الفيروس الجديد والانفلاونزا

اي احد دتطول اعراضه فوك ال ٧ ايام
خل يراجع طبيب باطنية
ويسوي X ray
حتى الواحد يتأكد ما صارت
secondary viral pneumonia
خاصة اذا عدكم احد جبير بالبيت ومناعتهم ضعيفة لان مضاعفاتها مزعجة ومتعبة * اذا بقت بدون علاج
وما راح يفيد وياها اي انتي بايتك لان هي فايرل مو بكتريل بهالحالة

42 Yrs Old Male with Chest Pain first time
Normal BP
PMH unremarkable
DDX

السلام عليكم👋🏻
نسولف طوارئ💛

Sob in ckd
اكثر مرضى اخاف منهم بالطوارئ اهل ckd
بحيث من يدخل اي مريض ckd حتى لو جاي tonsillitis ومر بطريقه للطوارئ
اعامله معامله emergency واستعبد شكو شي طارئ ( ابد ما ينحرزون فجأة مرات arrest)بحيث صار عندي شي اسمه ckd pt phobia او ckd pt trauma🫠

نكمل:

طبعا مرضى renal failure تعرفهم من الوجه
Earthy color
فمن يطب من بعيد تعرفله قبل لا يحجي حتى تخلي ببالك

المهم اجه المريض dyspnic وكال دكتورة ما اكدر انام ابد اختنك كلش وكل مرة اختنك هيج
يعني orthopnea
Pmh:dm, ht, ckd on dialysis, on diuretic use (2 tab/day)

On examination
🔹gcs15
Can’t lying flat
بحيث ردت اسويله تخطيط كال ما اكدر انام مستحيل
🔹Dyspnic
🔹Tachypnic

🔹Orthopnea
🔹Spo2 88%
🔹Pr 115
🔹Bp 130/90
🔹bilateral leg edema
طبعا ما يمر مريض ckd without chest auscultation
🔹looks for crepitation or diminished air entry or muffled heart sounds (to exclude pulmonary edema or pleural effusion or cardiac tamponade)

المريض جان بس crept chest
لهنا وصلت انو سبب dyspnea
Pulmonary edema due to ckd
🔺send for full investigations+ecg
اكيد التخطيط ضمن vital signs علمود hyperkalemia and mi

Mx:
بالبداية خليت عالمريض على O2 and semisetting position
الحمد لله ضغطه يسمح 130/90mmhg

تاخذ مدررات؟ اي ، شكد تاخذ؟
حباية باليوم 40mg orally

🔷 اذا المريض اصلاً ياخذ lasix الجرعة المطلوبة هي
👉🏻the dose is 1-2.5 times the pt previous total daily oral dose
👉🏻divided dose in half and administered iv bolus every 12 hours

المريض جان ياخذ 40mg , الجرعة المطلوبة هي.
👉🏻40- 100mg

🔺double the dose and repeated 30- 60minutes based on urine output
🔺maximal dose (160-200mg) per injection

انطيته
Lasix 3 ampoule
رجعت وره ساعه حتى اشوفه بعده المريض dyspnic , can’t lying flat
Uop 90cc/ hr
فضاعفت الجرعة وره ساعة
انطيته 120mg يعني 6amp

وشفته وره ساعة ونص
Wow 😮
🔹No sob
🔹Pt is lying flat
🔹Without o2
ولازم يبقى على lasix every 12 hr
بعدين طلعو على مسؤوليتهم من شافو صار زين وما قبلوا يبقون وكالوا اصلا عنده موعد غسل باجر ( جان عدهم جدول )

🔻اهم شي ننطي ال lasix خلال ٣ الى ٥ دقايق لان rapid injection induced tinnitus and hearing loss

🩵شي مهم :

اي مريض
Ckd
اشوفه يستحق غسل او لا من يدخل واكتب بالكارت
Need dialysis or not
يعني هذا المريض جان
🔹️Sk 4.5 so no refractory hyperkalemia
🔹️pulmonary edema response to tx so not refractory pulmonary edema
🔹️no uremic encephalopathy
صاحي وواعي ويحجي
Conscious, oriented،not irritable,

🔹️no uremic pericarditis
اصلا ما عنده chest pain

🔹️no severe acidosis
فجان ما يحتاج emergent dialysis
👋🏻👋🏻👋🏻

#CKD
#الكروب_الطبي_التعليمي

هذا التخطيط just for fun يعني😁
صراحة شفته منشور بالfacebook بدون جواب، كدعاية لاحد كورسات الECG، لذلك ما عندي قصة المريض الكاملة، بس هو التخطيط واضح وحلو.

ملاحظة: شوي غيرت هستري المريضة، بس هي المريضة صحيح عمرها 102😁

Left arm artefact !!

👆At first glance, the ECG looks scary, it looks like some form of regular wide complex tachycardia (regular WCT), but if you look at lead II, you can see that it is spared (green arrows) and does not show regular WCT. Why?

Let me tell you a little secret about lead II, in fact lead II is the only lead in the ECG that does not need electrical inputs from the left arm electrode, every other ECG lead is dependent directly or indirectly (via Wilson’s central terminal) on left arm electrode except lead II, as lead II is dependent only on the inputs coming from right arm and left leg electrodes.

Therefore, any continuous artefact coming from the left arm will be recorded by all 11 leads except lead II, things like tremor in the left arm can produce an artefact in the ECG that look like regular WCT. Spared lead II is a strong and simple observation that will save a lot of thinking and possibly unnecessary actions.

Another observation that strongly suggests an artefact, is that the amplitude of the waves in the limb leads is much larger than that in the chest leads (normally, cardiac electrical events should be more pronounced in the chest leads as the chest leads are more closer to the heart), it means that the source of these large waves is closer to the limbs compared to the heart (left arm tremor).
The waves in the chest leads are about 1/3 that in bipolar limb leads (lead I, II and III), while the waves in the unipolar limb leads (aVR, aVL, and aVF) are about 2/3 that in lead I, II and III. It means that these waves are not coming from the heart.

Let’s analyse lead II (fortunately lead II is the rhythm strip), you can see that the ventricular rate is around 30bpm, while the atrial rate is around 80bpm, and the P waves are upright (suggesting sinus origin) and regular (red arrows), there is clearly AV dissociation, as there is no relation between atrial and ventricular events, therefore, there is complete AV block, and the QRS complexes are either ventricular escape rhythm or junctional escape rhythm with some form of intrventricular conduction delay (I see slightly wide QRS complexes). I support junctional escape rhythm, as the T waves are concordant with the QRS in lead II. Beat #4 is a PVC.

This patient has Parkinson’s disease, knowing that would make the decision much clear and easier, but I avoided mentioning this important note in the presentation to raise the level of the challenge😁

Thank you for reading, I hope the above helps, I learned this from Dr. Ken Grauer, he kindly explained a similar case for me long time ago.

Ahmed Marai

Additional notes:
▫️Lead III, is the only lead in the ECG that does not depend on electrical inputs coming from right arm electrode
▫️Lead I, is the only lead in the ECG that does not depend on electrical inputs coming from left leg electrode

Young age male, heavy smoker, known case of asthma presented with sob for 3 days preceded by flu like illness
This is his ECG 🤝

Old age female, known case of HTN and IHD presented with 1 hour hx of chest pain, burning in nature, no radiation, associated with nausea without vomiting ?

A 72-year-old woman with a history of hypertension presented with an unpleasant awareness of her heartbeat and chest discomfort. On examination, her pulse rate was 30 bpm, with fine basal crackles and distant heart sounds. CXR showed Kerley B lines. One month earlier, she had an episode of palpitations and was diagnosed with paroxysmal atrial fibrillation, for which she was started on flecainide and bisoprolol.

This is a very interesting case. It was originally posted by Dr. Ali A. Rasheed, who kindly explained it to me a year ago.

Old age pt. With uncontrol HT presented to emergency department with sever headache and DLOC ?
BP 190/110
What happened?
Dx.?
How to deal with this pt. In ER ?

هذا المريض اجاني فقط
Sever headache

No chest pain , no dyspnea
PMH : DM , HTN
BP : 180/100

شتكولون شنسويله ؟
الكيس من د.حيدعبدالرضا 👏

#باطنية

Sent for CT هذا البيشنت لازم
طبعا ال SAH يجي ب finding of STEMI مو بس cerebral T wave

بالنتيجة المريض اندز CT و فعلا طلع SAH

Managment of HTN in patients with CKD

#cardionotes

#هام_جدا

المحكمة الاتحادية تقرّر إنهاء أعمال مجلس النواب وتحويل الحكومة إلى "حكومة تصريف أعمال" فيما يواصل رئيس الجمهورية ممارسة مهامه.

https://t.me/MydoctorA96

التعيين : سلملي

Very tough one⚡️⚡️⚡️

I would love to hear your interpretation, and learn from you, before I share my thoughts and first impression on this ECG.

In fact, this Case was posted by “ECG weekly” on facebook, unfortunately they don’t share the answer with the post.

👇This is my thoughts on this ECG

اغلب المرضى (حوالي ٧٠٪؜) اللي بيحصل لهم DKA مع ال SLG2is، السكر عدهم يكون اقل من ٢٥٠ وجزء كبير منهم السكر يكون اقل من ٢٠٠ (مو لازم السكر يكون مرتفع )

Risk factors of DKA with SGLT2 inhibitors include
Very-low-carbohydrate diets
Prolonged fasting
Dehydration
Excessive alcohol intake

#emergency_note

This post is for discussion, and I’d love to hear your thoughts.

We were always taught that thrombolytics are not indicated in patients with Non-STEMI. The usual explanations include that thrombolytics might worsen a partial occlusion into a complete one, or that they could generate emboli that block distal coronary vessels, among other explanations.

What do you think? Why are thrombolytics truly not recommended for patients with Non-STEMI?