ecg: atrial bigeminy with deep inverted t waves
TRANSCRIPT
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ECG of the Week!!!
Dr. K. Manoj KumarProf. Dr.Gowrishankar Unit
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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
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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
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ON INVESTIGATION Blood Sugar, Urea Creatinine levels are
within normal limits CBC with normal limits Chest X-Ray
Mild cardiomegalyLung fields clear
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ECG
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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
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DIFFERENTIAL DIAGNOSIS OF THIS ECG Hypertrophic cardiomyopathy lV SYSTOLIC OVERLOAD like
hypertension Myocardial ischemia CVA with qrs st pattern Valvular aortic stenosis
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HYPERTROPHIC CARDIOMYOPATHY 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
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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
3.1icknessPostwallth
knessSeptalThic
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PATHOPHYSIOLOGY 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
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EFFECT OF MANEUVER FOR HCM DIFFERENTIATION MANEUVER PHYSIOL EFFECT HCM AS
MR Valsalva vr,svr,co
squat&hand vr,svr,co Grip &phenyl
ephrine
Amylnitritevr, dec svr
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Parameters associated with sudden deathsurvivor of cardiac arrestSustained VTFamily history of premature sudden deathMassive degree of ventricular hypertrophyHypotensive response to exerciseMyocardial bridgingSeptal thickness > 30mm Troponin t mutation
Courtesy Braunwald heart diseases & Harrison Medicine
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ECHO FINDINGS 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
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ECHO CLASS OF LVH IN HOCM 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%
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COMPLICATIONS Sudden death Infective endocarditis Systemic embolism Atrial fibrillation High incidence of SVT 46%, PVC 43%,
VT 26% AF 25-30%
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TREATMENT 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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