Chapter 18: CNS Depressants & Sedative Medications

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Welcome back to the Deep Dive.

Today we are shifting gears a little bit.

We aren't just looking at a topic, we are stepping into a role.

I want you to imagine you are standing in a hospital corridor, it's maybe 2 .0 a .m., and you are holding that tiny little paper cup with a pill in it.

Yeah.

And that pill could be the difference between a patient getting the rest they desperately need to heal or, well, a patient ending up in respiratory arrest.

It sounds dramatic, but you're right, that is the reality of the medication cart.

Exactly.

So we're treating this session as a kind of survival guide for nursing students or really anyone who's fascinated by the high stakes world of medicine.

We are tackling one of the densest,

most intimidating topics in the whole curriculum.

Pharmacology.

And we're being very specific.

We are looking at Chapter 18 of Pharmacology, a patient -centered nursing process approach, the 12th edition.

The chapter title is Depressants.

Now I have to stop you right there because when a lay person hears depressants, they think sadness, they think, you know, clinical depression.

But we were talking about something mechanical here, completely different context.

Yeah.

In pharmacology, depression refers to a reduction in functional activity.

We are talking about depressing the central nervous system, the CNS.

We're literally slowing down the electrical firing of the brain.

So if the brain is a stereo system, we aren't changing the song to a sad ballad.

We are just turning the volume knob down.

That is the perfect analogy.

And this entire chapter is essentially about how far you turn that knob.

It's a spectrum.

Okay.

If you turn it down just tiny notch, you get sedation, you, you know, take the edge off anxiety, turn it down a bit more, you get sleep.

And if you just keep turning?

You get anesthesia, a total loss of consciousness.

And if you force that knob all the way to zero, that's coma, and then eventually death.

Our job today is to map that whole spectrum so you know exactly where your patient is.

Okay.

We have a lot to cover.

We're going to start at

the wild and sleep disorders and sedative hypnotics.

Then we're going to get into the historical heavyweights, the barbiturates and benzodiazepines.

And we'll really break down the mechanism of action there because if you don't get the chemistry, you won't understand the safety risks.

We also need to have a very serious conversation about older adults.

The text is very, very specific.

The rules of engagement change completely when the patient is over 65.

And then finally, we will go to the deep end of the pool, anesthetics, general surgery, spinal blocks, the whole thing.

It works.

So let's start at the beginning.

Before we can even think about drugging a patient to sleep, we need to understand what sleep actually is.

The physiology of it.

Right.

Sleep isn't just an off switch.

It's a really active biological cycle.

And the text points out that a staggering number of people have trouble with this.

It cites that what 10 % to 30 % of Americans suffer from insomnia.

And I think the CDC puts a number even higher for chronic sleep problems.

It's something like 70 million Americans.

That is just a massive patient population.

It is.

And statistically, you are going to see this more in female patients.

And it definitely increases as patients age.

The cost is huge.

Two billions in lost productivity.

So patients, they're desperate.

They are buying OTC aids.

They are asking for prescriptions.

But to treat it, you have to know the architecture.

The architecture of sleep.

The text breaks this down into two main phases, REM and NREM, rapid eye movement and non rapid eye movement.

Correct.

And they function in a cycle.

It's not like you just fall asleep and stay in one state.

You cycle through these phases at roughly 90 minute intervals.

Okay.

So walk me through that cycle.

How does it work?

You usually start with NREM and this has four stages getting progressively deeper.

Stage one is that light drifting off feeling you're not quite asleep yet.

The head bobbing stage.

Exactly.

By the time you hit stage three and four, you are in deep sleep.

This is the restorative stuff.

The body is repairing itself.

Then you shift gears into REM sleep.

Which is where the dreams happen.

Recallable dreams, yes.

And the physiology gets a little weird here.

In REM, it's actually quite hard to wake someone up.

The text notes that if you do manage to wake them, they might report these vivid, totally bizarre dreams.

You know, I always found it counterintuitive that sleepwalking happens in the deep sleep, not the dream sleep.

It surprises a lot of students.

Yeah.

You'd think sleepwalking is acting out a dream in REM, but no, the text is very specific.

Sleepwalking and even nightmares in children, they happen during NREM sleep.

Now you mentioned age matters.

How does this architecture change for say a 75 year old versus a seven year old?

And this is so crucial for nurses to be able to explain to families.

Children have very, very deep NREM sleep lots of stage three and four.

But as we age, we lose that depth.

Older adults experience a big decrease in deep sleep and an increase in these little waking periods throughout the night.

So grandpa waking up at 3 a .m.

isn't necessarily insomnia in the clinical sense.

It might just be the natural fragmentation of aging sleep.

Exactly.

And that distinction matters so much because we do not want to medicate a normal physiological process with heavy drugs if we can possibly avoid it.

Which leads us right to the big stop sign in the text.

Section one makes it so clear.

Drugs are not the first move.

Never the first move.

The nursing process demands non -pharmacologic interventions first.

We have to look at the patient's lifestyle.

The text provides a whole list of these interventions.

Some of them seem obvious, but let's look at the why behind them.

Arise at a specific time in the morning.

It's all about regularity.

You're regulating the circadian rhythm.

If you sleep until noon on Saturday, you're just not going to be tired Sunday night.

It totally disrupts the cycle.

Okay, that makes sense.

Avoid caffeine, alcohol, and nicotine six hours before bed.

Now, I want to pause on alcohol.

Culturally, the nightcap is probably the oldest sleep aid in the book.

You know, a shot of whiskey to help you sleep.

Why does the text flag this as a problem?

Because while alcohol is a depressant and it might help with induction, the falling asleep part,

it absolutely destroys the maintenance of sleep.

How so?

It suppresses REM sleep.

Then, as your body metabolizes it out of your system later in the night, you get this rebound effect.

You wake up often fragmented and just feeling unrefreshed.

So you pay for the easy onset with a terrible second half of the night.

Precisely.

The text also lists avoiding heavy meals and strenuous exercise right before bed.

And then you have the classic nursing advice,

warm milk.

Is that actually evidence -based or is that just an old wise tale that somehow made it into the textbook?

It's in the text, drink warm milk.

The biochemistry suggests that milk contains tryptophan, which is a precursor to serotonin and melatonin.

But really, the warmth and just the ritual itself can be very soothing.

The point is, try the milk, try the bath, try the quiet music before you call doctor for a prescription.

Okay, but let's say the warm milk failed.

The patient is exhausted, their healing is being compromised.

We have to intervene.

We enter the world of sedative hypnotics.

And we really need to define those terms because they're often used interchangeably, but there is a nuance.

Sedative versus hypnotic.

It's largely a matter of dose.

A sedative effect produces mild CNS depression.

It diminishes physical and mental responsiveness.

The patient is still conscious, just, less reactive.

It's great for treating tension and anxiety.

And hypnotic.

A hypnotic effect is stronger.

You're increasing the dose to induce what feels like natural sleep.

It shuts the system down just enough to allow sleep to take over.

So the same drug can be a sedative in the morning and a hypnotic at night.

Often, yes.

The text says, sedative hypnotic drugs are sometimes the same drug.

It all depends on how much you give.

Before we start throwing pills at the patient, though, we have to respect the effects and adverse reactions table.

Table 18 .1.

This isn't just a list.

It's basically a warning label for the entire profession.

It really is.

And the first concept to grasp is the hangover.

Which again, sounds a lot like alcohol.

It's a very similar mechanism.

Residual drowsiness.

You take a hypnotic at 10 .00 p .m.

By 7 a .m.

you want to be awake and alert.

But if the drug has a long half -life or if the liver produces these things called active metabolites.

So by still chemically active.

Exactly.

The drug is still working while you're trying to drive your car to work.

That is a massive safety risk.

Then there is REM rebound.

We just talked about how alcohol suppresses REM.

Well, a lot of hypnotics do the exact same thing.

So if you take them for a while and then stop abruptly, the brain tries to catch up on all the REM it missed.

It rubber bands back.

Yes.

And you get these vivid, intense, often nightmarish dreams.

It can be incredibly distressing for the patient, which then encourages them to take the drug again just to make the REM stop.

That's a classic cycle of dependence.

Speaking of dependence, the text makes a distinction between physical and psychological dependence.

Right.

Physical dependence is physiological.

The body has physically adapted to the drug.

If you stop, you get withdrawal symptoms.

Frimmers.

Twitching.

Dizziness.

The text notes withdrawal starts within 24 hours and can last for days.

And psychological.

That's the feeling.

The belief that you absolutely cannot function or sleep without the pill.

And tolerance.

What's happening there?

Tolerance is when the body just gets really good at neutralizing the drug.

You need a higher and higher dose to get the same sleep.

This is often due to something called enzyme induction.

The liver basically builds more workers to break down the drug faster.

But the big one, the one that scares every nursing instructor,

is respiratory depression.

This is the lethal line.

These drugs depress the CNS.

And the part of the can be depressed too much.

If that happens, the patient just stops breathing.

It is dose dependent, but it is the primary risk we are always watching for.

Okay, let's get into the specific classes.

We are going chronologically here.

First up, the barbiturates.

The early 1900s.

I mean, these were the miracle drugs of their time for anxiety and sleep.

But today you will almost never see them prescribed for sleep.

Why did they fall out of favor so dramatically?

Safety.

They have what's the difference between the dose that puts you to sleep and the dose that kills you is uncomfortably small.

Plus, the abuse potential is just incredibly high.

The text classifies them by their duration of action.

Let's run through these because the clinical uses are totally different based on the timing.

Right.

So first you have the long acting.

The prototype here is phenobarbital.

We do not use this for sleep.

We use it for seizure control in epilepsy.

It stays in the system for a very long time.

The text cites a half life of 53 to 118 hours.

That's days.

So you take one pill and it's basically in your system for a week.

Essentially, yeah.

Then you have intermediate acting like buddhabarbital.

These are sleep sustainers.

They take about an hour to kick in, but they last.

They are for the patient who can fall asleep okay, but then wakes up at 2 a .m.

Short acting.

That would be pentobarbital.

This is more for procedure sedation.

It works fast.

It is relatively fast.

And ultra short acting.

Mesohexidal.

This is for the operating room.

It's used for the induction of general anesthesia.

We are talking an immediate lights out effect.

There is a really critical interaction note in the text regarding barbiturates, specifically pentobarbital.

It mentions hepatic enzyme action.

We need to unpack this because it sounds like biochemistry jargon, but it directly affects patient safety.

This is absolutely vital.

Pentobarbital is an enzyme inducer.

It signals the liver to ramp up production of the enzymes that break down drugs.

Okay, so the liver becomes a hyper efficient shredder.

Exactly.

Now imagine your patient is also taking warfarin, which is a blood thinner to prevent clots.

The liver shreds that warfarin much faster because of the pentobarbital.

So the warfarin just stops working.

Or it works much, much less effectively.

The patient is suddenly at risk for blood clots, not because their warfarin dose changed, but because the barbiturate changed their liver.

Nurses have to be detectives for these kinds of interactions.

And the general rule for using barbiturates for sleep.

Short term only.

Two weeks.

Max.

The tolerance builds so fast that after two weeks they often stop working anyway and you're just left with all the side effects and the risk.

So barbiturates are the old guard.

Heavy blunt instruments.

Then in the 1960s we got something more precise.

The benzodiazepines.

The minor tranquilizers.

You know these names.

Alparzolam is Xanax.

Diazepam is Valium.

Lorazepam is Ativan.

The text explains their mechanism involving a neurotransmitter called GABA.

We need to go deep here.

I want to understand exactly what is happening at the neuron level.

Okay, let's visualize it.

GABA is the brain's primary inhibitory neurotransmitter.

It's the brain's breaking system.

The calm down signal.

Exactly.

When GABA binds to its receptor on a nerve cell, it opens a channel, specifically a chloride channel.

And chloride is a negative ion.

Right.

So all these negative ions rush into the cell.

This makes the inside of the cell more negative.

A state we call hyperpolarization.

A hyperpolarized neuron is stubborn.

It's much harder for it to fire an action potential.

It's sedated.

Okay, so GABA calms the neuron down.

What does the benzo do?

The benzo binds to that receptor complex, but at a different spot.

And it basically makes GABA better at its job.

It makes the receptor more sensitive, more attracted to GABA.

So it's like putting power steering on the brake pedal.

That's a perfect way to put it.

But here's the critical safety distinction between benzos and barbiturates.

Benzodiazepines increase the frequency of the channel opening, but they still need GABA to be there to work.

So there's a kind of ceiling to how much they can depress the CNS on their own.

And barbiturates.

Barbiturates do something different.

They keep the channel open longer, and at high enough doses, they can actually pop the channel open without any GABA around at all.

That's why barbiturates can kill you so much more easily.

They don't need the natural brake.

They just flood the engine.

That makes so much sense why benzos became the preferred choice.

It's just a safer profile.

Safer, yes, but certainly not risk -free.

The text highlights alprozolam, or Xanax, as the prototype.

It's a schedule fourth controlled substance.

We have to talk about the grapefruit rule.

It's a classic exam question, but what is the deal with grapefruit?

Grapefruit contains compounds that inhibit a specific set of enzymes in the liver called the CYP450 enzymes.

Those are the shredders we talked about.

If you inhibit the shredder, the alprozolam doesn't get broken down.

It builds up in the blood.

So you take a normal dose, but your body reacts like you took a triple dose.

It can quickly become toxic.

And green tea does the opposite.

Yes, green tea can induce the enzymes, basically speeding up the shredder and making the drug less effective.

It's a very delicate balance.

Let's look at the adverse effects of benzos.

We have the usual drowsiness, but there are some really bizarre neurological effects mentioned and tarot grade amnesia.

This is the blackout effect.

It's an impaired ability to recall events that happen after you've taken the dose.

You take the pill and it's like your memory recorder just stops taping for a while And sleep -related behaviors.

The text lists sleep driving, cooking meals, making phone calls.

It's a very strange dissociative state.

The motor centers of the brain are working, but the conscious executive function part is offline.

And you can imagine the danger of a patient cooking on a gas stove while they are technically asleep.

It's a major, major safety education point.

What happens if a patient overdoses?

With barbiturates, we're in big trouble.

But with benzos?

We have a parachute.

It's a drug called flumazenil.

The antidote.

Yes.

Flumazenil is a benzodiazepine antagonist.

It gets to the receptor and it competes for the spot and it basically kicks the benzo off.

It can wake the patient up very quickly.

That sounds like a miracle drug for the ER.

It is, but it comes with a huge warning label.

If the patient is chronically dependent on benzos and you just slam them with flumazenil, you rip away the brakes instantly.

Oh, life -threatening seizures.

You have to use it with extreme caution.

Okay.

Let's move to the next generation.

The text calls them the non -benzodiazepines.

These are sort of chemical cousins.

The big one is zolpidem, which you'll know as Ambien.

How does zolpidem differ from something like Xanax?

It targets the same GABA receptor complex, but it's much more selective.

It binds to a specific subunit that is thought to be more responsible for sedation rather than or muscle relaxation.

So it just puts you to sleep without as much of the other stuff, like the anti -anxiety effect.

Correct.

It's for short -term insomnia and the text says it should be used for less than 10 days.

The half -life is very short, around two to three hours or maybe up to eight hours for an extended release version.

The goal is to get you to sleep, but clear out by morning to prevent that hangover effect.

But the text mentions a crucial dosage adjustment for

Yes.

We absolutely must decrease the dose for the elderly.

We'll get into exactly why in a moment, but it's critical to remember.

Zolpidem hits older brains much, much harder.

There are two other categories mentioned that are gaining traction.

Melatonin agonists and orexin antagonists.

These are really exciting because they step away from that whole GABA depression model.

They work differently.

Let's start with Rammaltion or Rosrum.

This is a melatonin agonist.

It basically mimics the body's natural melatonin.

It targets the MT1 and MT2 receptors to help regulate your circadian rhythms.

And the text makes a point of saying it's not a controlled substance.

That is huge.

It means no abuse potential, no withdrawal symptoms, and it doesn't decrease REM sleep.

It's a very clean drug for sleep induction, though it doesn't really help much with staying asleep.

And the orexin antagonists.

The book mentions uvexin.

So this works on the

orexins are neuropeptides in the brain that act as the fuel line for wakefulness.

Suvexin blocks the orexin receptors.

So instead of hitting the brakes, like with GABA, we're cutting the fuel line to the engine.

That's a perfect analogy, but the text adds a very specific warning here.

It can worsen depression or suicidal tendencies.

So you have to monitor the patient's mood very closely.

This brings us to section six, which might be the most clinically important section for a working nurse,

sedatives and hypnotics for older adults.

This is where pharmacology meets the physiology of aging head on.

The text is extremely protective of this patient group.

So why is the older adults so uniquely vulnerable to these drugs?

It's what you could call the geriatric vicious cycle.

First, you have the liver and the kidneys.

Blood flow to the liver decreases with age, so metabolism slows way down.

The kidney filtration rate drops, so excretion also slows down.

The drug enters the body, but it has a much harder time leaving.

So it just accumulates.

It accumulates.

But there's another huge factor the text implies with pharmacokinetics, and that's protein binding.

Many of these drugs, like the benzos, right through the bloodstream, attach to proteins like albumin.

Okay, think of albumin like a bus.

Right.

And if the drug is on the bus, it's inactive.

It's just traveling.

Only the free drug, the passenger who gets off the bus, can cross into the brain and actually do its job.

And older adults.

They often have lower albumin levels, so fewer buses,

which means more passengers are walking around on the street.

You have more free drug hitting the brain at any given time.

So standard dose acts like an overdose because there's nothing there to buffer it.

Exactly.

And that is why the text is so emphatic.

Start with half the dose.

The mantra is always start low and go slow.

And there are some strict prohibitions in the text too.

Yes, no barbiturates.

They're just too dangerous for confusion and falls in this population.

And you have to avoid long -acting benzos like Tiazepam.

I mean, if the half -life is 40 hours in a young person, it could be 100 hours in an older adult.

It basically never leaves their system.

The text suggests using short -acting benzos like Tiazepam, if you absolutely must, but limited to maybe four times a week.

And always, always ask, is the insomnia caused by something else?

Is it caused by pain?

If grandma can't sleep because her arthritis hurts, give her an NSA aid, not a sleeping pill.

You have to treat the root cause.

Okay, we're going to leave the bedroom and wheel the gurney into the operating room.

Section seven, general anesthetics.

Now we're turning the volume knob all the way down.

General anesthesia is, for all intents and purposes, a drag -induced coma.

It alleviates pain, it depresses the CNS, and it causes a total loss of consciousness.

The text introduces this concept of balanced anesthesia.

This sounds like a cocktail approach.

It is.

In the old days, an anesthesiologist might just use a massive dose of a single agent, like ether, but that came with terrible side effects and very long nauseating recovery times.

Balanced anesthesia uses a combination of several different drugs to achieve the goal with lower, safer doses of each one.

So walk us through the cocktail that's mentioned in the text.

Well, it can start the night before with a hypnotic, just to ensure the patient gets some rest, then about an hour before surgery, pre -medication.

Okay.

This is often a narcotic analgesic, like morphine, or a benzo, like midazolam, to relax the patient, plus an anticholinergic.

An anticholinergic, like atropine or glycopyrrolate?

Why do they add that?

To dry up secretions.

You do not want the patient choking on their own saliva or mucus while they are unconscious and have a breathing tube in.

It's

Okay, so they're dry and relaxed.

What's next?

A short -acting nomborbitrate like propofol for induction.

This knocks them out very fast.

Then you might use an inhaled gas, like nitrous oxide with something else, to maintain the anesthesia.

And finally, a muscle relaxant.

Why the muscle relaxant?

Doesn't the anesthesia do that?

Not completely.

And surgeons need the body to be totally limp.

If the abdominal muscles are tight, they can't perform the surgery.

This combination allows for faster recovery and fewer side effects.

Now, once the drugs go in, the patient goes through specific stages.

Table 18 .4 outlines the four stages of anesthesia.

This is the road map of going under.

Every anesthesiologist knows this by heart.

Let's start with stage one, analgesia.

The patient is still conscious, but they're getting drowsy.

Speech becomes difficult.

Sensations of smell and pain start to fade.

They're just drifting.

Then stage two, excitement or delirium.

This sounds scary.

It is the danger zone.

The cerebral cortex, the higher thinking part of the brain, is depressed, but the lower centers can go haywire.

You might see confusion, excitement, muscle twitching, even fighting.

So the goal is to get through this stage as fast as humanly possible.

As fast as possible.

You want to slide right past delirium and into stage three.

Stage three, surgical anesthesia.

This is the sweet spot.

This is the goal.

Respirations are shallow but regular.

The muscles are relaxed.

The eyelid reflex is lost.

This is where the surgery happens.

And

medullary paralysis.

You went too far.

The respiratory centers and the brain stem shut down.

The heart can stop.

This is an overdose and it requires full life support.

The anesthesiologist's entire job is to keep the patient hovering perfectly in stage three and never ever let them slip into stage four.

Let's talk about the specific agents.

Section eight covers inhalation and 5E anesthetics.

Inhalation includes gases and volatile liquids.

Everyone knows nitrous oxide laughing gas.

Very rapid recovery but it's a great analgesic but a weak anesthetic.

You'd rarely use it alone for a major surgery.

Then you have the liquids.

Halothane, isoflurane, desflurane.

These are much more potent.

They provide a very smooth induction but they carry a rare absolutely terrifying risk.

Malignant hyperthermia.

The text puts a big warning box around this.

What is malignant hyperthermia?

It's a genetic reaction.

If a susceptible patient is exposed to these gases and also the muscle relaxin six in alkaline, their muscle metabolism just goes completely berserk.

What does that look like in the ill war?

Rigid contracted muscles.

A very high fever like spiking incredibly fast.

Tachycardia.

It's a life -threatening emergency.

You have to stop the drug immediately, cool the patient, and give a specific antidote.

Moving to the IV anesthetics.

The rock star here seems to be propofol.

Milk of amnesia.

It's called that because it actually looks like milk.

It's a lipid emulsion.

It's fat based.

And it's used for induction.

Yes, and also for conscious sedation.

It works incredibly fast.

But that milk aspect creates a really unique nursing problem.

Bacteria love fat.

So it's a petri dish.

Exactly.

The text warns that open vials of propofol must be discarded within six hours.

The tubing has to be changed every 12 hours.

If you leave propofol hanging for too long, you are risking sepsis for your patient.

I've heard patients complain about pain with propofol.

It burns going into the vein.

It really does.

Nurses will often mix it with a little bit of lidocaine to numb the vessel first.

The text also mentions mitazolam, which is first, and ketamine.

Right.

Mitazolam is the classic for conscious sedation, like for a colonoscopy.

You're awake enough to follow commands like turn on your side, but you won't remember a thing afterward.

Ketamine is very rapid.

But the text warns against using it patients with a psychiatric history because it can cause some pretty intense dissociation.

Finally, we have section nine.

Local, topical, and spinal anesthesia.

We aren't knocking the whole patient out.

We're just blocking a specific area.

Topical is the simplest.

Creams and sprays on the skin.

Local involves needles.

And the text divides local anesthetics into two chemical families.

The esters and the amides.

Why does the chemistry matter to a nurse on the floor?

Allergies.

The esters, like procaine, have a much higher rate of allergic reactions.

The amides, like lidocaine, have a very, very low allergic rate.

That's why lidocaine is the standard for almost everything today.

A lidocaine is everywhere.

Sutures, dental work.

Rapid onset, very stable duration.

It's reliable.

Now let's talk about the spine.

Spinal anesthesia.

This feels like very precision work.

It is.

The anesthesiologist injects local anesthetic directly into the upper acnoid space, where the cerebrospinal fluid is.

And the text is specific.

It says, below the first lumbar space, L1, in adults.

That's a critical landmark.

It's to avoid hitting the spinal cord itself.

You want to be in the fluid sac below where the solid cord ends.

What are the risks?

Gravity matters.

If the drug travels too high up the spinal column, it can hit the phrenic nerves that control the diaphragm.

And cause respiratory distress.

Exactly.

The patient can't breathe on their own.

And what about the headache?

The famous post -drill puncture headache.

This is classic mechanics.

You've made a tiny puncture in the dura mater, the sac holding the fluid.

Cerebrospinal fluid, or CSF, can leak out of that little hole.

This drops the pressure inside the skull.

So when the patient stands up, they get a splitting positional headache.

And the treatment for that?

Lay them flat, stop the leak, and increase fluids to help the body make more

Okay, section 10 wraps us all up with the nursing process.

The surgery is over.

The patient is in the PCU, the post -anesthesia care unit.

What are we doing now?

Monitoring.

The text is just relentless about this.

Constant monitoring.

First up, vital signs.

Hypotension, low blood pressure, and respiratory depression are the ghosts that can linger.

Just because the surgery is over doesn't mean the drug is done working.

You're an output.

Anesthesia puts the bladder to sleep too.

So veterinary retention is very common.

If your patient hasn't voided an eight -hours post -op, you have a problem you need to address.

And sensorium.

Their mental status.

Are they waking up appropriately?

Are they confused?

And safety.

You do not let a post -op patient get up and walk to the bathroom alone.

Their legs might feel fine to them, but the proprioception, their sense of where their body is in space, it isn't back yet.

They are a huge fall risk.

So bringing this all together, we've looked at the entire spectrum.

From a warm glass of milk for insomnia, to a benzodiazepine for anxiety, to a barbiturate for seizures,

all the way to a gas that induces a coma for surgery.

It is all about that volume knob.

And as a nurse, you are the guardian of that knob.

You are watching the breathing, checking the alertness, monitoring the liver function, anticipating the side effects.

It's a heavy responsibility.

A few milligrams difference can change a therapeutic drug into a lethal toxin.

That is the essence of pharmacology.

You have to respect the drug.

We hope this deep dive makes Chapter 18 feel a little more navigable for you.

Remember the case of Jay -Z in the text.

Always assess before you medicate.

And please remember that flumazenil is for benzos, not for opioids.

That's a classic mix up.

Good catch.

Thank you so much for listening.

Keep learning.

Thank you from the Last Minute Lecture Team.