In this high-impact episode of Think Like a Nurse, we break down the critical care triad: shock, SIRS, and sepsis — the emergencies every nurse must recognize early and act on fast. You’ll learn the three universal stages of shock, the big three shock types (empty tank, broken pump, leaky pipes), and exactly how to differentiate them within the first minutes at the bedside. We also walk through SIRS vs. Sepsis-3, the QS-SOFA bedside screen, and the defining criteria for septic shock. We share essential bedside pearls, including early clues nurses often miss, how to respond in a priority-driven sequence, and how to avoid the most dangerous treatment mistakes. If you want real clinical confidence in one of the highest-stakes areas of nursing, this is your guide.
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Core definition: inadequate tissue perfusion, leading to anaerobic metabolism, rising acid, cellular hypoxia, and eventual organ failure.
All shock types follow the same three-stage progression:
Stage 1: Compensated – tachycardia, tachypnea, cool pale skin, anxiety, decreased urine output; BP may still look normal.
Stage 2: Decompensated – severe tachycardia, severe tachypnea, drop in BP, narrowed pulse pressure, mental status changes, oliguria/anuria, metabolic acidosis.
Stage 3: Irreversible – refractory hypotension, multiorgan failure, disseminated intravascular coagulation, poor response to pressors or fluids.
Causes: bleeding, trauma, burns, dehydration, massive fluid shifts (DKA, vomiting, diarrhea).
Key assessment:
Pale, cool, clammy
Flat neck veins
Thready pulses
Low urine output
Lab clues:
Low hemoglobin/hematocrit (bleeding)
High hemoglobin/hematocrit (hemoconcentration from dehydration)
BUN-to-creatinine ratio over 20:1 → prerenal dehydration
Priority actions:
Two large-bore IVs, rapid fluid resuscitation
Blood products if bleeding
Keep patient warm; control source of fluid loss
Causes: massive heart attack, myocarditis, pulmonary embolism, cardiac tamponade.
Key assessment:
Cold + wet
Jugular vein distention
Crackles, pulmonary edema, pink frothy sputum
New S3 heart sound
Advanced hemodynamics:
High wedge pressure
Low cardiac index
Priority actions:
Avoid aggressive fluids
Reduce afterload
Start inotropes (dobutamine, milrinone)
Pressors if needed (norepinephrine is first-line)
Immediate cardiology intervention (cath lab, mechanical support)
Includes:
Septic
Anaphylactic
Neurogenic
Adrenal crisis
Early septic shock often looks warm:
Warm, flushed skin
Bounding pulses
Wide pulse pressure
High cardiac output, low vascular resistance
Neurogenic shock exception:
Warm, dry
Bradycardic
Caused by spinal cord injury above T6
SIRS (old criteria): too sensitive, not specific; triggered by many non-infectious conditions.
Sepsis-3 definition:
Life-threatening organ dysfunction caused by a dysregulated response to infection.
ICU tool measuring organ failure across six systems.
Suspected infection + 2 of 3:
Respiratory rate 22 or higher
Altered mentation
Systolic pressure 100 or less
→ Activate sepsis pathway immediately.
Sepsis PLUS:
Vasopressors needed to maintain a MAP of 65
Lactate level over 2 despite adequate fluid resuscitation
→ Mortality increases dramatically.
Airway, breathing, circulation first
High-flow oxygen
Two large-bore IVs immediately
Goal-directed fluids
Urine output target: 0.5–1 per hour → early marker of organ perfusion
Serial lactates
For sepsis:
Blood cultures before antibiotics if no delay
Broad-spectrum antibiotics within 60 minutes
Pressors through central line when possible
Maintain warmth; initiate stress-ulcer and DVT prevention
Hypovolemic: Cold + flat veins
Cardiogenic: Cold + wet lungs
Distributive (early septic): Hot + flushed
Neurogenic: Warm + bradycardic
Master these patterns → fast, accurate recognition.
Welcome to Think Like a Nurse. This conversation is part of the work created by Brooke Wallace, a 20-year ICU nurse, organ transplant coordinator, clinical instructor, and published author. We take really complex nursing topics and well, we try to make them a lot easier to understand. And today we are tackling a huge one, the critical care triad, shock, SERS, which we renounce sir, and sepsis. These are the emergencies that demand immediate and critical thinking from absolutely everyone on the team.
So, our mission today is to give you the fundamental knowledge and maybe more importantly those bedside pearls you need to not just recognize these conditions, but to manage them fast. And of course, if you want to dive deeper or review anything we talk about, you can always visit think like a nurse.org for more. Okay, so let's get into it. This is a massive topic. Where do we even start? Let's start with the absolute foundation. What is shock really at its core? At its core, shock is just inadequate tissue profusion. It sounds simple, but it's really a global crisis happening inside the body.
right? No matter what the cause is, the cells just aren't getting enough oxygen and that forces them into what's called anorobic metabolism, which creates acid that leads to cellular hypoxia and eventually organ dysfunction. And what's so critical for everyone to understand is that once that shock state starts, the body follows the exact same three universal stages of decline. It doesn't matter if it's from a bleed or an infection. Doesn't matter at all. The progression is the same. Stage one is compensated shock.
This is the one that's so hard to spot, right? Because the patient can look almost normal. Almost normal. Exactly. The sympathetic nervous system is working overtime just pumping out catacolamines to clamp down vessels and keep that heart rate up. So what are the subtle signs we should be looking for? You'll see tacocardia for sure, maybe a slight increase in their breathing rate, some tachypnia. Their skin might be cool and pale because blood is being shunted to the vital organs and their urine output.
It's starting to dip and you know the patient is often anxious. That anxiety is a huge sign of poor brain profusion even if their blood pressure is holding steady. That anxiety is a great pearl. You see a patient who's just a little edgy but their BP is say 110 over 70. Mhm. You can't just assume everything's fine. You absolutely can't because if you miss it, you're heading into stage two, decompensated shock. Some people call it progressive shock. And this is where the wheels really start to come off. This is where compensation fails completely. All those signs we were watching for, the tacic cardia, the tachchipnia, now they're severe.
And the blood pressure, now the blood pressure finally drops. The pulse pressure narrows and their mental status just falls off a cliff. They go from anxious to confused or worse. Exactly. Urine output becomes oliguric, maybe even anuric. And that anorobic metabolism we mentioned, it's just raging now, leading to a profound metabolic acidosis. Which brings us to stage three, the state we work so hard to prevent: irreversible shock. Mhm. This stage is really defined by a failure to respond. You have profound hypotension even with maxed out fluids and multiple pressers.
So nothing is working anymore. Nothing. Multiorgan failure is underway. You often see DIC disseminated intravascular coagulation where the body is clotting and bleeding at the same time. It's a catastrophic failure. At that point, the damage is just too widespread. It is. Even if you could magically restore profusion, the organs can't recover. It's when the entire focus of care can shift. Understanding that progression is so key. Okay, let's categorize the causes. For nurses, we often simplify shock into what we call the big three.
Yes, using some really helpful analogies. The empty tank, the broken pump, and the leaky pipes. I love these. They make it so much easier to visualize at the bedside. Let's start with the empty tank. The empty tank is hypoalmic shock. So, the tank is just empty. This could be from an absolute loss of volume like trauma, a GI bleed, maybe severe burns or it could be a relative loss. Massive fluid shifts like what you see in severe vomiting, diarrhea or even DKA. The mechanism here seems pretty straightforward.
It is preload is low because there's just not enough volume coming back to the heart. So stroke volume goes down and cardiac output plummets. And what does that patient look like? They are pale, cool, and clammy. That's from the shunting. Their neck veins are totally flat. Pulses are thready. And that urine output of less than.5 ml per kilo per hour is it's undeniable proof of poor kidney profusion. Okay, so the tank is empty. What are the labs telling us besides the obvious rising lactate?
Well, if they're bleeding, the hemoglobin and hematocrit will drop. But if it's dehydration, you often see the opposite hemo concentration. Okay, and here's a huge pearl, especially for students. Yeah, look at the BU to creatinine ratio. If it's greater than 20 to 1, that screams prenal failure from dehydration. The body is just desperately holding on to water. That makes so much sense. So the nursing priority is get volume back in fast. Fast. Two large bore IVs, aggressive crystalloid bololises, blood products if they're bleeding. Control the source of the loss and keep the patient warm.
All right, that's the empty tank. Now for the broken pump, cardiogenic shock. So now the volume might be fine. It might even be too high. But the heart itself, the pump has failed. The engine has seized up. Usually from a big heart attack, right? A massive MI is the classic cause. But also myocarditis or something physically blocking the pump like a huge PE or cardiac tamponade. This is where a nurse can get into big trouble if they just see a low BP and start pouring in fluids. Oh, absolutely. That is the critical mistake. If the pump is broken, adding more volume just backs everything up into the lungs.
So, the patient assessment is completely different. Instead of looking cold and dry, they look cold and wet. Perfectly said. You'll see distended neck veins, GVD. You listen to their lungs and you hear crackles from pulmonary edema, maybe even pink frothy sputum. Their extremities cool modeled because the cardiac output is just terrible. You might even hear a new S3 heart sound, which is a classic sign of heart failure. And what about the advanced numbers like PCWP or cardiac index? What do those mean at the bedside?
The PCWP or wedge pressure tells you the pressure on the left side of the heart. If the pump is failing, that pressure is high because blood is just pooling there. And the cardiac index that measures how well the heart is pumping for the patient's body size and in cardiogenic shock it will be very very low. It's a high pressure lowflow state. So our management has to be completely different. We're talking very cautious fluids if any very cautious. We focus on reducing afterload and then using medications that help the pump contract inotropes like dobutamine or milrenone.
and if any depressor for their blood pressure. Norpine is the first choice but really the ultimate fix for a broken pump is mechanical. They need to get to the cath lab immediately or maybe get support from a device like an IABP or an Impella. Time is muscle. Okay, that brings us to the third big one. The leaky pipes or distributive shock. This is a totally different problem. The pump is fine, the tank is full, but the pipes, the blood vessels are wide open. No, it's a problem of massive vasoddilation.
Exactly. This creates a relative hypoalmia. The blood just pulls out in the periphery and the systemic vascular resistance or SVR just plummets. The heart has no resistance to pump against. So the pressure drops. And under this umbrella, we find the big four, right? With septic shock being the most common, right? Septic, anaphylactic, neurogenic, and adrenal crisis. But here's a really important pearl. Early septic shock patients look different from the other types of shock. How so? They often look warm, flushed, even. They can have bounding pulses and a wide pulse pressure because all their vessels are so relaxed.
So they look hot instead of cold. But there's a huge exception in this group. You mentioned neurogenic shock. Yes. Neurogenic shock is unique. It's usually from a spinal cord injury typically above the T6 level. Okay. That injury severs the sympathetic chain. So you get massive vasoddilation. They're warm and dry. But without that sympathetic drive, the heart rate drops. They are profoundly brady cardartic. Wow. So warm skin but a slow heart rate. That's a key difference from the tacic cardia you see in almost every other shock state.
It's a defining feature. That's a perfect transition. because you said sepsis is the most common cause of distributive shock. Let's talk about how we define it now because the standards have really changed from the old SER days. They really have. You'll still hear people talk about SERS systemic inflammatory response syndrome. You know, the old criteria. Yeah. Two or more signs like weird temperature, high heart rate, fast breathing, or crazy white blood cell count. But the clinical world moved on from CERS back in 2016. Why? What was the problem?
The problem was it was just It was too sensitive, but not specific at all. I mean, almost anything could trigger SERS. A broken leg, a big surgery, pancreatitis. We had tons of SERS alerts on patients who weren't actually septic. Exactly. And on the flip side, some really sick septic patients, especially elderly or immuno compromised, wouldn't even meet the criteria. We needed a definition that focused on the actual damage being done. And that gave us the sepsis 3 definition. That's right. Sepsis is now defined as life-threatening organ dysfunction caused by a disregulated host response to infection. It's all about the organ damage.
and we measure that with something called the SOFA score. We do the SOFA score sequential organ failure assessment is the gold standard for tracking organ failure across six different systems in the ICU. But for a nurse on the floor or in the ED, we need something much faster. A quick screen. And that's where QS sofa comes in. The quick sofa. This is your simple rapid bedside tool. If you have a patient with a suspected infection and they meet two out of these three criteria, You need to call a code sepsis.
What are the three criteria? One, a respiratory rate of 22 or more. Two, altered mentation. And three, a systolic blood pressure of 100 or less. Two out of three. And you act immediately. Immediately. And when does that escalate to the diagnosis of septic shock? Septic shock is sepsis plus two critical failures. First, they need vasopressors just to keep their mean arterial pressure, their map, at 65 or higher. Okay? And second, their lactate levels persistently high, greater than two, even after you've given them adequate fluid resuscitation. That combination means profound circulatory failure, the mortality rate jumps to over 40%.
Wow. Okay. Now that we've defined all the stages and types, let's bring it all together. What are the core nursing actions for any shock state? This is all about prioritization. It's always ABC's first high flow oxygen and immediately get those two large bore IVs. You can't run a code through a tiny 20 2 gauge, right? Get the access you need up front and then you have to measure if what you're doing is working. So goal directed fluids come next. Get a fully catheter in right away because hourly urine output aiming for that 0.5 to 1 ml per kilo per hour is your best quickest window into organ profusion.
And for sepsis specifically, you mentioned serial lactates. You have to draw serial lactates because seeing that lactate number come down is a key goal of resuscitation. And what about antibiotics and suspected sepsis? That one-hour window is famous. It is non-negotiable. You have to get blood cultures before the antibiotics go in, but only if it doesn't cause a delay. Those broadspectctrum antibiotics have to be infusing within 60 minutes of recognition. It saves lives. Then vasopressors, if needed, ideally through a central line to keep that map above 65.
That's right. And beyond those immediate life-saving steps, there are other things that matter, too. Oh, absolutely. The meticulous care points keep the patient warm. Hypothermia makes everything worse. DBT and stress ulcer prophylaxis and tight glucose control all of it matters. So to give everyone the ultimate quick tool, let's go back to those analogies and boil it down into a visual triad. How to tell the difference in the first 5 minutes? This really summarizes the entire conversation.
Okay, for hypoalmic shock, the empty tank bleeding or dehydration equals cold and flat veins. They just look collapsed inside and out. For cardiogenic shock, the broken pump, a heart attack or heart failure equals cold and wet lungs. You've got distended veins and crackles. And finally, for distributive shock, specifically that early septic shock, the leaky pipes. An infection equals hot and flushed. Unless unless you're thinking spinal cord injury, then it's warm, but with a critically slow heart rate.
Master that visual triad. Knowing the difference between the cold, flat patient and the cold, wet patient. That's everything. It's the difference between giving the right treatment and causing harm. Early recognition rapid resuscitation and that precise nursing care. That's what separates survival from irreversible shock. If you can spot those three stages, use that QS sofa screen and tell the three shock types apart with that quick visual, you are truly thinking like a nurse. Learn it, own it, and apply it.
We hope you'll check in for more conversations like this one each week. And for more resources and to keep building your clinical knowledge, please visit think like nurse.org.