Electrocardiography. Dr.S Kesanakurthy Reviewed by Dr. Michael Jacobson. A Sequential Approach to Reading EKGâ€™s:. A Sequential Approach to Reading EKGâ€™s:. Gain familiarity with the "normal" EKG. Evaluate the rhythm.
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Dr. Michael Jacobson
3. Calculate rate and axis. Measure intervals. Consider the diagnostic possibilities suggested by abnormalities found, but do not make final diagnoses yet (except for left bundle branch block, which makes further interpretation impossible).
4. Evaluate each P wave, QRS, ST segment, T wave and U wave in the following lead order: I and aVL then II, III, and aVF then V1, V2, V3, V4, V5 and V6 (beginning with R wave progression), localizing and grouping all abnormalities.
5. Arrive at final diagnoses by critically evaluating each abnormality in relationship to all others and any available clinical data.
Each of the 12 leads represents a particular orientation in space, as indicated below (RA = right arm; LA = left arm, LF = left foot)
Bipolar limb leads (frontal plane): Lead I: RA (-) to LA (+) (Right Left, or lateral) Lead II: RA (-) to LF (+) (Superior Inferior) Lead III: LA (-) to LF (+) (Superior Inferior)
Augmented unipolar limb leads (frontal plane):
Lead aVR: RA (+) to [LA & LF] (-) (Rightward) Lead aVL: LA (+) to [RA & LF] (-) (Leftward) Lead aVF: LF (+) to [RA & LA] (-) (Inferior)
Unipolar (+) chest leads (horizontal plane): Leads V1, V2, V3: (Posterior Anterior) Leads V4, V5, V6:(Right Left, or lateral)
Ps in V1 and V2 are Diphasic, but never negative in V2
Q Wave: Amplitude of Q waves usually < 4mm in all leads except in III where it may reach 5 mm and the depth is < 25% of the R wave in all leads except III. R wave: Measures about 15 mm in lead I, 10mm in aVL and can be about 19mm in II, III & aVF. S wave: Most prominent in aVR about 16mm, 9mm in III & aVL, and <5mm in I, III and aVF. ST : 1mm elevation may be seen especially in the inferior leads, but ST depression is pathologic in any lead as long as the axis is directed inferiorly and leftward.
T wave: Always upright in I & II and inverted in aVR. Usually upright in aVF and inverted or upright in III & aVL. T wave is always upright in V5-6. Tallest in II,V2-3. <6mm in all limb leads., but not less than 0.5 mm in I & II
QT interval: The duration of the ventricular electrical systole. Normal QTc is about 0.39 secs in males and 0.41 secs in females. QTc > 0.44 secs is ABNORMAL.
U wave: Represent after potentials of ventricular myocardium.
P waves duration varies between 0.08 – 0.11 secs with an amplitude of 0.25mV and P wave axis is directed Inferiorly and leftward (00 – 750)
P waves are always upright in leads I and II, always inverted in aVR, diphasic in III, aVL, and V1, V2. A negative component of more than than one small square is considered abnormal. [left click once]
PR Interval is measured form the beginning of the P wave to the beginning of the QRS with a normal duration of 0.12 – 0.20 seconds. Lead II is usually used to measure PR interval.
Ventricular activation middle third of Left IV septum right septal surface RV leftward apex free walls of both ventricles basal portion of septum and the posterobasal portion of the free wall of LV are the last parts to be activated.
Left axis deviation
LVH, left anterior fasicular block, inferior wall MI
Right axis deviation
RVH, left posterior fascicular block, lateral wall MI
Normal axis (-30 to +90degrees)
Left axis deviation (-30 to -90) check lead II. To be true left axis deviation, it should also be down in lead II. If the QRS is upright in II, the axis is still normal (0 to -30).
.Right axis deviation
Indeterminate axis (-90 to -180)
If the axis is - 300 Biphasic in lead II, and negative in aVF
If the axis is <300 predominantly negative in lead II and aVF
Normal QRS width with an axis of >1000
Predominantly positive in leads II and III, and negative in aVL
Note diffuse J-point elevation, early R wave transition, with notched downstroke of R wave in lateral precordial leads. These changes are characteristic of early repolarization as seen in this EKG of a 28 year old African-American male.
Normal variants or artifacts
The specificity of ST-T and U wave abnormalities is provided more by the clinical circumstances in which the ECG changes are found than by the particular changes themselves.
Thus the term, nonspecific ST-T waveabnormalities, is frequently used when the clinical data are not available to correlate with the ECG findings. This does not mean that the ECG changes are unimportant!
It is the responsibility of the clinician providing care for the patient to ascertain the importance of the ECG findings.
Intrinsic myocardial disease (e.g., myocarditis, ischemia, infarction, infiltrative or myopathic processes) 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
E - ElectrolytesL - LBBBE - Early RepolarizationV - Ventricular hypertrophyA - AneurysmT - Treatment - PericardiocentesisI - Injury (AMI, contusion)O - Osborne waves (hypothermia)N - Non-occlusive vasospasm
Normal Variant “Early Repolarization”
Ischemic Heart Disease
Ischemic Heart Disease (usually convex upwards, or straightened) Acute transmural injury - as in this acute anterior MI
J-point is the point where S wave becomes isoelectric and joins the T wave.
ST segment elevation or depression is measured 2 small boxes away from the J-point and then, up or down the isoelectric line.
Normal variants or artifacts:
Subendocardial ischemia (exercise induced or during angina attack
“horizontal" ST depression in lead V6
Non Q-wave MI Reciprocal changes in acute Q-wave MI (e.g., ST depression in leads I & aVL
with acute inferior MI)
Ist Few Hours
First 24 Hours
First 72 Hours
Tomb stoning is less prominent with the onset of T wave inversions in the anterior precordium. Reciprocal changes are resolving.
Prominent Q waves have developed across the anterior precordium and leads I, aVL. However, ST segment elevation persists.
Q wave pattern in the anterolateral leads is well established.
Persistent ST segment elevation suggests complication by aneurysm or pericarditis
a) ST elevation and tall T waves
b) QS deflections in V1, V2 and V3 and V4
ST segment elevation in leads V4R and V5R reveals right ventricular involvement complicating the inferior infarct.
Note inferior ST segment elevation as well as atrioventricular dissociation secondary to complete heart block.
Note inferior ST segment elevation and Q waves as well as progressive prolongation of the PR interval followed by a dropped beat with grouped beating.
The "true" posterior MI is recognized by pathologic R waves in leads V1-2. These are the posterior equivalent of pathologic Q waves (seen from the perspective of the anterior leads). Tall T waves in these same leads are the posterior equivalent of inverted T waves in this fully evolved MI. The loss of forces in V6, I, aVL suggest a lateral wall extension of this MI.
ST segment elevation in leads I and aVL associated with inferior reciprocal changes along with poor R wave progression. Note preexisting anteroseptal MI.
Anterolateral ST segment depression is consistent with diffuse subendocardial ischemia vs. non-Q wave MI.
ST segment depression in leads V2 through V5 supports acute ischemic syndrome with no “Q” waves.
How to think about arrhythmias and conduction disturbances
A fully compensatory pause usually follows a premature complex, where the R - R interval produced by two sinus initiated QRS complexes on either side of the premature complex equals twice the normally conducted R - R interval
Premature Ventricular Complex
QRS complex appears bizarre usually greater than 120msec
T wave is large and opposite in direction to the QRS complex
A fully compensatory pause usually follows a PVC
a ventricular premature beat follows each normal beat
Atrial fibrillation (AF) is thought
to be due to multiple wavelets of conduction produced by reentry. Perpetuation of AF depends on
the relative dimensions of the atria and the size of the reentrant circuit. Compared with atrial flutter, in which there is one reentrant circuit and organized atrial activity, atrial fibrillation demonstrates no organized atrial contraction. This leads to blood stasis, the formation of clots, and the possibility of embolic events. Thus, most patients with chronic atrial fibrillation are given anticoagulants to reduce the risk of embolic events such as strokes.
No P waves. Narrow complex QRS with irregular RR intervals. Ventricular rate is controlled in this EKG.
Atrial Fib complicating inferior MI
The shortest RR interval is 190 msec, suggesting a high risk pathway that may be associated with rapid rates and degeneration to ventricular fibrillation. Catheter ablation should be strongly considered in patients such as this.WPW in Afib
Preexcited QRS complex with Atrial Fibrillation
Atrial Flutter circuit
Atrial flutter is a macro reentrant circuit in the right atrium. The circuit involves conduction in a counterclockwise (or clockwise) direction from the low posterior right atrium near the tricuspid valve annulus (TA), the posteroseptal region near the coronary sinus os, the interatrial septum, the high lateral right atrium, and down the crista terminalis to the isthmus between the inferior vena cava and the TA. The region of the posterior right atrium is thought to be the slow zone of conduction in the circuit. Evidence that supports this theory are data showing that atrial flutter can be entrained with atrial pacing. Electrophysiologists have developed techniques allowing to ablate the critical regions of the circuit causing atrial flutter, thus, rendering the circuit inoperable.
Atrial rate of 300 bpm with upright “FLUTTER” waves inferiorly. This is consistent with typical atrial flutter.
Atrial Flutter With 2:1 AV Conduction
Atrial flutter with 2:1 AV block is one of the most frequently missed ECG rhythm diagnoses because the flutter waves are often hard to find. In this example two flutter waves for each QRS are best seen in lead III and V1. The ventricular rate at 150 bpm should always prompt us to consider atrial flutter with 2:1 conduction as a diagnostic consideration.
1.Do you see any P waves?? How do they look? Are they upright, preceding, following or buried in relation to the QRS?
2. What is the ventricular rhythm? Look at the QRS and its duration?
3. Now wonder about the AV conduction with the above information!! Are the P and QRS related with normal intervals??
4. Are there any unusual complexes?
AVNRT—atrioventricular nodal reentry tachycardia
Narrow complex tachycardia
AVNRT—atrioventricular nodal reentry tachycardia
typical atrioventricular node reentrant tachycardia (AVNRT).
for atypical atrioventricular node reentrant tachycardia (AVNRT).AVN reentry
Diagram of atrioventricular (AV) nodal reentry
Slow pathway fibers begin in or around the coronary sinus (CS) or posteriorly and travel superiorly and anteriorly to converge on the compact AV node, which is in the superior interventricular septum. Fast pathway fibers travel superior and anterior to the compact AV node.
AV nodal reentry
a) Onset and termination are abrupt b) Episode ia initiated almost always by a premature atrial beat with a > PR interval c) Heart rate is usually between 140 and 220/min d) P - QRS complex resemble a junctional beat with inverted P in II, III, aVF. e) P waves may superimpose on, follow or rarely precede QRS f) QRS may be normal or wide secondary to an preexisting IVCD or secondary to an aberrant ventricular conduction.
a) Heart rate between 120/min and 220/min with minute to minute variations b) Normal QRS duration unless associated with aberrant conduction c) Rhythm generally regular, but may be irregular resembling A Fib or MAT d) Retrogade P wave may be seen following the QRS, but AV dissociation is common with slower rhythms
Wolf Parkinson White Syndrome
Wolf Parkinson White Syndrome
Wolf Parkinson White Syndrome
Conduction over an accessory pathway
WIDE COMPLEX TACHYCARDIA
SVT with aberrancy (atrial fibrillation/flutter)
Antidromic AV reentry via WPW accessory pathway
Atrial fibrillation, atrial flutter, atrial tachycardia, or AV nodal reentry in setting of WPW with rapid conduction down accessory pathway
Bundle branch reentry
Favors SVTwith Aberrancy
Duration: RBBB: QRS > 0.14 sec. < 0.14 sec. LBBB: QRS > 0.16 sec. < 0.16 sec.
Axis: QRS axis -90° to ±180° Normal
Morphology: Precordial concordance
If LBBB: V1 duration > 30 ms S wave > 70 ms S wave notched or slurred V6: qR or QR R wave monophasic
If RBBB: V1: monophasic R wave qR If triphasic, R > R1 R < R1 V6: R < S
Wide QRS - BBB(Aberrant conduction)
Wide QRS - Preexcitation(Conduction via AP)
Wide QRS - VT
Wide QRS Tachycardia may be of Ventricular or Supraventricular origin.
The main features of this wide QRS tachycardia that differentiate between ventricular and supraventricular origin are the presence of P waves and AV dissociation.
AV block is defined by PR intervals greater than 200 ms.
This may be caused by : drugs, such as digoxin;
excessive vagal tone
intrinsic disease in the AV junction or
bundle branch system
Second Degree AV Block: Type I Mobitz
Progressive PR segment prolongation prior to dropped QRS complex.
Dropped QRS wave with prolonged RR
AV conduction ratio 3:1 or higher
Left posterior fascicular block (posterior hemiblock, LPH) may be difficult to diagnose without prior ECGs. The QRS axis shifts substantially rightward. An axis of over +120, with no evidence of RVH or anterior infarction, is presumed LPH.
RS in I and aVL and a qR in Inferior leads are suggestive.
Left Bundle Branch Block
a) QRS duration > 0.12 secs b) Absence of “Q” waves in I,V5 & V6 c) Presence of a broad monophasic R in leads I, V5 & V6 which is usually notchedd) Displacement of ST segment and T wave in the opposite direction to the major deflection of the QRSe) Broad deep QS in V1 f) Delay of onset of the intrinsicoid deflection (R peak time) in V5 and V6
a) QRS duration > 0.12 secs b) Absence of “Q” waves in I,V5 & V6 c) Presence of a broad monophasic R in leads I, V5 & V6 which is usually notched d) Displacement of ST segment and T wave in the opposite direction to the major deflection of the QRS e) Broad deep QS in V1 f) Delay of onset of the intrinsicoid deflection (R peak time) in V5 and V6
a) Prolongation of QRS > 0.12 secs b) Secondary R (R’) in the right precordial leads with the R’ > than the initial R (rsR’) c) Delayed intrinsicoid deflection in the right precordial leads d) Wide S wave in leads I, V5 & V6
Normal PR interval
Intraventricular conduction block involving a RBBB with a division of the Left Bundle (either LAH or LPH) may be considered as a Bifascicular Block
A nice example of trifascicular block: Lead V1 shows RBBB; Lead II is mostly negative with an rS morphology suggesting left anterior fascicular block. Since Mobitz type II 2nd degree AV block is more often located in the bundle branch system, the only location left for this block is the left posterior division of the left bundle. Therefore all three ventricular conduction pathways are diseased.
RBBB- rsR’ in V1,V2
LAH qR in I, aVL
rS in II,III aVF
Frontal plane P wave vector > + 75ºRight Atrial Enlargement
high pointed P wave ³ 2,5 mm in II and/or aVF
Left atrial vectors travel posteriorly, leftward, and inferiorly and are reflected in the mid and late portions of the P wave. Left atrial enlargement causes an increase in the duration (time) of the vectors, but does not usually result in any significant shift of the axis of the P wave. This results in a broad, notched P wave in leads I and II, fre-quently with accompanying slurring of the terminal portion of the P wave. The distance between the two peaks of the notched P wave is usually longer ttotal duration of greater than0.12 seconds. Usually, the voltage (amplitude) of the P wave increases only slightly.
Left atrial enlargement and right ventricular hypertrophy have developed secondary to mitral stenosis causing fixed pulmonary hypertension
RVH: Right Axis Deviation > 1100or R/S ratio in V1 >1
R in V1 +S in V5or 6>11mm R in V1 >7mm S in V1 <2mm rSR’ in V1 >10mm
Left Ventricular Hypertrophy
Limb leads: R in lead I + S in lead III > 25 mm OR R in aVL > 11mm OR R in aVF >20mm OR S in aVR >14 Precordial leads: R in V5 or V6 >26mm OR R in V5 or V6 + S in V1 > 35mm OR largest R +largest S >45mm Supporting criteria: ST segment depression and T wave inversion in left precordial leads and in leads where QRS is upright (LV strain pattern).
The ST segment is depressed and the T wave is inverted. Note too that the R wave has become even taller.
Acute pulmonary embolus
S1 Q3 T3
a) Two sets of P waves b) RBBB – complete or incomplete c) Left anterior or posterior hemiblock d) ST segment and T wave elevation as in pericarditis, although transient e) Bradyarrhythmias, atrial, junctional or ventricular arrhythmias
a) ST segment depression, b) Decreased T wave amplitude c) Prominent U wave d) Prolongatiuon of QRS and P wave changes e) Cardiac Arrhythmias and AV blocks may occur
Marked widening of the QRS duration combined with tall, peaked T waves are suggestive of advanced hyperkalemia.
Note the absence of P waves, suggesting a junctional rhythm, but in hyperkalemia the atrial muscle may be paralyzed while still in sinus rhythm.
The sinus impulse conducts to the AV node through internodal tracts without activating the atrial muscle.
a) Diffuse ST segment elevation and T wave inversion in all leads
b) PR segment depression (>0.8mm) in all leads except aVR and occasionally V1. In aVR it is always elevated. These changes are attributed to subepicardial atrial injury
c) Low voltage QRS complexes & electrical alternans (with significant pericardial effusion)
Note upright QRS complex and P wave in lead aVR with inverted QRS in leads I and aVL.