Chapter 20: Trauma and Surgical Management

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So when you're standing in a quiet MedSerg unit, medicine can feel, I don't know, incredibly precise, almost like engineering, you know?

Oh, absolutely.

It's very linear.

Right.

Like a patient has an infection, you draw the labs, you identify the pathogen, hang specific antibiotic and just sort of monitor the steady recovery.

Yeah, it's controlled.

Exactly.

But the moment you step into the chaotic reality of severe trauma,

that illusion of orderly linear medicine just completely shattered.

Oh, it's gone.

It is the absolute definition of working in the clinical muddy waters.

Yeah, you're looking at a patient whose entire physiological system is rapidly decompensating in real time.

The landscape is just terrifyingly fast paced.

And your clinical judgment is often literally the only thing standing between stabilization and total system collapse.

Every single second dictates a physiological cascade.

Which brings us to you listening right now.

We know exactly who you are.

You're a college nursing student.

You've got a massive critical care exam looming and you're staring down Chapter 20.

Ah, yes.

Trauma and Surgical Management.

From Introduction to Critical Care Nursing, Seventh Edition.

That's the one.

So consider this deep dive your personal one -on -one tutoring session.

We aren't just going to like read a list of facts at you.

No, definitely not.

We are going to dive deep into the actual pathophysiology of trauma.

Right.

We'll trace the journey of a critically injured patient from, you know, the physics of the impact at the scene straight through the emergency resuscitation algorithms into the OR and finally into the ICU.

And by the time we finish today, the normal physiology you already know, the stuff you've already studied, will serve as your foundation for understanding this extreme instability.

You're going to understand the intricate cause and effect relationships that drive trauma care.

Oh, and by the end of this, you'll know exactly why a simple three -sided piece of tape can literally save a life.

Yes.

And why simply keeping a patient warm is honestly just as critical as stopping a massive bleed.

Totally.

But before we even touch a patient, we have to understand the broader landscape of trauma, like who it affects and the timeline of mortality.

Right.

The statistics in the text are pretty sobering.

Traumatic injury is the fifth leading cause of death in the U .S.

But what makes it devastatingly unique is that it's really a disease of the young.

It is.

It primarily claims lives between the ages of 16 and 54,

with males experiencing traumatic injuries at a two -to -one ratio compared to females.

Wow.

Two to one.

But what really dictates how we structure trauma care is this concept called the tremodal distribution of death.

Yeah, that tremodal distribution is basically the backbone of the entire trauma system.

It outlines three distinct peaks when patients are most likely to die.

Okay.

So let's break those down.

What's the first peak?

The first peak is immediate death.

This is occurring within seconds to minutes of the injury.

So we're talking about like catastrophic events here.

Exactly.

Massive traumatic brain injuries, a high cervical spinal cord severing, or a complete rupture of the aorta.

And those patients almost always pass away right at the scene, right?

Clinical intervention rarely saves them.

Unfortunately, yes.

The only real defense against this first peak is prevention.

Things like seat belts, helmets, you know, public safety measures.

Got it.

So the second peak is where critical care nursing truly begins.

Right.

This is early death occurring within minutes to a few hours post -injury.

You'll hear it referred to as the golden hour.

The famous golden hour.

Yeah.

And death here is typically driven by massive internal hemorrhage, right?

Like a shattered pelvis, a lacerated liver, ruptured spleen.

Exactly.

And then the third peak is late death.

This happens days or even weeks later in the ICU.

So the patient actually survived the initial trauma and the surgery, but...

But their body succumbs to secondary complications.

Things like sepsis or multiple organ dysfunction syndrome or M .O .D .S.

Man.

So the entire goal of our emergency and critical care interventions is basically to disrupt those second and third peaks.

Precisely.

And if we connect this to the bigger picture, this is exactly why the American College of Surgeons established the trauma center level system.

Right.

Levels I through five.

Yeah.

And a level I trauma center is designed specifically to intercept that golden hour.

It guarantees comprehensive immediate care.

Meaning like an attending surgeon is in -house 24 -7.

Yep.

And they will be physically present in the trauma bay within 15 minutes of the highest level activation.

They match the severity of the injury to the absolute highest level of resources.

OK.

So to stop that early peak of death, we have to look at the applied physics of the event.

The mechanism of injury or M .O .I.

Yeah.

Because knowing how the energy transferred into the patient tells the trauma team exactly what hidden damage to go hunting for.

And here's where it gets really interesting, because it's literally just physics.

Yes.

Energy always has to go somewhere.

The text categorizes this into blunt, penetrating, and blast mechanisms.

So blunt trauma is the most common, right?

Driven by acceleration and deceleration forces.

Right.

Think of a high -speed motor vehicle crash.

The car hits a concrete barrier and stops instantly.

The patient's body keeps moving at 60 miles per hour until the seatbelt violently halts their forward momentum.

But inside the body, the internal organs are still traveling at 60 miles per hour.

Exactly.

Until they smash into the inside of the skeleton.

Oh, man.

And this is how you get a coup contra coup brain injury, right?

Stod on.

The brain slams into the anterior skull.

That's the coup.

And then the sheer force causes it to rebound and slam into the posterior skull, the contra coup.

So you end up with bilateral brain contusions from just a single frontal impact.

Yeah.

And that same shearing force acts on the aorta, potentially tearing it right off its anchor points in the chest.

Terrifying.

So what about penetrating trauma?

That's a completely different kinetic profile.

It is.

The severity there is dictated by the velocity of the object and the specific organs in its trajectory.

And the textbook highlights this fascinating nuance about the history of the assault.

Oh, the gender differences.

Yeah.

Male and female assailants typically display completely different biomechanics during a stabbing.

Wait, really?

How so?

Well, women tend to stab with a downward thrust while men frequently use an upward thrust.

Wow.

So if you're the triage nurse receiving this handoff,

knowing the gender of the attacker completely shifts your internal map of which organs are likely lacerated based on that trajectory.

Exactly.

It completely changes your assessment priorities.

And then you have blast injuries, which just combine multiple mechanisms into one chaotic event.

The physics here are incredible.

You have the primary injury, which is the pressure wave itself.

Right.

And that sudden violent change in atmospheric pressure specifically targets gas -filled organs.

It'll rupture tympanic membranes, tear the alveoli in the lungs, causing pneumothoruses, and even perforate the bowels.

Then the secondary phase hits, where the explosion turns environmental debris into high velocity shrapnel.

Which causes penetrating trauma.

And the tertiary phase is the blast wind physically throwing the patient's body against a wall, causing blunt force trauma.

Yep.

And don't forget the quaternary phase.

That includes the chemical, thermal, and biological burns from the explosive material itself.

Okay.

I want to pause here because I genuinely struggle with the disaster triage protocols associated with mass casualty events like a blast.

It's a really tough mental shift.

It is.

Because as a nursing student, the entire foundation of your training is to run toward the most critical, unstable patient.

Right.

So if I'm on the scene of a factory explosion and I see a patient with a catastrophic, unsurvivable head wound, my autonomic reflex is to intervene and do everything I can to save them.

Tagging them black and physically walking away feels like a complete betrayal of the nursing ethos.

I completely understand that.

It is one of the most psychologically difficult transitions a clinician has to make.

How do you even do it?

Well, in standard emergency care, we operate under an individualistic ethical framework, meaning all resources go to the sickest person.

Yeah.

But in a mass casualty incident, that ethical framework abruptly shifts to utilitarianism.

The greatest good for the greatest number.

Exactly.

If you tie up three nurses, a physician, and all your blood products trying to resuscitate a patient with an unsurvivable injury, the black tag, you actively guarantee the deaths of five salvageable patients who are bleeding from femoral artery lacerations.

Man.

So those are your red tags.

Right.

Red tags are the emergent patients who have life -threatening but treatable injuries.

The yellow tags are urgent but can tolerate a slight delay, and the green tags are the walking wounded.

And to remove the emotional bias from these impossible choices, EMS relies on objective scoring systems, right?

Yes.

They use tools like the Glasgow Coma Scale, or GCS, to rapidly quantify neurologic deficits and the Injury Severity Score, the ISS, to predict mortality based on anatomical damage.

Okay, let's unpack this.

The triage is complete, the patient has been transported, and they hit the doors of the Level I Trauma Center.

Now the trauma team takes over.

Right.

This is where the nurse executes the primary survey.

And this isn't just some clipboard checklist, it's a physiological algorithm designed to find and fix immediate threats to life simultaneously.

The ABCDEFGs.

We begin with A and B, airway and breathing.

But we do so under the strict assumption that the patient has an unstable cervical spine fracture.

So you absolutely cannot do a standard head tilt chin lift.

No.

If you do that, you could sever their spinal cord.

Instead, you use the jaw thrust maneuver.

Okay.

So you place your fingers behind the angles of the lower jaw and physically displace the mandible forward.

Exactly.

This pulls the tongue away from the posterior pharynx, opening the airway while keeping the cervical spine perfectly neutral and immobilized.

And if their breathing is ineffective, you intervene instantly, which usually means rapid sequence intubation.

Got it.

So airway is secure, we move to C for circulation, and this is where we have to dive deep into the lethal triad.

Oh yes, the lethal triad.

If you take away one concept for your exam, make it this.

It's a devastating physiological feedback loop of hypothermia, acidosis, and coagulopathy.

So let's break down how this cascade starts.

When a patient is hemorrhaging, they are losing massive amounts of red blood cells.

Which means they are losing their oxygen carrying capacity.

Right.

And without adequate oxygen reaching the tissues, the cells are forced to switch from aerobic to anaerobic metabolism just to survive.

And the byproduct of anaerobic metabolism is lactic acid.

Yes.

As lactic acid floods the bloodstream,

the patient's blood pH plummets, causing profound metabolic acidosis.

Okay.

So that's the acidosis piece.

But simultaneously, because the patient is in hemorrhagic shock, their body cannot thermoregulate.

No, they lose heat rapidly, plunging into hypothermia.

And this leads to the third pillar, coagulopathy.

The enzymes in our blood that trigger the clotting cascade are incredibly temperamental, aren't they?

Very.

They require a normal core temperature and a normal pH to function.

When the blood becomes cold and acidic, the kinetic energy of those enzymatic reactions just drops.

The proteins denature.

The blood literally loses its ability to clot.

Exactly.

So the patient bleeds more, which means they lose more oxygen, which makes them more acidotic and colder.

Which further destroys their ability to clot.

It is literally a death spiral.

It really is.

And disrupting that spiral completely changed how we handle fluid resuscitation.

Yeah, because historically, if a patient was hypotensive from blood loss,

the protocol was to rapidly infuse liters of crystalloid fluids, like normal saline.

But normal saline doesn't carry oxygen and certainly doesn't contain clotting factors.

I always think of it like having a pot of rich chicken soup and pouring a gallon of cold tap water into it.

That's a great analogy.

Right.

You don't have more soup.

You just have a massive pot of watered down cold liquid.

By pumping a bleeding patient full of cold normal saline, we were actively dropping their core temp.

And diluting whatever native clotting factors they had left.

We were triggering dilutional coagulopathy ourselves.

Which led to the ProPiR trial, right?

This is heavily featured in an evidence -based practice box in the textbook.

Yes, the ProPiR trial revolutionized trauma care by establishing damage control resuscitation.

Now, instead of crystalloids, we initiate a massive transfusion protocol utilizing a one -to -one -to -one ratio.

Okay, explain that ratio.

For every one unit of packed red blood cells we give to restore oxygen -carrying capacity, we give one unit of fresh frozen plasma to restore clotting factors, and one unit of platelets to restore platelet plugs.

So we are meticulously attempting to mimic the physiological composition of whole blood.

Exactly.

To stop the lethal triad before it becomes irreversible.

Brilliant.

So as those blood products are hanging, we continue the survey.

D is for disability, right?

Just a rapid baseline neuro -assessment looking at pupillary response and the Glasgow Coma Scale.

Yep.

And E is for exposure.

You have to completely remove the patient's clothing to inspect every inch of their body for hidden injuries.

But wait, we just established how deadly hypothermia is.

Right.

Which is why exposure is immediately followed by aggressive, active rewarring.

We apply forced air -warring blankets, infuse warmed IV fluids, and literally crank up the ambient temperature of the trauma bay.

Okay, making sense.

Then F is for a full set of vital signs and facilitating family presence.

And G represents get resuscitation adjuncts.

The text categorizes this using the LMNOP mnemonic.

Okay.

L is for labs, most crucially an arterial blood gas and a serum lactate.

Yes.

That lactate level is your primary biomarker for tissue hypoxia.

If it's elevated, you have quantitative proof the patient is stuck in anaerobic metabolism.

Got it.

M is for monitor cardiac rhythm.

N is for nasogastric or orogastric tube placement to decompress the stomach.

To prevent aspiration, yeah.

Right.

O is for oxygen and ventilation assessment and P is for pain assessment and management.

And only after that primary survey is complete and the immediate threats are managed, do we move to the secondary survey.

Right.

Gathering a history using mist or sample and doing a meticulous head to toe.

And a critical nursing action here is coordinating the team to log roll the patient while maintaining spinal precautions.

You have to physically visualize the posterior surfaces.

Because a perfectly stable anterior chest assessment means nothing if there is an exit wound actively hemorrhaging into the stretcher pads beneath them.

Exactly.

And as you move through these surveys, the specific organ damage will start to reveal itself.

So what does this all mean for the nurse at the bedside?

Let's look at the chest cavity.

Cardiac tamponade is a prime example of obstructive shock here.

The heart is encased in a fibrous sac called the pericardium and that sac does not stretch.

So if a penetrating injury nicks a coronary vessel, blood rapidly fills that pericardial space.

Right.

And the rising pressure physically crushes the heart from the outside, preventing the right atrium and ventrothal from expanding to accept venous return.

And to identify this, the text highlights Beck's triad, right?

Hypotension because cardiac output drastically falls.

Muffled heart sounds because you are trying to listen to the valves through thick wall of blood and elevated central venous pressure, typically presenting as severely distended jugular veins.

The blood is trying to return to the heart, but hits a pressure wall and backs up into the neck.

Exactly.

And the definitive intervention there is a pericardial centesis where a physician uses ultrasound guidance to aspirate that trapped blood with a needle.

Instantly restoring cardiac compliance.

Now the lungs present their own distinct mechanical failures.

Yeah.

Let's talk about attention pneumothorax.

This occurs when a laceration in the lung tissue acts as a one -way valve.

So with every breath, air is forced into the pleural space, but it can't escape.

Right.

The intrapleural pressure climbs exponentially, collapsing the injured lung and violently shifting the entire mediastinum, the heart, the trachea, everything toward the uninjured side.

Which completely cuts off venous return to the heart.

That requires immediate needle thoracostomy to vent the trapped air.

Yes.

Now contrast that with an open pneumothorax or of sucking chest wound.

Here, a hole in the chest wall allows atmospheric air to rush directly into the pleural space.

And the nursing intervention here is that brilliant piece of applied physics we teased earlier.

You apply non -porous dressing and take it on exactly three sides.

Creating a functional one -way flutter valve.

Right.

So when the patient inhales, the negative pressure pulls the dressing flat against the wound, sealing it so air travels down the trachea.

But when they exhale, the positive pressure pushes the un -taped edge open, allowing the trapped air to escape.

It's so smart, because if you accidentally tape all four sides, you trap the air and rapidly convert an open pneumothorax into a deadly tension pneumothorax.

Exactly.

Now moving inferiorly, the abdomen is notorious for sequestering massive amounts of occult blood.

Enter the FAST exam, focused assessment with sonography for trauma.

Right.

This bedside ultrasound doesn't diagnose specific organ lacerations.

It just rapidly scans the dependent areas of the peritoneal cavity for a free -floating fluid.

Which, in a trauma context, is assumed to be blood.

Right.

And the liver and the spleen are highly vascular and highly susceptible to blunt force.

I definitely want to highlight a specific assessment finding for splenic rupture here.

CARES sign.

Oh, that's a localized pain in their left shoulder.

You have to recognize the underlying neuroanatomy.

Blood is pooling under the diaphragm, irritating the tissue.

And the diaphragm and the left shoulder share a common sensory pathway through the phrenic nerve.

Right.

So the brain receives the pain signal but misinterprets the origin, referring the diaphragmatic pain to the shoulder.

It's an immediate red flag for massive intra -abdominal hemorrhage.

We also have to address the pelvic ring.

The pelvis houses a massive venous plexus and major arterial branches.

So a disruption of the pelvic ring essentially turns the retroperitoneal space into an expandable reservoir that can hold liters of blood.

The mortality rate from hemorrhaging complex pelvic fractures approaches 50%.

50%.

That's insane.

So the critical nursing action is applying a commercial pelvic binder or even tightly wrapping a sheet around the greater trochanters?

Yes.

Yeah.

By physically compressing the pelvic ring back into its anatomical position, you reduce the volume of that retroperitoneal space and create tamponade pressure against the bleeding vessels.

Okay.

So with all this focus on the core organs, I feel like it's very easy to develop tunnel vision.

Like you might look at a fractured femur and think it's just a bone.

The leg can wait.

This raises an important question because the limbs can actually generate devastating, life -threatening systemic complications.

Right.

You have to constantly assess the extremities using the six P's pain, pallor, pulses, paresthesia, pressure, and paralysis.

And remember, the loss of a palpable pulse is an incredibly late and ominous sign.

Do not wait for pulselessness to intervene.

Good point.

So the first major complication is compartment syndrome.

Right.

Skeletal muscles are encased in a tough, fibrous fascia that lacks elasticity.

So if blunt trauma causes internal bleeding or massive edema within that muscle compartment, the pressure just skyrockets.

It literally chokes off the capillary beds supplying the muscle.

The hallmark clinical sign is deep, throbbing pain that is entirely out of proportion to the initial injury.

And crucially, ischemic nerve pain does not respond to opioid analgesics?

Not at all.

If you give a patient a heavy dose of fentanyl and they are still screaming in agony from their calf, suspect compartment syndrome, the only treatment is a surgical fasciotomy to open and release the pressure.

Wow.

The second complication is rhabdomyolysis.

When muscle tissue is subjected to prolonged crush injuries,

the cellular membranes rupture, dumping massive amounts of a protein called myoglobin into the systemic circulation.

And myoglobin is a large molecule.

As the kidneys attempt to filter it, it gets trapped, physically clogging the renal tubules.

So as the critical care nurse, you are monitoring the Foley catheter closely.

If the urine output drops and turns a dark, muddy brown or T color, that's myoglobinuria.

And your primary intervention is aggressive intravenous hydration to forcibly flush the kidneys before the patient spirals into acute renal failure.

And the third complication, fat embolism syndrome, is fascinating to me because of its delayed presentation.

Yeah, it doesn't happen right away.

When a large long bone like a femur fractures, yellow marrow fat droplets can be forced into the venous circulation.

These fat emboli travel through the right side of the heart and lodge in the microscopic pulmonary capillaries, creating a mechanical obstruction identical to a blood clot PE.

But again, this typically manifests 24 to 48 hours post -injury.

The patient will be recovering in the ICU, seemingly stable, and then abruptly develop profound hypoxemia, neurological changes, and a distinct patechial rash across their chest and axil.

And that delayed timing perfectly transitions us into the critical care phase because surviving the ED is really only the first hurdle.

Right.

The textbook uses an excellent case study of Mr.

M to illustrate this shift in strategy.

Yeah, Mr.

M is a 27 -year -old male who sustained a gunshot worn to the right chest.

He arrives in profound shock, hypotensive brady cardiac with a positive fast exam indicating massive abdominal bleeding.

So the team initiates the one -to -one -to -one massive transfusion protocol and rushes him straight to the OR.

But once inside the OR, the surgeons don't perform a meticulous anatomical reconstruction, do they?

No, they perform damage control surgery.

I always conceptualize damage control surgery by imagining a ship that has just taken a torpedo to the hull, water is flooding in, you do not start carefully remodeling the kitchen cabinets and painting the bulkheads.

Exactly.

You slap a crude steel patch over the hole just to keep the ship from sinking and you limp back to port.

Right.

And damage control surgery is executed in three distinct stages.

Stage one occurs in the OR.

The sole objective is to arrest the hemorrhage and control any spillage of bowel contents.

The surgeon might literally pack the abdomen with sponges, apply a temporary vacuum dressing, and leave the abdomen open.

Because keeping the patient on the operating table for a four -hour complex repair will guarantee their death from the lethal triad.

Right.

Stage two shifts the battlefield to the ICU.

This is critical care nursing takes the helm.

The goal here is aggressive physiological optimization.

You are actively rewarming the quartum, continuing volume resuscitation, and correcting that profound metabolic acidosis.

Mr.

M arrived with a highly acidotic blood pH of 7 .1 T and you have to reverse that.

And the nursing priorities during stage two are immense.

It begins with a meticulous handoff from the anesthesia team.

You manage continuous hemodynamic monitoring via arterial and central lines.

The textbook also emphasizes strict glycemic control here.

Yes.

Even in patients without diabetes, the massive physiological stress response triggers a surge of cortisol and epinephrine dumping glucose into the bloodstream.

And hyperglycemia heavily impairs immune function and wound healing.

So the evidence -based target is to maintain blood glucose between 140 and 180 milligrams per vesiliter using insulin protocols while strictly avoiding hypoglycemic events.

Then once the team has successfully re -warmed the patient, normalize their coagulation labs, and stabilize their hemodynamics, usually 24 to 48 hours later, we enter stage three.

The patient is transported back to the OR for definitive surgical repair.

The ship is finally safe in port and you can remodel the kitchen.

Exactly.

You know, Mr.

M was a healthy 27 -year -old, but the physiological response to trauma is heavily manipulated by the patient's baseline status.

Right.

You cannot apply standard hemodynamic metrics uniformly across all populations.

Let's look at the geriatric population.

Aging inherently stiffens the myocardium and the vascular bed.

And many older adults live with chronic hypertension.

If an elderly patient arrives after a fall with a blood pressure of 120 over 80, a novice might look at the monitor and think they are perfectly stable.

But if that patient's daily baseline is 170 over 90, a reading of 120 over 80 represents a massive sudden drop.

They are in profound hypovolemic shock.

And adding to that danger, many older adults are prescribed beta blockers.

Which chemically prevents the heart rate from rising.

Exactly.

The normal healthy physiological response to hemorrhage is compensatory tachycardia.

But with a beta blocker, that patient could be actively bleeding to death into their abdomen while displaying a reassuring, perfectly normal heart rate of 70 beats per minute.

That is terrifying.

Pregnant patients present an entirely different, highly deceptive physiological profile too.

Yeah.

During pregnancy, maternal plasma volume increases drastically.

And because she has so much excess reserve volume, and because maternal physiology prioritizes perfusion to her own brain and heart over the uterus, she can hemorrhage up to 40 % of her total circulating blood volume before you will see any significant drop in her systemic blood pressure.

By the time the monitor alarms for hypotension, she has exhausted every reserve,

and fetal demise may have already occurred.

And pediatric patients follow a similar deceptive pattern, don't they?

They do.

Children possess a higher basal metabolic rate and a much larger ratio of blood volume to body weight.

Their cardiovascular systems are incredibly robust and elastic.

So they'll maintain a normal blood pressure and look deceptively well perfused for an extended period.

Right, aggressively compensating for blood loss.

But once those compensatory mechanisms hit their limit, there is no gradual decline.

It is a physiological cliff.

They crash suddenly, rapidly, and catastrophically.

Yes.

Finally, we must anticipate the complications of substance abuse.

A significant percentage of traumatic injuries involve alcohol or illicit drugs.

So once the trauma team successfully stabilizes the physical injuries in the ICU, they have to for the profound neurochemical rebound of withdrawal.

You are managing a patient with an open abdomen who may suddenly develop violent seizures,

severe hallucinations, or extreme sympathetic spikes in heart rate and blood pressure from DTs.

Which can easily blow surgical anastomosis and completely derail the resuscitation effort.

It requires a highly coordinated pharmacological protocol just to manage the addiction safely while the body attempts to Man, we have covered an immense amount of ground today.

From the sheer physics of the traumatic impact, through the strict prioritization of the primary survey, to the granular critical thinking required to manage the lethal triad and damage control resuscitation.

We really explored how a nurse's anticipation of secondary complications like compartment syndrome or delayed fat embolican drastically alter patient outcomes.

And we spent so much time discussing how to spot those subtle microscopic shifts in the ICU to prevent that third peak of late trauma death.

But as we look toward the future of critical care, what if the next massive leap in trauma survival isn't a new surgical technique at all?

What do you mean?

Imagine the integration of predictive artificial intelligence into our bedside monitors.

Systems capable of analyzing tens of thousands of continuous micro fluctuations and heart rate variability and pulse pressure fluctuations totally invisible to human eye.

Oh, right.

To predict a septic cascade or a hemorrhagic crash hours before the standard 15 minute vital sign check ever triggers an alarm.

That is the future you are stepping into as a student.

You aren't just memorizing pathways.

You are learning to manage a rapidly shifting,

highly complex physiological landscape.

You understand the profound why the clinical what.

Absolutely.

From the last minute lecture team here at the deep dive.

Thank you so much for joining us and absolutely crush that exam.