Thursday, July 26, 2012

ECG Quiz 12

A 22 years old pregnant woman was admitted to the coronary care unit after she was found unconscious in her bed by her husband. Husband says he was in bed with his heavily pregnant wife and they had just finished having fight over picking a name for their yet to be born daughter which seemed to have taken emotional toll on both the partners. Soon after husband noticed that her wife started with jerking movements and he turned to see her exhibiting seizure like activity. Husband could not feel and pulse and being a paramedic himself performed CPR till ambulance arrived. On arrival patient was found to be in fast VT and was successfully defibrillated with one shock. She remained comatose and was intubated and transported to the hospital.

In the hospital initial history was un revealing except for the 12 lead ECG shown below. On physical exam she was intubated and withdrew to painful stimuli. Her pupils were dilated, but reactive to light symmetrically. She does have a 2/6 systolic murmur over the pre-cordium which increases slightly in intensity with inspiration. Her mother recalls couple of brief fainting episodes just like this one when the woman was younger in her teens. Mother and husband denies any foul play and denies that any drug is involved. Her urine toxicology screen comes back negative.

Her family history is notable for a her maternal grand father who was also deaf and died at young age few years after his marriage. Her maternal uncle also died at the age of 36 suddenly though they do not know the cause.



So answer the series of questions below.

Quiz - Question - 2

Quiz Question - 1 - Choose single best answer

1. What is the most likely diagnosis?

Brugada Syndrome

WPW with Aberrantly conducted tachycardia


Long QT Syndrome

Quiz - Question - 2

Quiz Question - 2 - Choose single best answer

1. What is the next step in her management?
Initiate beta blocker therapy
Cardiac sympathectomy
Send home with life-vest
ICD Implantation

Various types of Long QT syndromes are being diagnosed nearly everyday.At this time we know and have genetic testing for only about 2/3 rd of types of Long QTc Syndrome.

Till date 11 different types of Long QTc Syndromes have been identified wih their associated genes:

alpha subunit of the slow delayed rectifier potassium channel (KvLQT1 or KCNQ1)
The current through the heteromeric channel (KvLQT1 + minK) is known as IKs. These mutations often cause LQT by reducing the amount of repolarizing current. This repolarizing current is required to terminate the action potential, leading to an increase in the action potential duration (APD). These mutations tend to be the most common yet least severe. ASSOCIATED WITH CONGENITAL DEAFNESS – JARVELL-LANGE-NEILSEN SYNDROME. ASSOCIATED WITH EMOTIONAL EVENTS
alpha subunit of the rapid delayed rectifier potassium channel (hERG + MiRP1)
Current through this channel is known as IKr. This phenotype is also probably caused by a reduction in repolarizing current. AUDITORY STIMULI.
alpha subunit of the sodium channel (SCN5A)
Current through this channel is commonly referred to as INa. Depolarizing current through the channel late in the action potential is thought to prolong APD. The late current is due to the failure of the channel to remain inactivated. As a consequence, it can enter a bursting mode, during which significant current enters abruptly when it should not. These mutations are more lethal but less common. CAN BE ASSOCIATED WITH BRUGADA SYNDROME AND DILATED CARDIO-MYOPATHY. A/C SLEEP.
anchor protein Ankyrin B
LQT4 is very rare. Ankyrin B anchors the ion channels in the cell.
beta subunit MinK (or KCNE1), which coassembles with KvLQT1
CAN ALSO LEAD TO JERVELL-LANGE-NEILSEN - form of LQTS with associated congenital deafness. It is caused specifically by mutation of the KCNE1 and KCNQ1 genes In untreated individuals with JLNS, about 50 percent die by the age of 15 years due to ventricular arrhythmias.
beta subunit MiRP1 (or KCNE2), which coassembles with hERG
potassium channel KCNJ2 (or Kir2.1)
The current through this channel and KCNJ12 (Kir2.2) is called IK1. LQT7 leads to Andersen-Tawil syndrome.
alpha subunit of the calcium channel Cav1.2 encoded by the gene CACNA1c.
Leads to Timothy's syndrome. PATIENTS CAN HAVE SYNDACTYLY.





The diagnosis of LQTS is not easy since 2.5% of the healthy population have prolonged QT interval, and 10–15% of LQTS patients have a normal QT interval. A commonly used criterion to diagnose LQTS is the LQTS "diagnostic score". The score is calculated by assigning different points to various criteria (listed below). With four or more points, the probability is high for LQTS; with one point or less, the probability is low. A score of two or three points indicates intermediate probability.
  • QTc (Defined as QT interval / square root of RR interval)
    • >= 480 msec - 3 points
    • 460-470 msec - 2 points
    • 450 msec and male gender - 1 point
  • Torsades de pointes ventricular tachycardia - 2 points
  • T wave alternans - 1 point
  • Notched T wave in at least 3 leads - 1 point
  • Low heart rate for age (children) - 0.5 points
  • Syncope (one cannot receive points both for syncope and torsades de pointes)
    • With stress - 2 points
    • Without stress - 1 point
  • Congenital deafness - 0.5 points
  • Family history (the same family member cannot be counted for LQTS and sudden death)
    • Other family members with definite LQTS - 1 point
    • Sudden death in immediate family members (before age 30) - 0.5 points


-          Avoid drugs and situations that would prolong the QT interval further or lower the threshold for TDP.

Arrhythmia prevention

Avoid situations that create adrenergic surge.
Beta-blockers - Beta blockers are the first choice in treating Long QT syndrome.
 The presence of QTc >500ms and LQT2 and LQT3 genotype are associated with the highest incidence of recurrence. In these patients, primary prevention with ICD (Implantable cardioverter-defibrillator) implantation can be considered.
 Potassium supplementation: If the potassium content in the blood rises, the action potential shortens, and due to this reason it is believed that increasing potassium concentration could minimize the occurrence of arrhythmias. It should work best in LQT2, since the HERG channel is especially sensitive to potassium concentration, but the use is experimental and not evidence-based.
 Mexiletine, a sodium channel blocker: In LQT3, the problem is that the sodium channel does not close properly. Mexiletine closes these channels and is believed to be usable when other therapies fail. It should be especially effective in LQT3, but there is no evidence based documentation.
 Amputation of the cervical sympathetic chain (left stellectomy). This may be used as an add-on therapy to beta blockers, but modern therapy favors mostly ICD implantation if beta blocker therapy fails.

 Arrhythmia termination

Is by placement of an implantable cardioverter-defibrillator (ICD). Also, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with syncopes despite beta blocker therapy, and in patients having experienced a cardiac arrest.

The risk for untreated LQTS patients having events (syncopes or cardiac arrest) can be predicted from their genotype (LQT1-8), gender, and corrected QT interval.
 High risk (>50%)
 QTc>500 msec LQT1 & LQT2 & LQT3 (males)
 Intermediate risk (30-50%)
QTc>500 msec LQT3 (females)
QTc<500 msec LQT2 (females) & LQT3
 Low risk (<30%)
QTc<500 msec LQT1 & LQT2 (males)

Thursday, July 19, 2012

What is the Diagnosis? Answer the questions below - Quiz 11

A 21 years old CPA student was last seen by you in ER with her usual palpitations about 2 years ago comes across you in a hospital hallway. You remember from that episode that the episode of palpitation was self-terminated on that occasion. On closer inquiry she tell you that the she has had several such episodes since then and during one such episode a forceful sneeze terminated her palpitations. Since then she has learnt to self terminate her palpitations by blowing the trumpet which she has in her garage. She is embarassed that she had to blow the trumpet once or twice in the middle of night. She asks for your advice. She also hands you over her ECG taken from one of the hospital visits which is shown below.

Quiz - Question - 16

Quiz Question - 11 - Choose single best answer.

1. What is the most probable diagnosis in this person given the clinical history and the ECG?
Antidromic atri-ventricular reciprocating tachycardia
Atypical atrial flutter with 2:1 conduction
Mahaim Fiber Tachycardia
Atrial tachycardia with block
Typical AVNRT.

The impulse travels down the slow pathway and up the fast one leading to pseudo r and pseudo s.

Thanks to for images and illustration.

Thursday, May 10, 2012

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Sunday, December 4, 2011

33 years old female who presents with 4 year history of intermittent palpitations. She has otherwise been healthy, palpitations can come on at anytime without any pro-dromal symptoms. Extensive testing has been negative including thyroid function and holter monitoring have failed to reveal the cause and reason for palpitations. She has had couple of near syncopal episodes associated with palpitations but never actually passed out.What is the Diagnosis?
The Lown-Ganong-Levine syndrome (LGL) is a clinical syndrome consisting of paroxysms of tachycardia and electrocardiogram (ECG) findings of a short PR interval and normal QRS duration.

LGL is usually categorized in a class of preexcitation syndromes that includes the

Wolff-Parkinson-White syndrome (WPW)
LGL, and
Mahaim-type preexcitation.

in WPW accesory bundle involved is called Bundle of Kent. But very little is know with regards to accessory conduction in LGL.

Theories proposed to explain LGL have centered around the possible existence of intranodal or paranodal fibers that bypass all or part of the atrioventricular (AV) node.

Criteria for LGL include a PR interval less than or equal to 0.12 second (120 ms), normal QRS complex duration of less than 120 ms, and occurrence of a clinical tachycardia.

Sunday, November 20, 2011


What is the diagnosis? answer the poll.

Ok the answer is - b - There is clear cut ST segment elevation in leads I and aVL which are high lateral leads. In the setting of RBBB the st-t changes in antero-septal leads can lead to lots of confusion. In this 12 lead ecg there is also presence of subtle st elevation in lead V2 and st depression associated with inverted of t wave in lead v3. Though Q waves present in v1-v2 are pretty close to be pathological but not quite. (1x1 broad and deep). However there is no denying the fact that presence of RBBB in the setting of acute MI is not a good sign, particularly anterior MI. Presence of st elevation in V2 lead alone is of some concern, but anatomically looking what can give you st elevation in lead v2 alone?, perhaps occlusion of a small septal perfusing v2 area?. Debatable. The diagnosis of a Q wave MI can be made relatively easily in the presence of right bundle branch block (RBBB - provided they are pathological). RBBB affects primarily the terminal phase of ventricular depolarization, producing a wide R' wave in the right chest leads and a wide S wave in the left chest leads. These changes are due to delayed depolarization of the right ventricle, while depolarization of the left ventricle is not affected. MI usually involves the left ventricle and therefore affects the initial phase of ventricular depolarization, sometimes producing abnormal Q waves. Thus, these patterns are combined when complete RBBB and a Q wave infarct occur together: • The QRS complex will be abnormally wide (0.12 sec or more) due to the bundle branch block. • Lead V1 will show a terminal positive deflection. • Lead V6 will show a terminal negative deflection (wide S wave). • If the infarction is anterior, there will be a loss of R wave progression with abnormal Q waves in the anterior leads and characteristic ST-T changes. • If the infarction is inferior, Q waves will appear in leads II, III and aVF. The net effect is that the criteria for the diagnosis of a Q wave MI in a patient with RBBB are the same as in patients with normal conduction. RBBB is typically associated with secondary ST-T changes due to abnormal right ventricular repolarization. As an example, leads with an R' wave (leads V1, V2, and sometimes V3) will show T wave inversions. However, ST depressions or T wave inversions in leads with a terminal S wave (leads V5 and V6) cannot be attributed to the RBBB alone. Such primary ST-T changes may be due to ischemia, or other factors such as drug effects or electrolyte abnormalities. The above point was well summarized in HERO-2 trial by Wong et al.. Please click the above link to access the editorial comment which briefly summarizes the paper.

Wednesday, November 16, 2011

ECG Quiz - 9. What is the diagnosis?

Ok, 66 yo caucasian with known CAD, had a stent placed 4 years ago. Comes in with light headedness ongoing and worsening for past 3-4 weeks. Postural changes in BP +. Clinical and labwork did not reveal any infective focus.Patient never took digoxin was on short acting beta blocker which he had stopped taking 2-3 days ago.

Correct answer is b - Sins rhythm (sinus tachycardia), complete heart block with ventricular escape. Often it can be difficult to discern if the escape pattern is junctional versus ventricular one way of answering this is via an EP study. However in this patient the ventricular rate is too slow to be coming anywhere above the HIS bundle and qrs duration is also slightly prolonged. EP study in this person showed appropriately functioning sinus node with normal SNRT with CHB. Escape was from below the HIS bundle thus confirming Infra-Hisian origin of the ventricular escape. 

Thursday, November 10, 2011

ECG Quiz-8

What is the diagnosis? Alright and the answer is!!!! - Normal sinus rhythm!!!! - please look at the speed at which the ECG has been recorded, normal speed is 50 mm/second this one has been recorded at 50 mm/second, double the normal speed. So calculating the heart rate = 300/No. of large squares X 2 = 600/10 = HR = 60. P waves beside each qrs complex suggests normal sinus rhythm overall.

Now you know why it is important not to ignore basics whilst reading ECG. First check at standardization which is 10mm=1mv and speed = 25mm/second.

5 of you got it right but Dr. Grauer got it right at the very beginning.

CONGRATS to all those who got the right answer!!!.

Wednesday, November 9, 2011

ECG Quiz-7 What does this ecg show?

What does the ECG above show?. Answer the poll above.

Ok - Answer is sinus rhythm with bi-ventricular pacing + bi-atrial enlargement. - CORRECT ANSWER - D

Looking closely at ECG there are two spikes close by just before the qrs complexes and no pacing spike before p wave. p waves in inferior leads are 2.5 small squares long and measuring the negative portion of p wave in lead v1 is > 1 small square indicating both right and left atrial enlargement.

Tuesday, November 8, 2011

Differentiating Types of Narrow Complex Tachycardia.

General approach to the differential diagnosis of narrow complextachycardia

STEP 1:Is the tachycardia regular or irregular?

If irregular,the differential is limited to:
o Atrialfibrillation
o Atrialflutter with variable block
o Multifocalatrial tachycardia: defined as tachycardia with 3 or more different p wave
If regular,go to STEP 2

STEP 2:Where is the p wave?

Lookcarefully for the presence of p waves- they are often embedded at the end ofQRS
complexes or within the T waveso always compare the tachycardia ECG to the NSR ECG to look
for subtle changes in QRS/Twave morphology (e.g. in cases of atrial tachycardia with 2:1 block,
undetected “hidden” p wavesmay lead to an incorrect diagnosis of sinus tachycardia)
If the p waveis identified, measure the RP interval
If the RPinterval is < ½ the RR interval, this is a SHORT RP tachycardia
If the RPinterval is > ½ the RR interval, this is a LONG RP tachycardia
If the p waveis NOT found, one can probably assume that it is embedded within the QRS and is
therefore a SHORT RPtachycardia

Differentialdiagnosis for short RP tachycardia

Typical AVNRT(AV nodal reentry tachycardia)
o Ischaracterized by a reentrant circuit within an AV node with dual pathway (slowand fast
pathways) physiology
o Most commonform of PSVT (50%)
o Rates usually150-250 bpm with abrupt onset and termination
o Typical AVNRTinvolves a circuit that goes down the slow conductionpathway of the AV
node and goes up the fast conductionpathway which results in a short RP (the retrograde p
is formed after impulsestravels up the fast pathway)
o AtypicalAVNRT involves a circuit that goes down the fast pathway andgoes up the slow
pathway which results in alonger RP interval than that which is seen with typical AVNRT
OrthodromicAVRT (Atrioventricular reentrant tachycardia)
o Ischaracterized by reentrant circuit that includes the atria, normal AVnode/His-Purkinje
system, the ventricles and anaccessory pathway
o OrthodromicAVRT describes a circuit that goes down the AV node His-Purkinjesystem
ventricles retrograde up theaccessory pathway atria
o This is indistinction to an antidromic AVRT that would go down theaccessory pathway to
the ventricles and up theAV node resulting in a wide complex tachycardia
o NOTE: AVRT is ashort RP tachycardia but the retrograde p wave tends to be embedded
within the ST-T wave segmentdue to the time it takes for the circuit to go through the
ventricles and accessorypathway; AVNRT on the other hand tend to have even shorter RPs
because the circuit is muchsmaller (retrograde p’s are often seen at the terminal portion of
the QRS complex)
Atrialtachycardia with 1st degree AV delay

Differentialdiagnosis for long RP tachycardia

AtypicalAVNRT (AV nodal reentry tachycardia)
o Again ischaracterized by a reentrant circuit within an AV node with dual pathway (slowand
fast pathways) physiology
CornellCardiology Curriculum 2003-2004 40
o In contrastto typical AVRT, atypical AVNRT involves a circuit that goes down the fast
pathway and goes up the slow pathway whichresults in a longer RP interval due to the
longer time it takes for theretrograde p wave to form with respect to the timing of ventricular
PJRT(permanent junctional reciprocating tachycardia)
o Ischaracterized by reentrant circuit that includes the atria, normal AVnode/His-Purkinje
system, the ventricles and aserpiginous posteroseptal accessory pathway that delays
retrograde conduction enoughto produce a long RP tachycardia (in contrast to AVRT)
o Tends to beincessant or near incessant
o Presentsoften in children or young adults
o Due toincessant nature of the tachycardia, patients may have tachycardia-induced
o Unliketypical retrograde accessory pathways, the posteroseptal accessory pathway inPJRT
tend to decremental conductionproperties
Sinus nodereentry tachycardia


Medical therapy
Always run 12lead rhythm strips when attempting the following maneuvers to documenttermination
of tachycardia
In generalany tachycardia whose mechanism involves a reentrant circuit that goes throughthe AV
node should respond to vagalmaneuvers, adenosine or other nodal blocking agents
Focal atrialtachycardia tend to be adenosine-sensitive as well (Iwai et al., 2002)
Vagalmaneuvers: carotid sinus massage (R carotid generally 10x more effective than Lcarotid),
Adenosine 6mg IV PUSH (can halve dose if it is being given through a centralvenous line); if no
effect, can repeat at 12 mg x1
Radiofrequency ablation (isoften curative)
AVNRT: canablate the slow pathway of the AV node to break re-entrant circuit
AVRT: canablate accessory pathway to break re-entrant circuit
Atrialflutter: typical atrial flutter can often be cured with catheter ablation bytargeting the slow
conducting isthmus of atrialtissue between the IVC and tricuspid annulus
PJRT: canablate posteroseptal accessory pathway

Iwai et al. Response toadenosine differentiates focal from macroreentrant atrial tachycardia.Circulation
2002; 106: 2793.
Jackman et al. Three forms ofatrioventricular nodal (junctional) reentrant tachycardia. In Zipes &Jalife,
ed. Cardiac Electrophysiology:From Cell to Bedside. 3rd ed. W.B. Saunders Company, Phildelphia, PA
Miles et al. Atrioventricularreentry and variants: mechanisms, clinical features and management. In
Waldo, AL. Atrial flutter:mechanisms, clinical features and management. In Zipes & Jalife, ed.Cardiac
Electrophysiology: From Cellto Bedside. 3rd ed. W.B. Saunders Company, Phildelphia, PA 2000.
Zipes & Jalife, ed.Cardiac Electrophysiology: From Cell to Bedside. 3rd ed. W.B. Saunders Company,
Phildelphia, PA 2000.

Sunday, November 6, 2011

Management Lessons 1 to 4

ECG QUIZ-6 What is the Diagnosis? - Look at ECG-5 below as well.

Take a look at this 78 years old male who had this ecg taken on a routine visit to the hospital. He is completely asymptomatic.

What is the dignosis? Answer the poll above. YOu can also leave comments in the comment section.

Ok answer is atrial Bigeminy - Do not get confused with the SA nodal exit block presented in quiz-5, take a close look at the  p wave morphology there are two distinct type of p waves one sinus and the other ectopic which fires just before the second sinus beat leading to pause of after the third beat. Pretty benign condition usually does not need any treatment.


Wednesday, November 2, 2011

ECG QUIZ - 5, What is the diagnosis?

66 yo male presents with occasional feeling of lightheadedness ongoing for past several years, no real syncopal episodes.

Look at the ECG above. What is the diagnosis?

Alright - this is Sino-Atrial Exit Block.

Sinoatrial (SA) exit block is simply the failure of the sinus impulse to escape the SA node and enter the atrial conduction tissue. Much like atrioventricular block (heart block), there are 4 possible types of SA block:
  • First Degree is not detectable on the surface ECG
  • Second Degree Mobitz Type I is characterized by group beating, a shortening P-P interval with a constant P-R interval, and a P-P pause interval less than twice the usual P-P interval
  • Second Degree Mobitz Type II is characterized by a constant P-P interval with a P-P pause interval being approximately a precise multiple (within 0.10 seconds) of the usual P-P interval
  • Third Degree is not detectable on the surface EC
  • So this is SA node exit block second degree type-I (Wenckebach) - note that the P-P pause interval is less than twice the usual P-P interval. If it was twice the size (or atkleast 0.10 seconds on either side the diagnosis would have been type-2 second degree).

Tuesday, October 25, 2011

Whats going on with this ECG? - 75 Years old Male With Palpitations and Light Headedness!!!

This is a 75 years old Caucasian male who presented with sudden onset palpitations and light headedness whilst driving on an inter-state!!!.

He decided to stop his car at a gas station and after about 10 minutes his palpitations went away and he decided to drive on again. After about 30 minutes palpitations returned!!!. This time he decided to drive to the nearby hospital and presented to our University hospital!!!.

Here are his ECGS'. Closely look at ECG 1 and ECG 2 and Rhythm Strip.

His first ECG below was obtained when he came into ER. Then whilst in ER he started having palpitations and his second ECG below was taken when he was actually having palpitations!!!, we were also lucky to obtain rhythm strip demonstrating onset and termination of his rhythm during his ER stay.

What is the diagnosis???

The ECG below was obtained when he arrived into ER.
The ECG below was obtained shortly after the first ECG when he started experiencing palpitations in ER.

This is his rhythm strip whilst in ER showing both initiation and termination of the rhythm.

Tuesday, October 18, 2011

Board Questions - Question - 1


Tuesday, September 27, 2011

ECG CASE - 2 and 3

 What is the diagnosis? same patient two eg's were taken within few minutes? Answer in 48 hours.
So the diagnosis is - Atrial Tachycardia. One may get confused looking at the ECG-1, there are PVC's and associated pause but second ECG looks more like a AVNRT. But the very fact that the PVC does not reset the AV node indicates that this is atrial tachycardia. Also notice that in both ECG's there are tiny p waves which are most easily seen in V1 to V3, also observe that the isoelectric segment between two p waves is fairly straight which makes the atrial flutter unlikely.

Also observe the rate of atrial tachycardia is typically between 100-240 (some authors argue that it should be 250 bpm) and anything beyond this is unlikely to be atrial tachycardia. Why? because to generate rates beyond 220 one requires some form of re-entrant mechanism!!!. And atrial tachycardia persists despite the atrio-ventricular block created by pause induced by the ectopic ventricular beat.

Alright now all about atrial tachycardia. 

Atrial tachycardia can occur in both structurally normal heart as well as structurally abnormal heart.

  1. Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute (bpm). 
  2. The atrial rhythm is usually regular. 
  3.  The conducted ventricular rhythm is also usually regular but may become irregular, often at higher atrial rates because of variable conduction through the AV node, thus producing conduction patterns such as 2:1, 4:1, a combination of those, or Wenckeback AV Block
The P wave morphology as observed on the ECG may give clues to the site of origin and mechanism of the atrial tachycardia.In the case of a focal tachycardia, the P wave morphology and axis depend on the location in the atrium from which the tachycardia originates. In the case of macroreentrant circuits, the P wave morphology and axis depend on activation patterns.

Multifocal atrial tachycardia (MAT) is an arrhythmia with an irregular atrial rate greater than 100 bpm. Atrial activity is well organized, with at least 3 morphologically distinct P waves, irregular P-P intervals, and an isoelectric baseline between the P waves. Shine et al first proposed this definition in 1968.[1] 

Multifocal atrial tachycardia has previously been described by names such as chaotic atrial rhythm or tachycardia, chaotic atrial mechanism, and repetitive paroxysmal MAT.

A number of methods are used to classify atrial tachycardia, including origin as based on endocardial activation mapping data, pathophysiologic mechanisms, and anatomy.

Based on endocardial activation, atrial tachycardia may be divided into 2 groups.

  1. The first is focal atrial tachycardia, which arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum.
  2. The second group is the reentrant atrial tachycardias. These reentrant (usually macroreentrant) atrial tachycardias most commonly occur in persons with structural heart disease, complex heart disease, and particularly after surgery involving incisions or scarring in the atria (see Clinical Presentation).
Atrial tachycardia may be classified according to the following pathophysiologic mechanisms: enhanced automaticity, triggered activity, or reentry (see Pathophysiology). Anatomical classification of atrial tachycardia is based on the location of the arrhythmogenic focus.

A 12-lead electrocardiogram (ECG) is an important tool to help identify, locate, and differentiate atrial tachycardia. Laboratory studies may be indicated to exclude systemic disorders that may be causing the tachycardia. Electrophysiologic study may be required.

Treatment - Acute Atrial Tachycardia:

The primary treatment during a bout of atrial tachycardia is considered to be rate control using AV nodal blocking agents, such as beta-blockers or calcium channel blockers (see Medication).

Cardioversion should be considered for any patient in whom the rhythm is not tolerated well hemodynamically and in whom rate control drugs are ineffective or contraindicated.

Radiofrequency catheter ablation for atrial tachycardia has become a highly successful and effective treatment option for symptomatic, medically refractory patients or those who do not desire long-term antiarrhythmic therapy.

See the images below depicting atrial tachycardia.