1、 ArrhythmiaConduction and anatomy of heartConduction systemStable SVT is generally well tolerated in patients without underlying heart disease!?but may lead to myocardial ischemia or congestive heart failure in patients with coronary disease, valvular abnormalities, and systolic or diastolic myocard
2、ial dysfunction. Ventricular tachycardia, if lasting 1030 secs, often results in hemodynamic compromise and is more likely to deteriorate into ventricular fibrillation. RATE & RHYTHMRATE & RHYTHMAslow heart rates produce symptoms Aat rest or on exertion depends upon whether cerebral perfusion can be
3、 maintained, which is generally a function of whether the patient is upright or supine and whether left ventricular function is adequate to maintain stroke volume.A If the heart rate abruptly slows, as with the onset of complete heart block or sinus arrest, syncope or convulsions may result. RATE &
4、RHYTHM4Arrhythmias are detected either because they present with symptoms or detected during the course of monitoring. 4Arrhythmias causing sudden death, syncope, or near syncope require further evaluation and treatment unless they unlikely to recur (eg, electrolyte abnormalities or acute myocardial
5、 infarction).4Controversy over when and how to evaluate and treat rhythm disturbances that are not symptomatic but are possible markers for more serious abnormalities ( eg, nonsustained ventricular tachycardia). MECHANISMS OF ARRHYTHMIASuElectrophysiologic studies have greatly increased our understa
6、nding of the mechanisms underlying most arrhythmias. These includeu(1) disorders of impulse formation or automaticityu(2) abnormalities of impulse conduction,u(3) reentry, and u(4) triggered activity. uAltered automaticity is the mechanism for sinus node arrest, many premature beats, and automatic r
7、hythms as well as an initiating factor in reentry, arrhythmias. MECHANISMS OF ARRHYTHMIASAbnormalities of impulse conduction can occur at the sinus or atrioventricular node, in the intraventricular conduction system, and within the atria or ventricles. These are responsible for sinoatrial exit block
8、, for atrioventricular block at the node or below, and for establishing reentry circuits. MECHANISMS OF ARRHYTHMIASMECHANISMS OF ARRHYTHMIAS Triggered activity occurs when afterdepolarizations (abnormal electrical activity persisting after repelarization) reach the threshold level required to trigge
9、r a new depolarization. This may be the mechanism of ventricular tachycardia in the prolonged QT syndrome and in some cases of digitalis toxicity. TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCESElectrocardiographic MonitoringThe ideal way of establishin,g a causal relationship between a symptom and a
10、rhythm disturbance is to demonstrate the presence of the rhythm during the symptom, Unfortunately, this is not always easy because symptoms are usually sporadic.TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCESElectrocardiographic MonitoringPatients with SD and recent or recurrent syncope are often moni
11、tored . Outpatients. When episodes are infrequent, use of an event recorder is preferable to 24-hour continuous monitoring. Exercise testing may be helpful when the symptoms are associated with exertion or stress. Further electrophysielogic studies may be useful in evaluating ventricular tachyarrhyt
12、hmias. TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES4Electrocardiographic MonitoringElectrocardiographic MonitoringElectrocardiographic MonitoringTECHNIQUES FOR EVALUATING RHYTHM DISTURBANCESECG MonitoringlIn many cases, symptoms are due to a different arrhythmia or to noncardiac causes. lFor instan
13、ce, dizziness or syncope in older patients may be unrelated to concomitantly observed bradycardia, sinus node abnormalities, and ventricular ectopy. lAmbulatory monitoring is frequently used to quantify ventricular ectopy and detect asymptomatic ventricular tachycardia in post-myocardial infarction
14、or heart failure patients. lUnfortunately, while asymptomatic ventricular arrhythmias have negative prognostic implications, there are few-data to support specific therapeutic intervention. Thus, monitoring in asymptomatic individuals is usually not indicated. TECHNIQUES FOR EVALUATING RHYTHM DISTUR
15、BANCESHeart rate Variablityseveral studies have indicated that greater heart rate variability is associaled with a better prognosis and fewer life threatening arrhythmias in a variety of cardiac conditions.RR cycle length variability to provide indices of the relative balance between parasympathetic
16、 and sympathetic activity, with being considered to confer a better prognosis. postinfarction and patients with symptomatic arrhythmias, these Indices have had some prognostic value. However, adequate data are not yet available to support routine use of this technique in clinical practice. TECHNIQUE
17、S FOR EVALUATING RHYTHM DISTURBANCESSignal-Averaged ECG4Signal averaged ECG is new technique . 4To record 300 consecutive beats during basal conditions, Using appropriate electrical filtering and computer averaging of the signal, very law frequency signals called late potentials can be identified in
18、 the period following the QRS complex. 4Abnormal late potentials are considered markers for potential Ventricular ArrhythmiaTECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES Evaluation of recurrent syncope of possible cardiac origin, when the ambulatory ECG has not provided the diagnosis; Differentiatio
19、n of SVT from VA; Evaluation of therapy in patients with accessory atrioventricular pathways; Evaluation of the efficacy of pharmacotherapy in survivors of sudden death or other patients with symptomatic or life threatening VT; Evaluation of patients for catheter ablation procedures or antitachycard
20、ia devices. Autonomic Testing ( Tilt Table Testing )with recurrent syncope or near Syncope, arrhythmias are no cause. This is particularly true when the patient has no evidence of associated heart disease by history, examination, ECG, or noninvasive testing. Syncope may be neurocardiogenic in origin
21、, mediated by excessive vagal stimulation or an imbalance between sympathetic and parasympathetic autonomic activity. TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCESTECHNIQUES FOR EVALUATING RHYTHM DISTURBANCES4Autonomic Testing ( Tilt Table Testing )60 - 80TECHNIQUES FOR EVALUATING RHYTHM DISTURBANCE
22、SAntiarrhythmia drugMAntiarrhythmic drugs have limited efficacy and frequent side effects. They are often divided into four classes.MClass I agents block membrane sodium channels. Three subclasses are further defined by the effect of agents on the Purkinje fiber action potential MClass la drugs slow
23、 the rate of rise of the action potential (Vmax) and prolong its duration, thus slowing conduction and increasing refractorineas. MClass lb agents shorten action potential duration, they do not affect conduction or refractoriness. MClass Ic agents prolong Vmax and slow repolarization, thus slowing c
24、onduction and prolonging refractoriness, but more so than class la drugsAntiarrhythmia drug4Class II agents -beta-blockers Decrease automaticity, Prolong AV conduction, Prolong refractoriness. Antiarrhythmia drugClass III agents ABlock potassium channels AProlong repolarization, widening the QRS and
25、 prolonging the QT interval. ADecrease automaticity and conduction and prolong refractoriness. Antiarrhythmia drugClass IV agents - slow calcium channel blockers Decrease automaticity andAtrioventricular conduction DrugsWilliamsWilliams分类法：分类法：I：II：III：IV：A：QuinidineC： FlecainidePropranololAmiodaron
26、eVerapamil ProcainamideEncainideMetoprololSotalolDiltiazem ChangrolinPropafenoneEsmololBretyliumBepridilB：Lidocaine Atenolol Mexiletine Tocainide Moricizine PhenytoinAntiarrhythmia drug-Risk4The risk of antiarrhythmic agents has been highlighted by the Coronary Arrhythmia Suppression Trial (CAST). 4
27、Two class Ic agents (flecainide, encairfide) and a clam la agent (moficizine) increased mortality rates in patients with asymptonlatic ventricular ectapy after myocardial infarction. 4Therefore, these agents (any antiarrhythmic drug) should not be used except for life-threatening ventricular arrhyth
28、mias and symptomatic supraventricular tachyarrhythmias. Radiofrequency Ablation4Ablation has become the primary modality of therapy for many symptomatic SVT4Including AVNRT4AVRT -involving accessory pathways, paroxysmal atrial tachycardia, inappropriate sinus tachycardia, junctional tachycardia, Man
29、y laboratories have achieved reasonable success rates in preventing atrial flutter with rediofrequency techniques, and experience with atrial fibrillation is accumlating as well. Radiofrequency Ablation4Catheter ablation of VA has proved more difficult. Three specilic forms of VA proved to be amenab
30、le to radiofrequeney ablation. bundle branch reentry,VT originating in right ventricuiar outflow tract, VT originating in the left side of the interventricular septum. 4Other forms of VT, may be amenable to ablation, but experience thus far is limited. Radiofrequency Ablation4In addition, some proce
31、dures involve transseptal or retrograde left ventricular catheterization, with the attendant potential complications of aortic perforation, damage to the heart valves, or left-sided emboli. 4These procedures are generally safe, though there is a low incidence of perforation of the atria or right ven
32、tricle that results in pericardial tamponade and sufficient damage to the atriovantricular node to require permanent cardiac pacing. AVRT ablationAVNRT AblationAtrial tachycardia-ablationAtrial fibrillation accounts for 1/3 of all patient discharges with arrhythmia as principal diagnosis. 2% VFData
33、source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.34% Atrial Fibrillation18% Unspecified6% PSVT6% PVCs4% Atrial Flutter9% SSS8% Conduction Disease3% SCD10% VTSUPRAVENTRICULAR ARRHYTHMIAS sinus bradycardia4Causes of Slow Rhythms: Hypoxia Hyperkalemia Acute MI Heart Disease Increased parasympathetic
34、tone Drug effects from narcotics, benzodiazepines, digoxin, beta blockers, propranolol, or calcium channel blockersSinus Bradycardia4Decrease in the rate of atrial depolarization Rhythm is regular Rate 100 beats/minP wave, PR interval, and QRS complex are all normalSinus TachycardialTreatment:lAllev
35、iate the underlying causelinappropriate sinus tachycardia that may be very symptomatic or lead to LV contractile dysfunction. l Radiofrequeney modification of the sinus node has mitigated this problem ATRIAL PREMATURE BEATS4APB occur before the next sinus node impulse or a reentry_ circuit is establ
36、ished. 4P wave usually differs from the patients normal. 4R-R cycle length is usually unchanged or only slightly prolonged. 4premature beats occur in normal hearts and are never a sufficient basis heart disease. 4Speeding of the heart rate by any means usually abolishes most premature beats. 4Early
37、APB may cause aberrant QRS complexes or may be nonconducted to the ventricles because the latter are still refractory. Variability of Ventricular Ectopy with Age4Effect of age on probability (%) of having more than a given number ofPVCs per 24 hours in subjects with normal hearts.10-29 30-39 40-49 5
38、0-59 60-69Data from Kostis JB. Circulation. 1981;63(6):1353.AgeVENTRICULAR BEATS 4Distinction can be very difficult in patients with a wide QRS; it is important because of the differing prognostic and therapeutic implications of each type. ventricular origin include 4 atrioventricular dissociation;
39、4 a QRS duration exceeding 0.14 s; 4capture or fusion beats (infrequent); 4 left axis deviatinn with right bundle branch block morphology; 4 monophasic (R) or biphasic (qR, QR., or RS) complexes in V1,; and (6) a qR or QS complex in V6. VENTRICULAR BEATSSupraventricular origin is favorecl by 4a trip
40、hasic QRS complex, especially if there was initial negativity in leads I and V6; 4ventricular rates excceeding 170/min;4 QRS duration longer than 0.12 s but not longer than 0.14 s: 4 the presence of preexcitation syndrome. 4A single irritable focus within the ventricle fires prematurely giving rise
41、to an ectopic beat. QRS is wide If every other beat is PVC ventricular bigeminy If every third beat is a PVC ventricular trigeminy If every fourth beat is PVC ventricular quadrigeminy A PVC that falls on the T wave precipitates VT or VFVENTRICULAR BEATSVENTRICULAR BEATS4Treatment: PVCs which need to
42、 be treated are: Multifocal Occur in couplets Fall on or after the T wave That occur greater than 6 per minutePremature Ventricular Contraction 4Treatment Continued: In the setting of an acute MI, PVCs need to be aggressively treated with nitroglycerine, aspirin, morphine and oxygen. Lidocaine is th
43、e drug of choice to diminish PVCs, but does little to the underlying pathology. SUPRAVENTRICULAR TACHYCARDIA 4the commonest paroxysmal tachycardia and often occurs in patients without structural heart disease. 4Attacks begin and end abruptly and may last a few ,seconds to several hours or longer. 4H
44、r may be 140-240/mia (usually 160-220/min) and is perfectly regular (despite exercise or change in position). 4P wave usually differs in contour from shins beats. 4Asymptomatic, but some experience mild chest pain or shormess of breath, especially when episodes are prolonged, even in the absence of
45、associated cardiac abnormalities. 4PSVT may result from digitalis toxicity and then is commonly associated with atrioventricular block. SVTSVTSVT-Care4A Mechanical Measures: A variety of methods have been used to interrupt attacks, and patients may learn to perform these themselves. 4These include V
46、alsalvas maneuver, stretching the arms and body, lowering the head between the knees, coughing, and breath holding. SVT-treatment4B. Drug Therapy: If fail, rapidly intravenous agents will terminate more than 90% of episodes, 4Intravenous adenosine(or ATP) has a very brief duration of action and mini
47、mal negative inotropie activity, A 6-mg bolus is administered. 4If no response is observed after 10 minutes, a second and third 12- mg bolus shodld be given. Since the half- life of adenosine is less than 10 seconds, 4drug must be given rapidly (in 1 2 seconds from a peripheral intravenous line). Ad
48、enosine is very well tolerated, 4but nearly 20% -flushing, and some patients experience severe chest discomfort. SVTCare 4Calcium channel blockers also rapidly induce atrioventricular block and break most episodes of reentry SVT. 4IV verapamil may be given as a 2.5 mg-bolus, followed by additional d
49、oses of 2.5 to 5 mg every 1- 3 minutes up to a total of 20 mg if blood pressure and rhythm are stable. 4If the recurs, further doses can be given SVT-Care4 Cardioversion: If the patient is hemodynamically stable or if adenosine and vempamil are contraindicated or ineffective, synchronized electrical
50、 cardioversion (beginning at 100 J) is almost universally successful. 4If digitalis toxicity is present or strongly suspected, as in the case of paroxysmal tachycardia with block. electrical cardioversion should be avoided. Prevention of Attacks4A. Radiofrsquency Ablation: Safety and Less recurrent4
