Welcome back to the Deep Dive. Today we are shifting gears
retty significantly. Usually we take a bit of a
casual stroll through a topic, but today, today feels
different. We're not just browsing, we're
reing. I want you to imagine the lights
are bright, the air conditioning is humming and you are sitting
right across from a very stern faced examiner at Gujarat
University. That's exactly right.
We are simulating a high stakes pre exam study session.
This isn't just about learning for the sake of, you know,
curiosity. This is about survival, it's
about passing the MD anesthesiology exams.
We are really targeting that postgraduate student who's read
the books, who's been through the wards but now needs to
synthesize it all into a cohesive Viva ready performance.
And we have a massive stack of sources today.
I mean, we've got the heavy hitters like Miller's Anesthesia
and Morgan McHale. We've also got the objective
anesthesia review, piles of old DNB question bank papers, and
the the long and short cases text.
So our mission, our mission today is to take this mountain
of information and distill it into the ultimate audio guide on
chronic obstructive pulmonary disease.
COPD. And let's be absolutely clear
why we're tackling COPD In the world of anesthesia exams, this
is what we call a bread and butter topic.
It's fundamental. You will see it in your theory
papers. You will almost certainly get a
patient who smokes for your long case.
And if you survive all that, it will be waiting for you in the
Viva. Let me be blunt.
If you can't manage COPD, you can't be an anesthetist.
OK, so the stakes are set. I'm playing the role of the,
let's say, the exhausted resident.
I've read the chapters but the Physiology is all tangled up in
my head and frankly I'm terrified of saying the wrong
thing to the examiner. And I'm your senior faculty.
I'm here to guide you, to point out the exam traps, and most
importantly, to tell you exactly what the examiner wants to hear.
We're going to cover everything from the ground up,
pathophysiology, clinical features, investigations and of
course the all important anesthetic management.
OK, let's do it. Let's start with part A,
introduction and exam framing. So if I'm in the exam hall, I
draw that long question card and it just says obstructive lung.
Where do I begin without just rambling?
You start with precision, that's the key.
Don't jump straight into COPD as bad lungs, that's too
simplistic. You need to frame the territory
first. So you begin your answer with
the broad category obstructive lung diseases.
OK, defining the landscape first, not just this specific
town. Right.
And as per the standard texts and exam guides, you need to
classify this landscape, the classic exam duality.
The first thing you should write down is asthma versus COPD and.
The difference isn't just as simple as one is from allergies,
one is from smoking. Right?
That feels too basic for an MD level.
No, that's undergraduate level thinking.
For your MD exam, the critical distinction, the keyword is
reversibility. Asthma is characterized by
airflow obstruction that is for the most part reversible.
It comes and goes. It's triggered by inflammation,
but it can be reversed. But COPD, the definition you
absolutely must memorize, and this is straight from the
textbooks, is a disease state characterized by airflow
limitation that is not fully reversible.
Not fully reversible. That phrase, it feels like it's
doing a lot of heavy lifting. It sounds very deliberate.
It is. It does.
It implies that what we can help a bit with our bronchodilators.
The underlying architecture of the lung is permanently damaged.
It's broken. The airflow limitation is
usually progressive, and it's associated with an abnormal
inflammatory response of the lungs to, you know, noxious
particles or gases. Which brings us neatly to the
epidemiology in the exam. Do I need to be quoting precise
global statistics or is it more about the concept?
It's about acknowledging the burden.
You don't need another prevalence in every country, but
you need to state that smoking is the primary cause, accounting
for maybe 85 to 90% of cases. The key for us, for
anaesthetists, is the surgical population.
If you're working in any busy hospital, 20, maybe even 30% of
your elderly patients coming for surgery will have some degree of
COPD. So it's completely unavoidable.
It's not a rare disease we're preparing for.
Exactly, and that is precisely why it's an exam favorite.
It's not abstract. It tests your understanding of
respiratory Physiology, pharmacology, and critical care
all at once. You might get it as a short note
on a specific concept like auto peep or or flow volume loops.
You might get a 20 mark theory question on anesthetic
management of COPD OR. And this is the most likely
you'll get the long case A 65 year old chronic smoker coming
for a laparotomy. OK, I'm framed.
I think I understand the context, I know what it is, and
I know why it matters. So let's move to Part B
pathophysiology. The outline here says this is
absolutely essential. It is the absolute foundation.
If you don't understand the mechanics of what's broken in
the lung, you will. And I'm not being dramatic, you
will kill the patient with a ventilator for the exam.
You want to break the pathophysiology down into a very
specific, memorable framework. What's the framework?
How should I structure my answer?
Think of it as a detrap 4. Key components 1.
Chronic airflow limitation that's the hallmark 2.
Inflammation and remodeling 3. Mucus, hyper secretion and four
loss of elastic recoil. OK, let's unpack that second
one. Inflammation and remodeling.
I always picture just a swollen red airway, but it's more
complex than that, isn't it? It's much more, yeah.
This is where you can quote your reading from Miller.
It's not just simple edema. The chronic irritation, usually
from cigarette smoke, causes the bronchiolar smooth muscle, the
BSM, to increase in both tone and bulk.
It gets bigger and tighter. The actual wall of the airway
gets thicker. So the tube itself is physically
narrower even before mucus comes into play.
Yes, and then the lining of that tube changes.
You get something called goblet cell hyperplasia.
These are the cells that produce mucus.
So not only is the tube narrower and stiffer, but you're also
flooding it with secretions. That covers your Third Point,
mucus hypersecretion. That's the chronic bronchitis, a
component of the disease. Right now #4 loss of elastic
recoil. This is the one I always
struggle to explain clearly, even to myself sometimes.
I get that the lung is floppy, but why does that specifically
trap air? Let's use an analogy.
It's the best way to explain it in Aviva.
Imagine a brand new party balloon.
It has high elastic recoil. You blow it up.
You let go of the opening and snap.
The air rushes out forcefully. The rubber wants to collapse
back to its original state. Right, it empties itself.
Now imagine an old flabby balloon that's been
overstretched 1000 times. You blow it up, you let go, and
the air just sort of drifts out slowly, lazily.
That is the emphysematis lung. It has lost the intrinsic
driving pressure to exhale effectively.
OK, that makes sense. But there's another factor too,
right? I remember reading something
about the Airways themselves collapsing.
Correct, and this is a slightly more advanced concept, perfect
for scoring extra marks. It's the concept of radial
traction. In a healthy lung, the millions
of alveoli that surround the small Airways act like guy ropes
on a tent. They're all pulling out words,
holding the airway open, stenting it in emphysema.
You are pathologically destroying those alveolar walls.
You are in effect cutting the guy ropes.
So when the patient tries to exhale, the pressure from the
chest pushes on these unsupported Airways and they
just they flop shut. Exactly.
That is the definition of dynamic airway collapse.
The air is trapped by the closed door, and this single fact
dictates your entire anesthetic ventilation strategy.
You must give the patient a long, long time to get that air
out past that collapsing point. This leads us perfectly into
section three types of COPD. We often hear the old terms pink
puffer and blue bloater. Is that terminology still used?
Is it safe to use in an exam? It is, and examiners actually
love it because it represents 2 very distinct clinical
phenotypes, even if most real world patients are a mixture of
the two. Let's start with chronic
bronchitis. This is defined clinically.
Clinically, meaning it's based on symptoms, not a lab test.
Yes, the strict definition is a productive cough for three
months in each of two successive years in a patient in whom other
causes of chronic cough have been excluded.
These are your blue bloaters. And why blue?
Because they tend to become hypoxemic and cyanotic quite
early in the disease course, Their main problem is that the
tubes, the bronchi, are clogged with mucus, they have a profound
VQ mismatch, they often rely on their hypoxic drive to breathe,
they retain CO2, and they develop core poliola, right
heart failure, which leads to peripheral edema, hence
bloating. And the other side of the coin?
The Emphysema Group. This is defined pathologically.
It's not a symptom, it's a structural diagnosis.
It is the permanent destruction of the alveolar walls and
enlargement of the airspaces distal to the terminal
bronchioles. These are the pink puffers.
Pink because they managed to stay oxygenated.
For a very long time, yes. Their primary problem isn't
clogged tubes, It's the loss of surface area for gas exchange
and that loss of elastic recoil. They compensate by maintaining a
massive respiratory Dr. They hyperventilate to maintain their
PO2. They're often breathless, thin,
and cachectic because they're burning so many calories just in
the work of breathing. They're puffing to stay pink.
OK, that's a very clear distinction.
Let's go even deeper now into Section 4 effects on lung
mechanics. We've touched on resistance, but
what about compliance? This feels like a classic Viva
trap question. It is huge trap.
The examiner will lean forward and ask doctor is the compliance
high or low in COPD and there isn't one simple answer.
In pure chronic bronchitis, the compliance of the lung tissue
itself is often normal. The problem is purely high
resistance. However, in emphysema the static
compliance is actually increased.
That always confuses me. Increased compliance sounds like
a good thing. Compliant means easy, right?
Compliant means distensible. It's easy to blow air in.
That floppy old balloon is very compliant.
It expands with very little pressure.
The problem isn't getting air in, it's the lack of recoil to
get it out so high. Static compliance in this
context is deeply pathological. Which brings us to the monster
of this whole topic, Auto Peep, or as some books call it,
dynamic Hyperinflation. This is without a doubt the
single most critical concept for the statist in this entire
discussion. You understand this, You can
keep the patient safe. OK explain it to me like I'm in
the Viva and I'm starting to panic.
OK, take a breath. Respiration is a cycle.
Inspiration then expiration. Simple.
In a patient with COPD, expiration is pathologically
slow. This is due to the combination
of high airway resistance and low elastic recoil.
If you, the anesthetist controlling the ventilator,
initiate the next breath before the patient is fully finished
exhaling the previous breath, you trap a small residual volume
of air. You're stacking breaths on top
of each other. Precisely.
Breath after breath after breath, that trap volume
accumulates the patient's functional residual capacity.
FRC begins to rise. The pressure inside the alveoli,
the very end of expiration, is no longer zero.
It becomes positive. That positive pressure is
intrinsic PEEP or auto PEEP. And why is that so lethal?
I know it causes the blood pressure to crash, but why?
What is the mechanism? You must be able to explain the
hemodynamics clearly. The heart lives inside the chest
inside the thorax. Specifically, the superior and
inferior vena cava are low pressure vessels that have to
pass through the thorax to return blood to the heart.
If the lungs hyperinflate with trapped air, they physically
expand and compress everything around them.
They compress the vena cava and the heart itself, so
intrathoracic pressure rises dramatically.
This leads to a drop in the pressure gradient for venous
return. Less blood gets back to the
right ventricle, so preload drugs.
An empty heart can't pump what it doesn't have.
Exactly. An empty heart means no cardiac
outlet. And to make matters worse, at
the same time the hyperinflated lungs are squishing the tiny
pulmonary capillaries, which dramatically increases pulmonary
vascular resistance, or PVR. So the right ventricle is empty
and it's trying to pump against a brick wall.
This is a recipe for acute right ventricular failure and
cardiovascular collapse. The patient goes into PEA
pulseless electrical activity. That is a genuinely terrifying
image. OK, we'll definitely talk about
how to fix that in the management section, but that
mechanism is crystal clear. Now let's move on to Part C, gas
exchange and Physiology. Right.
And here we need to talk about VQ mismatch.
This is your Section 5. Ventilation versus perfusion,
the matching of air and blood. In COPD the lungs architecture
is destroyed and chaotic. You have some areas where there
is blood flow but no air getting in.
This is a shunt like effect. This is typical of a mucus plug
in bronchitis. And you have other areas where
there's plenty of air but no blood flow.
This is Dead Space. This happens because emphysema
destroys the capillary bed along with the alveoli.
And I see here the DNB questions source explicitly asks about the
clinical importance of anatomical and physiological
Dead Space. Yes, physiological Dead Space is
essentially wasted ventilation. You're moving air in and out of
a part of the lung that isn't participating in gas exchange.
But here is the anesthetic relevance you absolutely must
mention in your answer. Hypoxic pulmonary
vasoconstriction or HPV. The body's own defense mechanism
against this mismatch. Correct.
Normally if a part of the lung isn't getting oxygen, the body
is smart. It constricts the blood vessels
going to that hypoxic area to shunt blood towards the healthy,
well ventilated parts of the lung.
It tries to optimize the VQ matching.
But, and this is the crucial part, our volatile anesthetic
agents like isoflurane and suboflurane are vasodilators.
They inhibit HPV. So our anesthesia is actively
making the VQ mismatch worse. It can, yes.
It reopened those constricted vessels, sending blood back into
the poorly ventilated hypoxic areas of the lung.
This increases the shunt fraction and can cause a sudden
drop in the patient's oxygen saturation right after
induction. You need to be aware of this and
anticipate it. OK.
That's a huge point. Now Section 6 ABG changes.
This is an exam favorite, the whole acute versus chronic
thing. The hallmark of severe advanced
COPD is chronic CO2 retention. Their bodies get used to a high
level of CO2, but the body doesn't just let the blood
become acidic, it compensates. We call this compensated
respiratory acidosis. And how does the body
compensate? What's the mechanism?
The kidneys It's a slow but powerful process over days to
weeks. The kidneys respond to the
chronic high CO2 by retaining bicarbonate HCO 3, which is a
base. This buffers the acid.
So when you look at an arterial blood gas report, if the Paco 2
is high, let's say 60 millimilli HG, but the pH is in the normal
range, say 7.35 to 7.4 year, it is chronic.
The kidneys have done their job and the bicarbonate will be
high. But if the PECO 2 is high and
the pH is low, so acidotic it is acute, This is an acute
exacerbation and the kidneys haven't had time to catch up
yet. And that is a absolutely vital
distinction for determining if a patient is stable enough for an
elective surgery. Exactly.
An acute uncompensated acidosis is a huge red flag.
Stop optimize the patient. A chronic compensated acidosis
is often just that patient's baseline.
And just briefly to round out the section, Section 7, the
oxyhemoglobin dissociation curve, where does it?
It shifts to the right. You need to recall the bore
effect, the state of acidosis. So high H plus ions and
hypercapnea, high CO2 both cause the curve to shift to the right.
Right equals release. Correct.
It's an adaptive immunism. It means that for any given
partial pressure of oxygen, the hemoglobin has a lower affinity
for it. It gives up his oxygen more
easily to the tissues that desperately need it.
Perfect. OK, let's move to Part D,
clinical features and investigations.
We're at the bedside now in the pre op clinic.
What are the key things we are looking for?
The respiratory signs are obvious, the wheeze, the barrel
chest, the purse, lip, breathing, you'll see those from
the door. But the real money the marks are
in looking for the cardiovascular signs, you
absolutely must, must look for signs of core pulmonale.
Right sided heart failure caused by the lung disease.
Yes, and the long and Short cases textbook emphasizes this
over and over. You have to physically examine
the patient. Look for pedal edema, swelling
in the ankles, look for raised jugular venous pressure, the JVP
in the neck. Listen to the Heart for a loud
P2 heart sound. Why is this a fail?
If I miss it, why is it so critical?
Because the presence of corporal manal means the disease is
advanced and the cardiovascular system is already decompensated,
it drastically increases the risk of perioperative mortality
if you stand up in a long case presentation.
And you haven't mentioned checking the patient's ankles
for edema or looking at their JDP.
The examiner will stop you right there.
It shows you missed a critical risk factor.
OK, message received Section 9 Pulmonary function tests PFTS.
This is marked as absolutely essential.
Spirometry is the gold standard for diagnosis and severity
assessment. You need to know the numbers
cold. The key diagnostic ratio is FEV,
one FEC, the force expertory volume in one second divided by
the force vital capacity. If that ratio is less than .7 or
70%, that confirms the presence of an obstructive defect.
And how do we grade the severity?
The severity is then graded based on the FEV 1 as a
percentage of the predicted value for that patient's age,
sex, and height. Mild is an FEV one greater than
80%, predicted moderate is between 50 and 80%, severe is
between 30 and 50%, and very severe is less than 30%.
You need to memorize that table, no?
Excuses. What about the flow volume loop?
They often ask us to draw this in the exam.
What should it look like? OK, picture a normal loop.
The inspiration is a smooth semicircle and the expiration is
a straight sharp line going down to the baseline.
In COPD, the loop looks scooped out.
It becomes concave, curving inwards.
Why? Because as the patient tries to
exhale forcefully, their unsupported Airways start to
collapse. That dynamic compression we
talked about? This limits the flow rate and it
drops off drastically as they exhale.
Looks like someone took a bite out of a sandwich.
That's a great visual. The bitten sandwich loop.
I'll remember that and section 10 other investigations.
What should I look for on an ECG?
You're looking for evidence of chronic right heart strain.
The classic sign is P pulmonale. This is a tall peak P wave
greater than 2.5mm high, which you'll see best in the inferior
leads, so 2-3 and AVF. It signifies right atrial
enlargement. You might also see right axis
deviation or a right bundle branch block pattern.
These are all signs of right ventricular strain.
Excellent. Let's move into part E
preoperative assessment. We're back in the pre op clinic.
How do we properly assess the risk this patient poses?
The history is actually more important than any of the tests.
The textbooks are very clear on this.
You need to ask about their functional capacity.
Don't just ask are you breathless?
Ask practical questions. Can you climb two flights of
stairs without stopping to catch your breath?
Hunter piece? If they can do that, their
metabolic equivalent or me tease is likely greater than four and
they are probably a reasonable risk for most surgeries.
If they get breathless just walking from the waiting room to
your office, they're extremely high risk.
OK, now for Section 11, the slightly controversial topic,
smoking cessation. The patient is in front of you,
their surgery is next week. They ask you doctor, should I
stop smoking today? What's the right answer?
This is a classic exam trap and you have to explain the timeline
very carefully. There are different zones of
benefit and risk. Zone 1, the short term, we're
talking 12 to 24 hours. Does this help?
Yes, absolutely. It significantly reduces the
levels of carbon monoxide in the blood.
This shifts that dissociation curve back to the left,
improving oxygen carrying capacity, and it also reduces
the nicotine induced tachycardia.
So quitting the night before is definitely beneficial for oxygen
delivery. But then there's a period where
it's actually worse, right? The so-called danger zone.
Exactly. Zone 2, roughly 2 days to four,
maybe even six weeks. In this window the Airways start
to wake up. The cilia which were paralyzed
by the smoke start regenerating and beating again.
The volume of sputum they clear actually increases.
The Airways could become hyper reactive.
So, paradoxically, if you stop smoking just three or four days
before surgery, you might actually be more prone to
bronchospasm and mucus plugging than if you had just continued.
That is so counterintuitive, I can see how that would trip
someone up. It is so the ideal of course is
zone 3 greater than 8 weeks. That's the minimum time it takes
for the immune system to start normalizing and for sputum
volume and reactivity to genuinely decrease.
So for the exam, your answer is ideally the patient should stop
smoking at least 8 weeks before surgery.
If that is not possible, then quitting at least 12 to 24 hours
beforehand is beneficial. However, we must be very
cautious in the intermediate window of a few days to a few
weeks, as airway reactivity may increase.
Perfect. What about optimization?
What can we actively do in that pre op period to make them
safer? There are four key things.
One, bronchodilators make sure they are taking their prescribed
inhalers correctly and consistently optimize a regimen.
2 steroids. If they are actively wheezing or
have had a recent exacerbation, a short course of oral steroids
can significantly calm down the airway inflammation 3.
Physiotherapy. This is huge.
Teach them how to use an incentive spirometer before the
surgery so they know how to do it afterwards.
Teach them how to cough effectively.
The huff, cough and four Treat any active infection.
If their sputum is purulent so green or yellow, delay elective
surgery if possible and give them a course of antibiotics.
And for Section 12 risk stratification, what's the
bottom line? Remember that the surgical site
matters most. Upper abdominal and thoracic
surgeries carry the highest risk because the incision causes
pain, which leads to splinting, and they often involve cutting
through respiratory muscles. A knee replacement in the same
patient is a much, much safer proposition.
OK, Part F Anesthetic management, the main event,
Section 13. Choice of anesthesia.
The examiner looks at you and asks General or regional?
And you have to give a balanced answer for any peripheral
surgery. So limbs, lower abdomen,
regional anesthesia, RA is generally the preferred choice.
Because you completely avoid putting a tube in their very
reactive airway. Precisely no tube means no
instrumentation, no reflex bronchospasm and you avoid the
need for positive pressure ventilation or PPV, which
reduces the risk of barotrauma and that dreaded auto peep.
However, you must add a caveat. You have to be careful with the
level of the block. A high spinal or epidural, say
above T10, can start to paralyze the abdominal and intercostal
muscles. And COPD patients desperately
need those muscles to force the air out.
Correct. For them, expiration is an
active process. If you knockout their belly
muscles with a high block, they might not be able to exhale
effectively or clear secretions. So the answer is regional is
good, but keep the level as low as is practical for the surgery.
What about general anesthesia GA?
Sometimes it's just avoidable. A laparoscopic cholecystectomy,
for instance. Then we have a clear plan.
We move to Section 14 induction and airway management.
The primary goal is a smooth, deep induction.
You want to avoid any coughing, bucking or fighting on the tube
as this drives up intrathoracic pressure and can trigger severe
bronchospasm. LMA versus ETT, which is safer?
Well, the literature suggests the Laryngeal Matic Airway LMA
can be beneficial because it sits above the vocal cords.
It is a less stimulating device, so there is theoretically a
lower risk of triggering bronchospasm.
But you can only use it if you don't anticipate high airway
pressures and if the patient isn't at high risk of
aspiration. For many of these cases, you
will need a cuffed endotracheal tube ETT and if you are going to
intubate, ensure the patient is deeply anesthetized.
Using intravenous or topical lidocaine can be very helpful to
blunt the airway reflexes. OK, the patient is intubated
Section 15 intraoperative ventilation strategy.
This is marked very high yield. I am standing at the ventilator.
What numbers do I dial in? You have to remember the
pathophysiology we discussed. Air trapping.
Your entire strategy is designed to let the air out.
Number one, low respiratory rate.
This is the single most effective tool.
You have a rate of eight, maybe 10 breaths per minute.
Slower is better. This is the best way to increase
the available expiratory time #2A long IE ratio.
The ratio of inspiration time to expiration time normal is about
1:00 to 2:00. In a COPD patient, we dial in
one to three, one to four. In very severe cases, even 1:00
to 5:00. South a very quick breath in,
followed by a slow breath out. Exactly #3 permissive
hypercapnia. Because we are deliberately
breathing slowly for the patient, their entitle CO2 will
rise. We must accept this as long as
the arterial pH stays above a safe level, roughly 7.2 O or
7.25. We tolerated a high CO2, say 60
or 70 milli military in order to protect the lungs from the
Bureau trauma of auto PEEP. That's a critical trade off.
A bit of acidosis is much better than a popped lung or a cardiac
arrest. Exactly.
It's a lung protective strategy and #4 PEEP.
This is a bit controversial, but generally we apply a small
amount of extrinsic PEEP, maybe around 5 centimeter H2O.
The theory is that this helps to splint the small Airways open
during expiration and prevent that dynamic collapse we talked
about. Earlier.
Got it. OK, Section 16 drugs.
Let's run through the anaesthetic cart.
Inhalational agents, What's the best choice?
Civil fluorine is widely considered the agent of choice.
It's a potent bronchodilator and it's non pungent so it's very
smooth on the airway. You should definitely avoid
disflurane and probably isoflurane for induction as they
are pungent and can irritate the airway causing coughing and
laryngo spasm. Halothane, for the history
buffs, is a fantastic bronchodilator, but it
sensitizes the heart to catecholi means and can cause
arrhythmia, so it's very rarely used now.
OK, five induction agents. Propofol is an excellent choice.
It effectively suppresses laryngeal reflexes and provides
a very smooth induction. Ketamine is unique and very
useful option, especially in an emergency.
It has sympathomimetic properties.
It causes a release of endogenous catecholamines which
are potent beta 2 agonists and relax bronchial smooth muscle.
It's excellent for the actively wheezing or hypotensive patient.
And what about muscle relaxants? This is a common exam question.
The rule is simple, avoid anything that releases
histamine. So avoid atrocurium and
Vivicurium. Histamine causes
bronchoconstriction, which is the last thing you want.
Use rocaronium, vecaronium, or cisotracurium.
These are clean drugs from a histamine release perspective
and are much safer. Opioids.
Same principle. Same principle.
Morphine is known to cause histamine release.
Avoided. If possible, use a synthetic
opioid like fentanyl or sufentanyl.
And the big one, nitrous oxide and two OA.
Huge red flag in patients with emphysema.
If the patient has bullet which are large air filled cysts in
the lung, the late nitrous oxide will diffuse into these closed
air spaces faster than nitrogen can diffuse out.
The bullet will expand under pressure and can rupture,
causing attention to pneumothorax.
So the rule is strictly no nitrous in any patient with
known or suspected bullets. Emphysema.
OK. Part G Post operative in ICU
care. The surgery is over.
The patient is in recovery. The danger is absolutely not
over. The post op period is fraught
with risk. The main complications are
hypoventilation, bronchospasm and atelectasis, which is lung
collapse, and pain control which is section 18 is absolutely
huge. Because if it hurts to breathe,
they simply won't take a deep breath.
Exactly. That's called splinting, and
splinting leads to addalactasis, which creates a breeding ground
for bacteria and leads to pneumonia.
Thoracic epidural analgesia TEA is the gold standard for pain
relief after major abdominal or thoracic surgery.
It provides profound analgesia without the systemic respiratory
depression you get from high doses of IV opioids.
It allows the patient to cough, mobilize and breathe deeply.
What about NIV non invasive ventilation?
Things like Bipap. An absolute lifesaver in this
patient population. If the patient is struggling
after you've extubated them, don't wait.
Put them on Bipap immediately. It reduces their work of
breathing, it helps blow off any residual CO2, and it stents
their Airways open. It very often prevents the need
for re intubation. And if they do end up in the
ICU, Section 19 weaning from the ventilator.
Weaning can be very difficult and prolonged.
They have weak respiratory muscles and high airway
resistance. We often use modes like pressure
support, ventilation, PSV to help them overcome the
resistance of the breathing tube.
And you shouldn't be afraid to excavate them directly to NIV to
provide that bridge of support. Excellent.
OK, Part H exam integration. Let's bring it all home for the
exam Section 20 comparison tables.
Let's start with the classic asthma versus COPD.
OK, let's do this as a quick fire.
Age of onset asthma is typically early childhood.
COPD is midlife, almost always over 40 Etiology Asthma is often
allergic or atopic. COPD is overwhelmingly due to
smoking or noxious particle exposure.
Clinical course asthma is intermittent with symptom free
periods. COPD is chronic and progressive
and the big one, reversibility. In asthma, you see a significant
improvement in FEV, one more than 12% and 200 milliliters
after a bronchodilator. In COPD you see minimal or no
change. Perfect now for Section 21
common exam questions in Viva traps.
We touched on this earlier, but let's really hammer home the
hypoxic Dr. myth. A junior colleague says I won't
give the COPD patient much oxygen because they run on a
hypoxic Dr. and they'll stop breathing.
What is your response? My response is that this is a
partial truth that is used to justify dangerous practice.
Yes, it is true that in some chronic CO2 retainers the
primary stimulus to breathe is a low level of oxygen rather than
a high level of CO2. But if your patient is hypoxic
within this BO2 of 85%, you must give them oxygen.
Hypoxy kills in minutes. It causes brain death and fetal
arrhythmias. CO2 narcosis on the other hand
takes hours to develop and is reversible.
You always treat the more immediate threat to life.
Furthermore, the main reason their CO2 rises when you give
them oxygen is due to complex physiological effects like the
Haldane effect and reversing HPV which worsens VQ mismatch.
It's not just the brainstem shutting down.
So the safe gold standard exam answer.
Is I will administer controlled oxygen, for example via a 24 or
28% Venturi mask to maintain this BO2 in a target range of 88
to 92%. I will monitor the patient
closely for signs of rising CO2 and drowsiness, but I will never
withhold oxygen from a hypoxic patient.
That is the gold medal answer. I can hear the examiner nodding
and approval. OK, another trap.
The sudden intraoperative crash. We discussed how auto peep can
cause profound hypotension. What is the immediate management
algorithm? The first few steps.
Number one, instantly disconnect the breathing circuit from the
endotracheal tube. This immediately releases any
trap pressure. It treats auto peep and it also
rules out an equipment or ventilator failure #2 Start
bagging the patient manually with 100% oxygen.
This allows you to feel the compliance of the lungs in your
hand. Are they stiff?
Is it hard to bag #3 Listen to the chest with a stethoscope.
If you hear wheezing, it's likely bronchospasm.
If you hear silence on one side, you must suspect A pneumothorax
and #4 Look at your capnograph. A shark fin shape confirms
obstruction. A flat line means either there's
no cardiac output or you're disconnected.
Fantastic section 22 diagrams. What are the essential things I
should be prepared to draw? Three things.
One, the flow volume loop, you must draw the normal loop versus
the obstructive scooped out loop. 2, the captagraph trace,
draw a normal square wave trace next to the shark fin trace of
bronchospasm which has that slow sloping up stroke.
And three, a basic spherogram trace just showing a reduced FEV
1 and a reduced FEC. And finally, Section 23 summary
Exam conclusion. Give me the 62nd summary for the
listener who is walking from the canteen into the exam hall right
now. All right, here's your final
recap. One, define it.
It's a not fully reversible airflow limitation 2 pathology.
It's a mix of loss of recoil which is emphysema and mucus and
inflammation which is bronchitis.
Three key Physiology. Remember air trapping and auto
peep which cause hemodynamic collapse. 4 Pre op focus on
their functional capacity history.
Smoking cessation is best at more than 8 weeks or less than
24 hours. 5 Induction. Ensure deep anesthesia.
Avoid any histamine releasing drugs. 6 Maintenance seven floor
range is your friend. No nitrous oxide if they're a
bullet. 7 ventilation. The mantra is slow rate, long
expiratory time. Your IE ratio should be 1 to
3:00 or 1:00 to 4:00 except permissive hypercapnia 8 post op
and epidural for pain control is ideal.
Use early non invasive ventilation.
And the final word, the key, take away safety.
The examiner wants to know that you're a safe anesthetist.
They want to know you understand the risks.
So verbalize your safety checks. I am worried about auto peep so
I will monitor the flow curve. I will watch for new with
thorax. I'll be careful not to fluid
overload the right heart. Acknowledging the risks is how
you pass. Expert, thank you so much.
That was intense. It was thorough, but I feel like
I can actually visualize the lungs and the ventilator now.
It's a complex topic, there's no doubt about it, but if you stick
to the basic mechanics, the physics of flow and recoil, it
all starts to make sense. Good luck to our students out
there listening. Now grab a pen, draw that flow
volume, loop that bitten sandwich, and go crush that
exam. This has been the deep dive.
Goodbye. Wait wait, wait, hold on, we're
not done yet. That was the executive summary.
That was the high yield pass level stuff, but we have a full
hour to fill and frankly we just glossed over some really
important details, the kind of details that distinguish a pass
from a distinction. You're absolutely right.
We gave them the skeleton. This is a solid skeleton.
But now let's put some meat on those bones.
Let's circle all the way back to Part B pathophysiology.
We briefly mentioned it, but let's talk about A1 antitrypsin
deficiency. The genetic cause of COPD?
Yes. Most COPD is from smoking, but
if you see a young patient, say 35 or 40 years old, who has
never smoked but has severe emphysema, you must suspect
this. It's a deficiency of a crucial
protease inhibitor. Without it, an enzyme in the
lungs called elastase just runs rampant and literally eats the
elastic tissue in the lung. This leads to a specific type of
emphysema called panacinar emphysema, which
characteristically affects the lower lobes of the lungs.
You can compare that to smoking induced emphysema, which causes
sentry asinor emphysema and classically affects the upper
lobes. OK, that's a brilliant
distinction. So smoking equals smoke rises so
it hits the upper lobes in the center of the sinus or sentry
asinor. Genetic is systemic, gravity
wins so it affects the lower lobes and the whole is sinus so
panasinor. Exactly.
Dropping a Pearl like that in Aviva shows you aren't just
reciting the basics from a review book, it shows you've
read in depth. OK, let's dig deeper into Part D
investigations. We talked about the ECG.
What about echocardiography? If my patient has signs of core
pulmonale, what specific numbers am I looking for on that echo
report that will change my anesthetic plan?
An excellent question you are looking for.
The estimated pulmonary artery systolic pressure, or PASP
normal is less than 25 millimeter HG.
In a patient with severe core pulmonale.
It can be 5060 or even higher if that PSV starts to approach the
patient's systemic blood pressure.
The risk of acute right ventricular failure on induction
is absolutely massive. You're also looking for the TR
jet velocity from the tricuspid regurgitation and a key
measurement of RV function called Tape PSE, which stands
for a Tricuspid Annular Plane Systolic Excursion.
Tape PSE. That's a great keyword to use.
If the tape PSE is low, say less than 16mm, it means the right
ventricle is failing. It's weak.
You need to be incredibly gentle with your induction agents.
A standard dose of propofol might cause a complete
cardiovascular collapse. In that situation you might
choose Atomidate, which is famously cardio stable.
We're a very slow, careful titration of ketamine.
Let's revisit part E pre op optimization again.
We mentioned giving antibiotics for an infection.
Which bugs are we actually fighting?
What should I prescribe? The common community acquired
organisms are the usual suspects.
Streptococcus pneumonia, Hemophilus influenza and more
exelic Catarolis. But, and this is another
distinction level point, in a patient who has been in and out
of the hospital frequently, you must have a high index of
suspicion for Pseudomonas urugenosa.
Pseudomonas, the nasty one, the blue-green pots.
Yes, if they have risk factors for it like recent hospital
admission or previous courses antibiotics.
You need to ensure they have anti pseudomonal coverage.
Something like pipersilentasobectom or
siftazodime? And what about their nutritional
status? We see these emphysemedis
patients who are just skin and bones.
How much does that matter? It's a huge independent
predictor of poor post operative outcome.
A low serum albumin, say less than 3 point OGDL, is strongly
associated with poor wound healing, respiratory muscle
weakness, and an inability to wean from the ventilator.
If the surgery is elective, referring them to a dietitian
for a few weeks of high protein nutritional supplements can
genuinely change their outcome. OK, let's expand on Part F, the
intraoperative ventilation strategy.
We said use a low rate, but how do we decide on the exact rate?
Is it just a guess? It has to come down to the idea
of time constants. Right now we are talking
advanced respiratory physics. This is excellent.
Yes. The time constant, which is
often abbreviated as Tau, is a product of the lungs resistance
multiplied by its compliance. It is the time in seconds taken
for 63% of the lung volume to empty during a passive
exhalation. You need roughly three to four
time constants to empty 95 to 98% of the lung volume.
In COPD the resistance is very high and in emphysema the
compliance is also high. So the product Tau is huge.
It's a very long time constant. It takes seconds for their lungs
to empty. That is why we need to provide
four or five seconds of expiratory time.
And if you do the math, 60 seconds in a minute divided by,
say, one second for inspiration plus 5 seconds for expiration.
That's 6 seconds per breath. 60 / 6 is 10 breaths per minute.
That's where the math comes from.
So it's not a random guess, it's calculated based on the
patient's specific lung mechanics.
OK, and let's talk with the crisis intra operative
bronchospasm. We gave the initial algorithm
disconnect bag. Listen, but let's say it is
bronchospasm, the chest is tight and you can hear wheeze.
What is the pharmacological ladder?
What do you give and in what order?
A great question. This is your crisis management
drill #1 Deepen the level of anesthesia.
All volatile agents are bronchodilators.
Increase your several fluorine to two or three Mac if the blood
pressure allows or give a bolus of propofol or ketamine #2
Ensure you are on 100% oxygen #3 Give beta. 2 agonists
cellbutamol pus directly down the endotracheal tube.
You can use specific MDI connector or in an emergency
just disconnect and spray it right down the tube. 4 Add
anticholinergics. Hypertropium bromide works
synergistically with cellbutamol. 5 Intravenous
magnesium sulfate. A dose of 2 grams given over 10
to 15 minutes. It's a calcium antagonist and a
potent smooth muscle relaxant. Can be highly effective. 64V
steroids, hydrocortisone or dexamethasone.
They take hours to work, but you give them now to help with the
inflammation later on. And seven epinephrine.
This is the nuclear option. You can start with small IV
boluses of 10 to 20 micrograms or start a low dose infusion.
Epinephrine. Isn't that just for cardiac
arrest? That sounds quite extreme.
It is the most potent bronchodilator we have.
It is powerful beta 2 agonist effects.
In a severe life threatening silent chest scenario where no
air is moving, small doses of epinephrine can be life saving.
OK, let's talk about a very specific surgical scenario that
comes up all the time, laparoscopic surgery in a
patient with severe COPD. This feels like a double whammy
of problems. It is one of the most
challenging scenarios we face. First, you have the
pneumoperitoneum. The surgeon insufflates the
abdomen with carbon dioxide. This pushes the diaphragm up
into the chest, splitting it, and it compresses the lung
bases. This dramatically worsens
atlactasis. And second, you have CO2
absorption. The CO2 from the belly is
absorbed directly into the patient's bloodstream.
So you have a patient who is already struggling to exhale
their own CO2 because of their COPD, and now you are
systemically loading them with extra CO2 from the surgery.
The end title CO2 on the monitor is just going to skyrocket.
It will, and your natural instinct as a junior
anaesthetist is to see a high CO2 and want to increase the
ventilation to blow it off. Increase the rate.
But you can't. If you increase the rate you
cause auto peep. If you increase the tidal volume
you get dangerously high keek airway pressures.
You are trapped. So what do you do?
What's the strategy? One, you stick to your guns on
permissive hypercapnia, you let that CO2 rise as long as the pH
is safe. 2 Communication. You must speak to the surgeon.
Ask them to lower the insufflation pressure.
Can they operate at 12 millimill HG instead of 15?
Three, positioning. You had to avoid extreme
trendlenberg the head down position as that makes the
diaphragmatic splinting even worse.
And for conversion, if you simply cannot ventilate the
patient safely, you have to be brave enough to tell the surgeon
that they need to convert to an open procedure for the patient's
safety. That communication point is so
key for the oral exam. You have to show that you are
the captain of the ship in that room.
Absolutely. The anesthetist is the guardian
of the patient's Physiology. You have to advocate for it.
Let's just touch on regional anesthesia one more time with a
specific block, a brachial plexus block, specifically an
interscaling block for shoulder surgery.
Is that safe in a patient with severe COPD?
You need to be extremely careful, and interscaling block
because of where the local anesthetic spreads, almost
always causes a temporary frenic nerve palsy on the same side.
This means you paralyze that hemidiophram.
A healthy person can tolerate losing 50% of their
diaphragmatic function just fine.
They won't even notice. But a patient with severe COPD
who is already using every accessory muscle they have to
breathe, losing half their diaphragm might be the final
straw that pushes them into acute respiratory failure.
So the standard teaching is to strictly avoid interscaling
blocks in severe COPD. You'd want to use a
supraclavicular approach, though that has a risk of pneumothorax,
or an axillary approach if the surgery allows.
Fantastic. OK, let's do a true or false
rapid fire around from some of these question bangs just to
submit some of these concepts. OK #1 Routine use of
prophylactic post operative mechanical ventilation is
recommended for all patients with severe COPD.
False. The modern approach is to try
and extubate them as early as possible to avoid ventilator
associated pneumonia and ventilator dependency.
However, we have a very low threshold to use prophylactic
non invasive ventilation. So the strategy is extubate to
NIV or bi PAP, not leave them on the ventilator. #2 inhaled cell
butamol can cause hyperkalemia. False.
It causes hypokalemia. The beta 2 stimulation drives
potassium into the cells. This can be clinically
significant, especially if the patient is already on diuretics,
which also cause potassium loss. It can trigger arrhythmias.
OK #3 Aminopheline is the first line drug for treating severe
intraoperative bronchospasm. False.
It has a very narrow therapeutic index and a lot of side effects
like tachycardia and seizures. Is very much a second or third
line agent now. The inhaled beta agonists,
volatile agents, and magnesium are all superior and safer.
Last one, using a larger endotracheal tube, for example
size 8.5 versus A7 point O significantly reduces the work
of breathing during weaning. True, absolutely true.
You have to remember Poiseu's law resistance is inversely
proportional to the radius to the power of four.
A small increase in the tube's diameter drastically reduces the
resistance to airflow. This can make a huge difference
for a patient with weak respiratory muscles trying to
wean. Expert This has been incredibly
thorough. I feel like we have covered the
basics, the advanced Physiology, the pharmacology and the crisis
management. This is the whole package.
And we've tried to keep an exam focused at every step.
Just remember when you're in that exam, define your terms
clearly, always explain the why the underlying Physiology,
prioritize safety above all else, and don't fall for the
common traps like the hypoxic Dr. myth or the smoking
cessation timing. Thank you again for this master
class. To our listeners, you are now
armed with the knowledge to walk into that exam hall.
Take a deep breath, a long exhalation preferably, and own
the room. Review your notes, practice
drawing that bitten sandwich loop, and we will see you on the
next deep dive. Good luck to all of you.