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Welcome back to the Deep Dive. 
Today we're scrapping the usual 

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format. 
No broad overviews, no, you 

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know, casual skimming. 
We are simulating a pressure. 

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Cooker we certainly are. 
We are going right into the 

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operating theater or or maybe 
more to the point, the 

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examination hall. 
That's exactly right. 

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And look, I'm not just the 
expert today. 

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I want you to think of me as 
your external examiner. 

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I'm the senior faculty member 
from a neighboring Medical 

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College. 
I'm sitting across the table 

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from you, and frankly, I've 
heard every wrong answer in the 

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book. 
I have 0 patience for fluff. 

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My job today is to grill you, 
yes, but ultimately it's to get 

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you to pass. 
Because this topic we're 

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covering, it isn't just for 
marks. 

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It's the difference between a 
patient going home and a patient

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not. 
I'm ready. 

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I'm no longer the host. 
I'm the, let's say, the 

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terrified postgraduate student 
preparing for the Gujarat 

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University anesthesiology exams.
I've got my Miller, my Gaiden, 

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and my Stolting stacked right 
here. 

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Good. 
The topic is reflexes relevant 

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to anesthesia practice and 
specifically we're talking about

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the ones that kill the Bazol. 
Jairus reflex is the main event,

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but we'll hit the ocular 
cardiac, the Cushing, all of 

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them. 
This is high stakes Physiology, 

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so Doctors setup's great. 
Let's begin part 8, introduction

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and exam framing. 
Understood. 

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Let's do it all. 
Right. 

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Don't give me a dictionary 
definition. 

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In the context of our practice 
anesthesia, what is a 

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physiological reflex? 
OK, so a physiological reflex 

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is, well, it's basically an 
autonomic stimulus response 

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loop. 
It's the body's hardwired 

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attempt to maintain homeostasis.
A loop. 

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OK, yeah. 
And for the exam, I know I need 

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to be able to identify the four 
key components. 

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A sensor or receptor that 
detects a change, then an effort

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pathway that carries the to the 
CNSA central integrator, which 

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is usually the brain stem or 
medulla, and then finally the 

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efferent pathway that triggers 
an effective organ. 

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Fine, that's first year 
Physiology. 

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Yeah. 
Now tell me why I, as a senior 

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anesthetist, actually care about
this? 

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Why is this a question that 
comes up again and again in the 

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MD exams? 
Because, well, because 

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anesthesia is really the art of 
manipulating these reflexes. 

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We're either blunting them with 
our drugs or sometimes we 

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accidentally trigger them. 
And when we do, it's a disaster.

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These reflexes aren't just 
textbook trivia. 

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They are. 
I mean, they're the primary 

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cause of that sudden unexplained
intraoperative hemodynamic 

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collapse. 
Exactly the Oh my God, what's 

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happening moment, Yes. 
You can be cruising along in a 

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totally stable case, 
everything's perfect, and then 

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boom, assist alloy on the table.
Exactly. 

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Now in the Gudrat University 
exams and others, you're going 

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to see this in three places. 
First, the theory paper, write a

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short note on the Bizzle Geris 
reflex. 

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That's a classic 5 or 10 mark 
question, right? 

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Standard. 
Second, the OSCE station, you 

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might get a clinical scenario, 
you know, patient crashing 

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during eye surgery or maybe a 
shoulder Arthroscopy. 

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But the third place, that's the 
most dangerous, the Viva Viva, 

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the oral interrogation, right? 
I'll be sitting there and I'll 

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ask you, doctor, why did the 
heart rate drop? 

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And if you just say hypotension,
you fail. 

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It's an instant fail. 
Because it's not specific 

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enough. 
Not even close. 

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I'm looking for specific 
keywords. 

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I want to hear about the fibers,
the nuclei, the the paradox. 

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So with that in mind, let's dive
into the big one, Part B, the 

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bezel Gerish reflex. 
The BJR, the exam core, as you'd

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say. 
Absolutely. 

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So define it for me. 
I'm the examiner, I'm looking at

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my watch. 
Go. 

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The Bezel Gerish reflex is a a 
cardio inhibitory reflex. 

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The gold standard definition, 
the one from Miller's 

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anesthesia, is a triad. 
You see three things happen at 

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once. 
Name them hypotension, 

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bradycardia and and coronary 
artery dilatation. 

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Stop right there. 
You said coronary artery 

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dilatation. 
Why'd you include that? 

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Right. 
Most students, they forget that 

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last one. 
They just say hypotension and 

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bradycardia. 
Because that part, that's the 

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key to the whole 
cardioprotective theory. 

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It's what distinguishes the BJR 
from just a simple, you know, 

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vasovagal collapse. 
The dilation suggests the body 

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is actively trying to perfuse 
the myocardium even while it's 

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slowing everything else down. 
Good, you've read the big books,

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I can tell. 
Now give me the historical 

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context. 
Just briefly. 

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Examiners love it when you can 
drop a name or two. 

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OK, it was first described, I 
think, by von Bazold and Hurt 

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back in the 1860s, and then 
later clarified by Jerish. 

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But really, the key concept for 
the exam isn't the history, it's

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it's paradoxical nature. 
Explain that. 

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Why is it paradoxical? 
This is the aha man. 

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This is the whole point. 
It's paradoxical because it 

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completely contradicts the 
baroreceptor reflex. 

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I mean, normally if your blood 
pressure drops, the 

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baroreceptors in the carotid 
sinus and the aorta, they scream

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low pressure and the heart rate 
shoots up, you get tachycardia 

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to try and restore cardiac 
output. 

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That's the normal logical 
defense, right? 

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Your body hits the gas pedal. 
Exactly. 

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But with the BJR, the patient is
hypotensive, but instead of 

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speeding up, the heart slams on 
the brakes. 

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The rate plummets. 
You get a profound bradycardia 

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right in the face of 
hypotension. 

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It fundamentally works against 
the body's immediate attempt to 

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maintain its own perfusion 
pressure. 

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Precisely. 
It's a reflex that seems on the 

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surface to be sabotaging this 
systemic circulation. 

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Yeah, it makes no sense, which 
is why you need to understand 

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the mechanism. 
So let's get granular Section 3 

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receptors and pathway. 
Where are the sensors? 

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And don't just say the heart. 
OK. 

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Specifically, they are 
mechanoreceptors and 

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chemoreceptors located within 
the left ventricular wall. 

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Be more specific, which part of 
the wall? 

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Primarily the infer posterior 
wall of the left ventricle. 

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Correct. 
Now how does the signal get from

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that spot in the ventricle up to
the brain? 

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This is the specific phrase I 
have on my checklist. 

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I'm waiting for it. 
The signal travels via the vagus

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nerve, but specifically it's 
carried along unmyelinated vagal

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A front type C fibers. 
Boom, there it is, unmyelinated 

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C fibers. 
If you say those 3 words in the 

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Viva, I can take a box. 
I know you understand the 

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Physiology. 
Why does it matter that they're 

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unmyelinated? 
Well, unmyelinated fibers 

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usually imply a slower, more 
visceral type of transmission. 

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It's not like sharp pain or 
somatic sensation. 

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This is it's a deep distress 
signal. 

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Correct. 
So this distress signal travels 

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up the C fibers to the nucleus 
tractus solitarius, the NTS in 

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the medulla. 
And then what happens? 

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The NTS gets that signal and it 
it triggers a massive autonomic 

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shift, it cranks up the 
parasympathetic tone. 

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So the vagus nerve just hammers 
the SA node, which causes the 

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bradycardia, right? 
And at the exact same time it 

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causes a complete withdrawal of 
sympathetic tone from the blood 

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vessels. 
It causes. 

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Massive peripheral vasodilation.
The vessels all go floppy, blood

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pools in the periphery, so you 
end up with this slow heart 

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trying to pump into a completely
dilated, boggy system. 

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That's why the pressure crashes 
so profoundly. 

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And the coronary dilation you 
mentioned earlier? 

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That's part of the same process,
a mix of sympathetic withdrawal 

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and some direct vagal effects 
right on the coronary bed 

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itself. 
OK, you've nailed the mechanism,

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but the bigger question is why 
evolution usually doesn't design

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suicide switches. 
Miller talks about a theory for 

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the purpose of this reflex Why 
would the body want to shut the 

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heart down when the pressure is 
already dangerously low? 

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It's that hemorrhagic 
hibernation idea, or the 

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cardioprotective theory. 
The logic is that if the heart 

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is either ischemic or running on
empty, beating faster is 

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actually the most dangerous 
thing it can do. 

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Go on. 
Tachycardia just consumes a 

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massive amount of oxygen. 
If you're running on fumes, 

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sprinting is what's going to 
kill the engine for good. 

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Exactly so the BJR. 
The BJR acts like a circuit 

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breaker. 
It senses that extreme stress, 

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the ischemia or the violent 
squeezing of an empty chamber, 

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and it forces the heart to slow 
down. 

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It's basically screaming stop 
conserving of energy, dilate the

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coronaries, and just try to 
survive this insult. 

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So it sacrifices the system to 
save the organ. 

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Precisely, it sacrifices the 
systemic blood pressure to save 

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the heart muscle itself. 
A desperate last ditch effort. 

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Brilliant description. 
It sacrifices the Organism to 

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save the organ. 
You might also see apnea 

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mentioned in some textbooks, 
usually in animal models. 

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But let's be clear, in clinical 
practice, it's the hemodynamic 

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collapse that kills the patient.
Right. 

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Our focus is always on the 
circulation. 

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Now let's move to the most 
important part for us, Section 

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5, triggers and clinical 
scenarios. 

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This is where you earn your MDI.
Don't care about rats in the 

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lab? 
I care about the patient on my 

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operating table. 
When do we actually see this 

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reflex? 
The Interscalen Block, Miller 

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and Morgan are just full of 
warnings about this one, 

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specifically when the surgery is
done in the beach chair or 

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sitting position. 
Walk me through it step by step.

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Why does a numb shoulder lead to
a cardiac arrest? 

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It's the perfect storm. 
First you put the patient in a 

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sitting position. 
Gravity immediately pulls blood 

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down into the legs. 
You get venous pooling, so 

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venous return to the heart 
starts to drop, so the left 

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ventricle becomes underfilled. 
At the same time, the patient is

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usually awake or just lightly 
sedated. 

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They might be anxious so they 
have a high background 

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sympathetic tone. 
Adrenaline is flowing. 

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The heart is being told to beat 
hard and fast. 

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But the chamber is empty. 
Exactly. 

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It's hypercontractility against 
an empty chamber. 

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The ventricular walls are 
literally squeezing and rubbing 

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against each other. 
The mechanoreceptors embedded in

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the wall get crushed and 
squeezed. 

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And they misinterpret that 
signal. 

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Completely. 
They sense this violent 

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squeezing and they think, wow, 
the pressure in here must be 

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astronomical, even though the 
volume is critically low. 

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So they fire the C fibers. 
They fire the afferent loop. 

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The brain gets a false signal 
that the blood pressure is 

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dangerously high. 
So what does it do? 

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It triggers the BJR to lower the
pressure. 

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And the result. 
Massive vagal outflow. 

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The heart rate drops to 30, then
20, then a systole lights out. 

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And that right there is the 
empty heart theory. 

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The Mccanna receptors are 
tricked by the empty squeeze. 

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Now this brings us to the 
absolute favorite topic of the 

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Gujarat University examiners. 
It's a guaranteed question. 

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BJR in spinal anesthesia? 
Yes. 

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This is the big trap. 
I know this one. 

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It's a trap because it looks 
exactly like something else. 

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So I'll give you the scenario. 
You're the resident on call. 

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You give a spinal for a hip 
fracture. 

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The level comes up to T6. 
It's a perfect block. 

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Hemodynamics are rock solid. 
You relax. 

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You start filling out the chart 
20 minutes later. 

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Not immediately, but 20 minutes 
later. 

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The monitor alarms Heart rate 
40, blood pressure 60 / 30. 

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What happened? 
The knee jerk answer. 

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The wrong answer is high spinal.
And why is that the wrong 

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answer? 
Because a true high spinal where

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you've actually blocked the 
cardio accelerator fibers at T1 

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00:10:38,640 --> 00:10:41,880
to T4, that usually happens 
early as the block is setting up

233
00:10:42,640 --> 00:10:45,360
and the mechanism there is just 
a passive loss of synthetic 

234
00:10:45,360 --> 00:10:46,960
push. 
The heart slows down because 

235
00:10:46,960 --> 00:10:50,840
it's gas pedal has been cut off.
Correct, but in our scenario it 

236
00:10:50,840 --> 00:10:53,800
happened 20 minutes later. 
The key is the delay. 

237
00:10:53,880 --> 00:10:57,440
That's the signature of the BJR.
The spinal anesthetic caused 

238
00:10:57,440 --> 00:11:00,280
profound vasodilation in the 
legs in the abdomen. 

239
00:11:00,840 --> 00:11:03,760
Over those 20 minutes, blood 
just slowly pooled. 

240
00:11:04,520 --> 00:11:06,680
The central blood volume dropped
and dropped. 

241
00:11:06,680 --> 00:11:09,640
The ventricle got emptier and 
emptier until eventually it 

242
00:11:09,640 --> 00:11:11,600
crossed a critical threshold. 
The empty heart. 

243
00:11:11,600 --> 00:11:13,960
Threshold. 
Yes, the McCann receptors fired 

244
00:11:13,960 --> 00:11:15,960
and the vagus nerve attacked the
heart. 

245
00:11:16,120 --> 00:11:18,720
The vagus nerve attacked. 
I like that phrasing. 

246
00:11:18,880 --> 00:11:20,960
It implies an active aggressive 
process. 

247
00:11:21,480 --> 00:11:24,000
In a high spinal, the 
sympathetic system is simply 

248
00:11:24,000 --> 00:11:26,960
asleep. 
In the BJR, the parasympathetic 

249
00:11:26,960 --> 00:11:28,640
system is wide awake and 
aggressive. 

250
00:11:29,160 --> 00:11:31,520
That is the core distinction you
must make to pass the Viva. 

251
00:11:31,640 --> 00:11:35,560
So if the examiner asks, is the 
bradycardia in spinal anesthesia

252
00:11:35,560 --> 00:11:39,160
only due to a sympathetic block,
the answer is a hard no. 

253
00:11:39,160 --> 00:11:42,320
It's a combination, and in a 
delayed arrest it is almost 

254
00:11:42,320 --> 00:11:44,280
certainly the BJR. 
Exactly. 

255
00:11:44,440 --> 00:11:46,920
Now you've diagnosed it. 
Section 7 management. 

256
00:11:47,320 --> 00:11:48,720
You're the anesthetist in the 
room. 

257
00:11:48,840 --> 00:11:51,080
The patient is crashing. 
What do you do? 

258
00:11:51,280 --> 00:11:52,920
Don't give me a long list. 
Give me protocol. 

259
00:11:52,920 --> 00:11:56,080
OK, identify and act first. 
I know this isn't just simple 

260
00:11:56,080 --> 00:12:00,760
hypotension, this is a collapse.
So step one, restore preload 

261
00:12:00,960 --> 00:12:02,400
immediately. 
Get their legs up. 

262
00:12:02,440 --> 00:12:05,240
If they're in a beach chair, you
dump the bed flat as fast as you

263
00:12:05,240 --> 00:12:07,160
can. 
I have to fill that empty heart 

264
00:12:07,160 --> 00:12:08,920
to stop the mechanoreceptors 
from firing. 

265
00:12:08,920 --> 00:12:10,320
That's the root cause. 
Good. 

266
00:12:10,400 --> 00:12:11,920
What's next? 
Step 2. 

267
00:12:13,440 --> 00:12:16,640
Fluids open the IV wide. 
You have to treat the volume 

268
00:12:16,640 --> 00:12:18,560
deficit that started this whole 
cascade. 

269
00:12:18,560 --> 00:12:19,520
OK. 
And drugs. 

270
00:12:19,520 --> 00:12:22,200
Drugs, yes, atropine or 
glycopyrlate. 

271
00:12:22,480 --> 00:12:25,240
I need to block that efrain 
vagal limb that's going to deal 

272
00:12:25,240 --> 00:12:28,400
with the bradycardia. 
But the heart rate is 30, the BP

273
00:12:28,400 --> 00:12:30,720
is 50. 
Systolic atropine isn't working 

274
00:12:30,720 --> 00:12:33,200
fast enough. 
What is the drug of choice 

275
00:12:33,200 --> 00:12:35,800
according to Stolting in a 
severe collapse? 

276
00:12:35,800 --> 00:12:38,680
In a severe collapse, it's 
epinephrine adrenaline. 

277
00:12:38,840 --> 00:12:41,040
Why not ephedrine? 
We use ephedrine for spinal 

278
00:12:41,040 --> 00:12:44,080
hypotension all the time. 
Because ephedrine is an indirect

279
00:12:44,080 --> 00:12:47,560
act agent, it works by making 
your own nerve endings release 

280
00:12:47,560 --> 00:12:51,520
norepanifrin. 
But in a severe BJR or a high 

281
00:12:51,520 --> 00:12:55,440
spinal, the sympathetic system 
is already completely shut down 

282
00:12:55,440 --> 00:12:58,560
or exhausted. 
There's no norepinephrine left 

283
00:12:58,560 --> 00:13:00,240
to squeeze out. 
So it's useless. 

284
00:13:00,400 --> 00:13:02,480
Right, you need a direct 
agonist. 

285
00:13:03,000 --> 00:13:06,160
Epinephrine hits the alpha and 
beta receptors directly. 

286
00:13:06,160 --> 00:13:09,080
It completely bypasses the 
dysfunctional nerve ending, 

287
00:13:09,080 --> 00:13:11,280
correct? 
Do not tickle the patient with 

288
00:13:11,280 --> 00:13:15,520
ephedrine if they are dying. 
You give small repeated boluses 

289
00:13:15,520 --> 00:13:18,600
of epinephrine, it restores the 
vascular tone and it directly 

290
00:13:18,600 --> 00:13:20,920
kicks the heart rate up. 
And what about prevention? 

291
00:13:21,160 --> 00:13:24,400
Prevention is everything so Co 
loading you have to be 

292
00:13:24,400 --> 00:13:27,080
aggressive with hydration before
or during the block. 

293
00:13:27,400 --> 00:13:30,040
The key is to never let the 
heart get empty in the 1st place

294
00:13:30,280 --> 00:13:33,800
and be incredibly careful with 
sitting positions, especially in

295
00:13:33,800 --> 00:13:35,320
patients who might be 
dehydrated. 

296
00:13:35,520 --> 00:13:37,680
Very good. 
You pass the BJR station. 

297
00:13:37,920 --> 00:13:40,360
You know, the triad, the C 
fibers, the paradox, and the 

298
00:13:40,360 --> 00:13:42,920
management. 
But the exam isn't over. 

299
00:13:42,920 --> 00:13:45,520
Let's move to part C. 
Other important reflexes. 

300
00:13:45,520 --> 00:13:48,640
We can't ignore them. 
Let's start with the I the 

301
00:13:48,760 --> 00:13:53,840
ocular cardiac reflex OCR. 
Ah, the five and dime reflex. 

302
00:13:53,840 --> 00:13:56,200
And what do we call it that? 
It's just a mnemonic for the 

303
00:13:56,200 --> 00:13:57,560
cranial nerves that are 
involved. 

304
00:13:57,560 --> 00:13:59,840
The afferent limb is the 
trigeminal nerve. 

305
00:13:59,840 --> 00:14:05,000
That's cranial nerve 5 V and the
effort limb is the vagus nerve, 

306
00:14:05,000 --> 00:14:07,680
cranial nerve 10X5 and. 
Diamond. 

307
00:14:07,680 --> 00:14:10,160
It's acute mnemonic, but I'm an 
examiner who likes details. 

308
00:14:10,280 --> 00:14:13,320
Trace the path for me. 
OK, the stimulus is traction on 

309
00:14:13,320 --> 00:14:15,920
the extra ocular muscles. 
The books say the medial rectus 

310
00:14:15,920 --> 00:14:20,040
is the most potent trigger or 
direct pressure on the globe, 

311
00:14:20,040 --> 00:14:22,560
like during a retrobulbar block 
or from trauma. 

312
00:14:22,560 --> 00:14:25,040
And the signal goes where. 
The signal travels down the 

313
00:14:25,040 --> 00:14:27,320
optomic division of the 
trigeminal nerve to the 

314
00:14:27,320 --> 00:14:29,160
Gasserian ganglion. 
Keep going. 

315
00:14:29,280 --> 00:14:30,840
Where does it connect in the 
brain stem? 

316
00:14:31,080 --> 00:14:33,760
From there it goes to the main 
sensory nucleus of the 

317
00:14:33,760 --> 00:14:36,560
trigeminal nerve, which is in 
the floor of the 4th ventricle. 

318
00:14:36,920 --> 00:14:39,560
Yao and Artuzio is very specific
about that point. 

319
00:14:39,880 --> 00:14:43,680
Then it jumps across through 
interneurons to the vagomotor 

320
00:14:43,680 --> 00:14:45,080
nucleus. 
And the result of all that 

321
00:14:45,080 --> 00:14:48,160
wiring? 
Immediate profound bradycardia 

322
00:14:48,480 --> 00:14:50,400
or worse. 
You can see AV block, 

323
00:14:50,560 --> 00:14:53,320
ventricular ectopye, or it can 
go straight to a systole. 

324
00:14:53,320 --> 00:14:56,240
It's like a light switch. 
If the surgeon pulls the muscle,

325
00:14:56,240 --> 00:14:59,280
the heart stops. 
They let go, it starts again. 

326
00:14:59,320 --> 00:15:01,880
Which brings us to management. 
What is the very first thing you

327
00:15:01,880 --> 00:15:04,520
say in that situation? 
Stop, I tell the surgeon. 

328
00:15:04,720 --> 00:15:07,200
Stop traction. 
Let go of the muscle. 

329
00:15:07,560 --> 00:15:10,360
That is the single most 
effective treatment. 9 times out

330
00:15:10,360 --> 00:15:12,280
of 10, the rhythm returns 
immediately. 

331
00:15:12,360 --> 00:15:14,280
And if it keeps happening every 
time they pull? 

332
00:15:14,400 --> 00:15:16,320
Then I need to reassess my 
anesthetic. 

333
00:15:16,480 --> 00:15:20,120
First I check my depth light 
anesthesia makes this reflex 

334
00:15:20,120 --> 00:15:22,520
much worse. 
Then I check for hypoxia and 

335
00:15:22,520 --> 00:15:24,920
hypercarbia. 
Both of those things will 

336
00:15:24,920 --> 00:15:27,320
sensitize the heart to this 
vagal reflex. 

337
00:15:27,800 --> 00:15:30,200
And if everything is perfect, 
deep and aesthetic, good 

338
00:15:30,200 --> 00:15:33,360
ventilation and it's still 
happening, then I'll give a dose

339
00:15:33,360 --> 00:15:37,240
of atropine prophylactically. 
Good, now why do we see this so 

340
00:15:37,240 --> 00:15:40,440
much more in kids? 
Strabisma surgery is a classic 

341
00:15:40,440 --> 00:15:42,960
pediatric case. 
Because kids are vegatonic. 

342
00:15:43,000 --> 00:15:45,440
They're resting. 
Parasympathetic tone is just 

343
00:15:45,440 --> 00:15:48,840
much higher than in adults, and 
they really rely on their heart 

344
00:15:48,840 --> 00:15:52,400
rate for their cardiac output, 
so for them a sudden drop in 

345
00:15:52,400 --> 00:15:54,640
rate is hemodynamically 
devastating. 

346
00:15:54,680 --> 00:15:56,800
Very true. 
Now, briefly, what about the 

347
00:15:56,800 --> 00:16:00,120
variance mentioned in section 9?
Ocular Pulmonary. 

348
00:16:00,360 --> 00:16:02,600
Ocular gas. 
Right, it's the same trigger 

349
00:16:02,600 --> 00:16:06,000
traction on the eye muscles, but
the vagal output instead of just

350
00:16:06,120 --> 00:16:08,560
going to the heart, also goes to
the lungs, causing 

351
00:16:08,560 --> 00:16:12,080
bronchoconstriction, or to the 
stomach causing hypermotility 

352
00:16:12,080 --> 00:16:13,920
and nausea. 
And the clinical relevance of 

353
00:16:13,920 --> 00:16:15,680
that. 
It helps explain why these kids 

354
00:16:15,680 --> 00:16:18,200
often wake up vomiting after 
strabisma surgery. 

355
00:16:18,200 --> 00:16:20,840
It's not just the opioids or the
anesthetic, it's the reflex 

356
00:16:20,840 --> 00:16:23,280
itself kicking the stomach and 
making them feel sick. 

357
00:16:23,280 --> 00:16:25,320
Excellent point. 
That's a distinction level 

358
00:16:25,320 --> 00:16:27,640
insight. 
Now let's move down the anatomy,

359
00:16:27,720 --> 00:16:30,320
the airway, the laryngo cardiac 
reflex. 

360
00:16:30,320 --> 00:16:32,880
This is our bread and butter. 
This is laryngoscopy and 

361
00:16:32,880 --> 00:16:34,320
intubation. 
What's the pathway? 

362
00:16:34,520 --> 00:16:38,160
The afferent is the Vegas or the
glossopharyngeal nerve from 

363
00:16:38,160 --> 00:16:40,440
direct irritation of the larynx 
or the trachea. 

364
00:16:40,680 --> 00:16:43,040
The efferent again is the Vegas 
and the result? 

365
00:16:43,120 --> 00:16:47,000
Bradycardia and hypotension. 
Again, Miller really emphasizes 

366
00:16:47,000 --> 00:16:50,480
this is a pediatric issue. 
In adults, we usually see the 

367
00:16:50,480 --> 00:16:53,040
opposite, right? 
We see a huge sympathetic surge 

368
00:16:53,040 --> 00:16:56,880
from the pain of intubation. 
We get tachycardia and 

369
00:16:56,880 --> 00:16:58,640
hypertension. 
But in a baby? 

370
00:16:58,680 --> 00:17:02,120
But in a neonate, if you're too 
aggressive with the laryngoscope

371
00:17:02,120 --> 00:17:04,720
blade, they will Brady down on 
you in a second. 

372
00:17:04,920 --> 00:17:07,599
Which is why we used to 
premedicate all children with 

373
00:17:07,599 --> 00:17:10,560
atropine before induction. 
We don't do it routinely 

374
00:17:10,560 --> 00:17:13,359
anymore, but that knowledge is 
always in the back of our minds.

375
00:17:13,760 --> 00:17:17,839
What is the absolute number one 
rule for pediatric bradycardia? 

376
00:17:17,920 --> 00:17:20,480
Hypoxia until proven otherwise. 
See you again. 

377
00:17:20,720 --> 00:17:23,240
If a child has bradycardia, it 
is hypoxia. 

378
00:17:23,240 --> 00:17:25,400
Period. 
It's not the reflex, it's not 

379
00:17:25,400 --> 00:17:28,800
the drug, it's lack of oxygen. 
Check the tube position, check 

380
00:17:28,800 --> 00:17:32,160
the circuit, check their color. 
Only after you have definitively

381
00:17:32,160 --> 00:17:34,880
ruled out hypoxia can you start 
blaming a reflex. 

382
00:17:34,880 --> 00:17:38,960
Yeah, never, ever forget that. 
Now let's move to the neck, the 

383
00:17:38,960 --> 00:17:41,840
carotid sinus reflex. 
OK, this is a pure bear receptor

384
00:17:41,840 --> 00:17:43,600
reflex. 
Where are the sensors? 

385
00:17:43,800 --> 00:17:46,680
They're in the carotid sinus, 
which is a little bulge right at

386
00:17:46,680 --> 00:17:49,080
the bifurcation of the internal 
carotid artery. 

387
00:17:49,280 --> 00:17:51,400
They're stretch receptors. 
In the avrin nerve. 

388
00:17:51,560 --> 00:17:54,680
It's Herring's nerve, which is a
branch of the glossopharyngeal 

389
00:17:54,680 --> 00:17:55,720
cranial nerve. 
IX. 

390
00:17:56,240 --> 00:17:59,520
Good name. 
Drop Herring's nerve and the 

391
00:17:59,520 --> 00:18:02,160
response it generates. 
Well, its job is to regulate 

392
00:18:02,160 --> 00:18:05,520
blood pressure second by second.
If the systemic pressure is 

393
00:18:05,520 --> 00:18:08,840
high, the sinus stretches, 
herrings, nerve fires. 

394
00:18:09,400 --> 00:18:12,400
The brain then inhibits the 
vasoconstrictor center and 

395
00:18:12,400 --> 00:18:16,080
excites the vagal center. 
The result is vasodilation and 

396
00:18:16,080 --> 00:18:18,080
bradycardia to bring the 
pressure back down. 

397
00:18:18,240 --> 00:18:19,600
And the clinical relevance for 
us? 

398
00:18:19,600 --> 00:18:22,560
Neck surgery, especially carotid
indoorterectomy. 

399
00:18:22,840 --> 00:18:25,600
If the surgeon is dissecting 
around that carotid bifurcation,

400
00:18:25,600 --> 00:18:28,000
they can put pressure on the 
sinus and trick it into thinking

401
00:18:28,000 --> 00:18:31,520
the pressure is 2100 and boom, 
boom, sudden profound 

402
00:18:31,520 --> 00:18:35,280
hypotension and bradycardia. 
Also, Miller makes a point that 

403
00:18:35,280 --> 00:18:38,960
our volatile anesthetics like 
isoflurine actually depress this

404
00:18:38,960 --> 00:18:41,560
reflex. 
So under general anesthesia, 

405
00:18:41,560 --> 00:18:44,360
patients can't compensate for 
blood pressure swings as well as

406
00:18:44,360 --> 00:18:46,120
they can when they're awake. 
Correct. 

407
00:18:46,960 --> 00:18:48,680
OK, now let's go inside the 
skull. 

408
00:18:49,080 --> 00:18:52,360
The Cushing reflex. 
This one is the Grim Reaper of 

409
00:18:52,360 --> 00:18:54,480
reflexes. 
Yeah, this is a sign of 

410
00:18:54,480 --> 00:18:57,240
impending doom. 
It's the body's last ditch 

411
00:18:57,240 --> 00:19:00,840
physiological response to 
dangerously high intracranial 

412
00:19:00,840 --> 00:19:02,800
pressure. 
Give me the triad, the Cushing 

413
00:19:02,800 --> 00:19:05,640
triad. 
Hypertension, bradycardia, and 

414
00:19:05,640 --> 00:19:08,000
irregular respiration. 
Walk me through the mechanism. 

415
00:19:08,240 --> 00:19:10,560
Why on earth does the blood 
pressure skyrocket? 

416
00:19:10,600 --> 00:19:14,080
OK, so you have a bleed or a 
tumor or swelling inside the 

417
00:19:14,080 --> 00:19:16,880
skull. 
The ICP starts to rise of 

418
00:19:16,960 --> 00:19:19,200
essentially the pressure inside 
the skull gets higher than the 

419
00:19:19,200 --> 00:19:23,000
mean arterial pressure. 
The blood vessels inside the 

420
00:19:23,000 --> 00:19:25,760
brain get squashed flat. 
So blood can't get in. 

421
00:19:26,000 --> 00:19:28,160
Exactly. 
The brain starts to suffocate. 

422
00:19:28,160 --> 00:19:31,400
Cerebral ischemia. 
The brain stem is starving for 

423
00:19:31,400 --> 00:19:32,800
oxygen. 
And the brain panics. 

424
00:19:32,800 --> 00:19:35,560
It absolutely panics. 
It activates what Guyton calls 

425
00:19:35,560 --> 00:19:38,640
the CNS ischemic response. 
It initiates a massive, 

426
00:19:38,640 --> 00:19:41,560
overwhelming sympathetic outflow
to the entire body. 

427
00:19:42,080 --> 00:19:44,720
It clamps down on every 
peripheral blood vessel it can 

428
00:19:44,720 --> 00:19:46,880
find. 
It's trying to force the system 

429
00:19:47,120 --> 00:19:49,880
blood pressure up to make it 
higher than the intracranial 

430
00:19:49,880 --> 00:19:52,720
pressure. 
It's a brute force attempt to 

431
00:19:52,720 --> 00:19:55,560
restore its own blood flow. 
That's what causes the severe 

432
00:19:55,560 --> 00:19:57,360
hypertension. 
OK, that explains the 

433
00:19:57,360 --> 00:20:00,040
hypertension, but why the 
bradycardia? 

434
00:20:00,440 --> 00:20:03,080
Because the bear receptors in 
the aorta and the carotid are 

435
00:20:03,080 --> 00:20:06,080
still sitting there doing their 
job, they see the systemic blood

436
00:20:06,080 --> 00:20:10,600
pressure hit 2/21/20 and they 
scream way too high and they try

437
00:20:10,600 --> 00:20:13,520
to lower it by slowing the heart
down via the vagus nerve. 

438
00:20:13,680 --> 00:20:15,320
So you get this physiological 
war. 

439
00:20:15,400 --> 00:20:18,000
Exactly. 
The brain Brain is desperately 

440
00:20:18,000 --> 00:20:20,800
trying to drive the pressure up 
to save itself, and the body's 

441
00:20:20,800 --> 00:20:23,920
baroreceptors are desperately 
trying to bring it down to save 

442
00:20:23,920 --> 00:20:26,720
the system. 
The bradycardia is the result of

443
00:20:26,720 --> 00:20:29,000
that conflict. 
A terrible, futile war. 

444
00:20:29,680 --> 00:20:33,280
If you see this triad in a head 
trauma patient in the ER, what 

445
00:20:33,280 --> 00:20:35,520
does it mean? 
It means herniation is imminent,

446
00:20:35,520 --> 00:20:38,880
the brain stem is being crushed.
You need to hyperventilate them,

447
00:20:38,880 --> 00:20:41,720
give them manitol, call the 
neurosurgeon and get them to 

448
00:20:41,720 --> 00:20:44,480
drill a hole immediately. 
It is a true neurosurgical 

449
00:20:44,480 --> 00:20:46,280
emergency. 
OK, one last quick one. 

450
00:20:46,520 --> 00:20:48,840
The vagavogal reflex. 
This one's simple. 

451
00:20:48,840 --> 00:20:52,080
Vegas in, Vegas out. 
Usually peritoneal stretching. 

452
00:20:52,080 --> 00:20:54,920
The classic example is the 
insufflation of gas during 

453
00:20:54,920 --> 00:20:57,040
laparoscopy. 
The surgeon inflates the 

454
00:20:57,040 --> 00:20:59,160
abdomen, the peritonium gets 
stretched. 

455
00:20:59,360 --> 00:21:02,520
That sends a signal up the Vegas
and the heart slows down. 

456
00:21:02,520 --> 00:21:04,960
Simple enough. 
Now, Doctor, we're moving into 

457
00:21:04,960 --> 00:21:06,960
Part D comparison and 
integration. 

458
00:21:07,280 --> 00:21:10,360
This is where I separate the 
past students from the gold 

459
00:21:10,360 --> 00:21:12,840
medalists. 
I want you to visualize a table 

460
00:21:12,840 --> 00:21:14,400
in your mind. 
OK, I'm visualizing it. 

461
00:21:14,640 --> 00:21:17,880
Column one is the stimulus, 
column two is the response. 

462
00:21:18,120 --> 00:21:23,120
I want you to compare 3 reflexes
for me, BJR, the Bear receptor 

463
00:21:23,120 --> 00:21:25,360
reflex and the Bainbridge 
reflex. 

464
00:21:25,720 --> 00:21:27,760
The Bainbridge reflex. 
OK, that's the tricky. 

465
00:21:27,760 --> 00:21:29,880
One it is to find it first. 
We haven't touched on it yet. 

466
00:21:30,080 --> 00:21:33,040
The Bainbridge reflex is 
essentially the reverse of the 

467
00:21:33,040 --> 00:21:35,280
BJR. 
It's triggered not by low 

468
00:21:35,280 --> 00:21:38,840
volume, but by high volume. 
It's the stretch receptors in 

469
00:21:38,840 --> 00:21:41,840
the Atria that sense that the 
heart is being overfilled. 

470
00:21:41,840 --> 00:21:43,240
What's the response to that 
overfilling? 

471
00:21:43,960 --> 00:21:46,320
Tachycardia. 
The heart speeds up to try and 

472
00:21:46,320 --> 00:21:49,240
pump that extra fluid forward. 
It's a mechanism to prevent 

473
00:21:49,240 --> 00:21:51,600
blood from damming up in the 
venous system. 

474
00:21:51,600 --> 00:21:53,520
Good, so let's build that table 
biz. 

475
00:21:53,520 --> 00:21:57,680
Old gerish reflex stimulus is 
low volume. 

476
00:21:57,880 --> 00:22:01,960
The empty heart response is 
bradycardia now. 

477
00:22:02,280 --> 00:22:05,800
Bainbridge reflex stimulus. 
High volume and overfilled 

478
00:22:05,800 --> 00:22:07,320
heart. 
Response. 

479
00:22:07,360 --> 00:22:08,640
Tachycardia. 
Good. 

480
00:22:08,760 --> 00:22:10,800
Now boroceptor reflex stimulus 
is what? 

481
00:22:10,880 --> 00:22:13,440
Stimulus is a change in 
pressure, not volume, so let's 

482
00:22:13,440 --> 00:22:15,520
say low pressure. 
And the response to low 

483
00:22:15,520 --> 00:22:16,640
pressure. 
Tachycardia. 

484
00:22:16,640 --> 00:22:18,360
Excellent. 
Now synthesize that for me. 

485
00:22:18,360 --> 00:22:19,520
This is where it gets really 
interesting. 

486
00:22:19,600 --> 00:22:22,680
Let's say I start to hemorrhage.
I have a low volume and low 

487
00:22:22,680 --> 00:22:25,400
pressure. 
Which reflex wins? 

488
00:22:25,480 --> 00:22:28,840
This is the cool part initially 
as you bleed the bearer 

489
00:22:28,840 --> 00:22:30,160
receptor. 
Reflex wins. 

490
00:22:30,600 --> 00:22:33,600
The drop in pressure causes a 
compensatory tachycardia. 

491
00:22:33,880 --> 00:22:36,560
That's what we see first. 
But if the hemorrhage is severe 

492
00:22:36,560 --> 00:22:39,480
enough, if the volume loss 
becomes so critical that the 

493
00:22:39,480 --> 00:22:42,920
ventricle starts to run empty 
and the BJR takes over, it 

494
00:22:42,920 --> 00:22:45,360
overrides the baroreceptor 
reflex and the heart rate 

495
00:22:45,360 --> 00:22:47,600
suddenly crashes. 
That's the terminal event. 

496
00:22:47,760 --> 00:22:50,520
Brilliant synthesis. 
They're opposing forces and the 

497
00:22:50,520 --> 00:22:52,840
BJR is the last desperate one to
fire. 

498
00:22:54,040 --> 00:22:56,240
Now a final Viva question for 
this section. 

499
00:22:56,280 --> 00:22:59,360
A structured answer please. 
Doctor, you're in the OR. 

500
00:22:59,360 --> 00:23:02,720
Your patient's heart rate is 40.
List the differential diagnosis.

501
00:23:02,720 --> 00:23:04,520
Don't just ramble. 
Give me categories, OK? 

502
00:23:04,800 --> 00:23:07,120
I would use the examiner safe 
structure. 

503
00:23:07,200 --> 00:23:09,800
My category. 
My categories would be good 11 

504
00:23:09,920 --> 00:23:12,800
Reflex mediated. 
Is the surgeon pulling on the 

505
00:23:13,080 --> 00:23:16,200
eye OCR? 
Is the abdomen being insufflated

506
00:23:16,200 --> 00:23:20,120
vagovigal or is the heart empty 
from bleeding or venous bowling 

507
00:23:20,240 --> 00:23:23,440
BJR? 
Good category 2. 2 drug induced 

508
00:23:23,440 --> 00:23:26,600
did I just give a big bolus of 
fentanyl or Remi fentanyl? 

509
00:23:26,840 --> 00:23:29,080
Did I give a high dose of 
exmitotomidine? 

510
00:23:29,240 --> 00:23:31,240
Did I repeat a dose of 
succinylcholine? 

511
00:23:31,240 --> 00:23:34,080
Especially in a child. 
Excellent category 3. 3 

512
00:23:34,080 --> 00:23:37,240
Physiological and at the top of 
this list always is hypoxia, 

513
00:23:37,240 --> 00:23:41,160
especially in a child, then a 
high spinal blocking T1T4. 

514
00:23:41,200 --> 00:23:44,240
And the last one. 4 Surgical Is 
the surgeon physically 

515
00:23:44,240 --> 00:23:46,640
manipulating or compressing the 
vagus nerve in the neck or 

516
00:23:46,640 --> 00:23:48,240
chest? 
Direct stimulation. 

517
00:23:48,440 --> 00:23:51,880
That is a rock solid, safe and 
comprehensive answer. 

518
00:23:52,400 --> 00:23:53,880
It covers the common and the 
deadly. 

519
00:23:54,560 --> 00:23:56,800
Now Part E final exam 
integration. 

520
00:23:56,800 --> 00:23:58,840
Let's quickly review the common 
Viva traps. 

521
00:23:58,960 --> 00:24:03,400
Trap number one, I ask you, why 
did the patient arrest after the

522
00:24:03,400 --> 00:24:05,600
spinal was working perfectly for
20 minutes? 

523
00:24:06,040 --> 00:24:09,440
The answer is it's the BJR 
triggered by progressive venous 

524
00:24:09,440 --> 00:24:11,200
pooling leading to the empty 
heart state. 

525
00:24:11,520 --> 00:24:14,600
The delay is the clue. 
Perfect trap #2 is the 

526
00:24:14,600 --> 00:24:17,760
bradycardia seen in spinal 
anesthesia only due to the 

527
00:24:17,760 --> 00:24:20,120
sympathetic blockade. 
Answer No. 

528
00:24:20,440 --> 00:24:24,200
It is a combination of the 
direct sympathetic block at T1T4

529
00:24:24,200 --> 00:24:28,120
if the spinal is high and D the 
active reflex vagal activity 

530
00:24:28,120 --> 00:24:30,440
from the BJR if venous return is
poor. 

531
00:24:30,560 --> 00:24:32,000
Exactly. 
Trap number 3A. 

532
00:24:32,000 --> 00:24:34,720
More subtle one. 
How does the Valsalva maneuver 

533
00:24:34,720 --> 00:24:36,600
relate to all this? 
Miller mentions this. 

534
00:24:37,080 --> 00:24:40,320
A sustained Valsalva maneuver 
increases intrathoracic pressure

535
00:24:40,320 --> 00:24:43,280
which dramatically decreases 
venous return, so it can mimic 

536
00:24:43,280 --> 00:24:46,520
the empty heart Physiology and 
trigger similar baroreceptor and

537
00:24:46,520 --> 00:24:48,440
BJR like changes. 
Very good. 

538
00:24:48,440 --> 00:24:49,880
You're anticipating the 
curveballs now. 

539
00:24:49,880 --> 00:24:52,560
Section 17 diagrams. 
You have 10 minutes left in your

540
00:24:52,560 --> 00:24:54,360
theory paper. 
You need to draw the BJR 

541
00:24:54,360 --> 00:24:55,720
pathway. 
What do you put on the paper? 

542
00:24:55,960 --> 00:24:58,160
OK, simple as best. 
I draw a heart. 

543
00:24:58,600 --> 00:25:02,080
I labeled the left ventricle and
right mechanoreceptor schema 

544
00:25:02,080 --> 00:25:04,520
receptors on the infer posterior
wall. 

545
00:25:05,120 --> 00:25:07,880
From there I draw a line going 
up to the brain stem. 

546
00:25:08,080 --> 00:25:11,840
I label that line unmyelinated C
fibers afferent. 

547
00:25:11,880 --> 00:25:14,360
Keywords. 
Good in the brain stem I draw a 

548
00:25:14,360 --> 00:25:18,600
box and label it NTS in medulla.
Then I draw 2 lines coming out. 

549
00:25:18,600 --> 00:25:21,560
One goes back to the hearts 
essay node and I label it vagus 

550
00:25:21,560 --> 00:25:23,960
nerve vadycardia. 
The other line goes to the 

551
00:25:23,960 --> 00:25:26,920
peripheral blood vessels, and I 
label it sympathetic withdrawal,

552
00:25:27,120 --> 00:25:29,840
vasodilation, hypotension. 
And at the bottom. 

553
00:25:30,040 --> 00:25:33,320
At the bottom I write the triad 
in big bold letters. 

554
00:25:33,560 --> 00:25:36,440
Hypotension, Bradycardia, 
Coronary dilation. 

555
00:25:36,880 --> 00:25:38,920
Perfect. 
A clear, simple diagram like 

556
00:25:38,920 --> 00:25:41,200
that is worth 1000 words of 
messy handwriting. 

557
00:25:41,520 --> 00:25:43,960
So let's summarize this entire 
deep dive give you the final 

558
00:25:43,960 --> 00:25:46,560
take home exam points. 
This is the CHEAT SHEET you read

559
00:25:46,560 --> 00:25:48,120
right before you walk into the 
exam hall. 

560
00:25:48,120 --> 00:25:51,640
OK, the high yield recap. 
BJR definition is the triad 

561
00:25:52,040 --> 00:25:54,840
hypotension plus bradycardia 
plus coronary dilation. 

562
00:25:55,080 --> 00:25:57,520
Receptors are in the left 
ventricle, specifically the 

563
00:25:57,520 --> 00:26:00,600
inferior wall. 
Afrin pathway is unmyelinated. 

564
00:26:00,600 --> 00:26:04,640
C fibers say it over and over. 
Key triggers inferior wall MI, 

565
00:26:04,640 --> 00:26:07,600
the interscaling block in the 
sitting position, and spinal 

566
00:26:07,600 --> 00:26:09,520
anesthesia causing an empty 
heart. 

567
00:26:09,560 --> 00:26:11,720
Good. 
Keep going. 5 The spinal 

568
00:26:11,720 --> 00:26:14,640
mechanism is not just a 
sympathetic block, it's an 

569
00:26:14,640 --> 00:26:17,520
active vagal reflex due to an 
empty ventricle. 

570
00:26:17,600 --> 00:26:22,320
Treatment fluids first, preload 
is king, then epinephrine as the

571
00:26:22,320 --> 00:26:25,240
drug of choice for collapse. 
Atropine for the vagal 

572
00:26:25,240 --> 00:26:28,040
component. 
OCR triggered by traction on the

573
00:26:28,040 --> 00:26:31,040
medial rectus cranial nerve 5 
inches 10 out. 

574
00:26:31,720 --> 00:26:33,680
First action is to tell the 
surgeon to stop. 

575
00:26:33,760 --> 00:26:37,400
Cushing's triad. 
High ICP leads to high BP and 

576
00:26:37,400 --> 00:26:39,480
low heart rate. 
It's a sign of impending 

577
00:26:39,480 --> 00:26:41,600
herniation. 
Bainbridge is the opposite of 

578
00:26:41,600 --> 00:26:43,440
BJR. 
High volume leads to 

579
00:26:43,440 --> 00:26:44,880
tachycardia. 
You're ready. 

580
00:26:45,000 --> 00:26:46,720
That is a distinction level 
performance. 

581
00:26:46,720 --> 00:26:49,240
You didn't just memorize the 
names of the reflexes, you 

582
00:26:49,240 --> 00:26:51,520
understood the logic of the 
sensors in the pathways. 

583
00:26:51,520 --> 00:26:53,640
Thank you professor. 
Honestly, it feels less like 

584
00:26:53,640 --> 00:26:56,800
some terrifying magic now and 
more more like plumbing and 

585
00:26:56,800 --> 00:26:58,520
wiring. 
That is precisely what 

586
00:26:58,520 --> 00:27:01,240
anaesthesia is. 
It's applied Physiology in real 

587
00:27:01,240 --> 00:27:03,760
time. 
These reflexes, you see, they 

588
00:27:03,760 --> 00:27:06,440
aren't actually trying to kill 
the patient, they're trying to 

589
00:27:06,440 --> 00:27:08,640
save them, just in a very 
primitive way. 

590
00:27:08,640 --> 00:27:11,720
The BJR tries to save the heart 
muscle from ischemia. 

591
00:27:12,040 --> 00:27:15,040
The Cushing reflex tries to save
the brain from starvation. 

592
00:27:15,160 --> 00:27:18,080
But in the highly artificial 
environment of the operating 

593
00:27:18,080 --> 00:27:21,000
room, those primitive survival 
attempts can be lethal. 

594
00:27:21,120 --> 00:27:22,600
Correct. 
Which brings us to our 

595
00:27:22,600 --> 00:27:23,960
philosophical outro. 
Right. 

596
00:27:24,440 --> 00:27:27,680
We spend our entire careers 
fighting these reflexes. 

597
00:27:28,280 --> 00:27:31,320
The BJR is nature's way of 
saying the heart is tired and 

598
00:27:31,320 --> 00:27:33,840
ischemic, let it rest. 
And we come in and say 

599
00:27:33,840 --> 00:27:36,960
absolutely not, you're going to 
pump harder and here's a syringe

600
00:27:36,960 --> 00:27:38,360
full of adrenaline to make you 
do it. 

601
00:27:38,560 --> 00:27:40,840
It is a fundamental paradox of 
our specialty. 

602
00:27:40,840 --> 00:27:43,280
So the provocative question for 
you, the listener, to think 

603
00:27:43,280 --> 00:27:46,760
about is this. 
If the Bezel Jarish Reflex is an

604
00:27:46,760 --> 00:27:49,800
evolutionary masterpiece 
perfected over millions of years

605
00:27:49,800 --> 00:27:53,200
to protect a dying heart, are we
arrogant to so aggressively 

606
00:27:53,200 --> 00:27:55,320
abolish it? 
Or is the operating room a 

607
00:27:55,320 --> 00:27:57,920
unique place in the universe 
where the laws of nature and 

608
00:27:57,920 --> 00:28:00,280
evolution are suspended by the 
tip of a needle? 

609
00:28:00,360 --> 00:28:03,520
That is a fine question for the 
coffee room after the case, but 

610
00:28:03,520 --> 00:28:07,000
for the exam, treat the 
hypertension, save the patient 

611
00:28:07,000 --> 00:28:08,160
on the table. 
Deal. 

612
00:28:08,520 --> 00:28:11,320
Treat the patient first, pass 
the exam and then debate the 

613
00:28:11,320 --> 00:28:13,600
philosophy later. 
Good luck to everyone sitting 

614
00:28:13,600 --> 00:28:17,280
for the Gujarat University MD 
exams and any other anesthesia 

615
00:28:17,280 --> 00:28:19,920
exam. 
Keep your heads cool and your 

616
00:28:19,920 --> 00:28:22,800
atropine and epinephrine ready. 
Thanks for listening to this 

617
00:28:22,800 --> 00:28:24,280
deep dive. 
We'll see you next time.

