Diary of a Lost Student: From Theory to Practice -Foundational Anesthesia Concepts for All Providers

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Anesthesia pharmacology, physics, and physiology explained one idea at a time — for residents, SRNAs, CRNAs, anesthesia assistants, and anesthesiologists. The gas laws. Drug mechanisms. Where a drug came from and why it does what it does at three in the morning. Covered in anesthesia school — just not all the way down. This show goes underneath. One foundational anesthesia concept per episode. Under fifteen minutes. Twice a week. For anesthesia residents, SRNAs and CRNAs, student anesthesia assistants (AAs), practicing anesthesiologists, and anyone considering applying to anesthesia school. Not board prep. Just the moment a hard thing finally makes sense.

Recent Episodes

OCT 21, 2026
The Shunt Equation: Why More Oxygen Won't Fix True Shunt | Anesthesia Physics
Got something to say to this podcast? Send a voicemail, and you might hear yourself on the next episode! The Shunt Equation: Why More Oxygen Won't Fix True Shunt Every arterial blood gas is a mixture of two streams — blood that saw ventilated alveoli and picked up oxygen, and blood that skipped them entirely. The shunt equation solves for what fraction came from the second stream. This episode covers: the mass-balance algebra of Qs/Qt = (CcO₂ − CaO₂) / (CcO₂ − CvO₂); PAO₂ versus PaO₂; why normal shunt sits near 5% and anything above 10% is pathologic; true shunt versus V̇/Q̇ mismatch; the FiO₂ test; mixed venous sampling and why cardiac output changes the answer; the Riley–Cournand history; the perioperative causes — atelectasis, pneumonia, hemothorax, ARDS — and the anatomic ones: PFO, ASD, VSD, pulmonary AVM; and why PEEP — not more oxygen — is the response to true shunt. Against true shunt, extra FiO₂ is shouting at a room no one is in. Key Takeaways • Qs/Qt = (CcO₂ − CaO₂) / (CcO₂ − CvO₂) — the shunt fraction. • PAO₂ is calculated. PaO₂ is measured. • Normal shunt ≈ 5% — thebesian and bronchial veins. Above 10% is pathologic. • True shunt ignores FiO₂. V̇/Q̇ mismatch doesn't. • FiO₂ test: PaO₂ above 200 on 100% oxygen suggests mismatch; below 200 suggests true shunt. • Anatomic shunts — PFO, ASD, VSD, pulmonary AVM — ignore FiO₂ too. • A falling cardiac output deepens hypoxemia from an unchanged shunt. • PEEP reopens the lung. More oxygen doesn't. Timestamps 00:00 — Two pipes, one mixing chamber 01:53 — The equation, term by term 03:14 — PAO₂ versus PaO₂ 04:06 — Normal shunt and the 10% line 04:19 — True shunt versus V̇/Q̇ mismatch 05:08 — The FiO₂ test 05:24 — Why cardiac output changes the answer 05:56 — Riley, Cournand, and Swan-Ganz 06:48— From Theory to Practice If this made something click, leave a 5-star rating and follow the show. That's how other anesthesia providers — residents, SRNAs, SAAs, CRNAs, and anesthesiologists — find it. New episodes every week.
10 MIN
OCT 15, 2026
Massive Transfusion Protocol: The 1:1:1 Ratio, and the Diamond of Death | Anesthesia Clinical Concepts
Got something to say to this podcast? Send a voicemail, and you might hear yourself on the next episode! Massive Transfusion Protocol: The 1:1:1 Ratio, and the Diamond of Death | Anesthesia Clinical Concepts Ten units of red cells in 24 hours. That was the old definition — arbitrary, borrowed because ten units approximates one adult blood volume. It never accounted for rate. A patient can lose half their volume in an hour and never reach ten units before they arrest. Massive transfusion is not a number. It is a physiology problem with a clock attached. This episode covers the protocol from activation to deactivation — the ABC score, the 1:1:1 ratio, and what the PROPPR trial actually showed. Then the mechanism underneath: the lethal triad of hypothermia, acidosis, and coagulopathy, plus the fourth variable that turns a triad into a death spiral — ionized hypocalcemia from citrate. Viscoelastic testing, tranexamic acid, calcium, warming, and the team roles that decide outcomes. Key Takeaways • Massive transfusion is traditionally defined as 10 or more units of red cells in 24 hours. Modern practice favors dynamic criteria • The ABC score uses four bedside variables — penetrating mechanism, positive FAST, systolic BP ≤90, heart rate ≥120. Two or more activates the protocol. • Balanced resuscitation with a 1:1:1 ratio of plasma to platelets to red cells improves early hemorrhage control. The PROPPR trial showed no significant 24-hour mortality difference versus 1:1:2, but more patients in the 1:1:1 group achieved hemostasis and fewer died of exsanguination. • The lethal triad — hypothermia, acidosis, and coagulopathy. Citrate is the fourth variable that creates the diamond. Every unit of blood carries citrate that binds ionized calcium. Hypothermia and hypoperfusion slow citrate metabolism, prolonging hypocalcemia and worsening coagulopathy. • Transexamic acid works by blocking plasmin activation, preventing clot degradation rather than promoting clot formation. • Rapid infusers warm and deliver 200–1,200 mL/min. Warming is not comfort — it is coagulation management. Timestamps 00:00 — The falling wall 02:00 — 1:1:1 ratio 02:36 — The lethal triad and the diamond of death 03:33 — Calcium, Transexamic Acid, Cryoprecipitate 04:10 — The rediscovery of balance 05:05 — PROPPR Trial 05:31 — From Theory to Practice If this made something click, leave a 5-star rating and follow the show. That's how other anesthesia providers — residents, SRNAs, SAAs, CRNAs, and anesthesiologists — find it. New episodes Tuesday and Friday.
8 MIN
OCT 7, 2026
Phase II Conjugation: Glucuronidation and Why Some Drugs Last Longer | Anesthesia Foundational Concepts
Got something to say to this podcast? Send a voicemail, and you might hear yourself on the next episode! Phase 2 Conjugation: Glucuronidation and Why Some Drugs Last Longer | Anesthesia Foundational Concepts Imagine trying to catch a very slippery fish with your bare hands. It keeps slithering away. Now imagine someone glues a heavy, easy-to-grip handle onto the fish. Suddenly you can catch it. That is conjugation. Fat-soluble drug molecules are the slippery fish — they slip through the kidneys, get reabsorbed, and stick around in the body. Phase II enzymes glue a polar handle onto each drug molecule, usually glucuronic acid, and the resulting compound is water-loving enough for the kidneys to grab and flush out. This episode covers how that works, why almost every drug needs chemical alteration before it can leave the body, the difference between Phase I and Phase II and the role of glucuronidation. Then it follows conjugation to the bedside, where two stories anchor almost everything anesthesiology needs to know. Key Takeaways • Phase II conjugation attaches a large polar group to a lipid-soluble drug so the kidneys can excrete it. • Glucuronidation is the busiest pathway. • Morphine is the famous exception. • Morphine-6-glucuronide (M6G) is roughly twice as potent as morphine at the μ-opioid receptor and accounts for about 10 percent of metabolites. • Acetaminophen overdose works through the same machinery. Glucuronidation and sulfation saturate, more drug shunts through CYP2E1 to NAPQI, glutathione depletes, and NAPQI binds hepatocyte proteins. N-acetylcysteine replenishes glutathione so conjugation of NAPQI can resume. • Phase II is relatively preserved in liver disease. • Newborns have immature UGT capacity. That shortfall is behind neonatal jaundice. Timestamps 00:00 — The slippery fish 01:17 — Two fates, two phases 02:00 — Phase I versus Phase II 02:30 — Glucuronidation and the other tags 03:17 — Immature at birth: jaundice and gray baby 03:46 — The exception: morphine-6-glucuronide 04:55 — From Theory to Practice 05:06 — Morphine and renal failure 06:09 — Acetaminophen and NAPQI 07:19 — One habit of mind If this made something click, leave a 5-star rating and follow the show. That's how other anesthesia providers — residents, SRNAs, SAAs, CRNAs, and anesthesiologists — find it. New episodes Tuesday and Friday.
8 MIN