Electrocardiogram (ECG)

Overview and Recommendations

Background

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.

Indications for use

Screening healthy individuals for cardiovascular disease

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).

Patients with suspected or at high risk of cardiovascular disease

Obtain a baseline ECG in patients who (Strong recommendation):

have suspected or at high risk of cardiac disease or dysfunction due to presence of symptoms, abnormal physical exam or laboratory
findings, or a family history consistent with increased risk of cardiovascular disease
may have used cocaine, amphetamines, or other illicit drugs known to have cardiac effects
may have received an overdose of drug known to have a cardiac effect
Obtain serial ECGs in patients (Strong recommendation):
with suspected cardiac disease who are taking cardioactive drugs (such as beta blockers in patients with palpitation, tremor, or
migraine headache)
taking any agent known to cause cardiac abnormalities or ECG abnormalities (such as antineoplastic drugs, lithium, tranquilizers,
anticonvulsant drugs, or antidepressant drugs)

Patients with known cardiovascular disease

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

Preoperatively in patients undergoing noncardiac surgery

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).

ECG monitoring in hospitalized patients

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

standard 12-lead ECG signal(3)

ECG records potential differences between prescribed sites on body surface that vary during cardiac cycle
potential differences reflect differences in transmembrane voltages in myocardial cells that occur during depolarization and
repolarization within each cardiac cycle
ECG signal magnitude is related to spatial factors (such as projected boundary of differences in potential relative to area of sphere of
unit size) and nonspatial factors (such as magnitude of transmembrane potential differences across boundary within heart)
automated processing of ECG occurs in a series of steps, including(3)
signal acquisition (including filtering)
data transformation or preparation of data for further processing (including finding complexes, classification of complexes into
dominant and nondominant ectopic types and formation of average or median complex for each lead)
waveform recognition (process for identifying onset ans offset of diagnostic waves)
feature extraction (measurement of amplitudes and intervals)
diagnostic classification (may be heuristic or statistical in approach)

Proper lead electrode placement

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

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

misplacement of precordial leads can result in

poor reproducibility of precordial ECG amplitude measurements(3)
diagnostic errors, including(2, 3)
distorted R-wave progression, which simulates anteroseptal infarction
magnification of otherwise small terminal R' deflections and elevation of ST segments in V1 and V2, which confuses criteria for
diagnosis of left ventricular hypertrophy
precordial leads commonly misplaced by healthcare providers
based on cross-sectional study
119 healthcare providers completed a questionnaire marking placement of precordial leads V1-V6 on chest wall positions in
two bony landmark diagrams (anterior and lateral view)
healthcare providers included 10 cardiac technicians, 37 nurses, 52 noncardiac physicians, and 20 cardiologists
correct placement of lead V1 was identified by 90% of technicians, 49% of nurses, 31% of noncardiologists, 16% of cardiologists
most healthcare providers also misplaced leads V2-V6
Reference - Int J Clin Pract 2008 Jan;62(1):65, editorial can be found in Int J Clin Pract 2008 Jan;62(1):8
switching or transposition of limb or precordial leads(3)
switching left and right arm lead wires results in
inversion of limb lead I
switch of leads II and II
switch of leads aVR and aVL
no change in aVF
switching of right arm and right leg lead wires results in
very low amplitude in only lead II
inverted symmetry between standard lead I and lead III
switching of left arm and left leg lead wires difficult to recognize and results in subtle shift in axis and inversion of lead III
switching of lead wires to V1 and V2, to V2 and V3, or within all 3 leads results in reversal of R-wave progression that stimulates
anteroseptal wall infarction, but this error can be recognized by distorted progression of precordial P waves and T waves in same
leads
 use of standard interval durations (such as QT interval and QRS duration) derived from single-channel lead recordings instead of those
derived from newer digital electrocardiography(2)

Indications for Use

Screening healthy individuals for cardiovascular disease

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

In patients with known cardiovascular disease

American College of Cardiology/American Heart Association (ACC/AHA) recommendations

baseline or initial evaluation indicated in patients with known cardiovascular disease or dysfunction (ACC/AHA Class I)
serial ECG to evaluate response to therapy
indicated if (ACC/AHA Class I)
prescribed therapy known to produce ECG changes that correlate with therapeutic responses or progression of disease
therapy may produce adverse effects that may be predicted from or detected by ECG changes
serial ECG typically indicated until disease process and ECG response to therapy have stabilized
not indicated in patients receiving pharmacologic or nonpharmacologic therapy not known to produce ECG changes or to effect
conditions that may be associated with ECG changes (ACC/AHA Class III)
follow-up ECG
indicated in patients with (ACC/AHA Class I)
change in symptoms, signs, or relevant lab findings
implanted pacemaker or antitachycardia device
 preceding conditions (even in absence of new symptoms or signs) after interval of time appropriate for condition or
disease
not indicated in adults with (ACC/AHA Class III)
cardiovascular condition that are usually benign and unlikely to progress, such as patients with
asymptomatic mild mitral valve prolapse
minimal-to-mild arterial hypertension
premature contraction in absence of organic heart disease
chronic stable heart disease who are seen at frequent intervals (< 4 months) and who have new or unexplained
symptoms, physical exam, or lab findings, such as patients with
systemic arterial hypertension
chronic coronary artery disease
valvular heart disease
cardiomyopathy
lone atrial fibrillation
ECG before surgery
indicated in most patients with known cardiovascular disease or dysfunction (ACC/AHA Class I)
suggested in patients with (ACC/AHA Class II)
hemodynamically insignificant congenital or acquired heart disease
minimal-to-mild systemic arterial hypertension
infrequent premature complexes in absence of organic heart disease
Reference - Circulation 1992 Mar;85(3):1221

In patients with suspected or at high risk of cardiovascular disease

American College of Cardiology/American Heart Association (ACC/AHA) recommendations

baseline or initial evaluation indicated in patients who (ACC/AHA Class I)
have suspected or at high risk of cardiac disease or dysfunction due to presence of symptoms, abnormal physical exam or lab
findings, or family history consistent with increased risk of cardiovascular disease
may have used cocaine, amphetamines, or other illicit drugs known to have cardiac effects
may have received an overdose of drug known to have cardiac effect
serial ECG to evaluate response to therapy
indicated in patients (ACC/AHA Class I)
with suspected cardiac disease who are taking cardioactive drugs (such as beta blockers in patients with palpitation,
tremor, or migraine headache)
taking any agent known to cause cardiac abnormalities or ECG abnormalities (such as antineoplastic drugs, lithium,
tranquilizers, anticonvulsant drugs, or antidepressant drugs)
suggested in patients taking (ACC/AHA Class II)
any agent known to alter serum electrolyte concentrations (such as diuretic drugs in patients with hypertension)
agents that may alter potassium or magnesium concentration into or near an abnormal range
not indicated in patients taking agents not known to influence cardiac structure or function (ACC/AHA Class III)
follow-up ECG
indicated if (ACC/AHA Class I)
any changes in clinical status or lab findings suggest interval development of cardiac disease or dysfunction
increased risk for cardiac disease (ECG every 1-5 years in adults or more frequent in children < 2 years old)
patient followed for resolution of chest pain
ECG more than annually not indicated in patients who (ACC/AHA Class III)
remain clinically stable
are not at increased risk for cardiac disease
had no evidence of cardiac disease with previous disease
Reference - Circulation 1992 Mar;85(3):1221
review of cardiac effects of anticancer therapy in elderly patients can be found in J Clin Oncol 2014 Aug 20;32(24):2654
see Acquired long QT syndrome for medications known to prolong QT interval

Preoperative resting ECG in patients having noncardiac surgery

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

ECG monitoring in hospital setting

American Heart Association (AHA) recommendations for cardiac arrhythmia monitoring
monitoring indicated in most (if not all) patients at significant risk of immediate, life-threatening arrhythmia, including patients with
(AHA Class I)
previous resuscitation from cardiac arrest
early phase of ST-elevation myocardial infarction (STEMI) or acute coronary syndromes
unstable coronary syndromes and newly diagnosed high-risk coronary lesion
cardiac surgery (adults and children)
nonurgent percutaneous coronary intervention (PCI) with complications
implantation of defibrillator lead or pacemaker lead who are pacemaker dependent
temporary pacemaker or transcutaneous pacing pads
certain atrioventricular (AV) conduction disorders (such as Mobitz type II block, advanced second-degree block, or complete
block)
new onset bundle branch block in setting of acute (especially anterior) myocardial infarction
arrhythmias complicating Wolff-Parkinson-White syndrome with rapid anterograde conduction over accessory pathway
long QT syndrome and associated ventricular arrhythmias
intraaortic balloon pump (IABP) counterpulsation
acute heart failure/pulmonary edema
indication for intensive care
diagnostic/therapeutic procedures requiring conscious sedation or anesthesia
hemodynamically unstable arrhythmia
diagnosed with arrhythmia and are pediatric patients
indications for monitoring for QT prolongation
administration of antiarrhythmic medication known to cause QT prolongation with torasades de pointes
QTc monitoring recommended for patients with or without risk factors for torsades de pointes who are started on
anitarrhythmic drugs with known risk for torsades de pointes, including
dofetilide (AHA Class I, Level B)
ibutilide (AHA Class I, Level C)
sotalol (AHA Class I, Level C)
disopyramide (AHA Class I, Level C)
procainamide (AHA Class I, Level C)
quinidine (AHA Class I, Level C)
document QTc, including rhythm strip, at baseline and every 8-12 hours or more frequently if QTc prolongation occurs
during administration of drug
when increasing doses of drug
document QTc before and after increases in dose of QT-prolonging drugs
continue QTc monitoring for 48-72 hours when initiating or increasing dose of disopyramide, proacainamide,
quinidine, and sotalol
factors determining duration of QTc monitoring include
QTc return to baseline
drug half-life
time to drug elimination depending on hepatic or renal function
presence of QT-related arrhythmias
administration of antiarrhythmic medication with possible risk for torsades de pointes
QTc monitoring may be reasonable for patients with or without risk factors for torsades de pointes who are started on
antiarrhythmic drugs with possible risk for torsades de pointes, including
amiodarone (AHA Class IIb, Level C)
dronedarone (AHA Class IIb, Level C)
flecainide (AHA Class IIb, Level C)
administration of nonantiarrhythmic medication with known or possible risk for torsades de pointes
QTc monitoring recommended for patients with history of prolonged QTc or with general risk factors for torsades de
pointes who are started on nonantiarrhythmic drugs with known risk for torsades de pointes (AHA Class I, Level C) and
document QTc, including rhythm strip, at baseline and every 8-12 hours or more frequently if QTc prolongation occurs
during administration of drug
QTc monitoring reasonable for patients with history of prolonged QTc or with general risk factors for torsades de pointes
who are started on nonantiarrhythmic drugs with possible or conditional risk for torsades de pointes (AHA Class IIa, Level
C)
QTc monitoring not recommended for patients without history of prolonged QTc or without general risk factors for
torsades de pointes who are started on nonantiarrhythmic drugs with known, possible, or conditional risk for torsades de
pointes (AHA Class III, Level C)
additional indications for QTc monitoring not related to administration of medications associated with risk of torsades de
pointes
targeted temperature management
QTc monitoring recommended in patients undergoing targeted temperature management until (AHA Class I, Level C)
temperature normalizes
QTc interval in normal range
no evidence of QT-related arrhythmias
document QTc, including rhythm strip, at baseline and every 8-12 hours or more frequently if QTc prolongation
occurs during administration of drug
congenital long QT syndrome
QTc monitoring recommended in patients with congenital long QT syndrome who present with unstable ventricular
arrhythmias or medically- or metabolically-induced prolonged QT until (AHA Class I, Level C)
ventricular arrhythmia stabilizes
exacerbating medical or metabolic condition reverses
QTc interval returns to baseline
document QTc, including rhythm strip, at baseline and every 8-12 hours or more frequently if QTc prolongation
occurs during administration of drug
electrolyte disorders
 QTc monitoring recommended in patients with moderate to severe hypokalemia or hypomagnesemia in combination
with other risk factors for torsades de pointes until (AHA Class I, Level C)
electrolytes normalize
no evidence of QT-related arrhythmias
document QTc, including rhythm strip, at baseline and every 8-12 hours or more frequently if QTc prolongation
occurs during administration of drug
drug overdose
QTc monitoring recommended in patients with overdose of drug with known risk of torsades de pointes or overdose
with unknown drug until (AHA Class I, Level C)
QT-prolonging drug levels decrease
unknown drug identified as non-QT-prolonging
QTc interval in normal range
no evidence of QT-related arrhythmias
document QTc, including rhythm strip, at baseline and every 8-12 hours or more frequently if QTc prolongation
occurs during administration of drug
QT monitoring not recommended for patients with acute neurological events and no baseline QTc prolongation (AHA Class
III, Level C)
QTc monitoring in patients who develop QT prolongation
if QTc > 500 milliseconds develops, discontinue causative drug and continue QTc monitoring until drug washes out and
QTc decrease documented
if QTc prolonged but not ≥ 500 milliseconds, decision to hold drug depends on drug (may not need to hold amiodarone or
dronedarone) and expert consult may be needed
Reference - Circulation 2017 Nov 7;136(19):e273, see also Acquired long QT syndrome
monitoring may be beneficial in patients with (AHA Class II)
postacute myocardial infarction (within 24-48 hours)
chest pain syndromes
uncomplicated nonurgent percutaneous coronary interventions (PCI)
administration of antiarrhythmic drug or adjustment of drugs for rate control with chronic atrial tachyarrhythmias (Class I
indication if drug with known high risk of proarrhythmia - see monitoring for QT prolongation above for details)
implantation of pacemaker lead who are not pacemaker dependent
uncomplicated ablation of arrhythmia
routine coronary angiography
subacute heart failure
syncope
arrhythmias that cause discomfort who have do not resuscitate order - goal is to titrate antiarrhythmic drug dose for optimum
rate control instead of prevent sudden cardiac death
monitoring not indicated in patients at low-risk for cardiac arrhythmias, including patients (AHA Class III)
without heart disease who are
young and having uncomplicated procedures
obstetric patients
without permanent, rate-controlled atrial fibrillation
having hemodialysis
Reference - Circulation 2004 Oct 26;110(17):2721 full-text
ST-segment ischemia monitoring
monitor indicated in most (if not all) patients with (AHA Class I)
early phase of ST-elevation myocardial infarction (STEMI) or acute coronary syndromes
chest pain or anginal equivalent symptoms
nonurgent percutaneous coronary intervention (PCI) with suboptimal angiographic results
possible variant angina resulting from coronary vasospasm
monitoring may be beneficial in patients with (AHA Class II)
postacute myocardial infarction
nonurgent uncomplicated percutaneous coronary intervention (PCI)
high risk for ischemia after cardiac or noncardiac surgery
risk of ischemia or infarction resulting from congenital or acquired conditions in pediatric patients
monitoring not indicated in patients with (AHA Class III)
left bundle branch block
ventricular pacing rhythm
confounding arrhythmias that obscure ST segment
agitated behavior
Reference - Circulation 2004 Oct 26;110(17):2721 full-text

Standard ECG Features

General 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

Normal ECG waveform: A normal PQRST complex.

 Normal ECG: Sinus rhythm, normal intervals, normal QRS axis, no ST segment or T-wave abnormalities.

Abnormalities in ECG features

Ventricular repolarization abnormalities

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

ST elevation may reflect PR/TP depressions, true ST elevation, or combination of both(1)

when ST-segment deviation present, pay attention to QRS amplitude due to its effect on amplitude of ST-segment abnormalities(1)
displacement of ST segment usually measured at junction with end of QRS complex (J point) or 40-80 milliseconds after J point in some
cases (such as exercise testing)(1)
elevated ST segment can be described as upsloping, horizontal, or downsloping(1)
depressed ST segment may be further characterized as horizontal, downsloping, or upsloping (rapidly or slowly)(1)
ST-segment elevation(1)
in leads V1-V3
reference against elevation that usually occurs
elevation greater in
young and middle-aged men than women
black patients than white patients
in V2
elevation usually most pronounced
upper limit for J point elevation varies and depends on sex and race
important in setting of acute myocardial ischemia/infarction
threshold for abnormal J point elevation in leads V2 and V3
0.2 millivolts (mV) in men ≥ 40 years old
0.25 mV in men < 40 years old
0.15 mV in adult women
threshold for abnormal J point elevation in leads V1 and V4-V6 0.1 mV in men and women
when evaluating ST elevation, consider ST-segment waveform
ST segment in normal J point elevation in leads V1 and V2 generally sloping down steeply
normal ST elevation at 60 milliseconds past J point combined with upsloping ST segment (instead of horizontal ST segment
present in myocardial ischemia)
most common causes of ST elevation include
normal variant (referred to as early repolarization) commonly characterized by J point elevation and rapidly upsloping or
normal ST segment
injury currents (defined as flow of current across boundary between ischemic and nonischemic zones) associated with acute
ischemia or ventricular dyskinesis
injury currents associated with pericarditis
ST depression(1)
may be caused by various physiological, pathological, and pharmacological intervention that change plateau phase of ventricular
action potential (such as effects of ischemia, hypokalemia, and cardiac and noncardiac drugs)
may occur with T-wave changes (such as in setting of ST-segment depression associated with hypertrophy and secondary
repolarization abnormalities in ventricular conduction disturbances)

T-wave abnormalities

can occur with or without ST-segment abnormalities(1)

amplitude in limb leads influenced by frontal-plane T-axis, which is influenced by QRS axis(1)
in children > 1 month old, T wave often inverted in leads V1-V3(1)
in adolescents ≥ 12 years old and young adults < 20 years old, T wave may be slightly inverted in lead aVF and inverted in lead V2(1)
normal T-wave appearance on ECG in adults ≥ 20 years old(1)
inverted in lead aVR
upright or inverted in leads aVL, III, and V1
upright in leads I, II, and V3-V6
T-wave negativity in leads V5 and V6(1)
T wave slightly negative (< 0.1 mV) in 2% of white men and white women ≥ 60 years old, black men and black women ≥ 40 years old
T wave negative by ≥ 0.1 mV in 5% of black men and women ≥ 60 years old
 in normal adults, T-wave amplitude(1)
varies slightly based on age, gender, and race
most positive in lead V2 or V3
in lead V2 ranges from 1 to 1.4 mV in men and 0.7 to 1 mV in women
T-wave abnormalities may be qualitatively described as peaked, symmetrical, biphasic, flat, or inverted(1)
quantitative T-wave abnormalities(1)
T wave is inverted if amplitude ranges -1 mV to -0.5 mV in leads I, II, aVL, and V2-V6
T wave is deeply negative if amplitude < -1 mV
T wave is low if amplitude < 10% of R-wave amplitude in same lead
T wave is flat if peak T-wave amplitude ranges 0.1 to -0.1 mV in leads I, II, aVL (with R wave taller than 0.3 mV), and V4-V6
T-wave changes associated with hypertrophic, hypokalemia, and drugs can be attributed to secondary abnormalities in ventricular
conduction(1)
giant T-wave inversion usually due to hypertrophic cardiomyopathies, non-ST-elevation myocardial infarctions, or neurological events
(particularly intracranial hemorrhage)(1)
describe minor T-wave abnormalities as slight or indeterminate T-wave abnormality (determining cause of these abnormalities nearly
impossible and may be aided by comparison with prior ECG)(1)
notching of T wave(1)
rarely found in all 12 leads
interval between 2 summits of notched T wave usually less than interval between peak of monophasic T wave and U wave (usually >
150 milliseconds at heart rates of 50-100 beats/minute)
difficult to discriminate from superimposed U wave on downslope of upright T wave
T-wave alternans (defined as T-wave amplitude variations that alternate every second beat)(1)
usually not present at rest and requires special equipment and analysis software
presence indicates latent instability of repolarization predictive of malignant arrhythmias but clinical utility not fully defined (can
potentially identify patients at high risk of serious arrhythmic events)
usually observed as microvolt-level variation and most prominent in phase with respiration

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

indicate anatomic or physiological abnormalities in right or left atrium(4)

terms right or left atrial abnormality preferred over enlargement, overload, strain, or hypertrophy(4)
may be caused by any(4)
atrial dilation
atrial muscular hypertrophy
elevated atrial pressure
impaired ventricular distensibility
delayed intraatrial conduction
P-wave abnormalities may be due to combination of causes, which may not be distinguishable from each other(4)
recognition of P-wave abnormalities should include multiple ECG criteria(4)
intraatrial conduction delay should be recognized as category of atrial abnormality (particularly if P wave widening not accompanied by
increased amplitude of right or left atrial components)(4)
left atrial abnormality(4)
usually involves prolongation of total atrial activation time (due to left atrial activation beginning and ending later than right atrial
activation)
delay in left atrial activation tends to cause double-peaked or notched P wave (due to right and left atrial peaks becoming more
widely separated)
activation of left atrium more leftward and posterior than right atrium activation
ECG criteria for diagnosing left atrial abnormality
usually includes product of amplitude and duration of terminal negative component of P wave in lead V1 (P terminal force)
other features that may have value include
P-wave duration (≥ 120 milliseconds)
widely notched P wave (≥ 40 milliseconds)
left axis of terminal P wave (-30 to -90 degrees)
P-wave area
purely negative P wave in lead V1 suggests left atrial abnormality but can occur without increased P terminal force
right atrial abnormality(4)
typically manifests as increase in P-wave amplitude and rightward shift of P-wave vector
other ECG characteristics indicating right atrial abnormality include
tall upright P wave in lead II (> 0.25 millivolts) often with peaked or pointed appearance (may be due to summation of
enhanced right atrial component with simultaneous left atrial component)
prominent initial positivity in P wave in leads V1 or V2 (≥ 0.15 millivolts)
increased amplitude of initial P-wave forces
supportive ECG characteristics include
rightward axis of P wave
peaked form of P wave without increased amplitude
total P-wave duration typically normal except in patients with surgically repaired congenital heart disease (especially if single-
ventricle physiology) who may have significant P-wave prolongation, which may be risk factor for atrial tachyarrhythmia
combined atrial abnormality indicated by presence of some ECG features of both left and right atrial abnormality, but little evidence on
diagnostic performance of ECG criteria for diagnosing combined atrial abnormality(4)
QT interval prolongation

may be associated with increased risk of lethal ventricular arrhythmia(1)

may be due to(1)
acquired causes (such as QT-prolonging cardioactive drugs, hypokalemia, or hypocalcemia)
inherited causes (such as genetic mutations)
if identified on computer algorithm, validate visually(1)

Recommendations for reporting ECG 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)

ECG Characteristics by Condition

Electrical abnormalities and arrhythmias

Intraventricular conduction disorders

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

Atrioventricular (AV) conduction disorders

ECG findings by type of AV block

first-degree AV block (also called AV conduction delay)
abnormal prolongation of PR interval (> 200 milliseconds)
every P wave followed by QRS complex
First-degree AV block: sinus: Rhythm, first-degree AV block, PR interval 320 milliseconds, Morphology: narrow QRS, normal
axis, probable left ventricular hypertrophy, ST-segment depressions in II, aVF, V4-6.
First-degree AV block: sinus: Rhythm with first-degree AV block, PR interval 300 milliseconds, Morphology: narrow QRS, normal
axis.
 First-degree AV block, left anterior hemi block, right bundle branch block: Sinus rhythm, first-degree AV block, PR interval 300
milliseconds, QRS Axis: -79 Morphology: left anterior hemi block, right bundle branch block, T wave inversion in I, aVL, V5-6.

type I second-degree AV block

if Wenckebach - generally progressive (may be small) prolongation of PR interval followed by blocked P wave and resuming
with shortened PR interval while P-to-P interval remains constant
if 2:1 type - AV conduction ration 2:1 with constant PR interval
decremental conduction is not diagnostic of AV nodal block
 Mobitz type 1 second-degree AV block: Sinus rhythm, progressive PR prolongation followed by blocked P wave in a 4:3 pattern,
consistent with second-degree AV block type I. There is normal QRS duration and axis.

type II (Mobitz II) second-degree AV block in His bundle or His-Purkinje system

type II second-degree AV block
Wenckebach - generally progressive (may be small) prolongation of PR interval followed by blocked P wave and resuming with
shortened PR interval while P-to-P interval remains constant
2:1 type - AV conduction ratio > 2:1 with constant PR interval
sinus rate must usually be constant during ECG
block in His-Purkinje system can be tachycardia dependent with diagnosis made in setting of increased heart rate
block always infranodal

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.

advanced second-degree AV block

≥ 2 consecutive P-wave blocks
impossible to observe PR prolongation before block and cannot be described as type I or type II
conduction ratio can be
3:1 (2 consecutively blocked P waves)
4:1 (3 consecutively blocked P waves)
third-degree AV block
absence of AV conduction
atrial and ventricular activity completely dissociated (AV dissociation)
atrial rate > ventricular rate

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

diagnosis of preexcitation based on clinical findings and ECG with findings of

short PR interval
delta wave - initial slurry of QRS
wide QRS complex
 Wolff-Parkinson-White syndrome: Sinus rhythm with evident ventricular preexcitation via a left lateral bypass tract.

Preexcitation (Wolff-Parkinson-White pattern): Sinus rhythm with evident ventricular preexcitation via a posteroseptal bypass tract.

see Cardiac bypass tracts for details and additional information

Tachyarrhythmias

Atrial fibrillation

atrial fibrillation diagnosed based on ECG findings of

rapid oscillatory ('fibrillatory') baseline waves varying in amplitude, shape, and timing
absence of P waves
irregularly irregular ventricular responses
Atrial fibrillation: Rhythm: atrial fibrillation, Morphology: left bundle branch block.
Atrial fibrillation: Rhythm: atrial fibrillation, Morphology: narrow QRS, ST segment: nonspecific ST/T changes.
Atrial fibrillation: Rhythm: atrial fibrillation with rapid ventricular response; otherwise, normal intervals, normal QRS axis.

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.

see Atrial fibrillation for additional information

European Society of Cardiology (ESC) definition of atrial fibrillation
surface ECG shows absolutely irregular RR intervals
no distinct P waves on surface ECG, but some apparently regular atrial electrical activity may be seen in some leads, most often V1
see Atrial fibrillation for details and additional information

Atrial flutter

ECG findings by type of atrial flutter

typical atrial flutter
class saw-tooth flutter waves on inferior leads II, III, and aVF
atrial rates 240-300 beats/minute with variable block but often 2:1
low-amplitude biphasic F waves on leads I and aVL
upright F wave on precordial lead V1
inverted F wave on lead V6
atypical atrial flutter ECG findings are diverse
see Atrial flutter for details and additional information

Supraventricular tachycardia (SVT)

SVT diagnosed with tachycardia on ECG during acute episode of either

narrow QRS complex (< 120 milliseconds)
wide QRS complex (≥ 120 milliseconds) due to presence of either
bundle branch block
atrioventricular conduction over an accessory pathway
see Supraventricular tachycardia (SVT) for additional information
ECG findings by type of SVT
typical atrioventricular nodal reentrant tachycardia (AVNRT) findings
P wave buried in QRS complex
pseudo RSR' pattern in lead V1 often evidence of P wave absence
short RP tachycardia characterized by shorter RP interval than PR interval
adenosine usually terminates tachycardia
Atrial flutter: Typical counterclockwise atrial flutter with 2:1 ventricular conduction.
Atrial flutter: Atrial flutter with atypical features (cycle length < 200 milliseconds) and 5:1 ventricular response. There is
intermittent RBBB-type aberration. Abbreviation: RBBB, right bundle branch block.
Atrial flutter: Typical counterclockwise atrial flutter with 3:1 ventricular response and underlying RBBB. Abbreviation: RBBB,
right bundle branch block.
Atrial flutter: Probable clockwise atrial flutter with 6:1 ventricular response and underlying LBBB-type IVCD. Abbreviations:
IVCD, intraventricular conduction delay; LBBB, left bundle branch block.
 Atrial flutter: Probable atrial tachycardia with 1:1 ventricular response. Underlying LVH and ST-segment T-wave abnormalities.
Abbreviation: LVH, left ventricular hypertrophy.

atypical AVNRT findings

inverted P wave typically in middle or late in RR interval
long RP tachycardia characterized by longer RP interval than PR interval
atrioventricular reentrant tachycardia (AVRT) findings
short RP interval common but long RP can occur
adenosine usually terminates tachycardia
 orthodromic AVRT shows narrow QRS complex (< 120 milliseconds)
antidromic AVRT shows wide QRS complex (≥ 120 milliseconds) and delta wave in sinus rhythm
atrial tachycardia findings
RP interval often long
adenosine usually does not terminate tachycardia but may in case of a triggered atrial tachycardia
in multifocal atrial tachycardia ≥ 3 P-wave morphologies present
in focal atrial tachycardia
regular, well-defined P waves
rate can be close to sinus rhythm (100 beats/minute) or very high (≥ 200 beats/minute)
atrioventricular conduction not constant during tachycardia
if mechanism for tachycardia is abnormal automaticity, rate accelerates at beginning of tachycardia and decelerates
before spontaneous termination
sinus tachycardia
sinus rate > 100 beats/minute
upright P wave in leads I, II, and aVF
biphasic P wave in lead V1
see Supraventricular tachycardia (SVT) for details and additional information

Ventricular arrhythmias

ventricular arrhythmias (ventricular tachycardia [VT] and ventricular fibrillation [VF])

classification of ventricular arrhythmias
VT diagnosed based on ECG findings of ≥ 3 beats of wide QRS at rate > 100 beats/minute
types of VT
nonsustained VT
≥ 3 beats in duration terminating spontaneously in < 30 seconds
can be monomorphic (single QRS morphology) or polymorphic (changing QRS morphology at cycle length
between 180 and 600 milliseconds)
sustained VT
lasts > 30 seconds in duration or requires termination due to hemodynamic compromise in < 30 seconds
can be monomorphic (stable single QRS morphology) or polymorphic (changing or multiform QRS morphology
at cycle length between 180 and 600 milliseconds)
bidirectional VT (often associated with digitalis toxicity) shows beat-to-beat alternans in QRS frontal plane axis on
ECG
VF diagnosed based on ECG findings of
rapid heart rate (usually ≥ 300 beats/minute)
cycle length ≤ 180 milliseconds
grossly irregular rhythm with significant variability in QRS cycle length, morphology, and amplitude
ventricular flutter diagnosed based on ECG findings of
heart rate 300 beats/minute
regular arrhythmia (cycle length variability ≤ 30 milliseconds)
cycle length 200 milliseconds
monomorphic appearance
no isoelectric interval between successive QRS complexes
Reference - J Am Coll Cardiol 2006 Sep 5;48(5):e247 full-text

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.

idiopathic VT (VT in patients without overt structural heart disease)

most commonly originates from right ventricular or left ventricular outflow tracts (RVOT or LVOT)
other sites of origin include aortic sinuses of Valsalva, great cardiac veins, epicardial myocardium, aorta-mitral continuity, and
rarely pulmonary artery
ECG findings based on origin of tachycardia
outflow tract VT
ECG during sinus rhythm usually normal
episodes increase in frequency and duration during exercise and/or emotional stress
RVOT
left bundle branch block and inferior axis morphology
later R/S transition at lead V4 compares to LVOT
LVOT
inferior axis
early transition at leads V1/V2
LBBB pattern reported in 70% and RBBB reported in 30%
if VT arises from sinuses of Valsalva, broad QRS with early transition at leads V1-V2
if VT arises from pulmonary arteries (rare), LBBB with tall R waves in inferior leads and transition in V4/V5 usually
present
left ventricular VT
left posterior fascicular VT (most common)
right bundle branch block (RBBB) morphology
superior axis
narrow QRS complex
left anterior fascicular VT
RBBB morphology
right axis deviation
left anterior fascicular VT (rare)
narrow QRS complex
normal axis or right axis deviation
if VT arises from left posterior papillary muscle
RBBB morphology usually present
right or left superior QRS axis
QRS duration > 150 milliseconds
if VT arises from mitral annulus
QRS complex usually present with RBBB pattern
persistent S wave in leave V6
precordial R-wave transition in lead V1 (or between leads V1 and V2 in some cases)
if VT arises from tricuspid annulus, LBBB morphology and left axis deviation usually present
idiopathic VF is diagnosis of exclusion
ventricular arrhythmias associated with acute coronary syndromes
acute ischemia causes electrical instability and provokes ventricular arrhythmias, including
recurrent sustained VT that is usually polymorphic or recurrent ventricular fibrillation (VF)
recurrent VT or VF triggered by premature ventricular complexes (PVCs) arising from partially inured Purkinje fibres
PVCs and nonsustained VT
ventricular arrhythmias associated with cardiomyopathy
high PVC burden (> 24%) in patients with LV dysfunction and short coupling interval of PVC (< 300 milliseconds) suggests PVC-
induced cardiomyopathy
bundle branch tachycardia (rare) often associated with cardiomyopathy and shows LBBB morphology with left axis deviation
on ECG
VT in patients with arrhythmogenic right ventricular dysplasia
ventricular arrhythmia usually originates from RV with ECG showing
LBBB morphology
QRS axis may be different from that seen in RVOT
multiple QRS morphologies
Reference - Europace 2015 Nov;17(11):1601 full-text

Structural abnormalities

Coronary artery disease (CAD)

resting ECG findings that favor diagnosis of CAD include

evidence of left ventricular hypertrophy (LVH)
ST-T wave changes consistent with ischemia
evidence of previous Q wave myocardial infarction (MI)
conduction/rhythm disturbances
 Inverted T waves: Profound sinus bradycardia and sinus arrhythmia, with prolonged but varying PR interval likely due to changing
autonomic tone. Normal QRS, QT intervals, normal QRS axis. Low limb-lead QRS voltage. There are downsloping ST segments and T
wave inversions in leads I, II, III, aVF, V3, consistent with underlying myocardial ischemia.

see Coronary artery disease (CAD) for details and additional information

Acute coronary syndromes

ECG findings diagnostic of ST-elevation myocardial infarction (STEMI) include

ST elevation in absence of left ventricular hypertrophy (LVH) or left bundle branch block (LBBB)
new ST elevation at J point in ≥ 2 contiguous leads
in leads V2-V3 ≥ 2.5 mm (0.25 millivolts [mV]) in men < 40 years old, ≥ 2 mm (0.2 mV) in men > 40 years old, or 1.5 mm (0.15 mV)
in women
≥ 1 mm (0.1 mV) in other contiguous chest leads or limb leads
new or presumably new LBBB considered a STEMI equivalent, but most cases of LBBB at time of presentation are not known to be
old or new, ECG criteria for diagnosis of STEMI in setting of LBBB include any of
ST elevation ≥ 1 mm (0.1 mV) and concordant with QRS complex
ST depression ≥ 1 mm (0.1 mV) in V1, V2, or V3
ST elevation ≥ 5 mm (0.5 mV) and discordant with QRS complex
ST depression in ≥ 2 precordial leads (V1-V4) may indicate transmural posterior injury, additional posterior chest leads (V7-V9) with
ST elevation > 0.5 mm (0.05 mV) (or > 1 mm [0.1 mV] in men < 40 years old) is consistent with posterior myocardial infarction
see ST-elevation myocardial infarction (STEMI) for details and additional information
non-STEMI and unstable angina include
diagnostic ECG findings include
ST-segment depression
prominent T-wave inversion
absence of ST-segment elevation
suggestive ECG findings include
transient ST changes (≥ 0.5 mm [0.05 mV]) during symptoms at rest - suggestive of ischemia/underlying coronary artery disease
ST depression - suggestive of non-ST-elevation acute coronary syndrome
symmetrical precordial T-wave inversion (≥ 2 mm [0.2 mV]) - suggestive of acute ischemia, acute pulmonary embolism, or right-
sides ST-T changes
nonspecific ECG findings include
ST deviation < 0.5 mm (0.05 mV)
T-wave inversion < 2 mm (0.2 mV)
significant Q waves
isolated Q waves in lead III
see Acute coronary syndromes for details and additional information

Cardiomyopathies

hypertrophic cardiomyopathy ECG findings

12-lead ECG abnormal in 75%-95% of patients with hypertrophic cardiomyopathy, but abnormalities do not correlate with severity of
hypertrophy
atrial fibrillation is most common arrhythmia and occurs in about 20% of patients
see Hypertrophic cardiomyopathy for details and additional information
 Hypertrophic cardiomyopathy electrocardiogram: Sinus rhythm with normal intervals and normal QRS axis. There is underlying
LVH and nonspecific T-wave inversions. Abbreviation: LVH, left ventricular hypertrophy.

signs of dilated cardiomyopathy on ECG may include

atrioventricular (AV) block
accompanied by severe ventricular dilation, may suggest laminopathy, Emery-Dreifuss 1, myocarditis, sarcoidosis,
desminopathy, or myotonic dystrophy cause
accompanied by mild dilation, may suggest acute/subacute inflammation due to Lyme disease, giant cell myocarditis, or
sarcoidosis
supraventricular tachycardia (SVT)
ST-T wave changes
ventricular preexcitation pattern (may suggest storage disease or mitochondrial disorder cause)
low P-wave amplitude (may suggest Emery-Dreifuss 1 or 2 cause)
ventricular arrhythmias
postero-lateral infarction pattern (may suggest dystrophin-related cardiomyopathy, limb-girdle muscular dystrophy, or sarcoidosis
cause)
Goldberger triad
pseudo-infarction pattern in precordial chest leads
reduced voltage in limb leads
deep S waves in right precordial leads
very high QRS voltage (may suggest storage disease or preexcitation cause)
low QRS voltage may suggest amyloidosis (Eur Heart J 2013 May;34(19):1448 full-text)
low QRS voltage and atypical right bundle branch block (may suggest arrhythmogenic right ventricular dysplasia with biventricular
involvement)
very low QRS amplitude (may suggest very rare phospholamban mutation)
see Dilated cardiomyopathy for details and additional information
reported ECG changes in Takotsubo cardiomyopathy include
ST segment change mimicking acute anterior ST-elevation myocardial infraction (STEMI) reported in 11%-100%
shift is usually less pronounced than STEMI
ST depression reported in 5%-23%
ST segment changes often normalizes in subacute phase - by 1-2 days
T-wave inversion reported in 17%-100% (may be associated with poor prognosis) - may last 1-4 months
peaked T waves reported in 86%
long QTc interval reported in 50%-100%
pathological Q waves in 20%-63% - may be observed in chronic phase, resolves faster than with cardiac ischemia
reduction in R-wave progression in 7%-32%
most changes resolve in 3 weeks to 1 year
see Takotsubo cardiomyopathy for details and additional information
ECG findings suggestive of restrictive cardiomyopathy may include
nonspecific ST segment and T wave changes
depolarization abnormalities, such as
bundle branch block
ventricular hypertrophy
pathological Q waves
impaired atrioventricular conduction
see Restrictive cardiomyopathy for details and additional information
peripartum cardiomyopathy is diagnosis of exclusion (see Peripartum cardiomyopathy for details and additional information)

Channelopathies

congenital long QT syndrome

diagnosed based on heart rate-corrected QT interval (QTc) > 0.46 in females and > 0.45 seconds in males
 Prolonged QT: Sinus rhythm with normal PR and QRS intervals, normal QRS axis. There is significant QT interval prolongation.

morphology of T wave useful for diagnosis

precordial leads may show biphasic or notched T waves
T-wave alternans
in polarity or amplitude is diagnostic
is major marker of electrical instability and identifies patients at high risk
presence in patients being treated should alert clinician to persistent high risk and requires immediate reassessment of
treatment
sinus pauses (not related to sinus arrhythmia) are an additional warning signal, particularly for patients with SCN5A
mutations
see Congenital long QT syndrome for details and additional information
Brugada syndrome
diagnosed by ECG showing abnormal ST-segment morphology in right precordial leads, often in presence of right bundle branch
block in absence of acute cardiac ischemia
type 1 - coved ST-segment elevation in leads V1-V3 ≥ 0.2 mV suggests Brugada syndrome (Clin Med (Lond) 2014 Oct;14(5):482)
type 2 - saddle-back ST-segment elevation > 2.5 mm suggests Brugada syndrome
type 3 - coved or saddle-back ST-segment elevation < 2.5 mm suggests Brugada syndrome

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

ECG changes associated with hyperkalemia

relationship between degree of hyperkalemia and ECG changes variable
sever hypokalemia may rarely be associated with normal or near normal ECG
earliest ECG changes are peaked, narrow T waves and shortened QT interval
at plasma potassium concentration > 7 mEq/L (7 mmol/L)
widening of QRS complex
decreased amplitude and widening of P wave, with eventual loss of P wave
PR prolongation may occur
second- or third-degree atrioventricular block may follow PR prolongation
Hyperkalemia: Sinus rhythm, normal intervals, leftward QRS axis, and LVH with inverted T waves in I, aVL. There are narrow
and peaked T waves consistent with hyperkalemia. Abbreviation: LVH, left ventricular hypertrophy.
 Hyperkalemia: Sinus tachycardia with normal intervals and normal QRS axis. There are no diagnostic abnormalities. Relatively
tall T waves represent a normal variant and less likely hyperkalemia.

ECG findings may progress to

sine wave pattern with widening QRS complex merging with T wave
ventricular fibrillation or asystole

Hyperkalemia: Markedly wide-complex rhythm of unclear mechanism consistent with advanced hyperkalemia.

see Hyperkalemia for details and additional information

ECG changes associated with hypokalemia
not common with mild-to-moderate hypokalemia, usually occurs when serum potassium < 2.7 mEq/L (2.7 mmol/L)
most common changes
decreased T-wave amplitude (inverted or flat T waves)
ST-segment depression
presence of U wave (giant U waves may be mistaken for peaked T waves)
other findings (especially with concomitant hypomagnesemia) may include
QT interval prolongation
ventricular extrasystoles (with serum potassium < 2.5-3 mEq/L [2.5-3 mmol/L])
 ventricular arrhythmias
premature ventricular complexes
ventricular tachycardia
torsades de pointes
ventricular fibrillation
supraventricular arrhythmias
paroxysmal atrial tachycardia
multifocal atrial tachycardia
atrial fibrillation
atrial flutter
see Hypokalemia for details and additional information

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.

ECG changes associated with hypocalcemia

prolonged QT interval
prolonged ST interval
2:1 atrioventricular block

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

acquired long QT syndrome

prolonged heart-rate corrected QT (QTc) interval diagnosed based on ECG
for males
borderline prolonged QT interval defined as 430-450 milliseconds
 prolonged QT interval defined as > 450 milliseconds
for females
borderline prolonged QT interval defined as 450-470 milliseconds
prolonged QT interval defined as > 470 milliseconds
most commonly due to medications that either
block potassium channels and result in delay in phase 3 rapid repolarization of action potential
modify sodium channels and cause slowed intraventricular conduction due to increase in late sodium current
see Acquired long QT syndrome for details and additional information

Inflammation

acute pericarditis ECG findings

ST-segment elevation and PR-segment depression commonly observed in patients with acute pericarditis
4 stages of ECG finding in acute pericarditis (see in leads I, II, aVL, aVF, V3-V6)
stage I (hours to several days)
PR-segment depression (lead aVR shows PR-segment elevation) (Mayo Clin Proc 2010 Jun;85(6):572 full-text)
concave-upward ST-segment elevation with concordant (upright) T waves
absence of reciprocal ST-segment changes
leads aVR and V1 may have ST-segment depression
stage II (a few days to weeks)
ST and PR segment return to baseline
T waves progressively flatten and invert
stage III (several weeks) - T-wave inversion
stage IV (months)
gradual resolution of T-wave inversion
diffuse ST-segment depression and T-wave inversion may persist up to 3 months

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

Wellens' electrocardiography (ECG) pattern (also called Wellens' syndrome)

general information
Wellens' pattern or syndrome (also referred to as left anterior descending artery [LAD] coronary T wave syndrome) refers to T-wave
changes associated with critical stenosis in proximal left anterior descending (LAD) artery
critical LAD stenosis associated with risk for anterior wall myocardial infarction
Wellens' pattern or syndrome criteria
history of anginal chest pain
isoelectric or minimally elevated (< 1 mm) ST-segment with straight or convex morphology that leads to a negative (inverted) T
wave at an angle of 60-90 degrees
biphasic T waves in the right to midprecordial leads
absence of Q waves
normal precordial R wave progression
negative serum cardiac biomarker abnormalities (may be normal or minimally elevated)
T wave abnormalities may persist for hours to weeks (even in the absence of symptoms) and may have 2 observed ECG patterns,
including
Reference - Am J Emerg Med 2002 Nov;20(7):638
T wave abnormalities hypothesized to be associated with myocardial edema rather than systolic dysfunction (Heart Rhythm 2011
Oct;8(10):1629)
ECG and coronary angiography images of a 31-year-old man with Wellens' syndrome can be found in N Engl J Med 2015 Jan 1;372(1):66
Wellens' pattern associated with increased risk of significant stenosis in left anterior descending (LAD) artery and anterior wall
myocardial infarction in patients hospitalized for unstable angina
based on cohort study
145 consecutive patients (mean age 58 years) hospitalized for unstable angina were evaluated
26 patients had Wellens' pattern (abnormal ST-segment changes and inverted T waves in anterior chest leads without QRS changes)
within 24 hours of admission
22 patients had normal serial cardiac biomarker levels, including creatinine phosphokinase (CPK), serum glutamic oxaloacetic
transaminase (GOT), and lactic dehydrogenase (LDH)
13 patients had cardiac catheterization
12 had significant stenosis (defined as ≥ 70% luminal diameter stenosis), and all of these had ≥ 90% stenosis in the left
anterior descending (LAD) artery
1 patient had normal coronary arteries but prolapse of the posterior leaflet of the mitral valve
12 of 16 patients without surgical intervention developed anterior wall myocardial infarction within 39 days
2 patients died from congestive heart failure within 12 hours of myocardial infarction
1 patient died from ventricular tachycardia 6 weeks after myocardial infarction
9 patients who did not develop myocardial infarction had coronary artery bypass graft (CABG) mean 33 days after onset of
angina
Reference - Am Heart J 1982 Apr;103(4 Pt 2):730
Wellens' pattern associated with significant coronary artery stenosis and poor prognosis in patients treated medically
based on retrospective cohort study
118 consecutive patients with unstable angina were evaluated in coronary care unit for ≥ 48 hours and categorized by treatment
groups
42 patients had coronary angiography plus coronary artery bypass graft (CABG)
31 patients had coronary angiography plus medical treatment
45 patients did not have coronary angiography due to resolution of symptoms with drug therapy, age, or comorbidity that
precluded surgery and were treated medically
40% had Wellens' pattern with new T wave inversions (> 2 mm) with or without nonsignificant ST-segment depressions
mean follow-up 19 months in patients with CABG and 16 months in patients with medical treatment
all patients had negative cardiac biomarkers for myocardial infarction
 73 patients had coronary angiography, including 27 patients with Wellens' pattern
56 patients had significant stenosis (defined as ≥ 70% stenosis) of ≥ 1 coronary artery (48% had single vessel disease, 27% had
double vessel disease, and 25% had triple vessel disease)
3 patients had 50%-70% stenosis of 1 coronary artery
2 patients had < 50% stenosis of 1 coronary artery
12 patients had no stenosis
for predicting significant left anterior descending (LAD) artery stenosis, new T wave inversion had sensitivity 69% and specificity
89%
95% of patients completed follow-up
comparing patients with T wave inversion vs. patients without T wave inversion
significant stenosis in 87% vs. 62% (p < 0.001)
cardiac events (defined as cardiac death or myocardial infarction) in patients treated medically 38% vs. 16% (p < 0.05)
cardiac events in patients treated with CABG 18% vs. 11% (not significant)
Reference - Am J Cardiol 1983 Jul;52(1):14

Role in Detecting Ventricular Hypertrophy

Left ventricular hypertrophy (LVH)

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.

American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) recommendations(4)

ECG diagnosis of LVH should only use validated criteria without deviation from validated formulas
no single diagnostic criteria recommended over others
computer systems should use all criteria supported by valid evidence for identifying LVH
when diagnosing LVH on ECG, specify which criteria used and what findings were abnormal
adjust criteria for factors known to alter diagnostic performance (such as sex, race, and body habitus) when criteria have been
validated
do not use term strain, systolic, or diastolic in diagnostic statements related to LVH
use descriptors probable, possible, and borderline with caution
ECG criteria for diagnosing LVH based on QRS ECG feature(4)
influence of QRS voltages
 most commonly used criteria based on QRS voltages include
Cornell criteria diagnoses LVH if sum of S in lead V3 and R in lead aVL > 28 mm in men and > 20 mm in women
Sokolow-Lyon voltage criteria diagnosis LVH if sum of S in lead V1 and R in either lead V5 or V6 > 35 mm
QRS voltages also influenced by factors other than LV size or mass, including
age
QRS voltage tends to decline with increasing age
commonly used QRS voltage criteria apply to patients > 35 years old
QRS voltage standards for patients aged 16-35 years not well established, resulting in poor diagnostic performance of
criteria using only QRS voltage
sex (QRS voltage typically lower in women, even after adjustment for body size and cardiac mass)
race (compared to Euro-American patients, African American patients typically have higher QRS voltages and Hispanic
American patients typically have lower QRS voltages)
body habitus (obesity associated with increased LV mass on echocardiography but not increased QRS voltage)
influence of QRS duration
Cornell product ECG criteria based on Cornell voltage times QRS duration
QRS duration frequently increased in patients with LVH, which manifests as any
diffuse increase in QRS duration
increase in time from onset of QRS to R wave peak in leads V5 or V6
increased QRS duration may be due to increased thickness of LV wall and intramural fibrosis that distorts and prolongs
transmural impulse propagation
if ECG pattern of LVH present with widened QRS, septal Q wave may be absent and slurred R-wave upstroke may be present,
indicating associated incomplete left bundle branch block
other ECG criteria include indices based on any(4)
products of voltage and QRS duration
computation of QRS area
composite use of several criteria
scores derived from regression equations that incorporate multiple ECG and non-ECG factors
role of other ECG features in detecting LVH(4)
supportive but not diagnostic ECG features include
ST-T abnormalities
P-wave abnormalities (present frequently in patients with hypertension and may be early sign of hypertensive hear but also
present without LVH)
left axis deviation (may be associated with LVH but also occurs with left anterior fascicular block and other factors, such as
increasing age)
prolonged QT interval consistent with LVH but not supportive or diagnostic (may be associated with LVH or only secondary to
prolonged QRS duration)

Performance of diagnostic criteria

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

Diagnosis in presence of intraventricular conduction disorders

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

Right ventricular hypertrophy (RVH)

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

biventricular hypertrophy common in patients with heart disease of many types(4)

in presence of ECG criteria for left ventricular hypertrophy (LVH), ECG features suggesting concomitant presence of right ventricular
hypertrophy (RVH) include(4)
prominent S waves in lead V5 or V6
right axis deviation
unusually tall biphasic R/S complexes in several leads
signs of right atrial abnormality
in patients with congenital heart defects and RVH, presence of combined tall R waves and deep S waves in leads V2-V4 (combined
amplitude > 60 mm or 6 millivolts) may suggest concomitant RVH(4)
American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) recommendations(4)
biventricular hypertrophy suggested on basis of presence of accepted criteria for both LVH and RVH and low sensitivity of such
patterns should be noted
in presence of ECG criteria for LVH, right axis deviation and tall biphasic R/S complexes in several leads should be recognized as
suggestive of biventricular hypertrophy