Vital Flow

In Part 7 of the Local Anesthetics series, we’re breaking down epidural anesthesia from placement to troubleshooting.

We’ll cover how to confirm epidural catheter placement, the purpose and interpretation of the epidural test dose, and what intravascular or intrathecal signs should make you stop and reassess. Then we’ll walk through loading the epidural, incremental dosing, factors that influence block height and spread, choosing local anesthetic concentration and volume, and maintaining the block with top-ups or continuous infusions.

We’ll also tackle the epidural that just isn’t behaving: unilateral blocks, patchy blocks, inadequate sacral coverage, catheter migration, intravascular or intrathecal placement, breakthrough pain, and failed epidurals—including when to manipulate the catheter, redose, or replace it.

A practical, anesthesia-focused guide to understanding not just how to dose an epidural, but why it works—and what to do when it doesn’t.

In Part 6 of the Vital Flow Local Anesthetics series, we’re going beyond the local anesthetic and breaking down the drugs that can be added to spinal anesthesia to modify block quality, duration, and analgesia.

We’ll cover intrathecal opioids including fentanyl, sufentanil, and morphine, with a focus on lipophilicity, onset, duration, rostral spread, and important side effects like pruritus, nausea, urinary retention, and respiratory depression.

Then we’ll move into other intrathecal adjuvants, including epinephrine, dexmedetomidine (Precedex), dexamethasone (Decadron), clonidine, and neostigmine—what they do, why they may prolong or enhance spinal anesthesia, and the evidence and safety considerations behind their use.

A practical review of what we add to the spinal, why we add it, and what you need to know when choosing an intrathecal adjunct.

Spinal anesthesia is more than putting local anesthetic into the intrathecal space—the drug you choose, its baricity, the patient’s position, and the dose all influence where that block goes and how it behaves.

In Part 5 of the Local Anesthetics series, we break down the practical pharmacology behind spinal anesthesia and connect it directly to what happens in the OR.

We’ll cover:

• Hyperbaric, isobaric, and hypobaric solutions — what baricity actually means and how gravity affects distribution
• Patient positioning — how sitting, supine, lateral, and surgical positioning can influence block spread
• What determines spinal block height — including dose, baricity, anatomy, pregnancy, and other patient factors
• Bupivacaine, ropivacaine, lidocaine, chloroprocaine, and other intrathecal local anesthetics — how their onset, duration, potency, and clinical roles differ
• Choosing the right spinal drug and dose based on the procedure and expected surgical duration
• Why seemingly small changes in technique can produce very different blocks

Whether you’re studying for boards, learning spinal anesthesia for the first time, or just need a refresher before your next case, this episode brings the pharmacology and clinical decision-making together.

🎧 Vital Flow — anesthesia concepts made practical.

Episode Title

Local Anesthetics Part 4: LAST — When Local Anesthetics Become Toxic

Episode Description

In Part 4 of the Vital Flow Local Anesthetics series, we tackle one of the most important and potentially life-threatening complications of local anesthetic use: Local Anesthetic Systemic Toxicity, or LAST.

This episode walks through how LAST happens, which local anesthetics carry the greatest risk, and how toxicity progresses through the central nervous and cardiovascular systems. We’ll cover early warning signs, seizures, cardiovascular collapse, and why severe toxicity—particularly from bupivacaine—can be so difficult to treat.

Most importantly, we break down exactly what to do when LAST occurs, including airway and seizure management, modified ACLS considerations, lipid emulsion therapy, dosing, and when to consider cardiopulmonary bypass or ECMO.

We’ll also discuss prevention strategies, including incremental injection, aspiration, ultrasound guidance, epinephrine as an intravascular marker, and appropriate monitoring after local anesthetic administration.

Topics include:
• Pathophysiology of LAST
• CNS and cardiovascular signs and symptoms
• Risk factors and high-risk local anesthetics
• Bupivacaine cardiotoxicity
• Recognition of atypical and delayed presentations
• Immediate management of LAST
• 20% lipid emulsion therapy and dosing
• Modifications to standard ACLS
• Seizure management
• Prevention and monitoring
• When to escalate to cardiopulmonary bypass or ECMO

A high-yield episode for anesthesia providers covering how to recognize LAST early, treat it aggressively, and prevent it whenever possible.

In Part 3 of the Vital Flow Local Anesthetics series, we move from the pharmacology to the drugs themselves.

This episode breaks down the two major classes of local anesthetics—amides and esters—and walks through the individual agents anesthesia providers need to know. We’ll compare their metabolism, duration of action, clinical uses, dosing considerations, and the characteristics that make each drug unique.

We cover commonly used agents including lidocaine, bupivacaine, ropivacaine, mepivacaine, chloroprocaine, tetracaine, and cocaine, with a focus on how their pharmacology translates into real-world anesthetic practice.

You’ll learn how to quickly distinguish amides from esters, why their metabolism and allergy profiles differ, which drugs carry greater risks for cardiotoxicity and systemic toxicity, and how to choose the right local anesthetic based on the procedure, desired onset, and duration.

Whether you’re preparing for boards or making decisions in the OR, this episode ties the individual drugs together in a way that’s easier to remember—and easier to apply.

Topics include:​ Amides vs. esters• Metabolism and elimination• Allergy considerations• Lidocaine• Bupivacaine• Ropivacaine• Chloroprocaine• Cocaine• Clinical pearls and high-yield differences between agents

Why do some local anesthetics kick in faster, last longer, or produce a denser block than others? In Part 2 of our Local Anesthetics series, we break down the pharmacology that explains how local anesthetics actually behave in clinical practice.

We’ll cover differential blockade and why sympathetic, sensory, and motor function aren’t always lost—or recovered—at the same time. Then we’ll connect pKa to onset, explaining how the balance between ionized and nonionized drug determines how quickly a local anesthetic can cross the nerve membrane.

We’ll also tackle what determines potency and duration, including the roles of lipid solubility, protein binding, tissue vascularity, and local blood flow. Along the way, we’ll connect these concepts to the local anesthetics you use every day so they’re easier to remember when it matters.

By the end of this episode, you won’t just memorize which local anesthetic is fast, potent, or long-acting—you’ll understand why.

Vital Flow — anesthesia concepts that actually make sense.

In Part 1 of the Vital Flow Local Anesthetics series, we’re going back to the physiology that makes local anesthesia possible. We’ll break down how nerves generate and propagate action potentials, the role of sodium channels in depolarization, and exactly how local anesthetics interrupt nerve conduction.

We’ll also explore why some nerve fibers are blocked before others, how local anesthetics cross the nerve membrane, the importance of pKa and tissue pH, and why local anesthetics may be less effective in infected or acidic tissue.

By understanding what’s happening at the cellular level, the pharmacology of local anesthetics becomes much easier to predict and apply in clinical anesthesia.

🎧 In this episode:

• Resting membrane potential and action potentials
• Voltage-gated sodium channels
• How local anesthetics enter and block the sodium channel
• Ionized vs. nonionized drug
• The significance of pKa and pH
• Use-dependent (frequency-dependent) blockade
• Differential nerve blockade
• Why fiber size, myelination, and firing frequency matter
• Why local anesthetics work poorly in acidic/infected tissue
• How nerve physiology translates into clinical anesthesia

Master the physiology first—and the pharmacology starts to make sense.

Vital Flow is intended for educational purposes and does not replace clinical judgment, institutional protocols, or manufacturer recommendations.

Pneumoperitoneum changes more than the surgical view—it changes the physiology you’re managing. In this episode of Vital Flow, we break down the anesthesia considerations of laparoscopic surgery, from the cardiovascular and respiratory effects of increased intra-abdominal pressure to CO₂ absorption, positioning, ventilation, hemodynamic changes, and potential complications.

We’ll connect the physiology to what you actually see in the OR and discuss how anesthetic management can help anticipate and correct these changes. Whether you’re preparing for boards or managing your next laparoscopic case, this episode gives you a practical framework for understanding what happens when the abdomen is insufflated—and why it matters.

Because in laparoscopy, pressure changes everything.

Bradycardia in the OR. Copious secretions. Reversal with neostigmine. These are all situations where understanding anticholinergic pharmacology matters.

In this episode of Vital Flow, we break down the parasympathetic nervous system and anticholinergic medications from an anesthesia perspective. We’ll review acetylcholine, muscarinic receptors, and nicotinic receptors, then connect that physiology to the medications we use in everyday practice.

We’ll take a closer look at atropine and glycopyrrolate, including their mechanisms of action, dosing, onset and duration, effects on heart rate and secretions, and one of their most important differences: atropine crosses the blood-brain barrier, while glycopyrrolate does not.

We’ll also discuss how anticholinergics fit into the treatment of perioperative bradycardia, their role as antisialagogues, and why glycopyrrolate is paired with neostigmine during neuromuscular blockade reversal.

Along the way, we’ll connect the pharmacology to real clinical situations and review the adverse effects that come from blocking parasympathetic activity.

Whether you’re an SRNA learning autonomic pharmacology or an anesthesia provider looking for a high-yield refresher, this episode will help you understand not just when to give an anticholinergic, but what is happening physiologically when you do.

Blood pressure is falling. Heart rate is climbing. Do you reach for phenylephrine, ephedrine, norepinephrine—or a beta-blocker? The right drug starts with understanding the receptors.

In this episode of Vital Flow, we break down vasopressors, alpha-blockers, and beta-blockers through the physiology that actually matters in anesthesia. We’ll review alpha-1, alpha-2, beta-1, and beta-2 receptors and connect receptor activity to changes in vascular tone, heart rate, contractility, cardiac output, and blood pressure.

We’ll cover commonly used vasopressors including phenylephrine, ephedrine, norepinephrine, epinephrine, vasopressin, and dopamine, along with alpha- and beta-adrenergic blockers and how blocking these receptors changes the hemodynamic picture.

From treating anesthesia-induced hypotension and vasodilation to controlling hypertension and tachycardia, we’ll connect the pharmacology to real perioperative situations so you can understand not just what each drug does, but why it does it.

Whether you’re an SRNA learning adrenergic pharmacology or an anesthesia provider looking for a high-yield refresher, this episode is designed to make receptors, pressors, and blockers finally click.