زكاة العلم الدكتور محمد البيضاني

Ventricular ectopic beats blue one and supraventricular ectopic beats yellowish one

Sinus rhythm with supranational ( atrial ectopic beat bigmeni) Criteria of supranational ectopic beats - come early - preceded by abnormal P wave morphology or absent P wave - same shape of sinus beats as the ectopic beat above the AV node and pass through the AV node and take the same shape of sinus beat - post ectopic wide distance

Young age male presented with fever and chest pain. Patient get well with antipyretic and analgesia . Serial S troponine was negative Serial ECG ( after 8 hour there is resolution of ST change). At the beginning the ECG reveal picture of Brugada syndrome - pattern of RBBB(rSR pattern) -down sloping ST elevation in right pericardial lead - T wave inversion - absent slurred S wave in V6 which appear in true RBBB. ( in brugada there is pattern of RBBB not True RBBB. Note: brugada features not always appear in ECG. Patient may has brugada with normal ECG . Some conditions make brugada features obvious like chest pain , after correction of arrhythmia, after cardia arrest , ischmia , drugs, fever ,,,,,,, That’s why the changes appear with chest pain and fever and disappeared after stabilisation.

Brugada syndrome type A developed VF - rSr pattern in V1 partial RBBB with absent Slired S in lateral lead - ST elevation with down-sloping ST depression and T wave inversion. This is ECG of brugada type A .

35 years old male presented to the ED with dyspnea , tachypneic pale , sweaty . During examination there was chest crepitation and mild pitting odema . Normal pericardial examination. Renal indices was high , the family report history of renal problems before 4 weeks and refuse follow up. ECG was done and revel - flattening of P wave until losed in the baseline. - widening of QRS with formation of Sine wave - T wave from narrow base and peaked becomes wide base and and decrease the ampiltude . Conclusion: renal shutdown with hyperkalemia. emergency treatment - calcium gluconat 3 g ( three vial IV slowly ) - ventuline neubilizer - 50 ml of 50% GW with 10 unit insulin Complete the follow up with nephrologist.

MI get VF on ECG machine

By the way during my duty in general surgery I see this ECG - ST elevation in lead I and avL - ST depression in lead III This is called high lateral MI The occlusion occur in first diagonal branch of left anterior descending coronary artery

Atrial flutter 2/1 block Flutter wave appear clearly in the inferior lead ( downward fluttering) He take adenosine to increase the block and confirmation the atrial flutter Flutter wave appear clearly for few seconds and then return rapid atrial flutter My massages 1- any patient has heart rate about 150 bpm, narrow complex, no P wave is atrial flutter until prove otherwise 2- atrial flutter treatment as atrial fibrillation that mean need anticoagulant 3- echo study of patient with atrial flutter usually has atrial abnormality like dilation, valvular disease 4- something the patient diagnosis as AVNRT ( SVT) and when take adenosine the rhythm decrease and then re increase And misdiagnosed by doctor as resistant SVT 5- when you have any information try to share it with your friends .

Benign early repolorization syndrome 1 wide spread ST elevation. 2 ST elevation are concave upward. 3 notching at the J point 4 no reciprocal ST depression 5 no PR interval depression 6 asymmetrical large T wave 7 hight of ST / peak ofT wave <0. 25

Chest tightness with palpitations - look to the red arrow there are st elevation in inferior leads - looks to yellow arrows there are reciprocal st depression - look to black arrow there are three consecutive ventricular ectopic beats ( non sustained VT ) due to ischemia Conclusion: inferior STEMI with non sustained VT My messages: - search the cause of palpitations. - ectopic beats could be signs of ischmia even without st changes - be calm and well organised in the reading the ecg paper and put the priority to the clinical presentation

Inferior, posterior and lateral MI due to occlusion of circumflex artery. The circumflex artery supply the lateral wall, posterior wall and inferior wall. Occlusion of circumflex manifested by - ST elevation in lead II equal or more than lead III. - no reciprocal ST depression in lead I. - evidence of lateral wall infarction by ( ST elevation in lateral lead V5,6 or lead I and avL) . The right coronary artery also supply the inferior wall and posterior wall. And you can differentiate it from the circumflex by - ST elevation in lead III>lead II - reciprocal ST Depression in lead I - sometimes right ventricular involvement by ST elevation in V1 or avR or right side ECG.

Acute pericarditis ECG finding that pass with acute pericarditis - widespread ST elevation - PR interval depression (compare PR interval with TP segment) - ST depression and PR elevation in avR - no reciprocal ST depression - ST elevation not localised to specific area - T wave to too much prominent ( as in begin early repolorization ) - hight of ST / hight of T more than 0.25 - positive spodick sign ( TP segment sloping downward) - on serial ECG no dynamic st changes - negative Troponine titter

Anterior-inferior STEMI • ST elevation is present throughout the precordial and inferior leads • There are hyperacute T waves, most prominent in V1-3 • Q waves are forming in V1-3, as well as leads III and aVF • This pattern is suggestive of occlusion occurring in “type III” or “wraparound” LAD (i.e. one that wraps around the cardiac apex to supply the inferior wall)

Sinus tachycardia with LBBB and non sustained VT

Paroxysmal attacks of TDP

1- STEMI 2- VF

Sinus rhythm with first degree heart block. PR interval more than 0.20 second

Wellen syndrome type A

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