often the peak of R—and first check whether the spacing is regular.

At 25 mm/s, a large square lasts 0.20 seconds. There are 300 of these in one minute: for regular spacing, divide 300 by the number of large squares between R waves. Four large squares therefore give 75/min.

When spacing is irregular, one R–R interval is not representative. Count QRS over a known duration and multiply by 60 divided by that duration in seconds: 10 seconds ×6, or 6 seconds ×10. This estimates an average; a longer recording can help. Use the long rhythm strip when present, but verify its duration.

In adults, below 60/min and above 100/min are conventional descriptions of bradycardia and tachycardia. They do not identify the cause or establish illness. Count atrial activity separately when P waves and QRS are not linked; an ECG records electrical activation, not proof of a palpable pulse.

Find the origin, then describe the rate

A slow or fast rhythm may still start in the sinus node. “Sinus” describes the origin; the number of QRS complexes describes ventricular rate. To recognize the usual sequence, find P waves before deciding what the rate means.

Start in II, where P is often clear, and compare aVR and V1. Sinus P waves usually have a consistent shape, are upright in II and aVF, and negative in aVR. In uncomplicated sinus rhythm, one P precedes each QRS, each P conducts, and PR is stable.

The gaps can vary gradually with breathing, especially in younger people: respiratory sinus arrhythmia can be physiological. A rate of 60–100/min is the usual adult reference. Sinus bradycardia and sinus tachycardia keep a sinus origin; symptoms, medicines, activity and context help explain their rate.

These are recognition cues, not an absolute rule that every sinus P must conduct. Sinus atrial activity can coexist with AV block; we will examine that later. Always compare several beats rather than one small bump before a QRS.

One direction, several electrical views

The QRS axis summarizes the average direction of ventricular depolarization in the frontal plane. It is not the anatomical tilt of the heart. It helps put QRS changes into context, but an abnormal axis alone does not name a disease.

Look at the net QRS deflection in I and aVF: is the upward portion larger than the downward portion? If both are positive, the axis is between 0° and +90°. If I is positive and aVF negative, check II: a positive II can still indicate a normal leftward axis between −30° and 0°.

The usual adult range is −30° to +90°. Negative I with positive aVF suggests a rightward axis; both negative suggest an extreme axis. Near a boundary, small or nearly balanced QRS complexes require care. Check all limb leads and electrode placement before concluding.

Turn observations into an interpretation

A fixed sequence prevents one striking feature from distracting you from the rest. Before measuring, check identity, date, recording quality, speed and gain. An electrode error, movement or a wandering baseline can imitate disease; the automated diagnosis must also be checked.

Then assess rate, rhythm, axis, P, PR, QRS, QT/QTc and ST/T. For QRS, describe width, voltage, Q waves and the progression of R across V1–V6. Use II/V1 for atrial activity, the limb leads for axis, and all 12 leads for the full pattern.

Summarize what you observed before naming a diagnosis. For example, “regular rhythm with consistent P waves and narrow QRS” is a description, not a complete clinical conclusion. Compare with any previous ECG and the documented clinical context. A normal ECG does not exclude important disease.

More voltage is a clue, not a wall measurement

Hypertrophy means increased myocardial mass. It can change the balance of electrical forces, and therefore QRS voltage and axis. The ECG suggests an electrical pattern; it does not measure wall thickness or prove an anatomical diagnosis.

For LVH, look at S depth in V1 and R height in V5/V6. One voltage criterion adds S in V1 to the tallest R in V5 or V6: at 10 mm/mV, a sum of at least 35 mm meets that criterion. Always check gain before counting.

For RVH, look for a dominant R in V1 with a rightward axis and often deeper lateral S waves. Age, body habitus, electrode placement, RBBB and pre-excitation can alter these appearances. ST/T changes may accompany hypertrophy, but are not specific to it.

Neither high voltage alone nor a normal ECG settles the question. Consider the whole pattern and clinical context; imaging may be needed to assess ventricular structure.

Separate atrial activity from ventricular response

Arrhythmias involve changes in rhythm generation or conduction. Describe regularity, atrial activity and QRS width first, rather than naming a rhythm from its rate alone. Two common atrial rhythms are fibrillation and flutter.

In AF, atrial activation is disorganized: repeating discrete P waves are absent and ventricular R–R intervals are usually irregular. In flutter, atrial activation repeats in an organized circuit, often producing F waves with a sawtooth appearance. The AV node does not necessarily conduct every atrial activation.

Look carefully in II, III, aVF and V1 for atrial activity and use a long strip for R–R spacing. Flutter may conduct regularly or variably, so irregularity alone does not establish AF. Some F waves hide in QRS or T; 2:1 flutter may be less obvious than the classic sawtooth. Artefact and other rhythms can also mimic AF.

AF and flutter may be associated with arterial embolism and may coexist with acute ischemia. The ECG can identify the rhythm; it cannot, on its own, prove the source of an embolus or the reason the patient presented.

Follow P, then ask whether QRS follows

Conduction problems change the timing between atria and ventricles, or the spread within the ventricles. Begin with P waves in II or V1 and use a long strip to follow their relationship to QRS. The location of the delay matters more than the word “block” alone.

PR greater than 200 ms with every P conducted describes first-degree AV block—more precisely, AV delay. In second-degree block, some P waves do not conduct. In the usual Wenckebach pattern, PR lengthens before a nonconducted P, then the next conducted PR is shorter.

In Mobitz II, conducted PR intervals remain constant around an unexpectedly nonconducted P. An isolated 2:1 pattern cannot be labelled Mobitz I or II from PR behaviour alone. In complete AV block no atrial impulses conduct and an escape rhythm activates the ventricles independently. AV dissociation by itself is not proof of complete block.

Within the ventricles, delayed activation can widen QRS. Compare V1 with I and V6: RBBB typically adds a terminal R in V1 and a broad terminal S laterally; LBBB usually gives a mainly negative V1 and a broad lateral R. Width alone does not establish either diagnosis; inspect the full ECG.

Read ST and T in context

Ischemia is an imbalance between the heart muscle’s oxygen supply and its needs. It can change ventricular repolarization, especially ST and T. The ECG provides clues, but symptoms, timing, previous recordings and further clinical assessment determine their meaning.

Find the end of QRS: its junction with ST is the J point. Compare ST with an isoelectric reference, usually the TP segment when clearly visible. ST may be elevated or depressed. “Contiguous” leads view related anatomical regions, not simply adjacent boxes on the page: II/III/aVF are inferior; I/aVL/V5–V6 lateral; V1–V4 sample septal/anterior views.

Inspect all 12 leads for related and reciprocal changes. T inversion alone is not synonymous with ischemia: negative T is usual in aVR and can occur normally in V1 or III. Hypertrophy, bundle-branch block, pericarditis, early repolarization and electrolyte changes can also alter ST/T. Compare the whole pattern, not one isolated deflection.

An acute infarction cannot be dated or diagnosed from a historical dataset label. ST-elevation thresholds vary with lead, age and sex; this introductory demonstration is not a diagnostic cutoff exercise. Acute symptoms need prompt clinical assessment even when an ECG appears normal, with repeat ECGs and biomarkers when indicated.