see also: [[Atrial fibrillation]], [[Ventricular Tachycardia]], [[Syncope]] [bear syncope WOBBLER](bear://x-callback-url/open-note?id=47956F57-D397-46E1-B5C1-98CD3F2AF8CD-82152-00000F0418D1E7A8&header=ECG%20evaluation) > syncope and sudden death are on a spectrum of how lucky the patient is > [!Key Points] > **[[#Hypertrophic Cardiomyopathy]]** > - usually have abnormalities on ECG > - send for ECHO, avoid exertion, consider beta blockers > > **[[#Brugada]]** > - v1 and v2 rsr' with STE, often t inversion > - surprisingly common cause of sudden cardiac death > > **[[#WPW]]** > - if someone had resolved syncope and you find WPW on ECG, assume they had a malignant arrhythmia and admit > - causes two types of tachyarrhthmias: **SVT** or **rapid [[Atrial fibrillation|AF]]** > - AF is the bad one: identify if **changing morphologies** (some wide, some narrow, usually very fast) > - [[Cardioversion|cardiovert]] if in arrhythmia > - if in AF version of WPW, **can be made worse with AV nodal blockers** (digoxin, beta blocers, adenosine, and calcium channel blockers). > - procainamide and flecanide 150mg IV (2mg/kg) is OK, amiodarone likely OK but traditionally concern > > **[[#Long QT]]** > - major concern with [[Torsades de Pointes|TdP]] if QTc > 500ms > > **[[#ARVC]]** > - T inversion in right precordial leads > - Epsilon waves btwn QRS and T > - Prolonged s wave upstroke > [!tip]- WOBBLER causes of syncope > besides obvious ischemia, arrhythmias, or seizures, consider these: > > - WPW > - Obstruction of AV node > - Brugada > - Bifasicular block > - [[STEMI mimics|LVH]] > - Epsilon wave (ARVC) > - Repolarization (eg long QT) > > ![[Pasted image 20230517193841.png]] # Hypertrophic Cardiomyopathy - several names - anatomic abnormalities: - hypertrophies, non-dilated LV (normal CXR) - thickening usually prominent in the septum - only 55% cases fam history - average age of dx 30-40 years - definitive dx is doppler ECHO (or MRI now??) - can possibly happen in next day or two, but likely pt is getting admitted **caused by :** - hypertrophied septum causes obstruction to LV outflow - in times of exertion, patient can have sudden drop of cardiac output - can have VT --> degenerate to VF (sudden death) - if VT --> sinus it is **syncope** **clinical features:** - syncope, chest pain, palpitations, dysponea, sudden death - often associated with exertion (not always) - systolic murmur at left low sternal border - increases with valsalva and standing - decreases with squatting and trendelenburg - associated with [[Pulmonary Hypertension]] and diastolic heart failure **treatment:** - beta blockers - primarily a diastolic filling problem, systolic function is decent - so beta blockers help with diastolic filling - calcium channel blockers - Amiodarone if ventricular arrhythmias - ICD > [!danger]+ ECG features of HOCM > - **high voltage** most common > - Tall R wave in v1 (mimics posterior MI) > - **deep narrow Q waves** in inferior, lateral leads ("dagger-like") > - too narrow for old infarction Q waves ## HOCM examples 1. ![[Pasted image 20230517195820.png]] 29 yo w/ syncope, no med history. note dagger-like Q waves, LVH pattern. 2. ![[Pasted image 20230517201035.png]] high voltage, deep narrow qs in I, aVL, v5, v6 3. ![[Pasted image 20230517201202.png]] deep narrow qs in I, aVL, exertional syncope. 4. ![[Pasted image 20230517201329.png]] very deep narrow Q wavers again laterally! ## Apical HOCM - ECG: - Giant negative T-waves characteristic - voltage criteria for LVH, T-wave inversion - AF relatively common and non-sustained VT - localised hypertrophy of LV apex, causing an "ace of spades" configuration of the LV cavity ![[Pasted image 20241113145314.png]] ![[Pasted image 20241113145351.png]] # Brugada see [Brugada drugs](https://www.brugadadrugs.org/) for drugs that can unmask it - first described in 1992 - associated with sudden cardiac death (most commonly in sleep) - will go into **polymorphic VT** --> VF - **structurally normal** hearts; this is a ==purely electrical phenomenon== - fairly common cause of sudden death; ==possibly 1/25 cardiac arrests==[^1]! - also can cause sudden infant death syndrome in kids - also prone to AF and SVT - average age of first diagnosis ~40 years old - morality ~10%/year without ICD - more common when **febrile** - possibly why initially diagnosed in souteast asian area where it is hotter - no chest pain - **ECG findings can come and go** -- more commonly present around the time of the arrhythmia - therefore, if seeing it after a syncope, high concern **mechanism:** - **sodium channelopathy** - Na-channel blocker can bring out brugada pattern **treatment**: - **antiarrhythmics do not work** to prevent episodes - **ICD** is the only treatment that modifies mortality - sometimes isoprenaline infusion can suppress recurrent VF (but arrhythmogenic in own right) - ↑ Ca currents and thought to be helpful in tx of arrhythmia storm **diagnosis:** requires 2 parts: 1. typical ECG finding (especially coved) 2. clinical characteristics, 12 of the following: 1. history of VT/VF (usually polymorphic VT) 2. family history of sudden cardiac death age <45 3. FMx of coved-type ECG 4. agonal respirations during sleep 5. inducibility of VT/VF during EP study 6. Syncope **Disposition:** - Pt suspected of having a Brugada pattern ECG should be referred to a specialist Electrophysiologist Cardiologist - 1st deg relatives should also be considered for referral to electrophysiologist for genetic/electrophysiological testing - any patient with syncopal episode with known brugada syndrome, brugada ECG, or 1st deg relative with brugada syndrome should be *admitted to CCU* for ongoing cardiac monitoring and review by cardiologist > [!danger]+ Brugada ECG features > - **V1-V2 key leads** for this > - RBBB or IRBBB pattern BUT with ST elevation (rather than depression) > - Increased beta angle of r’ wave > - [[Osborn waves|J wave]] amplitude ≥ 2mm > > **2 patterns** of ST-segment elevation (type 1 and type 2): > 1. **coved pattern** (convex upwards, terminating in inverted t wave) -- most sensitive and specific > ![[Pasted image 20230517211237.png]] > ![[Pasted image 20230517211339.png]] > 2. **saddle pattern** - incomplete RBBB with concave upwards -- less sensitive/specific > ![[Pasted image 20230517211303.png]] > ![[Pasted image 20230517211437.png]] ==note that patients with RBBB or incomplete RBBB usually have ST depression, NOT ST elevation!== ![[Pasted image 20230517212836.png]] uncomplicated RBBB. note the difference: ST depression following rsR', not the STE seen in brugada! ## Brugada Examples 1. ![[Pasted image 20230517205851.png]] brugada. 30 year old woman syncope, asymptomatic. characteristic v1 v2 pattern 2. ![[Pasted image 20230517212531.png]] brugada. v1, v2 incomplete RBBB with STE terminating in inverted T wave 3. ![[Pasted image 20230517212603.png]] brugada. presented to her GP with syncope, note rsr' and standard T inversion 4. ![[Pasted image 20230517212736.png]] brugada. subtle STE v1 v2, this is atypical for incomplete RBBB. 5. ![[Pasted image 20230517213030.png]] brugada with "saddle" pattern in v2 and coved in v1 6. ![[Pasted image 20230517213059.png]] brugada. pt arrested and resused at outside hospital. cardio dxed as STEMI, but electrophysiologist recognised brugada. # WPW see also: - [WPW and AV re-enrant tachycardias](x-devonthink-item://EDA28672-626E-451F-B785-207874EC0BF5) - [Cameron WPW](x-devonthink-item://10DC3BB1-027C-40D6-BDB3-4AF0C6B160E6?page=255&start=921&length=32&search=%0APre-excited%20atrial%20fibrillation) - [Rosen pre-excitation syndromes](x-devonthink-item://F2F0190B-D639-41DF-9A27-931676B7B51A?page=20&start=1269&length=45&search=Preexcitation%20and%20Accessory%20Pathway%20Syndromes) [WPW ECG case sudden cardiac death](https://manualofmedicine.com/ecgs/ecg-interpretations/ecg-case-172-wolff-parkinson-white-pattern-intermittent/) - ventricular pre-excitation syndrome - if someone comes in with resolved syncope and you find WPW, assume they had a maligant arrhythmia > **causes two types of arrhthmias:** > 1. [[#SVT phenotype|SVT]] > 2. rapid [[Atrial fibrillation|AF]] (rates can be 300 bmp!) **pathophysiology:** - in normal conduction, pauses at AV node (accounts for PR interval) and then goes on to his-purkinje system - if you have an accessory pathway, an impulse bypasses AV node and hits the ventricle earlier and start myocyte conduction, causes shorted pr interval, and because this is less efficient than his-purkinje impulse-generation, you get slurring of the upstroke (**delta wave**), then signal from regular AV is conducted and the rest of atrium fires and the rest of the QRS is normal ![[Pasted image 20230517224355.png]] > [!Danger] WPW ECG findings > **classic triad:** > 1. **shortened PR interval** <120ms > 2. widened QRS interval (as a result of the delta wave) > 3. **delta wave** slurring of the upstroke of QRS ![[Pasted image 20230517224821.png]] short PR in many leads, slurring of upstroke (delta wave) ## SVT phenotype - treat as SVT (or VT if it looks like VT) - less scary variant of WPW tachyarrhythmia; medications are not unsafe (including adenosine) |orthodromic tachy| antidromic tachy| |---|---| |impulse down normal pathway, up accessory pathway to re-enter| impulse down accessory pathway and up the normal pathway| | regular, narrow complex |regular, wide QRS tachy. looks exactly like [[Ventricular Tachycardia]] | | responds to normal SVT treatment | responds to SVT or VT treatment | **Orthodromic tachycardia:** looks like any other SVT ![[Pasted image 20230517230101.png]] **Antidromic tachycardia:** ![[Pasted image 20230517230614.png]] ## atrial fibrillation phenotype ==bad arrhthmia for WPW== - *can be made worse* with digoxin, beta blockers, adenosine, and calcium channel blockers (*AV nodal blockers*) -- can cause **ventricular fibrillation** - ==procainamide 17mg/kg IV== over 30 min up to 50 mg/kg is OK. - ==Flecainide 150mg (2mg/kg)== IV over 30 min - [[Cardioversion|cardiovert]] if unstable - Amiodarone controversial - normal AF atrium 500-600 times per minute but ventricle only conducts ~150 BPM - rest of impulses are absorbed by the AV node - **Because WPW bypasses AV node, more atrial impulses get conducted to ventricle** - causes irregularly irregular broad complex rapid AF - **irregularity rules out VT** ![[Pasted image 20230517231808.png]] ![[Pasted image 20231010104429.jpg]] ### AF with accessory pathway vs bundle block? ![[Pasted image 20230518152232.png]] This is AF with a normal [[Right Bundle Branch Block|RBBB]]. Can tell it isn't an accessory pathway because the morphologies are NOT changing. ![[Pasted image 20230518152339.png]] This is AF with [[Left Bundle Branch Block|LBBB]], morphologies are the same (even though rate is irregular), therefore NO ACCESSORY PATHWAY. ### risks of adenosine / AV nodal blocker - In AF with an accessory pathway, many of the atrial impulses are still being stopped by the AV node. - if we block the AV node, then all that is left is the accessory pathway, and exacerbates the conduction of atrial impulses down the accessory pathway - rate goes from 200-300 to 600 --> ==ventricular fibrillation== - interestingly, if given digoxin, they tend to go into VF **a few hours later** ![[Pasted image 20230517232416.png]] In this case, adenosine was given and went right into ventricular fibrillation. ## WPW examples 1. ![[Pasted image 20230517223047.png]] AF with fast rates and changing morphology. changing morphology is concerning for pre-excitation syndrome 2. ![[Pasted image 20230517230738.png]] WPW with antidromic SVT. looks just like VT. can be treated as if it is VT (shock, amiodarone, etc). when they revert to sinus, you can see delta waves and short pr and dx WPW. 3. ![[Pasted image 20230517231905.png]] young nurse with AF phenotypes (irregularly irregular) broad complex tachycardia from WPW. 4. ![[Pasted image 20230517232732.png]] Looks like VT, but irregular, morphology changing. this is AF WPW. **do not give adenosine or any other AV nodal blocker**. patient will go into VF 5. ![[Pasted image 20230518151851.png]] Another example of AF with WPW (could easily be mistaken for polymorphic VT, but it is **irregular**. 1. ![[Pasted image 20230518151945.png]] got amiodarone and went into ventricular fibrillation 6. ![[Pasted image 20230517224217.png]] Rhythm irregularly irregular – atrial fibrillation. Ventricular rate variable – approx. 200-250/min – very fast. Left ward axis of broad complexes. 2 types QRS complex – narrow and broad (mostly) – represent different pathways of activation of ventricles – narrow through AV node, broad through accessory pathway. Hence AF with rapid ventricular response in pt with accessory pathway (WPW) Delta wave seen best in V4 # Long QT see also: [[Long QT]] - QT interval will vary based on rate. can use QTc to correct > $\textnormal{Corrected QT interval (\textbf{QTc}) Bazett} = \frac{QT}{\sqrt[]RR interval}$ - Bazettes over corrects QTc when HR > 110/min, under corrects when HR < 60/min. - Note that in tox cases, tend to use [[Classic tox ECGs#QT nomogram]]. > concern for [[Torsades de Pointes]] with QTc > 500ms ![[Long QT#Causes of prolonged QT]] ![[Pasted image 20240831165036.png]] ## Long QT examples 1. ![[Pasted image 20230518153945.png]] 2. ![[Pasted image 20230518160811.png]] psych patient (on antipsychotics) with syncope 1. ![[Pasted image 20230518160931.png]] patient went into torsades! 3. ![[Pasted image 20230518161302.png]] QTc 652. pt with gastroenteritis. 1. ![[Pasted image 20230518161625.png]] had runs of polymorphic VT 4. ![[Pasted image 20230518161644.png]] alcoholic QTc 520. 1. ![[Pasted image 20230518161726.png]] runs of polymorphic VT 5. ![[Pasted image 20230518162512.png]] mis-diagnosed as seizure 1. ![[Pasted image 20230518163429.png]] "seizures" on monitor 6. # ARVC - T-wave inversion in V1,V2, V3 (unlike Wellen’s that is V1-V4) - **epsilon wave** (looks like a reverse delta wave), with slurring of the downstroke of the QRS, from the nadir of the S wave to the isoelectric line +/- a notch - As ARVD is progressive, the changes on ECG evolve - RBBB, S wave slowing, T inversion. ![[ARVC-epsilon-wave.png.png]] [^1]: - [It is estimated to be responsible for 4%-12% of all sudden deaths and at least 20% of deaths in patients with structurally normal hearts](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8283591/). also 2004 paper: [Brugada syndrome--an under-recognized electrical disease in patients with sudden cardiac death.](bookends://sonnysoftware.com/ref/DL/56540)