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ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
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  3. 3. case<br />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.<br />
  4. 4. Typical configuration of outflow tract premature ventricular contraction (PVCs) in the 12-lead ECG.<br />Niwano S et al. Heart 2009;95:1230-1237<br />©2009 by BMJ Publishing Group Ltd and British Cardiovascular Society<br />
  5. 5. A diagnosis of VPC s have been made…..<br />Is it benign ?<br />Is it abnormal?<br />Does it need therapy after absence of heart disease?<br />Holter monitoring when is needed?<br />When do you call VT ?<br />Can you localise the origin of VPCs?<br />How to differentiate from APC s.<br />When there is a inferior wall MI what is its importance?<br />A student on ECG read as VPC with R on T phenomenon ..what will the importance of the word?<br />VPC s of ischemic heartdisease usually arise from ?<br />
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  10. 10. PREMATURE VENTRICULAR COMPLEXES<br />Occur before the next expected normal sinus impulse.<br />Not preceded by P waves.<br />Wide QRS complex >0.12 sec (0.14sec)---below bundle of HIS.<br />QRS is wide,slurred and notched.<br />Direct muscle to muscle transmission.<br />ST segment and T waves are discordant to QRS complex.<br />QRS complex followed by a compensatory pause.<br />
  11. 11. PVC s<br />Common<br />Increase with age.<br />Causes:<br />Anxiety<br />Caffeine intake<br />Aminophylline<br />Epinephrine<br />Isoproteronol<br />Digitalis <br />Valvular ,HTN,Ischemia,<br />Acute MI<br />Hypokalemia,hypomagnesemia,hypoxemia<br />
  12. 12. PVCs<br />They are called as ventricular extrasystoles.<br />Unifocal--- arise from a single location in the ventricle, uniform and have identical configuration. <br />Multifocal–two or more locations.<br />Interpolated PVCs – inserted between two sinus impulses without altering the basic sinus rate…it is not followed by a pause.<br />Fully compensatory pause--- does not discharge the sinus node prematurely…regularity of sinus impulse not altered– differentiates from premature atrial complex.<br />If conducted retrogradely to the atria –less then full compensatory pause.. <br />May suppress the SA node –more than full compensatory pause.<br />
  13. 13. Sinus beat following a interpolated VPC s has a prolonged PR interval.<br />Abnormal VPC S<br />Multifocal and VPC s in pairs<br />Unifocal abnormal in crops,bigeminy,>40 yrs ,assosciated cardiac disease.<br />Interpolated extrasystoles—bradycardia.<br />
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  18. 18. PVCs<br />Retrograde activation– leads to P wave formation –but may not be visible –buried in the PVCs<br />R on T phenomenon---- early PVC striking the T wave of the previous complex…short coupling interval..<br />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.<br />Coupling interval – distance between the PVC s and the preceding QRS complex…<br />Usually constant.<br />Short coupling interval <0.4 sec.<br />R on T phenomenon may trigger a potential arryhthmia.. <br />
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  22. 22. PVC s<br />Bigeminy --- if every other complex on the strip is a PVCs.<br />Trigeminy– if every third complex is a PVC.<br />It is also trigeminy if every two PVCs are followed by a sinus impulse.<br />Quadrigeminy– every fourth complex is a PVC.<br />Paired PVC –couplets consecutively.. <br />
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  26. 26. COUPLET<br />
  27. 27. APCs<br />
  28. 28. PVC s <br />
  29. 29. PVC s <br />Right ventricular PVC <br />Has a LBBB configuration.<br />RV apex – LBBB + LAD.<br />RV outflow --- LBBB + RAD<br />RV inflow --- LBBB + normal axis. (tricuspid area). <br />Just remember apex on left side,outflow on right side,inflow tricuspid valve in direction of lead II –normal axis.<br />
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  33. 33. PVC s<br />Left ventricular PVC s <br />Anterosuperior area --- RBBB +RAD supplied by anterior fascicle of the LBB.<br />Inferoposterior area – left posterior fascicle –RBBB +LAD. <br />
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  35. 35. VPC s without obvious cardiovascular heart diseases have RV origin >LV origin.<br />In with heart disease –LV origin<br />Apex and base of ventricle– heart disease.<br />LBB ---donot indicate cardiac disease.<br />
  36. 36. Treatment<br />Reversible cardiomyopathy –depressed LV function with bigeminy or freq non sustained VT<br />B Blockers in presence of STEMI .<br />Prognosis:<br />No prognostic significance in absence of structural heart disease.<br />Freq VPCs or runs of non sustained VT ---SCD in presence of heart disease.<br />No reduction in risk of arryhthmic death by use of antiarryhthmic drugs<br />Prophylactic pharmacotherapy c/I <br />
  37. 37. VENTRICULAR PARASYSTOLES<br />Independent ectopic impulse that competes with the sinus node as the pacemaker of the heart.<br />Located in the atria,AV junction or the ventricles.<br />Ventricular para systole is manifested when the sinus node fails. <br />The cells are protected and cannot be reset by the sinus impulse.<br />May or may not catch the ventricles depending upon the refractory period of the ventricles.<br />May result in fusion beats. <br />
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  39. 39. Consider as parasystole<br />Coupling intervals are variable.<br />Fusion complexes are present.<br />Mathematically related.<br />Longer are multiples of the shorter one..<br />
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  41. 41. parasystole<br />
  42. 42. Fusion beat<br />
  43. 43. Conduction of beats<br />
  44. 44. Capture beat<br />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.<br />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.<br />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. <br />
  45. 45. Capture beat<br />Two pacemakers discharge asynchronously.<br />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<br />Sinus impulse may reach the AV node when it is no longer refractory.<br />Able to penetrate the AV node and be conducted to and activate the ventricles.<br />Momentary activation of the ventricles by the sinus impulses in AV dissosciation is known as a ventricular capture beat.<br />It is an early beat..preceding p wave to be present.<br />
  46. 46. Capture beat<br />When a tachycardia with bizzare QRS complexes is complicated by capture beats…..see the morphology of the captured beat.<br />Capture beat has a normal or near normal narrow QRS configuration---the diagnosis of ectopic ventricular tachycardia is favoured.<br />Capture beat resembles the bizarre QRS pattern of the tachycardia,a diagnosis of SVT with aberration is favoured.<br />This because the course of activation of both the capturing and supraventricular ectopic impulse must be the same.<br />
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  48. 48. Capture beats<br />
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  51. 51. ACCELERATED IDIOVENTRICULAR RHYTHM<br />Ventricular rhythm<br />3 0r more complexes >40/min and <120 bpm<br />Abnormal automaticity<br />Benign rhythm<br />Gradual onset and offset<br />Brief,self limiting arryhthmia<br />
  52. 52. Idioventricular rhythm<br />
  53. 53. causes<br />Can be seen in absence of structural heart disease<br />Frequently seen in presence of acute MI<br />Cocaine intoxication<br />Acute myocarditis<br />Digoxin intoxication<br />Post operative cardiac surgery<br />Sustained forms--- acute MI ,POST OP,hemodynamiccompromise,AVdissosciation<br />
  54. 54. RVMI with proximal RCA occlusion has been more prone for bradyarryhthmias--------ventricular rhythm—AIVR ---hemodynamic compromise worsens<br />Treatment atrialpacing,atropine.<br />Overlap between AIVR and slow VT ---90-120 bpm<br />Slow VT has to be differentiated.<br />
  55. 55. answers<br />1. benign <br />2.not abnormal<br />3.no<br />4.frequent palpitations,syncope,chest pain<br />5. prsence of 3 0r more complexes,>100 bpm …<br />6.it is on outflow tract VPC with LAD.<br />7.absence of compensatory pause.<br />8.hypotension –atrial pacing required<br />9.risk of getting arryhthmia<br />10. left ventricle ---base and apex<br />
  56. 56. Diagnose…<br />
  57. 57. diagnose<br />
  58. 58. Take home message<br />VPC s may be in presence or absence of heart disease.<br />Only abnormal VPCs are to be treated<br />Prophylactic antiarryhthmic therapy is not indicated.<br />Ventricular parasystole diagnosed by varying coupling intervals and fusion complexes<br />B blockers can be given for VPC s in ischemia<br />AIVR is a benign rhythm usually self limited arryhthmia<br />Can be cause of hypotension in RVMI with RCA proximal occlusion.<br />Capture beats morhology differentiate VT and SVT<br />R on T phenomenon can cause arryhthmia<br />Three consequetive VPC s >100 bpm is VT.<br />
  59. 59. References<br />Leo SCHAMROTH an introdcution to electrocardiogarphy. ,7 thed<br />HARRISON’S principles of internal medicine,17 th ed.<br />Lifeinthefastlane/ecg library/clinical cases<br />Basic and bedside electrocardiography----- Romulo.F.Baltazar<br />
  60. 60. Thank you <br />sagittarian<br />