Torsades de pointes
- due to long QT
- causes ventricular tachycardia
- leads to sudden cardiac death due to asystole
Atrial arrhythmia
- SAN not used
- atria beat up to 300bpm
- electrical conduction through AVN is quicker so ventricles contract more
- causes palpitations
P wave
Depolarisation of atria
PR interval
Conduction through the AVN node
PR segment
Conduction through Bundle of His
q deflection
Conduction through interventricular septum
QRS
Ventricular depolarisation
S deflection
Conduction of ventricles up
T wave
Ventricular repolarisation
How are arrhythmias caused
- Pacemaker impulse formation - SAN/ AVN
- contraction impulse conduction - abnormal Bundle of His
- combination of both
Abnormal impulse generation:
- automatic rhythms - ectopic beat or enhance normal automaticity
- triggered rhythms - delayed/early afterdepolarisation
Abnormal conduction:
- reentry circuits
- conduction block
Fast cardiac action potential
In cardiac myocytes
Phase 0 - Na+ influx causes depolarisation
Phase 1 - Transient K+ efflux
Phase 2 - Ca2+ influx causes cardiac plateau
Phase 3 - K+ efflux - repolarisation
Phase 4 - Na+/K+ ATPase maintains the resting potential
Resting membrane potential in cardiac myocytes
- 90mv
Class 1 drugs
Block Na+ channels
Inhibit Na+ influx
Decreased speed of depolarisation, decreasing conduction velocity in tissue
Class 2 drugs
Beta blockers Inhibit Ca2+ influx Longer calcium plateau Prevents phase 4 depolarisation and automaticity Good for focal arrhythmias
Class 3 drugs
Block K+ channels
Inhibits K+ efflux
Longer time for repolarisation- extended refractory period
QT interval extended - can cause torsardes de pointes
Increases action potential duration
Class 4 drugs
Calcium channel blockers
Inhibit calcium influx
Decreases phase 4 spontaneous depolarisation
Slow cardiac action potential
In pacemaker cells - SAN/AVN
Phase 0 - Ca2+ influx causing depolarisation
Phase 3 - K+ efflux causing repolarisation
Phase 4 - pacemaker potential - HCN channels activate causing funny currents of sodium influx
- immediate depolarisation causing automaticity
Specialisation of pacemaker cells
Specialised myocytes
Spontaneous depolarisation
Less contractile machinery
Main classes of drugs that act on SAN/AVN
Class 2 - beta blockers
Class 4 - calcium channel blockers
Class 4 drugs on SAN
Slower conduction velocity as takes longer to depolarise
Increases the refractory period
Salbutamol side effect
Beta agonist
Can cause sinus tachycardia as can act on beta1 receptors
Increases calcium influx - increasing conduction velocity
Muscarinic agonists and adenosine
Decreased phase 0 depolarisation
Decreased conduction velocity
Wolf Parkinson white syndrome
- accessory pathway in the heart due to Bundle of Kent
- connects the atria and ventricles
- reentry circuit over and above the AVN
Slow fast reentry
50% of the population have slow and fast conduction pathways
- An ectopic beat travels via the slow pathway
- During its refractory period the rhythm goes back up the other way
- Constant loop causes reentry tachycardia
Micro reentry in MI
MI causes ischaemia and necrosis of heart tissue leading to a scar
Micro reentry can occur in the scar
Causing ventricular arrhythmias - e.g VT
Class 1b drugs examples
Lidocaine - IV form
Mexiletine - oral form
Class 1c drugs examples
Flecainide
Propafenone
Beta blocker examples
Bisoprolol
Metoprolol
Propranolol
Class III examples
Amiodarone (highest efficacy)
Sotalol
Class IV calcium channel blockers
Verapamil
Diltiazem
Class 1b
Mechanism:
- APD slightly decreased in normal tissue
- less Na+ influx
- decreased phase 0 conduction in fast beating of ischaemic tissue
- slower ventricular contraction
ECG:
- in fast beating or ischaemic patients - longer QRS
Used in: acute ventricular tachycardia especially during ischaemia
Side effects:
- less pro arrhythmic
- dizziness and drowsiness
- abdominal GI upset
Class 1c
Method:
- oral - prevention of arrhythmia
- IV - acute arrhythmia
Mechanism:
- substantially lower phase 0 - less Na+ influx
- decreased automaticity
- increased APD and increased refractory period
Uses: - wide spectrum - supraventricular arrhythmias - fibrillation and flutter - Wolf-Parkinson White syndrome - premature ventricular contractions ECG: - longer PR - longer QRS - longer QT
Sid effects of class 1c
- pro arrhythmia
- sudden death associated with chronic use and structural hearty disease
- flutter (1:1 ventricular response)
- CNS and gastrointestinal effects
When can fleconaide be used in structural heart disease patients
When the patient has an implantable cardiac defibrillator
Class II mechanism
Absorption and elimination:
- propanolol and metoprolol - IV or oral
- bisoprolol - oral
- esmolol - IV only (very short acting and short half life)
Effects:
- slower action potential duration in AV node therefore slows conduction velocity
ECG:
- Increased PR
- Decreased HR
Uses:
- sinus and catecholamine dependent tachycardia
- terminate reentrant arrhythmias at AV node
- protect ventricles from higher atrial rates in atrial flutter
Class II side effects
Bronchospasm
Hypotension
When should class II not be used
In partial AV block or acute heart failure
Class III mechanism
Taken: oral or IV via central line
Half life: 3 months
Effects:
- increases the refractory period and APD
- decreased speed of AV conduction
- decreases phase 0 and phase 4
Uses:
- wide spectrum for most arrhythmias
- especially VT
ECG:
- longer PR
- longer QRS
- longer QT
- decreased HR
Side effects of class III
Pulmonary fibrosis Hepatic injury Thyroid disease Increase LDL cholesterol Photosensitivity Optic neuritis when stopping medication
Sotalol
Taken: Orally
ECG:
- longer QT
- Lower HR
Uses:
- supraventricular and ventricular tachycardia
Side effects:
- pro arrhythmia
- fatigue
- insomnia
Class IV mechanism
Verapamil- oral or IV
Diltiazem - oral
Effects:
- slow conduction at AVN - terminates reentry circuit
- increases refractory at AVN
- slow HR as decreases phase 4 slope in SAN
ECG:
- increase PR
- Changes heart rate depending on blood pressure
Uses:
- supraventricular tachycardia
- re-entrant circuits at AVN
Side effects of class IV
- asystole if beta blocker also used with partial AVN block (only give if patient has pacemaker)
- gastrointestinal problems and constipation
Caution with:
- hypotension
- sick sinus
- decreased cardiac output
Adenosine
Administration: rapid IV bolus
Half life: very short (seconds)
Mechanism:
- natural nucleoside that binds to A1 receptors at the AVN, activating K+ currents in the AVN and SAN
- decreased action potential duration
- quicker hyperpolarisation
- decreased HR
- decreased Ca2+ - increased refractory period at AVN
Effects:
- slows conduction at AVN
Uses:
- re-entrant supraventricular arrhythmias
- Diagnosis of coronary artery disease
Vernakalant
Administration: IV bolus for 10 mins
Mechanism: blocks atrial specific K+ channels
Effects:
- slows atrial conduction
- increased potency with higher heart rates
Uses: converts rodent onset AF into sinus rhythm
Vernakalant side effects
Hypotension
AV block
Sneezing and taste disturbances
Ivabradine
Administration : oral
Mechanism:
- blocks funny currents in sinus node (no peripheral effect)
Effects:
- slows SAN firing but doesn’t effect BP
Uses:
- sinus tachycardia
- reduces heart rate in heart failure and angina
Side effects of ivabradine
- flashing lights
- teratogenic
Digoxin
Mechanism:
- enhances vagal activity
- increases K+ efflux and refractory period
- decreases Ca2+
- slows AV conduction and HR
Uses:
-reduces ventricularrate in AF and flutter
Contraindication
- renal failure as regally excreted
Atropine
Mechanism - selective muscarinic antagonist
Effects: blocks vagal activity to speed up AV conduction and increase HR
Uses: treat vagal bradycardia
AF drugs
Rate control:
- bisoprolol
- verapamil
- diltiazem
- digoxin
Rhythm control:
- sotalol
- flecainide with bisoprolol
- amiodarone
VT drugs
- metoprolol/ bisoprolol
- lignocaine/ mexilitine
- amiodarone
Wolf Parkinson White syndrome
Flecainide - nonstructural or ischaemic heart disease
Amiodarone
Re- entrant narrow complex tachycardia drugs
Acute (IV)
- adenosine
- verapamil
- flecainide
Chronic:
- bisoprolol and verapamil
- sotalol
- flecainide and procainamide
- amiodarone
Ectopic beat drugs
First line - bisoprolol
- flecainide
- sotalol
- amiodarone
Sinus tachycardiandrugs
Ivabradine
Bisoprolol
Verapamil