ECG: Atrial Bigeminy with deep inverted T waves

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ECG: Atrial Bigeminy with deep inverted T waves

  1. 1.  A 55yr old Male, c/o shortness of breath – 7 days; chest pain – 6days  No h/o syncope ; no h/o oliguria; no h/o fatigue  Not a known Diabetic; known hypertensive for 5yrs  No h/o similar illness in the family
  2. 2.  O/E Patient Conscious  Mildly dyspneic,tachypneic  Mild pallor – I0/PE0/L0/CL0  CVS S1 S2+ S4+; systolic murmur+ not radiating to carotid  RS NVBS heard  P/A soft  BP 130/80 mm hg  PR 76/min
  3. 3.  Blood Sugar, Urea Creatinine levels are within normal limits  CBC with normal limits  Chest X-Ray  Mild cardiomegaly  Lung fields clear
  4. 4.  ECG shows:  Rate : 75/min  Normal axis of 15 degree  Normal ST segment  PR interval normal  normal sinus beat followed by atrial ectopic  Atrial bigeminal rhythm  Tall R waves with deep symmetrical sharply pointed inverted T waves in the mid precordial leads  The initial horizontality of ST Segment with well developed ST T angle – ST Segment shelf is seen
  5. 5.  Hypertrophic cardiomyopathy  lV SYSTOLIC OVERLOAD like hypertension  Myocardial ischemia  CVA with qrs st pattern  Valvular aortic stenosis
  6. 6.  Inheritable autosomal dominant disease of heart muscle d/tmutation in beta mhc of chr14  characterized by thickened but non dilated left ventricle in the absence of another cardiac or systemic condition capable of producing magnitude of the hypertrophy evident  Small ventricular cavity and marked hypertrophy of myocardium with myofibril disarray w/wo dynamic outflow tract obstruction
  7. 7.  Most common cause of sudden cardiac death in young people including trained athelets  WHO designated with HCM to describe this unique process of primary muscle hypertrophy  M mode echo define ASH  Myocardial disarray of muscle fibre result in WHORLING characteristic of HCM
  8. 8.  Diastolic dysfunction  LV Out flow tract obstruction  Mitral regurgitation due to elongated mitral leaflets and chordae  Intramyocardial ischaemia due to partially obliterated intra mural coronary arteries  Arrythymias  Autonomic dysfunction – systolic BP↓ on exercise
  9. 9.  MANEUVER PHYSIOL EFFECT HCM AS MR Valsalva vr,svr,co squat&hand vr,svr,co  Grip &phenyl ephrine  Amylnitrite vr, dec svr
  10. 10.  Parameters associated with sudden death  survivor of cardiac arrest  Sustained VT  Family history of premature sudden death  Massive degree of ventricular hypertrophy  Hypotensive response to exercise  Myocardial bridging  Septal thickness > 30mm Troponin t mutation Courtesy Braunwald heart diseases & Harrison Medicine
  11. 11.  LV hypertrophy with septum >1.3times posterior LV wall thickness  Ground glass appearance of septum  Spade shaped LV Cavity  small lv cavity  SAM of mitral valve  septal immobility  premature closure of aortic valve  resting gradient>30mm  provocable gradient>50mm
  12. 12.  TYPE 1 ..ANT SEPTUM 10%  TYPE 2…ANT AND POST SEPTUM 20%  TYPE 3 ..ANT AND POST SEPTUM INCLUDING LAT.FREE WALL 52%  TYPE 4 ..REGION OTHER THAN SEPTUM AND POST FREE WALL 18%
  13. 13.  Sudden death  Infective endocarditis  Systemic embolism  Atrial fibrillation  High incidence of SVT 46%, PVC 43%, VT 26% AF 25-30%
  14. 14.  Screening Echo for first degree relatives  Avoid strenuous exercise  IE prophylaxis  Keep well hydrated  Medical therapy like Beta blockers, calcium channel blockers, diisopyramide  Surgical options include septal myectomy. Dual chamber pacing, septal ablation in patients not responding to surgery  AICD for prevention of sudden death

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