Sudden Cardiac Death

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  • Sudden Cardiac Death

    1. 1. Sudden Cardiac Death Rosco Gore
    2. 2. Definition <ul><li>The natural death from cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of an acute change in cardiovascular status. </li></ul>
    3. 3. Epidemiology <ul><li>300,000 cases per year </li></ul><ul><li>1-2/1000 </li></ul><ul><li>Bimodal distribution </li></ul>
    4. 4. Causes <ul><li>Long QT Syndrome </li></ul><ul><li>Brugada Syndrome </li></ul><ul><li>Hypertrophic Cardiomyopathy </li></ul><ul><li>Arrhythmogenic Right Ventricular Dysplasia </li></ul><ul><li>Commotio Cordis </li></ul><ul><li>Coronary Anomaly </li></ul>
    5. 5. Long QT Syndrome <ul><li>Autosomal Dominate- Romano-Ward </li></ul><ul><li>Autosomal Recessive- Jervell and Lange-Nielsen </li></ul><ul><li>Acquired </li></ul><ul><li>1/10,000 </li></ul>
    6. 7. Genetics <ul><li>Underlying mutations determine phenotypic expression </li></ul><ul><li>Variable penetrance </li></ul><ul><li>Compound mutations </li></ul>
    7. 9. Presentation <ul><li>Palpitations, Presyncope, Syncope, Seizures, or Cardiac arrest </li></ul><ul><li>Asymptomatic prolonged QTc </li></ul><ul><li>Referred by family members </li></ul><ul><li>Has a predilection for younger patient </li></ul>
    8. 12. QT interval <ul><li>Lead II </li></ul><ul><li>Include U wave if T/U wave merged and U wave >50% height of T wave </li></ul><ul><li>Correct for rate </li></ul><ul><ul><li>Bazett formula =QT/(RR)^1/2 </li></ul></ul><ul><ul><li>Fridericia’s cube-root =QT/(RR)^1/3 </li></ul></ul><ul><ul><li>Framingham Study Linear Regression Equation =QT + .154(1-RR) </li></ul></ul><ul><li>Average over 3-5 beats </li></ul>
    9. 13. http://www.torsades.org/
    10. 14. Diagnosis: Schwartz score
    11. 15. Prognosis <ul><li>Events increase w/ increasing QTc </li></ul>
    12. 16. Therapy <ul><li>NEJM 2008; 358:169-175 </li></ul>
    13. 18. Brugada Syndrome <ul><li>Autosomal dominate defect in cardiac Na channels- variable expression </li></ul><ul><li>0.4% US population </li></ul><ul><li>Male predominance </li></ul><ul><li>Average age of Dx=41 </li></ul>
    14. 19. Pathogenesis Texas Heart Inst J 2007;34:67-75
    15. 20. Presentation <ul><li>Funny looking EGKs </li></ul><ul><li>SCD/Syncope </li></ul><ul><li>Triggers </li></ul><ul><ul><li>Fever </li></ul></ul><ul><ul><li>Sleep </li></ul></ul><ul><ul><li>Glucose/insulin </li></ul></ul><ul><ul><li>Cocaine/ETOH </li></ul></ul><ul><ul><li>Electrolytes </li></ul></ul>
    16. 21. Unmasking Agents <ul><li>Na channel blockers </li></ul><ul><li>Calcium Channel blockers </li></ul><ul><li>Beta blockers </li></ul><ul><li>Nitrates </li></ul><ul><li>Tricyclics </li></ul><ul><li>SSRI </li></ul>
    17. 22. Diagnosis <ul><li>Type I ST pattern + one of </li></ul><ul><ul><li>Documented ventricular fibrillation </li></ul></ul><ul><ul><li>Self-terminating polymorphic ventricular tachycardia (VT) </li></ul></ul><ul><ul><li>Family history of sudden cardiac death at <45 years </li></ul></ul><ul><ul><li>Type 1 ST segment elevation in family members </li></ul></ul><ul><ul><li>Electrophysiologic inducibility of VT </li></ul></ul><ul><ul><li>Unexplained syncope suggestive of a tachyarrhythmia </li></ul></ul><ul><ul><li>Nocturnal agonal respiration </li></ul></ul><ul><li>Type II or III pattern + conversion to type I +one of the above </li></ul>
    18. 23. Prognosis <ul><li>SCD or VF </li></ul><ul><li>Syncope </li></ul><ul><li>Type I pattern </li></ul>
    19. 24. Treatment <ul><li>ACC/AHA- AICD </li></ul><ul><ul><li>Class I- Pt w/ previous cardiac arrest </li></ul></ul><ul><ul><li>Class IIa- Pt w/ previous syncope </li></ul></ul><ul><ul><li>Class IIa- Pt w/ previous VT </li></ul></ul><ul><li>Quinidine and hydroguinidine </li></ul>
    20. 26. Hypertrophic Cardiomyopathy <ul><li>AD defect in the myocardial contractile proteins </li></ul><ul><li>Defective sarcomers->Myocyte dissaray->…Ventricular hypertrophy </li></ul><ul><li>0.16-0.29% US population </li></ul>
    21. 31. Presentation <ul><li>SCD </li></ul><ul><li>DOE </li></ul><ul><li>Syncope </li></ul><ul><li>Heart failure </li></ul><ul><li>Chest Pain </li></ul><ul><li>Palpitation </li></ul><ul><li>Asymptomatic </li></ul>
    22. 32. Physical Exam <ul><li>Systolic Crescendo-decrescendo murmur LLSB/apex </li></ul><ul><li>Decreases w/ squatting, hand drip </li></ul><ul><li>Increase w/ standing </li></ul><ul><li>Bifid pulses </li></ul><ul><li>EKG-LVH </li></ul>
    23. 34. Ventricular Arrhythmias <ul><li>Contributing factors </li></ul><ul><ul><li>Myocardial hypertrophy </li></ul></ul><ul><ul><li>Myocardial disarray </li></ul></ul><ul><ul><li>Myocardial fibrosis </li></ul></ul><ul><ul><li>Myocardial ischemia </li></ul></ul><ul><ul><li>Autonomic disturbance </li></ul></ul><ul><li>SCD </li></ul><ul><ul><li>1% annual incidence </li></ul></ul>
    24. 35. Diagnosis <ul><li>ECHO </li></ul>
    25. 36. SCD Risk <ul><li>High risk= 6%+ </li></ul><ul><li>Low risk= 1% or < </li></ul>
    26. 37. Treatment <ul><li>Pharmocologic </li></ul><ul><ul><li>Verapamil </li></ul></ul><ul><ul><li>Beta blockers </li></ul></ul><ul><ul><li>Disopyramid </li></ul></ul><ul><li>ICD </li></ul><ul><ul><li>Class I- h/o sustained VT/VF </li></ul></ul><ul><ul><li>One or more major risk factor </li></ul></ul><ul><li>Ablation/Surgery </li></ul>
    27. 39. Arrhythmogenic Right Ventricular Dysplasia <ul><li>Defective Desmosome </li></ul><ul><li>Fibrofatty replacement of the RV myocardium </li></ul><ul><li>1:1000 </li></ul><ul><li>AD vs AR </li></ul>
    28. 41. Presentation <ul><li>Asymptomatic </li></ul><ul><li>Palpitation, syncope, atypical chest pain, dyspnea </li></ul><ul><li>Arrhythmias </li></ul><ul><li>SCD </li></ul><ul><ul><li>Exercise associated </li></ul></ul>
    29. 43. Diagnosis 2major or 1major + 2minor or 4minor
    30. 44. Treatment <ul><li>ICD: </li></ul><ul><ul><li>Class I: History of sustained VT/VF </li></ul></ul><ul><ul><li>Class IIa: extensive disease, LV involvement, family members w/ SCD, syncope </li></ul></ul><ul><li>Amiodarone or Sotalol-Class IIA </li></ul><ul><li>Ablation-Class IIA </li></ul>
    31. 45. Commotio Cordis <ul><li>SCD due to low-impact precordial trauma </li></ul><ul><li>Male predominance, young age </li></ul><ul><li>High mortality </li></ul><ul><li>Probability related to speed, time, hardness of object and location of impact </li></ul>
    32. 47. Commotio cordis <ul><li>Treatment </li></ul><ul><ul><li>CPR </li></ul></ul><ul><ul><li>Shock </li></ul></ul><ul><li>Prevention </li></ul><ul><ul><li>Safety baseballs </li></ul></ul><ul><ul><li>Chest protectors </li></ul></ul><ul><li>Follow up </li></ul><ul><ul><li>EKG </li></ul></ul><ul><ul><li>Holter </li></ul></ul><ul><ul><li>Echo </li></ul></ul>
    33. 50. Congenital Coronary Artery Anomalies <ul><li>Variation in the take off the Coronary Arteries </li></ul><ul><li>Incidence 5.6  0.17% </li></ul><ul><li>Deaths related to exertion </li></ul>
    34. 51. Presentation <ul><li>Angina </li></ul><ul><li>Atypical chest pain </li></ul><ul><li>Syncope </li></ul><ul><li>Palpitation </li></ul><ul><li>Dizziness </li></ul><ul><li>SCD </li></ul>
    35. 52. Pathophysiology <ul><li>Compression between the pulmonary artery and aorta </li></ul><ul><li>Acute angle take off </li></ul><ul><li>Myocardial necrosis </li></ul>
    36. 53. Diagnosis <ul><li>ECHO </li></ul><ul><li>Cardiac MRI </li></ul><ul><li>CT angiography </li></ul><ul><li>Cardiac Cath </li></ul>
    37. 54. Military Significance
    38. 57. Treatment <ul><li>Beta Blockers </li></ul><ul><li>Surgery </li></ul><ul><li>Coronary Stents </li></ul><ul><li>Avoid strenuous activities </li></ul>
    39. 58. What do you call 2 orthopedic surgeons reading an EKG? A double blind study!!!!
    40. 59. 0/1-not advisable, 2/3 intermediate risk, 4/5-permitted
    41. 60. 0/1-not advisable, 2/3 intermediate risk, 4/5-permitted
    42. 61. Athlete Screening <ul><li>ESC- EKG </li></ul><ul><li>Italian experience </li></ul><ul><ul><li>1979: 3.6/100K </li></ul></ul><ul><ul><li>2004: 0.4/100k </li></ul></ul>
    43. 62. A 32-year-old man is seen for an annual physical examination. There is no personal or family history of cardiovascular disease or symptoms. On physical examination, S1 and S2 are normal and there is an S4 present. There is a grade 2/6 crescendo-decrescendo systolic murmur heard best at the lower left sternal border. The murmur does not radiate to the carotid arteries. Valsalva maneuver increases the intensity of the murmur, and moving from a standing position to a squatting position, performing a passive leg lift while recumbent, and performing isometric handgrip exercises decreases the intensity. Rapid upstrokes of the peripheral pulses are present. A Mitral valve prolapse B Hypertrophic cardiomyopathy C Atrial septal defect D Ventricular septal defect E Aortic stenosis
    44. 63. A 32-year-old man is seen for an annual physical examination. There is no personal or family history of cardiovascular disease or symptoms. On physical examination, S1 and S2 are normal and there is an S4 present. There is a grade 2/6 crescendo-decrescendo systolic murmur heard best at the lower left sternal border. The murmur does not radiate to the carotid arteries. Valsalva maneuver increases the intensity of the murmur, and moving from a standing position to a squatting position, performing a passive leg lift while recumbent, and performing isometric handgrip exercises decreases the intensity. Rapid upstrokes of the peripheral pulses are present. A Mitral valve prolapse B Hypertrophic cardiomyopathy C Atrial septal defect D Ventricular septal defect E Aortic stenosis
    45. 64. A 23-year-old man is evaluated for palpitations that occur during exercise. He is otherwise healthy and takes no medications. Both the physical examination and the resting electrocardiogram are normal. A stress test demonstrates sustained monomorphic ventricular tachycardia at 201/min at peak exercise. There were no ischemic changes until the arrhythmia developed. The ventricular tachycardia had a left bundle and inferior axis morphology and terminated spontaneously after 7 minutes of rest. An echocardiogram is normal, and an MRI shows no abnormalities in the right or left ventricles. What is the most likely etiology of ventricular tachycardia in this patient? A Coronary spasm B Idiopathic C Arrhythmogenic right ventricular cardiomyopathy D Infiltrative heart disease E Anomalous origin of the coronary arteries
    46. 65. A 23-year-old man is evaluated for palpitations that occur during exercise. He is otherwise healthy and takes no medications. Both the physical examination and the resting electrocardiogram are normal. A stress test demonstrates sustained monomorphic ventricular tachycardia at 201/min at peak exercise. There were no ischemic changes until the arrhythmia developed. The ventricular tachycardia had a left bundle and inferior axis morphology and terminated spontaneously after 7 minutes of rest. An echocardiogram is normal, and an MRI shows no abnormalities in the right or left ventricles. What is the most likely etiology of ventricular tachycardia in this patient? A Coronary spasm B Idiopathic C Arrhythmogenic right ventricular cardiomyopathy D Infiltrative heart disease E Anomalous origin of the coronary arteries
    47. 66. A: ARVD B: Goldwire’s space re-entry vehicle C: Spaceballs hat hair
    48. 67. A: ARVD B: Goldwire’s space re-entry vehicle C: Spaceballs hat hair

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