Medical School · Year 1 · Cardiovascular · includes a quiz and discussion video

Lecture 3: Electrocardiography Basics

Unit 1.7: Cardiovascular System

Learning Objectives

By the end of this lecture, students will be able to:

1. Explain the principles of electrocardiography and lead placement
2. Identify the components of a normal ECG waveform
3. Calculate heart rate, axis, and intervals from an ECG
4. Describe the standard 12-lead ECG and lead orientation
5. Identify normal variants and basic ECG abnormalities
6. Apply a systematic approach to ECG interpretation

Principles of Electrocardiography

The electrocardiogram is a recording of the heart's electrical activity measured from the body surface. Understanding its principles requires grasping how cardiac depolarization creates electrical fields that can be detected by surface electrodes.

When a wave of depolarization spreads through cardiac tissue, it creates a moving front of electrical charge. Tissue ahead of the wave is polarized (resting, inside negative), while tissue behind the wave has been depolarized (inside now positive). This creates a dipole—a separation of positive and negative charges—that moves through the heart as depolarization spreads. An electrode positioned toward which the depolarization wave moves will record a positive (upward) deflection, while an electrode from which the wave moves away will record a negative (downward) deflection.

The heart's overall electrical activity at any moment can be represented as a single cardiac dipole, the vector sum of all individual cellular dipoles. The ECG measures the projection of this mean electrical vector onto different lead axes positioned around the body. Different leads "view" the heart from different angles, and the same electrical event will appear different in different leads depending on how the depolarization wave relates to each lead's axis.

Einthoven's triangle is a conceptual framework where the limb leads form an equilateral triangle with the heart at its center. Lead I measures voltage between the right arm (negative) and left arm (positive), providing a horizontal axis looking at the heart from the left side. Lead II measures between the right arm (negative) and left leg (positive), viewing the heart from below and to the left at a 60-degree angle. Lead III measures between the left arm (negative) and left leg (positive), viewing from below and to the right at 120 degrees.

<image>Panel A: Human torso with Einthoven's triangle superimposed connecting right arm, left arm, and left leg electrode positions with leads I, II, and III at their respective angles. Panel B: Heart positioned at triangle center with mean cardiac vector arrow pointing toward left leg (normal axis). Panel C: Three ECG traces showing the same vector appearing differently in each lead with Lead II showing tallest positive deflection, Lead I moderate, and Lead III smaller. Panel D: Inset demonstrating depolarizing wave moving toward electrode producing upward deflection and moving away producing downward deflection.</image>

ECG Lead Systems

The standard 12-lead ECG uses a combination of limb leads and precordial (chest) leads to view the heart from twelve different angles.

The bipolar limb leads (I, II, III) measure voltage differences between two limb electrodes. Lead I has positive polarity at the left arm and negative at the right arm, providing a horizontal viewpoint looking at the lateral heart. Lead II has positive polarity at the left leg and negative at the right arm, viewing the inferior and leftward heart. Lead III has positive polarity at the left leg and negative at the left arm, viewing the inferior heart.

The augmented unipolar limb leads (aVR, aVL, aVF) use one limb as the exploring electrode and a reference derived from the average of the other two limbs. Lead aVR has its positive electrode at the right arm and "looks" at the heart from the right shoulder toward the cardiac center—essentially viewing the inside of the heart cavities. Lead aVL has its positive electrode at the left arm, viewing the high lateral wall. Lead aVF has its positive electrode at the left foot, viewing the inferior wall directly.

The precordial leads (V1 through V6) are unipolar leads placed across the chest to view the heart in the horizontal plane. V1 is positioned at the fourth intercostal space at the right sternal border, viewing the septum and right ventricle. V2 is at the fourth intercostal space at the left sternal border, also a septal view. V3 is positioned between V2 and V4. V4 is at the fifth intercostal space at the midclavicular line, viewing the anterior wall. V5 is at the fifth intercostal space at the anterior axillary line, and V6 is at the fifth intercostal space at the midaxillary line, both viewing the lateral wall.

Leads can be grouped by the anatomical region they examine. The inferior wall is viewed by leads II, III, and aVF. The lateral wall is viewed by leads I, aVL, V5, and V6. The septal region is viewed by V1 and V2. The anterior wall is viewed by V3 and V4. The right ventricle is best viewed by V1 and additional right-sided leads such as V4R. The posterior wall is viewed by leads V7, V8, and V9, or indirectly through reciprocal changes in V1 through V3.

<image>Panel A: Human figure with limb lead positions showing RA (white), LA (black), LL (red), and ground (green) electrodes with leads I, II, III and their polarities. Panel B: Augmented leads shown with aVR viewing from right shoulder, aVL from left shoulder, and aVF from feet. Panel C: Anterior chest view with precordial electrode positions V1-V6 precisely marked at anatomical landmarks with ribs and sternum outlined. Panel D: Color-coded heart diagram showing lead territories: inferior in orange (II, III, aVF), lateral in blue (I, aVL, V5, V6), septal in green (V1, V2), and anterior in red (V3, V4).</image>

Normal ECG Waveform

The normal ECG waveform consists of several distinct components, each corresponding to specific electrical events in the cardiac cycle.

The P wave represents atrial depolarization. The SA node initiates the impulse, which spreads through both atria to produce this small, rounded deflection. The normal P wave duration is less than 120 milliseconds (three small boxes) and amplitude less than 2.5 millimeters. In sinus rhythm, the P wave should be upright in leads I, II, and aVF, reflecting the normal superior-to-inferior, right-to-left spread of atrial depolarization. In lead V1, the P wave is often biphasic—initially positive (right atrial depolarization toward V1) then negative (left atrial depolarization away from V1).

The PR interval extends from the beginning of the P wave to the beginning of the QRS complex. It includes atrial depolarization and the conduction delay through the AV node. The normal PR interval is 120 to 200 milliseconds (three to five small boxes). The PR segment, the isoelectric portion between the P wave and QRS, represents AV nodal conduction, which is too slow and involves too few cells to produce a detectable deflection.

The QRS complex represents ventricular depolarization. By convention, the Q wave is the first negative deflection (if present), the R wave is the first positive deflection, and the S wave is the negative deflection following the R wave. Additional deflections are labeled with primes (R', S'). A QS complex is entirely negative with no R wave. The normal QRS duration is less than 120 milliseconds. The morphology varies by lead, reflecting the direction of depolarization relative to each lead's axis.

The ST segment connects the QRS complex to the T wave and corresponds to the plateau phase of the ventricular action potential when all ventricular cells are depolarized. The J point marks the junction between the QRS and ST segment. Normally, the ST segment is isoelectric (at the baseline). The T wave represents ventricular repolarization and is normally upright in leads with upright QRS complexes. The U wave is a small deflection sometimes seen after the T wave, possibly representing repolarization of the Purkinje fibers or midmyocardial M cells.

The QT interval spans from the beginning of the QRS to the end of the T wave, encompassing all ventricular electrical activity. Because QT varies with heart rate (shorter at faster rates), the corrected QT (QTc) is calculated using formulas such as Bazett's: QTc equals QT divided by the square root of the RR interval in seconds. Normal QTc is less than 440 milliseconds in men and less than 460 milliseconds in women.

<image>Panel A: Normal ECG waveform on standard paper showing P wave with duration (< 120 ms) and amplitude (< 2.5 mm) criteria and PR interval with normal range (120-200 ms). Panel B: QRS complex with Q, R, and S waves identified, J point marked, and normal duration (< 120 ms) shown with ST segment highlighted as isoelectric. Panel C: T wave with asymmetric shape (gradual upstroke, rapid downstroke), small U wave indicated, and QT interval spanning from QRS onset to T wave end with QTc formula. Panel D: Standard calibration marks showing 0.04 sec per small box horizontally, 0.1 mV per small box vertically, and 1 mV calibration pulse.</image>

ECG Paper and Measurements

ECG paper is a standardized grid that allows precise measurement of both time (horizontal axis) and voltage (vertical axis).

The grid consists of small boxes 1 millimeter square. At the standard paper speed of 25 millimeters per second, each small box represents 0.04 seconds (40 milliseconds). Five small boxes form one large box of 5 millimeters, representing 0.20 seconds (200 milliseconds). At standard calibration of 10 millimeters per millivolt, each small box represents 0.1 millivolt, and each large box represents 0.5 millivolts. The calibration mark at the beginning of each lead should show a 10-millimeter deflection for the standard 1 millivolt pulse.

Heart rate can be calculated using several methods. For regular rhythms, the 300 method divides 300 by the number of large boxes between consecutive R waves. This works because 300 large boxes equal one minute at standard paper speed, so dividing by the number of large boxes per beat gives beats per minute. For more precision, the 1500 method divides 1500 by the number of small boxes between R waves. For irregular rhythms such as atrial fibrillation, the six-second method counts the number of R waves in six seconds (30 large boxes) and multiplies by ten.

Interval measurement requires identifying the beginning and end of each waveform. The PR interval is measured from the first deflection of the P wave to the first deflection of the QRS, whether that is a Q wave or R wave. The QRS duration is measured from the first QRS deflection to the final return to baseline. The QT interval is measured from the first QRS deflection to the end of the T wave, which can be difficult to define when the T wave merges with the U wave; the tangent method draws a line along the descending limb of the T wave to the baseline.

<image>Panel A: Magnified ECG grid paper showing small boxes (1 mm, 0.04 sec, 0.1 mV) and large boxes (5 mm, 0.20 sec, 0.5 mV) with standard calibration of 25 mm/sec and 10 mm/mV. Panel B: Heart rate calculation with 300 method (300 divided by large boxes between R waves) with memory aid sequence 300, 150, 100, 75, 60, 50 for 1-6 boxes. Panel C: 1500 method using small boxes and 6-second method counting R waves in 30 large boxes. Panel D: Interval measurement techniques showing PR interval, QRS duration, and QT interval with tangent method for defining T wave end.</image>

Cardiac Axis

The cardiac axis refers to the overall direction of ventricular depolarization in the frontal plane, representing the mean QRS vector.

In normal hearts, depolarization spreads from the AV node through the septum (left-to-right initially, then right-to-left), then through the ventricular free walls toward the apex. The large mass of the left ventricle dominates, so the mean QRS vector points leftward and inferiorly—toward the cardiac apex. Normal axis ranges from -30 to +90 degrees on the hexaxial reference system.

The hexaxial reference system positions the six limb leads in a circle, each 30 degrees apart. Lead I is at 0 degrees (horizontal, pointing left). Lead II is at +60 degrees, lead III at +120 degrees, aVF at +90 degrees (pointing straight down), aVL at -30 degrees, and aVR at -150 degrees (pointing rightward and upward).

Axis determination can be performed quickly using leads I and aVF. If the QRS complex is predominantly positive in both leads I and aVF, the axis lies in the normal quadrant (0 to +90 degrees). If the QRS is positive in lead I but negative in aVF, the axis is leftward—between 0 and -90 degrees. This is left axis deviation (LAD) when between -30 and -90 degrees. If the QRS is negative in lead I but positive in aVF, the axis is rightward, representing right axis deviation (RAD) between +90 and +180 degrees. If the QRS is negative in both leads I and aVF, the axis is in the extreme or northwest quadrant (-90 to -180 degrees).

Left axis deviation has several causes. Left anterior fascicular block produces marked LAD because activation of the anterior left ventricular wall is delayed, pulling the axis superiorly. Left ventricular hypertrophy may cause mild LAD due to increased leftward forces. Inferior myocardial infarction leaves electrical silence inferiorly, shifting the axis superiorly.

Right axis deviation may result from right ventricular hypertrophy (increased rightward forces), pulmonary embolism (acute right ventricular strain), left posterior fascicular block (delayed posterior wall activation), or lateral wall infarction (loss of leftward forces).

<image>Panel A: Hexaxial reference system circle with six limb leads at their angles (Lead I at 0 degrees, Lead II at +60, Lead III at +120, aVF at +90, aVL at -30, aVR at -150). Panel B: Axis ranges color-coded with normal (-30 to +90) in green, LAD (-30 to -90) in yellow, RAD (+90 to +180) in orange, and extreme axis in red. Panel C: Quadrant diagram for quick axis determination using leads I and aVF polarity patterns (positive both = normal, positive I/negative aVF = LAD, etc.). Panel D: Example ECG strips for each axis category showing leads I and aVF side by side with QRS polarity patterns and heart diagrams showing mean vector direction.</image>

P Wave and Atrial Abnormalities

Abnormalities in P wave morphology provide insight into atrial pathology.

The normal P wave represents sequential right then left atrial depolarization. The initial portion reflects right atrial activation (moving anteriorly and leftward toward V1 and leads I, II), and the terminal portion reflects left atrial activation (moving posteriorly and leftward away from V1). This sequence explains the biphasic P wave normally seen in V1—an initial positive deflection from right atrial activation followed by a small negative deflection from left atrial activation moving away from the anterior chest lead.

Right atrial enlargement (P pulmonale) produces tall, peaked P waves exceeding 2.5 millimeters in leads II, III, and aVF. The duration remains normal (less than 120 milliseconds) because conduction time through the right atrium is not prolonged. The increased amplitude reflects greater right atrial electrical mass or force. The name "P pulmonale" derives from the association with chronic lung disease causing pulmonary hypertension and right heart strain. Other causes include tricuspid stenosis and tricuspid regurgitation.

Left atrial enlargement (P mitrale) produces wide, often notched P waves exceeding 120 milliseconds in lead II. The two peaks represent sequential right and left atrial activation with a prolonged interval between them. In lead V1, the terminal negative deflection (representing left atrial forces directed posteriorly, away from V1) becomes prominent—greater than 1 millimeter deep and greater than 40 milliseconds wide. The name "P mitrale" reflects the association with mitral valve disease, though any cause of left atrial dilation or pressure overload produces these findings.

Biatrial enlargement combines features of both patterns: a tall, wide, notched P wave with prominent terminal negativity in V1.

<image>Panel A: Normal P wave morphology showing smooth rounded wave less than 2.5 mm tall and less than 120 ms wide in lead II, with small biphasic wave in V1. Panel B: P pulmonale (right atrial enlargement) with tall peaked P waves greater than 2.5 mm in leads II, III, aVF and diagram of enlarged right atrium generating increased forces. Panel C: P mitrale (left atrial enlargement) with wide notched P waves in lead II and prominent terminal negative deflection in V1 (greater than 1 mm deep, greater than 40 ms wide) with enlarged left atrium diagram. Panel D: Biatrial enlargement showing tall AND wide P waves combining features with V1 pattern showing increased initial positive and terminal negative components with clinical associations listed.</image>

QRS Complex Abnormalities

Abnormalities in QRS morphology indicate ventricular hypertrophy, conduction disturbances, or intraventricular conduction delays.

Left ventricular hypertrophy produces increased QRS voltage because the larger muscle mass generates larger electrical forces. Several voltage criteria have been developed. The Sokolow-Lyon criterion requires the sum of the S wave in V1 and the R wave in V5 or V6 to equal or exceed 35 millimeters. The Cornell criterion requires the sum of the R wave in aVL and the S wave in V3 to exceed 28 millimeters in men or 20 millimeters in women. These criteria have high specificity but only moderate sensitivity. Associated findings include left axis deviation and ST-T wave changes called "strain pattern"—downsloping ST depression and T wave inversion in the lateral leads, reflecting repolarization abnormalities secondary to hypertrophy.

Right ventricular hypertrophy is more difficult to detect because the normal ECG reflects left ventricular dominance. Findings suggesting RVH include tall R waves in V1 (greater than 7 millimeters), R/S ratio greater than 1 in V1, right axis deviation (greater than +110 degrees), and ST-T changes in the right precordial leads. The right ventricle must become substantially enlarged before its forces can overcome the normal left ventricular predominance.

Right bundle branch block (RBBB) occurs when conduction through the right bundle is blocked, causing delayed right ventricular activation. Depolarization proceeds normally through the left bundle to the left ventricle, then spreads slowly through the myocardium to the right ventricle. The QRS is widened to 120 milliseconds or more. The characteristic pattern is RSR' in V1 and V2 (the "rabbit ears" or "M-shaped" pattern), reflecting initial septal activation (R), then left ventricular activation (S), then delayed right ventricular activation (R'). Wide, slurred S waves appear in leads I and V6. T waves are inverted in V1 through V3 (secondary repolarization changes).

Left bundle branch block (LBBB) occurs when conduction through the left bundle is blocked. Right ventricular activation proceeds normally, then slow myocardial spread activates the left ventricle from right to left. The QRS is widened to 120 milliseconds or more. Broad, notched R waves appear in leads I, aVL, V5, and V6. Deep QS or rS patterns appear in V1 and V2. T waves are discordant—pointing opposite to the main QRS deflection.

<image>Panel A: Left ventricular hypertrophy with Sokolow-Lyon criterion (S in V1 plus R in V5 exceeding 35 mm) and Cornell criterion demonstrated with example showing ST-T strain pattern. Panel B: Right ventricular hypertrophy showing tall R wave in V1 with R/S ratio greater than 1 and axis diagram with marked right axis deviation (+120 degrees). Panel C: RBBB with RSR' M-shaped pattern in V1, wide slurred S waves in leads I and V6, and activation sequence diagram showing delayed RV. Panel D: LBBB with broad notched R in V6, QS in V1, discordant T waves, activation sequence showing delayed LV, and QRS duration greater than 120 ms emphasized.</image>

ST Segment and T Wave

The ST segment and T wave reflect ventricular repolarization and are sensitive markers of ischemia, injury, and other conditions.

The normal ST segment is isoelectric, at the same level as the baseline between the T wave and the next P wave. Minor deviations are acceptable: less than 1 millimeter of elevation or depression in limb leads, and less than 2 millimeters of elevation in leads V2 and V3 (up to 2.5 millimeters in men under 40 years). The normal T wave is upright in most leads where the QRS is upright and should not exceed 10 millimeters in precordial leads.

ST elevation has multiple causes. In ST-elevation myocardial infarction (STEMI), elevation appears in leads overlying the infarct territory, is convex upward (tombstone shape), and is accompanied by reciprocal depression in opposing leads. Acute pericarditis produces diffuse concave-upward (saddle-shaped) ST elevation affecting most leads, often accompanied by PR depression. Early repolarization is a benign normal variant in young, healthy individuals featuring a notched J point and elevation of the ST junction, usually most prominent in the precordial leads. Left ventricular aneurysm produces persistent ST elevation in the territory of a prior infarction, lasting indefinitely rather than evolving as in acute infarction. Brugada syndrome causes a distinctive coved ST elevation in V1 through V3 with a characteristic morphology.

ST depression has a different differential diagnosis. Ischemia produces horizontal or downsloping ST depression, often in multiple leads during demand ischemia. Strain pattern from ventricular hypertrophy produces asymmetric ST depression with the steeper slope on the upstroke (hockey stick shape) in leads overlying the hypertrophied ventricle. Digoxin effect creates a characteristic scooped or sagging ST segment resembling Salvador Dali's mustache. Hypokalemia causes ST depression with prominent U waves. Reciprocal changes are ST depression in leads opposite to those showing ST elevation in acute MI.

T wave abnormalities include inversion (associated with ischemia, post-MI evolution, cardiomyopathy, and many other conditions), peaking (seen in hyperkalemia and hyperacute myocardial infarction), flattening (hypokalemia, hypothyroidism), and biphasic patterns (Wellens syndrome in critical LAD stenosis features biphasic or deeply inverted T waves in V2-V3).

<image>Panel A: ST elevation patterns showing STEMI with convex/tombstone elevation in contiguous leads, acute pericarditis with diffuse concave/saddle-shaped elevation and PR depression. Panel B: Early repolarization with J-point notch and upward concavity, and Brugada Type 1 pattern with coved elevation in V1-V3. Panel C: ST depression patterns showing ischemia (horizontal/downsloping), LVH strain (asymmetric hockey stick), digoxin effect (scooped), and hypokalemia with prominent U wave. Panel D: T wave abnormalities showing normal T wave, tall peaked T (hyperkalemia, hyperacute MI), inverted T wave (ischemia), and Wellens Types A and B in V2-V3.</image>

Systematic ECG Interpretation

A systematic approach to ECG interpretation ensures that no abnormality is overlooked. While clinicians develop their own preferred sequence, the essential components must always be evaluated.

Begin with rate assessment. Determine if the rhythm is regular or irregular by comparing R-R intervals. Calculate the rate using the appropriate method—the 300 method or 1500 method for regular rhythms, the six-second method for irregular rhythms. Classify as bradycardia (less than 60 beats per minute), normal (60 to 100), or tachycardia (greater than 100).

Assess the rhythm by examining the relationship between P waves and QRS complexes. Is there a P wave before every QRS complex? Is there a QRS complex after every P wave? Are the P waves uniform in morphology? Is the rhythm regular or irregular? If irregular, is it irregularly irregular (suggesting atrial fibrillation) or regularly irregular (suggesting a pattern like second-degree block)?

Determine the axis using leads I and aVF as described above. Normal, left axis deviation, right axis deviation, and extreme axis each have different clinical implications.

Measure the intervals. The PR interval should be 120 to 200 milliseconds; shortening suggests pre-excitation (as in Wolff-Parkinson-White syndrome), while prolongation indicates first-degree AV block. The QRS duration should be less than 120 milliseconds; widening suggests bundle branch block or ventricular rhythm. The QT interval should be corrected for rate; prolongation predisposes to arrhythmias.

Examine the waves and segments systematically. Evaluate P wave morphology for atrial enlargement. Assess QRS amplitude for ventricular hypertrophy, and look for pathological Q waves indicating prior infarction. R wave progression across the precordial leads should show increasing R wave amplitude from V1 to V4-V5 and decreasing S wave depth. Evaluate ST segments for elevation or depression and T waves for inversion or peaking.

Finally, synthesize findings and correlate with the clinical presentation. Compare with prior ECGs when available to identify acute changes.

<image>Panel A: Rate assessment showing regular versus irregular determination, calculation methods (300/large boxes or 1500/small boxes), and classification (brady less than 60, normal 60-100, tachy greater than 100). Panel B: Rhythm assessment (P before every QRS, QRS after every P, regularity, P wave morphology) and axis determination using quadrant diagram with leads I and aVF. Panel C: Interval measurements (PR 120-200ms, QRS less than 120ms, QTc less than 440-460ms) and waves/segments checklist (P wave, QRS amplitude, Q waves, R progression, ST-T changes). Panel D: Example ECG strips showing abnormalities at each step with final synthesis box emphasizing clinical correlation and comparison to prior ECGs.</image>

Clinical Applications

Electrocardiography is essential in diagnosing acute coronary syndromes, electrolyte abnormalities, and drug effects.

In acute coronary syndromes, the ECG helps distinguish STEMI from NSTEMI and unstable angina. STEMI produces ST elevation in contiguous leads reflecting the coronary territory: anterior infarction from LAD occlusion shows changes in V1 through V4; lateral infarction from circumflex or diagonal branch occlusion affects leads I, aVL, V5, and V6; inferior infarction from RCA (or sometimes LCx) occlusion affects leads II, III, and aVF; posterior infarction produces reciprocal changes (ST depression and tall R waves) in V1 through V3 or direct changes in posterior leads V7 through V9. NSTEMI and unstable angina may show ST depression, T wave inversions, or can be normal, requiring serial ECGs and cardiac biomarkers for diagnosis.

Electrolyte abnormalities produce characteristic ECG changes. Hyperkalemia causes progressive changes as potassium rises: peaked, narrow-based T waves appear first, followed by P wave flattening and PR prolongation, then QRS widening, and finally a sinusoidal pattern approaching ventricular fibrillation or asystole. Hypokalemia produces flattened T waves, prominent U waves, and QT/QU prolongation, predisposing to torsades de pointes. Hypercalcemia shortens the QT interval by reducing the plateau phase. Hypocalcemia prolongs the QT interval.

Drug effects on the ECG are clinically important. Digoxin produces characteristic ST depression with a scooped appearance (Salvador Dali mustache) and shortens the QT interval; these are effects, not toxicity, but their presence confirms drug exposure. Class Ia and III antiarrhythmics (procainamide, sotalol, amiodarone) prolong the QT interval and can precipitate torsades de pointes. Beta-blockers cause sinus bradycardia and may prolong the PR interval. Tricyclic antidepressant overdose widens the QRS and prolongs the QT interval, with rightward axis shift in the terminal QRS.

<image>Panel A: Acute Coronary Syndromes showing heart diagram with coronary territories color-coded (LAD/anterior, LCx/lateral, RCA/inferior) matched to 12-lead ECG grid showing corresponding leads. Panel B: Example STEMI patterns for anterior MI (ST elevation V1-V4), inferior MI (ST elevation II, III, aVF), and posterior MI (ST depression and tall R in V1-V3 as reciprocal changes). Panel C: Electrolyte abnormalities showing hyperkalemia progression (peaked T to wide QRS to sinusoidal), hypokalemia (flat T, prominent U), hypercalcemia (short QT), and hypocalcemia (prolonged QT). Panel D: Drug effects showing digoxin (scooped ST), QT prolongation from Class III agents, and TCA toxicity (wide QRS, rightward terminal axis).</image>

Summary

The electrocardiogram records cardiac electrical activity via 12 leads, each viewing the heart from a different angle. The six limb leads (I, II, III, aVR, aVL, aVF) examine the frontal plane, while the six precordial leads (V1-V6) examine the horizontal plane. Standard calibration is 25 millimeters per second and 10 millimeters per millivolt.

Normal intervals are: PR interval 120 to 200 milliseconds, QRS duration less than 120 milliseconds, and QTc less than 440 to 460 milliseconds. The cardiac axis is quickly determined using leads I and aVF—positive in both indicates normal axis, positive I with negative aVF indicates left axis deviation, negative I with positive aVF indicates right axis deviation.

P wave abnormalities indicate atrial enlargement: tall peaked P waves suggest right atrial enlargement, while wide notched P waves suggest left atrial enlargement. QRS voltage criteria identify ventricular hypertrophy. QRS widening to 120 milliseconds or more suggests bundle branch block: RBBB produces RSR' in V1, while LBBB produces broad notched R waves in V6 with QS in V1.

ST elevation may indicate STEMI, pericarditis, early repolarization, or other conditions. ST depression suggests ischemia, strain, or drug effects. T wave changes including inversion and peaking have broad differential diagnoses including ischemia and electrolyte abnormalities.

A systematic approach to ECG interpretation—rate, rhythm, axis, intervals, and waves/segments—ensures thorough analysis that can be correlated with the clinical presentation.

Key Terms

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