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Cardiology > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Broad classification of antiarrhytmic drugs

A
  • Class 0 = HCN channel blockers (Ivabradine)
  • Class 1 = Na channel blockers
  • Class 2 = autnomic inhibitors and activators
  • Class 3 = potassium blockers/openers
  • Class 4 = Ca channel handling
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2
Q

Example of Class 0 antiarrhythmic in Vaughan William’s Classification, channel they work on and potential side effects

A

Ivabradine - acts on pacemaker channel HCN4 - slow heart rate
15% - luminous phenomena

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3
Q

Vaughan-Williams - examples of sodium channel blockers (Class I) and how they are classified

A

1a - intermediate binding - procainamide, quinidine

1b - rapid binding- lidocaine, mexeilitine (more effective in tachyarrhythmias than bradyarrhytmias)

1c - slow binding- flecainide, propaferone

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4
Q

Description of phases of cardiac action potential

A

Phase 0 - depolarisation - rapid entry of sodium through voltage dependent Na channels

Phase I - repolarisation - activation of outward potassium channel

Phase 2 - plataeu in repolarisation - late depolarising calcium and sodium currents balanced with repolarising potassium currents

Phase 3 and 4 - decay of calcium current and porgessive activation of repolarising potassium currents

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5
Q

Examples of Class III (potassium channel blockers) in Vaughan-William’s classification

A

Amiodarone, sotolol, dronedarone

Manifested by prolonged QT on ECG (amiodarone, dronedarone are exception - very little proarrhytmic activity)

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6
Q

Mechanism of action and pharmacokinetics of amiodarone

A

Actions

  • Class III → increased action potential duration
  • Class I → sodium channel blockers
  • Class II → non competitive beta blocker (and alpha)
  • Class IV → calcium channel blockers
  • Vasodilator
  • Net EP actions
    • Lengthen refactory period
    • Slow conduction
    • Reduce automaticity
  • Effective in all tachycardias

Pharmacokinetics

  • T ½ = 30 days
  • Bioavailability 35-65%
  • Hepatic excretion
  • Volume of distrubution = 60L/kg → marked tissue binding
  • Onset of action slow → IV hours, oral 2 days - 3 weeks
  • Pro-arrhythmia, also vasodilator
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7
Q

Notes on amiodarone and thyroid function

A
  • Decreases T3 production, blocks T3 receptor binding to nuclear receptors, direct toxic effect on thyroid follicular cells
  • Transient rise in TSH first few weeks very common
  • Hypothyroidism in 5-10% → replace with levothyroxine, continue amiodarone
  • Hyperthyroidism
    • Type 1 → increased synthesis T4 and T3 → treat with carbimazole
    • Type 2 → excess release of T4-T3 → destructive thyroiditis → treatment with glucocorticoids
    • May be able to continue amiodarone
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8
Q

Adverse Effects of Amiodarone

A
  • 75% have adverse effects by 5 years

Pulmonary chronic interstitial pneumoniitis

  • Delayed and dose dependent (rarely acute and idiosyncratic). Treatment with steroids and drug withdrawal

Thyroid - hypo- and hyper-thyroidism

  • Blocks conversion of T4 → T3

Cardiac - bradycardia and AV block, QT prolongation (incidence of TdP <1%)

Hepatic - symptomatic hepatitis <3%

Ocular - corneal microdepositis, optic neuropathy

Skin - Photosensitivity, bluish slate grey discolouration

Neurological - tremor, ataxia, peripheral neuropathy

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9
Q

Adverse drug-drug interactions with amiodarone

A

Highly bound to plasma protein

Digoxin- amiodarone: rasies plasma digoxin concentration

Warfarin-amiodarone - potentiates warfarin

Simvastatin - higher risk of rhabdomyolysis

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10
Q

Mechanism of action digoxin

A

Reversibly inhibit the Na-K-ATPase - increase intracellular sodium and decreases intracellular potassium - prevents sodium calcium antiporter expelling calcium from myocyte → increases intracellular calcium

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11
Q

Pharmcokinetics of digoxin - bioavailability, plasma binding, half life

A

Bioavailbility - 70%

Plasma binding 25%

Half life 50 hours

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12
Q

Potentiators of digoxin

A

Digoxin substrate of p-glycoprotein (efflux pump that excretes drugs into intesting or PCT thereby lowering derum concentrations

Inhibitors of p-glycoprotein potentiate digoxin

Amiodarone, quinidine, macrolides, itraconzole/ketoconazole, carvedilol, ciclosporin, ranolazine, ritonavir, verapamil

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13
Q

Drugs that will reduce serum concentrations of digoxin (inducers of p-glycoprotein)

A

Carbamazepine, phenytoin, rifampicin, St. John’s wort

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14
Q

Manifestations of digoxin toxicity

A

Cardiac - any arrhhthmia

Gastro - nasuea, vomiting, abdominal pain

Neurological - confusion, weakness

Visual - alterations in colour vision, diplopia, xanthopsia (objects appear yellow)

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15
Q

Significance of electrolyte disturbances in digoxin toxicity

A

Hyperkalaemia - predictor of mortality - secondary to inhibition of Na-K ATPase. K lowering agents do not reduce mortality

Hypo - K, Mg, Ca 0 increase susceptibility to effects of digoxin

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16
Q

Formula for QTc

A

QT/square root of R-R

Measure in leads II, V5

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17
Q

Management for acute rate control in AF

A
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18
Q

Management of Long-term rate control in AF

A
  • Note digoxin less efficacious in lowering exercise rate in comparison to beta blocker and verapamil
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19
Q

Factors favouring rhythm over rate control in AF

A

Patient preference

Highly symptomatic or physically active patients

Difficulty achieving rate control

LV dysfunction (mortality benefit)

Paroxysmal or early persistent AF

Absence of severe left atrial enlargement

Acute AF

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20
Q

Acute rhythm control in AF

A
  • Electrical cardioversion in unstable patients (can also consider in stable where pharamcological measures have failed)
  • Flecainide if no structural heart disease (B Blocker 30 minutes beforehand). Other options → propafenone, sotalol
  • Amiodarone if structural heart disease
  • Early cardioversion vs “wait and see” 48 hours
    • Reasonable to delay cardioversion 2 days → 69% spontaneously revert
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21
Q

Long-term rhythm control in AF

A
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22
Q

Indications for catheter ablation of AF

A
  • Younger patients (<75 years), symptomatic paroxsymal or persistent AF refactory or intolerant to at least one Class I or Class III antiarrhytmics. Absence of structural cardiac disease and co-morbidity.
  • Note - no actual mortality benefit but reduces symptom burden (though CASTLE- AF trial → patients with paroxsmal/persistent AF and heart failure → reduced death and hospitalised in ablation group)
  • Success rate 60-70% - second or third procedure may be required, more successful in paroxsymal vs persistent
  • Complications
    • Stroke, cardiac perforation, oesophageal fistula, pulmonary vein stenosis, phrenic nerve injury
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23
Q

Catheter abalation - factors for lower success rate/higher complication rate

A

Heart disease, obesity, OSA, LA enlargement, age, duration of time in continuous AF

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24
Q

When to start anticoagulation in AF following stroke/TIA

A

TIA - urgently

Moderate stroke - 5-7 days

Severe stroke - 10-14 days

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25
Q

Prescribing of DAPT/OAC in the setting of elective coronary stenting

A

Triple therapy for at least 1 week (up to one month). Then OAC plus single antiplatelet up to 1 year. Then OAC monotherapy long-term

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26
Q

Prescribing DAPT and OAC in patients with AF following ACS (with or without coronary stent)

A

Triple therapy for at least one month (up to six) followed by OAC plus single antiplatelet agent up to 12 months, then OAC alone

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27
Q

Notes on atrial flutter

A
  • Macro re-entrant circuit within the right atrium around the tricuspid annulus → 90% counter-clockwise
  • Electrical circuit must pass between the IVC and tricuspid annulus → ablation target
    • Class 1 indication for ablation
  • Wary of flecainide
    • Slows conduction velocity within flutter circuit, minimal effect on AV nodal conductino → could cause 1:1 conduction down AV node
28
Q

Causes of cardiac syncope

A

Arrhytmic

  • VT/VF
  • Complete heart block with ventricular standstill
  • Sinus node disease - sinus pauses
  • (Not AF, SVTs)

Structural

  • LVOT obstruction (severe AS, HOCM) - typically exertional syncope
  • Severe pulmonary hypertension
  • Major pulmonary embolism
29
Q

Notes on bifascicular block

A
  • RBBB + block of anterior (LAD) or posterior (RAD) fascicle of left bundle, or LBBB
  • Trifascicular block → bifascicular block + PR prolongation
  • Progression to CHB → 1% year asymptomatic, 5% year if symptomatic
  • If asymptomatic → no further evaluation
  • Pre-syncope/syncope
    • ECG/cardiac monitoring, +/- ECHO
    • Consider EPS
    • Consider implantable cardiac monitor
    • Consider up front permanent pacemarker
      • >50% end up with a pacemaker
30
Q

Definitions of sinus node disease

A

Sinus bradycardia <50bpm and pauses > 3 seconds and symptomatic

31
Q

Definition chronotropic incompetance

A

Failure to reach target heart rate with exertion relative to expected for age that is inadequate to meet metabolic demane

32
Q

Infectious/inflammatory conditions associated with bradycardia and conduction disorders

A

Chagas disease, diphtheria, infective endocarditis, lyme disease, myocarditis, sarcoidosis, toxoplasmosis

Rheum - RA, scleroderma, SLE

Infiltrative - amyloidosis, haemochromotosis, lymphoma

33
Q

Indications for permanent pacing in sinus node disease

A
  1. Symptoms directly attributable to SND
  2. Tachy-brady syndrome with symptoms of bradycardia
  3. Symptomatic chronotropic incompetance
34
Q

Permanent pacing techniques in sinus node disease

A

If normal Av conduction - dual chamber (RA, RV) or single atrial pacing (if dual selected and normal av conduction - program PPM to minimise ventricular pacing)

If life expectance < 1 year - single chamber RV pacing (unlikely to benefit from synchrony provided by dual pacemaker given increased risk of procedure)

35
Q

Adverse effects of single RV pacing/Pacemaker syndrome

A
  • Loss of AV synchonry with VVI
  • Adverse haemodynamics with normally functioning pacemaker resulting in symptoms or suboptimal status
    • Underfilled ventricle
    • Decreased cardiac output
    • High atrial pressure
    • Venous congestion
  • Symptoms → malaise, dyspnoea, dizziness, cough, atypical chest discomfort, throat fullness

Most consistent benefit of dual pacing over single chamber ventricular = reduction in incidence AF

36
Q

Definition high grade/high degree AV block

A

≥2 consecutive p waves at a normal rate are not conducted without complete loss of atrioventricular conduction

Generally considered to be intra- infra-Hisian and treated with pacing

(Progress more rapidly/unexpectedly, less likely to respond to atropine, more unpredictable ventricular escape rhythm)

37
Q

Indications for PPM in AV node disease

A
  1. Symptomatic/asymptomatic - mobitz II, high grade AV block, third degree AV block - for infiltrative diseases should also have defibb capacity
  2. Permanent AF with symptomatic bradycardia
  3. Could consider in marked symptomatic 1st degree/Mobitz I
  4. Bi, trifascicular block and recurrent unexplained syncope
38
Q

Potentially reversible cause for AV node disease that may negate need for PPM

A

Lyme disease

(Thyroid disease - AV conduction disturbance often doesn’t resolve after correcting TFTs)

39
Q

General indications for single chamber pacing

A

Frailty, significant comorbidities, advanced age, sedentary lifestyle, difficulty placing atrial lead, very infrequent episodes where pacing would be required

40
Q

Permanent pacing techniques in AV node disease

A

Generally dual chamber pacing over single chamber ventricular pacing (except when thought ventricular pacing will be minimal or life expectancy < 1 year)

41
Q

Notes on modes used in pacemakers

A

VVI

  • Sensing/pacing in the ventricle only
  • Generally used in temporary pacing wires

DDD

  • Most common
  • Sensing/pacing in atrium and ventricle

AAI

  • Sensing and pacing in atrium only → requires normal AV nodal conduction
  • Used for pure sinus node disease (but usually do insert ventricular lead also)
42
Q

Indications for cardiac resynchronisation therapy

A

Activates both the left and right ventricle simultaneously - the aim is to pace every beat

  • Improved functional capacity
  • Improved NYHA Functional class
  • Reduced mortality

Indications

  • Symptomatic heart failure, sinus rhythm with LVEF ≤35%, QRS duration ≥150 (consider if ≥130) and LBBB despite OMT
  • Atrial fibrillation → Symptomatic heart failure NYHA Class III or IV, QRS ≥130 (provided a strategy to ensure biventricular capture is in place)
43
Q

SVT - examples of long R-P (>90) and mechanism

A

AVRT, sinus tachycardia, atrial tachycardia

Accessory pathway - either manifest (delta wave) or concealed (conducts retrogradely ventricle → atrium)

Pre-excitation (delta wave) + tachyarrhythmias = WPW - usual rhythm AVRT - responsive to adenosine, can also get pre-excited AF

44
Q

Treatment of pre-excited AF

A

If sustained - DC cardioversion

Can give IV procainamide or Flecainide but avoid AV nodal blocking agents - will promote conduction down the accessory pathway

45
Q

Description of orthodontic and antidromic AVRT

A

Orthodromic → imprulse travels down the AV node through the His Purkinje system

Antidromic → less common, ventricle activated first - broad compex tachycardia, difficult to distinguish from VT

46
Q

Example of short R-P SVT (<90msec)

A

AVNRT - most common of SVTs

Typical → conducted down slow pathway - short R-P

Atypical → conducted down fast pathway and returns via slow - long R-P

47
Q

Notes on adenosine

A
  • Endogenous purine nucleotide, Half life 2-10 seconds
  • Acts on cardiovascular purine receptors
    • A1 → electrophysiological actions
    • A2 → coronary vasodilatation
    • Theophylline inhibits receptor binding
  • Electrophysiological actions
    • Suppresses automaticity at sinus node
    • Depressed conduction at AV node (terminate AVRT/AVNRT, slow AF)
    • Atrium → decreased action potential duration
    • No effect at level of ventricle/accessory pathways
  • Side effects
    • Flushing
    • Dsypnoea
    • Chest pain
    • Bronchospasm (asthmatics, especially if inhaled)
48
Q

Differential of wide complex tachycardia

A
  1. Ventricular tachycardia
  2. SVT with functional or fixed bundle branch block
  3. Pre-excited tachycardia
  4. Paced tachycardia
  5. Artefact
49
Q

Features of a wide complex tachycardia that would suggest pre-excited atrial fibrillation and treatment (and what not to treat with)

A

Irregular, beat to beat variation in morphology of QRS

Treatment - urgent cardioversion, pharmacotherapy would include flecainide, procainamide

Don’t use AV nodal blocking agents

50
Q

Features to help distinguish a VT from a SVT with bundle branch block

A

History of MI/dilated cardiomyopathy/non-ischaemic cardiomyopathy → VT

Variable intensity of 1st HS, canon A waves → VT

AV dissociation on ECG → VT

North-West axis on ECG → VT

All precordial QRS complexes pointing in same direction (downwards more helpful) → vt

Fusion and capture beats → VT

51
Q

Features of idiopathic ventricular arrhythmia syndromes

A

Majority present with frequent PVCs or bursts of NSVT, slightly more common in women

10% of all ventriculae arrhytmias

Usually due to focal triggered mechanisms

Known association with exercise (difficult to distinguish from arrhythmogenic RV cardiomyopathy)

Excellent prognosis

52
Q

Indications for treatment of idiopathic ventricular arrhythmia syndromes

A

Symptomatic VT or PVCs

Ectopy mediated cardiomyopathy - increasing burden of PVCs → decreased LV function, LV function improves post-ablation, anti-arrhythmic drugs don’t impact much on PVCs

53
Q

Treatment of scar-related VT

A

Electrical cardioversion - can trial one medication - sotolol, amiodarone, ligonocaine, procainamide

Never use verapamil

Nearly all have indication for ICD

Can consider catheter ablation first line for ischaemic cardiomyopathy

54
Q

Notes on sudden cardiac death

A
  • Definition → death <1 hour of symptoms
  • 75% male, 32% of all middle aged male deaths
  • 60% of all cardiovascular death s
  • 90% due to ischaemic heart disease - often first presentation IHD
    • Most rhythms VF, then bradys, VT, undertermined
  • Important causes of sudden death in young athletes
    • HOCM most common
    • Followed by commotio cordis and coronary artery anomalies
    • Myocarditis
    • Arrhythmogenic right ventricular cardiomyopathy
    • Dilated cardiomyopathy
    • Drug abuse
    • Long QT syndromes
    • Cardiac sarcoidosis
  • Other causes
    • WPW
    • Brugada
    • Congenital heart disease → complex, cyanosed, post-surgical, congenital complete heart block
    • SIDS
    • Myotonic dystrophy
  • Anti-arrhythmic drugs don’t improve mortality
55
Q

Indications for ICD

A

Secondary prevention

  • Resuscitated VT/VF arrest not due to a reversible cause (acute MI, drugs, metabolic)
  • VT sustained or symptomatic, not ablatable, associated with
    • Severe compromise or failed anti-arrhythmics or LVEF <40%

Primary prevention

  • Ischaemic cardiomyopathy → LVEF <30% >1 month post MI
  • CHF → LVEF <35%
  • Cardiomyopathy → LVEF <35%
  • Hereditary cardiac conditions at high risk. ofsudden cardiac death
    • HOCM
    • Long QT
    • Arrhythmogenic right ventricular cardiomyopathy
    • Brugada
56
Q

Predictors of sudden cardiac death in HOCM

A
  • Resuscitated cardiac arrest
  • Early symptom onset
  • Family history sudden cardiac death
  • Age
  • Septal hypertrophy >30mm
  • Outflow obstruction
  • Left atrial diameter
  • Non-sustained VT
  • Unexplained syncope
  • Exertional hypotension
  • Exertional ischaemia
  • MRI - late gadolinium enhancement

Indications for ICD

  • HCM Risk-SCD score ≥6% (consider if ≥4%)
57
Q

Notes on arrhymogenic right ventricular cardiomyopathy

A
  • Fibrous or fibro-fatty replacement of myocardium
  • RV primarily but also involves LV
  • AD in most forms
    • Mutations in desmosome related genes (cell adhesion)
  • Present with ventricular arrhythmias → cause of SCD
    • Can be exercise induced, exercise can influence disease development
  • ECG: prolonged S wave upstroke, anterior T wave inversion, epsilon wave
  • ECHO and MRI: RV dimension increases, wall motion abnormalities, aneursym
  • Treatment with beta blockers
  • ICD if cardiac arrest, VT, arrhytmic syncope, low EF
  • Prognosis influenced by genetics, potential indication for cardiac transplantation
58
Q

Features of Brugada Syndrome

A
  • Typical ECG features + asymptomatic = Brugada pattern
  • Autosomal dominant, males, South East Asian
    • Mutations in SCN5A/SCN10A - sodium channel genes
    • Can be subtle abnormalities of the RVOT
  • Presents with syncope, cardiac arrest or sudden cardiac death
    • Autonomic tone may be relevant → increased nocturnal events
    • Fever triggers ECG changes and arrhythmias
  • Provocative test with flecainide
  • Needs ICD - cardiac arrest survivros, arrhythmic syncope
59
Q

Notes on Long QT syndrome

A
  • Abnormal cardiac repolarisation, predipsose to Torsades-de-pointes VT
  • >0.45 seconds in men, >0.47 women
  • Acquired causes:
    • Bradycardia, cerebral events, drugs, metabolic, ischaemia, dietary
  • Congenital (adrenergic dependent)
    • Clinical classification → Romano Ward, Jervell Lange-Nielsen Syndromes
    • Channel/gene classification
60
Q

Drugs which lengthen QT

A
  • Antiarrhythmics → Class I, III
  • Antidepressants → TCAs,, SSRIs, MAOI
  • Pehnothiazines, haloperidol, lithium
  • Macrolides, cotrimoxazole, azoles
  • Diruretics → K+ wasting
  • Methadone
61
Q

Treatment of acquired long QT

A
  • Defibrillated sustained TdP
  • Correct cause
  • Increase heart rate
    • Pacing 90bpm
    • Isoprenaline
  • Magnesium 1g IV
62
Q

Notes on congenital long QT

A
  • 1:2000
  • Diagnosis difficult → QTC <440% in ⅓
    • Family history, syncope, genetic
    • ETT → QT > 0.38 @100bpm recovery
  • 50% symptomatic, onset typically < 40 years
    • Syncope, exertional, emotional, sudden fright
    • Mortality symptomatic untreated = 5%/year

LQT1

  • KCNQ1 gene
  • K current
  • Can be precipitated by swimming, exercise

LQT2

  • KCNH2 gene
  • K current
  • Precipitated by emotional stress, noise

LQT3

  • SCN5A gene
  • Na current
  • Precipitated by sleep

Risk factors for sudden death

QTC > 500, syncope, cardiac arrest, family history SCD, LQT3 males, LQT2 females, deafness, post partum, T wave alternans infants <1 year, neonates

Treatment

Avoid triggers, QT prolonging drugs and catecholamines

Beta blockers - nadalol for all symptomatic and most asymptomatic

Cervical sympathectomy

Pacing (rate >80bpm) occasionally used

ICD

63
Q
  • Notes on short QT syndromes
A
  • Overactivity K+ channels
  • QTC <330 @60bpm
  • → AF, SIDS, syncope, cardiac arrest
  • Treatment = Class I antiarrhythmics, ICD
64
Q

Signs of flecainide toxicity

A
  1. PR interval prolongation
  2. Widening of QRS complex
  3. Signs and symptoms of HF
  4. Torsades (though QT prolongation not noted)
65
Q

Actions of digoxin

A
  • Inhibits sodium-potassium ATPase
  • Reduces sympathetic outflow
  • Reduces renin secretion
  • Sensitizes cardiopulmonary baroreceptors
66
Q

Lown-Ganong-Levine syndrome

A

PR interval less than or equal to 0.12 second and a normal QRS upstroke and duration.(No Delta Waves)

Cardiology (9 decks)

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