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2) type 2: this is the most common form; it is observed in about 75% of cases; negative, deep, rather narrow and symmetrical T-waves, usually in V2, V3 but often in V1 and V4 and sometimes up to V5-V6; T wave changes can evolve over time from Type A to Type B pattern - An acute intracranial process (hemorrhage, trauma, carotid endarterectomy etc...) can cause dramatic T wave inversions and a prolonged QT interval on the ECG. # - Blocked premature atrial contractions occurring in a pattern of bigeminy can mimic sinus bradycardia. - Hyperacute T waves are large and broadly shaped occurring in the first few minutes of an acute myocardial infarction. -** - Electrical alternans occurs when every other QRS complex has varying amplitudes and is from the heart swaying within a large pericardial effusion,Another setting associated with electrical alternans is supraventricular tachycardia (SVT), especially when the rate is rapid. Although it has been suggested that electrical alternans during SVT is indicative of atrioventricular re-entrant tachycardia, this finding can be seen in any rapid SVT, we call it pseudoelectrical **alternans because it is disappeared once the arrhythmias aborted. - Bidirectional ventricular tachycardia occurs when every other beat has a different QRS morphology and each morphology meets VT criteria. This is caused most commonly by digoxin toxicity and also in catecholaminergic polymorphic ventricular tachycardia.The proposed arrhythmia mechanism is triggered activity arising alternately from the left anterior and posterior fascicle. - A fascicular block is a combination of a right bundle branch block with a left anterior or posterior fascicular block. # - A trifascicular block is a bifascicular block with a first degree AV block. - Ostium primum atrial septal defects cause an incomplete right bundle branch block with left axis deviation. Ostium secundum atrial septal defects cause an incomplete right bundle branch block with right axis deviation.

*Info copied from our another group* # # # ECG PEARLS**** # - The three irregularly irregularly irregular rhythms are atrial fibrillation, atrial flutter with variable conduction and multifocal atrial tachycardia (similar to wandering atrial pacemaker). # -Treat a wide-complex tachycardia like ventricular tachycardia until proven otherwise. Use the Brugada criteria to distinguish ventricular tachycardia from SVT with aberrancy. # - If no P waves can be seen and the QRS complexes are irregularly irregular, then atrial fibrillation is present. # - ST segment elevation from pericarditis is diffuse (all leads except aVR and V1) and concave upward. . PR segment depression can be from acute pericarditis or an atrial infarction. . Diffuse T wave inversion is stage III of the ECG changes in pericarditis. . Pericarditis can be distinguished from early repolarization by the ratio of the T wave to the ST elevation, in early repolarization (the ST elevation is < 25% of the T wave amplitude). The ST elevation from early repolarization resolves with exercise while that of pericarditis does not # - Acute myocardial infarction can be diagnosed on an ECG in the setting of a left bundle branch block (LBBB) on occasion using Sgarbossa Criteria or identifying Chapman’s sign or Cabrera’s sign. # - The causes of the R wave in lead V1 greater in amplitude than the S wave include right bundle branch block, posterior myocardial infarction, WPW type A, right ventricular hypertrophy, ventricular tachycardia with right bundle morphology and in ** Duchenne’s muscular dystrophy. - Epsilon wave (most specific finding, seen in 30% of (ARVD/C) patients ) a deflection after the J point at the beginning of the ST segment .It represents delayed activation of the right ventricular **in (ARVD/C) a “grassy knoll” # - An Osborne wave classically occurs in the setting of hypothermia and is seen as a spike at the end of the QRS complex. An Osborne wave can also occur from **hypercalcemia. ** - Hypercalcemia shortens the QT interval. -- A prolonged QT interval from hypocalcemia has a lengthened ST segment, then normal appearing T wave # - The most common ECG finding of an acute pulmonary embolism is sinus tachycardia, however the classic finding is an S wave in lead I, Q wave in lead III and inverted T waves in lead III (S1Q3T3 pattern). # - Clockwise atrial flutter causes positively deflected P waves in the inferior leads while counterclockwise atrial flutter causes negative deflected P waves in the inferior leads. # - Multifocal atrial tachycardia (MAT) requires 3 different P wave morphologies in 1 ECG with a QRS complex rate of > 100. - Wandering atrial pacemaker (WAP) requires 3 different P wave morphologies in 1 ECG with a **QRS complex rate of < 100. ** - Idioventricular rhythms meet criteria for ventricular tachycardia, but have a heart rate of** < 100. - Low voltage on the ECG can be caused by obesity, COPD, pericardial effusion, severe hypothyroidism, subcutaneous emphysema, massive myocardial damage/infarction**, or infiltrative/restrictive diseases such as amyloid cardiomyopathy. # - Dextrocardia shows negative QRS complex in lead I with negative P and T wave in this lead. There is low voltage in leads V4 through V6 (unlike limb lead reversal which has normal voltage in these leads, but negative QRS in lead I). # - Hypokalemia causes U waves in the ECG seen as a positive wave just after the T wave. - Hyperkalemia causes peaked T waves initially, then an intraventricular conduction delay with a widened QRS complex, then bradycardia and eventually a “sine wave” pattern ensues. - Wellens’ syndrome the changes in T-wave can take 2 forms: 1) type 1: observed in approximately 25% of Wellens’ syndrome cases; biphasic T-waves (initial positivity followed by negativity) most often in V2, V3 but occasionally in V1 and up to V5-V6;

👉 *IMPORTANT 48* 👈 *For station 2 n 5* Please remember For confirmation of diagnosis of seronegative spondylarthropathies presence of HLA B27 is mandatory ( alongwith negative automimune profile) so always mention it in investigation of these conditions as we may have patients having conditions mimicking them without HLA but we don't classify them as seronegative spondyarthropathy. Good luck

👉 *IMPORTANT 47* 👈 *HAS-BLED Score* Hypertension (systolic blood pressure >160 mmHg) 1 Abnormal renal and liver function* (1 point each) 1 or 2 Stroke 1 Bleeding tendency/predisposition* 1 Labile INRs (if on warfarin)* 1 Elderly (eg, age >65 y) 1 Drugs or alcohol (1 point each)* 1 or 2 A HAS-BLED score of ≥3 indicates that caution is warranted when prescribing oral anticoagulation and regular review is recommended. *Abnormal renal function is classified as the presence of chronic dialysis, renal transplantation, or serum creatinine ≥200 mmolL. Abnormal liver function is defined as chronic hepatic disease (eg, cirrhosis) or biochemical evidence of significant hepatic derangement (bilirubin 2 to 3 times the upper limit of normal, in association with aspartate aminotransferase/alanine aminotransferase/alkaline phosphatase 3 times the upper limit normal, etc), history of bleeding or predisposition (anemia), labile INR (ie, time in therapeutic range <60%), concomitant antiplatelets or nonsteroidal anti-inflammatory drugs, or excess alcohol. Good luck

☝️ *IMPORTANT 46* ☝️ *Some info about heart sounds* *The 1st heart sound (S1)* Represents closure of mitral and tricuspid valves. Splitting in inspiration may be heard and is normal. • *Loud S1* In mitral stenosis, because the narrowed valve orifice limits ventricular filling, there is no gradual decrease in flow towards the end of diastole. The valves are, therefore, at their maximum excursion at the end of diastole, and so shut rapidly leading to a loud S1 (the ‘tapping’ apex). S1 is also loud if diastolic filling time is shortened, eg if the PR interval is short, and in tachycardia. • *Soft S1* occurs if the diastolic filling time is prolonged, eg prolonged PR interval, or if the mitral valve leaflets fail to close properly (ie mitral incompetence). *The intensity of S1 is variable* in AV block, AF, and nodal or ventricular tachycardia. Good luck.

☝️ *IMPORTANT 45* ☝️ *Please remember for station 2 n 5* *Massive pulmonary embolism can cause fainting* and has appeared quite often as a cause of fainting. So plz be alert and always try to get hints from the history. Good luck.

☝️ *IMPORTANT 44* ☝️ *Some abnormalities of the JVP* • *Raised JVP with normal waveform* : Fluid overload, right heart failure. • *Fixed raised JVP with absent pulsation* : SVC obstruction. • *Large a wave* : Pulmonary hypertension, pulmonary stenosis. • *Cannon a wave* : When the right atrium contracts against a closed tricuspid valve, large ‘cannon’ a waves result. Causes—complete heart block, single chamber ventricular pacing, ventricular arrhythmias/ectopics. • *Absent a wave* : Atrial fibrillation. • *Large v waves* : Tricuspid regurgitation—look for earlobe movement. • *Constrictive pericarditis* : High plateau of JVP (which rises on inspiration—Kussmaul’s sign) with deep x and y descents. • *Absent JVP* : When lying flat, the jugular vein should be filled. If there is reduced circulatory volume (eg dehydration, haemorrhage) the JVP may be absent. Good luck.

☝️ *IMPORTANT 43* ☝️ Regarding JVP the pulsation is venous if it is • Usually impalpable, and obliterated by finger pressure on the vessel. • Rises transiently with pressure on abdomen (abdominojugular reflux) or on liver(hepatojugular reflux), and alters with posture and respiration (disappears when patient sits from lying flat). • Usually has a double pulse for every arterial pulse. ( Concomitantly palpate the arterial pulse ) Good luck.

Here is the recording of yesterday's session. Please try to listen the recording in 1 day as Zoom provides limited space and it automatically deletes the old recordings to keep space for new ones ..so the recording will not be available after 1 day☝️☝️☝️

16Ch+cW4

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*Announcement for Online Session No 69* *2 Oct 2022* DEAR DOCTORS : MAY I HAVE YOUR ATTENTION PLEASE : *Today we will have an online session on Zoom discussing 1 station 2 ( History Taking )* regarding our preparation for MRCP PACES ( UK ) TIMINGS : Saudia Arabia: 3 pm Pakistan : 5 pm Bangladesh : 6 pm India : 5 30 pm Singapore : 8 pm Hong Kong : 8 pm Malaysia : 8 pm Egypt : 2 pm Libya : 2 pm Bahrain : 3 pm Burma ( Myanmar ) :6 30 pm Sudan : 2 pm UAE : 4 pm UK : 1 00 pm Ireland ( Dublin ) : 1 00 pm Afghanistan : 4 30 pm Kenya : 3 00 pm Germany ( Berlin ) : 2 00 pm Nigeria : 1 00 pm Japan ( Tokyo ) : 9 00 pm Denmark : 3200 pm Qatar : 3 00 pm Oman : 4 00 pm Italy : 2 00 pm Indonesia : 7 00 pm Mauritius : 4 00 pm ( please Google for your local time zones to avoid any inconvenience ) Zoom meeting link will be shared 5 minutes before start time. The candidate for todays session has been selected. GOOD LUCK.

*Announcement for Online Session No 69* *2 Oct 2022* DEAR DOCTORS : MAY I HAVE YOUR ATTENTION PLEASE : *Tomorrow we will have an online session on Zoom discussing 1 station 2 ( History Taking )* regarding our preparation for MRCP PACES ( UK ) TIMINGS : Saudia Arabia: 3 pm Pakistan : 5 pm Bangladesh : 6 pm India : 5 30 pm Singapore : 8 pm Hong Kong : 8 pm Malaysia : 8 pm Egypt : 2 pm Libya : 2 pm Bahrain : 3 pm Burma ( Myanmar ) :6 30 pm Sudan : 2 pm UAE : 4 pm UK : 1 00 pm Ireland ( Dublin ) : 1 00 pm Afghanistan : 4 30 pm Kenya : 3 00 pm Germany ( Berlin ) : 2 00 pm Nigeria : 1 00 pm Japan ( Tokyo ) : 9 00 pm Denmark : 3200 pm Qatar : 3 00 pm Oman : 4 00 pm Italy : 2 00 pm Indonesia : 7 00 pm Mauritius : 4 00 pm ( please Google for your local time zones to avoid any inconvenience ) Zoom meeting link will be shared 5 minutes before start time. Any interested candidare may send a personal message to take the case GOOD LUCK.

☝️ *IMPORTANT 42* ☝️ Some Characters and volumes of pulse • *Bounding pulses* are caused by CO2 retention, liver failure, and sepsis. • *Small volume pulses* occur in aortic stenosis, shock, and pericardial effusion. • *Collapsing (‘waterhammer’) pulses* are caused by aortic incompetence, AV malformations, and a patent ductus arteriosus. • *Anacrotic (slow-rising) pulses* occur in aortic stenosis. • *Bisferiens pulses* occur in combined aortic stenosis and regurgitation. • *Pulsus alternans* (alternating strong and weak beats) suggests LVF, cardiomyopathy, or aortic stenosis. • *Jerky pulses* occur in HOCM. • *Pulsus paradoxus* (systolic pressure weakens in inspiration by >10mmHg) occurs in severe asthma, pericardial constriction, or cardiac tamponade Good luck.

☝️ *IMPORTANT 41* ☝️ *Xanthomata* are localized deposits of fat under the skin, occurring over joints, tendons, hands, and feet. *Xanthelasma* refers to xanthoma on the eyelid *Corneal arcus* is a crescentic-shaped opacity at the periphery of the cornea. Common in those over 60yrs, can be normal, but may represent hyperlipidaemia, especially in those under this age. Good luck.

*Info by courtesy of Dr Mustafa Abbass Othman* Elderly patients with BPH may be taking alpha 1 blocker drugs which may cause postural (orthostatic) hypotension. examples (tamsulosin, prazocin.....)

*POSTURAL HYPOTENSION* This is an important cause of falls and faints in the elderly. It is defined as a drop in systolic BP >20mmHg or diastolic >10mmHg after standing for 3min vs lying. Causes: Hypovolaemia (early sign); drugs, eg nitrates, diuretics, antihypertensives, antipsychotics; Addison’s ; hypopituitarism ( reduced ACTH); autonomic neuropathy ( DM, multisystem atrophy); after a marathon run (peripheral resistance is low for some hours); idiopathic. Treatment: • Lie down if feeling faint. • Stand slowly (with escape route: don’t move away from the chair too soon!). • Consider referral to a ‘falls clinic’, where special equipment is available for monitoring patient under various tilts. • Manage autonomic neuropathy, • increase in Water and salt ingestion can help (eg 150mmol Na+/day ), but Na+ has its problems. • Physical measures: leg crossing, squatting, elastic compression stockings (check dorsalis pedis pulse is present), and careful exercise may help. • If post-prandial dizziness, eat little and often; reduce carbohydrate and alcohol intake. • Head-up tilt of the bed at night increase renin release, so reduce fluid loss and imcrease standing BP. • 1st-line drugs: fludrocortisone (retains fluid) 50mcg/d; go up to 300mcg/24h PO only if tolerated. Monitor weight; beware if CCF, renal impairment, or reduced albumin as fludrocortisone worsens oedema. • 2nd-line drugs: sympathomimetics, eg midodrine (not always available) or ephedrine; pyridostigmine (eg if detrusor underactivity too).