Sinus tachycardia is considered physiological or "appropriate" when a reasonable stimulus, such as the catecholamine surge associated with fright, stress, or physical activity, provokes the tachycardia. It is distinguished by a presentation identical to a normal sinus rhythm except for its fast rate (>100 beats per minute in adults). It is generally not considered SVT.Sinoatrial node reentrant tachycardia (SANRT) is caused by a reentry circuit localised to the SA node, resulting in a normal morphology P-wave that falls before a regular, narrow QRS complex. It is therefore impossible to distinguish on the ECG from physiological sinus tachycardia unless the sudden onset is observed (or recorded on Holter monitor. It may sometimes be distinguished by its prompt response to vagal manoeuvres.Ectopic (unifocal) atrial tachycardia is tachycardia resultant from one ectopic focus within the atria, distinguished by a consistent P-wave of abnormal morphology that falls before a narrow, regular QRS complex. It is caused by "automaticity", or an impulsed generated by the heart muscle.Multifocal atrial tachycardia (MAT) is tachycardia resultant from at least three ectopic foci within the atria, distinguished by P-waves of at least three different morphologies that all fall before irregular, narrow QRS complexes.Atrial fibrillation is not, in itself, a tachycardia, but when it is associated with a rapid ventricular response greater than 100 beats per minute, it becomes a tachycardia. A-fib is characteristically an "irregularly irregular rhythm" both in its atrial and ventricular depolarizations. It is distinguished by fibrillatory P-waves that, at some point in their chaos, stimulate a response from the ventricles in the form of irregular, narrow QRS complexes.Atrial flutter, is caused by a re-entry rhythm in the atria, with a regular atrial rate often of about 300 beats per minute. On the ECG, this appears as a line of "sawtooth" P-waves. The AV node will not usually conduct such a fast rate, and so the P:QRS usually involves a 2:1 or 4:1 block pattern, (though rarely 3:1, and sometimes 1:1 in the setting of class IC antiarrhythmic drug use). Because the ratio of P to QRS is usually consistent, A-flutter is often regular in comparison to its irregular counterpart, A-fib. Atrial Flutter is also not necessarily a tachycardia unless the AV node permits a ventricular response greater than 100 beats per minute.AV nodal reentrant tachycardia (AVNRT) involves a reentry circuit forming just next to or within the AV node itself. The circuit most often involves two tiny pathways one faster than the other, within the AV node. Because the AV node is immediately between the atria and the ventricle, the re-entry circuit often stimulates both, meaning that a retrogradely conducted P-wave is buried within or occurs just after the regular, narrow QRS complexes.Atrioventricular reciprocating tachycardia (AVRT), also results from a reentry circuit, although one physically much larger than AVNRT. One portion of the circuit is usually the AV node, and the other, an abnormal accessory pathway (muscular connection) from the atria to the ventricle. Wolff-Parkinson-White syndrome is a relatively common abnormality with an accessory pathway, the Bundle of Kent crossing the AV valvular ring. In orthodromic AVRT, atrial impulses are conducted down through the AV node and retrogradely re-enter the atrium via the accessory pathway. A distinguishing characteristic of orthodromic AVRT can therefore be a P-wave that follows each of its regular, narrow QRS complexes, due to retrograde conduction.In antidromic AVRT, atrial impulses are conducted down through the accessory pathway and re-enter the atrium retrogradely via the AV node. Because the accessory pathway initiates conduction in the ventricles outside of the bundle of His, the QRS complex in antidromic AVRT is often wider than usual, with a delta wave.Finally, junctional ectopic tachycardia (JET) is a rare tachycardia caused by increased automaticity of the AV node itself initiating frequent heart beats. On the ECG, junctional tachycardia often presents with abnormal morphology P-waves that may fall anywhere in relation to a regular, narrow QRS complex. It is often due to drug toxicity.
ECG pattern of typical AVNRT. Panel A: 12-Lead ECG shows a regular SVT recorded at an ECG paper speed of 25 mm/sec. Note the pseudo r′ in V1 (arrow) and accentuated S waves in 2, 3, aVF (arrow). These findings are pathognomonic for AVNRT.
V4 = standard lead placementV’4 = one intercostal space belowV4’ = one intercostal space aboveV4M = one inch medial to V4V4L = one inch lateral to V4
Essentials of ecg interpretation aphrs
Essentials of ECG Interpretation :Pacemaker ECG, SVT & VT
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. "ECG- simplified. Aswini Kumar M.D". LifeHugger. Retrieved 2010-02-11.
Role of ECGIt helps in the detection of Heart Attack & Coronary Artery Disease (Ischaemia) Abnormal heartbeats (conduction system disorders) Bradycardia Tachycardia Enlargement of cardiac chambers Problems with the blood chemistry Image source : http://potomachospital.blogspot.tw
Conduction System Primary Pacemaker Rate / Min SA Node 60-100 Escape Pacemaker AV Node AV Junction HIS Bundle 40 - 60 Bundle Branches Ventricles Purkinje Fibres 20 - 40Image source : http://www.ekgguru.com/content/conduction-system-illustration
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 appropriate—not too fast, not too slow12 lead tracing source : http://meds.queensu.ca/courses/assets/modules/ts-ecg/Normal_ECG.bmp Video source : Youtube.com
ECG Interpretation• 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? Image source : www.broward.edu/cehealth
Step 1 : RateMethod 1 : Count the number of R waves for a six second intervaland multiply by ten. 6 sec 3 sec 3 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
Step 2 - Rhythm• Determine if the ventricular rhythm is regular or irregular• R-R intervals should measure the same• P-P intervals should also measure the same REGULAR IRREGULAR
STEP 3 : P Wave Morphology• Identify and examine P waves: • Present? • Appearance? • Consistency? • Relation to QRS?
Standard Morphologies Lea P- QRS T- d Wave Wave Limb Leads – Vertical Plane I II III Augmented Leads aVR aVF aVL Lea P-Wave QRS T-Wave dPrecordial Leads – Horizontal PlaneV1 /± Small R wave / QS V2 /± Small R wave / QS V3 Equiphasic QRS / V4 V5
Step 4 : PR IntervalConsistent PRI of <.20 secs is normalLengthening of PRI is indicative of AV Nodal disease Shortening of PRI is indicative of a bypass tract
Step 5 : QRS Duration• A narrow QRS complex (< 0.12), indicates the impulse has followed the normal conduction pathway• A widened QRS complex (> 0.12), may indicate the impulse was generated somewhere in the ventricles
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)
Function of a Pacemaker• Sense intrinsic activity• Pace the appropriate chamber
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?
ECG # 1• VVI.• Capture is present.• Sensing cannot be determined (this strip is all pacing).• The pacing interval corresponds to a rate of 72 ppm
Potential Problems Identifiable on an ECG• Undersensing• Oversensing• Noncapture• No output• Pseudomalfunction
Undersensing• An intrinsic depolarization that is present, yet not seen or sensed by the pacemaker P-wavenot sensed Atrial Undersensing Common Causes of Undersensing • Inappropriately programmed conductor fracture sensitivity • Lead maturation • Lead dislodgment • Change in the native signal • Lead failure: Insulation break;
Oversensing Markersensing of an The channel shows inappropriate signal ...Though no intrinsic activity... activity is present Ventricular Oversensing Can be physiologic or nonphysiologic Common Causes of Oversensing• Lead failure sensitivity• Poor connection at connector • Change in the native signal block• Exposure to interference• Inappropriately programmed
Non – Capture• No evidence of depolarization after pacing artifact Loss of capture Common Causes of Noncapture• Lead dislodgment • Poor connection at connector block• Low output • Lead failure• Lead maturation
Functional Non-Capture• Functional non-capture occurs when a pacing spike is delivered at a time when it could not possibly depolarize the heart (because the cardiac tissue is refractory)• However, had the pacing spike been more appropriately timed, it might have captured the heart• Functional non-capture is most often observed in asynchronous (non-sensing) modes, such as VOO or AOO
No Output Pacemaker artifacts do not appear on the ECG; rate is less than the lower rate Pacing output delivered; no evidence of pacing spike is seen Common Causes of No Output• Poor connection at connector block • Battery depletion• Lead failure • Circuit failure
Pseudomalfunction: Hysteresis• Allows a lower rate between sensed events to occur; paced rate is higher Lower Rate 70 ppm Hysteresis Rate 50 ppm
Fusion• Definition : The combination of an intrinsic beat and a paced beat• The morphology varies, a fusion beat doesnt really look like a paced beat or an intrinsic beat• Fusion beats contribute to the contraction of the chamber being paced• VOO pacing @ 80 bpm, so there is no sensing going on.• Capture is appropriate.• Beats 7 and 8 are fusion
Pseudofusion• The pacing pulse falls on an intrinsic beat• The pacing pulse is ineffective and does not contribute 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 of pseudofusion.
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?
Categorization of Tachycardia using 12 Lead ECGThe 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427–437
Supraventricular Tachycardia• Arrhythmia originates ―above the ventricles‖ • Usually has a rapid Narrow QRS (ventricular) response • Aberrant (abnormal appearing) conduction (SVTAC) can produce a wide-complex tachycardia that may mimic ventricular 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 sinus tachycardia or nodal reentry • If the atrial rate<ventricular rate, the rhythm is likely to be a VT
Common Forms of SVT• SVTs from a sinoatrial source: • Sinoatrial nodal reentrant tachycardia (SNRT)• SVTs from an atrial source: • Ectopic (unifocal) atrial tachycardia (EAT) • Multifocal atrial tachycardia (MAT) • Atrial fibrillation with a rapid ventricular response • Atrial flutter with a rapid ventricular response • Without rapid ventricular response, fibrillation and flutter are usually not classified as SVT• SVTs from an atrioventricular source (junctional tachycardia): • AV nodal reentrant tachycardia (AVNRT) or junctional reciprocating tachycardia (JRT) • Permanent (or persistent) junctional reciprocating tachycardia (PJRT), a form of JRT which occurs predominantly in infants and children but can occasionally occur in adults • AV reciprocating tachycardia (AVRT) - visible or concealed (including WPW syndrome) • Junctional ectopic tachycardia (JET)
Supraventricular TachycardiaNarrow complex, regular; retrograde P waves, rate <220
Differential Diagnosis for Narrow QRS Tachycardia Narrow QRS Tachycardia (QRS < 120 ms) Yes No Regular Rhythm No AF / AT / Flutter with Visible P waves variable AV conduction / Yes MAT No Atrial Rate > Ventricular Rate Yes No Atrial Flutter / AT Analyse RP Interval Yes Short (RP < PR) Long (RP > PR) Yes No RP > 70 AT / PJRT / Atypical RP < 70 ms AVNRT AVRT / AVNRT / AVNRT ATACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias∗—executive summary. J Am Coll Cardiol.2003;42(8):1493-1531. doi:10.1016/j.jacc.2003.08.013
AV Nodal Reentrant Tachycardia Slow pathway• 2 pathways within or limited to perinodal tissue • Anterograde conduction down fast pathway blocks with conduction down slow pathway, with retrograde conduction up fast pathway. Fast pathway
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 arrhythmias∗—executive summary. J Am CollCardiol. 2003;42(8):1493-1531. doi:10.1016/j.jacc.2003.08.013
WPW Pathophysiology• The atrial impulses are conducted partly or completely, prematurely, to the ventricles via a mechanism other than the normal AV-node * *Moss & Adams
Types of Accessory Pathway WPW - ORT WPW – Manifest AP WPW – ART Concealed AP URAPAccessory Pathway PJRT Mahaim
AVRT• Antidromic atrioventricular reentrant tachycardia,• Right posteroseptal accessory pathway.• Note the wide-complex, regular rhythm. The delta waves are more prominent because of maximal pre-excitation. The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427–437
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 an arrow.• No pseudo S/R’ waves are seen The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427–437
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
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
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
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) 427–437
P-Wave Morphology in Focal Atrial Tachycardia: J Am Coll Cardiol. 2006;48(5):1010-1017. doi:10.1016/j.jacc.2006.03.058
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 inferior wall • LV ―outflow tract‖ • LCC, RCC, NCC • coronary venous system • LV idiopathic VT (verapamil sensitive) • Basal LV • Papillary muscles
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 30 seconds.• Sustained VT- complexes lasting at least 30 seconds or that require intervention in less than 30 seconds.
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, retrograde conduction over the AV node does not occur. Thus if AV dissociation occurs during extrastimulus pacing but 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
QRS Complexes in different types of WCT Examples of leads V1 and V6 in both left bundle branch block and right bundle branch block types of QRS complexes in different types of wide complex tachycardia. ECG, electrocardiogram; SVT, supraventricular tachycardia; WPW, Wolff–Parkinson–White syndrome.Cara N. Pellegrini, Melvin M. Scheinman, Clinical Management of Ventricular Tachycardia, Current Problems in Cardiology, Volume 35, Issue 9,September 2010
QRS AxisThe mean QRS axis is determined by the anatomic positionof the heart and the direction in which the activation wavespreads through the ventricles.
Electrode Placements4th intercostal space Mason and Likar, Am Heart J 1966; Pahlm o, Am J Cardiol 1992; Pahlm O, J Eletrocardiol 2008
Lead MisplacementQRS-T changes secondary to shift of the V4 electrode
Depolarisation Tabatabaei and Asirvatham: Circ Arrhyth 2010
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 & see septal wall
Predictors of VT LBBB pattern In V1 : QS in V6 : QR / QS / QrS / Rr’Concordant pattern in precordials Common in VT -ve concordance in limb leads is another way of describing NW axis and suggests VT
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?
Ventricular Tachycardia in the Absence of Structural Heart Disease. Srivathsan K, Lester SJ, Appleton CP, ScottLR, Munger TM - Indian Pacing Electrophysiol J (2005)
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
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
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
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