WEBVTT

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Hey guys, this right here is going to be PALS,

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the Pediatric Advanced Life Support. And the

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way it's going to go is I'm going to try to keep

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it in this order. The systematic approach to

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the pediatric patients, pediatric shock recognition,

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pediatric management of shock, recognizing respiratory

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distress, managing respiratory distress. recognizing

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cardiac arrest, management of cardiac arrest,

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arrhythmias, recognition of those arrhythmias,

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and then management of those arrhythmias. I don't

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remember PALS being this deep, but again, it's

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been almost two years since I've taken PALS,

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but it seems like it's a lot more in depth than

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just your normal ACLS. So this material is coming

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straight from the book. For the course just make

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sure that you guys are reading that material

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Because I did not add some stuff in there like

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team dynamics or resources for respiratory care

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or Management of the post cardiac arrest, you

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know stuff like that. I didn't include that into

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this stuff So if you guys need that or want that,

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then by all means, read the book or, you know,

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Google it or whatever. But this right here is

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going to be the intro for the pals stuff. So

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I hope you guys enjoy the pediatric advanced

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life support material for the course. This is

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all going to happen super fast. Welcome to the

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emergency room. Welcome back to The Deep Dive.

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Today we are putting away the flashcards and

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really getting into the most critical zone of

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pediatric emergency care. If you're an ER nurse

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and you're gearing up for your PASS certification

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or maybe you just want to feel more confident

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when that pediatric respiratory call comes in,

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well, this Deep Dive is for you. That's absolutely

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right. And our focus today, it's not about just

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memorizing algorithms, not about where the arrows

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point on some flow chart. Our mission is to get

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into the path of physiology, the why behind the

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path of those guidelines. And we're going to

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be focusing specifically on that foundational

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pillar, which is recognizing and managing. pediatric

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respiratory distress and failure. We want to

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translate that textbook knowledge into what you

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actually do at the bedside. Exactly. And we're

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starting here for a reason, and it's, well, it's

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a bit grim, but it's absolutely essential. The

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pathos source material says this over and over

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again. Respiratory failure is the number one,

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the major cause of cardiac arrest in kids. It's

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the big one. It's not like adults, you know,

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where it's often a primary cardiac event. For

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kids, the arrest is usually the final step after

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they've been hypoxic for a while. And that means

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we have this tiny, tiny window to intervene,

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to do something before they code. Because once

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a child arrests, the outcomes, they're just dramatically

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worse. So the whole goal of PALLAS, especially

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for you, the ER nurse, is prevention. It's all

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about prevention. So if we can master spotting

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and aggressively managing that respiratory failure,

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we're actually changing the outcome. We're improving

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survival. We're improving survival and neurological

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outcomes. The difference between a good palace

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provider and a great one. It's often just speed

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and a systematic approach to breathing problems.

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OK, so let's unpack that, this clinical reality.

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You know, we're so often trained to think cardiac

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first with adults, but with a kid who's struggling

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to breathe, you're saying we have to flip that

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entire paradigm. What are the key physiological

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differences that make Pella so focused on respiratory

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first? Well, the differences are both anatomical

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and physiological. First off, just the anatomy.

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Kids, especially infants, they have much smaller

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airways. I mean, their trachea is shorter. It's

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narrower. So a little bit of swelling that an

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adult could handle is a huge deal. A huge deal.

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Think about croup. That little bit of swelling,

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which an adult might barely notice, becomes a

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life -threatening critical obstruction for a

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two -year -old. And second, they rely way more

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heavily on their diaphragm for breathing. Ah,

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which is why you see those retractions so clearly.

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Exactly. That's why seeing accessory muscle use,

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you know, the super sternal or subcostal retractions,

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that's an early and really significant sign of

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distress. And then there are the metabolic differences.

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I think this is where it gets really interesting.

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They have a higher metabolic rate. They just

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burn through oxygen faster. Precisely. So if

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they become hypoxemic, their oxygen reserves

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are depleted so, so rapidly. This is why that

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decline can be so fast. The kid looks distressed,

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then they get quiet, and then they crash. And

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that quiet phase is so dangerous. It's often

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mistaken for improvement, right? It's a classic,

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terrifying sign of fatigue and impending arrest.

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That shift from agitation to lethargy is a massive

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red flag. Recognizing that is absolutely fundamental.

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So we see the signs, we know we have to act fast.

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First step is always stabilization. Let's walk

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through that initial ABC framework. We stabilize

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oxygenation and ventilation, and only then do

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we hunt for the cause. Starting with A for airway

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interventions. What are the absolute non -negotiables

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to get that airway patent? Airway patency is

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everything. And, you know, the first, the simplest,

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and often the safest move is just allowing the

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child to find a position of comfort. So if they're

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sitting up, leaning forward in that tripod position,

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you just let them be. You let them be. Don't

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fight them. Anything you do that increases their

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agitation is going to increase their oxygen demand

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and can actually make the obstruction worse.

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But what if that's not enough? We have to intervene

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with maneuvers. The default is the head tilt

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chin lift, correct? Yes, that's the default.

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Unless, and this is a big dig, unless you have

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any suspicion of trauma or a C -spine injury.

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If that mechanism exists, you immediately switch

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to the jaw thrust maneuver without tilting the

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head. The goal is the same. Lift the tongue off

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the back of the pharynx. Beyond maneuvers, we

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have adjuncts. Let's get into the oropharyngeal

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airway, the OPA, and the nasopharyngeal, the

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NPA. They're crucial tools, but they come with

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risks, especially in kids. Absolutely. The OPA

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should only be used in a child who is deeply

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unconscious. I mean, truly flaccid, no gag reflex.

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And why is that so critical? Because if you stimulate

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that gag reflex, you're going to make them vomit.

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and that could lead to a lethal aspiration. And

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you have to size it right, from the corner of

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the mouth to the angle of the jaw. No guessing.

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And what about the MPA? It's usually better tolerated,

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right, even in a conscious child. But what are

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the big red flags that contraindications we have

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to look for? The MPA is great because it can

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bypass the tongue obstruction without causing

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that gagging. However, you have to use extreme

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caution if there's any known bleeding disorder,

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any significant facial trauma, or, critically,

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a suspected basal or skull fracture. Because

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you could actually insert it into the cranium.

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You could. It's a never event, but it's a known

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risk. And again, sizing is key. Tip of the nose

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to the tragus of the ear. Okay, that's A. Moving

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to B for breathing. We've got the pulse oxon,

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but we need to be thinking beyond that immediately.

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Immediately. You go straight to high -concentration

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oxygen with a non -rebreathing mask and NRB.

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We're aiming for 95 % saturation or higher. But

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you also need to be preparing for advanced respiratory

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monitoring. That means getting the end -title

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CO2 or ETQ -EROS monitor ready to go. because

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that tells you about ventilation and circulation.

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It gives you crucial data. And if it's indicated,

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say, a kid with a known history of asthma, you're

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giving inhaled meds right away. But the number

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one nursing priority here is preparation. You're

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always, always preparing for an advanced airway

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and the need for bag valve mask or BVM ventilation.

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Okay, I want to challenge that point a little

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because the second you bring out the BVM, you

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risk agitating the child. And you mentioned the

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risk of air trapping in some diseases. What's

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the clinical trigger? When do you make that leap

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from a non -rebreather to actually assisting

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their breaths with a BVM? That is a great question

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because you're right. The BVM is a high risk,

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high reward tool. The trigger is failing respiratory

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effort or a deteriorating mental status, even

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with high flow oxygen. If you see the child's

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respiratory rate plummeting. If they're becoming

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bradycardic, or if they just physically cannot

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maintain an adequate minute volume anymore, that's

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when you have to step in. So distress is one

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thing, but failure is the trigger. Distress is

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acceptable. Failure is not. That's the line.

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And C for circulation. Before we're even thinking

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about code meds, what's the ER nurse's first

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priority? You're monitoring the heart rate, the

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rhythm, the blood pressure, of course, but the

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absolute number one priority. is establishing

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vascular access, an IV or an intraosteus, an

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IO line immediately. Why so urgently? Because

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respiratory distress can progress to shock so

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fast. And if you wait until that child is hypotensive

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and crashing, their veins are going to collapse.

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Peripheral access becomes nearly impossible.

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You need that line ready for fluids and meds

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the second you need them, not a minute later.

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Let's isolate respiratory arrest for a moment.

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This is that critical point where The nurse is

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the only thing standing between the patient and

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a full cardiac arrest. How do we define it again,

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and what are the exact guidelines for rescue

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breathing? So respiratory arrest means the child

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is apneic, they're not breathing, but they still

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have a detectable pulse. There's still cardiac

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activity. Our job here is to profuse the brain

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and heart with oxygen before they also feel from

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the hypoxia. And the rhythm of those breaths.

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What's the specific rate? For infants and for

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children, you slow it way down compared to what

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you do in a full code. You're giving 12 to 20

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breaths per minute. That works out to one breath

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every three to five seconds. Okay, one breath

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every three to five seconds. Yep. And each breath

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should just take about one second to deliver,

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and you're just looking for visible chest rise.

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And of course, use oxygen as soon as you have

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it. So why is that three to five second interval

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so important? What's the physiology behind that

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specific timing? It's all about managing a delicate

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balance. You're trying to provide enough oxygen

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and allow for CO2 removal, but you're doing it

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without causing excessive gastric inflation.

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If you go too fast, you're just pumping air into

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the stomach. That can cause vomiting, aspiration,

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and it pushes up the diaphragm, which makes breathing

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even harder. It's a deliberate measured rate

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to maximize oxygen delivery and minimize those

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secondary problems. And how often do you check

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to see if things are changing? You have to check

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the pulse every two minutes. No longer. And if,

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during that check, the pulse is gone, or if the

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heart rate drops below 60 and you see signs of

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poor perfusion, you don't wait, you immediately

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transition, you shout for help, you start chest

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compressions, and you are now in the full CPR

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sequence, that rapid shift is essential because

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the clock on hypoxia is ticking down fast. OK,

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so once we've stabilized the ABCs, the Pale S

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framework tells us to get more specific with

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our management. We have to figure out which of

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the four big buckets this kid falls into. upper

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airway obstruction, lower airway obstruction,

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lung tissue disease, or disordered control of

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breathing. Let's start at the top. upper airway

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obstruction. Right. This involved the large airways,

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so the nose, the pharynx, the larynx. These are

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the patients we see all the time in the ER. And

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you have to remember, infants are so prone to

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this because their airways are just tiny and

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their tongue tends to fall back and obstruct

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when their muscle tone decreases. So the general

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management principles are all about keeping that

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airway open and, just as importantly, keeping

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the child calm. Beyond just positioning, what's

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the crisis pathway look like? Well, if those

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conservative measures aren't working and you

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see signs of pending respiratory failure, the

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conversation changes very quickly. You're moving

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towards advanced airway management, which means

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preparing for the possibility of a surgical airway

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like a tracheostomy or a crick. But thankfully,

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most cases will respond to the right medication

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for the specific cause. OK, let's drill into

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the classic example then, croup or laryngotracheal

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bronchitis. This viral infection causes swelling

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right below the vocal cords in the subglottic

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area, and that's what gives you that signature

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barking cough and stridor. How do you quickly

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assess how bad it is to guide your treatment?

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Severity assessment is everything because it

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can change so fast. You hear the barking cough,

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sure, but what you're really listening for is

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the stridor. Is it only there when the child

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is agitated or crying? Or is it present even

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when they're at rest? Stridor at rest is a big

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warning sign. A huge warning sign. Then you look

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at the retractions. Are they mild or are they

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deep and significant? And finally, what do you

00:13:17.470 --> 00:13:19.350
hear when you listen? How is their air entry?

00:13:19.450 --> 00:13:22.149
And the PAL -L -S guidelines give us a really

00:13:22.149 --> 00:13:24.629
clear tiered approach based on that assessment.

00:13:24.990 --> 00:13:26.830
Let's focus on that moderate to severe crude

00:13:26.830 --> 00:13:28.830
patient. You can hear the stridor at rest. You

00:13:28.830 --> 00:13:31.509
see significant retractions. What's the immediate

00:13:31.509 --> 00:13:34.309
game plan? The immediate game plan starts with

00:13:34.309 --> 00:13:37.509
humidified oxygen and you make them NPO, nothing

00:13:37.509 --> 00:13:41.029
by mouth. This minimizes aspiration risk and

00:13:41.029 --> 00:13:43.049
just reduces the work of breathing that comes

00:13:43.049 --> 00:13:45.570
with swallowing. The main medication, the one

00:13:45.570 --> 00:13:48.429
you go to right away, is nebulized epinephrine.

00:13:48.600 --> 00:13:52.259
Okay, so why nebulized epi and why is the follow

00:13:52.259 --> 00:13:54.659
-up period after you give it so incredibly important?

00:13:55.039 --> 00:13:58.080
Epinephrine is a powerful alpha adrenergic agonist.

00:13:58.360 --> 00:14:02.139
So when it's inhaled, it causes this rapid localized

00:14:02.139 --> 00:14:04.480
vasoconstriction in that swollen tissue in the

00:14:04.480 --> 00:14:06.940
subglottic area. It shrinks the swelling almost

00:14:06.940 --> 00:14:10.639
instantly. But, and this is a huge but, That

00:14:10.639 --> 00:14:13.200
effect is often temporary. It wears off. It wears

00:14:13.200 --> 00:14:15.340
off. And once that visa constriction is gone,

00:14:15.600 --> 00:14:17.460
usually within about two hours, the stridor can

00:14:17.460 --> 00:14:19.500
come right back. And sometimes it's even worse

00:14:19.500 --> 00:14:21.779
than before. And that is the essential clinical

00:14:21.779 --> 00:14:23.919
pearl for the ER nurse, isn't it? You cannot

00:14:23.919 --> 00:14:26.220
discharge or transfer that patient until they've

00:14:26.220 --> 00:14:28.440
been watched for at least two hours after that

00:14:28.440 --> 00:14:31.679
nebulized epi. Correct. That two hour observation

00:14:31.679 --> 00:14:34.700
period is completely non -negotiable. While the

00:14:34.700 --> 00:14:38.080
epi is giving you that rapid relief, you're simultaneously

00:14:38.080 --> 00:14:41.779
giving a systemic corticosteroid like dexamethasone,

00:14:42.059 --> 00:14:45.299
either PO, IV, or IM, to tackle the underlying

00:14:45.299 --> 00:14:47.899
inflammation with a longer -acting drug. Okay,

00:14:47.980 --> 00:14:51.039
now for the worst -case scenario. Impending respiratory

00:14:51.039 --> 00:14:54.700
failure and croup. The child is lethargic, pale,

00:14:54.970 --> 00:14:58.250
Maybe cyanotic. What now? Now is a full -blown

00:14:58.250 --> 00:15:00.669
emergency. You're continuing the high concentration

00:15:00.669 --> 00:15:03.210
oxygen, but you're probably providing assisted

00:15:03.210 --> 00:15:05.970
ventilation with a BVM to support that failing

00:15:05.970 --> 00:15:08.250
effort. You're given the dexamethasone, FETC,

00:15:08.429 --> 00:15:11.549
or IM for sure, and you are preparing for an

00:15:11.549 --> 00:15:14.549
advanced stairway for ET intubation. And is there

00:15:14.549 --> 00:15:16.990
a specific procedural trick for intubating a

00:15:16.990 --> 00:15:19.429
croup patient? There is. Because that swelling

00:15:19.429 --> 00:15:22.009
is subglottic, the airway below the vocal cords

00:15:22.009 --> 00:15:24.090
is much narrower than you'd expect. So you have

00:15:24.090 --> 00:15:26.129
to anticipate this and choose an endotracheal,

00:15:26.129 --> 00:15:29.409
or ET, tube that is often a half size to a full

00:15:29.409 --> 00:15:31.950
size, smaller than what the age -based formula

00:15:31.950 --> 00:15:33.830
would predict. Because if you try to force the

00:15:33.830 --> 00:15:35.929
predicted size, you could cause more trauma and

00:15:35.929 --> 00:15:37.909
completely obstruct the airway. You could make

00:15:37.909 --> 00:15:41.350
the situation a hundred times worse. Yeah. Let's

00:15:41.350 --> 00:15:44.139
shift gears to anaphylaxis. This also creates

00:15:44.139 --> 00:15:46.360
upper airway obstruction but through a totally

00:15:46.360 --> 00:15:49.259
different mechanism, a severe systemic allergic

00:15:49.259 --> 00:15:51.820
reaction. So we're dealing with both swelling

00:15:51.820 --> 00:15:55.539
or edema and bronchospasm, and it's often complicated

00:15:55.539 --> 00:15:58.899
by hypotension. Anaphylaxis is a multi -system,

00:15:59.360 --> 00:16:02.340
incredibly fast -moving emergency. For any moderate

00:16:02.340 --> 00:16:05.679
to severe reaction, the absolute undisputed first

00:16:05.679 --> 00:16:08.720
priority is epinephrine. And what are the details

00:16:08.720 --> 00:16:10.740
of that epi -administration? How is it given?

00:16:11.139 --> 00:16:14.070
Intramuscular. I am epinephrine right away, either

00:16:14.070 --> 00:16:16.110
with an auto injector or a standard syringe.

00:16:16.509 --> 00:16:18.509
And you can repeat it every 10 to 15 minutes

00:16:18.509 --> 00:16:20.350
as you need to. The mechanism is what makes it

00:16:20.350 --> 00:16:22.590
so perfect. It causes rapid vasoconstriction

00:16:22.590 --> 00:16:24.970
to reverse the hypotension and shrink that laryngeal

00:16:24.970 --> 00:16:27.549
edema. And it's also a bronchodilator to treat

00:16:27.549 --> 00:16:29.590
the wheezing. It is the single most important

00:16:29.590 --> 00:16:31.909
drug you will give. OK, so after the epine, we

00:16:31.909 --> 00:16:34.190
add the secondary meds to control that inflammatory

00:16:34.190 --> 00:16:36.970
response. Why this cocktail of steroids and two

00:16:36.970 --> 00:16:39.309
different kinds of antihistamines? We use IV

00:16:39.309 --> 00:16:42.009
corticosteroids like methylprednisolone. to prevent

00:16:42.009 --> 00:16:44.370
what's called a biphasic reaction, where the

00:16:44.370 --> 00:16:46.590
symptoms come back hours later, and to treat

00:16:46.590 --> 00:16:49.549
that underlying inflammation. And we aggressively

00:16:49.549 --> 00:16:52.509
treat the bronchospasm with continuous nebulized

00:16:52.509 --> 00:16:56.169
albuterol. And the antihistamines. We give diffenhydramine,

00:16:56.190 --> 00:16:58.649
which is an H1 blocker, but the guidelines also

00:16:58.649 --> 00:17:02.899
say to add an H2 blocker, like ranitidine. What's

00:17:02.899 --> 00:17:06.380
the rationale for the H2 blocker? Well, the defenhydramine,

00:17:06.380 --> 00:17:08.900
the H1 blocker, it targets the immediate symptoms

00:17:08.900 --> 00:17:11.980
like hives and itching. The H2 blockers help

00:17:11.980 --> 00:17:14.079
prevent the further release of histamine from

00:17:14.079 --> 00:17:16.420
mast cells, and they address the vasodilation

00:17:16.420 --> 00:17:18.380
and leaky capillaries that are contributing to

00:17:18.380 --> 00:17:21.259
the shock. The evidence for H2 blockers alone

00:17:21.259 --> 00:17:24.460
is a bit debated, but in PALS, the goal is comprehensive

00:17:24.460 --> 00:17:26.779
histamine blockade. What if the patient is already

00:17:26.779 --> 00:17:28.720
crashing into hypotensive shock? Fluid's the

00:17:28.720 --> 00:17:31.160
next step. What's the initial bolus? Immediate

00:17:31.160 --> 00:17:34.200
resuscitation. You lay the child flat, supine,

00:17:34.519 --> 00:17:37.420
and you give a 20 inoleller per kilogram bolus

00:17:37.420 --> 00:17:40.779
of an isotonic crystalloid. So normal saline

00:17:40.779 --> 00:17:43.019
or lactated ringers. And you have to be ready

00:17:43.019 --> 00:17:45.500
to repeat that bolus, sometimes two, three, even

00:17:45.500 --> 00:17:48.960
four times. Anaphylaxis causes a massive capillary

00:17:48.960 --> 00:17:51.779
leak, and these kids become profoundly volume

00:17:51.779 --> 00:17:54.819
depleted very, very quickly. And if the hypotension

00:17:54.819 --> 00:17:57.980
is just not responding to fluids and the IM epinephrine,

00:17:58.039 --> 00:18:00.079
what's the next escalation? You have to start

00:18:00.079 --> 00:18:03.119
a titratable IV epinephrine infusion, a continuous

00:18:03.119 --> 00:18:06.000
drip. You titrate it to achieve an adequate mean

00:18:06.000 --> 00:18:08.660
arterial pressure and good perfusion. And this

00:18:08.660 --> 00:18:10.140
just highlights why it's so critical to have

00:18:10.140 --> 00:18:13.420
that early IV or IO axis we talked about. Finally

00:18:13.420 --> 00:18:16.039
in this category, foreign body airway obstruction

00:18:16.039 --> 00:18:19.319
or FBAO. This might be the highest stress scenario

00:18:19.319 --> 00:18:22.259
because the fix is purely mechanical. We have

00:18:22.259 --> 00:18:25.019
to reinforce that key distinction. Responsive

00:18:25.019 --> 00:18:27.519
versus unresponsive. The PLS source material

00:18:27.519 --> 00:18:29.720
is crystal clear on this. If the child is responsive,

00:18:29.720 --> 00:18:31.619
they can make sounds or they're coughing forcefully.

00:18:31.980 --> 00:18:34.259
You do not intervene physically. You let them

00:18:34.259 --> 00:18:37.000
cough. Encourage them to keep coughing. Their

00:18:37.000 --> 00:18:38.900
own cough is almost always more effective than

00:18:38.900 --> 00:18:41.660
anything we can do manually. We only step in

00:18:41.660 --> 00:18:43.599
when that cough becomes silent or ineffective.

00:18:43.859 --> 00:18:46.559
They can't speak or you see poor air exchange.

00:18:46.920 --> 00:18:49.640
And the maneuvers themselves differ by age? They

00:18:49.640 --> 00:18:53.259
do. For an infant so younger than one year, you

00:18:53.259 --> 00:18:55.720
do a sequence of five rapid back slaps between

00:18:55.720 --> 00:18:58.460
the shoulder blades, followed by up to five chest

00:18:58.460 --> 00:19:00.799
thrusts, which are basically compressions. You

00:19:00.799 --> 00:19:03.240
repeat that cycle until the object is out or

00:19:03.240 --> 00:19:06.000
the infant becomes unresponsive. For a child,

00:19:06.259 --> 00:19:08.859
one year and older, you move to abdominal thrusts,

00:19:08.960 --> 00:19:11.960
the Heimlich maneuver. Again, you repeat until

00:19:11.960 --> 00:19:14.619
the object is expelled or they become unresponsive.

00:19:14.759 --> 00:19:16.779
And if they do become unresponsive, we immediately

00:19:16.779 --> 00:19:19.480
switch to our code protocol. What's that pathway?

00:19:19.660 --> 00:19:22.420
You activate EMS or your code team and you start

00:19:22.420 --> 00:19:25.819
CPR immediately. And this is important. You don't

00:19:25.819 --> 00:19:28.059
waste time with an initial pulse check if they're

00:19:28.059 --> 00:19:30.559
unresponsive and not breathing or only gasping.

00:19:30.859 --> 00:19:32.579
You just start compressions. Then every time

00:19:32.579 --> 00:19:34.380
you open the airway to give your two breaths,

00:19:34.579 --> 00:19:37.099
you look in the mouth for the object. And what's

00:19:37.099 --> 00:19:39.420
the clinical pearl about actually removing the

00:19:39.420 --> 00:19:41.759
object? You only attempt to remove it if you

00:19:41.759 --> 00:19:44.980
can clearly see it. The absolute rule is do not

00:19:44.980 --> 00:19:47.839
perform a blind finger sweep. You risk pushing

00:19:47.839 --> 00:19:50.859
that object deeper, turning a partial obstruction

00:19:50.859 --> 00:19:53.640
into a complete one, or causing serious trauma.

00:19:54.180 --> 00:19:57.119
If you see it, carefully remove it. If you don't,

00:19:57.259 --> 00:19:59.099
you just keep going with compressions and ventilation.

00:19:59.910 --> 00:20:02.250
Okay, let's move down the respiratory tract into

00:20:02.250 --> 00:20:04.690
lower airway obstruction, things like bronchiolitis

00:20:04.690 --> 00:20:07.450
and asthma. Now the problem is in those tiny

00:20:07.450 --> 00:20:09.910
distal airways, the bronchioles, deep inside

00:20:09.910 --> 00:20:12.170
the chest, this has to change our whole approach

00:20:12.170 --> 00:20:14.460
to ventilation, right? It changes everything.

00:20:14.839 --> 00:20:16.740
With lower airway obstruction, the problem isn't

00:20:16.740 --> 00:20:19.700
getting air in, it's getting air out. Those small

00:20:19.700 --> 00:20:21.940
downstream airways collapse during expiration

00:20:21.940 --> 00:20:24.299
and that leads to massive air trapping. So we

00:20:24.299 --> 00:20:27.319
have to completely rethink how we assist their

00:20:27.319 --> 00:20:29.599
breathing. This is where we need to talk about

00:20:29.599 --> 00:20:32.460
the huge life -threatening risks of hyperventilation.

00:20:33.079 --> 00:20:34.960
The PLS materials really stress this, but let's

00:20:34.960 --> 00:20:38.299
get into the physiological why. Why is the bag

00:20:38.299 --> 00:20:40.559
valve mask, if you use it wrong, maybe the most

00:20:40.559 --> 00:20:42.880
dangerous tool you have in a severe asthma attack?

00:20:43.460 --> 00:20:45.900
Because you're essentially forcing air into a

00:20:45.900 --> 00:20:48.759
closed off container. If you give too many breaths

00:20:48.759 --> 00:20:50.720
per minute or the breaths are too large, you

00:20:50.720 --> 00:20:52.539
just don't give the child enough time for passive

00:20:52.539 --> 00:20:55.660
expiration. This leads to a phenomenon called

00:20:55.660 --> 00:20:58.420
dynamic hyperinflation, where the lungs just

00:20:58.420 --> 00:21:01.059
get more and more full of trapped air with every

00:21:01.059 --> 00:21:03.059
breath you give. And what's the physiological

00:21:03.059 --> 00:21:05.420
cascade? How does that trapped air lead to a

00:21:05.420 --> 00:21:08.289
cardiac arrest? It causes a few catastrophic

00:21:08.289 --> 00:21:10.450
things to happen all at once. First, gastric

00:21:10.450 --> 00:21:12.710
distension, which increases aspiration risk.

00:21:13.250 --> 00:21:15.630
Second, the high pressures increase the risk

00:21:15.630 --> 00:21:18.170
of a pneumothorax, a collapsed lung. But the

00:21:18.170 --> 00:21:20.589
deadliest result is that the severe air trapping

00:21:20.589 --> 00:21:23.210
creates this massive increase in intra -thoracic

00:21:23.210 --> 00:21:25.509
pressure. And when that pressure inside the chest

00:21:25.509 --> 00:21:28.029
goes up, what does that do to the heart? The

00:21:28.029 --> 00:21:30.650
pressure physically squeezes the large veins,

00:21:31.470 --> 00:21:33.890
the superior and inferior vena cava that are

00:21:33.890 --> 00:21:35.509
returning blood to the right side of the heart.

00:21:35.799 --> 00:21:38.819
This crushes venous return, which means less

00:21:38.819 --> 00:21:41.819
preload, which instantly means less stroke volume,

00:21:42.180 --> 00:21:44.500
and therefore a sudden drop in cardiac output.

00:21:44.980 --> 00:21:47.700
It's basically a form of obstructive shock that

00:21:47.700 --> 00:21:50.240
we, the providers, are causing. The child can

00:21:50.240 --> 00:21:52.220
crash from that sudden drop in cardiac output

00:21:52.220 --> 00:21:54.920
and the worsening hypoxemia. So our attempt to

00:21:54.920 --> 00:21:57.339
save them with ventilation can actually be the

00:21:57.339 --> 00:21:59.680
thing that causes the arrest? It can precipitate

00:21:59.680 --> 00:22:02.740
the arrest, yes. That clinical reasoning is so

00:22:02.740 --> 00:22:05.140
important. The solution is slow, effective ventilation.

00:22:05.640 --> 00:22:08.059
We stick to that slow rate one breath every three

00:22:08.059 --> 00:22:10.380
to five seconds to give them as much time as

00:22:10.380 --> 00:22:12.460
possible for expiration to minimize that air

00:22:12.460 --> 00:22:14.660
trapping. Prioritize exhalation time. That's

00:22:14.660 --> 00:22:16.839
the mantra, absolutely. Don't rush the breaths.

00:22:17.119 --> 00:22:19.000
Okay, so let's apply that to managing an acute

00:22:19.000 --> 00:22:21.970
asthma attack. Assessment comes first. How does

00:22:21.970 --> 00:22:24.450
the PLS severity assessment guide our decisions?

00:22:24.829 --> 00:22:27.130
We use a set of objective criteria which are

00:22:27.130 --> 00:22:29.309
laid out right in the PAL materials. We look

00:22:29.309 --> 00:22:31.170
at their ability to speak. Can they speak in

00:22:31.170 --> 00:22:34.410
full sentences, phrases, or only single words?

00:22:34.930 --> 00:22:36.650
That tells you how much work it's taking them

00:22:36.650 --> 00:22:38.809
to breathe. We look at the respiratory rate.

00:22:38.990 --> 00:22:41.630
Anything over 30 per minute is severe. We look

00:22:41.630 --> 00:22:44.130
for accessory muscle use, but most importantly

00:22:44.130 --> 00:22:46.329
we look at the objective measures. What are the

00:22:46.329 --> 00:22:48.890
warning signs that just scream impending failure?

00:22:49.170 --> 00:22:51.970
An oxygen saturation below 90 % despite being

00:22:51.970 --> 00:22:54.569
on supplemental oxygen. That is a massive red

00:22:54.569 --> 00:22:57.089
flag. We can also look at peak expiratory flow

00:22:57.089 --> 00:22:59.849
or PEF if the child can cooperate. A reading

00:22:59.849 --> 00:23:02.230
below 60 % of their predicted value is a sign

00:23:02.230 --> 00:23:04.630
of a severe life -threatening attack. Well what's

00:23:04.630 --> 00:23:06.869
that critical cardiovascular sign? The one that

00:23:06.869 --> 00:23:09.640
means the child is right at the edge. bradycardia.

00:23:09.799 --> 00:23:11.980
If you see the heart rates start to drop in a

00:23:11.980 --> 00:23:14.420
patient who has been tachypneic and working this

00:23:14.420 --> 00:23:17.740
hard, it means they are exhausted. They are profoundly

00:23:17.740 --> 00:23:19.839
hypoxic and they are about to have a respiratory

00:23:19.839 --> 00:23:22.819
arrest. bradycardia in a pediatric respiratory

00:23:22.819 --> 00:23:25.460
patient should trigger an immediate code activation

00:23:25.460 --> 00:23:28.140
and prep for advanced interventions. Let's run

00:23:28.140 --> 00:23:30.319
through the interventions for a moderate to severe

00:23:30.319 --> 00:23:32.680
acute asthma attack. We're fighting two battles

00:23:32.680 --> 00:23:35.519
at once, inflammation and bronchoconstriction.

00:23:35.680 --> 00:23:38.099
So we give high concentration, humidified oxygen

00:23:38.099 --> 00:23:41.480
to keep their SO2 at 95 % or higher. We use inhaled

00:23:41.480 --> 00:23:44.200
bronchodilators, albuterol, often mixed with

00:23:44.200 --> 00:23:47.119
iprotropium bromide through a nebulizer or an

00:23:47.119 --> 00:23:51.359
MDI with a spacer. And we give oral or IV corticosteroids

00:23:51.359 --> 00:23:53.559
right away to break that inflammatory cycle.

00:23:54.019 --> 00:23:56.640
What about when the asthma is refractory? The

00:23:56.640 --> 00:23:59.240
child is failing despite all that standard therapy.

00:23:59.660 --> 00:24:02.220
We have to escalate. The first one is magnesium

00:24:02.220 --> 00:24:04.460
sulfate. What's its mechanism and what is the

00:24:04.460 --> 00:24:07.039
nurse's priority when giving it? Magnesium sulfate

00:24:07.039 --> 00:24:09.759
is a potent, smooth muscle relaxant. It acts

00:24:09.759 --> 00:24:12.680
as a secondary bronchodilator. It can be a true

00:24:12.680 --> 00:24:15.599
lifesaver in status osmaticus. The dose is given

00:24:15.599 --> 00:24:18.559
as an IV infusion over 15 to 30 minutes. And

00:24:18.559 --> 00:24:20.859
the critical nursing priority is continuous cardiac

00:24:20.859 --> 00:24:23.000
monitoring and frequent blood pressure checks.

00:24:23.359 --> 00:24:25.500
If you give it too fast, it can cause profound

00:24:25.500 --> 00:24:28.000
hypotension and bradycardia. So you have to be

00:24:28.000 --> 00:24:30.480
ready to slow the infusion or give fluids. And

00:24:30.480 --> 00:24:32.519
if they're still failing, even after the magnesium?

00:24:32.660 --> 00:24:35.180
At that point, we might consider subcutaneous.

00:24:35.119 --> 00:24:38.220
or IAM epinephrine or turbutaline, but really

00:24:38.220 --> 00:24:40.759
the next big step is moving to non -invasive

00:24:40.759 --> 00:24:44.119
positive pressure ventilation or NIV like CPAP

00:24:44.119 --> 00:24:47.359
to try and stent those airways open, or we prepare

00:24:47.359 --> 00:24:50.980
for ET intubation. And intubating a fever asthmatic

00:24:50.980 --> 00:24:53.380
has got to be one of the highest risk procedures

00:24:53.380 --> 00:24:55.799
in pediatric critical care. What are the key

00:24:55.799 --> 00:24:58.269
things to think about? You have to anticipate

00:24:58.269 --> 00:25:01.130
extremely high peak inspiratory pressures because

00:25:01.130 --> 00:25:03.650
of that severe airway resistance. The team needs

00:25:03.650 --> 00:25:06.589
to use paralytics carefully, ensure deep sedation,

00:25:06.690 --> 00:25:09.190
and be ready to use very slow ventilation rates

00:25:09.190 --> 00:25:11.450
once that tube is in place to allow for exhalation.

00:25:11.950 --> 00:25:14.529
The risk of barotrauma and causing a pneumothorax

00:25:14.529 --> 00:25:16.910
is incredibly high. It's a rescue procedure you

00:25:16.910 --> 00:25:19.569
perform with extreme caution. OK, let's shift

00:25:19.569 --> 00:25:22.029
to the next category, lung tissue disease or

00:25:22.029 --> 00:25:24.710
parenteral disease. This is when the alveoli

00:25:24.710 --> 00:25:26.809
themselves, the gas exchange units, are sick.

00:25:27.150 --> 00:25:29.170
So things like pneumonia, cardiogenic pulmonary

00:25:29.170 --> 00:25:32.210
edema or ARDS. The common thread here is severe

00:25:32.210 --> 00:25:34.410
hypoxemia that doesn't get better with just oxygen.

00:25:34.750 --> 00:25:36.569
Exactly. And the management for all of these

00:25:36.569 --> 00:25:39.269
fundamentally relies on supporting those failing

00:25:39.269 --> 00:25:42.789
alveoli. And that means using positive end -expertory

00:25:42.789 --> 00:25:46.190
pressure or PEEP. PEEP is what keeps those tiny

00:25:46.190 --> 00:25:48.269
airways and alveoli from collapsing at the end

00:25:48.269 --> 00:25:51.190
of expiration, and it maximizes the surface area

00:25:51.190 --> 00:25:53.910
you have for gas exchange. Let's compare two

00:25:53.910 --> 00:25:56.829
big causes where PEEP is used, but for slightly

00:25:56.829 --> 00:25:59.470
different reasons. In fact, just pneumonia and

00:25:59.470 --> 00:26:01.910
cardiogenic pulmonary edema. Let's start with

00:26:01.910 --> 00:26:04.450
pneumonia. For infectious pneumonia, you need

00:26:04.450 --> 00:26:08.150
urgent diagnostics, an ABG, a chest x -ray, blood

00:26:08.150 --> 00:26:10.910
cultures, and the nurse has to ensure that antibiotics

00:26:10.910 --> 00:26:13.509
are on board within the first hour, especially

00:26:13.509 --> 00:26:15.529
if you're worried about sepsis. You can treat

00:26:15.529 --> 00:26:18.009
any associated wheezing with albuterol, but the

00:26:18.009 --> 00:26:20.329
main supportive strategy is PEEP, delivered either

00:26:20.329 --> 00:26:23.730
via NIV or a ventilator, to overcome that alveolar

00:26:23.730 --> 00:26:26.269
collapse and fix the hypoxemia. You also have

00:26:26.269 --> 00:26:28.789
to aggressively manage any fever to reduce their

00:26:28.789 --> 00:26:31.430
metabolic demand. Now, cardiogenic pulmonary

00:26:31.430 --> 00:26:34.099
edema. This is fluid in the lungs because the

00:26:34.099 --> 00:26:36.259
heart's ventricle isn't working right. How does

00:26:36.259 --> 00:26:39.130
PEEP work here physiologically? This is a really

00:26:39.130 --> 00:26:41.789
elegant piece of clinical reasoning. In cardiogenic

00:26:41.789 --> 00:26:44.410
edema, yes, PEEP helps push fluid out of the

00:26:44.410 --> 00:26:46.869
lungs, but it also has a profound hemodynamic

00:26:46.869 --> 00:26:49.430
effect. By increasing the pressure inside the

00:26:49.430 --> 00:26:52.349
chest, PEEP actually helps reduce venous return.

00:26:52.670 --> 00:26:54.950
It decreases the preload to the failing left

00:26:54.950 --> 00:26:58.390
atrium. It essentially unloads the failing ventricle,

00:26:58.549 --> 00:27:00.609
which lowers the pressure in the capillaries

00:27:00.609 --> 00:27:02.930
and slows down the leakage of fluid into the

00:27:02.930 --> 00:27:05.130
lungs. So in this case, PEEP is acting a bit

00:27:05.130 --> 00:27:07.450
like a diuretic by lowering that hydrostatic

00:27:07.500 --> 00:27:09.859
pressure on top of helping with oxygenation.

00:27:10.680 --> 00:27:12.680
What other non -ventilatory treatments do we

00:27:12.680 --> 00:27:15.299
use? Diuretics are absolutely critical, something

00:27:15.299 --> 00:27:17.559
like furosemite, to quickly pull off circulating

00:27:17.559 --> 00:27:20.019
volume and lower that left atrial pressure. And

00:27:20.019 --> 00:27:21.880
if the ventricular dysfunction is really severe,

00:27:22.059 --> 00:27:24.839
we'd also consider inotropic support or actor

00:27:24.839 --> 00:27:28.160
load -reducing agents. And finally, ARDS, or

00:27:28.160 --> 00:27:30.950
acute respiratory distress syndrome. This is

00:27:30.950 --> 00:27:33.529
non -cardiogenic lung injury from something systemic

00:27:33.529 --> 00:27:36.329
like sepsis or major trauma. This is diffuse

00:27:36.329 --> 00:27:39.150
severe injury to the lungs. How do we define

00:27:39.150 --> 00:27:42.880
ARDS in the PLS world? ARDS is defined by its

00:27:42.880 --> 00:27:46.259
acute onset, severe hypoxemia, that is refractory

00:27:46.259 --> 00:27:49.819
to oxygen, and bilateral infiltrates, or whiteout,

00:27:49.920 --> 00:27:53.059
on a chest x -ray. We quantify that hypoxemia

00:27:53.059 --> 00:27:57.299
using the PO2 -FIO2 ratio. If that ratio is below

00:27:57.299 --> 00:28:00.539
300, it's suggestive of ARDS. The management

00:28:00.539 --> 00:28:02.460
strategy here is very specialized. It's called

00:28:02.460 --> 00:28:04.700
lung protective ventilation, which brings us

00:28:04.700 --> 00:28:07.279
to this complex idea of permissive hypercarbia.

00:28:07.420 --> 00:28:09.920
Why on earth would we intentionally let the carbon

00:28:09.920 --> 00:28:12.529
dioxide level in the blood get high? We accept

00:28:12.529 --> 00:28:15.089
that elevated PACO2, the hypercarbia, to protect

00:28:15.089 --> 00:28:16.990
the injured lungs from what's called ventilator

00:28:16.990 --> 00:28:20.049
-induced lung injury, or VILI. We do this by

00:28:20.049 --> 00:28:21.650
strictly limiting the amount of air we deliver

00:28:21.650 --> 00:28:24.230
with each breath, so low tidal volumes around

00:28:24.230 --> 00:28:26.849
5 to 8 millimals per kilo, and by keeping the

00:28:26.849 --> 00:28:29.299
peak inspiratory pressures low, If we try to

00:28:29.299 --> 00:28:31.819
blow off all that CO2 by pushing more air, we

00:28:31.819 --> 00:28:34.480
overstretch and damage the already injured alveoli,

00:28:34.480 --> 00:28:36.599
making everything worse. So we're trading a mild

00:28:36.599 --> 00:28:39.819
respiratory acidosis for mechanical safety. Exactly.

00:28:40.019 --> 00:28:42.420
We are prioritizing protecting the lung tissue

00:28:42.420 --> 00:28:45.619
over getting perfect lab numbers. We're deliberately

00:28:45.619 --> 00:28:47.599
setting the ventilator to be gentle, knowing

00:28:47.599 --> 00:28:50.819
that the priority is surviving the injury, not

00:28:50.819 --> 00:28:54.220
having a normal blood gas. Correcting the hypoxemia

00:28:54.220 --> 00:28:57.259
is still the number one priority, but we permit

00:28:57.259 --> 00:29:00.869
the CO2. The final big category of respiratory

00:29:00.869 --> 00:29:04.430
failure is disordered control of breathing. This

00:29:04.430 --> 00:29:06.569
is when the central or peripheral nervous system

00:29:06.569 --> 00:29:09.500
fails to actually run the show. Things like increased

00:29:09.500 --> 00:29:12.720
intracranial pressure or ICP and poisoning or

00:29:12.720 --> 00:29:15.599
drug overdose. Right. Starting with increased

00:29:15.599 --> 00:29:18.039
intracranial pressure. This can be from trauma,

00:29:18.259 --> 00:29:20.920
a hemorrhage, a severe infection. And the respiratory

00:29:20.920 --> 00:29:23.339
consequence is huge because it directly affects

00:29:23.339 --> 00:29:25.460
the central respiratory drive in the brain stem

00:29:25.460 --> 00:29:27.740
leading to weird breathing patterns or just stopping

00:29:27.740 --> 00:29:30.180
breathing altogether apnea. And the classic sign

00:29:30.180 --> 00:29:32.759
is Cushing's triad irregular breathing, hypertension,

00:29:33.140 --> 00:29:35.670
and bradycardia. but the Bilalosaurus gives a

00:29:35.670 --> 00:29:38.490
really important warning for kids. It does. While

00:29:38.490 --> 00:29:40.950
we all learn about bradycardia, children with

00:29:40.950 --> 00:29:43.589
a rapidly rising ICP might initially present

00:29:43.589 --> 00:29:46.109
with hypertension and tachycardia, or even a

00:29:46.109 --> 00:29:48.150
normal heart rate. They don't always show that

00:29:48.150 --> 00:29:51.230
profound bradycardia you see in adults. We can't

00:29:51.230 --> 00:29:53.009
wait for the heart rate to drop to intervene.

00:29:53.329 --> 00:29:55.769
If you see hypertension and a decreasing level

00:29:55.769 --> 00:29:58.750
of consciousness, you have to act. And the interventions

00:29:58.750 --> 00:30:02.410
are about optimization. Head midline, C -spine

00:30:02.410 --> 00:30:05.059
stabilization if needed, maintain an open airway.

00:30:05.539 --> 00:30:07.740
But the caution around hyperventilation here

00:30:07.740 --> 00:30:10.279
is maybe the most heavily emphasized point in

00:30:10.279 --> 00:30:12.900
the entire Pallas manual. It's the ultimate tightrope

00:30:12.900 --> 00:30:14.880
walk. You have to maintain the airway and ensure

00:30:14.880 --> 00:30:17.940
adequate ventilation, but you must, must avoid

00:30:17.940 --> 00:30:20.480
prophylactic severe hyperventilation. You cannot

00:30:20.480 --> 00:30:22.839
just start bagging them fast to drive that CO2

00:30:22.839 --> 00:30:25.640
down. Why is severe hyperventilation so dangerous

00:30:25.640 --> 00:30:28.660
when ICP is high? Because our main goal in ICP

00:30:28.660 --> 00:30:31.720
management is to maintain adequate cerebral perfusion

00:30:31.720 --> 00:30:35.220
pressure, or CPP, and CPP is your mean arterial

00:30:35.220 --> 00:30:38.380
pressure minus your ICP. Hyperventilation blows

00:30:38.380 --> 00:30:42.119
off CO2, and that causes rapid cerebral vasoconstriction.

00:30:42.559 --> 00:30:45.240
The blood vessels in the brain clamp down. While

00:30:45.240 --> 00:30:47.440
this does shrink the volume in the skull and

00:30:47.440 --> 00:30:51.019
acutely lowers the ICP, it also drastically reduces

00:30:51.019 --> 00:30:53.480
blood flow to the brain. So you're starving the

00:30:53.480 --> 00:30:56.099
already injured brain of oxygen and blood. You

00:30:56.099 --> 00:30:57.799
lower the pressure, but you reduce the supply.

00:30:58.160 --> 00:31:00.559
Precisely. You might get a great ICP number on

00:31:00.559 --> 00:31:02.640
the monitor, but you're actually making the underlying

00:31:02.640 --> 00:31:05.420
brain injury worse. That's why Pallas is so strict

00:31:05.420 --> 00:31:07.519
about avoiding severe hyperventilation after

00:31:07.519 --> 00:31:10.539
that initial 48 -hour period. So when is it okay

00:31:10.539 --> 00:31:13.720
to use mild hyperventilation? Only as a temporary

00:31:13.720 --> 00:31:16.579
last -ditch rescue therapy for acute deterioration.

00:31:16.799 --> 00:31:19.099
You see signs of impending brain herniation like

00:31:19.099 --> 00:31:21.880
a blown pupil or sudden bradycardia. It's a break.

00:31:21.769 --> 00:31:24.430
It buys you minutes while you get osmotic agents

00:31:24.430 --> 00:31:27.009
like mannitol or hypertonic saline ready. It

00:31:27.009 --> 00:31:29.450
is never a long -term strategy. Okay, let's move

00:31:29.450 --> 00:31:32.910
to poisoning or drug overdose. This usually causes

00:31:32.910 --> 00:31:36.230
respiratory failure by just depressing the central

00:31:36.230 --> 00:31:38.190
respiratory drive. Yeah, and supportive care

00:31:38.190 --> 00:31:40.690
is everything here. Airway and ventilation support

00:31:40.690 --> 00:31:42.910
are paramount because the patient can become

00:31:42.910 --> 00:31:45.789
apneic very, very quickly. You need to contact

00:31:45.789 --> 00:31:48.190
poison control immediately and you have to be

00:31:48.190 --> 00:31:51.029
ready for aggressive suctioning. Loss of consciousness

00:31:50.990 --> 00:31:54.210
means a huge risk of vomiting and aspiration.

00:31:54.450 --> 00:31:56.569
And the specific drug we often see used in the

00:31:56.569 --> 00:31:59.799
ER. If you suspect an opioid overdose and the

00:31:59.799 --> 00:32:01.599
patient is in respiratory arrest but still has

00:32:01.599 --> 00:32:05.460
a pulse, you give naloxone. The IM or intranasal

00:32:05.460 --> 00:32:07.759
routes are often faster than waiting to get an

00:32:07.759 --> 00:32:10.559
IV. But remember, if the patient is pulseless,

00:32:10.680 --> 00:32:12.700
you don't mess with naloxone, you go straight

00:32:12.700 --> 00:32:15.059
to CPR. And of course, you're sending off a whole

00:32:15.059 --> 00:32:17.960
panel of diagnostics, ABG, ECG, drug screens

00:32:17.960 --> 00:32:20.400
to guide the rest of the care. We've got a few

00:32:20.400 --> 00:32:23.140
crucial procedural airway perils that an ER nurse

00:32:23.140 --> 00:32:25.539
prepping for this exam has to have down cold,

00:32:25.680 --> 00:32:27.599
especially around and advanced airway management.

00:32:27.839 --> 00:32:30.059
First one is about cuffed ET tubes, which are

00:32:30.059 --> 00:32:32.700
now standard in pediatrics. The nursing team

00:32:32.700 --> 00:32:34.960
has to be meticulous about managing that cuff

00:32:34.960 --> 00:32:37.220
pressure. Why is that? What's the target range?

00:32:37.400 --> 00:32:39.759
You want to keep that cuff pressure between 20

00:32:39.759 --> 00:32:42.660
to 25 centimeters of water. If the pressure is

00:32:42.660 --> 00:32:45.059
too low, you get a big air leak around the tube,

00:32:45.460 --> 00:32:48.240
which means ineffective ventilation. That's especially

00:32:48.240 --> 00:32:51.180
bad in ARDS or asthma, where you need high pressures.

00:32:51.720 --> 00:32:53.839
But if the pressure is too high, you risk causing

00:32:53.839 --> 00:32:56.970
tracheal ischemia and long damage to the airway.

00:32:57.509 --> 00:32:59.470
It needs to be checked regularly with a cuff

00:32:59.470 --> 00:33:02.009
manometer. And another big procedural pearl is

00:33:02.009 --> 00:33:05.430
about using neuromuscular blocking agents paralytics

00:33:05.430 --> 00:33:08.470
for intubation, specifically succinylcholine.

00:33:08.599 --> 00:33:11.220
You have to be so cautious with succinylcholine

00:33:11.220 --> 00:33:13.839
in kids, especially if you suspect an underlying

00:33:13.839 --> 00:33:16.619
neuromuscular disease or in patients with burns,

00:33:16.880 --> 00:33:20.420
crush injuries, or prolonged immobility. Succinylcholine

00:33:20.420 --> 00:33:23.500
can cause a massive dangerous efflux of potassium

00:33:23.500 --> 00:33:26.500
from the cells. It can lead to severe hyperkalemia

00:33:26.500 --> 00:33:29.660
and fatal arrhythmias, or it can trigger malignant

00:33:29.660 --> 00:33:32.400
hyperthermia. And what's a key drug interaction

00:33:32.400 --> 00:33:34.740
pearl that relates to respiratory muscle weakness?

00:33:35.000 --> 00:33:37.220
The clinical pearl here is to remember that some

00:33:37.220 --> 00:33:41.309
of our most antibiotics, specifically amino glycosides

00:33:41.309 --> 00:33:44.490
like gentamicin and also vancomycin, they have

00:33:44.490 --> 00:33:47.029
some intrinsic neuromuscular blocking activity.

00:33:47.250 --> 00:33:49.630
So if you have a child with a known neuromuscular

00:33:49.630 --> 00:33:52.789
issue or even just a very septic kid who is already

00:33:52.789 --> 00:33:55.250
weak and struggling to breathe, giving these

00:33:55.250 --> 00:33:57.829
antibiotics can actually worsen their respiratory

00:33:57.829 --> 00:34:00.150
muscle weakness and make it harder to ventilate

00:34:00.150 --> 00:34:03.650
them. Lastly, let's just confirm the absolute

00:34:03.650 --> 00:34:06.750
necessity. of end -tidal CO2 monitoring across

00:34:06.750 --> 00:34:08.789
all of these different respiratory problems.

00:34:09.110 --> 00:34:11.750
ET Co -euros monitoring is completely essential

00:34:11.750 --> 00:34:15.030
and non -negotiable. It gives you instant continuous

00:34:15.030 --> 00:34:18.269
feedback on three critical things. First, ventilation

00:34:18.269 --> 00:34:20.289
effectiveness. It tells you if you're actually

00:34:20.289 --> 00:34:22.969
clearing CO2. This is so important when you're

00:34:22.969 --> 00:34:25.929
trying for permissive hypercarbia in ARDS or

00:34:25.929 --> 00:34:28.590
using those slow rates in asthma. Confirmation

00:34:28.590 --> 00:34:31.550
of tube placement. After you intubate, ET Co

00:34:31.550 --> 00:34:33.489
-euros is the gold standard for confirming that

00:34:33.489 --> 00:34:35.820
the tube is in the trachea and not in the esophagus.

00:34:36.000 --> 00:34:38.019
And third, it's an indicator of circulation,

00:34:38.079 --> 00:34:40.539
which is so important during an arrest. Yes.

00:34:41.300 --> 00:34:44.119
During a respiratory arrest or full -blown CPR,

00:34:44.559 --> 00:34:47.239
the ETKO level reflects pulmonary blood flow,

00:34:47.380 --> 00:34:49.519
which is directly tied to your cardiac output.

00:34:50.000 --> 00:34:53.760
A sudden drop in ETKO during CPR means your compressions

00:34:53.760 --> 00:34:56.800
are bad or circulation is failing. And on the

00:34:56.800 --> 00:35:00.320
flip side, a sudden sustained jump in ETKO is

00:35:00.320 --> 00:35:02.619
the earliest sign you'll get a return of spontaneous

00:35:02.619 --> 00:35:05.530
circulation. or ROSC. It connects the breath

00:35:05.530 --> 00:35:08.429
to the heart. So, to synthesize this whole respiratory

00:35:08.429 --> 00:35:11.269
management approach, PALIS success is overwhelmingly

00:35:11.269 --> 00:35:14.409
measured in prevention. We win when we recognize

00:35:14.409 --> 00:35:16.889
and manage that respiratory distress and impending

00:35:16.889 --> 00:35:19.489
failure long before the patient becomes pulseless.

00:35:19.750 --> 00:35:22.530
That shift from compensated distress to uncompensated

00:35:22.530 --> 00:35:25.429
failure is so fast, and it requires mastery of

00:35:25.429 --> 00:35:27.309
these targeted drugs and ventilation strategies.

00:35:27.409 --> 00:35:29.050
Okay, let's do a quick final review of the key

00:35:29.050 --> 00:35:30.989
pharmacological agents just to reinforce that

00:35:30.989 --> 00:35:33.130
structured PALIS thinking. will categorize them

00:35:33.130 --> 00:35:35.570
by the condition they treat. Perfect. For upper

00:35:35.570 --> 00:35:37.889
airway obstruction like croup, it's that one

00:35:37.889 --> 00:35:40.630
-two punch of rapid -acting nebulized epinephrine

00:35:40.630 --> 00:35:43.769
and the long -acting corticosteroids like dexamethasone.

00:35:44.210 --> 00:35:47.150
For anaphylaxis, immediate IM epinephrine, that's

00:35:47.150 --> 00:35:49.170
number one, followed by your bronchodilators,

00:35:49.389 --> 00:35:52.210
corticosteroids, and that dual anahistamine blockade.

00:35:52.400 --> 00:35:54.940
For lower airway obstruction, specifically that

00:35:54.940 --> 00:35:57.880
really bad refractory asthma, the foundation

00:35:57.880 --> 00:36:00.260
is still bronchodilators and corticosteroids,

00:36:00.280 --> 00:36:03.239
but the big rescue drug is that magnesium sulfate

00:36:03.239 --> 00:36:05.679
infuser. And for lung tissue disease, whether

00:36:05.679 --> 00:36:09.739
it's pneumonia, cardiogenic edema, or ARDS, the

00:36:09.739 --> 00:36:12.280
key mechanical support is PEEP. Then you add

00:36:12.280 --> 00:36:14.380
diuretics for the cardiogenic causes and, of

00:36:14.380 --> 00:36:17.480
course, antibiotics for infection. And for disordered

00:36:17.480 --> 00:36:19.860
control of breathing, the most critical interventions

00:36:19.860 --> 00:36:22.650
are defensive. You're avoiding hypoxia. avoiding

00:36:22.650 --> 00:36:25.389
severe hypercarbia, and avoiding hyperthermia

00:36:25.389 --> 00:36:27.630
in your ICP patients. And you're having the right

00:36:27.630 --> 00:36:29.869
antidote, like naloxone for an overdose, ready

00:36:29.869 --> 00:36:32.889
to go. And translating all this palace knowledge

00:36:32.889 --> 00:36:34.869
into the high -pressure world of the ER, the

00:36:34.869 --> 00:36:37.550
ICU, that really requires internalizing a few

00:36:37.550 --> 00:36:40.349
essential clinical pearls. Okay, first, let's

00:36:40.349 --> 00:36:43.510
hammer home the importance of constant, meticulous

00:36:43.510 --> 00:36:45.909
reassessment, especially after you've given certain

00:36:45.909 --> 00:36:49.400
drugs. never ever assume stability, especially

00:36:49.400 --> 00:36:51.840
with croup and asthma. We talked about that post

00:36:51.840 --> 00:36:53.940
-epinephrine observation for croup. They can

00:36:53.940 --> 00:36:56.739
rebound hard. And similarly, in severe asthma,

00:36:57.159 --> 00:36:59.679
a kid who goes from being anxious and fighting

00:36:59.679 --> 00:37:02.760
to being quiet and lethargic, that child is often

00:37:02.760 --> 00:37:04.440
entering the failure phase. They're just too

00:37:04.440 --> 00:37:06.679
tired to compensate anymore. The quiet child

00:37:06.679 --> 00:37:09.500
is the most frightening child. Second, the critical

00:37:09.500 --> 00:37:12.840
nursing priority of getting early vascular access

00:37:12.840 --> 00:37:15.639
in those moderate to severe cases. If you see

00:37:15.639 --> 00:37:18.440
a kid with moderate to severe anaphylaxis or

00:37:18.440 --> 00:37:21.159
status asthmaticus, your first thought after

00:37:21.159 --> 00:37:24.500
oxygen should be getting that IV or IO access

00:37:24.500 --> 00:37:26.920
immediately. You're going to need it for high

00:37:26.920 --> 00:37:29.619
volume fluid resuscitation, for continuous infusions

00:37:29.619 --> 00:37:33.039
of steroids, magnesium, maybe even IV epinephrine.

00:37:33.360 --> 00:37:35.860
If you wait until they're crashing, that peripheral

00:37:35.860 --> 00:37:38.099
vasoconstriction will make getting access nearly

00:37:38.099 --> 00:37:39.960
impossible and you'll have a critical delay.

00:37:40.340 --> 00:37:42.039
And finally, the need for concurrent management.

00:37:42.320 --> 00:37:44.340
You're treating the cause while aggressively

00:37:44.340 --> 00:38:04.320
providing support care at the same time. So mastering

00:38:04.320 --> 00:38:06.800
PALS respiratory management really means training

00:38:06.800 --> 00:38:09.420
your eye to see those subtle cues, the change

00:38:09.420 --> 00:38:11.559
in how they're speaking, the depth of the retractions,

00:38:11.880 --> 00:38:14.659
that slow shift toward bradycardia long before

00:38:14.659 --> 00:38:17.039
the patient ever needs chest compressions. That

00:38:17.039 --> 00:38:19.599
systemic physiologically based knowledge is your

00:38:19.599 --> 00:38:22.199
ultimate power in that critical moment. So as

00:38:22.199 --> 00:38:24.320
you take this deep dive and integrate it into

00:38:24.320 --> 00:38:27.420
your clinical prep, here's one final provocative

00:38:27.420 --> 00:38:30.000
thought for you to think about. This one is specifically

00:38:30.000 --> 00:38:32.460
about that high stakes procedure we discussed.

00:38:33.319 --> 00:38:36.360
Given the profound risks of hyperkalemia from

00:38:36.360 --> 00:38:39.340
using succinylcholine in certain pediatric patients,

00:38:40.039 --> 00:38:42.139
especially those with an unknown or underlying

00:38:42.139 --> 00:38:45.079
neuromuscular disease, and the absolute need

00:38:45.079 --> 00:38:48.519
for rapid paralysis for intubation, how does

00:38:48.519 --> 00:38:50.860
that risk assessment change your immediate choice

00:38:50.860 --> 00:38:54.920
of paralytic agent, say, rocoronium versus succinylcholine,

00:38:55.300 --> 00:38:58.300
during a non -traumatic severe status asthmaticus

00:38:58.300 --> 00:39:00.980
presentation in the chaos of the emergency department?

00:39:01.130 --> 00:39:03.030
Think about that clinical judgment call, the

00:39:03.030 --> 00:39:05.250
trade -off between speed and safety and how you

00:39:05.250 --> 00:39:07.349
prepare your drugs ahead of time. We'll catch

00:39:07.349 --> 00:39:09.170
you next time for the next Deep Dive.
