Welcome back to the Deep Dive. Today we are stripping away the
safety net. We aren't just exploring a
topic, we are entering a simulation.
That's right, today the stakes are significantly higher than
usual. I want you to visualize this.
You are an MD, anesthesiology postgraduate student.
You're sitting in the hot seat. It's the final practical exam
for Gujarat University. The air conditioning is humming,
your palms are sweating, and the external examiner is, you know,
staring at you over the rim of his glasses.
The case on the table is bronchial asthma.
And I'm stepping into the role of that senior faculty member.
I'm the internal examiner sitting next to you.
My job today isn't just to teach you the facts, It's to guide you
through the minefield. I'm here to point out the traps
that fail candidates and the precise gold medal answers that
distinguish the consultants from the students.
Our mission is to take this massive stack of source
material. We've compiled standard texts
like Miller, Morgan and McHale Gaytan for Physiology,
Harrison's for medicine, Robbins for pathology, and KD Tripathi
for pharmacology and distilled them into a single, cohesive,
exam winning narrative. We're really covering the full
spectrum here. Oh.
Yeah, from the cellular level of inflammation right up to the
terrifying silence of a status asthmatic.
His chest in the ICU. Precisely.
But I have to issue a disclaimer before we begin.
This is an exam preparation deep dive.
We are basing our discussions strictly on the provided source
texts. We all know clinical guidelines
evolve rapidly, but in the exam hall, these standard texts are
your Bible. So answer according to the book.
Answer according to the book, unless you have a landmark paper
in your back pocket to justify a deviation.
Understood. Let's set the stage then.
The exam usually begins with definitions.
It sounds simple, but I've seen students stumble right out of
the gate. We aren't just talking about
asthma yet. We're starting with the umbrella
category, Section 1, introduction to obstructive lung
diseases. How do we frame this for the
examiners to show we understand the physics of it?
Right. If the examiner asks what is
obstructive lung disease, do not just list diseases.
That's a classic mistake. You must focus on the
physiological defect. The core concept is flow
limitation. These are diseases characterized
by an increase in resistance to airflow due to partial or
complete obstruction at any level of the tracheobronchial
tree. So the problem isn't getting air
in. Exactly.
It's getting air out. And Robbins is very specific
about the classification. Here we refer to the BIG4.
Yes. In pathology, the big four are
emphysema, chronic bronchitis, asthma, and Bronchiectasis.
You should list these confidently.
It shows you've read beyond just the anesthesia texts.
But here is the pivot point for the anesthesiologist and
specifically for this exam topic.
We need to distinguish asthma from the rest, particularly from
COPD. What is the single most
important discriminator? The magic word is reversibility.
This is an exam tip right off the bat.
If you say asthma is airway obstruction, you're only half
right. You must say it is reversible
airway obstruction. So that's the keyword
reversible. Absolutely.
COPD, which is a clinical syndrome often comprising
emphysema and chronic bronchitis, is characterized by
persistent airflow limitation that is not fully reversible.
So conceptualizing this for the Viva, asthma is a dynamic state.
The airway clamps down, but it can open up again.
COPD is more of a fixed structural change.
That's a perfect way to put it, and you need to be precise with
the definition of asthma itself. It's not just wheezing.
That's a symptom, not a definition.
OK, so what's the full definition we should be giving?
Bronchial asthma is a chronic inflammatory disorder of the
Airways. This chronic inflammation causes
airway hyper responsiveness that leads to recurrent episodes of
wheezing, breathlessness, chest tightness and coughing,
particularly at night or in the early morning.
You've used two key terms there, inflammation and hyper
responsiveness, if we need to unpack.
Those we will. They're central to everything.
But first, let's touch on the epidemiology.
Why does this matter to us as anesthesiologists?
Is it just background noise or is there a real safety
implication? It's a massive safety issue.
I mean the global burden is around 300 million people.
It is likely the most common pulmonary comorbidity you will
encounter in your day-to-day practice.
So we're going to see it all the time.
All the time. And Miller explicitly points out
that about 9% of asthmatics may develop bronchospasm
perioperatively. 9% That's nearly one in 10.
That is a statistically significant risk for every
single list we run. Correct.
And intraoperative bronchospasm isn't a minor annoying it's not
just a bitter wheezing. In severe cases, it leads to
inability to ventilate, severe hypoxia, and potentially brain
damage or death. So this can be a true anesthetic
catastrophe. It can be, and you also need to
be attuned to the concept of the silent chest, which signifies
obstructions so severe that air movement is minimal.
If you're waiting for a wheeze to diagnose severity, you might
miss the patient who is about to arrest.
That is a terrifying concept to Silent Chest.
We will absolutely drill down into that later.
But first, let's look at the exam paper itself.
If I'm the student, what kind of questions am I anticipating?
You will see patterns for short notes.
They love mechanism based questions like pathophysiology
of asthma or equipment based ones like capnography and
bronchospasm. OK, short and focus.
Exactly for the long 10 to 20 mark questions, expect a high
stakes clinical scenario. Discuss the anesthetic
management of a case of status asthmaticus for emergency
surgery. The nightmare scenario.
The one that tests everything. And for the Viva or OSCE, be
ready to interpret flow volume loops or arterial blood gases on
the spot. OK, let's tackle that first
short note topic, Section 2, the pathophysiological basis of
asthma. This is the core of the exam,
isn't it? If you don't understand the
pathology, you can't justify your pharmacological choices
later. Absolutely.
The most common mistake students make is thinking asthma is just
bronchospasm, just muscle tightening.
It's not. It is fundamentally a disease of
chronic airway inflammation. So the muscle spasm is just the
symptom, the disease is the angry inflamed tissue
underneath. Exactly.
Even when the patient is asymptomatic, walking around
feeling fine, their airway is infiltrated with mast cells,
eosinophils, and T lymphocytes. This chronic state leads to what
we call airway remodeling. Remodeling sounds like a
construction project, but in this context I assume it's
destructive. It is maladaptive.
It's the body trying to repair pair itself but doing a bad job.
We see thickening of the sub basement membrane, hypertrophy
of the smooth muscle, and hyperplasia of the mucus glands.
So the airway is literally changing its structure for the
work. Precisely this structural change
makes the airway hyper responsive.
Define hyper responsiveness for me in an exam context.
Yeah. How do I explain that to a
junior colleague? It is the tendency of the
Airways to narrow excessively in response to triggers that
wouldn't affect a normal person. A little bit of cold air, a
specific or the mechanical touch of a laryngoscope blade that you
or I would ignore causes a massive disproportionate
reaction in an asthmatic A. Real overreaction of the area.
A huge overreaction and then we have the mucus.
This isn't just normal secretions, is it?
No, not at all. The mucus plugging in asthma is
nasty. It's thick, tenacious, and
incredibly difficult to suction. Pathology texts like Robbins
describes specific microscopic findings within this mucus.
Oh, this sounds like bonus points territory.
It is. You have Kirchman spirals, which
are these little whirls of shed epithelium, and charcoal Leiden
crystals which are composed of Eucenophil proteins.
Those sound like incredible buzzwords for a pathology
question. They are gold medal details.
Dropping charcoal Leiden crystals into your answer tells
the examiner you've read the pathology text.
It's not just the anesthesia summary.
OK, so Kirchman's spirals and charcoal Leiden crystals, but
what's the anesthetic relevance? The clinical relevance is this,
that inflammation makes the airway incredibly twitchy.
Instrumentation like putting in an endotracheal tube is a potent
trigger. You are essentially poking an
angry bear. An excellent analogy.
Moving on to Section 3, immunological mechanisms, this
is often labeled as exam gold. We need to understand the
mechanism to understand the drugs we use.
You need to know that it is predominantly an IG mediated
hypersensitivity or type hypersensitivity.
Walk us through the cellular level.
Who are the players? The star of the show is the mast
cell. Think of them as Sentinel cells
embedded in the submucosa, just waiting exactly in an atopic
individual, someone prone to allergies.
These cells are coated with Ige antibodies.
When an antigen, say pollen or a specific drug binds to that Ige,
it causes crosslinking. And crosslinking acts as the
trigger, like turning a key in a lock.
A perfect analogy. It triggers degranulation.
The mast cell essentially explodes, releasing a cocktail
of preformed inflammatory mediators.
The big one, of course, is histamine.
Which causes the immediate reaction we see on the table,
the wheezing, the pressure going.
Up right histamine causes rapid bronchoconstriction and mucosal
edema. That's the early phase, but you
also have the synthesis of new mediators like the leukotrienes,
which were formerly known as the slow reacting substance of
anaphylaxis. That's a great piece of medical
trivia. Slow reacting substance of
anaphylaxis. It is, and it tells you what it
does. Leukotrienes cause prolonged,
sustained bronchospasm. They are much more potent and
longer lasting than histamine. OK.
So that's the immediate problem, but you mentioned early versus
late phase reactions. Yes.
And this is a crucial conceptual leap for the anesthesiologist,
the early versus late phase reaction.
Why is this so clinically relevant for us?
The early phase happens in minutes.
That's the immediate bronchospasm you fight during
induction, but the late phase happens 2 to 8 hours later.
This is caused by the recruitment of inflammatory
cells like neutrophils and eosinophils into the Airways.
So. A patient could have a reaction
in the OT, You stabilize them, everything looks good, you send
them to the ward and then. And then six hours later in the
pay CU or on the floor they deteriorate.
They might look fine initially but crash post op because of
this late phase inflammatory bloom.
That is a Viva trap right there. Yeah.
Why did the patient deteriorate in the PCU despite a smooth
emergence? Exactly, if you can answer late
phase reaction due to inflammatory cell recruitment
you get full marks. It shows you're thinking beyond
the immediate crisis. Now let's connect this to
Section 4 effects on lung mechanics.
We talked about flow limitation. When the Airways narrow, what
happens to resistance? It's skyrockets and for the exam
you need to quote Kwizu's law. Oh, physics.
OK. It's simple but powerful.
Resistance is inversely proportional to the radius to
the power of 4. For laminar flow, the.
Power of four. Let's do the math on that if the
radius is halved. The resistance increases 16
fold. It's not a linear relationship,
it's exponential. 16 times harder to breathe.
Exactly. And if flow becomes turbulent,
which it often does in narrowed Airways, the dependence is on
the radius to the power of 5. This explains why breathing
becomes such incredibly hard work.
The patient has to generate massive negative pressure to
pull air in and massive positive pressure to push it out.
And specifically, expiration is affected more than inspiration,
correct? Why is that?
Yes, inspiration is an active process.
The chest wall expands and pulls the Airways open through
something called radial traction.
Expiration, however, is normally passive.
As the lung empties, the Airways naturally narrow a bit.
In asthma, this natural narrowing combined with the
pathology, the swelling, the mucus, the spasm leads to
premature airway closure. So the air gets trapped.
The air gets trapped. And this brings us to a critical
concept, dynamic hyperinflation or what we call auto peep.
Let's unpack auto peep. This is the term we hear in the
ICU all the time, but explaining it physically can be tricky.
Imagine breathing in through a very thin straw.
It's hard. Now imagine trying to breathe
out through that same straw, but before you have finished
exhaling, you are forced to take another breath in.
I'd still have air left in my lungs from the first breath.
I wouldn't have time to empty them completely.
Exactly. Air goes in, but it cannot get
out completely before the next breath starts.
This is air trapping. The lungs get bigger and bigger
with each breath. The functional residual
capacity, or FRC just keeps rising.
It sounds like it would increase pressure inside the chest quite
a bit. It does.
It increases intrathoracic pressure.
Now think about the hemodynamics.
What does high intrathoracic pressure do to the heart?
It acts like a tamponade. It squashes the great veins,
reducing venous return to the right heart.
Correct, it decreases venous return which decreases preload
which leads to hypotension. So here is the clinical Pearl.
If you are ventilating an asthmatic and their blood
pressure suddenly drops, you must immediately think of auto
peep. And the fix isn't fluids or
pressors initially. No, the immediate fix is to
treat the cause the trapped air. You disconnect the ventilator
from the endotracheal tube, you allow a long apnea period.
You might even gently push on the chest to help them exhale
that trapped gas. What happens when you do that?
You will hear a long hiss of air escaping and you'll see the
blood pressure come right back up.
It's dramatic and life saving. That's a practical save a life
tip disconnect and let them exhale.
Now Section 5 clinical features of asthma.
We know the classic triad, dyspnea, cough, wheezing, but
you mentioned the silent chest earlier.
Yes. In the exam, they will ask, is
the loudness of the wheeze a sign of severity?
The answer is an emphatic NO. Explain why that seems
counterintuitive. Because to make a wheeze, which
is a musical sound produced by turbulent flow through a narrow
tube, you need airflow. In severe obstruction there is
so little air moving that there is no sand generation.
A silent chest in a distressed tachypneic patient is a pre
terminal sign. So silence is worse than noise.
Silence is terrifying. It means imminent respiratory
arrest. What about triggers?
We know about pollen and dust. What about drugs?
This is crucial for our history taking.
Aspirin and other NSIS are classic triggers.
About 1% to 5% of asthmatics are sensitive.
This is sometimes known as Sampter's triad, which is
asthma. Aspirin sensitivity in nasal
polyps. What is the mechanism there?
It's not IG E mediated is it? No, it's not a true allergy.
It's biochemical. Nsiis inhibit the cyclooxygenase
or Cox enzyme. This blocks the production of
prostaglandins. However, the arachidonic acid
precursor has to go somewhere. So it gets diverted.
It gets shunted down the lipoxygenase pathway.
Which produces more? Leukotrienes and as we know from
our earlier discussion, leukotrienes cause potent
prolonged bronchospasm. So as a rule, avoid Toradol or
diclofenac in these patients unless you are absolutely
certain they are not aspirin sensitive.
In any asthmatic with a history of nasal polyps or known aspirin
sensitivity, absolutely avoid them.
It's not worth the risk. Let's talk investigations,
Section 6, pulmonary function tests, or PFTS.
This is absolutely essential for the exam.
You must know the spiromet findings cold.
The hallmark of any obstructive disease is a reduction in FEV
one the forced expiratory volume in one second.
The flow is slow. And the FVC, the forced vital
capacity, the total amount of air they can blow out.
It's usually normal or might be slightly reduced due to the air
trapping we talked about. But the key number, the one the
examiner wants to hear, is the FEV 1 FVC ratio.
In asthma and COPD this ratio is reduced, typically less than .7
or 70%. A normal person can blow out
most of their air in the first second and obstruct.
A person can't. And how do we prove it's asthma
and not COPD using just the PFT? Reversibility testing.
This is the gold standard for diagnosis.
You do the spirometry, then you give a bronchodilator like
cellbutamol, wait 15 minutes and repeat the test.
And what are we looking for? If the FEV 1 increases by more
than 12% ND more than 200 milliliters from the baseline,
that is a positive test. It confirms reversible
obstruction, which is the hallmark of asthma.
OK, 12% and 200 milliliters. Got it.
Now for the visual learners, imagine the flow volume loop you
are at the whiteboard and the Viva.
What are you drawing? You draw the axis with flow on
the axis and volume on the X axis.
You draw the inspiratory limb, which is usually a nice
symmetrical semicircle on the bottom.
Then you draw the expertory limb on top.
And for asthma? The expertory limb looks scooped
out. It has a concave appearance.
It starts with a sharp peak, but then the flow drops off very
quickly and tails off as the Airways collapse.
Unlike A restrictive disease. Right, A restrictive disease
like pulmonary fibrosis looks like a witch's hat.
It's narrow because the volumes are small, but the is preserved
and it's tall because the flows can be high relative to the
volume. Obstructive is scooped out.
Section 7. ABG changes in asthma.
This is an exam favorite. How does the ABG change as an
asthma attack progresses from mild to severe?
This is a classic progression that you must know in early or
mild asthma, the patient is anxious.
They feel short of breath, so they hyperventilate.
They're breathing fast. So what happens to their CO2?
They blow it off. So hypocapnia, which leads to a
respiratory alkalosis. Correct and usually mild
hypoxemia because of some VQ mismatch.
Now, as the attack gets more severe and the patient gets
tired, remember breathing through a straw is exhausting
work, The respiratory muscles begin to fatigue.
The rate might stay high, but the tidal volume drops.
The CO2 starts to rise. It returns to normal.
Wait, normal CO2 sounds good? If I see a PECO 2 of 40 milli
milli HG on an ABG, I'm usually pretty.
Happy. No.
That is the trap. A normal Peco 2, say 35 to 45
milli milli HG in a tachypneic, panting, distressed, asthmatic
is a huge danger sign. Why?
It implies that they can no longer maintain the work of
breathing needed to clear the CO2.
They are tiring out. They are failing.
So if I see a normal CO2 two in a distressed asthmatic, I
shouldn't be reassured, I should be worried.
You should be preparing for intubation.
It signals impending respiratory failure.
The next stage is hypercapnia, a high CO2 which causes a
respiratory acidosis and severe hypoxemia.
If you wait for the CO2 to be high, you have waited too long.
Let's move to Section 8, preoperative evaluation.
A patient comes to your clinic with a history of asthma,
scheduled for elective surgery. What are the high yield
questions? History is absolutely key.
You want to know the frequency of their inhaler use.
Are they using their rescue inhaler daily?
That's a bad sign. What else you need to know about
their history of hospitalizations?
Have they ever been admitted for asthma?
Ever been in the ICU? And the most critical question
Have they ever been intubated for their asthma?
Why is the intubation history so important?
If they've been intubated for asthma before, they are by
definition a high risk patient. It suggests their disease is
capable of becoming life threatening very quickly.
Also ask about recent upper respiratory infections or Uris.
Common cold. Exactly.
A Uri increases airway reactivity for weeks.
Some texts say up to six weeks post infection.
That's a long time. If they have a cold, do we
cancel the surgery? For elective surgery, yes.
The rule of thumb is that elective surgery should be done
when the patient is at their baseline symptom free.
If they are actively wheezing in the pre op Bay, you do not
induce, you postpone. If they had a Uri last week, you
postpone if possible. What about smoking cessation?
Always a good idea, but what's the timeline?
The longer the better, ideally 4 to 8 weeks.
What if they stopped just 48 hours before?
Does that do anything? It helps with carboxyhemoglobin
levels. It shifts the oxygen
dissociation curve back to the right, which improves oxygen
delivery to the tissues, but it doesn't do much for airway
reactivity or mucus claimants. In fact, sputum production might
increase initially as the cilia start to wake up and clear out
the gunk. So 4 to 8 weeks is the real
target for pulmonary benefit. Yes, that's when you start to
see restoration of mucosciliary transport and a reduction in
post op pulmonary complications. Let's look at Section 9, risk
stratification. How do we put all that
information together to decide who is going to have
bronchospasm on the table? The main predictors are a recent
Uri as we just discussed, active smoking and the type of surgery
and airway device. So instrumentation of the airway
matters a lot. It's a huge factor.
An endotracheal tube ETT is much more stimulating to the trachea
than a laryngeal mask, airway or LMA.
Also be aware that well controlled asthma carries a risk
that's pretty similar to non asthmatics.
It's the poorly controlled or symptomatic patient who is in
the danger zone. That leads us perfectly to
Section 10 choice of anesthesia. If you have a choice, regional
anesthesia is the gold standard for an asthmatic patient.
Why? What's the advantage?
It's simple. You avoid putting a tube in the
trachea. You avoid that direct mechanical
stimulation of the twitchy airway.
You bypass the main trigger entirely.
But there's a caveat, right? We can't just do a high spinal
block and relax. Correct.
You have to be careful. Avoid high blocks generally
above the T4 dermatome that might compromise the accessory
muscles of respiration, and asthmatic needs their
intercostals and abdominal muscles to actively exhale
against resistance. If you knock out their
intercostals with a high spinal, they might feel dysmayic even if
their oxygenation is perfectly fine.
But sometimes we have to do general anesthesia, laparoscopy
for instance, or major abdominal surgery.
Right. And if you must do GA, the goal
is deep anesthesia. You need to completely suppress
those airway reflexes before you touch the airway with a
laryngoscope or a tube. OK, let's talk about Section 11
premedication strategies. How do we set them up for
success before they even get to the OR?
First, anxiety triggers bronchospasm.
It's a physiological response via the parasympathetic system.
So anxiolysis with something like a small dose of midazolam
is very useful. And their inhalers, do they take
them on the day of surgery? Absolutely, they should continue
all their regular inhalers including their steroids and
long acting bronchodilators right up to the morning of
surgery. We often give a prophylactic
nebulization with cell butamol in the pre op area as well.
And. What about steroids?
The systemic ones. This is key.
If they are on chronic systemic steroids, their own adrenal axis
is suppressed. You must give them a stress dose
of steroids, usually hydrocortisone 100 milligram IV
at induction and then continue at post op and.
What if they're not on chronic steroids, but they're actively
wheezing before an urgent surgery?
In that case we might start a short course of oral steroids
for three to five days pre op to really calm the inflammation
down before the surgery date. Now the moment of truth.
Section 12. Induction in airway management.
We want a smooth, gentle induction.
What drugs are we reaching for? Propofol is a great choice.
It has mild bronchodilating properties and it suppresses the
laryngeal reflexes very well. It's a very smooth induction.
What about ketamine? I always hear about ketamine for
asthmatics. Ketamine is the theoretical
exeriencer for the actively wheezing patient.
It is an excellent bronchodilator.
It works via a sympathomimetic action.
It increases circulating catecholamines, which relax the
bronchial smooth muscle. It's the agent of choice and a
hypotensive asthmatic or someone in the middle of a severe
bronchospasm. Were there any downside to
ketamine? Yes, the big one is increased
secretions. You might need to give an
antisalagon like glycopyrrolate alongside it to keep the airway
dry. And what do we avoid for
induction? The classic one to avoid is
thiopentone. Historically it's associated
with histamine release in an exam.
If you suggest thiopentone for an asthmatic, you might get a
frown from the examiner. Even if the evidence is a bit
weak. Even then, why take the risk
when propofol exists? It's about choosing the safest
possible option. Airway device you mentioned an
LMA is better. An LMA sits above the glottis.
It doesn't stimulate the trachea itself, so it is much less
stimulating and preferred if there is no contraindication
like a high risk of aspiration or if you need high ventilatory
pressures. But if we need an ETT for a lap
coal for example. Then you must ensure the patient
is deep. I can't stress this enough.
Deep volatile anesthesia. Or you can use IV lidocaine,
about 1.5 milligrams given 90 seconds before you intubate to
blunt the airway. Reflexes.
Do not intubate a light asthmatic.
That is asking for disaster. Once the tube is in, we have to
ventilate them. Section 13 Interoperative
ventilation strategy. This is marked as very high
yield. It is.
The entire strategy can be summed up in 3 words.
Avoid air trapping. Prevent that auto peep we talked
about. So how do we set the ventilator
to do that? We need to give them a long time
to exhale. Remember, their expiration is
prolonged and difficult, so we use a low respiratory rate,
maybe 6 to 10 breaths per minute, and we deliberately
prolong the expiratory time. So the IE ratio.
Instead of the usual 1.2, we go for 1.2.51.3 or even 1.4.
In severe cases. We want the expiratory phase to
be long enough for the expiratory flow to return to 0
before the next breath is delivered.
But if we breathe them that slowly, their CO2 will rise.
And that is OK. That is the concept of
permissive hypercapnia. We accept a higher CO2 as long
as the pH say is above roughly 7.2 in exchange for lower airway
pressures and avoiding Barra trauma or the hemodynamic
collapse from auto PEEP. We prioritize lung mechanics
over blood gas chemistry. And the tidal volume?
Moderate 6 to 8 milligrams of ideal body rate.
Don't use large tidal volumes that could over distend the
lungs. Section 14.
Anesthetic drug considerations. We're in the maintenance phase
of anesthesia. Which gas are we using?
Civil fluorine. It's an excellent bronchodilator
and it's non irritant. It's sweet smelling.
It is the agent of choice for maintenance.
What about dysplorine? Absolutely not.
Dysplorine is pungent. It irritates the airway and can
cause coughing, laryngospasm and bronchospasm.
Avoided in asthmatics. It's a key drug to avoid.
And muscle relaxants we've induced, now we need to keep
them relaxed. Avoid the histamine releases.
That means Actrocurium and its cousin Mevacurium are out.
So what are the safe choices? Rocuronium, vecuronium or
sesatrocurium. They are historically very safe.
Regarding histamine release, stick to those.
Analgesics. Fentanyl versus morphine.
Fentanyl and its derivatives are safe.
Morphine is a known histamine releaser.
So in the exam you say you will avoid morphine.
OK, we're in the middle of surgery.
We've done everything right, but suddenly the peak pressures go
up, The alarms are blaring. Section 15.
Recognition of intraoperative bronchospasm.
Clinically, you might hear a wheeze with your stethoscope,
but remember with the noise of the OT and the surgical drapes,
you might miss it. The most reliable sign is on
your monitor. Look at the Capna graph.
The waveform. Yes, you will see a classic
shark fin pattern. Describe that for the listener
who has to draw it in an exam. Normally the expertory waveform
is a nice square box. You have a shop up stroke, a
flat plateau and a sharp down stroke.
In bronchospasm. The up stroke, which is phase
two, becomes slow and slurred because of the obstruction and
the alveolar plateau phase three slopes steeply upward because
the alveoli are emptying at different rates.
So it looks like a shark's dorsal fin.
Exactly. Pointing to the left on most
monitors, it's an unmistakable sign of expiratory airflow
obstruction. And we need to verify this with
the vimilator pressures. Yes, you will see a High Peak
inspiratory pressure PIP but, and here is the key
discriminator for the Viva, the plateau pressure P plat will be
normal or only slightly elevated.
Why is the plateau pressure normal?
Because plateau pressure reflects the compliance of the
lung parenchyma and the chest wall, the static compliance in
asthma, the compliance of the lungs themselves is generally
OK. The problem is the resistance in
the conducting Airways. So to summarize for the exam.
A High Peak pressure with a normal plateau pressure means a
resistance problem. Think asthma, A kinked tube or a
mucus plug. A High Peak pressure with a high
plateau pressure means a compliance problem.
Think pneumothorax, pulmonary edema, or abdominal
insufflation. That is a crucial distinction.
It helps you build a differential diagnosis in
seconds. It helps you rule out a life
threatening pneumothorax very quickly.
So we have identified bronchospasm.
The shark fin is there, the pressures are up.
Section 16. Management of acute bronchospasm
give us the examiner safe algorithm step by step.
OK Step 1 deepen anesthesia. Light anesthesia is the most
common cause of bronchospasm under GA.
Turn up the CEVA flaring to 3 or 4% or give a bolus of propofol
step 200% oxygen and switch to manual ventilation.
Get your hand on the bag. You can feel the compliance and
resistance much better than the machine can tell you.
It also helps you rule out a ventilator malfunction.
Step 3. Pharmacology.
Beta 2 agonists. You have cellbutamol.
You can puff it directly down the ETT using a specific adapter
or use a nebulizer. In the breathing circuit, give 6
to 8 puffs and assess the response.
Step 4. Add anticholinergics like
ipratropium bromide. It's often given together with
the cellbutamol for a synergistic effect on
bronchodilation step. Five if things aren't improving.
4 Steroids hydrocortisone hundred 200 milligram or
dexamethasone. Remember this takes hours to
work so it won't fix the spasm now, but you must give it early
to treat the underlying inflammation and prevent that
late phase reaction. Step 6. 5V Magnesium sulfate 2G
infused intravenously over about 20 minutes.
How does magnesium work here? It acts as a smooth muscle
relaxant. It interferes with calcium
uptake and signaling in the bronchial smooth muscle cells,
causing them to relax. It's very effective in severe
refractory cases. Is there a role for epinephrine?
Yes, in refractory life threatening cases, if the blood
pressure is dropping and you can't break the spasm, give low
dose IV epinephrine. You can give it in small boluses
of say 10 to 20 micrograms at a time, or as a continuous
infusion. In ketamine.
If you haven't already used it for induction, a bolus of
ketamine, say .5 milligram, can also help break the.
Spasm. The surgery is done, you've
managed the spasm. Time to wake them up.
Section 17 and 18. Post operative complications in
management. The main post op complications
are a recurrence of bronchospasm, especially during
extubation, hypoxia due to ongoing VQ mismatch, and
atelactasis. Those mucus plugs can easily
collapse segments of the lung. And the extubation itself.
This is always a tense moment. It is This is the great debate.
Deep versus awake extubation. So deep extubation means taking
the tube out while they are still deeply anesthetized?
Yeah, and Gwettel's stage 3 so they don't cough on the tube.
Right, it's elegant when it works.
No coughing, no bucking, no bronchospasm triggered by the
tube. But you lose your airway
protection immediately If they vomit or have a lot of
secretions they can aspirate. It requires an expert hand and a
guaranteed easy airway. And awake extubation.
This is safer from an aspiration point of view, but they will
almost certainly cough on the tube, and that coughing is a
powerful trigger for bronchospasm.
So what's the exam answer? There's no perfect choice.
The safe answer for a generalist and for the exam is usually
awake but smooth. This is the middle ground.
You utilize Ivy to cane or small doses of opioids to suppress the
cough reflex, but you ensure they are fully awake, following
commands and breathing adequately before you pull the
tube. However, you should mention that
deep extubation is an option in carefully selected patients.
Post op pain control matters too I assume.
Absolutely. If they are in pain, they
splint. They don't take deep breaths.
That worsens atelectasis and mucus plugging.
Epidurals are fantastic for thoracic or major abdominal
surgery and asthmatics because they provide excellent pain
relief without respiratory depression.
Let's briefly touch on Section 19 ICU management for severe
asthma or status asthmaticus. When do we decide to intubate a
patient with severe asthma in the ICU?
It's a last resort. We try everything else first.
Bipap, high flow oxygen, continuous nibs.
The indications for intubation are a rising Paco 2 indicating
fatigue, a deteriorating level of consciousness, or of course,
cardiorespiratory arrest. But ventilation and status
asthmaticus is famously dangerous.
Extremely, the risk of barotrauma like causing a
pneumothorax and severe hypotension from auto PEEP is
very high. We use the strategy of
controlled hypovilation. We deliberately allow the CO2 to
rise permissive hypercapnia to keep the airway pressures down.
We prioritize keeping the plateau pressure below 30
centimeter HA2O overachieving a normal pH.
And constantly watching for that auto P.
Constantly. If they suddenly become
hypotensive on the ventilator, your first move is to disconnect
the circuit and manually decompress the chest.
Before we wrap up, let's hit Section 20 comparison tables.
These are high yield for the Viva voce.
Let's do a quick fire round. Asthma versus COPD.
Age of onset asthma is usually childhood or early adulthood.
COPD is midlife or later. Asthma is associated with
allergy, atopy, eczema. COPD is overwhelmingly
associated with smoking. Asthma shows significant
reversibility with bronchodilators.
COPD shows minimal or only partial reversibility.
DLCO, diffusion capacity. This is a key differentiator.
It is normal and pure asthma because the lung parenthema, the
alveoli are intact. It is decreased in emphysema
predominant COPD because the parenchema is destroyed.
That DLCO point is a great Viva nugget.
It shows a deep physiological understanding.
It separates the students who've read deeply from those who have
just skimmed the summary chapter.
Let's review Section 21 common exam questions in Viva drafts.
We've covered a few trap one. Is wheezing a sign of severity?
No, a silent chest is far worse. Trap 2A normal ABG in a panting
asthmatic. It's a sign of impending
failure, not stability. Trap 3 Using Atrocurium for
muscle relaxation. Don't say it.
It's a known histamine releaser. Stick to rocaronium or
vecaronium. And the Examiner's favorite
waveform? The Kapnograph in bronchospasm,
the shark fin be able to draw it and explain why Phase 2 is
prolonged and phase 3 is upsloping due to uneven alveolar
emptying. Section 22 Diagrams In a written
exam, what should we definitely draw?
Definitely draw the flow volume loop showing this scooped out
appearance of obstruction. And for a management question,
draw the bronchospasm management algorithm as a flow chart.
It saves time, it's clear and it looks professional.
Let's summarize Section 23 summary and exam conclusion.
Give us the final high yield. Recap the take home points.
OK one, asthma is fundamentally a disease of inflammation and
hyper reactivity. It's not just about muscle
spasm. 2 Preoperative optimization is mandatory before
any elective surgery. Symptom free is the goal.
Three avoid histamine releasing drugs like thiopentone,
atrocurium, and morphine 4. Deep anesthesia before any
airway manipulation is non negotiable.
Light anesthesia is your enemy. 5 And finally, permissive
hypercapnia is your friend. When ventilating a severe
asthmatic, prioritize low pressures over a normal CO2.
That is a solid foundation if you can articulate those five
points clearly in a very good position.
Mastering this topic gives you confidence.
It's a common clinical case, but when managed poorly, it's a
nightmare. When you manage it well, it's
smooth sailing. Good luck to everyone preparing
for the Gujarat University exams or for any anesthesiology board
exam for that matter. You have the tools now.
My advice? Go practice drawing those flow
volume loops in the shark fin capnograph right now.
Don't wait. Get it into your muscle memory.
Next time, we tackled the Cardiac Risk Index.
Until then, keep diving deep.