I. The Standard 12 Lead ECG
Professor of Medicine
University of Utah School of Medicine
QRS complex: right and left ventricular depolarization (normally the ventricles are activated simultaneously)
ST-T wave: ventricular repolarization
U wave: origin for this wave is not clear – but probably represents “afterdepolarizations” in the ventricles
PR interval: time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)
QRS duration: duration of ventricular muscle depolarization
QT interval: duration of ventricular depolarization and repolarization
RR interval: duration of ventricular cardiac cycle (an indicator of ventricular rate)
PP interval: duration of atrial cycle (an indicator of atrial rate)
Lead II: RA (-) to LF (+) (Superior Inferior)
Lead III: LA (-) to LF (+) (Superior Inferior)
Lead aVL: LA (+) to [RA & LF] (-) (Leftward)
Lead aVF: LF (+) to [RA & LA] (-) (Inferior)
Leads V4, V5, V6:(Right Left, or lateral)
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
PR interval (from beginning of P to beginning of QRS)
QRS duration (width of most representative QRS)
QT interval (from beginning of QRS to end of T)
QRS axis in frontal plane (go to: “How To Determine Axis”)
Go to: ECG Measurement Abnormalities (Lesson IV) for description of normal and abnormal measurements
Identify additional rhythm events if present (e.g., “PVC’s”, “PAC’s”, etc)
Consider all rhythm events from atria, AV junction, and ventricles
Go to: ECG Rhythm Abnormalities (Lesson V) for description of arrhythmias
The diagram illustrates the normal cardiac conduction system.
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AV block (lesson VI): 1st, 2nd (type I vs. type II), and 3rd degree
IV blocks (lesson VI): bundle branch, fascicular, and nonspecific blocks
Exit blocks: blocks just distal to ectopic pacemaker site
(Go to ECG Conduction Abnormalities (Lesson VI) for a description of conduction abnormalities)
QRS complexes: look for pathologic Q waves (lesson IX), abnormal voltage (lesson VIII), etc.
ST segments (lesson X): look for abnormal ST elevation and/or depression.
T waves (lesson XI): look for abnormally inverted T waves.
U waves (lesson XII): look for prominent or inverted U waves.
Old anteroseptal MI
Left anterior fascicular block (LAFB)
Left ventricular hypertrophy (LVH)
Nonspecific ST-T wave abnormalities
Any rhythm abnormalities
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
QRS Duration: 0.06 – 0.10 sec
QT Interval (QTc < 0.40 sec)
Poor Man’s Guide to upper limits of QT: For HR = 70 bpm, QT<0.40 sec; for every 10 bpm increase above 70 subtract 0.02 sec, and for every 10 bpm decrease below 70 add 0.02 sec. For example:
QT < 0.42 @ 60 bpm
The P waves in leads I and II must be upright (positive) if the rhythm is coming from the sinus node.
Both the PR interval and QRS duration should be within the limits specified above.
It is important to remember that the P wave represents the sequential activation of the right and left atria, and it is common to see notched or biphasic P waves of right and left atrial activation.
P amplitude < 2.5 mm
Frontal plane P wave axis: 0o to +75o
May see notched P waves in frontal plane
QRS Complex
The QRS represents the simultaneous activation of the right and left ventricles, although most of the QRS waveform is derived from the larger left ventricular musculature.
QRS amplitude is quite variable from lead to lead and from person to person. Two determinates of QRS voltages are:
Proximity of chest electrodes to ventricular chamber (the closer, the larger the voltage)
Frontal plane leads:
Normal q-waves reflect normal septal activation (beginning on the LV septum); they are narrow (<0.04s duration) and small (<25% the amplitude of the R wave). They are often seen in leads I and aVL when the QRS axis is to the left of +60o, and in leads II, III, aVF when the QRS axis is to the right of +60o. Septal q waves should not be confused with the pathologic Q waves of myocardial infarction.
Precordial leads: (see Normal ECG)
In reverse, the s-waves begin in V6 or V5 and progress in size to V2. S-V1 is usually smaller than S-V2.
The usual transition from S>R in the right precordial leads to R>S in the left precordial leads is V3 or V4.
Small “septal” q-waves may be seen in leads V5 and V6.
ST Segment and T wave
In a sense, the term “ST segment” is a misnomer, because a discrete ST segment distinct from the T wave is usually absent. More often the ST-T wave is a smooth, continuous waveform beginning with the J-point (end of QRS), slowly rising to the peak of the T and followed by a rapid descent to the isoelectric baseline or the onset of the U wave. This gives rise to an asymmetrical T wave. In some normal individuals, particularly women, the T wave is symmetrical and a distinct, horizontal ST segment is present.
The normal T wave is usually in the same direction as the QRS except in the right precordial leads. In the normal ECG the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR.
U wave direction is the same as T wave direction in that lead
U waves are more prominent at slow heart rates and usually best seen in the right precordial leads.
Origin of the U wave is thought to be related to afterdepolarizations which interrupt or follow repolarization.
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Short PR: < 0.12s
AV Junctional Rhythms with retrograde atrial activation (inverted P waves in II, III, aVF): Retrograde P waves may occur before the QRS complex (usually with a short PR interval), in the QRS complex (i.e., hidden from view), or after the QRS complex (i.e., in the ST segment).
Ectopic atrial rhythms originating near the AV node (the PR interval is short because atrial activation originates close to the AV node; the P wave morphology is different from the sinus P)
Normal variant
Prolonged PR: >0.20s
Slowed conduction in AV node (most common site)
Slowed conduction in His bundle (rare)
Slowed conduction in bundle branch (when contralateral bundle is blocked)
Second degree AV block (PR interval may be normal or prolonged; some P waves do not conduct)
Type II (Mobitz): Fixed PR intervals plus nonconducted P waves
AV dissociation: Some PR’s may appear prolonged, but the P waves and QRS complexes are dissociated (i.e., not married, but strangers passing in the night).
Prolonged QRS Duration (>0.10s):
Nonspecific intraventricular conduction delay (IVCD)
Some cases of left anterior or posterior fascicular block
QRS duration > 0.12s
Nonspecific IVCD
Ectopic rhythms originating in the ventricles (e.g., ventricular tachycardia, pacemaker rhythm)
Long QT Syndrome – “LQTS” (based on upper limits for heart rate; QTc > 0.47 sec for males and > 0.48 sec in females is diagnostic for hereditary LQTS in absence of other causes of increased QT)
Electrolyte abnormalities ( K+, Ca++, Mg++)
CNS disease (especially subarrachnoid hemorrhage, stroke, trauma)
Hereditary LQTS (e.g., Romano-Ward Syndrome)
Coronary Heart Disease (some post-MI patients)
Normal: -30 degrees to +90 degrees
Abnormalities in the QRS Axis:
Some cases of inferior MI with Qr complex in lead II (making lead II ‘negative’)
Inferior MI + LAFB in same patient (QS or qrS complex in lead II)
Some cases of LVH
Some cases of LBBB
Ostium primum ASD and other endocardial cushion defects
Some cases of WPW syndrome (large negative delta wave in lead II)
Right Axis Deviation (RAD): > +90o (i.e., lead I is mostly ‘negative’)
High lateral wall MI with Qr or QS complex in leads I and aVL
Some cases of RBBB
Some cases of WPW syndrome
Children, teenagers, and some young adults
Bizarre QRS axis: +150o to -90o (i.e., lead I and lead II are both negative)
Dextrocardia
Some cases of complex congenital heart disease (e.g., transposition)
Some cases of ventricular tachycardia
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Premature junctional complexes
Atrial fibrillation
Atrial flutter
Ectopic atrial tachycardia and rythm
Multifocal atrial tachycardia
Paroxysmal supraventricular tachycardia
Junctional rhythms and tachycardias
Aberrancy vs. ventricular ectopy
Ventricular tachycardia
Differential diagnosis of wide QRS tachycardias
Accelerated ventricular rhythms
Idioventricular rhythm
Ventricular parasystole
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Type I (Wenckebach) 2nd Degree AV Block
Type II (Mobitz) 2nd Degree AV Block
Complete (3rd Degree) AV Block
AV Dissociation
Left Bundle Branch Block
Left Anterior Fascicular Block
Left Posterior Fascicular Block
Bifascicular Blocks
Nonspecific Intraventricular Block
Wolff-Parkinson-White Preexcitation
The pause duration is less than the two preceding PP intervals
The PP interval following the pause is greater than the PP interval just before the pause
Differential Diagnosis: sinus arrhythmia without SA block. The following rhythm strip illustrates SA Wenckebach with a ladder diagram to show the progressive conduction delay between SA node and the atria. Note the similarity of this rhythm to marked sinus arrhythmia. (Remember, we cannot see SA events on the ECG, only the atrial response or P waves.)
The pause is approximately twice the basic PP interval
His bundle (uncommon)
Bundle branch and fascicular divisions (in presence of already existing complete bundle branch block)
1st Degree AV Block: PR interval > 0.20 sec; all P waves conduct to the ventricles.
In “classic” Type I (Wenckebach) AV block the PR interval gets longer (by shorter increments) until a nonconducted P wave occurs. The RR interval of the pause is less than the two preceding RR intervals, and the RR interval after the pause is greater than the RR interval before the pause. These are the classic rules of Wenckebach (atypical forms can occur). In Type II (Mobitz) AV block the PR intervals are constant until a nonconducted P wave occurs. There must be two consecutive constant PR intervals to diagnose Type II AV block (i.e., if there is 2:1 AV block we can’t be sure if its type I or II). The RR interval of the pause is equal to the two preceding RR intervals.
Type I AV block is almost always located in the AV node, which means that the QRS duration is usually narrow, unless there is preexisting bundle branch disease.
Narrow QRS rhythm suggests a junctional escape focus for the ventricles with block above the pacemaker focus, usually in the AV node.
Wide QRS rhythm suggests a ventricular escape focus (i.e., idioventricular rhythm). This is seen in ECG ‘A’ below; ECG ‘B’ shows the treatment for 3rd degree AV block; i.e., a ventricular pacemaker. The location of the block may be in the AV junction or bilaterally in the bundle branches.
May be complete or incomplete. In complete AV dissociation the atria and ventricles are always independent of each other. In incomplete AV dissociation there is either intermittent atrial capture from the ventricular focus or ventricular capture from the atrial focus.
There are three categories of AV dissociation (categories 1 & 2 are always incomplete AV dissociation):
In the above example of AV dissociation (3rd degree AV bock with a junctional escape pacemaker) the PP intervals are alternating because of ventriculophasic sinus arrhythmia (phasic variation of vagal tone in the sinus node depending on the timing of ventricular contractions and blood flow near the carotid sinus).
Close examination of QRS complex in various leads reveals that the terminal forces (i.e., 2nd half of QRS) are oriented rightward and anteriorly because the right ventricle is depolarized after the left ventricle. This means the following:
Terminal S waves in leads I, aVL, V6 indicating late rightward forces
Terminal R wave in lead aVR indicating late rightward forces
The frontal plane QRS axis in RBBB should be in the normal range (i.e., -30 to +90 degrees). If left axis deviation is present, think about left anterior fascicular block, and if right axis deviation is present, think about left posterior fascicular block in addition to the RBBB.
“Incomplete” RBBB has a QRS duration of 0.10 – 0.12s with the same terminal QRS features. This is often a normal variant.
The “normal” ST-T waves in RBBB should be oriented opposite to the direction of the terminal QRS forces; i.e., in leads with terminal R or R’ forces the ST-T should be negative or downwards; in leads with terminal S forces the ST-T should be positive or upwards. If the ST-T waves are in the same direction as the terminal QRS forces, they should be labeled primary ST-T wave abnormalities.
The ECG below illustrates primary ST-T wave abnormalities (leads I, II, aVR, V5, V6) in a patient with RBBB. ST-T wave abnormalities such as these may be related to ischemia, infarction, electrolyte abnormalities, medications, CNS disease, etc. (i.e., they are nonspecific and must be correlated with the patient’s clinical status).
Close examination of QRS complex in various leads reveals that the terminal forces (i.e., 2nd half of QRS) are oriented leftward and posteriorly because the left ventricle is depolarized after the right ventricle.
Terminal R waves in lead I, aVL, V6 indicating late leftward forces; usually broad, monophasic R waves are seen in these leads as illustrated in the ECG below; in addition, poor R progression from V1 to V3 is common.
“Incomplete” LBBB looks like LBBB but QRS duration = 0.10 to 0.12s, with less ST-T change. This is often a progression of LVH.
rS complexes in leads II, III, aVF
Small q-wave in leads I and/or aVL
R-peak time in lead aVL >0.04s, often with slurred R wave downstroke
QRS duration usually <0.12s unless coexisting RBBB
Usually see poor R progression in leads V1-V3 and deeper S waves in leads V5 and V6
May mimic LVH voltage in lead aVL, and mask LVH voltage in leads V5 and V6.
In this ECG, note -75 degree QRS axis, rS complexes in II, III, aVF, tiny q-wave in aVL, poor R progression V1-3, and late S waves in leads V5-6. QRS duration is normal, and there is a slight slur to the R wave downstroke in lead aVL.
rS complex in lead I
qR complexes in leads II, III, aVF, with R in lead III > R in lead II
QRS duration usually <0.12s unless coexisting RBBB
Must first exclude (on clinical grounds) other causes of right axis deviation such as cor pulmonale, pulmonary heart disease, pulmonary hypertension, etc., because these conditions can result in the identical ECG picture!
Features of RBBB plus frontal plane features of the fascicular block (axis deviation, etc.)
The above ECG shows classic RBBB (note rSR’ in V1) plus LAFB (note QRS axis = -45 degrees, rS in II, III, aVF; and small q in aVL).
Criteria for specific bundle branch or fascicular blocks not met
Causes of nonspecific IVCD’s include:
Myocardial infarction (so called periinfarction blocks)
Drugs, especially class IA and IC antiarrhythmics (e.g., quinidine, flecainide)
Hyperkalemia
QRS complex represents a fusion between two ventricular activation fronts:
Ventricular activation through the normal AV junction, bundle branch system
ECG criteria include all of the following:
- Short PR interval (<0.12s)
- Initial slurring of QRS complex (delta wave) representing early ventricular activation through normal ventricular muscle in region of the accessory pathway
- Prolonged QRS duration (usually >0.10s)
- Secondary ST-T changes due to the altered ventricular activation sequence
Delta waves, if negative in polarity, may mimic infarct Q waves and result in false positive diagnosis of myocardial infarction.
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Better criteria can be derived from the QRS complex; these QRS changes are due to both the high incidence of RVH when RAE is present, and the RV displacement by an enlarged right atrium.
QRS voltage in V1 is <5 mm and V2/V1 voltage ratio is >6 (Sensitivity = 50%; Specificity = 90%)
In the above ECG, note the tall P waves in Lead II, and the Qr wave in Lead V1.
Terminal P negativity in lead V1 (i.e., “P-terminal force”) duration >0.04s, depth >1 mm.
Sensitivity = 50%; Specificity = 90%
P wave in lead II >2.5 mm tall and >0.12s in duration
Initial positive component of P wave in V1 >1.5 mm tall and prominent P-terminal force
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
- Introduction
- Left Ventricular Hypertrophy (LVH)
- Right Ventricular Hypertrophy (RVH)
- Biventricular Hypertrophy
Delayed intrinsicoid deflection in V6 (i.e., time from QRS onset to peak R is >0.05 sec)
Widened QRS/T angle (i.e., left ventricular strain pattern, or ST-T oriented opposite to QRS direction)
Leftward shift in frontal plane QRS axis
Evidence for left atrial enlargement (LAE) (lessonVII)
ESTES Criteria for LVH (“diagnostic”, >5 points; “probable”, 4 points)
+ECG Criteria
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Points
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Voltage Criteria (any of):
a. R or S in limb leads >20 mm
b. S in V1 or V2 > 30 mm
c. R in V5 or V6 >30 mm
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3 points
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ST-T Abnormalities:
Without digitalis With digitalis |
3 points
1 point |
Left Atrial Enlargement in V1
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3 points
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Left axis deviation
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2 points
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QRS duration 0.09 sec
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1 point
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Delayed intrinsicoid deflection in V5 or V6 (>0.05 sec)
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1 point
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CORNELL Voltage Criteria for LVH (sensitivity = 22%, specificity = 95%)
S in V3 + R in aVL > 20 mm (women)
Other Voltage Criteria for LVH
R in I + S in III >25 mm
Chest-lead voltage criteria:
Example 1: (Limb-lead Voltage Criteria; e.g., R in aVL >11 mm; note wide QRS/T angle)
(Note also the left axis deviation of -40 degrees, and left atrial enlargement)
Tall R-waves in RV leads; deep S-waves in LV leads
Slight increase in QRS duration
ST-T changes directed opposite to QRS direction (i.e., wide QRS/T angle)
May see incomplete RBBB pattern or qR pattern in V1
Evidence of right atrial enlargement (RAE) (lessonVII)
Specific ECG features (assumes normal calibration of 1 mV = 10 mm):
R in aVR > 5 mm, or
R in aVR > Q in aVR
Any one of the following in lead V1:
qR pattern
R > 6 mm, or S < 2mm, or rSR’ with R’ >10 mm
Other chest lead criteria:
R/S ratio in V5 or V6 < 1
R in V5 or V6 < 5 mm
S in V5 or V6 > 7 mm
ST segment depression and T wave inversion in right precordial leads is usually seen in severe RVH such as in pulmonary stenosis and pulmonary hypertension.
Example #1: (note RAD +105 degrees; RAE; R in V1 > 6 mm; R in aVR > 5 mm)
S in V5 or V6 > 6 mm
RAD (>90 degrees)
LVH criteria met and RAD or RAE present
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
- Introduction (Read this first)
- Inferior Q-Wave MI Family
- Anterior Q-Wave MI Family
- MI + Bundle Branch Block
- Non Q-Wave MI
- The Pseudoinfarctions
- Miscellaneous QRS Abnormalities
In general, the more leads of the 12-lead ECG with MI changes (Q waves and ST elevation), the larger the infarct size and the worse the prognosis. Additional leads on the back, V7-9 (horizontal to V6), may be used to improve the recognition of true posterior MI.
B. Hyperacute T wave changes – increased T wave amplitude and width; may also see ST elevation
C. Marked ST elevation with hyperacute T wave changes (transmural injury)
D. Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis)
F. Pathologic Q waves, upright T waves (fibrosis)
Q waves usually largest in lead III, next largest in lead aVF, and smallest in lead II
Example #1: frontal plane leads with fully evolved inferior MI (note Q-waves, residual ST elevation, and T inversion in II, III, aVF)
R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)
Hyperacute ST-T wave changes: i.e., ST depression and large, inverted T waves in V1-3
Late normalization of ST-T with symmetrical upright T waves in V1-3
Often seen with inferior MI (i.e., “inferoposterior MI”)
Example #1: Acute inferoposterior MI (note tall R waves V1-3, marked ST depression V1-3, ST elevation in II, III, aVF)
ST elevation, >1mm, in right chest leads, especially V4R (see below)
Evolving ST-T changes
Example: Fully evolved anteroseptal MI (note QS waves in V1-2, qrS complex in V3, plus ST-T wave changes)
(Note also the slight U-wave inversion in leads II, III, aVF, V4-6, a strong marker for coronary disease)
Example #1: Inferior MI + RBBB (note Q’s in II, III, aVF and rSR’ in lead V1)
Suggested ECG features, not all of which are specific for MI include:
Notching of the downstroke of the S wave in precordial leads to the right of the transition zone (i.e., before QRS changes from a predominate S wave complex to a predominate R wave complex); this may be a Q-wave equivalent.
Notching of the upstroke of the S wave in precordial leads to the right of the transition zone (another Q-wave equivalent).
rSR’ complex in leads I, V5 or V6 (the S is a Q-wave equivalent occurring in the middle of the QRS complex)
RS complex in V5-6 rather than the usual monophasic R waves seen in uncomplicated LBBB; (the S is a Q-wave equivalent).
“Primary” ST-T wave changes (i.e., ST-T changes in the same direction as the QRS complex rather than the usual “secondary” ST-T changes seen in uncomplicated LBBB); these changes may reflect an acute, evolving MI.
Although it is tempting to localize the non-Q MI by the particular leads showing ST-T changes, this is probably only valid for the ST segment elevation pattern
Evolving ST-T changes may include any of the following patterns:
Convex upwards or straight ST segment elevation only (uncommon)
Symmetrical T wave inversion only (common)
Combinations of above changes
Example: Anterolateral ST-T wave changes
IHSS (septal hypertrophy may make normal septal Q waves “fatter” thereby mimicking pathologic Q waves)
LVH (may have QS pattern or poor R wave progression in leads V1-3)
RVH (tall R waves in V1 or V2 may mimic true posterior MI)
Complete or incomplete LBBB (QS waves or poor R wave progression in leads V1-3)
Pneumothorax (loss of right precordial R waves)
Pulmonary emphysema and cor pulmonale (loss of R waves V1-3 and/or inferior Q waves with right axis deviation)
Left anterior fascicular block (may see small q-waves in anterior chest leads)
Acute pericarditis (the ST segment elevation may mimic acute transmural injury)
Central nervous system disease (may mimic non-Q wave MI by causing diffuse ST-T wave changes)
Poor R Wave Progression – defined as loss of, or no R waves in leads V1-3 (R £2mm):
LVH (look for voltage criteria and ST-T changes of LV “strain”)
Complete or incomplete LBBB (increased QRS duration)
Left anterior fascicular block (should see LAD in frontal plane)
Emphysema and COPD (look for R/S ratio in V5-6 <1)
Diffuse infiltrative or myopathic processes
WPW preexcitation (look for delta waves, short PR)
Prominent Anterior Forces – defined as R/S ration >1 in V1 or V2
True posterior MI (look for evidence of inferior MI)
RVH (should see RAD in frontal plane and/or P-pulmonale)
Complete or incomplete RBBB (look for rSR’ in V1)
WPW preexcitation (look for delta waves, short PR)
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Drugs (e.g., digoxin, quinidine, tricyclics, and many others)
Electrolyte abnormalities of potassium, magnesium, calcium
Neurogenic factors (e.g., stroke, hemorrhage, trauma, tumor, etc.)
Metabolic factors (e.g., hypoglycemia, hyperventilation)
Atrial repolarization (e.g., at fast heart rates the atrial T wave may pull down the beginning of the ST segment)
Ventricular conduction abnormalities and rhythms originating in the ventricles
“Secondary” ST-T Wave changes (these are normal ST-T wave changes solely due to alterations in the sequence of ventricular activation)
ST-T changes seen in fascicular block
ST-T changes seen in nonspecific IVCD
ST-T changes seen in WPW preexcitation
ST-T changes in PVCs, ventricular arrhythmias, and ventricular paced beats
“Primary” ST-T Wave Abnormalities (ST-T wave changes that are independent of changes in ventricular activation and that may be the result of global or segmental pathologic processes that affect ventricular repolarization)
Electrolyte abnormalities (e.g., hypokalemia)
Ischemia, infarction, inflammation, etc
Neurogenic effects (e.g., subarrachnoid hemorrhage causing long QT)
ST elevation may also be seen as a manifestation of Prinzmetal’s (variant) angina (coronary artery spasm)
ST elevation during exercise testing suggests extremely tight coronary artery stenosis or spasm (transmural ischemia)
Acute Pericarditis
No reciprocal ST segment depression (except in aVR)
Unlike “early repolarization”, T waves are usually low amplitude, and heart rate is usually increased.
May see PR segment depression, a manifestation of atrial injury
Other Causes:
Left bundle branch block (in right precordial leads with large S-waves)
Advanced hyperkalemia
Hypothermia (prominent J-waves or Osborne waves)
Physiologic J-junctional depression with sinus tachycardia (most likely due to atrial repolarization)
Hyperventilation-induced ST segment depression
Ischemic heart disease
Note: “horizontal” ST depression in lead V6
Note: “Upsloping” ST depression is not an ischemic abnormality
Reciprocal changes in acute Q-wave MI (e.g., ST depression in leads I & aVL with acute inferior MI)
Nonischemic causes of ST depression
Digoxin effect on ECG
Hypokalemia
Mitral valve prolapse (some cases)
CNS disease
Secondary ST segment changes with IV conduction abnormalities (e.g., RBBB, LBBB, WPW, etc)
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Subacute or old pericarditis
Myocarditis
Myocardial contusion (from trauma)
CNS disease causing long QT interval (especially subarrachnoid hemorrhage; see below):
Mitral valve prolapse
Digoxin effect
RVH and LVH with “strain” (see below: T wave inversion in leads aVL, V4-6 in LVH)
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Hypokalemia (remember the triad of ST segment depression, low amplitude T waves, and prominent U waves)
Quinidine and other type 1A antiarrhythmics
CNS disease with long QT intervals (often the T and U fuse to form a giant “T-U fusion wave”)
(E.g., lead II, III, V4-6)
Mitral valve prolapse (some cases)
Hyperthyroidism
Negative or “inverted” U waves
During episode of acute ischemia (angina or exercise-induced ischemia)
Post extrasystolic in patients with coronary heart disease
During coronary artery spasm (Prinzmetal’s angina)
Nonischemic causes
Some patients with LQTS (see below: Lead V6 shows giant negative TU fusion wave in patient with LQTS; a prominent upright U wave is seen in Lead V1)
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