ECG Signs, Scores, Tips, Tricks Flashcards

1
Q

ECG in Pericarditis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ECG on paper analysis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ECG in pulmonary embolism
Various Presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ECG in Dextrocardia

A

= 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

STE in lead aVR

A
1. Left main obstruction 2. Acute pericarditis 3. TCA poisoning 4. AVRT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

STE in aVR - mechanism

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

STE in aVR - Causes

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

STE in aVR- Example 2

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

STE in aVR- Example 3

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

STE in aVR- Example 4

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

STE in aVR- Example 5

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

STE in aVR- Example 6

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

STE in aVR- Example 7

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

STE in aVR- Example 8

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

RBBB pattern wide complex VTach- criteria’s in favor of VTach

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Broad complex tachycardia with LBBB criteria’s

A

Lead V1:
- rS or QS with time to S wave nadir is < 70 ms

Lead V6:
- R wave with no Q wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Tachyarrhythmia as likely VTach

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Irregular Broad Tachycardia Types

A
  1. Atrial fibrillation with aberration
  2. Atrial flutter with aberration
  3. Multifocal atrial tachycardia with BBB
  4. Pre-excited AF (WPW)
  5. Torsade de pointes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Monomorphic Ventricular Tachycardia Rx

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Brugada syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Brugada Syndrome Types

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

QTc formulas

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

QTc nomogram

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

LVH criteria

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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.
26
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
27
HOCM ECG
Deep septal Q waves in I, aVL, V4V5V6 LVH findings: LAD
28
**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
29
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
30
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
31
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
32
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
33
Josephson sign
Notching/slurring near nadir of S wave in V2
34
Vereckei algorithm - to determine VT/SVT in a wide tachycardia
35
Findings favouring VT during tachycardia rather than SVT
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
36
Spodick sign
Down sloping TP segment is seen in 30% of cases of pericarditis as an early manifestation.
37
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
38
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)
39
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
40
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
41
Osborn or J wave
Small notch at end of S wave Seen in : Hypothermia mainly but also in: Hypercalcemia, Brugada syndrome, neurological injury
42
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,
43
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
44
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**
45
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
46
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
47
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
48
ECG in pericarditis
49
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
50
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
51
modified Sgarbossa ECG
52
Managing AFib with WPW
- urgent **Sync-Cardioversion** - Avoid BB, CCB, Adenosine -
53
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)
54
ECG in Hypercalcemia
very **short QT** interval bizarre looking QRS **J waves** as in Hypothermia at end of QRS, best seen in V1
55
Bazzet formula for corrected QTc
QTc = QT interval / square root of RR interval normal QTc < 440 seconds Prolonged QTc risk of torsade de pointes
56
Fridericia formula for corrected QTc
QTc = QT interval/ (RR)rest to 1/3
57
Framingham formular for QTc
QTc = QT + 154 x (1-RR)
58
Hodges formula for QTc
QTc = QT + 1.75 x {(60/RR) - 60 }
59
Rautaharju formula for QTc
QTc = QT x (120 +HR) / 180
60
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
61
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
62
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
63
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**
64
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
65
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.
66
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
67
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
68
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
69
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
70
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
71
Pacing Recommendations in SA blocks
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
72
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
73
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.
74
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
75
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
76
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
77
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
78
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
79
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
80
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
81
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
82
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
83
Heart rhythm disorders: **supra-HIS or infra-HIS**
84
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
85
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)
86
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
87
PR versus RP intervals
88
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
89
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
90
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
91
**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
92
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)
93
Different forms of **VTach**
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
94
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)
95
Marriot Sign in ECG
Presence of less aberrant rabbit ear in QRS morphology ie R > R' favors VTach and oppostite favors (r < R') SVT
96
Rabbit sign in ECG
97
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
98
Basel Algorithm
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
99
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%
100
Axis determination in ECG: Method 2
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
101
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
102
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
103
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
104
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
105
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
106
Indications for ICD placement
107
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.
108
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)**
109
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
110
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
111
Diagnostic recommendations for Brugada Syndrome
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
112
Early Repolarization **J wave** syndrome
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
113
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
114
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
115
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)
116
Causes of Left Axis deviation
1. Inferior wall MI 2. Left anterior Hemiblock: most common cause, blocked left anterior-superior division of
117
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)
118
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.
119
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.
120
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.
121
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**
122
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**
123
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
124
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.
125
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.
126
Causes of long QTc
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
127
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
128
Axis in ECG: Method 01
*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
129
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.
130
Right axis deviation in ECG
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
131
T wave axis determination
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.
132
P waves in ECG
• 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)
133
Morris index (P terminal force)
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
134
P wave: RA abnormality
• 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 •
135
ECG manifestations of LVH due to systolic overload/pressure/resistance
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
136
V6 leads in LVH of pressure versus Volume overload
137
Ventricular activation time
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.
138
Romhilt - Estes LVH point score system
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
139
Total QRS voltage
Total QRS voltage, combined for all 12 leads with normal standardisation is **17.5 mV or 175 mm** More than this indicates LVH.
140
T3 taller than T1 syndrome
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.
141
Sokolov Lyon index
SV1 + RV5/V6 > 35 mm and Indicates LVH Underestimates LVH in the presence of obesity.
142
Cornell voltage product
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.
143
LVH with diastolic overload: ECG changes: with AR/MR/PDA/VSD
# 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