Cardiology 1 - Arrhythmias Flashcards

1
Q

What are risk factors for Atrial Fibrillation?

A

Age: 80 1:10
Gender - 30% higher risk in males
Hypertension 1.5x greater risk (V. significant RF)
Valvular heart disease - 30-70% of pt with rheumatic HD have AF
HCM (10-30% of cases)
Hyperthyroidism (8-10%)
Cardiopulmonary disease (congenital, PE, COPD)
Obesity
Diabetes
(NO strong link w ischaemic heart disease)

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2
Q

What is highly suggestive of HOCM?

A

TWI in inferolateral leads in young patients

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3
Q

What is the effect of lifestyle modification on AF recurrence?

A

LEGACY study showed that with increasing weight loss, there was a reduction in ablation/drug free AF freedom, in addition to total AF freedom - greater than the effect of medical therapy

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4
Q

What is the effectiveness of exercise in reducing AF?

A

Increasing exercise level by 2 METS leads to reduction in recurrence by approximately ~50%

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5
Q

What is the relationship between AF and mortality?

A

associated with 1.5-2x increase in overall mortality

Due to thromboembolic events, heart failure and disease associations.

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6
Q

What are presumed pathogenic causes of AF?

A

Haemodynamic - LA stretch
Genetic - 1st degree relatives = 1.4 time risk, polygenic
Inflammation
Metabolic syndrome

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7
Q

What are the stages of AF development?

A

Stage 1 - arrhythmic foci within muscular sleeves extending into pulmonary veins (Paroxysmal -

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8
Q

What is the basic management of AF?

A

If new onset (48hrs or uncertain - TOE, revert and anticoagulate for at least 6 weeks. OR if thrombus, no toe AC for 4-6 weeks then revert.

Urgent cardioversion - if unstable (hypotensive, uncontrolled HF, active ischaemia) - pre-excitation

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9
Q

What are strategies for SR maintenance in paroxysmal AF?

A

Pill in pocket - flecainide +/- betablocker
sotalol is effective, but least well tolerated b-blocker (not good at REVERTING AF)
Amiodarone - most effective, but SEs (thyroid, pulmonary, hepatic and occular toxicity)
dronederone - deriv of amio, increased mortality in HF

B-blockers, verapamil, diltiazem and digoxin have nil efficacy

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10
Q

What were the outcomes of the RACE and AFFIRM studies?

A

found that there was non-inferiority when rate and rhythm control strategies were compared in both studies.

Sinus rhythm and warfarin were independent predictors of improved survival in AF.

Benefit of antiarrhythmics in attaining SR were offset by their SEs

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11
Q

What is the principle of lenient vs strict rate control in chronic AF?

A

Aiming to reduce the risk of tachycardia related cardiomyopathy
RACE I trial found that lenient control (

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12
Q

What is the efficacy of agents in rate control in AF?

A

B-blockers - 59%
Non-dihydropyridine CCB - 38% verapamil > diltiazem
Dig + B-blocker/CCB 60%
MOST EFFECTIVE - Dig + B-blocker + CCB 70%
(verapamil + dig increases drug level)
Verapamil and diltiazem should not be used in HF
Increased risk of heart block and PPM with increasing rate retarding agents.

  • lenient rate control
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13
Q

What are indications for AF abaltion?

A
for patients with Sx+ AF refractory to medical therapy
Does not improve outcomes
does not change indications for Anticoag
60-70% successful
expensive, requires multiple procedures
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14
Q

What are pathological features of A flutter?

A

macro reentrant circuit in the RA, between IVC and tricuspid valve
typical counter-clockwise pattern with downward p-waves in II, III, aVF

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15
Q

What is the treatment of choice in A flutter?

A

ablation of macroreentrant circuit - acceptable to cease anticoagulation if succssful on EP study

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16
Q

What is the complication associated with flecainide in AF?

A

can organise AF to Aflutter and lead to 1:1 conduction to ventricles.
need to co prescribe with b-blocker

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17
Q

When is CHA2DS2-Vasc indicated?

A

In patients who are low risk, i.e. with CHADS2 0-1

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18
Q

What is the relationship between CHADS2 score and bleeding?

A

increasing CHAD2 score has higher rates of bleeding in anticoagulation - those who need to be anticoagulated most are most at risk of AEs.
Can use HASBLED score to assess risk

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19
Q

What are components of HASBLED score?

A

Hypetension, impaired renal function, impaired liver function, Hx stroke, Hx bleeding, Labile INR, Elderly >65, Drugs (NSAIDs, antiplt), Alcohol consumption

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20
Q

What is the mechanism of AVNRT?

A

2 conducting pathways in node - fast and slow
Slow pathway has short refractory time - if premature atrial beat, can conduct down slow during refractory period of fast - leading to reentrant pathway.
P-waves are either not seen or very close to the QRS

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21
Q

What are treatment options in AVNRT?

A

therapy which increased AV nodal delay

vagal manoeuvres, carotid massage
adenosine
diltiazem/verapamil
b-blockers
Rarely DCR

Valsalva with leg raising (40mmHg valsalva for 15 seconds) is better than valsalva without (43% reversion vs 17%)

22
Q

What are differences between orthodromic and antidromic tachycardia in WPW?

A

Orthodromic is narrow-complex, with QRS-P >100ms, treat with AV nodal blockade.

Antidromic is broad complex (difficult to distinguish from VT) - do not give AV node blockers

23
Q

What is a significant complication of WPW?

A

AF conduction down accessory pathway w short refractory time

Rx with IV flecainide, or DCR if unstable.

24
Q

What is the rationale for EP risk stratification?

A

What is the shortest pre-excited RR interval? If >250msec, has excellent NPV,

25
Q

What is the current recommendation for EP risk stratification?

A

EST is new 1st line - loss of pre-excitation during exercise (~20%) is an excellent predictor of low risk

26
Q

What are causes of VT with structural heart disease?

A
Post AMI
Ischaemic CM
Non-ischaemic DCM
Inherited CM - HCM, ACM
Myocarditis
Infiltrative diseases (sarcoid, amyloid, fabry's, metastatic ca)
27
Q

What is the mainstay of treatment of symptomatic VT w structural heart disease?

A

ICD - if sustained VT, pre/syncope due to VT in context of structural HD, ?unexplained syncope

No prognostic benefit with antiarrhythmics, only to prevent Sx and ICD discharge

28
Q

What is the only antiarrhythmic shown to prevent VT and SCD post AMI?

A

B-blockers

29
Q

When is an AICD indicated post AMI?

A

If LVEF 40 days following AMI on medical therapy.

30
Q

What are primary prevention measures in non-ischaemic CM?

A

B-blockers only antiarrhythmic indicated (flecainide C/I)
ICD has mortality benefit
CRT-Defib in those with QRS >120msec 10%ARR
CRT only in those with class IV heart failure

31
Q

What are features of Hypetrophic CM?

A

Clinical Dx - ECG, Echo/CMR, FHX
Autosomal Dominant
Most common cause of SCD age

32
Q

What is the most Sn test in HCM?

A

ECG - but still misses 10%

No single specific echo or CMR finding

33
Q

What are treatment options for HCM?

A

B-blockers indicated in all patients
Risk stratify for ICD implantation:

Major RFs: LV wall thickness >=30mm, FHx premature cardiac death 50mmHg at rest or with provocation

34
Q

How is the Dx of ARVC made?

A
Combination of:
structural/functional studies
histology
repolarisation/depolarisation
arrhythmias
FHx/genetics
35
Q

What are the genetics of AVRC?

A

familial associations in 50%
genetic mutations in desmosomal proteins found in 40-60% (incomplete penetrance)
- desmoplakin and plakoglobin gene mutations

36
Q

What are features of cardiac sarcoid?

A

difficult to diagnose, ECG is non-specific
echo shows wall motion abnormalities, thinning in non-coronary distribution
thallium - intriguing reverse perfusion, but Sn only 60%
CMR is gold standard for diagnosis - role of ICD not clearly established

37
Q

What are causes of VT without structural heart disease?

A

Channelopathies

Outflow tract VT

38
Q

What are primary genes associated with Long QT syndorme?

A

LQT1 (KCNQ1), LQT2 (KCNH2), LQT3 (SCN5A) are assoc with 90%
Autosomal dominant
70-80% positive on gene testing

39
Q

What are features of different subtypes of LQT?

A

LQT1 - most events are caused by exercise, esp swimming/emotional stress
LQT3 - most events during sleep/rest or by loud noises

Longer QTs have worse prognosis.
QTc >500ms represents greatest risk of symptomatic arrhthmias

40
Q

In what congenital LQT patients are B-blockers indicated?

A

ALL

41
Q

What features make ICD indicated in LQT?

A

Previous VT
high risk feat with no prev VT
- QTc >500
- LQT1, LQT2, Male sex LQT3 (female is intermediate risk) for LQT3 with QTc >500)

42
Q

What are features of brugada syndrome?

A

Autosomal dominant
Peak incidence of SCD in 4th decade
ECG changes with septal downsloping ST elevation
May be elicited with flecainide challenge

43
Q

What are features of catecholaminergic polymorphic VT?

A

positive family history
multiple and frequent ventricular arrhythimas on stress testing
treatment is with flecainide, sympathectomy, ICD

44
Q

What are features of idiopathic VT?

A

generally an excellent prognosis
Most frequently RVOT or LVOT tachycardia
ablation is usually efficacious

45
Q

What are types of sinus node dysfunction?

A
Sinus bradycardia
Sinus arrest
Brady-tachy syndrome
Chronotropic incompetence
- treatment - PPM if symptomatic
46
Q

What are features of 1st degree AV block?

A

PR interval >0.2 seconds
benign unless there is associated bifascicular block, where progression to more advanced block may occur
no indication for PPM

47
Q

What are features of 2nd degree AV block?

A

Mobitz I - usually benign, normally in young fit patients and no indication for PPM (resolves with eST, vagally mediated)

Mobitz II - no variation in PR interval, non-conducted P-waves, significant risk of progression to CHB - PPM indicated regardless of Sx

48
Q

When is pacing indicated in 3rd degree heart block?

A

When symptomatic, or rate is

49
Q

What are features of neuro-cardiogenic syncope?

A

cause unknown

teenagers and

50
Q

what are the 3 main types of neurogenic syncope?

A

Cardioinhibitory (HR drops)
Vasodilatatory (BP drops)
Both
tilt table only 70% Sn/Sp

51
Q

What occurs with RV pacing?

A

increased rates of heart failure, increased mortality

BiV pacing in Class I-III HF leads to improved event free survival and is preferred in heart failure with heart block