ECG  BASICS By  Dr .Mahipal Reddy
ECG machine
Lead Position <ul><li>Four limb leads </li></ul><ul><li>Six chest leads </li></ul><ul><li>V1- 4th intercostal space to the...
Horizontal plane - the six chest leads 6.5 V1 V1 V2 V2 V3 V3 V4 V4 V5 V5 V6 V6 RA LA LV RV
Colour codes given by AHA
ECG paper and timing <ul><li>ECG paper speed  = 25mm/sec </li></ul><ul><li>Voltage calibration 1 mV  =  1cm </li></ul><ul>...
ECG paper 5 Large squares = 1 second Time 1 Large square = 0.2 second 1 Small square = 0.04 second 2 Large squares = 1 cm ...
STANDARDISATION ECG amplitude scale Normal amplitude 10 mm/mV Half amplitude 5 mm/mV Double amplitude 20 mm/mV
ECG WAVES
The Normal ECG Normal Intervals: PR 0.12-0.20s QRS duration <0.12s QTc 0.33-0.43s
NSR
P-wave <ul><li>Normal values </li></ul><ul><li>up in all leads except aVR. </li></ul><ul><li>Duration.   < 2.5 mm. </li></...
 
 
 
 
 
 
 
 
NORMAL P-R INTERVAL <ul><li>PR interval time  0.12 seconds to 0.2 seconds. </li></ul><ul><li>That is three small squares t...
PR interval <ul><li>Definition:  the time interval between beginning of P-wave to beginning of QRS complex. </li></ul><ul>...
 
 
PR interval <ul><li>Definition:  the time interval between beginning of P-wave to beginning of QRS complex. </li></ul><ul>...
Q WAVES <ul><li>Q waves <0.04 second. </li></ul><ul><li>That’s is less than one small square duration. </li></ul><ul><li>H...
Normal Q wave
Q wave in MI
Q wave in septal hypertrophy
                                                                     
QRS COMPLEX <ul><li>QRS duration <0.11 s </li></ul><ul><li>That is less than almost three small squares </li></ul><ul><li>...
QRS complex <ul><li>Normal values </li></ul><ul><li>Duration : < 2.5 mm. </li></ul><ul><li>Morphology :   progression from...
Small voltage QRS <ul><li>Defined as < 5 mm peak-to-peak in all limb leads or <10 mm in precordial leads. </li></ul><ul><l...
V 1 V 2 V 3 V 4 V 5 V 6 The R wave in the precordial leads must grow from V1 to at least V4
 
 
J  point Q S ST
L V H-Voltage Criteria <ul><li>In adult with normal chest wall </li></ul><ul><li>SV1+RV5 >35 mm </li></ul><ul><li>or </li>...
LEFT VENTRICULAR HYPERTROPHY
Dominant R wave in V1 <ul><li>RBBB </li></ul><ul><li>Chronic lung disease, PE Posterior MI WPW Type A Dextrocardia Duchenn...
Right Ventricular Hypertrophy <ul><li>WILL SHOW AS </li></ul><ul><li>Right axis deviation (RAD) </li></ul><ul><li>Precordi...
 
Right Ventricular Hypertrophy
Right ventricular hypertrophy <ul><li>Right ventricular hypertrophy (RVH) increases the height of the R wave in V1. An R w...
Right Ventricular Hypertrophy <ul><li>Other findings in RVH include right axis deviation, taller R waves in the right prec...
Right Ventricular Hypertrophy <ul><li>True posterior infarction may also cause a tall R wave in V1, but the T wave is usua...
Right Ventricular Hypertrophy <ul><li>A large R wave in V1, when not accompanied by evidence of infarction, nor by evidenc...
Right Ventricular Hypertrophy <ul><li>RVH Criteria </li></ul><ul><li>R in V1 > 7 mm or > S wave </li></ul><ul><li>T in V1 ...
Right Ventricular Hypertrophy <ul><li>Right axis deviation </li></ul><ul><li>Right atrial enlargement </li></ul><ul><li>Do...
Right Ventricular Hypertrophy
Left Ventricular Hypertrophy
Left Atrial Enlargement Criteria P wave duration in II  ≥ 120ms or Negative component of biphasic P wave in V 1   ≥  1 “sm...
Right Atrial Enlargement Criteria P wave height in II ≥ 2.4mm or Positive component of biphasic P wave in V 1  ≥ 1 “small ...
Left Ventricular Hypertrophy
RHV-Any one of the following in lead V1 <ul><li>R/S ratio > 1 and negative T wave  </li></ul><ul><li>qR pattern  </li></ul...
ECG criteria for RBBB <ul><li>•(1) QRS duration exceeds 0.12 seconds </li></ul><ul><li>•(2) RSR complex in V1 </li></ul><u...
RBBB & MI <ul><li>If abnormal Q waves are present they will not be masked by the BBB pattern. </li></ul><ul><li>•This is b...
Significance of RBBB <ul><li>RBBB is seen in :- </li></ul><ul><li>(1) occasional normal subjects </li></ul><ul><li>(2) pul...
Partial / Incomplete RBBB <ul><li>is diagnosed when the pattern of RBBB is present but the duration of the QRS does not ex...
ECG criteria for LBBB <ul><li>(1)Prolonged QRS complexes, greater than 0.12 seconds </li></ul><ul><li>(2)Wide, notched QRS...
Significance of LBBB <ul><li>LBBB is seen in :- </li></ul><ul><li>(1) Always indicative of organic heart disease </li></ul...
Partial / Incomplete LBBB <ul><li>is diagnosed when the pattern of LBBB is present but the duration of the QRS does not ex...
NORMAL ST- SEGMENT <ul><li>it's isoelectric.   </li></ul><ul><li>[i.e. at same level of PR or PQ segment at least in the  ...
NORMAL CONCAVITY OF S-T SEGMENT <ul><li>It then gradually slopes upwards making concavity upwards and not going more than ...
Abnormalities <ul><li>ST elevation: </li></ul><ul><li>More than one small square </li></ul><ul><li>Acute MI. </li></ul><ul...
 
 
Stress test ECG – note the ST Depression
 
Note the arrows pointing ST depression
ST depression & Troponin T  positive is NON STEMI
Coving of S-T segment <ul><li>Concavity lost and convexity appear facing upwards. </li></ul>
Diagnostic criteria for AMI <ul><li>Q wave duration of more than 0.04 seconds </li></ul><ul><li>Q wave depth of more than ...
Abnormalities of ST- segment acute MI pericarditis early repolariz. ischemia
Q waves in myocardial infarction                                                                        
 
T-wave <ul><li>Normal values. </li></ul><ul><li>1.amplitude:   </li></ul><ul><li>< 10mm in the chest leads. </li></ul><ul>...
QT- interval   <ul><li>Definition :  Time interval between beginning of  </li></ul><ul><li>QRS complex to the end of T wav...
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval -
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval - QT  interval
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval - QT  interval
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval - QT  interval R R
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval - QT  interval R R
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval - QT  interval R R
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval - QT  interval 65 - 90 bpm R R
QT  Interval -  Should  be  <  1/2  preceding  R to R  interval - QT  interval 65 - 90 bpm Normal  QT c  =  0.46 sec R R
M
Atrioventricular (AV) Heart Block
Classification of AV Heart Blocks Degree AV Conduction Pattern 1 St  Degree Block Uniformly prolonged PR interval 2 nd  De...
AV Blocks <ul><li>First Degree </li></ul><ul><ul><li>Prolonged AV conduction time </li></ul></ul><ul><ul><li>PR interval >...
1 st  Degree AV Block Prolongation of the PR interval, which is constant All P waves are conducted
<ul><li>1st degree AV Block : </li></ul><ul><li>Regular Rhythm </li></ul><ul><li>PRI > .20 seconds or 5 small squares  and...
First Degree Block <ul><li>prolonged PR interval </li></ul>
Analyze the Rhythm
AV Blocks <ul><li>Second Degree </li></ul><ul><ul><li>Definition </li></ul></ul><ul><ul><ul><li>More Ps than QRSs </li></u...
Second-Degree AV Block <ul><li>There is intermittent failure of the supraventricular impulse to be conducted to the ventri...
Second Degree <ul><ul><li>Types </li></ul></ul><ul><ul><ul><li>Type I </li></ul></ul></ul><ul><ul><ul><ul><li>Wenckebach p...
Type I Second-Degree AV Block: Wenckebach Phenomenon <ul><li>ECG findings  </li></ul><ul><li>1.Progressive lengthening of ...
2nd degree AV Block (“Mobitz I” also called  “Wenckebach”) : Pattern Repeats…………. PRI = .24 sec PRI = .36 sec PRI = .40 se...
 
Type II Second-Degree AV Block: Mobitz Type II <ul><li>ECG findings  </li></ul><ul><li>1.Intermittent or unexpected blocke...
 
Second Degree AV Block <ul><li>Mobitz type I or Winckebach </li></ul><ul><li>Mobitz type II </li></ul>
Type 1 (Wenckebach) Progressive prolongation of the PR interval until a P  wave is not conducted. Constant PR interval wit...
Mobitz Type I
MOBITZ TYPE 1
<ul><li>2nd degree AV Block (“Mobitz II”) :   </li></ul><ul><li>Irregular Rhythm  </li></ul><ul><li>QRS complexes may be s...
Analyze the Rhythm
Second Degree Mobitz <ul><ul><li>Characteristics </li></ul></ul><ul><ul><ul><ul><li>Atrial rate > Ventricular rate </li></...
Analyze the Rhythm
Mobitz II <ul><li>Definition: Mobitz II is characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave wi...
Mobitz Type II
Mobitz Type II <ul><li>Sudden appearance of a single, non-conducted sinus P wave... </li></ul>
Advanced Second-Degree AV Block Two or more consecutive nonconducted sinus P waves
Complete AV Block <ul><ul><li>Characteristics </li></ul></ul><ul><ul><ul><li>Atrioventricular dissociation </li></ul></ul>...
3 rd  Degree (Complete) AV Block EKG Characteristics: No relationship between P waves and QRS complexes Relatively constan...
Complete heart block <ul><li>P waves are not conducted to the ventricles because of block at the AV node. The P waves are ...
<ul><li>3rd degree AV Block (“Complete Heart Block”) :  </li></ul><ul><li>Irregular Rhythm  </li></ul><ul><li>QRS complexe...
Third-Degree (Complete) AV Block
Third-Degree (Complete) AV Block <ul><li>The P wave bears no relation to the QRS complexes, and the PR intervals are compl...
30 AV Block <ul><li>AV dissociation </li></ul><ul><li>atria and ventricles beating on their own </li></ul><ul><li>no relat...
Key points <ul><li>Wenckebach </li></ul><ul><li>look for group beating & changing PR </li></ul><ul><li>Mobitz II </li></ul...
 
Left Anterior Fascicular Block  <ul><li>Left axis deviation , usually -45 to -90 degrees  </li></ul><ul><li>QRS duration u...
<ul><li>Left Anterior Hemiblock (LAHB) :  </li></ul><ul><li>Left axis deviation (> -30 degrees) will be noted and there wi...
Left Posterior Fascicular Block <ul><li>Right axis deviation  </li></ul><ul><li>QR pattern in inferior leads (II,III,AVF) ...
<ul><li>Left Posterior Hemiblock (LPHB) :  </li></ul><ul><li>Right axis deviation and there will be a prominent S-wave in ...
Bifascicular  Bundle Branch Block <ul><li>RBBB with either left anterior or left posterior fascicular block </li></ul><ul>...
Trifascicular Block <ul><li>The combination of RBBB, LAFB and long PR interval  </li></ul><ul><li>Implies that conduction ...
Indications For Implantation of  Permanent Pacing in Acquired AV Blocks <ul><li>1.Third-degree AV block, Bradycardia with ...
Cardiac Pacemakers <ul><li>Definition </li></ul><ul><ul><li>Delivers artificial stimulus to heart </li></ul></ul><ul><ul><...
Cardiac Pacemakers <ul><li>Types </li></ul><ul><ul><li>Fixed </li></ul></ul><ul><ul><ul><li>Fires at constant rate </li></...
Cardiac Pacemakers
Cardiac Pacemakers <ul><li>Demand Pacemaker Types </li></ul><ul><ul><li>Ventricular </li></ul></ul><ul><ul><ul><li>Fires v...
Cardiac Pacemakers <ul><li>Demand Pacemaker Types </li></ul><ul><ul><li>Atrial Synchronous </li></ul></ul><ul><ul><ul><li>...
Cardiac Pacemakers <ul><li>Problems </li></ul><ul><ul><li>Failure to capture </li></ul></ul><ul><ul><ul><li>No response to...
Cardiac Pacemakers <ul><li>Problems </li></ul><ul><ul><li>Failure to sense </li></ul></ul><ul><ul><ul><li>Spike follows QR...
Implanted Defibrillators <ul><li>AICD </li></ul><ul><ul><li>Automated Implanted Cardio-Defibrillator </li></ul></ul><ul><l...
Implanted Defibrillators <ul><li>Programmed at insertion to deliver predetermined therapies with a set order and number of...
Implanted Defibrillators <ul><li>Potential Complications </li></ul><ul><ul><li>Fails to deliver therapies as intended </li...
Sinus Exit Block <ul><li>Due to abnormal function of SA node </li></ul><ul><li>MI, drugs, hypoxia, vagal tone </li></ul><u...
Sinus block
ARRTHYMIAS AND ECTOPIC BEATS
normal (&quot;sinus&quot;) beats sinus node doesn't fire leading to a period of asystole (sick sinus syndrome) p-wave has ...
there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin an...
actually a &quot;retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles,...
Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery The “Re-Entry” Mechanism of Ectopic Beats & Rhythms ...
Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Premature Beat Impulse Cardiac Conduction Tissue <ul...
<ul><ul><ul><li>3.  The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathwa...
<ul><ul><ul><li>4.  On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the w...
Recognizing and Naming Beats & Rhythms <ul><li>Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles) :  </li></...
Recognizing and Naming Beats & Rhythms <ul><li>Characteristics of PVC's  </li></ul><ul><li>PVC’s don’t have P-waves unless...
<ul><li>PVC's are Dangerous When : </li></ul><ul><li>They are frequent (> 30% of complexes) or are increasing in frequency...
Recognizing and Naming Beats & Rhythms <ul><li>Notes on V-tach : </li></ul><ul><li>Causes of V-tach </li></ul><ul><ul><li>...
Recognizing and Naming Beats & Rhythms <ul><li>Premature Atrial Contractions (PAC’s) :  </li></ul><ul><li>An ectopic focus...
<ul><li>Premature Junctional Contractions (PJC’s) :  </li></ul><ul><li>An ectopic focus in or around the AV junction disch...
Recognizing and Naming Beats & Rhythms <ul><li>Multifocal Atrial Tachycardia (MAT) :  </li></ul><ul><li>Multiple ectopic f...
Recognizing and Naming Beats & Rhythms <ul><li>Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) :  </li></...
Sinus arrest or exit block
PAC
Junctional Premature Beat <ul><li>single ectopic beat that originates in the AV node or </li></ul><ul><li>Bundle of His ar...
Junctional Escape Beat
Junctional  Rhythm <ul><li>Rate : 40 to 60 beats/minute (atrial and ventricular) </li></ul><ul><li>• Rhythm : regular atri...
Junctional  Rhythm
MaligMalignant PVC   patterns <ul><li>Frequent PVCs </li></ul><ul><li>Multiform PVCs </li></ul><ul><li>Runs of consecutive...
 
 
Types of PVCs <ul><li>Uniform </li></ul><ul><li>Multiform </li></ul><ul><li>PVC rhythm patterns </li></ul><ul><li>–  Bigem...
Junctional Escape Rhythm
Ventricular tachycardia (VTach) <ul><li>3 or more PVCs in a row at a rate of 120 to 200 bts/min-1 </li></ul><ul><li>Ventri...
 
Torsades de Pointes <ul><li>Type of VT known as “twisting of the points.” </li></ul><ul><li>Usually seen in those with pro...
ECG Paper: Dimensions 5 mm 1 mm 0.1 mV 0.04 sec 0.2 sec Speed = rate Voltage ~Mass
Why “1500 / X”? <ul><li>Paper Speed: 25 mm/ sec </li></ul><ul><li>60 seconds / minute </li></ul><ul><li>60 X 25 = 1500 mm ...
Atrial Fibrillation :
Regular “Irregular” <ul><li>Premature Beats: PVC </li></ul><ul><ul><li>Widened QRS, not associated with preceding P wave <...
Notice a Pattern in the PVC’s?
Identifying AV Blocks:  Name Conduction PR-Int R-R Rhythm Regular (20-40 bpm) Grossly  Irregular P > R 3°: Regular Constan...
Most Important Questions of Arrhythmias <ul><li>What is the mechanism? </li></ul><ul><ul><li>Problems in impulse formation...
QRS Axis <ul><li>Check Leads:  </li></ul><ul><li>1 and AVF </li></ul>
Interpreting Axis Deviation: <ul><li>Normal Electrical  Axis:  </li></ul><ul><ul><li>(Lead I + / aVF +) </li></ul></ul><ul...
NW Axis (No Man’s Land) <ul><li>Both I and aVF are – </li></ul><ul><li>Check to see if leads are transposed (- vs +) </li>...
Determining Regions of CAD: ST-changes in leads… <ul><li>RCA: Inferior myocardium </li></ul><ul><ul><li>II, III, aVF </li>...
Regions of the Myocardium: Inferior II, III, aVF Lateral I, AVL,  V5-V6 Anterior /  Septal V1-V4
Sinus Arrhythmia
Sinus Arrest/Pause
Sinoatrial Exit Block
Premature Atrial Complexes (PACs)
Wandering Atrial Pacemaker (WAP)
Supraventricular Tachycardia (SVT)
Wolff-Parkinson-White Syndrome (WPW)
Atrial Flutter
Atrial Fibrillation (A-fib)
Premature Junctional Complexes (PJC)
Junctional Rhythm
Junctional Rhythm
Accelerated Junctional Rhythm
Junctional Tachycardia
Premature Ventricular Complexes (PVC's) Note –  Complexes  not    Contractions
PVC’s <ul><li>Uniformed/Multiformed </li></ul><ul><li>Couplets/Salvos/Runs </li></ul><ul><li>Bigeminy/Trigeminy/Quadragemi...
Uniformed PVC’s
R on T Phenomena
Multiformed PVC’s
PVC Couplets
PVC Salvos and Runs
Bigeminy PVC’s
Trigeminy PVC’s
Quadrageminy PVC’s
Ventricular Escape Beats
Idioventricular Rhythm
Ventricular Tachycardia (VT) <ul><li>Rate:   101-250 beats/min </li></ul><ul><li>Rhythm:  regular </li></ul><ul><li>P wave...
Ventricular Tachycardia (VT)
V Tach
Torsades de Pointes (TdeP) <ul><li>Rate:   150-300 beats/min </li></ul><ul><li>Rhythm:   regular or irregular </li></ul><u...
Torsades de Pointes (TdeP)
Ventricular Fibrillation (VF) <ul><li>Rate:   CNO as no discernible complexes </li></ul><ul><li>Rhythm:   rapid and chaoti...
Ventricular Fibrillation (VF)
Ventricular Fibrillation (VF)
Asystole  (Cardiac Standstill) <ul><li>Rate:   none  </li></ul><ul><li>Rhythm:   none </li></ul><ul><li>P waves:   none </...
Asystole  (Cardiac Standstill)
Asystole The Mother of all Bradycardias
Atrial Pacemaker  (Single Chamber) pacemaker <ul><li>Capture? </li></ul>
Ventricular Pacemaker  (Single Chamber) pacemaker
Dual Paced Rhythm pacemaker
Pulseless Electrical Activity (PEA) <ul><li>The absence of a detectable pulse and blood pressure </li></ul><ul><li>Presenc...
ventricular bigeminy <ul><li>The ECG trace below shows ventricular bigeminy, in which every other beat is a ventricular ec...
ventricular bigeminy
ventricular trigeminy ;  <ul><li>The occurrence of more than one type of ventricular ectopic impulse morphology is evidenc...
ventricular trigeminy
ventricular trigeminy
QUESTIONS?
Thank you all
MYOCARDIAL INFARACTION
Diagnosing a MI <ul><li>To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 1...
ST Elevation <ul><li>One way to diagnose an acute MI is to look for elevation of the ST segment. </li></ul>
ST Elevation (cont) <ul><li>Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocard...
Anterior Myocardial Infarction <ul><li>If you see changes in leads V 1  - V 4  that are consistent with a myocardial infar...
Putting it all Together <ul><li>Do you think this person is having a myocardial infarction. If so, where? </li></ul>
Interpretation <ul><li>Yes , this person is having an acute anterior wall myocardial infarction. </li></ul>
Putting it all Together <ul><li>Now, where do you think this person is having a myocardial infarction? </li></ul>
Inferior Wall MI <ul><li>This is an inferior MI. Note the ST elevation in leads II, III and aVF. </li></ul>
Putting it all Together <ul><li>How about now? </li></ul>
Anterolateral MI <ul><li>This person’s MI involves  both  the anterior wall (V 2 -V 4 ) and the lateral wall (V 5 -V 6 , I...
NORMAL RULE
Rule 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated I II III aVR aVL aVF V1  V2 V3...
Characteristic changes in AMI <ul><li>ST segment elevation over area of damage </li></ul><ul><li>ST depression in leads op...
ST elevation hyperacute phase <ul><li>Occurs in the early stages </li></ul><ul><li>Occurs in the leads facing the  infarct...
Deep Q wave <ul><li>Only diagnostic change of myocardial infarction </li></ul><ul><li>At least 0.04 seconds in duration </...
T wave changes <ul><li>Late change </li></ul><ul><li>Occurs as ST elevation is returning to normal </li></ul><ul><li>Appar...
Bundle branch block I II III aVR aVL aVF V1  V2 V3 V4  V5 V6 I II III aVR aVL aVF V1  V2 V3 V4  V5 V6 Anterior wall MI Lef...
Sequence of changes in evolving AMI 1 minute after onset 1 hour or so after onset A few hours after onset A day or so afte...
Anterior infarction Anterior infarction Left  coronary  artery I II III aVR aVL aVF V1  V2 V3 V4  V5 V6
Inferior infarction Inferior infarction Right  coronary  artery I II III aVR aVL aVF V1  V2 V3 V4  V5 V6
Lateral infarction Lateral  infarction Left  circumflex coronary  artery I II III aVR aVL aVF V1  V2 V3 V4  V5 V6
Diagnostic criteria for AMI <ul><li>Q wave duration of more than 0.04 seconds </li></ul><ul><li>Q wave depth of more than ...
Surfaces of the Left Ventricle <ul><li>Inferior - underneath </li></ul><ul><li>Anterior - front </li></ul><ul><li>Lateral ...
Inferior Surface <ul><li>Leads  II, III and avF  look UP from below to the inferior surface of the left ventricle </li></u...
Inferior Leads <ul><ul><li>II </li></ul></ul><ul><ul><li>III </li></ul></ul><ul><ul><li>aVF </li></ul></ul>
Anterior Surface <ul><li>The  front  of the heart viewing the left ventricle and the septum </li></ul><ul><li>Leads  V2 , ...
Anterior Leads <ul><ul><li>V2 </li></ul></ul><ul><ul><li>V3 </li></ul></ul><ul><ul><li>V4 </li></ul></ul>
Lateral Surface <ul><li>The left sided wall of the left ventricle </li></ul><ul><li>Leads  V5  and  V6, I  and  avL  look ...
Lateral Leads V5, V6,  I, aVL
Posterior Surface <ul><li>Posterior wall infarcts are rare </li></ul><ul><li>Posterior diagnoses can be made by looking at...
Inferior  II, III, AVF Antero-Septal V1,V2, V3,V4 Lateral  I, AVL, V5, V6 Posterior  V1, V2, V3 RIGHT LEFT
ST Segment Elevation <ul><li>The ST segment lies above the isoelectric line: </li></ul><ul><li>Represents myocardial injur...
ST-Segment Elevation
 
T wave inversion in an evolving MI
The ECG in  ST Elevation MI
The Hyper-acute Phase <ul><li>Less than 12 hours </li></ul><ul><li>“ ST segment elevation is the hallmark ECG abnormality ...
 
The Fully Evolved Phase <ul><li>24 - 48 hours from the onset of a myocardial infarction </li></ul><ul><li>ST segment eleva...
The Chronic Stabilised Phase <ul><li>Isoelectric ST segments </li></ul><ul><li>T waves upright. </li></ul><ul><li>Patholog...
 
Reciprocal Changes <ul><li>Changes occurring on the opposite side of the myocardium that is infarcting </li></ul>
Reciprocal Changes ie S-T depression in some leads in MI
Non ST Elevation MI <ul><li>Commonly ST depression and deep T wave inversion </li></ul><ul><li>History of chest pain typic...
Changes in NSTEMI
Action potentials and electrophysiology + + + + _ _ _ _ 3.2 Ca   in(slow) ++ K   out + Na   in + Resting Depolarised Repol...
LVH and strain pattern Ventricular Strain   Strain is often associated with ventricular hypertrophy Characterized by moder...
Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026 Non-ischaemic ST segment changes: in p...
Examples of T wave abnormalities Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026
Sick Sinus Syndrome Sinoatrial block (note the pause is twice the P-P interval)  Sinus arrest with pause of 4.4 s before g...
Bundle Branch Block
Left Bundle Branch Block <ul><li>Widened QRS (> 0.12 sec, or 3 small squares) </li></ul><ul><li>Two R waves appear – R and...
Right Bundle Branch Block
Where’s the MI?
Where’s the MI?
Where’s the MI?
Final one…
 
Which one is more tachycardic during this exercise test?
Any Questions?
Thanks for paying attention. I hope you have found this session useful.
 
 
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Ecgrevised2 090808155046 Phpapp01

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  • Horizontal plane - the six chest leads Each of the six chest leads has a fixed position. In order to place the precordial leads correctly the fourth intercostal space needs to be identified. The ribs form convenient horizontal landmarks. In order to count them, feel for the ridge with marks the junction of the manubrium and the body of the sternum. When this has been found, run the finger outwards until it reaches the second costal cartilage, which articulates with the sternum at this level. The space immediately above this is the first intercostal space. The spaces should then be counted downwards, well away from the sternum, as they are more easily felt here. V 1 right sternal margin at fourth intercostal space V 2 left sternal margin at fourth intercostal space V 3 midway between V 2 and V 4 V 4 intersection of left midclavicular line and fifth intercostal space V 5 intersection of left anterior axillary line with a horizontal line through V 4 V 6 intersection of mid-axillary line with a horizontal line through V 4 and V 5 . V 1 and V 2 face and lie close to the free wall of the right ventricle, V 3 and V 4 lie near to the interventricular septum with V 4 usually at the cardiac apex, and V 5 and V 6 face the free wall of the left ventricle but are separated from it by a substantial distance. Together the chest leads observe changes in the anterior and lateral aspects of the heart, giving detailed information about the myocardium of the area they lie over.
  • ECG paper The electrocardiogram (ECG) is a recording of the electrical activity of the heart. It records the wave of depolarisation that spreads across the heart. The ECG is recorded from two or more simultaneous points of skin contact (electrodes). When cardiac activation proceeds towards the positive contact, an upward deflection is produced on the ECG. As the activation moves away from the electrode, a downward deflection is seen. The neutral position on the ECG is known as the isoelectric line, and is where the tracing rests when there is no electrical activity in the muscle. There are many types of ECG machine, including 3, 6, and 12 channel machines. The ECG trace is printed out on paper composed of a number of 1 and 5 mm squares. The height of each complex represents the amount of electrical potential involved in each complex and an impulse of 1 mV causes a deflection of 10 mm. Horizontally each millimetre represents 0.04 second and each 5 mm represents 0.2 second.
  • Rule 6 The normality of QRS complexes recorded from the precordial leads is dependent on both morphological and dimensional criteria.
  • Diagnostic criteria for AMI Myocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis. Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves. Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.
  • Rule 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated.
  • Characteristic changes in AMI The 12-lead ECG is the most useful investigation for confirming the diagnosis of acute myocardial infarction, locating the site of the infarct and monitoring the progress. It is therefore very important to know the changes that occur in this situation. The only diagnostic evidence of a completed myocardial infarction seen on the ECG are those in the QRS complexes. In the early stages changes are also seen in the ST segment and the T wave, and these can be used to assist diagnosis of myocardial infarctions. Shortly after infarction there is an elevation of the ST segment seen over the area of damage, and opposite changes are seen in the opposite leads. Several hours later pathological Q waves begin to form, and tend to persist. Later the R wave becomes reduced in size, or completely lost. Later still, the ST segment returns to normal, and at this point the T wave also decreases, eventually becoming deeply and symmetrically inverted. Although these changes occur sequentially, it is very unlikely they will all be clearly observed by the paramedic or GP. A patient can present at any stage and a progression through the ECG changes will not be seen. It is important to recognise these features as they occur rather than in association with each other. All these changes imply myocardial infarction, and will be discussed in more detail over the next few slides.
  • ST elevation ST segment elevation usually occurs in the early stages of infarction, and may exhibit quite a dramatic change. ST elevation is often upward and concave, although it can appear convex or horizontal. These changes occur in leads facing the infarction. ST elevation is not unique to MIs and therefore is not confirming evidence. Basic requirements of ST changes for diagnosis are: elevation of at least 1 mm in two or more adjoining leads for inferior infarctions (II, III, and aVF), and at least 2 mm in two or more precordial leads for anterior infarction. You should be aware that ST elevation can be seen in leads V 1 and V 2 normally. However, if there is also elevation in V 3 the cause is unlikely to be physiological.
  • Deep Q wave The only diagnostic changes of acute myocardial infarction are changes in the QRS complexes and the development of abnormal Q waves. However, this may be a late change and so is not useful for the diagnosis of AMI in the pre-hospital situation. Remember that Q waves of more than 0.04 seconds , or 1 little square, are not generally seen in leads I, II or the precordial leads.
  • T wave inversion The T wave is the most unstable feature of the ECG tracing and changes occur very frequently under normal circumstances, limiting their diagnostic value. Subtle changes in T waves are often the earliest signs of myocardial infarction. However, their value is limited for the reason above, but for approximately 20 to 30% of patients presenting with MI, a T wave abnormality is the only ECG sign. The T wave can be lengthened or heightened by coronary insufficiency. T wave inversion is a late change in the ECG and tends to appear as the ST elevation is returning to normal. As the ST segment returns towards the isoelectric line, the T wave also decreases in amplitude and eventually inverts.
  • Bundle branch block Bundle branch block is the pattern produced when either the right bundle or the entire left bundle fails to conduct an impulse normally. The ventricle on the side of the failed bundle branch must be depolarised by the spread of a wave of depolarisation through ventricular muscle from the unaffected side. This is obviously a much slower process and usually the QRS duration is prolonged to at least 0.12 seconds (for right bundle branch block) and 0.14 seconds (for left bundle branch block). The ECG pattern of left bundle branch block (LBBB) resembles that of anterior infarction, but the distinction can readily be made in nearly all cases. Most importantly, in LBBB the QRS is widened to 140 ms or more. With rare exceptions there is a small narrow r wave (less than 0.04 seconds) in V 1 to V 3 which is not usually seen in anteroseptal infarction. There is also notching of the QRS best seen in the anterolateral leads, and the T wave goes in the opposite direction to the QRS in all the precordial leads. This combination of features is diagnostic. In the rare cases where there may be doubt assume the correct interpretation is LBBB. This will make up no difference to the administration of a thrombolytic on medical direction but for the present will be accepted as a contraindication for paramedics acting autonomously (see later slide). Right bundle branch block is characterised by QRS of 0.12 seconds or wider, an s wave in lead I, and a secondary R wave (R’) in V1. As abnormal Q waves do not occur with right bundle branch block, this remains a useful sign of infarction.
  • Sequence of changes in evolving AMI The ECG changes that occur due to myocardial infarction do not all occur at the same time. There is a progression of changes correlating to the progression of infarction. Within minutes of the clinical onset of infarction, there are no changes in the QRS complexes and therefore no definitive evidence of infarction. However, there is ST elevation providing evidence of myocardial damage. The next stage is the development of a new pathological Q wave and loss of the r wave. These changes occur at variable times and so can occur within minutes or can be delayed. Development of a pathological Q wave is the only proof of infarction. As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually persist. The late change is the inversion of the T wave and in a non-Q wave myocardial infarct, when there is no pathological Q wave, this T wave change may be the only sign of infarction. Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves and reduced voltage R waves persist. In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main change to look for on the ECG is ST segment elevation.
  • Location of infarction and its relation to the ECG: anterior infarction As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V 1–6 ) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V 5 and V 6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V 2–6 , with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V 1–6 , I, and aVL.
  • Location of infarction and its relation to the ECG: inferior infarction ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node.
  • Location of infarction and its relation to the ECG: lateral infarction Occlusion of the left circumflex artery may cause lateral infarctions. Lateral infarctions are diagnosed by ST elevation in leads I and aVL.
  • Diagnostic criteria for AMI Myocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis. Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves. Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.
  • Action potentials and electrophysiology The heart is a hollow organ with walls made of specialised cardiac muscle. When excited, these muscles shorten, thicken and squeeze on the hollow cavities, forcing blood to flow in directions permitted by the valves (as described in the last slide). An action potential refers to the voltage changes occurring inside a cell when it is electrically depolarised, due to ionic movements into and out of the cell. Cardiac muscles can be electrically excited and show action potentials that propagate along the surface membrane, carrying excitation to all parts of the muscle. Cardiac muscle cells (cardiomyocytes) are interconnected by gap junctions, allowing action potentials to pass from one cell to the next. This ensures that the heart as a whole participates in each contraction, making the heartbeat an “all or none” response. The basic ventricular action potential is due to three voltage-dependent currents: sodium, potassium, and calcium. The very rapid rise of the initial spike of an action potential is due to the opening of the sodium channels, allowing sodium ions to rush into the cell from the outside, depolarising the cell further. The sodium channels then inactivate, and calcium channels activate. There is now a small flow of calcium ions flowing into the cell, balancing the small amounts of potassium ions leaking out. This results in the membrane potential being held in a suspended plateau. The potassium channels then open, and the calcium channels close, causing a rush of potassium ions out of the cell and the membrane being rapidly repolarised. The action potential does vary throughout the heart due to the presence of different ion channels. In the cells of the sino-atrial (SA node) and atrioventricular nodes (AV node) calcium channels, rather than sodium channels, are activated by membrane depolarisation, resulting in a different shape of the action potential. A recording of the electrical changes that accompany the cardiac cycle is called an electrocardiogram (ECG). Each cardiac cycle produces three distinct waves, designated P, QRS and T. It should be noted that these waves are not action potentials, they represent any electrical activity within the heart as a whole.
  • Ecgrevised2 090808155046 Phpapp01

    1. 1. ECG BASICS By Dr .Mahipal Reddy
    2. 2. ECG machine
    3. 3. Lead Position <ul><li>Four limb leads </li></ul><ul><li>Six chest leads </li></ul><ul><li>V1- 4th intercostal space to the right of sternum </li></ul><ul><li>V2- 4th intercostal space to the left of sternum </li></ul><ul><li>V3- halfway between V2 and V4 </li></ul><ul><li>V4- 5th intercostal space in the left mid-clavicular line </li></ul><ul><li>V5- 5th intercostal space in the left anterior axillary line </li></ul><ul><li>V6- 5th intercostal space in the left mid axillary line </li></ul>
    4. 4. Horizontal plane - the six chest leads 6.5 V1 V1 V2 V2 V3 V3 V4 V4 V5 V5 V6 V6 RA LA LV RV
    5. 5. Colour codes given by AHA
    6. 6. ECG paper and timing <ul><li>ECG paper speed = 25mm/sec </li></ul><ul><li>Voltage calibration 1 mV = 1cm </li></ul><ul><li>ECG paper - standard calibrations </li></ul><ul><ul><li>each small square = 1mm </li></ul></ul><ul><ul><li>each large square = 5mm </li></ul></ul><ul><li>Timings </li></ul><ul><ul><li>1 small square = 0.04sec </li></ul></ul><ul><ul><li>1 large square = 0.2sec </li></ul></ul><ul><ul><li>25 small squares = 1sec </li></ul></ul><ul><ul><li>5 large squares = 1sec </li></ul></ul>
    7. 7. ECG paper 5 Large squares = 1 second Time 1 Large square = 0.2 second 1 Small square = 0.04 second 2 Large squares = 1 cm 6.1
    8. 8. STANDARDISATION ECG amplitude scale Normal amplitude 10 mm/mV Half amplitude 5 mm/mV Double amplitude 20 mm/mV
    9. 9. ECG WAVES
    10. 10. The Normal ECG Normal Intervals: PR 0.12-0.20s QRS duration <0.12s QTc 0.33-0.43s
    11. 11. NSR
    12. 12. P-wave <ul><li>Normal values </li></ul><ul><li>up in all leads except aVR. </li></ul><ul><li>Duration. < 2.5 mm. </li></ul><ul><li>Amplitude. </li></ul><ul><li>< 2.5 mm. </li></ul><ul><li>Abnormalities </li></ul><ul><li>1. Inverted P-wave </li></ul><ul><li>Junctional rhythm. </li></ul><ul><li>2. Wide P-wave (P- mitrale) </li></ul><ul><li>LAE </li></ul><ul><li>3. Peaked P-wave (P-pulmonale) </li></ul><ul><li>RAE </li></ul><ul><li>4. Saw-tooth appearance </li></ul><ul><li>Atrial flutter </li></ul><ul><li>5. Absent normal P wave </li></ul><ul><li>Atrial fibrillation </li></ul>
    13. 21. NORMAL P-R INTERVAL <ul><li>PR interval time 0.12 seconds to 0.2 seconds. </li></ul><ul><li>That is three small squares to five small squares. </li></ul>
    14. 22. PR interval <ul><li>Definition: the time interval between beginning of P-wave to beginning of QRS complex. </li></ul><ul><li>Normal PR interval </li></ul><ul><li>3-5mm (0.12-0.2 sec) </li></ul><ul><li>Abnormalities </li></ul><ul><li>1. Short PR interval </li></ul><ul><li>WPW syndrome </li></ul><ul><li>2. Long PR interval </li></ul><ul><li>First degree heart block </li></ul>
    15. 25. PR interval <ul><li>Definition: the time interval between beginning of P-wave to beginning of QRS complex. </li></ul><ul><li>Normal PR interval </li></ul><ul><li>3-5mm (0.12-0.2 sec) </li></ul><ul><li>Abnormalities </li></ul><ul><li>1. Short PR interval </li></ul><ul><li>WPW syndrome </li></ul><ul><li>2. Long PR interval </li></ul><ul><li>First degree heart block </li></ul>
    16. 26. Q WAVES <ul><li>Q waves <0.04 second. </li></ul><ul><li>That’s is less than one small square duration. </li></ul><ul><li>Height < 1 / 4 of R wave height. </li></ul>
    17. 27. Normal Q wave
    18. 28. Q wave in MI
    19. 29. Q wave in septal hypertrophy
    20. 30.                                                                      
    21. 31. QRS COMPLEX <ul><li>QRS duration <0.11 s </li></ul><ul><li>That is less than almost three small squares </li></ul><ul><li>Some books write 2 and a half small squares. </li></ul><ul><li>Height of R wave is (V1-V6) >8 mm in at least one of chest leads. </li></ul>
    22. 32. QRS complex <ul><li>Normal values </li></ul><ul><li>Duration : < 2.5 mm. </li></ul><ul><li>Morphology : progression from Short R and deep S (rS) in V1 to tall R and short S in V6 with small Q in V5-6 (qRs). </li></ul><ul><li>Abnormalities : </li></ul><ul><li>1. Wide QRS complex </li></ul><ul><li>Bundle branch block. </li></ul><ul><li>Ventricular rhythm . </li></ul><ul><li>2. Tall R in V1 </li></ul><ul><li>RVH. </li></ul><ul><li>RBBB. </li></ul><ul><li>Posterior MI. </li></ul><ul><li>WPW syndrome. </li></ul><ul><li>3. abnormal Q wave </li></ul><ul><li>[ > 25% of R wave] </li></ul><ul><li>MI. </li></ul><ul><li>Hypertrophic cardiomyopathy. </li></ul><ul><li>Normal variant. </li></ul>
    23. 33. Small voltage QRS <ul><li>Defined as < 5 mm peak-to-peak in all limb leads or <10 mm in precordial leads. </li></ul><ul><li>Chronic causes — pulmonary disease, hypothyroidism, obesity, cardiomyopathy. </li></ul><ul><li>Acute causes — pleural and/or pericardial effusions </li></ul>
    24. 34. V 1 V 2 V 3 V 4 V 5 V 6 The R wave in the precordial leads must grow from V1 to at least V4
    25. 37. J point Q S ST
    26. 38. L V H-Voltage Criteria <ul><li>In adult with normal chest wall </li></ul><ul><li>SV1+RV5 >35 mm </li></ul><ul><li>or </li></ul><ul><li>SV1 >20 mm </li></ul><ul><li>or </li></ul><ul><li>RV6 >20 mm </li></ul>
    27. 39. LEFT VENTRICULAR HYPERTROPHY
    28. 40. Dominant R wave in V1 <ul><li>RBBB </li></ul><ul><li>Chronic lung disease, PE Posterior MI WPW Type A Dextrocardia Duchenne muscular dystrophy </li></ul>
    29. 41. Right Ventricular Hypertrophy <ul><li>WILL SHOW AS </li></ul><ul><li>Right axis deviation (RAD) </li></ul><ul><li>Precordial leads </li></ul><ul><li>In V1, R wave > S wave </li></ul><ul><li>In V6, S wave > R wave </li></ul><ul><li>Usual manifestation is pulmonary disease or </li></ul><ul><li>congenital heart disease </li></ul>
    30. 43. Right Ventricular Hypertrophy
    31. 44. Right ventricular hypertrophy <ul><li>Right ventricular hypertrophy (RVH) increases the height of the R wave in V1. An R wave in V1 that is greater than 7 boxes in height, or larger than the S wave, is suspicious for RVH. Other findings are necessary to confirm the ECG diagnosis. </li></ul>
    32. 45. Right Ventricular Hypertrophy <ul><li>Other findings in RVH include right axis deviation, taller R waves in the right precordial leads (V1-V3), and deeper S waves in the left precordials (V4-V6). The T wave is inverted in V1 (and often in V2). </li></ul>
    33. 46. Right Ventricular Hypertrophy <ul><li>True posterior infarction may also cause a tall R wave in V1, but the T wave is usually upright, and there is usually some evidence of inferior infarction (ST-T changes or Qs in II, III, and F). </li></ul>
    34. 47. Right Ventricular Hypertrophy <ul><li>A large R wave in V1, when not accompanied by evidence of infarction, nor by evidence of RVH (right axis, inverted T wave in V1), may be benign “counter-clockwise rotation of the heart.” This can be seen with abnormal chest shape. </li></ul>
    35. 48. Right Ventricular Hypertrophy <ul><li>RVH Criteria </li></ul><ul><li>R in V1 > 7 mm or > S wave </li></ul><ul><li>T in V1 inverted </li></ul><ul><li>Right axis deviation </li></ul><ul><li>S waves in V5-V6 </li></ul>
    36. 49. Right Ventricular Hypertrophy <ul><li>Right axis deviation </li></ul><ul><li>Right atrial enlargement </li></ul><ul><li>Downsloping ST depressions in V 1 -V 3 (a.k.a. RV strain pattern) </li></ul><ul><li>Tall R wave in V 1 </li></ul>Although there is no widely accepted criteria for detecting the presence of RVH, any combination of the following EKG features is suggestive of its presence:
    37. 50. Right Ventricular Hypertrophy
    38. 51. Left Ventricular Hypertrophy
    39. 52. Left Atrial Enlargement Criteria P wave duration in II ≥ 120ms or Negative component of biphasic P wave in V 1 ≥ 1 “small box” in area
    40. 53. Right Atrial Enlargement Criteria P wave height in II ≥ 2.4mm or Positive component of biphasic P wave in V 1 ≥ 1 “small box” in area
    41. 54. Left Ventricular Hypertrophy
    42. 55. RHV-Any one of the following in lead V1 <ul><li>R/S ratio > 1 and negative T wave </li></ul><ul><li>qR pattern </li></ul><ul><li>R > 6 mm, or S < 2mm, or rSR' with R' >10 mm </li></ul>
    43. 56. ECG criteria for RBBB <ul><li>•(1) QRS duration exceeds 0.12 seconds </li></ul><ul><li>•(2) RSR complex in V1 </li></ul><ul><li>•(3) Delayed S wave in Ι, V5, V6 </li></ul><ul><li>•(4) ST/T must be opposite in direction to the terminal QRS(is secondary to the block and does not predispose primary ST/T changes) </li></ul>
    44. 57. RBBB & MI <ul><li>If abnormal Q waves are present they will not be masked by the BBB pattern. </li></ul><ul><li>•This is because there is no alteration of the initial part of the complex RS (in V1) and abnormal Q waves can still be seen. </li></ul>
    45. 58. Significance of RBBB <ul><li>RBBB is seen in :- </li></ul><ul><li>(1) occasional normal subjects </li></ul><ul><li>(2) pulmonary embolus </li></ul><ul><li>(3) coronary artery disease </li></ul><ul><li>(4) ASD </li></ul><ul><li>(5) active carditis </li></ul><ul><li>(6) RV diastolic overload </li></ul>
    46. 59. Partial / Incomplete RBBB <ul><li>is diagnosed when the pattern of RBBB is present but the duration of the QRS does not exceed 0.12 seconds. </li></ul>
    47. 60. ECG criteria for LBBB <ul><li>(1)Prolonged QRS complexes, greater than 0.12 seconds </li></ul><ul><li>(2)Wide, notched QRS (M shaped) V5, V6 </li></ul><ul><li>(3)Wide, notched QS complexes are seen in V1 (due to spread of activation away from the electrode through septum + LV) </li></ul><ul><li>(4)In V2, V3 small r wave is seen due toactivation of paraseptalregion </li></ul>
    48. 61. Significance of LBBB <ul><li>LBBB is seen in :- </li></ul><ul><li>(1) Always indicative of organic heart disease </li></ul><ul><li>(2) Found in ischemic heart disease </li></ul><ul><li>(3) Found in hypertension. </li></ul><ul><li>MI should not be diagnosed in the presence of LBBB ->Q waves are masked by LBBB pattern </li></ul><ul><li>Cannot diagnose the presence of MI with LBBB </li></ul>
    49. 62. Partial / Incomplete LBBB <ul><li>is diagnosed when the pattern of LBBB is present but the duration of the QRS does not exceed 0.12 seconds. </li></ul>
    50. 63. NORMAL ST- SEGMENT <ul><li>it's isoelectric. </li></ul><ul><li>[i.e. at same level of PR or PQ segment at least in the beginning] </li></ul>
    51. 64. NORMAL CONCAVITY OF S-T SEGMENT <ul><li>It then gradually slopes upwards making concavity upwards and not going more than one small square upwards from isoelectric line or one small square below isoelectric line. </li></ul><ul><li>In MI this concavity may get lost and become convex upwards called coving of S-T segment. </li></ul>
    52. 65. Abnormalities <ul><li>ST elevation: </li></ul><ul><li>More than one small square </li></ul><ul><li>Acute MI. </li></ul><ul><li>Prinzmetal angina. </li></ul><ul><li>Acute pericarditis. </li></ul><ul><li>Early repolarization </li></ul><ul><li>ST depression: </li></ul><ul><li>More than one small square </li></ul><ul><li>Ischemia. </li></ul><ul><li>Ventricular strain. </li></ul><ul><li>BBB. </li></ul><ul><li>Hypokalemia. </li></ul><ul><li>Digoxin effect. </li></ul>
    53. 68. Stress test ECG – note the ST Depression
    54. 70. Note the arrows pointing ST depression
    55. 71. ST depression & Troponin T positive is NON STEMI
    56. 72. Coving of S-T segment <ul><li>Concavity lost and convexity appear facing upwards. </li></ul>
    57. 73. Diagnostic criteria for AMI <ul><li>Q wave duration of more than 0.04 seconds </li></ul><ul><li>Q wave depth of more than 25% of ensuing r wave </li></ul><ul><li>ST elevation in leads facing infarct (or depression in opposite leads) </li></ul><ul><li>Deep T wave inversion overlying and adjacent to infarct </li></ul><ul><li>Cardiac arrhythmias </li></ul>
    58. 74. Abnormalities of ST- segment acute MI pericarditis early repolariz. ischemia
    59. 75. Q waves in myocardial infarction                                                                       
    60. 77. T-wave <ul><li>Normal values. </li></ul><ul><li>1.amplitude: </li></ul><ul><li>< 10mm in the chest leads. </li></ul><ul><li>Abnormalities: </li></ul><ul><li>1. Peaked T-wave: </li></ul><ul><li>Hyper-acute MI. </li></ul><ul><li>Hyperkalemia. </li></ul><ul><li>Normal variant </li></ul><ul><li>. </li></ul><ul><li>2. T- inversion: </li></ul><ul><li>Ischemia. </li></ul><ul><li>Myocardial infarction. </li></ul><ul><li>Myocarditis </li></ul><ul><li>Ventricular strain </li></ul><ul><li>BBB. </li></ul><ul><li>Hypokalemia. </li></ul><ul><li>Digoxin effect. </li></ul>
    61. 78. QT- interval <ul><li>Definition : Time interval between beginning of </li></ul><ul><li>QRS complex to the end of T wave. </li></ul><ul><li>Normally: At normal HR: QT ≤ 11mm (0.44 sec) </li></ul><ul><li>Abnormalities : </li></ul><ul><li>Prolonged QT interval: hypocalcemia and congenital long QT syndrome. </li></ul><ul><li>Short QT interval: hypercalcemia. </li></ul>
    62. 79. QT Interval - Should be < 1/2 preceding R to R interval -
    63. 80. QT Interval - Should be < 1/2 preceding R to R interval - QT interval
    64. 81. QT Interval - Should be < 1/2 preceding R to R interval - QT interval
    65. 82. QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R
    66. 83. QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R
    67. 84. QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R
    68. 85. QT Interval - Should be < 1/2 preceding R to R interval - QT interval 65 - 90 bpm R R
    69. 86. QT Interval - Should be < 1/2 preceding R to R interval - QT interval 65 - 90 bpm Normal QT c = 0.46 sec R R
    70. 87. M
    71. 88. Atrioventricular (AV) Heart Block
    72. 89. Classification of AV Heart Blocks Degree AV Conduction Pattern 1 St Degree Block Uniformly prolonged PR interval 2 nd Degree, Mobitz Type I Progressive PR interval prolongation 2 nd Degree, Mobitz Type II Sudden conduction failure 3 rd Degree Block No AV conduction
    73. 90. AV Blocks <ul><li>First Degree </li></ul><ul><ul><li>Prolonged AV conduction time </li></ul></ul><ul><ul><li>PR interval > 0.20 seconds </li></ul></ul>
    74. 91. 1 st Degree AV Block Prolongation of the PR interval, which is constant All P waves are conducted
    75. 92. <ul><li>1st degree AV Block : </li></ul><ul><li>Regular Rhythm </li></ul><ul><li>PRI > .20 seconds or 5 small squares and is CONSTANT </li></ul><ul><li>Usually does not require treatment </li></ul>PRI > .20 seconds
    76. 93. First Degree Block <ul><li>prolonged PR interval </li></ul>
    77. 94. Analyze the Rhythm
    78. 95. AV Blocks <ul><li>Second Degree </li></ul><ul><ul><li>Definition </li></ul></ul><ul><ul><ul><li>More Ps than QRSs </li></ul></ul></ul><ul><ul><ul><li>Every QRS caused by a P </li></ul></ul></ul>
    79. 96. Second-Degree AV Block <ul><li>There is intermittent failure of the supraventricular impulse to be conducted to the ventricles </li></ul><ul><li>Some of the P waves are not followed by a QRS complex.The conduction ratio (P/QRS ratio) may be set at 2:1,3:1,3:2,4:3,and so forth </li></ul>
    80. 97. Second Degree <ul><ul><li>Types </li></ul></ul><ul><ul><ul><li>Type I </li></ul></ul></ul><ul><ul><ul><ul><li>Wenckebach phenomenon </li></ul></ul></ul></ul><ul><ul><ul><li>Type II </li></ul></ul></ul><ul><ul><ul><ul><li>Fixed or Classical </li></ul></ul></ul></ul>
    81. 98. Type I Second-Degree AV Block: Wenckebach Phenomenon <ul><li>ECG findings </li></ul><ul><li>1.Progressive lengthening of the PR interval until a P wave is blocked </li></ul>
    82. 99. 2nd degree AV Block (“Mobitz I” also called “Wenckebach”) : Pattern Repeats…………. PRI = .24 sec PRI = .36 sec PRI = .40 sec QRS is “dropped” <ul><li>Irregular Rhythm </li></ul><ul><li>PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse) </li></ul><ul><ul><li>PRI is NOT CONSTANT </li></ul></ul>Pause 4:3 Wenckebach (conduction ratio may not be constant)
    83. 101. Type II Second-Degree AV Block: Mobitz Type II <ul><li>ECG findings </li></ul><ul><li>1.Intermittent or unexpected blocked P waves you don’t know when QRS drops </li></ul><ul><li>2.P-R intervals may be normal or prolonged,but they remain constant </li></ul><ul><li>4. A long rhythm strip may help </li></ul>
    84. 103. Second Degree AV Block <ul><li>Mobitz type I or Winckebach </li></ul><ul><li>Mobitz type II </li></ul>
    85. 104. Type 1 (Wenckebach) Progressive prolongation of the PR interval until a P wave is not conducted. Constant PR interval with unexpected intermittent failure to conduct Type 2
    86. 105. Mobitz Type I
    87. 106. MOBITZ TYPE 1
    88. 107. <ul><li>2nd degree AV Block (“Mobitz II”) : </li></ul><ul><li>Irregular Rhythm </li></ul><ul><li>QRS complexes may be somewhat wide (greater than .12 seconds) </li></ul><ul><li>Non-conducted sinus impulses appear at unexpected irregular intervals </li></ul><ul><ul><li>PRI may be normal or prolonged but is CONSTANT and fixed </li></ul></ul><ul><li>Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart block (3rd degree block) </li></ul><ul><li>It’s appearance in the setting of an acute MI identifies a high risk patient </li></ul><ul><li>Cause: anterioseptal MI, </li></ul><ul><li>Treatment: may require pacemaker in the case of fibrotic conduction system </li></ul>Non-conducted sinus impulses “ 2:1 block ” “ 3:1 block” PRI is CONSTANT
    89. 108. Analyze the Rhythm
    90. 109. Second Degree Mobitz <ul><ul><li>Characteristics </li></ul></ul><ul><ul><ul><ul><li>Atrial rate > Ventricular rate </li></ul></ul></ul></ul><ul><ul><ul><ul><li>QRS usually longer than 0.12 sec </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Usually 4:3 or 3:2 conduction ratio (P:QRS ratio) </li></ul></ul></ul></ul>
    91. 110. Analyze the Rhythm
    92. 111. Mobitz II <ul><li>Definition: Mobitz II is characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave will be constant for each QRS </li></ul><ul><li>. EKG Characteristics:Atrial and ventricular rate is irregular. P Wave: Present in two, three or four to one conduction with the QRS. PR Interval constant for each P wave prior to the QRS. QRS may or may not be within normal limits. </li></ul>
    93. 112. Mobitz Type II
    94. 113. Mobitz Type II <ul><li>Sudden appearance of a single, non-conducted sinus P wave... </li></ul>
    95. 114. Advanced Second-Degree AV Block Two or more consecutive nonconducted sinus P waves
    96. 115. Complete AV Block <ul><ul><li>Characteristics </li></ul></ul><ul><ul><ul><li>Atrioventricular dissociation </li></ul></ul></ul><ul><ul><ul><li>Regular P-P and R-R but without association between the two </li></ul></ul></ul><ul><ul><ul><li>Atrial rate > Ventricular rate </li></ul></ul></ul><ul><ul><ul><li>QRS > 0.12 sec </li></ul></ul></ul>
    97. 116. 3 rd Degree (Complete) AV Block EKG Characteristics: No relationship between P waves and QRS complexes Relatively constant PP intervals and RR intervals Greater number of P waves than QRS complexes
    98. 117. Complete heart block <ul><li>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. </li></ul>
    99. 118. <ul><li>3rd degree AV Block (“Complete Heart Block”) : </li></ul><ul><li>Irregular Rhythm </li></ul><ul><li>QRS complexes may be narrow or broad depending on the level of the block </li></ul><ul><li>Atria and ventricles beat independent of one another (AV dissociation) </li></ul><ul><ul><li>QRS’s have their own rhythm, P-waves have their own rhythm </li></ul></ul><ul><li>May be caused by inferior MI and it’s presence worsens the prognosis </li></ul><ul><li>Treatment: usually requires pacemaker </li></ul>QRS intervals P-wave intervals – note how the P-waves sometimes distort QRS complexes or T-waves
    100. 119. Third-Degree (Complete) AV Block
    101. 120. Third-Degree (Complete) AV Block <ul><li>The P wave bears no relation to the QRS complexes, and the PR intervals are completely variable </li></ul>
    102. 121. 30 AV Block <ul><li>AV dissociation </li></ul><ul><li>atria and ventricles beating on their own </li></ul><ul><li>no relation between P’s & QRS’s </li></ul><ul><li>Atrial rate is different from ventricular </li></ul><ul><li>ventricular rate: 30-60 bpm </li></ul><ul><li>Rhythm is regular for both </li></ul><ul><li>QRS can be narrow or wide </li></ul><ul><li>depends on site of pacemaker! </li></ul>
    103. 122. Key points <ul><li>Wenckebach </li></ul><ul><li>look for group beating & changing PR </li></ul><ul><li>Mobitz II </li></ul><ul><li>look for reg. atrial rhythm & consistent PR </li></ul><ul><li>3o block </li></ul><ul><li>atrial & ventricular rhythm regular </li></ul><ul><li>􀂾 rate is different!!! </li></ul><ul><li>no consistent PR </li></ul>
    104. 124. Left Anterior Fascicular Block <ul><li>Left axis deviation , usually -45 to -90 degrees </li></ul><ul><li>QRS duration usually <0.12s unless coexisting RBBB </li></ul><ul><li>Poor R wave progression in leads V1-V3 and deeper S waves in leads V5 and V6 </li></ul><ul><li>There is RS pattern with R wave in lead II > lead III </li></ul><ul><li>S wave in lead III > lead II </li></ul><ul><li>QR pattern in lead I and AVL,with small Q wave </li></ul><ul><li>No other causes of left axis deviation </li></ul>
    105. 125. <ul><li>Left Anterior Hemiblock (LAHB) : </li></ul><ul><li>Left axis deviation (> -30 degrees) will be noted and there will be a prominent S-wave in Leads II, and III </li></ul>LPIF LASF LBB 1. 2. Lead III Lead I Lead AVF
    106. 126. Left Posterior Fascicular Block <ul><li>Right axis deviation </li></ul><ul><li>QR pattern in inferior leads (II,III,AVF) small q wave </li></ul><ul><li>RS patter in lead lead I and AVL(small R with deep S) </li></ul>
    107. 127. <ul><li>Left Posterior Hemiblock (LPHB) : </li></ul><ul><li>Right axis deviation and there will be a prominent S-wave in Leads I. Q-waves may be noted in III and AVF. </li></ul><ul><li>Notes on (LPHB) : </li></ul><ul><li>QRS is normal width unless BBB is present </li></ul><ul><li>If LPHB occurs in the setting of an acute MI, it is almost always accompanied by RBBB and carries a mortality rate of 71% </li></ul>LPIF LASF LBB 1. 2. Lead III Lead I Lead AVF
    108. 128. Bifascicular Bundle Branch Block <ul><li>RBBB with either left anterior or left posterior fascicular block </li></ul><ul><li>Diagnostic criteria </li></ul><ul><li>1.Prolongation of the QRS duration to 0.12 second or longer </li></ul><ul><li>2.RSR’ pattern in lead V1,with the R’ being broad and slurred </li></ul><ul><li>3.Wide,slurred S wave in leads I,V5 and V6 </li></ul><ul><li>4.Left axis or right axis deviation </li></ul>
    109. 129. Trifascicular Block <ul><li>The combination of RBBB, LAFB and long PR interval </li></ul><ul><li>Implies that conduction is delayed in the third fascicle </li></ul>
    110. 130. Indications For Implantation of Permanent Pacing in Acquired AV Blocks <ul><li>1.Third-degree AV block, Bradycardia with symptoms </li></ul><ul><li>Asystole </li></ul><ul><li>e.Neuromuscular diseases with AV block (Myotonic muscular dystrophy) </li></ul><ul><li>2.Second-degree AV block with symptomatic bradycardia </li></ul>
    111. 131. Cardiac Pacemakers <ul><li>Definition </li></ul><ul><ul><li>Delivers artificial stimulus to heart </li></ul></ul><ul><ul><li>Causes depolarization and contraction </li></ul></ul><ul><li>Uses </li></ul><ul><ul><li>Bradyarrhythmias </li></ul></ul><ul><ul><li>Asystole </li></ul></ul><ul><ul><li>Tachyarrhythmias (overdrive pacing) </li></ul></ul>
    112. 132. Cardiac Pacemakers <ul><li>Types </li></ul><ul><ul><li>Fixed </li></ul></ul><ul><ul><ul><li>Fires at constant rate </li></ul></ul></ul><ul><ul><ul><li>Can discharge on T-wave </li></ul></ul></ul><ul><ul><ul><li>Very rare </li></ul></ul></ul><ul><ul><li>Demand </li></ul></ul><ul><ul><ul><li>Senses patient’s rhythm </li></ul></ul></ul><ul><ul><ul><li>Fires only if no activity sensed after preset interval (escape interval) </li></ul></ul></ul><ul><ul><li>Transcutaneous vs Transvenous vs Implanted </li></ul></ul>
    113. 133. Cardiac Pacemakers
    114. 134. Cardiac Pacemakers <ul><li>Demand Pacemaker Types </li></ul><ul><ul><li>Ventricular </li></ul></ul><ul><ul><ul><li>Fires ventricles </li></ul></ul></ul><ul><ul><li>Atrial </li></ul></ul><ul><ul><ul><li>Fires atria </li></ul></ul></ul><ul><ul><ul><li>Atria fire ventricles </li></ul></ul></ul><ul><ul><ul><li>Requires intact AV conduction </li></ul></ul></ul>
    115. 135. Cardiac Pacemakers <ul><li>Demand Pacemaker Types </li></ul><ul><ul><li>Atrial Synchronous </li></ul></ul><ul><ul><ul><li>Senses atria </li></ul></ul></ul><ul><ul><ul><li>Fires ventricles </li></ul></ul></ul><ul><ul><li>AV Sequential </li></ul></ul><ul><ul><ul><li>Two electrodes </li></ul></ul></ul><ul><ul><ul><li>Fires atria/ventricles in sequence </li></ul></ul></ul>
    116. 136. Cardiac Pacemakers <ul><li>Problems </li></ul><ul><ul><li>Failure to capture </li></ul></ul><ul><ul><ul><li>No response to pacemaker artifact </li></ul></ul></ul><ul><ul><ul><li>Bradycardia may result </li></ul></ul></ul><ul><ul><ul><li>Cause: high “threshold” </li></ul></ul></ul><ul><ul><ul><li>Management </li></ul></ul></ul><ul><ul><ul><ul><li>Increase amps on temporary pacemaker </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Treat as symptomatic bradycardia </li></ul></ul></ul></ul>
    117. 137. Cardiac Pacemakers <ul><li>Problems </li></ul><ul><ul><li>Failure to sense </li></ul></ul><ul><ul><ul><li>Spike follows QRS within escape interval </li></ul></ul></ul><ul><ul><ul><li>May cause R-on-T phenomenon </li></ul></ul></ul><ul><ul><ul><li>Management </li></ul></ul></ul><ul><ul><ul><ul><li>Increase sensitivity </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Attempt to override permanent pacer with temporary </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Be prepared to manage VF </li></ul></ul></ul></ul>
    118. 138. Implanted Defibrillators <ul><li>AICD </li></ul><ul><ul><li>Automated Implanted Cardio-Defibrillator </li></ul></ul><ul><li>Uses </li></ul><ul><ul><li>Tachyarrhythmias </li></ul></ul><ul><ul><li>Malignant arrhythmias </li></ul></ul><ul><ul><ul><li>VT </li></ul></ul></ul><ul><ul><ul><li>VF </li></ul></ul></ul>
    119. 139. Implanted Defibrillators <ul><li>Programmed at insertion to deliver predetermined therapies with a set order and number of therapies including: </li></ul><ul><ul><li>pacing </li></ul></ul><ul><ul><li>overdrive pacing </li></ul></ul><ul><ul><li>cardioversion with increasing energies </li></ul></ul><ul><ul><li>defibrillation with increasing energies </li></ul></ul><ul><ul><li>standby mode </li></ul></ul><ul><ul><ul><li>Effect of standby mode on Paramedic treatments </li></ul></ul></ul>
    120. 140. Implanted Defibrillators <ul><li>Potential Complications </li></ul><ul><ul><li>Fails to deliver therapies as intended </li></ul></ul><ul><ul><ul><li>worst complication </li></ul></ul></ul><ul><ul><ul><li>requires Paramedic intervention </li></ul></ul></ul><ul><ul><li>Delivers therapies when NOT appropriate </li></ul></ul><ul><ul><ul><li>broken or malfunctioning lead </li></ul></ul></ul><ul><ul><ul><li>parameters for delivery are not specific enough </li></ul></ul></ul><ul><ul><li>Continues to deliver shocks </li></ul></ul><ul><ul><ul><li>parameters for delivery are not specific enough and device senses a reset </li></ul></ul></ul><ul><ul><ul><li>may be shut off (not standby mode) with donut-magnet </li></ul></ul></ul>
    121. 141. Sinus Exit Block <ul><li>Due to abnormal function of SA node </li></ul><ul><li>MI, drugs, hypoxia, vagal tone </li></ul><ul><li>Impulse blocked from leaving SA node </li></ul><ul><li>usually transient </li></ul><ul><li>Produces 1 missed cycle </li></ul><ul><li>can confuse with sinus pause or arrest </li></ul>
    122. 142. Sinus block
    123. 143. ARRTHYMIAS AND ECTOPIC BEATS
    124. 144. normal (&quot;sinus&quot;) beats sinus node doesn't fire leading to a period of asystole (sick sinus syndrome) p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. It is therefore called an &quot;atrial&quot; beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Atrial Escape Beat Recognizing and Naming Beats & Rhythms
    125. 145. there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction. The beat is therefore called a &quot;junctional&quot; or a “nodal” beat Junctional Escape Beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Recognizing and Naming Beats & Rhythms
    126. 146. actually a &quot;retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles QRS is wide and much different (&quot;bizarre&quot;) looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a “ventricular” beat Ventricular Escape Beat there is no p wave, indicating that the beat did not originate anywhere in the atria Recognizing and Naming Beats & Rhythms
    127. 147. Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery The “Re-Entry” Mechanism of Ectopic Beats & Rhythms Electrical Impulse Cardiac Conduction Tissue <ul><li>Tissues with these type of circuits may exist: </li></ul><ul><ul><li>in microscopic size in the SA node, AV node, or any type of heart tissue </li></ul></ul><ul><ul><li>in a “macroscopic” structure such as an accessory pathway in WPW </li></ul></ul>
    128. 148. Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Premature Beat Impulse Cardiac Conduction Tissue <ul><ul><ul><li>1. An arrhythmia is triggered by a premature beat </li></ul></ul></ul><ul><ul><ul><li>2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only </li></ul></ul></ul>Repolarizing Tissue (long refractory period) The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
    129. 149. <ul><ul><ul><li>3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway </li></ul></ul></ul>Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
    130. 150. <ul><ul><ul><li>4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit </li></ul></ul></ul>Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
    131. 151. Recognizing and Naming Beats & Rhythms <ul><li>Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles) : </li></ul><ul><li>A ventricular ectopic focus discharges causing an early beat </li></ul><ul><li>Ectopic beat has no P-wave (maybe retrograde), and QRS complex is &quot;wide and bizarre&quot; </li></ul><ul><li>QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant) </li></ul><ul><li>In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion </li></ul><ul><li>PVC’s are sometimes described by lay people as “skipped heart beats” </li></ul>
    132. 152. Recognizing and Naming Beats & Rhythms <ul><li>Characteristics of PVC's </li></ul><ul><li>PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave) </li></ul><ul><li>T-waves for PVC’s are usually large and opposite in polarity to terminal QRS </li></ul><ul><li>Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle </li></ul><ul><li>Every other beat being a PVC (bigeminy) may indicate coronary artery disease </li></ul><ul><li>Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s </li></ul>Interpolated PVC – note the sinus rhythm is undisturbed The classic PVC – note the compensatory pause
    133. 153. <ul><li>PVC's are Dangerous When : </li></ul><ul><li>They are frequent (> 30% of complexes) or are increasing in frequency </li></ul><ul><li>The come close to or on top of a preceding T-wave (R on T) </li></ul><ul><li>Three or more PVC's in a row (run of V-tach) </li></ul><ul><li>Any PVC in the setting of an acute MI </li></ul><ul><li>PVC's come from different foci (&quot;multifocal&quot; or &quot;multiformed&quot;) </li></ul><ul><li>These dangerous phenomenon may preclude the occurrence of deadly arrhythmias: </li></ul><ul><li>Ventricular Tachycardia </li></ul><ul><li>Ventricular Fibrillation </li></ul>Recognizing and Naming Beats & Rhythms sinus beats Unconverted V-tach r V-fib V-tach “ R on T phenomenon” time The sooner defibrillation takes place, the increased likelihood of survival
    134. 154. Recognizing and Naming Beats & Rhythms <ul><li>Notes on V-tach : </li></ul><ul><li>Causes of V-tach </li></ul><ul><ul><li>Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause) </li></ul></ul><ul><li>Typical V-tach patient </li></ul><ul><ul><li>MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm) </li></ul></ul><ul><li>V-tach complexes are likely to be similar and the rhythm regular </li></ul><ul><ul><li>Irregular V-Tach rhythms may be due to to: </li></ul></ul><ul><ul><ul><li>breakthrough of atrial conduction </li></ul></ul></ul><ul><ul><ul><ul><li>atria may “capture” the entire beat beat </li></ul></ul></ul></ul><ul><ul><ul><ul><li>an atrial beat may “merge” with an ectopic ventricular beat (fusion beat) </li></ul></ul></ul></ul>Fusion beat - note p-wave in front of PVC and the PVC is narrower than the other PVC’s – this indicates the beat is a product of both the sinus node and an ectopic ventricular focus Capture beat - note that the complex is narrow enough to suggest normal ventricular conduction. This indicates that an atrial impulse has made it through and conduction through the ventricles is relatively normal.
    135. 155. Recognizing and Naming Beats & Rhythms <ul><li>Premature Atrial Contractions (PAC’s) : </li></ul><ul><li>An ectopic focus in the atria discharges causing an early beat </li></ul><ul><li>The P-wave of the PAC will not look like a normal sinus P-wave (different morphology) </li></ul><ul><li>QRS is narrow and normal looking because ventricular depolarization is normal </li></ul><ul><li>PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s) </li></ul><ul><li>PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco </li></ul><ul><li>PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy </li></ul><ul><li>PAC’s may also precede PSVT </li></ul>PAC Non conducted PAC Non conducted PAC distorting a T-wave
    136. 156. <ul><li>Premature Junctional Contractions (PJC’s) : </li></ul><ul><li>An ectopic focus in or around the AV junction discharges causing an early beat </li></ul><ul><li>The beat has no P-wave </li></ul><ul><li>QRS is narrow and normal looking because ventricular depolarization is normal </li></ul><ul><li>PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm </li></ul>Recognizing and Naming Beats & Rhythms PJC
    137. 157. Recognizing and Naming Beats & Rhythms <ul><li>Multifocal Atrial Tachycardia (MAT) : </li></ul><ul><li>Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles </li></ul><ul><ul><li>QRS complexes are almost identical to the sinus beats </li></ul></ul><ul><li>Rate is usually between 100 and 200 beats per minute </li></ul><ul><li>The rhythm is always IRREGULAR </li></ul><ul><li>P-waves of different morphologies (shapes) may be seen if the rhythm is slow </li></ul><ul><ul><li>If the rate < 100 bpm, the rhythm may be referred to as “wandering pacemaker” </li></ul></ul><ul><li>Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF </li></ul><ul><li>Treatments: Ca ++ channel blockers,  blockers, potassium, magnesium, supportive therapy for underlying causes mentioned above (antiarrhythmic drugs are often ineffective) </li></ul>Note IRREGULAR rhythm in the tachycardia Note different P-wave morphologies when the tachycardia begins
    138. 158. Recognizing and Naming Beats & Rhythms <ul><li>Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) : </li></ul><ul><li>A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted normally to the ventricles (usually initiated by a PAC) </li></ul><ul><ul><li>QRS complexes are almost identical to the sinus beats </li></ul></ul><ul><li>Rate is usually between 150 and 250 beats per minute </li></ul><ul><li>The rhythm is always REGULAR </li></ul><ul><li>Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope ( d Q ) </li></ul><ul><li>Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter </li></ul><ul><li>May be terminated by carotid massage </li></ul><ul><ul><li>u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction </li></ul></ul><ul><li>Treatment: ablation of focus, Adenosine ( d AV conduction), Ca ++ Channel blockers </li></ul>Note REGULAR rhythm in the tachycardia Rhythm usually begins with PAC
    139. 159. Sinus arrest or exit block
    140. 160. PAC
    141. 161. Junctional Premature Beat <ul><li>single ectopic beat that originates in the AV node or </li></ul><ul><li>Bundle of His area of the condunction system </li></ul><ul><li>– Retrograde P waves immediately preceding the QRS </li></ul><ul><li>– Retrograde P waves immediately following the QRS </li></ul><ul><li>– Absent P waves (buried in the QRS) </li></ul>
    142. 162. Junctional Escape Beat
    143. 163. Junctional Rhythm <ul><li>Rate : 40 to 60 beats/minute (atrial and ventricular) </li></ul><ul><li>• Rhythm : regular atrial and ventricular rhythm </li></ul><ul><li>• P wave : usually inverted, may be upright; may precede, </li></ul><ul><li>follow or be hidden in the QRS complex; may </li></ul><ul><li>be absent </li></ul><ul><li>• PR interval : not measurable or less than .20 sec. </li></ul>
    144. 164. Junctional Rhythm
    145. 165. MaligMalignant PVC patterns <ul><li>Frequent PVCs </li></ul><ul><li>Multiform PVCs </li></ul><ul><li>Runs of consecutive PVCs </li></ul><ul><li>R on T phenomenon – PVC that falls on a T </li></ul><ul><li>wave </li></ul><ul><li>PVC during acute MI </li></ul>
    146. 168. Types of PVCs <ul><li>Uniform </li></ul><ul><li>Multiform </li></ul><ul><li>PVC rhythm patterns </li></ul><ul><li>– Bigeminy – PVC occurs every other complex </li></ul><ul><li>– Couplets – 2 PVCs in a row </li></ul><ul><li>– Trigeminy – Two PVCs for every three complexes </li></ul>
    147. 169. Junctional Escape Rhythm
    148. 170. Ventricular tachycardia (VTach) <ul><li>3 or more PVCs in a row at a rate of 120 to 200 bts/min-1 </li></ul><ul><li>Ventricular fibrillation (VFib) </li></ul><ul><li>No visible P or QRS complexes. Waves appear as fibrillating waves </li></ul>
    149. 172. Torsades de Pointes <ul><li>Type of VT known as “twisting of the points.” </li></ul><ul><li>Usually seen in those with prolonged QT intervals caused by </li></ul>
    150. 173. ECG Paper: Dimensions 5 mm 1 mm 0.1 mV 0.04 sec 0.2 sec Speed = rate Voltage ~Mass
    151. 174. Why “1500 / X”? <ul><li>Paper Speed: 25 mm/ sec </li></ul><ul><li>60 seconds / minute </li></ul><ul><li>60 X 25 = 1500 mm / minute </li></ul><ul><li>Take 6 sec strip (30 large boxes) </li></ul><ul><li>Count the P/R waves X 10 </li></ul>OR
    152. 175. Atrial Fibrillation :
    153. 176. Regular “Irregular” <ul><li>Premature Beats: PVC </li></ul><ul><ul><li>Widened QRS, not associated with preceding P wave </li></ul></ul><ul><ul><li>Usually does not disrupt P-wave regularity </li></ul></ul><ul><ul><li>T wave is “inverted” after PVC </li></ul></ul><ul><ul><li>Followed by compensatory ventricular pause </li></ul></ul>
    154. 177. Notice a Pattern in the PVC’s?
    155. 178. Identifying AV Blocks: Name Conduction PR-Int R-R Rhythm Regular (20-40 bpm) Grossly Irregular P > R 3°: Regular Constant P > R 2°:Mobitz II Irregular Progressive P > R 2°:Mobitz I Regular > .20 P = R 1°:
    156. 179. Most Important Questions of Arrhythmias <ul><li>What is the mechanism? </li></ul><ul><ul><li>Problems in impulse formation? (automaticity or ectopic foci) </li></ul></ul><ul><ul><li>Problems in impulse conductivity? (block or re-entry) </li></ul></ul><ul><li>Where is the origin? </li></ul><ul><ul><li>Atria, Junction, Ventricles? </li></ul></ul>
    157. 180. QRS Axis <ul><li>Check Leads: </li></ul><ul><li>1 and AVF </li></ul>
    158. 181. Interpreting Axis Deviation: <ul><li>Normal Electrical Axis: </li></ul><ul><ul><li>(Lead I + / aVF +) </li></ul></ul><ul><li>Left Axis Deviation: </li></ul><ul><ul><li>Lead I + / aVF – </li></ul></ul><ul><ul><li>Pregnancy, LV hypertrophy etc </li></ul></ul><ul><li>Right Axis Deviation: </li></ul><ul><ul><li>Lead I - / aVF + </li></ul></ul><ul><ul><li>Emphysema, RV hypertrophy etc. </li></ul></ul>
    159. 182. NW Axis (No Man’s Land) <ul><li>Both I and aVF are – </li></ul><ul><li>Check to see if leads are transposed (- vs +) </li></ul><ul><li>Indicates: </li></ul><ul><ul><li>Emphysema </li></ul></ul><ul><ul><li>Hyperkalemia </li></ul></ul><ul><ul><li>VTach </li></ul></ul>
    160. 183. Determining Regions of CAD: ST-changes in leads… <ul><li>RCA: Inferior myocardium </li></ul><ul><ul><li>II, III, aVF </li></ul></ul><ul><li>LCA: Lateral myocardium </li></ul><ul><ul><li>I, aVL, V5, V6 </li></ul></ul><ul><li>LAD: Anterior/Septal myocardium </li></ul><ul><ul><li>V1-V4 </li></ul></ul>
    161. 184. Regions of the Myocardium: Inferior II, III, aVF Lateral I, AVL, V5-V6 Anterior / Septal V1-V4
    162. 185. Sinus Arrhythmia
    163. 186. Sinus Arrest/Pause
    164. 187. Sinoatrial Exit Block
    165. 188. Premature Atrial Complexes (PACs)
    166. 189. Wandering Atrial Pacemaker (WAP)
    167. 190. Supraventricular Tachycardia (SVT)
    168. 191. Wolff-Parkinson-White Syndrome (WPW)
    169. 192. Atrial Flutter
    170. 193. Atrial Fibrillation (A-fib)
    171. 194. Premature Junctional Complexes (PJC)
    172. 195. Junctional Rhythm
    173. 196. Junctional Rhythm
    174. 197. Accelerated Junctional Rhythm
    175. 198. Junctional Tachycardia
    176. 199. Premature Ventricular Complexes (PVC's) Note – Complexes not Contractions
    177. 200. PVC’s <ul><li>Uniformed/Multiformed </li></ul><ul><li>Couplets/Salvos/Runs </li></ul><ul><li>Bigeminy/Trigeminy/Quadrageminy </li></ul>
    178. 201. Uniformed PVC’s
    179. 202. R on T Phenomena
    180. 203. Multiformed PVC’s
    181. 204. PVC Couplets
    182. 205. PVC Salvos and Runs
    183. 206. Bigeminy PVC’s
    184. 207. Trigeminy PVC’s
    185. 208. Quadrageminy PVC’s
    186. 209. Ventricular Escape Beats
    187. 210. Idioventricular Rhythm
    188. 211. Ventricular Tachycardia (VT) <ul><li>Rate: 101-250 beats/min </li></ul><ul><li>Rhythm: regular </li></ul><ul><li>P waves: absent </li></ul><ul><li>PR interval: none </li></ul><ul><li>QRS duration: > 0.12 sec. often difficult to differentiate between QRS and T wave </li></ul><ul><li>Note: Monomorphic - same shape </li></ul><ul><li>and amplitude </li></ul>
    189. 212. Ventricular Tachycardia (VT)
    190. 213. V Tach
    191. 214. Torsades de Pointes (TdeP) <ul><li>Rate: 150-300 beats/min </li></ul><ul><li>Rhythm: regular or irregular </li></ul><ul><li>P waves: none </li></ul><ul><li>PR interval: none </li></ul><ul><li>QRS duration: > 0.12 sec. gradual alteration in amplitude and direction of the QRS complexes </li></ul>
    192. 215. Torsades de Pointes (TdeP)
    193. 216. Ventricular Fibrillation (VF) <ul><li>Rate: CNO as no discernible complexes </li></ul><ul><li>Rhythm: rapid and chaotic </li></ul><ul><li>P waves: none </li></ul><ul><li>PR interval: none </li></ul><ul><li>QRS duration: none </li></ul><ul><li>Note: Fine vs. coarse? </li></ul>
    194. 217. Ventricular Fibrillation (VF)
    195. 218. Ventricular Fibrillation (VF)
    196. 219. Asystole (Cardiac Standstill) <ul><li>Rate: none </li></ul><ul><li>Rhythm: none </li></ul><ul><li>P waves: none </li></ul><ul><li>PR interval: not measurable </li></ul><ul><li>QRS duration: absent </li></ul>
    197. 220. Asystole (Cardiac Standstill)
    198. 221. Asystole The Mother of all Bradycardias
    199. 222. Atrial Pacemaker (Single Chamber) pacemaker <ul><li>Capture? </li></ul>
    200. 223. Ventricular Pacemaker (Single Chamber) pacemaker
    201. 224. Dual Paced Rhythm pacemaker
    202. 225. Pulseless Electrical Activity (PEA) <ul><li>The absence of a detectable pulse and blood pressure </li></ul><ul><li>Presence of electrical activity of the heart as evidenced by ECG rhythm, but not VF or VT </li></ul>= 0/0 mmHg +
    203. 226. ventricular bigeminy <ul><li>The ECG trace below shows ventricular bigeminy, in which every other beat is a ventricular ectopic beat. These beats are premature, wider, and larger than the sinus beats. </li></ul>
    204. 227. ventricular bigeminy
    205. 228. ventricular trigeminy ; <ul><li>The occurrence of more than one type of ventricular ectopic impulse morphology is evidence of multifocal ventricular ectopics. In this example, the ventricular ectopic beats are both wide and premature, but differ considerably in shape </li></ul>
    206. 229. ventricular trigeminy
    207. 230. ventricular trigeminy
    208. 231. QUESTIONS?
    209. 232. Thank you all
    210. 233. MYOCARDIAL INFARACTION
    211. 234. Diagnosing a MI <ul><li>To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. </li></ul>Rhythm Strip 12-Lead ECG
    212. 235. ST Elevation <ul><li>One way to diagnose an acute MI is to look for elevation of the ST segment. </li></ul>
    213. 236. ST Elevation (cont) <ul><li>Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction. </li></ul>
    214. 237. Anterior Myocardial Infarction <ul><li>If you see changes in leads V 1 - V 4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction. </li></ul>
    215. 238. Putting it all Together <ul><li>Do you think this person is having a myocardial infarction. If so, where? </li></ul>
    216. 239. Interpretation <ul><li>Yes , this person is having an acute anterior wall myocardial infarction. </li></ul>
    217. 240. Putting it all Together <ul><li>Now, where do you think this person is having a myocardial infarction? </li></ul>
    218. 241. Inferior Wall MI <ul><li>This is an inferior MI. Note the ST elevation in leads II, III and aVF. </li></ul>
    219. 242. Putting it all Together <ul><li>How about now? </li></ul>
    220. 243. Anterolateral MI <ul><li>This person’s MI involves both the anterior wall (V 2 -V 4 ) and the lateral wall (V 5 -V 6 , I, and aVL)! </li></ul>
    221. 244. NORMAL RULE
    222. 245. Rule 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
    223. 246. Characteristic changes in AMI <ul><li>ST segment elevation over area of damage </li></ul><ul><li>ST depression in leads opposite infarction </li></ul><ul><li>Pathological Q waves </li></ul><ul><li>Reduced R waves </li></ul><ul><li>Inverted T waves </li></ul>
    224. 247. ST elevation hyperacute phase <ul><li>Occurs in the early stages </li></ul><ul><li>Occurs in the leads facing the infarction </li></ul><ul><li>Slight ST elevation may be normal in V 1 or V 2 </li></ul>R P Q ST
    225. 248. Deep Q wave <ul><li>Only diagnostic change of myocardial infarction </li></ul><ul><li>At least 0.04 seconds in duration </li></ul><ul><li>Depth of more than 25% of ensuing R wave </li></ul>R P Q T ST
    226. 249. T wave changes <ul><li>Late change </li></ul><ul><li>Occurs as ST elevation is returning to normal </li></ul><ul><li>Apparent in many leads </li></ul>R P Q T ST
    227. 250. Bundle branch block I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Anterior wall MI Left bundle branch block
    228. 251. Sequence of changes in evolving AMI 1 minute after onset 1 hour or so after onset A few hours after onset A day or so after onset Later changes A few months after AMI Q R P Q T ST R P Q ST P Q T ST R P S T P Q T ST R P Q T
    229. 252. Anterior infarction Anterior infarction Left coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
    230. 253. Inferior infarction Inferior infarction Right coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
    231. 254. Lateral infarction Lateral infarction Left circumflex coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
    232. 255. Diagnostic criteria for AMI <ul><li>Q wave duration of more than 0.04 seconds </li></ul><ul><li>Q wave depth of more than 25% of ensuing r wave </li></ul><ul><li>ST elevation in leads facing infarct (or depression in opposite leads) </li></ul><ul><li>Deep T wave inversion overlying and adjacent to infarct </li></ul><ul><li>Cardiac arrhythmias </li></ul>
    233. 256. Surfaces of the Left Ventricle <ul><li>Inferior - underneath </li></ul><ul><li>Anterior - front </li></ul><ul><li>Lateral - left side </li></ul><ul><li>Posterior - back </li></ul>
    234. 257. Inferior Surface <ul><li>Leads II, III and avF look UP from below to the inferior surface of the left ventricle </li></ul><ul><li>Mostly perfused by the Right Coronary Artery </li></ul>
    235. 258. Inferior Leads <ul><ul><li>II </li></ul></ul><ul><ul><li>III </li></ul></ul><ul><ul><li>aVF </li></ul></ul>
    236. 259. Anterior Surface <ul><li>The front of the heart viewing the left ventricle and the septum </li></ul><ul><li>Leads V2 , V3 and V4 look towards this surface </li></ul><ul><li>Mostly fed by the Left Anterior Descending branch of the Left artery </li></ul>
    237. 260. Anterior Leads <ul><ul><li>V2 </li></ul></ul><ul><ul><li>V3 </li></ul></ul><ul><ul><li>V4 </li></ul></ul>
    238. 261. Lateral Surface <ul><li>The left sided wall of the left ventricle </li></ul><ul><li>Leads V5 and V6, I and avL look at this surface </li></ul><ul><li>Mostly fed by the Circumflex branch of the left artery </li></ul>
    239. 262. Lateral Leads V5, V6, I, aVL
    240. 263. Posterior Surface <ul><li>Posterior wall infarcts are rare </li></ul><ul><li>Posterior diagnoses can be made by looking at the anterior leads as a mirror image. Normally there are inferior ischaemic changes </li></ul><ul><li>Blood supply predominantly from the Right Coronary Artery </li></ul>
    241. 264. Inferior II, III, AVF Antero-Septal V1,V2, V3,V4 Lateral I, AVL, V5, V6 Posterior V1, V2, V3 RIGHT LEFT
    242. 265. ST Segment Elevation <ul><li>The ST segment lies above the isoelectric line: </li></ul><ul><li>Represents myocardial injury </li></ul><ul><li>It is the hallmark of Myocardial Infarction </li></ul><ul><li>The injured myocardium is slow to repolarise and remains more positively charged than the surrounding areas </li></ul><ul><li>Other causes to be ruled out include pericarditis and ventricular aneurysm </li></ul>
    243. 266. ST-Segment Elevation
    244. 268. T wave inversion in an evolving MI
    245. 269. The ECG in ST Elevation MI
    246. 270. The Hyper-acute Phase <ul><li>Less than 12 hours </li></ul><ul><li>“ ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction” (Quinn, 1996) </li></ul><ul><li>The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal </li></ul><ul><li>Usually occurs within a few hours of infarction </li></ul><ul><li>May vary in severity from 1mm to ‘tombstone’ elevation </li></ul>
    247. 272. The Fully Evolved Phase <ul><li>24 - 48 hours from the onset of a myocardial infarction </li></ul><ul><li>ST segment elevation is less (coming back to baseline). </li></ul><ul><li>T waves are inverting. </li></ul><ul><li>Pathological Q waves are developing (>2mm) </li></ul>
    248. 273. The Chronic Stabilised Phase <ul><li>Isoelectric ST segments </li></ul><ul><li>T waves upright. </li></ul><ul><li>Pathological Q waves. </li></ul><ul><li>May take months or weeks. </li></ul>
    249. 275. Reciprocal Changes <ul><li>Changes occurring on the opposite side of the myocardium that is infarcting </li></ul>
    250. 276. Reciprocal Changes ie S-T depression in some leads in MI
    251. 277. Non ST Elevation MI <ul><li>Commonly ST depression and deep T wave inversion </li></ul><ul><li>History of chest pain typical of MI </li></ul><ul><li>Other autonomic nervous symptoms present </li></ul><ul><li>Biochemistry results required to diagnose MI </li></ul><ul><li>Q-waves may or may not form on the ECG </li></ul>
    252. 278. Changes in NSTEMI
    253. 279. Action potentials and electrophysiology + + + + _ _ _ _ 3.2 Ca in(slow) ++ K out + Na in + Resting Depolarised Repolarised Plateau + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + Ca ++ K + K + Na + _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _
    254. 280. LVH and strain pattern Ventricular Strain Strain is often associated with ventricular hypertrophy Characterized by moderate depression of the ST segment.
    255. 281. Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026 Non-ischaemic ST segment changes: in patient taking digoxin (top) and in patient with left ventricular hypertrophy (bottom)
    256. 282. Examples of T wave abnormalities Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026
    257. 283. Sick Sinus Syndrome Sinoatrial block (note the pause is twice the P-P interval) Sinus arrest with pause of 4.4 s before generation and conduction of a junctional escape beat Severe sinus bradycardia
    258. 284. Bundle Branch Block
    259. 285. Left Bundle Branch Block <ul><li>Widened QRS (> 0.12 sec, or 3 small squares) </li></ul><ul><li>Two R waves appear – R and R’ in V5 and V6, and sometimes Lead I, AVL. </li></ul><ul><li>Have predominately negative QRS in V1, V2, V3 (reciprocal changes). </li></ul>
    260. 286. Right Bundle Branch Block
    261. 287. Where’s the MI?
    262. 288. Where’s the MI?
    263. 289. Where’s the MI?
    264. 290. Final one…
    265. 292. Which one is more tachycardic during this exercise test?
    266. 293. Any Questions?
    267. 294. Thanks for paying attention. I hope you have found this session useful.

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