Chapter 12: General & Local Anaesthetics

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Okay, let's unpack this.

We are undertaking a deep dive into one of the most critical and frankly high stakes areas of healthcare, the tools we use to manage pain and consciousness,

anesthetics.

Specifically, we're diving into chapter 12 on general and local anesthetics from Lily's Pharmacology for Canadian healthcare practice.

And our goal today really is to give you, the learner, a bit of a shortcut.

We want to synthesize the core pharmacology, you know, the clinical realities and those absolutely vital nursing responsibilities that come with anesthetic drugs.

We need to go beyond just listing facts and really get into the why the mechanisms of action, the MOA, and crucially the safety implications.

Yeah, and the vocabulary is probably the best place to start.

When we talk about anesthesia, we're simply talking about losing the ability to feel pain through drug administration, but it immediately splits off, doesn't it?

It really does.

You've got the whole body approach.

General anesthesia or GA, this is a drug -induced state, needs total system control,

complete loss of consciousness, affects the whole body, and this is key, it depresses the normal respiratory drive.

Okay, total shutdown, then there's the more targeted approach, local anesthesia, LA.

Exactly.

Here, we're just altering peripheral or spinal nerve impulses, so you get sensation reduction in a specific area, but, and this is the big difference, the patient stays conscious.

They maintain control over their body systems.

It seems like, though, modern practice isn't usually just one GA drug, is it?

No, rarely.

Yeah.

It's all about balanced anesthesia, using helper drugs, adjuncts from different classes.

This synergy lets practitioners use lower doses of those really potent GA agents.

Which means better control.

Better control and drastically reducing the overall toxic load on the patient.

It's a much safer approach overall.

Okay, so if we're looking at the drugs used for that total system shutdown, the GA, there are two main routes,

inhaled and correntral, meaning IV.

What are the key differences there?

Well, the inhaled agents, these are volatile liquids or gases mixed with oxygen.

They're really about precise control.

Take sevalfluorine, for instance, it has a rapid onset and, just as importantly, rapid elimination.

The patient wakes up faster.

Which makes it good for...

Excellent choice for outpatient surgery.

Pediatrics, too, partly because it's less irritating to the airway.

Then you've got nitrous oxide at the other end of the spectrum.

It's the weakest GA, really.

Laughing gas, right?

Yeah, mostly used as a supplement to other agents or for, you know, minor dental work.

Okay, then on the parenteral side, the IV drugs, we see some real heavy hitters like propofol and ketamine.

But before we get into specifics, we should probably touch on how these drugs actually work on the nervous system.

The Overton -Meyer theory comes up here.

Ah, yes.

This is fundamental to understanding GA mechanism of action.

The theory basically states that potency is directly linked to lipid solubility.

Lipid solubility.

And fat solubility.

Exactly.

Your nerve cell membranes, the blood -brain barrier, they're essentially layers of fat.

So the more fat -soluble the anesthetic drug is, the easier it crosses those barriers, the more it concentrates in the nervous system, and therefore the stronger its effect.

Simple chemistry.

Really powerful biological effect.

And the goal of that chemistry is massive depression of the central nervous system.

The source material really emphasizes that GA causes a progressive reduction of function.

Sensory and motor control go first.

What's the critical bit about what goes last?

The functions controlled way down in the medulla, so cardiac function and pulmonary function.

Those are the absolute last things to be interrupted by the anesthetic.

That seems crucial for safety.

It is.

It tells you the clinical goal.

We're intentionally shutting down non -essential systems, metabolism, muscle tone, even some blood flow regulation, while carefully protecting that final line of defense.

But, and this can't be stressed enough because respiratory drive is suppressed,

mechanical ventilation is absolutely non -negotiable with GA.

Okay, let's zoom in on those IV agents then.

Propofol.

It seems to be everywhere.

Induction, maintenance, even long -term sedation in the ICU.

What's its profile?

Propofol works by enhancing GABA activity.

GABA is like the brain's main off switch.

Its primary inhibitory neurotransmitter.

So, propofol turns up the off switch.

Pretty much, yeah.

It leads to profound sedation.

But the critical point for anyone administering it or caring for the patient is that it has no analgesic properties.

None at all.

So, it stops movement in memory, but not the pain signal itself.

Exactly.

That's why it's often given with an opioid.

Also remember, it's in a lipid emulsion, that moky white stuff.

Right.

So, you have to monitor serum lipids, especially with longer infusions.

And the biggest safety watch out, it's dose -dependent reduction in blood pressure and cardiac output You have to watch hemodynamics very closely.

Okay.

Contrast that with ketamine.

The book calls it unique.

Works on different receptors and MDA receptors involved in pain.

What's the trade -off?

Ketamine's great because it often maintains cardiovascular function better than propofol.

That makes it popular for procedural sedation,

like setting a complex fracture in the emergency department.

But its major downside is the potential for disturbing psychomimetic effects.

Things like hallucinations, vivid dreams, general disorientation.

That sounds unpleasant.

It can be.

Fortunately, giving a benzodiazepine alongside it usually lessens that risk quite a bit.

And finally, under GA, we have to talk about the ultimate danger, the one always flagged as high alert, malignant hyperthermia, MH.

Yes.

This is the most acute, life -threatening emergency in anesthesia.

It's genetic.

A rapid, potentially fatal metabolic reaction.

Triggered by?

Triggered specifically by volatile inhaled anesthetics like sevilleflurane or the neuromuscular blocker succinylcholine.

You'll see a sudden rapid rise in temperature, extreme muscle rigidity, fast heart rate, fast breathing.

Tachycardia, tachypnea.

Right.

You must know the treatment.

Immediate supportive care, cooling measures, and the specific antidote, the muscle relaxant dantrolene sodium.

Every place using these triggering agents has to have dantrolene immediately available.

Okay, so we've covered GA, the complete shutdown.

But what about times when you just need the patient relaxed, pain -free, maybe a bit forgetful, but still fundamentally stable?

That's procedural sedation, isn't it?

Exactly.

Sometimes called conscious sedation, though procedural sedation is the preferred term now.

It's like a milder form of GA, aiming for that sweet spot.

Sweet spot meaning?

Meaning the patient might lose consciousness partially or even completely, but, and this

advantage,

it generally preserves the normal respiratory drive.

The patient can usually maintain their own airway, maybe even respond to commands.

So procedures like endoscopies, cardioversions, things you couldn't do easily on someone wide awake but don't need full GA for.

Precisely.

It's a massive win for safety.

You get much faster recovery times and significantly lower risks to the heart and lungs compared to full general anesthesia.

And how is it usually achieved?

Is there a standard approach?

There's a very common combination, kind of a standard cocktail,

a benzodiazepine, usually minazolam, for amnesia and anxiety reduction.

Makes sense.

Plus an opioid, often fentanyl or morphine, for the pain relief.

But the crucial detail here is dosing.

Because these drugs potentiate each other to make each other stronger,

the doses of both drugs need to be cut back significantly, usually by 30 to 50 % when you use them together.

To avoid over sedation.

Exactly.

To avoid dangerous respiratory depression or cardiovascular instability.

It requires careful titration.

Alright, so we've covered general control.

Now let's switch gears entirely to local control.

How do local anesthetics actually stop a nerve signal cold?

The mechanism, the MOA, for LA's is quite elegant actually.

They work by stabilizing the nerve membrane itself.

Stabilizing how?

They physically block the movement of critical ions, sodium, potassium, and calcium, across the nerve cell membrane.

These ions are absolutely necessary for generating and conducting that electrical nerve impulse.

So no ion movement, no signal.

No signal.

Simple as that.

The nerve impulse just can't propagate past the blocked area.

What's fascinating clinically is that the effect isn't random.

There's a predictable order to how function is lost and regained, right?

Yes, absolutely.

Autonomic functions, things like sensing temperature or vasodilation control, those are lost first.

Then pain sensation and other sensory functions get blocked.

Motor activity, the ability to move muscles is always the last thing to go.

And recovery?

Happens in the exact reverse order.

Motor function comes back first, then sensory, then autonomic.

Knowing that sequence is really important for assessing recovery.

Okay.

Now LA's fall into two main chemical classes,

esters and amides.

Lidocaine, probably the most common one we use, is an amide.

Why do we need to know about esters versus amides?

It really boils down to allergies.

Esters get metabolized into a compound called PAVA, paraminobenzoic acid.

And PAVE is much more commonly associated with true allergic reactions compared to the amide breakdown products.

So if someone has a true allergy to, say, an ester type.

You can usually safely switch to an amide, like Lidocaine, without worrying about cross reactivity and vice versa.

It gives you options.

Makes sense.

Let's talk about how they're given.

The central injections sound like they carry pretty significant risk.

Oh, absolutely.

These are high stakes procedures.

Central injections are either spinal, also called intrathecal,

that's injecting directly into the subarachnoid space where the cerebrospinal fluid is, often used for a major abdominal or lower limb surgery, or c -sections.

Okay.

Or it could be epidural, where a small catheter is placed just outside the dura into the epidural space.

This is very common for labor pain relief or managing post -operative pain over a longer period.

Then moving away from the spine for peripheral use, we often see infiltration.

That's just small amounts injected right into the tissue.

Yeah, exactly.

Like numbing up skin before stitching a cut.

And often it's combined with a vasoconstrictor, usually epinephrine.

Why epinephrine?

The epinephrine constricts the local blood vessels.

Two main benefits.

Yeah.

First, it keeps the local anesthetic concentrated right there, reducing how much gets absorbed into the bloodstream systemically.

Second, it reduces bleeding at the site.

Handy.

And the other peripheral type.

Ervblox.

This is where you inject the LA near major nerve trunks to numb up a whole region, like an entire arm or leg, for surgery.

Okay.

Now, one specific adverse effect of those central injections, particularly after the dura, might get punctured during an epidural or spinal.

The spinal headache.

The book mentions it can happen quite often.

Yeah.

Incidents can be surprisingly high, sometimes up to 70 % after certain procedures involving

The symptom is classic.

The headache is awful when the patient sits or stands up, but gets much better when they lie down flat.

What's the treatment?

It starts with conservative things.

Bedrest, hydration, caffeine, sometimes helps constrict cranial vessels.

But the most effective treatment, if those fail, is something called a blood patch.

A blood patch.

Yeah, they draw some of the patient's own blood and carefully inject it back into the epidural space near the puncture site.

Yeah.

The idea is it forms a clot and physically seals the hole where cerebrospinal fluid was leaking out.

It'd be remarkably effective.

Wow.

Okay, that brings up a huge safety point mentioned in the text.

Anticoagulants before any spinal anesthesia.

Critical point.

Anticoagulant therapy,

including the newer direct oral anticoagulants, the DOACs, must be stopped for a prolonged period beforehand.

We're talking potentially 12 hours, maybe even up to 92 hours, depending on the drug and renal function.

Why so long?

The risk of bleeding into that confined space around the spinal cord could be catastrophic.

A spinal hematoma can cause permanent neurological damage.

It's just too high a risk.

Got it.

And just to circle back quickly, you mentioned lidocaine as the common amide.

It pops up elsewhere too, doesn't it?

It does.

It's incredibly versatile.

We use it topically, often mixed with prelocaine and e -malay cream for numbing skin before heavy starts.

Besides infiltration and nerve blocks, its IV form is a class IB antiarrhythmic drug used to treat certain ventricular heart rhythm problems.

Our last big category of drugs, and maybe the trickiest conceptually, neuromuscular blocking drugs, NMBDs.

These aren't anesthetics themselves, right?

They're adjuncts.

Exactly.

They don't cause sedation or pain relief.

Their sole purpose is to cause muscle paralysis, usually for surgery, to relax the muscles for better access, or to facilitate mechanical ventilation in the ICU.

And because of that effect, they are definitely high alert drugs.

Absolutely top tier high alert.

They paralyze all skeletal muscles, including the diaphragm and intercostal muscles needed for breathing.

So mechanical ventilation is absolutely required, mandatory, non -negotiable.

That's the core physical safety point.

But there's a psychological one too.

Yes.

And it's vital.

A patient receiving an NMBD, even though they can't move, can often still hear and potentially still feel pain, if not adequately managed.

They must receive adequate sedation and analgesia concurrently.

Imagine being awake but unable to move or breathe on your own, terrifying.

OK.

The mechanism of action here gets really interesting because there are two fundamentally different ways these drugs work.

That's right.

It's fascinating.

First, you have the depolarizing NMBDs.

There's only one clinically relevant drug in this class, cystealcholine.

Cycatincholine.

How does it work?

It actually acts as an agonist at the acetylcholine, or AKC, receptors on the muscle.

It mimics AC, binds to the receptor, and causes the muscle cell membrane to depolarize, leading to contraction.

Wait.

It causes contraction.

I thought it caused paralysis.

It does both.

Initially, it causes depolarization and contraction.

You often see this as muscle fasciculations, like little twitches all over.

Right.

Phase one.

But cystealcholine isn't broken down by the normal enzyme at the junction, so it hangs around, keeping the membrane depolarized.

The muscle can't repolarize, so it can't contract again.

It enters a state of flaccid paralysis phase two.

Its effect is very fast onset but also very short duration, usually five to nine minutes.

OK.

So it forces contraction, then exhaustion.

What about the other class?

The other, much larger class, are the non -depolarizing NMBDs.

Think drugs like vecuronium, rocuronium.

These work as straightforward antagonists.

Blockers.

Exactly.

They physically sit on the AC receptors and block AC from binding.

No ACE binding means no depolarization, which means no muscle contraction.

They just prevent the go signal from getting through.

These have varying durations, intermediate or long -acting.

And just like with local anesthetics, there's a predictable sequence to the paralysis.

Yes, there is.

Small, rapidly moving muscles, fingers, eyes get paralyzed first.

Then the limbs, neck, and trunk muscles.

Finally, the intercostal muscles and the diaphragm, the main muscles of breathing, are paralyzed last.

And recovery.

Reverse order again.

Diaphragm function returns first, then trunk limbs, then the small muscles.

Monitoring this sequence helps assess when the patient might be ready to breathe on their own again.

Now what if you need to reverse the paralysis quickly,

specifically for those non -depolarizing blockers like rocuronium?

We have antidotes.

We use anticholinesterase drugs like neostigmine.

How do they work?

They don't kick the blocker off the receptor directly.

No, they work indirectly.

They inhibit the enzyme, acetylcholinesterase, which normally breaks down A in the...

So they stop the clean -up crew.

Essentially, yes.

By stopping the breakdown of A, say, the concentration of AET builds up significantly at the neuromuscular junction.

Eventually, there's so much natural AC that it outcompetes the non -depolarizing blocker for the receptor sites, displaces it, and restores muscle function.

Okay, wrapping this all together for you, the learner.

These final points are about what this means in daily clinical practice.

When dealing with any anesthetic or NMBD, what's the absolute top priority assessment?

It always, always comes back to the ABCs.

Airway, breathing, circulation.

That's your constant immediate check during induction, maintenance, and emergence from anesthesia.

But backing that up, a thorough baseline assessment before any drugs are given is paramount.

What kind of baseline?

You absolutely need to document baseline neurological function, level of consciousness, motor strength, sensory function, even swallowing ability before the procedure.

This gives you something concrete to compare against afterwards.

And what specific history elements are crucial to get?

Well, allergies, obviously.

But also, any history of substance use, particularly alcohol and nicotine.

Nicotine use is highly relevant.

Why nicotine specifically?

Because chronic smoking paralyzes the tiny cilia in the respiratory tract that normally

This significantly boosts the risk of post -operative respiratory complications like atelectasis, where lung segments collapse, and pneumonia.

Good point.

What about lab work, beyond just checking liver and kidney function for drug clearance?

Electrolytes are key,

specifically potassium and magnesium levels.

Imbalances, either high or low, can drastically alter how patients respond to NMBDs and other CNS depressants, potentially prolonging paralysis or causing arrhythmias.

And of course, for any female patient of childbearing age, a pregnancy test is standard protocol before administering drugs that could potentially harm a fetus.

We also need to remember specific populations are at higher risk, right?

Older adults and children.

Absolutely.

Older adults often have some degree of generalized organ deterioration, maybe reduced liver or kidney function, maybe increased CNS sensitivity.

This puts them at higher risk for drug toxicity and prolonged effects.

And kids?

Children, especially infants and neonates, have immature liver and kidney function, affecting drug metabolism and excretion.

Their airways are smaller and more reactive, too, increasing risks like laryngospasm.

Dosing needs to be very precise and monitoring extra vigilant.

When it comes to actually giving these drugs, implementation safety is everything.

Resuscitation gear must be right there, ready to go.

But focusing again on the patient getting an NMBD, you mentioned educating them beforehand.

Why is that so critical?

Because they need to understand what's going to happen.

They need to know that even if they feel paralyzed, unable to move or speak or signal distress,

that the team knows this and will be giving them medications to manage anxiety and pain.

Reassurance is key.

Critical.

And continuing to talk to them calmly, explaining what's happening, even if they appear unconscious, is vital.

It helps minimize the potential psychological trauma of that paralyzed state.

And then post -anesthesia care, this really falls heavily on the nursing team, doesn't it?

It really does.

Encouraging, frequent turning, coughing, deep breathing exercises.

That's essential to prevent those respiratory complications like pneumonia and adellectasis and getting the patient moving, ambulating, even with assistance, as soon as it's safe and ordered.

To prevent blood clots.

Exactly.

To prevent DVTs, deep vein thrombosis, and promote overall circulation and lung expansion.

We as nurses are often that final safety net, constantly watching for those subtle changes from baseline, a slight dip in oxygen saturation, a small rise in temperature that could signal early MH, slow return of bowel sounds.

It's continuous assessment.

So what does this all mean?

Let's recap.

We've covered the big differences.

GA means system shutdown, needs breathing support.

LA is targeted pain control, patients awake.

We highlighted those two opposite ways muscles get paralyzed.

Sustenal choline forces, depolarization, then exhaustion.

The agonist approach.

Right.

While drugs like rocuronium just block the receptor the antagonist way.

And we absolutely hammered home the signs, the triggers, and the critical rapid treatment needed for malignant hyperthermia with bantraline.

Crucial takeaways.

Yeah.

You know, if we loop back to that idea of procedural sedation where we get amnesia, reduced anxiety, good stability, rapid recovery, it does raise an interesting point for you to think about.

Well, if a patient is amnestic for the procedure and their vital signs bounce back to normal very quickly,

how do we truly gauge their full psychological recovery from the, you know, the significant physiological stress the body just went through?

Does that quick physical recovery always mean they've fully recovered emotionally and psychologically?

Or is there maybe a hidden stressor, a sort of subclinical impact that we need to be more aware of in our post procedure care and follow up?

That's a really interesting thought.

Something beyond just checking the boxes for vital signs and motor function.

Exactly.

Something to mull over.

Definitely something to carry with you as you integrate all this pharmacological knowledge.

Thank you so much for joining us on this deep dive into the source material.