Chapter 58: Adult & Pediatric Emergency Drug Therapy

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Welcome back to the Deep Dive.

Today, we are doing something very specific and honestly something I think is going to be incredibly valuable for a huge chunk of our audience.

We are doing what we're calling a Last Minute Lecture.

It's a bit of a specialized mission today.

We are essentially, you know, cramming.

We are.

So if you are a nursing student standing outside the exam hall or maybe you're a new grad about to start your first shift in the ER or the ICU,

this one is absolutely for you.

We are taking Chapter 58 of Pharmacology, a patient -centered nursing process approach, the 12th edition.

A beast of a chapter.

A huge one.

And we are going to unpack it line by line.

Yeah, the timer is titled Adult and Pediatric Emergency Drugs.

And the goal here isn't just to, you know, list off a bunch of dosages that we will get to that, but to really build that mental framework you need for when things go sideways.

Exactly.

The whole premise is that we're going to walk through this chapter in the exact order it's presented in the text.

We're covering the concepts, the mechanisms, the math, and I think most importantly, those critical nursing safety alerts that usually end up being questions on the board exams.

And honestly, those safety alerts are the things that save lives in practice, so you should really consider this your audio study guide.

No fluff, just the chapter translated into plain English.

Okay, let's set the stage.

The text introduces these medications as first -line agents, but I feel like there is a bit of a misconception about where these drugs are actually used.

When we say emergency drugs, I think we all picture the trauma bay.

Right, picture the ER, you know, the lights, the sirens, all the drama.

But the chapter introduction makes a really, really important point right off the bat.

Medical and surgical emergencies happen everywhere.

Everywhere.

They happen in the clinic, they happen on a quiet med surg floor at three in the morning, they happen out in the community.

So if you're working on a general floor, you can't just have the mindset of, oh, the code team handles that.

You absolutely can't.

The author emphasizes that learning the implications of these drugs before the crisis hits is what allows you, the nurse, to function at your highest level.

I mean, think about it.

When a patient's heart stops or they stop breathing,

your adrenaline just spikes.

Oh, yeah.

Your fine motor skills degrade.

Your cognitive bandwidth, it just narrows to a pinpoint.

That is not the time to be cracking open the textbook to see if you should push a drug fast or slow.

You need to know the how way before the what even happens.

Precisely.

You need that muscle memory.

It has to be automatic.

Before we dive into the specific agents, we really need to define our patients.

The text gives us very specific definitions for dosing populations, and they might be a little different than what you'd see in, say, a pediatrics textbook.

So let's clarify what this text uses for this chapter.

Yeah, this is so crucial for the math and for the protocols.

So for this chapter,

an infant is anyone younger than one year old.

Okay.

Under one.

Then you have a child, which is defined as one year old all the way up to adolescence or puberty.

And adults are generally considered anyone who is an adolescent or older.

But and this is a really important little nuance, the text notes that for advanced life support, the ALS guidelines, adult protocols usually kick in for anyone older than eight years.

Whoa, okay.

That's a big distinction.

So for general pharmacology, an 11 year old might be considered a child.

But if you're actually running a code algorithm, they might be treated as an adult.

In terms of certain things like defibrillation energy or some drug protocols.

Yes, it's a good reminder that, you know, age is just a number, but the physiology is really the guide.

But the bottom line is to always check your specific hospital policy.

But for any exam based on this book, you have to know those definitions.

Got it.

Okay, let's dive into section one.

It is the most commonly used drug in the hospital, but I feel like we so rarely respect it as a medication.

We're talking about oxygen.

Yeah.

And the text is very, very explicit here.

Oxygen is a drug.

It is not just air.

And like any other drug, it has a mechanism of action, it has therapeutic effects, and it has adverse effects.

So let's get out on the physiology for just a second.

What is oxygen actually doing to our blood vessels?

This is actually fascinating.

So oxygen acts as a pulmonary vasodilator.

That means it opens up the blood vessels in the lungs, which you know, that makes sense.

You want to blood flow to the area where you're doing gas exchange.

Right.

But systemically and specifically in the brain, it acts as a vasoconstrictor.

It constricts vessels in the body.

It does.

It tightens them up.

And the urgency for using it is just crystal clear.

The text states that without oxygen, brain death begins within six minutes.

So it is the ultimate first line agent.

There's nothing more important.

Now there's a concept here that the text calls the hypoxemia rule.

And honestly, this sounds like common sense.

But I think a lot of us, myself included, miss the nuance and the heat of the moment.

It is common sense, but it gets lost in the panic.

The rule is really simple.

Treat the hypoxemia to treat the physiological disturbance.

Okay, break that down for me.

What does that mean in practice?

Okay, so imagine you have a patient who is having chest pain, or maybe their heart rate has dropped down into the 40s, their brady cardiac.

Your first instinct might be to grab the morphine for the pain.

Right.

Or the atropine for the heart rate.

You want to fix the symptom that you see right in front of you.

Right.

I see a slow heart.

I want to speed it up.

It makes perfect sense.

But the text is basically saying, stop, take a breath, look at the oxygen saturation first.

Because if that chest pain is happening because the heart muscle is literally starving for oxygen, or if that bradycardia is the heart's response to certification, then the drug is just a band -aid.

It's like putting a band -aid on a bullet hole.

It doesn't fix the core problem.

If you fix the oxygen, if you treat the hypoxemia, the chest pain often just resolves on its own.

The bradycardia resolves.

You fix the root cause instead of chasing symptoms.

So oxygen is the foundation.

And if the foundation is cracked, it really doesn't matter what fancy drugs you throw at the house.

Exactly.

But, and this is a massive but, in this 12th edition, it's a huge change.

Do not fall into the trap of more is better.

This is the liberal oxygen warning.

Yeah.

I have to say, this actually surprised me when I was reading it.

It's a huge shift in nursing culture.

I mean, we used to slap high flow oxygen on absolutely everyone who walked through the door.

Totally.

Chest pain, oxygen, sprained ankle.

Yeah.

Here, have some oxygen.

Right.

But the evidence that's cited in the text now suggests that if a patient is not hypoxemic, so if they're just sitting there at 98 % saturation and you put them on high flow oxygen, you might actually be increasing their mortality risk.

That seems so counterintuitive.

How does giving someone oxygen kill them?

Well, remember that mechanism we just talked about?

Cerebral vasoconstriction.

Too much oxygen can actually cause the blood vessels in the heart and the brain to clamp down, which reduces blood flow precisely where you need it most.

Plus, hyperoxia leads to the release of free radicals, which damage tissue at a cellular level.

So the big takeaway is target the saturation.

Don't just max out the dial on the wall.

Okay.

So we need specific targets.

What does the textbook define as normoxemia for a standard patient?

For a standard patient, normoxemia is defined as a saturation between 94 % and 99%.

Okay.

What about in those really high stakes scenarios?

Let's say we just got a pulse back after a cardiac arrest.

What's the target then?

In post -cardiac arrest resuscitation, the target is actually 92 % to 98%.

You want to actively avoid 100 % because of that reperfusion injury from the free radicals.

Interesting.

And for a stroke patient?

The target is greater than 94%.

Now, we rely so heavily on the pulse oximeter, that little glowing clip on the finger, but the text warns us that it can be, well, a liar.

It can absolutely lie to you.

The pulse ox works by measuring hemoglobin saturation based on light absorption and importantly, pulsatile flow.

So if you have cold extremities, the blood isn't really flowing there.

If you have severe vasoconstriction or the patient is in shock, the sensor just can't pick up a good signal.

And there's one specific poison mentioned in the chapter that tricks the machine entirely.

Carbon monoxide.

This is a huge one.

If a patient has been in a fire or exposed to exhaust fumes, the carbon monoxide binds to the hemoglobin.

The pulse ox just sees red hemoglobin and it reads it as 100 % saturated.

Oh, wow.

Meanwhile, the patient is literally suffocating because that hemoglobin can't carry oxygen.

You cannot trust the spio -2 reading in carbon monoxide poisoning, ever.

That is such a critical safety tip.

Okay.

Let's talk delivery methods.

Room air is about 21 % IO2.

If we have a patient in severe distress shock,

major trauma, cardiac arrest, what are we reaching for?

In those really severe cases, we aren't worrying about oxygen toxicity yet.

The mission is to save the brain.

You are targeting an FIO2 that's approaching 100 % and the device of choice is a non -rebreather mask at 10 to 15 liters per minute.

That's the mask with the reservoir bag hanging off of it, right?

And a little practical tip from the field, make sure you inflate that bag with your thumb over the valve before you put it on the patient's face.

Otherwise, they're just sucking on plastic for the first few breaths.

Good tip.

And if the patient isn't breathing effectively on their own, you switch to a bag valve mask.

The AMBU bag also cranked up to 15 liters per minute.

Now, here is the classic, the all -time nursing school exam question,

the COPD patient.

Ah, yes, the hypoxic drive.

This is the concept where patients with chronic lung disease who live with chronically high CO2 levels, eventually their drive to breathe switches, it stops responding to high CO2 and starts responding to low oxygen.

So the fear is if we give them too much oxygen, their brain thinks, oh, we have plenty of air now and they just stop breathing.

That is the fear, yes.

But the text is very, very clear on the nursing implication here.

You never deny oxygen to a patient who needs it, regardless of their COPD history.

If they're turning blue, you give them the oxygen, period.

But you have to be ready for the consequence.

Exactly.

You treat the life -threatening emergency in front of you.

If their respiratory drive does knock out, you must be prepared to ventilate them manually with a bag valve mask.

You don't let a patient die of hypoxia just because you're scared of messing up the respiratory drive.

That's a great way to put it.

Okay, for the less severe situations, we have the nasal cannula and simple face mask.

Right.

The nasal cannula gives you about 24 % to 44 % oxygen at flows of 1 to 6 liters.

And the simple face mask bumps that up to maybe 40, 60 % at flows of 6 to 10 liters.

There's a really nice pediatric tip in the text regarding masks.

Yes.

Little kids, they hate masks.

It feels suffocating.

It's scary.

The text suggests using a face tent, it's kind of shaped like a shovel that sits under their chin and just blows a cloud of oxygen up toward their nose and mouth.

It's much less claustrophobic.

And you run that at a pretty high flow.

Yeah.

You run that at high flow, 10 to 15 liters to make sure you're creating that oxygen -rich environment around their face.

And finally, a word on oxygen toxicity.

The text notes that prolonged FiO2 greater than 50 % can lead to lung damage things like atelectasis and surfactant disruption.

So the rule is use what you need to stabilize, but then titrate down to that 94, 99 % target range as soon as you can.

Okay.

Moving on to section two, this is the heavyweight division of the chapter, emergency drugs for cardiac disorders.

Yeah, this is a big one.

The text organizes these essentially by the M -Mone acronym for chest pain and then by different heart rhythms.

It's a ton of information, so let's just take it one drug at a time.

Perfect.

First up, aspirin.

Aspirin is the first line drug for acute coronary syndromes and myocardial infarction, you know, heart attacks.

It works by decreasing platelet aggregation.

Essentially, it just makes the platelets slippery so the clot that's blocking the artery doesn't get any bigger.

The dose listed is 162 to 325 milligrams,

but the administration instruction here is absolutely vital.

The patient must chew the tablet.

By chewing.

I mean, why not just swallow it with a little bit of water?

Because we are racing the clock, a swallowed tablet has to dissolve in the stomach, then it has to pass into the intestines, then it has to get absorbed.

That all takes time that the heart muscle just doesn't have.

So chewing bypasses some of that.

Completely.

Chewing breaks it down, it increases the surface area, and it allows absorption to begin immediately through the buccal mucosa in the mouth.

It just speeds up the anti -platelet effect significantly.

What are the contraindications?

When do we not give it?

A true allergy, of course, but also if there is a cerebral hemorrhage, a bleeding stroke, you definitely do not want to be thinning the blood.

And also, a recent GI bleed is a big one.

Okay, next up is nitroglycerin.

Nitro is sort of the plumber of the heart.

It dilates the coronary arteries, which improves blood flow to the ischemic muscle, but it also dilates the veins in the rest of the body, and that reduces preload, the amount of blood returning to the heart.

This makes it really excellent for acute cardiogenic pulmonary edema because it stops the heart from being overwhelmed by fluid.

Now, we absolutely have to talk about the red flag.

This is probably the most famous contraindication in emergency cardiology, but the text emphasizes that you have to be really active about looking for it.

Right.

You absolutely cannot give nitroglycerin if the patient has taken phosphoesterase inhibitors, which are erectile dysfunction drugs, within the last 24 to 48 hours.

We're talking about droves like Viagra, which is sildenafil, Cialis, which is didalafil.

Correct.

And here's the functional challenge.

A 65 -year -old man comes in with crushing chest pain.

He's scared.

His wife is standing right there at the bedside.

Is he going to volunteer that he took a Viagra last night?

Probably not.

Probably not.

So you cannot just ask, are you on any other medications?

You have to be specific, and sometimes you have to be discreet about it.

You have to ask, have you taken any medications for erectile dysfunction?

Because if you miss this and you give that nitro— What's the actual physiology there?

Why is it so incredibly dangerous?

It's a complete double whammy of vasodilation.

The ED drugs work by keeping the vessels open.

Nitro works by forcing the vessels open.

When you combine the two of them, the vascular resistance just collapses.

You just bottom out the blood pressure.

Profound refractory hypotension.

And refractory is a really scary word there.

It means it doesn't respond to treatment.

You can give fluids, you can give pressors, but that blood pressure just stays in the basement.

It can be fatal.

So the awkward question is always better than the fatal mistake.

Every single time.

So assuming they're clear on that front, let's talk about dosing.

If their systolic BP is greater than 90, you can use the sublingual tablet or the spray.

And the protocol is one tablet or one spray every five minutes, up to a total of three doses.

Are there any specific administration tips for the spray?

Because I feel like that can be confusing.

Yes.

Do not inhale it.

It is not an asthma inhaler.

You spray it under the tongue and you tell the patient not to swallow for at least 10 seconds to let it absorb properly.

And for IV administration?

That's usually for unstable angina or if the sublinguals don't work.

You start at about five micrograms per minute and you titrate up based on their pain and their blood pressure.

But you have to watch that BP like a hawk.

Hypotension is the major adverse effect.

And if the BP does drop, what's the first move?

First thing you do is stop the drip,

then lay the patient's supine and elevate their legs to return blood flow to the heart.

And you have to warn them about the headache.

Oh, the nitro headache is brutal.

It's because it dilates the vessels in the brain, too.

It's actually a sign that the drug is working, but it is really, really unpleasant for the patient.

Okay.

So we've given aspirin, we've given nitro, the chest pain is still there.

Now we bring in morphine sulfate.

Morphine is indicated for chest pain that's unrelieved by nitro.

And specifically for an ST segment elevation MI or STEMI, it acts on the central nervous system to relieve the pain, but it also has the nice side effect of dilating venous vessels, which further reduces the cardiac workload.

What are we monitoring for when we give it?

The big two are respiratory depression and hypotension.

You always administer it slowly, about one to four milligrams 5E over one to five minutes.

And if we do suppress their respirations too much,

what's the plan?

You need to have the rescue drug ready to go.

That's naloxone.

We'll talk more about that in the overdose section, but it should always, always be within arm's reach when you are pushing opioids.

Okay.

Let's switch gears from pain to heart rate.

The patient is bradycardic.

The heart is beating way too slow to maintain their blood pressure.

The go -to drug for symptomatic bradycardia is atropine sulfate.

It works by inhibiting the vagus nerve.

The vagus nerve is like the brake pedal for the heart.

So atropine essentially takes the foot off the brake and lets the heart speed up.

Now the text gives a very specific dosing rule for adults that feels like a classic trap for new nurses.

It is a total trap.

The minimum adult dose is 0 .5 milligrams.

So what happens if I want to be super cautious and I just give, say, 0 .25 milligrams?

You might cause paradoxical bradycardia.

A dose that's too small can actually stimulate the vagal center in the brain before it blocks the nerve at the heart.

And that causes the heart rate to drop even lower.

Wow.

So 0 .5 milligrams is the floor.

Do not go under it.

And what's the ceiling?

The max dose is 3 milligrams.

After you've given a total of 3 milligrams, the vagus nerve is fully blocked.

Giving any more won't do anything helpful.

It'll just cause toxicity.

Is there any exception to that max dose?

Yes, there is one big one.

Organophosphate poisoning.

So if a farmer comes in covered in pesticide or someone is exposed to a nerve gas, they are in a massive cholinergic crisis.

They need massive, massive doses of atropine to dry up all their secretions.

The 3 milligram limit goes completely out the window in that specific case.

What about the pediatric nuance?

This seems really important.

It's critical.

In infants, cardiac output is almost entirely rate dependent.

They can't really increase their stroke volume very much.

So if their rate drops, their output just plummets.

So if the heart rate is less than 60 in an infant who has poor perfusion, you don't just give drugs.

You start CPR.

CPR first.

And for neonates, it's even more specific.

For neonates, if the rate is less than 80, the text says you actually give epinephrine before you give atropine.

Why epi first in a newborn?

It's because a stressed neonate burns through their endogenous catecholamines, their own adrenaline reserves, incredibly fast.

Their heart isn't slowing down because of the vagus nerve.

It's slowing down because the engine is just running out of gas.

They need the epinephrine to restart the whole system.

Okay, now let's go the other way.

The heart is racing.

Proxysmal supraventricular tachycardia or PSVT.

The first line drug, the one you go to immediately, is adenosine.

Let's talk about the administration because adenosine is famous for being, well, high stakes.

You don't just casually hang this in a drip.

The text describes a very specific technique.

Yeah, you might hear this called the slam in clinical practice.

And that is not an exaggeration.

The half -life of adenosine is less than five seconds.

Five seconds.

So by the time I finish this sentence, the drug is essentially gone from the body.

Exactly.

And because of that, if you push this slowly,

the enzymes in the blood, specifically adenosine deminase, will just eat it up before it ever reaches the heart.

It will do absolutely nothing.

So walk me through the choreography here.

I'm at the bedside.

I've got the drug.

What do I do?

Okay, first you need an IV site that's as close to the heart as possible.

The anticubital fossa, the crook of the elbow is standard.

You do not want to be using an IV in the hand.

Just too much travel time.

Way too much travel time.

So you have your six milligrams of adenosine in one syringe and a 20 -millilow saline flush right behind it in another syringe.

You push the drug as hard and as fast as that plunger allows, and you immediately, I mean, immediately slam that saline flush right behind it.

It's like a train pushing the drug down the track.

Exactly.

And then as soon as that's in, you lift their arms straight up in the air.

Gravity helps race that bolus down to the right atrium.

The moment everyone in the room dreads.

The pause, the assistily.

The text warns about this, but it doesn't quite capture the feeling in the room when that monitor goes flat.

It feels like an eternity.

Adenosine works by completely blocking electrical conduction through the AV node.

So for about six to maybe 15 seconds, the monitor might go completely flat.

The patient often feels this massive thud in their chest or a sense of impending doom they might gasp.

It is terrifying if you are not expecting it.

So the nursing implication here isn't just push fast, it's warn the patient.

100%.

You have to tell them you are going to feel very funny for a few seconds, like a kick in the chest.

We'll be right here with you and it will pass very quickly.

If you don't warn them, they will think they are dying.

And for a few seconds, their heart has technically stopped.

And if that six milligram dose doesn't work?

You can repeat with the 12 milligram dose.

But if that doesn't work, you stop.

Higher doses aren't recommended and you need to move on to something else.

What if adenosine fails?

Or what if the rhythm is something like atrial fibrillation or atrial flutter?

Then we move on to our second line agent, which is diltizum.

It's a calcium channel blocker.

It works by slowing the ventricular rate, basically controlling how many of those chaotic impulses get through the AV node down to the ventricles.

Are there any major contraindications for diltiazum?

Yes, a big one.

Do not mix it with beta blockers.

The text warns that the effects are synergistic.

Since both drugs depress the heart muscle and slow conduction, using them together can cause severe bradycardia or even throw the patient into heart failure.

Okay, let's get into the truly life -threatening rhythms.

Ventricular tachycardia, V -tach, and ventricular fibrillation, V -fib.

The big guns,

amiodarone.

Amiodarone is a total powerhouse.

It has alpha and beta blocking effects, and it affects the sodium, potassium, and calcium channels.

It's the first line antidisrhythmic in the cardiac arrest algorithm for a reason.

The dosing for it depends entirely on the patient's status, right?

Pulse or no pulse?

Correct.

You have two very distinct scenarios.

Scenario A.

The patient is in cardiac arrest.

They are pulseless.

You give 300 milligrams as a rapid IV push.

You just want to get it in there as fast as possible.

Okay.

And scenario B.

Scenario B.

The patient has a pulse, but they are in a dangerous, unstable rhythm.

In that case, you give 150 milligrams mixed in a bag, and you run it over 10 minutes, much more controlled.

What are the main adverse effects we're watching for?

Hypotension and bradycardia are the big, immediate ones you have to look out for.

And always remember, amiodarone has an incredibly long half -life.

It stays in the body for weeks, so its effects can linger.

The alternative to amiodarone in the algorithm is lidocaine.

Right.

Lidocaine isn't just for numbing up skin for stitches.

It exerts a local anesthetic effect directly on the heart muscle itself, which decreases irritability and calms down those extra beats.

I love the term the text uses for lidocaine toxicity here.

Lidocaine crazies.

It sounds like a bad 80s band name, but it's actually really serious.

What does that look like in a patient?

It's all signs of neurotoxicity.

So you're looking for confusion, drowsiness, maybe hearing impairment,

muscle twitching, and eventually it can progress to seizures.

If you see your patient on a lidocaine drip getting twitchy or confused, you need to stop the drip and call the provider.

And if the patient has liver issues?

That's a huge consideration.

You need to reduce the dose by as much as 50 % because the liver is what metabolizes lidocaine.

If the liver is broken, the drug just builds up to toxic levels incredibly fast.

Next on the list is prokainamide.

Prokainamide is used for V -tach and PVCs that are unresponsive to adenosine.

But this is a drug that requires really intense monitoring.

You have to know the stop points.

Okay, these are the conditions where you must immediately stop the infusion.

What are they?

Okay, there are four.

Number one, the dysrhythmia resolves.

That's the good one.

That means it worked.

Right.

Number two, hypotension develops.

That's bad you stop.

Number three, the total load of 17 milligrams per kilogram is reached.

That's your max dose.

And number four, and this is the big ECG one, the QRS complex widens by more than 50 % of its original width.

Why is that QRS widening so scary?

What's happening?

Because the widening indicates that conduction through the ventricles is slowing down dangerously.

If you widen it too much, you are setting the stage for a systole or V -fib.

It is a major sign of toxicity.

And you should never ever give brucanamide if the patient has.

Torsades de pointes.

It prolongs the QT interval, which will just make torsades even worse.

Speaking of torsades de pointes, the text points out that there is a specific cure for that particular rhythm.

Magnesium sulfate.

It is the drug of choice, hands down.

Torsades is a specific type of twisting ventricular tachycardia that's often caused by low magnesium levels.

So giving magnesium acts kind of like a calcium channel blocker and it stabilizes the cardiac membrane.

But you have to be careful about pushing it too fast.

Right.

If you push it too fast and a patient who has a pulse, you can cause hypotension.

And if you give too much, if you cause hypermagnesemia, you get loss of deep tendon reflexes and respiratory depression.

You can essentially paralyze them.

Okay.

Two more drugs in the cardiac section.

The one we all know.

Epinephrine.

Epi.

It's an incredibly potent vasoconstrictor.

In cardiac arrest, we aren't really using it to start the heart.

We are using it to clamp down on all the blood vessels in the body to shunt what little blood flow there is to the brain and the heart.

There's a critical safety alert in the book regarding concentrations.

This is a do not kill the patient moment.

Absolutely.

This is the deadly decimal point.

There are two main concentrations you'll see.

There's 1 .7 thousand.

This is a large volume of fluid with a small amount of drug.

This is the cardiac concentration for a single IV push dose.

And the other one.

The other one is 1 .1 thousand.

This is highly, highly concentrated.

This is used for IM injection and anaphylaxis or for mixing continuous infusions.

If you accidentally push the 1 .1 thousand concentration IV, you are giving a massive overdose that can cause a stroke or a fatal dysrhythmia.

So always, always check the box.

And what about compatibility?

Never mix epinephrine with sodium bicarbonate in the same line.

The alkaline solution completely inactivates the epinephrine.

It basically turns your life -saving drug into useless water.

Which brings us nicely to our last cardiac drug, sodium bicarbonate.

It's used for severe metabolic acidosis, sometimes for hyperkalemia or for a tricyclic antidepressant overdose.

But the text makes a big point that it is not a first line drug for cardiac arrest anymore.

Why did it fall out of favor?

We used to give it all the time.

Because while it fixes the acid number in the blood, it can cause metabolic alkalosis, which shifts the oxygen dissociation curve and actually makes it harder for oxygen to release from the hemoglobin into the tissues.

Plus, it's really hard to reverse alkalosis.

So the current practice is you only use it if acidosis is confirmed by lab work.

All right, that was a marathon cardiac section.

Let's move to the brain.

Section three, intracranial hypertension.

The drug here is mannitol.

Mannitol is an osmotic diuretic.

It's used when you have cerebral edema swelling of the brain from a head trauma or after brain surgery.

So how does it work?

How does it get the swelling down?

Think of the brain like a wet sponge inside a fixed box, which is the skull.

Mannitol makes the blood incredibly salty or hyperosmolar.

This high osmolality in the blood vessels draws water out of the brain cells and into the blood, where it then travels to the kidneys and gets peed out.

It literally shrinks the sponge.

There is a very specific, very important nursing safety step here that involves the equipment you use.

Yes, this is a big one.

Mannitol is a sugar alcohol.

In cool temperatures, it crystallizes.

You can pick up the vial and it looks like it has rock candy or glass shards inside of it.

You absolutely cannot inject crystals into a patient's vein.

It would act like an embolus.

So what do you do if you see that?

You have to warm the vial up to dissolve the crystals.

But critically, you must use a filter needle to draw the medication up just to catch any microscopic crystals you can't see.

And then you have to use a new filter needle or an inline filter on the IV tubing to inject it into the patient.

No filter, no mannitol.

That's the rule.

That is the absolute rule.

Okay, section four, emergency drugs for drug overdose.

We touched on this briefly with morphine, but let's talk specifically about naloxone or Narcan.

Naloxone is the classic opioid antagonist.

It reverses morphine, heroin, fentanyl, you name it.

The typical dosing is 0 .4 to 2 milligrams for free.

But there is a huge trap here.

The book calls it the recurrence trap.

This is so crucial for nurses to understand.

The half -life of naloxone is very short, maybe 30 to 45 minutes.

But the half -life of morphine, or especially methadone, is hours and hours.

So the Narcan wears off while the opioid is still in the system just throwing a party.

Exactly.

So you give the Narcan, the patient wakes up, they're breathing again.

You think, great, my job is done.

You walk away.

But 45 minutes later, the Narcan fades.

The opioid rebinds to the receptors, and the patient stops breathing all over again.

You have to monitor for that recurrence of respiratory depression.

And what's the patient like when they wake up initially?

You need to watch out.

It precipitates acute, immediate withdrawal.

They don't wake up thanking you for saving their life.

They wake up in excruciating pain.

They're vomiting, and they're often very combative.

So stand back.

What about for benzodiazepines?

Things like Valium or Versed?

The reversal agent for benzos is flumazenil.

But there is a significant risk with this one, too.

A big black box warning.

Seizures.

Benzodiazepines work by raising the seizure threshold.

If a patient is a chronic user, say they take Xanax every day for anxiety, and you suddenly strip all of that away with flumazenil, their brain can go into the state of chaotic excitability.

You can trigger intractable seizures that are very difficult to stop.

So you have to use it with extreme caution.

And what about for ingested poisons?

For that, we use activated charcoal.

It basically stays in the gut, and it binds to toxins like a sponge, which prevents them from being absorbed into the bloodstream.

It looks pleasant, I'm sure.

It looks like black sludge.

And getting a patient to drink it is a challenge.

What's the major safety consideration with charcoal?

Vomiting.

If you force a patient to drink this slurry and they are drowsy, they are at a huge risk of vomiting.

If they aspirate that charcoal into their lungs, it can cause a fatal chemical pneumonia or ARDS.

So you do not give it if their gag reflex is absent, or if they're too sleepy, unless you have intubated them first to protect the airway.

Okay, section five.

Emergency drugs for shock.

The text starts with a golden rule about using drugs versus fluids.

The rule is, drugs are secondary.

Imagine a car with an empty gas tank.

It doesn't matter how hard you push the gas pedal, which are the drugs.

The car is not going to go.

In hypovolemic shock, the tank is empty.

You must fill the tank with fluids or blood first.

Pressors only work if there is actually fluid in the pipes to squeeze.

So once the tank is full, if we still need to raise the blood pressure, we might look at dopamine.

Right.

Dopamine is a sympathomimetic, and it's interesting because its effects are dose dependent.

At lower doses, it primarily hits the beta -1 receptors, so it increases heart rate and contractility.

At higher doses, it hits the alpha receptors and causes vasoconstriction to raise the BP.

But there is a really nasty hazard if the IV leaks out of the vein.

Extravagation.

If dopamine leaks into the surrounding tissue, it causes profound vasoconstriction locally.

It literally strangles the skin cells of their blood supply.

You can get severe tissue necrosis and even gain green.

If that happens, is there an antidote?

Yes, there is.

It's fentolamine, which is also known as regutine.

And the technique for giving it is very specific.

You don't just put it in a new IV.

You take a syringe and you inject the fentolamine directly into the skin all around the swollen infiltrated site to force those vessels to open back up and save the tissue.

Okay, let's talk about a specific type of shock.

Anaphylactic shot.

We're back to using epinephrine.

But notice the critical route change here.

For cardiac arrest, we went IV.

For anaphylaxis, the preferred route is IM intramuscular, right into the thigh, the vivastus lateralis muscle.

Why IM instead of VA?

Because in anaphylactic shock, the patient is so vasodilated that their peripheral veins are often collapsed and really hard to find.

The muscle is highly vascular and it provides rapid predictable absorption.

And we use the concentrated 1 .1 ,000 solution here.

And for anaphylaxis, we also use adjuncts, right?

Other drugs to help.

For sure.

You'll give albuterol nebulizers to reverse the bronchoconstriction.

And you'll give diphenhydramine benadryl to help with the swelling and the itching.

There is a fantastic assessment tip in the text regarding albuterol and wheezing.

Yes, this is one that trips up a lot of new nurses.

We get scared when we hear wheezing.

But imagine a patient with a silent chest.

No air is moving at all.

That patient is about to die.

So you give them an albuterol treatment and suddenly you hear loud wheezing.

Which sounds worse.

It sounds worse, but it's actually so much better.

It means that air is finally moving through those narrowed airways enough to create the sound.

The silent chest becoming a wheezy chest is a sign of improvement.

That is a great clinical pearl.

One more shock type.

Insulin shock or severe hypoglycemia?

If they have an IV, you give dextrose 50 % or D50.

It's basically thick, concentrated sugar syrup.

But it's very irritating to veins, so you have to watch closely for phlebitis.

And if you can't get an IV?

Then you give glucagon.

You can give it IM or sub -Q.

It stimulates the liver to break down its stored glycogen into glucose.

But it takes about 10 to 15 minutes to work, so you don't get that instant wake -up effect that you get with D50.

Okay, last big section.

Section 6.

Emergency drugs for hypertensive crises.

The BP is through the roof.

The text says a diastolic over will 120.

The first drug listed is labetalol.

It's an alpha and beta blocker.

It's great for hypertensive crises and some types of stroke.

But because it blocks beta receptors in the lungs too, you want to avoid it in patients with asthma or severe COPD because it can cause bronchospasm.

Then there is nitroproside sodium.

This is a very potent, immediate arterial and venous vasodilator.

But it has some really quirky handling requirements that you have to know.

The foil wrapper.

Yes, it is rapidly inactivated by light.

You must wrap the IV bag in foil or some other opaque material that comes with it.

If you see the solution has turned blue or brown, it has degraded and you have to throw it out.

And what about toxicity?

This is a wild one.

It actually metabolizes into thiocyanate and cyanide.

Yes, cyanide.

If you use it for too long, more than three days or at very high doses, you can actually poison the patient.

You look for metabolic acidosis and this is a distinct sign.

An almond smell on their breath.

Wow.

Okay.

And finally, furosemide or Lasix.

A classic loop diuretic.

It's often used for acute pulmonary edema that's associated with a hypertensive crisis.

How does it help immediately?

I mean, diuresis takes a little bit of time to kick in.

That's a great question.

The text notes that furosemide actually causes some vasodilation before the diuresis even starts.

That helps lower the BP right away.

But you have to push it slowly.

The book says 20 milligrams over one to two minutes.

Why so slow for Lasix?

Ototoxicity.

If you slam Lasix in too fast, you can cause permanent hearing loss.

Okay.

Section seven, clinical judgment and case studies.

Let's wrap up by looking at the text's Tums patient.

A total classic.

It's a 42 -year -old man who thinks he has indigestion and he's been taking Tums.

It's actually an MI.

He gets the full workup.

Oxygen, aspirin, nitro.

But the chest pain is refractory.

It's not going away.

So that's when morphine is indicated.

Correct.

And when he complains of a bad headache, the Sharp nurse recognizes that is a common side effect of the nitro, not a sign of a new stroke.

And the trauma patient, DWT.

He has that weird combination of hypotension and bradycardia.

That specific combo points to neurogenic shock.

A loss of sympathetic tone from a spinal injury.

He needed mannitol for his head injury.

And you have to remember the filter needle.

And he needed dopamine for his pressure.

And you have to watch for extravization.

It really does a great job of tying it all together.

It does.

It shows how in one patient, you might need a presser one minute and an antihistamine the next.

It's all about knowing your options.

We have covered a ton of ground.

Oxygen, cardiac meds for rhythm and flow, brain meds like mannitol, antidotes, shock pressers, and BP lowering agents.

My final thought on all this.

In an emergency, knowing what the drug does is only half the battle.

You have to know the logistics.

Where is the filter needle on the unit?

What is the correct concentration?

Can I mix these two drugs in the same line?

That practical knowledge is what makes you a safe and effective nurse.

That is some critical advice.

Thanks for listening to this deep dive.

Good luck on your exams.

And remember to be the calm and the chaos.

A warm thank you from the last minute lecture team.

We'll see you next time.