ECG Signs, Scores, Tips, Tricks Flashcards

Question

Limb leads

Answer 1

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.

Answer 2

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

Answer 3

Deep septal Q waves in I, aVL, V4V5V6 LVH findings: LAD

Answer 4

- 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

Answer 5

- 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

Answer 6

**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

Answer 7

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

Answer 8

- 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

Answer 9

Notching/slurring near nadir of S wave in V2

Answer 10

1. Broad QRS > 160 ms 2. Rabbit ear R waves ie R>R’ 3. AV dissociation present 4. Northwestern, 270 degree ie ‘No man’s land’ axis 5. Any q wave present in V6 6. 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

Answer 11

Down sloping TP segment is seen in 30% of cases of pericarditis as an early manifestation.

Answer 12

= 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

Answer 13

**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)

Answer 14

**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

Answer 15

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

Answer 16

Small notch at end of S wave Seen in : Hypothermia mainly but also in: Hypercalcemia, Brugada syndrome, neurological injury

Answer 17

**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,

Answer 18

- 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

Answer 19

**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**

Answer 20

- 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

Answer 21

**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

Answer 22

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

Answer 23

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

Answer 24

**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

Answer 25

- urgent **Sync-Cardioversion** - Avoid BB, CCB, Adenosine -

Answer 26

**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)

Answer 27

very **short QT** interval bizarre looking QRS **J waves** as in Hypothermia at end of QRS, best seen in V1

Answer 28

QTc = QT interval / square root of RR interval normal QTc < 440 seconds Prolonged QTc risk of torsade de pointes

Answer 29

QTc = QT interval/ (RR)rest to 1/3

Answer 30

QTc = QT + 154 x (1-RR)

Answer 31

QTc = QT + 1.75 x {(60/RR) - 60 }

Answer 32

QTc = QT x (120 +HR) / 180

Answer 33

**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

Answer 34

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

Answer 35

**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

Answer 36

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**

Answer 37

**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

Answer 38

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.

Answer 39

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

Answer 40

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

Answer 41

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

Answer 42

**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

Answer 43

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

Answer 44

1. Recommended when symptomatic bradycardia: Class 1/ Level B 2. Recommended in tachycardia:Bradycardia form of sinus node disease (SND) to control bradycardia and enable drugs for tachycardia at same time (alternate - ablation) 3. **NOT Recommended** for bradycardia in SND due to reversible causes

Answer 45

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

Answer 46

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.

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

Aortic stenosis Ischaemic Heart disease Hypertension Dilated cardiomyopathy Anterior MI Hyperkalemia Digoxin Toxicity **Lenegre-Lev disease**: primary degenerative disease (fibrosis) of the conducting system

Answer 53

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

Answer 54

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

Answer 55

**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

Answer 56

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

Answer 57

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)

Answer 58

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

Answer 59

**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

Answer 60

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

Answer 61

**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

Answer 62

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

Answer 63

**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)

Answer 64

1. Monomorphic VT with structural heart disease: = Bundle Branch Re-entrant tachycardia 2. Monomorphic VT without structural heart disease: = Outflow tract VT, Verapamil sensitive LV VT 3. Polymorphic VT without QT prolongation 4. Polymorphic VT with acquired QT prolongation ie TdP (Torsades) 5. Polymorphic VT with congenital QT prolongation ie Long QT syndromes 6. Bidirectional VT 7. Accelerated idioventricular rhythm

Answer 65

**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)

Answer 66

Presence of less aberrant rabbit ear in QRS morphology ie R > R' favors VTach and oppostite favors (r < R') SVT

Answer 67

**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

Answer 68

Simplified algorithm for differential diagnosis of wide complex tachycardia 1. Structural Heart disease present(MI, CHF, ICD or CRT present) ++ 2. Lead II: Time to first peak > 40 ms ++ 3. Lead aVR: Time to first peak > 40 ms > 2 criteria present = VT 0/1 criteria only = SVT

Answer 69

**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%

Answer 70

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

Answer 71

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

Answer 72

- 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

Answer 73

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

Answer 74

**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

Answer 75

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

Answer 76

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.

Answer 77

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)**

Answer 78

**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

Answer 79

first degree AV block F-QRS Prominent R wave in aVR lead QRS duration > 110 ms wide deep S wave in I/II

Answer 80

Type 1 Spontaneous ECG pattern & no other heart disease ------------------------------ 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 ------------------------- Genetic testing for SCN5A positive ----------------------------- 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

Answer 81

J point elevation > 0.1 mV, notched/ slurred S in > 2 inferior/lateral leads ----------------------- 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 ---------------------- 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

Answer 82

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

Answer 83

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

Answer 84

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)

Answer 85

1. Inferior wall MI 2. Left anterior Hemiblock: most common cause, blocked left anterior-superior division of

Answer 86

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)

Answer 87

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.

Answer 88

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.

Answer 89

Positive small upward after T wave Best seen in V2 to V4 Considered as due to late depolarisation of mid-myocardial M cells.

Answer 90

Horizontal heart position - represent left axis deviation - **qR in aVL** Vertical heart position - represents right or inferior axis deviation **qR in aVF**

Answer 91

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**

Answer 92

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

Answer 93

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.

Answer 94

**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.

Answer 95

1. During sleep 2. Acute myocarditis specially acute rheumatic carditis 3. Hypo-calcemia 4. Hypothermia 5. Complete AV block 6. Acute MI 7. Drugs: Quinidine, Procainamide, TCA 8. Cerebral injury, sympathetic stimulation 9. Hypertrophic cardiomyopathy 10. Congenital long QT syndromes

Answer 96

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

Answer 97

*How to determine ECG axis:* *Step 1:* Look at leads 1,2,3 and aVR, aVL and aVF. *Step 2*: determine most equiphasic QRS deflection ie R and S waves are of almost equal heights, usually this one is in aVL. *Step 3:* Look at perpendicular lead to previous one, in our case lead II (perpendicular to aVL), Axis should be parallel to this lead II *Step 4:* If QRS predominantly positive in lead II, axis is directed towards positive pole of this lead II Refer to hexaxial system and look at positive pole of this lead II which is 60’ which is our axis

Answer 98

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.

Answer 99

1. -**RV dominance** as in: - RVH in CHD, - Pulmonary embolism - cor pulmonary 2. **AnteroLateral MI**: QRS forces directed away from infarcted area 3. **WPW syndrome**, certain forms with left sided accessory tract where QRS vector is directed towards right 3. **Left posterior hemiblock** where only left anterior tract is active and directs QRS to right

Answer 100

Step 1. Consider most equiphasic T wave deflection ie not too positive and not too negative, usually seen in Lead III Step 2. Look at perpendicular lead to this lead, here lead aVR Step 3. Look at positive pole of this lead , here aVR if T wave positive in first lead (III) ie to 30 degrees Step 4. As T wave is not exactly equiphasic but more positive in III, we have to adjust its axis. So axis must be slightly deviated to positive pole of III but not exactly perpendicular to it, so around 40’ instead of 30 Other rule: T wave axis always moves away from pathology, as in LVH (due to AS or HTN) it will directed to right.

Answer 101

• Best seen in lead II • biphasic in V1: initial +ve (up) as vector comes from sinus node in RA towards V1 lead and later is negative/down as goes away from V1 lead • Height < 2.5 mm in II normally • Notching of P in II suggests LA abnormality (P mitrale) as second half of vector affected, moves away and notching occurs. Same way height of P > 2.5mm suggests RA abnormality (P pulmonale)

Answer 102

P wave depth in mm x duration in seconds, Unit mm.sec Example: 1mm x 0.03 sec = 0.03 mm.secs Normal < 0.003 mm.s > 0.03 indicates LA abnormality ie P mitrale present and look for it in ECHO

Answer 103

• tall P in II > 2.5 mm • initial +ve part of P in V1 more tall > 40 ms (pointed) RA enlarged • Intrisicoid P deflection < 0.03 ie slope of P wave •

Answer 104

Causes/conditions: **AS, HTN, HOCM, Coarctation** 1. Abnormalities of QRS: - increase in total QRS duration/widening - counterclockwise axis ie to left - attenuation ie loss of initial q waves in left oriented leads V5V6 (SV1+RV6) 2. Abnormalities if ST segments, T waves 3. Inversion of U waves in V5V6 - sensitive sign of impaired Left ventricle specially with Aortic regurgitation. 4. Left atrial abnormality, notched P in II 5. Abnormalities of axis of T/QRS waves

Answer 105

Also known as **time of onset of the intrinsicoid deflection** and it is: Time from start of QRS complex to height of R wave and is **normally < 40 ms**. It increase in LVH specially systolic pressure overload type and becomes > 50 ms.

Answer 106

1. Increased QRS magnitude/height = 3 points 2. ST-T abnormality ie inversions = 3 points 3. P wave of signifying LAE (notched in II or more deeper second half in V1) = 3 points 4. Left axis deviation present = 2 points 5. Increased VAT > 45 ms = 1 point Total possible : 12 points > 5 points = LVH Mainly applicable for LVH due to pressure overload ie AS/HTN/HOCM etc

Answer 107

Total QRS voltage, combined for all 12 leads with normal standardisation is **17.5 mV or 175 mm** More than this indicates LVH.

Answer 108

Occurs in LVH Progressive lowering of T wave occurs in lead I causing T wave in Lead III seem or become taller than T wave in lead I. As LVH progresses - T wave axis moves away from disease LV ie to right and QRS-T angle increases > 45 degrees - reflected by lowering if T in I.

Answer 109

SV1 + RV5/V6 > 35 mm and Indicates LVH Underestimates LVH in the presence of obesity.

Answer 110

SV3 + R in aVL > 28 mm in men in LVH > 20 mm in women in LVH Cornell voltage X QRS duration > 2440 mm.ms = LVH Example: 28 mm x 120 ms = 3360 mm.ms Overestimates LVH in the presence of obesity.

Answer 111

# Tall R waves in left oriented leads ie V5V6, may reach 40-50 mm RV6 may be > RV5 # no deep S in V1 with severe Mitral regurgitation as it causes giant LA which displaces heart forward, changing QRS vector orientation. S may be attenuated/lost. # deep S is largest in LVH due to AR or PDA (no giant LA here) # deep q waves present in V5, V6 and reflects hypertrophied basal septum. Can be 0.2/0.5 or 1.0 mV (they are lost in pressure overload LVH) # tall pointed T waves in V5V6 (rather than inverted in pressure LVH) # ST segment 1-2 mm concave up elevated in V5V6 # inverted u waves in V4/5/6, reflects more compromised LV and occurs in both, diastolic as well as systolic LVH