This episode breaks down three of the most dangerous respiratory emergencies nurses face: ARDS, cardiogenic pulmonary edema, and tension pneumothorax. Using clear bedside cues and rapid-action frameworks, you learn how to spot these crises early, understand the physiology driving them, and take the immediate steps that prevent collapse. From pink frothy sputum to tracheal deviation to refractory hypoxia, this conversation turns complex pathology into a simple action plan rooted in airway-first priorities, lung-protective strategies, and critical “never delay” rules. By the end, you’ll know exactly how to differentiate a mechanical problem, a cardiac overload problem, and an inflammatory lung problem—and what to do the moment each one appears.
Welcome to Think Like a Nurse.
We're so glad you're here.
This is the show where we really try to take the most complex uh clinical topics and just distill them down into knowledge that actually sticks.
Right. The goal is to help you prioritize and act when you know every single second counts.
And all of this this whole approach, it comes from our creator, Brooke Wallace,
a 20-year ICU nurse, organ transplant coordinator, clinical instructor,
and a published author. She's really the mind behind this mission.
And today we are getting laser focused on the immediate life-saving steps for some really critical respiratory emergencies.
We're talking about ARDS, cardiogenic pulmonary edema, and tension pneumathorax.
And our mission really is to turn all that complex criteria into uh a clear action plan you can use. So for more on this and other topics, definitely visit think likeanurse.org.
But before we dive into any specific diagnosis, we have to set the stage. There's one universal priority
always
airway and breathing. It is always without question priority one. If the patient can't get oxygen in, literally nothing else we do matters.
That's the foundation for everything.
Mhm.
So, let's talk about the red flags. What are those, you know, visual cues that tell us a patient is actively losing the fight to breathe?
You're really looking for a whole picture of distress. Um, it usually starts with an altered mental status. The brain just isn't getting enough oxygen,
confusion, agitation.
Exactly. Then you'll see accessory muscle use. They're straining their neck, their abdominal muscles. anything to lift that chest wall.
And of course, the dreaded tripod position.
Yes, the tripod position is such a bad sign because it means they're trying to use every single muscle they have just to increase their chest diameter.
It's pure air hunger.
It is. It's metabolically expensive and it tells you they are desperate. You might also see, you know, cyanosis, nasal flaring, retractions.
And what about the numbers? When do the alarms on the monitor really start to mean something urgent?
Well, if O2 saturation drops below 90%, event, you're officially in crisis territory. Clinically though, we look at the PO2,
the oxygen in their arterial blood,
right? If that number drops below 60 mm of mercury, that patient has entered respiratory failure. Full stop.
And then there's that idea of refractory hypoxmia. That's the really scary part, isn't it? When you turn up the oxygen and nothing happens.
Refractory hypoxmia is the clue that the problem isn't a lack of oxygen supply. It's a physi ical barrier
like a dam.
A dam is a great way to put it. It's usually a massive shunt preventing gas exchange. So when you hit 100% FiO2 on the ventilator and the sat doesn't budge.
Yeah.
You know you need a mechanical solution, not just more O2.
Okay, let's unpack two of those immediate life threats, the ones that need intervention in like seconds. First up, the mechanical killer tension pumathorax.
This is such a deadly trap because the physiology is so brutally simple.
Air gets into the plural space
through a hole in the lung or the chest wall,
right? But it acts like a one-way valve. Air gets in, but it absolutely cannot get out. And this just dramatically increases pressure inside the chest.
And that pressure, it doesn't just collapse the lung on that one side.
No. And that's the difference between a simple pneumo and a tension pumo. The pressure gets so high, it physically pushes the entire central part of the chest, the mediainum, the heart, the great vessel, all of it pushes it away from the affected side. And that shift kinks the superior and inferior venneava. shut,
which means blood can't get back to the heart.
Exactly. The heart can't fill. So, you get this instantaneous loss of Venus return, which leads to profound hypotension. It's obstructive shock.
So, for a nurse at the bedside, what's the fastest way to spot this? How do you know it's tension?
You have your classic signs, right? Sudden severe dispnnea, hypotension, and when you listen,
nothing.
Absent breath sounds. The chest might even sound hyper resonant like a drum. But the two late crucial signs that scream act now are a deviated trachea
pushed away from the bad side
away from the bad side and distended neck veins JVD those are the signs of total collapse from the pressure
okay so the patient is crashing this is no time for a long diagnostic workup what is the single immediate life-saving thing you do
needle decompression period and the critical rule and this is a huge decision point is you do not delay for imaging
no waiting for a chest x-ray
you do not wait if those tension signs are present you act. Time is tissue. Time is life.
It's a high states procedure to do emergently. How is it done safely?
Well, you're aiming for the second intercostal space, mid-clavicular line or uh sometimes the fourth or fifth intercostal space at the anterior axillary line. That was often preferred now.
A bit safer.
A little safer. Yeah. You use a large bore needle. You insert it and you listen for that whoosh of air. That sound tells you you've relieved the pressure and it buys you precious time. time until a chest tube can be placed.
All right, let's pivot. We're going from a mechanical pressure problem to a uh a circulatory disaster, cardiogenic pulmonary edema, CPE.
This is a fluid backup, plain and simple. Okay,
the root cause is massive left ventricular failure. The left side of the heart just can't pump blood out effectively.
And that's often triggered by what? An MI.
An acute MI is a huge one. Or just completely uncontrolled hypertension that's been going on for years.
So all that pressure backs up all the way from the heart into the lungs. How do we, you know, quantify that?
We look at the pulmonary capillary wedge pressure, the PCWP. Normally, it's pretty low, but in CPE, it just surges. It goes above 18 mm of mercury,
and that pressure literally forces fluid out of the blood vessels and into the lungs,
into the alvoli themselves. The patient is, for all intents and purposes, flash drowning in their own fluid.
Wow. And the assessment findings here are just so classic. What do we see? see in here.
What you see is the big one, the pithognemonic sign. Pink frothy sputum.
Can't miss it.
You can't. That's fluid mixed with blood and air. What you hear are bilateral crackles. They usually start at the bases and you can literally hear them climbing up towards the apes as it gets worse.
And sometimes a heart sound.
You might hear an S3 gallop, which is a key sign of severe heart failure.
Okay, so we've identified it. We need to act fast. There's a great pneummonic for this, right?
Yes. Lnop. It's Perfect for biting your immediate treatment.
Let's walk through it. L
L is for Lasix or fioamide. 40 to 80 milligrams IV stats. You have to get that fluid off.
M is for morphine. 2 to 4 milligrams IV slow push. Morphine is fantastic here. It decreases preload and afterload. So it eases the heart's workload and it also calms the patient's panic.
Okay. N is for nitro.
Nitroglycerin. Either sublingual or uh more likely an IV infusion. It's a powerful vasod dilator. So it drops the preload dramatically. Less blood returns to the failing heart which stops the backup.
No.
O is for oxygen. High flow or even better non-invasive ventilation. NIV
like BiPAP or CPAP.
Exactly. That positive pressure helps physically push the fluid out of the alvola and keep them open.
And finally P.
P is for position. Get them sitting up. High Fowler's position. Gravity is your friend here. It reduces Venus return and makes it easier for them to expand their chest.
And there's one critical never do this rule here. Oh, absolutely. Fluids are completely totally 100% contraindicated in CPE. You are trying to dry this patient out. An IV fluid bullis could be fatal.
Okay, let's move into something more complex. ARDS, acute respiratory distress syndrome. This patient is usually already critically ill, probably intubated. How do we recognize it?
We use what's called the Berlin criteria. First, it has to be acute. The onset is within one week of some known insult like SEP is severe pneumonia, trauma,
something that kicked it all off,
right? Second, the chest X-ray has to show bilateral fluffy infiltrates.
And the third piece is the most specific. It's about their oxygenation.
That's the PF ratio. You take their P2 and divide it by their FiO2. And that ratio has to be 300 or less.
And there's one more piece to that.
Yes. And the patient has to be on at least 5 cm of water of PEEP.
Okay, let's break those terms down really fast. P2 is the oxygen in the blood. What is FiO2 and PEEP?
FiO2 is just the fraction of inspired oxygen. Room air is 21%. On a ventilator, it could be anywhere up to 100%. PEEP is positive and expiratory pressure.
So, pressure left in the lungs after you breathe out.
Exactly. It's there to keep those sick, damaged alvoli from just collapsing completely.
And that PF ratio, it tells you how bad it is, right? What are the numbers we need to know?
They're pretty easy to remember. Mild ARDS is a PF ratio of 2011 to 300. Moderate is 101. 200
and severe
severe is anything 100 or less. And if you see that ratio dropping into the double digits, you know you're dealing with a profound life-threatening shunt.
So once we confirm ARDS, the game changes. Now it's about protecting the lungs from us from the ventilator.
The mantra is lung protective ventilation. We have to minimize barat trauma and volt trauma damage from too much pressure and too much volume.
So what does that look like in practice?
It means we use a really low tidal volume. That's the amount of air with each breath. We're talking 4 to 8 milliliters per kilogram of their ideal body weight,
not their actual weight.
No, ideal body weight. That's critical. And the other number we watch like a hawk is the plateau pressure.
And that has to stay below
30. We have to keep the plateau pressure at 30 cm of water or less. Going above that just dramatically increases the risk of injuring the lungs further.
But if we're using such low volumes, that must mean their CO2 is going to climb.
It will. And we let it. It's called permissive hypercapnea.
So we're letting them get a little acidotic on purpose.
We are because we're prioritizing protecting the lungs physical structure over having a perfect acidbased balance. Barat trauma kills a little bit of respiratory acidosis we can manage.
That makes sense. Now, another big game changer for moderate to severe ARDS is proning. Literally flipping the patient onto their stomach. Why on earth does that work so well?
Proning is amazing. It works because it dramatically improves what we call VQ matching ventilation and profusion.
Okay. When a patient is lying on their back, the weight of their heart and everything in the middle of their chest just squashes the back parts of their lungs.
So no air gets in there,
right? But by proning them for at least 16 hours a day, you redistribute everything. You recruit those posterior areas that were collapsed and suddenly you have way more lung to work with.
And we saw this in that case study, the 38-year-old.
Yeah, that was a powerful example. He had severe ARDS. His PF ratio was a terrifying 54. We couldn't oxygenate him. But after just one 16-hour cycle of proning,
the numbers changed
dramatically. His P2 jumped from 54 to 112. We were able to wean his FiO2 way down. The response can be just life-saving.
Yeah, this is a really critical distinction, especially now. Not all ARDS is the same. The treatment can be really different, especially with viral causes.
This is so vital to know. Classic ARDS, you know, from bacteria aspiration, it usually presents with a very stiff lungs. low compliance right away
and it responds well to PEEP and pronun
extremely well but viral pathogens they play by different rules.
Let's start with CO 19 ARDS.
So CO 19 ARDS especially in its later stages it starts to look and act a lot like classic ARDS but the medication rules are specific.
Okay, what are they?
You need to give dexamethasone 6 milligrams a day for 10 days and therapeutic anti-coagulation is key plus remesae if you catch it early.
Now compared Compare that to severe influenza ARDS.
Influenza pneumonia often acts like classic ARDS right from the get-go. Stiff lungs, good response to proning. But the cornerstone antiviral is early assult tummy 75 to 150 milligrams twice a day.
And this is where it gets really really important. The divergence on steroids.
This is a non-negotiable point of practice. For severe influenza ARDS, systemic corticoststeroids are actually harmful.
Harmful.
Yes. They have to be strictly avoided. They impair the body's ability to clear the virus. So knowing which virus you're treating is everything because the standard of care completely flips. So to really lock all this in, let's do a rapid fire review connecting the symptom to the immediate action.
I love this. Okay, scenario one. You walk in, you see pink frothy sputum and you hear crackles climbing up the lungs. What is it? What do you do?
Cardiogenic pulmonary adure. Action. Give fosomide first and get that LMOP protocol started.
Next Sudden shortness of breath. Blood pressure is in the tank. And you see the trachea is shifted to one side.
Tension pneumoththorax action. Needle decompress immediately. Do not wait for an X-ray.
Okay. Your patient's on a vent. Their PF ratio is say 140 and their plateau pressure is 32.
That's moderate to severe ARDS with lung injury. Action. Immediately lower the title volume. Increase the PEEP and start making calls to get the team ready to prone.
Patients intubated positive for CO. 19. What medicine do they need?
Dexamethasone 6 milligs a day.
And what if that intubated patient is positive for severe influenza?
Give us and make absolutely sure there are no systemic steroids on the order set.
Perfect. Let's finish by reinforcing those two absolute never rules.
Cursed.
Never give fluids and cardiogenic pulmonary edema. You will make everything worse. And never delay needle decompression for an X-ray when you see the signs of attention pumthorax. That delay can be fatal.
That's it. That's how you think like a nurse in these crises.
This has been such a focused, practical look at navigating these emergencies. From LMO P to PF ratios, you now have the tools to act with confidence when the pressure is on.
That ability to quickly tell the difference between a mechanical problem, a cardiac problem, and an inflammatory lung problem. That is your most powerful tool.
Thank you so much for joining us for this conversation. We really hope you'll check in for more conversations each week.
And for more resources and fantastic nursing guidance from Brooke Wallace, please be sure to visit Think like a nurse.org.