Download
slide1 n.
Skip this Video
Loading SlideShow in 5 Seconds..
Normal Sinus Rhythm PowerPoint Presentation
Download Presentation
Normal Sinus Rhythm

Normal Sinus Rhythm

917 Views Download Presentation
Download Presentation

Normal Sinus Rhythm

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

    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 Sins masaji Sins tasikardisi Kalp hizinda yavas ve geici yavaslama AT (paroksismal) Etki yok veya tasikardi sonlanir AT(devamli) Etki yok veya ventrikler hizda geici yavaslama Atriyal flutter Etki yok veya ventrikler hizda geici 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 Locations Accessory 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 patients left apical septal VT.Demonstrates the morphology of a patients 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. Ventrikler 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 (1029/h) ..............Sinif D Sregen Olmayan VT Sinif IV Sik (>30/h) ..............................Sinif E Sregen VT Sinif V , F Ani Kardiyak lm Geirme

    56. Yapisal Bozukluk Olmadan (?) Gelisen Ventrikler Tasiaritmiler 1. Tekrarlayan Monomorfik VT - Nonsustained- Sustained VT (Tetiklenmis aktiviteyle) - Adenozin, beta blokr, verapamile duyarli - Sag veya sol ventrikl ikis yolundan kken alir ? Sol dal blogu ve inferiyor aks paterni - Direnli olgularda RF Ablasyon

    57. Yapisal Bozukluk Olmadan (?) Gelisen Ventrikler Tasiaritmiler 2. Sol Septal Ventrikler Tasikardi - Nonsustained-sustained VT (Tetiklenmis aktivite veya re-entry ile) - Sag dal blogu ve sol aks paternli - IV Verapamile kismen duyarli - Direnli olgularda RF ablasyon, Class III ila (?) 3. Idiyopatik VF a. Normal EKG ile (Belhassen) b. Sag dal blogu ve sag prekodiyallerde ST yksekligi ile (Brugada) (A+) c. Uyku-lm Sendromu; sag dal blogu ve sag prekordiyallerde ST yksekligi (Aponte)(A-)

    58. Brugada Sendromu

    62. Genis QRSli Tasikardiler DZENLI DZENSIZ Ventrikler Tasikardi Atriyal Fibrilasyon WPW (Antidromik) Intraventrikler ileti defekti Aberan Iletili Supra-VT Atriyal Flatter Atriyal Flatter (degisken bloklu) Genis QRSli WPW (Antidromik) WPW Antidromik Intraventrikler 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 Faktrler Siklikla kullanilan Class IA Antiaritmikler (Nadiren Sotalol, Amiadaron) Hipokalemi, hipomagnesemi, hipokalsemi (?) Fenotiyazinler, trisiklik antidepresanlar Eritromisin, ketakonazol Prenilamin, lidoflazin Miyakard iskemi/infarkts Myokardit

    73. QT Araligini Uzatan Faktrler 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 amplitd ve morfolojisinde tipik degisme QT uzamis Genellikle VPBs ile baslar (uzun RR araligi sonrasinda) Hiz 150-300/dak 30 snden kisa veya uzun Kendiliginen sonlanabilir veya VFye dejenere olabilir Konjenital : a. Romano-Ward (OD) b.Jervell-Lange-Nielsen (OR, isitme kaybi) Edinsel uzun QT

    94. VENTRIKLER ARTMILERDE ILA KULLANIMI Ila Negatif Kalp Yetmezligi Ciddi ldrc Inotropik Etki Presipitasyonu? Yan Etki Aritmide Etkinlik Kinidin ............... + ............. EF <%25 ....................... Proaritmi ++++ (TDP) ......... Minimal Trombositopeni Prokainamid ... IV +++, Oral ++ ....... EF < %40 ......................Agranlositoz . .................. Zayif Lupus, TDP Dizopromid ........ ++++ ............ EF < %40 .................... TDP .................. Zayif Mexiletin ......... + ............. EF < %25 ................... Minor yan etki yksek .......Minimal Proaritmi + Flekainid ........... +++ ............. EF < %35 .................... Proaritmi +++ ............... EF < %35 nerilmez Propafenon ...... +++ ............ EF < %35 ................... Agranlositoz + ............. EF < %35 Proaritmi ++ nerilmez Amiadaron ..... + (?) ........... EF < %25 (?) ............... Sik, Proaritmi + .............. +++ Beta Blker .... ++ ........... EF < %35 ................ Yok ................ +++ Sotalol ........ + ............ EF < %35 ................. Proaritmi ++ ................ ++ (?) + Minimal Etki, ++++ Maksimal Etki TDP; Torsades des Pointes

    95. Aritmilerde Acil Tedavi 1. Hemodinamik Durum ? - Hipotansiyon - Periferik hipoperfzyon 2. Semptomlar ? - Ggs agrisi - Nefes darligi - Presenkop - Senkop - Bilin bulanikligi 3. Kardiyak Dekompanzasyon ? - Kalp yetmezligi

    96. Aritmilerde Acil Tedavi 1. Hemodinamik Durum ? - Hipotansiyon - Periferik hipoperfzyon 2. Semptomlar ? - Ggs agrisi - Nefes darligi - Presenkop - Senkop - Bilin bulanikligi 3. Kardiyak Dekompanzasyon ? - Kalp yetmezligi

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

    98. Aritmiye Yolaan 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 geirme (VT, VF) Uzun QT (hipokalemi, bradikardi) LV Disfonksiyonu (zellikle EF< %30)

    100. Proaritmi Sonulari VPBs artisi, nonsustained VT sikliginda artma Yeni olusan VT veya VF Antiaritmik lm Erken dnemde proaritmi olusmamasi ge dnemde olusmayacaginin gstergesi degil (CAST) Ge proaritmi, sik Holter veya EPS ile kestirilemez Mevcut verilerle;- Beta-blokerler gvenli - Amiadaron, ve mexiletin kismen gvenli - Kinidin, Class Ic tehlikeli - Digerleri ?

    101. PM-EKG

    102. PM-EKG

    103. PM-EKG