Ventricular arrhythmias

Transcription

1 Ventricular arrhythmias Assoc.Prof. Lucie Riedlbauchová, MD, PhD Department of Cardiology University HospitalMotol and2nd FacultyofMedicine, Charles University in Prague

2 Definition and classification Ventricular arrhythmia = cardiac rhythm disturbance originating in the ventricular myocardium in the conduction system below the Hiss bundle Clasification of ventricular arrhythmias: Ventricular prematur Accelerated idiovent Ventricular tachycard Ventricular flutter/ fib

3 Ventricular premature beats (VPBs) Characteristics: 1. prematurity 2. wide QRS complex 3. complete compensatory pause (4. P wave is hidden in or follows QRS complex) 2100ms 2100ms 1050ms 620ms

4 Ventricular premature beats (VPBs) Relationship between P wave and VPB Coincidence of sinus P wave and VPB VPB conducted retrogradelly into the atrium Sinus P wave in ST/T segment of VPB AVB II Mobitz! 1465ms 1465ms x

5 Ventricular premature beats (VPBs) Morphology: Relationship: Monomorphic VPB Bigeminy Polymorphic VPBs Trigeminy Isolated VPB Cuplets of VPBs Triplets of VPBs

6 Ventricular premature beats (VPBs) Hierarchic clasification (Lown-Wolf) Degree Definition 0 Absence of VPBs 1 < 30 VPBs/hour 2 30 VPBs/hour 3 Polytopic VPBs 4a Couplets of VPBs 4b Ventricular tachycardia 5 R on T VPBs It doesn t reflect presence and severity of the underlying heart disease Complexity of VPBs may vary in time No prognostic importance Therapy of VPBs: Asymptomatic VPBs no therapy Symptomatic VPBs betablockers (or another antiarrhythmic drug in the absence of structural heart disease) amiodarone RF ablation

7 Accelerated idioventricular rhythm Ectopic ventricular rhythm (>3 beats) with rate > sinus rhythm rate and slower than the heart rate of monomorphic VT (usually bpm) Characteristics: wide QRS complexes regular rhythm, sometimes wide acceleration at the beginning and decceleration before termination (increased automaticity) heart rate ± 10% of normal sinus rhythm usually spontaneous termination possible fusion beats, coincidence with sinus P waves Therapy: 0 (procainamid, ajmalin)

8 Ventricular tachycardias (VTs) Organised ventricular activity ( 3 beats) with heart rate > 100 bpm QRS > 120ms (QRS < 120ms in 4% - VT originating in the conduction system distally to Hiss) QRS 180ms QRS > 120ms

9 Ventricular tachycardias (VTs) VT classification 1. Arrhythmogenic mechanism (reentry, triggered activity, abnormal automaticity ) 2. VT duration/ haemodynamic consequence Nonsustained VT < 30 s Sustained VT > 30s or immediate hemodynamic deterioration 3. Morphology of the QRS complexes Monomorphic VT polymorphic KT

10 Ventricular tachycardias 1. Idiopatic VTs 2. VTs in the presence of structural heart disease - Ischemic heart disease - Dilated cardiomyopathy - Hypertrofic cardiomyopathy - Arhythmogenic cardiomyopathy of the right ventricle - Another structural heart diseases 3. VTs in the presence of channelopathies - Long QT syndrome (LQTS) - Brugada syndrome - Catecholaminergic polymorphic ventricular tachycardia (CPVT) - Short QT syndrome (SQTS) - Syndrom of early repolarization

11 Prognostic clasification of VTs Malignant ventricular arrhythmias Ventricular fibrilation/ flutter Sustained VT Torsade de pointes in LQTS Benign ventricular arrhythmia - no structural heart disease - no pathology of repolarization Potentially malignant ventricular arrhythmias Isolated VPBs Short runs of VPBs Idiopathic VT from RVOT/ LVOT - up to 65% of all ventricular arrhythmias - evaulation of potential malignity of the arrhythmia based on the type and severity of the underlying heart disease

12 1. Idiopatic ventricular tachycardia - 10% of all sustained VTs - monomorphic VT in patients without structural heart disease - focal origin - rather younger individuals Benign prognosis Clasification (based on the ECG/ site of origin) VT from RVOT (right ventricular outflow tract) VT from LVOT (left ventricular outflow tract) Paroxysmal form Repetitive form Verapamil-sensitive Adenosin-sensitive Propranolol-sensitive

13 Idiopathic VT from RVOT - 70% of all idiopathic VTs - women > men - typical trigger = exercise arrhythmogenic mechanism catecholamine-triggered activity? abnormal automaticity? LBBB morphology Right axis deviation

14 Idiopathic VTs from LVOT RBBB morphology Left axis deviation Verapamil-sensitive VT (fascicular reentry tachycardia) - intrafascicular reentry - men > women Adenosin-sensitive VT - triggered activity from septum or LVOT, physical activity Propranolol-sensitive VT - catecholamine-enhanced automaticity from various places of LV Therapy: - only in symptomatic pts. BB, sotalol (verapamil, IC antiarrhythmic drugs - RFA indicated in symptomatic pt., drug resistance, development of tachycardic CMP

15 2. VT in structural heart disease Ischemic heart disease (IHD) Myocardial infarction (MI) Chronic form of IHD Monomorphic sustained VT Polymorphic sustained VT Ventricular flutter/ fibrilation Acute phase of MI (<48 hrs) - Ischemia - Trimecain (Mesocain) - Revascularization Polymorphic sustained VT Ventricular fibrilation (Monomorphic sustained VT - 0,5%) VT in the acute phase of MI doesn t carry higher risk of reccurent arrhythmia in the long-term perspective. Subacute phase of MI (3 60 days) Multivessel disease, LV dysfunction - Amiodarone - Revascularization Monomorphic sustained VT (Polymorphic sustained VT)

16 2. VT in structural heart disease Ischemic heart disease (IHD) Chronic form of IHD Monomorphic sustained VTs Acute treatment: - Amiodarone - Overdrive pacing - DC cardioversion Revascularization Amiodarone ICD RF substrate modification

17 2. VT in structural heart disease Idiopathic dilated cardiomyopathy Definition: ventricular dilatation with systolic dysfunction in the absence of IHD of such an extent that may cause given degree of dysfunction and in the absence of hemodynamic reasons (hypertension, valvular diseases) Sustained monomorphic VT caused by intramyocardial microreentry Bundle-branch reentry

18 Thank you for attention The static electricity is an awfull stuff. Come back when the drought is not so strong.