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Electrocardiography Dr.S Kesanakurthy Reviewed by  Dr. Michael Jacobson
A  Sequential Approach to Reading  EKG’s: ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],A Sequential Approach to Reading EKG’s:
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 .
Lead placement
Lead placement
Orientation of the 12 Lead ECG: ,[object Object],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)          Right        Left         Superior        Inferior         Anterior        Posterior
Standard Limb Leads
Right Sided Leads
normal ECG ,[object Object],[object Object],[object Object],[object Object],[object Object],ST segment
normal ECG ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Normal Sinus Rhythm ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Normal EKG Ps in I, II and aVF are always upright and always inverted in aVR Ps in V1 and V2 are Diphasic, but never negative in V2 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 (0 0  – 75 0 )   P waves are always upright in leads I and II, always inverted in aVR, diphasic in III, aVL, and V 1 , V 2.  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. 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.
AXIS AXIS Normal axis -30 0  to 120 0 Left axis deviation -30 0  to -90 0 Right axis deviation 120 0  to 180 0 Indeterminate (extreme)  axis deviation -90 0  to 180 0
AXIS   Lead I Lead aVF 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 Differential Diagnosis Left axis deviation LVH, left anterior fasicular block, inferior wall MI Right axis deviation RVH, left posterior fascicular block, lateral wall MI
NORMAL AXIS
LEFT AXIS DEVIATION If the axis is - 30 0     Biphasic in lead II, and negative in aVF If the axis is <30 0     predominantly negative in lead II and aVF
RIGHT AXIS DEVIATION Normal QRS width with an axis of  >100 0 Predominantly positive in leads II and III, and negative in aVL
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
ischemia Ischemia
ST Segment 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 wave   abnormalities , 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.          General Introduction to ST, T, and U wave abnormalities
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 ,[object Object],[object Object]
&quot;Primary&quot; ST-T Wave Abnormalities ,[object Object],[object Object]
Causes of ST Elevation &quot;ELEVATION&quot;  E  - Electrolytes L  - LBBB E  - Early Repolarization V  - Ventricular hypertrophy A  - Aneurysm T  - Treatment - Pericardiocentesis   I  -  Injury (AMI, contusion) O  - Osborne waves (hypothermia) N  - Non-occlusive vasospasm
Differential Diagnosis of ST Segment Elevation Normal Variant “Early Repolarization” Ischemic Heart Disease Acute Pericarditis Other Causes
&quot;Early Repolarization&quot;: ,[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object]
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 ,[object Object],[object Object],Normal variants or artifacts: ,[object Object],[object Object]
Non-ischemic causes of ST depression ,[object Object],[object Object]
Ischemic heart disease Subendocardial ischemia (exercise induced or during angina attack “ horizontal&quot; 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 Ist Few Hours First 24 Hours First 72 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 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 Q wave pattern  in the anterolateral leads is well established.  Persistent ST segment elevation suggests complication by aneurysm or pericarditis
Acute anteroseptal myocardial infarction a)  ST elevation and tall T waves b)  QS deflections  in V1, V2 and V3 and V4
Right sided EKG lead placement
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 Note inferior ST segment elevation as well as atrioventricular dissociation secondary to complete heart block.  AV dissociation
Acute inferior myocardial infarction complicated by Wenkebach 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.  wenckebach
Inferoposterior MI ,[object Object],[object Object],Tall R in V2,R/S >1
Postero-lateral MI The &quot;true&quot; 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 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 Anterolateral ST segment depression  is consistent with diffuse subendocardial ischemia vs. non-Q wave MI.
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 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Non-Q Wave MI ,[object Object],[object Object],[object Object]
pseudoinfarcts ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Arrhythmias ARRHYTHMIAS
Arrhthmia algo How to think about arrhythmias and conduction disturbances
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
APC ,[object Object],[object Object],[object Object],[object Object],Atrial Premature Beat (APB)
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
PVC ,[object Object],[object Object]
Bigeminy Ventricular Bigeminy a  ventricular premature beat  follows each normal beat
QT prolongation ,[object Object],[object Object],[object Object]
A Fib 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.  Atrial Fibrillation
A Fib No P waves. Narrow complex QRS with irregular RR intervals. Ventricular rate is controlled in this EKG.   Atrial Fibrillation
A Fib Atrial Fib complicating  inferior MI
WPW in Afib Preexcited QRS complex with  Atrial Fibrillation ,[object Object],[object Object]
AFlutter 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 Flutter circuit
A Flutter Atrial rate of 300 bpm with upright “FLUTTER” waves inferiorly. This is consistent with typical atrial flutter.   Atrial Flutter “ F” waves
A Flutter 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.  Atrial Flutter With 2:1 AV Conduction
SVT Supraventricular Rhythms
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?
SVT SVT
SVT Supraventricular Tachycardia ,[object Object],[object Object]
SVT Supraventricular Tachycardia
Narrow complex Tachycardia ,[object Object],[object Object],[object Object],[object Object],Electrocardiographic patterns of narrow complex tachycardia AVNRT—atrioventricular nodal reentry tachycardia
Narrow complex tachycardia ,[object Object],[object Object],[object Object],[object Object],Electrocardiographic patterns of narrow complex tachycardia AVNRT—atrioventricular nodal reentry tachycardia Narrow complex tachycardia
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. Schema for  typical atrioventricular node reentrant tachycardia (AVNRT). Schema  for atypical atrioventricular node reentrant tachycardia (AVNRT).
AVNRT 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 .   150 /min Inverted P
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
WPW ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Wolf Parkinson White Syndrome
WPW Wolf Parkinson White Syndrome
WPW Wolf Parkinson White Syndrome ,[object Object],[object Object],[object Object],[object Object],[object Object]
Conduction over an accessory pathway ,[object Object],[object Object],[object Object],[object Object],Conduction over an accessory pathway
Conduction over an accessory pathway ,[object Object],[object Object],[object Object]
Wide complexd tachycardia WIDE COMPLEX TACHYCARDIA
Differential Diagnosis of Wide-Complex Tachycardia ,[object Object],[object Object],[object Object],[object Object],[object Object]
EKG Distinction of VT from SVT with 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: V 1  duration > 30 ms S wave > 70 ms S wave notched or slurred V 6 : qR or QR R wave monophasic If RBBB: V 1 : monophasic R wave qR If triphasic, R > R 1 R < R 1   V 6 : R < S Favors VT Favors SVT with Aberrancy
A-V Dissociation, Fusion, and Capture Beats in VT ECTOPY FUSION CAPTURE C E F
Wide QRS Tachycardia Wide QRS - Preexcitation (Conduction via AP) Narrow QRS Wide QRS - BBB (Aberrant conduction) Wide QRS - VT
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 Rhythms
Ventricular tachycardia ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Idioventricular Rhythm
Torsade de pointes ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Conduction blocks Conduction Blocks
Conduction blocks
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 ,[object Object],[object Object],[object Object],[object Object],Second Degree AV Block: Type I Mobitz
Second Degree AV Block: Type I Mobitz Progressive PR segment prolongation prior to dropped QRS complex.
Second Degree AV Block: Type II Mobitz Dropped QRS wave with prolonged RR P waves
High Grade AV block AV conduction ratio 3:1 or higher
Complete Heart Block ,[object Object],[object Object],[object Object]
Junctional Rhythm Junctional Rhythm
HEMIBLOCKS
Left Anterior Hemiblock (LAH) ,[object Object],[object Object],[object Object]
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.
Bundle Branch Blocks
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 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
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 delayed intrinsicoid deflection
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
RBBB complicating Inferior Wall MI
Bifascicular block Intraventricular conduction block involving a RBBB with a division of the Left Bundle (either LAH or LPH) may be considered as a Bifascicular Block  LAH RBBB Normal PR interval
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 Block ,[object Object],LAH  qR  in I, aVL rS in II,III aVF RBBB- rsR’ in V1,V2
Trifascicular Block
SPECIFIC DISORDERS
Right Atrial Enlargement high pointed P wave ³ 2,5 mm in II and/or aVF     high P wave in V1 or V2; positive part > then 1,5 mm     Frontal plane P wave vector > + 75 º
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  t total duration of  greater than   0.12 seconds. Usually, the voltage (amplitude) of the P wave increases only slightly.
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 > 110 0   or R/S ratio in V 1  >1   R in V1 +S in V 5   or 6 >11mm R in V 1  >7mm  S in V 1  <2mm  rSR’ in V 1  >10mm
Left Ventricular Hypertrophy 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). > 35mm > 26mm
Left Ventricular Hypertrophy
LVH strain pattern LV Strain Pattern The ST segment is depressed and the T wave is inverted. Note too that the R wave has become even taller.  ,[object Object],[object Object]
Acute pulmonary embolus ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],S1 Q3 T3 Acute pulmonary embolus
Chronic Obstructive Pulmonary Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Digitalis  toxicity ,[object Object],[object Object],[object Object],[object Object],“ U”
Digitalis Effect on Rhythm and Conduction
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 ,[object Object],[object Object]
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 ,[object Object],[object Object],[object Object],[object Object],[object Object]
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) ,[object Object],[object Object],[object Object],[object Object],[object Object]
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 V 1.  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 ,[object Object]
DEXTROCARDIA
DEXTROCARDIA
DEXTROCARDIA
Left vs Right sided leads in Dextrocardia
Demand Pacing
Limb Lead Reversal Note upright QRS complex and P wave in lead aVR with inverted QRS in leads I and aVL.

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Ekg Tutorial

  • 1. Electrocardiography Dr.S Kesanakurthy Reviewed by Dr. Michael Jacobson
  • 2.
  • 3. 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 .
  • 6.
  • 9.
  • 10.
  • 11.
  • 12. Normal EKG Ps in I, II and aVF are always upright and always inverted in aVR Ps in V1 and V2 are Diphasic, but never negative in V2 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 (0 0 – 75 0 ) P waves are always upright in leads I and II, always inverted in aVR, diphasic in III, aVL, and V 1 , V 2. 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. 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.
  • 13. AXIS AXIS Normal axis -30 0 to 120 0 Left axis deviation -30 0 to -90 0 Right axis deviation 120 0 to 180 0 Indeterminate (extreme) axis deviation -90 0 to 180 0
  • 14. AXIS Lead I Lead aVF 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 Differential Diagnosis Left axis deviation LVH, left anterior fasicular block, inferior wall MI Right axis deviation RVH, left posterior fascicular block, lateral wall MI
  • 16. LEFT AXIS DEVIATION If the axis is - 30 0  Biphasic in lead II, and negative in aVF If the axis is <30 0  predominantly negative in lead II and aVF
  • 17. RIGHT AXIS DEVIATION Normal QRS width with an axis of >100 0 Predominantly positive in leads II and III, and negative in aVL
  • 18. 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.
  • 19. Normal variants or artifacts Normal variants or artifacts
  • 22. 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 wave abnormalities , 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.      General Introduction to ST, T, and U wave abnormalities
  • 23. 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
  • 24.
  • 25.
  • 26. Causes of ST Elevation &quot;ELEVATION&quot; E - Electrolytes L - LBBB E - Early Repolarization V - Ventricular hypertrophy A - Aneurysm T - Treatment - Pericardiocentesis I - Injury (AMI, contusion) O - Osborne waves (hypothermia) N - Non-occlusive vasospasm
  • 27. Differential Diagnosis of ST Segment Elevation Normal Variant “Early Repolarization” Ischemic Heart Disease Acute Pericarditis Other Causes
  • 28.
  • 29.
  • 30.
  • 31. 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.
  • 32.
  • 33.
  • 34. Ischemic heart disease Subendocardial ischemia (exercise induced or during angina attack “ horizontal&quot; 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)
  • 35. Stages of Acute Q-Wave MI Ist Few Hours First 24 Hours First 72 Hours
  • 36. 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.
  • 37. 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.
  • 38. 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
  • 39. Acute anteroseptal myocardial infarction a) ST elevation and tall T waves b) QS deflections in V1, V2 and V3 and V4
  • 40. Right sided EKG lead placement
  • 41. Right ventricular infarction (Rt.sided leads) ST segment elevation in leads V4R and V5R reveals right ventricular involvement complicating the inferior infarct.
  • 42. Complicated Acute inferior myocardial infarction Note inferior ST segment elevation as well as atrioventricular dissociation secondary to complete heart block. AV dissociation
  • 43. Acute inferior myocardial infarction complicated by Wenkebach 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. wenckebach
  • 44.
  • 45. Postero-lateral MI The &quot;true&quot; 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.
  • 46. 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.
  • 47. Subendocardial Ischemia Anterolateral ST segment depression is consistent with diffuse subendocardial ischemia vs. non-Q wave MI.
  • 48. Unstable angina vs. non-Q wave myocardial infarction ST segment depression in leads V2 through V5 supports acute ischemic syndrome with no “Q” waves.
  • 49.
  • 50.
  • 51.
  • 53. Arrhthmia algo How to think about arrhythmias and conduction disturbances
  • 54. 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
  • 55.
  • 56. 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
  • 57.
  • 58. Bigeminy Ventricular Bigeminy a ventricular premature beat follows each normal beat
  • 59.
  • 60. A Fib 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. Atrial Fibrillation
  • 61. A Fib No P waves. Narrow complex QRS with irregular RR intervals. Ventricular rate is controlled in this EKG. Atrial Fibrillation
  • 62. A Fib Atrial Fib complicating inferior MI
  • 63.
  • 64. AFlutter 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 Flutter circuit
  • 65. A Flutter Atrial rate of 300 bpm with upright “FLUTTER” waves inferiorly. This is consistent with typical atrial flutter. Atrial Flutter “ F” waves
  • 66. A Flutter 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. Atrial Flutter With 2:1 AV Conduction
  • 68. 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?
  • 70.
  • 72.
  • 73.
  • 74. 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. Schema for typical atrioventricular node reentrant tachycardia (AVNRT). Schema for atypical atrioventricular node reentrant tachycardia (AVNRT).
  • 75. AVNRT 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 . 150 /min Inverted P
  • 76. 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
  • 77.
  • 78. WPW Wolf Parkinson White Syndrome
  • 79.
  • 80.
  • 81.
  • 82. Wide complexd tachycardia WIDE COMPLEX TACHYCARDIA
  • 83.
  • 84. EKG Distinction of VT from SVT with 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: V 1 duration > 30 ms S wave > 70 ms S wave notched or slurred V 6 : qR or QR R wave monophasic If RBBB: V 1 : monophasic R wave qR If triphasic, R > R 1 R < R 1 V 6 : R < S Favors VT Favors SVT with Aberrancy
  • 85. A-V Dissociation, Fusion, and Capture Beats in VT ECTOPY FUSION CAPTURE C E F
  • 86. Wide QRS Tachycardia Wide QRS - Preexcitation (Conduction via AP) Narrow QRS Wide QRS - BBB (Aberrant conduction) Wide QRS - VT
  • 87. 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.
  • 89.
  • 90.  
  • 92.
  • 95. 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
  • 96.
  • 97. Second Degree AV Block: Type I Mobitz Progressive PR segment prolongation prior to dropped QRS complex.
  • 98. Second Degree AV Block: Type II Mobitz Dropped QRS wave with prolonged RR P waves
  • 99. High Grade AV block AV conduction ratio 3:1 or higher
  • 100.
  • 103.
  • 104. 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.
  • 106. 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 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
  • 107. 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 delayed intrinsicoid deflection
  • 108. 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
  • 110. Bifascicular block Intraventricular conduction block involving a RBBB with a division of the Left Bundle (either LAH or LPH) may be considered as a Bifascicular Block LAH RBBB Normal PR interval
  • 111. 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.
  • 112.
  • 115. Right Atrial Enlargement high pointed P wave ³ 2,5 mm in II and/or aVF     high P wave in V1 or V2; positive part > then 1,5 mm     Frontal plane P wave vector > + 75 º
  • 116. 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 t total duration of greater than 0.12 seconds. Usually, the voltage (amplitude) of the P wave increases only slightly.
  • 117. 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 > 110 0 or R/S ratio in V 1 >1 R in V1 +S in V 5 or 6 >11mm R in V 1 >7mm S in V 1 <2mm rSR’ in V 1 >10mm
  • 118. Left Ventricular Hypertrophy 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). > 35mm > 26mm
  • 120.
  • 121.
  • 122.
  • 123.
  • 124. Digitalis Effect on Rhythm and Conduction
  • 125. 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
  • 126.
  • 127. 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
  • 128.
  • 129. 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.
  • 130.
  • 131. 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 V 1. 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)
  • 132.
  • 136. Left vs Right sided leads in Dextrocardia
  • 138. Limb Lead Reversal Note upright QRS complex and P wave in lead aVR with inverted QRS in leads I and aVL.