Chapter 45: Care of Patients With Emergent Conditions, Trauma, and Shock

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You know, usually when we talk about a medical diagnosis, there's this expectation of clinical precision.

Feels almost like engineering, right?

Like, a patient comes in with a broken arm, the x -ray shows that stark jagged white line across the radius, and the provider just points at the screen and says, well, there it is.

Right, it's binary.

Broken or not broken, it's clean.

Exactly, and it's comforting.

Yeah, in healthcare, we naturally gravitate toward things that are visible.

We easily categorize problems with standard linear solutions.

But then you step through the double doors of the emergency department.

You enter this world of emergent conditions, complex trauma and shock, and suddenly, that metaphorical x -ray machine of easy answers is just, it's broken.

Completely broken.

You're looking at a diagnostic landscape that is entirely murky.

I mean, a patient rolls in unconscious and there's no flashing neon sign telling you whether it's a traumatic brain injury, massive internal hemorrhage, a metabolic crash, or a drug overdose.

It is the absolute definition of diagnostic muddy waters.

And you know, you're entering this field at a particularly critical time in healthcare.

Emergency nursing isn't just about the adrenaline rush of running down hallways with a crash cart.

Right, definitely not like the movie.

No, not at all.

It requires a level of flawless assessment and rapid, almost instinctual clinical decision making.

Because right now, hospitals are facing an unprecedented crisis.

Over 90 % of hospital emergency department directors report that overcrowding and agonizingly long wait times are a massive systemic issue.

Wow, 90%.

Yeah.

It's gotten to the point where reducing these wait times is a formalized focus for healthy people 2030.

And organizations like the Joint Commission are holding facilities strictly punitively accountable for their throughput efficiency.

So because of that overcrowding, you as the nursing student stepping into this role, you do not have a luxury of time.

You have to prioritize care effectively the moment a patient arrives.

And that's really the mission of our deep dive today.

We're going to conquer chapter 45, care of patients with emergent conditions, trauma and shock from medical surgical nursing.

And we're going to break this dense material down sequentially, turning all those pathophysiological concepts into practical clinical reasoning.

Right, linking assessments directly to safe, prioritized nursing care.

Welcome, by the way, to this special one -on -one tunering session from the last minute lecture team.

Glad to be here.

So to start, we actually have to take a step back.

Because before a patient even reaches the triage desk or the trauma bay,

an emergency always has a context.

We often think of trauma as starting at the hospital doors, right?

We do.

But the reality is the vast majority of these emergencies begin in the home.

Which is a sobering reality, honestly.

If you look at box 45 .1 in the text, accidents in the home and within the community consistently rank as the fourth leading cause of death across all age groups.

Fourth leading cause, that's massive.

It is.

And the epidemiological data shows the principal victims are starkly clustered at the extremes of age.

So children younger than five and adults older than 65.

If we could drastically improve our attention to home safety for these specific populations, we could prevent a huge percentage of these fatalities before an ambulance is ever even called.

So as a nurse, you aren't just treating the acute injury.

Patient education is a massive preventative part of your scope of practice.

Absolutely.

You're gonna be having conversations with families, trying to identify and mitigate these risks.

For instance, something as simple as cooking.

You need to be teaching families to always use vents or flues for stoves to prevent carbon monoxide buildup.

Right, or smoke buildup.

Exactly.

And you have to constantly remind parents of toddlers to keep the handles of pots and pans turned inward, away from the edge of the stove.

That's a huge one.

A toddler's center of gravity and natural curiosity means they'll just reach up, grab that handle, and pull boiling water or hot oil directly down onto their face and chest.

Causing devastating life -altering burns.

Yeah, it really comes down to anticipating the developmental level or the physical limitations of the patient.

For children, it extends to storing highly toxic household poisons like bleach or drain cleaner in cabinets equipped with actual child safety locks, not just placed out of sight.

Because they will find them.

They always do.

And for the older adult population, the risks shift toward mobility and sensory deficits.

So using non -slip rubber mats in bathtubs and showers is absolutely crucial to prevent falls.

Which are a primary cause of those devastating hip fractures.

Exactly.

And subsequent decline in the elderly.

It also means keeping all medications tightly capped, clearly labeled, and completely out of reach.

Oh, and physical safety measures too.

Yeah.

Like teaching people to safely dispose of broken glass by placing it in heavy paper sacks before putting it in the trash.

Right, so it doesn't slice through a plastic garbage bag and sever a tendon in the leg of whoever's taking out the trash.

Ouch.

But despite our best efforts at preventative education,

accidents will happen.

They will.

The preventative measures fail and the patient arrives at the ED doors.

This is where the triage process acts as the critical gatekeeper.

The detective work begins.

Yes.

When you're the triage nurse, you are the first line of defense.

Yeah.

And the tech says you have to use three very specific elements to make a clinical decision.

Preceding events,

the mechanism of injury or MOI, and your index of suspicion.

Let's break down how you actually use these in the real world.

Think about preceding events.

If EMS brings in a young woman found unresponsive with vomit around her mouth and the friends report a preceding event of, well, heavy drinking and taking unknown pills at a party.

Okay, that preceding event immediately points your clinical reasoning toward aspiration, CNS depression, and a toxicological overdose.

Right, your pathway is clear.

But what if EMS brings in an older man, also unresponsive, found in a grocery store parking lot and a bystander reports that the preceding event was the man clutching his chest, complaining of severe pain, and frantically reaching into his pocket for a pill bottle.

It's the exact same physical presentation and unresponsive patient.

But the preceding event points to a completely different path of physiology.

Exactly.

That second scenario is an acute cardiac event.

Likely a massive MI leading to cardiac arrest.

The preceding events give you the vital context to start your initial algorithms.

Then we have the mechanism of injury, the MOI, paired with your index of suspicion.

This is where my detective analogy really comes in.

You have to look past the obvious.

Let's say a panicked parent runs in holding a three -year -old.

The toddler has this giant, incredibly dramatic purple goose egg swelling on their forehead.

The parent is terrified because it looks monstrous.

Of course.

But the parent tells you the MOI.

The toddler was running across the living room rug and tripped, hitting their head on the flat surface of a wooden coffee table.

See, that mechanism of injury tells an experienced triage nurse a lot.

A trip and fall onto a flat surface from a toddler's height generates a relatively low amount of kinetic energy.

Right.

The superficial blood vessels in the scalp bleed profusely, which creates that terrifying goose egg.

But the actual risk of a severe traumatic brain injury or skull fracture is relatively low.

So it looks terrible, but your index of suspicion for a life -threatening internal injury remains low.

Exactly.

Now flip the scenario.

A 25 -year -old guy walks up to the triage desk.

She drove himself to the hospital.

He's talking to you normally.

His skin looks fine.

No visible blood, no dramatic swelling.

He just looks a little pale.

Okay.

But he tells you the MOI.

He was in a bar fight an hour ago and took three or four incredibly heavy direct punches from a large man right to his upper abdomen.

Oh, wow.

Yeah, that is precisely where your index of suspicion must skyrocket.

It has to.

That mechanism of injury involves massive focused kinetic energy delivered directly to the solid organs of the abdomen, the liver, and the spleen.

And those organs are highly vascular.

While the external skin might not even have a bruise yet, that blunt force could have caused a deep laceration or a subcapsular hematoma in the spleen.

He could be actively slowly bleeding to death into his abdominal cavity while standing right in front of you complaining about the wait time.

And in a busy ED where everyone in the waiting room is anxious, the charge nurse is stressed,

you cannot let a stable external appearance fool you.

A high index of suspicion is your defense against complacency.

It really forces you to anticipate the hidden internal damage based entirely on the physics of the MOI.

So once you've triaged the patient and moved them into a trauma bay,

you transition from that detective work into a highly structured unyielding protocol, the primary and secondary surveys.

Right.

You have to rapidly identify and neutralize immediate threats to life.

And the primary survey is universally structured around the ABCDE assessment framework.

You do not deviate from this.

It's systematic.

You fix any life threat you find in one letter before you're allowed to move on to the next, right?

Always.

Let's walk through it.

A is for airway.

Without an open airway, nothing else matters.

You are physically looking, listening, and feeling.

Assessing for gasping, choking, or agonal respirations.

Listening for wheezing or gurgling, which indicates fluid or blood pooling in the back of the throat.

And you are hypovigilant for stridor.

Stridor, that is a very specific, high -pitched, harsh whistling sound, right?

Yes.

It happens when air is being forced through a severely narrowed upper airway.

It means there's a partial obstruction, maybe from a foreign body or swelling from a burn.

It's a massive red flag that the airway is about to close completely.

Exactly.

And securing that airway in a trauma patient requires immense caution.

And this is something I want to push back on because it trips up a lot of students.

In a basic community CPR class, they teach you to tilt the head back and lift the chin to open the airway.

The standard head tilt chin lift.

Right.

But the tech says in emergency trauma nursing, doing that maneuver on a trauma victim could literally kill them or render them a quadriplegic.

Why is that specific maneuver so dangerous here?

It all comes down to the cervical spine, the C -spine.

In any patient who has suffered a traumatic mechanism of injury, you must operate under the absolute assumption that they have an unstable fracture of their cervical vertebrae.

Okay.

If one of those neck bones is broken and you tilt their head back to open their airway,

the jagged edge of that fractured bone could easily slice directly through the spinal cord.

Oh, wow.

Yeah.

And if you sever the cord at the cervical level, you destroy the phrenic nerve pathway, which controls the diaphragm.

The patient will instantly lose the ability to breathe on their own and they'll be permanently paralyzed from the neck down or die.

So if you can't move their neck, how do you open the airway of an unconscious trauma patient whose tongue is blocking their throat?

You use the jaw thrust maneuver.

You place your fingers behind the angles of the patient's lower jaw and physically push the jaw forward and upward.

Okay, so that lifts the tongue out of the back of the throat without bending the neck.

Someone holds strict manual inline stabilization of the head and neck while the airway is secured.

Okay, so once A is clear, we move to B, breathing.

Because having an open airway doesn't mean the lungs are actually working.

You're assessing for rhythmic, symmetric rise and fall of the chest and abdomen.

Checking the rate and quality.

Right.

Are they using accessory muscles in their neck to heave air in?

You also need to look at the geometry of the chest.

If you see asymmetric chest rise, meaning the right side expands when they inhale, but the left side does nothing, something is critically wrong within that pleural cavity.

Like a collapsed lung or blood accumulating.

Or a flail chest.

You also look closely at the trachea in the front of the neck.

It should be perfectly midline.

If the trachea is physically deviated, pushed to one side, you are looking at a late, highly lethal sign of a tension pneumothorax.

Terrifying.

So after breathing, we hit C.

Circulation and hemorrhage.

You're checking central pulses, like the carotid in the neck or the femoral in the groin.

Right, because if there is no central pulse, the patient is in cardiac arrest or profound obstructive shock, you immediately initiate CPR.

But if there is a pulse, you rapidly assess its quality.

The quality tells you the hemodynamic story.

A rapid bounding pulse might just be massive, sympathetic nervous system stimulation.

You know, pure terror and adrenaline from the accident.

Makes sense.

But a rapid, thready pulse is dangerous.

It feels like a tiny thread vibrating under your fingers.

Weak, fast, easily compressible.

That tells you the heart is beating frantically to compensate, but the actual volume of blood inside the vessels is dangerously low.

They're bleeding out.

Actively bleeding out, either internally or externally, heading straight for hypovolemic shock.

And this is also where you do a rapid check for catastrophic external hemorrhage.

If they're bleeding heavily from a limb, you don't wait.

You apply immediate direct pressure or place a tourniquet high and tight.

You stop the bleeding right there in the C -step.

Next is D, which stands for disability.

In the primary survey, disability refers entirely to their neurologic status.

Right, assessing their level of consciousness.

Are they alert and oriented?

You check their response to verbal stimuli or they only respond to pain.

And you calculate a baseline Glasgow Coma Scale or GCS score.

Measuring eye -opening verbal response and motor response.

Yeah.

The highest is a 15, meaning normal.

But the text says a score of eight or less indicates a severe coma.

And the golden rule is less than eight intubate because they can't protect their own airway.

Exactly, alterations in their neurologic status here could be a traumatic brain injury, but it could also be a massive stroke, profound hypoglycemia, hypoxia, or an overdose.

So you're also scanning for medical alert bracelets.

Finally, E, exposure environmental controls.

The rule is you cannot treat what you cannot see.

You have to use trauma shears to completely remove the patient's clothing.

Because an unconscious patient can't tell you they have a stab wound in their back.

Right, but this introduces a massive secondary risk.

While you are stripping them down in a cold trauma bay, you must protect them from hypothermia.

Cover them with warm blankets or use forced air warming devices as soon as the assessment is done.

Because hypothermia in a trauma patient is part of the lethal triad, right?

When they get cold, their blood stops clotting properly, which makes them bleed more, which makes them colder.

It's a fatal cycle.

A vicious cycle.

So the ABCDE primary survey is complete.

Life threats neutralized.

Now you transition to the secondary survey.

This is the comprehensive systematic head to toe assessment.

Starting at the head, feeling the skull for step off fractures, reassessing the neck while maintaining C -spine precautions,

auscultating lung fields.

Then you move down to the abdomen and the genitourinary system.

Listening for bowel sounds, gently palpating for rigidity or guarding.

Checking the urinary meatus for blood, indicating a torn urethra.

And when examining the abdomen, you must be hypervigilant for two very specific clinical cues that signal massive internal hemorrhage.

First is the Cullen sign.

This is a bluish, purplish tinge or bruising directly around the umbilicus, the belly button.

Wait, if the bleeding is from a ruptured organ deep in the back of the abdomen, why does the bruising show up right at the belly button?

Because of the fascial planes.

When you have severe bleeding in the retroperitoneal space, say, from a ruptured pancreas, that free blood physically tracks along the anatomical planes of the abdominal fascia, it migrates toward the anterior abdominal wall and pools subcutaneously around the umbilicus.

Oh, I see.

The blood follows the path of least resistance.

Exactly.

And the second cue is the Gray -Turner sign.

Essentially the same physiological process, but the bruising appears along the flanks, the sides of the abdomen.

Both Cullen and Gray -Turner signs are massive red flags.

The patient is bleeding out internally.

The secondary survey also involves checking all four limbs, peripheral circulation,

pulses distal to any suspected fracture.

And then the log roll.

Right, because you haven't seen their back yet.

To do this safely, it takes a coordinated team of at least four people.

One person is positioned at the head of the bed.

Their entire job is to rigidly hold the patient's head and neck.

On the leader's count, the team gently log rolls the patient onto their side as a single unit.

So you can check the spine, buttocks, and back of the head, looking for hidden fractures or in penetrating trauma, exit wounds.

A bullet can bounce around and exit anywhere.

Now, before we move on to specific injuries,

there's a really strict clinical standard the text points out regarding interprofessional management and how the team communicates during these codes.

On TV, it looks like people are just shouting random verbal orders.

Right, pure chaos.

But the team is actually operating off well -established algorithms like ACLS.

And as the nurse administering medications, you are strictly responsible for seeking clarification of orders.

Absolutely.

Misunderstanding a verbal order because the room was loud is never an acceptable excuse for a medication error.

You must implement closed -loop communication.

If the doctor says, give one milligram of epinephrine IV push, you look at them and say, drawing up one milligram of epinephrine for IV push.

Confirm it before you do it, no excuses.

Okay, so we've assessed the patient.

Let's move to section three, the pathophysiology and management of specific traumas, starting with bleeding.

Hemorrhage control.

You have to differentiate between arterial and venous bleeding.

Arterial blood is bright red because it's oxygenated and it's under high pressure from the heart.

It will literally spurt out of the wound in a rhythmic pattern.

Very aggressive.

Extremely.

Venous blood is dark red and under much lower pressure.

It doesn't spurt, it oozes or leaks steadily.

Less dramatic, but still lethal if ignored.

The intervention for both is applying firm direct pressure exactly over the site and universally donning your PPE gloves, face shields before touching a bleeding patient.

Moving down to the chest cavity.

The pathophysiology here is incredibly complex.

Let's talk about a flail chest.

Okay, this usually results from massive blunt force like a steering wheel to the chest.

The pathophysiology is defined by the bones.

It occurs when three or more adjacent ribs are broken and each of those ribs is broken in two or more separate places.

So you've effectively created a free -floating segment of bone and muscle.

The chest wall becomes unstable.

And that destroys the physics of ventilation.

Normally you inhale, your chest expands, creating negative pressure to vacuum air in.

But with a flail chest, because that broken segment is detached, it moves paradoxically.

Paradoxical motion.

When the patient breathes in, the negative pressure sucks the flail segment inward, painfully compressing the lung.

When they exhale, the pressure pushes it outward.

It's moving opposite to the rest of the chest.

It makes it impossible to pull enough air in.

It leads to profound hypoxia.

The treatment is to take over the work of breathing.

The patient requires endotracheal intubation and mechanical ventilation.

The ventilator pushes air in under positive pressure, which internally splints the chest wall open.

And you give heavy sedatives so they don't fight the ventilator and damage their lungs.

Next is pneumothorax or hemothorax.

The lungs are surrounded by the pleural cavity, which exists under negative pressure to keep the lung expanded.

If a penetrating injury creates a hole, a sucking chest wound air gets vacuumed into that space.

That's an open pneumothorax.

Or if blood fills it, it's a hemothorax.

As air or blood accumulates, the lung collapses inward.

Assessment cues are labored breathing, maybe bubbling blood from the wound, and lack of chest movement on one side.

For positioning, you want them in a semi -fowler position to let gravity pull the abdominal organs down.

The definitive treatment is a chest tube to pull the air or blood out and restore negative pressure.

But we have to distinguish that from a tension pneumothorax, which is a lethal cardiovascular crisis.

In a tension pneumothorax, air enters the pleural space when they inhale, but a flap of torn tissue acts as a one -way check valve.

The air goes in, but when they exhale, it gets trapped.

So pressure builds exponentially, collapsing the lung, but it also pushes against the mediastinum.

A mediastinal shift.

The immense pressure shoves the heart, the vena cava, the trachea over to the unaffected side.

And the vena cava relies on low pressure to dump blood into the heart.

If it's kinked by this high -pressure air, blood can't return, the heart gets squeezed so tightly it can't fill.

Cardiac output drops to almost zero.

They go into obstructive shock and will die in minutes.

The emergent treatment is a needle thoracostomy.

Plunging a large bore IV needle directly through the chest wall to vent that trapped air.

You literally hear a hiss as the air escapes.

Then we have cardiac chroma.

Blunt force can cause a myocardial contusion, bruising the heart muscle, causing lethal arrhythmias mimicking an MI.

But penetrating trauma causes cardiac tamponade.

Blood hemorrhages rapidly into the sealed pericardial sac surrounding the heart.

It crushes the heart muscle.

The ventricles can't relax and fill.

And the clinical cues form Beck's triad.

First, muffled distant heart sounds because the heart is drowning in blood.

Second, severe hypotension because it can't pump.

And third, jugular vein distension or JVD because the right side of the heart can't accept venous blood, so it backs up into the neck.

Another form of obstructive shock.

The treatment is a pericardiocentesis, aspirating that blood with a long needle.

Moving below the diaphragm to abdominal trauma.

This is a black box.

Blunt trauma, like from a seatbelt, can tear the liver or spleen.

You have to do serial assessments looking for a rigid, board -like abdomen.

Diagnostically, we relied on the FAST exam.

Focus assessment with sonography for trauma.

A portable ultrasound looking for free fluid, which is assumed to be blood.

Interventions include two large bore IVs, an NG tube, a Foley catheter, and sending blood for a type in cross -match immediately.

Oh, and multiple trauma.

Common in car crashes.

Airway is always the priority.

Always.

Now, let's shift focus to section four, medical and metabolic emergencies.

Sometimes the body's internal systems just crash.

Let's start with severe hypoglycemia.

The pathophysiology is all about the brain.

Brain cells can't store glucose.

If systemic levels drop, the brain sarps.

The vasomotor center fails.

Blood vessels dilate.

BP drops.

The body panics and dumps epinephrine to try to release stored sugar.

This adrenaline dump causes the classic cues.

Altered LOC, dizzy, tachycardic, and cold, clammy, profuse sweat.

So nursing interventions must be immediate.

If they're awake, give fast -acting oral carbs.

Juice, milk, hard candy.

But here's a crucial pushback from the text.

Why does it warn against giving orange juice to a patient with chronic renal failure?

This is a critical clinical cue.

Orange juice is exceptionally high in potassium.

A renal failure patient can't excrete that potassium effectively.

A massive bolus of OJ can drive their potassium to a toxic point and trigger lethal cardiac dysrhythmias.

Like ventricular fibrillation, wow.

Yeah, give apple, cranberry, or grape juice instead.

And if they have a decreased LOC, give IVD50 or IM -glucogon, then follow up with a protein meal.

Let's transition to toxicological emergencies.

Poisoning.

Older adults are uniquely at risk for accidental overdoses because of decreased liver and kidney function, right?

Exactly.

A normal therapeutic dose can accumulate into a toxic overdose simply because they can't clear the drug from their system.

Symptoms vary by toxidrome.

Opioid overdose presents with pinpoint pupils, profound unconsciousness, and respiratory depression.

Whereas organophosphate poisoning, like from pesticides, causes massive parasympathetic overstimulation.

Salivation, tearing, vomiting, and uniquely a strong garlic odor on the breath.

The interventions.

Ensure ABCs first.

Listen to family for clues.

And call poison control immediately.

1 -800 -222 -1222.

Have all the patient's stats ready.

Okay, section five.

Basic life support and CPR algorithms.

If the heart stops, you step into resuscitation mode.

The AHA emphasizes CAB chest compressions, airway breathing.

Push hard, push fast.

And the text breaks down lay rescuer versus healthcare provider.

Lay rescuers do hands -only CPR, no airway maneuvers.

But providers use head tilt chin lift or jaw thrust to see spine injury at 30 to two ratio and a bag valve mask.

And use the AED as soon as possible because if it's ventricular fibrillation, only electricity can fix it.

Which brings us to section six.

The central concept.

Shock, the ultimate common pathway.

Shock starts at the cellular level.

The hallmark is a lack of adequate perfusion to tissues.

Lack of oxygen forces the body into anaerobic metabolism, right?

Yes, producing lactic acid, causing metabolic acidosis and eventually multi -organ dysfunction.

I love the analogy for perfusion.

Think of it like a city's water supply.

The reservoir is your blood volume.

The pipes are your blood vessels.

The pumping station is your heart.

For the houses to have water pressure, all three must work.

If the reservoir drains or the pipes expand too much or the pump breaks, pressure drops.

The body tries to compensate, leading to the three stages of shock.

First is compensated shock.

The body maintains BP through vasoconstriction and increased heart rate.

Cues are tachycardia and cool skin.

But if not fixed, they crash into decompensated shock.

Oxygen lack hits the central organs.

Cues are confusion, diaphoresis, rapid thready pulse, hypotension, narrowing pulse pressure, and urine output less than 20 mB each hour.

And finally, irreversible shock.

Tissue damage is beyond repair.

Recovery is impossible.

So in section seven, we diagnose the four types of shock.

First, hypovolemic shock.

Low volume.

The reservoir is empty.

Caused by bleeding, vomiting, diarrhea,

burns.

At 40 % loss, BP drops.

At 50%, death is imminent.

But here's another clinical judgment scenario.

A patient vomits massive amounts of blood, but their pulse stays between 50 and 60.

Why no compensatory tachycardia?

Check the medication history.

They might be on antihypertensives like beta blockers that physically block the heart from speeding up.

It masks how close to decompensation they are.

For management, stop the fluid loss.

Establish two large boar IVs.

Administer crystalloids or colloids.

And always give oxygen.

Second is cardiogenic shock.

Pump failure.

Usually in MI.

We use vasopressors and inotropes, like dogutamine, to increase contractility.

But wait, if the heart is damaged, aren't we making it work too hard by forcing it to squeeze harder?

Yes, which is why we also judiciously use vasodilators like nitroglycerin to decrease afterload.

It makes the vessels wider so the heart doesn't have to push against as much resistance.

Third is obstructive shock.

The blockage.

Tension pneumothorax, tamponade, or pulmonary embolism.

Management is eliminating the source.

Needle thoracostomy, et cetera.

And fourth is distributive shock.

The volume is normal, but the vessels are too wide.

Relative hypovolemia.

Three subtypes.

First, neurogenic shock from spinal injury.

Sympathetic impulses are blocked.

The unique cues are a triad of hypotension, hypothermia, and bradycardia, unlike other shocks where the heart races.

Second, anaphylactic shock.

Massive allergic reaction releasing histamine, causing vasodilation and capillary permeability.

Treat with epinephrine.

And third, septic shock.

Starts with an infection.

Progresses to a dysregulated inflammatory response.

Starts as SARS, then sepsis.

We use QSOFED now, right?

Yes, the QSOFED criteria.

Altered mental status.

Cystolic BP under 100.

Respiratory rate over 22.

If they remain hypotensive despite fluids and lactate is over two, it's septic shock.

Capillaries leak and clot everywhere called DIC.

Disseminated intravascular coagulation.

They're clotting internally, but bleeding externally.

Recognize early.

Implement the sepsis bundle.

Fluids, blood cultures, broad spectrum antibiotics within one hour, and norepinephrine.

Which brings us to section eight.

Priority nursing care and evaluation.

Applying the care plan to Bob Jones, blunt force abdominal trauma.

Priority problems.

Fluid volume deficit, impaired gas exchange, fear of death, interventions.

Monitor VS every five minutes.

Patent IVs for boluses.

Lay patient flat and elevate legs 10 to 12 inches to redistribute central volume.

Unless they're in cardiogenic shock, don't do that then.

Right.

KEEPO2 over 95 % offer calm presence.

Evaluation.

Cystolic BP over 90.

Cap refill under three seconds.

And urine output returns to 20 to 30 millidellio jar, indicating kidney perfusion.

To wrap up, imagine an 85 -year -old female in a car crash.

History of stroke, ruptured bowel, femur fractures, and a tense pneumothorax.

A single patient can be at risk for multiple types of shock simultaneously.

Hypothelemic from the femurs, obstructed from the pneumothorax, distributed from the ruptured bowel.

The emergency nurse must constantly connect the ducts between the MOI and the shifting vitals.

It requires relentless vigilance.

It really does.

Well, on behalf of the last minute lecture team, we wanna thank you for joining us for this deep dive.

We wish you luck on your exams and future shifts.

Remember, strong foundational concepts are the key to saving lives at the bedside.

Keep pushing hard, keep pushing fast, and we will see you next time.