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Electrophysiology Flashcards

1
Q

What is the prevalence of congenital LQTS?

A

1 in 2000

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2
Q

Describe Jervell Lange Nielsen Syndrome.

A

Autosomal recessive congenital LQTS with associated sensorineural deafness. Associated with malignant course, cardiac events precipitated by emotional or physical stress.

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3
Q

What is the rate of SCD in those with Lange jervell Nielsen Syndrome?

A

25%

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4
Q

In those with jervell Lange Nielsen Syndrome, what were the event rates for those aged 1, 3 and 18?

A

15, 50, 90%

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5
Q

How does pregnancy influence risk of events in those with LQTS (particularly LQTS2)

A

Higher risk of events 6-9 months post partum.

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6
Q

Describe pause dependence.

A

Duration of repolarisation is dependent on the duration of the preceding RR interval

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7
Q

What are the external triggers that classically exacerbate LQTS?

A

LQT1 - exercise, swimming, diving

LQT2 - noise, emotion

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8
Q

What preceding symptoms prior to syncope/seizure is highly suggestive of LQTS?

A

Emotional stress

Physical exertion

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9
Q

What types of LQTS have triggered events during sleep?

A

LQT2 and 3

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10
Q

Describe Andersen Tawil Syndrome.

A

Autosomal dominant condition characterised by episodes of potassium related paralysis, ventricular arrhythmia (LQT) and dysmorphic features.

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11
Q

What is the Schwartz score and what is it’s clinical use?

A

Estimate of the clinical likelihood of LQTS based on ECG, clinical and family history.

Used to guide investigation with genetic testing.

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12
Q

What is the role of ecg stress testing in those with suspected LQTS?

A

Exercise associated arrhythmias
Change in T wave morphology
Maladaptive QT response during recovery

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13
Q

What are the maladaptive T wave changes during recovery after ecg stress testing in a patient with LQTS?

A

QTc >470 at 2-4 mins - 70% PPV for LQT1

QTC >470 a 5 min - 70% PPV for LQT2

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14
Q

In what type of LQT is stress ecg not helpful and why?

A

LQT3 - QTc is short in exercise and recovery

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15
Q

What is the management of patients with symptomatic congenital LQTS?

A
  1. General measures (avoid drugs, electrolyte optimisation, AED plan)
  2. Lifelong beta blockade - propranolol (nadolol and metoprolol)
  3. ICD as secondary prevention
  4. ICD or sympathetic denervation if recurrent events despite maximum beta blockade
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16
Q

What is the rate of cardiac events in athletes with LQTS who chose to remain in competitive athletics?

A

Genotype pos/phenotype negative - 0% after 5 years (70 patients)

Genotype and phenotype pos - 1 in 60 after five years

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17
Q

How does type of LQTS inform on management?

A

LQT1 - better to avoid competitive athletics
LQT2 - avoid loud alarms, acute arousal events
LQT3 - less benefit with beta blockade. Consider adding mexilitine

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18
Q

When are ICDs recommended in Long QT?

A
  1. Sudden cardiac arrest for secondary prevention
  2. Recurrent cardiac syncope despite beta blockers and LCSD
  3. Recurrent cardiac syncope despite beta blockers in those not a candidate for LCSD
  4. Asymptomatic patient with LQT2/3 with resting QTc of 550
  5. Post pubertal women LQT2 QTc>500
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19
Q

When is family history of LQTS associated SCD an indication for ICD?

A

Never

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20
Q

What is the rate of major complications from ICD placement over 5 years?

A

31% (infection, lead fracture, dislodgement, inappropriate discharges, psychiatric)

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21
Q

What percentage of congenital LQTS will require ICD?

A

10%

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22
Q

Describe Romano Ward Syndrome.

A

Autosomal dominant LQTS

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23
Q

Describe Brugada Syndrome.

A

Autosomal dominant disorder with variable expression characterised by characteristic ECG findings with risk of ventricular arrhythmias.

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24
Q

What percentage of patients with Brugada pattern ECGs will have an event in 2.5 years?

A

10%

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25
Q

What mental health disease is associated with high rates of Brugada pattern on ECG?

A

Schizophrenia even after controlling for sodium channel blockers

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26
Q

What genes are causative of Brugada?

A

SCN5A

SCN10A

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27
Q

What channels are associated with Brugada?

A

Sodium channels 50%
Calcium channels 10%
Potassium channels

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28
Q

What a drugs are associated with transient Brugada pattern?

A

Cocaine - sodium channel blockade
TCA
Neuroleptic Drugs

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29
Q

How does autonomic tone influence Brugada Syndrome?

A

increased arrhythmia at night suggests parasympathetic worsening of Brugada

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30
Q

What is the incidence of AF in Brugada?

A

20%

Increased disease severity and higher risk of VF

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31
Q

What is the significance of agonal nocturnal breathing in a patient with suspected cardiac arrhythmia?

A

Equivalent of syncope/ventricular arrhythmia. ?aborted event

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32
Q

How does fever influence Brugada?

A

Reduction in sodium current resulting in predisposition to ventricular arrhythmia

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33
Q

What is the diagnostic criteria for type 1 Brugada Syndrome?

A
  1. Symptomatic
    - Type 1 Brugada pattern (V1 or V2) at rest or with flecainide challenge
  2. Asymptomatic
    - type 1 Brugada pattern with
    - first degree block, LAD
    - atrial fibrillation
    - late potentials, fragmented qrs, st-t wave alternans with VEB
    - absence of structural heart disease
    - absence of coronary artery disease
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34
Q

What is the definition of “symptomatic” in patients with Brugada?

A 
VF/VT
Inducible VT on EP
Unexplained syncope 
Nocturnal agonal respiration 
Family history of SCD <45 years 
Family history Type 1 Brugada pattern
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35
Q

What is the definition of Type 2 Brugada?

A
  1. Type 2 Brugada pattern
  2. Conversion to Type 1 with flecainide challenge
  3. Additional feature listed below
    - VF/VT
    - inducible VT on EP
    - family history SCD <45
    - family history of Type 1 ECG
    - agonal respiration
    - unexplained syncope
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36
Q

What is the evaluation of suspected Brugada Syndrome?

A

Echo
+/-CMR
Stress testing/imaging

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37
Q

In the setting of wide complex tachycardia, what are the features suggestive of VT over SVT with aberrant conduction?

A

Capture beat
Fusion beat
Positive or negative concordance in QRS in chest leads
No mans land axis (pos aVR and neg aVF and lead 1)
RSR pattern with taller left rabbit ear
Absence of typical LBBB or RBBB pattern

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38
Q

How do you risk assess people with Brugada pattern without symptoms?

A

Family history
Cardiac imaging - echo/MRI
Drug Challenge if Type 2
Signal averaged ECG
Consider EP study in Type 1 asymptomatic patients
Genetic testing if mutation identified in family

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39
Q

What are the indications for Flecanide challenge in those with Type 2 brugada pattern?

A

Family history of SCD<45 years
Family history of Type 1 pattern

No family history, recommend against challenge

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40
Q

What is the sensitivity of flecainide drug challenge in patients with Type 2 Brugada for Type 1 pattern?

A

15-100%

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41
Q

What are the indications to stop a drug challenge for ?Brugada?

A

Type 1 brugada pattern
>2mm increase in ST elevation with Type 2
Ventricular premature beats
QRS widening >30%

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42
Q

What is the rate of sustained ventricular arrhythmia following drug challenge?

A

1-2%

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43
Q

What is the duration of ECG monitoring post Flecainide challenge for Brugada?

A

30min if IV
4 hours if oral
ECG at 90 min is useful

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44
Q

VT on exertion makes you suspicious of what diseases?

A

HOCM

CPVT

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45
Q

What proportion of patients with Brugada pattern ECG with inducible VT on EP studies will develop and arrhythmic event?

A

3.3%

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46
Q

What is the management of Brugada Syndrome?

A
  1. Treat pyrexia
  2. ICD implantation
  3. Antiarrrhythmics indicated if refusing ICD or multiple shocks (quinidine or amiodarone)
  4. Avoid sodium channel blockers (apart from quinidine)
  5. Catheter ablation - if recurrent events
  6. Family Testing
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47
Q

What is the family testing in a patient with Brugada Syndrome?

A

ECG and clinical history

If negative for repeat assessment every 1-2 years as may still develop disease

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48
Q

What are the rates of complications with ICD placement over 6 years?

A

37% inappropriate shock

30% lead issues

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49
Q

What is the incidence of AF >30s in patients in sinus with mitral stenosis on holter?

What is the rate of TIA/stroke?

A

29%

5.7%

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50
Q

What are the ecg features of RVOT VT?

A 
LBBB morphology 
Rightward axis (positive inferior leads)
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51
Q

Physiology of typical slow fast AVNRT

A

Atrial premature beat allows slow pathway conduction while fast is refractory.

Slow pathway then is able to conduct through to the fast pathway resulting in AVNRT

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52
Q

Which has the shorter refractory period, slow or fast pathway of AVN?

A

Slow pathway - short refractory period

Fast pathway - long refractory period

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53
Q

What are the potential triggers for AVNRT?

A

nicotine, alcohol, stimulants, exercise

54
Q

ECG features of Typical AVNRT

A

P waves close to QRS (commonly after)

Retrograde P waves

55
Q

ECG features of Atypical AVNRT

A

Very late retrograde p waves often shortly before the next QRS

56
Q

What is the modified valsalva?

A

Exhaling against a closed glottis for 15 seconds

Followed by supine re-positioning with passive leg raise for 15 seconds

57
Q

What is the adenosine dose for a patient with SVT with orthotopic heart transplant

58
Q

What is the acute arrhythmic management of AVNRT?

A
  1. Modified valsalva twice
  2. Adenosine if no contraindication
  3. IV beta blockers of calcium channel blocker
59
Q

Long term management of recurrent AVNRT

A
  1. Patient education on modified valsalva and pill in pocket
  2. Chronic suppressive therapy with anti arrhythmics
  3. Catheter ablation 95% success
60
Q

What are the differentials for SVT with retrograde p waves with short RP interval

A

Typical AVNRT

AVRT with accessory pathway

61
Q

What is the definition of short RP interval?

62
Q

What causes SVT with abnormal p waves with short RP interval

A

Atrial tachycardia with AV nodal conduction delay

63
Q

What are the differentials for SVT with retrograde p waves with a long RP interval

A

Atypical AVNRT

AVRT with slow accessory pathway

64
Q

What are retrograde p waves on ECG?

A

Inverted p waves in inferior leads

65
Q

What are the differentials for SVT with abnormal p waves with a long RP interval

A

Atrial tachycardia

Uncommonly from atypical AVNRT

66
Q

What are the important ECG features to assess in SVT?

A

Atrial Rate
P wave morphology
RP relationship
AV relationship

67
Q

What is the most common side for antidromic AVRT?

A

Left sided as needs 4cm between AV node and bypass tract

68
Q

What is the acute arrhythmic management of orthodromic AVRT?

A
  1. Modified Vagal
  2. Adenosine
  3. Verapamil
  4. Beta Blocker/Procainamide
69
Q

What is the acute arrhythmic management of antidromic AVRT?

A

Procainamide

If known to be AVRT then adenosine, verapamil, IV beta blockers

70
Q

What is the medical treatment for recurrent AVRT?

A
  1. Flecainide

2. Proprafenone

71
Q

What are the contraindications to flecainide?

A

Heart block
Heart failure
Structural heart disease
Ischaemic heart disease

72
Q

What are the contraindications to propafenone?

A

Bradycardia
Brugada syndrome
Heart failure
Chronic airways disease

73
Q

What are the contraindications to procainamide?

A

Heart block
SLE
Torsades

74
Q

What is the rate of stroke when cardioverting AF of >48 hours without preceding anti-coagulation?

75
Q

What are the ECG features which increase the likelihood of VT?

A 
Capture beat, fusion beat
AV dissociation
Positive of negative concordance in chest leads 
Absence of typical RBBB/LBBB
Extreme axis 
Complexes >160
76
Q

What is brugada sign? What does it indicate

A

Distance from start of QRS to nadir of S wave is 100ms

More likely VT

77
Q

What is Josephson sign?

A

Notching near nadir of s wave, likely VT

78
Q

What does an RSR with a taller left rabbit ear indicate?

A

Specific for VT

79
Q

What is the use of the Vereckei Algorithm?

A

Used to diagnose VT over SVT with aberancy

80
Q

Describe the steps of the Vereckei Algorithm?

A
  1. AV Dissociation
  2. Initial R wave in AVR
  3. Atypical BBB pattern
  4. Vi/Vt <1

Yes to any of these is VT

81
Q

Describe the steps of the Brugada Algorithm?

A
  1. Absence of RS complex in all precordial leads
  2. R to S intercal >100ms in one precordial lead
  3. AV dissociation
  4. Morphology criteria for VT present in V1 and V6
82
Q

What are the morphological criteria for RBBB morphology VT in the chest leads?

A

V1
Smooth monophasic R wave
Notched downslope of R wave (taller left rabbit ear)
qR complex in V1

V6
negative QS complex
R/S ratio <1 (small R big S)

83
Q

What are the morphological criteria for LBBB morphology VT in the chest leads?

A

V1
R wave >30-40ms
Notching of S wave
RS interval >60-70ms

V6
QS wave (highly specific)
qR pattern (small q large R)
84
Q

What is ohms law formula?

A

Voltage = current * resistance

85
Q

What is the resistance aimed for at pacemaker lead tips?

86
Q

What is the purpose for high resistance in pacemaker leads?

A

Preserve battery life

87
Q

What is the typical amplitude ranges for signals recorded from atrial and ventricular leads?

A

1.5-5 and 5-25mV

88
Q

What occurs if the atria and ventricular signals have amplitudes lower than the respective amplitude ranges?

A

Undersensing and potential inappropriate delivery of pacing pulses

89
Q

Yield of holter monitor in syncope?

A

2%

Useful to fund cardiologists’ Ferrari’s

90
Q

Yield of telemetry monitoring in syncope?

91
Q

What is the progression from bifasicular to trifasicular block per year?

A

1% Asymptomatic

5% symptomatic

92
Q

What is the progression from bifasicular to trifasicular block per year?

A

1% Asymptomatic

5% symptomatic

93
Q

What are the two mutations associated with CPVT?

A 
Ryanodine receptor (autosomal dominant)
Calsequestrin 2 gene (autosomal recessive)
94
Q

What is the pathophysiology of CPVT?

A

Sarcoplasmic reticulum calcium release during diastole

95
Q

What is the molecular pathophysiology of bidirectional VT?

A

Intracellular calcium overload

96
Q

What are the causes of bidirectional VT?

A

Digitalis intoxication

CPVT

97
Q

What is the preferred beta blocker in CPVT?

A

Propranolol

98
Q

How does one achieve a unipolar intracardiac electrogram?

A
  1. Wilson’s central terminal

2. Indifferent electrode

99
Q

What are the features of myocardial scar on intracardiac electrograms?

A

Low amplitude

Fractionated

100
Q

What pacemaker mode is required in a patient with chronic atrial arrhythmias with chronotropic incompetence?

101
Q

What pacemaker mode is required in a patient with paroxysmal atrial arrhythmias with chronotropic incompetence?

102
Q

What pacemaker mode is required in a patient with intact AV node function with chronotropic incompetence?

A

AAIR

But realistically DDDR in real world to ensure covering ventricular pacing if needed

103
Q

What pacemaker mode is required in a patient with poor AV node function with chronotropic incompetence?

104
Q

How do you electrically detect lead insulation failure?

A

Impedance drops, normally <200 ohms

105
Q

How do you identify a conductor fracture of the lead electrically?

A

Increased impedance >2000 ohms

106
Q

How do you electrically localise conductor fracture of a lead?

A

If high impedance is found should

  1. test impedance in unipolar
    2 if returns to normal issue is with the anode.
  2. If does not return to normal, problem is with cathode or both anode and cathode conductor wires
107
Q

What are the causes of high lead impedance?

A

Conductor fracture

Bad lead connection with pacemaker block (?loose screw)

108
Q

What are the components of the threshold of a pacemaker?

A 
Amplitude (Voltage)
Pulse width (time)
109
Q

What is the formula for energy?

A

Energy = ((voltage)2 * time) / resistance

110
Q

To ensure adequate threshold to provide capture, is it more energy effective to increase voltage or pulse width?

A

Pulse width

111
Q

What is the threshold safety margin for voltage and pulse width respectively?

A

2 times voltage

3 times pulse width

112
Q

What is the safety margin for pacemaker sensing?

A

Half the measures impulse

113
Q

What are the three types of upper rate behaviour?

A

2:1 block
Pacemaker Wenckebach
Pacemaker mediated tachycardia

114
Q

How do you calculate pacemakers 2:1 block point?

A

60000/TARP

115
Q

TARP

A

Total atrial refractory period

116
Q

What is the cause of pacemaker wenckebach?

A

Maximum track rate (upper rate limit) delays ventricular pacing

P wave comes during PVARP resulting in “non conducting” p wave

117
Q

What is the formula to calculate pacemaker TARP?

A

Atrial refractory period + post ventricular atrial refractory period

118
Q

How can you manage upper rate behaviour?

A
  1. Decrease TARP total duration

2. Rate response mode

119
Q

What is the mechanism of pacemaker mediated tachycardia?

A

Ventricular ectopic that conducts retrograde through electrical system ultimately leading to an atrial senses beat.
This then triggers a ventricular paces beats which has retrograde conduction again etc

120
Q

What are the conditions that must be present for pacemaker mediated tachycardia to occur?

A
  1. Loss of AV synchrony
  2. Intact V-A retrograde conduction
  3. VA conduction time must be greater than the programmed PVARP
121
Q

What are the causes of undersensing of a pacemaker?

A
  1. Insensitive lead
  2. Lead displacement
  3. Insulation failure
  4. Lead fracture
122
Q

What are the general sensing cut offs for the p and r waves?

123
Q

What proportion of patients with unpaced sick sinus syndrome will develop systemic thromboembolism?

124
Q

What is the benefit of atrial based pacing (AAI or DDD) compared to VVI alone?

A

Reduction in stroke and AF

125
Q

What are the causes of compromising bradycardia?

A

Drugs
Ischaemia
Intoxication
Electrolyte disturbance

126
Q

What is a normal HV interval?

127
Q

What are the long RP interval SVT?

A

Atrial tachy
AVRT
Atypical AVNRT

128
Q

What are the short RP interval SVT?

A

Typical AVNRT
AVRT delta pathway
Atrial tachycardia

129
Q

What is a normal SNRT?

130
Q

What is the formula for CSNRT?

131
Q

What is a normal CSNRT?

RACP Cardio AT (13 decks)

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