ECG Signs, Scores, Tips, Tricks Flashcards
ECG in Pericarditis
ECG in Pericarditis
= PR depression
= Concave ST elevation global
= PR elevation in aVR/V1
= Sinus tachycardia
= AFib, Flutter, APC’s
= Spodick sign ie downsloping TP
= Late: flat T and then inversion
ECG on paper analysis
The rate of paper (i.e. of recording of the EKG) is 25 mV/s which results in:
1 mm = 0.04 sec (or each individual block)
5 mm = 0.2 sec (or between 2 dark vertical lines)
Distance between Tick marks = 3 seconds (in the rhythm strip)
The voltage recorded from the leads is also standardized on the paper where 1 mm = 1 mV (or between each individual block vertically) This results in:
1 mm = 0.1 mV
5 mm = 0.5 mV (or between 2 dark horizontal lines)
10 mm = 1.0 mV
ECG in pulmonary embolism
Various Presentation
Sinus tachycardia most common
Tall R in V1
RV strain -
= ST down T down in V1V2V3
= ST down T down in II/ III/ aVF
Right BBB
T inversions in V1V2V3
S1S2S3 - deep S in 1/2/3 leads
S1Q3T3 - deep S1, Q in 3, T inv in 3
Inferior STEMI - rarely
ECG in Dextrocardia
= Right axis deviation
= Positive QRS complexes (with upright P + T) in aVR (reversed)
= Lead I: inversion of all complexes, aka ‘global negativity’ (inverted P, negative QRS, inverted T)
= Absent R-wave progression in the chest leads (dominant S waves throughout)
= Normal life exceptancy if no other abnormalities and equal frequency in Male:females
Associations:
= Kartagener syndrome with situs inversus + bronchiectasis + recurrent sinusitis + dextrocardia
STE in lead aVR
STE in aVR - mechanism
STE in aVR - Causes
STE in aVR- Example 2
STE in aVR- Example 3
STE in aVR- Example 4
STE in aVR- Example 5
STE in aVR- Example 6
STE in aVR- Example 7
STE in aVR- Example 8
RBBB pattern wide complex VTach- criteria’s in favor of VTach
Lead V1:
- rSR’ with R’ > r
- RS with R > S
Lead V6:
- if a Q wave is present - it must be 40 ms and < 0.2 mV
Broad complex tachycardia with LBBB criteria’s
Lead V1:
- rS or QS with time to S wave nadir is < 70 ms
Lead V6:
- R wave with no Q wave
Tachyarrhythmia as likely VTach
- broad QRS > 140 ms or 3.5 small squares
- markedly negative LAD
- < 40 ms R-R variation
- QRS concordance in chest leads is mainly positive side
- capture beats, fusion beats
- known CHF or poor LVEF
Irregular Broad Tachycardia Types
- Atrial fibrillation with aberration
- Atrial flutter with aberration
- Multifocal atrial tachycardia with BBB
- Pre-excited AF (WPW)
- Torsade de pointes
Monomorphic Ventricular Tachycardia Rx
Precordial thump
Unsynchronised cardioversion 200 J
If stable -
- IV Amiodarone or
- IV Sotalol or
- IV Procainamide
- Lidocaine or beta blockers 2nd line
- IV Magnesium 8 mmols over 5 min followed by 60 mmols in 50 ml glucose over 24 Hrs if at risk of low Mg (on diuretics, alcoholics)
Think of need for PCI
- correct UE and acidosis
Brugada syndrome
ST coving elevation in V1-V3
ST elevation might need a trigger as fever
Can be induced with Na channel blockers
Risks: Sudden death, Cardiac syncope due to arrhythmia
Autosomal dominant, SCN5a mutation
Diagnostic tests - additional 1mm STE in V1-V3 after iv Flecainide 2mg/kg or Procainamide 10 mg/kg in 10 minutes
Rx - Quinidine, promt fever control, ICD,
Avoid Brugada drugs
Brugada Syndrome Types
Type 1: coved ST elevation in V1V2V3 > 2mm at least 2 leads followed by negative t waves
Type 2: horizontal saddle type ST elevation > 2mm in at least 1 of V1V2V3
Type 3: either type morphology of 1 or 2 types but elevation is < 2mm in V1V2V3
QTc formulas
QTc nomogram
LVH criteria
LVH: Voltage criteria:
- tallest R (v4-v6) + deepest S (v1-v3) > 40
SV1 + RV6 > 35 - tallest R (v4-v6) > 27 mm
- deepest S (v1-v3) > 30 mm
- R in aVL > 13 mm
- QRS > 0.08
- abnormal ST depression or T inversion in V4-V6
Limb leads
Lead I: negative right arm, positive left arm
Lead II: negative right arm, positive left leg
Lead III: negative left arm, positive left leg
All axis forms an equilateral triangle called Einthoven’s triangle.
Augmented leads
All unipolar leads are termed V leads and includes augmented & precordial leads.
aVR - faces heart from right shoulder
aVF - faces heart from left foot
aVL - faces heart from left arm
HOCM ECG
Deep septal Q waves in I, aVL, V4V5V6
LVH findings: LAD
Brugada algorithm for VT determination
- no precordial lead has both R and S
- onset of R to nadir of S > 100 ms in any V1 - V6
- AV dissociation present
-
Morphological criteria ++ for VT
V1 = monophasic R or biphasic QRS or R>R’ ie rabbit ear pattern
V2 = R<S or dominant Q or monophasic R
Likely VT in ECG
- negative QRS in precordials v1-v6
- QRS > 160 ms always VT
- QRS in RBBB type > 140 ms
- axis - northwest ie > 270* suggests VT
- morphological criteria positive
Morphological criteria for VT
RBBB type VT:
V1 lead = monophasic R or biphasic QRS or R>R’ (rabbit ear)
V6 lead = R< S or QS/QR with dominant Q or monophasic R (no q/s/r’)
—————
LBBB type VT :
V1 or V2 lead =
Initial r>30ms or
onset of r to nadir of S > 60 ms or
Notched downstroke
V6 lead=
Any q wave or
QS or QR present
Kindwall criteria for VT/SVT
Decides VT rather than SVT present
In LBBB type:
V1 lead
Notched downstroke QRS
R wave in V1V2 > 30 ms
Start of r to nadir of S >60 ms
V2 lead:
Any q present
Brugada sign of VTach
- r wave length > 30 ms favours VT
- Distance from onset of R wave to nadir of S wave is > 100 ms in leads V1-V6 favours VT
- notching or slurring along downstroke of QRS favours VT
Josephson sign
Notching/slurring near nadir of S wave in V2
Vereckei algorithm - to determine VT/SVT in a wide tachycardia
Findings favouring VT during tachycardia rather than SVT
- Broad QRS > 160 ms
- Rabbit ear R waves ie R>R’
- AV dissociation present
- Northwestern, 270 degree ie ‘No man’s land’ axis
- Any q wave present in V6
- R wave>30 ms + notching of downstroke in S wave + start of r wave to end of S wave > 60 ms in V1 /V2 lead
Spodick sign
Down sloping TP segment is seen in 30% of cases of pericarditis as an early manifestation.
Tilt Table testing for syncope evaluation
= keep fasting for 2 hours
= keep in a dark quiet room (reduces sympathetic drive)
= five minutes supine before tilting to 70 degrees head up
= keep head up 20 minutes then give GTN spray
Interpretations:
1. Old age effect: exaggerates hypotension without Bradycardia
2. Ortho static Hypotension: Hypotension > 20 mmHg without bradycardia or has tachycardia
3. Neurally mediated syncope: Hypotension along with bradycardia (inappropriate)
Mechanism : along with hypotension - medullary vasodepressor region is stimulated through C fibres which causes inappropriate bradycardia through vagus and also sudden vasodilation by reduction in sympathetic tone leading to hypotension + bradycardia + syncope
Responses to Tilt-table testing in neurocardiogenic syncope
Type 1
Mixed bradycardia & vasodepressor response
Bradycardia but remains above 40/minute
Rx - cardiac pacing
Type 2A:
Bradycardia rate below 40/minute > 10 seconds but No asystole
Rx with cardiac pacing for carotid sinus hypersensitivity (CSH)
Type 2B:
Asystole occurs > 3 seconds
Rx - cardiac pacing for CSH
Type3:
Vasodepressor response, no cardio inhibition
Hypotension > 50% but heart rate doesnot drop > 10%
Rx- Compression stockings, Salt tablets, Fluodrocortisone, SSRI, betablockers (paradoxical effect)
Hypokalemia effects on ECG
Biphasic T waves: initial T wave goes down then goes up (Opposite happens with ischemia, T goes up & then down)
- Progressive flattening of T waves
- Small u waves after T waves
- peaked P waves when severe
- ST depression
Bradycardia: Causes
Causes of Bradycardia:
- Cardiomyopathy
- Vagal Stimulation: Vomiting
- Glaucoma
- Hyperkalemia
- Hypothyroidism
- Hypothermia
- Raised Intracranial pressure
- Inferior wall STEMI
- SA node disease
- Myocarditis
Drugs causing Bradycardia: Betablockers, CCB, Digoxin, Lithium, Amiodarone, Timolol Eye drops
Osborn or J wave
Small notch at end of S wave
Seen in : Hypothermia mainly but also in: Hypercalcemia, Brugada syndrome, neurological injury
Brugada drugs (to avoid)
Na channel blockers: Ajmaline, Flecainide, Procainamide, Propafenone
Psychotropics: Amitryptiline, Clomipramine, Lithium, Oxcarbazepine
Anaesthestics/ Analgesics: Bupivacaine, Procaine, Propofol
Other substances: Alcohol, Acetyl choline, Cannabis, Cocaine, Ergonovine,
Wellen’s Syndrome
- Biphasic (Pattern A) or deeply inverted (pattern B) T waves in V2V3 - This pattern persists even when patient pain free.
- Isoelectric or minimally elevated ST <1mm
- No q waves in precordial leads
- Preserved R wave progression ie R in V3 > 3mm
- Recent anginal chest pain with normal or slightly elevated Troponins
- LAD Lesion, may be significant stenosis
de-Winter T waves
anterior STEMI equivalent
- tall, prominent, symmetrical T waves in precordial leads with
- upsloping ST depression > 1mm @ J point in precordial leads
- absent STE in precordial leads
- reciprocal STE in aVR, 0.5-1 mm
Typical STEMI may follow this pattern
Wolf-Parkinson-White (WPW) syndrome
- short PR < 120 ms
- delta wave ie slurring of upstroke of R wave due to conduction through accessory tract
- QRS > 110 ms
- discordant ST-T opposite to QRS complex
- Pseudo-infarction pattern in 70% ie pseudo q waves in inferior/ anterior leads OR prominent R waves in V1V2V3 mimicking posterior infarction
WPW syndrome Types
Type A WPW-
Left sided accessory tract present
positive delta wave in all precordial leads
R-S > 1 in V1
Type B WPW-
- Right sided accessory tract present
- negative delta wave in V1V2
short PR in both types
Accessory tract can be bidirectional, anterograde or retrograde conductor
Lown-Ganong-Lewine (LGL) syndrome
pre-excitation type with ** intra-nodal** accessory tract composed of James fibres
- short PR interval < 120 ms
- normal P wave axis
- normal/narrow QRS < 110 ms
- can cause paroxysmal SVT
ECG in pericarditis
ECG in TCA overdose
TCA’s are Na channel blockers:
- QRS duration >100 ms in lead II
- Terminal R wave > 3mm in aVR
or
R/S ration > 0.7 in aVR
Sinus tachycardia due to muscarinic blockade
Sgarbossa criteria in LBBB
modified Sgarbossa:
1. Concordant ST elevation > 1mm in leads with a positive QRS ie STE is in same direction as +ve qrs complexes
2. Concordant ST depression > 1 mm in V1V2V3 ie ST goes down same as negative QRS
3. ST elevation at J point relative to QRS onset, is at least 1mm AND has an amplitude at least 25% of the preceding S wave
consider ACS in a pre-existing LBBB case
modified Sgarbossa ECG
Managing AFib with WPW
- urgent Sync-Cardioversion
- ## Avoid BB, CCB, Adenosine
Brugada Criteria
Brugada Sign: coved ST elevation >2mm in V1V2v3 followed by inverted T wave
and must have -
- past documented VF/ VTach
- family H/o sudden death
- Brugada type ECG in family members
- H/o Syncope
- nocturnal agonal breaths
- inducibility of VTach with brugada drugs (avoid them)
ECG in Hypercalcemia
very short QT interval
bizarre looking QRS
J waves as in Hypothermia at end of QRS, best seen in V1
Bazzet formula for corrected QTc
QTc = QT interval / square root of RR interval
normal QTc < 440 seconds
Prolonged QTc risk of torsade de pointes
Fridericia formula for corrected QTc
QTc = QT interval/ (RR)rest to 1/3
Framingham formular for QTc
QTc = QT + 154 x (1-RR)
Hodges formula for QTc
QTc = QT + 1.75 x {(60/RR) - 60 }
Rautaharju formula for QTc
QTc = QT x (120 +HR) / 180
Tachycardia: Regular vs Irregular types
Regular tachycardias:
- Sinus tachycardia
- Atrial flutter with 2:1 block
- Atrio-ventricular Reentry tachycardia through AP (AVRT), ex- WPW
- AV nodal Reentry tachycardia (AVNRT) - p waves inverted/ incorporates in QRS
- Intra-atrial reentry tachycardia
—————————-
Irregular Tachycardias:
- Atrial fibrillation
- Atrial flutter with variable block
- Multi-focal atrial tachycardia: > 3 morphologies of P waves seen
Various MI-Involved ECG leads-Coronaries
Septal MI - V1V2 - proximal LAD
Anterior MI - V3V4 - LAD
Lateral mi = V5V6, I , aVL = LCx
Anteroseptal = V1 TO V4 = LAD
Inferior MI = II, III, aVF, Reciprocal changes I, aVL = RCA
Posterior MI = V7V8V9, Reciprocal in V1V2V3 = RCA or LCx
JVP waveforms
Ascent waves:
A - atrial contraction
C - Tricuspid elevation into Rt atrium
V - back pressure from blood filling RA
Descent waves:
X - downward movement as RV contracts
Y - opening of tricuspid in early RV diastole
ECG in posterior MI
Reciprocal ST depression in V1-V4
Tall broad R wavesin V1V2, R/s ratio > 1
Upright T waves in V1V2
Dominant R wave in V2
STE in V7V8V9
SA block types
First degree: normal ECG
Second Degree: dropped p wave, Type I & 2
Third Degree: no p waves in ECG, junctional bradycardia, retrograde negative P waves in inferior leads, II, III, aVF
SA nodal Block: Second degree
sinus impulses are intermittently blocked within SA (sino-atrial) junction and does not cross it - causing dropped P wave
This is followed by prolonged next PP interval - this one shoulder be twice the normal PP interval.
SA block: Type 1: Second Degree
Progressive prolongation of SA conduction
progressive slowing of SA conduction
progressive shortening of PP intervals (one P to next P) - then failure of conduction of P wave and - dropped P wave with long pause ie long P-P interval (less than double the normal PP).
Fault is in SA junction conduction with progressive prolongation like 50-70-80 etc
PP interval shortnes like 850-830-810 then drops
Long PP interval 1520 is shorter than double of normal PP 850
SA block: Type 2: Second degree
intermittent conduction block at SA junction
No progressive shortening PP interval
sudden dropped P wave
Long PP interval double the normal PP
then conduction resumes normally
SA Block: Third Degree
no P waves conducted in SA junction
junctional rhythm takes over
retrograde P waves can be found comming from junction
bradycardia as junctional rhythm is slow
SA Block: Extrinsic causes
Drugs: BB, CCB, Digoxin, Amiodarone, Ivabradine, Sotalol
Physical training - marathon runners
Vagal effects
Obstructive sleep apnea (OSA)
Hypo - kalemia,
Hyper-calcemia/ Kalemia/ Magnesemia
Hypo - thyroidism
Hypo-xia
Hypo-thermia
Anorexia, Acidosis, Raised ICT
Temporal Lobe epilepsy
SA block: Intrinsic Causes
CABG, Valve replacement, Maze operation, Heart transplant, TAVI
Aging, degenerative changes: MI, Cardiomyeopathies, Ischemia, Genetic
Congenital Heart diseases
Chagas disease
Sinus tachycardia ablation
Radiation therapy
Infiltration: Sarcoidosis, Amyloidosis, Haemochromatosis
Collagen Vascular diseases: RA, Scleroderma, SLE
Storage diseases, NMD’s
Pacing Recommendations in SA blocks
- Recommended when symptomatic bradycardia: Class 1/ Level B
- Recommended in tachycardia:Bradycardia form of sinus node disease (SND) to control bradycardia and enable drugs for tachycardia at same time (alternate - ablation)
- NOT Recommended for bradycardia in SND due to reversible causes
Pacemaker Syndrome
Pacemaker syndrome is most commonly seen in the setting of a single chamber device with ventricular sensing and pacing lead. Since there is no atrial sensing lead to guide the ventricle, the ventricle contracts at the programmed rate regardless of the timing of atrial contraction. This leads to loss of AV synchrony which leads to a loss in stroke volume and cardiac output. VA conduction, which is usually a ventricular beat finding its way upwards to the atria also leads to a mistimed atrial contraction and produces similar effects.
Symptoms - syncope, CHF symptoms, Fatigue, Low pulse volume, Hypotension,
Rx - dual chamber pacing
AV block: Second Degree: Wenkebach/ Mobitz I
progressive prolongation of PR interval followed by no conduction at all ie dropped P wave and QRS complex (no p-qrs-t) then pattern resumes
Pacing recommended if symptomatic or block noted at or infra HIS levels in EP studies.
AV Block: Third degree: CHB
sinus wave is not conducted through AV node and escape rhythm takes over which can be
- broad QRS, slow escape rhythm
- narrow QRS, relatively rapid escape rhythm
Left Posterior Hemiblock
posterior branch of LBB blocked
- Right axis (RAD) between 90 and 140
- QRS duration < 120 ms
- rS pattern in lead I, aVL
- qR pattern in leads II, III, aVF
prolonged R wave peak time > 45 ms in aVF
Left Anterior Hemiblock (LAHB)
anterior branch of LBBB blocked
- Left axis deviation, -30 to -90
- QRS duration < 120 ms
- rS in II, III, aVF deep S in II, III
- qR in leads I, aVL
- no other cause for LAD like LVH or Inferior MI
Left Bundle branch block (LBBB)
QRS > 120 ms ie broad
Axis usually Left (LAD)
QS or rS in V1 (W type) with positive T wave and ST slightly elevated
uniq M shaped R wave in V6 with negative T
(W in V1 and M in V6)
positive broad R in I, aVL with negative T wave
QS in aVR with positive T wave
Incomplete LBBB
QRS between 110-120
Prolonged R peak time in V4V5V6 > 60 ms
no Q waves in I, V5V6
slurring of ascending R wave in left precordials
LVH pattern
Causes of LBBB
Aortic stenosis
Ischaemic Heart disease
Hypertension
Dilated cardiomyopathy
Anterior MI
Hyperkalemia
Digoxin Toxicity
Lenegre-Lev disease: primary degenerative disease (fibrosis) of the conducting system
ECG in RBBB
QRS > 120 ms
Right axis deviation if LPHB +
Left axis if LAHB +
** rsR’ in V1** and usually also in V2
asymmetrical negative T wave in V1V2
QR in aVR with slurring in R
negative T wave and qRs in lead I, aVL with slurring in S wave
causes of RBBB
Right ventricular hypertrophy / cor pulmonale
Pulmonary embolus
Ischaemic heart disease
Rheumatic heart disease
Congenital heart disease (e.g. atrial septal defect)
Myocarditis
Cardiomyopathy
Lenègre-Lev disease: primary degenerative disease (fibrosis) of the conducting system
Analysis of Leads polarity in accessory tract situations
Step 1: look at leads V1V2V3 (positive or negative) - if + ve - AP is located on left side along mitral ring
Step 2: look at leads II, III, aVF
Step 3: look at leads I, aVL
Heart rhythm disorders:
supra-HIS or infra-HIS
Orthodromic AVRT (WPW)
narrow QRS tachycardia
rhythm travels down normal AV nodal pathway but comes up through accessory pathway (AP)
long RP interval > 90 ms
no delta wave on ECG but can be present if second AP is present
Antidromic AVRT (WPW)
broad QRS tachycardia
rhythm travels through AP first and comes back through AV node, so inverted P waves
Long RP > 90 ms (peak of R to peak of next P)
AV nodal Re-entry Tachycardia (AVNRT)
narrow complex tachycardia
short RP < 90 ms (not PR)
syncope, palpitations
Re entry happens within AV node and not through Accessory pathway (not WPW)
Atypical presentation
Long RP > 90 ms
Slow-slow or fast-slow
PR versus RP intervals
Atrial Tachycardia Types
Sinus: Physiological, Inappropriate, Sinus nodal Re-entrant tachycardia
Focal atrial tachycardia
Multifocal atrial tachycardia
Macro-Re-entrant atrial tachycardia (MRAT)
- Cavo-tricuspid isthmus dependant MRAT
- non-cavo-tricuspid isthmus dependant MRAT
Atrial fibrillation
AV Junctional Tachycardias
AV nodal re-entrant tachycardias (AVNRT)
- Typical
- Atypical
Non Re-entrant junctional Tachycardia
- Junctional ectopic/ focal tachycardia
- other non re-entrant tachycardia
AV Re-entrant tachycardias:
- Orthodromic
- Antidromic
Adenosine Responses in narrow QRS tachy
no effect to adenosine:
- inadequate dose
- not rapid enough delivery
- High septal VTach
Gradual slowing then Re acceleration:
- Sinus tachycardia
- Automatic focal Atrial tachy
- Junctional ectopic tachy
Sudden termination:
- AVNRT
- AVRT
- Sinus nodal re-entry tachy
- Triggered focal Atrial tachy
Persistent atrial Tachycardia with transient high grade AV block:
- Atrial flutter
- Micro re0entrant focal AT
Isthmic flutter
Macro re entry around tricuspid valve, counterclockwise wave,
300 beats/min atrial rate
Saw tooth flutter in inferior leads with negative polarity
Clockwise flutter has positive P wave in inferior leads and negative P wave in V1
P wave position interpretation
P waves
1. > 90 ms after QRS onset instead before it = suggests presence of accessory pathway
2. > 200 ms after QRS = AP with slow conduction or atrial tachycardia
3. within QRS = intra nodal tachycardia (AVNRT)
Different forms of VTach
- Monomorphic VT with structural heart disease: = Bundle Branch Re-entrant tachycardia
- Monomorphic VT without structural heart disease: = Outflow tract VT, Verapamil sensitive LV VT
- Polymorphic VT without QT prolongation
- Polymorphic VT with acquired QT prolongation ie TdP (Torsades)
- Polymorphic VT with congenital QT prolongation ie Long QT syndromes
- Bidirectional VT
- Accelerated idioventricular rhythm
Fusion beat vs Capture beats
Fusion beats are fusion of both, sinus beat and ectopic ventricular beat - with morphology of both in one, favors VT.
Capture beat is a normal sinus beat appearing on the VT rhythm momentarily(normal narrow QRS amongst otherwise broad vpc rhythm)
Marriot Sign in ECG
Presence of less aberrant rabbit ear in QRS morphology ie R > R’ favors VTach and oppostite favors (r < R’) SVT
Rabbit sign in ECG
Prague ICU Algorithm for VT
Step 1
Absent RS complexes in precordial leads ie either all R-waves or all S-waves present.
Positive concordance in chest leads = not VT
Negative concordance in chest leads = VT
Step 2
If any RS complex in V1 to V6 = check if RS > 100 ms in one precordial lead
Step 3
If RS < 100 ms: check if any AV dissociation (notching of QRS at various points, due to super imposed P wave)
Fusion Beats present (favors VT)
Capture beats present (normal narrows QRS in between broad QRS favors VT)
Step 4
If no signs of AV dissociation, look for V1V2 and V6 features: RBBB vs LBBB morphology
RBBB morphology:
3 patterns in V1V2 favors VT
- smooth monophasic R wave
- Marriot Sign: Tall Left rabbit ear R>R’
- qR in V1
2 patterns in V6 favors VT
- QS complex in V6 ie no R waves
- rS favors VT if LAD also +
LBBB morphology
3 patterns in V1V2 favors VT
- initial R wave > 30 ms
- notching of S wave (Josephson sign)
- RS > 70 ms
2 patterns in V6 favors VT
- QS complex (same as in RBBB)
- qR in V6
Basel Algorithm
Simplified algorithm for differential diagnosis of wide complex tachycardia
- Structural Heart disease present(MI, CHF, ICD or CRT present)
++ - Lead II: Time to first peak > 40 ms
++ - Lead aVR: Time to first peak > 40 ms
> 2 criteria present = VT
0/1 criteria only = SVT
Major sites of Ventricular arrhythmia Origin
RVOT (around PV) 60%
RV intra cavitary 14%
LVOT (AV) 10%
LV Intracavitary 10%
Left Bundle fascicles 10%
Mitral and Tricuspid annular, 5-10%
LV summit 3%
Epicardial Foci 3-5%
Axis determination in ECG
Look at Leads I and aVF
Positive QRS in Lead I = axis directed to I
Positive QRS in aVF = axis to the aVF
——————–
combine information from both leads
Both positive - normal axis - 0 to +90
Both negative - extreme deviation: -90 to -180
Positive in I & negative in aVF: RAD > +90
Negative in I & Positive in aVF: LAD < -30
Outflow Tract VPC/VT with - R/S transition in V3
Looks at Leads V3:
- VPC/VT beat transition later than SR
if YES: RVOT is the origin of VT
if NO:
look at Lead V2:
Calculate Transition ratio: C/D DIVIDED BY A/B
if < 0.6 = RVOT origin
if > 0.6 = LVOT origin
Epicardial origin VT/ VPC
- QRS duration > 200 ms
- Pseudo delta waves durstion > 34 ms
- Delayed intrinsicoid deflection > 85 ms
- RS complex duration > 121 ms
- Maximum deflection index, MDI > 0.54
- QS in I, aVF suggests epicardial origin on the LV free wall or ventricular posterior wall
MDI - dividing the shortest time from QRS onset to the max deflection in any of the pre cordial leads by total QRSd
Discordance in inferior leads:
QRS going opposite in II and III
Opposite depolarisation vecotr slong biplolar limb leads = Ventricular arrhythmia’s originating from mid cavitary structres (IVS, Moderator band, Lateral valvular annuli & Anterior papillary muscle)
Two types:
1. Positive in II/ Negative in III - RV structure origin - LBBB
2. Negative in II/ Positive in III - LV structures, RBBB
Long QT syndrome diagnosis:
ECG QT > 480 or Score > 3
Genetics positive whatever QTc
QTc > 460 but < 48o with H/o Syncope
ECG criteria
QTc: > 480 = 3.5 points
QTc: 460-479 = 2 points
QTc: 450-459 = in males = 01 point
QTc: > 480 ms during 4th minutes of recovery from exercise test = 01 point
Torsade de pointes (TdP) = 02 pts
T wave alterans = 01 pt
Notched T wave in 3 leads = 01 pt
Low Heart rate for age = 0.5 pt
————————–
Syncope with stress = 02 pt
Syncope without stress = 01 pt
—————————-
Family member with LQTS = 01
Unexplained SCD in first degree relative< 30 yrs = 01 pt
——————–
Pathogenic mutation detected =3.5 pts
Long QT syndromes
3 major genotypes:
LQTS type 1:
- KCNQ1 P.(Lys557Glu)
- broad based T waves
- arrhythmic syncope during exercise 85%
LQTS type 2:
- KCNH2 P.(Thr613Met)
- T wave with low amplitues, notches or humps
- sleep arrhythmias 50%, 29% emotional stress
LQTS Type 3:
- SCN5A P.(insAsp1795)
- Long ST segment
- T wave later and pointed
- sleep arrhtyhmias 64%
ClinGen curated Genes:
KCNQ1, KCNH2
SCN5A
CALM 1-3
TRDN, KCNJ2, CACNA1C
Indications for ICD placement
Anderson Tawil Syndrome
Also known as Long QT syndrome 7
Dysmorphic Features: Broad forehead, Broad nasal bridge, Hypertelorism (wide gap between two eyes), Low Set ears, Micrognathia (small jaw), Clinodactyly (curved 5th finger to other fingers), Syndactyly ie fused 2/3 toes,
ECG: VT: bidirectional (up & down complexes)
Amiodarone is contraindicated.
Short QTc syndrome
Short QT < 320 ms - diagnostic
Short QT between 320 - 360 + arrhythmic syncope
Short QTc < 360 ms and
one or more of following:
- Pathogenic mutation +
- family H/o Short QTS
- Survival from VT/VF without heart disease
Genetic testing indicated: KCNH2 P.(sER981Gly)
Scoring for Short QT syndrome
ECG criteria:
QTc < 370 = 01 point
QTc < 350 = 02 point
QTc < 330 = 03 point
J pt to T peak interval < 120 ms
Clinical history:
Sudden cardiac death history = 02
H/o VF/ Polymorphic VT = 02
Unexplained syncope = 01
Atrial fibrillation = 01
Family history:
1/2 degree relqative with SQTS = 01
1/2 degree relative, autopsy negative SCD = 01
SIDS in family = 01
Genotype:
Positive for SQTS = 01
VUS in a culprit gene = 01
High probability > 4 point, Low < 2
High Risk Fatures inf Brugada Syndrome
first degree AV block
F-QRS
Prominent R wave in aVR lead
QRS duration > 110 ms
wide deep S wave in I/II
Diagnostic recommendations for Brugada Syndrome
Post cardiac arrest survived case from VF/VT with Type 1 brugada pattern induced by Noa channel blocking drug like Flecainide or during fever with no other heart disease
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Genetic testing for SCN5A positive
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Positive induced Brugada Type 1 ECG + No other heart disease + any one of:
- Arrhythmic syncope history
- Agonal nocturnal breaths seen
- Family H/o BrS
- Family H/o sudden death < 45 yr old with autopsy negative & circumstance S/o BrS
Early Repolarization J wave syndrome
J point elevation > 0.1 mV,
notched/ slurred S
in > 2 inferior/lateral leads
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ECG:
short coupled VPB’s
Dynamic J wave
Widespread j wave
Associated: BrS, SHD, Fragmented QRS, LQTS
Amplitude > 2mm of J point
Horizontal/Descending ST segment
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Clinical: increased risk of arrhythmia:
Cardiac arrest
Family H/o SCD
Syncopes with high risk features: agonal breaths during syncope, injuries suffered, convulsions, Urine loss
Catecholaminergic Polymorphic VT
a genetic disorder: Presentation: Black outs, SCD
(typically during exercise/stress when catecholamine levels are high)
cause: mutations affecting proteins that regulate the concentrations of calcium, the most commonly identified gene is RYR2, which encodes a protein, ryanodine receptor; which releases calcium from the sarcoplasmic reticulum, during every heartbeat.
Genes: RYR2, CASQ2(AD/AR), TRDN (AR), TECRL (AR), CALM1-3
Rx :
- BB, CCB, Flecainide
- ICD placement
- Sympathetic deneration of heart
DPP6 haplotype risk of idiopathic VF
Overexpression of DPP6, which encodes dipeptidyl-peptidase 6, a putative component of the transient outward current (Ito) channel complex in the heart, was proposed as the likely pathogenetic mechanism. DPP6 significantly alters the inactivation kinetics of both Kv4.2 and Kv4.3 and promotes expression of these alpha subunits in the cell membrane. Clinical evaluation of 84 risk-haplotype carriers and 71 noncarriers revealed no ECG or structural parameters indicative of cardiac disease. Penetrance of idiopathic VF was high; 50% of risk-haplotype carriers experienced (aborted) SCD before the age of 58 years.113
Left oriented leads: (V6, I, aVL)
A lead oriented to LV free wall, such as V6/ I/aVL senses initial small septal vector, (Lt to right in septum) away from lead - hence initial small negative q recoded in those leads followed by large Rt to Lt free wall vector recoded as upward R wave (qR complex in I, V4V5V6)
Causes of Left Axis deviation
- Inferior wall MI
- Left anterior Hemiblock: most common cause, blocked left anterior-superior division of
Right oriented leads: (V1V2)
A lead oriented to RV ie V1, detects first small septal vector (Lt to Rt) directed to it hence records small positive r wave and then detects large LV free wall vector (Rt to Lt) and records large negative S wave as opposite to lead (rS pattern in v1v2)
Transition zone in ECG, V3V4
Reflects transition from rS pattern of right oriented leads (V1V2) )
to
qR pattern of left oriented leads (V6V5, I, aVL)
And
Has RS pattern in them.
Leads aVR and V1
Lead aVR: directed to the cavity of the heart hence all vectors directed away from it hence all waves are negative
Lead V1: directed to the lead are atrial vectors (positive P) and septal vector( positive initial small r wave).
Abnormality should not be read into those leads unless grossly positive.
U wave
Positive small upward after T wave
Best seen in V2 to V4
Considered as due to late depolarisation of mid-myocardial M cells.
Heart Positions in leads
Horizontal heart position - represent left axis deviation - qR in aVL
Vertical heart position - represents right or inferior axis deviation
qR in aVF
Counterclockwise Electrical rotation
Around an oblique axis from base to apex of heart - brings LV more anterior - hence V1V2 lead would be oriented to RV recording rS and - V4/5/6 would be facing LV recording qR
Clockwise Electrical Rotation
Around oblique axis from base to apex of heart position- brings RV more anterior - hence most or all of precordial leads V1-V5 records r/s or RS complexes in V6 and transitions zone shifts to V5/6
Intrinsic or intrinscicoid deflection
Downstroke of the QRS complex, change from maximum positivity of the R wave returning to the baseline or below. It represents ventricular activation time (VAT) and should not exceed 40 ms in left oriented leads (V6, I) and 20 ms in right oriented leads V1/2.
Determining frontal plane QRS axis
Step 01 - look at frontal plane leads I, II, III, aVR, aVL and aVF
Step 02
Determine most equiphasic QRS deflection ie R and S same size,
for example - if aVL is most equiphasic - means vector is perpendicular to aVL - which means it is parallel to right angles lead of aVL which is lead II and should show large complex - now
Step 03
Look at this perpendicular lead, ie lead II in our example - if complex is mainly positive - means vector goes to positive pole which is +60 which is our axis.
Causes of long QTc
- During sleep
- Acute myocarditis specially acute rheumatic carditis
- Hypo-calcemia
- Hypothermia
- Complete AV block
- Acute MI
- Drugs: Quinidine, Procainamide, TCA
- Cerebral injury, sympathetic stimulation
- Hypertrophic cardiomyopathy
- Congenital long QT syndromes
Congenital Long QT syndrome
Labelled LQTS 1- 13
Jervil-Lange-Nelson syndrome: autosomal recessive, congenital deafness + syncope attacks + long QTc, risk of sudden death
Romano-Ward syndrome:
Without deafness but otherwise same as JLN.
Anderson-Tawil syndrome: dysmorphic features, Long QT, hypertelorism, low set ears, micrognathia, clinodactyly, syndactyly of toes, KCN5 gene mutation
Null deflection
If a vector is directed at right angles or perpendicular to a particular lead axis, the net impression on that lead will be be nil.
In other words, the deflection in that lead is usually small & equiphasic so that positive and negative deflections cancel each other and referred as null deflection
Evident in perpendicular leads, for example Lead I and aVF, if one is large other will be small.
