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Electrocardiogram (ECG) is the most commonly used diagnostic test to measure the electrical activity of the heart.
It is essential for diagnosing and promptly starting therapy in patients with acute coronary syndromes, and ventricular conduction
disturbances, and arrhythmias.
Do not use ECG to screen asymptomatic adults at low risk for coronary artery disease (Strong recommendation).
Use ECG in addition to history and physical in young athletes prior to participation in competitive sports (Strong recommendation).
Consider screening in young persons aged 12-25 years to identify patients at risk for sudden cardiac death (SCD) but be aware of
limitations of 12-lead ECG as a population screening test (Weak recommendation).
Perform a baseline ECG in patients with a known cardiovascular disease (Strong recommendation).
Perform follow-up ECGs in patients with a known cardiovascular disease and (Strong recommendation):
a change in symptoms, signs, or relevant laboratory findings
an implanted pacemaker or antitachycardia device
Do not obtain serial ECGs in patients with a cardiovascular condition that is usually benign and unlikely to progress, such as patients with
(Strong recommendation):
asymptomatic mild mitral valve prolapse
minimal-to-mild arterial hypertension
premature contraction in absence of organic heart disease
Do not obtain a preoperative ECG in asymptomatic patients undergoing low-risk surgical procedures.
Consider performing a preoperative ECG in patients with clinical risk factors or a known cardiovascular disease undergoing intermediate
or high-risk surgery (Weak recommendation).
Use ECG monitoring in hospitalized patients at significant risk of immediate, life-threatening arrhythmias including but not limited to
those (Strong recommendation):
with acute coronary syndromes
undergoing cardiac surgery
with implantation of pacemakers that are pacemaker-dependent
with high-degree atrioventricular block or new-onset bundle branch block
with long QT syndrome with associated arrhythmias
Consider ECG monitoring in selected hospitalized patients with (Weak recommendation):
chest pain syndromes
uncomplicated coronary angiography or percutaneous interventions
implantation of pacemaker
Do not perform ECG monitoring in patients at low risk for cardiac arrhythmias, including those without heart disease who are (Strong
recommendation):
young and having uncomplicated procedures
obstetric patients
Related Summaries
Cardiac telemetry monitoring
Cardiac stress testing
Overview
ECG is most commonly used cardiovascular diagnostic test that is essential for diagnosing and promptly starting therapy in patients with
acute coronary syndromes and most accurate for diagnosing conduction disturbances and arrhythmias
indications for ECG may include
screening healthy individuals for cardiovascular disease (including athletes)
obtaining baseline or follow-up ECG to diagnose cardiovascular disease or drug-induced cardiac abnormalities in patients with
known cardiovascular disease
suspected or at high-risk of cardiovascular disease
preoperative resting ECG to evaluate patients with known coronary artery disease, significant arrhythmia, or other significant
structural heart disease before having noncardiac intermediate- or high-risk noncardiac surgical procedures
ECG monitoring in hospital setting to detect drug-induced cardiac abnormalities (such as in patients taking antiarrhythmic drugs) or
monitor response to therapy in patients at significant risk of immediate, life-threatening arrhythmia (such as in patients with ST-
elevation myocardial infarction [STEMI])
ECG also plays a role in detecting
electrical abnormalities and arrhythmias
tachyarrhythmias
structural abnormalities
metabolic conditions
drug effects
inflammation
Description
most commonly used cardiovascular diagnostic test that measures the electrical activity of the heart(3)
is essential for diagnosing and promptly starting therapy in patients with acute coronary syndromes and most accurate for diagnosing
intraventricular and atrioventricular conduction disturbances and arrhythmias(3)
other uses of ECG include monitoring patients taking antiarrhythmic and other drugs, preoperative assessment of patients undergoing
noncardiac surgery, and screening individuals in high-risk occupations or athletes for participation in sports(3)
see Cardiac telemetry monitoring for ambulatory ECG monitoring
Basic Principles
standard 12-lead ECG contains(3)
6 limb leads (3 established and 3 augmented leads) and 6 precordial leads
8 independent pieces of information, including
2 measured potential differences in limb leads (which can be used to calculate remaining 4 limb leads)
6 independent precordial leads
leads(3)
defined as pairs of electrodes and tracing that results from their use
lead axis
defined as straight line connecting lead electrode to the heart
projection by heart vector onto lead axis explains voltage and direction in lead axis
lead vector
has both magnitude and electrical direction that is different from lead axis
voltage in any lead is projection of heart vector on lead vector multiplied by magnitude of lead vector
lead vector direction and magnitude depend on geometry of body and varying electric impedances of tissue on torso
lead polarity
American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society (AHA/ACCF/HRS) discourages
use of the terms unipolar or bipolar when describing leads
all leads are effectively bipolar
describing augmented limb leads or precordial leads as unipolar lacks precision
frontal plane defined by 4 limb leads originally defined by Einthoven(3)
right leg lead acts as electronic reference to improve common mode (unwanted noise) rejection
3 pairs of electrodes are connected in closed electrical loop and generate 6 waveforms
within each pair of connected leads electrodes
one electrode is positive end - current flow is toward lead electrode in upward (or positive) direction
other electrode is negative end - current flow is exact opposite waveform of positive electrode (current flow is away from lead
electrode in downward [or negative] direction)
of 6 waveforms generated, 3 are established as standard limb leads, including
lead I defined as potential difference between left arm and right arm (LA-RA)
lead II defined as potential difference between left leg and right arm (LL-RA)
lead III defined as potential difference between left leg and left arm (LL-LA)
Einthoven law
at any instant in the cardiac cycle, standard lead II = lead I + lead III
any 1 standard limb lead can be mathematically derived from other 2 leads, resulting in only 2 independent pieces of
information from 3 standard limb leads
independent of Einthoven triangle, which denotes lead electrode placement
vectoral perspective within frontal plane defined by 3 augmented limb leads (aVR, aVL, and aVF)(3)
does not contain new information (can be mathematically derived from any 2 of standard limb leads) but provides new views of
cardiac electrical activity
augmented limb leads use derived electrode to serve as opposing electrode of lead pair
Wilson Central Terminal (WCT)
obtained as average potential of RA, LA and LL electrodes
potential at WCT
equals (RA + LA + LL)/3
not required to be zero or remain constant throughout cardiac cycle
6 standard precordial leads(3)
are based on potential differences between exploring electrode on chest wall and original WCT
each precordial lead (symbolized by Vi) represents potential difference given by Vi - WCT
each precordial lead provides unique measured potential differences at recording site with reference to central terminal
basic electrocardiogram
deflections on ECG(3)
positive voltage deflection in recorded waveform defined as net current flow toward first or positive electrode within each
standard lead
negative voltage deflection in recorded waveform defined as net current flow away from the first or positive electrode within
each standard lead
direction of repolarization and depolarization(1)
ventricular repolarization proceeds from epicardium to endocardium and ventricular depolarization proceeds in opposite
direction (endocardium to epicardium)
difference in spatial sequence of depolarization and repolarization in left ventricular free wall reflects inverse relationship
between activation time and action potential durations
Technical Aspects
ECG signal and processing
preparing skin with cleaning and gentle abrasion can reduce noise and improve quality of recorded ECG(3)
placement of 4 limb lead electrodes that make up frontal plane(3)
right leg lead electrode acts as reference
Einthoven triangle denotes placement of 3 standard limb leads electrodes (leads I, II, and III) at apices of equilateral triangle
Einthoven triangle: Einthoven triangle forms the basis of ECG analysis. The projection of the depolarization vector onto each lead
determines the amplitude and polarity of waveform deflection. A depolarization vector directed toward the positive end of a lead
will produce an upward (positive) deflection of the waveform on that lead. Abbreviation: ECG, electrocardiogram.
placement of 4 limb lead electrodes can be either distal to shoulder and hips or proximal on wrists and ankles, but clearly document
precise location (effect of distal versus proximal limb lead electrode placement remains unknown)
historically, limb lead electrodes placed at wrists and ankles (proximal placement)
recently, limb lead electrodes placed at upper arms in effort to reduce motion artifacts (distal placement)
placement of 6 precordial lead electrodes (V1-V6) that make up horizontal plane(3)
in women, place lead electrodes under breast instead of on top of breast
V1 - in fourth intercostal space at right sternal border
V2 - in fourth intercostal space at left sternal border
V3 - midway between V2 and V4
V4 - in fifth intercostal space in midclavicular line
V5 - in horizontal plane of V4 at anterior axillary line (or midway between V4 and V6 if anterior axillary line is ambiguous)
V6 - in horizontal plane of V4 at midaxillary line
alternative lead applications are not equivalent to standard 12-lead ECG and cannot be used to replace or directly compare to standard 12-
lead ECG(3)
Mason-Likar monitoring and modified lead placement during ambulatory and exercise ECG(3)
limb leads placed onto torso to reduce noise from motion of arms and legs
arm electrodes placed in infraclavicular fossae medial to deltoid insertions or over outer clavicles in more recent applications of
Mason-Likar monitoring
left leg electrode placed midway between costal margin and iliac crest in left anterior axillary line
precordial leads placed in standard positions
QRS morphology may be effected by altered lead position, resulting in possible false-negative and false-positive infarction criteria
reduced lead sets(3)
reduced lead sets can be used to mathematically construct a synthesized 12-lead ECG
synthesized 12-lead ECG tracings can differ from standard 12-lead ECG tracing in interval duration and amplitude
Frank lead system (used for vectorcardiography) involves 7 electrodes, including
5 electrodes placed at points in horizontal plane that intersect fifth intercostal space at left sternal border
A at left midaxillary line
C on anterior left chest wall halfway between E and A
E at mid sternum anteriorly
I at right midaxillary line
M at mid spine posteriorly
electrode H placed at junction of neck and torso posteriorly
electrode F placed on left foot
EASI lead system (used to allow patients to move around without intolerable noise) involves 5 electrodes, including
electrodes E, A, and I from Frank lead system
electrode S placed at top of mid sternum
ground reference electrode to provide orthogonally oriented signals
expanded lead sets(3)
hybrid lead system involves standard 12-lead set plus 3 electrodes from Frank lead system and can be useful for some
electrocardiograms
additional chest precordial leads may be useful for investigating acute coronary syndromes and ST-elevation myocardial infarction
(STEMI)
4 additional right-sided precordial leads (V3R, V4R, V5R, and V6R) placed on right side in mirror image of standard lead
positions
3 additional posterior chest precordial leads (V7, V8, and V9) may help identify ST-elevation events in posterior wall
V7 placed at posterior axillary line
V8 placed below scapula
V9 placed at paravertebral border
Common errors
ECG can raise suspicion for or detect certain genetic cardiovascular diseases, including(2)
ion channelopathies
hypertrophic cardiomyopathy
screening in adult persons
guidelines consistently recommend against screening healthy adult individuals for coronary heart disease using ECG
United States Preventative Services Task Force (USPSTF) recommendations for screening with resting or exercise ECG for
prediction of coronary heart disease events
screening not recommended in asymptomatic adults at low risk for coronary heart disease (USPSTF Grade D)
insufficient evidence to recommend for or against screening in asymptomatic adults at intermediate or high risk for
coronary heart disease events (USPSTF Grade I)
Reference - Ann Intern Med 2012 Oct 2;157(7):512
American College of Preventive Medicine (ACPM) recommends against routine screening of general adult population for
coronary heart disease using ECG (Am J Prev Med 2011 Mar;40(3):381.e1)
no guidelines recommending cardiac screening of low-risk adult patients found in systematic review evaluating guidelines from
primary care, cardiology, and radiology (Ann Intern Med 2015 Mar 17;162(6):438)
screening in young persons aged 12-25 years to identify patients at risk for sudden cardiac death (SCD)(2)
American College of Cardiology/American Heart Association (ACC/AHA) recommendations
screening with 12-lead ECGs in association with history and physical exam to identify or raise suspicion of genetic/congenital
and other cardiovascular abnormalities may be considered in relatively small cohorts (such as in high schools,
college/universities, or local communities) as long as physician closely involved and quality control can be achieved (ACC/AHA
Class IIb, Level C)
if screening initiative chosen, be aware of limitations of 12-lead ECG as population screening test, including expected frequency
of false-positive and false-negative results (ACC/AHA Class IIb, Level C)
mandatory and universal mass screening with 12-lead ECG in large general populations to identify genetic/congenital and other
cardiovascular abnormalities not recommended (ACC/AHA Class III, Level C)
general considerations for screening
low prevalence of cardiovascular disease responsible for sudden cardiac death (SCD)
patients diagnosed with cardiovascular disease at low risk for SCD
includes large population of people
diagnostic performance of 12-lead ECG depends on
purpose of acquisition
technical quality of recording
selection of study population
distinguishing factors within population subgroups (such as age, sex, race, and level of physical activity)
quality of interpretive analysis
ECG diagnostic ability to detect prognostically important abnormalities
factors compromising reliability of ECG diagnostic criteria
changes in ECG in healthy young individuals can overlap with (sometimes indistinguishable from) cardiovascular disease that
cause SCD (especially hypertrophic cardiomyopathy)
sensitivity for detecting channelopathies and cardiomyopathies difficult to determine due to variations in ECG abnormalities as
a result of heterogeneous disease severity
sensitivity for detecting preexcitation syndromes in healthy screening populations may be reduced by
changing day-to-day fusion of normal and accessory pathway conduction that usually presents as normal ECG tracing
questionably slurred waveform upstrokes that occasionally present in midprecordial leads in healthy individuals
effects of ECG diagnostic performance on screening utility
even at low false-positive rate (about 5%), large number of patients would be referred for additional testing to rule out
cardiovascular disease
false-negative tests limit utility of ECG as screening modality (for example, ECG reported to have low sensitivity for detecting
inherited coronary anomalies [ECG reported to be normal in ≥ 90% of patients])
positive predictive value very low due to low prevalence of disease
screening in athletes
preparticipation cardiovascular screening for athletes aims to identify individuals with cardiovascular abnormalities potentially
associated with sudden cardiac death (SCD) with goal of reducing risk for SCD in these persons by disqualifying them from
competitive sports
history and physical exam
guidelines consistently agree that preparticipation screening for cardiovascular abnormalities in competitive athletes should
include history and physical exam focused on assessing cardiac risk
American Heart Association/American College of Cardiology (AHA/ACC) recommends use of AHA/ACC 14-point screening
guideline in conjunction with history and physical exam to detect or raise suspicion of genetic/congenital cardiovascular
abnormalities (AHA/ACC Class I, Level C)
European Society of Cardiology (ESC) recommends systematic preparticipation cardiovascular screening of young
competitive athletes for timely detection of cardiovascular abnormalities that includes complete personal and family
history and physical exam with blood pressure measurement
2 standardized forms have been developed by guideline organizations (14-element American Heart Association questionnaire
and preparticipation physical evaluation monograph fourth edition)
preparticipation screening with history and physical has poor sensitivity but strong specificity for detecting cardiac
abnormalities in college athletes (level 1 [likely reliable] evidence)
guidance mixed for addition of 12-lead electrocardiogram (ECG) to preparticipation cardiovascular screening with history and
physical exam
guidelines are not in agreement on mandatory use of ECG as part of preparticipation screening
AHA/ACC concludes screening with 12-lead ECG in conjunction with history and physical exam should be considered in
select cohorts of young healthy people aged 12-25 years, not necessarily limited to competitive athletes, provided that
close physician involvement and quality control achieved
known limitations (such as false-positive and false-negative rates) considered (AHA/ACC Class IIb, Level C)
ESC concludes initial cardiovascular evaluation should include 12-lead ECG in addition to history and physical exam
general considerations for screening with ECG
low prevalence of cardiovascular disease responsible for SCD, and patients diagnosed with cardiovascular disease at low
risk for SCD
factors compromising reliability of ECG diagnostic criteria
changes in ECG in healthy young individuals can overlap with (sometimes indistinguishable from) cardiovascular
disease that causes SCD (especially hypertrophic cardiomyopathy)
sensitivity for detecting channelopathies, preexcitation syndromes, and cardiomyopathies difficult to determine due
to variations in ECG abnormalities resulting from heterogeneous disease severity
effects of ECG diagnostic performance on screening utility
even at low false-positive rate (about 5%), large number of patients would be referred for additional testing to rule
out cardiovascular disease
false-negative tests limit utility of ECG as screening modality (ECG reported to be normal in most patients with
inherited coronary anomaly)
positive predictive value very low due to low prevalence of disease
effect on mortality
preparticipation athletic screening with exam and ECG associated with reduced rate of sudden cardiovascular death in
Italy (level 2 [mid-level] evidence)
preparticipation screening with exam plus ECG and disqualification of young athletes with hypertrophic cardiomyopathy
reported to have prevented sudden death in Italy (level 3 [lacking direct] evidence)
several criteria for interpreting ECG in athletes have been proposed to distinguish between normal training-related ECG
findings and abnormal ECG findings not related to training
training-related ECG findings do not require further evaluation
abnormal ECG findings require further evaluation and additional testing is specific to abnormal finding
ESC recommends
imaging with echocardiography as first test in patients with ECG findings suggestive of structural heart disease
other testing, such as exercise ECG and 24-hour ECG monitoring, in patients with suspected conduction
abnormalities, preexcitation syndromes, or channelopathies
proposed criteria include
2005 and 2010 ESC criteria
Seattle criteria
2014 Refined criteria
diagnostic performance of proposed criteria
compared to history and physical alone
33% of athletes reported to have ECG abnormalities requiring additional evaluation using 2010 ESC criteria
addition of ECG to preparticipation screening history and physical can significantly increase detection of cardiac
abnormalities in college athletes, but also increases false-positive rate (level 1 [likely reliable] evidence)
compared to each other
2014 refined ECG criteria increases specificity of preparticipation cardiovascular screening with ECG in male athletes
compared to 2010 ESC and Seattle criteria (level 1 [likely reliable] evidence)
compared to 2010 ESC criteria, Seattle criteria for evaluating ECG in athletes may
reduce false-positive rate in black and white elite athletes (level 2 [mid-level] evidence)
reduce number of athletes needing additional cardiac evaluation with echocardiography after abnormal ECG
on preparticipation screening (level 2 [mid-level] evidence)
routine echocardiogram screening appears to offer little benefit for detecting clinically significant cardiac pathology compared to
preparticipation screening with history, physical, and ECG
see Preparticipation cardiovascular screening for athletes for details
many cardiologists and noncardiologists incorrectly classify QT interval
based on cohort study
902 physicians from 12 countries (25 QT experts, 106 arrhythmia specialists, 329 cardiologists, and 442 noncardiologists) interpreted
ECG from 2 healthy women and 2 patients with long QT syndrome
corrected QT interval was calculated correctly by > 80% of arrhythmia experts, < 50% of cardiologists, and < 40% of noncardiologists
correct classification of QT interval as long or normal was made by 96% of QT experts, 62% of arrhythmia experts, and < 25% of
cardiologists and noncardiologists
Reference - Heart Rhythm 2005 Jun;2(6):569, editorial can be found in Heart Rhythm 2005 Jun;2(6):575
recommendations
American College of Cardiology/American Heart Association (ACC/AHA) 2014 recommendations
preoperative resting 12-lead ECG
not indicated in asymptomatic patients having low-risk surgical procedures (ACC/AHA Class III, Level B)
reasonable in patients with known coronary artery disease, significant arrhythmia, peripheral arterial disease,
cerebrovascular disease, or other significant structural heart disease if having intermediate- or high-risk surgical
procedures (ACC/AHA Class IIa, Level B)
may be reasonable in asymptomatic patients if not having low-risk surgical procedures (ACC/AHA Class IIb, Level B)
European Society of Cardiology/European Society of Anaesthesiology (ESC/ESA) recommendations for preoperative risk assessment
and cardiac risk stratification
routine preoperative ECG
recommended for patients with clinical risk factors who are having intermediate- or high-risk surgery (ESC/ESA Class I,
Level C)
may be considered for patients with clinical risk factors if having low-risk surgery or for patients without clinical risk
factors who are > 65 years old and having intermediate-risk surgery (ESC/ESA Class IIb, Level C)
not recommended for patients without clinical risk factors who are having low-risk surgery (ESC/ESA Class III, Level B)
Canadian Anesthesiologist Society recommends against ordering baseline ECG for asymptomatic patients undergoing low-risk
noncardiac surgery
see Perioperative cardiac management for noncardiac surgery for additional information
T wave(1)
refers to phase of rapid repolarization (phase 3) of ventricular action potential
during phase 3 of repolarization in normal physiological conditions, the transmembrane action potential repolarizes from its plateau
voltage of about 10 to -10 millivolts (mV) to its resting level of about -85 mV
T wave is generated as intraventricular and interventricular voltage gradients are created (due to myocardial cells undergoing rapid
sequential repolarization)
configuration determined by spatial-temporal characteristics of ventricular repolarization (particularly asynchrony of phase 3 of
ventricular action potentials)
ST segment(1)
refers to plateau phase of ventricular transmembrane action potential
in normal physiological conditions, only small voltage gradients present on ECG (due to transmembrane voltage changing slowly and
remaining at about same level in all ventricular myocardial cells)
TP segment(1)
refers to electric diastole (end of repolarization to onset of next depolarization)
in normal physiological conditions, voltage gradient nearly flat (due to ventricular myocardial cells being at resting transmembrane
potential of about -85 mV)
in normal physiological conditions, ST segment and TP segment are isoelectric due to lack of significant voltage gradients in ventricular
myocardial cells during phases of cardiac cycle which they measure(1)
U wave(1)
most likely represents mechanoelectric phenomenon occurring after repolarization that leads to low amplitude, low frequency
deflection after T wave
frequently absent in limb leads and most evident in leads V2 and V3 where its amplitude has been reported to be about 0.33 mV or
11% of T-wave amplitude
presence on ECG is heart rate dependent and rarely seen at heart rates > 95 beats/minute
enhances with bradycardia and seen often at heart rates < 65 beats/minute
usually associated with depression of ST segment and decrease in T-wave amplitude, which may due to any
cardioactive drugs with potassium channel blocking effects
hypokalemia (U-wave amplitude may exceed T-wave amplitude in same lead if advanced hypokalemia or potassium < 2.7
mmol/L)
fusion of U wave and T wave may occur in association with increase in sympathetic tone and in presence of significantly prolonged
QT interval
QT interval(1)
QT interval refers to onset of QRS complex to end of T wave (or earliest indication of ventricular depolarization to latest indication of
ventricular repolarization)
problems associated with measuring QT interval include
recognizing onset of QRS complex and end of T wave
determining appropriate leads for measuring
onset of QRS complex tends to be 20 milliseconds earlier in leads V2 and V3 compared to limb leads
QT interval differences between leads measuring up to 50 milliseconds may be normal
if using individual leads when reporting QT interval
use lead showing longer QT interval (typically lead V2 or V3), but consider using interval measured from other leads
if interval > 40 milliseconds than other leads
use lead not showing U wave if T wave and U wave are superimposed and cannot be separated (usually leads aVR
and aVL)
adjusting for sex, increases in QRS duration, and heart rate
QT interval adjustments
QT correction for rate
Bazett formula most commonly used
other formulas developed include Fridericia formula and linear regression functions
correction of QT interval should not be done if RR interval has large variability (such as with atrial fibrillation) or if end of
T wave cannot be reliably identified
adjust QT interval for sex
adjust for QRS duration if ventricular conduction defects present
QT dispersion refers to difference between longest and shortest QT intervals(1)
QRS complex
represents intraventricular propagation of supraventricular impulse through His-Purkinje conduction system
is wider in precordial leads than in limb leads
Reference - J Am Coll Cardiol 2009 Mar 17;53(11):976 full-text
QRS duration
is influenced by age and gender
may increase with increasing heart size
Reference - J Am Coll Cardiol 2009 Mar 17;53(11):976 full-text
P wave
represents atrial impulse conduction through atrioventricular node into ventricle
Reference - Rev Esp Cardiol (Engl Ed) 2012 Jul;65(7):656
PR interval
represents onset of atrial and ventricular conduction
Reference - Circulation 2013 Jan 22;127(3):e283 full-text
abnormalities in ST segment, T wave, and duration of QT interval indicate abnormalities in ventricular repolarization(1)
abnormalities in T wave and ST segment(1)
may occur with or without abnormal voltage gradients
can be caused by either
abnormal voltage gradients during plateau and rapid repolarization phases of action potential
changes in sequence of repolarization
often associated with variety of well-defined anatomic, pathological, physiological, and pharmacological events
distinguishing primary from secondary repolarization abnormalities(1)
primary (but not secondary) repolarization abnormalities indicate changes in repolarization features of ventricular myocytes
primary repolarization abnormalities
include abnormalities in ST segment and T wave due to changes in shape and/or duration of repolarization phases of
transmembrane action potential without changes in depolarization
may be localized or diffuse
may be caused by any
ischemia
myocarditis
drugs
toxins
electrolyte abnormalities (particularly abnormalities in serum calcium and potassium)
abrupt change in heart rate
hyperventilation
changes in body position
catecholamines
sympathetic stimulation or ablation of stellate ganglion
temperature changes
secondary repolarization abnormalities
include abnormalities in ST segment and T wave due to changes in QRS shape and/or duration (due to changes in sequence
and/or duration of ventricular depolarization)
may be caused by voltage gradients that normally cancel out but become manifest when changes in sequence of depolarization
alter repolarization sequence
examples include ST segment and T wave changes associated with bundle branch blocks, ventricular preexcitation, and ectopic
or paced ventricular complexes
ST-segment abnormalities
T-wave abnormalities
U-wave abnormalities
inverted U wave in leads V2-V5 may appear transiently during acute ischemia or in presence of hypertension(1)
abnormalities usually subtle and rarely appear without other abnormalities on ECG(1)
P-wave abnormalities
American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) recommendations for reporting ECG
abnormalities
for reporting ST-segment abnormalities(1)
include qualitative description of ST segment with consideration to patient age and gender
note if ST depression ≥ 0.1 millivolts (mV)
include possible causes
for evaluating ST elevation, use computer algorithm that includes reference values established in large population and
stratified by age, sex, and race
for reporting T-wave abnormalities, include(1)
description of abnormalities
identification of associated ST-segment changes (if present)
whether cause indeterminate or likely associated with specific cause
include U-wave abnormalities in ECG report if any(1)
inverted U wave
U wave merged with T wave
U-wave amplitude greater than T-wave amplitude
if QT interval prolongation reported by computer algorithm, visually validate the QT interval (temporally aligned superimposed ECG
leads may be used to facilitate QT measurements and validate onset and end points of the interval)(1)
do not include QT dispersion on routine ECG reports(1)
for reporting P-wave abnormalities, terms right or left atrial abnormality preferred over enlargement, overload, strain, or
hypertrophy(4)
American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society (AHA/ACCF/HRS) ECG diagnostic criteria
for intraventricular conduction disorders
complete right bundle branch block (RBBB)
QRS duration
≥ 120 milliseconds in adults
≥ 100 milliseconds in children aged 4-16 years
≥ 90 milliseconds in children < 4 years old
QRS morphology
rsr', rsR', or rSR' in leads V1 or V2 (R' or r' deflection usually wider than initial R wave)
minority of patients may have wide and often notched R-wave pattern in leads V1 and/or V2
S-wave duration > R-wave duration or > 40 milliseconds in leads I and V6 in adults
normal R peak time in leads V5 and V6
R peak time > 50 milliseconds in lead V1
Right bundle branch block electrocardiogram: Sinus rhythm, normal PR interval, underlying RBBB with normal QRS axis.
Abbreviation: RBBB, right bundle branch block.
Right bundle branch block electrocardiogram: Sinus rhythm, normal PR interval, underlying RBBB with an indeterminate
QRS axis. There are nonspecific T-wave abnormalities. Abbreviation: RBBB, right bundle branch block.
incomplete RBBB
same QRS morphology as for complete RBBB but QRS duration between
110 and 120 milliseconds in adults
90 and 100 milliseconds in children aged 4-16 years
86 and 90 milliseconds in children < 8 years old
terminal rightward deflection < 40 milliseconds but ≥ 20 milliseconds in children
may be present without heart disease (especially when V1 lead recorded higher than or to right of normal position and r' < 20
milliseconds)
complete left bundle branch block (LBBB)
QRS duration
≥ 120 milliseconds in adults
≥ 100 milliseconds in children aged 4-16 years
≥ 90 milliseconds in children < 4 years old
QRS morphology
broad notched or slurred R wave in leads I, aVL, V5, and V6
occasional RS pattern in leads V5 and V6 (due to displaced transition in QRS complex)
absent q waves in leads I, V5, V6, and aVL (narrow q wave may be present in lead aVL in absence of myocardial
pathology)
R peak time > 60 milliseconds in leads V5 and V6 but normal in leads V1, V2, and V3 when small initial r waves can be
discerned
ST and T waves inverted relative to QRS complex
positive T wave may be normal in leads with upright QRS complex (positive concordance)
depressed ST segment and/or negative T wave in leads with negative QRS complex are abnormal (negative concordance)
appearance of LBBB may change mean QRS axis in frontal plane to right, left, or superior (can be rate-dependent)
Left bundle branch block electrocardiogram: Sinus rhythm, normal PR interval, underlying LBBB, leftward QRS axis.
Abbreviation: LBBB, left bundle branch block.
Left bundle branch block electrocardiogram: Sinus rhythm, borderline PR prolongation, left atrial abnormality,
underlying LBBB, leftward QRS axis, nonspecific ST-segment T-wave abnormalities. Abbreviation: LBBB, left bundle
branch block.
incomplete LBBB
QRS duration between
110 and 119 milliseconds in adults
90 and 100 milliseconds in children aged 4-16 years
80 and 90 milliseconds in children < 8 years old
QRS morphology
left ventricular hypertrophy pattern
R peak time > 60 milliseconds in leads V4, V5, and V6
absent q waves in leads I, V5, V6
left anterior fascicular block (LAFB) (not applicable to patients with congenital heart disease who have left-axis deviation in infancy)
QRS duration < 120 milliseconds
frontal plane left axis deviation
significant deviation between -45 and -90 degrees
moderate deviation between -30 and -45 degrees
QRS morphology
qR pattern in lead aVL
R peak time ≥ 45 milliseconds in lead aVL
left posterior fascicular block (LPFB)
QRS duration < 120 milliseconds
frontal plane right axis deviation
between +90 and +180 degrees in adults
more rightward in children ≤ 16 years old (only when distinct rightward change in axis documented)
QRS morphology
rS pattern in leads I and aVL
qR pattern in leads III and aVF
nonspecific intraventricular conduction disturbance is absence of criteria for RBBB or LBBB with QRS duration
> 110 milliseconds in adults
> 90 milliseconds in children aged 8-16 years
> 80 milliseconds in children < 8 years old
Reference - J Am Coll Cardiol 2009 Mar 17;53(11):976 full-text
Second-degree heart block type 2: Sinus rhythm with AV Wenckebach and 2:1 AV block, likely Mobitz I given the progressive PR
prolongation and relative sinus bradycardia due to vagotonia on the basis of an acute inferior-posterior wall myocardial
infarction (ST segment elevations inferiorly and reciprocal ST segment depressions in aVL and V2).
Second-degree AV block with 2:1 conduction: Sinus rhythm with 2:1 AV block, with prolonged conducted PR interval at 500
milliseconds, and narrow QRS. Given the relatively fast sinus rate of about 90 bpm, the likely type of block is Mobitz II.
Abbreviation: bpm, beats per minute.
Second-degree AV block, type II: Sinus tachycardia with 3:2 AV Wenckebach, underlying LVH with RBBB and LAHB. The
presence of sinus tachycardia and minimal PR prolongation during the Wenckebach cycle indicate a Mobitz II type of block.
Abbreviations: LAHB, left anterior fascicular block; LBBB, left bundle branch block; LVH, left ventricular hypertrophy.
Third-degree heart block: Sinus rhythm and underlying complete heart block with a narrow-complex ventricular escape
mechanism.
Third-degree heart block: Sinus tachycardia and underlying complete heart block with a narrow-complex ventricular escape
mechanism at approximately 70 bpm suggesting the higher junction as a site of origin. Abbreviation: bpm, beats per minute.
Third-degree AV block: Sinus or atrial tachycardia with underlying complete heart block and a wide-complex ventricular
escape of LBBB-morphology likely originating from the right bundle. Abbreviation: LBBB, left bundle branch block.
see Atrioventricular (AV) conduction disorders for details and additional information
Preexcitation
Preexcitation (Wolff-Parkinson-White pattern): Sinus rhythm with evident ventricular preexcitation via a posteroseptal bypass tract.
Tachyarrhythmias
Atrial fibrillation
Atrial fibrillation: Atrial fibrillation with rapid ventricular response. There are normal intervals. Occasional aberration is seen.
Atrial fibrillation with aberrant conduction: Atrial fibrillation with ventricular preexcitation and very rapid ventricular response.
Atrial flutter
Ventricular arrhythmias
Ventricular tachycardia: Ventricular tachycardia originating from the inferior wall/inferior septum (QS complexes in II, III,
aVF).
Ventricular tachycardia: Wide-complex tachycardia with extreme right superior axis consistent with VT, likely originating from
the inferoposterolateral wall. Abbreviation: VT, ventricular tachycardia.
Ventricular tachycardia: Wide-complex tachycardia of RBBB-type, right superior axis morphology, consistent with VT.
Abbreviations: RBBB, right bundle branch block; VT, ventricular tachycardia.
Structural abnormalities
see Coronary artery disease (CAD) for details and additional information
Cardiomyopathies
Channelopathies
Brugada syndrome: Sinus rhythm, normal PR interval, rightward QRS axis, and RBBB with ST-segment elevation in V1
consistent with Brugada syndrome. Abbreviation: RBBB, right bundle branch block.
for asymptomatic patients with type 1 ECG findings, additional ECG findings consistent with Brugada syndrome include
cessation of ST-segment elevation at peak of exercise test, with reappearance during recovery phase
first-degree atrioventricular block and left axis QRS deviation
atrial fibrillation
signal-averaged ECG with late potentials
fragmented QRS
ST-T alternans, spontaneous left bundle branch block ventricular premature beats during prolonged ECG recording
see Brugada syndrome for details and additional information
other inherited arrhythmia syndromes
catecholaminergic polymorphic ventricular tachycardia
diagnosed on ECG with findings during exercise of
bidirectional ventricular tachycardia
polymorphic ventricular premature beats
ventricular tachycardia
arrhythmias show typical pattern of development during exercise, progressing from supraventricular and ventricular beats or
couplets to bidirectional ventricular tachycardia that return to baseline at interruption of exercise
short QT syndrome
diagnosed based on QTc interval ≤ 330 milliseconds
most patients show
tall, peaked, narrow T waves
almost absent ST segment
relatively long Tpeak-Tend interval
progressive cardiac conduction disease diagnosed based on prolonged P-wave duration, prolonged PR interval, and QRS widening
with axis deviation (associated with atrioventricular conduction disorders and atrial and ventricular arrhythmias)
see Inherited arrhythmia syndromes for details and additional information
Metabolic conditions
Hyperkalemia: Markedly wide-complex rhythm of unclear mechanism consistent with advanced hyperkalemia.
Hypokalemia on ECG: Sinus rhythm with normal PR and QRS intervals. There is extreme QT interval prolongation and T wave
abnormality consistent with profound hypokalemia. 2 APBs are seen. Abbreviations: APB, atrial premature beat.
Hypokalemia: Rhythm: sinus bradycardia, normal PR, QRS intervals, normal QRS axis. Presence of U wave consistent with
hypokalemia.
Hypocalcemia-induced electrocardiographic changes: Sinus rhythm, normal PR, QRS intervals, normal QRS axis, nonspecific T-wave
abnormality in I, aVL. There is abnormally prolonged QT interval for given heart rate, primarily due to prolongation of the ST-
segment which is consistent with hypocalcemia.
Drug effect
Inflammation
Acute pericarditis electrocardiogram: Sinus rhythm with sinus arrhythmia, normal intervals, and normal QRS axis. There
is diffuse concave ST-segment elevation consistent with pericarditis.
Pericarditis electrocardiogram: Sinus rhythm with normal intervals and normal QRS axis. There is diffuse concave ST-
segment elevation, PR segment depression in II, aVF, and PR-segment elevation in aVR, all consistent with pericarditis.
Pericarditis electrocardiogram: Sinus rhythm with normal intervals and normal QRS axis. There is diffuse concave mild
ST-segment elevation, PR-segment depression in II, aVF, and PR-segment elevation in aVR, all consistent with pericarditis.
see Acute and recurrent pericarditis for details and additional information
constrictive pericarditis ECG may be normal or show
low QRS voltage
generalized T-wave inversion or flattening
interatrial block
atrioventricular block, intraventricular conduction defects (especially in patients with myocardial fibrosis and calcifications)
left atrium abnormalities
atrial fibrillation
pseudoinfarction pattern (rare)
see Constrictive pericarditis for details and additional information
pericardial effusion and tamponade ECG findings may include
low QRS voltage (absence does not preclude tamponade)
PR-segment depression
ST-segment elevation
bundle branch block
fluctuating QRS amplitude (rare without tamponade; indicates swinging heart in pericardial fluid)
end-stage bradycardia
sinus tachycardia
see Pericardial effusion and tamponade for details and additional information
Diagnostic criteria
detection of LVH important to prevent or delay adverse clinical outcomes by reversing LVH with therapy(4)
LVH definitive diagnosis made using imaging (echocardiography, computed tomography, or magnetic resonance imaging) or
measurement of ventricular mass at autopsy, but ECG has a role in detecting LVH due to widespread availability, convenience, and low
cost(4)
principal ECG features associated with LVH include(4)
increase in QRS amplitude and duration
changes in instantaneous and mean QRS vectors
abnormalities in
ST segment
T wave
P wave
Left ventricular hypertrophy: Sinus rhythm with normal intervals and leftward QRS axis. There are occasional blocked APBs.
There are prominent QRS voltages in I and aVL indicative of LVH. There are diffuse T-wave abnormalities consistent with LVH,
cardiomyopathy, or myocardial ischemia. Abbreviations: APB, atrial premature beat; LVH, left ventricular hypertrophy.
Left ventricular hypertrophy: Normal sinus rhythm with normal intervals and normal QRS axis. There are tall R waves in I,
aVL, and delayed intrinsicoid deflection, all consistent with LVH. Abbreviation: LVH, left ventricular hypertrophy.
Sinus bradycardia with left ventricular hypertrophy: Sinus bradycardia with borderline PR prolongation, normal QRS width
and axis. There is probable RA abnormality. There are prominent QRS voltages in the precordium consistent with LVH. There
are diffuse ST-segment T-wave abnormalities consistent with LVH and/or cardiomyopathy. Abbreviation: LVH, left ventricular
hypertrophy.
sensitivity generally low for all criteria (reported to be < 50%) but specificity generally high (reported range 85%-90%)(4)
body size-adjusted Cornell product criteria may improve LVH detection compared to adjusted Cornell voltage criteria in both men
and women (level 2 [mid-level] evidence)
based on diagnostic cohort study without independent validation
3,351 adults with ECG and echocardiographic measurements were evaluated for LVH using 10 ECG diagnostic criteria
17% had LVH (defined as LV mass indexed to height > 143 g/m in men and > 102 g/m in women) on echocardiography (reference
standard)
ECG diagnostic criteria were adjusted to body size using regression analysis to improve correlation with LV mass
comparing adjusted Cornell product vs. adjusted Cornell voltage at fixed specificity of 95% for detecting LVH
sensitivity in women 51% vs. 46% (p < 0.001)
sensitivity in men 39% vs. 32% (p < 0.001)
Reference - J Am Coll Cardiol 1995 Oct;26(4):1022 full-text
Cornell product criteria may improve LVH detection compared to other ECG diagnostic criteria when LV mass indexed to body
size (level 2 [mid-level] evidence)
based on retrospective diagnostic cohort study with unclear blinding
212 patients who had 12-lead ECG of adequate technical quality within mean 16 days of death were evaluated for LVH using ECG
diagnostic criteria
19% were overweight to mildly obese (body mass index [BMI] > 27.8 kg/m2 in men and 27.3 kg/m2 in women)
reference standard was LV mass index measured by chamber partition method on autopsy and indexed to measures of body size
prevalence of LVH on reference standard was
43% when indexed to body surface area (defined as LV mass index > 118 g/m2 in men and > 104 g/m2 in women)
42% when indexed to height (defined as LV mass/height > 143 g/m in men and > 102 g/m in women)
38% when indexed to height2.7 (defined as LV mass/height2.7 > 50 g/m2.7 in men and > 47 g/m2.7 in women)
when all specificities fixed at 95%, Cornell product had increased sensitivity compared to other ECG criteria for detecting LVH
using LV mass indexed to body surface area
Cornell product sensitivity 52%
Sokolow-Lyon voltage sensitivity 30% (p < 0.001 compared to Cornell product)
Cornell voltage sensitivity 45% (p < 0.05 compared to Cornell product)
Framingham-adjusted Cornell voltage 24% (p < 0.001 compared to Cornell product)
using LV mass indexed to height
Cornell product sensitivity 43%
Sokolow-Lyon voltage sensitivity 22% (p < 0.001 compared to Cornell product)
Cornell voltage sensitivity 35% (p < 0.05 compared to Cornell product)
Framingham-adjusted Cornell voltage 33% (no p value reported compared to Cornell product)
using LV mass indexed to height2.7
Cornell product sensitivity 39%
Sokolow-Lyon voltage sensitivity 22% (p < 0.01 compared to Cornell product)
Cornell voltage sensitivity 36% (no p value reported compared to Cornell product)
Framingham-adjusted Cornell voltage 29% (p < 0.05 compared to Cornell product)
Reference - J Am Coll Cardiol 1996 Jan;27(1):124 full-text
in obese patients
body mass index adjustments of Sokolow-Lyon index voltage criteria may increase sensitivity with minimal loss of specificity
for patients with overweight and obesity (level 2 [mid-level] evidence)
based on diagnostic cohort study with unclear inclusion criteria
derivation cohort included 821 adults in Oxford, United Kingdom being evaluated for left ventricular hypertrophy having ECG
and cardiovascular magnetic resonance imaging (MRI) (reference standard)
patients were classified based on BMI, with normal weight defined as 18.5-24.9 kg/m2 (32%), overweight as 25-29.9 kg/m2
(36%), and obese as > 30 kg/m2 (32%)
patients were excluded for contraindications to MRI (pregnancy, claustrophobia, or metallic foreign body), complete left
or right bundle branch block, chronic obstructive pulmonary disease, evidence of myocardial infarction on imaging,
hypertrophic cardiomyopathy, or pericardial effusion > 1 cm
21% had left ventricular hypertrophy by reference standard in derivation cohort
increased BMI associated with significant decrease in Sokolow-Lyon index voltage criteria
adjustment factors for Sokolow-Lyon index voltage criteria developed for patients with overweight or obese BMI in derivation
cohort
+ 4 mm for overweight BMI
+ 8 mm for obese BMI
validation cohort included 520 similar patients (39.6% normal BMI, 32.5% overweight BMI, 27.9% obese BMI) in Cape Town,
South Africa
9.3% had left ventricular hypertrophy by reference standard in validation cohort
performance of Sokolow-Lyon index voltage criteria adjustment factors in validation cohort
Positive Negative Predictive
Sensitivity Specificity
Predictive Value Value
Normal BMI Unadjusted 39% 95.4% 35.7% 95.9%
+4 adjustment 39.1% 93.1% 47.4% 90.1%
Overweight BMI
Unadjusted 8.3% 98.6% 50.1% 87.1%
+8 adjustment 25% 97.3% 72.7% 81.5%
Obese BMI
Unadjusted 9.4% 99.1% 75% 79%
Abbreviation: BMI, body mass index.
compared to unadjusted criteria, adjusted criteria had significantly higher sensitivities and lower specificities in patients with
overweight or obese BMIs
Reference - Heart 2016 Oct 1;102(19):1566 full-text
Cornell voltage criteria may be more sensitive than Sokolow-Lyon voltage criteria for detecting LVH in obese patients with
hypertension (level 2 [mid-level] evidence)
based on diagnostic cohort study with unclear blinding
349 patients with hypertension with adequate quality echocardiography for LV mass calculation (reference standard) were
evaluated for LVH using ECG Cornell voltage criteria and Sokolow-Lyon voltage criteria
30% of patients were obese (BMI ≥ 27.8 kg/m2 in men and 27.3 kg/m2 in women)
prevalence of LVH on reference standard when LV mass indexed to
body surface area (LVH defined as LV mass index > 125 g/m2 in men and > 110 g/m2 in women)
16.3% in obese women and 13.7% in nonobese women
27.9% in obese men and 24.5% in nonobese men
height (LVH defined as LV mass/height > 136 g/m in men and > 120 g/m in women)
30.2% in obese women and 13.7% in nonobese women
36.1% in obese men and 28% in nonobese men
height2.7 (LVH defined as LV mass/height2.7 > 56 g/m2.7 in men and > 49 g/m2.7 in women)
48.8% in obese women and 18.6% in nonobese women
32.8% in obese men and 21.7% in nonobese men
comparing sensitivity of Cornell voltage criteria vs. Sokolow-Lyon voltage criteria for detecting LVH when specificity fixed at
95% in obese patients
using LV mass indexed to body surface area
23.4% vs. 8.7% in men (no p value reported)
36.3% vs. 10.9% in women (no p value reported)
using LV mass indexed to height
27.6% vs. 9.9% in men (no p value reported)
33.5% vs. 5.5% in women (no p value reported)
using LV mass indexed to height2.7
18.1% vs. 9.5% in men (no p value reported)
20.5% vs. 3.2% in women (no p value reported)
Reference - Am J Cardiol 1996 Apr 1;77(9):739
compared to normal weight patients, prevalence of LVH in obese and overweight patients increased using Sokolow-Lyon
voltage criteria and reduced using Cornell product criteria in patients with hypertension
based on cohort analysis of randomized trial
8,417 patients (mean age 67 years, 54% women) with hypertension randomized to losartan or atenolol with ECG available were
evaluated for LVH using Cornell voltage-duration product and Sokolow-Lyon voltage criteria
1,573 patients were obese (BMI > 31 kg/m2 for men and > 32.3 kg/m2 for women) and 2,519 patients were overweight (BMI 27.8-
31 kg/m2 for men and 27.3-32.3 kg/m2 for women)
prevalence of LVH
using Sokolow-Lyon voltage criteria > 38 mm
10.9% in obese patients (p < 0.001 compared to normal weight patients)
16.2% in overweight patients (p < 0.001 compared to normal weight patients)
31.4% for normal weight patients (reference)
using Cornell product criteria > 1,713 mm milliseconds in women and > 2,674 mm milliseconds in men
75.1% in obese patients (p < 0.001 compared to normal weight patients)
69.9% in overweight patients (p < 0.001 compared to normal weight patients)
60.7% (reference)
Reference - Hypertension 2000 Jan;35(1 Pt 1):13 full-text
DynaMed commentary – no gold standard applied to determine diagnosis of LVH so unable to distinguish between
underdiagnosis by Sokolow-Lyon criteria or overdiagnosis by Cornell criteria
make diagnosis of LVH in presence of left branch bundle block with caution due to conflicting evidence of diagnostic performance in this
setting(4)
diagnosing LVH in presence of intraventricular conduction disorders(4)
in setting of left anterior fascicular block
R-wave amplitudes in leads I and aVL are no longer reliable for diagnosing LVH due to shift in QRS vector (in posterior and
superior direction) that results in
larger R wave in leads I and aVL
smaller R wave but deeper S waves in leads V5 and V6
LVH diagnostic criteria that include S wave in left precordial leads improve LVH detection
in setting of left bundle branch block
diagnosis should not be attempted unless presence of all
left atrial P-wave abnormality
QRS duration > 155 milliseconds
precordial lead voltage criteria
in setting of right bundle branch block
amplitude of S wave reduced in right precordial leads
ECG criteria for LVH have poor performance for detecting LVH in presence of right bundle branch block (level 1 [likely reliable]
evidence)
based on 2 diagnostic cohort studies
100 patients (mean age 67 years) with right bundle branch block and technically satisfactory ECGs were evaluated for LVH using 36
standard diagnostic criteria
56% had LVH on echocardiography using Penn method and LV mass index > 132 g/m2 in men and 109 g/m2 in women
(reference standard)
diagnostic performance of ECG criteria with highest sensitivity
SIII plus (R+S) maximal precordial lead ≥ 30 mm had sensitivity 68% and specificity 66%
left axis deviation of -30 to -90 degrees had sensitivity 59% and specificity 71%
combination of left axis deviation and SIII plus (R+S) maximal precordial lead ≥ 30 mm had sensitivity 52% and specificity
84%
diagnostic performance of ECG criteria with specificity ≥ 90%
left axis deviation of -30 to -90 degrees with SV1 > 2 mm had sensitivity 34%
point-score system, RaVL > 12 mm, and RI + SIII > 25 mm each had sensitivity 27%
Reference - Am J Cardiol 1989 May 1;63(15):1080
62 adults aged 41-94 years with right bundle branch block were evaluated for LVH using ECG criteria
56% had LVH on echocardiography using Penn method and LV mass ≥ 215 g (reference standard)
ECG criteria with highest sensitivity
mean QRS axis ≤ -30 degrees had sensitivity 52%
excessive P terminal force had sensitivity 28%
ECG criteria with highest specificity
Sokolow index ≥ 35 mm had specificity 100%
RV5 or RV6 ≥ 25 mm had specificity 96.3%
RI plus SIII ≥ 25 mm had specificity 92.6%
intrinsicoid deflection ≥ 0.05 seconds had specificity 88.5%
Reference - Am J Cardiol 1988 Sep 15;62(9):590
Prognostic implication
electrocardiographically identified LVH and echocardiographically identified LVH each may independently indicate increased
risk for all-cause mortality in older men
based on retrospective population-based cohort study
475 men aged 70 years who had technically satisfactory echocardiographic exams included
median follow-up 5.2 years
44 patients died during follow-up (18 deaths from cardiovascular disease)
after adjustment for 9 cardiovascular risk factors, all-cause mortality increased in patients with LVH on
ECG when using
Sokolow-Lyon criteria QRS voltage ≥ 3.5 millivolts (mV) (adjusted hazard ratio [HR] 2.12, 95% CI 1.05-4.29)
Cornell criteria QRS voltage > 2.8 mV (adjusted HR 2.53, 95% CI 1.21-5.29)
Cornell product > 244 mcvolt seconds (adjusted HR 3.75, 95% CI 1.99-7.07)
echocardiography when using left ventricular mass index (LVMI) ≥ 150 g/m2 (adjusted HR 1.61, 95% CI 1.23-2.12)
after further adjustment for ECG and echocardiographic factors, increase in all-cause mortality remained significant in patients with
LVH on
ECG using Cornell product > 244 mcvolt seconds (adjusted HR 2.89, 95% CI 1.4-5.95)
echocardiography using LVMI (adjusted HR 1.44, 95% CI 1.09-1.91)
cardiovascular mortality varies based on criteria used for diagnosis of LVH
ECG using Cornell product > 244 mcvolt seconds associated with increased cardiovascular mortality (adjusted HR 3.41, 95% CI
1.17-9.92)
ECG using Sokolow-Lyon criteria QRS voltage ≥ 3.5 mV or Cornell criteria QRS voltage > 2.8 mV not associated with
cardiovascular mortality
Reference - Circulation 2001 May 15;103(19):2346 full-text
secondary ST-T abnormalities associated with increased cardiovascular mortality and events in hypertensive patients treated
with atenolol or losartan
based on cohort analysis of randomized trial
8,854 hypertensive patients with LVH on ECG who were randomized to treatment with atenolol vs. losartan analyzed
LVH on ECG diagnosed using Cornell voltage-duration product or Sokolow-Lyon voltage criteria
971 patients (11%) had secondary ST-T abnormalities (defined as downsloping convex ST segment with inverted asymmetrical T
wave opposite to QRS axis in leads V5 or V6)
1,035 patients (11.7%) reached composite endpoint of cardiovascular death or nonfatal myocardial infarction or stroke
after adjustment for treatment effect, secondary ST-T abnormalities associated with increased
composite outcome (adjusted hazard ratio [HR] 1.99, 95% CI 1.7-2.33)
cardiovascular death (adjusted HR 2.26, 95% CI 1.78-2.86)
fatal/nonfatal myocardial infarction (adjusted HR 2.16, 95% CI 1.67-2.8)
fatal/nonfatal stroke (adjusted HR 1.76, 95% CI 1.39-2.21)
after adjustment for standard cardiovascular risk factors, secondary ST-T abnormalities remained significantly associated with
increased composite outcome, cardiovascular mortality, and myocardial infarction
Reference - Hypertension 2004 Jul;44(1):48 full-text
decrease in Cornell product on ECG associated with reduced risk of hospitalization for new-onset heart failure in patients with
hypertension treated with atenolol or losartan
based on cohort analysis of randomized trial
8,479 hypertensive patients without history of heart failure randomized to losartan vs. atenolol were analyzed
214 patients (2.5%) were hospitalized for heart failure during mean follow-up of 4.7 years, of whom 77 patients had decrease in
Cornell product > 236 mm milliseconds
each 817 mm millisecond decrease in Cornell product on ECG associated with reduced risk of hospitalization for heart failure
(adjusted hazard ratio 0.81, 95% CI 0.77-0.85)
Reference - Ann Intern Med 2007 Sep 4;147(5):311
RVH difficult to detect on echocardiography due to complex 3-dimensional shape of RV and difficulty measuring thickness of RV free
wall(4)
ECG features associated with RVH may include(4)
displacement of QRS vector toward right and in anterior direction
delay in R wave peak in right precordial leads
American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) recommendations(4)
no single ECG criteria or limited set of ECG criteria recommended
adjust ECG criteria for age, gender, race, and body habitus
use ancillary clinical diagnoses (such as congenital heart disease, valvular heart disease, or chronic pulmonary disease) to adjust
probability estimates for RVH diagnosis
many ECG diagnostic criteria have been derived using(4)
amplitude of R and S in leads I, V1, and V6
R wave peak time in lead V1
sensitivity of diagnostic criteria usually low but some reported to have high specificity
diagnosing RV in presence of other conditions(4)
right axis deviation and prominent anterior forces in right precordial leads required for ECG diagnosis of RVH in all clinical
scenarios but is not specific to RVH due to other potential causes (such as normal variant)
ECG diagnostic criteria may be helpful in diagnosing RVH in setting of congenital heart disease, acquired heart disease, and primary
pulmonary hypertension in adults
in setting of congenital heart disease, ECG pattern in patients with RVH often classified on basis of contrasting ECG patterns
pattern similar to right bundle branch block suggests volume overload
pattern consisting of predominantly tall R wave (as part of Rs, R, or Qr complexes) in right precordial leads suggests
pressure overload
ECG diagnostic criteria reported to have poor performance in presence of chronic lung disease
in patients with chronic nonobstructive lung disease, ECG often shows right axis deviation and deep S wave in precordial leads
in patients with chronic obstructive lung disease
RVH suggested only if R-wave amplitude in V1 relatively decreased
ECG pattern often reflects mainly low diaphragm due to increased lung volume
ECG pattern includes
low voltage in limb leads
frontal plane QRS axis that is rightward, superior, and indeterminate
rightward P wave axis (> 60 degrees)
persistent S waves in all precordial leads
low R-wave amplitude in lead V6
Biventricular hypertrophy