Ebook Electrocardiography of arrhythmias - A comprehensive review: Part 2

(BQ) Part 2 book Electrocardiography of arrhythmias - A comprehensive review presents the following contents: Atrial tachycardia, atrial flutter, atrial fibrillation, atrial fibrillation, ventricular tachycardia in structural heart disease, ventricular tachycardia in the absence of structural heart disease,...

7 ATRIAL TACHYCARDIA Atrial tachycardia (AT) is defined as a regular atrial rhythm originating from the atrium at 100 bpm to 240 bpm The presence of an atrial rate above 100 bpm with three different P wave morphologies signifies different foci of atrial depolarization and is called a multifocal atrial tachycardia (MAT) Previous classifications of AT had been based exclusively on the routine electrocardiogram (ECG) with a constant rate and an isoelectric line between the two consecutive P waves Atrial flutter (AFL) is typically a reentrant arrhythmia defined as having a pattern of regular tachycardia with a rate above 240 bpm without an isoelectric baseline between deflections The typical (cavotricuspid dependent) AFL usually shows sawtooth pattern in inferior ECG leads ATs can also have a reentrant mechanism, usually seen around a scar in the atrium The ECG pattern can mimic an atypical (noncavotricuspid dependent) AFL However, neither rate nor lack of isoelectric baseline is specific for any tachycardia mechanism A rapid AT in a scarred atrium can mimic AFL, and, on the other hand, a typical AFL can show distinct isoelectric intervals between flutter waves, in diseased atria, or in the presence of antiarrhythmic drug therapy Therefore it becomes a matter of semantics to define an AT or an atypical AFL AT can result from a focal mechanism such as abnormal automaticity or triggered activity Unlike prior definitions stating that focal ATs have a constant rate, a focal AT can show a significant cycle length (>15%) variation, more than that seen in a reentrant AT, and can also occur in diseased atria Table 7-1 shows the classification of AT/AFL Focal automatic ATs occur mostly in children and young adults Focal automatic ATs begin with a P wave identical to the P wave during the arrhythmia, and the rate generally increases gradually (warms up) over the first few seconds Automatic ATs are catecholamine sensitive and cannot be induced or terminated by programmed electrical stimulation (PES) ATs resulting from triggered activity can arise anywhere in the atria but most commonly originate from the crista terminalis, tricuspid annulus, and mitral annulus These ATs can be induced and terminated with PES The majority of focal ATs caused by triggered activity are adenosine sensitive Rarely, a microreentrant AT can appear to be focal in origin during mapping, but its reentrant mechanism can be elu­ cidated after a careful electrophysiology study including entrainment Macroreentrant AT and AFL are discussed in detail in Chapter ATRIAL TACHYCARDIA The location of the focal source of an AT is determined by P wave morphology and vector on 12-lead ECG (Figures 7-1 and 7-2) Focal AT can arise anywhere in the atrium, pulmonary veins (PVs), and venae cavae (Figures 7-3 through 7-9) Focal ATs usually have discrete P waves at rates of 110 to 240 bpm, but AT/AFL arising from PVs can be as fast as 300 bpm Antiarrhythmic drugs can slow the AT/AFL rate by decreasing the conduction velocity or increasing the refractory period of the reentrant circuit, and an isoelectric line between two P waves can be seen Shorter atrial activation with a shorter P wave duration and longer diastolic intervals on the ECG distinguishes a focal from a macroreentrant AT with 90% sensitivity and specificity Careful analysis of the 12-lead ECG and rhythm strips as well as vagal maneuvers and drug interventions (adenosine and atrioventricular [AV] nodal blockers) help in determining the mechanism of an AT An electrophysiology study is helpful in determining the focus of an AT or the isthmus of a reentrant AT (Figures 7-10 through 7-18) P AND QRS RELATIONSHIP DURING ATRIAL TACHYCARDIA ATs usually have a long R-P′ tachycardia but can have a short R-P′ tachycardia in the presence of significant first-degree heart block at baseline or in the presence of dual AV nodal physiology with AV conduction via the slow pathway The atrial to ventricular relationship depends on the ability of the AV node conduction during tachycardia It is usually 1 : 1 conduction during ATs; however, Wenckebach pattern or 2 : 1 AV block can occur The presence of AV block during supraventricular tachycardia strongly suggests AT and excludes an AV reentrant tachycardia Rarely, an AV nodal reentrant tachycardia with lower common pathway block or His-Purkinje 187 188 CHAPTER 7  Atrial Tachycardia TABLE  7-1  Classification of atrial tachycardia and atrial flutter TYPE Focal Macroreentrant AT and AFL MECHANISM Abnormal automaticity Triggered activity MAPPING PROPERTIES A focal in origin A focal in origin INDUCTION Spontaneous, catecholamine PES Microreentry A focal in origin but careful mapping shows an area of continuous or mid-diastolic potential PAC, PES TERMINATION Beta blockers Adenosine, calcium blocker PES Cavotricuspid dependent right AFL Typical counterclockwise Typical clockwise Lower-loop reentry Double-loop reentry Intra-isthmus reentry Upper-loop reentry (see Chapter 8) Lesional (incision related) Scar related (congenital heart disease, cardiac surgery, cardiomyopathy) Postablation PES, PAC, PVC (rarely) PES Noncavotricuspid isthmus dependent Left atrial or biatrial Around scar or anatomic structures PES Postatrial fibrillation catheter ablation or maze procedure Perimitral, peripulmonary vein posttransplant, septal reentry PES PES AFL, Atrial flutter; AT, atrial tachycardia; PAC, premature atrial complex; PES, programmed electrical stimulation; PVC, premature ventricular complex disease may show AV block and variable relation of P waves with QRS Termination of a supraventricular tachycardia without a following QRS practically rules out an AT EFFECT OF DRUG THERAPY ON ATRIAL TACHYCARDIA AND ATRIAL FLUTTER With AV nodal disease or AV nodal drug therapy, 4 : 1 or variable AV block is seen In the presence of antiarrhythmic drug therapy, the cycle length of AFL can prolong or atrial fibrillation can organize to a relatively slower flutter that allows the AV node to conduct 1 : 1, resulting in a rapid ventricular response and increased risk for life-threatening ventricular arrhythmia Adenosine can terminate focal ATs resulting from triggered activity LOCALIZATION OF FOCAL ATRIAL TACHYCARDIAS Several algorithms have been proposed for ECG localization of focal AT using the P wave morphology and axis on a 12-lead ECG (see Figures 7-1 and 7-2) However, sometimes P wave morphology can be difficult to determine on account of the partial masking by ST segment/T wave Simple vagal maneuvers or intravenous adenosine admini­ stration during 12-lead ECG rhythm strip recording can separate the P wave from T wave Alternatively, a post– premature ventricular contraction compensatory pause can separate the P wave from the T wave and delineate P wave morphology ECG lead V1 is the most useful in identifying the likely anatomic site of origin for a focal AT The right atrium (RA) is an anterior structure, and the left atrium (LA) is a posterior structure The lead V1 is located to the right and anteriorly in relation to the atria Therefore P wave morphology in lead V1 plays a vital role in determining the origin of focal ATs A right AT originating from the tricuspid annulus or crista terminalis has negative P waves in lead V1 because the atrial activation travels away from lead V1.1,2 P waves in lead V1 are positive for ATs originating from the PVs because of the posterior location in the chest In general, negative P waves in the anterior precordial leads suggest an anterior RA or LA free wall location Negative P waves in the inferior leads suggest a low (inferior) atrial origin One study showed that ATs originating from PVs are significantly faster (mean cycle lengths: 289 ± 45 ms and 280 ± 48 ms in patients without and with PV ablation for atrial fibrillation, respectively) compared with left ATs (mean cycle lengths: 392 ± 106 ms and 407 ± 87 ms, patients without and with PV ablation for atrial fibrillation, respectively).3 P waves in focal PV ATs usually have longer duration (≥110 ms) A prior catheter ablation of atrial fibrillation or reentrant AT, maze procedure, and surgery for congenital heart disease can affect the localization of the AT/AFL focus or circuit RIGHT ATRIAL TACHYCARDIA A negative or biphasic (positive, then negative) P wave in lead V1 has a 100% specificity and positive predictive value for ATs arising from the RA (Figures 7-19 through 7-30; see also Figures 7-9 through 7-18) P waves during ATs arising near the septum are generally narrower than those CHAPTER 7  Atrial Tachycardia arising in the RA or LA free wall because of a relatively rapid activation from the midline to both atria, whereas the impulse from ATs with a right or left lateral atrial origin has to travel a longer distance to excite the whole contralateral atria SINUS NODE REENTRY TACHYCARDIA Sinus node reentry is defined as a reentrant tachycardia involving the sinus node and perinodal tissue that is induced and terminated with PES and is adenosine sensitive However, there has not been recent confirmation of this entity in the literature It is possible that sinus node reentry tachycardia may represent a high cristal AT originating near the sinus node that is adenosine sensitive if the mechanism of the tachycardia is triggered activity Alternatively, it is an AT owing to microreentry in tissue near the sinus node or perinodal region (superior crista terminalis) that is responsive to adenosine because of involvement of sinus nodal tissue The P wave morphology during the tachycardia is identical to that seen during sinus rhythm INAPPROPRIATE SINUS TACHYCARDIA Inappropriate sinus tachycardia (see Figure 7-12) is defined as a persistent increase in the resting sinus rate (usually >80-90 bpm) unrelated to, or out of proportion with, the level of physical, emotional, pathologic, or pharmacologic stress, or an exaggerated heart rate response to minimal exertion or a change in body posture It occurs in a disproportionately high number among health care professionals The tachycardia originates at the superior part of the sinus node and is refractory to medical therapy During electrophysiology study it is mapped at the sinus node at the superior part of the crista terminalis CRISTAL ATRIAL TACHYCARDIA In cristal AT (see Figures 7-4 and 7-18 through 7-22), P waves are biphasic in lead V1 and negative in lead aVR The presence of negative P waves in aVR identifies cristal ATs with 100% sensitivity and 93% specificity P waves are positive and broad in leads I and II, as well as positive in lead aVL, owing to right-to-left activation High, mid, or low cristal ATs can be identified according to the P wave polarity in the inferior leads TRICUSPID ANNULAR AND LATERAL RIGHT ATRIAL TACHYCARDIA Tricuspid annular and lateral right ATs (see Figures 7-4 and 7-22 through 7-26) have negative P waves in lead V1 The P wave polarity in inferior leads helps to differentiate the inferior from the superior location of the AT ATs originating from superior sites closer to the interatrial septum have transition from negative in lead V1 through biphasic to upright in the lateral precordial leads An anteroinferior AT usually has inverted P waves across the precordial leads and in inferior leads SEPTAL ATRIAL TACHYCARDIA AND ATRIAL TACHYCARDIAS ORIGINATING FROM CORONARY SINUS The predictive value of P wave morphology for localizing the atrium of origin is more limited because of a variation of activation of atrial pattern of both atria Those ATs are associated with variable P wave morphology, with considerable overlap for tachycardias located on the left and right side of the septum The P wave during the AT is approximately 20 ms narrower than the sinus P wave and is negative or biphasic in lead V1 These ATs can mimic AV nodal reentrant tachycardia (AVNRT) or orthodromic AV reentrant tachycardia (AVRT) associated with a septal bypass tract, depending on the site of origin ATs originating above the membranous septum, between the membranous septum and coronary sinus, and below and around the coronary sinus ostium are designated as high, mid, and low septal ATs, respectively (Figure 7-31; see also Figures 7-4 through 7-6 and 7-27 through 7-29) HIGH SEPTAL ATRIAL TACHYCARDIA High septal ATs with a relatively long P-R interval can mimic slow-fast AVNRT or orthodromic AVRT with superoparaseptal accessory pathways MIDSEPTAL ATRIAL TACHYCARDIA Midseptal ATs can mimic fast-intermediate AVNRT or orthodromic AVRT with midseptal accessory pathway POSTEROSEPTAL ATRIAL TACHYCARDIA Posteroseptal ATs have P waves positive in lead V1, negative in the inferior leads, and positive in leads aVL and aVR These ATs can mimic fast-slow AVNRT or orthodromic AVRT using a posteroseptal accessory pathway or persistent form of junctional reciprocating tachycardia Anteroseptal and midseptal right ATs have a biphasic or negative P wave morphology in lead V1 The combination of a negative or biphasic P wave in V1 and a positive or biphasic P wave in all inferior leads favors an anteroseptal AT, whereas the presence of a negative or biphasic P wave in V1 and a negative P wave in at least two of the three inferior leads favors a midseptal AT The presence of a positive P wave in V1 and a negative P wave in all three inferior leads favors a posteroseptal AT The electrophysiology study is critical for differentiating these tachycardias from atypical AV node reentry or a septal accessory pathway In several series, 27% to 35% of patients had ATs originating from this region AORTIC CUSP Atrial musculature has not been demonstrated to extend into the aortic coronary cusps of the sinus of Valsalva (Figure 7-32; see also Figure 7-7) However, the origin of focal ATs can be mapped from the aortic sinus of Valsalva because of its close relation with right and left atrial 189 190 CHAPTER 7  Atrial Tachycardia myocardium behind the thin aortic wall at the level of the sinotubular junction Most of the ATs reported are from the noncoronary cusp but rarely can arise from the left or the right coronary cusp P wave morphology in ATs originating from the noncoronary cusp of the aorta is negativepositive in leads V1 and V2, predominantly upright or biphasic in inferior leads and lead aVL, and negative in aVR.4 The precordial leads are negative-positive in V1 and V2, negative-positive or positive in leads V3-V5, and positive in lead V6 LEFT ATRIAL TACHYCARDIA Left-sided ATs can arise anywhere from the LA, but PVs and the mitral valve annulus are the main sources A positive or biphasic (negative, then positive) P wave in lead V1 is associated with a 100% sensitivity and negative predictive value for ATs originating in the LA (Figures 7-33 through 7-42; see also Figures 7-8 and 7-9) ATRIAL TACHYCARDIAS ARISING FROM MITRAL ANNULAR AND LEFT ATRIAL APPENDAGE AND CORONARY SINUS1 Mitral annular ATs mostly originate from the superior aspect of the mitral annulus in close proximity to the aortomitral continuity P waves of AT originating from this area have an initial narrow negative deflection followed by a positive deflection in lead V1, negative/isoelectric in lead aVL, negative in leads I, and isoelectric or slightly positive in the inferior leads The positivity of the P wave becomes progressively less from V1 through V6 ATs originating from anterolateral mitral annulus and LA appendage have P wave positive in lead V1 and inferior leads (lead III >II), and negative in lateral leads (I and aVL) with a deeply negative P wave in lead I ATs arising from coronary sinus or posterior mitral annulus have bifid-positive P waves in leads V1, aVL, and negative P waves in the inferior leads (Figures 7-43 and 7-44; see also Figures 7-36 through 7-42) ATRIAL TACHYCARDIAS ARISING FROM PULMONARY VEINS ATs arising from PVs (Table 7-2; see also Figures 7-8, 7-9, 7-37 through 7-40) are characterized by entirely positive P waves in lead V1 in 100%, isoelectric or negative in lead aVL in 86%, and negative in lead aVR in 96% of cases ATs originating from the superior PVs have larger amplitude P waves in the inferior leads than those in ATs arising from the inferior PVs P wave morphology and polarity of ATs TABLE  7-2  Right superior pulmonary vein atrial tachycardias versus left superior pulmonary vein atrial tachycardias P WAVE Lead V1 RIGHT SUPERIOR PV AT Biphasic or positive LEFT SUPERIOR PV AT Broad P waves Lead I Isoelectric Isoelectric or negative Lead aVL Positive or biphasic Negative Inferior leads Positive Positive Amplitude in lead III versus II Equal III/II ratio >0.8 Positive notching Present in ≥2 leads AT, Atrial tachycardia; PV, pulmonary vein originating from right superior PVs can mimic ATs from the superior region of RA, except that it is positive in V1 It is unlike negative P waves in lead V1 in right ATs or a biphasic (positive-negative) P wave in ATs originating from posterior RA P wave morphology generally is of greater accuracy in distinguishing right-sided from left-sided PVs in contrast to superior from inferior PVs ATs arising from inferior PVs generally show lesser amplitude (or negative P waves in inferior leads) than ATs arising from superior PVs REFERENCES Kistler PM, Roberts-Thomson KC, Haqqani HM, et al P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin J Am Coll Cardiol 2006;48:1010-1017 Teh AW, Kistler PM, Kalman JM Using the 12-lead ECG to localize the origin of ventricular and atrial tachycardias Part 1: focal atrial tachycardia J Cardiovasc Electrophysiol 2009;20:706-709; quiz 705 Bazan V, Rodriguez-Font E, Vinolas X, et al Atrial tachycardia originating from the pulmonary vein: clinical, electrocardiographic, and differential electrophysiologic characteristics Rev Esp Cardiol 2010;63:149-155 Zhou YF, Wang Y, Zeng YJ, et al Electrophysiologic characteristics and radiofrequency ablation of focal atrial tachycardia arising from non-coronary sinuses of valsalva in the aorta J Interv Card Electrophysiol 2010;28:147-151 Kistler PM, Fynn SP, Haqqani H, et al Focal atrial tachycardia from the ostium of the coronary sinus: electrocardiographic and electrophysiological characterization and radiofrequency ablation J Am Coll Cardiol 2005;45:1488-1493 CHAPTER 7  Atrial Tachycardia – or P in aVL + P in V1 Yes No RA focus LA focus + P in I >50 mcV + P in V1 >80 ms – P in aVR Yes Non-PV foci LSPV, LIPV No Cristal AT RSPV, RIPV + P in II, III, aVF TA or septal – P in II, III, aVF – or –/+ P in >3 leads V2–V6 P in lead II >100 mcV LSPV, RSPV Superolateral + P in V5, V6; P duration in SVT