KNOW YOUR ECG G. Somasekhar MD DM FEp

Consultant Electro physiologist,

Aayush Hospital,

Vijayawada

CASE DETAILS

A 48-year-old female non hypertensive, non diabetic presented with history of shortness of breath class III in congestive heart failure.

H/O of intermittent palpitations with near syncope.

H/O of cardiovertion 6 to 7 times in another facility before transferring to us for further management.

Diagnosis of above ECG

1. Coarse Atrial fibrillation

2. Atrial flutter with variable blocks

3. Atrial fibrillation with preexitation

4. Ischemic Cardiomyopathy with Atrial

fibrillation

Correct Answer : Coarse Atrial fibrillation

Investigations

2D echo showed global hypokinesia with severe Left ventricular systolic dysfunction.

Coronary angiogram showed normal coronaries.

Patient received treatment with decongestive and rate control therapy with Amiodarone, Furosemide, Aldactone.

Subsequent ECG is depicted below.

What is the diagnosis?

1. Inferior wall ischemia with Complete AV block

2. Evolved Anterior wall MI with ventricular ectopics

3.Sinus pauses with acquired long qt causing Ventricular ectopics

4.Inferior wall MI with Ventricular couplets

Episodes recurred after stopping of amiodarone

Serum potassium was normal.

Tachycardia episodes stopped after overdrive temporary pacing.

Correct answer : As episodes recurred after stopping of amiodarone, we came to conclusion Polymorphic Ventricular tachycardia is secondary to acquired Long QT secondary to Sinus node dysfunction.

ECG showing occasional P waves (Astrick), junctional escape (Arrow), R on T ectopics by after depolarisations (Broad Arrow), Prolonged QT

> 600 m sec (Double Arrow)

Follow up

Due to financial constraints, we did permanent Atrial pacing at rate 90/min and started her back on Amiodarone as rhythm control strategy to prevent A fibrillation episodes.

ECG showing Atrial paced rhythm

SINUS NODE DYSFUNCTION VARIED MANIFESTATIONS

Pss choudary, Purna Chandra Rao Kondru,Gopalakrishna koduru, Somasekhar Ghanta

Polymorphic Ventricular tachycardia

Polymorphic Ventricular tachycardia is a ventricular

tachycardia where ECG changes in QRs amplitude axis and

duration which is commonly seen in setting of myocardial

ischemia.

Torsades pointes is a form of polymorphic VT seen in context

of Long QT, whether it be congenital or acquired.

Acquired long QT is commonly seen than congenital.

Commonly seen Long QT causing Torsades is secondary due

to drugs or dyselectrolytemia (Hypokalaemia,

hypomagnesemia, Hypocalcaemia).

Polymorphic Ventricular tachycardia

Sometimes Torsades can be precipitated in

congenital long QT cases by

dyselectrolytemia/drugs.

Bradycardia is also less common cause of acquired

long QT and so Torsades.

In cases of long QT, due to prolonged

repolarisations, early after depolarisations can be

seen which manifest as U waves and if reach

threshold can cause ventricular premature

contractions.

Polymorphic Ventricular tachycardia

It can harbinger polymorphic VT if Short long short

sequence supervenes whether by Atrial/

ventricular ectopic.

Polymorphic VT can sometimes degenerate to VF

and cause cardiac arrest.

Most common cause of death in CHB is

polymorphic VT due to bradycardia.

Present case - Conclusion

Here in the above case Sinus node dysfunction manifested as tachy brady syndrome and brady episodes manifested as sinus pauses with junctional escape, short coupled ventricular ectopics by early after depolarisations and due to prolonged QT early after depolarisations seen as R on T ectopics sometimes deteriorated to PVT and VF requiring cardioversion.

Over drive Pacing will shorten refractory period and QT interval treating such episodes.

Along with overdrive pacing we need to correct causes of bradycardia if it is due to drugs/ ischemia/ degenerative conduction system disease.

The END