slide1 n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Electrocardiography PowerPoint Presentation
Download Presentation
Electrocardiography

Loading in 2 Seconds...

play fullscreen
1 / 138

Electrocardiography - PowerPoint PPT Presentation


  • 164 Views
  • Uploaded on

Electrocardiography. Dr.S Kesanakurthy Reviewed by Dr. Michael Jacobson. A Sequential Approach to Reading EKG’s:. A Sequential Approach to Reading EKG’s:. Gain familiarity with the "normal" EKG. Evaluate the rhythm.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Electrocardiography' - abraham-nichols


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
slide1

Electrocardiography

Dr.S Kesanakurthy

Reviewed by

Dr. Michael Jacobson

a sequential approach to reading ekg s

A Sequential Approach to Reading EKG’s:

A Sequential Approach to Reading EKG’s:
  • Gain familiarity with the "normal" EKG.
  • Evaluate the rhythm.
    • It is best to evaluate rhythm on a rhythm strip. If this is not available, look at "pieces" of the rhythm in each lead (II and V1 generally have prominent P waves).
    • Determine if the rhythm is regular or irregular.
    • For irregular rhythms determine if the rhythm is completely irregular ("irregularly irregular") or if the irregularity is caused by additional or dropped complexes superimposed on an underlying regular rhythm.
    • For all rhythms, look for and evaluate P waves in the underlying rhythm first, and then in relation to any additional or dropped beats
    • Look at QRS complex morphology, first in the underlying rhythm and then in any additional beats.
    • At each step consider the two main questions of rhythm interpretation: where has impulse formation occurred and how has conduction proceeded.
a sequential approach to reading ekg s1
A Sequential Approach to Reading EKG’s:

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.

orientation of the 12 lead ecg
Orientation of the 12 Lead ECG:

   Right

Left

  Superior

Inferior

 Anterior

Posterior

  • It is important to remember that the 12-lead ECG provides spatial information about the heart's electrical activity in 3 approximately orthogonal directions:

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)

normal ecg
normal ECG

ST segment

  • The normal ECG has the following features:
    • P wave - due to atrial depolarization
    • PR interval (due to delayed conduction through the AV node) 0.12 - 0.20 seconds
    • QRS complex - due to ventricular depolarization
    • T wave due to ventricular repolarization
normal ecg1
normal ECG
  • The P wave represents atrial activation
  • the PR interval is the time from onset of atrial activation to onset of ventricular activation. (from the sinus node to the His Bundle purkinje fibers)
  • The QRS complex represents electrical ventricular activation; the QRS duration is the duration of ventricular activation.
  • The ST-T wave represents ventricular repolarization.
  • The QT interval is the duration of ventricular activation and recovery.
  • The U wave probably represents "after-depolarization" in the ventricles.
normal sinus rhythm
Normal Sinus Rhythm
  • A normal sinus rhythm one would expect the following:
    • an ECG with P waves
    • a PR interval of 0.12 - 0.20 seconds
    • a regular interval between each QRS complex (R-R interval) of 0.60 - 1.0 secs
    • a distinct a wave in the CVP trace due to atrial contraction
    • there may be minor regular variation in heart rate and pulse pressure associated with respiration (sinus arrhythmia)
normal ekg

Ps in I, II and aVF are always upright and always inverted in aVR

Normal EKG

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.

slide13

Normal axis

-300 to 1200

AXIS

Left axis deviation

-300 to -900

Right axis deviation

1200 to 1800

Indeterminate (extreme) axis deviation

-900 to 1800

AXIS
slide14

Differential Diagnosis

Lead I

Lead aVF

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)

Positive

Positive

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).

Positive

Neg

.Right axis deviation

Neg

Positive

Indeterminate axis (-90 to -180)

Neg

Neg

AXIS
left axis deviation
LEFT AXIS DEVIATION

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

right axis deviation
RIGHT AXIS DEVIATION

Normal QRS width with an axis of >1000

Predominantly positive in leads II and III, and negative in aVL

early repolarization
Early Repolarization

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
Normal variants or artifacts

Normal variants or artifacts

ischemia
ischemia

Ischemia

slide22

General Introduction to ST, T, and U wave abnormalities

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.

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, 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

secondary st t wave changes
“Secondary” ST-T Wave changes
  • “Secondary" ST-T Wave changes (these are ST-T wave changes solely due to alterations in the sequence of ventricular activation)      ST-T changes seen in bundle branch blocks (generally the ST-T polarity is opposite to the major or terminal deflection of the QRS) ST-T changes seen in fascicular block ST-T changes seen in nonspecific IVCD ST-T changes seen in WPW pre-excitation ST-T changes in PVCs, ventricular arrhythmias, and ventricular paced
  • beats
primary st t wave abnormalities
"Primary" ST-T Wave Abnormalities
  •  "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)
  •      Drug effects (e.g., digoxin, quinidine, etc)     Electrolyte abnormalities (e.g., hypokalemia)      Ischemia, infarction, inflammation, etc      Neurogenic effects (e.g., subarachnoid hemorrhage causing long QT)
causes of st elevation
Causes of ST Elevation

"ELEVATION"

E - ElectrolytesL - LBBBE - Early RepolarizationV - Ventricular hypertrophyA - AneurysmT - Treatment - PericardiocentesisI - Injury (AMI, contusion)O - Osborne waves (hypothermia)N - Non-occlusive vasospasm

differential diagnosis of st segment elevation
Differential Diagnosis of ST Segment Elevation

Normal Variant “Early Repolarization”

Ischemic Heart Disease

Acute Pericarditis

Other Causes

early repolarization1
"Early Repolarization":
  • Normal Variant "Early Repolarization" (usually concave upwards, ending with large symmetrical,, upright T waves)     
    • "Early Repolarization": note high take off of the ST segment in leads V4-6.
    • The ST elevation in V2-3 is generally seen in most normal ECG's.
    • The ST elevation in V2-6 is concave upwards, another characteristic of this normal variant.
slide29

Ischemic Heart Disease (usually convex upwards, or straightened) Acute transmural injury - as in this acute anterior MI

  • Persistent ST elevation after acute MI suggests ventricular aneurysm     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)
slide30

Acute Pericarditis

  • Concave upwards ST elevation in most leads except aVR      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 ventricular hypertrophy (in right precordial leads with large S-waves)      Left bundle branch block (in right precordial leads with large S-waves)      Advanced hyperkalemia      Hypothermia (prominent J-waves or Osborne waves)
slide31

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.

differential diagnosis of st segment depression
Differential Diagnosis of ST Segment Depression

Normal variants or artifacts:

  • Pseudo-ST depression (wandering baseline due to poor skin- electrode contact)     Physiologic J-junctional depression with sinus tachycardia (most likely due to atrial repolarization)     Hyperventilation-induced ST segment depression
  • Ischemic heart disease
  • Nonischemic causes of ST depression
non ischemic causes of st depression
Non-ischemic causes of ST depression
  • RVH (right precordial leads) or LVH (left precordial leads, I, aVL)      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)
ischemic heart disease
Ischemic heart disease

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)

stages of acute q wave mi
Stages of Acute Q-Wave MI

Ist Few Hours

First 24 Hours

First 72 Hours

evolution of acute anterolateral myocardial infarction at 3 hours
Evolution of acute anterolateral myocardial infarction at 3 hours

Tomb stoning is less prominent with the onset of T wave inversions in the anterior precordium. Reciprocal changes are resolving.

evolution of acute anterolateral myocardial infarction at 24 hours
Evolution of acute anterolateral myocardial infarction at 24 hours

Prominent Q waves have developed across the anterior precordium and leads I, aVL. However, ST segment elevation persists.

evolution of acute anterolateral myocardial infarction at 72 hours
Evolution of acute anterolateral myocardial infarction at 72 Hours

Q wave pattern in the anterolateral leads is well established.

Persistent ST segment elevation suggests complication by aneurysm or pericarditis

acute anteroseptal myocardial infarction
Acute anteroseptal myocardial infarction

a) ST elevation and tall T waves

b) QS deflections in V1, V2 and V3 and V4

right ventricular infarction rt sided leads
Right ventricular infarction (Rt.sided leads)

ST segment elevation in leads V4R and V5R reveals right ventricular involvement complicating the inferior infarct.

complicated acute inferior myocardial infarction
ComplicatedAcute inferior myocardial infarction

AV dissociation

Note inferior ST segment elevation as well as atrioventricular dissociation secondary to complete heart block.

acute inferior myocardial infarction complicated by wenkebach
Acute inferior myocardial infarction complicated by Wenkebach

wenckebach

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.

inferoposterior mi

Tall R in V2,R/S >1

Inferoposterior MI
  • Q waves in leads II, III & aVF
  • Tall R wave in lead V2 with a duration of > 0.04 secs and R/S ratio equal to or >1 (in patients over 30 years of age without RVH)
postero lateral mi
Postero-lateral MI

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.

lateral myocardial infarction
Lateral myocardial infarction

ST segment elevation in leads I and aVL associated with inferior reciprocal changes along with poor R wave progression. Note preexisting anteroseptal MI.

subendocardial ischemia
Subendocardial Ischemia

Anterolateral ST segment depression is consistent with diffuse subendocardial ischemia vs. non-Q wave MI.

unstable angina vs non q wave myocardial infarction
Unstable angina vs. non-Q wave myocardial infarction

ST segment depression in leads V2 through V5 supports acute ischemic syndrome with no “Q” waves.

non q mi
Non Q MI
  • Non-Q Wave MI
  • Recognized by evolving ST-T changes over time without the formation of pathologic Q waves (in a patient with typical chest pain symptoms and/or elevation in myocardial-specific enzymes)  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 downward ST segment depression only (common)
  • Convex upwards or straight ST segment elevation only (uncommon)
  • Symmetrical T wave inversion only (common)
  • Combinations of above changes
non q wave mi
Non-Q Wave MI
  •  Convex downward ST segment depression only (common)
  • Convex upwards or straight ST segment elevation only (uncommon)
  • Symmetrical T wave inversion only (common)
pseudoinfarcts
pseudoinfarcts
  • The Pseudoinfarcts
  • These are ECG conditions that mimic myocardial infarction either by simulating
      • pathologic Q or QS waves or mimicking the typical ST-T changes of acute MI.
      • IHSS (may make normal septal Q waves "fatter" 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 V1-V3)
      • Pneumothorax (loss of right precordial R waves)
      • Left anterior fascicular block (may see small q-waves in anterior chest leads)
      • Acute pericarditis (the ST segment elevation may mimic acute transmural injury)
      • CNS disease (may mimic non-Q wave MI by causing diffuse ST-T wave changes)
      • COPD and cor pulmonale (loss of R waves V1-3 and/or inferior Q waves with RAD)
arrhythmias
Arrhythmias

ARRHYTHMIAS

arrhthmia algo
Arrhthmia algo

How to think about arrhythmias and conduction disturbances

pauses
pauses

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

slide55

Atrial Premature Beat (APB)

APC
  • an abnormal P wave
  • as P waves are small and rather shapeless the difference in an APB is usually subtle. The one shown here is a clear example.
  • occurs earlier than expected
  • followed by a pause - but not a full compensatory pause
slide56
PVC

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

slide57

Interpolated PVC

  • Sinus rhythm with a PVC that has no effect on the sinus rate. Although not easily seen, there is often PR prolongation due to retrograde concealed penetration into the AV node.
PVC
bigeminy
Bigeminy

Ventricular Bigeminy

a ventricular premature beat follows each normal beat

qt prolongation
QT prolongation
  • Marked QT Prolongation
  • ECG rhythm strip of a 12 year old male with recurrent unexplained syncope and Long QT syndrome. ECG strip shows marked QT prolongation.
  • Low amplitude notched T waves are often associated with LQT type 2, associated with HERG gene mutations that cause defects in IKr.
a fib
A Fib

Atrial Fibrillation

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.

a fib1
A Fib

Atrial Fibrillation

No P waves. Narrow complex QRS with irregular RR intervals. Ventricular rate is controlled in this EKG.

a fib2
A Fib

Atrial Fib complicating inferior MI

wpw in afib

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

aflutter
AFlutter

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.

a flutter
A Flutter

Atrial Flutter

“F” waves

Atrial rate of 300 bpm with upright “FLUTTER” waves inferiorly. This is consistent with typical atrial flutter.

a flutter1
A 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.

slide67
SVT

Supraventricular Rhythms

slide68
SVT

Supraventircular Rhythms

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?

slide69
SVT

SVT

slide70
SVT

Supraventricular Tachycardia

  • P waves follow the QRS
  • QRS regular with a normal duration
slide71
SVT

Supraventricular Tachycardia

narrow complex tachycardia

Electrocardiographic patterns of narrow complex tachycardia

Narrow complex Tachycardia
  • The most important clue to the mechanism of a narrow complex tachycardia is the relationship of the P wave to the QRS complex.
  • No visible P wave often means that the P wave is buried in the QRS complex. This is usually due to typical atrio-ventricular (AV) nodal reentry.
  • With typical AV nodal reentry, the P wave may also be located just at the start or end of the QRS complex, giving a qRs or Rsr′ pattern.
  • When the P wave is located close to the previous QRS complex, it is identified as a short-RP tachycardia. This is often seen with accessory pathway–mediated tachycardia and is due to retrograde atrial activation over the accessory pathway.

AVNRT—atrioventricular nodal reentry tachycardia

narrow complex tachycardia1

Electrocardiographic patterns of narrow complex tachycardia

Narrow complex tachycardia
  • The most important clue to the mechanism of a narrow complex tachycardia is the relationship of the P wave to the QRS complex.
  • The P wave may also be far from the previous QRS complex and are classified as a
  • long-RP tachycardia.
  • If the P wave is inverted, it may be the result of atypical AV node reentry, or it may be using a slowly conducting accessory pathway in the retrograde direction.

Narrow complex tachycardia

AVNRT—atrioventricular nodal reentry tachycardia

avn reentry

Schema for

typical atrioventricular node reentrant tachycardia (AVNRT).

Schema

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.

avnrt
AVNRT

AV nodal reentry

Inverted P

150 /min

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.

junctional tachycardia
Junctional Tachycardia

Junctional Tachycardia

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

slide77
WPW

Wolf Parkinson White Syndrome

  • The short PR interval is due to a bypass track, also known as the Kent pathway.
  • By bypassing the AV node the PR shortens.
  • The delta wave represents early activation of the ventricles from the bypass tract.
  • The fusion QRS is the result of two activation sequences, one from the bypass tract
  • and one from the AV node.
  • The ST-T changes are secondary to changes in the ventricular activation sequence.
slide78
WPW

Wolf Parkinson White Syndrome

slide79
WPW

Wolf Parkinson White Syndrome

  • A PR interval of <0.12 sec, with normal P wave
  • Abnormally wide QRS complex with a duration of 0.11 sec or more
  • The presence of an initial slurring of the QRS complex, The delta Wave
  • Secondary ST segment and T wave changes
  • The frequency association of paroxysmal tachycardia
conduction over an accessory pathway
Conduction over an accessory pathway

Conduction over an accessory pathway

  • The morphology of a QRS complex in patients with an accessory pathway (AP) is an excellent example of fusion.
  • Conduction over an AP is influenced by drugs, sympathetic states, and its location along the atrioventricular annulus. If there is no antegrade conduction, the AP may still conduct in the retrograde direction but is considered concealed, because it is not apparent on the ECG.
  • When conduction over the AP is minimal and atrioventricular (AV) node conduction predominates, the QRS becomes a fusion of conduction over the AV node–His-Purkinje system and the AP.
  • H-P—His Purkinje; LA—left atrium; LV—left ventricle; PVC—premature ventricular complex; RA—right atrium; RV—right ventricle.
conduction over an accessory pathway1
Conduction over an accessory pathway
  • When conduction to the ventricle over the AP predominates compared with AV nodal conduction, the QRS represents a fusion of conduction over the AV node–HPS and the AP, but the larger the portion of the ventricle activated by the AP, the wider the QRS complex appears.
  • If ventricular activation is only over the AP, as with maximally preexcited tachycardias, it is difficult to distinguish the complex from ventricular tachycardia.
  • H-P—His Purkinje; LA—left atrium; LV—left ventricle; PVC—premature ventricular complex; RA—right atrium; RV—right ventricle.
wide complexd tachycardia
Wide complexd tachycardia

WIDE COMPLEX TACHYCARDIA

differential diagnosis of wide complex tachycardia
Differential Diagnosis of Wide-Complex Tachycardia

VT

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

ekg distinction of vt from svt with aberrancy
EKG Distinction of VT from SVT with Aberrancy

Favors SVTwith Aberrancy

Favors VT

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 tachycardia
Wide QRS Tachycardia

Wide QRS - BBB(Aberrant conduction)

Narrow QRS

Wide QRS - Preexcitation(Conduction via AP)

Wide QRS - VT

wide qrs tachycardia1
Wide QRS Tachycardia

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.

ventricular tachycardia
Ventricular tachycardia
  • Abnormal and wide QRS complexes with secondary ST segment and T wave changes
  • A ventricular rate usually between 140 and 200 beats/min
  • A regular or slightly irregular rhythm
  • Abrupt onset and termination
  • AV dissociation
  • f) Capture beats g) Fusion beats
torsade de pointes
Torsade de pointes
  • Polymorphous ventricular tachycardia
    • This is a form of VT where there is usually no difficulty in recognising its ventricular origin.
    • wide QRS complexes with multiple morphologies
    • changing R - R intervals
    • the axis seems to twist about the isoelectric line
    • it is important to recognise this pattern as there are a number of reversible causes
      • heart block
      • hypokalaemia or hypomagnesaemia
      • drugs (e.g. tricyclic antidepressant overdose)
      • congenital long QT syndromes
      • other causes of long QT (e.g. IHD)
conduction blocks
Conduction blocks

Conduction Blocks

first degree av block
First Degree AV Block

AV block is defined by PR intervals greater than 200 ms.

This may be caused by : drugs, such as digoxin;

excessive vagal tone

ischemia or

intrinsic disease in the AV junction or

bundle branch system

second degree av block type i mobitz
Second Degree AV Block: Type I Mobitz

Second Degree AV Block: Type I Mobitz

  • The 3 rules of “classic AV Wenckebach” are:
  • decreasing RR intervals until pause
  • the pause is less than preceding 2 RR intervals
  • 3) the RR interval after the pause is greater than the RR interval just prior to pause.
second degree av block type i mobitz1
Second Degree AV Block: Type I Mobitz

Progressive PR segment prolongation prior to dropped QRS complex.

second degree av block type ii mobitz
Second Degree AV Block: Type II Mobitz

P waves

Dropped QRS wave with prolonged RR

high grade av block
High Grade AV block

AV conduction ratio 3:1 or higher

complete heart block
Complete Heart Block
  • Complete Heart Block
    • a) P waves are not conducted to the ventricles because of block at the AV node. The P waves are indicated below and show no relation to the QRS complexes. They 'probe' every part of the ventricular cycle but are never conducted.
    • b) The ventricles are depolarized by a ventricular escape rhythm
junctional rhythm
Junctional Rhythm

Junctional Rhythm

left anterior hemiblock lah
Left Anterior Hemiblock (LAH)
  • Displacement of the mean QRS axis in the frontal plane to between –300 and –900 ( abnormal Left axis deviation )
  • A qR complex ( or an R ) in I and aVL, an rS in II, III and aVF
  • Normal or slightly prolonged QRS
left posterior hemiblock
Left Posterior Hemiblock

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
Left Bundle Branch Block

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

left bundle branch block1

delayed intrinsicoid deflection

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 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

right bundle branch block
Right Bundle Branch Block

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

bifascicular block
Bifascicular block

RBBB

LAH

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

trifascicular block
Trifascicular 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.

trifascicular block1
Trifascicular Block

RBBB- rsR’ in V1,V2

LAH qR in I, aVL

rS in II,III aVF

  • PR prolongation b) RBBB with a left anterior hemiblock (LAH) or left posterior hemiblock (LPH) OR Left Bundle Branch Block
right atrial enlargement

high P wave in V1 or V2; positive part > then 1,5 mm

Frontal plane P wave vector > + 75º

Right Atrial Enlargement

high pointed P wave ³ 2,5 mm in II and/or aVF

left atrial enlargement
Left Atrial Enlargement

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 with rvh
Left Atrial Enlargement with RVH

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
Left Ventricular Hypertrophy

Left Ventricular Hypertrophy

> 35mm

> 26mm

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).

lvh strain pattern
LVH strain pattern

LV

Strain Pattern

  • LVH only
  • LVH with 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
Acute pulmonary embolus

Acute pulmonary embolus

S1 Q3 T3

  • The following often transient, changes may be seen in a large pulmonary embolus
      • S1Q3T3 pattern ( a classic finding, not frequently seen )
      • Prominent S wave in lead I
      • Q wave and inverted T wave in lead III
      • Sinus tachycardia
      • T wave inversion in leads V1 - V3
      • Right Bundle Branch Block
      • low amplitude deflections
chronic obstructive pulmonary disease
Chronic Obstructive Pulmonary Disease
  • P waves >2.5mm in II, III, aVF with a axis of > 700 in frontal plane
  • Lead I sign with an isoelectric P and a QRS amplitude < 1.5mm
  • QRS amplitude < 5mm in all limb leads
  • R/S ratio of <1 in V5 and V6
  • S1S2S3 Syndrome with an R/S ratio of <1 in leads I, II and III
digitalis toxicity
Digitalis toxicity

“U”

  • ST segment depression
  • Decreased amplitude of T wave which may be biphasic
  • Shortening of QT interval
  • Increased amplitude of U wave
ekg in heart transplant
EKG in Heart Transplant

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

hypocalcemia
Hypocalcemia
  • Prolongation of QTc interval secondary to an increased duration of the ST segment with no change in the duration of the T wave ( morphology of “T” may alter - peaked or flattening or inversion). Similar changes may be seen only with hypothermia.
  • QTc is directly proportional to the ionic calcium level and seldom exceeds 140msec. If QTc is > 140 msec, consider other associated abnormalities.
hypokalemia
Hypokalemia

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

hyperkalemia
Hyperkalemia
  • The following changes may be seen in hyperkalemia
    • wide, tall and tented T waves
    • wide QRS
    • atrial fibrillation
    • ventricular fibrillation
advanced hyperkalaemia
Advanced Hyperkalaemia

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.

neurogenic t waves osborne waves
Neurogenic T waves (Osborne waves)
  • Large , upright or deeply inverted T waves
  • Prominent U waves
  • Prolongation of QTc interval
  • Abnormal Q waves, diffuse ST elevation or depression may also be seen
  • mimic ischemic changes
acute pericarditis
Acute Pericarditis

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)

low voltage ekg
Low Voltage EKG
  • Uniform Reduction of QRS voltage in all leads b) ST segment and T wave changes
limb lead reversal
Limb Lead Reversal

Note upright QRS complex and P wave in lead aVR with inverted QRS in leads I and aVL.