ECG Flashcards
What is the diagnostic criteria for STEMI
> 20 minutes of pain and persistent ECG changes for >20 minutes with ST elevation in >2 contiguous leads
> 2.5mm STE in V2/3 in Men<40
2mm STE in V2/3 in Men>40
1.5mm STE in V2/3 Women
1mm STE in other leads
New onset LBBB
What is the Smith modified Sgarbossa Criteria
Concordant STE >/= 1mm in >/=1 lead (5 points)
Concordant STD >/=1mm in>/=1 lead V1-3 (3 points)
Proportionally excessive (>/=25% preceding S wave) discordant STE in >=/-1lead with >=/1mm STE (2points)
Original Sgarbossa criteria defines excessive discordant STE as >5mm
3 points needed for AMI on old
Both original and modifieid highly specifici ~95%
Smith modified has higher sensitivity (80% vs 30%)
What is the Barcelona Criteria
New criteria to diagnose AMI in LBBB but yet to be externally validated
In internal validation study has sensitivity and specificity ~93%
Difference to Modified Sgarbossa is concordant STD can happen in any lead (not just V1-3) and discordant ST deviation of >/=1mm in any lead when R or S wave is </=6.
LMCA occlusion
Widespread ST depression most prominent in I, II and V4-6
ST elevation > 1mm aVR
ST elevation in aVR > V1
Can also be due to post cardiac arrest, severe anaemia/hypoxia, triple vessel disease
LAD occlusion
ST elevation aVR > 1mm
ST elevation often also in V1-3
Widespread ST depression
Can also be severe triple vessel disease
Raised ICP
Giant cerebral T wave inversion in multiple leads
QT prolongation
Bradycardia
Diffuse ST elevation (STEMI mimic)
General rhythm disturbance
Right heart strain pattern
ST depression and T wave inversion in R precordial leads V1-3 +/- V4
Also inferior leads most pronounced to lead III
S1 Q3 T3
TWI in lead 3 and V1 suspicious for PE
Signs associated with RVH:
Right axis deviation
RBBB (Dominant R wave in V1 and Persistent S wave V6)
What are some causes of R heart strain
Acute cor pulmonale
- PE
- Severe pneumonia
- Exacerbation of COPD/Asthma
- Ptx
- Pneumonectomy
- Upper airway obstruction
Chronic
- Recurrent small PEs
- Cystic fibrosis
- Severe kyphosis
- OSA
- Intersitial lung disease
Diagnostic criteria for LVH
Sokolow-Lyon criteria most frequent with high specificity but poor sensitivity
S wave in V1 + R wave in V5-6 >35mm
Modified Cornell
R wave aVL >12mm
Romhilt Estes score system has best sensitivity 60%
Tall R waves in L sided leads (V4-6) >26mm
Deep S waves in R leads (aVR, V1-3) >14mm
Non voltage criteria
Increased R wave peak time >50ms V5 or V6
Discordant ST segment depression and T wave inversion in L sided (lateral) leads
Discordant STE may be seen in V1-3
PE changes on ECG and how to differentiate from ACS?
Sinus tachycardia most common (44% of cases)
Right ventricular strain - T wave inversion V1-4 and inferior leads (34%)
S1 Q3 T3 20%
RBBB associated with increased mortality 18%
RAD 16%
P pulmonale 9% (R atrial enlargement)
Clockwise rotation - shift of R/S transition towards V6 with persistent S wave in V6 8%
Atrial tachycardias 8%
Dominant R wave V1
Non specific ST and T wave changes in 50%
Completely normal ECG in 18%
Tachycardia is rarely assosciated with ACS and TWI in leads III and V1 is highly specific 99% for PE
TWI in inferior and R recording leads, V1-4, most specific for PE (up to 99%)
What are the diagnostic features of Wolff Parkinson White
Short PR interval < 120
Delta waves (look in inferior leads)
QRS prolongation > 110
ST segment and T wave discordant changes
Pseudo infarction pattern due to negatively deflected delta waves (70% pseudo q waves inferior anterior leads and prominent R waves in V1-3)
Describe the accessory pathway of WPW
AP (bundle of Kent) is bidirectional in majority of cares, retrograde in 15% (also known as concealed pathway as no preexcitation occurs and therefore no features on ECG) and anterograde rarely
Can also be:
Left sided - Type A pattern with positive delta in precordial leads with dominant R wave in V1
Right sided - Type B pattern with negative delta in V1-2
What tachyarrhythmias is WPW susceptible towards
AF or Aflutter - due to direct conduction from atria to ventricles via AP bypassing the AV node
AVRT - formation of re-entry circuit involving the AP
What are the diagnostic features of Hypertrophic cardiomyopathy present on ECG?
Left ventricular hypertrophy
Deep narrow dagger like Q waves lateral +/- inferior leads (1, aVL, V5-6)
Often non specific ST/T wave abnormalities
P mitrale
Short PR and delta waves (WPW) seen in 33%
Dysthrythmias - AF, SVT, PAC, PVC, VT
Clinical features - presyncope/syncope, palpitations, chest pain, pulmonary congestion
What is the Brugada pattern on ECG?
Type 1 pattern
Coved ST elevation > 2mm in at least 1 of V1-3 followed by negative T wave
Must also have one of the following clinical criteria:
- documented VF or polymorphic VT
- FH sudden death < 45
- syncope
- nocturnal agonal respiration
- other family members with ECG changes
- VT induced
Type 2
>2mm of saddleback shaped ST elevation.
Type 3 either type 1 or 2 but <2mm STE
Can be unmasked by fever, hypothermia, ischaemia, hypo/hyperkalaemia, cocaine, alcohol, cardiac drugs (na block, beta block, ccb, alpha agonists, nitrates)
What are some differentials for Irregular supraventricular tachycardia?
Atrial origin, narrow complex
- atrial fibrillation - no p waves, variable rate
- atrial flutter with variable block - no p waves, saw tooth pattern
- multifocal atrial tachycardia - at least 3 distinct p wave morphologies in same lead
What are some differentials for regular supraventricular tachycardia
Sinus tachycardia
Atrial tachycardia
Atrial flutter with fixed AV block
AV nodal re-entrant tachycardia (classical SVT - regular 140-280, narrow complex, buried p waves so appear absent)
AV re-entrant tachycardia (WPW)
What are some differentials for Regular broad complex tachycardia?
VT
SVT with aberrant conduction due to BBB
SVT with aberrant conduction due to WPW
Accelerated idioventricular rhythm
VT vs SVT ECG features (if clinical features/doubt then treat as VT!!)
Absence typical LBBB (if originating from the R, negative complexes in V1 and 2) or RBBB morphology
Extreme axis deviation (north west axis) with QRS positive in aVR and negative in 1 and aVF
Very broad complexes > 160
AV dissociation
Capture beats
Fusion beats
Positive concordance throughout precordial leads
Negative concordance throughout precordial leads
RSR complexes with taller left rabbits ear
Brugada sign - distance from onset of R wave to nadir of S wave is >100ms in V1-6
Josephson sign - notching/slurring near nadir of S wave
What are some clinical factors that increase likelihood or VT or SVT with aberancy
VT
- Age >35 (PPV of 85%)
- Structural heart disease
- IHD or previous MIs
- Family hx of sudden cardiac death
SVT with aberrancy
- Previous BBB
- Previous WPW
- Paroxysmal tachycardias successfully terminated with adenosine or vagal manoevres
What is the Brugada Algorithm in context of VT
Used in difficult cases to help distinguish VT and SVT with aberrancy
Name another algorithm other than the Brugada Algorithm for diagnosing VT
The Vereckei Algorith is single lead (aVR) algorthim
What is RVOT tachycardia
Monomorphic VT origination from the RVOT or tricuspid annulus
LBBB
Inferior axis
rS complex in V1 and R complex V6
Precordial transition usually >/= V3 with exception of the septal origin which occurs at </= V3
Most commonly idiopathic VT and arrhythmogenic right ventrciular dysplasia
Idiopathic can terminate with vagal maneuvers and adenosine
ARVD RVOT tachy does not
Arryhthmogenic right ventricular dysplasia
Autosomal dominant, second most common sudden cardiac death in young people (after HCM), often associated FH
Fatty infiltration of RV free wall, predisposing to paoxysmal ventricular arrhythmias, sudden cardiac deat and biventricular failure
T wave inversion V1-3 without RBBB (85%) Epsilon wave best seen V1/2 (most specific, seen in 50%) - Fontaine leads to help QRS widening V1-3 >110ms Frequent PVCs Paroxysmal VT with LBBB morphology (right ventricular outflow tract obstruction)
What are some differentials for Irregular broad complex tachycardia?
VF
Torsdaes de pointes
Polymorphic VT
AF with WPW
AF with BBB
What is Mobitz I heart block?
Usually benign with low risk of haemodynamic compromise or third degree HB
Also called Wenckebach and commonly a reversible functional suppression of AV conduction
Progressive prolongation PR interval culminating in non conducted P wave (Progressive fatigue of AV nodal cells)
P-P ratio remains constant
Causes
Drugs : b-blockers, CCB, Digoxin, Amiodarone
Increased Vagal tone
Inferior MI
Myocarditis
Following cardiac surgery
Asymptomatic pts do not require treatment
Responds to atropine and PPM rarely required
What is Mobitz II
Intermittent non conducted P waves with PR interval remaining normal
(all or nothing phenomenon with His-Purkinje cells suddenly and unexpectedly failing)
Causes
Anterio MI (necrosis of bundle branches)
Auto immune (SLE, Sclerosis)
Inflammatory (Rheumatic fevers, Myocarditits, Lyme disease)
Infiltrative (Amyloidosis, haemochromatosis, sarcoidosis)
HyperKalemia
Drugs: b-blockers, CCB, digoxin, amiodarone
Much more likely to cause haemodynamic compromise, severe bradycardia and 3rdHB then mobitiz 1
Sudden and unexpected instability or collapse
Risk asystole 35% per year
Immediate cardiac admission and temporary pacing with definitive PPM
What is 3rd degree or complete heart block
Complete AV dissociation with independent atrial and ventricular rates
Causes
- inferior MI
- Drugs : b-blockers, CCB, digoxin)
- Idiopathic degeneration (lenegre or Levs disease)
How can you distinguish between Mobitz 1 and 2?
Mobitiz 1 would have lengthening PR interval however in 2:1 block this cannot be seen
Long rhythm strip looking for other non-conducted P waves and woudl suggest Mobitz 1
Carotid massage or atropine, if response then suggests Mobitz 1 (mobitz 2 block occurs just past the AV node which these methods work on)
Invasive EP study to determine level of block
What is sinoatrial exit block and how do they present on ECG
Failed propagation of pacemaker impulse beyond SA node causing intermittent failure of atrial depolarization (dropped p waves)
Similar pattern to AV block and only second degree SA block (type 1 and 2) can be distinguished on ECG and can be found by examining timing of p waves
Causes
- Sick sinus syndrome
- Increased vagal tone (athletes)
- Vagal stimulation (surgery or pain)
- Inferior MI
- Myocarditis
- Drugs: digoxin, b-blockers, CCB, amiodarone
What is sick sinus syndrome and list some causes
Abnormal sinus node function with resultant bradycardia and cardiac insufficiency
Commonly seen in elderly with syncope, dizzines, palpitations or fatigue
ECG can show
Sinus brady
Sinus arrhythmia
SA exit block
Sinus arrest - pause >3 seconds
Slow AF
Tachy brady syndrome
Causes are intrinsic and extrinsic
INTRINSIC
Idiopathic degenerative fiborsis (most common)
Ischemia
Cardiomyopathy
Infiltrative disease (sarcoidosis, haemochromatosis)
Congenital abnormalitis
EXTRINSIC
Drugs (digoxin, b-blockers, CCB)
Autonomic dysfunction
Hypothyroid
HyperK
Right ventricular infraction
Inferior STEMI with
- STE in V1
- STE in V1 and STD in V2 (highly specific for RV infarct)
- Isolectric ST in V1 with marked STD in V2
- ST elevation in III>II
Diagnosis is confirmined with STE in R sided ECG (V3R - V6R)
May be preload dependent and can have hypotension in response to nitrates however this is under contention
How to distinguish culprit vessel in Inferior STEMI
RCA 80%
STE lead III>II
Reciprocal STD in lead 1
Signs of RV infarct
LCx 18%
STE lead II>III
Absence of reciprocal STD in lead I
Signs of lateral infract STE 1, aVL, V5-6
How does a High Lateral STEMI present
South African Flag sign with STE in 1, aVL and V2 with STD in lead III
Caused by LAD-D1 occulsion
LCx can cause STE in 1 and AVL but along with V5 /6
Posterior STEMI
Horizontal flat ST depression V1-3 with upright T waves
Tall broad R waves V1-3 (>30ms)
Dominant R wave V2 (R/S ratio>1 )
Do posterior leads - STE can be 0.5mm
3-11% isolated posterior infracts
Otherwise extension from inferior or lateral infarct and can take up large percentage of LV increasing risk fo LV dysfunction and death
What to think if narrow complex tachycardia rate 150
Atrial flutter with 2:1 block (elderly, IHD)
SVT
AV reentry in WPW
Sinus tachycardia
30, 40/50 junction rhythm
75, 100, 150, 200 atrial flutters
300 WPW or sotolol/flecainde
What to look for in syncope
- Too fast - VT, VF, torsades
- Too slow - sinus bradycardia, pauses, heart block (Mobitz II or 3rd degree)
- Pump failure - MI, PE
- Electrical problems - electrolytes (hypo/hyperkalaemia), pacemaker failure
- Syncope syndromes - long QT, short QT, WPW, Brugada, HOCM, ARVD
What is the Digoxin effect (not toxicity) on ECG
Down sloping ST depression (reverse tick)
Flattened, inverted or biphasic T waves
Shortened QTc
Prominent U waves
PR prolongation
Shortening of atrial and ventricular refractory period and increased vagal tone
ECG in digoxin toxicity
Supra ventricular tachycardia due to increased automaticity (intracellular Ca) and slow ventricular response due to decreased AV conduction (increased vagal tone) or features of both
Most commonly
- frequent PVCs/bigeminy/trigeminy
- sinus bradycardia
- slow AF
- AV block of any type
- VT (bidirectional most commonly seen in severe digoxin toxicity)
Other clinical features
GIT - N/V/D
Visual 0- Blurred vision, yellow/green discolouration, haloes
CVS - Palpitations, syncope, dyspnoea
CNS - Confusion, delirium, faitgue
Left axis deviation
QRS positive lead I and aVL and negative in lead aVF (also in II and III)
Causes LBBB inferior MI LVH Left anterior fasicular block Paced rhythm WPW
Left Anterior Fascicular block
LAD
qR in leads 1 and aVL
rS in II, III, aVF
Prolonged R wave peak time in aVL>45ms
Right axis deviation
QRS positive in aVF (also II and III), negative in I
Causes Right ventricular hypertrophy PE COPD Left posterior fasicular block WPW Hyper kalaemia Sodium channel blocker toxicity
Left posterior fascicular block
RAD
rS in leads I and aVL
qR in leads II, III, aVF
Prolonged peak R wave time in aVF
There should be no other cause for RAD (PE, TCA overdose, lateral STEMI) or evidence of RVH
More commonly with RBBB in context of bifascicular block
Paediatric ECG
Dominant R in V1 (RSR pattern) T wave inversion V1-3 May have right axis deviation Often shorter PR Can have sinus arrhythmia
STEMI mimics
Benign early early repolarisation
LVH
LBBB
Paced rhythm
Pericarditis
Left ventricular aneurysm
Brugada
Takatsubo
Increased intracranial pressure
HyperK
Osborn wave of hypothermia
Describe benign early repolarization
Diffuse STE with upward concavity at the initial segment of ST
Notching of the J point
Maximal in V2-V5
Symmetrical concordant T waves with large amplitude
Stable over time but might regress with old age
What are some features that help distinguish ischemic vs normal variant ST elevation
Straight or convex ST segments in 1 or more precordial leads
STE at least 5mm in V2-V4
STD in any lead
TWI in any lead
Q waves in V2-V4
Any terminal QRS distortion in V2/3 (lack of S or J wave dropping below isolelectric line)
Causes of long QTc
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
Hypothermia
Myocardial ischaemia
Post ROSC
Raised ICP
Congenital
Drugs - antipsychotics, TCAs, type Ia (procainimide), Ic (flecanide), III (sotalol, amiodarone), citalopram, venlafaxine, quinine, macrolides
What are the OMI that are often missed signs of ACS
- Inferior wall MI (subtle inferior lead STE with STD in aVL)
- Posterior MI
- New bifascicular block (RBBB and LAFB. Any Concordant STE in RBBB is concerning for ACS)
- Hyperacute T waves (Wider and symmetrical T waves, larger in amplitude of preceding complex)
What are the 5 Ps of pacemaker classification
Position 1 - Chambers paced
Position 2 - Chambers sensed
Position 3 - Response to sensing (does sensed activity trigger or inhibit pacemaker activity)
Position 4 - Rate modulation (can the PPM modulate HR to meet physiological needs by responding to variable including vibrations, respiration or acid base status
Position 5 - Multisite stimulation for more than 1 pacing site within one anatomical area
What are some common pacing modes
AAI
- For sinus node dysfunction with intact AV conduction
- Sensed atrial activity and if present PPM is inhibited, if not then atrial pacing initiated
VVI or VVIR
- Used in chronic AF or A flutter
- Sensed ventricular acitivty, if present PPM is inhibited, if not then ventricular pacing initiated
- Simple and low cost but has fixed rate and risk of pacemaker syndrome
- VVIR is rate responsive but required advanced programming
DDD
- Most common mode and used often used for complete heart block
- Atrial pacing if no native activity
- Ventricular pacing if no native activity AFTER atrial activity
- Atrial tracking restores normal physiology but has no rate responsiveness and required 2 leads with advanced programming
DDDR
- Used for sinus node dysfunction and when rate responsiveness AV block
- Universal pacer with all options of pacing programming avaible
- Complexity, cost and advanced programming with frequent follow up evaluations needed
Magnet mode
- Applying magnet to PPM usually initiates asynchronous pacing AOO, VOO or DOO
- Constant firing rate despite native activity and therefore can set off PPM induced ventricular arrhythmia
- Different from magnet on ICD which deactivates the defib
What are De Winter T waves
Anterior STEMI equivalent OMI which requires immediate reperfusion
Tall prominent, symmetrical T waves in precordial leads
Upsloping STD>1mm at J point
Absence of STE in precordial leads but reciprocal STE (0.5-1mm) in aVR
Typical STEMI morphology may precede or follow this
What are the common pacemaker malfunctions
PROBLEMS WITH SENSING
Undersensing
- fails to sense native cardiac activity causing asynchronous pacing
- pacing spike within QRS is suggestive
- Caused by exit block, poor lead contact, new BBB or program problems
Oversensing
- Inappropriately recognizes artifact (large P or T waves or skeletal muscle activity) as native cardiac activity inhibiting pacing
PROBLEMS WITH PACING
Failure to capture
- Stimulus does not result in myocardial depolarization
- Electrode displacement, lead disconnection, wire fractures, electrolyte disturbance, MI or exit block
Output failure
- Paced stimulus is not generated
- Caused by battery depletion, oversensing, wire fracture, lead displacement or interference
What are the common pacemaker associated dysrhythmias
What is Wellens Syndrome
Biphasic or deeply inverted T waves in V2-3 with recent hx of chest pain that is NOW resolved
Highly specific for critical stenosis of LAD and pts high risk for extensive anterior wall MI within days to weeks
Type A (25%) - Biphaisc with initally positive, terminally negative T waves
Type B (75%) - Deeply symmetrical TWI
Occurs following transient anterior STEMI with reperfusion of LAD (spontaneous clot lysis or aspirin) which resolves symptoms and causes T wave changes similar to reperfusing PCI (biphasic or inverted initially with progression to deeply inverted and symmetrical overtime).
Reocculsion can pseudo-normalisation of T waves due to hyperactue STEMI so ECG MUST be taken in pain free state for diagnosis
Poor response to medical management
MI or cardiac arrest if given stress test
What are some mimics of Wellens Syndrome
LVH/RVH
Raised ICP
Brugada syndrome
Hypokalemia
PE
RBBB
What are AVRT and AVNRT and how to differentiate between them
AVRT - Atrioventricular Re-entry tachycardia - is SVT from accessory pathways which can be Orthodromic (anterograde conduction through AV node) or Antidromic (retrograde conduction through AV node)
Orthodromic AVRT
- Rate 200-300
- Retrograde p waves with long RP interval
- Narrow QRS unless preexisting BBB or aberrant conduction
- QRS alternans (different from electrical alternans as has normal amplitude)
- Rate related ischemia is common
Antidromic AVRT
- More rare, only 5% of tachyarrhythmia from WPW
- Rate 200-300
- Wide QRS from abnormal ventricular depolarization via AP
- Difficult to distinguish from VT
- AV blocking agents have small chance of inducing AF and subsequent cardiac arrest
AVNRT
- Retrograde p waves occur early, so either buried in QRS or partially seen as pseudo r’ wave at terminal QRS
- p waves in AVRT occur later with RP interval >70ms
Anterior ST depression
LAD infarct
Posterior STEMI
Infer/pos/lateral reciprocal
What are pathological q waves
Normally not seen in R heart leads (V1-3) but should be seen in V5/6
- otherwise there is LBBB
Deeper q waves (>2mm) in leads III and aVR is a normal variant
PATHOLOGICAL
>40ms (1mm) wide
>2mm deep
>25% of depth of QRS complex
Seen in leads V1-3
Caused by
MI
Cardiomyopathy - Hypertrophic or infiltrative
Extreme rotation
Lead placement errors
What are the causes of polymorphic VT
What are the ECG changes seen in Takotsubo and how do you distinguish them from ACS
What is accelerated iodioventricular rhythm
Automatic ventricular rhythm from enhanced automaticity faster then normal ventricular escpate (>50) but slower then classic ventricular tachycardia (<120)
Wide complex with classic morphology of tall monophasic upright QRS complexes in inferior leads
Can have capture beats and fusion beats
Typically, benign and transient but can be secondary to significant underlying pathology
- reperfusion of OMI (most common)
- ROSC post arrest
- digoxin toxicity
- sympathetic overload (cocaine, adrenaline, isoprenaline)
- electrolyte abnormalities
- Cardiomyopathy, myocarditis
- Athletic heart
Resolves when sinus rate exceeds ventricular foci
Low cardiac output states (Biventricular failure) may need atropine to restore AV synchrony and restore atrial kick
Antiarrhythmics can cause severe bradycardia and asystole.
ISCHEMIC CHANGES
