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Atrial Tachycardia

Atrial activity is most prominent in lead V1. Note that the P wave is closer to the next QRS
complex than the previous QRS complex; a socalled “long-RP tachycardia.
Atrial Fibrilation

Characteristic findings are the absence of P waves, with disorganized electrical activity in
their place, and irregular R-R intervals due to irregular conduction of impulses to the
ventricles.[1] At very fast heart rates (400- 600 bpm) atrial fibrillation may look more
regular which may make it more difficult to separate from SVT or ventricular tachycardia

Atrioventricular nodal reentrant tachycardia (AVNRT) is a common arrhythmia,

comprising approx 60% of cases of PSVT. Retrograde P waves are evident as deflections at the
junction of the QRS complex and ST segment. Pseudo S waves are evident in leads II, III, and
aVF, while pseudo R′ waves are seen in aVR and V1. narrow QRS complex with a rate between
130 and 240 beats per minute (BPM).
Wolf Parkinson White

ECG in a patient with WPW. Note the short PR interval and delta wave reflective of ventricular
pre-excitation. In this case, the pathway is right septal.
Antidromic AVRT

QRS morphology is wide and bizarre, an exaggeration of the delta wave seen during sinus
rhythm. Retrograde atrial activation is via the AV node, and is not evident in this tracing.

ECG in a patient with WPW who presented after a syncopal spell. AF is present, with
extremely rapid pre-excited QRS complexes. Cardiac arrest occurred moments after this
ECG was recorded. The patient was successfully resuscitated, and underwent successful
catheter ablation of a left septal pathway.
Atypical AVNRT

Note the deeply inverted P waves relatively close to the next QRS complex, a so-called
“long RP” tachycardia
Typical Atrial Flutter

Common atrial flutter with characteristic negative “sawtooth” flutter waves in leads II, III,
and AVF and positive flutter waves in V1. Atrial rate is 280/min with variable conduction
to the ventricle
Ventricle Premature Contraction

frequent PVCs in a pattern of ventricular bigeminy

NS Torsades de Pointes pada LQTS

Torsades de pointes PVT in a patient with acquired LQTS caused by quinidine therapy. Note
the recurrent paroxysms of NSVT following “long-short” sequences
Monomorphic VT

Monomorphic NSVT in a patient with underlying nonischemic cardiomyopathy and AF. Note
that the PVC that initiates NSVT has a different morphology than the subsequent salvo of NSVT
Polymorphic VT

Polymorphic NSVT in a patient with acute MI. Although the morphology is suggestive of
torsades, marked QT prolongation is absent. The etiology was believed to be acute ischemia.
Brugada syndrome
STEMI Inferior + VF
VT during Exercise

Young athlete with palpitations during exercise. Work-up was negative for structural heart
disease. During a treadmill exercise test, this rhythm was recorded. VT seemed to be triggered
by sinus rates above 160 BPM. The patient was treated with a beta-blocker, and was unable to
achieve this sinus rate. He has done well, without symptomatic VT recurrences
Accessory Pathway

Pre-excitation WPW Orthrodromic Antidromic