زكاة العلم الدكتور محمد البيضاني

what is your First action to the patient?

ECG show 1- No p wave 2- rapid heart rate about 165 bpm 3- regular 4- left axis deviation 5- upper normal QRS duration between 0.1– 0.14 seconds 6- pattern of RBBB ( rsR in V1) Conclusion: as the patient young age , negative history of IHD, SHD ,,,,, . ECG show tachycardia, No p wave , slightly wide QRS , left axis deviation and RBBB These features pass with idiopathic ventricular tachycardia type ( left anterior fascicular tachycardia) Acute treatment - vagal nerve stimulation - adenosine - beta blocker - CCB especially verapamil which is treatment of choice according to this the pathway responsible for tachycardia called verapamil reentry circut - sometime lidocaine, amidarone - synchronised DC shock Definitive treatment is ablation Notes - this condition usually miss diagnosed as SVT with block. - after termination of tachycardia these no RBBB pattern unless there is already block - it is difficult to distinguish the fascicular from VT after age 45 as the patient may had ischemia , structural abnormalities that make the decision difficult - idiopathic VT ( 90% right ventricular outflow tachycardia, 10% fascicular tachycardia. Left anterior fascicular tachycardia take 9% of fascicular tachycardia and left posterior tachycardia take 1% of fascicular tachycardia).

20 years old male with negative history of Ischmic heart disease, structural heart disease, valvular heart disease and congenital heart disease. Presented with palpitations, he report history of palpitations two times before 6 months that pass spontaneously. Any how the S electrolytes was normal and previous ECG was sinus rhythm without bundle block. See the explanation in the first comment 😹

In general Features pass with VT ( not all present in this ECG). - old age - history of IHD - don’t had history of palpitations since young age that passed spontaneously or with IV medication - extreme left axis deviation - QRS in pericardial leads in same direction ( concordanc). - fusion beats - capture beats - WRS duration more than 4 small square.

Old age male with history of IHD Presented with palpitations.

Ventricular tachycardia in patient with heart failure treatment with synchronised DC shock. After DC shock the ECG show - frequent ventricular ectopy which is the source of VT - Q wave and poor progression of R wave in pericardial indicate old ischemic which is the causes of VT.

1- flattening of P wave until loss in baseline which appears in Lead II (black) 2- peak T wave which becomes wide base ongoing decrease in hight as S k increase (red) 3- QRS become wide (green) 4- impending Sine wave formation which appears clearly in lead I (yellow). هذا قرائتي الشخصيه للتخطيط ممكن صح وممكن لا يقال المريض اتوفا ورا لحضات من استلامه وتعالج على اساس shockable VT سالت احد اخصائي القلبيه كال VT with Lbbb بس اني مصر انو hyperkalemia ولو مستلم المريض تحت كل الضروف انطي كالسيوم. كلامي لايعتبر حجه شرعيه تكدرون تستفسرون بس اني مصر و جدا على رائي ولو مستلم المريض اعالجه ك hyperkalemia until prove otherwiseا منو يشاركني برائي

الي يحلل التخطيط عظيم؟

6 years old presented with fever and tachycardia. ECG show T wave inversion in right pericardial leads ( juvenile T wave inversion which is normally up to 18 years old, sometimes persistent up to 45 years old and called persistence juvenile T wave inversion). No juvenile T wave inversion above 45 years old.😜

ECG (1):is AVNRT. ECG (2): atrial fibrillation. The patient had chronic AF and develop SVT. After the metoprolol The patient return to original rhythm which is AF.

45 years old men with hypertension and smoking presented with palpitations as in ECG (1). He take metoprolol ampull and the result ECG (2) What’s your interpretation of the case?

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

50 years old smoker presented with chest tightness and palpitation ?

ECG Features demonstrating the Digoxin Effect( not toxicity). Digoxin effect refers to the presence on the ECG of: • Downsloping ST depression with a characteristic “reverse tick” or “Salvador Dali sagging” appearance • Flattened, inverted, or biphasic T waves • Shortened QT interval Other Digoxin effect features Additional ECG Features • Mild PR interval prolongation, up to 240 ms (due to increased vagal tone) • Prominent U waves • Peaking of the terminal portion of the T waves • J point depression (usually in leads with tall R waves)

60 years old presented with abdominal pain?

30 years old developed syncopal attack during football match . In the ED he develop VF and take 150J and asynchoronised DC shock. His father was dead at 37 years old. ECG show typical features of Brugada syndrome type 1 . Permanent ICC was implemented later on 😁.

-(2)- - Brugada syndrome: is due to a mutation in the cardiac sodium channel gene. This is often referred to as a sodium channelopathy. Over 60 different mutations have been described so far and at least 50% are spontaneous mutations, but familial clustering and autosomal dominant inheritance has been demonstrated. - brugada syndrome has structurally normal heart. Clinical features - asymptomatic - syncopal attack - VT - VF - sudden death Type 1 • Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave. • This is the only ECG abnormality that is potentially diagnostic. Type 2 • Brugada Type 2 has >2mm of saddleback shaped ST elevation. Type 3 • Brugada type 3: can be the morphology of either type 1 or type 2, but with <2mm of ST segment elevation ECG abnormality must be associated with one of the following clinical criteria to make the diagnosis: • Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT). • Family history of sudden cardiac death at <45 years old . • Coved-type ECGs in family members. • Inducibility of VT with programmed electrical stimulation . • Syncope. • Nocturnal agonal respiration ECG changes can be transient with Brugada syndrome and can also be unmasked or augmented by multiple factors: • Fever • Ischaemia • Multiple Drugs ◦ Sodium channel blockers eg: Flecainide, Propafenone ◦ Calcium channel blockers ◦ Alpha agonists ◦ Beta Blockers ◦ Nitrates ◦ Cholinergic stimulation ◦ Cocaine ◦ Alcohol • Hypokalaemia • Hypothermia • Post DC cardioversion Definitive treatment is implemented cardiac defibrillator

(1) - 80% of causes of sudden cardiac death related to ischemic heart disease. -Those with MI and heart failure have structural changes in the wall of the heart. - the ischemic wall trigger for arrhythmia and VF. The necrotic wall become thin fibrosed which also trigged for arrhythmia. So the patient develop ventricular ectopic beat , non sustained VT , sustained VT and VF. - Those with heart failure and EF less than 35% are risky for VF thats why we implant intracardiac defibrillator to prevent sudden death

التلغرام شغال عدكم!

حياكم الله ودكم نحجي على sudden cardiac death هيج لمحات بسيطه باوقات مختلفه بس اريد تكونون متفاعلين