心臟電生理及射頻消融基礎(chǔ)

1、電生理相關(guān)資料 1Cardiac vein stenosisPTCA with 3.5 mm balloonFinal result2 Modified Seldinger technique for percutaneous catheter sheath introduction3 4 Sequence of P Wave GenerationSinus Node SAJunctionAtrium(P wave)Non-visible process on the EKG5 AV node“Slowzone”IVCLead II6 SUMMARYMechanisms of SVTAtria

2、l TachycardiaAVNRTAVRTFPSP7 Differential Diagnosis of NCTShort RPAVRTATSlow-Slow AVNRTLong RPATAtypical AVNRTPJRTP buried in QRSTypical AVNRTATJET8 SUMMARYObtain a 12 lead ECG. The location of the P wave will dictate the differential diagnosisIf hemodynamically unstable (chest pain, heart failure, h

3、ypotension)- CARDIOVERSIONIf hemodynamically stable -AV NODAL AGENTLong term therapy depends on mechanism and can be conservative, pharmacologic or invasive EP study often needed for definitive characterization of mechanism and can cure most SVTs with 90% success rate9 AVNRT10 11 Atrial flutter sawt

4、ooth or picket fence12 Atrial flutter with rapid response13 Arrhythmias: SA BlockPQRS T14 Arrhythmias: Atrial Flutter15 Steps to reading ECGsWhat is the rate? Both atrial and ventricular if they are not the same. Is the rhythm regular or irregular? Do the P waves all look the same? Is there a P wave

5、 for every QRS and conversely a QRS for every P wave?Are all the complexes within normal time limits?Name the rhythm and any abnormalities.16 17 18 RateLook at complexes in a 6-second strip and count the complexes; that will give you a rough estimate of rateCount the number of large boxes between tw

6、o complexes and divide into 300 Count the number of small boxes between two complexes and divide into 1500 Estimate rate by sequence of numbers (see next slide)19 Bundle branch blocksLook at the QRS morphology in V1 and V620 AVNRTAcute treatment ATP or Verapamil Cardioversion if BP Long term Drugs,

7、verapamil or b-blocker EPS and RFA21 AVRTWPW or concealed accessory pathwayacute and chronic treatment similar to AVNRTavoid b-blocker and verapamil in known WPW22 Atrial FlutterMarcoreentrant circuit in RAterminate by cardioversion with high success ratepoorly controlled by medical therapyEPS + RFA

8、23 “Typical isthmus dependent atrial flutter” is due to a macro reentrant circuit around the tricuspid valve This rhythm can be stopped by pacing and cured with ablation Embolic risk may be less than in fibrillation, but same recommendations applyElectrophysiology II Supraventricular ArrhythmiasAtri

9、al Flutter24 Ventricular rate 150 bpm“Saw tooth” p wavesAtrial FlutterElectrophysiology II Supraventricular Arrhythmias25 Atrioventricular Nodal Reentrant Tachycardia(AV Node Reentry or AVNRT) Most common cause of paroxysmal SVT in the young adult Occurs over a small reentrant circuit located near t

10、he AV node The circuit consists of a fast and slow pathway connected by a common top and bottom pathwayElectrophysiology II Supraventricular Arrhythmias26 AV Node Reentry TachycardiaRate of 145 bpm(Short RP tachycardia)Electrophysiology II Supraventricular ArrhythmiasRetrograde p wavesRP = 60 msec27

11、 Ectopic Atrial Tachycardia(Long RP tachycardia) Uncommon cause of paroxysmal SVT in the young adult (0.09s預(yù)激波額面電軸右偏（90120度）94 右側(cè)房室旁路的定位標(biāo)準(zhǔn)V1導(dǎo)聯(lián)QRS波主波方向向下（多呈rS型）V1導(dǎo)聯(lián)P波和QRS波融合，二者間無(wú)等電位線，PR0.07s預(yù)激波額面電軸左偏（3060度）95 右后、右側(cè)游離壁： 、aVL、V5、V6導(dǎo)聯(lián)預(yù)激波正向， 、aVF導(dǎo)聯(lián)預(yù)激波負(fù)向或正負(fù)雙向。右前游離壁： 、aVF導(dǎo)聯(lián)預(yù)激波正向或正負(fù)雙向。96 前間隔房室旁路的定位標(biāo)準(zhǔn)V1導(dǎo)聯(lián)QRS

12、波主波方向向下（多呈rS型）V1導(dǎo)聯(lián)P波和QRS波融合，二者間無(wú)等電位線，PR0.21 would be classified as first degree block. Usually this block is above His bundle 112 Second degree - some P waves are not followed by QRS. Often has a regular sequence, i.e., 2:1 or 3:2. The first number is the number of P waves present and the second is

13、the number of QRSs. What is this?113 Mobitz I (Wenckebach) the PR progressively lengthens with one P wave for every QRS until a beat is dropped. Usually the block is above His bundle. This is common in coronary patients and is caused by increased vagal tone and usually eventually disappears with no

14、problems 114 115 Mobitz II the PR is constant but with occasional dropped beats. This is a more serious arrhythmia because the injury is probably in fast conducting tissue below the His bundle which is not under vagal control.116 This is unambiguously Mobitz IIIt is a dangerous arrhythmia because th

15、e heart may suddenly start beating very slowly or even stop.117 Complete heart block. Since there is no conduction down the AV node pathway atria and ventricles beat regularly but at different rates. 118 Slow ventricular rateUsually treated with pacemakerMay be temporary or intermittent. Can be indu

16、ced by drugs that cause increased vagotonia119 WPW: Normally conducting cardiac muscle bridges the gap between atria and ventricles. The accessory pathway activates the ventricle before normal activation via the AV node.120 The PR interval is 100b/min1. Normal P waves2. Normal or shortened PR interv

17、al3. QRS and T vectors are normal4. ST segments are normal5. RR interval short 15mm1500/100 = 15124 Fig 3Normal sinus rhythmSinus tachycardiaSinus bradycardiaSinus Bradycardia 25mm1500/60 = 25125 Premature ventricular contraction (PVC) 1. Arises from ectopic focus in ventricles2. Early QRS not prece

18、ded by a P wave (see fig 4)3. Will have an unusual QRS shapea) odd vectorb) prolonged QRS duration 126 Premature ventricular contraction (PVC) 1. Arises from ectopic focus in ventricles2. Early QRS not preceded by a P wave (see fig 4)3. Will have an unusual QRS shapea) odd vectorb) prolonged QRS dur

19、ation 4. A compensatory pause127 Multifocal PVCs. Two separate foci are originating PVCsIrritable ventricleIF all PVC are identical it is from one ectopic site (Unifocal).128 Premature atrial contraction (PAC)1. Arises from an ectopic focus in the atria.2. Will have an identifiable P wave but the sh

20、ape of the P wave may be altered3. May have a normal QRS 4. May have a compensatory pause129 The QRS may be altered if some of the ventricle is still in its refractory period.The compensatory pause is lacking because the SA node was reset.The rhythm has been shifted.130 Atrial fibrillation1. Irregul

21、arly irregular2. No P waves131 The AV node keeps the ventricular rate lowMay be treated with drugs to depress AV conduction and slow the ventricular rhythm: Beta blockers, calcium channel blockers132 Common: will occur in about 1/3 of the populationNot a serious arrhythmia unless in WPW133 Electrica

22、l reentry can cause fibrillations and tachycardias. 134 Ventricular tachycardia (Fig 9)1. Regularly occurring rhythm originating from a regular ventricular ectopic focus.2. QRS morphology is usually like a PVC135 Because the cardiac output is very low it usually produces myocardial ischemia and ofte

23、n progresses to ventricular fibrillation 136 Ventricular fibrillation (VF)1. Thought to be a reentrant excitation of the ventricles; premature impulse may arise during vulnerable period2. Irregular baseline with no identifiable waves137 3. No cardiac output. Usually the cause of sudden death4. May b

24、e the result of ischemia, lightning strike, electrocution, chest trauma, or drugs5. Requires CPR and electrical difibrillation. Patients do not spontaneously recover.138 Extended phase two cause long QT syndrome.139 Q-T interval is rate- dependent and is an index of the duration of phase 2 in the ve

25、ntricular AP12 x 40 = 480 ms12 blocks140 Long QT syndromeProlonged duration of phase 2 causes an early afterdepolarization. That can trigger an early action potential causing a reentrant tachycardia Patients may experience attacks of VT with torsades de pointes - a waxing and waning of the QRS morph

26、ology (as if circling around a point). 141 3. Long QT is induced by some drugs and can be due to genetic abnormalities in some potassium and calcium channels. At present 5 separate genetic defects have been identified which cause long QT 142 14 STEPS TO ASSURE A SUCCESSFUL READING AND UNDERSTANDING

27、OF AN UNKNOWN ECG1. Is the ventricular rhythm regular?2. Are there P waves?3. Is the atrial rhythm regular?4. Is there one P wave for each QRS?5. What are the atrial and ventricular rates?6. What is the P-R interval?7. Is the P-R interval constant?8. Are there extra or premature beats?9. What is the

28、 QRS duration?10. Does the QRS morphology indicate presence of a conduction defect?11. What is the mean electrical QRS axis?12. What is the mean electrical P wave axis?13. Is there S-T segment deviation?14. Are there pathologic Q waves?143 Fig 12 a summary of heart blocks.144 a summary of other arrh

29、ythmias145 146 RALALVRVTypes of Supraventricular TachyarrhythmiasSinus Node ReentryAtrial FlutterAutomatic Atrial TachycardiaReentrant Atrial TachycardiaAtrioventricular NodalReentry (AVNRT)AV Reentry via an AccessoryAV Connection (AVRT)Atrial Fibrillation (Not Shown)147 Types of Paroxysmal Supraven

30、tricular TachycardiaAV NodalReentryAV ReciprocatingTachycardiaSinus Nodal ReentryIntra-atrial ReentryAutomatic AtrialTachycardia148 Mechanisms of Paroxysmal Supraventricular TachycardiasEnhanced Automaticity:Paroxysmal and AcuteChronicRe-entry without Bypass Tracts:AV Nodal Re-entry: Slow Fast/Fast

31、SlowSinoatrial Nodal Re-entryIntra-atrial Re-entryRe-entry in Association with Bypass Tracts:Re-entry with Anterograde AV Conduction (Orthodromic)With Evidence of Pre-excitation of 12-Lead ECGConcealed WPW (Bypass Tract Conducting only Retrogradely )Re-entry with Anterograde Conduction Over Bypass tract (Antidromic) During Tachycardia149 Accessory Pathways: Concealed Bypass Tract AV Reentrant TachycardiaAV NodeBundle of HisLeft Bundle BranchPRight Bundle