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Anti dysrhythmics

Physiology and Pharmacology

QuestionAnswer
Storm warnings Atrial fibrillation Nodal escape rhythms Ventricular extrasystoles Ventricular tachycardia Ventricular fibrillation Atrial are more common and less severe
Atrial fibrillation Age related Affects ventricular rate Palpitations if episodic
Ventricular fibrillation Usually indicates pathology May progress to fatal VF - especially if older
Causes of dysrhythmia Abnormal initiation - abnormal excitability and cellular uncoupling Abnormal propagation - Altered conductivity, obstacle in the path and abnormal anatomy
Abnormal initiation Electrolyte disturbances Sympathetic drive Ischaemia Stretch and uncoupling e.g. atrial dilation from mitral stenosis
Abnormal propagation Ischaemia through cellular uncoupling Anatomical obstacles - scars Abnormal anatomy - WPW, HOCM
Re entry model Wave front progresses around heart in a circle Takes so long to get round that cells have stopped depolarising before it gets back
Criteria of the re entry model No short cuts Conduction time must exceed refractory period Minimum wavelength = cv x rp
Breaking the circle Supress impulse generation - membrane stabilisers Block abnormal circuits - lengthen refractory period, increase conduction velocity
Common causes of dysrhythmia Nothing Electrolyte disturbances Sympathetic stimulation Ischaemia
Dysrhythmia in health Self terminating - very common, not a sign of disease Occasional fatal VF - same origin but not self terminating - sudden cardiac death syndrome
Dysrhythmic electrolytes Potassium - hyperkalaemia depolarises membrane so fires spontaneously - hypokalaemia does the same Calcium - after depolarisations - accumulates at surface to cause small depolarisations Magnesium appears to protect against this
Sympathetic dysrhythmia Increased oxygen debt Pacemaker currents Shortened AP - not all by same time so fire independently Potassium disturbance Increased in cold weather = more infarction
Ischaemic dysrhythmia No O2 caused Na K ATPase to stop - build up of calcium under membrane - generated after depolarisations Increased K at rest Increased Ca - cellular uncoupling Increased sympathetic drive - ischaemia and pacemaker currents
R on T phenomenon When a second AP arrives during the T wave the heart is particularly vulnerable - ventricular tachycardia Can be terminated by DC shock - resets system and stops VF temporarily
Antidysrhythmic drugs Local anaesthetics Beta blockers - acute Amiodarone - acute Verapamil
Early antidysrhythmic Quinidine - d-quinone Lidocaine - LA still used today Phenytoin Mexiletine Work via extending the refractory period
Local anaesthetic effects Block Na channels Gradual dissociations = gradual recovery from inactivation Becomes frequency dependent - AP can be generated with drug partially bound but is smaller and slower Reduces chance of RonT rhythms
Local anaesthetics Reduce abnormal impulses - reduce availability of sodium channels Reduce abnormal propagation - extends effective refractory period and decreases conduction velocity
Classifications of Na blockers Fast - lidocaine intermediate - quinidine Slow - flecainide Fast dissociation are most effective as dissociate 1/2 way through cardiac cycle
Local anaesthetics and calcium Reduce Na influx so increase Na gradient More calcium extruded - less available in cell Reduces contractility
Side effects of lidocaine Cardiac failure Ischaemia Dysrhythmia
Acute beta blockade Reduce oxygen demand Reduce pacemaker currents reduce disparity and shortening of action potentials
Amiodarone Lengthens action potential - potassium channel inactivation with a long onset time Antisympathetic Weak local anaesthetic
Calcium antagonists Reduce cellular uncoupling Reduce after depolarisations Must be cardioselective - verapamil used to avoid hypotension
Antidysrhythmic problems Negative inotropic effect Local anaesthetics vis NA/Ca exchange Beta blockers through reduced sympathetic drive Verapamil via reduced Ca entry
Implantable cardioverter defibrillators Detect dysrhythmia Deliver DC shock Only effective in AF if given quickly - atria remodel so fibrillation becomes permanent
Secondary prophylaxis Chronic beta blockade Reduces cardiac workload Reduces sympathetic drive Reduces platelet activation Reduces risk of ischaemia Lengthens AP
Atrial fibrillation Age related problem Risk of stroke - thrombus in left atrial appendage Risk of cardiac syncope - fast ventricular rate
Rate control in AF Bisoprolol - beta blocker Flecainide - local anaesthetic Amiodarone Glycosides
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