Arrhythmias Flashcards
Broad classification of antiarrhytmic drugs
- 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
Example of Class 0 antiarrhythmic in Vaughan William’s Classification, channel they work on and potential side effects
Ivabradine - acts on pacemaker channel HCN4 - slow heart rate
15% - luminous phenomena
Vaughan-Williams - examples of sodium channel blockers (Class I) and how they are classified
1a - intermediate binding - procainamide, quinidine
1b - rapid binding- lidocaine, mexeilitine (more effective in tachyarrhythmias than bradyarrhytmias)
1c - slow binding- flecainide, propaferone
Description of phases of cardiac action potential
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
Examples of Class III (potassium channel blockers) in Vaughan-William’s classification
Amiodarone, sotolol, dronedarone
Manifested by prolonged QT on ECG (amiodarone, dronedarone are exception - very little proarrhytmic activity)
Mechanism of action and pharmacokinetics of amiodarone
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
Notes on amiodarone and thyroid function
- 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
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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
Adverse Effects of Amiodarone
- 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
Adverse drug-drug interactions with amiodarone
Highly bound to plasma protein
Digoxin- amiodarone: rasies plasma digoxin concentration
Warfarin-amiodarone - potentiates warfarin
Simvastatin - higher risk of rhabdomyolysis
Mechanism of action digoxin
Reversibly inhibit the Na-K-ATPase - increase intracellular sodium and decreases intracellular potassium - prevents sodium calcium antiporter expelling calcium from myocyte → increases intracellular calcium
Pharmcokinetics of digoxin - bioavailability, plasma binding, half life
Bioavailbility - 70%
Plasma binding 25%
Half life 50 hours
Potentiators of digoxin
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
Drugs that will reduce serum concentrations of digoxin (inducers of p-glycoprotein)
Carbamazepine, phenytoin, rifampicin, St. John’s wort
Manifestations of digoxin toxicity
Cardiac - any arrhhthmia
Gastro - nasuea, vomiting, abdominal pain
Neurological - confusion, weakness
Visual - alterations in colour vision, diplopia, xanthopsia (objects appear yellow)
Significance of electrolyte disturbances in digoxin toxicity
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
Formula for QTc
QT/square root of R-R
Measure in leads II, V5
Management for acute rate control in AF
Management of Long-term rate control in AF
- Note digoxin less efficacious in lowering exercise rate in comparison to beta blocker and verapamil
Factors favouring rhythm over rate control in AF
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
Acute rhythm control in AF
- 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
Long-term rhythm control in AF
Indications for catheter ablation of AF
- 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
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Complications
- Stroke, cardiac perforation, oesophageal fistula, pulmonary vein stenosis, phrenic nerve injury
Catheter abalation - factors for lower success rate/higher complication rate
Heart disease, obesity, OSA, LA enlargement, age, duration of time in continuous AF
When to start anticoagulation in AF following stroke/TIA
TIA - urgently
Moderate stroke - 5-7 days
Severe stroke - 10-14 days
Prescribing of DAPT/OAC in the setting of elective coronary stenting
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
Prescribing DAPT and OAC in patients with AF following ACS (with or without coronary stent)
Triple therapy for at least one month (up to six) followed by OAC plus single antiplatelet agent up to 12 months, then OAC alone
Notes on atrial flutter
- 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
Causes of cardiac syncope
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
Notes on bifascicular block
- 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
Definitions of sinus node disease
Sinus bradycardia <50bpm and pauses > 3 seconds and symptomatic
Definition chronotropic incompetance
Failure to reach target heart rate with exertion relative to expected for age that is inadequate to meet metabolic demane
Infectious/inflammatory conditions associated with bradycardia and conduction disorders
Chagas disease, diphtheria, infective endocarditis, lyme disease, myocarditis, sarcoidosis, toxoplasmosis
Rheum - RA, scleroderma, SLE
Infiltrative - amyloidosis, haemochromotosis, lymphoma
Indications for permanent pacing in sinus node disease
- Symptoms directly attributable to SND
- Tachy-brady syndrome with symptoms of bradycardia
- Symptomatic chronotropic incompetance
Permanent pacing techniques in sinus node disease
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)
Adverse effects of single RV pacing/Pacemaker syndrome
- 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
Definition high grade/high degree AV block
≥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)
Indications for PPM in AV node disease
- Symptomatic/asymptomatic - mobitz II, high grade AV block, third degree AV block - for infiltrative diseases should also have defibb capacity
- Permanent AF with symptomatic bradycardia
- Could consider in marked symptomatic 1st degree/Mobitz I
- Bi, trifascicular block and recurrent unexplained syncope
Potentially reversible cause for AV node disease that may negate need for PPM
Lyme disease
(Thyroid disease - AV conduction disturbance often doesn’t resolve after correcting TFTs)
General indications for single chamber pacing
Frailty, significant comorbidities, advanced age, sedentary lifestyle, difficulty placing atrial lead, very infrequent episodes where pacing would be required
Permanent pacing techniques in AV node disease
Generally dual chamber pacing over single chamber ventricular pacing (except when thought ventricular pacing will be minimal or life expectancy < 1 year)
Notes on modes used in pacemakers
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)
Indications for cardiac resynchronisation therapy
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)
SVT - examples of long R-P (>90) and mechanism
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
Treatment of pre-excited AF
If sustained - DC cardioversion
Can give IV procainamide or Flecainide but avoid AV nodal blocking agents - will promote conduction down the accessory pathway
Description of orthodontic and antidromic AVRT
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
Example of short R-P SVT (<90msec)
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
Notes on adenosine
- Endogenous purine nucleotide, Half life 2-10 seconds
- Acts on cardiovascular purine receptors
- A1 → electrophysiological actions
- A2 → coronary vasodilatation
- Theophylline inhibits receptor binding
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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
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Side effects
- Flushing
- Dsypnoea
- Chest pain
- Bronchospasm (asthmatics, especially if inhaled)
Differential of wide complex tachycardia
- Ventricular tachycardia
- SVT with functional or fixed bundle branch block
- Pre-excited tachycardia
- Paced tachycardia
- Artefact
Features of a wide complex tachycardia that would suggest pre-excited atrial fibrillation and treatment (and what not to treat with)
Irregular, beat to beat variation in morphology of QRS
Treatment - urgent cardioversion, pharmacotherapy would include flecainide, procainamide
Don’t use AV nodal blocking agents
Features to help distinguish a VT from a SVT with bundle branch block
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
Features of idiopathic ventricular arrhythmia syndromes
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
Indications for treatment of idiopathic ventricular arrhythmia syndromes
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
Treatment of scar-related VT
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
Notes on sudden cardiac death
- 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
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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
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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
Indications for ICD
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
Predictors of sudden cardiac death in HOCM
- 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%)
Notes on arrhymogenic right ventricular cardiomyopathy
- 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
Features of Brugada Syndrome
- 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
Notes on Long QT syndrome
- Abnormal cardiac repolarisation, predipsose to Torsades-de-pointes VT
- >0.45 seconds in men, >0.47 women
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Acquired causes:
- Bradycardia, cerebral events, drugs, metabolic, ischaemia, dietary
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Congenital (adrenergic dependent)
- Clinical classification → Romano Ward, Jervell Lange-Nielsen Syndromes
- Channel/gene classification
Drugs which lengthen QT
- Antiarrhythmics → Class I, III
- Antidepressants → TCAs,, SSRIs, MAOI
- Pehnothiazines, haloperidol, lithium
- Macrolides, cotrimoxazole, azoles
- Diruretics → K+ wasting
- Methadone
Treatment of acquired long QT
- Defibrillated sustained TdP
- Correct cause
- Increase heart rate
- Pacing 90bpm
- Isoprenaline
- Magnesium 1g IV
Notes on congenital long QT
- 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
- Notes on short QT syndromes
- Overactivity K+ channels
- QTC <330 @60bpm
- → AF, SIDS, syncope, cardiac arrest
- Treatment = Class I antiarrhythmics, ICD
Signs of flecainide toxicity
- PR interval prolongation
- Widening of QRS complex
- Signs and symptoms of HF
- Torsades (though QT prolongation not noted)
Actions of digoxin
- Inhibits sodium-potassium ATPase
- Reduces sympathetic outflow
- Reduces renin secretion
- Sensitizes cardiopulmonary baroreceptors
Lown-Ganong-Levine syndrome
PR interval less than or equal to 0.12 second and a normal QRS upstroke and duration.(No Delta Waves)
