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Welcome back to the Deep Dive. 
Today we are stripping away the 

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safety net. 
We aren't just exploring a 

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topic, we are entering a 
simulation. 

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That's right, today the stakes 
are significantly higher than 

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usual. 
I want you to visualize this. 

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You are an MD, anesthesiology 
postgraduate student. 

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You're sitting in the hot seat. 
It's the final practical exam 

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for Gujarat University. 
The air conditioning is humming,

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your palms are sweating, and the
external examiner is, you know, 

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staring at you over the rim of 
his glasses. 

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The case on the table is 
bronchial asthma. 

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And I'm stepping into the role 
of that senior faculty member. 

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I'm the internal examiner 
sitting next to you. 

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My job today isn't just to teach
you the facts, It's to guide you

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through the minefield. 
I'm here to point out the traps 

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that fail candidates and the 
precise gold medal answers that 

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distinguish the consultants from
the students. 

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Our mission is to take this 
massive stack of source 

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material. 
We've compiled standard texts 

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like Miller, Morgan and McHale 
Gaytan for Physiology, 

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Harrison's for medicine, Robbins
for pathology, and KD Tripathi 

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for pharmacology and distilled 
them into a single, cohesive, 

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exam winning narrative. 
We're really covering the full 

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spectrum here. 
Oh. 

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Yeah, from the cellular level of
inflammation right up to the 

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terrifying silence of a status 
asthmatic. 

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His chest in the ICU. 
Precisely. 

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But I have to issue a disclaimer
before we begin. 

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This is an exam preparation deep
dive. 

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We are basing our discussions 
strictly on the provided source 

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texts. 
We all know clinical guidelines 

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evolve rapidly, but in the exam 
hall, these standard texts are 

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your Bible. 
So answer according to the book.

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Answer according to the book, 
unless you have a landmark paper

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in your back pocket to justify a
deviation. 

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Understood. 
Let's set the stage then. 

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The exam usually begins with 
definitions. 

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It sounds simple, but I've seen 
students stumble right out of 

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the gate. 
We aren't just talking about 

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asthma yet. 
We're starting with the umbrella

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category, Section 1, 
introduction to obstructive lung

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diseases. 
How do we frame this for the 

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examiners to show we understand 
the physics of it? 

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Right. 
If the examiner asks what is 

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obstructive lung disease, do not
just list diseases. 

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That's a classic mistake. 
You must focus on the 

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physiological defect. 
The core concept is flow 

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limitation. 
These are diseases characterized

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by an increase in resistance to 
airflow due to partial or 

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complete obstruction at any 
level of the tracheobronchial 

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tree. 
So the problem isn't getting air

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in. 
Exactly. 

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It's getting air out. 
And Robbins is very specific 

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about the classification. 
Here we refer to the BIG4. 

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Yes. 
In pathology, the big four are 

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emphysema, chronic bronchitis, 
asthma, and Bronchiectasis. 

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You should list these 
confidently. 

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It shows you've read beyond just
the anesthesia texts. 

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But here is the pivot point for 
the anesthesiologist and 

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specifically for this exam 
topic. 

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We need to distinguish asthma 
from the rest, particularly from

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COPD. 
What is the single most 

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important discriminator? 
The magic word is reversibility.

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This is an exam tip right off 
the bat. 

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If you say asthma is airway 
obstruction, you're only half 

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right. 
You must say it is reversible 

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airway obstruction. 
So that's the keyword 

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reversible. 
Absolutely. 

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COPD, which is a clinical 
syndrome often comprising 

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emphysema and chronic 
bronchitis, is characterized by 

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persistent airflow limitation 
that is not fully reversible. 

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So conceptualizing this for the 
Viva, asthma is a dynamic state.

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The airway clamps down, but it 
can open up again. 

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COPD is more of a fixed 
structural change. 

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That's a perfect way to put it, 
and you need to be precise with 

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the definition of asthma itself.
It's not just wheezing. 

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That's a symptom, not a 
definition. 

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OK, so what's the full 
definition we should be giving? 

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Bronchial asthma is a chronic 
inflammatory disorder of the 

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Airways. 
This chronic inflammation causes

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airway hyper responsiveness that
leads to recurrent episodes of 

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wheezing, breathlessness, chest 
tightness and coughing, 

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particularly at night or in the 
early morning. 

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You've used two key terms there,
inflammation and hyper 

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responsiveness, if we need to 
unpack. 

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Those we will. 
They're central to everything. 

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But first, let's touch on the 
epidemiology. 

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Why does this matter to us as 
anesthesiologists? 

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Is it just background noise or 
is there a real safety 

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implication? 
It's a massive safety issue. 

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I mean the global burden is 
around 300 million people. 

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It is likely the most common 
pulmonary comorbidity you will 

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encounter in your day-to-day 
practice. 

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So we're going to see it all the
time. 

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All the time. 
And Miller explicitly points out

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that about 9% of asthmatics may 
develop bronchospasm 

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perioperatively. 9% That's 
nearly one in 10. 

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That is a statistically 
significant risk for every 

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single list we run. 
Correct. 

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And intraoperative bronchospasm 
isn't a minor annoying it's not 

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just a bitter wheezing. 
In severe cases, it leads to 

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inability to ventilate, severe 
hypoxia, and potentially brain 

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damage or death. 
So this can be a true anesthetic

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catastrophe. 
It can be, and you also need to 

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be attuned to the concept of the
silent chest, which signifies 

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obstructions so severe that air 
movement is minimal. 

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If you're waiting for a wheeze 
to diagnose severity, you might 

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miss the patient who is about to
arrest. 

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That is a terrifying concept to 
Silent Chest. 

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We will absolutely drill down 
into that later. 

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But first, let's look at the 
exam paper itself. 

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If I'm the student, what kind of
questions am I anticipating? 

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You will see patterns for short 
notes. 

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They love mechanism based 
questions like pathophysiology 

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of asthma or equipment based 
ones like capnography and 

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bronchospasm. 
OK, short and focus. 

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Exactly for the long 10 to 20 
mark questions, expect a high 

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stakes clinical scenario. 
Discuss the anesthetic 

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management of a case of status 
asthmaticus for emergency 

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surgery. 
The nightmare scenario. 

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The one that tests everything. 
And for the Viva or OSCE, be 

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ready to interpret flow volume 
loops or arterial blood gases on

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the spot. 
OK, let's tackle that first 

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short note topic, Section 2, the
pathophysiological basis of 

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asthma. 
This is the core of the exam, 

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isn't it? 
If you don't understand the 

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pathology, you can't justify 
your pharmacological choices 

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later. 
Absolutely. 

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The most common mistake students
make is thinking asthma is just 

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bronchospasm, just muscle 
tightening. 

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It's not. 
It is fundamentally a disease of

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chronic airway inflammation. 
So the muscle spasm is just the 

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symptom, the disease is the 
angry inflamed tissue 

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underneath. 
Exactly. 

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Even when the patient is 
asymptomatic, walking around 

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feeling fine, their airway is 
infiltrated with mast cells, 

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eosinophils, and T lymphocytes. 
This chronic state leads to what

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we call airway remodeling. 
Remodeling sounds like a 

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construction project, but in 
this context I assume it's 

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destructive. 
It is maladaptive. 

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It's the body trying to repair 
pair itself but doing a bad job.

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We see thickening of the sub 
basement membrane, hypertrophy 

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of the smooth muscle, and 
hyperplasia of the mucus glands.

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So the airway is literally 
changing its structure for the 

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work. 
Precisely this structural change

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makes the airway hyper 
responsive. 

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Define hyper responsiveness for 
me in an exam context. 

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Yeah. 
How do I explain that to a 

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junior colleague? 
It is the tendency of the 

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Airways to narrow excessively in
response to triggers that 

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wouldn't affect a normal person.
A little bit of cold air, a 

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specific or the mechanical touch
of a laryngoscope blade that you

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or I would ignore causes a 
massive disproportionate 

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reaction in an asthmatic A. 
Real overreaction of the area. 

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A huge overreaction and then we 
have the mucus. 

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This isn't just normal 
secretions, is it? 

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No, not at all. 
The mucus plugging in asthma is 

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nasty. 
It's thick, tenacious, and 

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incredibly difficult to suction.
Pathology texts like Robbins 

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describes specific microscopic 
findings within this mucus. 

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Oh, this sounds like bonus 
points territory. 

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It is. 
You have Kirchman spirals, which

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are these little whirls of shed 
epithelium, and charcoal Leiden 

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crystals which are composed of 
Eucenophil proteins. 

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Those sound like incredible 
buzzwords for a pathology 

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question. 
They are gold medal details. 

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Dropping charcoal Leiden 
crystals into your answer tells 

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the examiner you've read the 
pathology text. 

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It's not just the anesthesia 
summary. 

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OK, so Kirchman's spirals and 
charcoal Leiden crystals, but 

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what's the anesthetic relevance?
The clinical relevance is this, 

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that inflammation makes the 
airway incredibly twitchy. 

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Instrumentation like putting in 
an endotracheal tube is a potent

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trigger. 
You are essentially poking an 

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angry bear. 
An excellent analogy. 

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Moving on to Section 3, 
immunological mechanisms, this 

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is often labeled as exam gold. 
We need to understand the 

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mechanism to understand the 
drugs we use. 

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You need to know that it is 
predominantly an IG mediated 

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hypersensitivity or type 
hypersensitivity. 

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Walk us through the cellular 
level. 

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Who are the players? 
The star of the show is the mast

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cell. 
Think of them as Sentinel cells 

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embedded in the submucosa, just 
waiting exactly in an atopic 

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individual, someone prone to 
allergies. 

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These cells are coated with Ige 
antibodies. 

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When an antigen, say pollen or a
specific drug binds to that Ige,

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it causes crosslinking. 
And crosslinking acts as the 

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trigger, like turning a key in a
lock. 

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A perfect analogy. 
It triggers degranulation. 

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The mast cell essentially 
explodes, releasing a cocktail 

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of preformed inflammatory 
mediators. 

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The big one, of course, is 
histamine. 

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Which causes the immediate 
reaction we see on the table, 

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the wheezing, the pressure 
going. 

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Up right histamine causes rapid 
bronchoconstriction and mucosal 

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edema. 
That's the early phase, but you 

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also have the synthesis of new 
mediators like the leukotrienes,

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which were formerly known as the
slow reacting substance of 

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anaphylaxis. 
That's a great piece of medical 

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trivia. 
Slow reacting substance of 

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anaphylaxis. 
It is, and it tells you what it 

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does. 
Leukotrienes cause prolonged, 

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sustained bronchospasm. 
They are much more potent and 

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longer lasting than histamine. 
OK. 

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So that's the immediate problem,
but you mentioned early versus 

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late phase reactions. 
Yes. 

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And this is a crucial conceptual
leap for the anesthesiologist, 

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the early versus late phase 
reaction. 

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Why is this so clinically 
relevant for us? 

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The early phase happens in 
minutes. 

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That's the immediate 
bronchospasm you fight during 

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induction, but the late phase 
happens 2 to 8 hours later. 

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This is caused by the 
recruitment of inflammatory 

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cells like neutrophils and 
eosinophils into the Airways. 

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So. 
A patient could have a reaction 

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in the OT, You stabilize them, 
everything looks good, you send 

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them to the ward and then. 
And then six hours later in the 

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pay CU or on the floor they 
deteriorate. 

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They might look fine initially 
but crash post op because of 

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this late phase inflammatory 
bloom. 

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That is a Viva trap right there.
Yeah. 

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Why did the patient deteriorate 
in the PCU despite a smooth 

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emergence? 
Exactly, if you can answer late 

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phase reaction due to 
inflammatory cell recruitment 

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you get full marks. 
It shows you're thinking beyond 

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the immediate crisis. 
Now let's connect this to 

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Section 4 effects on lung 
mechanics. 

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We talked about flow limitation.
When the Airways narrow, what 

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happens to resistance? 
It's skyrockets and for the exam

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you need to quote Kwizu's law. 
Oh, physics. 

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OK. 
It's simple but powerful. 

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Resistance is inversely 
proportional to the radius to 

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00:10:42,040 --> 00:10:44,320
the power of 4. 
For laminar flow, the. 

235
00:10:44,360 --> 00:10:46,800
Power of four. 
Let's do the math on that if the

236
00:10:46,800 --> 00:10:49,880
radius is halved. 
The resistance increases 16 

237
00:10:49,880 --> 00:10:52,640
fold. 
It's not a linear relationship, 

238
00:10:52,680 --> 00:10:55,520
it's exponential. 16 times 
harder to breathe. 

239
00:10:55,600 --> 00:10:58,720
Exactly. 
And if flow becomes turbulent, 

240
00:10:58,720 --> 00:11:01,960
which it often does in narrowed 
Airways, the dependence is on 

241
00:11:01,960 --> 00:11:05,800
the radius to the power of 5. 
This explains why breathing 

242
00:11:05,800 --> 00:11:07,520
becomes such incredibly hard 
work. 

243
00:11:07,800 --> 00:11:10,280
The patient has to generate 
massive negative pressure to 

244
00:11:10,280 --> 00:11:13,560
pull air in and massive positive
pressure to push it out. 

245
00:11:13,680 --> 00:11:16,680
And specifically, expiration is 
affected more than inspiration, 

246
00:11:16,680 --> 00:11:17,600
correct? 
Why is that? 

247
00:11:17,760 --> 00:11:20,520
Yes, inspiration is an active 
process. 

248
00:11:20,680 --> 00:11:23,600
The chest wall expands and pulls
the Airways open through 

249
00:11:23,600 --> 00:11:25,160
something called radial 
traction. 

250
00:11:25,360 --> 00:11:27,320
Expiration, however, is normally
passive. 

251
00:11:27,680 --> 00:11:30,720
As the lung empties, the Airways
naturally narrow a bit. 

252
00:11:31,080 --> 00:11:33,640
In asthma, this natural 
narrowing combined with the 

253
00:11:33,640 --> 00:11:36,800
pathology, the swelling, the 
mucus, the spasm leads to 

254
00:11:36,800 --> 00:11:39,160
premature airway closure. 
So the air gets trapped. 

255
00:11:39,360 --> 00:11:42,880
The air gets trapped. 
And this brings us to a critical

256
00:11:42,880 --> 00:11:47,560
concept, dynamic hyperinflation 
or what we call auto peep. 

257
00:11:47,800 --> 00:11:50,880
Let's unpack auto peep. 
This is the term we hear in the 

258
00:11:50,880 --> 00:11:54,160
ICU all the time, but explaining
it physically can be tricky. 

259
00:11:54,600 --> 00:11:57,040
Imagine breathing in through a 
very thin straw. 

260
00:11:57,400 --> 00:11:59,480
It's hard. 
Now imagine trying to breathe 

261
00:11:59,560 --> 00:12:02,080
out through that same straw, but
before you have finished 

262
00:12:02,080 --> 00:12:05,160
exhaling, you are forced to take
another breath in. 

263
00:12:05,280 --> 00:12:07,880
I'd still have air left in my 
lungs from the first breath. 

264
00:12:07,880 --> 00:12:09,680
I wouldn't have time to empty 
them completely. 

265
00:12:09,680 --> 00:12:11,960
Exactly. 
Air goes in, but it cannot get 

266
00:12:11,960 --> 00:12:14,000
out completely before the next 
breath starts. 

267
00:12:14,080 --> 00:12:17,080
This is air trapping. 
The lungs get bigger and bigger 

268
00:12:17,080 --> 00:12:19,160
with each breath. 
The functional residual 

269
00:12:19,160 --> 00:12:21,920
capacity, or FRC just keeps 
rising. 

270
00:12:21,920 --> 00:12:24,520
It sounds like it would increase
pressure inside the chest quite 

271
00:12:24,520 --> 00:12:25,480
a bit. 
It does. 

272
00:12:25,560 --> 00:12:27,600
It increases intrathoracic 
pressure. 

273
00:12:27,960 --> 00:12:29,680
Now think about the 
hemodynamics. 

274
00:12:29,760 --> 00:12:32,800
What does high intrathoracic 
pressure do to the heart? 

275
00:12:33,120 --> 00:12:37,040
It acts like a tamponade. 
It squashes the great veins, 

276
00:12:37,400 --> 00:12:39,560
reducing venous return to the 
right heart. 

277
00:12:39,840 --> 00:12:43,120
Correct, it decreases venous 
return which decreases preload 

278
00:12:43,240 --> 00:12:47,520
which leads to hypotension. 
So here is the clinical Pearl. 

279
00:12:47,880 --> 00:12:50,240
If you are ventilating an 
asthmatic and their blood 

280
00:12:50,240 --> 00:12:53,440
pressure suddenly drops, you 
must immediately think of auto 

281
00:12:53,440 --> 00:12:55,840
peep. 
And the fix isn't fluids or 

282
00:12:55,840 --> 00:12:58,680
pressors initially. 
No, the immediate fix is to 

283
00:12:58,680 --> 00:13:02,640
treat the cause the trapped air.
You disconnect the ventilator 

284
00:13:02,640 --> 00:13:06,040
from the endotracheal tube, you 
allow a long apnea period. 

285
00:13:06,400 --> 00:13:09,280
You might even gently push on 
the chest to help them exhale 

286
00:13:09,280 --> 00:13:11,400
that trapped gas. 
What happens when you do that? 

287
00:13:11,440 --> 00:13:14,000
You will hear a long hiss of air
escaping and you'll see the 

288
00:13:14,000 --> 00:13:15,440
blood pressure come right back 
up. 

289
00:13:15,480 --> 00:13:18,480
It's dramatic and life saving. 
That's a practical save a life 

290
00:13:18,480 --> 00:13:20,920
tip disconnect and let them 
exhale. 

291
00:13:21,560 --> 00:13:24,760
Now Section 5 clinical features 
of asthma. 

292
00:13:24,760 --> 00:13:27,800
We know the classic triad, 
dyspnea, cough, wheezing, but 

293
00:13:27,800 --> 00:13:29,960
you mentioned the silent chest 
earlier. 

294
00:13:29,960 --> 00:13:32,280
Yes. 
In the exam, they will ask, is 

295
00:13:32,280 --> 00:13:34,280
the loudness of the wheeze a 
sign of severity? 

296
00:13:34,440 --> 00:13:37,720
The answer is an emphatic NO. 
Explain why that seems 

297
00:13:37,720 --> 00:13:40,520
counterintuitive. 
Because to make a wheeze, which 

298
00:13:40,520 --> 00:13:43,600
is a musical sound produced by 
turbulent flow through a narrow 

299
00:13:43,600 --> 00:13:47,520
tube, you need airflow. 
In severe obstruction there is 

300
00:13:47,520 --> 00:13:50,440
so little air moving that there 
is no sand generation. 

301
00:13:50,800 --> 00:13:54,400
A silent chest in a distressed 
tachypneic patient is a pre 

302
00:13:54,400 --> 00:13:56,760
terminal sign. 
So silence is worse than noise. 

303
00:13:56,760 --> 00:13:59,960
Silence is terrifying. 
It means imminent respiratory 

304
00:13:59,960 --> 00:14:02,240
arrest. 
What about triggers? 

305
00:14:02,600 --> 00:14:05,160
We know about pollen and dust. 
What about drugs? 

306
00:14:05,720 --> 00:14:07,440
This is crucial for our history 
taking. 

307
00:14:07,520 --> 00:14:10,160
Aspirin and other NSIS are 
classic triggers. 

308
00:14:10,360 --> 00:14:13,560
About 1% to 5% of asthmatics are
sensitive. 

309
00:14:13,880 --> 00:14:16,280
This is sometimes known as 
Sampter's triad, which is 

310
00:14:16,280 --> 00:14:18,680
asthma. 
Aspirin sensitivity in nasal 

311
00:14:18,680 --> 00:14:20,600
polyps. 
What is the mechanism there? 

312
00:14:20,600 --> 00:14:23,640
It's not IG E mediated is it? 
No, it's not a true allergy. 

313
00:14:23,640 --> 00:14:27,280
It's biochemical. 
Nsiis inhibit the cyclooxygenase

314
00:14:27,280 --> 00:14:30,160
or Cox enzyme. 
This blocks the production of 

315
00:14:30,160 --> 00:14:32,440
prostaglandins. 
However, the arachidonic acid 

316
00:14:32,440 --> 00:14:34,680
precursor has to go somewhere. 
So it gets diverted. 

317
00:14:34,720 --> 00:14:37,040
It gets shunted down the 
lipoxygenase pathway. 

318
00:14:37,040 --> 00:14:40,000
Which produces more? 
Leukotrienes and as we know from

319
00:14:40,000 --> 00:14:42,520
our earlier discussion, 
leukotrienes cause potent 

320
00:14:42,520 --> 00:14:46,360
prolonged bronchospasm. 
So as a rule, avoid Toradol or 

321
00:14:46,360 --> 00:14:49,320
diclofenac in these patients 
unless you are absolutely 

322
00:14:49,320 --> 00:14:51,080
certain they are not aspirin 
sensitive. 

323
00:14:51,160 --> 00:14:54,520
In any asthmatic with a history 
of nasal polyps or known aspirin

324
00:14:54,520 --> 00:14:56,280
sensitivity, absolutely avoid 
them. 

325
00:14:56,360 --> 00:14:58,680
It's not worth the risk. 
Let's talk investigations, 

326
00:14:58,680 --> 00:15:01,760
Section 6, pulmonary function 
tests, or PFTS. 

327
00:15:01,800 --> 00:15:04,520
This is absolutely essential for
the exam. 

328
00:15:04,640 --> 00:15:06,720
You must know the spiromet 
findings cold. 

329
00:15:06,800 --> 00:15:09,880
The hallmark of any obstructive 
disease is a reduction in FEV 

330
00:15:09,920 --> 00:15:12,440
one the forced expiratory volume
in one second. 

331
00:15:12,960 --> 00:15:15,840
The flow is slow. 
And the FVC, the forced vital 

332
00:15:15,840 --> 00:15:18,360
capacity, the total amount of 
air they can blow out. 

333
00:15:18,840 --> 00:15:21,960
It's usually normal or might be 
slightly reduced due to the air 

334
00:15:21,960 --> 00:15:24,400
trapping we talked about. 
But the key number, the one the 

335
00:15:24,400 --> 00:15:28,080
examiner wants to hear, is the 
FEV 1 FVC ratio. 

336
00:15:28,400 --> 00:15:32,920
In asthma and COPD this ratio is
reduced, typically less than .7 

337
00:15:32,920 --> 00:15:35,720
or 70%. 
A normal person can blow out 

338
00:15:35,720 --> 00:15:37,720
most of their air in the first 
second and obstruct. 

339
00:15:37,720 --> 00:15:39,840
A person can't. 
And how do we prove it's asthma 

340
00:15:39,840 --> 00:15:43,960
and not COPD using just the PFT?
Reversibility testing. 

341
00:15:44,160 --> 00:15:46,560
This is the gold standard for 
diagnosis. 

342
00:15:47,080 --> 00:15:50,200
You do the spirometry, then you 
give a bronchodilator like 

343
00:15:50,200 --> 00:15:53,360
cellbutamol, wait 15 minutes and
repeat the test. 

344
00:15:53,680 --> 00:15:56,680
And what are we looking for? 
If the FEV 1 increases by more 

345
00:15:56,680 --> 00:15:59,960
than 12% ND more than 200 
milliliters from the baseline, 

346
00:16:00,120 --> 00:16:03,040
that is a positive test. 
It confirms reversible 

347
00:16:03,040 --> 00:16:04,960
obstruction, which is the 
hallmark of asthma. 

348
00:16:05,120 --> 00:16:07,800
OK, 12% and 200 milliliters. 
Got it. 

349
00:16:08,160 --> 00:16:11,040
Now for the visual learners, 
imagine the flow volume loop you

350
00:16:11,040 --> 00:16:12,480
are at the whiteboard and the 
Viva. 

351
00:16:12,520 --> 00:16:15,800
What are you drawing? 
You draw the axis with flow on 

352
00:16:15,800 --> 00:16:18,080
the axis and volume on the X 
axis. 

353
00:16:18,080 --> 00:16:20,440
You draw the inspiratory limb, 
which is usually a nice 

354
00:16:20,440 --> 00:16:22,720
symmetrical semicircle on the 
bottom. 

355
00:16:23,080 --> 00:16:25,160
Then you draw the expertory limb
on top. 

356
00:16:25,280 --> 00:16:27,640
And for asthma? 
The expertory limb looks scooped

357
00:16:27,640 --> 00:16:29,480
out. 
It has a concave appearance. 

358
00:16:29,480 --> 00:16:32,600
It starts with a sharp peak, but
then the flow drops off very 

359
00:16:32,600 --> 00:16:35,240
quickly and tails off as the 
Airways collapse. 

360
00:16:35,360 --> 00:16:38,360
Unlike A restrictive disease. 
Right, A restrictive disease 

361
00:16:38,360 --> 00:16:40,840
like pulmonary fibrosis looks 
like a witch's hat. 

362
00:16:41,120 --> 00:16:44,520
It's narrow because the volumes 
are small, but the is preserved 

363
00:16:44,760 --> 00:16:47,440
and it's tall because the flows 
can be high relative to the 

364
00:16:47,440 --> 00:16:49,480
volume. 
Obstructive is scooped out. 

365
00:16:49,840 --> 00:16:52,600
Section 7. 
ABG changes in asthma. 

366
00:16:52,800 --> 00:16:56,200
This is an exam favorite. 
How does the ABG change as an 

367
00:16:56,200 --> 00:16:58,640
asthma attack progresses from 
mild to severe? 

368
00:16:58,800 --> 00:17:02,320
This is a classic progression 
that you must know in early or 

369
00:17:02,320 --> 00:17:04,240
mild asthma, the patient is 
anxious. 

370
00:17:04,240 --> 00:17:06,240
They feel short of breath, so 
they hyperventilate. 

371
00:17:06,520 --> 00:17:09,280
They're breathing fast. 
So what happens to their CO2? 

372
00:17:09,359 --> 00:17:12,440
They blow it off. 
So hypocapnia, which leads to a 

373
00:17:12,440 --> 00:17:15,440
respiratory alkalosis. 
Correct and usually mild 

374
00:17:15,440 --> 00:17:17,599
hypoxemia because of some VQ 
mismatch. 

375
00:17:18,000 --> 00:17:20,480
Now, as the attack gets more 
severe and the patient gets 

376
00:17:20,480 --> 00:17:23,200
tired, remember breathing 
through a straw is exhausting 

377
00:17:23,200 --> 00:17:25,760
work, The respiratory muscles 
begin to fatigue. 

378
00:17:26,119 --> 00:17:29,120
The rate might stay high, but 
the tidal volume drops. 

379
00:17:29,320 --> 00:17:31,920
The CO2 starts to rise. 
It returns to normal. 

380
00:17:31,920 --> 00:17:35,400
Wait, normal CO2 sounds good? 
If I see a PECO 2 of 40 milli 

381
00:17:35,400 --> 00:17:37,440
milli HG on an ABG, I'm usually 
pretty. 

382
00:17:37,440 --> 00:17:37,800
Happy. 
No. 

383
00:17:37,920 --> 00:17:41,840
That is the trap. 
A normal Peco 2, say 35 to 45 

384
00:17:41,840 --> 00:17:45,480
milli milli HG in a tachypneic, 
panting, distressed, asthmatic 

385
00:17:45,480 --> 00:17:47,000
is a huge danger sign. 
Why? 

386
00:17:47,200 --> 00:17:49,720
It implies that they can no 
longer maintain the work of 

387
00:17:49,720 --> 00:17:51,480
breathing needed to clear the 
CO2. 

388
00:17:51,560 --> 00:17:53,240
They are tiring out. 
They are failing. 

389
00:17:53,240 --> 00:17:56,200
So if I see a normal CO2 two in 
a distressed asthmatic, I 

390
00:17:56,200 --> 00:17:58,040
shouldn't be reassured, I should
be worried. 

391
00:17:58,200 --> 00:18:00,200
You should be preparing for 
intubation. 

392
00:18:00,200 --> 00:18:02,560
It signals impending respiratory
failure. 

393
00:18:03,080 --> 00:18:07,040
The next stage is hypercapnia, a
high CO2 which causes a 

394
00:18:07,040 --> 00:18:09,960
respiratory acidosis and severe 
hypoxemia. 

395
00:18:10,240 --> 00:18:14,080
If you wait for the CO2 to be 
high, you have waited too long. 

396
00:18:14,360 --> 00:18:17,040
Let's move to Section 8, 
preoperative evaluation. 

397
00:18:17,840 --> 00:18:20,640
A patient comes to your clinic 
with a history of asthma, 

398
00:18:20,800 --> 00:18:23,360
scheduled for elective surgery. 
What are the high yield 

399
00:18:23,360 --> 00:18:25,760
questions? 
History is absolutely key. 

400
00:18:25,760 --> 00:18:27,840
You want to know the frequency 
of their inhaler use. 

401
00:18:27,840 --> 00:18:29,880
Are they using their rescue 
inhaler daily? 

402
00:18:30,040 --> 00:18:32,400
That's a bad sign. 
What else you need to know about

403
00:18:32,400 --> 00:18:33,920
their history of 
hospitalizations? 

404
00:18:33,920 --> 00:18:35,720
Have they ever been admitted for
asthma? 

405
00:18:35,720 --> 00:18:39,040
Ever been in the ICU? 
And the most critical question 

406
00:18:39,520 --> 00:18:42,200
Have they ever been intubated 
for their asthma? 

407
00:18:42,200 --> 00:18:44,360
Why is the intubation history so
important? 

408
00:18:44,400 --> 00:18:47,000
If they've been intubated for 
asthma before, they are by 

409
00:18:47,000 --> 00:18:50,240
definition a high risk patient. 
It suggests their disease is 

410
00:18:50,240 --> 00:18:52,720
capable of becoming life 
threatening very quickly. 

411
00:18:53,200 --> 00:18:57,080
Also ask about recent upper 
respiratory infections or Uris. 

412
00:18:57,080 --> 00:18:58,680
Common cold. 
Exactly. 

413
00:18:58,960 --> 00:19:02,240
A Uri increases airway 
reactivity for weeks. 

414
00:19:02,240 --> 00:19:04,920
Some texts say up to six weeks 
post infection. 

415
00:19:05,120 --> 00:19:07,480
That's a long time. 
If they have a cold, do we 

416
00:19:07,480 --> 00:19:10,240
cancel the surgery? 
For elective surgery, yes. 

417
00:19:10,320 --> 00:19:12,920
The rule of thumb is that 
elective surgery should be done 

418
00:19:12,920 --> 00:19:15,560
when the patient is at their 
baseline symptom free. 

419
00:19:15,840 --> 00:19:18,800
If they are actively wheezing in
the pre op Bay, you do not 

420
00:19:18,800 --> 00:19:22,280
induce, you postpone. 
If they had a Uri last week, you

421
00:19:22,280 --> 00:19:24,920
postpone if possible. 
What about smoking cessation? 

422
00:19:25,160 --> 00:19:26,800
Always a good idea, but what's 
the timeline? 

423
00:19:27,000 --> 00:19:29,680
The longer the better, ideally 4
to 8 weeks. 

424
00:19:30,360 --> 00:19:32,600
What if they stopped just 48 
hours before? 

425
00:19:33,040 --> 00:19:36,280
Does that do anything? 
It helps with carboxyhemoglobin 

426
00:19:36,280 --> 00:19:38,160
levels. 
It shifts the oxygen 

427
00:19:38,160 --> 00:19:41,800
dissociation curve back to the 
right, which improves oxygen 

428
00:19:41,800 --> 00:19:44,960
delivery to the tissues, but it 
doesn't do much for airway 

429
00:19:44,960 --> 00:19:49,120
reactivity or mucus claimants. 
In fact, sputum production might

430
00:19:49,120 --> 00:19:52,000
increase initially as the cilia 
start to wake up and clear out 

431
00:19:52,000 --> 00:19:54,280
the gunk. 
So 4 to 8 weeks is the real 

432
00:19:54,280 --> 00:19:57,600
target for pulmonary benefit. 
Yes, that's when you start to 

433
00:19:57,600 --> 00:20:00,960
see restoration of mucosciliary 
transport and a reduction in 

434
00:20:00,960 --> 00:20:04,840
post op pulmonary complications.
Let's look at Section 9, risk 

435
00:20:04,840 --> 00:20:06,800
stratification. 
How do we put all that 

436
00:20:06,800 --> 00:20:09,160
information together to decide 
who is going to have 

437
00:20:09,160 --> 00:20:12,600
bronchospasm on the table? 
The main predictors are a recent

438
00:20:12,640 --> 00:20:17,320
Uri as we just discussed, active
smoking and the type of surgery 

439
00:20:17,320 --> 00:20:20,040
and airway device. 
So instrumentation of the airway

440
00:20:20,040 --> 00:20:22,040
matters a lot. 
It's a huge factor. 

441
00:20:22,360 --> 00:20:27,200
An endotracheal tube ETT is much
more stimulating to the trachea 

442
00:20:27,200 --> 00:20:29,920
than a laryngeal mask, airway or
LMA. 

443
00:20:30,680 --> 00:20:33,760
Also be aware that well 
controlled asthma carries a risk

444
00:20:33,760 --> 00:20:36,120
that's pretty similar to non 
asthmatics. 

445
00:20:36,360 --> 00:20:39,440
It's the poorly controlled or 
symptomatic patient who is in 

446
00:20:39,440 --> 00:20:41,240
the danger zone. 
That leads us perfectly to 

447
00:20:41,240 --> 00:20:45,080
Section 10 choice of anesthesia.
If you have a choice, regional 

448
00:20:45,080 --> 00:20:47,920
anesthesia is the gold standard 
for an asthmatic patient. 

449
00:20:48,160 --> 00:20:49,480
Why? 
What's the advantage? 

450
00:20:49,480 --> 00:20:51,600
It's simple. 
You avoid putting a tube in the 

451
00:20:51,600 --> 00:20:53,840
trachea. 
You avoid that direct mechanical

452
00:20:53,840 --> 00:20:55,760
stimulation of the twitchy 
airway. 

453
00:20:55,920 --> 00:20:58,040
You bypass the main trigger 
entirely. 

454
00:20:58,160 --> 00:21:00,920
But there's a caveat, right? 
We can't just do a high spinal 

455
00:21:00,920 --> 00:21:02,240
block and relax. 
Correct. 

456
00:21:02,240 --> 00:21:05,160
You have to be careful. 
Avoid high blocks generally 

457
00:21:05,160 --> 00:21:08,760
above the T4 dermatome that 
might compromise the accessory 

458
00:21:08,760 --> 00:21:12,160
muscles of respiration, and 
asthmatic needs their 

459
00:21:12,160 --> 00:21:15,240
intercostals and abdominal 
muscles to actively exhale 

460
00:21:15,240 --> 00:21:17,640
against resistance. 
If you knock out their 

461
00:21:17,640 --> 00:21:21,080
intercostals with a high spinal,
they might feel dysmayic even if

462
00:21:21,080 --> 00:21:23,400
their oxygenation is perfectly 
fine. 

463
00:21:23,400 --> 00:21:26,200
But sometimes we have to do 
general anesthesia, laparoscopy 

464
00:21:26,200 --> 00:21:28,080
for instance, or major abdominal
surgery. 

465
00:21:28,120 --> 00:21:31,120
Right. 
And if you must do GA, the goal 

466
00:21:31,120 --> 00:21:34,360
is deep anesthesia. 
You need to completely suppress 

467
00:21:34,360 --> 00:21:37,360
those airway reflexes before you
touch the airway with a 

468
00:21:37,360 --> 00:21:40,600
laryngoscope or a tube. 
OK, let's talk about Section 11 

469
00:21:40,880 --> 00:21:43,600
premedication strategies. 
How do we set them up for 

470
00:21:43,600 --> 00:21:45,400
success before they even get to 
the OR? 

471
00:21:45,560 --> 00:21:47,840
First, anxiety triggers 
bronchospasm. 

472
00:21:48,360 --> 00:21:51,400
It's a physiological response 
via the parasympathetic system. 

473
00:21:51,400 --> 00:21:54,280
So anxiolysis with something 
like a small dose of midazolam 

474
00:21:54,320 --> 00:21:56,400
is very useful. 
And their inhalers, do they take

475
00:21:56,400 --> 00:21:59,360
them on the day of surgery? 
Absolutely, they should continue

476
00:21:59,360 --> 00:22:02,080
all their regular inhalers 
including their steroids and 

477
00:22:02,080 --> 00:22:04,800
long acting bronchodilators 
right up to the morning of 

478
00:22:04,800 --> 00:22:07,200
surgery. 
We often give a prophylactic 

479
00:22:07,200 --> 00:22:10,160
nebulization with cell butamol 
in the pre op area as well. 

480
00:22:10,160 --> 00:22:11,600
And. 
What about steroids? 

481
00:22:11,680 --> 00:22:13,480
The systemic ones. 
This is key. 

482
00:22:13,800 --> 00:22:17,480
If they are on chronic systemic 
steroids, their own adrenal axis

483
00:22:17,480 --> 00:22:20,240
is suppressed. 
You must give them a stress dose

484
00:22:20,240 --> 00:22:23,400
of steroids, usually 
hydrocortisone 100 milligram IV 

485
00:22:23,480 --> 00:22:26,200
at induction and then continue 
at post op and. 

486
00:22:26,280 --> 00:22:29,240
What if they're not on chronic 
steroids, but they're actively 

487
00:22:29,240 --> 00:22:31,040
wheezing before an urgent 
surgery? 

488
00:22:31,120 --> 00:22:33,920
In that case we might start a 
short course of oral steroids 

489
00:22:33,920 --> 00:22:37,040
for three to five days pre op to
really calm the inflammation 

490
00:22:37,040 --> 00:22:39,920
down before the surgery date. 
Now the moment of truth. 

491
00:22:40,360 --> 00:22:43,040
Section 12. 
Induction in airway management. 

492
00:22:43,520 --> 00:22:45,360
We want a smooth, gentle 
induction. 

493
00:22:45,360 --> 00:22:48,240
What drugs are we reaching for? 
Propofol is a great choice. 

494
00:22:48,320 --> 00:22:51,720
It has mild bronchodilating 
properties and it suppresses the

495
00:22:51,720 --> 00:22:54,800
laryngeal reflexes very well. 
It's a very smooth induction. 

496
00:22:54,800 --> 00:22:56,880
What about ketamine? 
I always hear about ketamine for

497
00:22:56,880 --> 00:22:59,320
asthmatics. 
Ketamine is the theoretical 

498
00:22:59,320 --> 00:23:02,160
exeriencer for the actively 
wheezing patient. 

499
00:23:02,600 --> 00:23:04,680
It is an excellent 
bronchodilator. 

500
00:23:05,080 --> 00:23:07,800
It works via a sympathomimetic 
action. 

501
00:23:08,320 --> 00:23:11,560
It increases circulating 
catecholamines, which relax the 

502
00:23:11,560 --> 00:23:14,960
bronchial smooth muscle. 
It's the agent of choice and a 

503
00:23:14,960 --> 00:23:17,960
hypotensive asthmatic or someone
in the middle of a severe 

504
00:23:17,960 --> 00:23:20,280
bronchospasm. 
Were there any downside to 

505
00:23:20,280 --> 00:23:23,120
ketamine? 
Yes, the big one is increased 

506
00:23:23,120 --> 00:23:25,440
secretions. 
You might need to give an 

507
00:23:25,440 --> 00:23:29,480
antisalagon like glycopyrrolate 
alongside it to keep the airway 

508
00:23:29,480 --> 00:23:31,080
dry. 
And what do we avoid for 

509
00:23:31,080 --> 00:23:33,360
induction? 
The classic one to avoid is 

510
00:23:33,520 --> 00:23:35,800
thiopentone. 
Historically it's associated 

511
00:23:35,800 --> 00:23:38,120
with histamine release in an 
exam. 

512
00:23:38,120 --> 00:23:41,040
If you suggest thiopentone for 
an asthmatic, you might get a 

513
00:23:41,040 --> 00:23:43,520
frown from the examiner. 
Even if the evidence is a bit 

514
00:23:43,520 --> 00:23:45,680
weak. 
Even then, why take the risk 

515
00:23:45,680 --> 00:23:48,280
when propofol exists? 
It's about choosing the safest 

516
00:23:48,280 --> 00:23:50,720
possible option. 
Airway device you mentioned an 

517
00:23:50,720 --> 00:23:53,480
LMA is better. 
An LMA sits above the glottis. 

518
00:23:53,480 --> 00:23:56,080
It doesn't stimulate the trachea
itself, so it is much less 

519
00:23:56,080 --> 00:23:59,120
stimulating and preferred if 
there is no contraindication 

520
00:23:59,120 --> 00:24:03,080
like a high risk of aspiration 
or if you need high ventilatory 

521
00:24:03,080 --> 00:24:05,320
pressures. 
But if we need an ETT for a lap 

522
00:24:05,320 --> 00:24:07,800
coal for example. 
Then you must ensure the patient

523
00:24:07,800 --> 00:24:10,040
is deep. 
I can't stress this enough. 

524
00:24:10,480 --> 00:24:14,080
Deep volatile anesthesia. 
Or you can use IV lidocaine, 

525
00:24:14,080 --> 00:24:18,440
about 1.5 milligrams given 90 
seconds before you intubate to 

526
00:24:18,440 --> 00:24:19,800
blunt the airway. 
Reflexes. 

527
00:24:20,200 --> 00:24:22,000
Do not intubate a light 
asthmatic. 

528
00:24:22,080 --> 00:24:25,320
That is asking for disaster. 
Once the tube is in, we have to 

529
00:24:25,320 --> 00:24:28,360
ventilate them. 
Section 13 Interoperative 

530
00:24:28,360 --> 00:24:30,960
ventilation strategy. 
This is marked as very high 

531
00:24:30,960 --> 00:24:32,200
yield. 
It is. 

532
00:24:32,240 --> 00:24:34,720
The entire strategy can be 
summed up in 3 words. 

533
00:24:34,920 --> 00:24:38,120
Avoid air trapping. 
Prevent that auto peep we talked

534
00:24:38,120 --> 00:24:39,520
about. 
So how do we set the ventilator 

535
00:24:39,520 --> 00:24:41,360
to do that? 
We need to give them a long time

536
00:24:41,360 --> 00:24:43,520
to exhale. 
Remember, their expiration is 

537
00:24:43,520 --> 00:24:46,480
prolonged and difficult, so we 
use a low respiratory rate, 

538
00:24:46,960 --> 00:24:49,800
maybe 6 to 10 breaths per 
minute, and we deliberately 

539
00:24:49,800 --> 00:24:52,320
prolong the expiratory time. 
So the IE ratio. 

540
00:24:52,400 --> 00:24:57,040
Instead of the usual 1.2, we go 
for 1.2.51.3 or even 1.4. 

541
00:24:57,040 --> 00:24:59,560
In severe cases. 
We want the expiratory phase to 

542
00:24:59,560 --> 00:25:01,920
be long enough for the 
expiratory flow to return to 0 

543
00:25:01,920 --> 00:25:03,280
before the next breath is 
delivered. 

544
00:25:03,400 --> 00:25:06,680
But if we breathe them that 
slowly, their CO2 will rise. 

545
00:25:06,840 --> 00:25:09,560
And that is OK. 
That is the concept of 

546
00:25:09,560 --> 00:25:13,720
permissive hypercapnia. 
We accept a higher CO2 as long 

547
00:25:13,720 --> 00:25:18,000
as the pH say is above roughly 
7.2 in exchange for lower airway

548
00:25:18,000 --> 00:25:21,040
pressures and avoiding Barra 
trauma or the hemodynamic 

549
00:25:21,040 --> 00:25:24,160
collapse from auto PEEP. 
We prioritize lung mechanics 

550
00:25:24,160 --> 00:25:26,840
over blood gas chemistry. 
And the tidal volume? 

551
00:25:27,080 --> 00:25:29,960
Moderate 6 to 8 milligrams of 
ideal body rate. 

552
00:25:29,960 --> 00:25:32,600
Don't use large tidal volumes 
that could over distend the 

553
00:25:32,600 --> 00:25:34,280
lungs. 
Section 14. 

554
00:25:34,600 --> 00:25:37,720
Anesthetic drug considerations. 
We're in the maintenance phase 

555
00:25:37,720 --> 00:25:40,080
of anesthesia. 
Which gas are we using? 

556
00:25:40,200 --> 00:25:43,120
Civil fluorine. 
It's an excellent bronchodilator

557
00:25:43,120 --> 00:25:45,480
and it's non irritant. 
It's sweet smelling. 

558
00:25:45,680 --> 00:25:47,680
It is the agent of choice for 
maintenance. 

559
00:25:48,120 --> 00:25:50,160
What about dysplorine? 
Absolutely not. 

560
00:25:50,160 --> 00:25:52,600
Dysplorine is pungent. 
It irritates the airway and can 

561
00:25:52,600 --> 00:25:55,360
cause coughing, laryngospasm and
bronchospasm. 

562
00:25:55,600 --> 00:25:58,240
Avoided in asthmatics. 
It's a key drug to avoid. 

563
00:25:58,360 --> 00:26:01,120
And muscle relaxants we've 
induced, now we need to keep 

564
00:26:01,120 --> 00:26:02,920
them relaxed. 
Avoid the histamine releases. 

565
00:26:02,920 --> 00:26:05,880
That means Actrocurium and its 
cousin Mevacurium are out. 

566
00:26:05,880 --> 00:26:09,040
So what are the safe choices? 
Rocuronium, vecuronium or 

567
00:26:09,040 --> 00:26:11,520
sesatrocurium. 
They are historically very safe.

568
00:26:11,520 --> 00:26:13,320
Regarding histamine release, 
stick to those. 

569
00:26:13,600 --> 00:26:16,320
Analgesics. 
Fentanyl versus morphine. 

570
00:26:16,360 --> 00:26:18,320
Fentanyl and its derivatives are
safe. 

571
00:26:18,680 --> 00:26:21,040
Morphine is a known histamine 
releaser. 

572
00:26:21,040 --> 00:26:24,120
So in the exam you say you will 
avoid morphine. 

573
00:26:24,120 --> 00:26:25,800
OK, we're in the middle of 
surgery. 

574
00:26:26,040 --> 00:26:29,040
We've done everything right, but
suddenly the peak pressures go 

575
00:26:29,040 --> 00:26:32,200
up, The alarms are blaring. 
Section 15. 

576
00:26:32,600 --> 00:26:35,520
Recognition of intraoperative 
bronchospasm. 

577
00:26:36,120 --> 00:26:39,080
Clinically, you might hear a 
wheeze with your stethoscope, 

578
00:26:39,480 --> 00:26:42,760
but remember with the noise of 
the OT and the surgical drapes, 

579
00:26:42,880 --> 00:26:45,680
you might miss it. 
The most reliable sign is on 

580
00:26:45,680 --> 00:26:47,840
your monitor. 
Look at the Capna graph. 

581
00:26:47,840 --> 00:26:50,200
The waveform. 
Yes, you will see a classic 

582
00:26:50,200 --> 00:26:53,200
shark fin pattern. 
Describe that for the listener 

583
00:26:53,200 --> 00:26:56,240
who has to draw it in an exam. 
Normally the expertory waveform 

584
00:26:56,240 --> 00:26:58,920
is a nice square box. 
You have a shop up stroke, a 

585
00:26:58,920 --> 00:27:00,840
flat plateau and a sharp down 
stroke. 

586
00:27:01,120 --> 00:27:03,520
In bronchospasm. 
The up stroke, which is phase 

587
00:27:03,520 --> 00:27:07,040
two, becomes slow and slurred 
because of the obstruction and 

588
00:27:07,040 --> 00:27:10,080
the alveolar plateau phase three
slopes steeply upward because 

589
00:27:10,080 --> 00:27:12,240
the alveoli are emptying at 
different rates. 

590
00:27:12,360 --> 00:27:13,800
So it looks like a shark's 
dorsal fin. 

591
00:27:14,240 --> 00:27:16,120
Exactly. 
Pointing to the left on most 

592
00:27:16,120 --> 00:27:19,480
monitors, it's an unmistakable 
sign of expiratory airflow 

593
00:27:19,480 --> 00:27:21,920
obstruction. 
And we need to verify this with 

594
00:27:21,920 --> 00:27:25,360
the vimilator pressures. 
Yes, you will see a High Peak 

595
00:27:25,360 --> 00:27:29,160
inspiratory pressure PIP but, 
and here is the key 

596
00:27:29,160 --> 00:27:33,000
discriminator for the Viva, the 
plateau pressure P plat will be 

597
00:27:33,000 --> 00:27:35,360
normal or only slightly 
elevated. 

598
00:27:35,520 --> 00:27:37,280
Why is the plateau pressure 
normal? 

599
00:27:37,720 --> 00:27:40,480
Because plateau pressure 
reflects the compliance of the 

600
00:27:40,480 --> 00:27:44,960
lung parenchyma and the chest 
wall, the static compliance in 

601
00:27:44,960 --> 00:27:47,840
asthma, the compliance of the 
lungs themselves is generally 

602
00:27:47,840 --> 00:27:50,280
OK. 
The problem is the resistance in

603
00:27:50,280 --> 00:27:53,400
the conducting Airways. 
So to summarize for the exam. 

604
00:27:53,560 --> 00:27:56,360
A High Peak pressure with a 
normal plateau pressure means a 

605
00:27:56,360 --> 00:28:00,000
resistance problem. 
Think asthma, A kinked tube or a

606
00:28:00,000 --> 00:28:02,880
mucus plug. 
A High Peak pressure with a high

607
00:28:02,880 --> 00:28:05,120
plateau pressure means a 
compliance problem. 

608
00:28:05,520 --> 00:28:08,720
Think pneumothorax, pulmonary 
edema, or abdominal 

609
00:28:08,720 --> 00:28:11,040
insufflation. 
That is a crucial distinction. 

610
00:28:11,040 --> 00:28:13,000
It helps you build a 
differential diagnosis in 

611
00:28:13,000 --> 00:28:14,880
seconds. 
It helps you rule out a life 

612
00:28:14,880 --> 00:28:16,720
threatening pneumothorax very 
quickly. 

613
00:28:16,720 --> 00:28:18,560
So we have identified 
bronchospasm. 

614
00:28:18,560 --> 00:28:20,320
The shark fin is there, the 
pressures are up. 

615
00:28:20,520 --> 00:28:23,200
Section 16. 
Management of acute bronchospasm

616
00:28:23,200 --> 00:28:26,000
give us the examiner safe 
algorithm step by step. 

617
00:28:26,240 --> 00:28:31,480
OK Step 1 deepen anesthesia. 
Light anesthesia is the most 

618
00:28:31,480 --> 00:28:33,920
common cause of bronchospasm 
under GA. 

619
00:28:34,480 --> 00:28:38,560
Turn up the CEVA flaring to 3 or
4% or give a bolus of propofol 

620
00:28:38,560 --> 00:28:42,920
step 200% oxygen and switch to 
manual ventilation. 

621
00:28:43,240 --> 00:28:45,960
Get your hand on the bag. 
You can feel the compliance and 

622
00:28:45,960 --> 00:28:48,280
resistance much better than the 
machine can tell you. 

623
00:28:48,600 --> 00:28:51,040
It also helps you rule out a 
ventilator malfunction. 

624
00:28:51,040 --> 00:28:52,320
Step 3. 
Pharmacology. 

625
00:28:52,600 --> 00:28:54,920
Beta 2 agonists. 
You have cellbutamol. 

626
00:28:54,920 --> 00:28:58,120
You can puff it directly down 
the ETT using a specific adapter

627
00:28:58,280 --> 00:29:00,880
or use a nebulizer. 
In the breathing circuit, give 6

628
00:29:00,880 --> 00:29:02,600
to 8 puffs and assess the 
response. 

629
00:29:02,600 --> 00:29:04,960
Step 4. 
Add anticholinergics like 

630
00:29:05,040 --> 00:29:07,600
ipratropium bromide. 
It's often given together with 

631
00:29:07,600 --> 00:29:09,560
the cellbutamol for a 
synergistic effect on 

632
00:29:09,560 --> 00:29:12,360
bronchodilation step. 
Five if things aren't improving.

633
00:29:12,800 --> 00:29:16,080
4 Steroids hydrocortisone 
hundred 200 milligram or 

634
00:29:16,080 --> 00:29:18,480
dexamethasone. 
Remember this takes hours to 

635
00:29:18,480 --> 00:29:21,160
work so it won't fix the spasm 
now, but you must give it early 

636
00:29:21,160 --> 00:29:23,360
to treat the underlying 
inflammation and prevent that 

637
00:29:23,360 --> 00:29:27,680
late phase reaction. 
Step 6. 5V Magnesium sulfate 2G 

638
00:29:27,680 --> 00:29:29,960
infused intravenously over about
20 minutes. 

639
00:29:30,120 --> 00:29:33,440
How does magnesium work here? 
It acts as a smooth muscle 

640
00:29:33,440 --> 00:29:36,120
relaxant. 
It interferes with calcium 

641
00:29:36,120 --> 00:29:39,320
uptake and signaling in the 
bronchial smooth muscle cells, 

642
00:29:39,560 --> 00:29:42,960
causing them to relax. 
It's very effective in severe 

643
00:29:42,960 --> 00:29:45,720
refractory cases. 
Is there a role for epinephrine?

644
00:29:46,200 --> 00:29:50,080
Yes, in refractory life 
threatening cases, if the blood 

645
00:29:50,080 --> 00:29:53,160
pressure is dropping and you 
can't break the spasm, give low 

646
00:29:53,160 --> 00:29:56,440
dose IV epinephrine. 
You can give it in small boluses

647
00:29:56,440 --> 00:30:00,480
of say 10 to 20 micrograms at a 
time, or as a continuous 

648
00:30:00,480 --> 00:30:01,680
infusion. 
In ketamine. 

649
00:30:02,000 --> 00:30:04,120
If you haven't already used it 
for induction, a bolus of 

650
00:30:04,120 --> 00:30:07,120
ketamine, say .5 milligram, can 
also help break the. 

651
00:30:07,120 --> 00:30:08,800
Spasm. 
The surgery is done, you've 

652
00:30:08,800 --> 00:30:10,760
managed the spasm. 
Time to wake them up. 

653
00:30:10,920 --> 00:30:13,960
Section 17 and 18. 
Post operative complications in 

654
00:30:13,960 --> 00:30:16,320
management. 
The main post op complications 

655
00:30:16,320 --> 00:30:19,000
are a recurrence of 
bronchospasm, especially during 

656
00:30:19,000 --> 00:30:22,720
extubation, hypoxia due to 
ongoing VQ mismatch, and 

657
00:30:22,720 --> 00:30:25,720
atelactasis. 
Those mucus plugs can easily 

658
00:30:25,720 --> 00:30:28,200
collapse segments of the lung. 
And the extubation itself. 

659
00:30:28,200 --> 00:30:30,880
This is always a tense moment. 
It is This is the great debate. 

660
00:30:30,880 --> 00:30:35,240
Deep versus awake extubation. 
So deep extubation means taking 

661
00:30:35,240 --> 00:30:38,120
the tube out while they are 
still deeply anesthetized? 

662
00:30:38,120 --> 00:30:40,840
Yeah, and Gwettel's stage 3 so 
they don't cough on the tube. 

663
00:30:40,960 --> 00:30:42,760
Right, it's elegant when it 
works. 

664
00:30:42,960 --> 00:30:45,960
No coughing, no bucking, no 
bronchospasm triggered by the 

665
00:30:45,960 --> 00:30:48,520
tube. 
But you lose your airway 

666
00:30:48,520 --> 00:30:51,240
protection immediately If they 
vomit or have a lot of 

667
00:30:51,240 --> 00:30:55,000
secretions they can aspirate. 
It requires an expert hand and a

668
00:30:55,000 --> 00:30:58,240
guaranteed easy airway. 
And awake extubation. 

669
00:30:58,320 --> 00:31:01,160
This is safer from an aspiration
point of view, but they will 

670
00:31:01,160 --> 00:31:03,960
almost certainly cough on the 
tube, and that coughing is a 

671
00:31:03,960 --> 00:31:06,080
powerful trigger for 
bronchospasm. 

672
00:31:06,080 --> 00:31:08,760
So what's the exam answer? 
There's no perfect choice. 

673
00:31:08,920 --> 00:31:12,680
The safe answer for a generalist
and for the exam is usually 

674
00:31:12,720 --> 00:31:15,400
awake but smooth. 
This is the middle ground. 

675
00:31:15,760 --> 00:31:19,520
You utilize Ivy to cane or small
doses of opioids to suppress the

676
00:31:19,520 --> 00:31:22,840
cough reflex, but you ensure 
they are fully awake, following 

677
00:31:22,840 --> 00:31:25,040
commands and breathing 
adequately before you pull the 

678
00:31:25,040 --> 00:31:27,040
tube. 
However, you should mention that

679
00:31:27,040 --> 00:31:30,800
deep extubation is an option in 
carefully selected patients. 

680
00:31:30,840 --> 00:31:32,800
Post op pain control matters too
I assume. 

681
00:31:32,880 --> 00:31:34,800
Absolutely. 
If they are in pain, they 

682
00:31:34,800 --> 00:31:36,680
splint. 
They don't take deep breaths. 

683
00:31:36,680 --> 00:31:39,000
That worsens atelectasis and 
mucus plugging. 

684
00:31:39,240 --> 00:31:42,760
Epidurals are fantastic for 
thoracic or major abdominal 

685
00:31:42,760 --> 00:31:45,800
surgery and asthmatics because 
they provide excellent pain 

686
00:31:45,800 --> 00:31:47,480
relief without respiratory 
depression. 

687
00:31:47,760 --> 00:31:51,560
Let's briefly touch on Section 
19 ICU management for severe 

688
00:31:51,560 --> 00:31:55,400
asthma or status asthmaticus. 
When do we decide to intubate a 

689
00:31:55,400 --> 00:31:57,400
patient with severe asthma in 
the ICU? 

690
00:31:57,440 --> 00:31:59,680
It's a last resort. 
We try everything else first. 

691
00:31:59,800 --> 00:32:02,560
Bipap, high flow oxygen, 
continuous nibs. 

692
00:32:02,960 --> 00:32:06,960
The indications for intubation 
are a rising Paco 2 indicating 

693
00:32:06,960 --> 00:32:10,920
fatigue, a deteriorating level 
of consciousness, or of course, 

694
00:32:11,080 --> 00:32:13,640
cardiorespiratory arrest. 
But ventilation and status 

695
00:32:13,640 --> 00:32:15,480
asthmaticus is famously 
dangerous. 

696
00:32:15,480 --> 00:32:18,480
Extremely, the risk of 
barotrauma like causing a 

697
00:32:18,480 --> 00:32:21,240
pneumothorax and severe 
hypotension from auto PEEP is 

698
00:32:21,240 --> 00:32:23,160
very high. 
We use the strategy of 

699
00:32:23,160 --> 00:32:26,400
controlled hypovilation. 
We deliberately allow the CO2 to

700
00:32:26,400 --> 00:32:29,920
rise permissive hypercapnia to 
keep the airway pressures down. 

701
00:32:30,120 --> 00:32:32,880
We prioritize keeping the 
plateau pressure below 30 

702
00:32:33,000 --> 00:32:36,040
centimeter HA2O overachieving a 
normal pH. 

703
00:32:36,160 --> 00:32:37,880
And constantly watching for that
auto P. 

704
00:32:37,880 --> 00:32:39,800
Constantly. 
If they suddenly become 

705
00:32:39,800 --> 00:32:42,800
hypotensive on the ventilator, 
your first move is to disconnect

706
00:32:42,800 --> 00:32:45,080
the circuit and manually 
decompress the chest. 

707
00:32:45,240 --> 00:32:48,080
Before we wrap up, let's hit 
Section 20 comparison tables. 

708
00:32:48,080 --> 00:32:49,400
These are high yield for the 
Viva voce. 

709
00:32:49,680 --> 00:32:52,400
Let's do a quick fire round. 
Asthma versus COPD. 

710
00:32:52,600 --> 00:32:56,080
Age of onset asthma is usually 
childhood or early adulthood. 

711
00:32:56,640 --> 00:32:59,400
COPD is midlife or later. 
Asthma is associated with 

712
00:32:59,400 --> 00:33:03,720
allergy, atopy, eczema. 
COPD is overwhelmingly 

713
00:33:03,720 --> 00:33:06,640
associated with smoking. 
Asthma shows significant 

714
00:33:06,640 --> 00:33:08,680
reversibility with 
bronchodilators. 

715
00:33:08,880 --> 00:33:11,760
COPD shows minimal or only 
partial reversibility. 

716
00:33:12,040 --> 00:33:15,800
DLCO, diffusion capacity. 
This is a key differentiator. 

717
00:33:16,080 --> 00:33:19,320
It is normal and pure asthma 
because the lung parenthema, the

718
00:33:19,320 --> 00:33:23,120
alveoli are intact. 
It is decreased in emphysema 

719
00:33:23,120 --> 00:33:25,840
predominant COPD because the 
parenchema is destroyed. 

720
00:33:26,160 --> 00:33:28,760
That DLCO point is a great Viva 
nugget. 

721
00:33:28,760 --> 00:33:30,960
It shows a deep physiological 
understanding. 

722
00:33:31,040 --> 00:33:33,320
It separates the students who've
read deeply from those who have 

723
00:33:33,320 --> 00:33:35,400
just skimmed the summary 
chapter. 

724
00:33:35,600 --> 00:33:39,000
Let's review Section 21 common 
exam questions in Viva drafts. 

725
00:33:39,000 --> 00:33:43,240
We've covered a few trap one. 
Is wheezing a sign of severity? 

726
00:33:43,240 --> 00:33:47,920
No, a silent chest is far worse.
Trap 2A normal ABG in a panting 

727
00:33:47,920 --> 00:33:49,560
asthmatic. 
It's a sign of impending 

728
00:33:49,560 --> 00:33:53,080
failure, not stability. 
Trap 3 Using Atrocurium for 

729
00:33:53,080 --> 00:33:54,600
muscle relaxation. 
Don't say it. 

730
00:33:54,600 --> 00:33:57,520
It's a known histamine releaser.
Stick to rocaronium or 

731
00:33:57,520 --> 00:33:59,840
vecaronium. 
And the Examiner's favorite 

732
00:33:59,840 --> 00:34:01,920
waveform? 
The Kapnograph in bronchospasm, 

733
00:34:02,080 --> 00:34:05,760
the shark fin be able to draw it
and explain why Phase 2 is 

734
00:34:05,760 --> 00:34:09,199
prolonged and phase 3 is 
upsloping due to uneven alveolar

735
00:34:09,199 --> 00:34:12,639
emptying. 
Section 22 Diagrams In a written

736
00:34:12,639 --> 00:34:14,960
exam, what should we definitely 
draw? 

737
00:34:15,159 --> 00:34:17,639
Definitely draw the flow volume 
loop showing this scooped out 

738
00:34:17,639 --> 00:34:20,639
appearance of obstruction. 
And for a management question, 

739
00:34:20,639 --> 00:34:23,560
draw the bronchospasm management
algorithm as a flow chart. 

740
00:34:23,840 --> 00:34:26,440
It saves time, it's clear and it
looks professional. 

741
00:34:26,440 --> 00:34:29,760
Let's summarize Section 23 
summary and exam conclusion. 

742
00:34:29,920 --> 00:34:32,960
Give us the final high yield. 
Recap the take home points. 

743
00:34:32,960 --> 00:34:36,760
OK one, asthma is fundamentally 
a disease of inflammation and 

744
00:34:36,760 --> 00:34:38,840
hyper reactivity. 
It's not just about muscle 

745
00:34:38,840 --> 00:34:42,800
spasm. 2 Preoperative 
optimization is mandatory before

746
00:34:42,800 --> 00:34:45,360
any elective surgery. 
Symptom free is the goal. 

747
00:34:45,880 --> 00:34:48,920
Three avoid histamine releasing 
drugs like thiopentone, 

748
00:34:48,920 --> 00:34:52,880
atrocurium, and morphine 4. 
Deep anesthesia before any 

749
00:34:52,880 --> 00:34:54,880
airway manipulation is non 
negotiable. 

750
00:34:55,040 --> 00:34:58,640
Light anesthesia is your enemy. 
5 And finally, permissive 

751
00:34:58,640 --> 00:35:01,240
hypercapnia is your friend. 
When ventilating a severe 

752
00:35:01,240 --> 00:35:04,920
asthmatic, prioritize low 
pressures over a normal CO2. 

753
00:35:05,200 --> 00:35:07,680
That is a solid foundation if 
you can articulate those five 

754
00:35:07,680 --> 00:35:09,280
points clearly in a very good 
position. 

755
00:35:09,400 --> 00:35:11,440
Mastering this topic gives you 
confidence. 

756
00:35:11,800 --> 00:35:14,520
It's a common clinical case, but
when managed poorly, it's a 

757
00:35:14,520 --> 00:35:16,960
nightmare. 
When you manage it well, it's 

758
00:35:16,960 --> 00:35:19,680
smooth sailing. 
Good luck to everyone preparing 

759
00:35:19,680 --> 00:35:23,720
for the Gujarat University exams
or for any anesthesiology board 

760
00:35:23,720 --> 00:35:25,560
exam for that matter. 
You have the tools now. 

761
00:35:25,560 --> 00:35:28,360
My advice? 
Go practice drawing those flow 

762
00:35:28,360 --> 00:35:31,040
volume loops in the shark fin 
capnograph right now. 

763
00:35:31,480 --> 00:35:33,760
Don't wait. 
Get it into your muscle memory. 

764
00:35:33,800 --> 00:35:36,200
Next time, we tackled the 
Cardiac Risk Index. 

765
00:35:36,480 --> 00:35:38,320
Until then, keep diving deep.
