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16 Cards in this Set
- Front
- Back
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Heart block |
•Damage to the conducting system ofheart •Fibrosis or ischaemic damagenormally cause•Total heart block, atria andventricles beat independently •Rate determined by pacemaker that isdistal to condition block •Sporadic complete block treated bypacemaker |
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Delayed after-depolarization |
•Delayed after-depolarizationtriggers ectopic beats •Associated with elevated [Ca2+]i •Hypercalcaemia •Hypokalaemia •Many drugs trigger this phenomenonby binding to cardiac ion channels •Long QT syndrome e.g. hERGchannel in drug development |
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Re-entry |
•Normally action potential dies out inventricles as surrounding tissue is still in refractory period•Damage can mean APs re-excite areas thatrefractory period has ended, termed re-entry or “circus movement” •Ischaemic damage a common cause |
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Ectopic pacemaker activity |
•Pacemaker activityfrom areas other than SAN •Sympathetic activity can promoteectopic activity •Tachyarrhythmia (e.g. AF)can be triggered - Associated with increased sympatheticactivity e.g. pain, hyperthyroidism (thyrotoxosis)etc. •Ischaemia - partial depolarisation triggers abnormalpacemaker activity |
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Vaughn Williams classification |
•Class I - Sodium channel blockers •Class II - Beta Blockers •Class III - Amiodaronelike drugs •Class IV - Calcium channel blockers |
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Class ISodium channel blockers |
•Block voltage gated sodium channelsphase 0 of the cardiac action potential •Block is usedependent Class Ia e.g.Disopyramide •Intermediate kinetics Class Ib e.g.Lidocaine •Fast kinetics- block open channel duringphase 0 reducing max depolarization, dissociate before next beat Class Ic Flecainide •Slow kinetics steady state of block•Block during whole cardiac cycle |
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Class IIBeta blockers |
•Block action ofadrenaline/noradrenaline on heart preventtachyarrhythmias •supress actions of sympatheticnervous system, reducing depolarization in phase 4 of the cardiac AP •slow HR and force of contraction |
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Class III amiordarone-like |
•Originally based on action ofamiordarone (now others inc. Stall) •Complex action involving more thanone mechanism •Solatalalso has Class II properties •Prolong the cardiac AP increasingthe refractory period •Inhibit potassium channels involved inphase 3 •Serious potential adverse effects •Can lead to pro-arrhythmic effects suchby prolonging Q-T interval |
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Class IV Calcium channel blockers |
•Block L-Type VGCC •slow conduction in SA and AV nodewhere AP depends on calcium entry verapamil the main used(in some cases diltiazem) •Reduce duration of Plateau (phase2) of AP •Reduce force of heart beat •Also reduce after-depolarizationpreventing ectopic beats •dihydropyridines pro-arrhythmic •reflex tachycardia esp.nifedipine |
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Supraventricular -Atrial fibrillation |
•Most common Sustained arrhythmia •atrial rate of 350>360 bpm •often caused by re-entry atrial contraction essentially unable to occur •ventricular contraction normally <200 •AVN cannotconduct all impulses•Blood pools in systemic circulation- oedema and thrombotic events, Leading cause of strokein elderly |
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CHA2DS2-VAScand stroke/thromboemolism risk in AF |
Congestive heart failure High blood pressure Age-75+ 65-74 Diabetes Previous stroke to TIA Vascular disease Female |
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AF treatment |
Rhythm control •Beta blocker (class II) or calcium antagonist (class IV) •Sedentary patients digoxin (AVNconduction) Rate control •Electrical cardioversion •Class I(c), flecinamideor class III amiloridone/sotalol •Controlof Thromboembolism/stroke •Also remember - Eliminate the cause E.g. Hyperthyroidism, previous MI |
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SupraventricularAtrial Flutter |
•Like AF normally caused by re-entryevents •Intermediate treatment is torestore ventricular rate •Class II or Class IV (verapamil) •Intravenous preferred for rapid control •Conversion to sinus rhythm can bedone by cardioversion or catheter ablation of damaged region •Pharmacologically class Iato be avoided (can cause sudden death) class II better but pharmacologicaltreatments often fail •Stroke risk assessed and antithrombotictreatment should be considered |
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SupraventricularAVNRT and AVRT |
•Often termed paroxysmal supraventricular tachycardia •Atrioventricular nodal re-entrant tachycardia (AVNRT) •Atrioventricular re-entrant tachycardia (AVRT) •Often terminated by non-pharmacological means •carotid massage or reflex vagal simulation (e.g. immersion of face in cold water) •Adenosine terminates this as well (effect on KATP channels) •Class 1c (flecainide) Class II |
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Ventricular tachyarrhythmiasVT and VF (Cardiac Arrest |
•Ventricular tachycardia (VT) resting HR >100 bpm •Various causes including: Congenital heart disease, Drugs that prolong long QT interval, Changes in blood pH, ionic balance, etc •Ventricular fibrillation (VF)seriously reduces blood pumped emergencysituation (Cardiac Arrest) •VT and especially VF major cause ofsudden cardiac death |
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Treatment of VT and VF |
•Cardioversion to restore sinusrhythm •Sustained VT - Type III (amiodarone) class 1c (flecainide) or 1b (lidocaine) •Non-sustained - Class II (beta blocker) or solotal•Implantable cardioversion, catheterablation - often in combination with drugs |
