1、Supraventricular arrhythmias,Jerry John July 29, 2009,Objectives,Supraventricular Arrhythmias How do supraventricular arrhythmias manifest? What are the common supraventricular arrhythmias? What is the mechanism of atrioventricular arrhythmias? Which drugs are used in the management of supraventricu
2、lar arrhythmias? Which patients should be offered catheter ablation? Atrial Fibrillation and Atrial Flutter What are the incidence and prevalence of atrial fibrillation? What are the major sequelae of atrial fibrillation? What are the risk factors for stroke in atrial fibrillation? What are the trea
3、tment options for patients with atrial fibrillation?,History,F M (2:1) AVNRT M F AVRT Posture Menses 3rd trimester pregnancy Neck pulsations (“Frog sign”) Age of onset (10 year difference AVNRT(39) vs. AVRT (26) Thyroid symptoms Acute precipiants (post op, PE, drug withdrawal, ischemia),JACC 2009; 5
4、3:2353-58,EKG,AV node dependent (Y/N) Re-entrant circuit (Y/N) Circuit (Macro/Micro) Anatomic (e.g. previous ASD repair, CVTI) Accessory pathway ( WPW, Mahaim, etc. ) P wave Rate Morphology (Sinus/Retrograde/abnormal): look at the T waves and the psuedo R (V1) and psedo S (inferior leads) Conduction
5、 (2:1; 3:1, etc.) Response to AV Block VA conduction (i.e. R-P relationship): (short/long) Initiation (PAC or PVC) & Termination (P wave or QRS),Anatomy & Physiology,SA node 1 mm subendocardial near RSPV AV node Decremental conduction properties His-Purkinje Accessory pathways No decremental conduct
6、ion AV conduction 10-20 ms,AVNRT,Atach (reentry or automaticity),ORT,Non paraoxysmal junctional tach,AV Node Depdendence (Y/N),AV nodal dependent arrhythmias AVNRT (micro-reentrant circuit) AVRT (macro-reentrant circuit): anti/orthodromic JET (junctional ectopic tachycardia) - childhood and associat
7、ed with congenital heart disease AV nodal independent arrhythmias Atrial tachycardia Inappropriate Sinus Tachycardia Sinus Node Reentrant Tachycardia Atrial flutter Atrial fibrillation,RP relationship,Short “RP” Tachycardias:Typical AVNRTAVRT Long “RP” Tachycardias:Atrial TachycardiaAtypical AVNRTAV
8、RT with long retrograde conductionPJRT,Wheres the P wave,Valsalva Carotid sinus massage Slows SA nodal; and/or AV nodal conduction Adenosine Slows sinus rate Increases AV nodal conduction delay T 5 seconds 6 or 12 mg bolus Effect blocked by theophylline, methylxanthines (caffeine); and potentiated b
9、y dipyridamole,P waves,Rate Morphology (Sinus/Retrograde/abnormal) Conduction (2:1; 3:1, etc.) Response to AV Block VA conduction (i.e. R-P relationship): (short/long),P waves,(-) Inferior leads atrial activation from low to high: AVNRT, atypical AVNRT; AVRT Right atrial focus: 1) (-/+) in aVL right
10、 atrium activated first and then left atrium) 2) (-) or biphasic in V1 Left atrial focus: 1) (-) or isoelectric in aVL 2) (+) V1 suggests back to front,Tachycardia onset,Most SVTs triggered by a PAC If the PAC conducts with a long PR, dual AV nodal physiology is suggested with the conduction being t
11、hrough the slow pathway If a PVC initiates SVT, it is likely to be AV node dependent,Tachycardia termination,Ends with a P wave: suggests an AV nodal dependent arrhythmia because the generation of the P wave without a QRS suggests block in the AV node this is more likely to be AVNRT or AVRT AVNRT p
12、waves however can be buried in the QRS if VA conduction is very short Ends with a QRS : almost always atrial tachycardia (some rare AV node dependent tachycardias can terminate in this manner),AVNRT,Most common cause of a regular narrow complex tachycardia Involves a slow and a fast pathway in the r
13、egion of the AV node Turn around point appears above the bundle of His 160-190 bpm but may exceed 200 bpm Slow-fast form accounts for 90% of AVNRT Fast-slow or slow-slow AVNRT accounts for 10% Pseudo r in V1, pseudo S wave in 2,3,avf, and p wave absence help distinguish AVNRT from AVRT and atrial ta
14、chycardia,AVNRT,Initiation and termination by APDs, VPDs or atrial pacing during AVW Dual AVN physiology Initiation depends on critical A-H delay Concentric retrograde atrial activation(V-A -42 to 70 msec) Retrograde P wave within QRS with distortion of terminal portion of the QRS Atrium, His bundle
15、 and ventricle not required , vagal maneuvers slow and then terminate SVT,Atypical AVNRT,Initiation and termination by APDs, VPDs, or ventricular pacing during retrograde AVW Dual retrograde AVN physiology Initiation dependent on critical H-A delay Earliest retrograde activation at CS os Retrograde
16、P wave with long R-P interval Atrium, His bundle, and ventricle not required, vagal , maneuvers slow and then terminate SVT, always in the retrograde slow pathway,AVNRT Treatment,Low threshold for catheter ablation given long term success rate 90% and low risk of complications AV nodal blocking agen
17、ts (diagnosis/treatment) Adenosine BB/CCB Digoxin Anti-arrhythmics (third choice) Procainamide Amiodarone Disopyramide Flecainide/Propafenone,AVRT,Activation sequence is ventricle via atria; therefore P wave often in the ST or T Left lateral AP: (+) Delta V1; (-) Delta I Right sided AP: (-) Delta V1
18、 QS pattern; (+) Delta I Concealed AP implies only retrograde conduction; i.e. no pre-excitation and only orthodromic AVRT. Rapidly conducted Afib occurs may occur for 2 reasons: 1) AP may have a short refractory period ; 2) AP does not exhibit decremental conduction properties like the AV node Flec
19、ainide and Propafenone preferred as they prolong the effective refractory period,BBB on tachycardia,Interval development of BBB and increased tachycardia cycle length suggests contralateral AVRT Pre-existing BBB Rate related BBB: will look like a conventional BBB Accessory pathway,AVRT,Use of Adenos
20、ine or Verapamil There is a small risk (3-5%) of preferential conduction down the accessory pathway, and ibutilide or procainamide, or electric cardioversion should be immediately available,Asymptomatic WPW,165 children (5-12 years) screened 60 randomized, 3 withdrew: 20 ablation and 27 no ablation
21、1 child in ablation group had arrhythmia (5%) and 12 of 27 in control group ( 44% ) 2 children in control group had VF and one diedPappone et al; NEJM 2004;351:1197-05,AVRT Treatment,Low threshold for catheter ablation given long term success rate 90% and low risk of complications Posteroseptal path
22、ways have less success rates L sided AV nodal blocking agents (diagnosis/treatment) Adenosine BB orCCB in conjunction with Flecainide or Propafenone,Atrial tachycardia,Older patients - related to atrial stretch or scarring If conduction to the ventricle via the AV node, variable AV block may occur A
23、 bystander (accessory) pathway may be used to conduct antegrade to the ventricles; i.e. the accessory pathway is not what is causing the atria to beat so fast Tachycardia may be incessant: “the ventricle is a slave to the atrium” Procainamide may be considered to achieve immediate control AV nodal b
24、locking agents and sotalol may be considered for chronic treatment,Irregular SVT,AV block Wenckebach Variable block (e.g. atrial tachycardias) 2:1 with typical flutter; odd multiples with atypical flutter Multifocal atrial tachycardia (MAT) Atrial Fibrillation (with or w/o pre-excitation),Focal Atri
25、al Tachycardia,Incessant or paroxysmal atrial rhythms 120-250 bpm Demographic profile similar to reentrant AT, but less likely to have cardiac surgery Typically 1:1 conduction P wave morphology different from sinus Typically terminate or transiently suppress with adenosine Centrifugal activation Can
26、not be entrained,Focal Atrial Tachycardia,Three Subgroups: Cristal Tachycardia- Initiated and terminated with PES- Arise along crista - P wave similar to NSR- Terminates with adenosine Repetitive monomorphic AT- Repetitive runs of nonsustained AT- Suppress with adenosine- Variable locations Automati
27、c AT- Incessant AT- Transient suppression with adenosine,Macroentrant Atrial Tachycardia,Incessant or Paroxysmal atrial rhythms 120-250 bpm Demographic similar to focal atrial tach but more likely to have had cardiac surgery P wave morphology usually differs from sinus Typically are insensitive to a
28、denosine Demonstrate features specific for reentry- concealed or manifest entrainment- fractionated mid diastolic EGMs- concealed activation during diastole,Junctional Tachycardia,Nonparoxysmal Junctional Tachycardia Junctional Ectopic Tachycardia Congenital Automatic Junctional Tachycardia,Nonparox
29、ysmal Junctional Tachycardia,70-120 bpm Generally regular with VA conduction Seen with dig toxicity, ischemia, COPD, metabolic disturbances, carditis and after cardiac surgery Mechanism is triggered activity due to DADs,Junctional Ectopic Tachycardia (JET),Following surgery for congenital heart dise
30、ase 3% of VSD repairs, 10% of TGV, 7% of TOF and 2% of Fontan Perinodal trauma Procainamide and cooling, amiodarone,Congenital Automatic Junctional Tachycardia, 1% of pediatric SVTs Average HR 230 bpm (140-370) Infants 6 months old High mortality. Less malignant older the child is Triggered activity
31、, enhanced automaticity Amiodarone, ablation with PM,Orthodromic reciprocating tachycardia Earliest retrograde activation in proximal CS Tachycardia terminates with adenosine with retrograde AP block HIS refractory PVC advances atrial activation,Atrial Flutter,Typical or type I atrial flutter:Counte
32、r clockwise atrial activation manifested as - P waves in II,III,avf and + in VI with transition to - P in V6Clockwise with reverse activation Atypical or type II atrial flutterAlso called as fib flutter In the absence of AFib symptomatic Aflutter is often amenable to ablation (success rates 90%),Afi
33、b,What are the incidence and prevalence of atrial fibrillation? What are the major sequelae of atrial fibrillation? What are the risk factors for stroke in atrial fibrillation? What are the treatment options for patients with atrial fibrillation?,Afib epidemiology,Age adjusted incidence has been inc
34、reasing from 1980 to 2000: 3.2 million in 1980; 5.1 million in 2000The detection of Afib requires symptoms and asymptomatic PAF may go undetected Current estimates at the Mayo Clinic would suggest 2.3 million Americans. Afib prevalence increases with age: 0.1% 55 years; at 9% in octogenerians. At yo
35、unger ages (70), Afib has a greater prevalence among males (5.8%) than females (2.8%) based on data from CHS The lifetime risk based on the Framingham cohort is 23-26% among 40 year olds.,Circulation 2006; 114(2):119-125. ;Am J Cardiol 1994; 74:236-241).; JAMA 2004; 292:2471-2477; JACC 2007; 49:565-
36、571).,Afib epidemiology,Age alone does not explain the increased incidence: an increase in obesity accounted for 60% of the age adjusted increase in AF incidence HTN and Diastolic dysfunction Obesity has been associated with new onset Afib in the Framingham and other cohorts OSA, Etoh, Anger, ethnic
37、ity, and genetic influences have been reported to be associated with incident Afib. Appropriately treated OSA reduces AFib recurrence after cardioversion AA race is associated with less Afib than whites. Afib and CAD are co-existent Rheumatic heart disease and valvular heart disease,Circulation 2006
38、; 114(2):119-125. ;Am J Cardiol 1994; 74:236-241).; JAMA 2004; 292:2471-2477; JACC 2007; 49:565-571; Circ 2003; 107:2589-2594).,Afib categories,Lone atrial fibrillation: no structural heart disease (usually 1 year and CV not attempted or failed. * Episodes 30 seconds unrelated to a reversible cause
39、(cardiac surgery, pericarditis, MI, hyperthyroidism, PE),What are the major sequelae of atrial fibrillation?,Worsened heart failure Afib begets afib leading to electrical and structural remodeling Tachycardia induced cardiomyopathies Stroke Decreased quality of life and exercise tolerance Acute hemo
40、dynamic compromise,CHADS2,. Risk of Stroke: (CHAD score ranges from 0-6; 2 points for prior TIA or stroke, 1 for HTN, CHF, DM, Age75, JAMA 2001; 285:28 64-70). Annual risk of stroke: (non-rheumatic Afib) 0=1.9% 1=2.8% 2=4.0% 3=5.9% 4=8.5% 5=12.5% 6=18.2%,Afib treatment options,Rate control AV nodal
41、agents AV node ablation and pacemaker Rhythm control Cardioversion: chemical or electrical; +/- TEE Anti-arrhythmics Catheter Ablation MAZE Anticoagulation ASA ASA + clopidogrel Warfarin,Irregularly irregular rhythms,MAT Afib ATach with variable conduction,Pregnancy and SVTs,50% have SV ectopics Sus
42、tained arrhythmia rare (2-3/1000) Symptomatic increase in 20% Risk to mother and fetus No controlled study and there would be none AA drugs toxic and should be reserved for only highly symptomatic patients Role of RF ablation,Antiarrhythmic drugs in Pregnancy,Radiofrequency Catheter Ablation,Who sho
43、uld be referred? What arryhthmias should be referred for ablation? What are the success rates? What are the risks of ablation?,Who should be referred?,Symptomatic patients AVNRT (90% succes rates) WPW and symptomatic AVRT (CCB ; BB and Dig not appropriate as sole therapy) (90%) Aflutter(90%) AFib (4
44、0-70%) High risk for sudden death AFib with WPW and cycle length 250 ms Not amenable to catheter ablation MAT Reversible causes (thryotoxicosis; PE; post-op),Question 1,A 35-year old woman with unrepaired Ebsteins anomaly is evaluated in the emergency department for recurrent tachycardia episodes. S
45、everal episodes occur while she is being evaluated. She notes that she feels somewhat lightheaded. The patients blood pressure is 110/60 mm Hg. She is acyanotic and afebrile. Cardiac examination demonstrates a brief systolic murmur along the lower left sternal border, which increases with inspiratio
46、n. The jugular venous pressure is elevated. The electrocardiogram shows a short PR interval, an abnormal initial portion of the QRS complex, and right bundle branch block. The tachycardia is wide-complex and regular at a rate of 190/min. What is the most appropriate acute treatment of choice? A Aden
47、osine B Procainamide C Digoxin D Direct-current cardioversion,Question 2,A 26-year-old nurse is evaluated in the emergency department after an episode of syncope. While working in the intensive care unit, she developed tachycardia and then lost consciousness. She admits to having a stressful day and
48、 having had more caffeine than normal. She has had brief episodes of tachypalpitations in the past but no prior syncope. Physical examination is unremarkable and the patient is in sinus rhythm. The chest radiograph is unremarkable. The electrocardiogram initially demonstrates sinus rhythm and is unr
49、emarkable. Ten minutes later, the patient develops an episode of brief tachycardia. Shortly after the tachycardia episode, a repeat electrocardiogram is performed and is shown (Figure 122). What is the most likely diagnosis in this patient?A Atrioventricular nodal reentrant tachycardia B Accelerated
50、 idioventricular tachycardia C Atrioventricular reentrant tachycardia D Multifocal atrial tachycardia,Question 3,A 68-year-old woman comes to the emergency department because of a racing heart for the past 2 hours. She reports a 2-year history of similar episodes, for which her physician instructed
51、her to cough or strain. The episodes usually terminate after a few minutes of following her physicians instructions, but the current episode is persisting. She does not have chest pain, and she has no other cardiac history. The physical examination demonstrates a blood pressure of 110/60 mm Hg, hear
52、t rate of 165/min, respiratory rate of 20/min, clear lungs, and no murmurs or gallop. After the carotids are auscultated and the presence of bruit excluded, carotid sinus massage is attempted, but the tachycardia persists. The electrocardiogram obtained in the emergency department is shown .Which is the drug of choice for terminating this patients arrhythmia?A Metoprolol B Verapamil C Adenosine D Digoxin,
