1.ECG BASICS By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associate Professor Medicine Email drbashir123@gmail.com

2. From Right to Left Dr.Smitha associate prof gynae Dr Bashir associate professor Medicine Dr Udaman neurologist Dr Patnaik HOD ortho Dr Tin swe aye paeds 3. From RT to Lt Professor Dr Datuk rajagopal N Dr Bashir associate professor medicine Dr Urala HOD gynae Dr Nagi reddy tamma HODopthomology Dr Setharamarao Prof ortho 4. ELECTROGRAPHY MADE EASY ULTIMATEAIM TO HELP PATIENTS 5. ECG machine 6. Limb and chest leads Whenan ECG is taken we put 4 limb leads or electrodes with different colour codes on upper and lower limbs one each at wrists and ankles by applying some jelly for close contact. We also put six chest leads at specific areas over the chest So in reality we see only 10 chest leads. 7. Position of limb and chest leads Four limb leadsSix chest leads V1- 4th intercostal space to the right of sternum V2- 4th intercostal space to the left of sternum V3- halfway between V2 and V4 V4- 5th intercostal space in the left mid-clavicular line V5- 5th intercostal space in the left anterior axillary line V6- 5th intercostal space in the left mid axillary line 8. Horizontal plane - the six chest leads LA RA V1V2LV RVV6V3 V4 V5 V6 V5 V4 V1V2V36.5 9. Colour codes given by AHA 10. ECG Paper: Dimensions 5 mm 1 mm0.1 mV0.04 sec 0.2 secSpeed = rateVoltage ~Mass 11. ECG paper and timing ECG paper speed Voltage calibration 1 mV= 25mm/sec = 1cmECG paper - standard calibrations each small square = 1mm each large square = 5mmTimings 1 small square 1 large square 25 small squares 5 large squares= = = =0.04sec 0.2sec 1sec 1sec 12. Afterapplying these leads on different positions then these leads are connected to a connector and then to ECG machine. The speed of machine kept usually 25mm/second.calibration or standardization done while machine is switched on. 13. ECG paper 1 Small square = 0.04 second2 Large squares = 1 cm1 Large square = 0.2 second5 Large squares = 1 secondTime6.1 14. Thefirst step while reading ECG is to look for standardization is properly done. Look for this mark and see that this mark exactly covers two big squares on graph. 15. STANDARDISATION ECG amplitude scaleNormal amplitudeHalf amplitudeDouble amplitude10 mm/mV5 mm/mV20 mm/mV 16. ECG WAVES Youwill see then base line or isoelectric line that is in line with P-Q interval and beginning of S-T segment. From this line first positive deflection will arise as P wave then other waves as shown in next slide. Small negative deflections Q wave and S wave also arise from this line. 17. ECG WAVES 18. The Normal ECGNormal Intervals: PR 0.12-0.20s QRS duration than 2 and half small squares with notched p wave or Negative component of biphasic P wave in V1 1 small box in area 32. Right Atrial Enlargement Criteria P wave height in II >2 and half small squares and are also tall and peaked. or Positive component of biphasic P wave in V1 > 1 small box in area 33. Slide 15 34. Atrial fibrillation Pwaves thrown into number of small abnormal P waves before each QRS complex The duration of R-R interval varies The amplitude of R-R varies Abnormal P waves dont resemble one another. 35. Slide 41 36. Atrial flutter TheP waves thrown into number of abnormal P waves before each QRS complex. But these abnormal P waves almost resemble one another and are more prominent like saw tooth appearance. 37. Slide 40 38. Junctional rhythm InJunctional rhythm the P waves may be absent or inverted.in next slide u can see these inverted P waves. 39. Slide 43 40. Paroxysmal atrial tachycardia TheP and T waves you cant make out separately The P and T waves are merged in one The R-R intervals do not vary but remain constant and same. The heart rate being very high around 150 and higher. 41. Slide 39 42. NORMAL P-R INTERVAL PRinterval seconds. Thattime 0.12 seconds to 0.2is three small squares to five small squares. 43. PR interval Definition: the time interval between beginning of P-wave to beginning of QRS complex. Normal PR interval 3-5mm or 3-5 small squares on ECG graph (0.12-0.2 sec)Abnormalities 1. Short PR interval WPW syndrome 2. Long PR interval First degree heart block 44. Short P-R interval ShortP-R interval seen in WPW syndrome or preexcitation syndrome or LG syndrome P-R interval is less than three small squares. The beginning of R wave slopes gradually up and is slightly widened called Delta wave. There may be S-T changes also like ST depression and T wave inversion. 45. Slide 17 46. Lengthening of P-R interval Occursin first degree heart block. The P-R interval is more than 5 small squares or > than 0.2 seconds. This you will see in all leads and is same fixed lengthening . 47. Slide 44 48. Q WAVES Qwaves 25% of R wave] MI. Hypertrophic cardiomyopathy. Normal variant. 55. Small voltage QRS Definedas < 5 mm peak-to-peak in all limb leads or 35 mm or SV1 >20 mm or RV6 >20 mm 60. Left ventricular hypertrophy-Voltage Criteria Countsmall squares of downward R wave in V1 plus small squares of R wave in V5 . If it comes to more than 35 small squares then it is suggestive of LVH. 61. LEFT VENTRICULAR HYPERTROPHY 62. Right ventricular hypertrophy Normallyyou see R wave is downward deflection in V1.but if you see upward R wave in V1 then it is suggestive of RVH etc. 63. Dominant or upward R wave in V1 Causes RBBB Chroniclung disease, PE Posterior MI WPW Type A Dextrocardia Duchenne muscular dystrophy 64. Right Ventricular Hypertrophy WILLSHOW AS Right axis deviation (RAD) Precordial leads In V1, R wave > S wave In V6, S wave > R wave Usual manifestation is pulmonary disease or congenital heart disease 65. Right Ventricular Hypertrophy 66. Right ventricular hypertrophy Rightventricular hypertrophy (RVH) increases the height of the R wave in V1. And R wave in V1 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. 67. Right Ventricular Hypertrophy Otherfindings in RVH include right axis deviation, taller R waves in the right precordial leads (V1-V3), and deeper S waves in the left precordial (V4-V6). The T wave is inverted in V1 (and often in V2). 68. Right Ventricular Hypertrophy Trueposterior 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). 69. Right Ventricular Hypertrophy Alarge 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 counterclockwise rotation of the heart. This can be seen with abnormal chest shape. 70. Right Ventricular HypertrophyAlthough there is no widely accepted criteria for detecting the presence of RVH, any combination of the following EKG features is suggestive of its presence: TallR wave in V1 Rightaxis deviation Right atrial enlargement Down sloping ST depressions in V1-V3 ( RV strain pattern) 71. Right Ventricular Hypertrophy 72. Left Ventricular Hypertrophy 73. Left Ventricular Hypertrophy 74. ECG criteria for RBBB (1)QRS duration exceeds 0.12 seconds or 2 and half small squares roughly in V1 and may also see it in V2. (2) RSR complex in V1 may extend to V2. 75. ECG criteria for RBBB ST/Tmust be opposite in direction to the terminal QRS(is secondary to the block and does not mean primary ST/T changes). Ityou meet all above criteria it is then complete right bundle branch block. In incomplete bundle branch block the duration of QRS will be within normal limits. 76. RBBB & MI Ifabnormal Q waves are present they will not be masked by the RBBB pattern. 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. 77. Significance of RBBB RBBBis seen in : (1) occasional normal subjects (2) pulmonary embolus (3) coronary artery disease (4) ASD (5) active Carditis (6) RV diastolic overload 78. Partial / Incomplete RBBB isdiagnosed when the pattern of RBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and a half small squares. 79. In next slide you will see ECGcharacteristics of a typical RBBB showing wide QRS complexes with a terminal R wave in lead V1 and slurred S wave in lead V6. Also you see R wave has become upright in V1.QRS duration has also increased making it complete RBBB. 80. 81. ECG criteria for LBBB (1)ProlongedQRS complexes, greater than 0.12 seconds or roughly 2 and half small squares in all leads almost. (2)Wide, notched QRS (M shaped) V5, V6 (3)Wide, notched QS complexes are seen in V1 (due to spread of activation away from the electrode through septum + LV) (4)In V2, V3 small r wave may be seen due to activation of para septal region 82. ECG criteria for LBBB Solook in all leads for QRS duration to make it complete LBBB or incomplete LBBB as u did in RBBB. Look in V5 and V6 for M shaped pattern at summit or apex of R wave. Look for any changes as S-T depression and T wave in inversion if any. 83. Significance of LBBB LBBBis seen in : (1) Always indicative of organic heart disease (2) Found in ischemic heart disease (3) Found in hypertension. MI should not be diagnosed in the presence of LBBB Q waves are masked by LBBB pattern Cannot diagnose the presence of MI with LBBB 84. Partial / Incomplete LBBB isdiagnosed when the pattern of LBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and half small squares. 85. NORMAL ST- SEGMENT it's isoelectric. [i.e. at same level of PR or PQ segment at least in the beginning] 86. NORMAL CONCAVITY OF S-T SEGMENT Itthen 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. In MI this concavity may get lost and become convex upwards called coving of S-T segment. 87. Abnormalities ST elevation: More than one small square 1. Acute MI. Prinzmetal angina. Acute pericarditis. Early repolarizationST depression: More than one small square Ischemia. Ventricular strain. BBB. Hypokalemia. Digoxin effect. 88. Slide 11 89. Slide 12 90. Stress test ECG note the ST Depression 91. Note the arrows pointing ST depression 92. ST depression & Troponin T positive is NON STEMI 93. Coving of S-T segment Concavityupwards.lost and convexity appear facing 94. Diagnostic criteria for AMI Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias 95. Abnormalities of ST- segment 96. Q waves in myocardial infarction 97. T-wave Normal values. 1.amplitude: < 10mm in the chest leads.. 2. T- inversion:Abnormalities:1. Peaked T-wave: Hyper-acute MI. Hyperkalemia. Normal variant Ischemia. Myocardial infarction. Myocarditis Ventricular strain BBB. Hypokalemia. Digoxin effect. 98. QT- interval Definition: Time interval between beginning of QRS complex to the end of T wave. Normally: At normal HR: QT 11mm (0.44 sec)Abnormalities: 1. 2.Prolonged QT interval: hypocalcemia and congenital long QT syndrome. Short QT interval: hypercalcemia. 99. QT Interval - Should be < 1/2 preceding R to R interval - 100. QT Interval - Should be < 1/2 preceding R to R interval -QT interval 101. QT Interval - Should be < 1/2 preceding R to R interval -QT interval 102. QT Interval - Should be < 1/2 preceding R to R interval RQT intervalR 103. QT Interval - Should be < 1/2 preceding R to R interval RQT intervalR 104. QT Interval - Should be < 1/2 preceding R to R interval RQT intervalR 105. QT Interval - Should be < 1/2 preceding R to R interval 65 - 90 bpmRQT intervalR 106. QT Interval - Should be < 1/2 preceding R to R interval 65 - 90 bpmRQT intervalNormal QTc = 0.46 secR 107. Atrioventricular (AV) Heart Block 108. Classification of AV Heart Blocks DegreeAV Conduction Pattern1St Degree BlockUniformly prolonged PR interval2nd Degree, Mobitz Type IProgressive PR interval prolongation2nd Degree, Mobitz Type IISudden conduction failure3rd Degree BlockNo AV conduction 109. AV Blocks FirstDegree Prolonged AV conduction time PR interval > 0.20 seconds 110. 1st Degree AV BlockProlongation of the PR interval, which is constant All P waves are conducted 111. 1st degree AV Block: Regular Rhythm PRI > .20 seconds or 5 small squares and is CONSTANT Usually does not require treatmentPRI > .20 seconds 112. First Degree Blockprolonged PR interval 113. Analyze the Rhythm 114. AV Blocks SecondDegree Definition More Ps than QRSs Every QRS caused by a P 115. Second-Degree AV Block Thereis intermittent failure of the supraventricular impulse to be conducted to the ventricles Someof 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 116. Second Degree Types Type I Wenckebach phenomenon Type II Fixed or Classical 117. Type I Second-Degree AV Block: Wenckebach Phenomenon ECGfindings 1.Progressive lengthening of the PR interval until a P wave is blocked 118. 2nd degree AV Block (Mobitz I also called Wenckebach): Irregular Rhythm PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse) PRI is NOT CONSTANTPRI = .24 secPRI = .36 secPRI = .40 secQRS is droppedPause 4:3 Wenckebach (conduction ratio may not be constant)Pattern Repeats. 119. Type II Second-Degree AV Block: Mobitz Type II ECG findings1.Intermittent or unexpected blocked P waves you dont know when QRS drops 2.P-R intervals may be normal or prolonged,but they remain constant 4. A long rhythm strip may help 120. Second Degree AV BlockMobitz type I or Winckebach Mobitz type II 121. Type 1 (Wenckebach) Progressive prolongation of the PR interval until a P wave is not conducted.Type 2Constant PR interval with unexpected intermittent failure to conduct 122. Mobitz Type I 123. MOBITZ TYPE 1 124. 2nd degree AV Block (Mobitz II): Irregular Rhythm QRS complexes may be somewhat wide (greater than .12 seconds) Non-conducted sinus impulses appear at unexpected irregular intervals PRI may be normal or prolonged but is CONSTANT and fixed Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart block (3rd degree block) Its appearance in the setting of an acute MI identifies a high risk patient Cause: anterioseptal MI, Treatment: may require pacemaker in the case of fibrotic conduction systemPRI is CONSTANTNon-conducted sinus impulses2:1 block3:1 block 125. Analyze the Rhythm 126. Second Degree Mobitz Characteristics Atrial rate > Ventricular rate QRS usually longer than 0.12 sec Usually 4:3 or 3:2 conduction ratio (P:QRS ratio) 127. Analyze the Rhythm 128. Mobitz II 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 . 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. 129. Mobitz Type II 130. Mobitz Type IISudden appearance of a single, nonconducted sinus P wave... 131. Advanced Second-Degree AV BlockTwo or more consecutive nonconducted sinus P waves 132. Complete AV Block Characteristics Atrioventricular dissociation Regular P-P and R-R but without association between the two Atrial rate > Ventricular rate QRS > 0.12 sec 133. 3rd Degree (Complete) AV BlockEKG Characteristics:No relationship between P waves and QRS complexes Relatively constant PP intervals and RR intervals Greater number of P waves than QRS complexes 134. Complete heart block Pwaves 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. 135. 3rd degree AV Block (Complete Heart Block) : Irregular Rhythm QRS complexes may be narrow or broad depending on the level of the block Atria and ventricles beat independent of one another (AV dissociation) QRSs have their own rhythm, P-waves have their own rhythm May be caused by inferior MI and its presence worsens the prognosis Treatment: usually requires pacemakerQRS intervalsP-wave intervals note how the P-waves sometimes distort QRS complexes or T-waves 136. Third-Degree (Complete) AV Block 137. Third-Degree (Complete) AV BlockThe P wave bears no relation to theQRS complexes, and the PR intervals are completely variable 138. 30 AV Block AV dissociation atria and ventricles beating on their own no relation between Ps & QRSs Atrial rate is different from ventricular ventricular rate: 30-60 bpm Rhythm is regular for both QRS can be narrow or wide depends on site of pacemaker! 139. Key points Wenckebach look for group beating & changing PR Mobitz II look for reg. atrial rhythm & consistent PR 3o block atrial & ventricular rhythm regular rate is different!!! no consistent PR 140. Left Anterior Fascicular Block Left axis deviation , usually -45 to -90 degreesQRS duration usually lead III S wave in lead III > lead II QR pattern in lead I and AVL,with small Q wave No other causes of left axis deviation 141. LBB LPIFLead ILeft Anterior Hemiblock (LAHB): 1.Left axis deviation (> -30 degrees) will be noted and there will be a prominent S-wave in Leads II, and III1.LASF2.Lead IIILead AVF 142. Left Posterior Fascicular Block Rightaxis deviation QR pattern in inferior leads (II,III,AVF) small q wave RS patter in lead lead I and AVL(small R with deep S) 143. Lead ILBB LPIFLeft Posterior Hemiblock (LPHB): 1.1.Right axis deviation and there will be a prominent S-wave in Leads I. Q-waves may be noted in III and AVF.Notes on (LPHB): QRS is normal width unless BBB is presentIf LPHB occurs in the setting of an acute MI, it is almost always accompanied by RBBB and carries a mortality rate of 71%LASF 2. Lead IIILead AVF 144. Bifascicular Bundle Branch Block RBBB with either left anterior or left posterior fascicular block Diagnostic criteria 1.Prolongation of the QRS duration to 0.12 second or longer 2.RSR pattern in lead V1,with the R being broad and slurred 3.Wide,slurred S wave in leads I,V5 and V6 4.Left axis or right axis deviation 145. Trifascicular Block Thecombination of RBBB, LAFB and long PR interval Impliesthat conduction is delayed in the third fascicle 146. Indications For Implantation of Permanent Pacing in Acquired AV Blocks 1.Third-degree AV block, Bradycardia with symptoms Asystole e.Neuromuscular diseases with AV block (Myotonic muscular dystrophy) 2.Second-degree AV block with symptomatic bradycardia 147. Cardiac Pacemakers Definition Delivers artificial stimulus to heart Causes depolarization and contraction Uses Bradyarrhythmias Asystole Tachyarrhythmias (overdrive pacing) 148. Cardiac Pacemakers Types Fixed Fires at constant rate Can discharge on T-wave Very rare Demand Senses patients rhythm Fires only if no activity sensed after preset interval (escape interval) Transcutaneous vs Transvenous vs Implanted 149. Cardiac Pacemakers 150. Cardiac Pacemakers DemandPacemaker Types Ventricular Fires ventricles Atrial Fires atria Atria fire ventricles Requires intact AV conduction 151. Cardiac Pacemakers DemandPacemaker Types Atrial Synchronous Senses atria Fires ventricles AV Sequential Two electrodes Fires atria/ventricles in sequence 152. Cardiac Pacemakers Problems Failure to capture No response to pacemaker artifact Bradycardia may result Cause: high threshold Management Increase amps on temporary pacemaker Treat as symptomatic bradycardia 153. Cardiac Pacemakers Problems Failure to sense Spike follows QRS within escape interval May cause R-on-T phenomenon Management Increase sensitivity Attempt to override permanent pacer with temporary Be prepared to manage VF 154. Implanted Defibrillators AICD AutomatedImplanted CardioDefibrillatorUses Tachyarrhythmias Malignantarrhythmias VT VF 155. Implanted Defibrillators Programmedat insertion to deliver predetermined therapies with a set order and number of therapies including: pacing overdrive pacing cardioversion with increasing energies defibrillation with increasing energies standby mode Effect of standby mode on Paramedic treatments 156. Implanted Defibrillators PotentialComplications Fails to deliver therapies as intended worst complication requires Paramedic intervention Delivers therapies when NOT appropriate broken or malfunctioning lead parameters for delivery are not specific enough Continues to deliver shocks parameters for delivery are not specific enough and device senses a reset may be shut off (not standby mode) with donut-magnet 157. Sinus Exit Block Dueto abnormal function of SA node MI, drugs, hypoxia, vagal tone Impulse blocked from leaving SA node usually transient Produces 1 missed cycle can confuse with sinus pause or arrest 158. Sinus block 159. ARRTHYMIAS AND ECTOPIC BEATS 160. Recognizing and Naming Beats & Rhythms Atrial Escape BeatQRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normalnormal ("sinus") beatssinus 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 "atrial" beat 161. Recognizing and Naming Beats & RhythmsJunctional Escape BeatQRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normalthere 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 "junctional" or a nodal beat 162. Recognizing and Naming Beats & RhythmsVentricular Escape BeatQRS is wide and much different ("bizarre") 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 beatthere is no p wave, indicating that the beat did not originate anywhere in the atria actually a "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 163. The Re-Entry Mechanism of Ectopic Beats & Rhythms Electrical Impulse Cardiac Conduction Tissue Fast Conduction Path Slow RecoverySlow Conduction Path Fast RecoveryTissues with these type of circuits may exist: in microscopic size in the SA node, AV node, or any type of heart tissue in a macroscopic structure such as an accessory pathway in WPW 164. The Re-Entry Mechanism of Ectopic Beats & Rhythms Premature Beat Impulse Cardiac Repolarizing Tissue Conduction (long refractory period) Tissue Fast Conduction Path Slow RecoverySlow Conduction Path Fast Recovery1. An arrhythmia is triggered by a premature beat 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 165. The Re-Entry Mechanism of Ectopic Beats & Rhythms Cardiac Conduction Tissue Fast Conduction Path Slow RecoverySlow Conduction Path Fast Recovery3. 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 166. The Re-Entry Mechanism of Ectopic Beats & Rhythms Cardiac Conduction Tissue Fast Conduction Path Slow RecoverySlow Conduction Path Fast Recovery4. 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 167. Recognizing and Naming Beats & Rhythms Premature Ventricular Contractions (PVCs, VPBs, extrasystoles) : A ventricular ectopic focus discharges causing an early beat Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre" QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant) In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion PVCs are sometimes described by lay people as skipped heart beatsR on T phenom em onM u lt if o c a l P V C 'sC o m p e n s a to ry p a u s e a fte r th e o c c u r a n c e o f a P V C 168. Recognizing and Naming Beats & Rhythms Characteristics of PVC's PVCs dont have P-waves unless they are retrograde (may be buried in T-Wave) T-waves for PVCs are usually large and opposite in polarity to terminal QRS Wide (> .16 sec) notched PVCs may indicate a dilated hypokinetic left ventricle Every other beat being a PVC (bigeminy) may indicate coronary artery disease Some PVCs come between 2 normal sinus beats and are called interpolated PVCsThe classic PVC note the compensatory pauseInterpolated PVC note the sinus rhythm is undisturbed 169. Recognizing and Naming Beats & Rhythms PVC's are Dangerous When: They are frequent (> 30% of complexes) or are increasing in frequency The come close to or on top of a preceding T-wave (R on T) Three or more PVC's in a row (run of V-tach) Any PVC in the setting of an acute MI PVC's come from different foci ("multifocal" or "multiformed") These dangerous phenomenon may preclude the occurrence of deadly arrhythmias: Ventricular Tachycardia Ventricular FibrillationThe sooner defibrillation takes place, the increased likelihood of survivalR on T phenomenon timesinus beatsV-tachUnconverted V-tach r V-fib 170. Recognizing and Naming Beats & Rhythms Notes on V-tach: Causes of V-tach Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause) Typical V-tach patient MI with complications & extensive necrosis, EF .20R-R RhythmRegular2:Mobitz P > R IProgressive Irregular2:Mobitz P > R IIConstantRegular3:Grossly IrregularRegularP>R(20-40 bpm) 191. Most Important Questions of Arrhythmias What is the mechanism? Problems in impulse formation?(automaticity or ectopic foci) Problems in impulse conductivity? (block or re-entry) Whereis the origin? Atria, Junction, Ventricles? 192. QRS Axis Check Leads: 1 and AVF 193. Interpreting Axis Deviation: NormalElectrical Axis: (Lead I + / aVF +) LeftAxis Deviation: Lead I + / aVF Pregnancy, LV hypertrophy etc RightAxis Deviation: Lead I - / aVF + Emphysema, RV hypertrophy etc. 194. NW Axis (No Mans Land) BothI and aVF are Check to see if leads are transposed (- vs +) Indicates: Emphysema Hyperkalemia VTach 195. Determining Regions of CAD: ST-changes in leads RCA:Inferior myocardium II, III, aVF LCA:Lateral myocardium I, aVL, V5, V6 LAD:Anterior/Septal myocardium V1-V4 196. Regions of the Myocardium: Lateral I, AVL, V5-V6 Inferior II, III, aVFAnterior / Septal V1-V4 197. Sinus Arrhythmia 198. Sinus Arrest/Pause 199. Sinoatrial Exit Block 200. Premature Atrial Complexes (PACs) 201. Wandering Atrial Pacemaker (WAP) 202. Supraventricular Tachycardia (SVT) 203. Wolff-Parkinson-White Syndrome (WPW) 204. Atrial Flutter 205. Atrial Fibrillation (A-fib) 206. Premature Junctional Complexes (PJC) 207. Junctional Rhythm 208. Junctional Rhythm 209. Accelerated Junctional Rhythm 210. Junctional Tachycardia 211. Premature Ventricular Complexes (PVC's)Note Complexes not Contractions 212. PVCs Uniformed/Multiformed Couplets/Salvos/Runs Bigeminy/Trigeminy/Quadrageminy 213. Uniformed PVCs 214. R on T Phenomena 215. Multiformed PVCs 216. PVC Couplets 217. PVC Salvos and Runs 218. Bigeminy PVCs 219. Trigeminy PVCs 220. Quadrageminy PVCs 221. Ventricular Escape Beats 222. Idioventricular Rhythm 223. Ventricular Tachycardia (VT) Rate:101-250 beats/min Rhythm: Pregularwaves: absent PRinterval: none QRSduration: > 0.12 sec. often difficult to differentiate between QRS and T wave Note: Monomorphic - same shape and amplitude 224. Ventricular Tachycardia (VT) 225. V Tach 226. Torsades de Pointes (TdeP) Rate:150-300 beats/min Rhythm: Pregular or irregularwaves: none PRinterval: none QRSduration: > 0.12 sec. gradual alteration in amplitude and direction of the QRS complexes 227. Torsades de Pointes (TdeP) 228. Ventricular Fibrillation (VF) Rate:CNO as no discernible complexes Rhythm: Prapid and chaoticwaves: none PRinterval: none QRSduration: none Note: Fine vs. coarse? 229. Ventricular Fibrillation (VF) 230. Ventricular Fibrillation (VF) 231. Asystole (Cardiac Standstill) Rate:none Rhythm: Pnonewaves: none PRinterval: not measurable QRSduration: absent 232. Asystole (Cardiac Standstill) 233. Asystole The Mother of all Bradycardias 234. Atrial Pacemaker (Single Chamber)pacemakerCapture? 235. Ventricular Pacemaker (Single Chamber)pacemaker 236. Dual Paced Rhythmpacemaker 237. Pulseless Electrical Activity (PEA) Theabsence of a detectable pulse and bloodpressure Presenceof electrical activity of the heart asevidenced by ECG rhythm, but not VF or VT += 0/0 mmHg 238. ventricular bigeminy TheECG 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. 239. ventricular bigeminy 240. ventricular trigeminy; Theoccurrence 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 241. ventricular trigeminy 242. ventricular trigeminy 243. MYOCARDIAL INFARACTION 244. Diagnosing a MI To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. 12-Lead ECGRhythm Strip 245. ST Elevation One way to diagnose an acute MI is to look for elevation of the ST segment. 246. ST Elevation (cont) Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction. 247. Anterior Myocardial Infarction If you see changes in leads V1 - V4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction. 248. Putting it all Together Do you think this person is having a myocardial infarction. If so, where? 249. Interpretation Yes, this person is having an acute anterior wall myocardial infarction. 250. Putting it all Together Now, where do you think this person is having a myocardial infarction? 251. Inferior Wall MI This is an inferior MI. Note the ST elevation in leads II, III and aVF. 252. Putting it all Together How about now? 253. Anterolateral MI This persons MI involves both the anterior wall (V2V4) and the lateral wall (V5-V6, I, and aVL)! 254. I II IIIaVR aVL aVFV1 V2 V3V4 V5 V6The ST segment should start isoelectric except in V1 and V2 where it may be elevated 255. Characteristic changes in AMI ST segment elevation over area of damage ST depression in leads opposite infarction Pathological Q waves Reduced R waves Inverted T waves 256. ST elevation hyperacute phase Occurs in the early stagesR ST PQ Occurs in the leads facing the infarction Slight ST elevation may be normal in V1 or V2 257. Deep Q wave Only diagnostic change of myocardial infarctionR ST At least 0.04 seconds in durationP T Q Depth of more than 25% of ensuing R wave 258. T wave changes Late change R Occurs as ST elevation is returning to normalSTP Apparent in many leads T Q 259. Bundle branch block Anterior wall MI I II IIIaVR aVL aVFV1 V2 V3Left bundle branch block V4 V5 V6I II IIIaVR aVL aVFV1 V2 V3V4 V5 V6 260. Sequence of changes in evolving AMI RR TRSTSTPPPQSTQ1 minute after onsetQ1 hour or so after onsetA few hours after onsetR STPP TQA day or so after onsetSTTP TQLater changesQA few months after AMI 261. Anterior infarction Anterior infarctionI II IIILeft coronary arteryaVR aVL aVFV1 V2 V3V4 V5 V6 262. Inferior infarction Inferior infarctionI II IIIRight coronary arteryaVR aVL aVFV1 V2 V3V4 V5 V6 263. Lateral infarction Lateral infarctionI II IIILeft circumflex coronary arteryaVR aVL aVFV1 V2 V3V4 V5 V6 264. Diagnostic criteria for AMI Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias 265. Surfaces of the Left Ventricle Inferior - underneathAnterior - frontLateral - left sidePosterior - back 266. Inferior Surface Leads II, III and avF look UP from below to the inferior surface of the left ventricle Mostly perfused by the Right Coronary Artery 267. Inferior Leads II III aVF 268. Anterior Surface The front of the heart viewing the left ventricle and the septum Leads V2, V3 and V4 look towards this surface Mostly fed by the Left Anterior Descending branch of the Left artery 269. Anterior Leads V2 V3 V4 270. Lateral Surface The left sided wall of the left ventricle Leads V5 and V6, I and avL look at this surface Mostly fed by the Circumflex branch of the left artery 271. Lateral Leads V5, V6,I, aVL 272. Posterior Surface Posterior wall infarcts are rare Posterior diagnoses can be made by looking at the anterior leads as a mirror image. Normally there are inferior ischaemic changes Blood supply predominantly from the Right Coronary Artery 273. RIGHTInferior II, III, AVFPosterior V1, V2, V3LEFTAntero-Septal V1,V2, V3,V4Lateral I, AVL, V5, V6 274. ST Segment Elevation The ST segment lies above the isoelectric line: Representsmyocardial injury It is the hallmark of Myocardial Infarction The injured myocardium is slow to repolarise and remains more positively charged than the surrounding areas Other causes to be ruled out include pericarditis and ventricular aneurysm 275. ST-Segment Elevation 276. T wave inversion in an evolving MI 277. The ECG in ST Elevation MI 278. The Hyper-acute Phase Less than 12 hours ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction (Quinn, 1996) The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal Usually occurs within a few hours of infarction May vary in severity from 1mm to tombstone elevation 279. The Fully Evolved Phase 24 - 48 hours from the onset of a myocardial infarction ST segment elevation is less (coming back to baseline). T waves are inverting. Pathological Q waves are developing (>2mm) 280. The Chronic Stabilised Phase IsoelectricST segments T waves upright. Pathological Q waves. May take months or weeks. 281. Reciprocal Changes Changesoccurring on the opposite side of the myocardium that is infarcting 282. Reciprocal Changes ie S-T depression in some leads in MI 283. Non ST Elevation MI CommonlyST depression and deep T waveinversion History of chest pain typical of MI Other autonomic nervous symptoms present Biochemistry results required to diagnose MI Q-waves may or may not form on the ECG 284. Changes in NSTEMI 285. + + + + _ _ _ _ _ _ _ _ _ + + + ++ + ++ + _ + __ + +Action potentials and electrophysiology +Na_ _ _ _ __ _ + + + + + _ + + _ _ + + + + + _ _ _ _ _ _ +_ _ _ + + + + + _ + + _ + + + + + _ _ _ _ _ _+K_ _ _ _ _+ + _ _ + _ + ++ + + + _ _ _ _ _ _ _ _ _ + + + ++ + +KRestingDepolarisedCa +Na++ in(slow)inK++Ca+ outPlateauRepolarised3.2 286. LVH and strain pattern Ventricular Strain Strain is often associated with ventricular hypertrophy Characterized by moderate depression of the ST segment. 287. Non-ischaemic ST segment changes: in patient taking digoxin (top) and in patient with left ventricular hypertrophy (bottom)Channer, K. et al. BMJ 2002;324:1023-1026 Copyright 2002 BMJ Publishing Group Ltd. 288. Examples of T wave abnormalitiesCopyright 2002 BMJ Publishing Group Ltd.Channer, K. et al. BMJ 2002;324:1023-1026 289. 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 beatSevere sinus bradycardia 290. Bundle Branch Block 291. Left Bundle Branch Block WidenedQRS (> 0.12 sec, or 3 smallsquares) Two R waves appear R and R in V5 and V6, and sometimes Lead I, AVL. Have predominately negative QRS in V1, V2, V3 (reciprocal changes). 292. Right Bundle Branch Block 293. Wheres the MI? 294. Wheres the MI? 295. Wheres the MI? 296. Final one 297. Which one is more tachycardic during this exercise test? 298. Any Questions? 299. I hope you have found this session useful.