Normal Sinus Rhythm

1. Normal Sinus Rhythm

22. AF � VF The bipolar electrogram of AF is seen on the bottom of the tracing. There is evidence for rapid accessory pathway conduction, ultimately leading to ventricular fibrillation. The bipolar electrogram of AF is seen on the bottom of the tracing. There is evidence for rapid accessory pathway conduction, ultimately leading to ventricular fibrillation.

23. Recommendations for Management of Atrial Fibrillation < 48 Hours

24. Recommendations for Management of Atrial Fibrillation > 48 Hours

25. Timing of Cardioversion for Atrial Fibrillation

29. AV Nodal Reentry Tachycardia This demonstrates the mechanisms for two forms of AV nodal reentry SVT: typical and atypical AV nodal reentry.This demonstrates the mechanisms for two forms of AV nodal reentry SVT: typical and atypical AV nodal reentry.

30. AVNRT Demonstrates AV nodal reentry SVT. It is non-specific. ST changes.Demonstrates AV nodal reentry SVT. It is non-specific. ST changes.

31. AV Nodal Reentry: Slow and Fast Pathways This slide illustrates the triangle of Koch, and anatomical landmarks used to visualize the location of the AV nodal tracts. The three sides of the triangle are defined by the tricuspid valve annulus, the tendon of Tornado, and the ostium of the coronary sinus. The fast AV nodal pathway lies near the compact AV node along the tendon of Todaro. The slow AV nodal pathway is located along the tricuspid valve annulus near the ostium of the coronary sinus.This slide illustrates the triangle of Koch, and anatomical landmarks used to visualize the location of the AV nodal tracts. The three sides of the triangle are defined by the tricuspid valve annulus, the tendon of Tornado, and the ostium of the coronary sinus. The fast AV nodal pathway lies near the compact AV node along the tendon of Todaro. The slow AV nodal pathway is located along the tricuspid valve annulus near the ostium of the coronary sinus.

32. AV Nodal Reentry This slide demonstrates a catheter placed in a potentially successful spot for performance of slow pathway ablation. This is at the entry site into the area of the slow pathway with a sharp potential seen right after the atrial electrogram on the ablation catheter (labeled HRADIST). During delivery of the RF in the slow pathway the patient generally develops an accelerated junctional rhythm as is shown here. This rhythm with rapid conduction back to the atrium is indicative of forming ablation in a potentially successful spot. One thing to keep a careful eye on is the presence of retrograde conduction via the fast pathway.This slide demonstrates a catheter placed in a potentially successful spot for performance of slow pathway ablation. This is at the entry site into the area of the slow pathway with a sharp potential seen right after the atrial electrogram on the ablation catheter (labeled HRADIST). During delivery of the RF in the slow pathway the patient generally develops an accelerated junctional rhythm as is shown here. This rhythm with rapid conduction back to the atrium is indicative of forming ablation in a potentially successful spot. One thing to keep a careful eye on is the presence of retrograde conduction via the fast pathway.

34. Karotid Sin�s masaji Sin�s tasikardisi Kalp hizinda yavas ve ge�ici yavaslama AT (paroksismal) Etki yok veya tasikardi sonlanir AT(devamli) Etki yok veya ventrik�ler hizda ge�ici yavaslama Atriyal flutter Etki yok veya ventrik�ler hizda ge�ici yavaslama AVNRT Etki yok veya tasikardi sonlanir CMT Etki yok veya tasikardi sonlanir

38. Site of Slow Pathway Ablation To ablate the slow pathway, the tip electrode of the ablation catheter is positioned along the tricuspid annulus, near the ostium of the coronary sinus. The boundaries of the triangle of Koch guide precise catheter placement. To ablate the slow pathway, the tip electrode of the ablation catheter is positioned along the tricuspid annulus, near the ostium of the coronary sinus. The boundaries of the triangle of Koch guide precise catheter placement.

39. �Typical� AV Nodal Reentry This tracing demonstrates initiation of AVNRT with a premature atrial beat. Notice the large jump in the AH interval. At this point, conduction is blocked in the fast pathway, and �jumps� to the slower pathway. This tracing demonstrates initiation of AVNRT with a premature atrial beat. Notice the large jump in the AH interval. At this point, conduction is blocked in the fast pathway, and �jumps� to the slower pathway.

40. AVNRT Ablation Demonstrates positioning of the catheters usually used for ablation of AV nodal reentry supraventricular tachycardia. This is an RAO projection showing the catheter in the coronary sinus, one in the HIS bundle position, and one in the slow pathway location.Demonstrates positioning of the catheters usually used for ablation of AV nodal reentry supraventricular tachycardia. This is an RAO projection showing the catheter in the coronary sinus, one in the HIS bundle position, and one in the slow pathway location.

41. Kalp transplantasyonu-EKG

42. Kalp transplantasyonu-EKG

43. Digoksin- EKG

45. Digoksin-EKG

46. Anatomic LocationsAccessory Pathways Bypass tracts are categorized based on their location. This graphic reviews the anatomical location of bypass tracts in relation to the mitral valve annulus, the tricuspid valve annulus, the coronary sinus and the bundle of His. Generally, left-sided bypass tracts may course through the AV groove obliquely and may be composed of multiple fiber bundles. Right-sided bypass tracts appear to cross the AV groove through an area where the tricuspid annulus is structurally deficient. Right-sided bypass tracts are challenging ablations because of the absence of venous structure along the annulus. Bypass tracts are categorized based on their location. This graphic reviews the anatomical location of bypass tracts in relation to the mitral valve annulus, the tricuspid valve annulus, the coronary sinus and the bundle of His. Generally, left-sided bypass tracts may course through the AV groove obliquely and may be composed of multiple fiber bundles. Right-sided bypass tracts appear to cross the AV groove through an area where the tricuspid annulus is structurally deficient. Right-sided bypass tracts are challenging ablations because of the absence of venous structure along the annulus.

47. Pre-excitation This EKG demonstrates evidence for ventricular pre-excitation. There is a delta wave with a short PR-interval seen in all 12 leads of electrocardiogram. This is a right-sided accessory pathway.This EKG demonstrates evidence for ventricular pre-excitation. There is a delta wave with a short PR-interval seen in all 12 leads of electrocardiogram. This is a right-sided accessory pathway.

48. WPW sendromu

49. WPW sendromu

50. WPW sendromu

51. WPW: Case Study ECG Demonstrates the morphology of a patient�s left apical septal VT.Demonstrates the morphology of a patient�s left apical septal VT.

52. Orthodromic Reciprocating Tachycardia This tachycardia is an SVT with an apparent P-wave buried in the ST segment suggestive of orthodromic AV reciprocating tachycardia.This tachycardia is an SVT with an apparent P-wave buried in the ST segment suggestive of orthodromic AV reciprocating tachycardia.

53. AF with Multiple Accessory Pathways There is evidence for AF with an irregular ventricular response rate and at least two QRS morphologies, suggestive of at least two accessory pathways during AF.There is evidence for AF with an irregular ventricular response rate and at least two QRS morphologies, suggestive of at least two accessory pathways during AF.

55. Ventrik�ler Aritmilerde Siniflama SIKLIK SEKIL Sinif 0 � 0.................................................Sinif A � Uniformik Sinif I � Nadir ......................................... Sinif B � Multiformik Sinif II � Seyrek (1-9/h)...........................Sinif C � Pespese 2-5 Sinif III � Orta Siklik (10�29/h) ..............Sinif D � S�regen Olmayan VT Sinif IV � Sik (>30/h) ..............................Sinif E � S�regen VT Sinif V , F � Ani Kardiyak �l�m Ge�irme

56. Yapisal Bozukluk Olmadan (?) Gelisen Ventrik�ler Tasiaritmiler 1. Tekrarlayan Monomorfik VT - Nonsustained- Sustained VT (Tetiklenmis aktiviteyle) - Adenozin, beta blok�r, verapamil�e duyarli - Sag veya sol ventrik�l �ikis yolundan k�ken alir ? Sol dal blogu ve inferiyor aks paterni - Diren�li olgularda RF Ablasyon

57. Yapisal Bozukluk Olmadan (?) Gelisen Ventrik�ler Tasiaritmiler 2. Sol Septal Ventrik�ler Tasikardi - Nonsustained-sustained VT (Tetiklenmis aktivite veya re-entry ile) - Sag dal blogu ve sol aks paternli - IV Verapamil�e kismen duyarli - Diren�li olgularda RF ablasyon, Class III ila� (?) 3. Idiyopatik VF a. Normal EKG ile (Belhassen) b. Sag dal blogu ve sag prekodiyallerde ST y�ksekligi ile (Brugada) (A�+) c. Uyku-�l�m Sendromu; sag dal blogu ve sag prekordiyallerde ST y�ksekligi (Aponte)(A�-)

58. Brugada Sendromu

62. Genis QRS�li Tasikardiler D�ZENLI D�ZENSIZ Ventrik�ler Tasikardi Atriyal Fibrilasyon WPW (Antidromik) Intraventrik�ler ileti defekti Aberan Iletili Supra-VT Atriyal Flatter Atriyal Flatter (degisken bloklu) Genis QRS�li WPW (Antidromik) WPW Antidromik Intraventrik�ler Ileti defekti WPW (Antidromik) Polimorfik VT

63. Monomorfik VT Benzer QRS morfolojisinde Dissosiye P dalgalari sekli kismen degistirebilir Genellikle MI komsulugunda LV anevrizmasi Dilate Kardiyomiyopati Nadiren yapisal kalp hastaligi olmadan ?Genelde Reentry ile olusur

71. T wave alternans & QT uzamasi

72. QT Araligini Uzatan Fakt�rler Siklikla kullanilan Class IA Antiaritmikler (Nadiren Sotalol, Amiadaron) Hipokalemi, hipomagnesemi, hipokalsemi (?) Fenotiyazinler, trisiklik antidepresanlar Eritromisin, ketakonazol Prenilamin, lidoflazin Miyakard iskemi/infarkt�s� Myokardit

73. QT Araligini Uzatan Fakt�rler Uzun QT ile birlikte bradikardi Klorakin, pentolamin Organik fosforlu insektisitler Astemizol, terfenadin (diger antihistaminikler ?) Adenozin Sivi protein diyeti Subaraknoid kanama Kokain kullanimi

76. Polimorfik VT Vurudan vuruya QRS morfolojisi farkli Uzun QT ile � Torsades de Pointes Normal QT ile Genelde Tetiklenmis Aktivite ile olusur

79. Torsades de Pointes (Atipik VT) QRS amplit�d ve morfolojisinde tipik degisme QT uzamis Genellikle VPBs ile baslar (uzun RR araligi sonrasinda) Hiz 150-300/dak 30 sn�den kisa veya uzun Kendiliginen sonlanabilir veya VF�ye dejenere olabilir Konjenital : a. Romano-Ward (OD) b.Jervell-Lange-Nielsen (OR, isitme kaybi) Edinsel uzun QT

94. VENTRIK�LER ARTMILERDE ILA� KULLANIMI Ila� Negatif Kalp Yetmezligi Ciddi �ld�r�c� Inotropik Etki Presipitasyonu? Yan Etki Aritmide Etkinlik Kinidin ............... + ............. EF <%25 ....................... Proaritmi ++++ (TDP) ......... Minimal Trombositopeni Prokainamid ... IV +++, Oral ++ ....... EF < %40 ......................Agran�lositoz . .................. Zayif Lupus, TDP Dizopromid ........ ++++ ............ EF < %40 .................... TDP .................. Zayif Mexiletin ......... + ............. EF < %25 ................... Minor yan etki y�ksek .......Minimal Proaritmi + Flekainid ........... +++ ............. EF < %35 .................... Proaritmi +++ ............... EF < %35 �nerilmez Propafenon ...... +++ ............ EF < %35 ................... Agran�lositoz + ............. EF < %35 Proaritmi ++ �nerilmez Amiadaron ..... + (?) ........... EF < %25 (?) ............... Sik, Proaritmi + .............. +++ Beta Bl�ker .... ++ ........... EF < %35 ................ Yok ................ +++ Sotalol ........ + ............ EF < %35 ................. Proaritmi ++ ................ ++ (?) + Minimal Etki, ++++ Maksimal Etki TDP; Torsades des Pointes

95. Aritmilerde Acil Tedavi 1. Hemodinamik Durum ? - Hipotansiyon - Periferik hipoperf�zyon 2. Semptomlar ? - G�g�s agrisi - Nefes darligi - Presenkop - Senkop - Bilin� bulanikligi 3. Kardiyak Dekompanzasyon ? - Kalp yetmezligi

96. Aritmilerde Acil Tedavi 1. Hemodinamik Durum ? - Hipotansiyon - Periferik hipoperf�zyon 2. Semptomlar ? - G�g�s agrisi - Nefes darligi - Presenkop - Senkop - Bilin� bulanikligi 3. Kardiyak Dekompanzasyon ? - Kalp yetmezligi

97. Aritmiyi Olusturan Fakt�rler - Iskemi -SSS-AV Blok -Hipomagnezemi -Reperf�zyon -Kalp Yetmezligi -Hiperkalemi -Hipotansiyon -Hipokalemi -Alkalemi -Asidemi -Hipokalsemi -Infeksiyon -Otonomik tonus degisikligi -Akut kan kaybi -Tirotoksikoz -Digoksin toksisitesi -Proaritmik ila�

98. Aritmiye Yola�an Kardiyak Patolojiler Iskemik Kalp Hastaligi Kardiyomiyopati (Aritmojenik RV Dispalizi) RKH Myokardit SSS Kardiyak Aksesuar Yol Konjenital Kalp Hastaligi

99. Anti-aritmiklerde Proaritmik Riskin Arttigi Durumlar Kardiyak arrest ge�irme (VT, VF) Uzun QT (hipokalemi, bradikardi) LV Disfonksiyonu (�zellikle EF< %30)

100. Proaritmi Sonu�lari VPBs artisi, nonsustained VT sikliginda artma Yeni olusan VT veya VF Antiaritmik �l�m Erken d�nemde proaritmi olusmamasi ge� d�nemde olusmayacaginin g�stergesi degil (CAST) Ge� proaritmi, sik Holter veya EPS ile kestirilemez Mevcut verilerle;- Beta-blokerler g�venli - Amiadaron, ve mexiletin kismen g�venli - Kinidin, Class Ic tehlikeli - Digerleri ?

101. PM-EKG

102. PM-EKG

103. PM-EKG