Emergency Medicine Mnemonics

When the heart rate blasts past 150, our reflex is often to grab a syringe—diltiazem, metoprolol, something to slow things down. But here’s the hard truth: if the patient is in sick-tachy—tachycardia as a secondary compensation—slamming them with rate control can be catastrophic. That racing heart rate may be the only thing keeping them alive. Pausing to ask “sick-tachy or tachy-sick?” is what separates the new learner from the confident emergency clinician.This episode is all about STOP-ping before you treat the number. STOP is your mnemonic for the must-consider secondary compensations that drive tachycardia in the ED. Each of these can mimic or mask primary arrhythmias, and missing them can lead to disaster:⸻🛑 STOP MnemonicS – Sepsis • Tachycardia is often the earliest sign of infection. • Always check a lactate—“Lactic Acid” should be etched in your mind. • Bundle: fluids + source control. • Be cautious in elderly or vague abdominal presentations; tachycardia may be your only clue.T – Thyroid Storm • Look for agitation, fever, tremor, weight loss history. • Order TSH/T3/T4. • Treatment anchor: Beta-blockers (BB) are first-line for rate control here—unique compared to other scenarios. • Missing thyroid storm means missing a reversible cause of near-fatal tachycardia.O – HypOvolemia • Think bleeding (low H/H), dehydration, or anemia. • Visual: half water / half blood glass—“Fill the Tank.” • Don’t just reach for meds—give fluids, transfuse, and stabilize volume first. • Remember also anxiety/pain can amplify sympathetic tone.P – Pulm/Cards (Cardiopulmonary) • Pneumonia – fever, infiltrate, hypoxia. • Pneumothorax – sudden pleuritic chest pain, absent breath sounds. • PE – unexplained hypoxia, pleuritic pain, risk factors. • CHF (low EF) – the most dangerous one to miss before you push AV nodal blockers. • Workup tools: ABG, BNP, CTPA, CXR, POCUS.⸻🧠 Why This Matters • Sinus tachycardia is often appropriate—but it can mask life-threatening systemic illness. • Medicating away compensation without treating the cause can pull the plug on the patient’s only survival mechanism. • STOP first before flipping to tachyarrhythmia algorithms (SVT, AFib w/ RVR, VT, Torsades, VF).⸻⚡ Clinical Pearls • Always ask: Stable or unstable? Unstable → Shock immediately per ACLS. • If stable → STOP. Consider secondary compensations before rhythm drugs. • POCUS is your left-hand tool—look for low EF before you dare to push AV nodal blockers. • Gradual vs sudden onset helps distinguish sick-tachy (gradual, compensatory) from tachy-sick (primary arrhythmia, often sudden). • Repetition is your friend—STOP, STOP, STOP until it becomes second nature.⸻🎧 In this episode, you’ll learn how to build a jetpack framework for HR >150 that keeps you calm under pressure, helps you avoid rookie mistakes, and makes sure you never miss the underlying killer hiding beneath “just a fast heart rate.”STOP first. Then treat.

In a cardiac emergency, pattern recognition saves lives. The ability to rapidly identify ST-elevation myocardial infarctions (STEMIs) — and recognize their reciprocal changes — is one of the most high-yield clinical skills you can master. But memorizing lead groupings, artery territories, and reciprocal zones can feel abstract… until now.This podcast brings EKGs to life inside a colorful, stadium-themed world where each ECG lead is a character in the crowd — making it dramatically easier to remember the key patterns of ischemia and their reciprocals. Whether you’re a student, clinician, or educator, this episode transforms clinical EKG interpretation into vivid, unforgettable storytelling.🧠 Characters You’ll Meet: • Inferior Peasants (II, III, aVF) — Dirty, disheveled townsfolk crowd-surfing with broken RC cars (Right Coronary Artery), holding crossed-out nitro packs to remind us: No nitro in RCA infarcts! • Royal Ladder Holders (I, aVL, V5, V6) — Crowned kings and queens dropping through trapdoors as reciprocal ST depression hits the lateral leads, each holding golden ladders labeled Left Circumflex. • Cavemen with Septal Bones (V1–V2) — Giant-nosed, primitive figures gripping a huge bone marked SEPTAL, standing just in front of… • Shirtless Musclemen (V3–V4) — Tattooed with the word Anterior, these strongmen are chained to a floating AC unit labeled Left Ventricle — representing the LAD (Widowmaker). • Posterior Posts (V7–V9) — Hydraulic pylons rising behind the wall, symbolizing posterior MI that’s often missed without reciprocal signs.🎯 Quick Reference Patterns Covered in the Episode:⸻✅ Inferior MI (II, III, aVF)• ST elevation: Inferior leads• Reciprocal depression: I, aVL (high lateral)→ “When the peasants rise, the royals fall.”✅ High Lateral MI (I, aVL)• ST elevation: High lateral leads• Reciprocal depression: III, aVF→ Works both ways: “The balcony royals rise, the peasants fall.”✅ Posterior MI (V7–V9)• ST elevation: Posterior wall (not on standard 12-lead!)• Reciprocal depression: V1–V3→ “When posterior posts rise, septal cavemen drop.”✅ Anterior MI (V2–V4)• ST elevation: Anterior leads• Possible reciprocal depression: II, III, aVF→ Sometimes: “When the chest heroes rise, peasants tremble.”✅ Low Lateral MI (V5–V6)• ST elevation: Low lateral leads• Reciprocal depression: V1–V2 (septal)→ “Kings and queens rise, cavemen fall.”⸻🔥 Bonus Insights: • Why reciprocal changes matter: They can confirm a true STEMI, suggest a larger infarct area, and sometimes reveal hidden infarctions (like posterior MIs). • LBBB & Reciprocal Thinking: LBBB distorts ST segments, but understanding the mirror logic behind “William” (LBBB) and “Marrow” (RBBB) helps clarify expected patterns. ST depression in V1–V2? May just be part of LBBB — unless it’s concordant…📌 Use this episode as your visual and verbal anchor. Once you’ve seen the peasants, the royalty, the cavemen, and the Left Vent AC unit, you’ll never look at a 12-lead the same way again.

This is the most basic, essential framework for EKG interpretation — built for emergency medicine clinicians who need clarity, speed, and confidence in the heat of the moment.Our brains are wired for movement and story. Just like remembering your morning routine — wake up, brush teeth, grab caffeine — we naturally recall sequences that follow a simple, visual narrative. In this episode, we harness that power by turning EKG interpretation into Evel Knievel’s most daring stunt ride. It’s not just a fun story — it’s a high-yield, easy-to-remember mental checklist that sticks, even under pressure.🏥 Why it works in the ED:In emergency medicine, chaos is the norm. We don’t have time to think academically when a STEMI or arrhythmia is staring us in the face. That’s why we built this vivid, memorable sequence — rooted in the high-performance principle Michael Phelps used to win 23 Olympic gold medals: a set routine. You don’t rise to the occasion. You fall back on your training.🏁 What you’ll hear in this episode:​ 🏍️ Evel Knievel enters the EKG stadium: First, he scans for the big stuff — STEMI and reciprocal changes.​ 🛠️ Check engine light: T-wave inversions on his digital monitor.​ 📈 RPMs climbing: Smooth R-wave progression across the precordial leads.​ 🔍 Arrhythmia check: Is there a P for every QRS?​ 📏 The perfect ramp: PR interval = Evel’s takeoff — 120–200 ms.​ 🛵 Mobitz moped warning: PR lengthens before crashing (Wenckebach).​ ❌ Sudden moped disappearance: Mobitz II.​ ⚫ Unicycle of doom: Third-degree block — P and QRS totally disconnected.​ 🧠 Anomalies & Final Scan: Brugada, hyperkalemia (peaked Ts), Osborn waves, and when to order a posterior EKG.🚨 Key Takeaways to Remember:​ This story is your reliable sequence: scan for ischemia → check for arrhythmia → assess intervals.​ STEMI? Look for elevation + reciprocal depression — including the often-missed posterior wall (V7–V9).​ Rhythm? Ask: Is there a P for every QRS?​ PR = takeoff ramp. QT = safe landing zone.​ Mobitz I = gradual PR lengthening → dropped beat.​ Mobitz II = PR stays the same → sudden drop.​ Third-degree block = P and QRS divorced — high risk of instability.​ Brugada = beware of the “grave cross” in V1–V2. Ask about family history of sudden cardiac death.​ Prolonged QT = risk of torsades, syncope, or V-fib — know when to shock.🎧 This is your EKG blueprint. Your Michael Phelps routine. Your Evel Knievel ride to interpretation mastery.Let’s ride.

In the fast-paced, high-stakes world of emergency medicine, every second matters—especially when it comes to sickle cell crisis. This podcast takes you straight to the heart of what matters most for ED clinicians, walking you through the essential “4 R’s” that can mean the difference between stabilization and rapid deterioration: • Recognize — Identify the telltale signs of sickle cell crises early. Understand presentations like acute pain episodes, acute chest syndrome, stroke, and splenic sequestration, and learn how to differentiate these from other causes of acute pain or respiratory distress. • Reverse — Act fast to correct life-threatening complications. From oxygen and aggressive IV fluids to urgent infection management, you’ll get evidence-based, bedside-ready strategies to halt progression. • Radiology — Know when and why to image. From chest X-rays in acute chest syndrome to brain imaging for suspected stroke, we’ll break down which modalities to order—and how to interpret findings in the sickle cell patient. • Refer — Recognize when escalation of care is critical. Whether to hematology, critical care, or transfer to a higher-level facility, we’ll cover the decision-making process and timing.Hosted with a focus on clinically relevant, ED-ready pearls, each episode blends: • Case-based storytelling — Putting you in the room with the patient, step-by-step. • Mnemonic-rich recall tools — Like our “crime scene outline” visual, with key stickers marking the 4 R’s across the patient’s limbs for fast memory anchoring. • Practical takeaways — What you can do immediately, what you must watch for, and what to avoid.The principles behind the Sickle Cell 4 R’s is delivered in a no-fluff, high-yield format designed for busy clinicians who want to sharpen their edge in real emergencies.Whether you’re a seasoned emergency medicine provider, a resident looking to solidify your sickle cell knowledge, or simply someone passionate about critical care, Sickle Cell Crisis: The 4 R’s will give you the skills and confidence to take decisive action when it matters most.

Step aboard the Anemia Train and enter the Normocytic Skeleton Car—the middle car of your anemia mind palace—designed specifically for busy ED clinicians who need fast recall without flipping through textbooks.In this episode, you’ll: • 🧠 Visualize the Normocytic Train Car: Skeleton passengers holding reticulocyte balloons, split by a divider wall between low retic (front) and high retic (back). • 🎈 Lock in Retic Logic for the ED: • Low retic = Hypoproliferative (CKD with low EPO / Aplastic with high EPO but no marrow response) • High retic = Hyperproliferative (Hemolysis vs. Acute Blood Loss) • 🩸 Master Key ED Presentations: • CKD skeleton with sagging balloon (↓EPO), struggling for signal on a dead cell phone • Aplastic skeleton with a ringing phone he can’t answer, sitting on a frying pan (pancytopenia) • Hemolytic skeleton with bursting balloons, a Reuben sandwich with a lemon (↑LDH), stepping on a smiley‑face sticker (↓haptoglobin) • Acute Blood Loss skeleton in a puddle of blood, holding a GBS ping‑pong paddle (Glasgow‑Blatchford), with a soft BP cuff falling off his arm reminding you to check code status and be MTP ready • 🧳 Tour the Hemolytic Suitcases (final segment): 1. TTP/HUS VW suitcase with 5 bullet holes and brown diarrhea door → plasmapheresis + fluids 2. Autoimmune suitcase: Warm IGG sun w/ spleen & butterfly, Cold IGM iceberg with blue hand → consult heme 3. G6PD suitcase: G6 Police Dept badge, fava beans, Heinz ketchup bite cap, “Radical” free radical sticker → stop offending agents 4. Medical Sales suitcase: Heart valve + ECMO plush lungs, cola urine bottle, business card for cardiology → check hemolysis panel & hemodynamics⸻Why It Matters in the ED • 🚨 Rapid Retic Check = Life‑Saving Triage: Quickly determine production vs. destruction vs. loss • ⚡ Know When to Act: • Hyperproliferative side = ED danger zone (hemolysis & acute blood loss) • Hypoproliferative side = usually outpatient follow‑up unless profoundly symptomatic or pancytopenic • 💉 Immediate Actions: • Transfuse if symptomatic or unstable • Initiate MTP for massive GI bleeds • Call heme or GI early for high‑risk or crashing patients • 📊 ED Labs to Prioritize: CBC w/ indices + retic, hemolysis panel, type & screen, stool/urine checks as indicated⸻Disclaimer:This podcast is for educational purposes only. Always check local ED protocols and consult specialists for patient‑specific management.

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.—🧠 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 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. ELEVATIONElectrolytes (Hyperkalemia), Left Bundle Branch Block, Early Repolarization, Ventricular Hypertrophy (Left), Aneurysm (Ventricular), Thailand (Brugada Syndrome), Inflammation (Pericarditis), Osborn J Wave, Non-Ischemic VasospasmWe 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.

E-MOTIVE Mnemonic for Postpartum Hemorrhage: A Lifesaving StrategyThe 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.

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 FluidsC – CalciumB – Beta-2 AgonistsB – BicarbonateI – Insulin & GlucoseK – Kayexalate (Sodium Polystyrene Sulfonate)D – DiureticsD – Dialysis1. 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.

The GOLD MARK causes are divided into three major pathophysiologic groups based on the source of the acid production:​ 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.​ 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.​ Metabolic Causes → Endogenous Acid Production​ L-lactate → Type A (ischemia), Type B (mitochondrial dysfunction)…L for Loser anaerobic (super winded loser in the race: anaerobic)​ D-lactate → Short gut syndrome, bacterial overgrowth …GI can think “diet for D”​ Renal Failure → Uremia, organic acids​ Ketones → Starvation, alcohol, diabetic ketoacidosis (DKA) think… Keytones are SAD ​ 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 PhysiciansIn the ED, when a patient has metabolic acidosis with an elevated anion gap, think:​ 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​ 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).

To determine if the patient requires admission or can be discharged, the Glasgow-Blatchford Score (GBS) is used. Here’s the ABCDEF mnemonic and why these factors increase the risk of an upper GI bleed:​ A - Active: Conditions like syncope or melena indicate ongoing or significant bleeding, increasing risk severity.​ B - Blood Urea Nitrogen: Levels ≥ 7 mg/dL suggest impaired kidney function, which is often associated with poor systemic clearance and bleeding risk.​ C - Circulation: A systolic blood pressure ≥ 110 mm Hg may reflect hemodynamic instability or stress response to bleeding.​ D - Drop in Hemoglobin: Hemoglobin levels ≤ 12.9 g/dL (men) or ≤ 11.9 g/dL (women) indicate anemia, suggesting significant blood loss.​ E - Elevated Pulse: A pulse rate ≥ 100/min signals compensatory tachycardia, often a response to blood loss.​ F - Failure: Cardiovascular or liver disease impairs clotting and hemodynamic stability, exacerbating bleed risk.Developed in Scotland, the GBS is a risk assessment tool for upper GI bleeds and considers symptoms, vital signs, and lab values on admission. Key factors in the score include melena, syncope, liver disease, heart failure, heart rate, blood pressure, hemoglobin, and BUN levels. Points are assigned based on these variables to assess the severity of bleeding and volume loss.For example:​Melena suggests significant GI bleeding, whereas isolated hematemesis (like coffee-ground emesis) has no scoring points.​Syncope, tachycardia, hypotension, and changes in Hb/BUN levels suggest volume loss.​Comorbid conditions (e.g., liver disease) may indicate a need for admission, especially if variceal bleeding is suspected.Discharge criteria also include access to follow-up care, a support system, and a nearby hospital for emergency returns if symptoms worsen.For more on current recommendations, consult the 2021 American Journal of Gastroenterology guidelines on upper GI bleeding.

The “H’s and T’s” refer to a mnemonic used in medicine to help healthcare professionals quickly recall the most common causes of cardiac arrest during a code (a medical emergency requiring CPR). Memorizing these is crucial because identifying and addressing these causes rapidly can improve the chances of saving a patient’s life. Here’s a breakdown:The H’s: OK TVHypoxia - Lack of oxygen to tissues can lead to a heart stopping, so ensuring proper oxygenation is key.Hypo-/Hyperkalemia - Abnormal potassium levels affect the heart’s electrical activity, potentially causing it to stop.Hypothermia - Low body temperature can slow heart function and lead to cardiac arrest.Hypovolemia - Loss of blood or fluids can lead to insufficient circulation and cardiac arrest.Hydrogen ion (acidosis) - A build-up of acid in the blood (often due to respiratory failure or shock) can disrupt heart function.The T’s: THROW TEN TOXIC TAMPONSThrombosis (pulmonary or coronary) - Blood clots in the lungs (pulmonary embolism) or heart (myocardial infarction) can obstruct blood flow, leading to cardiac arrest.Tension Pneumothorax - Air trapped in the chest cavity compresses the heart and lungs, affecting circulation.Toxins - Certain substances (medications, drugs, poisons) can disrupt heart rhythms.Tamponade (cardiac) - Accumulation of fluid around the heart prevents it from pumping effectively.Importance of Memorizing the H’s and T’s:These causes cover many reversible conditions that may lead to cardiac arrest. During a code, time is critical, so having these potential causes at the top of your mind helps quickly assess and treat the patient. Remembering the “H’s and T’s” mnemonic ensures that a healthcare provider methodically works through possible causes and provides the best chance of resuscitation.

The “KEEP” mnemonic is a tool to remember the most common organisms causing urinary tract infections (UTIs). Here’s how the mnemonic breaks down, followed by key information relevant for emergency medicine boards:K - Klebsiella species • Relevance: Klebsiella is the second most common organism causing UTIs, especially hospital-acquired infections. • Key Points: • Gram-negative rod. • Often seen in patients with underlying conditions like diabetes, or those with urinary catheters. • Resistant to many antibiotics, so susceptibility testing is important. • Treatment Options: Cephalosporins (like ceftriaxone), carbapenems in resistant cases.E - Escherichia coli (E. coli) • Relevance: The most common organism causing both community-acquired and some hospital-acquired UTIs. • Key Points: • Gram-negative rod. • Responsible for approximately 70-90% of uncomplicated UTIs. • Often originates from the gut. • Can exhibit antibiotic resistance, particularly to trimethoprim-sulfamethoxazole. • Treatment Options: Trimethoprim-sulfamethoxazole (Bactrim), nitrofurantoin, fosfomycin, or ciprofloxacin based on resistance patterns.E - Enterococcus species • Relevance: More common in complicated UTIs, particularly in hospital settings. • Key Points: • Gram-positive cocci. • Often found in patients with catheters, immunocompromised status, or structural abnormalities in the urinary tract. • Can be resistant to many antibiotics, including vancomycin-resistant Enterococcus (VRE). • Treatment Options: Ampicillin or amoxicillin when susceptible; for resistant cases, vancomycin or linezolid.P - Proteus species • Relevance: Known for causing complicated UTIs and is associated with kidney stones. • Key Points: • Gram-negative rod. • Produces urease, which increases urine pH and can lead to the formation of struvite stones. • Can cause upper UTIs and is known to colonize catheters. • Treatment Options: Ciprofloxacin, trimethoprim-sulfamethoxazole, cephalosporins; nitrofurantoin is usually not effective.Summary of the Mnemonic ‘KEEP’ • Klebsiella: Second most common UTI organism; hospital-acquired; antibiotic resistance common. • E. coli: Most frequent cause of UTIs; community-acquired; potential resistance to some antibiotics. • Enterococcus: Complicated and hospital-acquired UTIs; often found in patients with urinary abnormalities. • Proteus: Associated with kidney stones; catheter-related UTIs; produces urease.By remembering “KEEP,” you can recall the key organisms responsible for UTIs and their relevance to diagnosis and treatment in emergency settings.