Understanding Electrocardiography

• Electrocardiography is a graphical representation of electrical activity in

the heart detected by electrodes attached to the extremities and chest wall.
• ECG leads are configured to display differences in potential between
specific pairs of electrodes, making it noninvasive, inexpensive, and
versatile.
• The depolarization, stimulation, and recovery potentials generated by atrial
and ventricular myocardium are recorded by ECG, revealing arrhythmias,
myocardial ischemia, and life-threatening metabolic disturbances or
increased susceptibility to sudden cardiac arrest.
• Cardiac pacemaker cells, specialized conduction tissue, and heart muscle
itself produce the electric currents that spread through the heart and are
recorded by the ECG.
• The depolarization wave for the normal heartbeat originates in the
sinoatrial node, followed by stimulation of specialized conduction tissue in
the atrioventricular nodal and His-bundle areas, before the depolarization
wavefronts spread through the ventricular wall.
• The direction and magnitude of the depolarization and repolarization waves
can be represented by vectors.
• The ECG waveforms labeled alphabetically, beginning with the P wave,
representing atrial depolarization, followed by QRS complex representing
ventricular depolarization, and the ST-T-U complex representing ventricular
repolarization.
Basic ECG Waveforms and Intervals
• The J point is the junction between the end of the QRS complex and the
beginning of the ST segment.
• Atrial repolarization waveforms (ST-T ‚) may become apparent in specific
conditions like acute pericarditis, atrial infarction, and AV heart block.
• The QRS-T waveforms of the surface ECG correspond to the different
phases of simultaneously obtained ventricular action potentials.
• Factors that decrease the slope of phase 0 by impairing the influx of Na*
tend to increase QRS duration.
• Conditions that prolong phase 2 or 3 increase the QT interval.
• The ECG graph measures the amplitude of a specific wave or deflection.
• There are four major sets of ECG intervals: RR, PR, QRS, and QT/QTc.
• The instantaneous heart rate can be computed from the interbeat (RR)
interval.
• The QRS interval reflects the duration of ventricular depolarization.
• The QT interval subtends both ventricular depolarization and repolarization
times and varies inversely with the heart rate.

Notes on Electrocardiography
• QT/VRR has systematic errors and the Framingham formula is an
alternative with upper normal limits proposed.
• QT/QTc measurement limitations should be considered for precise
determination from standard ECG waveform.
• The 12 ECG leads are divided into limb and chest leads and provide a
three-dimensional representation of electrical activity.
• The frontal plane leads are shown on a hexaxial diagram with spatial
orientation and polarity.
• The horizontal plane leads are obtained with electrodes and right chest
leads may enhance detection of right ventricular involvement.
• Additional posterior leads are sometimes placed on the same horizontal
plane as V4 to facilitate detection of acute posterolateral infarction.
Understanding Electrocardiography (ECG) Leads and Depolarization Process
• ECG leads are equivalent to separate video angles, monitoring atrial and
ventricular depolarization from various spatial positions.
• Biphasic deflection in a lead is recorded when the depolarization vector is
at right angle to that lead axis.
• A positive (upright) deflection in a lead signifies that the depolarization
wave is moving towards the positive pole and vice versa.
• Normal P wave in lead V • may be biphasic with a positive component (right
atrial depolarization) followed by a small (<1 mm²) negative component (left
atrial depolarization).
• QRS complex represents two sequential phases of ventricular
depolarization; the first phase is depolarization of the interventricular
septum, while the second phase is the simultaneous depolarization of both
the ventricles.
• Vector 2 in QRS complex points leftward and posteriorly, and it is
dominated by the more massive left ventricle.

Understanding Electrocardiography
• Intermediate leads show a relative increase in R-wave amplitude and a
decrease in S-wave amplitude progressing across the chest from right to
left.
• The lead where the R and S waves are of about equal amplitude is referred
to as the transition zone.
• Ventricular depolarization can be divided into two major phases, each
represented by a vector denoting depolarization of the ventricular septum,
beginning on the left side and spreading to the right.
• Simultaneous depolarization of the LV and RV constitutes the second
phase, reflected by vectors representing these two phases in reference to
the horizontal plane leads.
• Normal electrocardiogram consists of sinus rhythm with normal R-wave
progression with the transition zone (R wave S wave) in lead V3.
• The QRS pattern in the extremity leads may vary considerably and ranges
from "30° to +100°, referred to as left or right axis deviation.
ECG abnormalities associated with cardiac enlargement and hypertrophy
• Left axis deviation is commonly associated with left ventricular
hypertrophy, left anterior fascicular block, or inferior myocardial infarction.
Right axis deviation may be a normal variant or caused by right ventricular
overload, lateral infarction, or dextrocardia.
• The normal QRS-T-wave vector concordance indicates repolarization
normally proceeds in the reverse direction from depolarization. An abnormal
increase in U-wave amplitude may be caused by drugs or hypokalemia.
• Right atrial overload may cause tall, peaked P waves, while left atrial
abnormality may cause broad, often notched P waves and a biphasic P wave
in lead V •.
• Right ventricular hypertrophy due to a severe pressure load is
characterized by a tall R wave in lead V • with right axis deviation.

Electrocardiography: Common ECG Patterns

• Right ventricular hypertrophy (RVH) can cause ST depression and T-wave
inversion in the right to mid-precordial leads, and a rightward QRS axis.
• Left ventricular hypertrophy (LVH) causes ST-segment depression and
T-wave inversion in leads with prominent R waves.
• Acute cor pulmonale due to pulmonary thromboembolism may present as
normal ECG or with the S •Q3T3 pattern and slow R-wave progression.
• Chronic cor pulmonale due to obstructive lung disease can cause small
right precordial R waves, slow R-wave progression, and low-voltage
complexes.
• Multiple voltage criteria for LVH include tall left precordial R waves and
deep right precordial S waves (e.g., SV • + [RV5 or RV6] >35 mm).
ECG Findings and Their Interpretation
• Repolarization abnormalities may appear in leads with prominent R waves,
but are not always indicative of left ventricular hypertrophy.
• Precordial voltages may occur as a normal variant, especially in athletic or
young individuals.
• The presence of left atrial abnormality increases the likelihood of
underlying left ventricular hypertrophy.
• Conventional voltage criteria for left ventricular hypertrophy are less
sensitive in middle-aged and obese individuals or those with right bundle
branch block.
• ECG evidence for left ventricular hypertrophy is a noninvasive marker of
increased risk of cardiovascular morbidity and mortality rates.
• Intrinsic impairment of conduction in either the right or the left bundle
system leads to prolongation of the QRS interval.
• With complete bundle branch blocks, the widest QRS interval is "e120 ms in
duration; with incomplete blocks, the QRS interval is between about 110 and
120 ms.
• Left bundle branch block generates wide, predominantly negative (QS)
complexes in lead V • and entirely positive (R) complexes in V6.
• Electronic right ventricular pacing can produce waveform patterns
identical to left bundle branch block.
• Biventricular pacing usually produces a right bundle branch morphology
along with a wide R wave in lead aVR.
Bundle Branch Block and Electrocardiography Notes
• Bundle branch block is a condition that can occur due to a variety of
underlying heart conditions.
• Right bundle branch block is more common in subjects without structural
heart disease than left bundle branch block.
• Left bundle branch block is a marker of coronary heart disease,
hypertensive heart disease, aortic valve disease, or cardiomyopathy.
• Bundle branch blocks can be chronic or intermittent and may be
rate-related.
• Bundle branch blocks and depolarization abnormalities due to pacemakers
affect both ventricular depolarization and secondary repolarization.
• T-wave discordance with the last deflection of the QRS is typically seen
with bundle branch blocks.
• Primary repolarization abnormalities are independent of QRS changes
while secondary ones are caused by altered depolarization.
• T-wave inversions in precordial leads with bundle branch block may
indicate underlying ischemia or other abnormalities.
• Partial blocks in the left bundle system are associated with shifts in the
frontal plane QRS axis.
• Left anterior fascicular block is the most common cause of marked left axis
deviation in adults.
• Intraventricular conduction delays can be caused by toxic factors that slow
ventricular conduction.
Interpretation of ECG changes in Ischemic Heart Disease
• Prolongation of QRS duration does not always indicate conduction delay
but can be due to preexcitation of the ventricles via a bypass tract like
Wolff-Parkinson-White (WPW) pattern.
• Ischemia has time-dependent effects on myocardial cells, lowering the
resting membrane potential and shortening the duration of the action
potential, causing a voltage gradient between normal and ischemic zones.
These currents of injury are represented in the ECG by deviation of ST
segment.
• In transmural acute ischemia, the ST vector usually shifts outward,
producing ST elevations and sometimes hyperacute T waves. In
subendocardial ischemia, the ST vector shifts towards the inner layer of the
affected ventricle and ventricular cavity, causing ST depression.
• ST segment elevation in multiple leads indicates severe ischemia. Non-ST
elevation type is not consistent efficacy of emergency reperfusion therapy.
• ECG leads can localize regions of ST elevation than non-ST elevation
ischemia. Acute transmural anterior wall ischemia can be reflected by ST
elevations or increased T-wave positivity in one or more of the precordial
leads (V •-V) and leads I and aVL. Inferior wall ischemia produces changes in
leads II, III, and aVF.
Electrocardiography for Diagnosing Acute Coronary Syndrome
• Reciprocal ST depressions in V • to V ƒ may indicate inferior involvement
and constitute an ST elevation "equivalent" acute coronary syndrome.
• Acute right ventricular ischemia leads to ST elevations in right-sided chest
leads.
• Ischemic ST elevations typically are followed by evolving T-wave
inversions and often by Q waves in the same lead distribution.
• Transient ST-segment elevations caused by coronary vasospasm may
occur without developing Q waves.
• Severe obstruction in the left anterior descending coronary artery can
cause deep T-wave inversions in multiple precordial leads with or without
cardiac enzyme elevations.
• Prominent T-wave inversions in V • to V „, I, and aVL (Wellens T waves) are
usually associated with a high-grade stenosis of the left anterior descending
coronary artery.
• Depolarization (QRS) changes may accompany repolarization (ST-T)
abnormalities in infarction.
• Abnormal Q waves are not exclusive to transmural myocardial infarction
and can occur with subendocardial infarcts.
• Loss of depolarization forces due to posterior or lateral infarction may
cause reciprocal increases in R-wave amplitude in V • and V ‚ without
diagnostic Q waves in conventional leads.
• Persisting ST-segment elevations after a Q-wave infarct usually indicate a
severe underlying wall motion disorder but not necessarily a frank
ventricular aneurysm.
Electrocardiography in the Diagnosis of Ischemic Heart Disease
• The sequence of depolarization and repolarization changes with anterior
and inferior wall Q-wave infarctions.
• Anterior infarcts are characterized by ST elevations in leads I and aVL and
precordial leads, accompanied by reciprocal ST depressions in leads II, III,
and aVF.
• Reciprocal ST depressions in leads V • to V3 are associated with acute
inferior or posterolateral infarcts.
• The ECG has limitations in sensitivity and specificity in diagnosing acute
and chronic ischemic heart disease.
• A single normal ECG does not exclude ischemia, while a normal ECG
through the course of an acute infarct is rare.
• Acute or evolving ischemia may be masked by the presence of left bundle
branch block, electronic ventricular pacemaker patterns, and
Wolff-Parkinson-White preexcitation.
• Clinicians may overdiagnose ischemia or infarction based on the presence
of ST-segment elevations or depressions.
• ST-segment elevations simulating acute ischemia may be caused by acute
pericarditis or myocarditis, COVID-19 infections, normal variants, or other
conditions.
• Tall T waves do not always indicate hyperacute ischemic changes but may
be due to normal variants, hyperkalemia, cerebrovascular injury, or other
causes.
Electrocardiography and The Effects of Metabolic Abnormalities and Drugs
• ST-segment elevations and tall, positive T waves commonly found in leads
V • and V ‚ are associated with left bundle branch block or left ventricular
hypertrophy in the absence of ischemia.
• A variety of factors such as ventricular hypertrophy, hypokalemia, and
drugs such as digoxin can cause ST-segment depressions that mimic
subendocardial ischemia.
• Prominent T-wave inversions can be caused by various factors including
ventricular hypertrophy, cardiomyopathies, and myocarditis.
• Metabolic abnormalities such as hyperkalemia, hypokalemia, and
hypocalcemia along with certain drugs can alter the ECG, usually changing
the duration of repolarization.
• The earliest ECG change with hyperkalemia is usually the peaking of T
waves, with further increases in serum potassium concentration leading to
widening QRS complexes, decrease in amplitude or P waves, and eventually,
a sine-wave pattern that leads to asystole unless emergency therapy is
given.
Electrocardiogram (ECG) Changes and Their Causes
• Various metabolic disturbances, drugs, and other factors can cause
ventricular repolarization prolongation with QT prolongation or prominent U
waves, leading to increased susceptibility to ventricular tachycardia.
• Systemic hypothermia can cause a distinctive convex "hump" at the J
point (Osborn wave, arrow) due to altered ventricular action potential
characteristics.
• Tricyclic antidepressant overdose can lead to QRS and QT prolongation
along with sinus tachycardia.
• Hypocalcemia causes the prolongation of the Q-T interval while
hypercalcemia can cause abbreviation of the ST segment and relative or
absolute shortening of the QT interval.
• Non-specific ST-T wave changes may occur with electrolyte and acid-base
disturbances, infectious or inflammatory processes, central nervous system
disorders, endocrine abnormalities, many drugs, ischemia, hypoxia, and
virtually any type of cardiopulmonary abnormality.
• Low QRS voltage may occur with pericardial or pleural effusions, chronic
obstructive pulmonary disease, infiltrative cardiomyopathies, and anasarca,
among other causes.

Electrocardiography and Pericardial Effusion

• Classic triad for pericardial effusion with cardiac tamponade: sinus
tachycardia, low QRS voltages, and electrical alternans.
• Electrical alternans-a beat-to-beat alternation in one or more components
of the ECG signal-is a common type of nonlinear cardiovascular response to
a variety of hemodynamic and electrophysiologic perturbations.
• P-QRS-T electrical alternans with sinus tachycardia is a relatively specific
sign of pericardial effusion, usually with cardiac tamponade.
• Accurate analysis of ECGs requires thoroughness and care, including
analyzing 14 points, along with the patient's age, gender, and clinical status.
• Computerized systems are widely used for immediate retrieval of ECG
records, but fully automated computerized ECG analyses still have major
limitations and should not be accepted without careful clinician review.
• Further reading is recommended with reliable sources being available to
those seeking in-depth knowledge regarding the subject.
Updates on Electrocardiographic Monitoring Standards
• Sandauke KE et al. published an update to the practice standards for
electrocardiographic monitoring in hospital settings in 2017 under the
American Heart Association’s scientific statement.
• Sharma S et al. released international recommendations for
electrocardiographic interpretation in athletes in 2017 via the J Am Coll
Cardiol.
• Chapter 240 of Ary L. Goldberger's book "Electrocardiography" is available
on McGraw Hill and covers the subject.
• Surawicz B and Knilans T's "Chou's Electrocardiography in Clinical
Practice: Adult and Pediatric," 6th ed. explores electrocardiography
standards for adult and pediatric patients.