1.Essentials of ECGInterpretation :Pacemaker ECG, SVT &VT

2. ElectrocardiographyElectrocardiography (ECG) is a transthoracic interpretation of the electrical activity of the heart over a period of time, as detected byelectrodes attached to the outer surface of the skin and recorded by a device external to the body.[1]"ECG- simplified. Aswini Kumar M.D". LifeHugger. Retrieved 2010-02-11. 3. Role of ECGIt helps in the detection ofHeart Attack & Coronary Artery Disease (Ischaemia)Abnormal heartbeats (conduction system disorders)BradycardiaTachycardiaEnlargement of cardiac chambersProblems with the blood chemistryImage source : http://potomachospital.blogspot.tw 4. Conduction System Primary Pacemaker Rate / Min SA Node 60-100Escape Pacemaker AV Node AV Junction HIS Bundle40 - 60 Bundle Branches Ventricles Purkinje Fibres20 - 40Image source : http://www.ekgguru.com/content/conduction-system-illustration 5. Normal Sinus Rhythm 1:1 AV synchrony (one atrial event for each ventricular event) Stable rhythm with repeating patterns (60 100 bpm) Morphologies of beats should be similar from complex to complex Rate should be appropriatenot too fast, not too slow12 lead tracing source : http://meds.queensu.ca/courses/assets/modules/ts-ecg/Normal_ECG.bmp Video source : Youtube.com 6. ECG Complex 7. ECG Interpretation Step 1: What is the rate? Step 2: Is the rhythm regular orirregular? Step 3: Is the P wave normal? Step 4: P-R Interval/relationship? Step 5: Normal QRS complex? Image source : www.broward.edu/cehealth 8. Step 1 : RateMethod 1 : Count the number of R waves for a six second intervaland multiply by ten.6 sec 3 sec3 sec Tachycardia exists if the rate is greater than 100 bpm. Bradycardia exists if the rate is less than 60 bpm. 3 1 1Method 2 : 0 5 0 7 6 5 0 0 0 5 0 0 9. Step 2 - Rhythm Determine if the ventricular rhythm is regular orirregular R-R intervals should measure the same P-P intervals should also measure the same REGULAR IRREGULAR 10. STEP 3 : P Wave Morphology Identify and examine P waves: Present? Appearance? Consistency? Relation to QRS? 11. Standard MorphologiesLea P- QRST-d WaveWaveLimb Leads Vertical PlaneI II III Augmented LeadsaVR aVF aVL Lea P-WaveQRST-Wave dPrecordial Leads Horizontal PlaneV1 / Small R wave / QS V2 / Small R wave / QS V3Equiphasic QRS / V4 V5 12. Step 4 : PR IntervalConsistent PRI of 0.12), may indicate theimpulse was generated somewhere in the ventricles 14. Abnormal Cardiac Rhythm Abnormally shaped waves Lack of 1:1 AV synchrony Rapid cardiac activity, even if otherwise stable Very slow cardiac activity, even if otherwise stable Irregular cardiac activity Variability in PR interval Pauses Premature beats (oddly timed events) 15. Conduction Blocks 16. Function of a Pacemaker Sense intrinsic activity Pace the appropriate chamber 17. Systematic Approach Identify pacing mode Is there capture? Is there sensing? What is the pacing interval? Are there rate variations and can we account for them? Is hysteresis present? Is fusion or pseudofusion happening? 18. ECG # 1 VVI. Capture is present. Sensing cannot be determined (this strip is allpacing). The pacing interval corresponds to a rate of 72 ppm 19. Potential Problems Identifiableon an ECG Undersensing Oversensing Noncapture No output Pseudomalfunction 20. Undersensing An intrinsic depolarization that is present, yet notseen or sensed by the pacemaker P-wavenot sensed Atrial Undersensing Common Causes of Undersensing Inappropriately programmedconductor fracture sensitivity Lead maturation Lead dislodgment Change in the native signal Lead failure: Insulation break; 21. OversensingMarkersensing of anThe channel shows inappropriate signal ...Though nointrinsic activity...activity is present Ventricular OversensingCan be physiologic or nonphysiologic Common Causes of Oversensing Lead failure sensitivity Poor connection at connector Change in the native signalblock Exposure to interference Inappropriately programmed 22. Non Capture No evidence of depolarization after pacing artifact Loss of captureCommon Causes of Noncapture Lead dislodgment Poor connection atconnector block Low output Lead failure Lead maturation 23. Functional Non-Capture Functional non-capture occurs when a pacing spikeis delivered at a time when it could not possiblydepolarize the heart (because the cardiac tissue isrefractory) However, had the pacing spike been moreappropriately timed, it might have captured the heart Functional non-capture is most often observed inasynchronous (non-sensing) modes, such as VOO orAOO 24. No OutputPacemaker artifacts do not appear on the ECG; rate isless than the lower ratePacing output delivered;no evidence of pacingspike is seen Common Causes of No Output Poor connection at connector block Battery depletion Lead failure Circuit failure 25. Pseudomalfunction: Hysteresis Allows a lower rate between sensed events to occur;paced rate is higher Lower Rate 70 ppm Hysteresis Rate 50 ppm 26. Fusion Definition : The combination of an intrinsic beat and a paced beat The morphology varies, a fusion beat doesnt really look like a pacedbeat or an intrinsic beat Fusion beats contribute to the contraction of the chamber beingpaced VOO pacing @ 80 bpm, so there is no sensing going on. Capture is appropriate. Beats 7 and 8 are fusion 27. Pseudofusion The pacing pulse falls on an intrinsic beat The pacing pulse is ineffective and does notcontribute to the contraction of the chamber VVI, pacing @ 72 bpm Capture is present. Sensing is appropriate. Beats 3 and 6 are fused beats; beat 4 is an example ofpseudofusion. 28. Remember Identify pacing mode Is there capture? Is there sensing? What is the pacing interval? Are there rate variations and can we account for them? Is hysteresis present? Is fusion or pseudofusion happening? 29. Categorization of Tachycardiausing 12 Lead ECGThe 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427437 30. Mechanism of Arrhythmia Abnormal heart pulse formation Sinus pulse Ectopic pulse Triggered activity Abnormal heart pulse conduction Reentry Conduct block 31. SUPRAVENTRICULARTACHYCARDIA 32. Supraventricular Tachycardia Arrhythmia originates above the ventricles Usually has a rapid Narrow QRS (ventricular) response Aberrant (abnormal appearing) conduction (SVTAC) canproduce a wide-complex tachycardia that may mimicventricular tachycardia (VT). To differentiate SVTs from true VTs If atrial rate>ventricular rate, the rhythm is likely to be an SVT If atrial rate=ventricular rate, the rhythm is likely to be a sinustachycardia or nodal reentry If the atrial rate Ventricular Rate YesNoAtrial Flutter / ATAnalyse RP IntervalYesShort (RP < PR)Long (RP > PR) Yes No RP > 70AT / PJRT / AtypicalRP < 70 msAVNRTAVRT / AVNRT /AVNRTATACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmiasexecutive summary. J Am Coll Cardiol.2003;42(8):1493-1531. doi:10.1016/j.jacc.2003.08.013 36. AV Nodal Reentrant TachycardiaSlow pathway 2 pathways within orlimited to perinodaltissue Anterograde conductiondown fast pathway blockswith conduction down slowpathway, with retrogradeconduction up fastpathway. Fast pathway 37. ECG Pattern of Typical AVNRT12-Lead ECG shows a regular SVT recorded at an ECG paper speed of 25mm/sec. Note the pseudo r in V1 (arrow) and accentuated S waves in II, II, aVF(arrow). These findings are pathognomonic for AVNRT.ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmiasexecutive summary. J Am CollCardiol. 2003;42(8):1493-1531. doi:10.1016/j.jacc.2003.08.013 38. WPW Pathophysiology The atrial impulses areconducted partly orcompletely, prematurely,to the ventricles via amechanism other thanthe normal AV-node * *Moss & Adams 39. Types of AccessoryPathway WPW - ORTWPW Manifest AP WPW ARTConcealed AP URAPAccessory PathwayPJRT Mahaim 40. Algorithms 41. AVRT Antidromic atrioventricular reentrant tachycardia, Right posteroseptal accessory pathway. Note the wide-complex, regular rhythm. The delta waves are more prominentbecause of maximal pre-excitation.The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427437 42. AVRT Orthodromic atrioventricular reentrant tachycardia. Note the narrow, regular, rapid tachycardia. The P waves buried in the ST segment (short-RP interval) are marked with anarrow. No pseudo S/R waves are seenThe 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427437 43. Atrial Flutter P waves are present but have a characteristic saw tooth appearance Two types of flutter Type I is organized i.e., saw tooth appearance Type II is disorganized and appears as a fib/flutter Best observed in leads II, III, and aVF.Normal sinus rhythm Result of reentry within the atria Atrial rate is usually range between 220 - Atrial Flutter 350 44. Atrial Flutter This atrial flutter shows distinctive atrial beats and the characteristic sawtooth pattern Atrial rate here is 250 bpm Only every other atrial beat conducts down to the ventricles, so the ventricular rate is 125 bpm P-waves are evident There are four p-waves to every ventricular beat (4:1 conduction) The atrial rate here is 280 bpm Atrial flutter with irregular ventricular response P-waves are evident; these are flutter waves with the characteristic flutter pattern Not every P-wave conducts but there is no regular pattern; this indicates AV block 45. Atrial Fibrillation (AF) Disorganized, rapid atrial rhythm P-waves not clearly discernible Ventricular response is often rapid,may be erratic Three main types of AF Paroxysmal Starts suddenly, resolves spontaneously, short episodes, asymptomatic Persistent Longer duration, requires medical intervention, likely symptomatic Permanent Chronic, medically refractory, often severely symptomatic 46. Atrial TachycardiaEctopic foci within the atria, distinguished by a consistent p-wave ofabnormal morphology that fall before a narrow, regular QRS complex.The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427437 47. P-Wave Morphology in FocalAtrial Tachycardia: J Am Coll Cardiol. 2006;48(5):1010-1017. doi:10.1016/j.jacc.2006.03.058 48. Ventricular Tachycardia 49. Ventricular Tachycardia(VT)A VT is an abnormally fast rhythm that originates withinthe ventricles, or more specifically in the region belowthe His bundle. 50. Ventricular Tachycardia 51. Classification : Etiology Ischemic (Post MI) Idiopathic VT Scar related Not associated with any SHD unknown cause Slow conduction pathways Usually Focal mechanism Re-entry mechanism Monomorphic RVOT (85%), RV inflow, RV inferiorwallLV outflow tract LCC, RCC, NCC coronary venous systemLV idiopathic VT (verapamil sensitive)Basal LVPapillary muscles 52. Classification : Morphology & Duration Monomorphic VT - has one QRS shape or morphology Polymorphic VT - has more than one QRS shape. Nonsustained VT - short bursts of complexes lasting less than 30seconds. Sustained VT- complexes lasting at least 30 seconds or that requireintervention in less than 30 seconds. 53. Distinguishing VT from SVTVentricular tachycardia (VT) is diagnosed by demonstrating that the atria are not part of the VT mechanism.Since all VTs are potentially life-threatening, it is critical to distinguish VT from SVT with aberrantconduction. AV dissociation is present in 50% of patients with VT. It is never present in SVT. During VT, retrogradeconduction over the AV node does not occur. Thus if AV dissociation occurs during extrastimulus pacingbut the tachycardia continues, the rhythm is almost always VT (Murgatroyd 2002). The table provides information for distinguishing VT from SVT with aberrancy.More than 95% of patients with previous myocardial infarction and wide-complex QRS have VT regardless 54. QRS Complexes in different types of WCTExamples of leads V1 and V6 inboth left bundle branch blockand right bundle branch blocktypes of QRS complexes indifferent types of wide complextachycardia. ECG,electrocardiogram; SVT,supraventricular tachycardia;WPW, WolffParkinsonWhitesyndrome.Cara N. Pellegrini, Melvin M. Scheinman, Clinical Management of Ventricular Tachycardia, Current Problems in Cardiology, Volume 35, Issue 9,September 2010 55. QRS AxisThe mean QRS axis is determined by the anatomic positionof the heart and the direction in which the activation wavespreads through the ventricles. 56. Electrode Placements4th intercostal space Mason and Likar, Am Heart J 1966; Pahlm o, Am J Cardiol 1992; Pahlm O, J Eletrocardiol 2008 57. Lead MisplacementQRS-T changes secondary to shift of the V4 electrode 58. DepolarisationTabatabaei and Asirvatham: Circ Arrhyth 2010 59. Lead Groups Inferior Leads II, III, aVF View from Left Leg Inferior wall of left ventricle Lateral Leads I, aVL, V5 and V6 View from Left Arm Left lateral chest wall /ventricle Anterior Leads V3, V4 Left anterior chest electrode on anterior chest Septal Leads V1, V2 Along sternal borders Look through right ventricle & seeseptal wall 60. Predictors of VT 61. Predictors of VTLBBB pattern In V1 : QS in V6 : QR / QS / QrS / RrConcordant pattern in precordialsCommon in VT-ve concordance in limb leads is another way of describingNW axis and suggests VT 62. VT LocalisationThe steps to finding the exit site are: What is the bundle branch block (BBB) configuration? What is the inferior lead QRS complex polarity? What is the lead I QRS complex polarity? What is the lead aVL QRS complex polarity? What is the lead aVR QRS complex polarity? Where is the R-wave transition point? 63. Ventricular Tachycardia in the Absence of Structural Heart Disease. Srivathsan K, Lester SJ, Appleton CP, ScottLR, Munger TM - Indian Pacing Electrophysiol J (2005) 64. Localization of VTUsing the twelve-lead electrocardiogram to localize the site of origin of ventricular tachycardia. Mark E. Josephson, MD,a David J.Callans, MDb 65. Localization of VTUsing the twelve-lead electrocardiogram to localize the site of origin of ventricular tachycardia. Mark E. Josephson, MD,a David J.Callans, MDb 66. Conclusion Always follow a systematic approach to reading ECGs Step 1: What is the rate? Step 2: Is the rhythm regular or irregular? Step 3: Is the P wave normal? Step 4: P-R Interval/relationship? Step 5: Normal QRS complex? Determine the site of origin of the arrhythmia Interpret the Waveform morphologies 67. A Warm Invitation.to an UnforgettableExperience !