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Clinical Cardiology Update 2010

Clinical Cardiology Update 2010. INTERACTIVE ECG SESSION. Dr J.EZHILAN Senior Consultant Cardiologist. ECG NO 1. 27 year old man with h/o syncope. 1)What is your diagnosis 2)What is the mechanism for this disease? 3)how do you classify this condition?

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Clinical Cardiology Update 2010

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  1. Clinical Cardiology Update 2010 INTERACTIVE ECG SESSION Dr J.EZHILAN Senior Consultant Cardiologist

  2. ECG NO 1

  3. 27 year old man with h/o syncope

  4. 1)What is your diagnosis • 2)What is the mechanism for this disease? • 3)how do you classify this condition? • 3)How do drugs influence this condition?

  5. RBBB patternST elevation in V1-V3Type I Brugadas Syndrome

  6. BRUGADAS SYNDROME Aeitology • 1)Genetic mutation causing decrease in sodium current (Ina), leading to premature shortening of action potential and reentry. • 2)Conduction delay in the RVOT compared with the RV free wall. Dr Pedro Brugada

  7. 4 TYPES BASED ON TRANSMEMBRANE ACTION POTENTIAL

  8. 3 TYPES BASED ON ECG

  9. Brugada Leads

  10. BRUGADAS SYNDROME Influence of drugs • APPARENT Na channel Blockers 1)Flecainide 2)Procainamide 3)Ajmaline • INCREASED 1)Beta blockers • DECREASED 1)Isoprenaline

  11. ECG NO 2

  12. 47 yr old women c/o irregular pulse

  13. ECG findings • Q waves in L2 L3 and avf. • T inversion in L3 and avf. • R waves in V1 & V2 is 0.04 sec in duration & R in V2 is greater than S • Upright T in V1. • Inferior wall infarction • Posterior wall infarction • Type I – Second degree AV Block • Wenchebachs phenomenon

  14. WENCHEBACHS PHENOMENON • 1)Progressive PR prolongation • 2)Progressive diminution of PR increments • 2)Progressive shortening of RR interval • 3)Greatest increase in PR occurs in the 2nd conducted P after the pause. • 4)RR interval encompassing the blocked P wave is shorter than the sum of 2 PP intervals 5)RR interval following the pause is larger than RR interval preceding the pause

  15. 1) Progressive PR interval prolongation .20 .24 .26 .28 seconds

  16. 2) Progressive dimunition of PR increment .20 .24 .26 .27 .04 .02 .01 seconds

  17. 3)Greatest increase in PR occurs in the 2nd conducted P after the pause. .20 .24 .26 .28 seconds

  18. 4)R-R interval encompassing the blocked p wave is less than the sum of 2 PP interval 1800 ms 1680 ms

  19. 5)RR interval following the pause is larger than RR interval preceding the pause 680 ms 760 ms

  20. ECG NO 3

  21. 20 Year old boy with breathlesness & cardiomegaly

  22. What are the chambers involved ? • Criteria for LAE? • Most sensitive LAE criteria? • Most specific LAE criteria? • What are the indexes measured in LAE? • What are the types of P wave?

  23. MACRUZ INDEX • Measures the ratio between the duration of P wave and PR segment. Normally it is 1-1.6. In LAE P wave duration increases whereas PR interval tends to remain same thus Macruz index becomes large.

  24. MORRIS INDEX • It is the algebric product of the duration of the terminal P wave force and the amplitude of the force in lead V1. • In normal atrial size the algebric product is -10 to +10 msec. • In LAE it is > 40 msec.

  25. Criteria for LAE SEN SPE • 1)Duration of –ve phase of P in V1 > 40 ms 83 80 • 2)Notched P waves with interpeak duration 40 ms 15 100 • 3)Morris index-Pterminal force depthXduration>40ms 69 93 • 4)Depth of –ve phase of P in V1>1 mm 60 93 • 5)Total P wave duration in any standard lead >110 ms • 6)Macruz index – Total P wave duration >1.6 31 64 PR segment

  26. P wave types • P MITRALE – LAE in RHD – MS • P PULMONALE – RAE in Pulmonary disease • P Congenitale – RAE due to CHD • P Tricuspidale – RAE due to TV disease • HIMALAYAN P – RAE in Ebsteins anomaly • Pseudo P pulmonale - RAE in Left heart disease

  27. ECG NO 4

  28. 73 year old man with palpitation

  29. Rhythm is irregularly irregular • No P waves are seen • Fibrillatory waves are seen in V1 • Atrial fibrillation • Complexes 12 & 19 show RBBB aberration.

  30. Ashmans phenomenon • Long cycle, short cycle- aberrancy. • Prolonged refractory period due to a long cycle folowed by early excitation due to a short cycle leads to aberrancy. • The aberrancy is usually RBBB because the right bundle has a longer refractory period than the left.

  31. Ashmans phenomenon 19 12

  32. How will you differentiate Ashmans from VPC?

  33. Differentiating Ashmans from VPC • 1) VENTRICULAR RATE Phasic aberrancy occurs at relatively faster ventricular rartes where as VPC occurs with slower ventricular rates • 2)QRS MORPHOLOGY Phasic aberrancy usually results in RBBB where as in VPC LBBB & RBBB are seen with equal frequency but usually it is not typical LBBB or RBBB morphology. • 3)QRS VARIABILITY All gradations of variability is seen in Ashmans, VPCs on the otherhand have 1or 2 fixed patterns.

  34. Differentiating Ashmans from VPC • 4)COUPLING INTERVAL VPCs have fixed coupling order where as Ashmans has variable coupling intervals • 5)COMPENSATORY PAUSE VPC is followed by a long pause where as in Ashmans there is no attempt for a compensatory pause. • 6)LONG-SHORT CYCLE Ashmans has long-short cycle where as in VPC also a long preceding cycle(Rule of Bigeminny) favours occurance of VPC. Hence this does not help to differentiate

  35. ECG NO 5 Early Repolarization syndrome

  36. 64 yr old hypertensive African-Americans preoperative ECG for emergency abdominal surgery April 17 2009

  37. LVH with strain • Early Repolarization syndrome • D/D 1)AMI 2)Pericarditis

  38. Part 4 Tracing 6a July 17 2005

  39. Healthy young men Exercise normalises ST Isoprenaline norma ST Beta blocker inc ST Sudden death Healthy young men Exercise normalises ST Isoprenaline norma ST Beta blocker inc ST No Sudden death Brugadas ERS

  40. Healthy young men Exercise normalises ST Isoprenaline norma ST Beta blocker inc ST Sudden death Healthy young men Exercise normalises ST Isoprenaline norma ST Beta blocker inc ST No Sudden death Brugadas ERS Brugadas ERS Long QT Syn

  41. ECG NO 6 Hyperkalemia with Hypocalcemia

  42. 29 year old woman with nausea

  43. ECG FINDINGS • Sinus rhythm • Broad Low amplitude P waves are difficult to identify in limb leads • PR interval is prolonged (0.24sec) • QRS complex is widened (0.20 sec) • Left axis deviation (-15 degrees) • T waves are peaked • QT is prolonged (500 ms)

  44. Hyperkalemia + Hypocalcemia Renal Failure

  45. What could be her serum K level?

  46. 6-7 Peaking of T waves • 7-8 Taller & more peaked • >8 P wave amplitude decreases • PR interval widens • QRS complex widens • >10 P wave disappears(Sinoventricular Rhythm • QRS becomes sinusoid • Ventricular fibrillation

  47. ECG NO 7

  48. 80 year old woman with confusion

  49. III degree AV Block Junctional escape rhythmVPC Bigeminny / Digitalis toxicity • Atrial rhythm is sinus at 70/mt • QRS complexes are in pairs with a fairly constant coupling interval (VPC Bigeminny) • AV dissociation • III degree AV block • The first beat of the pair is narrow with some morphology variation throughout • The second beat of the pair is consistently wide with some variation as well

  50. Arrythmias not caused by digitalis ?

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