Sunday ECG ACADEMICs

Decoding the ECG in Brugada syndrome:A step towards understanding
By DR. D.P. KHAITAN,
MD (MEDICINE) FCGP (IND) FIAMS (MEDICINE) FICP FICCMD,FIACM, Gayajee, India
@EcgsOnly
@ecgandrhythmRoe @smithECGBlog

▪️In the normal ventricle , the epicardial and endocardial action potentials maintain a harmonious symmetry without disturbing the electrical field balance across the wall –translating on the surface ECG as an isoelectric ST segment , as a part imprint of cardiac electrical journey during repolarization.

▪️A different gesture exists with ‘Brugada syndrome’ , a genetically inherited ECG abnormality. Every Brugada pattern is a whisper of warning from the heart asking for decoding its waves on ECG and its recognition before the life is lost in silence.

▪️To decode Brugada is to hear the language of sodium current – the silent spark in the epicardial territory of RVOT as coved ST elevation in leads V1,V2 and V3 with a recognized pattern on ECG.

▪️The volcano of arrhythmia may erupt at any time , which can end the life suddenly

▪️Every clinician must be acquainted with this abnormal electrical activity occurring in the right ventricle with BrS , signifying its association with high risk of malignant ventricular
arrhythmias , a gigantic turmoil snatching the life from the sufferers

🔦Now see the attached ECG
Findings :

Coved ST elevation in V1-V2 > 2 mm.
This coved upper convex pattern with smooth , oblique descend into an inverted Twave – without an intervening gap in between two.

It is the hallmark of Type 1 Brugada pattern

Early repolarization (ERS) is seen in lateral chest leads V4-V6 as a overlap part.

Prolonged PR interval is also seen , most obvious over lead V3 indicating first degree AV block.

Comments :

Coved ST elevation in >2 mm in right precordial leads (V1-V2) is sufficient enoughto classify the pattern as Type 1 Brugada.

Early repolarization in lateral leads V4-V6 with BrS as an overlapping J-wave syndrome.

Prolonged PR interval here in association reflects extension of sodium channel dysfunction into the conduction system.

✈️Take Home Message

🚦Brugada syndrome (BrS) is fundamentally a channelopathy primarily due to loss-offunction mutations of the cardiac sodium channel (SCN5A → Naᵥ1.5), leading to
reduced INa and conduction delay, most pronounced in the right ventricular outflow tract (RVOT) epicardium.


🚦The RVOT epicardium exhibits a prominent Ito current, making it highly vulnerable to the loss of the action potential dome to the extent of its collapsing (prominent Ito
current reduces the activation of ICa current with the loss of dome pattern). Endocardium retains the dome, while the epicardium loses it, thereby creating a transmural voltage gradient during early repolarization.

🚦The resulting outward current (endo → epi) is directed toward the chest leads
(V1–V3), producing the characteristic coved-type ST-segment elevation available on the ECG to be interpreted.

🚦The basic diagnostic dictum in Type-1 Brugada syndrome – Coved-ST segment elevation > 2 mm > 1 of V1-3 , immediately merging with the following negative T-wave.

🚦Type 2 and Type 3 only serve as pointing clues ; pharmacological challenge with sodium channel blockers or high-lead replacement in needed to unmask the type 1
morphology if it is masked therein.

🚦The resultant transmural voltage gradient is the basis of re-entry mechanism providing the substrate for ventricular tachycardias, explaining the syndrome’s arrhythmogenic potential despite structurally normal hearts.

🚦Recognition of the ECG pattern in the background of clinical context, avoidance of sodium-channel blocking drugs, fever control, and use of ICD therapy in high-risk patients remain the cornerstone of management.

🚦Lastly to say the understanding of Brugada syndrome depends upon how much one grasps its electro-ionic basis , which transforms ECG pattern into a meaningful electrophysiological story.

Next🧵🧵 Keypoints
@EkgHacks @googledocs @medflutter_ @ECG_BUDDY_ARPI
o Brugada syndrome , first shared globally in 1992 by ‘Brugada brothers’ (Pedro, Josep, and Ramon, three Spanish cardiologists) is a major electrophysiological abnormality
causing sudden cardiac death (SCD) , syncope and even ventricular tachyarrhythmias in young population with no structural heart disease.

o There is a genetically determined ionic derangement over the right ventricular outflow tract (RVOT) epicardial cells to the extent of the loss of harmony in between EPI-ENDO action potentials , endangering the life by setting in of high degree of transmural voltage gradient which might result in ventricular tachyarrhythmias.

o By the further turning of the pages of history it was found to be first described in 1917 in the Philippines as Bengungut referring to sudden death in apparently healthy young males , occurring at night during sleep with revealing no pathological changes on
autopsy as the cause of death. The same disease entity was nomenclatured as ‘Laitai’ (‘death during sleep’) in Thailand, ‘Pokkuri’ (sudden and unexcepted ceased
phenomenon) death syndrome’ in Japan , ‘Dolyeonsa death syndrome’ in Korea , ‘Dream disease’ in Hawai or ‘Sudden Manhood Death Syndome’ in China .
All these nomenclatures indicate the occurrence of death during resting or sleeping hours , suggesting a possible association with Bradycardia and Vagal events.

These incidences point towards the occurrence of this unexplained nocturnal death syndrome in Southeast Asian ethnic group and it is also a fact that this entity is highly prevalent in this global zone.

2. Biostatistics
Its prevalence varies from one in five thousand to one in two thousand.

The age in diagnosis ranging from 2 days to 84 years. It is 8 to 10 times more prominent in males compared to females.

The incidence of SCD in young males is having the highest occurrence those under 40 years of age.

Women and elderly patients are considered to be in lower risk group.
In 1997, Brugada syndrome was recognized as an entity with sudden unexplained nocturnal death syndrome

The first genetic alteration was identified in 1998 (It is well known that BrS is consistent with an autosomal dominant inheritance having variable expressions).

Next🧵🧵🚦

CME INDIA Sunday ECG ACADEMICs

The Normal T-wave : A Path to Better Understanding
ByDR. D.P. KHAITAN,MD (MEDICINE) FCGP(IND) FIAMS(MEDICINE) FICP FICCMD,FIACM(Gayajee,Bharat)
@ECG_BUDDY_ARPI @ecgchallenge
@EcgsOnly @ecgandrhythmRoe
@smithECGBlog @EcgOxford @EkgHacks @link_ecg @NTFabiano
@TrackYourHeart @DFCapodanno
@escardio @JElectrocardiol @EcgImaging
Catching a wave and observing it with mindfulness is a meaningful metaphor. Waves rise and fall like tides, and it takes genuine effort to understand them.

By recognising their nature and characteristics, we become more acquainted with them. Every wave is a challenge unless and unit we don’t know about it fully.

The waves on ECG are a continuous disciplined series of depolarizing and replolarizing events. T-wave , the repolarizing wave needs a special reference.

The event of repolarization starts from the point where the depolarizing wave
QRS gets ended and then it moves towards the epicardium.

Epicardial cells repolarize earlier than endocardial cells , with its initial and rapid spread in the similar direction as that of the QRS complex – the result is a positive T-wave deflection.

🌼There is a dire need of being acquainted with the morphology of normal T-wave , then it would be possible to differentiate it from abnormal T-waves whenever they are met with.
Let us scan this ECG

Interpretation :

Positive T in V1 with more amplitude compared to that of V6. This indicates a high likelihood of coronary artery disease.

🚦What to Learn Today

▪️The T-wave is the repolarizing event on ECG , formed at the end of ST segment.

▪️Normal T-wave is slightly asymmetrical in shape, with a rounded apex that occurs closer to its end than its beginning.

▪️Exploring the fact leading to T-wave morphogenesis

▪️Normally the myocardial cells are having uniform and isotropic conductivity, practically with no or low dispersion , hence having no impact on the shape of the T-wave

▪️It is the rate of repolarization over the epicardium and endocardium which determines the asymmetrical nature of the T-wave.

▪️The descending limb of the T-wave is steeper because the rate of repolarization accelerates as the endocardium completes its recovery.

▪️T-wave amplitude < 5 mm in limb leads , <10 mm in precordial leads (10 mm males , 8 mm females) – usually one-tenth of the preceding R-wave amplitude.

▪️The width of T-wave is not measured by its width at the base , QTc measurement serves the purpose.
(QTc is directly proportional to the base-width of the corresponding T-wave)

▪️The T vector is oriented leftward , inferiorly and anteriorly over the frontal plane(normally T-wave vector ranges from +150 to +750)

▪️Since the repolarization starts first at the posterobasal region of the left ventricle , the T-wave polarity is tilted towards the left precordial leads i.e. T-wave polarity in lead V6 is larger than in V1. This entire concept is known as precordial T-wave balance.

▪️Loss of precordial T-wave balance (T-wave in V1 is larger than that in V6) usually indicates a high likelihood of coronary artery disease , and when new it implies acute ischemia.

🌄More Learning 🧵🧵 The T-wave is the repolarizing event on ECG , formed at the end of ST-segment.

When the phase of ventricular systole (coinciding with ST segment of phase 2 , as illustrated below) gets ended , there is a need of returning back to the initial polarized state of the cardiac
membrane.

In other words , it can be stated that this part of ventricular repolarization is the process by which the ventricular myocytes are returned to their positive resting potential , so that they can again restart the journey.

Normally , there is a cessation of Ca2+ inflow but with the continuation of K
+ ions outflow from intracellular compartment to extracellular compartment during the phase 3 , interrupting
| 2the isoelectric ST segment – the resultant situation causes upright T wave.

Sunday ECG ACADEMICS

Wellens’ Syndome : A Dynamic ECG Signature of Occlusion MI
A Narrative Review   DR. D.P. KHAITAN,
MD (MEDICINE) FCGP (IND) FIAMS (MEDICINE) FICP FICCMD
FIACM
@ECG_BUDDY_ARPI @EcgHackers
@EcgsOnly @ecgandrhythmRoe @smithECGBlog @EcgOxford @ecgchallenge
Two phenomena – protection and destruction have been chasing each other since time immemorial.

Protection keeps us alive and luminous in life– upholding our bio-tissues to run
smoothly with heroic strength.

On the contrary , the destruction does the reverse and the hour of adversity sets in life. These are two sides of the same coin.

The heart is shielded from the throttling grip of thrombosis in coronary circulation
through the process of auto-thrombolysis with reperfusion – but might be ruined
again by the gloomy blow with the recurrent thrombosis.

Thus , auto-thrombolysis is the comedy, while reocclusion is the tragedy.

So is the essence of Wellens’ syndrome – protection is chased by destruction.

A pre-infarction state may , in a cruel turn, progress into a full-blown infarction.

Let us scan ECG 1

This ECG was recorded in a middle aged smoker male with a preceding history of chest pain with Trop I negative.

Findings :

Biphasic T-wave with initial positivity and terminal negativity in leads V2-V3.

Absence of precordial poor R wave progression.

T-waves inversion in leads V4-V5 , also in lead aVL.

Discussion :

These T-wave changes are more widely spread along the precordial leads. Therefore ,
the lesion is more proximal in the LAD.

Since the lesion is admixture of both biphasic and negative T-wave in precordial leads, this indicates the lesion is progressing towards the next phase Type B.

Now ECG 2 in next thread... This ECG 2 shows :

Deeply inverted T-waves in leads V2-V6 with minimally elevated ST segment less than
1 mm.

The absence of precordial poor R wave progression

Troponin I : normal

Discussion :

The findings are consistent with Type B Wellens’ syndrome.

Now scan ECG 3 in next...