Methylene blue is used in vasoplegic shock when high-dose norepinephrine, vasopressin, and steroids fail to maintain MAP ≥ 65 mmHg. It works by inhibiting nitric oxide (NO)-mediated vasodilation, helping restore vascular tone.

Indications for Methylene Blue in Septic Shock

• Refractory Septic Shock (MAP < 65 mmHg despite high-dose vasopressors).
• Vasoplegia (Distributive Shock) with High Cardiac Output, Low SVR.
• Septic Shock with Profound Acidosis (Lactate > 4 mmol/L, pH < 7.2).
• Post-cardiopulmonary bypass vasoplegia (if refractory to catecholamines).

For the Infusion Protocol

1. Loading Dose (Slow IV Bolus Over 15-30 Minutes):
   • 1–2 mg/kg IV over 15–30 minutes
   • Dilution: Mix 50 mg (5 mL) of 1% methylene blue in 100 mL Normal Saline (NS) or D5W.
   • Infusion rate: Administer at 200–300 mL/hour to avoid hypotension.

2. Continuous Infusion (If Needed):
   • 0.25–0.5 mg/kg/hour IV infusion for 6–12 hours.
   • Dilution: Prepare 50 mg in 500 mL NS or D5W and run at 2–5 mL/hour (titrate based on response).

For Monitoring & Precautions
Monitor BP every 5 minutes during bolus → Rapid infusion may cause paradoxical hypotension.
Check methemoglobin levels if prolonged infusion (>6 hrs).
Watch for rebound hypotension after stopping infusion.
Monitor renal & hepatic function (risk of toxicity in dysfunction).

still my best stimulant video

Premature ventricular contractions (PVCs) can be due to automaticity or reentry. They are often sensitive to sympathetic stimulation and can be a sign of increased sympathetic tone; myocardial ischemia; hypoxia; electrolyte abnormalities, particularly hypokalemia; or underlying heart disease.

During myocardial ischemia or in association with other heart disease, PVCs can be a harbinger of sustained ventricular tachycardia or ventricular fibrillation.

The ECG characteristics of the arrhythmia are often suggestive of whether structural heart disease is present.
PVCs with smooth uninterrupted contours and sharp QRS deflections suggest an ectopic focus in relatively normal myocardium, whereas broad notching and slurred QRS deflections suggest a diseased myocardial substrate.

The QRS morphology also suggests the likely site of origin within the ventricle. PVCs that have a dominant S wave in V1 , referred to as left bundle branch block–like configuration, originate from the right ventricle or interventricular septum. Those with a dominant R wave in V 1 originate from the left ventricle.
A superior frontal plane axis (negative in II, III, and aVF) indicates initial depolarization of the inferior wall (diaphragmatic aspect of the heart), whereas an inferior frontal plane axis (positive in II, III, and aVF) indicates an origin in the cranial aspect of the heart.

The location of arrhythmia origin often suggests the nature of underlying heart disease.
Most ventricular arrhythmias that are not associated with structural heart disease have a left bundle branch block–like configuration. PVCs with right bundle branch configuration are more likely to be associated with structural heart disease.
Multiple morphologies of PVCs (multifocal PVCs) are also more likely to indicate structural heart disease.

Approach to Fluid overload that is refractory to usual diuretics therapy:

1. Start Furosemide infusion (5-40 mg/hr).
   Some recommends oral torasemide 100 mg/12 hrs.

2. If still no response, start with sequential nephronal block:
   -- add oral metolazone 5-10 mg/day given 30 min before loop diuretics.
   -- add spironolactone 25-100 mg/day.

3. Maintain serum albumin higher than 2.5 g/dL by infusion of 50-100% ml 25% albumin infusion.

4. Restrict sodium: <2 g/day.
   Restrict fluids to (urine output - 500).

5. Correct hypokalemia and hypomagnesemia to enhance diuretic efficacy.

6. if hyponatremia developed, tolvaptan (ADH antagonist) can be used.

7. For refractory cases, consider ultrafiltration in settings like congestive heart failure or renal failure when diuretics fail to mobilize fluid.

Massive Transfusion Protocol (MTP):

MTP is a systematic approach to the resuscitation of patients with massive hemorrhage, often defined as requiring the replacement of one blood volume within 24 hours, >10 units of packed red blood cells (PRBCs) within 24 hours, or >3 units in 1 hour with continued bleeding.

Goals:

Restore hemodynamic stability.

Achieve and maintain hemostasis.

Minimize complications such as coagulopathy, hypothermia, and acidosis (the "lethal triad").

Components of MTP:

1. Initial Activation Criteria

Suspected massive hemorrhage (e.g., trauma, obstetric hemorrhage, GI bleed).

Clinical signs: hypotension, tachycardia, or clinical shock with uncontrolled bleeding.

Laboratory triggers:

Base deficit >6 mmol/L.

INR >1.5.

Hemoglobin <7 g/dL.

1. Resuscitation Ratios

Administer blood products in a balanced ratio to prevent coagulopathy:

PRBCs : Fresh Frozen Plasma (FFP) : Platelets = 1:1:1 or 2:1:1.

PRBCs: To restore oxygen-carrying capacity.

FFP: To replenish coagulation factors (start with 4 units after 4 PRBCs).

Platelets: Maintain platelet count >50,000/μL (>100,000/μL in neurosurgical or obstetric cases).

1. Adjunctive Therapies

Tranexamic Acid (TXA):

Dose: 1 g IV over 10 minutes, followed by 1 g over 8 hours.

Administer within 3 hours of trauma if indicated.

Cryoprecipitate: Administer if fibrinogen <100-150 mg/dL.

Dose: 10 units or target fibrinogen >200 mg/dL.

Calcium Replacement:

Use calcium gluconate or calcium chloride to prevent hypocalcemia from citrate in blood products.

Goal ionized calcium >1.1 mmol/L.

Correct Hypothermia:

Use warming devices to keep body temperature >36°C.

Correct Acidosis:

Target pH >7.2 using bicarbonate if necessary.

1. Laboratory Monitoring

Perform serial labs every 30–60 minutes or after every major intervention:

Complete blood count (CBC).

Coagulation studies (PT/INR, aPTT).

Fibrinogen levels.

Electrolytes, calcium, and lactate.

1. Endpoints of Resuscitation

Hemodynamic stability achieved.

Control of bleeding (surgical or radiologic).

Normalization of lab parameters:

INR <1.5.

Fibrinogen >200 mg/dL.

Platelets >50,000/μL.

Complications to Monitor For:

Volume overload (e.g., pulmonary edema).

Hyperkalemia or citrate toxicity.

Disseminated Intravascular Coagulation (DIC).

Cessation of MTP:

Stop MTP when bleeding is controlled, or laboratory targets are met.

Transition to standard care for anemia and ongoing management.

This protocol is adapted and customizable to institutional policies and patient-specific factors.

Insulin in DKA:

1. the initial dose is 0.1 unit/kg, with target RBS refuction by 50-90 mg/dl per hr.
   No max dose.
   و يا ريت العالم تقتنع بهالشي.
   بيشنت الرندوم ماله ما ينزل عن 500، و مبقينه 7 وحدات بالساعة، من تحاجيهم يبقى يعترض بشي هو اصلا جاهل بيه.

2. Adminstration:
   IV route is preferred.
   SC or IM route can be used in mild to moderate DKA.

IV:
The preferred way is to add 50 units insulin in 50 cc NS (final conc is 1 unit/1 ml).
الكثير يخلي 50 وحده ب 500 سيسي.
يعني اذا تريد تنطي 14 وحده انسولين، لازم تنطي 140 سيسي
و هذا يعتبر
hidden not calculated fluid
ممكن يدخل البيشنت بمضاعفات انت ما ماخذ بالك منها.
فمن تنطي 140 سيسي، لازم الفلود الي حاسبه تقلل منه 140، و هذا الشي لم و لن يطبق.

1. contraindications:
   insulin should be #discontinued if serum K was <3.3 even if he has severe acidosis !!!!

According to UpToDate, the target of albumin therapy is not primarily to normalize serum albumin levels. Instead, the goals depend on the clinical context:

A. Restoring intravascular volume: In cases like shock or hypovolemia, the focus is on improving hemodynamic stability and maintaining adequate perfusion, rather than achieving a specific serum albumin level.

B. Managing hypoalbuminemia in specific conditions: In conditions such as nephrotic syndrome or liver disease, albumin therapy is used to help maintain oncotic pressure, reduce edema, and improve fluid balance, not necessarily to normalize serum albumin.

C. Post-paracentesis in cirrhosis: Albumin is given to prevent circulatory dysfunction and renal impairment after large-volume paracentesis rather than targeting albumin levels.

In summary, the therapeutic aim is usually symptom control (e.g., stabilizing circulation, reducing edema) and preventing complications rather than strictly normalizing serum albumin levels. Monitoring clinical response (e.g., blood pressure, urine output) is often more critical than achieving a target albumin concentration.