JIPMER, Cardiology clinics

In this book, I am writing all the clinical cases discussed during my cardiology training at JIPMER, Pondicherry, India. There are theory question papers of cardiology at the end of this book.  This book is useful for DM cardiology residentss, MD medicine residents, MRCP cardiology residents, DNB Cardiology residents and or anyone who is preparing for any cardiology practical and theory exam.

Available of amazon

https://www.amazon.in/dp/B078LHRQB3/ref=sr_1_1?s=books&ie=UTF8&qid=1514171953&sr=1-1&keywords=JIPMER%2CCARDIOLOGY+CLINICS

Thank you

Praveen Gupta

Cardiology MCQ Book

Cardiology MCQ book 

released on Dec 22 December 2017

Available online on Bluerose publisher website (http://bluerosepublishers.com/product/64-cardiology-mcq-aiims-dm-cardiologydecember-2014-solved-paper/) Amazon, Flipkart, Shopclues. In this book I am going to discuss AIIMS, New Delhi, Dec 2014 cardiology DM entrance exam paper with colored picture, full explanation, and references

Thank you

Praveen Gupta

SVT with aberrancy

A 65-years old female came with a history of palpitation  since last 3 years.  Patient went to the local hospital and was diagnosed as a case of PSVT and was on oral medication.  Patient was a known case of Diabetes mellitus and hypertension for which she was on oral medication. There was no history of coronary artery diseases.

ECG during tachycardia (Click on the image to enlarge it)

ECG is showing broad complex regular tachycardia @ 200 beats per minute, QRS duration140 msec, QRS morphology is typical LBBB, Left axis deviation, no P wave seen, No AV dissociation, no capture beat, no fusion beat.

ECG diagnosis Broad complex regular tachycardia. 

Differential diagnosis: Ventricular tachycardia (Bundle branch reentrant tachycardia), or SVT with underlying aberrancy or  SVT (AVRT OR AVNRT)with rate related aberrancy or AVRT with accessory pathway conduction(Mahaim fiber tachycardia in view of LBBB morphology) or antidromic AVRT over the right accessory pathway.

However, in ECG there is no evidence of Brugada or avR criteria for VT seen. Also, morphological criteria for VT in the tachycardia ECG is not seen. The initial activation of the ventricle is rapid as evidenced by sharp activation in lead V1. All these favors SVT rather than a VT.

The patient was given injection adenosine, following which her tachycardia subsided. Sinus ECG is shown below.

ECG during sinus rhythm (Click on the image to enlarge it)

ECG is showing sinus rhythm at the rate of 82 beats per minute, normal axis, no ST-T wave changes seen.
The final diagnosis is SVT with aberrancy. The patient underwent an Electrophysiological study which showed Atrioventricular reentrant tachycardia with left-sided accessory pathway with orthodromic conduction. The patient underwent successful radiofrequency ablation. 

Let's discuss how to differential SVT with aberrancy from VT.

Thank you

Praveen Gupta

PSVT (AVNRT)

A 46 years old male came with a history of palpitation for the last 6 months. ECG during tachycardia is shown below.

ECG (Click on the image to enlarge it)

ECG is showing narrow QRS complex, regular tachycardia @ 200 beats per minute, normal axis, no P wave seen, no ST-T wave changes seen.  

Diagnosis of the ECG Narrow QRS regular tachycardia (Short RP tachycardia)

Differential diagnosis  Atrioventricular nodal reentrant tachycardia(AVNRT) or Atrioventricular reentrant tachycardia (AVRT) or Atrial tachycardia (AT).

Patient was given carotid massage, following which his tachycardia subsided. Post tachycardia ECG  is shown below.

ECG (Click on the ecg to enlarge it)

ECG is showing sinus rhythm @115 beats per minute, normal axis, PR interval of 160 msec, there are no other ST- T wave changes.

Patient underwent Electrophysiological study which showed AVNRT with dual AV nodal physiology with a Slow-fast pathway. The patient underwent successful radiofrequency ablation and later was discharged in stable condition.

Let's discuss how to approach in a patient with narrow QRS complex tachycardia

Thank you

Praveen Gupta

Trifascicular block with sinus bradycardia

 A70 years old female came with a history of giddiness since one week. She had a history of two episode of syncope with transient loss of consciousness over last one week. During the evaluation in the emergency, patient pulse was 40 beats per minute. Patient ECG is shown below.

ECG 1(Click on the image to enlarge it)

ECG is showing sinus bradycardia @ 48 beats per minute,  left axis deviation (LAD), rS complex in lead II, III, avF suggestive of left anterior hemiblock(LAHB), PR interval is 280 msec, suggestive of first degree AV block, QT interval is 560 msec, corrected QT interval is 501 msec, QRS complex of RBBB morphology, QRS duration120 msec, no other ST- T wave changes.  ECG is suggestive of trifasicular block. 

ECG 2 (Click on the image to enlarge it)

ECG is showing sinus bradycardia with a heart rate of 45 beats per minute, there is LAD, LAHB, RBBB. 

Diagnosis is Trifasicular block. Patient was put on single-chamber ventricular pacemaker (VVI)  in view of high-grade AV block and later discharged in stable condition.

Let's discuss Trifasicular block

Trifascicular block indicates conduction abnormality in all the three fascicles of cardiac conduction system (Right fascicle, left anterior fascicle and left posterior fascicle). It will manifest on the ECG in the form of RBBB with Left anterior hemiblock with prolonged PR interval or 1 degree AV block or RBBB with left posterior hemiblock with prolonged PR interval.

Thank you

Praveen Gupta

Pacemaker failure to capture

A 78-years old female came with a history of giddiness on and off and dyspnoea on exertion since last one week. She was also complaining of orthopnoea and paroxysmal nocturnal dyspnoea. Patient was a known case of diabetes mellitus and hypertension since last 20 years. The patient had the history of coronary artery diseases twenty years back for which she underwent CABG at outside hospital. Patient also had history of complete heart block for which she underwent pacemaker implantation (Medtronic ) with VVI mode 25years back. Patient had history of pacemaker battery replacement 4 years back. At the time of admission patient blood pressure was 178/100 mmHg, pulse was 40 beats per minute, Respiratory system examination showed right-sided basal crepitation, CVS S1S2 heard. ECG of the patient is shown below.

ECG (Click on the image to enlarge it)

ECG is showing pacemaker spikes with intermittent intrinsic QRS complexes, Ventricle rate @ 40 beats per minute, absence of QRS complex after few pacemaker spikes suggestive of there is proper pacing by pacemaker (in view of presence of pacemaker spikes) but loss of capture( as spikes are not followed by QRS complexes)

Another ECG of the patient without magnet (Click on the image to enlarge it)

ECG is showing the heart rate of 60 beats per minute. Pacemaker spikes are followed by QRS complex suggestive of both normal pacings, sensing and capture by a pacemaker.

ECG with magnet (Click on the image to enlarge it)

ECG is showing heart rate of 100 beats per minute with normal pacemaker pacing and capture.

Final diagnosis was intermittent failure to capture.

Patient pacemaker device interrogation was done which showed pacemaker battery lifespan of 8 months suggestive of End of life pacemaker with pacing threshold of 5.5V. The patient is presently planned for new pacemaker implantation.


Thank you

Praveen Gupta

Hyperkalemia induced high grade AV block

A 62-year-old female came with a history of giddiness and vomiting since last two days. Patient was a known case of diabetes mellitus and hypertension. Patient pulse during the time of admission was 24 beats per minute. Patient serum creatinine was 4, serum potassium was 6.6mq/dl. Patient ECG is shown below,

1 st ECG of the patient (Click on the ecg to enlarge it)

ECG is showing severe bradycardia with heart rate around 20 beats per minute, there is complete AV dissociation with atrial rate around 100 beats per minutes, QRS morphology is showing incomplete RBBB pattern, QT interval of 600 msec, corrected QTc of 346 msec, there are peaked, tall, tenting T wave of amplitude greater than QRS complex seen in lead V3-V6 so the ecg is suggestive of Complete heart block due to hyperkalemia. 

Patient was given hyperkalemia correction in the form of dextrose insulin drip, injection lasix, and calcium gluconate. Patient repeat ECG is shown below.

ECG of the patient

ECG is showing bradycardia with a heart rate around 50 beats per minute, there is a sudden loss of QRS complex for every 3rd P wave suggestive of 3.1 AV block suggestive of Mobitz type II AV block.

Repeat ECG of the patient after half an hour later of the second ECG 

ECG is showing normal sinus rhythm with tall tenting P wave in lead V2 only, with normal PR interval and RBBB block. Patient serum potassium during this time was 4.9.

Lets discuss ECG changes in hyperkalemia

In hyperkalemia earliest ECG changes seen is narrow and peaking T wave. There is a shortening of QT interval along with the widening of QRS duration. There is a decrease in the P wave amplitude along with prolongation of PR interval, which leads to second or third degree atrioventricular block. There will be a complete loss of P wave along with junctional escape rhythm or so
called sinoventricular rhythm.
In the latter instance, sinus rhythm persists with conduction between the sinoatrial and atrioventricular nodes and occurs without producing an overt P wave. Moderate to severe hyperkalemia occasionally induces ST elevations in the right precordial leads (V1 and V2), simulating an ischemic current injury or Brugada-type patterns. Very marked hyperkalemia leads to eventual asystole, sometimes preceded by a slow undulatory (or sine wave) ventricular flutter like pattern.


Thank you

Praveen Gupta