Chapter 11: General and Local Anesthetics

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Welcome back to The Deep Dive.

Today, we're really getting into something quite technical, but absolutely critical,

perioperative pharmacology.

Yeah.

So we're going to unpack how these drugs work, the ones that let doctors temporarily switch off pain, sensation, even consciousness itself.

It sounds almost like science fiction, but it's everyday medicine.

It is.

And our goal today for you listening is clarity.

We've looked at the sources, focusing on the three big categories, general, local, and moderate sedation.

We'll cover how they work, the specific drugs, the big safety issues, and what nurses really need to know.

Exactly.

Starting with the basics.

Anesthesia just means the loss of the ability to feel pain because of a drug.

But it's not just one thing, is it?

It's a whole spectrum.

Definitely.

At one end, you've got general anesthesia, GA.

That's a drug -induced reversible state, total CNS depression.

Meaning?

Complete loss of consciousness, no memory of the event, and crucially, loss of body reflexes.

That includes the drive to breathe.

So under GA, you absolutely need a ventilator.

Correct.

Mechanical or manual support is essential.

The body's own systems are offline.

Okay.

And the other end of the spectrum, local anesthesia, LA.

Right.

LA is very targeted.

It knocks out pain only in a specific area, like where nerves are being directly numbed.

No loss of consciousness at all.

But you wouldn't do major surgery with just LA, usually.

Not typically on its own, no.

Which leads us to the sort of hybrid approach.

Ah, like monitored anesthesia care?

Or MS?

Precisely.

EMBA combines local anesthesia with some sedation and pain relief.

So the patient is relaxed, maybe a bit sleepy, but importantly, they can still breathe on their own and respond if you talk to them.

Makes sense.

And underpinning a lot of this is the idea of balanced anesthesia, using combinations of different drugs.

Why do that?

Well, you get better control, a more stable anesthetic state, and you can often use lower doses of each drug.

That usually means fewer side effects overall.

Okay.

So GA is the full shutdown, total CNS depression.

How do the drugs actually do that?

Our sources mention different types.

Yeah, mainly two delivery methods.

You've got the inhalational ones, gases,

or volatile liquids mixed with oxygen.

Think civil fluorine, nitrous oxide.

Stuff you breathe in.

Exactly.

And then parenteral given by IV.

Drugs like propofol or ketamine, these are often used to get things started for induction or to keep the anesthesia going.

And they don't work alone, right?

There are helper drugs.

Adjunct anesthetics.

Things like benzodiazepines, mitazolam is common to reduce anxiety.

Opioids like fentanyl for pain.

Even antibiotics for nausea.

So you have gases, liquids,

chemically quite different.

Is there a common thread for how they knock out the CNS?

There is, and it's fascinating.

It largely comes down to the Overton -Meier theory.

This theory basically says anesthetic potency is directly linked to how well the drug dissolves in lipids, or fats.

Why lipids?

Because nerve cell membranes, the brain itself, the blood -brain barrier, they're all rich in lipids.

Fat -soluble drugs cross these barriers easily.

So wait, are you saying the drugs that work fastest, like propofol for quick IV induction, are essentially just the greasiest ones?

Is it that simple?

Um, in a fundamental way, yes.

That's a good way to think about it.

Highly fat -soluble drugs get into those nerve membranes quickly and effectively.

Stronger, faster anesthetics.

And the overall effect is shutting down CNS functions?

Progressively, yes.

Sensory motor functions go first.

Importantly, the functions controlled by the brainstem, like heart rate and breathing, are the last to be affected.

That's a key safety feature.

Right.

Let's talk specifics.

Propofol is common for induction, but what about something like ketamine?

When would you use that?

Ah, ketamine.

It's a bit different.

A dissociative anesthetic.

Very lipid -soluble, very fast onset.

But here's the really interesting clinical nugget.

Ketamine actually dilates the bronchioles.

Bronchodilating.

So good for asthma patients.

Exactly.

It can be an excellent choice for someone with asthma or COPD needing general anesthesia.

A major plus.

But what about the side effects?

The hallucinations, the psychomimetic stuff it's known for?

That's a definite consideration.

It can cause some disturbing emergence reactions.

That's why it's very often given alongside a benzodiazepine, like metazolam.

To sort of smooth things out.

Precisely.

The benzo helps lessen the chance and intensity of those effects.

Okay.

Another one mentioned is dexmitetamidine, or Presedex.

What's the deal with that one?

Presedex is interesting.

It's an alpha -2 agonist.

Popular because it provides sedation and pain relief without causing significant respiratory depression.

That's a huge advantage in many cases.

No respiratory depression.

Sounds great.

Any catches?

Yes.

A big one.

The dosing.

It's a high alert medication because of this.

Presedex is dosed in micrograms per kilogram per hour.

Per hour.

Not per minute.

Correct.

Most other potent IV drips are memigio kilominit.

Mixing up hour and minute with Presedex could be catastrophic.

Very easy mistake to make if you're not vigilant.

Wow.

Okay.

Critical detail.

Speaking of critical.

Malignant hyperthermia.

MH.

Yeah.

That sounds terrifying.

It is.

It's rare, thankfully, but potentially fatal.

It's a genetically linked metabolic reaction to certain anesthetics.

Which ones trigger it?

Classically, the volatile inhalational gases we mentioned earlier and also a specific muscle relaxant called succinylcholine.

And what does it look like?

How would you know?

The signs are pretty dramatic.

A very rapid rise in body temperature, heart racing, fast breathing,

muscles becoming rigid.

What's the treatment?

Immediate, aggressive, supportive care managing breathing, circulation, and administering a specific drug, a skeletal muscle relaxant called dantrolene.

Facilities using these anesthetics are required by law to have dantrolene readily available.

Good to know.

And quickly, before we move on, any special considerations for older adults with GA?

Absolutely.

They often have reduced liver and kidney function, meaning they metabolize and excrete drugs more slowly.

So higher risk of toxicity.

Yes.

Increased risk of drug toxicity and overdose.

Plus, they often have existing heart or lung conditions, putting them at higher risk for complications like arrhythmias or pneumonia.

And polypharmacy interactions with their other medications is always a concern.

Okay, let's shift gears to that middle ground.

Moderate sedation, also called procedural sedation.

Right.

Here, the goal is different.

You want the patient comfortable, maybe sleepy, maybe even having a partial loss of consciousness.

But, and this is key, they must be able to maintain their own airway.

And they should respond if you talk to them?

Yes, they should be able to respond purposefully to verbal commands or light touch.

What drugs are typically used for this?

The classic combo is a short -acting benzodiazepine, usually midazolam, paired with a short -acting opioid like fentanyl or sometimes morphine.

Midazolam and fentanyl.

Okay.

Important, flaky point here from the sources.

Oh, yes.

The dosing.

If you combine midazolam with an opioid like fentanyl, you need to reduce the midazolam dose.

By how much?

Typically by 30 % to 50%.

Using them together significantly boosts the sedative effect, so you need less of the benzo.

Very important to remember.

Got it.

Midazolam often causes some amnesia too, doesn't it?

It often does, yes.

Mild amnesia is common and often desirable for the procedure, but you can't guarantee it.

So the takeaway for staff is...

Always act and speak professionally, as if the patient is fully awake and can remember everything.

Because they might.

Standard of care.

And this isn't something just anyone can administer, right?

There are rules.

Definitely.

The person giving the drugs needs advanced training, typically ACLS, Advanced Cardiac Life Support,

and critically, there must be one person whose only job is to monitor the patient.

Vitals, oxygen levels, responsiveness, no other tasks.

Dedicated monitor person.

That makes sense.

What about kids?

Pediatrics often involves oral metazolam syrup.

Dosing is strictly by weight, but kids' responses can vary a lot.

So start low.

Best practice is to start with the lowest recommended dose, or even half, and carefully titrate upwards based on response.

And you absolutely must have the reversal agents ready.

Meloxone for the opioid, flumazanil for the benzo.

Immediately available, non -negotiable.

All right, let's zoom in on local anesthetics, LA's.

We said they block pain locally, no loss of consciousness.

How did they actually stop that nerve signal?

They're known as membrane -stabilizing drugs.

It's all about ion movement across the nerve cell membrane.

Ions like sodium.

Exactly.

To fire an impulse, nerves need ions like sodium, potassium, and calcium to move across their membranes.

LA's interfere primarily with sodium influx.

They block the sodium channels.

So no sodium gets in?

The nerve can't depolarize?

And the signal can't be transmitted.

Pain signal blocked.

Does it affect everything at once, like feeling touch versus pain?

No.

There's a predictable sequence.

Autonomic functions go first, changes in temperature sensation, maybe some numbness.

Then pain and other sensory functions are lost.

Motor activity, the ability to move muscles, goes last.

And recovery.

Happens in the reverse order.

Motor function comes back, then sensory, then autonomic.

We see LA's used in different ways, right?

Topical creams, injections.

Like a Lididerm patch or EMLA cream on the skin.

Infiltration, which is small injections into the tissue, like for stitching a cut.

And sometimes combined with something else.

I remember reading about epinephrine.

Ah, yes.

For infiltration anesthesia, LA's are very often mixed with a vasoconstrictor, usually epinephrine.

Why add adrenaline?

It constricts the local blood vessels.

This does two things.

It keeps the anesthetic right there in the tissue longer, prolonging the effect, and it reduces bleeding at the site.

Makes sense.

But is there a risk?

What if that epinephrine gets absorbed systemically?

Big risk.

That's the caveat.

You wouldn't use epinephrine in areas with poor circulation already, like fingers or toes, or in patients with severe high blood pressure or heart disease.

Systemic absorption could cause dangerous spikes in blood pressure or heart rate.

Good point.

Now, the sources mention two chemical classes, esters and amides.

Why is that important?

It's crucial for allergies.

Knowing the class helps you avoid giving a drug someone's allergic to.

How do you tell them apart?

It's actually pretty simple based on the name.

Amides all have the letter I appearing before the kaia suffix.

Think lidocaine, bupivacaine, they're mostly metabolized by the liver.

Okay, amides have an I before kaian, and esters?

Esters do not have that extra I, like procaine, cocaine, tetrocaine.

These are broken down differently by enzymes called cholinesteroses into compounds called paba, para -aminobenzoic acid, and it's often these paba compounds that people are actually allergic to.

Ah, so if someone's allergic to an ester, like procaine, you can likely safely give them an amide, like lidocaine.

Exactly.

The cross allergy between the classes is rare because the allergy is usually tied to that paba byproduct of ester metabolism, which amides don't produce.

Very useful clinical pearl.

Definitely.

One last thing on LAs, that dreaded spinal headache.

What causes that?

That can happen after spinal or epidural anesthesia if the needle accidentally punctures the dura, the membrane around the spinal cord, causing cerebrospinal fluid, CSF, to leak out.

And it feels worse when you sit up?

Characteristically, yes.

The headache is often severe, worse when upright, and gets better when lying flat.

The pressure change from the CSF leak causes it.

How do you treat it?

Usually conservative first.

Bed rest, lots of fluids, caffeine sometimes helps constrict blood vessels.

If it's persistent or severe, they might do a blood patch.

Injecting the patient's own blood.

Yes.

They draw some of the patient's venous blood and inject it into the epidural space near the puncture site.

The blood clots and effectively patches the hole, stopping the leak.

Okay, now we get to a class of drugs where the safety warnings are, like flashing red lights, neuromuscular blocking drugs, NMBDs, things like rocoronium or succinylcholine.

Yes.

This is arguably the highest alert category we've discussed.

The warning cannot be emphasized enough.

Because they paralyze muscles?

All skeletal muscles, including the diaphragm and the intercostal muscles you need to breathe.

So NMBDs must never ever be given to a patient unless they are already intubated and being mechanically ventilated.

Because otherwise they suffocate.

Correct.

And terrifyingly, these drugs do not affect consciousness or pain sensation.

The patient would be completely aware, unable to move, unable to breathe.

It's a horrific scenario.

So sedation and pain management aren't just optional alongside NMBDs, they're absolutely mandatory.

Every single second the NMBD is active.

Okay, pharmacologically there are two main types.

Depolarizing and non -depolarizing.

Right.

Succinylcholine is the main depolarizing one used.

It actually mimics acetylcholine, the natural neurotransmitter, at the muscle junction.

It binds to the receptor and causes depolarization.

So what does that look like clinically?

Initially you see muscle fasciculations visible twitching as the muscles fire.

That's phase one.

This is quickly followed by phase two where the muscles become resistant to further stimulation leading to flaccid paralysis.

Why use something that causes twitching first?

Its main advantage is its incredibly fast onset, less than a minute and very short duration, maybe four to six minutes.

That makes it ideal for emergency intubations where you need paralysis quickly but briefly.

Okay and the non -depolarizing NMBDs, like rocoronium.

Those are competitive antagonists.

They simply block acetylcholine from binding to its receptor at the neuromuscular junction.

No binding, no muscle contraction.

Do they cause twitching?

No, they don't cause the initial fasciculations, they just produce paralysis directly.

Is there a pattern to the paralysis?

Yes, it follows a predictable sequence.

Weakness starts first, then total flaccid paralysis.

It typically affects the small, rapidly moving muscles, first eyes, fingers, then moves to the limbs, neck, trunk.

And breathing muscles.

The intercostals and diaphragm are usually the last muscles to be paralyzed.

And thankfully, the first to recover as the drug wears off.

What happens if someone gets too much or the paralysis lasts too long?

Are there antidotes?

Yes.

The primary concern is prolonged respiratory paralysis.

For the non -depolarizing drugs, like rocoronium, vecuronium, we can use anti -cholinesterase drugs like neostigmine.

How do those work?

They inhibit the enzyme that breaks down natural acetylcholine.

So more acetylcholine builds up at the junction and competes with the blocking drug, eventually overcoming the blockade.

Are there newer options?

Yes.

There's a newer agent called Sugimadex, which works differently.

It directly binds to and inactivates rocoronium or vecuronium molecules, providing a more rapid and complete reversal for those specific drugs.

Okay, let's bring this all together for the nursing perspective.

Assessment priorities.

Where do you start?

Always, always with the ABCs, airway, breathing, circulation, baseline vitals, oxygen saturation, that's fundamental.

And history -taking.

Absolutely thorough.

You need the medical history, allergies, current meds.

Critically, you must ask about any family history of malignant hyperthermia.

Because it's genetic.

Exactly.

Also, you need to ask about alcohol and, importantly, nicotine use.

Smoking is a big one.

Why nicotine specifically?

Nicotine paralyzes the tiny cilia in the respiratory tract that normally sweep out mucus and debris.

So smokers have a much higher risk of mucus plugging, adelictasis, collapsed lung sections, and pneumonia after surgery.

Good point.

What else in assessment?

Baseline neurological status is crucial.

Level of consciousness, motor strength, sensation, gag reflex.

You need that starting point.

And check recent labs, especially electrolytes.

High electrolytes.

Imbalances, particularly in potassium and magnesium, can really increase the patient sensitivity to NMBDs, potentially leading to prolonged paralysis or toxicity.

Okay.

Moving to implementation.

Safety first.

Always.

Resuscitative equipment, airway supplies, suction, emergency drugs, defibrillator must be immediately accessible whenever these anesthetics or NMBDs are used, and the reversal agents we talked about.

And after the procedure,

post -anesthesia care.

Monitor closely for side effects,

especially hypotension.

Watch for orthostatic hypotension when they first get up.

Encourage turning, coughing, deep breathing exercises early on.

To prevent lung issues.

Yes, prevent adelictasis.

And early ambulation, getting them walking, helps prevent that and reduces the risk of deep vein thrombosis, blood clots.

What about specific patient teaching for NMBDs?

This is so important.

If a patient is paralyzed with an NMBD but potentially still aware due to insufficient sedation, you must educate the family.

Let them know the patient can likely still hear them.

So they should talk to the patient normally.

Yes.

Reassure them.

Explain what's happening.

It can significantly reduce anxiety for both the patient and the family.

Don't talk about the patient as if they aren't there.

Okay.

And for spinal anesthesia, any specific monitoring?

Continuous monitoring for the return of sensation and motor function below the level of the block.

Keep the head of the bed elevated as ordered, usually slightly, to prevent the anesthetic from drifting higher up the spinal cord, which could affect breathing.

And watch blood pressure very closely.

Spinal blocks can cause vasodilation and sudden drops in BP.

One last crucial point.

Herbal medications.

Oh yes.

Patients need to be upfront about everything they take, including herbals and supplements.

Many interact dangerously with anesthetics.

Like which ones?

While things like fever -few, garlic and ginger can increase the risk of bleeding, cava and St.

John's wort can significantly increase the sedative effects, potentiating the anesthesia.

Honesty is key for safety.

Hashtag outro.

So, to kind of wrap up this deep dive, the big contrast to keep straight are general versus local anesthesia, think consciousness on or off.

Depolarizing versus non -depolarizing NMVDs, think initial twitching or just blockade.

And the constants.

The absolute constants are prioritizing the ABCs, knowing how to spot high alert conditions like malignant hyperthermia immediately, and the unwavering rule about mechanical ventilation with NMVDs.

Those are paramount.

You know, it's really striking we have these incredibly sophisticated drugs targeting specific ion channels or brain receptors with amazing precision.

The pharmacology is remarkable.

And yet, some of the most serious complications we've discussed, MH,

the heightened risks in older adults, they often come back to things we can't fully control beforehand, like genetics or existing health problems.

That's true.

Patient variability is huge.

It makes you think, doesn't it?

Even with perfect drugs, how much of successful pharmacology still depends on really understanding the individual patient before you even give the first dose, on getting that history right.

That's a really powerful point to end on.

The assessment piece is just as critical as knowing the drug itself.

Indeed.

Well, thank you for joining us for this deep dive into the complex world of perioperative pharmacology.

Hope it was helpful.

We'll see you next time on The Deep Dive.