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

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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

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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.

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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.


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Praveen Gupta

Ventricular flutter in a patient with anterior wall myocardial infarction

A 29 years old male who had the history of acute onset retrosternal chest pain of two hours duration, went to outside hospital.  The patient had the history of recently diagnosed diabetes mellitus and family history of coronary artery diseases.

ECG of the patient  is shown below

 
ECG is showing sinus tachycardia with a heart rate around 130 beats per minute, normal axis, PR interval of 160 msec, there is marked ST-segment elevation seen in lead V2-V6, I, avL, II, III, avF, QT interval of 320 msec suggestive of extensive anterior wall myocardial infarction.
Patient was immediately thrombolysed. ECHO suggestive of severe left ventricular systolic dysfunction. Post thrombolysis coronary angiogram of the patient showed mid LAD Total occlusion. PCI  with stenting to LAD done. Post PCI patient develops acute onset episode of palpitations and giddiness.

ECG of the patient after stenting

ECG is showing sine wave pattern with no clearly seen QRS complex or P wave or ST segment or T wave. Heart rate around 300 beats per minute so the ECG is suggestive of ventricular flutter.

Another ECG of the patient

ECG is showing ventricular flutter. The patient develops hypotension. The patient was immediately given DC shock, injection amiodarone, and CPR but he could not be revived and he died due to cardiac arrest.


Thank you

Praveen Gupta

Left ventricular hypertrophy with LV strain pattern

A 51 years old male who was a known hypertensive since last 10 years, came for routine evaluation. Patient ECG is shown below

ECG (Click on the image to enlarge it)

ECG is showing Sinus rhythm at rate 80 beats per minutes, PR interval 160 msec, QT interval 320 msec, there is ST-segment depression with T wave inversion seen in lead II, III, aVF, V5-V6, S wave height in V1 is 6 square boxes( 3 mv) and in V2 it is 9 squares boxes (4.5 mv), R wave height in lead V5 and V6 is 7 square boxes (3.5 mv) so, the sum of  S wave in lead V1 and V6 is 6.5 mv suggestive of concentric type of Left ventricular hypertrophy with left ventricular strain pattern. The patient underwent ECHO, which was suggestive of severe concentric left ventricular hypertrophy with grade 1 diastolic dysfunction.

Let's discuss ECG criteria for Left ventricular hypertrophy

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Praveen Gupta

WPW syndrome with atrial fibrillation

A 37 years old male came with the history of acute onset palpitation of two hours duration. Tachycardia ECG is shown below.

Tachycardia ECG (Click on the image to enlarge it)

ECG is showing broad QRS complex tachycardia, irregularly irregular @ 200 beats per minutes, No AV dissociation no fusion beats no capture beats seen, QRS is showing RBBB morphology in lead V1, variable QRS morphology, negative delta wave in lead II,III, avF,  Positive delta wave are seen in lead I, avL, V1 to V4 

ECG Diagnosis: Broad complex tachycardia, irregularly irregular suggestive

Differential diagnosis: Pre-excited tachycardia, Atrial fibrillation with underlying aberrancy.

Another tachycardia ECG of the patient

Another tachycardia ECG of the patient

Patient was given injection amiodarone but his tachycardia did not subside. DC cardioversion was done. Post cardioversion sinus ECG is shown below

Sinus ECG(Click on the image to enlarge it)

ECG is showing sinus rhythm @ 80 bpm, PR  60 msec, Left axis deviation, Negative delta wave seen in lead II, III, avF, Positive delta wave seen in lead V2-V5. Ecg is suggestive of WPW syndrome. As the delta wave is negative in lead 2, it is most likely pathway from coronary sinus diverticulum.
The patient underwent electrophysiological study which showed WPW syndrome with pathway originating from Coronary sinus diverticulum.

Lets discuss pathway localization for WPW syndrome.

Thank you

Praveen Gupta

Atrial flutter

A 64-year-old male came with a history of acute onset palpitation along with dyspnoea, orthopnea, and paroxysmal nocturnal dyspnoea. The patient was a known case of severe aortic valve stenosis with aortic valve regurgitation with moderate mitral regurgitation and was on medical follow up. ECG of the patient during tachycardia is shown below.

ECG is showing heart rate of 156 beats per minutes, narrow QRS complex, irregularly irregular, P wave is seen, RP interval is long then PR interval, there is ST segment depression in lead V4-V6, so the ECG is suggestive of  narrow QRS complex irregularly irregular, long RP tachycardia with visible P wave,  so the most likely differential diagnosis atrial tachycardia or atrial flutter with 1:1 AV conduction.

Another ECG Of the patient taken five minutes after first ECG

ECG is showing heart rate of 98 beats per minutes, irregularly irregular, there are P wave present which is of Sawtooth appearance, P wave is  positive in lead 2,3,avF, there is ST segment depression seen in lead I,II, III, V5,V6 so the ECG is suggestive of atrial flutter with variable block.

Lets discuss how to approach in a patient with narrow QRS complex tachycardia

Thank you

Praveen Gupta

Posterior wall myocardial infarction with inferior wall myocardial infarction

A 45 years old male came with the history of acute onset retrosternal chest pain of 3 hours duration. The patient was a chronic smoker. ECG is shown below

ECG 1

ECG is showing bradycardia with heart rate of 38 beats per minute, regular in nature, no clearly visible P wave seen, there is ST segment elevation in lead 2,3,avF with marked ST-segment depression in lead V1-V5, also in lead V6, there is prominent R wave seen in lead V2, V3 along with upright T wave seen in lead V2-V5.  ECG is suggestive of acute inferior wall myocardial infarction with posterior wall myocardial infarction with junctional bradycardia.

ECG 2

ECG is showing ST-segment elevation in lead 2,3,avF with marked ST-segment depression in lead V1-V4 also in lead V5, there is prominent R wave seen in lead V1- V4 suggestive of R/S ratio > 1 along with upright T wave in lead V2-V6, suggestive of posterior wall myocardial infarction. 

The patient was immediately started on streptokinase thrombolytic therapy. Post thrombolysis ECG is shown below.

 ECG 3 (Post thrombolysis)

 ECG after thrombolysis was still showing ST-segment elevation in lead 2,3,avF with ST-segment depression in lead V1-V5 suggestive of failed thrombolysis. The patient was immediately taken for Rescue PCI which was suggestive of Co-dominant coronary circulation with both RCA and LCX dominance with TIMI 3 flow so further intervention was deferred. The patient was started on medical therapy and planned for delayed Percutaneous intervention.

Little bit about Posterior wall myocardial infarction

Posterior wall myocardial infarction (MI) occur due to occlusion of either the left circumflex or the right coronary artery. It most commonly occur with acute inferior or lateral MI; but isolated posterior wall MI can occur. 

Electrocardiographic abnormalities suggestive of acute posterior wall MI include  (in leads V1, V2, or V3): 

(1) Horizontal ST segment depression

(2) Tall, upright T wave;

 (3) Tall, wide R wave

 (4) R/S wave ratio greater than 1.0 (in lead V2 only). 

Combination of horizontal ST segment depression with an upright T wave increased the diagnostic accuracy of these two separate electrocardiographic findings. 

The additional-lead electrocardiogram using left posterior thorax leads is potentially helpful; ST segment elevation greater than 1 mm in this distribution suggests an acute posterior wall MI

Reference
Brady WJ. Acute posterior wall myocardial infarction: electrocardiographic manifestations. The American journal of emergency medicine. 1998 Jul 1;16(4):409-13.
Thank you
Praveen Gupta

Inferior wall myocardial infarction with variable block

A 55 years old male came with a history of acute onset chest pain of 2 hours duration along with giddiness. The patient was a known case of diabetes mellitus and hypertension. Patient ECG is shown below.

ECG 1

ECG is showing bradycardia @ 36 beats per minute,  AV dissociation, P wave @ 100bpm, ST- segment elevation in lead II, III, avF, ST-segment depression in  avL, V2-V6 

ECG diagnosis: Acute ST-elevation myocardial infarction with complete heart block.

Another ecg of the patient taken after ten minute

ECG is showing dissociation of P wave and QRS complex suggestive of complete heart block. There is ST- segment elevation in lead II, III,avF with ST-segment depression in lead I, avL, V2-V6 

Diagnosis: Acute ST-elevation inferior wall myocardial infarction with complete heart block.

The patient was immediately thrombolysed and there is the resolution of ST-elevation and complete heart block after thrombolysis.

Thank you

Praveen Gupta

Left anterior fascicular ventricular tachycardia

A 23 years old male came with the history of palpitation of one-hour duration. There was no history of giddiness, syncope dyspnoea or past history of any heart diseases. ECG of the patient is shown below.

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

ECG is showing wide complex regular tachycardia at heart rate of 186 beats per minute, there is right axis deviation, QRS morphology is RBBB, QRS duration 200 msec, visible P wave are seen after QRS merged into the ST-segment, there was no capture beat no fusion beat seen, there was no AV dissociation seen. So ECG diagnosis was wide complex tachycardia with a possibility of either supraventricular tachycardia or ventricular tachycardia arising from left posterior fascicule.

 Sinus ECG of the patient

Sinus ECG is showing normal sinus rhythm at a rate around 78 beats per minutes, normal axis, No ST-T wave changes seen.

The patient underwent electrophysiological study which showed left anterior fascicular tachycardia. The patient underwent successful radiofrequency ablation.

Let's discuss how to approach in patient with wide complex tachycardia

A Little bit about Fascicular tachycardia.

Idiopathic fascicular left ventricular tachycardia (IFLVT) is the most common idiopathic ventricular tachycardia of left ventricle. It is characterized by right bundle branch block (RBBB) morphology and left axis deviation on the ECG. The QRS duration during the time of tachycardia is relatively narrow.  This tachycardia is highly sensitive to verapamil. It is originating near the posterior fascicle.

It occurs mainly in young adults (15 to 40 years) and mainly affects males (60-80%0. The patient most frequently present with paroxysmal episodes of palpitation. Although most episodes occur at rest, exercise, emotional stress, and catecholamine infusion can act as triggers.

Electrocardiographic features

Baseline ECG is normal in most patient though it may present T-wave inversion immediately after tachycardia (cardiac memory).

 IFLVT usually shows a QRS complex duration inferior to 140-150 ms and fast initial forces (RS interval of 60-80 ms). 

The ECG varies depending on the site of origin of the tachycardia:

1. Posterior fascicular ventricular tachycardia (P-IFLVT). It is characterized by right bundle branch block (RBBB) morphology and left axis suggesting that the exit of the circuit is located in the inferoposterior septum.It occurs in 90-95% of cases. 
2. Anterior fascicular ventricular tachycardia (A-IFLVT). It is the second variant in terms of frequency. Its ECG pattern typically shows RBBB morphology and right axis. The earliest activation has been described in the anterolateral wall of the left ventricle.
3. Upper septal fascicular ventricular tachycardia. This presentation is exceptional. As a general rule, it presents RBBB but a few cases with the morphology of left bundle branch block have also been described. 

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Praveen Gupta

Programming AICD

Problem associated with Drug eluting stent

Atrial fibrillation in a patient with inferior wall myocardial infarction

A 50 years old male came to the emergency with chief complaints of acute onset retrosternal chest pain radiating to left arm along with palpitation and perspiration. ECG of the patient is shown below.

ECG 1 (Click on the ecg to enlarge it)

ECG is showing heart rate of 120 beats per minute, irregularly, irregular, no visible P wave seen, left axis deviation, narrow QRS, there is 2-3 mm ST segment visible in lead II,III, avF, V5,V5 along with ST segment depression in lead I, avL so the ecg is suggestive of acute inferolateral wall myocardial infarction with atrial fibrillation.

ECG 2  (Click on the ecg to enlarge it)

.
Patient was successfully thrombolysed with injection streptokinase therapy after ruling out contraindication.

Final diagnosis of the patient is Inferior wall myocardial infarction with atrial fibrillation with successful thrombolysis.


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AVNRT presenting as Wide complex tachycardia

A 52 years old male came to the emergency with history of palpitation of one hour duration. There was no history of  Diabetes mellitus, hypertension or coronary artery diseases. ECG of the patient is shown below.

ECG 1(Click on the ecg to enlarge it)

ECG is showing wide QRS complex tachycardia at the rate of 230 beats per minutes, right axis, QRS is of RBBB morphology, after each qrs complex ?? small P waves were seen which were merged into the ST segment,RP interval is 80 msec, shorter than PR interval of 240 mse there is no Fusion complex, no capture beat. Also there is no AV dissociation. So the differential diagnosis of the ECG is either Atrioventricular nodal reentrant tachycardia (AVNRT) or Atrioventricular reentrant tachycardai (AVRT) or rare possibility of ventricular tachycardia (VT).

ECG 2 (Another tachycardia ECG of the patient) 

Sinus ECG

 
ECG is showing normal sinus rhythm at 90 beats per minute, normal axis, no significant ST-T wave changes seen.

Patient underwent Electrophysiological study which showed AVNRT with slow-fast pathway. Patient underwent successful slow pathway ablation.

Lets discuss how to diagnose AVNRT

Thank you.

Praveen Gupta

How to prepare for DM/MCH entrance exam: AIIMS/PGIMER/JIPMER/NEET All India

 How to prepare for DM/Mch entrance exam?. Available on amazon.com. 

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Dr. Praveen Gupta

Assistant professor

Department of Cardiology

VMMC & Safdarjung Hospital

New Delhi, India

WPW syndrome, left posterior pathway, intermittent pre-excitation

A 19 years old male came with the history of palpitation on and off since last six months.  There was no history of giddiness or syncope. Patient ECG is shown below.

ECG (Click on the image to enlarge it)

ECG is showing sinus rhythm at rate 64 beats per minutes, left axis (as lead I is positive and lead avF is equivocal) PR interval is 80 msecs, positive delta wave present in lead I, V1, negative delta waves are present in lead III,avF so the ECG is suggestive of pre-excitation with short PR interval or WPW syndrome. Now if we apply Arruda algorithm then because V1 is positive with R/S >1 so accessory pathway is located on the left side. Now because the lead avF is negative so the pathway is located in the left posterior or left posterolateral in location.

ECG of the patient was showing intermittent pre-excitation. The second ECG of the patient does not shows any pre-excitation. 

ECG 2(Click on the image to enlarge it)  

ECG is showing normal sinus rhythm at rate 110 beats per minute, normal axis, PR interval 160 msec, there is no evidence of any delta wave or pre-excitation in this ECG.

So the final diagnosis is WPW syndrome with left posterior pathway with intermittent pre-excitation.

Lets discuss how to localise pathway in WPW syndrome.

There are two algorithm.

First one

Another algorithm

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Praveen Gupta