In this high-yield episode, we build a visual memory palace down the “Highway to Hell” of emergency thrombocytopenia syndromes. Each stop reveals a unique and dangerous cause of low platelets you’ll encounter in the ED—brought to life through vivid storytelling, unforgettable characters, and layered mnemonics.

🚑 What You’ll Learn (Quick Hits):

• TTP – Thrombotic Thrombocytopenic Purpura

⚠️ Medical emergency! Think fever, renal failure, confusion, and schistocytes. LDH ↑, haptoglobin ↓. No platelets? No transfusions—start plasma exchange.

• HUS – Hemolytic Uremic Syndrome

👶 Usually in kids post-E. coli O157:H7 diarrhea. Watch for MAHA, AKI, and thrombocytopenia. Supportive care is key.

• ITP – Immune Thrombocytopenic Purpura

🍽 Isolated platelets on the floor. In kids: post-viral; in adults: chronic. No MAHA. Often treated with steroids or IVIG.

• DIC – Disseminated Intravascular Coagulation

🎲 The DIC casino. Caused by trauma, sepsis, OB complications, or malignancy. PT/PTT ↑, D-dimer ↑, fibrinogen ↓, schistocytes present. Treat the cause!

• HELLP – Hemolysis, Elevated Liver Enzymes, Low Platelets

🔥 Pregnant patient near the end of the road—hypertension, RUQ pain, and MAHA. Delivery is the only definitive treatment.

• HIT – Heparin-Induced Thrombocytopenia

🕷 A clotting catastrophe. 5–10 days post-heparin. Watch for new clots and falling platelets. Stop heparin and start a direct thrombin inhibitor like argatroban.

💡 Distinctions to Remember:

• MAHA: Present in TTP, HUS, DIC, HELLP (look for schistocytes, LDH ↑, haptoglobin ↓).

• Isolated thrombocytopenia: Think ITP.

• Timing: HIT = 5–10 days after heparin; HUS = 5–10 days after diarrheal illness.

• Treatment: TTP = plasma exchange, DIC = treat cause + FFP/cryoprecipitate, HELLP = deliver, HIT = stop heparin.

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🧠 Bonus: Visual mnemonics and character scenes help lock it all in. This episode blends storytelling, pathophys, and pattern recognition so you’ll never forget what each condition looks like in real life.

📌 Save it. Share it. Pass your boards. Help your patients.

In this unforgettable bloody podcast, we bring the clotting cascade to life through a cast of hilarious and high-yield characters designed to make clinical recall effortless under pressure.

Play Table Tennis = PTT = Inside = Intrinsic.

Play Tennis = PT = Outside = Extrinsic.”

You’ll meet:

🟢 Lucky Number 7 — our tennis-playing war cry–shouting Factor VII who kicks off the extrinsic pathway by yelling “This is WAR!” 🎾 Warfarin is his signature drug, and he’s monitored using PT/INR.

🔵 Inside, we find our Intrinsic Table Tennis Team:

• Factor XII – Haggard from Hogwarts: Looks impressive but doesn’t cause bleeding (aPTT prolonged, no clinical bleeding).

• Factor XI – The Ashkenazi Post-Op Guy: Mild bleeding, especially post-surgery.

• Factor IX – Hemophilia B Player: Jersey with a bold upside-down 9 (“B”) — classic for Hemophilia B (X-linked, prolonged aPTT, normal PT).

• Factor VIII – “Dave the ATE Guy”: Sporting an “ATE” shirt and bitten fruit logo — he’s your clue for Hemophilia A (treated with Factor VIII or DDAVP).

“Ate = Eight = Hemophilia A” and “B = looks like upside-down 9 = Hemophilia B.”

🔴 In the Commons, you’ll meet:

• Jason from Friday the 13th: Our grim reaper of clotting, holding the bills for Factors 10, 5, 2, 1, and 13.

• Prothrombin (Factor II) — aka “Thumb Bill”: Turns into thrombin (the $2 bill with a big thumbprint) and activates fibrinogen (the $1 bill made of fiber) into fibrin.

• Factor XIII (Jason again) then seals the clot with a sticky web. The clot is locked. Game over.

🌿 Then enters Heparin: A barefoot hippie who amplifies Antithrombin the Ferret 🐾, whose collar reads “10 & 2 Stopper.”

• Heparin inactivates Factor 10a and Thrombin (2a), preventing the clot entirely.

• Heparin’s work is monitored by aPTT (not PT/INR).

Mnemonic: “Check the aPTT!” echoes across the commons as the web dissolves.

✅ Quick Clinical Takeaways:

• Hemophilia A = Factor VIII deficiency → Treat with Factor VIII or DDAVP

• Hemophilia B = Factor IX deficiency → Treat with Factor IX

• Both: X-linked, prolonged aPTT, normal PT

• Heparin = Acts on Factors 2a & 10a, monitored by aPTT

• Warfarin = Inhibits Factor VII, monitored by PT/INR

👨‍⚕️ Built for emergency physicians and learners who want fast recall, sticky mnemonics, and a clotting cascade you’ll never forget.

In this episode, we tackle STEMI mimics—conditions that mimic ST-segment elevation myocardial infarction on an EKG but aren’t always a heart attack.

Why’s it critical? Because ST elevation doesn’t always mean STEMI, and misdiagnosis can waste time or miss critical conditions.

ELEVATION

Electrolytes (Hyperkalemia),

Left Bundle Branch Block,

Early Repolarization,

Ventricular Hypertrophy (Left),

Aneurysm (Ventricular),

Thailand (Brugada Syndrome),

Inflammation (Pericarditis),

Osborn J Wave,

Non-Ischemic Vasospasm

We use the ELEVATION mnemonic to guide you through each mimic with clear explanations, repeated key points, and rapid-fire quizzes to lock in your recall.

How to Mix Push-dose Epi: One out, one in — makes ten

Goal concentration: 10 mcg/mL

Step-by-Step Mixing:

1. Start with a 10 mL syringe of normal saline (NS)

• empty 1 mL to retain 9 mL of NS in the syringe.

2. Use the code cart 1:10,000 epi (100 mcg/mL)

• This is the standard “cardiac arrest epi” amp (usually 1 mg in 10 mL)…the 1:10,000 prefilled syringe used during ACLS

3. Withdraw 1 mL of the 1:10,000 epi (this gives you 100 mcg) using 3 mL syringe.

4. Inject that 1 mL (100 mcg) into your syringe of 9 mL NS.

• Now you have 10 mL of epinephrine at 10 mcg/mL — ready to use.

So what we just did is the mnemonic: One out, one in — makes ten

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• What’s the concentration of the code cart epi?

• How much do you withdraw?

• What do you inject it into?

• What’s the final concentration?

You should be able to say it out loud, now. If not — just repeat the podcast a couple of times to get it solid.

⸻

How to Administer:

• Dose: 1–2 mL IV push every 1–5 minutes PRN hypotension

• That’s 5 to 20 micrograms per dose — meaning 0.5 to 2 mL of your push-dose epi, depending on the patient’s response.

• Titrate to clinical effect (aim for MAP >65 or ROSC support)

E-MOTIVE Mnemonic for Postpartum Hemorrhage: A Lifesaving Strategy

The E-MOTIVE mnemonic stands for a six-component bundle aimed at tackling postpartum hemorrhage (PPH), a major cause of maternal death, especially in low-resource settings. This approach, tested in a cluster-randomized trial across 80 hospitals in Kenya, Nigeria, South Africa, and Tanzania, was published in the New England Journal of Medicine in 2023. Here’s what E-MOTIVE stands for and why it matters:

• E – Early Detection: Uses a calibrated blood-collection drape to objectively measure blood loss after vaginal delivery. This ensures PPH (blood loss ≥500 ml) is identified quickly and accurately, unlike visual estimation, which can be unreliable.

• M – Massage: Uterine massage is performed to stimulate contractions and control bleeding, particularly for uterine atony, the most common cause of PPH.

• O – Oxytocic Drugs: Administers drugs like oxytocin to promote uterine contractions and reduce bleeding. These are critical for managing uterine atony effectively.

• T – Tranexamic Acid: An antifibrinolytic drug given to stabilize clots and reduce bleeding, especially when administered early after PPH onset.

• I – Intravenous Fluids: Provides fluids to maintain blood volume and prevent shock in women experiencing significant blood loss.

• V – Vaginal Examination and Escalation: Involves a thorough genital tract exam to identify trauma or retained tissue, with escalation to surgical or advanced care if bleeding persists.

• E – Effective Teamwork: Emphasizes communication, cooperation, and rapid response among healthcare providers to ensure all components are delivered promptly.

Why It’s a Game-Changer: The trial showed that E-MOTIVE reduced the risk of severe PPH (blood loss ≥1000 ml), laparotomy for bleeding, or maternal death by 60% compared to usual care.

PPH was detected in 93.1% of cases in the intervention group versus 51.1% in the control group, and the treatment bundle was used in 91.2% of cases versus 19.4%.

This bundle ensures evidence-based interventions are applied consistently and concurrently, saving lives by addressing PPH faster and more effectively.

E-MOTIVE is a practical, scalable solution, especially for low- and middle-income countries where PPH is deadliest. Its use of low-cost tools like the blood-collection drape makes it accessible, while the mnemonic simplifies training and implementation for healthcare teams under pressure.

This summary is based on the New England Journal of Medicine article.

This is a Neonatal Resuscitation Algorithm flowchart, specifically the NRP (Neonatal Resuscitation Program), published by the AHA in 2020. It provides a step-by-step guide for healthcare providers to follow during the resuscitation of a newborn immediately after birth, focusing on stabilizing the infant’s breathing, heart rate, and oxygenation.

Starting Point

• Antenatal Counseling and Team Briefing: Before birth, the team prepares and checks equipment.

• Birth: The process begins at the moment of birth.

Initial Assessment (Within the First Minute)

1 Term Gestation? Good Tone? Breathing or Crying?

◦ If Yes: The infant stays with the mother for routine care (warming, maintaining normal temperature, positioning airway, clearing secretions if needed, drying, and ongoing evaluation).

◦ If No: Proceed to resuscitation steps.

2 Apnea or Gasping? HR Below 100/min?

◦ If Yes:

▪ Start PPV (Positive Pressure Ventilation) using a SpO₂ monitor and consider an ECG monitor.

▪ Check if the heart rate (HR) is still below 100/min after PPV.

◦ If No:

▪ Check for Labored Breathing or Persistent Cyanosis.

3 Labored Breathing or Persistent Cyanosis?

◦ If Yes:

▪ Position and clear the airway, monitor SpO₂, and provide supplementary O₂ as needed. Consider CPAP (Continuous Positive Airway Pressure).

▪ Follow up with post-resuscitation care and team debriefing.

◦ If No: Continue with routine care as described earlier.

Further Resuscitation (If HR Remains Low)

4 HR Below 100/min After PPV?

◦ If Yes:

▪ Check chest movement and take corrective ventilation steps if needed (e.g., using an endotracheal tube (ETT) or laryngeal mask).

◦ If No: Monitor and continue care.

5 HR Below 60/min?

◦ If Yes:

▪ Intubate if not already done.

▪ Start chest compressions coordinated with PPV using 100% O₂.

▪ Use an ECG monitor and consider an umbilical venous catheter (UVC) for access.

◦ If No: Continue monitoring.

6 HR Still Below 60/min After Compressions?

◦ If Yes:

▪ Administer IV Epinephrine.

▪ If HR remains persistently below 60/min, consider hypovolemia (low blood volume) or pneumothorax (collapsed lung) as potential causes.

Additional Information

• Targeted Preductal SpO₂ After Birth: The chart lists target oxygen saturation (SpO₂) levels for a newborn at different time intervals post-birth:

◦ 1 min: 60%–65%

◦ 2 min: 65%–70%

◦ 3 min: 70%–75%

◦ 4 min: 75%–80%

◦ 5 min: 80%–85%

◦ 10 min: 85%–95%

Context

This algorithm is used in clinical settings, particularly in delivery rooms or neonatal intensive care units (NICUs), to guide healthcare providers in managing newborns who aren’t breathing adequately or have a low heart rate at birth. It emphasizes rapid assessment and intervention to ensure the infant stabilizes within the critical first minutes of life.

The 3-Step Approach to Acute Hyperkalemia

1. Stabilize: the Heart (If ECG changes) → Calcium

2. Shift: K+ Into Cells → Insulin + Glucose, Albuterol, Bicarb (if acidotic)

3. Send-it: Remove K+ From Body → Diuretics (if making urine), Kayexalate (if GI motility intact), Dialysis (if severe/refractory)

I – IV Fluids

C – Calcium

B – Beta-2 Agonists

B – Bicarbonate

I – Insulin & Glucose

K – Kayexalate (Sodium Polystyrene Sulfonate)

D – Diuretics

D – Dialysis

1. First Step: Assess ECG & Risk of Arrhythmia

• Peaked T waves, QRS widening, sine wave = Give Calcium ASAP

• Calcium doesn’t lower K+, but it prevents cardiac arrest.

2. Temporary vs. Definitive Treatments

• Shifting K+ into cells (Beta-agonists, Bicarb, Insulin) buys time.

• Excreting K+ (Diuretics, Dialysis, Kayexalate) removes K+.

3. Timing of Interventions:

• Calcium: Immediate (stabilizes heart).

• Insulin/Albuterol/Bicarb: 15–30 min (shifts K+).

• Diuretics/Kayexalate: 1–6 hours (removes K+).

• Dialysis: Immediate, definitive.

4. Common Pitfalls & Pro Tips

• Insulin can cause hypoglycemia – recheck glucose in 30 minutes.

• Albuterol requires high doses – typical 2.5 mg nebs won’t cut it.

• Bicarb only works if acidotic – don’t rely on it in normotensive patients.

• Kayexalate is slow & controversial – consider patiromer or zirconium cyclosilicate instead in chronic cases.

• If oliguric or ESRD → Straight to dialysis.

USED CARS mnemonic for non-anion gap metabolic acidosis (NAGMA):

Why “USED CARS”?

• Ureterosigmoidostomy

• Saline & Chloride infusion (excessive).. chloride offsets AG

• Endocrine disorders (Addison’s disease aka adrenal insufficiency, hypoaldosteronism)

• Diarrhea

• Carbonic anhydrase inhibitors

• Ammonium chloride

• Renal tubular acidosis

• Spironolactone

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U – Ureteroenteric fistula (or diversion surgery)

• Why NAGMA?

• Ureter attached directly to colon; bicarbonate lost into bowel, chloride absorbed, causing hyperchloremic acidosis.

• Symptoms:

• History of bladder/colon surgery, urine-like smell from stool, chronic acidosis.

• Labs: Normal AG, elevated chloride, chronic metabolic acidosis.

• ED Management:

• Identify, refer to urology or general surgery for definitive repair.

• Correct electrolyte disturbances (usually potassium, bicarbonate).

⸻

S – Saline Infusion (Excessive)

• What: Excessive infusion of normal saline (0.9% NaCl).

• Why (Pathophysiology): High chloride content of NS dilutes bicarbonate → hyperchloremic metabolic acidosis (common in hospitalized patients).

• Symptoms: Usually subtle (fatigue, mild confusion, fluid overload signs).

• Labs: Normal AG, hyperchloremia, normal renal function initially.

• ED Management:

• Switch to balanced solutions (Lactated Ringer’s, Plasmalyte).

• Monitor fluid and electrolyte balance.

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E – Endocrine Disorders (Addison’s Disease/Adrenal Insufficiency):

• Why: Lack of aldosterone = inability to excrete acid & retain sodium.

• Clinical Clues: Weakness, fatigue, low BP, dizziness, hyperpigmentation (skin darkening), abdominal pain.

• Labs: Low sodium, high potassium, normal anion gap, metabolic acidosis.

• ED Management:

• IV fluids (Normal saline), hydrocortisone, monitor electrolytes closely.

• Admit for adrenal crisis management.

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D – Diarrhea

• Pathophysiology: Loss of bicarbonate-rich fluids via stool → bicarbonate depletion.

• Clinical Clues: Frequent watery stools, dehydration signs (tachycardia, low BP).

• Labs: Normal anion gap, hypokalemia common, hyperchloremia.

• ED Management:

• Aggressive fluid resuscitation (often NS or LR).

• Electrolyte replacement (especially potassium).

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C – Carbonic Anhydrase Inhibitors (Acetazolamide)

• Mechanism: Prevent bicarbonate reabsorption → bicarbonate loss → acidosis.

• Clinical clues: Medication history (glaucoma treatment, altitude sickness prophylaxis, idiopathic intracranial hypertension).

• Labs: Normal AG, mild hypokalemia, mild hyperchloremia.

• ED Management:

• Stop offending medication, supportive care, and electrolyte replacement.

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A – Ammonium Chloride Ingestion

• Mechanism: Direct chloride ingestion overwhelms bicarbonate buffers.

• Rare cause today, often historical or industrial exposure.

• Clinical clues: History of ingestion, occupational exposures, metabolic symptoms (nausea, vomiting, confusion).

• Labs: Normal AG, hyperchloremia.

• ED Management:

• Supportive care, stop exposure.

• Correct metabolic acidosis if severe (sodium bicarbonate IV if severe).

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R – Renal Tubular Acidosis (RTA)

• Mechanism: Kidneys fail to reabsorb bicarbonate or excrete acid properly.

• Bicarbonate replacement.

• Potassium correction (careful monitoring).

• Referral to nephrology.

⸻

R – Renal Tubular Acidosis (Already covered above)

• Included in detail in the “A” section, given its complexity.

⸻

S – Spironolactone (and other Aldosterone Antagonists)

• Mechanism: Blocks aldosterone receptors → reduced acid and potassium excretion.

• Clinical clues:

Use in CHF, cirrhosis, hypertension treatment.

• Hold spironolactone, manage hyperkalemia aggressively (calcium gluconate, insulin/dextrose, albuterol, kayexalate).

• Consider bicarbonate if severely acidotic.

The GOLD MARK causes are divided into three major pathophysiologic groups based on the source of the acid production:

1. Alcohols (Toxic Ingestions) → Emergency Toxins

• Glycols → Ethylene glycol (antifreeze) and propylene glycol

• Methanol → Windshield washer fluid, homemade alcohol substitutes

• Why grouped together?

• Common in suicide attempts, accidental ingestions, or chronic alcoholics.

• Key labs: Serum osmolality, anion gap, osmolar gap.

• Imaging: Calcium oxalate crystals on urine microscopy (ethylene glycol).

• Treatment: Fomepizole or ethanol (blocks alcohol dehydrogenase), hemodialysis in severe cases.

2. OTCs & Medication-Related Causes → Common but Easily Missed

• Oxoproline → Chronic acetaminophen (Tylenol) use, often in malnourished patients

• Aspirin → Salicylates, including bismuth subsalicylate (Pepto-Bismol)

• Why grouped together?

• Often overlooked in chronic users or the elderly.

• Key signs: Tachypnea (respiratory alkalosis), tinnitus (aspirin), altered mental status.

• Key labs: Salicylate level, ABG (mixed acid-base disorder).

• Treatment: Alkalinization (sodium bicarb drip), dialysis for severe cases.

3. Metabolic Causes → Endogenous Acid Production

• L-lactate → Type A (ischemia), Type B (mitochondrial dysfunction)

• D-lactate → Short gut syndrome, bacterial overgrowth

• Renal Failure → Uremia, organic acids

• Ketones → Starvation, alcohol, diabetic ketoacidosis (DKA)

• Why grouped together?

• These involve internal production of acids due to organ dysfunction.

• Key labs:

• Lactate level (for sepsis, ischemia).

• BHB (beta-hydroxybutyrate) for DKA.

• BUN/Cr for renal failure.

• Urinalysis (ketones, glucose, uremia markers).

• Treatment:

• Fluids, treat underlying cause (DKA → insulin drip, renal failure → dialysis).

Clinically Important Considerations for EM Physicians

In the ED, when a patient has metabolic acidosis with an elevated anion gap, think:

1. What is the patient’s history?

• Suicide attempt or confusion? → Alcohols, aspirin

• Chronic Tylenol use or malnourished? → Oxoproline

• Sepsis, shock, ischemia? → L-lactate

• Short gut, diarrhea, recent antibiotics? → D-lactate

• Known diabetes, alcoholism, or fasting? → Ketones

• Chronic kidney disease? → Uremia

2. What tests should I order immediately?

• ABG/VBG → Confirms metabolic acidosis.

• Anion gap calculation → Determines if the acidosis is anion gap or non-anion gap.

• Serum osmolality & osmolar gap → Alcohol toxicity (ethylene glycol, methanol).

• Lactate level → Sepsis, ischemia, mitochondrial dysfunction.

• BHB (Beta-hydroxybutyrate) → DKA vs. alcoholic/starvation ketosis.

• Salicylate level & acetaminophen level → Toxic ingestion screening.

• CMP (BUN/Cr, glucose, liver enzymes, electrolytes) → Renal failure, DKA, liver dysfunction.

Takeaway: What’s an Emergency?

• Dialysis Emergencies → Methanol, ethylene glycol, severe aspirin toxicity, uremia.

• Toxin Emergencies → Alcohols (treat with fomepizole), salicylates (alkalinization & dialysis).

• Septic Shock / Tissue Hypoxia → Elevated L-lactate = immediate resuscitation with fluids & source control!

• DKA → Fluids, insulin drip, and monitor for electrolyte shifts (esp. potassium).

Mister Ronald McDonald (MR RM) is a helpful flowchart for interpreting acid-base disorders, specifically for determining whether a patient’s condition is due to a metabolic (M) or respiratory (R) cause:

1. Check the pH (7.4 is the cutoff)

• pH > 7.4 → Alkalosis

• pH < 7.4 → Acidosis

2. Assess Carbon Dioxide (CO₂) Levels (PaCO₂)

• The key threshold is 40 mmHg:

• If CO₂ > 40 mmHg, this suggests respiratory acidosis or metabolic alkalosis.

• If CO₂ < 40 mmHg, this suggests respiratory alkalosis or metabolic acidosis.

3. Determine the Cause

• In Alkalosis:

• If CO₂ > 40, the cause is Metabolic (M) Alkalosis.

• If CO₂ < 40, the cause is Respiratory (R) Alkalosis.

• In Acidosis:

• If CO₂ > 40, the cause is Respiratory (R) Acidosis.

• If CO₂ < 40, the cause is Metabolic (M) Acidosis.

Key Takeaway

• The chart helps determine whether a patient’s acid-base imbalance is due to a metabolic or respiratory cause by analyzing pH and CO₂ levels.