Locals: Whats the deal?

Local anesthetics are a valuable part of anesthesia care. This class of medication proves to be extremely beneficial for patients whether it's a spinal, epidural or a peripheral nerve block. Listen and get a basic understanding of how local anesthetics work, what is pKa and what is local anesthetic systemic toxicity. Let's Go!

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Welcome to Bent on Education Podcast, a podcast focusing on evidence-based review of physiology, pharmacology, pathophysiology, and other anesthesia-related topics. I'll discuss being a clinical preceptor, a mentor, and a leader. This podcast is by CRNA for SRNAs and others seeking to build their basic knowledge base. So let's get bent on education. Well, welcome back to Bent on Education Podcast. So today we're going to talk about a pretty important topic within anesthesia, local anesthetics. So whether you're in clinical and you're putting in an epidural or you're helping or doing a peripheral nerve block or a spinal, um, understanding how the pain pathways work, local anesthetics are really one of the foundations of nurse anesthesia practice. So for many of the sRNAs out there, local anesthetics can seem super intimidating. And mostly because there are so many different ones, so many concentrations, dosing recommendations, and things like that. And of course, toxicity concerns. But hopefully, I can simplify the topic a little bit and give you a solid knowledge base that you can build upon throughout your training as an SRNA and of course going into anesthesia practice. So we want to talk about a couple things like how do locals work and what makes us know how quickly they're going to work? What determines how long the local is going to last and things like that. So let's go ahead and get started. So before we discuss like pharmacology, we have to remember why local anesthetics are such an important part of our practice. Um, regional anesthesia gives really good postoperative pain control to patients. The other thing, too, is that we're able to reduce some of the opioid consumption that is out there, helps our patients maybe mobilize a little bit quicker, depending on what kind of block they have, of course. Um, decreases in nausea and vomiting. Uh, post-operative nausea and vomiting is one of those big topics within anesthesia. And potentially for those who are staying overnight in a hospital, maybe they get a little bit of a shorter stay in, you know, in the hospital setting. So as someone who is around local anesthetics, as a CRNA, locals allow us to give anesthesia while minimizing, if you will, systemic medication requirements. So those opioid requirements. Every time in our practice we perform a spinal or an epidural or a tap block or adduct or canal block or anything like that, we rely on our understanding of how local anesthetics work. Let's talk a little bit about nerve transmission signals. So, in order to understand local anesthetics, we first have to understand what they're trying to stop. Um, so the nerves communicate, of course, using electrical impulses, and those impulses are called action potentials. So, when the action potential, or I should say when the nerves are at rest, um the nerve cells remain in a negative electrical charge that's inside the cell. So a couple of things happen when they are stimulated. Sodium channels open, sodium enters the cell, depolarization can then occur, and the electrical signal travels down the nerve. So you have to think, I guess broadly, that sodium channels are like the door that allows a message to move from one part of a nerve to another part of a nerve. And what happens is if we block that door, the message cannot travel, right? So no message means that there's no pain transmission. It means that there is no temperature sensation and no motor function if enough of those fibers are affected. So this is exactly what local anesthetics do. Now, as we get into the nitty-gritty, it's really important for us to understand what the mechanism of action is as well. So the primary mechanism of a local anesthetic is to block the voltage-gated sodium channels, which we talked a bit about those sodium channels earlier. So local anesthetics will enter the nerve and bind to the sodium channels from the inside. Now, when sodium cannot enter, what happens? Depolarization is prevented, um, action potentials can't propagate a signal, and nerve conduction stops. So a phrase that many students memorize is local anesthetics prevent sodium influx. And that statement is absolutely correct. So when no sodium influx happens, then no nerve signal can happen either. And no nerve signal happening means that there is no sensation as well. So as we talk about local anesthetics, we also need to talk about which nerve fibers are blocked first. One of the really fascinating things about locals is that not all nerve fibers are blocked equally or to the same uh depth, if you will. So generally, the smaller fibers are blocked before the larger fibers. Pain fibers tend to disappear before motor function. Now, the typical progression when we're looking at fibers that are blocked is pain first, temperature second, then touch, then pressure, then motor function. So this explains why patients might say I can't feel the pain, but they can still move that extremity. As the block becomes denser, the motor function will also disappear, or may also disappear. Now, looking at the chemical structure of our local anesthetics, you have to remember that every local anesthetic has three components. One is the lipid soluble aromatic ring. Um, the second is an amine group, and the third is an intermediate chain. Now, the intermediate chain is what determines whether the local anesthetic is an ester or if it's an amide. So this is one of the most commonly tested concepts uh in anesthesia education when we're talking about local anesthetics. Let's talk about esters versus amides. It's simple to remember, or a simple way to differentiate the two is to know that amides has or amides have two eyes. So some of the examples of amides include lidocaine, ropivacaine, bupivacaine, mepivacaine, and prilocaine. And some of the examples of ester local anesthetics would be like procaine, chloroprocaine, tetracaine. So why does this really matter? The reason why it matters is because the two classes are metabolized very differently. Esters are metabolized primarily by our plasma choline esterases, but our amides are metabolized primarily in the liver. So what does this mean for us clinically? Clinically, it means that patients with severe hepatic dysfunction may have like an altered metabolism of our amide local anesthetics. Fortunately for us, the majority of our local anesthetics we use now are amides. Now, one of the parts of learning about local anesthetics is PKA. And it's not anyone's favorite part of learning about locals for sure. So when we think about PKA, you want to think about the onset of your local students and cRNAs alike struggle with PKA, but let's try and put it a little bit in a simplified form. So I teach pharmacology to our first-year nurse anesthesia students. And I'm not saying that I'm, you know, this pharmacology PKA guru, but I understand it to somewhat of a level that I can teach it to our students. So local anesthetics exist in two forms. One is an ionized form and one is an unionized form. So the unionized form crosses nerve membranes. Now the ionized form actually blocks the sodium channel. So the closer a drug's pKa is to physiologic pH, the more unionized drug will be available. So more unionized drug means that there's faster membrane penetration and a faster onset as well. This is why lidocaine generally works faster than bupivacaine. So for clinical practice, just remember this: that the lower the pKa means that there's a faster onset of that local anesthetic. Another aspect of you know understanding local anesthetics would be understanding lipid solubility. So this is a major property as well. Highly lipid soluble drugs penetrate nerve membranes more effectively and you know more quickly. So the greater lipid solubility generally means that the local is more potent and it has better nerve penetration, like I said before. Bupivacaine and its S isomer, rhopivacaine, are highly lipid soluble, and therefore those two local anesthetics are very potent. Another piece of the puzzle would be protein binding. So protein binding largely determines the duration of action of our local anesthetic. The more protein bound a local anesthetic is, the longer it tends to remain associated with the receptors and with the tissues. When we look at protein binding, the greater protein bound means longer duration and more prolonged analogesia for the patient. Bupivacaine is a very highly protein-bound local anesthetic, and so it's gonna last much longer than lidocaine. Other aspects that we need to look at are vasodilation and the absorption of our medication. Most of our local anesthetics cause a degree of vasodilation. So when blood vessels dilate, the drug is absorbed a little bit more rapidly and the duration then shortens. And systemic levels of that medication will be increased. This is why epinephrine is often added to our local anesthetics. As opposed to the vasodilation that our local anesthetic causes, epinephrine causes vasoconstriction. Now, the benefit of adding um epinephrine to our local anesthetic is that it helps prolong the duration of action, it reduces that systemic absorption of our local anesthetic, and potentially it proves to be a way by reducing the toxicity of our local anesthetic as well. You can kind of think of it in a way that epinephrine helps the local anesthetic kind of stay where you want it. Now, we're going to talk about some of the most commonly used local anesthetics because it's worth like kind of giving you a brief on some of the medication that in this class that we use more often than others. So, lidocaine. It's probably one of the most known uh local anesthetics. It's probably one that most students will encounter first, right? So, what are some of the characteristics of lidocaine? It has a fast onset, intermediate duration, and it's highly versatile. So, what do I mean by that? Uh, you've probably heard of controlling like arrhythmias with lidocaine. So it's a very versatile um medication. Why do we use lidocaine in the OR or for patients? Um, we use them as a local infiltration. You're gonna put an IV in, so maybe you infiltrate a little lidocaine first. Um, we use them for peripheral nerve blocks, we use lidocaine for epidurals and intravenous regional anesthesia, like a beer block or something like that. Lidocaine is very dependable, it's pretty predictable, and it honestly remains one of the workhorses of um our local anesthetic agents. Now, bupivacaine is another major local anesthetics that we encounter constantly as well. One of the things about bupivacaine and how it differentiates from lidocaine is that it has a slower onset, a much longer duration of action, and a very dense sensory blockade. So it's frequently used for epidurals, spinals, nerve blocks. I mean, at the end of a case, a surgeon may infiltrate bupivacaine into the incision. One of the major concerns, though, that we have with bupivacaine is that it is uh cardiotoxic. So, compared with other local anesthetics, bupivacaine actually has a greater potential for severe cardiac complications if systemic toxicity does occur with it. This is one of the major reasons why every anesthesia provider has to be comfortable recognizing uh local anesthetic toxicity or last. Now, another local anesthetic that has really been in favor is uh rhopivacaine. So, rupivacaine was developed really to provide prolonged analoggesia, and it really has an improved um patient safety profile over bupivacaine. So, compared with bupivacaine, it has a similar duration of action. It's slightly less potent and less cardiotoxic. So many providers will favor rhopivacaine for peripheral nerve blocks because it's an excellent sensory blocker. And again, that favorable safety characteristic of the medication. Chloroprocaine kind of deserves like an honorable mention here as well. Um, the characteristics of chloroprocaine is that it has a very rapid onset and a very uh short duration of action. Because it's rapidly metabolized by our plasma cholinesterases, it can be used um when a short duration uh local anesthetic or anesthesia is desired. Now, as most of us know, when we talk about spinal anesthesia, so we'll talk about spinal anesthesia, we'll talk about um epidural anesthesia as well. But when we infiltrate our local anesthetic into our cerebral spinal fluid, we produce what's called spinal anesthesia. So some of the factors that affect the spread of our spinal anesthetic are the dose of the medication we're giving, um, the baricity or how heavy, for lack of better words, how heavy that local anesthetic is, the patient's position after we deliver the local anesthetic, and injection characteristics as well. So a spinal block produces pretty profound sensory and motor blockade because the local anesthetic directly bathes the nerve roots. This is why relatively small doses can create a dramatic effect in patients. Now, epidural anesthesia is different from spinal anesthesia. Instead of directly entering the cerebral spinal fluid, local anesthetic is placed into the epidural space, and the epidural space is a potential space. So the drug has to diffuse across tissues before it reaches the nerve roots. As a result of that, larger doses of the local anesthetic is needed, the onset is slower, and the blocks can be titrated. We can give more medication through an epidural, whereas a spinal is a single shot, unless you're doing a second spinal. So this flexibility makes our epidurals very useful for like laboring analoggesia and major surgical procedures and even postoperative, you know, uh care if we needed it for postoperative analogesia. Peripheral nerve blocks. Peripheral nerve blocks have gained a lot of popularity and it continues to grow as well. Using ultrasound guidance, we can place local anesthesia precisely around the nerves. So some examples of peripheral nerve blocks that are utilized are interscaline blocks, femoral blocks, adductor canal blocks, adductor canal blocks. Sorry, say that three times fast, tap blocks, and popliteal blocks. So understanding local anesthetic pharmacology helps us choose the correct agent based on the anticipated duration of pain. So, what are some of the factors though that affect the block quality? Many students assume that every block should work perfectly. I mean, that's the plan, but that doesn't always work as planned. But in reality, block success depends on a couple factors too. A patient's anatomy, the technique that's used, um, the selection of the drug, the volume of the anesthetic that we're delivering, of course, the concentration and the tissue environment as well. Infected or inflamed tissues can be acidic. So when we're considering an acidic environment, acidic environments reduce the amount of unionized drug that's available. So as a result of that, local anesthetics often work less effectively in affected tissues if they work at all. So this is just a classic clinical, you know, teaching that we all should know about and understand why it happens like that as well. So local anesthetic systemic toxicity. This is a complication that every sRNA should be able to recognize, or you know, you want to be able to recognize that so we can treat the patient. So local anesthetic systemic toxicity occurs when an excessive amount of local anesthetic enters systemic circulation. So this can occur from accidental intravascular injection. Excessive dosing of a local anesthetic or rapid absorption of that anesthetic. Although it is common, it is life-threatening. So we need to understand and see what the signs are of last. So some of the early neurological symptoms may include circumoral numbness. And that's something our patient can tell us if they're awake. Of course, that metallic taste in the mouth, ringing in the ears, dizziness, and just overall agitation. These are warning signs. If we recognize these signs early, we can intervene before cardiovascular collapse potentially can develop. So what is the progression of toxicity? And as this worsens, patients may develop seizures, altered mental status, of course, some compromise in their respiratory drive and respiratory system. From a cardiovascular standpoint, some of the effects may include hypotension, of course, brachycardia, ventricular arrhythmias, and potential cardiac arrest. Remember, I said earlier that bupivicine is particularly notorious for severe cardiac toxicity. So, how is last treated? Every anesthesia professional should know the treatment algorithm for LAST. What are the key steps? Stopping that local injection, right? Stop injecting local anesthesia. We don't want to continue to inject our local anesthetic if our patient is having an issue. We want to call for help. Of course, manage the patient's airway and oxygenation. If the patient were to have seizures, you want to make sure that you treat those seizures uh quickly and promptly and begin lipid emuls therapy. Now, lipid emulsion therapy has dramatically improved the outcomes for patients who develop local anesthetic systemic toxicity. Many people describe it as kind of a lipid sink, if you will. The concept is that the lipids will help to sequester lipophilic local anesthesia molecules and reduce their toxic effect. So know where your intralipids are. There are some providers that I work with that they will not do a block or anything like that unless they have lipids in the room with them before they're doing the block. So some practical pearls, if you will, for students as we are wrapping up here. Number one, you want to understand the concept before memorizing doses. Of course, you have to memorize doses of things, but understand concepts before memorizing doses. You want to be able to differentiate between lidocaine, bupivacaine, and ropivacaine. Um, three, always calculate the maximum safe dose before performing any block because maybe you know someone does the block, they're like, oh, I think I need more, I didn't get a good spread on the um ultrasound. But you want to make sure that you know your maximum safe dose, both in milligrams and in MLs. Of course, number four, like any anesthetic, we want to respect our local anesthetics. They are an incredibly useful medication, but they can become dangerous when we use them improperly. And number five, this is probably the biggest thing, is never stop learning about regional anesthesia. It is one of the fastest growing and most rewarding areas of anesthesia practice. Um, you know, it's so helpful for our patients, and we just want to make sure that it's something that we continue to learn and grow with. So we discussed how these locals work by blocking sodium channels, um, reviewed some of the differences between esters and amides. Remember that amides has two eyes. Um, we also explored some of the factors that affect the onset and duration of our local anesthetic. So if you are an sRNA out there listening to this episode, share it with a friend. Um, and my advice is simple focus on understanding the big picture. So when you understand that sodium channel blockade, pKa, uh protein binding and toxicity, the rest of local anesthetic pharmacology becomes a little bit easier to learn. Um, again, if you found this episode to be helpful for you, please subscribe, leave a review, share it with a classmate or um, you know, another friend, and we'll just continue to learn. So until next time, get in on education.