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Cardiology > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

Broad complex tachycardia differential:

A

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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2
Q

In which lead are flutter waves best seen?

A

V1

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3
Q

Sick sinus syndrome:

A

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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4
Q

5 causes of 1deg heart block:

A

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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5
Q

2deg heart block:

A

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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6
Q

Complete heart block:

A

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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7
Q

Management options in unstable bradycardia:

A

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

OR

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

OR

  • 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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8
Q

Bradycardia aetiology DDx:

A

‘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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9
Q

DDx narrow complex tachycardia:

A

REGULAR
- Sinus tachy
- SVT
- Flutter
- Junctional tachycardia

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

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10
Q

DDx broad complex tachycardia:

A

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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11
Q

DDx narrow complex bradycardia

A

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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12
Q

DDx broad complex bradycardia

A

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

  • Hyperkalaemia
  • Hypothermia

IRREGULAR

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13
Q

VT vs SVT with aberrancy:

A

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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14
Q

What overall % of broad, regular tachy is VT?

A

70%

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15
Q

APPROACH to broad complex tachycardia:

A

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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16
Q

Define non-sustained VT:

A

3 or more PVCs
but < 30 secs duration

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17
Q

Management of monomorphic VT:

A

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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18
Q

Management of Torsades (long QT PMVT):

A

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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19
Q

What is Torsades?

A

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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20
Q

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

A

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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21
Q

What is this ECG finding?

A

Epsilon wave

Blip in ST segment

ARVD

22
Q

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

A

Brugada
Long QT syndrome
ARVD
HOCM
WPW

23
Q

ECG features of WPW:

A

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)

24
Q

Discuss the use of antiarrhythmics in symptomatic WPW:

A

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.

25
Q
A

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

26
Q

3 drugs that prolong QT:

A

Antipsychotics
Antidepressants
Antihistamines
Macrolides
Class 1 and 3 antiarrythmics

27
Q

ECG findings in HOCM:

A

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

28
Q

Clinical manifestations of HOCM (HCM):

A

Most common cause of young cardiac death

  • Exertional syncope (dynamic LV obstruction)
  • Angina (abnormal coronaries)
  • Diastolic failure
  • Arrythmia/ SCD
29
Q

Management of SVT:

A

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

30
Q

Treatment of SVT in pregnancy:

A

DCR
Vagal
Adenosine

Avoid verapamil first trimester. Okay thereafter.

31
Q

Treatment of SVT in children:

A

DCR 1-2J/kg
Vagal: incl. diving, icepack, handstand

Adenosine
AVOID VERAPAMIL
–> Will kill infants
–> Not recommended for children (HD collapse)

32
Q

Describe the REVERT trial valsalva:

A

-Sit up 30deg
-Blow 10ml syringe 15secs
-Lie back and legs up 15 secs
-Sit up again

43% success
NNT 3

33
Q

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

A
  • Confirm AF
  • Evidence structural change: LA dilation, RVH, LVH
  • Conduction abnormality: AV block, BBB, QTc (may make worse with meds)
  • ## Accessory pathway
34
Q

Main AF acute treatment options, with doses:

A

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

35
Q

When might you choose rhythm control, over rate?

A

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

36
Q

Preferred AF Tx in critically unwell/ HD unstable:

A

DCR
Amiodarone

Second line: digoxin

BB and CCB (++) are negative inotropes. Digoxin unlikely effective

37
Q

When is anticoagulation indicated prior to cardioversion in AF?

A

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

38
Q

Preferred rate control options in stable AF:

A

BB
CCB

Amiodarone shouldn’t be first choice- long term toxicities

39
Q

Preferred AF Tx in pregnancy:

A

DCR

Try to avoid meds: all class C

40
Q

Preferred AF Tx in asthma:

A

CCB first line
Digoxin second line
Amiodarone is option

(Bronchospasm with BB)

41
Q

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

A

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.

42
Q

When is discharge anticoagulation recommended?

A

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

43
Q

Target HR for maintenance therapy:

A

80- 110 at rest

Lower end if CAD, CCF

44
Q

HASBLED score:

A

3 or more = ‘high risk’

45
Q

CHA2DS2 VASc score:

A

Recommended
- Female 3
- Male 2

Consider if 1 point below

46
Q

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

A

2-3%

47
Q

Treatment of flutter:

A

Same as AF!

48
Q

Antiarrythmics: classes and drugs

A

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

49
Q

Antiarrythmics: classes and effects on the heart

A
  • 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)
50
Q

Which antiarrhythmics are options for VENTRICULAR arrhythmia?

A

Amiodarone
Sotalol
Lignocaine
Procainamide

Lignocaine is only safe one for Torsades and TCA OD.

Cardiology (14 decks)

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