ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar... any queries...

1. VENTRICULARARRYHTHMIAS Dr.PRAVEEN NAGULA

2. INTRODUCTION 1.PREMATURE VENTRICULAR COMPLEXES. 2.IDIOVENTRICULAR RHYTHM 3.NONSUSTAINED VT MONOMORPHIC POLYMORPHIC 4.SUSTAINED VT MONOMORPHIC POLYMORPHIC 5.BUNDLE BRANCH REENTRANT TACHYCARDIA 6.BIDIRECTIONAL VT 7.TORSADES DE POINTES 8.VENTRICULAR FLUTTER 9.VENTRICULAR FIBRILLATION

3. case A 39-year-old lady presents to you with frequent palpitations lasting a few months, which are not associated with dizziness, syncope or angina. She has enjoyed good health and is not on any medication or herbal medicine. She is a non-smoker and has no known diabetes, hypertension or hypercholesterolaemia. Her menses is regular and physical examination is unremarkable other than a few premature beats. This is her ECG.

4. Typical configuration of outflow tract premature ventricular contraction (PVCs) in the 12-lead ECG. Niwano S et al. Heart 2009;95:1230-1237 ©2009 by BMJ Publishing Group Ltd and British Cardiovascular Society

5. A diagnosis of VPC s have been made….. Is it benign ? Is it abnormal? Does it need therapy after absence of heart disease? Holter monitoring when is needed? When do you call VT ? Can you localise the origin of VPCs? How to differentiate from APC s. When there is a inferior wall MI what is its importance? A student on ECG read as VPC with R on T phenomenon ..what will the importance of the word? VPC s of ischemic heartdisease usually arise from ?

6. VENTRICULAR ACTION POTENTIAL

7. VULNERABLE PERIOD

8. WHERE THERE IS A POSSIBILITY

10. PREMATURE VENTRICULAR COMPLEXES Occur before the next expected normal sinus impulse. Not preceded by P waves. Wide QRS complex >0.12 sec (0.14sec)---below bundle of HIS. QRS is wide,slurred and notched. Direct muscle to muscle transmission. ST segment and T waves are discordant to QRS complex. QRS complex followed by a compensatory pause.

11. PVC s Common Increase with age. Causes: Anxiety Caffeine intake Aminophylline Epinephrine Isoproteronol Digitalis Valvular ,HTN,Ischemia, Acute MI Hypokalemia,hypomagnesemia,hypoxemia

12. PVCs They are called as ventricular extrasystoles. Unifocal--- arise from a single location in the ventricle, uniform and have identical configuration. Multifocal–two or more locations. Interpolated PVCs – inserted between two sinus impulses without altering the basic sinus rate…it is not followed by a pause. Fully compensatory pause--- does not discharge the sinus node prematurely…regularity of sinus impulse not altered– differentiates from premature atrial complex. If conducted retrogradely to the atria –less then full compensatory pause.. May suppress the SA node –more than full compensatory pause.

13. Sinus beat following a interpolated VPC s has a prolonged PR interval. Abnormal VPC S Multifocal and VPC s in pairs Unifocal abnormal in crops,bigeminy,>40 yrs ,assosciated cardiac disease. Interpolated extrasystoles—bradycardia.

18. PVCs Retrograde activation– leads to P wave formation –but may not be visible –buried in the PVCs R on T phenomenon---- early PVC striking the T wave of the previous complex…short coupling interval.. End diastolic PVC s --- if it occurs late in the diastole such that already P wave of the sinus impulse is formed…fusion complex..long coupling interval. Coupling interval – distance between the PVC s and the preceding QRS complex… Usually constant. Short coupling interval <0.4 sec. R on T phenomenon may trigger a potential arryhthmia..

22. PVC s Bigeminy --- if every other complex on the strip is a PVCs. Trigeminy– if every third complex is a PVC. It is also trigeminy if every two PVCs are followed by a sinus impulse. Quadrigeminy– every fourth complex is a PVC. Paired PVC –couplets consecutively..

26. COUPLET

27. APCs

28. PVC s

29. PVC s Right ventricular PVC Has a LBBB configuration. RV apex – LBBB + LAD. RV outflow --- LBBB + RAD RV inflow --- LBBB + normal axis. (tricuspid area). Just remember apex on left side,outflow on right side,inflow tricuspid valve in direction of lead II –normal axis.

33. PVC s Left ventricular PVC s Anterosuperior area --- RBBB +RAD supplied by anterior fascicle of the LBB. Inferoposterior area – left posterior fascicle –RBBB +LAD.

35. VPC s without obvious cardiovascular heart diseases have RV origin >LV origin. In with heart disease –LV origin Apex and base of ventricle– heart disease. LBB ---donot indicate cardiac disease.

36. Treatment Reversible cardiomyopathy –depressed LV function with bigeminy or freq non sustained VT B Blockers in presence of STEMI . Prognosis: No prognostic significance in absence of structural heart disease. Freq VPCs or runs of non sustained VT ---SCD in presence of heart disease. No reduction in risk of arryhthmic death by use of antiarryhthmic drugs Prophylactic pharmacotherapy c/I

37. VENTRICULAR PARASYSTOLES Independent ectopic impulse that competes with the sinus node as the pacemaker of the heart. Located in the atria,AV junction or the ventricles. Ventricular para systole is manifested when the sinus node fails. The cells are protected and cannot be reset by the sinus impulse. May or may not catch the ventricles depending upon the refractory period of the ventricles. May result in fusion beats.

39. Consider as parasystole Coupling intervals are variable. Fusion complexes are present. Mathematically related. Longer are multiples of the shorter one..

41. parasystole

42. Fusion beat

43. Conduction of beats

44. Capture beat When interference dissosciation occurs between sinus rhythm and a faster subsidiary(ventricular or AV nodal rhythm),the mutual impedence or interference occurs within the AV node. The ventricular or AV nodal impulses cannot be conducted retrogradely---upper AV nodal refractoriness consequent to partial penetration of the sinus impulse to AV node. Sinus impulses cannot be conducted anterogradely to the ventricles,as a result of lower AV nodal refractoriness consequent to retrograde penetration of ventricular impulses to AV node.

45. Capture beat Two pacemakers discharge asynchronously. Sinus impulse occurs progressively later in relation to the AV nodal or ventricular discharge----p wave falls away from the QRS complex of the subsidiary rhythm Sinus impulse may reach the AV node when it is no longer refractory. Able to penetrate the AV node and be conducted to and activate the ventricles. Momentary activation of the ventricles by the sinus impulses in AV dissosciation is known as a ventricular capture beat. It is an early beat..preceding p wave to be present.

46. Capture beat When a tachycardia with bizzare QRS complexes is complicated by capture beats…..see the morphology of the captured beat. Capture beat has a normal or near normal narrow QRS configuration---the diagnosis of ectopic ventricular tachycardia is favoured. Capture beat resembles the bizarre QRS pattern of the tachycardia,a diagnosis of SVT with aberration is favoured. This because the course of activation of both the capturing and supraventricular ectopic impulse must be the same.

48. Capture beats

51. ACCELERATED IDIOVENTRICULAR RHYTHM Ventricular rhythm 3 0r more complexes >40/min and <120 bpm Abnormal automaticity Benign rhythm Gradual onset and offset Brief,self limiting arryhthmia

52. Idioventricular rhythm

53. causes Can be seen in absence of structural heart disease Frequently seen in presence of acute MI Cocaine intoxication Acute myocarditis Digoxin intoxication Post operative cardiac surgery Sustained forms--- acute MI ,POST OP,hemodynamiccompromise,AVdissosciation

54. RVMI with proximal RCA occlusion has been more prone for bradyarryhthmias--------ventricular rhythm—AIVR ---hemodynamic compromise worsens Treatment atrialpacing,atropine. Overlap between AIVR and slow VT ---90-120 bpm Slow VT has to be differentiated.

55. answers 1. benign 2.not abnormal 3.no 4.frequent palpitations,syncope,chest pain 5. prsence of 3 0r more complexes,>100 bpm … 6.it is on outflow tract VPC with LAD. 7.absence of compensatory pause. 8.hypotension –atrial pacing required 9.risk of getting arryhthmia 10. left ventricle ---base and apex

56. Diagnose…

57. diagnose

58. Take home message VPC s may be in presence or absence of heart disease. Only abnormal VPCs are to be treated Prophylactic antiarryhthmic therapy is not indicated. Ventricular parasystole diagnosed by varying coupling intervals and fusion complexes B blockers can be given for VPC s in ischemia AIVR is a benign rhythm usually self limited arryhthmia Can be cause of hypotension in RVMI with RCA proximal occlusion. Capture beats morhology differentiate VT and SVT R on T phenomenon can cause arryhthmia Three consequetive VPC s >100 bpm is VT.

59. References Leo SCHAMROTH an introdcution to electrocardiogarphy. ,7 thed HARRISON’S principles of internal medicine,17 th ed. Lifeinthefastlane/ecg library/clinical cases Basic and bedside electrocardiography----- Romulo.F.Baltazar

60. Thank you sagittarian