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1、Copyright 2003 St. Jude Medical Cardiac Rhythm Management Division心动过速的发生机制心动过速的发生机制SJM internal use ONLY SJM internal use ONLY 目标目标描述传导的解剖和特性描述传导的解剖和特性了解动作电位和自主神经系统在心动过速中的作用了解动作电位和自主神经系统在心动过速中的作用了解心律失常的机制和类型了解心律失常的机制和类型了解药物对心律失常的影响和作用了解药物对心律失常的影响和作用SJM internal use ONLY 内容内容心脏传导心脏传导动作电位动作电位心动过速的发生机
2、制心动过速的发生机制复习药物复习药物复习心律失常复习心律失常总结总结心脏的传导心脏的传导心脏组织的特性:选择性通透选择性通透The process by which cell membranes allow certain molecules or charged ions to pass through it.兴奋性兴奋性Ions shift across the cell membrane in response to a stimulus creating measureable electrical potential changes and causing contraction传导
3、性传导性The ability to transmit an electrical impulse from one cell to the next自律性自律性The ability of the cardiac muscles to depolarize spontaneously. i.e without external electrical stimulation SJM internal use ONLY Selective PermeabilityThe process by which cell membranes allow certain molecules or char
4、ged ions to pass through it.SJM internal use ONLY Excitability and ConductivityExcitabilityIons shift across the cell membrane in response to a stimulus creating measureable electrical potential changes and causing contractionConductivityThe ability to transmit an electrical impulse from one cell to
5、 the nextSJM internal use ONLY AutomaticityThe ability of the cardiac muscles to depolarize spontaneously. i.e without external electrical stimulationCardiac Action PotentialA measureable wave of electrical discharge that travels along the membrane of a cellAction Potential graphic depiction of elec
6、trical activity of one cardiac cellSurface ECG graphic depiction of sum of all electrical signalsCardiac cells go both ways:Depolarization and RepolarizationSJM internal use ONLY Action Potential - DepolarizationSJM internal use ONLY Action Potential - RepolarizationSJM internal use ONLY Action Pote
7、ntial Localized Differences in Conduction 0.2 meters/second in the AV node 0.4 meters/second in ventricular muscle 1 meter/second in atrial muscle 4 meters/second in the Purkinje fibersConduction velocity within cardiac tissue varies from slowest to fastest as follows:Why do we need to understand ac
8、tion potentials?Direct relationship on the cardiac rhythm mechanismsDirect relationship to drug and shock therapyCardiac Action PotentialSJM internal use ONLY Pharmacology ReviewPrimary Actions of Anti-Arrhythmic Drugs Cell Membrane Activity Affect Na+, Ca+, and K+ Ion channelsAutonomic Nervous Syst
9、em InnervationsSympathetic and ParasympatheticSJM internal use ONLY Pharmacology Review Autonomic Nervous System Consists of motor neurons that control internal organs Two divisions: 1. Sympathetic = Adrenergic 2. Parasympathetic = CholinergicSJM internal use ONLY Pharmacology ReviewCell Membrane Ac
10、tivity Affects the ion transport mechanisms/channels that directly impact rate of depolarization and repolarizationSlows conduction velocityIncrease or decrease refractory periodsDepress automaticity of SA/AV nodeSJM internal use ONLY Pharmacology ReviewAutonomic Nervous System Beta ReceptorStimulat
11、ion B1 - Increases heart rate, myocardial contractility and enhances AV conductionB2 - Dilates bronchial tubes to allow increased oxygenationCardioselective versus non-cardioselectiveSJM internal use ONLY Pharmacology ReviewAutonomic Nervous System- Parasympathetic Compensatory mechanism for sympath
12、etic systemRelease of neurotransmitter, acetylcholine (cholinergic)Stimulation causes decrease in heart rate conduction, and force of contractionVagus Nerve SJM internal use ONLY Pharmacology ReviewVaughan Williams Classification of Antiarrhythmic Drugs Class I Fast Na+ ion channel-decrease speed of
13、 depolarizationClass IIBeta blocking action-decrease sympathetic toneClass IIINa+ and Ca+ channel effects- Increases action potential duration Class IVSlow Ca+ ion channel- Mainly effects SA and AV nodes by slowing automaticity and conduction timeClass VIncreases Parasympathetic affectsSJM internal
14、use ONLY Fogoros,R. Practical Cardiac Diagnosis Electrophysiology Testing. 3rd Ed. Pg 25. Blackwell Science, 1999.Cell Membrane ActivityClass Ia DrugsClass Ib DrugsClass Ic DrugsClass III DrugsClass IV Drugs(AV node action potential)= Normal Activity= Drug-Influenced ActivityPharmacology ReviewSJM i
15、nternal use ONLY Pharmacology ReviewClass IA ACTION: Na+ Channel Moderately prolongs refractoriness and decreases conduction velocity (increases QRS and prolongs QT interval) DRUGS: Procainamide, Disopyriamide (Norpace), QuinidineCONSIDERATIONS:Can use for atrial and ventricular arrhythmiasTosade de
16、 pointe- monitor QRS width and prolongation of QTMay slow VT rates- ATP therapy and detection ratesCan enhance AV conduction- may need to use with rate slowing drugsSJM internal use ONLY Pharmacology ReviewClass IB ACTION: Na+ ion channel Mildly Decreases action potential duration and shorten refrac
17、tory periodDRUGS: Lidocaine, Mexilitine, Tocainide, Phenytoin (Dilantin)CONSIDERATIONS:Used only for ventricular arrhythmiasMay slow VT rate- ATP and detection rate adjustmentsCNS side effects- Dizziness, depressed level of consciousness, tingling/numbness of extremitiesLidocaine used for short term
18、 IV therapy/ common with AMISJM internal use ONLY Pharmacology ReviewClass IC ACTION: Na+ channel blockade- Pronounced depression of action potential conduction velocity with little effect on refractory periodsDRUGS: Flecainide, Encainide, Propafenone (Rhythmol)CONSIDERATIONS:Can use for atrial and
19、life threatening ventricular arrhythmiasGenerally used for patients WITHOUT structural heart diseaseIncrease risk of Sudden Death when used in patients with ischemia and structural heart disease, LV dsyfunction (CAST-Cardiac Arrhythmia Suppression Trial) PROARRYTHMIC EFFECTSSlow VT rates- ATP and de
20、tection rate programmingFlecainide- Known for increasing pacing thresholdsSJM internal use ONLY Pharmacology ReviewClass II ACTION: Blocks Sympathetic Beta ReceptorsDRUGS: Beta Blockers- Commonly end in “ol”Propranolol (Inderal), Pindilol, Sectral, Atenolol, MetoprololCONSIDERATIONS:Slows AV Conduct
21、ionMay not be tolerated in COPD and asthma patientsCardioselective (B1) vs. Noncardioselective (B1 and B2 properties)SJM internal use ONLY Pharmacology ReviewClass III ACTIONS: Increase action potential duration and refractory periodsDRUGS: Amiodarone (Cordarone), Sotalol, Ibutilide, DofetilideCONSI
22、DERATIONS: Used for atrial and ventricular arrhythmiasSotalol - LOWERS ventricular DFT/ can increase pacing thresholdAmiodarone - INCREASES ventricular DFTSlow VT rates - ATP and detection rate programming45 day half life; requires long loading period before adequate blood levels are achievedRequire
23、s frequent drug levels and routine eye, lung and blood tests due to possible toxic build up in body tissueSJM internal use ONLY Pharmacology ReviewClass IV ACTIONS: Ca+ channel blockade. The slower Ca+ channel affects mainly the SA and AV node.DRUGS: Verapamil (Calan, Isoptin), Diltiazim (Cardiazem)
24、CONSIDERATIONS: Used for SVT, no proarrhythmic profileVarious degrees of Heart Block can occurSJM internal use ONLY Pharmacology ReviewACTIONS: Depends on the Drug Class V (Other Drugs) DRUGS: Digoxin - (Lanoxin) Increases parasympathetic activity. Slows atrial rate and AV conduction. Increases cont
25、ractile force. One of the standard drugs for HF therapyAdenosine - Potent depressive effects on AV node - used in terminating PSVTCONSIDERATIONS:Used primarily for atrial arrhythmiasAdenosine must be given rapid IV bolus with flush of fluid or may have decreased or inappropriate effect on slowing of
26、 AV conduction. Very short half life (30 sec)SJM internal use ONLY SJM internal use ONLY Mechanisms of ArrhythmiasEnhanced Automaticity An abnormal acceleration of phase 4 of the action potential that may be caused by an increase in the inward calcium currentTriggered Automaticity Has features of au
27、tomaticity Affects Phase 4 of the action potentialHas a warm-up periodHas features of reentryCan be provoked by premature beatsReentry Most common mechanism for arrhythmiasRequires that three components be present:Area of slow (scar/disease) conductionTwo limbs with different refractory periodsOne c
28、onducts more slowly but has shorter refractory periodOther conducts more quickly but has longer refractory periodUnidirectional blockSJM internal use ONLY “Sinus”“Reentry”Slow conduction / Fast recoverySlow PathwayFast PathwayFast Conduction / Slow recoveryMechanisms of ArrhythmiasTachycardiaMechani
29、smReentry80 -90%Non-reentryTorsade de pointesAcute ischemiaMechanismsSJM internal use ONLY Normal HeartScarring Due to Myocardial InfarctionIschemic Re-entryMechanismsSJM internal use ONLY MechanismsGray areas represent scarSJM internal use ONLY MechanismsSJM internal use ONLY MechanismsEnhanced Aut
30、omaticityTriggeredReentryArrhythmiasSVT (usually not fatal)VT (can be deadly)Arrhythmia ReviewSJM internal use ONLY Arrhythmia ReviewTreatment optionsDrugsAblationDevicesSJM internal use ONLY Objectives in SummaryDescribe the anatomy and properties of conduction Understand the role of the action potential and the autonomic nervous system in tachycardiaUnderstand the mechanisms and types of arrhythmiasUnderstand the effects and role of drugs on arrhythmias
