Antihypertensive medications don’t have to feel overwhelming or memorization-heavy. In this solo lecture, Chloe Gomez, DNP, CRNA breaks down antihypertensive pharmacology through physiology, mechanisms of action, and real-world anesthesia implications - exactly what SRNAs, CRNAs, and anesthesia providers need for boards and the operating room.

This episode walks through the major classes of antihypertensives, focusing on how each drug lowers blood pressure rather than relying on disconnected lists. You’ll learn how antihypertensives interact with preload, afterload, heart rate, contractility, and systemic vascular resistance, and why those effects matter during induction, maintenance, and emergence from anesthesia.

Key topics covered include:

• Beta blockers (β₁ vs β₂ effects, perioperative continuation, blunted sympathetic response)

• ACE inhibitors (ACE-Is) & ARBs: RAAS physiology, vasodilation, and refractory hypotension

• Calcium channel blockers (DHP vs non-DHP): vascular vs nodal effects

• Alpha agonists and antagonists

• How antihypertensives alter MAP, CO, SVR, and reflex tachycardia

• Why certain antihypertensives increase the risk of induction hypotension

• What to hold, continue, or anticipate on the day of surgery

Throughout the episode, complex pharmacology is tied directly to:

• Hemodynamic management in anesthesia

• Common board scenarios and NBCRNA-style reasoning

• Vasopressor choice and response

• Drug interactions with propofol, volatile agents, opioids, and neuraxial anesthesia

This lecture emphasizes understanding over memorization, helping anesthesia learners build a framework they can use in high-stakes clinical moments - not just exam day.

🎧 Antihypertensives explained for anesthesia learners - fewer flashcards, more confidence, safer patients.

Antiarrhythmics don’t have to feel like chaos. In this solo lecture, CRNA educator Chloe Gomez, DNP, CRNA breaks down antiarrhythmic pharmacology using clear physiology, memorable frameworks, and anesthesia-specific clinical relevance - perfect for SRNAs, CRNAs, and anesthesia providers preparing for boards and clinical practice.

This episode walks step-by-step through the Vaughan Williams classification system (Class I–IV) and explains why these drugs work, not just what list they belong to. You’ll learn how antiarrhythmics interact with sodium, potassium, calcium channels, and beta receptors, and how those effects translate to changes in phase 0 depolarization, action potential duration, refractory periods, and conduction velocity.

Key topics covered include:

• Class I sodium channel blockers (IA, IB, IC): how they alter phase 0, QRS width, and conduction

• Class II beta blockers: AV node effects, rate control, and anesthesia considerations

• Class III potassium channel blockers: action potential prolongation, QT interval risk, and torsades

• Class IV calcium channel blockers: nodal suppression and hemodynamic effects

• Why electrolytes (K⁺, Mg²⁺) matter when using antiarrhythmics

• How antiarrhythmics can become pro-arrhythmic

• What anesthesia providers must watch for in the OR, ICU, and PACU

This lecture emphasizes mechanism-based understanding, tying pharmacology directly to:

• ECG changes

• Perioperative risk stratification

• Volatile anesthetics and arrhythmia risk

• Drug interactions common in anesthesia practice

• Board-style clinical reasoning for the NBCRNA NCE

If you’ve ever memorized the Vaughan Williams classes and immediately forgotten them, this episode is designed to finally make antiarrhythmics stick - so you can reason through arrhythmias with confidence instead of panic.

🎧 Antiarrhythmics decoded for anesthesia learners - fewer tables, more understanding, safer practice.

Anticoagulants don’t have to feel overwhelming. In this solo episode, CRNA educator Chloe Gomez, DNP, CRNA breaks down the coagulation cascade and anticoagulant pharmacology in a clear, intuitive way designed for SRNAs, CRNAs, and anesthesia providers preparing for boards and real-world clinical practice.

We start with a simple, step-by-step walkthrough of the intrinsic, extrinsic, and common pathways, then connect that physiology directly to how commonly used anticoagulants work — including unfractionated heparin (UFH), low-molecular-weight heparin (LMWH), warfarin (Coumadin), and direct oral anticoagulants (DOACs).

This episode goes beyond memorization and focuses on mechanism-based understanding, explaining:

• Why heparin potentiates antithrombin III and primarily inhibits factor IIa (thrombin) and factor Xa

• Why PT/INR rises first with warfarin due to factor VII’s short half-life — not because warfarin “blocks the extrinsic pathway”

• How DOACs selectively target factor Xa or thrombin

• Which labs actually reflect drug effect (aPTT, PT/INR, ACT, anti-Xa)

• How electrolyte imbalances can turn anticoagulants into pro-arrhythmics or bleeding risks

We also cover high-yield anesthesia considerations, including:

• Neuraxial anesthesia timing and safety

• ASRA-aligned anticoagulant hold times

• Reversal agents (protamine, vitamin K, PCCs, andexanet alfa, idarucizumab)

• Practical OR case scenarios you are likely to see in real practice

If you’re studying for the NBCRNA NCE, teaching anesthesia pharmacology, or just want anticoagulants to finally make sense, this episode is designed to help you stop memorizing tables - and start building safe anesthetic plans.

🎧 Educational, board-relevant, and clinically grounded - this is anticoagulation for anesthesia providers who want to truly understand the “why.”