ECG

ESSENTIALS
BY DR ARYAN ARORA
MBBS – GOLD MEDALIST – 10/19 SUBJECTS
RANK 1 – ALL 4 MBBS YEARS
DISTINCTION – 16/19 SUBJECTS
NEET PG 2024 RANK (1ST ATTEMPT) – 1105
INICET MAY 2024 RANK (1ST ATTEMPT) – 513

COMPREHENSIVE ECG NOTES BASED ON

1. HARRISON’S PRINCIPLES OF INTERNAL MEDICINE – 21ST EDITON

2. ECG MADE EASY – JOHN HAMPTON

3. THE ONLY ECG BOOK YOU WILL EVER NEED – MALCOM S THALER
 HOW TO USE THIS?

THESE NOTES ARE AN ADJUNCT TO THE ABOVE-MENTIONED

TEXTBOOKS. ONLY IF YOU HAVE READ THE ABOVE BOOKS OR
HAVE A PRE- EXISTING THOROUGH KNOWLEDGE OF THE ECG,
THEN ONLY THESE WILL HELP YOU.

VIDEOS ADJUNCT TO THESE NOTES WILL ALSO BE COMING

OUT SOON

NOTE – THESE ARE IN NO SENSE THE REPLACEMENT OF ANY

TEXTBOOK.

FOR ANY CORRECTIONS/ADDITIONS KINDLY CONTACT –

INSTAGRAM –
@DOCTORMISNOMER
@DR.AARYYANN9

EMAIL - DRARYAN.ARORAPG96@GMAIL.COM
 CHAPTER 1 – BASICS OF ECG

ELECTRO-CARDIO-GRAM – GRAPH OF THE ELECTRICAL ACTIVITY OF THE HEART

ELECTRO-CARDIO-GRAPH – MACHINE USED TO RECORD THE ELECTRICAL ACTIVITY OF HEART

CELL AND CHARGE –

RESTING STATE DEPOLARISATION REPOLARISATION

WAVE MAKING –

1. POSITIVE CHARGE MOVES

TOWARDS POSITIVE
ELECTRODE
2. NEGATIVE CHARGE MOVES
TOWARDS NEGATIVE

POSITIVE WAVE

3. POSITIVE CHARGE MOVES

TOWARDS NEGATIVE
ELECTRODE
4. NEGATIVE CHARGE MOVES
TOWARDS POSITIVE
ELECTRODES
NEGATIVE WAVE
 5. POSITIVE ELECTRODE IN THE
MIDDLE –

A. POSITIVE CHARGE MOVES

TOWARDS POSITIVE
ELECTRODE
B. POSITIVE CHARGE MOVES
AWAY FROM POSITIVE
ELECTRODE

BIPHASIC WAVE

TYPES OF CELLS IN HEART –

CELL FUNCTION
1. PACEMAKER CELL STARTS THE ACTION POTENTIAL
2. CONDUCTING CELL FASTLY SPREAD THE ACTION POTENTIAL ➔
NARROW COMPLEX
3. MYOCARDIAL CELL SLOWLY SPREAD THE ACTION POTENTIAL ➔
WIDE COMPLEX

CONDUCTING SYSTEM –
 12 VIEWS OF THE HEART –

A. 6 LIMB LEADS B. 6 PRE- CORDIAL LEADS

- FRONTAL PLANE - HORIZONTAL PLANE

1. STANDARD LEADS/ 2. AUGMENTED LEADS/
EINTHOVAN LEADS GOLDBERGER LEADS
I, II, III AVR, AVL, AVF V1-V6

A. 6 LIMB LEADS –

1. STANDARD LEADS/ EINTHOVAN LEADS –

EINTHOVAN’S LAW –
LEAD I + LEAD III = LEAD II

2. AUGMENTED LEADS/ GOLDBERGER LEADS –

AUGMENTATION – 1.5 TIMES

COMBINATION –
B. PRE – CORDIAL LEADS –

➢ HOW TO PUT THE LEADS –

➢ EXTRA LEADS –

A. RIGHT SIDED LEADS FOR RV/INFERIOR WALL MI

B. POSTERIOR LEADS FOR POSTERIOR MI –

➢ VIEWS AND LEADS –

SUPER SUMMARY –

VIEW LEADS
1. ANTERIOR V1-V4
2. POSTEIOR/INFERIOR II, III, AVF
3. LEFT LATERAL V5, V6, I, AVL
4. RIGHT LATERAL AVR

ECG PAPER –

SPEED – 25 MM/S

(IF 50 MM/S = WIDE QRS COMPLEX = FACTITIOUS ECG)

GLOSSARY –

NON-ISO ELECTRIC LINES WAVES/COMPLEXES

ISO ELECTRIC LINE SEGEMENTS
WAVES/COMPLEX + SEGEMENT INTERVAL
WAVES OF ECG –

LEADS NORMAL P WAVE AMPLITUDE NORMAL T WAVE AMPLITUDE

LIMB LEADS < 2.5 MM < 5 MM
CHEST LEADS < 1.5 MM < 10 MM
BAZZET FORMULA =

NORMAL = ≤ 0.44 SECONDS

NORMAL IN MEN – 0.45 SECONDS

NORMAL IN WOMEN – 0.46 SECONDS

OTHER FORMULA –

1. FRAMHINGHAM FORMULA –

QTC = QT + 0.15 (1000 – RR)

2. FRIDERICIA FORMULA

3. HODGES FORMULA

➢ WHAT TO DO WITH QT INTERVAL WITH U WAVE –

A. SMALL U WAVE (< 1 MM) + NOT FUSED B. LARGE U WAVE (> 1 MM) + FUSED
WITH T WAVE WITH T WAVE
= CALCULATE QT INTERVAL = CALCULATE QU INTERVAL
INTERPRETATION OF ECG WAVES –

RHYTHM STRIP = LEAD 2

WAVE INTERPRETATION
1. P WAVE ATRIAL DEPOLARISATION

NO ATRIAL DEPOLARISATION SEEN ➔ DUE TO SMALL

AMPLITUDE (< 0.1 MV) – MASKED BY QRS

ATRIAL DEPOLARISATION SEEN IN –

A. ACUTE PERICARDITIS
B. ATRIAL INFARCTION
C. AV BLOCK

2. PR SEGMENT AVN DELAY = 0.10 SECONDS ➔ TO ALLOW BOTH ATRIA TO

CONTRACT ➔ COMPLETE FILLING OF VENTRICLE
3. QRS COMPLEX
1. Q WAVE = SEPTAL DEPOLARISATION

2. R WAVE = MAJOR VENTRICULAR DEPOLARISATION

3. S WAVE = BASE OF HEART DEPOLARISATION

Q WAVE – NORMALLY SEEN IN I/AVL/V5/V6 ONLY

MEANING OF QRS COMPLEX –

VARIANTS –

R WAVE PROGRESSION ➔

V1 → V6 (V5>V6) ➔ INCREASE IN AMPLITUDE

 POOR R WAVE PROGRESSION = R IN V3 < 3MM

1. AWMI
2. RVHT

TRANSITION ZONE ➔ V3/V4

4. ST SEGMENT INTERVAL B/W VENTRICULAR DEPOLARISATION AND

REPOLARISATION ➔ NO CURRENT FLOW

IF CURRENT FLOW + = INJURY CURRENT = MI

5. T WAVE VENTRICULAR REPOLARISATION

NOTE – 1ST REPOLARISATION BEGINS IN THE LAST AREA OF

DEPOLARISATION

6. U WAVE PAPILLARY MUSCLE REPOLARISATION

DISEASES WITH U WAVE –

1. HYPOKALEMIA
2. CNS DISEASE
3. PRECURSOR TO QT PROLONGATION
4. ANTI ARRYTHMICS – IA/III
 HOW TO CALCULATE HR?

Figure 2
Figure 1

CAUSES OF DOMINANT R WAVE IN –

V1 AVR
1. RVHT 1) DEXTROCARDIA
2. RBBB 2) TCA
3. PWMI 3) LEAD REVERSAL
4. HOCM 4) V. TACHYCHARDIA
5. DMD
6. V. TACHYCHARDIA
7. NORMAL IN CHILD
 CHAPTER 2 – DILATION AND HYPERTROPHY

NORMAL AXIS AND DEVIATION –

NORMAL AXIS = 0 – 90 DEGREE (PRECISE = -30 TO 100 DEGREE)

TO CALCULATE AXIS ➔ DO R – S IN LEAD I AND AVF

I AVF INTERPRETATION
+ + NORMAL
- + RAD
+ - LAD
- - EAD

CAUSES OF –

LAD RAD
1. NORMAL 1. NORMAL
2. LVHT 2. RVHT
3. LAF BLOCK 3. LPF BLOCK
4. INFERIOR MI 4. ANTERIOR MI
5. DEXTROCARDIA OR LEAD REVERSAL
 ➢ DIFFERENCE B/W HYPERTROPHY AND DILATION –

HYPERTROPHY DILATION
= INCREASED THICKNESS DUE TO ➔ PRESSURE = INCREASED CAVITY SIZE DUE TO ➔ VOLUME
OVERLOAD OVERLOAD
MC – VENTRICLE MC – ATRIA
THUS SEE – QRS COMPLEX THUS SEE – P WAVE
COMMON = INCREASED CELLS =

1. MORE TIME FOR CURRENT TO FLOW = INCREASED DURATION

2. INCREASED CURRENT = INCREASED VOLTAGE = INCREASED AMPLITUDE

3. AXIS DEVIATION

1. ATRIAL DILATION –

SEEN IN –

A. LEAD II = MAXIMUM POSITIVE DEFLECTION

B. V1 = BIPHASIC ➔ THUS EASY DEMARCATION

RA ENLARGEMENT LA ENLARGEMENT
1. KNOWN AS P – PULMONALE (MCC – COR P – MITRALE (MCC – MITRAL
PULMONALE) STENOSIS)

2. AMPLITUDE

A. LIMB LEAD INCREASED (> 0.25 MV) INCREASED (> 0.25 MV)
B. CHEST LEAD INCREASED (> 0.15 MV) INCREASED (> 0.15 MV)

DEEP & WIDE LA’S P WAVE

= P TERMINAL FORCE

3. DURATION SAME A. INCREASED (> 0.12 S)

REASON – B. DISTANCE B/W 2 PEAKS

AS ATRIAL DEPOLARISATION > 0.4 SECONDS
ENDS WITH LA DEPOLARISATION
C. LA DURATION > 0.4 S
4. AXIS DEVIATION RAD + (> 75) LAD + ( -30 TO -45)
5. ECG

2 INDICES IN MITRAL STENOSIS DEPECTING LA ENLARGEMENT –

1. MARCUZ INDEX 2. MORRIS INDEX

IN V1 – WIDTH X DEPTH = Z MM/S

P DURATION
PR SEGMENT DURATION

NORMAL – 1- 1.6 WIDTH = > 0.4 SECONDS

IN MS = > 1.6 DEPTH = > 2 MM

 2. VENTRICULAR HYPERTROPHY –

RVHT LVHT
1. LIMB LEADS A. LAD
RAD (MC CHANGE)
B. R (I) + S (III) > 25 MM

2. PRE-CORDIAL LEADS A. RBBB A. LBBB

B. R WAVE PROGRESSION B. R (V5/V6) + S (V1/V2)

IS LOST > 35 MM = SOKOLOV
LYON’S CRTIERIA
3. PRIMARY
REPOLARISATION
CHANGES/STRAIN
PATTERN = V1/V2 V5/V6
INDEPENDENT OF QRS
CHANGES –

A. ST DEPRESSION

B. GRADUAL T WAVE
INVERSION

DD OF STRAIN PATTERN –
I. ISCHEMIA
II. DIGOXIN
III. ELECTROLYTE
DISTURBANCES

OTHER CRITERIAS –

1. RVHT 2. LVHT
ALL INDICATE POOR R WAVE PROGRESSION

A. CORNELL – VOLTAGE CRITERIA – BEST

V1 V5/V6 CRTIERIA OVERALL =
A. R > 7 MM A) S > 7 MM
B. R/S > 1 B) R/S < 1 R (AVL) + S (V3) =
C) QRS – NORMAL
MEN > 20 MM
WOMEN > 28 MM

BUTTLER – LEGGET FORMULA – B. ROM – HILT SCORE

R (V1/V2) + S (V5/V6) – S (V1/V2) = > 7MM

 CHAPTER 3 – AVN AND AVN DISORDERS - CONDUCTION BLOCK

LOCATION OF AV NODE –

AT THE APEX OF TRIANGLE OF KOCH – AT RA ENDOCARDIUM

PARTS OF AVN = ELECTRICAL GATE KEEPER OF HEART -

A. COMPACT AV NODE B. LOWER NODAL BUNDLE

AV JUNCTION –

NOTE – TRANSITIONAL CELL ZONE ➔ HALLMARK – RECREMENTAL CONDUCTION – AS STIMULATION

➔ CONDUCTION DECREASES
FLOW –

SIZE OF AV NODE – 1 X 3 X 5 MM

FLOW –

COMPACT AV NODE ➔ PENETRATING AV BUNDLE ➔ TRAVERSE THE CENTRAL FIBROUS BODY AND
ANNULUS OF TV ➔ COMES OUT AS “BUNDLE OF HIS” ➔

A. RBB ➔ MODERATE BAND ➔ B. LBB ➔ PURKINJEE FIBRES

PURKINJEE FIBRES

BLOOD SUPPLY OF CONDUCTION SYSTEM –

BLOOD SUPPLY NERVOUS SUPPLY

1. SAN 60 % - RCA SNS/PSNS

40 % - LCA
2. AVN 90 % - RCA SNS/PSNS

10 % - LEFT CIRCUMFLEX
ARTERY

1% - 1ST SEPTAL PERFORATOR

OF LADA
3. BUNDLE OF HIS PDA AND LADA NO ANS SUPPLY
CAUSES OF CONDUCTION BLOCK –

CONGINENTAL ACQUIRED = “IF”

1. MATERNAL LUPUS I – IATROGENIC –

I. VALVULAR SURGERY – AV AND TV

II. ABLATIVE THERAPY
III. DRUGS – BCD
IV. RADIO/CHEMOTHERAPY
2. CHD I – ISCHEMIA = MI

INFERIOR MI (MC) ANTERIOR MI

1) RCA 1) LCA
2) AVN BLOCK 2) BOH/BB
BLOCK
3) NARROW 3) WIDE QRS
QRS
4) STABLE ➔ 4) UNSTABLE ➔
NO TEMP TEMP PACING
PACING
3. GENETIC – SCN5A I – INFECTION –

A. LYME’S DISEASE – MCC OF REVERSIBLE

3RD DEGREE BLOCK
B. IE + PERI VALVULAR ABSCESS
C. CHAGAS DISEASE
D. TOXOPLASMOSIS
E. VIRAL MYOCARDITIS
4. NM DISORDERS – I – INFILTERATIVE DISORDERS –

MYOTONIC DYSTROPHY / KEARN SAYRE A. HYPOTHYROIDISM

SYNDROME / ERBS DYSTROPHY B. AMYLOIDOSIS
C. SARCOIDOSIS
D. LYMPHOMA

I – INFLAMMATION –

A. ARF
B. SLE
C. SS
D. RA
I – INCREASED VAGAL TONE
F – FIBROSIS OF CONDUCTION TISSUE

– MCC OVERALL
 A. LEV’S B. LENEGRE
DISEASE DISEASE
1. OLD 1) YOUNG
PATIENTS PATIENTS
1. PROXIMAL 2) DISTAL BBB
BBB

C. CALCIFICATION OF ANNULUS – AV > MV

1. ATRIO – VENTRICULAR NODE (AVN) BLOCK –

BLOCK PR INTERVAL P: QRS DROPPED ECG

BEAT
1ST DEGREE BLOCK INCREASED 1:1 NO
(> 0.2 S)
= AVN DELAY QRS –
NORMAL

2ND DEGREE BLOCK

A. MOBLITZ KEEPS ON 4:3 YES

TYPE 1/ INCREASING
WENCKEBACH QRS –
BLOCK NORMAL

= AVN BLOCK

B. MOBLITZ SAME 3:2 YES

TYPE 2
QRS –
= INFRA NODAL WIDE
BLOCK COMPLEX
C. 2:1 BLOCK SAME 2:1 YES
 ➢ MOBLITZ TYPE 1 VS MOBLITZ TYPE 2 BLOCK –

MOBLITZ TYPE 1 MOBLITZ TYPE 2

1. COMMON MORE LESS
2. LOCATION AVN BUNDLE OF HIS
3. NATURE BENIGN ➔ DOESN’T GO SERIOUS ➔ AS IT GOES
INTO 3RD DEGREE HEART INTO 3RD DEGREE HEART
BLOCK ➔ NO PACEMAKER BLOCK ➔ PACEMAKER YES
4. VAGUS INCREASES THE BLOCK DECREASES THE BLOCK
STIMULATION

2. 3RD DEGREE BLOCK / COMPLETE HEART BLOCK –

PATHOGENESIS –

NO CONDUCTION FROM ATRIA → VENTRICLE ➔ ESCAPE RHYTHM – JUNCTIONAL OR VENTRICULAR

➔ ATRIA CONTRACT AT DIFFERENT RATE AND VENTRICLE AT DIFFERENT RATE = AV DISSOCIATION

NOTE – LOWER IN CONDUCTION SYSTEM ESCAPE RHYTHM OCCURS ➔ LOWER RELIABILITY IT HAS

NORMAL P-P INTERVAL

NORMAL R-R INTERVAL
ABNORMAL P-R INTERVAL
CLF = STOKES ADAM SYNDROME –

COMPLETE HEART BLOCK ➔ DECREASED CO ➔ CEREBRAL ANOXIA ➔ ANOXIC SEZUIRE ➔ ESCAPE

RHYTM ➔ NORMALISES CO ➔ RECOVERY
 BUNDLE BRANCH BLOCKS

TYPES –

1. FIXED 2. INTERMITTENT/RATE RELATED

AS HR INCREASES ➔ CELLS STILL IN
REPOLARISATION ➔ BLOCK PATTERN

NOTE – BBB AFFECTS – QRS COMPLEXES ➔ THUS, DIFFICULT DIAGNOSIS OF MI AND HYPERTROPHY

CAUSES –

RBBB LBBB
1. NORMAL
2. MI 1. MI
3. RVHT 2. LVHT
4. ASD 3. HOCM
5. MYOCARDITIS 4. DIGOXIN
6. DEGENERATIVE DISEASE OF
CONDUCTION SYSTEM = LEVS AND
LENEGRE DISEASE

COMMON FINDING ➔ DUE TO BLOCK ➔ EARLY ACTIVATION OF ONE CHAMBER AND DELAYED
ACTIVATION OF OTHER CHAMBER =

WIDE QRS COMPLEX= > 0.12 SECONDS

COMPLETE VS INCOMPLETE BBB –

COMPLETE BBB INCOMPLETE BBB

QRS DURATION >0.12 SECONDS 0.11 – 0.12 SECONDS

DD – PACING –

RIGHT VENTRICULAR PACING BI- VENTRICULAR PACING

LBBB PATTERN RBBB PATTERN
 RBBB LBBB
1. PATHOGENESIS RBBB ➔ COMPENSATORY LEFT → RIGHT LBBB ➔ COMPENSATORY RIGHT → LEFT
DEPOLARISATION DEPOLARISATION

2. V1/V2 M PATTERN/RABBIT EARS/RSR’ PATTERN W PATTERN/ DEEP S WAVES

3. V5/V6 (& I/AVL) W PATTERN/ DEEP S WAVES M PATTERN/RABBIT EARS/RSR’ PATTERN

4. SECONDARY V1/V2 V5/V6 (& 1/AVL)

REPOLARISATION
ABNORMALITIES
= OPPOSITE TO QRS
COMPLEX –

ST DEPRESSION AND
GRADUAL T WAVE
INVERSION
5. AXIS DEVIATION ABSENT LAD +

6. MNEMONIC
 HEMIBLOCKS (OBVIOUSLY AT LEFT SIDE)

LAF BLOCK LPF BLOCK

PATHOGENESIS DEPOLAIRSATION WAVE FROM ➔ DEPOLARISATION WAVE FROM ➔
INFERIOR → SUPERIOR SUPERIOR → INFERIOR

AXIS LAD RAD

DEVIATION
COMMON MORE LESS

DUE TO –
A. THIN AND LONG
B. MORE BLOOD SUPPLY
POSITIVE QRS I/AVL/V5/V6 II/III/AVF
COMPLEX

NEGATIVE QRS II/III/AVF I/AVL/V5/V6

COMPLEX

QRS/ST NOT PRESENT

SEGMENT/T
WAVE CHANGE

SEEN WITH NORMAL AND DISEASED HEARTS DISEASED HEARTS

MCC OF MARKED LAD IN ADULTS

NOTE – BEFORE DIAGNOSIS OF HEMIBLOCKS ➔ R/O OTHER CAUSES LAD/RAD

 A. BIFASICULAR BLOCK
=

A. RBBB + LAF BLOCK B. RBBB + LPF BLOCK

B. TRI FASICULAR BLOCK

=
RBBB + LAF BLOCK + LPF BLOCK
=
3RD DEGREE BLOCK> 1ST/2ND DEGREE BLOCK + BIFASICULAR BLOCK

DIAGNOSING MI IN PRESNCE OF LBBB –

SGARBOSSA CRITERIA

ST ELEVATION ST DEPRESSION
CONCORDANT >1 MM (5 POINTS) >1 MM IN V1-V3 (2 POINTS)
DIS CORDANT >5 MM (3 POINTS) -
DIAGNOSIS SCORE > 3

NOTE – SECONDARY REPOLARISATION ABNORMALITIES = QRS & ST-T DISCORDANCE

➔ IN VENTRICULAR PACING

➔ IS K/A CARDIAC MEMORY EFFECT

APPROACH TO THE PATIENT –
 ➢ NODAL VS INFRA NODAL BLOCK –

NODAL BLOCK INFRA NODAL BLOCK

1. VAGAL STIMULATION INCREASES THE BLOCK DECREASES THE BLOCK

2. ATROPINE/ISO DECREASES THE BLOCK INCREASES THE BLOCK

PRENALINE /
EXERCISE

➢ HIS BUNDLE ECG –

PROCEDURE – CATHETER AT SUPERIOR MARGIN OF TV ANNULUS

HIS BUNDLE ECG –

AH INTERVAL HV INTERVAL

= CONDUCTION VIA AV NODE = INFRA NODAL CONDUCTION

INCREASE AH INTERVAL = NODAL BLOCK INCREASED HV INTERVAL = INFRA NODAL BLOCK

NOTE – INCREASED HV INTERVAL ➔ > 100 MS ➔ INCREASE RISK OF PROGRESSION TO HIGHER

GRADE BLOCKS ➔ 10% RISK OF COMPLETE HEART BLOCK ➔ THUS INDICATION OF PACEMAKER
TREATMENT –

1. TEMPORARY PACING –

INDICATION –

A. BASED ON SYMPTOMS
B. BASED ON HEMODYANMIC STATUS
C. BASED ON LEVEL OF BLOCK

TYPES –

1. TRANS CUTANEOUS PACING 2. TRANS VENOUS PACING

LESS STABLE MORE STABLE

CATHODE – APEX OF HEART = LEFT INFRA MAMMARY AREA

ANODE – B/W LEFT SCAPULA AND SPINE

 2. PERMANENT PACING –

CLASS - 1 CLASS - 2A CLASS - 2B

A) CHB A. SYMPTOMATIC A. ASYMPTOMATIC 1ST
MOBLITZ TYPE 1 BLOCK DEGREE BLOCK + NMD

B) MOBILITIZ TYPE 2 B. SYMPTOMATIC 1ST

DEGREE BLOCK

C) INFRA NODAL BLOCK B. ASYMPTOMATIC 1ST

DEGREE BLOCK +
LAMININ A/C DEFECT

D) WIDE QRS COMPLEX + C. ASYMPTOMATIC BI/TRI

2/3 DEGREE BLOCK FASICULAR BLOCK +
INTERMITTEN CHB/
MOBLITZ TYPE 2 BLOCK

E) SYMPTOMATIC BI OR
TRI FASICULAR BLOCK

F) MOBLITZ TYPE 1 BLOCK

+ NMD/ LAMININ A/C
DEFECT

PHYSIOLOGICAL PACING OF VENTRICLE = > 40 % TIME – VENTRICULAR PACING

INDICATION – EF < 50 % + AV BLOCK

TECHNIQUE –

METHOD AREA
1. CRT ADD LEAD IN LEFT BRANCH OF CORONARY
SINUS ➔ SIMUTANEOUS RV + LV
OR CONTRACTION

2. HIS BUNDLE PACING TV ANNULUS

OR

3. LBB AREA PACING PROXIMAL IVS REGION

 CHAPTER 4 – PRE-EXCITATION SYNDROMES

HALLMARK = ABNORMALITY DISAPPEARS DURING EXERCISE AS AVN CONDUCTION >>> CONDUCTION

VIA ACESSORY PATHWAY

ASSOCIATION OF PRE- EXCITATION SYNDROMES WITH –

1. EBSTIEN ANOMALY
2. HOCM WITH – PRKAG2 MUTATION
3. DANNON’S DISEASE
4. FABRY’S DISEASE

NORMAL ABNORMAL
AVN DELAY (0.10 S) ➔ DUE TO TRAVEL VIA AVN NO DELAY ➔ DUE TO TRAVEL VIA ACCESSORY
PATHWAY
= PR SEGMENT/INTERVAL- NORMAL = PR SEGMENT/INTERVAL – SHORT ➔ PRE-
EXCITATION SYNDROMES

TYPES OF ACCESSORY PATHWAYS –

BUNDLE OF KENT JAMES FIBRES

1. NAME OF PRE- WOLF – PARKINSON WHITE (WPW) LOWN – GANONG – LEVINE
EXCITATION SYNDROME (LGL) SYNDROME
SYNDROME
2. LOCATION OF INTRA NODAL ➔ THUS,
ACCESSORY A. TYPE A = LEFT SIDED (LA ➔ LV) BYPASS THE AV NODE
PATHWAY – MOST COMMON

B. TYPE B = RIGHT SIDED (RA ➔

RV)

OTHERS – POSTERO SEPTAL > ANTERO

SEPTAL

3. DIAGRAM
4. PR INTERVAL BY PASS THE AVN ➔ SHORT PR BY PASS THE AVN ➔ SHORT
INTERVAL PR INTERVAL

5. DELTA WAVE THEN CURRENT CONDUCTIONS VIA THEN CURRENT CONDUCTS

ABNORMAL PATHWAY ➔ PREMATURE VIA NORMAL PATHWAY ➔
ACTIVATION OF VENTRICULAR NO PRE-MATURE
MYOCARDIUM ➔ DELTA WAVE ACTIVATION OF
VENTRICULAR
MYOCARDIUM ➔ NO DELTA
WAVE

6. QRS COMPLEX ➔BROAD QRS COMPLEX ➔NORMAL QRS COMPLEX

7. SECONDARY ➔ST SEGMENT DEPRESSION AND ➔NORMAL ST SEGEMENT
REPOLARISATIO GRADUAL T WAVE INVERSION AND T WAVE
N OPPOSITE TO QRS COMPLEX
ABNORMALITY
8. BBB A. LEFT SIDED – RBBB NORMAL

B. RIGHT SIDED – LBBB

9. ECG

10. TOC RF/CATHETER ABLATION

NOTE –

ATRIAL – FASICULAR PATHWAY = MAHAIM FIBRES

➔ CONNECT RA → RBB
➔ PRE-EXCITATION OF RV + LBBB PATTERN
COMPLICATION OF WPW SYNDROME –

= ARRYTHMIAS

WHY? –

AS BOK IS

1. FAST CONDUCTION
2. BUT – HIGH REFRACTORY PERIOD

THUS, NORMAL SINUS RHYTHM ➔ ATRIAL PMB ➔ RE- ENTRY CIRCUIT

A. ORTHO-DROMIC AVRT B. PRE-EXCITATION

TACHYCHARDIAS

TYPES MC TACHYCARDIA ASSOCIATED WITH

ACCESSORY PATHWWAY 1) ANTI- DROMIC AVRT –
MC TYPE OF PRE-
EXCITATION
TACHYCARDIA

2) PRE-EXCITED ATRIAL
TACHYCHARDIAS –

A.FIB/A.FLUTTER/AVNRT ➔
CONDUCTS VIA BYSTANDER AP ➔ RR
INTERVAL < 0.25 S ➔ CONVERTS TO
V.TACH/V.FIB

ECG OF PRE EXICTED A.FIB –

1. IRREGULARLY – IRREGULAR
RHYTHM
2. WIDE QRS COMPLEX
3. BIZZARE QRS COMPLEX –
BEAT TO BEAT CHANGE

CI = AVN BLOCK ➔ AS IT DOESN’T

PASSES VIA AVN & WORSENS IT.

DOC – IV PROCAINAMIDE/ IV
IBUTILIDE

TOC – CARDIOVERSION
 PATHOGENESIS STARTS VIA AVN ➔ ACTIVATION OF STARTS VIA VENTRICLE ➔
BOH AND PURKINJEE SYSTEM ➔ ACTIVATION OF AVN ➔
ACTIVATION OF ATRIA ACTIVATION OF ATRIA
P WAVES RETEROGRADE P WAVES RETEROGRADE P WAVES
& &
AFTER QRS BEFORE QRS

THUS PR INTERVAL >>> RP INTERVAL

DELTA WAVE ABSENT PRESENT
QRS COMPLEX NORMAL DURATION WIDE COMPLEX
AVN BLOCK WILL TERMINATE IT SINCE IT PASSES VIA AVN

NOTE – RETEROGRADE CONDUCTION VIA SLOW ACCESSORY PATHWAY ➔ MC IN SEPTAL REGION

➔ RE- ENTERY CIRCUIT

➔ PERMANENT JUNCTIONAL RECIPROCATING TACHYCARDIA
➔ TACHYCARDIA INDUCED CARDIOMYOPATHY
➔ IOC – EP STUDY
MANAGEMENT OF ACCESSORY PATHWAYS –
 CHAPTER 5 – MYOCARDIAL INFARCTION

1. T WAVE 2. ST SEGMENT 3. Q WAVE

1. DIAGNOSTIC ISCHEMIA INJURY INFARCTION
OF
2. REPRESENT REVERSIBLE CHANGE IRREVERSIBLE
CHANGE
3. EARLY HYPERACUTE T WAVES ELEVATION = PARDEE -
= BROAD TALL T SIGN
WAVES
FUSION OF T WAVES +
DD – J POINT ST SEGMENT = DOME
ELEVATION – SHAPED/CONVEX
SHAPE
A. NO FUSION
B. NORMAL T
WAVE
4. LATE SYMMETRICAL T NORMAL DEEP Q WAVES
WAVE INVERSION

PERSISTANT ST ALWAYS LOOK FOR

ELEVATION = RECIPROCAL CHANGES
VENTRICULAR IN DIAGONALLY
ANEURSYM OPPOSITE LEADS

SIGNIFICANT DEEP Q WAVES/PATHOLOGICAL Q WAVES –

1. AMPLITUDE 2. DURATION
A. >25% OF R WAVE >0.04 SECONDS
B. > 2 MM
 FUNDA OF DEEP Q WAVES –

DD OF DEEP/PATHOLOGICAL Q WAVES –

1. MI –

A. FULLY EVOLVED ACUTE MI – WITH ST-T CHANGES

B. OLD MI – W/O ST-T CHANGES

2. HOCM

3. LEAD REVERSAL

4. ROTATION OF HEART/ DEXTROCARDIA

DEFINATION OF ST ELEVATION IN MI – IN >2 CONTIGOUS LEADS – AMPLITUDE –

LIMB LEADS - > 1 MM

CHEST LEADS – > 2 MM

FUNDA OF ST SEGMENT ELEVATION AND DEPRESSION – CONCEPT OF CURRENT OF INJURY

FUNDA OF RECIPROCAL LEADS –

 ➢ TYPES OF INFARCTS –

STEMI NSTEMI
CAUSE TRANS MURAL INFARCT SUB ENDOCARDIAL INFARCT
ST SEGMENT ELEVATION DEPRESSION
T WAVE INVERSION INVERSION

➢ Q WAVE VS NON-Q WAVE INFARCTION –

Q WAVE INFARCTION NON-Q WAVE INFARCTION

INITIAL MORTALITY MORE LESS
RISK FOR FURTHER INJURY LESS MORE

➢ NON-Q WAVE INFARCTION VS ANGINA –

NON-Q WAVE INFARCTION ANGINA

1. ST SEGMENT DEPRESSION DEPRESSION

EXCEPT – ELEVATION IN
PRINZMETAL ANGINA
2. ST SEGMENT AFTER 48 HOURS IMMEDIATELY
NORMALISES
3. T WAVE INVERSION INVERSION
4. ENZYMES RAISED NORMAL

WELLEN’S SYNDROME –

WHAT IS IT?

SEVERE LADA BLOCK ➔ UNSTABLE ANGINA ➔

ECG DURING ATTACK ECG NOT DURING ATTACK

ST SEGMENT ST DEPRESSION ST – NORMAL
T WAVE T WAVE INVERSION TYPE A WELLENS – BIPHASIC T
WAVES

TYPE B WELLENS – DEEP T

WAVES

IN V2- V3

SIGNIFICANCE – SEVERE ANTERIOR WALL ISCHEMIA

➢ LOCALISATION OF INFARCT –

TYPE OF MI LEADS ARTERY

1. ANTERIOR MI V1-V4 LADA ➔ ANTERIOR
INTERVENTRICULAR ARTERY
ASSOCIATED WITH – LOSS OF R
WAVE PROGRESSION
2. LATERAL MI V5, V6, I, AVL LEFT CIRCUMFLEX ARTERY
3. ANTERO-LATERAL MI / V1- V6 + I, AVL LEFT CORONARY ARTERY
EXTENSIVE ANTERIOR
MI / WIDOW MAKER
4. INFERIOR MI II, III, AVF RCA

NOTE – Q WAVE LASTS ONLY

FOR 6 MONTHS
5. POSTERIOR MI V7, V8, V9 – ST ELEVATION RCA ➔ POSTERIOR
INTERVENTRICULAR ARTERY
OR

RECIPROCAL CHANGE IN V1 –
V3 = ST ELEVATION
EQUIVALENT ACS (SEACS)

1. TALL R WAVE IN V1-V3

2. ST DEPRESSION IN V1
– V3
3. R/S > 1 IN V1-V3
6. RIGHT VENTRICULAR V3R-V6R – ST ELEVATION
MI
OR

ST ELEVATION IN LEAD –

A. V1/V2
B. III> II
DD OF ST SEGMENT ELEVATION –

E ELECTROYLTE – HYPERKALEMIA
AND HYPER CALCEMIA
L LBBB
E EARLY REPOLARISATION – J POINT ELEVATION
V VENTRICULAR ANEURYSM
A A. ANTI – ARRYTHMICS – IC
B. AFTER DC CARDIOVERSION
C. ACUTE PULMONARY EMBOLISM
T TAKATSOBU CARDIOMYOPATHY
I A. INFARCTION – MI = STEMI

B. INFLAMMATION – PERCARDITIS AND

MYOCARDITIS

C. INJURY – MYOCARDIAL INJURY

O OSBORN WAVE
N NON ARTHEROSCLEROTIC ANGINA –
VASOSPASTIC ANGINA

MC AFFECTS – RIGHT CORONARY ARTERY

S SCD ➔ DUE TO BRUGADA SYNDROME

DD OF ST SEGEMENT DEPRESSION –

A. UP SLOPING B. HORZONTAL OR C. CURVED

DOWN SLOPING

>0.5 MM IN >2 CONTIGOUS

LEADS = ISCHEMIA

1) NORMAL – EXERCISE/ 1. UA/SA DIGOXIN

HYPERVENTILATION

2) HYPOKALEMIA 2. NSTEMI
3) REPOLARISATION 3. PWMI
ABNORMALITIES – PRIMARY +
SECONDARY
4) LADA ISCHEMIA = 4.
DE- WINTER SIGN

UP SLOPING ST ELEVATION +
PROMINENT T WAVES
DD OF T WAVE INVERSION –

1. NORMAL IN CHILDREN
2. NORMAL IN LEAD AVR AND V1
3. ALL TYPES OF ANGINAS
4. ALL TYPES OF MI
5. REPOLARISATION ABNORMALITIES – BOTH PRIMARY AND SECONDARY
6. PULMONARY EMBOLISM
7. HOCM
8. TAKATSOBU CARDIOMYOPATHY
9. BRAIN BLEEDS – MC – SAH
 CHAPTER 6 – MISCELLANOUS

1. HYPERKALEMIA –

SERUM POTASSIUM LEVELS ECG CHANGE DIAGRAM

1. 5.5-6.5 HYPERACUTE T WAVES

2. 6.5-7.5 FLAT P WAVE + INCREASED PR

INTERVAL

3. 7-8 WIDE QRS COMPLEX

ST ELEVATION

4. > 8 SINE WAVE

 2. HYPOKALEMIA –

3. CALCIUM AND MAGNESIUM DISTURBANCES –

HYPOCALCEMIA/ QT PROLONGATION
HYPOKALEMIA/HYPOMAGNESIMIA
HYPERCALCEMIA QT DECREASE

4. HYPOTHERMIA –

A. GENERALISED SLOWING = ALL INTERVALS/ WAVES/COMPLEXES INCREASES

B. ST ELEVATION = OSBORNE WAVE

 C. MC ARRYTHMIA – ATRIAL FIBRILLATION

D. MUSCLE TREMOR ARTIFACT ➔ DUE TO SHIVERRING

E. INCREASED QT INTERVAL

5. DIGITALIS –

THERAPEUTIC = DIGITALIS EFFECT TOXICITY

1. GRADUAL ST DEPRESSION A. PSNS + ➔ ALL TYPES OF CONDUCTION
BLOCKS EXCEPT – MOBLITZ TYPE 2
2. GRADUAL T WAVE INVERSION

K/A SALVOR- DALI – MUSTACHE SIGN/ SCOOPED

PATTERN

3. DECREASED QT INTERVAL B. SNS + ➔

4. INCREASED PR INTERVAL MC – PVCS ➔ MC – VENTRICULAR BIGEMINY

LEAST COMMON – ATRIAL FIBRILLATION

MOST SPECIFIC – PAT + SECOND DEGREE BLOCK

6. COPD –

A. HYPERINFLATED LUNG ➔ LOW VOLTAGE ECG

B. RVHT ECG CHANGE
C. RA DILATION ECG CHANGE

7. MYOCARDITIS ➔ CONDUCTION BLOCKS

8. CNS BLEEDS – MC – SAH

A. SINUS BRADYCARDIA
B. U WAVES +
C. GIANT INVERTED T WAVES = CVA – T WAVE PATTERN
D. INCREASED QT INTERVAL

9. PULMONARY EMBOLISM –

➢ MC SIGN – SINUS TACHY CHARDIA

➢ MOST SPECIFIC SIGN – S1/Q3/T3 PATTERN AKA MC- GINN WHITE SIGN
10. ACUTE PERICARDITIS –

ACUTE PERICARDITIS MI
1. ST CONCAVE ELEVATION CONVEX/DOME SHAPED
SEGMENT ELEVATION
2. T WAVE DIFFUSE T WAVE INVERSION LOCALISED T WAVE INVERSION
3. ORDER ST ELEVATION + NORMAL T WAVES ➔ ST ELEVATION + HYPERACUTE T
ST NORMAL + INVERTED T WAVES WAVES ➔ ST NORMAL +
INVERTED T WAVES
4. Q WAVE ABSENT PRESENT
5. PR DEPRESSED NORMAL
INTERVAL
6. ECG

11. PERICARDIAL EFFUSION –

MILD PERICARDIAL EFFUSION LARGE PERICARDIAL EFFUSION/ CARDIAC

TAMPONADE
LOW VOLTAGE ECG ELECTRICAL ALTERANS ➔ AXIS CHANGE WITH
EACH BEAT ➔ VARYING QRS AMPLITUDE WITH
EACH BEAT
 12. LOW VOLTAGE ECG –

DEFINATION –

LEADS QRS
LIMB LEADS < 5 MM
CHEST LEADS < 10 MM

CAUSES –

CARDIAC LUNG OTHERS

1. PERICARDIAL EFFUSION 1) PLEURAL EFFUSION 1. ANASARCA
2. INFILTERATIVE 2) PNEUMOTHORAX 2. OBESITY
CARDIOMYOPATHIES
3. EXTENSIVE MI 3) COPD

13. ELECTRICAL ALTERANS SYNDROME –

A. TOTAL ELECTRICAL ALTERANS B. PARTIAL ELECTRICAL ALTERANS

= P + QRS + T WAVES = ST-T OR U WAVES
= CARDIAC TAMPONADE = PRECEDE VENTRICULAR TACHYCARDIA

14. HOCM –

ECG –

A. LVHT
B. SEPTAL HYPERTROPHY ➔ DEEP Q WAVES = DAGGERED SHAPED Q WAVES

IMPORTANT FUNDA –

DRUGS DECREASING PRELOAD (EG – NITRATES) ➔ DECREASES VR ➔ DECREASES LV VOLUME ➔

INCREASES OBSCTRUCTION ➔ DECREASES CO ➔ WORSEN ANGINA ➔ THUS CI
 15. DEXTROCARDIA VS LEAD REVERSAL –

DEXTROCARDIA LEAD REVERSAL

1. GLOBAL DECREASE IN YES YES
R WAVE AMPLITUDE
EXCEPT AVR
2. AVR – DOMINANT R YES YES
WAVES
3. RAD YES YES
4. R WAVE POOR NORMAL
PROGRESSION

16. VENTRICULAR ANEURSYM –

DIAGNOSIS –

PERSISTANT -ST ELEVATION > 2 WEEKS AFTER MI – THAT IS -

A. CONCAVE/CONVEX
B. MC – PRECORDIAL LEADS
C. QRS DISCORDANCE PRESENT
 CHAPTER 7 – ARRYTHMIAS

CHAPTER 7A – CARDIAC ELECTROPHYSIOLOGY

A. CARDIAC CELL ACTION POTENTIAL –

PHASE KNOWN AS CHANGE CHANNEL GENE

O DEPOLARISATION SODIUM INFLUX INA SCN5A
1 POTASSIUM EFFLUX ITO KCND3
2 POTASSIUM EFFLUX I CA-L CACNA1
REPOLARISATION = CA INFLUX
3 POTASSIUM EFFLUX IKR KCNH2
IKS KCNQ1
4 RMP NO CHANGE IK1 KCNJ2

DEPOLARISATION REPOLARISATION

ENDOCARDIUM ➔ EPICARDIUM EPICARDIUM ➔ ENDOCARDIUM

FAST = SHARP QRS COMPLEX SLOW = CURVED T WAVE

OPPOSITE VECTORS IN OPPOSITE DIRECTION, THUS QRS AND T WAVE CONCORDANCE

NOTE – MAXIMUM CONDUCTION VELOCITY IN HEART = PURKINJEE FIBRES = 1-3 M/S ➔ DUE TO
MAXIMUM -CONNEXIN 40 ➔ MAINTAINS CARDIAC SYNCHRONY
 B. PACEMAKER POTENTIAL (SAN AND AVN) –

PHASE KNOWN AS CHANGE CHANNEL GENE

0 DEPOLARISATION CALCIUM INFLUX ICA-L CACNA1
3 REPOLARISATION POTASSIUM IKR KCNH2
EFFLUX IKS KCNQ1
IKACh
4 AUTOMATICITY A. IF – NA + K IF
INFLUX
B. ICA-T – ICA – T
CALCIUM
INFLUX
C. INCX – NA INCX SLC8A1
INFLUX – CA
EFFLUX

ION CHANNELS –
 1. PORE / P- DOMAIN 2. REGULATORY SUB 3. GATE
UNIT
LOOP B/W 5 AND 6 OPEN/CLOSE IN RESPONSE TO
MEMBRANE SPANNING MEMBRANE POTENTIAL
SEGMENT ➔ ALLOW IONS TO CHANGES/LIGAND ETC
PASS

PORE REGULATORY GATE DRUGS

SUBUNIT BIND
1. POTASSIUM 4 ALPHA 1 BETA VOLTAGE/LIGAND
CHANNEL
2. SODIUM 1 ALPHA (4 1 BETA VOLTAGE 6TH
CHANNEL HOMOLOGOUS MEMBRANE
DOMAINS) SPANNING
UNIT
3. CALCIUM 1 ALPHA (4 BETA/GAMMA/DELTA VOLTAGE ALPHA 1
CHANNEL HOMOLOGOUS
DOMAINS)

• VOLTAGE SENSOR – S4 SEGMENT/ 4TH OF THE 6TH SEGMENT

• INACTIVATION GATE IN SODIUM CHANNEL – LINKED B/W 3RD AND 4TH MEMBRANE
SPANNING UNIT

MECHANISMS OF CARDIAC ARRYTHMIAS –

A. BRADY – ARRYTHMIAS B. TACHY – ARRYTHMIAS

1. ABNORMALITY IN 1. ABNORMALITY IN 2. ABNORMALITY IN A/V
CONDUCTION TISSUE CONDUCTION TISSUE TISSUE

METHODS –

I. ABNORMAL AUTOMATICITY
II. TRIGERRED ACTIVITY
III. RE – ENTERY CIRCUITS
METHODS OF TACHY – ARRYTHMIAS –

METHODS SPECIFIC MECHANISM EXAMPLES

1. ABNORMAL A. ENHANCED 1. IDIOPATHIC VT
AUTOMATICITY AUTOMATICITY ➔
PHASE 4 STIMULATION 2. ATRIAL TACHYCARDIA

3. ATRIAL FIBRILLATION
B. INHIBTIED 1. SAN DYSFUNCTION
AUTOMATICITY ➔
PHASE 4 INHIBITION

2. TRIGERRED ACTIVITY A. EAD ➔ PHASE 2/3 1. PVC

2. TDP

B. DAD ➔ PHASE 4 1. REPERFUSION

INDUCED
ARRYTHMIAS

2. DIGITALIS INDUCED
ARRYTHMIAS
3. RE – ENTERY CIRCUIT 1. AVNRT

2. AVRT

3. ATRIAL FLUTTER

4. ATRIAL FIBRILLATION

5. SCARRED V.
TACHYCARDIA

1. ABNORMAL AUTOMATICITY / SPONTAENOUS DEPOLARISATION / SPONATENOUS PHASE 4

➔ IN NODAL TISSUE

SNS PSNS

➔STIMULATE L- CA CHANNELS ➔ INCREASED ➔STIMULATE IK-ACH CHANNELS ➔ INCREASED

CALCIUM INFLUX ➔ STIMULATE PHASE 4 POTASSIUM EFFLUX ➔ HYPERPOLARISATION ➔
INHIBIT PHASE 4
 FUNDA OF INTRINSIC HEART RATE –

IHR = PURE SAN RATE (W/O ANS INPUT) = 30 – 220 B/MIN ➔ AVERAGE = 100 B/MIN

EVERY 10 YEARS ➔ DECREASED IHR ➔ 5 BEATS/MIN

MAXIMUM IHR = 118 – 0.5 X AGE

NORMALLY, ANS INPUT IS PRESENT ➔ PSNS >> SNS ➔ HR = 60-100 B/MIN

SITES FOR INCREASED AUTOMATICITY –

1. NODAL TISSUE
2. PULMONARY VEINS
3. CORONARY SINUS
4. SVC
5. VENTRICULAR OUTFLOW TRACTS
6. ISCHEMIC MYOCARDIUM = POST MI ARRYTHMIAS
7. INJURED MYOCARDIUM = POST REPERFUSION INJURY ARRYTHMIAS

DOC FOR ENHANCED AUTOMATICITY ➔ BLOCK NODAL TISSUE’S PHASE 4 DEPOLARISATION –

A. BETA BLOCKERS
B. CCB
C. IVABRADINE

2. TRIGGERED AUTOMATICITY/ AFTER DEPOLARISATIONS –

MECHANISM – INCREASED CALCIUM INFLUX ➔ ACTIVATE AFTER DEPOLARISATIONS

TOC FOR TRIGGERED AUTOMATICITY = TREAT THE CAUSE

3. RE – ENTERY CIRCUITS –
 RE – ENTERY CIRCUITS ACROSS –

FIXED ANATOMICAL BARRIER = ANATOMICAL REFRACTORY BARRIER = FUNCTIONAL

RE – ENTERY (MORE COMMON) RE – ENTERY

1. MORE STABLE ➔ LESS DANGEROUS 1. LESS STABLE ➔ SPONTANEOUSLY TERMINATE/ RESTART ➔

MORE DANGEROUS
2. ABNORMAL AREA IS DEFINED ➔ ABLATION 2. ABNORMAL AREA IS NOT DEFINED ➔ ABLATION NOT EASY
EASY
3. SEEN IN – 3. SEEN IN –

A. AVRT A. A.FIB
B. AVNRT B. V.FIB
C. A. FLUTTER
D. SCAR ASSOCIATED VT
 ƛ = VELOCITY (THETA) X REFRACTORY PERIOD (Tr)

IF LENGTH OF CIRCUIT > LAMBDA = EXCITATION GAP ➔ RE- ENTERY CIRCUIT

ISCHEMIA/ INJURY TO MYOCARDIUM ➔ CAN LEAD TO BOTH ANATOMICAL AND FUNCTIONAL RE – ENTERY –

1. ANTOMICAL RE – ENTERY ➔ SCAR FORMATION

2. FUNCTIONAL RE – ENTERY ➔ CHRONIC ISCHEMIA → DOWN REGULATION OF CONNEXIN → SLOW IMPULSE

PROPOGATION

DOC FOR RE – ENTERY CIRCUITS ➔

A. DRUGS THAT INCREASE REFRACTORY B. DRUGS THAT DECREASE VELOCITY =

PERIOD = POTASSIUM CHANNEL SODIUM CHANNEL BLOCKERS
BLOCKERS

INCREASED LAMBDA ➔ LAMBDA > LENGTH OF DECREASE LAMBDA ➔ L> LAMBDA ➔ EXCITATION
CIRCUIT ➔ DECREASES EXCITATION GAP ➔ HALTS GAP INCREASES ➔ PRO – ARRYTHMIC
RE-ENTERY CIRCUIT ➔ THUS DOC

CLINICAL FEATURES OF ARRYTHMIAS –

1. IRREGULAR RATE PALPATATIONS

2. DECREASED CARDIAC OUTPUT A. SYNCOPE
B. DYSPNEA
C. EXERCISE INTOLERENCE
D. FATIGUE

3. EXACERBATES PRE-EXISTING HEART A. ANGINA

DISEASE B. CHF

4. SCD MOST IMPORTANT SYMPTOM INDICATING SCD =

SYNCOPE

BENIGN ARRYTHMIA MALIGNANT ARRYTHMIA

LESS DECREASE IN CO MORE DECREASE IN CO
 APPROACH TO THE PATIENT WITH ARRYTHMIAS -

➢ HISTORY TAKING – FAMILY HISTORY/ DRUG HISTORY / AGE / GENDER/ RACE

➢ EXTRA ECG BASED INVESTIGATIONS –

A. HOLTER
B. MOBILE CARDIAC TELEMETRY
C. WEARABLE DEVICES
D. EVENT MONITORS
E. IMPLANTABLE MONITORS
F. TREADMIL TESTING ➔ TO KNOW THE MAXIMUM HEART RATE
 ➢ INVASIVE ELECTRO – PHYSIOLOGICAL STUDY (EPS) –

USE – TELLS THE EXACT MECHANISM OF ARRYTHMIAS ➔ THUS GOLD STANDARD TEST

PROCEDURE –

CATHETER BASED RECORDING OF INTRA CARDIAC ECG ➔ F/B CATHETER ALBATION ➔ EPS
EVALUATES THE EFFICACY OF ABLATION

TREAMTMENT OF ARRYTHMIAS –

1. ANTI – ARRYTHMIC DRUGS – (AAD) -

3 MAIN PROBLEMS ASSOCIATED WITH AAD ➔ THUS LESS USED ➔

I. PRO ARRYTHMIOGENIC POTENTIAL

II. LONG TERM SIDE EFFECTS
III. BRADYCARDIA → REQUIRING PACEMAKER

2. CATHETER ABLATION –

INDICATIONS –

A. ENHANCED AUTOMATICITY INDUCED ARRYTHMIAS

B. ANATOMICAL RE – ENTERY CIRCUITS BASED ARRYTHMIAS

PROCEDURE –

2 MAIN METHODS TO FOR CATHETER TO ENTER THE HEART -

1. ENDOCARDIAL ARRYTHMIOGENIC 2. SUB EPICARDIAL ARRYTHMIOGENIC
SOURCE ➔ TRANS VENOUS METHOD SOURCE ➔ PERCUTANEOUS
PERICARDIAL PUNCTURE

1. CATHETER ➔ FV ➔ IVC ➔ RA/RV/BUNDLE OF HIS/ LA

2. USE ADDITIONAL METHODS TO LOCALISE THE EXACT SOURCE OF ABNORMALITY –
 A. EAMS – ELECTRO ANATOMICAL MAPPING SYSTEM –

I. REAL TIME CONSTRUCTION OF HEART CHAMBERS

II. IDENTIFY THE ARRYTHMIOGENIC TISSUE

B. ICE – INTRA CARDIAC ECHOCARDIOGRAPHY

C. INTRA CARDIAC ECG & SURFACE ECG

3. ABLATE THE TISSUE VIA DIFFERENT MECHANISMS –

A. RADIO FREQUENCY ABLATION – MOST COMMON OVERALL

FREQUENCY – 300-550 KHZ

B. LASER ABLATION
C. USG
D. MICRO WAVE ABLATION
E. CRYOTHERMY = - 40 DEGREE C ➔ MC – PAROXYSMAL ATRIAL ABLATION
F. PULSE FIELD ELECTROPORATION ➔ TARGETS LIPID CELL MEMBRANE

COMPLICATIONS –

1. INFECTION AND BLEEDING

2. CARDIAC TAMPONADE
3. PHRENIC NERVE INJURY
4. CHF
5. STUNNING OF CHAMBER ➔ EMBOLISM ➔ STROKE

3. STEREO- TACTIC – EBRT –

ADVANTAGE – FOR PLACES WHERE CATHETER CAN NOT REACH

4. IMPLANTED ELECTRICAL DEVICE THERAPY –

A. PACEMAKERS B. ICD

A. PACEMAKERS –

INDICATION – TOC FOR BRADY - ARRYTHMIAS

TYPES OF PACEMAKERS –

1. TEMPORARY PACEMAKERS 2. PERMANENT PACEMAKERS

PARTS OF PACEMAKER –

1. PULSE GENERATOR – BATTERY +

CIRCUIT ➔ MC SITE – PREPECTORAL
SPACE
2. LEADS
3. ELECTRODES – ANODES AND
CATHODES

METHOD OF INSERTION –

A. PER – CUTANEOUS PACEMAKERS B. LEADLESS PACEMAKERS

1. TRANS VENOUS PACEMAKERS –

SUB CLAVIAN VEIN ➔ SVC ➔ RA ➔ RV FV ➔ IVC ➔ RV ENDOCARDIUM

2. EPICARDIAL PACEMAKERS

I. MORE CHANCE OF INFECTION I. LESS CHANCE OF INFECTION

II. MORE LEAD FRACTURE II. LESS LEAD FRACTURE

MC – ATRIAL BASED PM MC – VENTRICULAR BASED PM + ATRIAL

SENSING ➔ MAINTAINS AV SYNCRONY
NOMENCLATURE OF PACEMAKERS –

1. CHAMBER 2. CHAMBER 3. SENSED 4. RATE

PACED SENSED EVENT RESPONSE

GOAL – TO MIMIC
PHYSIOLOGICAL
INCREASE IN HR IN
RESPONSE TO
EXERCISE ➔ MOST
IMPORTANT IN
CHRONOTROPIC
INCOMPETENCE

O – NONE O – NONE ON
A – ATRIAL I – INHIBITION OFF
V – VENTRIULAR T – TRIGERRED
D – DUAL D – DUAL
S- SINGLE

EG – D D D R (ON)
BEST – DUAL CHAMBER PACING (DDDR) ➔ AS MANTAINS AV SYNCHRONY

SINGLE ATRIAL CHAMBER PACING – YOUNG PATIENTS WITH PURE SNS DYSFUNCTION

SINGLE VENTRICULAR CHAMBER PACING (VVI) – IN PATIENTS WITH CO MORBIDITIES/ELDERLY

COMPLICATIONS OF PACEMAKERS –

ACUTE CHRONIC
1. INFECTION AND BLEEDING 1) INFECTION AND EROSION
2. PERFORATION OF – 2) LEAD FAILURE
LUNG/HEART/DIAPHRAGM

3. LEAD DISLODGEMENT 3) TWIDDLER SYNDROME –

WRAPPING OF LEADS AROUND PULSE

GENERATOR ➔ PM DYSFUNCTION

4) PACEMAKER SYNDROME –
CAN’T MAINTAIN AV SYNCHRONY
 B. ICD – IMPLANTABLE CARDIOVERTER DEFIBRILATOR –

INDICATION – DETECT SUSTAINED V. TACHYCHARDIAS ➔ DE FIBRILLATE ➔ PREVENT SCD

NOTE – INSERT ICD ONLY IF – 1 YEAR SURVIVAL + ACCEPTABLE FUNCTIONING

EXCEPT – END STAGE HEART DISEASE + LBBB OR AWAITING CARDIAC TRANSPLANT

PARTS OF ICD –

1. PULSE GENERATOR – BATTERY + CIRCUIT

2. LEADS
3. ELECTRODES – ANODES AND CATHODES

METHOD OF INSERTION –

1. PER-CUTANEOUS ICD 2. SUB – CUTANEOUS ICD

I) TYPES -
A. TRANS VENOUS ICD

SUB CLAVIAN VEIN ➔ SVC ➔ RA

➔ RV

B. EPI- CARIDAL ICD

II) PACING PRESENT ABSENT

MODE
III) ANTI – PRESENT PRESENT
TACHYCARDI
A PACING
(ATP)

ADVANTAGE – RAPID
PACING FASTER THAN
 MONOMORPHIC VT ➔
TERMINATES VT
IV) S/E 1. MORE INFECTION 1. LESS INFECTION
2. MORE LEAD RELATED 2. LESS LEAD RELATED
COMPLICATES COMPLICATION
V) PHOTO

NOTE 1 – WEARABLE ICD/ EXTERNAL ICD –

INDICATION – SHORT TERM USE ➔ PENDING DECISION TO PUT PERMANENT ICD

NOTE 2 – ICD HAS ELECTRO- GRAM (RECORDING OF EPISODES BY ICD) ➔ INTERO- GRAM (RETRIVE
THE EPISODE’S INFORMATION)

COMPLICATIONS OF ICD –

1. PROCEDURE RELATED

2. NON-PROCEDURE RELATED –

MC COMPLICATION – UNNECESSARY SHOCKS >> ATP ➔

A. RECURRENT V. TACH
B. WORSENS CHF

THUS, INCREASED RISK OF DEATH

THUS, IN CASE OF RECURRENT UNNECESSARY SHOCKS, GIVE ➔

 1. CATHETER ABLATION – TOC 2. AAD

DOC – SOTALOL + AMIODARONE

PREVENTION - PROGRAMME ICD TO GIVE SHOCKS ➔ > 220 BEATS/MIN

OTHER COMPLICATIONS –

I. PAIN
II. PTSD
 CHAPTER 7 B – BRADY-ARRYTHMIAS – SAN DISORDERS

SAN – LOCATION AND STRUCTURE –

A. LOCATION – LATERAL JUNCTION OF RA AND SVC ➔ AT CRISTA TERMINALIS ➔ AT

EPICARDIUM

B. STRUCTURE –

1. SAN ARTERY 2. SAN CELLS/ 3. ECM/CT

PACEMAKER CELLS

A. 60% = RCA A) NO IC DISCS FUNCTION – INSULATES SAN

FROM HYPERPOLARISING
B. 40 % = LCA B) NO T TUBULES INFLUENCE OF ATRIA

C) NO SERCA PUMP

SAN DYSFUNCTION / SICK SINUS SYNDROME –

CL/F – DECREASED CO

CAUSES –

A. IDIOPATHIC – MUTATION OF SCN5A/ HCN4 (IF) CHANNEL / ANKB

B. IRREVERSIBLE – STRUCTURAL HEART DISORDERS

C. REVERSIBLE CAUSES

REVERSIBLE CAUSES OF SAN DYSFUNCTION

DISEASE DRUGS
1. HYPOTHYROIDISM A–

A. ANTI ARRYTHMICS – IA/IC/III

B. ANTI PSYCHOTICS
C. ANESTHESIA – PROPOFOL
D. ALPHA – METHYL DOPA

2. HYPOXIA B – BETA BLOCKERS

3. HYPOTHERMIA C - CCB
4. HYPERTENSION OF BRAIN ➔ D – DIGOXIN
INCREASED ICP ➔ CUSHINGS REFLEX
5. HYPER ACTIVE VAGUS ➔ VAGAL REFLEX
6. HYPER TROPHIC PATIENT ➔ OSAS ➔
INCREASED VAGAL TONE

SSS/ SAN DYSFUNCTION SUB TYPES –

1. SAN EXIT BLOCK VS SINUS ARREST –

SINUS ARREST SAN EXIT BLOCK

IMPULSE DOESN’T FORM IMPULSE FORMS BUT CAN’T EXIT SAN

IN BOTH ➔ ASYSTOLE/PAUSE ➔JUNCTIONAL ESCAPE RHYTHM ➔ RETEROGRADE P WAVES ➔ + IN

AVR AND – IN LEAD 2 ➔ BEFORE, AFTER OR MERGED WITH QRS
TYPES OF SAN EXIT BLOCK – (EXACTLY LIKE AVN BLOCK) –

TYPE OF BLOCK FEATURE PP INTERVAL MISSED BEAT IDENTIFICATION

ST
1 DEGREE BLOCK FIXED DELAY OUT SAME NONE EPS
OF SAN
2ND DEGREE BLOCK
A. MOBLITZ INCREASING KEEPS YES PROGRESSIVE
TYPE 1 DELAY OUT OF DECREASING HR DECREASE
SAN
B. MOBLITZ FIXED BLOCK OUT SAME YES SUDDEN
TYPE 2 OF SAN DECREASE IN
HR ➔
SUDDENNLY,
100 B/MIN ➔
50 B/MIN
3RD DEGREE BLOCK EPS

2. TACHY – BRADY SYNDROME –

MC TYPE OF TACHYCARDIA – ATRIAL FIBRILLATION

TREATMENT –

A. TREAT TACHYCARDIA ➔ SPONTANEOUS RESOLUTION OF BRADYCARDIA

B. TOC – PACEMAKER

3. CHRONOTROPIC INCOMPETENCE (CI) –

PATHOGENESIS –
 4. SAN FIBROSIS –

MC – OLD PATIENTS (ALSO HAVE – DECREASED SAN CELLS)

5. SAN ISCHEMIA/INFARCTION –

CAUSES –

A. POSTERIOR/INFERIOR MI ➔ RCA B. POST ABLATION OF AFIB/A.FLUTTER

INVOLVEMENT

MECHANISM – DAMAGE TO SAN ARTERY

6. CAROTID HYPERSENSTIVITY –

PATHOGENESIS – CAROTID HS ➔ STIMULATE VAGUS ➔ NEURAL MEDIATED BRADYCARDIA ➔ VASO-

VAGAL SYNCOPE

TOC – PACEMAKER

COMPLICATION OF SSS –

ATRIAL STANDSTILL ➔ STASIS OF BLOOD ➔ THROMBO- EMBOLISM

APPROACH TO THE PATIENT WITH SAN DYSFUNCTION –
 INDICATION OF PACEMAKERS –

TEMPORARY PACEMAKERS PERMANENT PACEMAKERS

1. N/R AFTER TREATING CAUSES 1) SYMPTOMATIC SND
2. POST CARDIAC TRANSPLANT - 2) SYMPTOMATIC SND DUE TO DRUGS BUT
CAN’T STOP DRUG
A. SAN INJURY
B. AMIODARONE ACCUMULATION

3. POST SPINAL CORD INJURY – 3) SYMPTOMATIC TACHY- BRADY

SYNDROME
ANS DYSFUNCTION

4) SYMPTOMATIC CI
5) HR < 40

NOTE – MORE CORRELATION B/W SYMPTOMS AND BRADYCARDIA ➔ MORE CHANCES OF

IMPROVEMENT POST PACEMAKER

PRE – MATURE ATRIAL CONTRACTION

HALLMARK – P WAVE OF DIFFERENT MORPHOLOGY

CAUSES –

1. CAFFEINE
2. ALCOHOL
3. STRESS
 CHAPTER 7 C – APPROACH TO SUPRA VENTRICULAR TACHYCARDIA /
NARROW COMPLEX TACHYCARDIA = QRS < 0.12 S

CLASSIFICATION –

TYPES –

1. NON-SUSTAINED VS SUSTAINED

A. NON-SUSTAINED B. SUSTAINED
LASTS < 30 SECONDS OR SELF TERMINATES LASTS > 30 S OR REQUIRES INTERVENTION

2. PAROXYSMAL VS PERSISTANT
APPROACH TO THE PATIENT –

➢ REGULAR RATE VS IRREGULAR RATE –

A. IRREGULAR RATE –

1. ATRIAL FIBRILLATION
2. MFAT

B. REGULAR RATE –

A: V 1:1 2/3:1 1:2/3

ARRYTHMIA A. AVNRT ATRIAL FLUTTER JUNCTIONAL

B. AVRT TACHYCARDIA
C. FAT
VAGAL MANEUVRE / AVN BLOCKING AGENTS –

1. VALSALVA MANEUVRE 2. BREATHING INTO A 3. SUDDEN LEG RAISE

SYRINGE HELD
AGAINST PRESSURE
4. DIVER’S REFLEX – FACE 5. CAROTID SINUS 6. DRUGS –
INTO COLD WATER MASSAGE ADENOSINE/BETA
BLOCKERS/ CCB/
CI = ATHEROSCLEROSIS DIGOXIN

EFFECT OF AVN BLOCKING ON ARRYTHMIAS –

1. INCREASED 2. NO EFFECT 3. DECREASE SVT 4. SVT 5. ATRIAL RATE

SVT SVT TERMINATED CONTINUES
WITH AV
BLOCK

PRE – EXCITATION VENTRICULAR A. SINUS 1. AVNRT 1. A. FLUTTER

TACHYCARDIA TACHYCARDIA TACHYCARDIA
2. ORTHO – 2. FAT
B. JUNCTIONAL AVRT
TACHYCARDIA
 CHAPTER 7 D – SINUS TACHYCARDIA

DEFINATION – HR > 100 B / MIN

PHYSIOLOGICAL TACHYCARDIA NON-PHYSIOLOGICAL/ IN- APPROPRIATE

TACHYCARDIA
APPROPRIATE RESPONSE TO A STIMULUS SPONTAENOUS TACHYCARDIA OR
EXAGGERATED RESPONSE TO A STIMULUS
1. EMOTIONS A. DISEASE –

1) FEVER
2) HYPERTHYROIDISM
3) ANEMIA
4) CUSHING SYNDROME
5) LUNG/HEART DISEASE
6) AS A COMPENSATORY RESPONSE TO
DECREASE BP
2. EXERCISE B. TOXINS –

1) COCAINE
2) AMPHETAMINE
3) LSD
4) MDMA/ECSTASY
C. DRUG –

1) SNS +/ B1 AGONIST
2) PSNS BLOCK / ATROPINE
3) METHYLXANTHINE/ CAFFINE
4) DAUXO/ DAUNORUBICIN

POTS – POSTURAL ORTHOSTATIC TACHYCARDIA –

DEFINATION – PR > 120 B/MIN OR INCREASE IN > 30 B/MIN WITHIN 10 MINUTES OF STANDING W/O
HYPOTENSION

PATHOGENESIS – VIRAL INFECTION INDUCED ANS DYSFUNCTION

TOC = INCREASE BP ➔ DECREASE HR

 1. SALT SUPPLEMENTATION
2. ORAL FLUDROCORTISONE
3. MIDODRINE
4. COMPRESSION STOCKINGS
5. EXERCISE TRAINING

APPROACH AND MANAGEMENT OF SINUS TACHYCARDIA –

 CHAPTER 7 E – FOCAL ATRIAL TACHYCARDIA

ORIGIN – ONE FOCUS IN ATRIA

MECHANISM –

1. ABNORMAL 2. TRIGGERRED ACTIVITY 3. RE – ENTERY CIRCUIT

AUTOMATICITY

LOCATION –

1. ATRIAL TISSUE 2. EXTRA ATRIAL TISSUE

A. SVC
B. CORONARY SINUS
C. PLUMONARY VEIN

CAUSES –

1. SECONDARY ATRIAL FIBROSIS 2. DIGOXIN –

MOST SPECIFIC ARRYTHMIA – FAT + AV BLOCK

TYPES –

1. SUSTAINED VS NON-SUSTAINED

2. PAROXYSMAL VS PERSISTANT

CLINICAL FEATURE –

1. FOCAL AND ATRIAL = ABNORMAL P WAVE MORPHOLOGY BUT CONSISTENT THROUGHOUT

EXPOSE P WAVES = AVN BLOCKING MANUVRES ➔ INCREASED ATRIAL CONTRACTION + AVN BLOCK

2. TACHYCARDIA

WARM UP PHASE (INCREASING HR) ➔ FAT (SUSTAINED INCREASED HR) ➔ COOL DOWN PHASE
(DECREASING HR)
DIFFERENCE FROM SINUS TACHYCARDIA –

1. ABNORMAL P WAVE MORPHOLOGY

2. ABRUPT ONSET AND OFF SET

COMPLICATION –

1. ATRIAL FIBRILLATION/ ATRIAL FLUTTER

2. ATRIAL TACHYCARDIA INDUCED CARDIOMYOPATHY

TREATMENT –
 CHAPTER 7 F – PAROXYSMAL SUPRA VENTRICULAR TACHYCARDIA /
PSVT

HALLMARK –

1. PAROXYSMAL SUPRA VENTRICULAR = NARROW QRS COMPLEX = < 0.12 S

2. TACHYCARDIA = HR > 100 B/MIN

TYPES –

1. AVNRT 2. JUNCTIONAL 3. ACCESSORY PATHWAY

TACHYCARDIA ASSOCIATED
TACHYCARDIA

1. AVNRT –

➢ MC FORM OF PSVT
➢ MC – 20 – 40 YEARS
➢ MC – FEMALES >> MALES

MECHANISM –
NET VECTOR DIRECTION =

THUS, NEGATIVE P WAVES/ RETROGRADE P WAVES ➔ 2/3/AVF ➔ MAY OR MAY NOT BE SEEN.

SOMETIMES, SIMULTANEOUS A-V CONTRACTION ➔ CANNON A WAVES ON JVP ➔ STIMULATE

ANP/BNP ➔ POST TACHYCARDIA INDUCED DIURESIS

ECG –

JUNCTIONAL ECTOPIC ACCELERATED JUNCTIONAL

TACHYCARDIA = JET RHYTHM = AJR
1. MECHANISM INCREASED AUTOMATICITY
2. CAUSE A. MCC – POST SURGERY A. MC – AFTER PVC
FOR CHD
B. INCREASED SNS TONE
B. INCREASED SNS TONE
– MC AFTER POST
CATHETER ABLATION +
ISOPRENALINE

3. HR >100 B/MIN 60-100 B/MIN

4. P WAVES A-V BLOCK = AV DISSOCIATION AV CONDITION PRESENT ➔
➔ NO P WAVES RETEROGRADE P WAVES
5. QRS COMPLEX NARROW NARROW
TREATMENT –

ADENOSINE IN PSVT –

A. DOSE 6 MG ➔ N/R ➔ 12 MG
B. ROUTE IV BOLUS PUSH AS T1/2 = 6 SECONDS DUE TO
RAPID UPTAKE BY ALL CELLS
C. SIDE EFFECTS 1. BRONCHOSPASM
2. PRECIPITATES ATRIAL FIBRILLATION
(THUS DON’T USE IN WPW SYNDROME
+ AFIB)

MECHANISM – ADENOSINE ACTS VIA Gi ➔ K

EFFLUX ➔ EARLY REPOLARISATION ➔ EARLY
DEPOLARISATION
D. CI TRANSPLANTED HEARTS ➔ DUE TO SNS
DENERVATION HYPERSENSITIVITY ➔ CARDIAC
ARREST
DD OF WIDE COMPLEX TACHYCARDIA –

1. VENTRICULAR TACHYCARDIA

2. SVA + BBB

3. PRE – EXCITED SYNDROME ASSOCIATED TACHYCARDIAS = SVA + ABBERANCY

4. RAPID PACING IN PPM/ICD PATIENT

TREAT THEM LIKE VENTRICULAR TACHYCARDIA, UNTIL PROVEN OTHERWISE.

VT VS SVA + ABBERANCY – HOW TO DIFFERENTIATE -

1. AV DISSOCIATION
2. POSITIVE R WAVE IN AVR
3. POSITIVE R WAVE IN V1

IF ANY 1 IS SEEN ➔ VT MORE LIKELY

IF NONE IS SEEN ➔ SVT + ABBERACY MORE LIKELY

GOLD STANDARD TEST - EPS

 CHAPTER 7 G – ATRIAL FIBRILLATION
INTRODUCTION –

➢ MC SUSTAINED ARRYTHMIA

RISK FACTORS OF ATRIAL FIBRILLATION –

A. NON-MODIFIABLE B. MODIFIABLE
1. AGE – SINGLE MOST IMPORTANT RF I. CARDIAC CAUSES –

MC > 60 YEARS 1) CAD - 2ND MOST IMPORTANT MODIFIABLE

CAUSE
2) RHD
3) HOCM
4) CHF
5) CARDIAC SURGERY

2. MALES > FEMALES II. LUNG –

1) PE
2) COPD
3) OSAS

3. WHITES > BLACKS III. SYSTEMIC DISEASES –

1) HYPERTENSION – MOST IMPORTANT

MODIFIABLE CAUSE
2) DM
3) OBESITY
4) CKD
5) HYPERTHYROIDISM

4. GENETIC IV. OTHERS –

1) ALCOHOL
2) CAFFINE
3) SMOKING

OVERALL, MOST IMPORTANT CAUSES – HIGHLIGHTED

CLASSIFICATION OF ATRIAL FIBRILLATION –

PAROXYSMAL PERSISTANT LONG STANDING

1. LASTS FOR < 1 WEEK OR SELF 1WEEK – 1 YEAR >1 YEAR
TERMINATING
2. LA SIZE MINIMUM MODERATE MAXIMUM
3. LA SCAR MINIMUM MODERATE MAXIMUM
4. AAD EFFICACY MAXIMUM MODERATE MINIMUM
5. ABLATION MAXIMUM MODERATE MINIMUM
BENEFIT
6. ABLATION PV SOURCE ONLY PV + NON-PV SOURCE PV + NON-PV SOURCE
TECHNIQUE + LA SCAR ABLATION
7. NO OF MINIMUM MODERATE MAXIMUM
ABLATION
PROCEDURES
RECURRENT ATRIAL FIBRILLATION ➔ > 2 EPISODES
PERMANENT ATRIAL FIBRILLATION ➔ > 1 YEAR + UN – EFFECTIVE RHYTHM CONTROL METHODS

PATHOGENESIS –

STAGE 1 STAGE 2 STAGE 3

SOURCE OF AUTOMATICITY TISSUE REMODELLING FIBROSIS
FOCUS –

PV >>> NON-PULMONARY
SOURCE

NON-PULMONARY SOURCE –
IDENTIFICATION – FIRE IN
RESPONSE TO ISOPRENALINE

1. SVC
2. CORONARY SINUS
3. REMANENT VEIN OF
MARSHALL

PV ➔ ENHANCED TISSUE REMODELLING ➔ LA FIBROSIS ➔ LA

AUTOMATICITY ➔ ECTOPIC SHORTENS THE ATRIAL TISSUE ENLARGEMENT
BEATS/PRE-MATURE ATRIAL REFRACTORY PERIOD ➔ RE-
CONTRACTION ➔ ATRIAL ENTERY CIRCUIT ➔ SUSTAINED
TACHYCARDIA ➔ NON- ATRIAL FIBRILLATION
SUSTAINED ATRIAL FIBRILLATION
FEATURES –

INVESTIGATION –

A. ECG –

B. ECHOCARDIOGRAPHY – TEE> TTE

ATRIAL FIBRILLATION AND VENTRICULAR RATE –

A. ATRIAL B. ATRIAL C. ATRIAL D. ATRIAL

FIBRILLATION FIBRILLATION FIBRILLATION FIBRILLATION WITH
WITH SLOW WITH WITH FAST SUSTAINED
VENTRICULAR CONTROLLED VENTRICULAR VENTRICULAR RATE
RATE VENTRICULAR RATE
RATE

<60 B/MINUTE 60 – 100 B/MINUTE 100-200 B/MINUTE >200 B/MINUTE

ASSOCIATED WITH
CONDUCTION BLOCKS

CLINICAL FEATURES –

1. IRREGULAR RATES PALPATATIONS – MC CLINICAL FEATURE

2. HEMO – DYNAMIC CONSEQUENCE DUE A. EXERCISE INTOLERENCE
TO VARIABLE STROKE VOLUME
B. FATIGUE/WEAKNESS

C. SYNCOPE

D. DYSPNEA

E. EXACERBATION OF PRE-EXISTING HEART

DISEASE

3. CARDIO – EMBOLIC PHENOMENON – PATHOGENESIS –

MOST LIFE THREATINING AND MOST
SIGNIFICANT COMPLICATION OF ATRIAL LOSS OF ORGANISED ATRIAL CONTRACTION ➔
FIBRILLATION BLOOD STASIS ➔ THROMBUS (MC – LA
APPENDAGE) ➔ EMBOLISE ➔

1. ISCHEMIC STROKE – MC
2. VASCULAR DEMENTIA

4. COMPLICATION A. RAPID VENTRICULAR RATE ➔

TACHYCARDIA INDUCED
CARDIOMYOPATHY

B. STIFF LA SYNDROME ➔ LEFT SIDED

HEART FAILURE
ASHMAN PHENOMENON/ ANTICIPATION SYNDROME –

PATHOGENESIS –

AFIB

➔ LONG PAUSE

➔ NORMAL SINUS WAVE

➔ BUNDLE BRANCH THINKS THAT ONE MORE PAUSE WILL COME

➔ SLOWS CONDUCTION, MC – RBB > LBB

➔ ABNORMAL WAVE – NORMAL P WAVE + BROAD AND ABNORMAL QRS

TREATMENT OF ATRIAL FIBRILLATION –

CARDIOVERSION AND ANTI COAGULATION –

ONSET OF ATRIAL FIBRILLATION

A. < 48 HOURS / NO HIGH-RISK FACTORS B. > 48 HOURS / HIGH RISK FACTORS PRESENT –
PRESENT
1. MS
2. HOCM
3. H/O EMBOLIC STROKE

= LESS RISK OF THROMBO – EMBOLISM AFTER = HIGH RISK OF THROMBO – EMBOLISM AFTER
CARDIO VERSION CARDIO VERSION
= DO CARDIOVERSION STAT = 2 MAIN APPROACHES TO DO CARDIOVERSION -

1. 3 WEEKS ANTI 2. TEE/ HR CARDIAC CT

COAGULATION ➔ STAT TO SEE
CARDIOVERSION ➔ 4 THROMBUS ➔ IF NO
WEEKS ANTI THROMBUS ➔
COAGULATION CARDIOVERSION ➔ 4
WEEKS ANTI
COAGULATION

CHRONIC MANAGEMENT OF ATRIAL FIBRILLATION –

1. CONTROL SYMPTOMS A. RATE CONTROL

B. RHYTHM CONTROL

2. THROMBO- EMBOLIC RISK

MANAGEMENT
3. RISK FACTORS MANAGEMENT TO HALT THE PROGRESSION OF DISEASE
1. CONTROL OF SYMPTOMS –

A) VENTRICULAR RATE CONTROL –

ACUTE CHRONIC
GOAL – INCREASE DIASTOLIC FILLING ➔ GOAL –
INCREASED CO ➔ DECREASE SYMPTOMS
A. INCREASE DIASTOLIC FILLING ➔
INCREASED CO ➔ DECREASE SYMPTOMS
B. DECREASE COMPLICATIONS

DOC – DOC –

A. W/O CHF – BETA BLOCKERS/ CCB BETA BLOCKERS/ CCB

B. WITH CHF – DIGOXIN (AS NO ADEQUATE RATE CONTROL –

IONOTROPIC EFFECT)
1. RESTING HR - < 80
2. LIGHT EXERTION HR - < 100

OVERALL ACCEPTABLE HR CONTROL - < 110

N/R – N/R –

DOC – BB/CCB + DIGOXIN TOC = ABLATE AND PACE STATERGY

ABLATE – AV JUNCTION

PACE – PERMANENT PM

MC – BIVENTRICULAR PACING / HIS BUNDLE

PACING / LBB PACING ➔ TO DECREASE
VENTRICULAR DYSYNCHRONY
 B) RHYTHM CONTROL –

1. ABLATION = TOC 2. AAD

INDICATION – INDICATION –

1. HFREF + AFIB 1. SYMPTOMATIC PAROXYSMAL AFIB

2. RECURRENT 2. N/R TO RATE CONTROL
SYMPTOMS +
PERSISTANT AFIB
METHOD – A. W/O STRUCTURAL B. WITH STRUCTURAL
HEART DISEASE = IA/IC HEART DISEASE = III
1. CATHETER ABLATION

FV ➔ TRANS ATRIAL SEPTAL

PUNCTURE ➔ PV >> NON-PV
SITE ABLATION

2. SURGICAL ABLATION

MC DONE DURING CAD

SURGERY/ VALVE SURGERY

3. HYBRID PROCEDURE –

CATHETER ALBATION +
SURGICAL ABLATION

INDICATION – PERMANENT
AFIB

COMPLICATION –

SAN INJURY ➔ PERMANENT

PM IMPLANTATION

NOTE – IN ATRIAL FLUTTER – I. DISOPYRIMIDE I. SOTALOL

ALBATE CAVO – TRICUSPID II. FLECANIDE II. DOBUTILIDE
ISTHMUS III. PROPAFENONE III. AMIODARONE

SPECIFIC COMPLICATION DURING CATHETER ABLATION FOR ATRIAL FIBRILLATION –

1. PV STENOSIS
2. ESOPHAGUS INJURY ➔ ULCERS ➔ ESOPHAGEAL – ATRIAL FISTULA

CL/F – IE/STROKE 1-3 WEEKS LATER

IOC – CECT – ORAL + IV CONTRAST

TOC – EMERGENCY OPEN SURGERY

 2) THROMBO – EMBOLIC RISK MANAGEMENT –

A. VALVULAR AFIB = AFIB IN – B. NON-VALVULAR AFIB

MS/HOCM/HO OF STROKE

START ANTI COAGULATION IRRESPECTIVE OF CALCULATE RISK OF STROKE VS RISK OF

ANYTHING BLEEDING

DRUGS INCLUDE - NSAIDS/DAPT

0 = NO THERAPY

1 = ORAL ANTI COAGULATION > ANTI PLATLET

SCORE > 3 = INCREASED RISK OF BLEEDING
>2 = ORAL ANTI COAGULATION

NOTE – SCORE 1 SHOULDN’T ONLY BE DUE TO

FEMALE GENDER.
 ORAL ANTI COAGULATION THERAPY
CLASS DOAC VITAMIN K ANTAGONIST
1. DRUGS 1. ORAL XA INHIBITORS – WARFARIN
APIXABAN/RIVAROXABAN/EDOXABAN

2. ORAL DTI - DABIGATRAN

2. USE 1. DOC IN NON VAVLULAR AFIB 1. DOC IN VALVULAR
AFIB

2. DOC IN
MECHANICAL
HEART VALVES +
AFIB

3. DOC IN ESRD
(EGFR < 15)

3. MONITORING NOT REQUIRED PT – INR

THERAPEUTIC EFFECT –
INR – 2-3
4. RISK OF LESS MORE
BLEEDING
5. DOC FOR 1. ORAL XA INHIBITOR – ANDEXANET 1. PCC
TOXICITY 2. FFP
2. ORAL DTI – IDARUCIZUMAB 3. VITAMIN K

INDICATION OF DOSE MODIFICATION OF DOAC –

1. AGE > 80
2. WEIGHT< 60
3. CREATINE CLEARANCE 15-50
4. S. CREATINE > 1.5

DABIGATRAN RIVAROXABAN EDOXABAN APIXABAN

STANDARD DOSE 150 MG BD 20 MG QID 60 MG QID 5 MG BD

MODIFIED DOSE 110 MG BD 15 MG QID 30 MG QID 2.5 MG BD

IN PATIENTS WITH, CI TO CHRONIC ANTI COAGULATION –

1. LA APPENDAGE REMOVAL + ATRIAL MAZE SURGERY

2. LAA DEVICES – TO BLOCK THROMBUS FROM COMING IN LA

WATCHMAN DEVICE/ AMPLATZER DEVICE / LARIAT DEVICE

3. PER – CUTANEOUS LIGATION OF LA APPENDAGE

 3) RISK FACTOR MANAGEMENT –

1. EXERCISE –

MALES FEMALES

2. MODERATE CAFFEINE INTAKE ➔ MODERATE REDUCTION IN AFIB RISK

DIFFERENT TYPES OF RHYTHM –

 CHAPTER 7 H – MACRO- RE- ENTERANT ATRIAL TACHYCARDIA & MFAT

DEFINATION OF MRAT – MACRO – RE- ENTERANT ATRIAL TACHYCARDIA:

ATRIAL SCAR ➔ MACRO – RE – ENTERANT CIRCUIT ➔ TACHYCARDIA = ATRIAL FLUTTER

TYPES OF ATRIAL FLUTTER –

A. COMMON/ TYPICAL B. ATYPICAL ATRIAL

ATRIAL FLUTTER FLUTTER
1. SITE OF MACRO – RE- CAVO – TRICUSPID ISTHMUS/ SUB NOT CAVO – TRICUSPID ISTHMUS
ENTERY CIRCUIT – EUSTACHIAN
2. MC SITE RA RA OR LA

3. MC AFTER 4. RA SURGERY RA – POST RA ATRIOTOMY

5. RIGHT SIDED HEART LA – POST ABLATION
DISEASE
6. IC/III ANTI ARRYTHMIC
DRUGS

MC ASSOCIATION – ATRIAL
FIBRILLATION

BOUNDRIES OF CAVO – TRICUSPID ISTHMUS/ SUB- EUSTACHIAN ISTHMUS –

ANTERIOR – TV ISTHMUS

POSTERIOR – IVC AND FUNCTIONAL BLOCK IN CRISTA TERMINALIS

PATHOGENESIS –

RHYTHM IN ATRIAL FLUTTER –

IRREGULARLY – REGULAR IRREGULARLY - IRREGULAR

= A. FLUTTER + FIXED AV BLOCK A. FLUTTER + VARIABLE AV BLOCK

ECG –

RE – ENTERY CIRCUIT = COUNTER CLOCKWISE DIRECTION ➔

NEGATIVE P WAVES POSITIVE P WAVES

IN II/III/AVF = SAW TOOTH FLUTTER WAVES V1

NOTE – INCREASE THE AV NODAL BLOCK ➔ EXPOSE THE FLUTTER WAVES

TREATMENT – SAME AS ATRIAL FIBRILLATION

 MFAT – MULTI FOCAL ATRIAL TACHYCARDIA

DEFINATION –

MULTI – FOCAL = > 3 DIFFERENT P WAVE MORPHOLOGY

TACHYCARDIA = HR > 100-150 B/MIN

MECHANISM –

TRIGGERED AUTOMATICITY FROM MULTIPLE FOCI

CAUSES –

1. COPD MC CAUSE OVERALL

2. ACUTE FEBRILE ILNESS/ SEPSIS 2ND MC CAUSE OVERALL
3. DRUGS A. MC – THEOPHYLINE
B. BETA AGONISTS
C. DIGOXIN

4. ELECTROLYTES A. HYPOKALEMIA
B. HYPO – MG

ECG –

RHYTHM – IRREGULARLY – IRREGULAR

TREATMENT –

1. TREAT THE CAUSE

2. DOC – CCB/ BB (BB – CI IN COPD)

3. IF N/R ➔ DOC = AMIODARONE

 CHAPTER 7 I – APPROACH TO VENTRICULAR ARRYTHMIAS

HALLMARK –

1. VENTRICULAR CONDUCTION = SLOW ➔ BROAD QRS COMPLEX = > 0.12 SECONDS

2. NO RESPONSE TO AVN BLOCK

ORIGIN –

A. FOCAL B. DIFFUSE
1. AUTOMATICITY RE – ENTERY CIRCUIT
2. TRIGERRED ACTIVITY
MC SITE – MYOCARDIUM / PURKINJEE CELLS MC SITE – SCAR

TYPES –

1. PVC
2. VENTRICULAR TACHYCARDIA

A. MONOMORPHIC VTACH (MMVT)

B. POLYMORPHIC VTACH (PMVT) / TDP

3. VENTRICULAR FIBRILLATION
4. IDIOPATHIC VENTRICULAR ARRYTHMIAS

EVALUATION OF THE PATIENT –

1. DETERMINE IF V. ARRYTHMIA IS THE HISTORY/PHYSICAL EXAMINATION / ECG /

CAUSE OF SYMPTOMS OTHER ECG BASED INVESTIGATION

2. PRE – EXISTING CARDIAC DISEASE OR CARDIAC IMAGING

NOT

3. DETERMINE RISK OF A. SCD

B. RECURRENCE

TREATMENT –

1. ANTI ARRYTHMIC DRUGS

2. ICD
3. CARDIAC ABLATION
4. SURGERY SURGICAL CRYOABLATION + ANEURSYMECTOMY
 CHAPTER 7 J – PVC/ NON-SUSTAINED V. TACHYCARDIA AND AIVR

PVC – MOST COMMON VENTRICULAR ARRYTHMIA

HALLMARKS OF PVC –

TYPES –

1. UNI FOCAL VS MULTI FOCAL PVC

2. BIGEMINY VS TRIGEMINY –

BIGEMINY TRIGEMINY
PVC: NORMAL QRS 1: 1 1: 2
RATIO
ECG

HALL MARK OF PVCS –

PSEUDO- BRADYCARDIA = FALSE LOW PULSE BUT HR = NORMAL ➔ K/A PULSE DEFECIT –

CAUSES ATRIAL FIBRILLATION VPCS

DEFECIT >10 B/MIN <10 B/MIN
MECHANISMS –

1. INCREASED 2. TRIGGERED 3. RE – ENTERY CIRCUITS

AUTOMATICITY ACTIVATION

CAUSES –

1. MI 2. ELECTROLYTE 3. STRUCTURAL 4. INFLAMMATION

HEART INDUCED PVC
DISEASES
MC – HYPOKALEMIA EG – MVP ➔ PAPILARY LATEST MECHANISM
MUSCLE INITITATE PVC
➔ SCD

MOST IMPORTANT TRIGGER = SNS ACTIVATION

NON-DANGEROUS PVC DANGEROUS PVC

1. SEEN IN NORMAL HEARTS DISEASED HEARTS
2. QRS A. SMOOTH CONTOURS A. NOTCHED CONTOURS
B. SHARP B. SLURRED

3. BBB PATTERN LBBB PATTERN RBBB PATTERN

4. MC SITE LV/RV OUTFLOW TRACT ➔ MULTIFOCAL
THUS MC – SUPERIOR ORIGIN

5. OTHER SITES A. PAPILLARY MUSCLE A. MV/TV

B. FASICLES B. MODERATOR BAND
C. EPICARDIAL SURFACE

6. MORPHOLOGY MONO MORPHIC POLY MORPHIC

7. HR < 200 >200
8. SHORT COUPLED PVC/ NOT SEEN SEEN
R ON T PHENOMENON
SITE –

ORIGIN ECG PATTERN LEADS

1. RV LBBB V1
2. LV RBBB V1
3. SUPERIOR = TALL R WAVES 2/3/AVF
OUTFLOW TRACT ➔
AXIS IS DOWN
4. INFERIOR ➔ AXIS IS TALL/DEEP S WAVES 2/3/AVF
UP

COMPLICATION OF PVCS = PVC INDUCED VENTRICULAR DYSFUNCTION

HOW? = IF PVC = 20 % OF TOTAL BEATS IN 24 HOURS

MECHANISM –

1. TACHYCARDIA INDUCED CARIDOMYOPATHY = TICM

2. VENTRICULAR DYS-SYNCHRONY

BOTH 1 AND 2 ➔ DEPRESS VENTRICULAR FUNCTION ➔ HEART FAILURE

 ➢ PVC AND GENETIC SYNDROMES –

1. LONG QT SYNDROME
2. ARVC
3. HOCM

SIGNIFICANCE = INCREASED RISK OF SCD

➢ PVC AND ACS –

A. PERI – INFARCT PVC B. POST RECOVERY PVC

SIGNIFICANCE LESS DANGEROUS IF > 10 PVC / HOUR +
SYMPTOMATIC ➔
DEPPRESSED VENTRICULAR
FUNCTION ➔ INCREASED
MORTALITY
DOC BETA BLOCKERS + T/T AMIODARONE
HYPOKAELMIA AND HYPO –
MG
MAIN GOAL = DECREASE V. FIB ➔ DECREASE SCD

IN BOTH SUSPECTED STRUCTURAL HEART DISEASE/ GENETIC SYNDROME ➔ ADVANCED CARDIAC

IMAGING DONE
MANAGEMENT –

ROLE OF ICD ➔ PREVENT SCD

INDICATIONS –

1. > 40 DAYS POST MI + LVEF < 30 %

2. > 5 DAYS POST MI + NSVT/ INDUCIBLE VT ON EPS
3. NYHA 2/3 CHF + LVEF < 35 %
4. PATIENTS WITH INCREASED RISK OF SCD
 ACCLERATED IDIO – VENTRICULAR RHYTHM – AIVR

AIVR VENTRICULAR TACHYCARDIA

PVC >3 >3
HR <100 >100

MECHANISM – ENHANCED AUTOMATICITY >>> RE – ENTERY CIRCUIT

CAUSES –

1. MI ➔ MC – POST REPERFUSION WITH THROMBOLYTIC THERAPY

2. HOCM
3. OSAS
4. SINUS BRADYCARDIA

ECG –

TREATMENT –

1. TREAT THE CAUSE

2. DOC FOR BRADYCARDIA = ATROPINE

 CHAPTER 7 K - SUSTAINED MONOMORPHIC VENTRICULAR TACHYCARDIA –
MMVT

SUSTAINED VS NON-SUSTAINED VT

NON - SUSTAINED VT SUSTAINED VT

LASTS < 30 S OR SELF TERMINATING LASTS > 3O S OR REQUIRES INTERVENTION TO

TERMINATE

CLASSIFICATION OF VENTRICULAR TACHYCARDIAS –

A. MONO-MORPHIC VENTRICULAR B. POLYMORPHIC VENTRICULAR

TACHYCARDIAS = MMVT TACHYCARDIAS = PMVT / TDP
1. FAST 2. SLOW SINUSOIDAL
SINUSOIDAL RATE
RATE =
VENTRICULAR
FLUTTER
CAUSE –

I. HYPOKAELMIA
II. DRUGS – IC
AND TCA

HOW DO YOU DIAGNOSE SCARS?

1. ECG Q WAVES

2. ECHO RWMA

3. GE – MRI DELAYED GADOLINIUM ENHANCEMENT

FORMATION OF MMVT –

R ON T PHENOMENON/ SHORT COUPLED PVC ➔ > 3 PVC ➔ MMVT

ECG HALLMARKS OF MMVT –

1. BROAD COMPLEX TACHYCARDIA

2. AV DISSOCIATION = PATHOGNOMIC

DD OF AV DISSOCIATION –

1. COMPLETE HEART BLOCK 2. VENTRICULAR TACHYCARDIA

AV DISSOCIATION ➔ IF ATRIA AND VENTRICLE CONTRACT TOGETHER ➔ ATRIA CONTRACTS AGAINST

CLOSED TV ➔ BACKFLOW OF BLOOD INTO IJV ➔ CANNON A WAVES

3. FUSION BEAT VS CAPTURE BEAT –

FUSION BEAT CAPTURE BEAT

ATRIAL BEAT IS FUSED WITH V. TACH WAVE ATRIAL BEAT IS VISIBLE DISTINCTLY FROM
VTACH WAVE
CAUSES OF SUSTAINED VENTRICULAR ARRYTHMIAS –

A. MMVT B) PMVT/ TDP ➔ VFIB

1. IDIOPATHIC VT 1) HOCM
2. ISCHEMIC CARDIOMYOPATHY 2) GENETIC ARRYTHMIAS
3. NON – ISCHEMIC CARDIOMYOPATHY 3) IDIOPATHIC PMVT/VFIB
4. ARVC
5. REPAIRED TOF

TYPES OF MMVT –

NORMAL HEART DISEASED HEART

MECHANISM A. INCREASED A. RE- ENTERY CIRCUIT
AUTOMATICITY IN AROUND SCARS
PURKINJEE SYSTEM

B. RE-ENTERY CIRCUIT IN
PURKINJEE SYSTEM
MC CLF PALPATATIONS SYNCOPE
RISK OF VFIB = RISK OF SCD LESS MORE

1. IDIOPATHIC VT

BENIGN CONDITON WITH -

A. NORMAL ECG
B. NO STRUCTURAL HEART DISEASES
C. NO GENETIC SYNDROMES
D. NO RISK OF SCD

HALLMARK – SNS SENSITIVE

TYPES –

ORIGIN

1. OUTFLOW TRACT – MOST COMMON RV LV

OVERALL LBBB PATTERN + RBBB PATTERN +
SUPERIOR ORIGIN SUPERIOR ORIGIN
= SUPERIOR ORIGIN (SINCE OUTFLOW = UP)
2. LV FASICLE – 2ND MOST COMMON
OVERALL = K/A BELHASSEN VT / MC – LAF BLOCK ➔ RBBB PATTERN + LAD
VERAPAMIL SENSITIVE VT

= RBBB PATTERN (SINCE FROM LV)

3. PAPILLARY MUSCLE ANTERO – LATERAL POSTERO – MEDIAL

RBBB PATTERN + RBBB PATTERN +
= RBBB PATTERN (SINCE FROM LV)
POSITIVE R IN LEAD 3 MONOPHASIC R
AND NEGATIVE R IN WAVES
LEAD 1

COMPLICATION –

REPEATED BURSTS OF VT ➔ TACHYCARDIA INDUCED CM ➔ DEPRESSED LV FUNCTION

TREATMENT –

DOC – BETA BLOCKERS/ CCB

N/R
DOC – FLECANIDE
N/R
TOC – CATHETER ABLATION

NOTE – ICD IS NOT INDICATED

2. ISCHEMIC CARDIOMYOPATHY –

CAUSE – SCAR ➔ THUS PATIENT HAS A H/O PREVIOUS MI

CLINICAL CASE – PATIENT WITH PREVIOUS H/O OF MI ➔ PRESENTS WITH ➔ MMVT

TREATMENT –

TOC = ICD >>> AAD

S/E OF ICD –

UNNECCESARY SHOCKS ➔ INCREASED RATES OF CHF AND RECURRENT VT ➔ INDICATION TO START

ADDITIONAL THERAPY –

1. BETA BLOCKERS + ACEI/ARBS

2. TOC – CATHETER ABLATION >>>> AAD

TRIALS – VANISH AND BERLIN VT

3. NON-ISCHEMIC CARDIOMYOPATHY –

CAUSES –

GENETIC ACQUIRED
LAMININ A/C MUTATION 1. POST VIRAL
2. INFLAMMATION –

A. MYOCARDITIS
B. SARCOIDOSIS
C. CHAGAS DISEASE

MECHANISM - SCAR

MC SITE OF SCAR – INTRA MURAL / SUB EPICARDIAL SCAR

IOC – ENDOMYOCARDIAL BIOPSY

TREATMENT – SAME AS ABOVE ➔ EXCEPT – LESS ROLE OF CATHETER ABLATION

 4. ARRYTHMIOGENIC RV DYSPLASIA – ARVD

GENETIC MUTATION –

AD AR

1. NAXOS SYNDROME 2. CARVAJAL SYNDROME

DESMOSOME PLAKOPHILLIN 2/ PLAKOGLOBIN DESMOPLAKIN

PATHOGENESIS –

RV → REPLACED BY FIBRO-FATTY TISSUE

A. DELAYED ACTIVATION OF RV ➔ LBBB PATTERN – IN V1-V3

1. BROAD QRS COMPLEX 2. T WAVE INVERSION 3. NOTCHED UPSTROKED

WITH WILLIAM S WAVE = EPSILON
PATTERN WAVE

B. RE – ENTERY CIRCUITS AROUND FIBRO – FATTY RV ➔ MMVT + LBBB PATTERN – MC

ARRYTHMIA IN ARVD

TREATMENT – SAME AS ABOVE

 5. REPAIRED TOF –

CAUSE - POST VENTRICULOTOMY >>>> HT VENTRICLE

MECHANISM – SCAR ➔ STEROTYPED RE – ENTERY CIRCUIT ➔ RV ORIGIN ➔ MMVT + LBBB PATTERN

TREATMENT – SAME AS ABOVE

OVERALL MANAGEMENT OF MMVT –

 CHAPTER 7 L – PMVT AND VFIB

CAUSES OF PMVT –

1. MI
2. HOCM
3. IDIOPATHIC PMVT
4. CHANNELOPATHIES / GENETIC SYNDROMES –

A. LONG QT B. BRUGADA C. CATACHOLAMINERGIC D. SHORT QT

SYNDROME SYNDROME VT SYNDROME

5. EARLY REPOLARISATION SYNDROME

MECHANISM OF PMVT –

1. MULTIPLE RE – ENTERY CIRCUITS

2. MULTIPLE RE – ENTERY FOCI

COMPLICATION OF PMVT/TDP –

PMVT/TDP ➔ VENTRICULAR FIBRILLATION ➔ SCD

ECG OF PMVT –
 1. MI AND PMVT –

MAX RISK – 1ST HOUR = GOLDEN HOUR

MAX RISK OF MORTALITY DUE TO PMVT - < 48 HOURS

TREATMENT –

ACUTE CHRONIC
A. ACLS ICD
B. TREAT THE CAUSE – T/T MI AND
CORRECT ELECTROLYTES

2. HOCM –

MOST COMMON CARDIAC GENETIC DISEASE

MC ARRYTHMIA – ATRIAL FIBRILLATION

MCC OF SCD - PMVT >>> MMVT DUE TO APICAL ANEURSYM SCAR

HIGH RISK OF SCD –

1. YOUNG
2. NON-SUSTAINED VT
3. FAILURE OF RISE OF BP DURING EXERCISE
4. WITHIN 6 MONTHS OF SYNCOPE
5. VENTRICULAR WALL THICKNESS > 3 CM
6. SEVERE LVOO
7. TRANSCORTICAL ETHANOL SEPTAL ABLATION >>> SURGICAL MYOMECTOMY

TOC – ICD

3. IDIOPATHIC PMVT –

MCC - PVC

MC SITE – LAF BLOCK ➔ LAD + RBBB PATTERN

 4. CHANNELOPATHIES –

A. LONG QT SYNDROME –

DEFINATION –

MALES FEMALES
QTC >0.44 S >0.46 S

TYPES –

1. CONGINENTAL LONG QT SYNDROME

2. ACQUIRED LONG QT SYNDROME

 CONGINENTAL LONG QT SYNDROME

CLASSIFICATION –

A. GENES B. INHERITENCE C. MULTISYSTEM

DISORDER WITH LONG
QT SYNDROME

A. GENES –

I. MAJOR LONG QT SYNDROME – 75%

LONG QT 1 LONG QT 2 LONG QT 3

GENE KCNQ1 - LOF KCNH2 - LOF SCN5A - GOF
MUTATED
CHANNEL IKS IKR INA
AFFECTED
% 35 30 10
ARRYTHMIA EXERTION SUDDEN AUDITORY/ SLEEP
PPT BY EMOTIONAL STIMULUS
MC – SWIMMING
T WAVE

BROAD BASED T WAVE NOTCHED T WAVE NARROW BASED T WAVE

TREATMENT T/T THE CAUSE + DOC = NON-SELECTIVE BETA BLOCKERS ➔ N/R ➔ ICD

INCREASED RISK OF SCD –

1. QTC > 500 MS

2. FEMALE GENDER
3. H/O SYNCOPE
4. H/O CARDIAC ARREST

II. MINOR LONG QT SYNDROME – 25 %

 B. INHERITENCE –

AD AR
1. ROMANO – WARD SYNDROME – MC 1. JERVEL – LANGE – NEILSON SYNDROME
OVERALL
2. DEAFNESS NOT PRESENT 2. DEAFNESS PRESENT

C. MULTI SYSTEM DISORDERS WITH LONG QT SYNDROME –

1. TIMOTHY SYNDROME – LONG QT SYNDROME 8

C CACN1 MUTATION IN EXON 8A AND EXON 8

A AUTISM SPECTRUM DISORDER
R ROUND FACES
D DIGITS ABNORMAL = SYNDACTYLY ➔ IF ABSENT
= ATYPICAL TIMOTHY SYNDROME ➔ ONLY
EXON 8 MUTATION

DECREASE GLUCOSE = HYPOGLYCEMIA

I IMMUNOSUPRESSED
AC CARDIAC ARRYTHMIA –

A. FETAL AV BLOCK
B. TDP
C. MARCOSCOPIC T WAVE ALTERANS

DOC – BETA BLOCKERS /CCB

2. ANDERSON TAWI SYNDROME – LONG QT SYNDROME 7

GENETICS – TYPICAL ATS/ ATS1 ➔ CHROMSOME 17 ➔ KCNJ2 LOF MUTATION ➔ AFFECTS KIR 2.1
CHANNEL’S ALPHA SUBUNIT – C TERMINAL END ➔ PRESENT IN –

A. BRAIN
B. HEART
C. SKELETAL MUSCLE
 A ARRYTHMIAS –

MC – VPCS + U WAVE

THUS, INCREASED QU INTERVAL

N NERVOUS SYSTEM – EPILEPSY
D DYSMORPHIC FEATURES
E EPISODIC/ PERIODIC PARALYSIS

DOC FOR ARRYTHMIAS – BETA BLOCKERS/ CCB

DOC FOR PERIODIC PARALYSIS – CA INHIBITORS

3. ANKYRIN B SYNDROME - LONG QT SYNDROME 4

 ACQUIRED LONG QT SYNDROME

CAUSES – NICED -

N = NUTRITIONAL 1. ANOREXIA
2. STARVATION
3. BYPASS SURGERY
4. CELIAC DISEASE
I = INTRA CRANIAL INCREASED ICP
C = CARDIAC 1. MI
2. MYOCARDITIS
3. MARKED BRADYCARDIA
4. STRESS CARDIOMYOPATHY
E = ELECTROLYTES 1. HYPOKALEMIA
2. HYPOCALCEMIA
3. HYPOMAGNESEMIA
E = ENDOCRINE 1. HYPOTHYROIDISM
2. HYPER PTH
3. PHEOCHROMOCYTOMA
4. HYPERALDOSTERONISM
D = DRUGS A = ANTI ARRTHMIC = IA/III

B = ANTI BIOTICS -

I. MACROLIDES
II. FQ
III. CLINDAMYCIN
IV. CQ
V. AMANTIDINE
VI. KEOTCONAZOLE

C = CNS INHIBITORS – ANTI PSYCHOTICS AND TCA

D = DIURETICS

E = ANTI EMETIC – ONDENSETRON

F = FAALTU –

I. CITRATE POST MBT

II. COCAINE
III. METHDONE

H = HISTAMINE BLOCKERS – CAT DRUGS

ECG –

TREATMENT –

1. T/T THE CAUSE

2. 2 GRAMS MGSO4

MOA = INHIBIT PVC

N/R
3. INCREASE HR = OVERDRIVE PACING ➔ 100-120 B/MIN ➔ INHIBIT PVC

DOC = ISOPRENALINE
 B. BRUGADA SYNDROME –

GENETICS – SCN5A LOF MUTATION

MC – MALES > FEMALES

PRECIPITATED BY – SLEEP / FEVER

CL/F –

Q R ST
INCREASED QT INTERVAL ➔ RBBB ST ELEVATION + T WAVE
PMVT/TDP INVERSION IN V1 – V3

TYPES OF BRUGADA SYNDROME –

ST ELEVATION T WAVE INVERSION ECG

TYPE 1 COVED ST ELEVATION > T WAVE INVERSION
2MM

TYPE 2 SADDLE BACK ST BI PHASIC T WAVE

ELEVATION > 1 MM

TYPE 3 1 OR 2 WITH < 1 MM

NOTE – UNMASK THE ST ELEVATION VIA IA/IC DRUGS

TREATMENT –

1. QUINIDINE/CCB + ISOPRENALINE
N/R
2. CATHETER ABLATION OF EPICARDIAL RV FREE WALL
N/R
3. TOC = ICD

C. CATACHOLAMINERGIC PMVT –

LARGEST ION CHANNEL = RYR2

GENETIC –

AD AR
RYR 2 MUTATION – MC OVERALL CALSEQUESTRIN 2 AND TRIADIN MUTATION

PATHOGENESIS –

NOTE – QT INTERVAL = NORMAL

CL/F – EXERCISE/ EMOTION INDUCED SYMPTOMS

TREATMENT –

A. DRUGS B. SURGERY C. ICD

1. DOC = BETA BLOCKERS LEFT CARDIAC SNS TOC
DENERVATION
2. CCB
3. FLECANIDE

D. SHORT QT SYNDROME –

DEFINATION –

QT INTERVAL - < 360 MS

QTC INTERVAL - < 300 MS

CAUSES –

GENETIC ACQUIRED
GOF MUTATION IN IKR 1. HYPERCALCEMIA
2. DIGOXIN

CL/F –

1. ATRIAL FIBRILATION
2. PMVT ➔ SCD

4. EARLY REPOLARISATION SYNDROME –

GENETICS – KCNJ8 MUTATION

SEEN WITH –

1. NORMAL PEOPLE
2. BRUGADA SYNDROME
3. POST RECOVERY FROM VFIB

CL/F – EARLY REPOLARISATION PATTERN + VFIB ➔ SCD

 EARLY REPOLARISATION PATTERN = MC – FARLANE CRITERIA –

1. J POINT ELEVATION > 1 MM

2. QTS < 120 MS

IN > 2 CONTIGOUS LEADS – MC - INFERIOR LEADS

TOC – ICD IF H/O CARDIAC ARREST

 VENTRICULAR FIBRILLATION

MECHANISM –

1. SPIRAL WAVE RE- ENTERY

2. MULTIPLE CIRCUIT RE – ENTERY

MCC OVERALL – ISCHEMIA

ECG -

AFIB/A. FLUTTER V.TACH V.FIB

P WAVE/T WAVE FIBRILLATORY/ NOT PRESENT NOT PRESENT
FLUTTER WAVES

QRS COMPLEX NARROW COMPLEX BROAD COMPLEX NOT PRESENT

MANAGEMENT –

1. MANAGE ACCORDING TO ACLS PROTOCOL – DEFIBRILLATION

2. T/T CAUSE

3. IF NO CAUSE – TOC = ICD

 CHAPTER 7 M – ELECTRICAL STORM AND INCESSANT VENTRICULAR
TACHYCARDIA

ELECTRICAL STORM INCESSANT VTACH

>3 EPISODES OF VTACH/VFIB IN 24 HOURS THAT RECURRENCE OF VT SHORTLY AFTER
REQUIRES TERMINATION TERMINATION

CAUSES OF ELECTRICAL STORM –

1. MI – ISCHEMIC CARDIOMYOPATHIES
2. PVC INDUCED
3. LONG QT SYNDROME
4. INFLAMMATORY CARDIOMYOPATHIES

NOTE – PURKINJEE FIBRES ➔ MOSTLY ‘SURVIVE’ ACUTE ISCHEMIA DUE TO –

1. INCREASED GLYCOGEN STORES

2. DIFFUSED OXYGEN FROM LV CAVITY

THUS, ON RE VASCULARISATION ➔ PURKINJEE FIBRES INITITATE PVC ➔ VFIB ➔ ELECTRICAL STORM

MANAGEMENT –

A. STABLISE B. RELIEVE TRIGGERS C. DECREASED

RHYTHM SNS TONE

EARLY ACLS PROTOCOL – 1. ELECTROLYTE 1. SEDATION AND

DEFIBRILLATE INTUBATION
2. CORONARY RE-
VASCULARISATION 2. BETA BLOCKERS
LATE 1. ANTI ARRYTHMIC 1) OVERDRIVE 1. STELLATE
– IA PACING GANGLION BLOCK
➔ SNS BLOCK
2. TOC – CATHETER 2) ECMO/IABP
ABLATION 2. SURGICAL SNS
DENERVATION
3) ANTI
INFLAMMATORY 3. UPPER THORACIC
THERAPY EPIDURAL
ANESTHESIA
 OVERALL APPROACH TO PATIENT WITH ECG
= RAHIM
1. R – RATE –

NORMAL HR = 60-100 B/MIN

2. R – RHYTHM –

NORMAL RHYTHM – SINUS RHYTHM

3 QUESTION RULE FOR ASSESING RHYTHM –

QUESTION 1 –

QUESTION 2 –
QUESTION 3 –

REGULAR RHYTHM IRREGULAR RHYTHM

REGULAR R-R INTERVAL IRREGULAR R-R INTERVAL

A - ALL CHECKING –

PR AND QT INTERVAL ➔ P: QRS ➔ P WAVE ➔ QRS ➔ ST SEGMENT ➔ T WAVE

A – AXIS – I AND AVF

H – HYPERTROPHY – ATRIA AND VENTRICLE

I – INFARCTION

M – MISCELLANEOUS