Arrythmia Step 1

Is every P wave followed by a QRS complex? And every QRS preceded by a P wave? What is the PR interval and does it change?

What is the ventricular heart rate?

>100 bpm = tachycardia <60 bpm = bradycardia Are there extra beats? -> Ectopic Beats

Step 4 What is the QRS width?

Step 2 find the P waves.

If the QRS < 120ms (i.e. a narrow complex), then it is either a sinus arrhythmia,supraventricular rhythm or a junctional tachycardia. In tachycardias, this flowchart will lead to the right diagnosis.[1] If the QRS > 120ms it is either a ventricular tachycardia or a supraventricular rhythm with additional bundle branch block. This is a challenging diagnosis. Therefore a flowchart which incoporates the Brugada criteria for VT should be used.[2] Another method to discriminate VT from SVT has been proposed by Vereckei et al.[3]In that paper an excellent review is given on the subject by Dendi and Josephson.[4]

Do you see P waves? Leads II and V1 are often most suitable to find P waves. What is the rate of the P waves? What is the P wave morphology?

Step 3

What is the relationship between P waves and QRS complexes?

Is there a 1:1 relation between P waves and QRS complexes? If not there may beAV dissociation due to a Ventricular Arrhythmias or AV block

Supraventricular Arrythmia

Ventricular Tachycardia

Atrial fibrilasi

Atrial fibrillation can be catechorized as follows: First documented episode Recurrent atrial fibrillation: after two or more episodes. Paroxysmal atrial fibrillation: if recurrent atrial fibrillation spontaneously converts to sinus rhythm. Persisting atrial fibrillation: if an episode of atrial fibrillation persists more than 7 days. Permanent atrial fibrillation: if atrial fibrillation persists after an effort of electrical or chemical cardioversion

Treatment strategies include:

[3][4][5]

Rate control: accept atrial fibrillation and focus on symptom relief and prevention of tachycardias. Typically with beta-blockers and digoxin. Target rate is < 100 bpm. Rhythm control: trying to keep the patient in normal sinus rhythm. Typically with anti-arrhythmics like amiodarone, flecainide, and sotalol, or electrical cardioversion, or with radiofrequency catheter ablation.

In both cases anti-coagulants are needed to prevent embolic stroke.

Ventricular tachycardia can be catechorized as follows: Non-sustained VT: three or more ventricular beats with a maximal duration of 30 seconds. Sustained VT: a VT of more than 30 seconds duration (or less if treated by electrocardioversion within 30 seconds). Monomorphic VT: all ventricular beats have the same configuration. Polymorphic VT: the ventricular beats have a changing configuration. The RR interval is 180-600 ms (comparable to a heart rate of 100-333 bpm). Biphasic VT: a ventricular tachycardia with a QRS complex that alternates from beat to beat. Associated with digoxin intoxication and long QT syndrome.

Ventricular tachycardia can be difficult to diagnose when confronted with a wide complex tachycardia. A seperate chapter deals with ECG algorithms to analyze wide complex tachycardias.

Torsade de Pointes (TdP) is a form of polymorphic ventricular tachycardia associated with a long QT interval on the resting ECG. Torsade de Pointes is typically initiated by a short-long-short interval. A ventricle extrasystole (first beat: short) is followed by a compensatory pause. The following beat (second beat: long) has a longer QT interval. If the next beat follows shortly thereafter, ther is a good chance that this third beat falls within the QT interval, resulting in the R on T phenomenon and subsequent Torsades de Pointes. During Torsades de Pointes the ventricles depolarize in a circular fashion resulting in QRS complexes with a continuously turning heart axis around the baseline (hence the name Torsade de Pointes). Read the chapter on the Long QT Syndrome for [1] an list of causes. Also, a more rare form of short coupled Torsades de Pointes has been observed. Treatment
[2]

Withdrawal of any offending drugs and correction of electrolyte abnormalities (potassium repletion up to 4.5 to 5 mmol/liter). Acute and long-term cardiac pacing in patients with TdP presenting with heart block and symptomatic bradycardia. Intravenous magnesium sulfate for patients with QT prolongation and few episodes of TdP. Acute and long-term cardiac pacing for patients who have recurrent, pause-dependent TdP. Beta blockers combined with cardiac pacing as acute therapy for patients with TdP and sinus bradycardia. Isoproterenol as temporary treatment in patients with recurrent pause-dependent TdP who do not have congenital long QT syndrome.
[3]

There has been much debate in the Circulation journal among French and American scientist whether one should write Torsades de Pointes orTorsade de Pointes. As for now Torsade is prefered (unless one sees rotations around more than one axis in one episode), but both forms are used in similar [4] frequency.