5 Classification of antiarrhythmics (based on mechanisms of action) Class I – blocker’s of fast Na+ channelsSubclass IACause moderate Phase 0 depressionProlong repolarizationIncreased duration of action potentialIncludesQuinidine – 1st antiarrhythmic used, treat both atrial and ventricular arrhythmias, increases refractory periodProcainamide - increases refractory period but side effectsDisopyramide – extended duration of action, used only for treating ventricular arrthymias
6 Classification of antiarrhythmics (based on mechanisms of action) Subclass IBWeak Phase 0 depressionShortened depolarizationDecreased action potential durationIncludesLidocane (also acts as local anesthetic) – blocks Na+ channels mostly in ventricular cells, also good for digitalis-associated arrhythmiasMexiletine - oral lidocaine derivative, similar activityPhenytoin – anticonvulsant that also works as antiarrhythmic similar to lidocane
7 Classification of antiarrhythmics (based on mechanisms of action) Subclass ICStrong Phase 0 depressionNo effect of depolarizationNo effect on action potential durationIncludesFlecainide (initially developed as a local anesthetic)Slows conduction in all parts of heart,Also inhibits abnormal automaticityPropafenoneAlso slows conductionWeak β – blockerAlso some Ca2+ channel blockade
8 Classification of antiarrhythmics (based on mechanisms of action) Class II – β–adrenergic blockersBased on two major actions1) blockade of myocardial β–adrenergic receptors2) Direct membrane-stabilizing effects related to Na+ channel blockadeIncludesPropranololcauses both myocardial β–adrenergic blockade and membrane-stabilizing effectsSlows SA node and ectopic pacemakingCan block arrhythmias induced by exercise or apprehensionOther β–adrenergic blockers have similar therapeutic effectMetoprololNadololAtenololAcebutololPindololStalolTimololEsmolol
9 Classification of antiarrhythmics (based on mechanisms of action) Class III – K+ channel blockersDeveloped because some patients negatively sensitive to Na channel blockers (they died!)Cause delay in repolarization and prolonged refractory periodIncludesAmiodarone – prolongs action potential by delaying K+ efflux but many other effects characteristic of other classesIbutilide – slows inward movement of Na+ in addition to delaying K + influx.Bretylium – first developed to treat hypertension but found to also suppress ventricular fibrillation associated with myocardial infarctionDofetilide - prolongs action potential by delaying K+ efflux with no other effects
10 Classification of antiarrhythmics (based on mechanisms of action) Class IV – Ca2+ channel blockersslow rate of AV-conduction in patients with atrial fibrillationIncludesVerapamil – blocks Na+ channels in addition to Ca2+; also slows SA node in tachycardiaDiltiazem
19 Proarrhythmia effect of antiarrhythmia agents Ia, Ic class: Prolong QT interval, will cause VT or VF in coronary artery disease and heart failure patientsIII class: Like Ia, Ic class agentsII, IV class: Bradycardia
20 Non-drug therapyCardioversion: For tachycardia especially hemodynamic unstable patientRadiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT, AF, AFL)Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular arrhythmia patients.
23 Sinus Bradycardia Sinus rate < 60 beats/min Normal variant in many normal and older peopleCauses: Trained athletes, during sleep, drugs (ß-blocker) , Hypothyriodism, CAD or SSSSymptoms:Most patients have no symptoms.Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope.Needn’t specific therapy, If the patient has severe symptoms, planted an pacemaker may be needed.
24 Sinus Arrest or Sinus Standstill Sinus arrest or standstill is recognized by a pause in the sinus rhythm.Causes: myocardial ischemia, hypoxia, hyperkalemia, higher intracranial pressure, sinus node degeneration and some drugs (digitalis, ß-blocks).Symptoms: dizziness, amaurosis, syncopeTherapy is same to SSS
25 Sinoatrial exit block (SAB) SAB: Sinus pulse was blocked so it couldn’t active the atrium.Causes: CAD, Myopathy, Myocarditis, digitalis toxicity, et al.Symptoms: dizziness, fatigue, syncopeTherapy is same to SSS
26 Sinoatrial exit block (SAB) Divided into three types: Type I, II, IIIOnly type II SAB can be recognized by EKG.
27 Sick Sinus Syndrome (SSS) SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node automaticity and SA conduction.Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor, trauma and congenital disease.With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythmsBradycardia-tachycardia syndrome
28 Sick Sinus Syndrome (SSS) EKG Recognition:Sinus bradycardia, ≤40 bpm;Sinus arrest > 3sType II SABNonsinus tachyarrhythmia ( SVT, AF or Af).SNRT > 1530ms, SNRTc > 525msInstinct heart rate < 80bmp
32 Premature contractions The term “premature contractions” are used to describe non sinus beats.Common arrhythmiaThe morbidity rate is 3-5%
33 Atrial premature contractions (APCs) APCs arising from somewhere in either the left or the right atrium.Causes: rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemiaSymptoms: many patients have no symptom, some have palpitation, chest incomfortable.Therapy: Needn’t therapy in the patients without heart disease. Can be treated with ß-blocker, propafenone, moricizine or verapamil.
35 Atrial tachycardia May occur transient; intermittent; or persistent. Symptoms: palpitation; chest uncomfortable, tachycardia may induce myopathy.Auscultation: the first heart sound is variable
36 Intra-atrial reentry tachycardia (IART) ECG characters:Atrial rate is around bpm;P’ wave is different from sinus P wave;P’-R interval ≥ 0.12”Often appear type I or type II, 2:1 AV block;EP study: atrial program pacing can induce and terminate tachycardia
37 Automatic atrial tachycardia (AAT) ECG characters:Atrial rate is around bpm;Warmup phenomenaP’ wave is different from sinus P wave;P’-R interval≥ 0.12”Often appear type I or type II, 2:1 AV block;EP study: Atrial program pacing can’t induce or terminate the tachycardia
39 Chaotic atrial tachycardia (CAT) Also termed “Multifocal atrial tachycardia”.Always occurs in COPD or CHF,Have a high in-hospital mortality ( 25-56%). Death is caused by the severity of the underlying disease.ECG characters:Atrial rate is around bpm;The morphologies P’ wave are more than 3 types.P’-P’, P’-R and R-R interval are different.Will progress to af in half the casesEP study: Atrial program pacing can’t induce or terminate the tachycardia
41 TherapyIRAT: Esophageal Pulsation Modulation, RFCA, Ic and IV class anti-tachycardia agentsAAT: Digoxin, IV, II, Ia and III class anti-tachycardia agents; RFCACAT: treat the underlying disease, verapamil or amiodarone.Associated with SSS: Implant pace-maker.
42 Atrial flutter Etiology: It can occur in patients with normal atrial or with abnormal atrial.It is seen in rheumatic heart disease (mitral or tricuspid valve disease), CAD, hypertension, hyperthyroidism, congenital heart disease, COPD.Related to enlargement of the atriaMost AF have a reentry loop in right atrial
44 Atrial flutterSymptoms: depend on underlying disease, ventricular rate, the patient is at rest or is exertingWith rapid ventricular rate: palpitation, dizziness, shortness of breath, weakness, faintness, syncope, may develop angina and CHF.
45 Atrial flutter Therapy: Treat the underlying disease To restore sinus rhythm: Cardioversion, Esophageal Pulsation Modulation, RFCA, Drug (III, Ia, Ic class).Control the ventricular rate: digitalis. CCB, ß-blockAnticoagulation
46 Atrial fibrillationSubdivided into three types: paroxysmal, persistent, permanent.Etiology:Morbidity rate increase in older patientsEtiology just like atrial flutterIdiopathicMechanism:Multiple wavelet re-entry;Rapid firing focus in pulmonary vein, vena cava or coronary sinus.
48 Atrial fibrillation Manifestation: Affected by underlying diseases, ventricular rate and heart function.May develop embolism in left atrial. Have high incidence of stroke.The heart rate, S1 and rhythm is irregularly irregularIf the heart rhythm is regular, should consider about (1) restore sinus rhythm; (2) AF with constant the ratio of AV conduction; (3) junctional or ventricular tachycardia; (4) slower ventricular rate may have complete AV block.
51 Atrioventricular junctional premature contractions Etiology and manifestation is like APCsTherapy the underlying diseaseNeedn’t anti-arrhythmia therapy.
52 Nonparoxysmal AV junctional tachycardia Mechanism: relate to hyper-automaticity or trigger activity of AV junctional tissueEtiology: digitalis toxicity; inferior MI; myocarditis; acute rheumatic fever and postoperation of valve diseaseECG: the heart rate ranges bpm or more, regular, normal QRS complex, may occur AV dissociation and wenckebach AV block
53 Nonparoxysmal AV junctional tachycardia Therapy:Treat underlying disease; stopping digoxin, administer potassium, lidocaine, phenytoin or propranolol.Not for DC shockIt can disappear spontaneously. If had good tolerance, not require therapy.
54 Paroxysmal tachycardia Most PSVT (paroxysmal supraventricular tachycardia) is due to reentrant mechanism.The incidence of PSVT is higher in AVNRT (atrioventricular node reentry tachycardia) and AVRT (atioventricular reentry tachycardia), the most common is AVNRT (90%)Occur in any age individuals, usually no structure heart disease.
55 Paroxysmal tachycardia Manifestation:Occur and terminal abruptly.Palpitation, dizziness, syncope, angina, heart failure and shock.The sever degree of the symptom is related to ventricular rate, persistent duration and underlying disease
56 Paroxysmal tachycardia ECG characteristic of AVNRTHeart rate is bpm, regularQRS complex is often normal, wide QRS complex is with aberrant conductionNegative P wave in II III aVF, buried into or following by the QRS complex.AVN jump phenomena
57 Paroxysmal tachycardia ECG characteristic of AVRTHeart rate is bpm, regularIn orthodromic AVRT, the QRS complex is often normal, wide QRS complex is with antidromic AVRTRetrograde P’ wave, R-P’>110ms.
58 Paroxysmal tachycardia Therapy:AVNRT & orthodromic AVRTIncrease vagal tone: carotid sinus massage, Valsalva maneuver.if no successful,Drug: verapamil, adrenosine, propafenoneDC shockAntidromic AVRT:Should not use verapamil, digitalis, and stimulate the vagal nerve.Drug: propafenone, sotalol, amiodaroneRFCA
59 Pre-excitation syndrome (W-P-W syndrome) There are several type of accessory pathwayKent: adjacent atrial and ventricularJames: adjacent atrial and his bundleMahaim: adjacent lower part of the AVN and ventricularUsually no structure heart disease, occur in any age individual
60 WPW syndrome Manifestation: Palpitation, syncope, dizziness Arrhythmia: 80% tachycardia is AVRT, 15-30% is AFi, 5% is AF,May induce ventricular fibrillation
61 WPW syndromeTherapy:Pharmacologic therapy: orthodrome AVRT or associated AF, AFi, may use Ic and III class agents.Antidromic AVRT can’t use digoxin and verapamil.DC shock: WPW with SVT, AF or Afi produce agina, syncope and hypotensionRFCA
63 Ventricular Premature Contractions (VPCs) Etiology:Occur in normal personMyocarditis, CAD, valve heart disease, hyperthyroidism, Drug toxicity (digoxin, quinidine and anti-anxiety drug)electrolyte disturbance, anxiety, drinking, coffee
64 VPCs Manifestation: palpitation dizziness syncope loss of the second heart sound
65 PVCs Therapy: treat underlying disease, antiarrhythmia No structure heart disease:Asymptom: no therapySymptom caused by PVCs: antianxiety agents, ß-blocker and mexiletine to relief the symptom.With structure heart disease (CAD, HBP):Treat the underlying diseasß-blocker, amiodaroneClass I especially class Ic agents should be avoided because of proarrhytmia and lack of benefit of prophylaxis
67 Ventricular tachycardia Torsades de points (Tdp): A special type of polymorphic VT,Etiology:congenital (Long QT),electrolyte disturbance,antiarrhythmia drug proarrhythmia (IA or IC),antianxiety drug,brain disease,bradycardia
68 Ventricular tachycardia Accelerated idioventricular rhythm:Related to increase automatic toneEtiology: Often occur in organic heart disease, especially AMI reperfusion periods, heart operation, myocarditis, digitalis toxicity
69 VT Manifestation: Nonsustained VT with no symptom Sustained VT : with symptom and unstable hemodynamic, patient may feel palpitation, short of breathness, presyncope, syncope, angina, hypotension and shock.
70 VT ECG characteristics: Monomorphic VT: bpm, occur and terminate abruptly,regularAccelerated idioventricular rhythm: a runs of ventricular beats, rate of bpm, tachycardia is a capable of warm up and close down, often seen AV dissociation, fusion or capture beatsTdp: rotation of the QRS axis around the baseline, the rate from bpm, QT interval prolonged > 0.5s, marked U wave
71 Treatment of VT Treat underlying disease Cardioversion: Hemodynamic unstable VT (hypotension, shock, angina, CHF) or hemodynamic stable but drug was no effectPharmacological therapy: ß-blockers, lidocain or amiodaroneRFCA, ICD or surgical therapy
72 Therapy of Special type VT Accelerated idioventricular rhythm:usually no symptom, needn’t therapy.Atropine increased sinus rhythmTdp:Treat underlying disease,Magnesium iv, atropine or isoprenaline, ß-block or pacemaker for long QT patienttemporary pacemaker
73 Ventricular flutter and fibrillation Often occur in severe organic heart disease: AMI, ischemia heart diseaseProarrhythmia (especially produce long QT and Tdp), electrolyte disturbanceAnaesthesia, lightning strike, electric shock, heart operationIt’s a fatal arrhythmia
74 Ventricular flutter and fibrillation Manifestation:Unconsciousness, twitch, no blood pressure and pulse, going to dieTherapy:Cardio-Pulmonary Resuscitate (CPR)ICD
76 Atrioventricular Block AV block is a delay or failure in transmission of the cardiac impulse from atrium to ventricle.Etiology:Atherosclerotic heart disease; myocarditis; rheumatic fever; cardiomyopathy; drug toxicity; electrolyte disturbance, collagen disease, lev’s disease.
77 AV Block AV block is divided into three categories: First-degree AV blockSecond-degree AV block: further subdivided into type I and type IIThird-degree AV block: complete block
78 AV Block Manifestations: First-degree AV block: almost no symptoms; Second degree AV block: palpitation, fatigueThird degree AV block: Dizziness, agina, heart failure, lightheadedness, and syncope may cause by slow heart rate, Adams-Stokes Syndrome may occurs in sever case.First heart sound varies in intensity, will appear booming first sound
79 AV BlockTreatment:I or II degree AV block needn’t antibradycardia agent therapyII degree II type and III degree AV block need antibradycardia agent therapyImplant Pace Maker
81 Intraventricular Block Etiology:Myocarditis, valve disease, cardiomyopathy, CAD, hypertension, pulmonary heart disease, drug toxicity, Lenegre disease, Lev’s disease et al.Manifestation:Single fascicular or bifascicular block is asymptom; tri-fascicular block may have dizziness; palpitation, syncope and Adams-stokes syndrome
82 Intraventricular Block Therapy:Treat underlying diseaseIf the patient is asymptom; no treat,bifascicular block and incomplete trifascicular block may progress to complete block, may need implant pace maker if the patient with syncope