Sino-Atrial Exit Block Sino-Atrial Exit Block (SA Block): (SA Block):

22ndnd Degree SA Block: this is the only Degree SA Block: this is the only degree of SA block that can be degree of SA block that can be recognized on the surface ECG (i.e., recognized on the surface ECG (i.e., intermittent conduction failure between intermittent conduction failure between the sinus node and the right atrium). the sinus node and the right atrium). There are two types, although because There are two types, although because of sinus arrhythmia they may be hard of sinus arrhythmia they may be hard to differentiate. Furthermore, the to differentiate. Furthermore, the differentiation is differentiation is electrocardiographically interesting but electrocardiographically interesting but not clinically important not clinically important

Type I (SA Wenckebach): the following 3 rules represent the Type I (SA Wenckebach): the following 3 rules represent the classic rules of Wenckebach, which were originally described for classic rules of Wenckebach, which were originally described for Type IType I AVAV block. The rules are the result of decremental block. The rules are the result of decremental conduction where the conduction where the incrementincrement in conduction delay for in conduction delay for each subsequent impulse gets smaller until conduction each subsequent impulse gets smaller until conduction failure finally occurs. This declining increment results in failure finally occurs. This declining increment results in the following findingsthe following findings

1.1. PP intervals gradually shorten until a pause occurs (i.e., the PP intervals gradually shorten until a pause occurs (i.e., the blocked sinus impulse fails to reach the atria) blocked sinus impulse fails to reach the atria)

2.2. The pause duration is The pause duration is less thanless than the two preceding PP the two preceding PP intervalsintervals

3.3. The PP interval following the pause is The PP interval following the pause is greater thangreater than the PP the PP interval just before the pauseinterval just before the pause

Differential Diagnosis: Differential Diagnosis: sinus arrhythmia without SA block. The sinus arrhythmia without SA block. The following rhythm strip illustrates SA Wenckebach with a ladder following rhythm strip illustrates SA Wenckebach with a ladder diagram to show the progressive conduction delay between SA diagram to show the progressive conduction delay between SA node and the atria. Note the similarity of this rhythm to marked node and the atria. Note the similarity of this rhythm to marked sinus arrhythmia. (Remember, we cannot see SA events on the sinus arrhythmia. (Remember, we cannot see SA events on the ECG, only the atrial response or P waves.) ECG, only the atrial response or P waves.)

Type II SA Block Type II SA Block

PP intervals fairly constant (unless PP intervals fairly constant (unless sinus arrhythmia present) until sinus arrhythmia present) until conduction failure occursconduction failure occurs

The pause is approximately The pause is approximately twicetwice the basic PP intervalthe basic PP interval

Atrio-Ventricular (AV) Block Atrio-Ventricular (AV) Block

Possible sites of AV blockPossible sites of AV block

1.1. AV node (most common)AV node (most common)

2.2. His bundle (uncommon)His bundle (uncommon)

3.3. Bundle branch and fascicular Bundle branch and fascicular divisions (in presence of already divisions (in presence of already existing complete bundle branch existing complete bundle branch block) block)

1st Degree AV Block1st Degree AV Block: PR interval > 0.20 sec; : PR interval > 0.20 sec; allall

P waves conduct to the ventriclesP waves conduct to the ventricles

2nd Degree AV Block2nd Degree AV Block: The diagram below illustrates the : The diagram below illustrates the difference between Type I (or Wenckebach) and Type II AV difference between Type I (or Wenckebach) and Type II AV

blockblock. .

In "classic" Type I In "classic" Type I (Wenckebach) (Wenckebach) AV block the AV block the PR interval gets longer PR interval gets longer (by shorter (by shorter increments)increments) until a nonconducted P wave until a nonconducted P wave occurs. The RR interval of the pause is occurs. The RR interval of the pause is less less thanthan the two preceding RR intervals, and the the two preceding RR intervals, and the RR interval after the pause is RR interval after the pause is greater thangreater than the RR interval before the pause. These are the RR interval before the pause. These are the the classicclassic rules of rules of WenckebachWenckebach (atypical (atypical forms can occur). In Type II forms can occur). In Type II (Mobitz)(Mobitz) AV block AV block the PR intervals are constant until a the PR intervals are constant until a nonconducted P wave occurs. There must be nonconducted P wave occurs. There must be two consecutive constanttwo consecutive constant PR intervals to PR intervals to diagnose Type II AV block (i.e., if there is 2:1 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). AV block we can't be sure if its type I or II). The RR interval of the pause is The RR interval of the pause is equal toequal to the the two preceding RR intervalstwo preceding RR intervals

Type I (Wenckebach) AV block (note the RR Type I (Wenckebach) AV block (note the RR

intervals in ms durationintervals in ms duration Type I AV block is Type I AV block is almost alwaysalmost always

located in the AV node, which located in the AV node, which means that the QRS duration is means that the QRS duration is usually narrow, unless there is usually narrow, unless there is preexisting bundle branch preexisting bundle branch diseasedisease

Type II (Mobitz) AV block(note there are two consecutive Type II (Mobitz) AV block(note there are two consecutive

constant PR intervals before the blocked P waveconstant PR intervals before the blocked P wave Type II AV block is Type II AV block is almost almost

alwaysalways located in the located in the bundle branches, which bundle branches, which means that the QRS means that the QRS duration is wide duration is wide indicating complete indicating complete block of one bundle; the block of one bundle; the nonconducted P wave is nonconducted P wave is blocked in the other blocked in the other bundle. In Type II block bundle. In Type II block several consecutive P several consecutive P waves may be blocked waves may be blocked

as illustrated belowas illustrated below

Complete (3rd Degree) AV BlockComplete (3rd Degree) AV Block Usually see Usually see complete AV complete AV

dissociationdissociation because the because the atria and ventricles are atria and ventricles are each controlled by separate each controlled by separate pacemakerspacemakers

Narrow QRS rhythm suggests Narrow QRS rhythm suggests a junctional escape focus for a junctional escape focus for the ventricles with block above the ventricles with block above the pacemaker focus, usually the pacemaker focus, usually in the AV nodein the AV node

Wide QRS rhythm suggests a Wide QRS rhythm suggests a ventricular escape focus (i.e., ventricular escape focus (i.e., idioventricular rhythmidioventricular rhythm). ). This is seen in ECG 'A' This is seen in ECG 'A' below; ECG 'B' shows the below; ECG 'B' shows the treatment for 3rd degree treatment for 3rd degree AV block; i.e., a AV block; i.e., a ventricular ventricular pacemaker. pacemaker. The location of The location of the block may be in the AV the block may be in the AV junction or bilaterally in the junction or bilaterally in the bundle branchesbundle branches

AV DissociationAV Dissociation (independent (independent rhythms in atria and ventricles): rhythms in atria and ventricles):

NotNot synonymous with 3 synonymous with 3rdrd degree AV block, degree AV block, although AV block is although AV block is oneone of the causes. of the causes.  May be May be

complete complete or or incomplete. incomplete. In In completecomplete AV AV dissociation the atria and ventricles are dissociation the atria and ventricles are always independent of each other. always independent of each other.

In In incompleteincomplete AV dissociation there is either AV dissociation there is either intermittent atrial intermittent atrial capturecapture from the from the ventricular focus or ventricular ventricular focus or ventricular capturecapture from from the atrial focus. the atrial focus.

 There are  There are three categoriesthree categories of AV of AV dissociation (categories 1 & 2 are always dissociation (categories 1 & 2 are always incompleteincomplete AV dissociation AV dissociation

Slowing of the primary pacemaker (i.e., SA node); Slowing of the primary pacemaker (i.e., SA node);

subsidiary subsidiary escapeescape pacemaker takes over by pacemaker takes over by defaultdefault

Acceleration of a subsidiary pacemaker faster than sinus Acceleration of a subsidiary pacemaker faster than sinus

rhythm; takeover by rhythm; takeover by usurpationusurpation

22ndnd or 3 or 3rdrd degree AV block with escape rhythm from degree AV block with escape rhythm from

junctional focus or ventricular focusjunctional focus or ventricular focus In the below example of AV dissociation (3In the below example of AV dissociation (3rdrd

degree AV bock with a junctional escape degree AV bock with a junctional escape pacemaker) the PP intervals are alternating pacemaker) the PP intervals are alternating because of because of ventriculophasic sinus arrhythmiaventriculophasic sinus arrhythmia (phasic variation of vagal tone in the sinus (phasic variation of vagal tone in the sinus node depending on the timing of ventricular node depending on the timing of ventricular contractions and blood flow near the carotid contractions and blood flow near the carotid

sinus).sinus).

Intraventricular Blocks Intraventricular Blocks

Right Bundle Branch Block Right Bundle Branch Block (RBBB)(RBBB)

"Complete" RBBB has a QRS duration "Complete" RBBB has a QRS duration >>0.12s0.12s Close examination of QRS complex in various Close examination of QRS complex in various

leads reveals that the terminal forces (i.e., 2leads reveals that the terminal forces (i.e., 2ndnd half of QRS) are oriented half of QRS) are oriented rightwardrightward and and anteriorlyanteriorly because the right ventricle is because the right ventricle is depolarized depolarized afterafter the left ventricle. This the left ventricle. This means the followingmeans the following

1.1. Terminal R' wave in lead V1 (usually see rSR' Terminal R' wave in lead V1 (usually see rSR' complex) indicating late complex) indicating late anterior anterior forcesforces

2.2. Terminal S waves in leads I, aVL, V6 indicating Terminal S waves in leads I, aVL, V6 indicating late late rightwardrightward forces forces

3.3. Terminal R wave in lead aVR indicating late Terminal R wave in lead aVR indicating late rightwardrightward forces forces

The frontal plane QRS axis in RBBB should be in the normal The frontal plane QRS axis in RBBB should be in the normal range (i.e., -30 to +90 degrees). If left axis deviation is range (i.e., -30 to +90 degrees). If left axis deviation is present, think about present, think about leftleft anterioranterior fascicularfascicular blockblock, and if , and if right axis deviation is present, think about right axis deviation is present, think about leftleft posteriorposterior fascicularfascicular blockblock in addition to the RBBB in addition to the RBBB

Incomplete" RBBB has a QRS duration of 0.10 - 0.12s with Incomplete" RBBB has a QRS duration of 0.10 - 0.12s with the same terminal QRS features. This is often a normal the same terminal QRS features. This is often a normal variantvariant

The "normal" ST-T waves in RBBB should be oriented The "normal" ST-T waves in RBBB should be oriented opposite to the direction of the terminal QRS forces; i.e., in opposite to the direction of the terminal QRS forces; i.e., in leads with terminal R or R' forces the ST-T should be leads with terminal R or R' forces the ST-T should be negative or downwards; in leads with terminal S forces the negative or downwards; in leads with terminal S forces the ST-T should be positive or upwards. If the ST-T waves are in ST-T should be positive or upwards. If the ST-T waves are in the the same directionsame direction as the terminal QRS forces, they as the terminal QRS forces, they should be labeled should be labeled primary ST-T wave abnormalitiesprimary ST-T wave abnormalities

The ECG below illustrates 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 (leads I, II, aVR, V5, V6) in a patient with RBBB. ST-T wave abnormalities such as these may be related to ischemia, abnormalities such as these may be related to ischemia, infarction, electrolyte abnormalities, medications, CNS infarction, electrolyte abnormalities, medications, CNS disease, etc. (i.e., they are disease, etc. (i.e., they are nonspecificnonspecific and must be and must be correlated with the patient's clinical status).correlated with the patient's clinical status).

  Left Bundle Branch BlockLeft Bundle Branch Block (LBBB) (LBBB)

"Complete" LBBB" has a QRS duration "Complete" LBBB" has a QRS duration >>0.12s0.12s Close examination of QRS complex in various Close examination of QRS complex in various

leads reveals that the terminal forces (i.e., 2leads reveals that the terminal forces (i.e., 2ndnd half of QRS) are oriented half of QRS) are oriented leftwardleftward and and posteriorlyposteriorly because the left ventricle is depolarized because the left ventricle is depolarized afterafter the the right ventricle.right ventricle.

1.1. Terminal S waves in lead V1 indicating late Terminal S waves in lead V1 indicating late posteriorposterior forces forces

2.2. Terminal R waves in lead I, aVL, V6 indicating late Terminal R waves in lead I, aVL, V6 indicating late leftward leftward forces; usually broad, monophasic forces; usually broad, monophasic R waves are seen in these leads as R waves are seen in these leads as illustrated in the ECG below; in addition, illustrated in the ECG below; in addition, poor R progression from V1 to V3 is commonpoor R progression from V1 to V3 is common

The "normal" ST-T waves in LBBB should be oriented The "normal" ST-T waves in LBBB should be oriented opposite to the direction of the terminal QRS forces; opposite to the direction of the terminal QRS forces; i.e., in leads with terminal R or R' forces the ST-T i.e., in leads with terminal R or R' forces the ST-T should be downwards; in leads with terminal S forces should be downwards; in leads with terminal S forces the ST-T should be upwards. If the ST-T waves are in the ST-T should be upwards. If the ST-T waves are in the the same directionsame direction as the terminal QRS forces, as the terminal QRS forces, they should be labeled they should be labeled primary ST-T wave primary ST-T wave abnormalities.abnormalities. In the above ECG the ST-T In the above ECG the ST-T waves are "normal" for LBBB; i.e., they are waves are "normal" for LBBB; i.e., they are secondarysecondary to the change in the ventricular to the change in the ventricular depolarization sequencedepolarization sequence

"Incomplete" LBBB looks like LBBB but QRS duration "Incomplete" LBBB looks like LBBB but QRS duration = 0.10 to 0.12s, with less ST-T change. This is often = 0.10 to 0.12s, with less ST-T change. This is often a progression of LVH a progression of LVH

Left Anterior Fascicular BlockLeft Anterior Fascicular Block (LAFB)... (LAFB)... the most common intraventricular the most common intraventricular

conduction defectconduction defect Left axis deviation in frontal plane, usually -45 to -90 Left axis deviation in frontal plane, usually -45 to -90

degreesdegrees rS complexes in leads II, III, aVFrS complexes in leads II, III, aVF Small q-wave in leads I Small q-wave in leads I and/orand/or aVL aVL R-peak time in lead aVL >0.04s, often with slurred R R-peak time in lead aVL >0.04s, often with slurred R

wave downstroke wave downstroke QRS duration usually <0.12s unless coexisting QRS duration usually <0.12s unless coexisting

RBBBRBBB Usually see poor R progression in leads V1-V3 and Usually see poor R progression in leads V1-V3 and

deeper S waves in leads V5 and V6deeper S waves in leads V5 and V6 May May mimicmimic LVH voltage in lead aVL, and LVH voltage in lead aVL, and maskmask LVH LVH

voltage in leads V5 and V6voltage in leads V5 and V6

In this ECG, note -75 In this ECG, note -75 degree QRS axis, rS degree QRS axis, rS complexes in II, III, complexes in II, III, aVF, tiny q-wave in aVF, tiny q-wave in aVL, poor R aVL, poor R progression V1-3, and progression V1-3, and late S waves in leads late S waves in leads V5-6. QRS duration is V5-6. QRS duration is normal, and there is a normal, and there is a slight slur to the R slight slur to the R wave downstroke in wave downstroke in lead aVL lead aVL

Left Posterior Fascicular BlockLeft Posterior Fascicular Block (LPFB).... Very rare (LPFB).... Very rare

intraventricular defectintraventricular defect! ! Right axis deviation in the frontal plane (usually > +100 Right axis deviation in the frontal plane (usually > +100

degrees)degrees)

 rS complex in lead I  rS complex in lead I

 qR complexes in leads II, III, aVF, with R in lead III > R in  qR complexes in leads II, III, aVF, with R in lead III > R in lead IIlead II

 QRS duration usually <0.12s unless coexisting RBBB  QRS duration usually <0.12s unless coexisting RBBB

   Must first exclude (on clinical grounds) other Must first exclude (on clinical grounds) other causes of right axis deviation such as cor pulmonale, causes of right axis deviation such as cor pulmonale, pulmonary heart disease, pulmonary hypertension, pulmonary heart disease, pulmonary hypertension, etc., because these conditions can result in the etc., because these conditions can result in the identical ECG picture!identical ECG picture!

Bifascicular BlocksBifascicular Blocks RBBB plus either LAFB RBBB plus either LAFB

(common) (common) ororLPFB LPFB (uncommon) (uncommon)

Features of RBBB plus Features of RBBB plus frontal plane features frontal plane features of the fascicular block of the fascicular block (axis deviation, etc.)(axis deviation, etc.)

The above ECG shows The above ECG shows classic RBBB (note classic RBBB (note rSR' in V1) rSR' in V1) plusplus LAFB LAFB (note QRS axis = -45 (note QRS axis = -45 degrees, rS in II, III, degrees, rS in II, III, aVF; and small q in aVF; and small q in aVL). aVL).

Nonspecific Intraventricular Nonspecific Intraventricular Conduction Defects (IVCD)Conduction Defects (IVCD)

QRS duration >0.10s indicating slowed QRS duration >0.10s indicating slowed conduction in the ventriclesconduction in the ventricles

Criteria for specific bundle branch or fascicular Criteria for specific bundle branch or fascicular blocks not met blocks not met

Causes of nonspecific IVCD's includeCauses of nonspecific IVCD's include1.1. Ventricular hypertrophy (especially LVH)Ventricular hypertrophy (especially LVH)2.2. Myocardial infarction (so called Myocardial infarction (so called periinfarction periinfarction

blocksblocks))3.3. Drugs, especially class IA and IC Drugs, especially class IA and IC

antiarrhythmics (e.g., quinidine, flecainide)antiarrhythmics (e.g., quinidine, flecainide)4.4. Hyperkalemia Hyperkalemia

Wolff-Parkinson-White Wolff-Parkinson-White PreexcitationPreexcitation

Although not a true IVCD, this condition causes widening of Although not a true IVCD, this condition causes widening of QRS complex and, therefore, deserves to be considered QRS complex and, therefore, deserves to be considered herehere

QRS complex represents a QRS complex represents a fusionfusion between between twotwo ventricular ventricular activation frontsactivation fronts

1.1. Early ventricular activation in region of the accessory AV Early ventricular activation in region of the accessory AV pathway (pathway (Bundle of KentBundle of Kent))

2.2. Ventricular activation through the normal AV junction, Ventricular activation through the normal AV junction, bundle branch systembundle branch system

3.3. ECG criteria include all of the followingECG criteria include all of the followingShort PR interval (<0.12s) Short PR interval (<0.12s) Initial slurring of QRS complex (Initial slurring of QRS complex (delta wavedelta wave) representing early ) representing early

ventricular activation through normal ventricular muscle in ventricular activation through normal ventricular muscle in region of the accessory pathway region of the accessory pathway

  Prolonged QRS duration (usually >0.10s) Prolonged QRS duration (usually >0.10s)   Secondary ST-T changes due to the altered ventricular Secondary ST-T changes due to the altered ventricular

activation sequence activation sequence

QRS morphology, including polarity of QRS morphology, including polarity of delta wave depends on the particular delta wave depends on the particular location of the accessory pathway as location of the accessory pathway as well as on the relative proportion of the well as on the relative proportion of the QRS complex that is due to early QRS complex that is due to early ventricular activation (i.e., degree of ventricular activation (i.e., degree of fusion).fusion).

delta waves, if negative in polarity, may delta waves, if negative in polarity, may mimic infarct Q waves and result in false mimic infarct Q waves and result in false positive diagnosis of myocardial positive diagnosis of myocardial infarction infarction

Right Atrial Enlargement (RAE) Right Atrial Enlargement (RAE) P wave amplitude >2.5 mm in II and/or >1.5 mm P wave amplitude >2.5 mm in II and/or >1.5 mm

in V1 (these criteria are not very specific or in V1 (these criteria are not very specific or sensitive)sensitive)

Better criteria can be derived from the QRS Better criteria can be derived from the QRS complex; these QRS changes are due to both the complex; these QRS changes are due to both the high incidence of RVH when RAE is present, and high incidence of RVH when RAE is present, and the RV displacement by an enlarged right atriumthe RV displacement by an enlarged right atrium

1.1. QR, Qr, qR, or qRs morphology in lead V1 (in QR, Qr, qR, or qRs morphology in lead V1 (in absence of coronary heart disease)absence of coronary heart disease)

2.2. QRS voltage in V1 is <5 mm QRS voltage in V1 is <5 mm andand V2/V1 voltage V2/V1 voltage ratio is >6 (Sensitivity = 50%; Specificity = 90%) 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. .

Left Atrial Enlargement (LAE) Left Atrial Enlargement (LAE)

P wave duration P wave duration >> 0.12s in frontal plane (usually 0.12s in frontal plane (usually lead II)  Notched P wave in limb leads with the lead II)  Notched P wave in limb leads with the inter-peak duration inter-peak duration >> 0.04s 0.04s

Terminal P negativity in lead V1 (i.e., "P-terminal Terminal P negativity in lead V1 (i.e., "P-terminal force") duration force") duration >>0.04s, depth 0.04s, depth >>1 mm.1 mm.

Sensitivity = 50%; Specificity = 90%Sensitivity = 50%; Specificity = 90%

Bi-Atrial Enlargement (BAE) Bi-Atrial Enlargement (BAE)

Features of both RAE and LAE in Features of both RAE and LAE in same ECGsame ECG

P wave in lead II >2.5 mm tall P wave in lead II >2.5 mm tall andand >>0.12s in duration0.12s in duration

Initial positive component of P wave Initial positive component of P wave in V1 >1.5 mm tall in V1 >1.5 mm tall andand prominent P- prominent P-terminal force terminal force

Introduction to ECG Recognition of Introduction to ECG Recognition of Myocardial Infarction Myocardial Infarction

When myocardial blood supply is abruptly reduced or cut When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events off to a region of the heart, a sequence of injurious events occur beginning with subendocardial or transmural occur beginning with subendocardial or transmural ischemia, followed by necrosis, and eventual fibrosis ischemia, followed by necrosis, and eventual fibrosis (scarring) if the blood supply isn't restored in an (scarring) if the blood supply isn't restored in an appropriate period of time. Rupture of an atherosclerotic appropriate period of time. Rupture of an atherosclerotic plaque followed by acute coronary thrombosis is the usual plaque followed by acute coronary thrombosis is the usual mechanism of acute MI. The ECG changes reflecting this mechanism of acute MI. The ECG changes reflecting this sequence usually follow a well-known pattern depending on sequence usually follow a well-known pattern depending on the location and size of the MI. MI's resulting from total the location and size of the MI. MI's resulting from total coronary occlusion result in more homogeneous tissue coronary occlusion result in more homogeneous tissue damage and are usually reflected by a damage and are usually reflected by a Q-wave MI patternQ-wave MI pattern on the ECG. MI's resulting from subtotal occlusion result in on the ECG. MI's resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by more heterogeneous damage, which may be evidenced by a a nonnon Q-waveQ-wave MI MI pattern on the ECG. pattern on the ECG. Two-thirds of MI's Two-thirds of MI's presenting to emergency rooms evolve to non-Q presenting to emergency rooms evolve to non-Q wave MI's, most having ST segment depression or T wave MI's, most having ST segment depression or T wave inversionwave inversion

Most MI's are located in the Most MI's are located in the left ventricleleft ventricle. In the setting of a . In the setting of a proximal right coronary artery occlusion, however, up to 50% may proximal right coronary artery occlusion, however, up to 50% may also have a component of also have a component of rightright ventricularventricular infarctioninfarction as well. as well. Right-sided chest leads are necessary to recognize RV MI.Right-sided chest leads are necessary to recognize RV MI.

In general, the more leads of the 12-lead ECG with MI changes (Q 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 waves and ST elevation), the larger the infarct size and the worse the prognosis. Additional leads on the back, V7-9 (horizontal to the prognosis. Additional leads on the back, V7-9 (horizontal to V6), may be used to improve the recognition of true posterior MIV6), may be used to improve the recognition of true posterior MI

The left anterior descending coronary artery (LAD) and it's The left anterior descending coronary artery (LAD) and it's branches usually supply the anterior and anterolateral walls of the branches usually supply the anterior and anterolateral walls of the left ventricle and the anterior two-thirds of the septum. The left left ventricle and the anterior two-thirds of the septum. The left circumflex coronary artery (LCX) and its branches usually supply circumflex coronary artery (LCX) and its branches usually supply the posterolateral wall of the left ventricle. The right coronary the posterolateral wall of the left ventricle. The right coronary artery (RCA) supplies the right ventricle, the inferior artery (RCA) supplies the right ventricle, the inferior (diaphragmatic) and true posterior walls of the left ventricle, and (diaphragmatic) and true posterior walls of the left ventricle, and the posterior third of the septum. The RCA also gives off the AV the posterior third of the septum. The RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX. 10-15%, this artery is a branch of the LCX.

Usual ECG evolution of a Q-wave MI; not all of the Usual ECG evolution of a Q-wave MI; not all of the following patterns may be seen; the time from onset of MI following patterns may be seen; the time from onset of MI to the final pattern is quite variable and related to the to the final pattern is quite variable and related to the size of MI, the rapidity of reperfusion (if any), and the size of MI, the rapidity of reperfusion (if any), and the location of the MI.location of the MI.

1.1. A. Normal ECG prior to MIA. Normal ECG prior to MI2.2. B. Hyperacute T wave changes - increased T wave B. Hyperacute T wave changes - increased T wave

amplitude and width; may also see ST elevationamplitude and width; may also see ST elevation3.3. C. Marked ST elevation with hyperacute T wave changes C. Marked ST elevation with hyperacute T wave changes

(transmural injury)(transmural injury)4.4. D. Pathologic Q waves, less ST elevation, terminal T wave D. Pathologic Q waves, less ST elevation, terminal T wave

inversion (necrosis)  (Pathologic Q waves are usually inversion (necrosis)  (Pathologic Q waves are usually defined as duration defined as duration >>0.04 s or >25% of R-wave 0.04 s or >25% of R-wave amplitude)amplitude)

5.5. E. Pathologic Q waves, T wave inversion (necrosis and E. Pathologic Q waves, T wave inversion (necrosis and fibrosis)fibrosis)

6.6. F. Pathologic Q waves, upright T waves (fibrosis) F. Pathologic Q waves, upright T waves (fibrosis)

Inferior MI Family of Q-wave MI's Inferior MI Family of Q-wave MI's

includes inferior, true posterior, and right includes inferior, true posterior, and right ventricular MI's)ventricular MI's)

Inferior MIInferior MI1.1. Pathologic Q waves and evolving ST-T Pathologic Q waves and evolving ST-T

changes in leads II, III, aVFchanges in leads II, III, aVF2.2. Q waves usually largest in lead III, next Q waves usually largest in lead III, next

largest in lead aVF, and smallest in lead IIlargest in lead aVF, and smallest in lead II3.3. Example #1: frontal plane leads with fully Example #1: frontal plane leads with fully

evolved inferior MI (note Q-waves, residual evolved inferior MI (note Q-waves, residual ST elevation, and T inversion in II, III, aVF) ST elevation, and T inversion in II, III, aVF)

Old inferior MI (note largest Q in lead III, Old inferior MI (note largest Q in lead III,

next largest in aVF, and smallest in lead II)next largest in aVF, and smallest in lead II)

True posterior MI True posterior MI ECG changes are seen in anterior precordial ECG changes are seen in anterior precordial

leads V1-3, but are the leads V1-3, but are the mirror imagemirror image of an of an anteroseptal MIanteroseptal MI

1.1.   Increased R wave amplitude and duration (i.e., Increased R wave amplitude and duration (i.e., a "pathologic R wave" is a mirror image of a a "pathologic R wave" is a mirror image of a pathologic Q)pathologic Q)

2.2. R/S ratio in V1 or V2 >1 (i.e., prominent anterior R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)forces)

3.3. Hyperacute ST-T wave changes: i.e., ST Hyperacute ST-T wave changes: i.e., ST depression and large, inverted T waves in V1-3depression and large, inverted T waves in V1-3

4.4. Late normalization of ST-T with symmetrical Late normalization of ST-T with symmetrical upright T waves in V1-3 upright T waves in V1-3

Acute Acute inferoposterior MI inferoposterior MI (note tall R waves (note tall R waves V1-3, marked ST V1-3, marked ST depression V1-3, depression V1-3, ST elevation in II, ST elevation in II, III, aVF) III, aVF)

Old inferoposterior Old inferoposterior MI (note tall R in MI (note tall R in V1-3, upright T V1-3, upright T waves and inferior waves and inferior Q waves) Q waves)

Old posterolateral Old posterolateral MI (precordial MI (precordial leads): note tall R leads): note tall R waves and upright waves and upright T's in V1-3, and T's in V1-3, and loss of R in V6 loss of R in V6

Right Ventricular MI (only seen with proximal right coronary Right Ventricular MI (only seen with proximal right coronary

occlusion; i.e., with inferior family MI's)occlusion; i.e., with inferior family MI's) ECG findings usually ECG findings usually

require additional require additional leads on right chest leads on right chest (V1R to V6R, (V1R to V6R, analogous to the left analogous to the left chest leads)chest leads)

ST elevation, ST elevation, >>1mm, in right 1mm, in right chest leads, chest leads, especially V4R (see especially V4R (see below) below)

Anterior Family of Q-wave MI's Anterior Family of Q-wave MI's

Anteroseptal MI  Q, QS, or qrS complexes in leads Anteroseptal MI  Q, QS, or qrS complexes in leads V1-V3 (V4)V1-V3 (V4)

Evolving ST-T changesEvolving ST-T changes ExampleExample: Fully evolved anteroseptal MI (note QS : Fully evolved anteroseptal MI (note QS

waves in V1-2, qrS complex in V3, plus ST-T wave waves in V1-2, qrS complex in V3, plus ST-T wave

changes)changes)

Anterior MI (similar changes, but Anterior MI (similar changes, but usually V1 is spared; if V4-6 involved usually V1 is spared; if V4-6 involved call it "anterolateral") call it "anterolateral") ExampleExample: : Acute anterior or anterolateral MI Acute anterior or anterolateral MI (note Q's V2-6 plus hyperacute ST-T (note Q's V2-6 plus hyperacute ST-T changes) changes)

High Lateral MI (typical MI features High Lateral MI (typical MI features seen in leads I and/or aVL)seen in leads I and/or aVL)

ExampleExample: note Q-wave, slight ST : note Q-wave, slight ST elevation, and T inversion in lead aVL elevation, and T inversion in lead aVL

MI + Left Bundle Branch Block MI + Left Bundle Branch Block Often a difficult ECG diagnosis because in Often a difficult ECG diagnosis because in

LBBB the LBBB the right ventricleright ventricle is activated first is activated first and and left ventricularleft ventricular infarct Q waves may not infarct Q waves may not appear at the beginning of the QRS appear at the beginning of the QRS complex (unless the septum is involved). complex (unless the septum is involved).

Suggested ECG features, not all of which Suggested ECG features, not all of which are specific for MI include:  Q waves of any are specific for MI include:  Q waves of any size in size in twotwo or more of leads I, aVL, V5, or V6 or more of leads I, aVL, V5, or V6 (See below: one of the most reliable signs (See below: one of the most reliable signs and probably indicates and probably indicates septalseptal infarction, infarction, because the septum is activated early from because the septum is activated early from the right ventricular side in LBBB) the right ventricular side in LBBB)

Reversal of the usual R wave progression in precordial leads (see above )Reversal of the usual R wave progression in precordial leads (see above ) Notching of the downstroke of the S wave in precordial leads to the right of 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 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 complex to a predominate R wave complex); this may be a Q-wave equivalent.equivalent.

Notching of the upstroke of the S wave in precordial leads Notching of the upstroke of the S wave in precordial leads to the right of the transition zone (another Q-wave to the right of the transition zone (another Q-wave equivalent).equivalent).

  rSR' complex in leads I, V5 or V6 (the S is a Q-wave rSR' complex in leads I, V5 or V6 (the S is a Q-wave equivalent occurring in the middle of the QRS complex)equivalent occurring in the middle of the QRS complex)

RS complex in V5-6 rather than the usual monophasic R RS complex in V5-6 rather than the usual monophasic R waves seen in uncomplicated LBBB; (the S is a Q-wave waves seen in uncomplicated LBBB; (the S is a Q-wave equivalent).equivalent).

"Primary" ST-T wave changes (i.e., ST-T changes in the "Primary" ST-T wave changes (i.e., ST-T changes in the same direction as the QRS complex rather than the usual same direction as the QRS complex rather than the usual "secondary" ST-T changes seen in uncomplicated LBBB); "secondary" ST-T changes seen in uncomplicated LBBB); these changes may reflect an acute, evolving MI. these changes may reflect an acute, evolving MI.

Non-Q Wave MI Non-Q Wave MI

Recognized by evolving ST-T changes over Recognized by evolving ST-T changes over time without the formation of pathologic Q time without the formation of pathologic Q waves (in a patient with typical chest pain waves (in a patient with typical chest pain symptoms and/or elevation in myocardial-symptoms and/or elevation in myocardial-specific enzymes)specific enzymes)

Although it is tempting to localize the non-Although it is tempting to localize the non-Q MI by the particular leads showing ST-T Q MI by the particular leads showing ST-T changes, this is probably only valid for the changes, this is probably only valid for the ST segment elevation patternST segment elevation pattern

Evolving ST-T changes may include any of Evolving ST-T changes may include any of the following patterns: the following patterns:

Convex downward ST segment Convex downward ST segment depression only (common)depression only (common)

Convex upwards or straight ST Convex upwards or straight ST segment elevation only (uncommon)segment elevation only (uncommon)

Symmetrical T wave inversion only Symmetrical T wave inversion only (common)(common)

Combinations of above changesCombinations of above changes Example:Example: Anterolateral ST-T wave Anterolateral ST-T wave

changes changes

The Pseudoinfarcts The Pseudoinfarcts These are ECG conditions that mimic myocardial infarction either by These are ECG conditions that mimic myocardial infarction either by

simulating pathologic Q or QS waves or mimicking the typical ST-T simulating pathologic Q or QS waves or mimicking the typical ST-T changes of acute MIchanges of acute MI

1.1. WPW preexcitation (WPW preexcitation (negativenegative delta wave may mimic pathologic Q delta wave may mimic pathologic Q waves)waves)

2.2. IHSS (septal hypertrophy may make normal septal Q waves "fatter" IHSS (septal hypertrophy may make normal septal Q waves "fatter" thereby mimicking pathologic Q waves)thereby mimicking pathologic Q waves)

3.3. LVH (may have QS pattern or poor R wave progression in leads V1-3) LVH (may have QS pattern or poor R wave progression in leads V1-3) 4.4. RVH (tall R waves in V1 or V2 may mimic true posterior MI) cRVH (tall R waves in V1 or V2 may mimic true posterior MI) c5.5. Complete or incomplete LBBB (QS waves or poor R wave progression in Complete or incomplete LBBB (QS waves or poor R wave progression in

leads V1-3)leads V1-3)6.6.   Pneumothorax (loss of right precordial R waves)Pneumothorax (loss of right precordial R waves)7.7.   Pulmonary emphysema and cor pulmonale (loss of R waves V1-3 and/or Pulmonary emphysema and cor pulmonale (loss of R waves V1-3 and/or

inferior Q waves with right axis deviation)inferior Q waves with right axis deviation)8.8. Left anterior fascicular block (may see small q-waves in anterior chest Left anterior fascicular block (may see small q-waves in anterior chest

leads)leads)9.9. Acute pericarditis (the ST segment elevation may mimic acute Acute pericarditis (the ST segment elevation may mimic acute

transmural injury)transmural injury)10.10. Central nervous system disease (may mimic non-Q wave MI by causing Central nervous system disease (may mimic non-Q wave MI by causing

diffuse ST-T wave changes) diffuse ST-T wave changes)

Miscellaneous Abnormalities of the Miscellaneous Abnormalities of the QRS Complex QRS Complex

The differential diagnosis of these The differential diagnosis of these QRS abnormalities depend on other QRS abnormalities depend on other ECG findings as well as clinical ECG findings as well as clinical patient informationpatient information

Poor R Wave Progression - defined as Poor R Wave Progression - defined as loss of, or no R waves in leads V1-3 loss of, or no R waves in leads V1-3 (R <2mm): (R <2mm):

Normal variant (if the rest of the ECG is normal)Normal variant (if the rest of the ECG is normal) LVH (look for voltage criteria and ST-T changes of LVH (look for voltage criteria and ST-T changes of

LV "strain")LV "strain") Complete or incomplete LBBB (increased QRS Complete or incomplete LBBB (increased QRS

duration)duration) Left anterior fascicular block (should see LAD in Left anterior fascicular block (should see LAD in

frontal plane)frontal plane) AnteriorAnterior oror anteroseptalanteroseptal MI MI Emphysema and COPD (look for R/S ratio in V5-6 Emphysema and COPD (look for R/S ratio in V5-6

<1)<1) Diffuse infiltrative or myopathic processesDiffuse infiltrative or myopathic processes WPW preexcitation (look for WPW preexcitation (look for delta wavesdelta waves, short PR) , short PR)

Prominent Anterior Forces - defined as Prominent Anterior Forces - defined as R/S ration >1 in V1 or V2R/S ration >1 in V1 or V2

1.1. Normal variant (if rest of the ECG is Normal variant (if rest of the ECG is normal)normal)

2.2. TrueTrue posteriorposterior MI MI (look for evidence of (look for evidence of inferior MI)inferior MI)

3.3. RVH (should see RAD in frontal plane RVH (should see RAD in frontal plane and/or P-pulmonale)and/or P-pulmonale)

4.4. Complete or incomplete RBBB (look for Complete or incomplete RBBB (look for rSR' in V1)rSR' in V1)

5.5. WPW preexcitation (look for WPW preexcitation (look for delta wavesdelta waves, , short PR) short PR)

General Introduction to ST, T, and General Introduction to ST, T, and U wave abnormalities U wave abnormalities

Basic Concept:Basic Concept: the the specificityspecificity of ST-T and of ST-T and U wave abnormalities is provided more by U wave abnormalities is provided more by the the clinical circumstancesclinical circumstances in which the in which the ECG changes are found than by the ECG changes are found than by the particular changes themselves. Thus the particular changes themselves. Thus the term, term, nonspecific ST-T wave abnormalitiesnonspecific ST-T wave abnormalities, , is frequently used when the clinical data is frequently used when the clinical data are not available to correlate with the ECG are not available to correlate with the ECG findings. This does not mean that the ECG findings. This does not mean that the ECG changes are unimportant! It is the changes are unimportant! It is the responsibility of the clinician providing responsibility of the clinician providing care for the patient to ascertain the care for the patient to ascertain the importance of the ECG findings importance of the ECG findings

Factors affecting the ST-T and U wave configuration include Factors affecting the ST-T and U wave configuration include   Intrinsic myocardial disease (e.g., myocarditis, ischemia, Intrinsic myocardial disease (e.g., myocarditis, ischemia,

infarction, infiltrative or myopathic processes) infarction, infiltrative or myopathic processes)

 Drugs (e.g., digoxin, quinidine, tricyclics, and many others)  Drugs (e.g., digoxin, quinidine, tricyclics, and many others)

 Electrolyte abnormalities of potassium, magnesium, calcium  Electrolyte abnormalities of potassium, magnesium, calcium

 Neurogenic factors (e.g., stroke, hemorrhage, trauma,  Neurogenic factors (e.g., stroke, hemorrhage, trauma, tumor, etc.) tumor, etc.)

 Metabolic factors (e.g., hypoglycemia, hyperventilation)  Metabolic factors (e.g., hypoglycemia, hyperventilation)

 Atrial repolarization (e.g., at fast heart rates the atrial T  Atrial repolarization (e.g., at fast heart rates the atrial T wave may pull down the beginning of the ST segment) wave may pull down the beginning of the ST segment)

 Ventricular conduction abnormalities and rhythms  Ventricular conduction abnormalities and rhythms originating in the ventricles originating in the ventricles

Secondary" ST-T Wave changes (these are Secondary" ST-T Wave changes (these are normalnormal ST-T ST-T wave changes solely due to alterations in the sequence of wave changes solely due to alterations in the sequence of ventricular activationventricular activation

ST-T changes seen in bundle branch blocks (generally the ST-T changes seen in bundle branch blocks (generally the ST-T polarity is opposite to the major or terminal deflection ST-T polarity is opposite to the major or terminal deflection of the QRS) of the QRS)

 ST-T changes seen in fascicular block  ST-T changes seen in fascicular block

 ST-T changes seen in nonspecific IVCD  ST-T changes seen in nonspecific IVCD

 ST-T changes seen in WPW preexcitation  ST-T changes seen in WPW preexcitation

 ST-T changes in PVCs, ventricular arrhythmias, and  ST-T changes in PVCs, ventricular arrhythmias, and ventricular paced beats ventricular paced beats

Primary" ST-T Wave Abnormalities (ST-T wave Primary" ST-T Wave Abnormalities (ST-T wave changes that are independent of changes in changes that are independent of changes in ventricular activation and that may be the result ventricular activation and that may be the result of global or segmental pathologic processes that of global or segmental pathologic processes that affect ventricular repolarization) affect ventricular repolarization)

Drug effects (e.g., digoxin, quinidine, etc) Drug effects (e.g., digoxin, quinidine, etc)

 Electrolyte abnormalities (e.g., hypokalemia)  Electrolyte abnormalities (e.g., hypokalemia)

 Ischemia, infarction, inflammation, etc  Ischemia, infarction, inflammation, etc

 Neurogenic effects (e.g., subarrachnoid  Neurogenic effects (e.g., subarrachnoid hemorrhage causing long QT) hemorrhage causing long QT)

Differential Diagnosis of ST Segment Differential Diagnosis of ST Segment Elevation Elevation

Normal Variant "Early Repolarization" Normal Variant "Early Repolarization" (usually concave upwards, ending (usually concave upwards, ending with symmetrical, large, upright T with symmetrical, large, upright T waves) waves)

Example #1Example #1: "Early Repolarization": note high : "Early Repolarization": note high take off of the ST segment in leads V4-6; the ST take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal elevation in V2-3 is generally seen in most normal ECG's; the ST elevation in V2-6 is concave ECG's; the ST elevation in V2-6 is concave upwards, another characteristic of this normal upwards, another characteristic of this normal variant variant

Ischemic Heart Disease (usually Ischemic Heart Disease (usually convex upwards, or straightened) convex upwards, or straightened)

Acute transmural Acute transmural injury - as in this injury - as in this acute anterior MI acute anterior MI

Persistent ST elevation after acute MI Persistent ST elevation after acute MI suggests ventricular aneurysm suggests ventricular aneurysm

 ST elevation may also be seen as a  ST elevation may also be seen as a manifestation of Prinzmetal's (variant) manifestation of Prinzmetal's (variant) angina (coronary artery spasm) angina (coronary artery spasm)

 ST elevation during exercise testing  ST elevation during exercise testing suggests extremely tight coronary suggests extremely tight coronary artery stenosis or spasm (transmural artery stenosis or spasm (transmural ischemia ischemia

Acute Pericarditis Acute Pericarditis Concave upwards ST elevation in most Concave upwards ST elevation in most

leads except aVR leads except aVR

 No reciprocal ST segment depression  No reciprocal ST segment depression (except in aVR) (except in aVR)

 Unlike "early repolarization", T waves are  Unlike "early repolarization", T waves are usually low amplitude, and heart rate is usually low amplitude, and heart rate is usually increased. usually increased.

 May see PR segment depression, a  May see PR segment depression, a manifestation of atrial injury manifestation of atrial injury

Other Causes Other Causes Left ventricular hypertrophy (in right Left ventricular hypertrophy (in right

precordial leads with large S-waves) precordial leads with large S-waves)

 Left bundle branch block (in right  Left bundle branch block (in right precordial leads with large S-waves) precordial leads with large S-waves)

 Advanced hyperkalemia  Advanced hyperkalemia

 Hypothermia (prominent J-waves or  Hypothermia (prominent J-waves or Osborne waves) Osborne waves)

Differential Diagnosis of ST Differential Diagnosis of ST Segment Depression Segment Depression

Normal variants or artifacts:  Pseudo-ST-Normal variants or artifacts:  Pseudo-ST-depression (wandering baseline due to depression (wandering baseline due to poor skin-electrode contact) poor skin-electrode contact)

 Physiologic J-junctional depression with  Physiologic J-junctional depression with sinus tachycardia (most likely due to atrial sinus tachycardia (most likely due to atrial repolarization) repolarization)

 Hyperventilation-induced ST segment  Hyperventilation-induced ST segment depression depression

Ischemic heart disease Ischemic heart disease

Subendocardial ischemia (exercise Subendocardial ischemia (exercise induced or during angina attack - as induced or during angina attack - as illustrated below) illustrated below)

Nonischemic causes of ST depression  RVH (right Nonischemic causes of ST depression  RVH (right precordial leads) or LVH (left precordial leads, I, aVL) precordial leads) or LVH (left precordial leads, I, aVL)

 Digoxin effect on ECG  Digoxin effect on ECG

 Hypokalemia  Hypokalemia

 Mitral valve prolapse (some cases)  Mitral valve prolapse (some cases)

 CNS disease  CNS disease

 Secondary ST segment changes with IV conduction  Secondary ST segment changes with IV conduction abnormalities (e.g., RBBB, LBBB, WPW, etc) abnormalities (e.g., RBBB, LBBB, WPW, etc)

Differential Diagnosis of T Wave Differential Diagnosis of T Wave Inversion Inversion

Q wave and non-Q wave MI (e.g., evolving Q wave and non-Q wave MI (e.g., evolving anteroseptal MI): anteroseptal MI):

Myocardial ischemia Myocardial ischemia

 Subacute or old pericarditis  Subacute or old pericarditis

 Myocarditis  Myocarditis

 Myocardial contusion (from trauma)  Myocardial contusion (from trauma)

 CNS disease causing long QT interval  CNS disease causing long QT interval

Idiopathic apical hypertrophy (a rare Idiopathic apical hypertrophy (a rare form of hypertrophic form of hypertrophic cardiomyopathy) cardiomyopathy)

 Mitral valve prolapse  Mitral valve prolapse

 Digoxin effect  Digoxin effect

 RVH and LVH with "strain  RVH and LVH with "strain

Differential Diagnosis of U Wave Differential Diagnosis of U Wave Abnormalities Abnormalities

Prominent upright U waves  Sinus bradycardia Prominent upright U waves  Sinus bradycardia accentuates the U wave accentuates the U wave

 Hypokalemia (remember the triad of ST  Hypokalemia (remember the triad of ST segment depression, low amplitude T waves, segment depression, low amplitude T waves, and prominent U waves) and prominent U waves)

 Quinidine and other type 1A antiarrhythmics  Quinidine and other type 1A antiarrhythmics

 CNS disease with long QT intervals (often the  CNS disease with long QT intervals (often the T and U fuse to form a giant "T-U fusion T and U fuse to form a giant "T-U fusion wave") wave")

LVH (right precordial leads with deep LVH (right precordial leads with deep S waves) S waves)

 Mitral valve prolapse (some cases)  Mitral valve prolapse (some cases)

 Hyperthyroidism  Hyperthyroidism

Negative or "inverted" U waves Negative or "inverted" U waves Ischemic heart disease (often indicating left Ischemic heart disease (often indicating left

main or LAD disease)  Myocardial infarction main or LAD disease)  Myocardial infarction (in leads with pathologic Q waves) (in leads with pathologic Q waves)

 During episode of acute ischemia (angina  During episode of acute ischemia (angina or exercise-induced ischemia) or exercise-induced ischemia)

 Post extrasystolic in patients with  Post extrasystolic in patients with coronary heart disease coronary heart disease

 During coronary artery spasm  During coronary artery spasm (Prinzmetal's angina) (Prinzmetal's angina)

Nonischemic causes Nonischemic causes

Some cases of LVH or RVH (usually in Some cases of LVH or RVH (usually in leads with prominent R waves) leads with prominent R waves)

 Some patients with LQTS (see  Some patients with LQTS (see below: Lead V6 shows giant negative below: Lead V6 shows giant negative TU fusion wave in patient with LQTS; TU fusion wave in patient with LQTS; a prominent upright U wave is seen a prominent upright U wave is seen in Lead V1 in Lead V1