Ventricular tachycardia Ventricular fibrillation and ICD

Transcription

1 EKG Conference Ventricular tachycardia Ventricular fibrillation and ICD Samsung Medical Center CCU D.I. Hur Ji Won

2 Ventricular tachyarrhythmia ventricular tachycardia ventricular fibrillation ventricular flutter

3 Ventricular Premature Complexes (VPCs) wide (usually >0.14 s), bizarre QRS complexes that are not preceded by P waves Single ventricular ectopy

4 VPCs may occur singly in patterns of bigeminy, in which every sinus beat is followed by a VPC in trigeminy, in which two sinus beats are followed by a VPC in quadrigeminy, etc. Two successive VPCs are termed pairs or couplets while three or more consecutive VPCs are termed ventricular tachycardia when the rate exceeds 100 beats/min morphologies Similar: monomorphic, or uniform Different: polymorphic, or multiformed

5 Sustained ventricular Definition tachycardia persists for >30 s requires termination because of hemodynamic collapse

6 Associated with some form of structural heart disease most commonly chronic ischemic heart disease associated with a prior myocardial infarction nonischemic cardiomyopathies metabolic disorders drug toxicity prolonged QT syndrome

7 Nonsustained VT Definition three beats to 30 s Compared with sustained VT occurs in cardiac disease s absence more often than the sustained arrhythmia usually does not produce symptoms

8 The ECG diagnosis of VT a wide-complex QRS tachycardia at a rate exceeding 100 beats/min The QRS configuration during any episode of VT uniform (monomorphic) vary from beat to beat (polymorphic)

9 ECG CRITERIA that favor VT AV dissociation QRS width > 0.14 s with RBBB configuration > 0.16 s with LBBB configuration QRS axis Left axis deviation with RBBB morphology Extreme left axis deviation (northwest axis) with LBBB morphology Concordance of QRS in precordial leads Morphologic patterns of the QRS complex RBBB: Mono- or biphasic complex in V 1 RS (only with left axis deviation) or QS in V 6

10 Ventricular tachycardia with AV dissociation P waves are dissociated from the underlying wide complex rhythm (best seen on lead V 1 )

11 Clinical features depend on the ventricular rate duration of the tachycardia presence and extent of underlying cardiac disease the tachycardia is rapid and associated with severe myocardial dysfunction and cerebrovascular disease hypotension and syncope are common the presence of hemodynamic stability does not preclude a diagnosis of VT

12 Treatment asymptomatic, nonsustained VT need not be treated (d/t their prognosis will not be affected) But, with congenital long QT syndrome recurrent polymorphic VT and a high mortality from sudden death if untreated with sustained VT in the absence of heart disease usually require therapy (d/t the arrhythmia causes symptoms) beta blockers; verapamil; class IA, IC, or III agents; or amiodarone

13 promptly terminated by (DC) cardioversion with VT and organic heart disease if marked hemodynamic compromise is present if there is evidence of ischemia, CHF, or central nervous system hypoperfusion pharmacologic therapy may be tried with organic heart disease tolerates the VT well Procainamide is probably the most effective agent for acute therapy In stable patients in whom these drugs do not terminate the arrhythmia a pacing catheter can be inserted pervenously into the right ventricular apex

14 Torsades de pointes VT characterized by polymorphic QRS complexes that change in amplitude and cycle length, giving the appearance of oscillations around the baseline result from electrolyte disturbances (particularly hypokalemia and hypomagnesemia) use of a variety of antiarrhythmic drugs (especially quinidine), phenothiazines and tricyclic antidepressants liquid protein diets intracranial events, and bradyarrhythmias (particularly third-degree AV block)

15 Rhythm strips of patients with drug (disopyramide)-induced torsades de pointes The polymorphic ventricular tachycardia is associated with very long QT intervals.

16 Ventricular fibrillation nonischemic VF the onset usually begins with a short run of rapid VT(initiated by a relatively late coupled VPC) acute myocardial infarction or ischemia VF usually precipitated by a single early ventricular complex beat falling on the T wave (the vulnerable period), which produces a rapid VT that degenerates into VF The clinical setting in which VF occurs is important primary VF within the first 48 h of the onset of AMI have a good long-term prognosis (with a very low rate of recurrence or sudden cardiac death) VF unassociated with the development of AMI have a recurrence rate of 20 to 30% in the year following the event

17 In a patient with coronary disease, ventricular fibrillation is initiated by an early ventricular premature complex that produces a rapid polymorphic ventricular tachycardia, which rapidly degenerates to ventricular fibrillation (note the undulating baseline with indistinguishable systole and diastole)

18 Implantable cardioverter defibrillators(icd) promptly recognize and terminate life-threatening ventricular arrhythmias deliver <1 to 40 W s, the amount of which can be programmed antitachycardia pacing capabilities such that VT can be sensed and terminated without resorting to a painful shock

19 Guidelines for ICD Implantation Cardiac arrest due to VF or VT (not due to a transient or reversible cause) Spontaneous sustained VT in association with structural heart disease Syncope of undetermined origin with clinically relevant, hemodynamically significantly sustained VT or VF induced at EPS (when drug therapy is ineffective, not tolerated, or not preferred) Nonsustained VT in patients with coronary disease(prior M.I., LV dysfunction) and inducible VT or sustained VT at EPS (not suppressible by a class I antiarrhythmic drug) Spontaneous sustained VT in patients who do not have structured heart disease(not amenable to other treatments)

20 Reference Harrison's Principles of Internal Medicine, 16th Edition Dennis L. Kasper, Eugene Braunwald, Anthony S. Fauci, Stephen L. Hauser, Eds. Part 8. Disorders of the Cardiovascular System 순환기학 임상심장학. 서울 : 고려의학, 이원로편저. 김수겸, 김준수. 심실성부정맥.

21 Thank you!