ECG Flashcards

Question

What are some differentials for Irregular broad complex tachycardia?

Answer 1

VF Torsdaes de pointes Polymorphic VT AF with WPW AF with BBB

Answer 2

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

Answer 3

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

Answer 4

Complete AV dissociation with independent atrial and ventricular rates Causes - inferior MI - Drugs : b-blockers, CCB, digoxin) - Idiopathic degeneration (lenegre or Levs disease)

Answer 5

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

Answer 6

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

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

Atrial flutter with 2:1 block (elderly, IHD) SVT AV reentry in WPW Sinus tachycardia

Answer 13

30, 40/50 junction rhythm 75, 100, 150, 200 atrial flutters 300 WPW or sotolol/flecainde

Answer 14

- 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

Answer 15

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

Answer 16

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

Answer 17

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 ```

Answer 18

LAD qR in leads 1 and aVL rS in II, III, aVF Prolonged R wave peak time in aVL>45ms

Answer 19

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 ```

Answer 20

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

Answer 21

``` Dominant R in V1 (RSR pattern) T wave inversion V1-3 May have right axis deviation Often shorter PR Can have sinus arrhythmia ```

Answer 22

Benign early early repolarisation LVH LBBB Paced rhythm Pericarditis Left ventricular aneurysm Brugada Takatsubo Increased intracranial pressure HyperK Osborn wave of hypothermia

Answer 23

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

Answer 24

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)

Answer 25

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

Answer 26

- 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)

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

LVH/RVH Raised ICP Brugada syndrome Hypokalemia PE RBBB

Answer 33

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

Answer 34

LAD infarct Posterior STEMI Infer/pos/lateral reciprocal

Answer 35

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

Answer 36

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.