Arrhythmia Flashcards by Melanie Thomas

Broad complex tachycardia differential:

8 DIFFERENTIALS

SVT (any) with aberrancy
BBB morphology
Lack of VT features

AF with WPW
Irregular (may be subtle)
Rate >200

Na channel blockade
Terminal R wave aVR

HyperK
More typically brady

Accelerated IV rhythm
Differentiated on RATE- 50-120bpm
Patient stable
Typically post thrombolysis/ reperfusion

VT
Patient factors
ABDDEF+ on ECG
Rate >100/150
Variable patient state
polymorphic irregular, monomorphic reg

VF
Chaotic, no complexes
Rate 150-500
Patient arrested

Runaway PPM

________________________________________
Clinically, main things are:
- IS THIS AF WITH WPW:
?irregular ?rate 200+
Avoid drugs, partic AV blockers
- IF IN DOUBT, SHOCK.
- If want to avoid DCR and SURE not WPW, adenosine may help differentiate.

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In which lead are flutter waves best seen?

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Sick sinus syndrome:

Diseased SA node- typically surrounding fibrosis with old age.

ECG:
Sinus brady
Intermittent SA nodes failure (no P) –> sinus arrest (long pause) –> +/- escape rhythm/ tachy-brady –> resumption of sinus rhythm.

Can have collapse, instability

Mx:
Avoid antiarrythmics- all can make worse
- Atropine/ adren/ dobut/ isopren/ transcut as required
- PPM

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5 causes of 1deg heart block:

PR= 3-5 sml (120 - 200ms)

Vagal tone
Drugs: CCB, BB, digoxin, amiodarone

Rarely, signifies a problem like ischaemia, myocarditis, valve disease.

No specific Tx required.

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2deg heart block:

Mobitz I (Wenkebach)
Progressive lengthening
- Block AT the node. Mostly benign.
- Mx cause- avoid AV blockers etc.
- PPM if symptomatic only

Mobitz II
Regular drop
—> Not good. Structural damage BEYOND node.
–> High risk of deterioration to complete HB.
–> Admit, +- pace, PPM

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Complete heart block:

Escape rhythm may be narrow (junctional) or wide (ventricular)

Unstable/ at risk sudden death

Trial atropine whilst setting up pacing (in case issue AT node)
Can trial Isoprenaline to enhance perfusingg escape rhythm
Pace, Urgent PPM

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Management options in unstable bradycardia:

When vagally mediated:
- ATROPINE 20microg/kg, repeat Q10min

….OFTEN FAILS. Doesn’t work well when the SA or AV itself is dysfunctional (eg. heart block)
______

Next line (or if hypotensive +):

ADRENALINE 0.1microg/kg/min + titrate, max 20
Preferred in ISCHAEMIA- preserves coronary perfusion

DOBUMATINE 2.5 microg/kg/min + titrate, max 10

ISOPRENALINE 0.5 - 2 microg/min + titrate, max 10
Contraindicated in digoxin
Only useful one in heart transplant

…Change to central access ASAP.
_________

Transcutaneous pacing
Transvenous pacing
PPM

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Bradycardia aetiology DDx:

‘Normal’
- Vagal (eg. vomit)
- Fit, young

Cardiac
- Heart block
- Ischaemia (incl inf AMI)
- Myocarditis
- Cardiomyopathy
- Fibrosis, infiltrative

Metabolic
- Hypothyroid
- Hypothermia
- Hypoglycaemia
- HypoMg
- Hypo/ hyper K

Acidosis
Hypoxia

Medication
- BB
- CCB
- Amiodarone
- Digoxin
- Na channel blockers *(TCA, amitrip/ nortrip)
- Clonidine
- Opioids

Toxicological
- Organophosphate

Raised ICP/ Cushing’s

VAGAL predominance vs SYMPATHECTOMY vs ESCAPE RHYTHM ETC.

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DDx narrow complex tachycardia:

REGULAR
- Sinus tachy
- SVT
- Flutter
- Junctional tachycardia

IRREGULAR
- AF
- SVT/ AF/ flutter with variable block
- MAT
- Dig toxicity

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DDx broad complex tachycardia:

REGULAR
- VT (monomorphic)
- SVT with aberrancy
- Accelerated idioventric

Na channel blockade
Post-cardioversion
HyperK (usually brady)
Pacemaker tachycardia

IRREGULAR
- VF
- Polymorphic VT (incl. Torsades)
- AF with WPW
- AF with aberrancy

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DDx narrow complex bradycardia

REGULAR
- Sinus brady
- Junctional
- 1st degree block
- Complete block
- Flutter with high degree block

IRREGULAR
- Sinus arrythmia
- Sinus pause/ arrests
- Slow AF
- Flutter with variable block
- Second degree heart block

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DDx broad complex bradycardia

REGULAR
- Sinus brady with aberrhancy
- Idioventricular
- Ventricular escape
- Paced

Hyperkalaemia
Hypothermia

IRREGULAR

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VT vs SVT with aberrancy:

IN SUPPORT OF VT:

Patient:
Age > 35 (PPV 85%)
Structural heart disease
IHD- active or past
FHX sudden cardiac death

ECG
ABCDEF+
A: Northwest/extreme axis (1 neg, aVf neg, aVr pos), Abscence of BBB
B: Broad >200ms
C: Concordance (+-, v1-6, no RS complexes), Capture beats
D: Dissociation (Ie. P waves)
E: Ear: LEFT rabbit ear V1 (as opposed to right in RBBB)
F: Fusion beats
+:
Josephson’s sign (notching of S wave nadir)
RS interval >100ms (‘Brugada Sign’) in a praecordial lead

If ANY of these present, 90-100% specific

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What overall % of broad, regular tachy is VT?

70%

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APPROACH to broad complex tachycardia:

Main question: Could this be AF with WPW

Avoid drugs- partic AV blockers.
–> If happens to be WPW, will precipitate VF.

If in doubt, shock.

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Define non-sustained VT:

3 or more PVCs
but < 30 secs duration

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Management of monomorphic VT:

1- AMIODARONE
5mg/kg IV stat –> 15mg/kg in 24-hour infusion

2- LIGNOCAINE
1mg/kg
Repeat 10 minutely up to 3x
–> 1-4mg/kg/hr infusion

3- SOTALOL
1mg/kg

DCR 100 –> 150 –> 200J
Overdrive pacing
Optimise myocardial responsiveness (acidosis, hypoxia, temp)
________

STABLE:
–> Amiodarone

UNSTABLE: chest pain, ischaemia, syncope, hypoTN
–> 1- Synchronised DCR plus amiodarone
–> 2- Repeat DCR up to 3, second line agents (sotalol, ligno)
–> 3- Overdrive pace

PULSELESS:
–> ACLS
–> 3x unsynchronised stacked if monitored, witnessed

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Management of Torsades (long QT PMVT):

Notoriously difficult to treat

1- UNSYNCHRONISED DCR if unstable
—> Lignocaine 1.5mg/kg is only safe antiarrhythmic (shortens QT)

2- MAGNESIUM
2g IV over 2 mins
–> 2g/hr infusion
(0.2mmol/kg kids)
Stop if Mg levels >=3mmol

3- Optimise QT
- Correct K, Ca
- Cease culprit meds
- Keep pulse rate >90
–> Isoprenaline
–> Overdrive pacing

_______
Pulseless: ACLS
Unstable: Unsynch DCR 200J
Stable: meds

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What is Torsades?

Polymorphic VT in setting of QT prolongation

QT prolongation may be congenital, or acquired.

May be perfusing. But, can degenerate to RonT —> VF

Management is MAGNESIUM and OPTIMISE QT
(correct K, Ca, stop meds, increase PR- isoprenaline or pacing)

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What 4 causes must be considered in the young person with VT? How can these be diagnosed?

1- Arrhythmogenic RV Dysplasia (ARVD)
- Fibrofatty deposits –> conduction disturbance
- Exertional
- VT with RVH and epsilon wave, RV strain
- Mx ablation

2- 1- Right Ventricular Outflow Tract VT (RVOT)
- Idiopathic
- Exertional or random
- VT with LBBB
- Mx as per SVT

3- Catecholaminergic polymorphic VT
- Dx in childhood
- Exertion, emotion or stress
- *Mx Beta blockers

4- Congenital long QT with Torsades

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What is this ECG finding?

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Epsilon wave

Blip in ST segment

ARVD

What cardiac conditions are associated with ‘FHx of sudden cardiac death’:

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Brugada
Long QT syndrome
ARVD
HOCM
WPW

ECG features of WPW:

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BASELINE
Short PR interval (<120ms)
Delta wave
Prolonged QRS

SYMPTOMATIC
- Broad complex tachy
with variable QRS morphology,
at rates >180 (if down accessory)
OR
- Narrow complex tachys (if down AV)

Discuss the use of antiarrhythmics in symptomatic WPW:

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3 tachyarrhythmias can occur in WPW:

1-AF
–> Most via AV, some via acc
–> QRS complexes vary in appearance
–> Rates high (200+)
2- Orthodromic SVT
–> Down AV, back up acc
–> Will look like normal, narrow SVT
3- Antidromic SVT
–> Down acc, back up AV
–> Will be broad and fast, hard to tell from AF WPW/ VT

____________

Normal, narrow SVT in WPW can be managed the usual way: val salva, adenosine, DCR.
….But DCR still safer.

AF in WPW is the scary one
+ wide, antidromic SVT should always be considered to be this, just in case.

AV BLOCKERS CONTRAINDICATED or they will force AF (with its atrial rate of 300) down the acc pathway and precipitate VF arrest.

DO NOT USE:
- BB
- CCB
- Adenosine
- Digoxin

….Just DCR.

If absolutely have to try meds:
Procainamide 30mg every minute, (to max 17/kg) IS RECOMMENDED.

**Brugada** Syndrome **Sodium channelopathy** **SE Asia** common 50% familial ECG changes unmasked by: *Fever, isch, K, ETOH, drugs* _____________________ ***ECG criteria:*** - Type 1: **Coved STE >2mm V1 - V3**, followed by TWI *--> 'Brugada sign'* - Type 2: **Saddle-back STE** - Type 3: Coved, or saddleback, but **<2mm** **PLUS** ***Clinical Criteria*** One of: - VF/ polymorphic VT - FHx sudden death <45 - FHx 'coved' ECGs - Syncope - Agonal resps at night - Positive EPS Needs **ICD**

3 drugs that prolong QT:

Antipsychotics Antidepressants Antihistamines Macrolides Class 1 and 3 antiarrythmics

ECG findings in HOCM:

**LVH** Narrow, **dagger Q waves in lateral (+\- inferior) leads**

Clinical manifestations of HOCM (HCM):

**Most common cause of young cardiac death** - Exertional syncope (dynamic LV obstruction) - Angina (abnormal coronaries) - Diastolic failure - Arrythmia/ SCD

Management of SVT:

**DCR at 50J** **Vagal Manoeuvres** --> *REVERT valsalva, carotid massage, handstand, diving* **ADENOSINE 100microg/kg --> 200 --> 200** (Max 6mg, 12, 12) OR **VERAPAMIL** **2.5 -5mg IV over 3 mins Can repeat 30 minutely Max dose 20mg** -Not for kids, *KILLS INFANTS* *Other options: - Diltiazem - Flecainide - Beta blockers (not as good)* On discharge: - Refer cardio for EPS - Teach vagal manoeuvres - If recurrent: PO verapamil 80mg TDS

Treatment of SVT in pregnancy:

DCR Vagal Adenosine **Avoid verapamil first trimester**. Okay thereafter.

Treatment of SVT in children:

DCR **1-2J/kg** Vagal: *incl. diving, icepack, handstand* Adenosine **AVOID VERAPAMIL** --> Will kill infants --> Not recommended for children (HD collapse)

Describe the REVERT trial valsalva:

-Sit up 30deg -Blow 10ml syringe 15secs -Lie back and legs up 15 secs -Sit up again 43% success NNT 3

What are you looking for on an ECG for suspected AF?

- **Confirm AF** - Evidence **structural change**: LA dilation, RVH, LVH - **Conduction abnormality**: AV block, BBB, QTc *(may make worse with meds)* - **Accessory pathway** -

Main AF acute treatment options, with doses:

*TRIAL OF NOTHING* - 80% convert within 48 hours *(optimise hydration, electrolyets etc.)* ___________ RATE ***BETA BLOCKERS*** - **Metoprolol** 25-50mg PO 2.5 - 5mg IV (max 15) - **Sotalol** 80mg PO 1mg/kg IV or ***CALCIUM CHANNEL BLOCKERS (nondi)*** - **Verapamil** PO 80- 160mg 5-10mg IV - **Diltiazem** 60mg PO 0.25mg/kg IV Second-line: -**DIGOXIN** IV load: 500 microg --> 250microg 6-hourly x2 -**AMIODARONE** IV 5mg/kg stat --> 15mg/kg over 24hr __________ RHYTHM - **FLECAINIDE** PO 200mg IV 2mg/kg (over 30mins) Second-line: - **AMIODARONE** -**DCR** --> ED synch at 200J --> Delayed TOE -**Overdrive pacing** -**Ablation**

When might you choose rhythm control, over rate?

Unstable Young Active Highly symptomatic First episode Structural normal heart likely / not chronic Known not to have a clot, or low risk

Preferred AF Tx in critically unwell/ HD unstable:

DCR Amiodarone Second line: digoxin *BB and CCB (++) are negative inotropes. Digoxin unlikely effective*

When is anticoagulation indicated prior to cardioversion in AF?

In AF **>=48 hours** or unknown --> Either prove no thrombus with TOE and DCR in DEM with clexane or —> Home on DOAC, return to cardio clinic for synchronised TOE/DCR --> Anticoagulate fully with NOAC (3 weeks), return for delayed DCR

Preferred rate control options in stable AF:

BB CCB *Amiodarone shouldn't be first choice- long term toxicities*

Preferred AF Tx in pregnancy:

DCR Try to avoid meds: *all class C*

Preferred AF Tx in asthma:

CCB first line Digoxin second line Amiodarone is option (Bronchospasm with BB)

When should a patient go home on an antiarrythmic? Which one?

The only time they *shouldn't*, is resolved lone AF *(ie. stimulant, sepsis)* 'Pill in pocket'- flec/ amiod *shouldn't be given from ED*- needs echo first. BB, CCB, dig, amiodarone all options.

When is discharge anticoagulation recommended?

**AF > 48 hours** = ALL, for *at least* 4 weeks **AF < 48 hours** = Only consider if likely to be recurrent, persisent, or high risk. --> *Use Cha2ds2vasc/ HASBLED* _____________ NOAC if: **Male, CHA2DSvasc 2**+ **Female, CHA2DSvasc 3**+ *Consider* if 1 point below **HASBLED 3 or more = high risk**

Target HR for maintenance therapy:

**80- 110** at rest Lower end if CAD, CCF

HASBLED score:

3 or more = 'high risk'

CHA2DS2 VASc score:

**Recommended - Female 3 - Male 2** *Consider* if 1 point below

What is the annual stroke risk for CHA2DS2 vasc 2 or more (when anticoag recommended), without treatment?

**2-3%**

Treatment of flutter:

Same as AF!

Antiarrythmics: classes and drugs

Class I- **Na Channel** blockers **1a**: PROLONG QT - *Procainamide, quinidine* **1b**: SHORTEN QT - *Lignocaine* **1c**: QT NEUTRAL (still prolongs a bit) - *Flecainide* Class II- **Beta Blockers** Class III- **K+ channel blockers** *Sotalol, amiodarone* Class IV- **Calcium Channel** blockers - **Non-dihydro**: Diltiazem, Verapamil - **Dihydro**: (antiHTN only) + Adenosine + Digoxin

Antiarrythmics: classes and effects on the heart

- All are pro-arrhythmic - Most reduce PR --> *Except Na chann + amiodarone* - All are negative inotropes --> *Except digoxin (use in CCF)* - All are AV blockers --> *Except Na chann blockers (use procainamide in WPW)* - All prolong the QT --> *Except lignocaine which shortens (use in Torsades)* - ONLY Na channel blockers prolong QRS (incl. flecainide)

Which antiarrhythmics are options for VENTRICULAR arrhythmia?

Amiodarone Sotalol Lignocaine Procainamide Lignocaine is only safe one for Torsades and TCA OD.

Arrhythmia Flashcards

(50 cards)