Hello and welcome back to the Dee Dive.
Today we are shifting gears. We are moving away from general
curiosity and stepping right into the high pressure, high
stakes environment of the medical examination hall.
That's right. Specifically, we are simulating
a hardcore prep session for a Gujarat University MD
Anesthesiology student. Right.
And if you are listening to this, you likely have the
distinct pleasure or terror of facing a thoracic anesthesia
case in your practicals or staring down a 20 mark long
theory question on this exact topic.
Exactly. So for the next hour, I'm going
to adopt the persona of your senior faculty member, maybe
even that slightly intimidating external examiner sitting across
the table peering over their glasses for you to slip up.
And I'll be the learner, the resident who has, you know,
frantically read Miller Morgan and Mikhail and Yao and Artuzio
the night before, but needs to synthesize all that dense text
into a coherent, passing answer. It's a lot to bring together
under pressure. It really is.
Our mission today is crystal clear.
We are cracking the code on one lung ventilation or OLV.
We are going to cover the indications, the incredibly
complex Physiology, the hardware and, of course, the management
of that dreaded intraoperative hypoxia.
It is the absolute bread and butter of thoracic anesthesia.
I mean, if you cannot manage OLV, you simply cannot call
yourself a thoracic anesthetist. It's that fundamental.
It is, and from an exam perspective, this topic is a
goldmine for examiners. It tests your Physiology, your
pharmacology, your physics, and your crisis management all at
once. So let's get serious.
Let's do it. Let's jump right into Part A,
introduction and exam framing. If I'm sitting in the exam hall
and I get a question on OLV or the examiner asked me to define
it, how do I set the scene? I need a definition that you
know, screams competence. You need to be crisp and
academic. Do not just say breathing with
one lung, that's too simplistic. One lung ventilation is defined
as the mechanical separation of the two lungs to allow
ventilation of one lung while the other is allowed to
collapse. Separation and isolation, those
are the keywords. Those are the keywords.
It shows you understand the core principle.
You're not just turning 1 lung off, you're creating a physical
barrier between the two. And strictly speaking, why do we
do it? I mean, biologically, we're
designed to use both lungs. Collapsing one seems completely
counterintuitive. It is, and that's the central
challenge, but it's the defining skill of our subspecialty
because it achieves 2 absolutely critical things.
First, it provides a still surgical field, the so-called
quiet lung. Right, the surgeon needs to see
what they're doing. They do modern thoracic surgery,
especially video assisted techniques.
VATS is impossible if the lung is inflating and deflating in
the surgeon's face. They're working with long
instruments through tiny ports. They need a motionless target.
And the second reason. The 2nd and arguably more
critical reason for patient safety is it protects the
healthy lung from contamination. Contamination like from blood or
pus? Exactly.
We'll get into the specific indications, but imagine one
lung is full of infectious material or is bleeding
massively. Without isolation, that material
would immediately spill into the healthy, dependent lung and
you'd have an absolute catastrophe on your hands.
But physiologically, this is a disaster, isn't it?
I remember reading in Miller's Anesthesia that thoracic
anesthesia is often described as a physiological trespass.
That is the perfect phrase to use in an introduction
physiological trespass. It shows the examiner you
appreciate the gravity of what you're doing.
So what does that mean exactly? Think about it.
We are deliberately creating a massive right to left
intrapulmonary shunt. We are collapsing a lung, so
ventilation the V in VQ becomes 0.
The blood flow continued. But perfusion the Q continues to
that lung. So we are actively taking venous
blood, running it through a lung that has no oxygen oxygen, and
then mixing that unoxygenated blood right back into the
arterial circulation. It's a controlled physiological
crisis. Controlled crisis is a great way
to put it. Our entire job during OLV is to
manage that crisis and keep the patient safe despite the
trespass we've committed. I like that framing.
Before we get into the weeds of how we survive that crisis,
let's look at the exam patterns. Looking at the DMB questions and
some Gudrat University past papers, how does this topic
usually appear? You need to be ready for three
distinct formats. First, the long question.
This is your 10 or 20 marker. Discuss indications, Physiology
and management of hypoxia during OLV that requires A structured,
logical essay. So a full on brain dump but
organized. Organized is the key.
You need headings, subheadings. You can't just ramble second,
you'll see it as short notes. OK, like 5 markers.
Exactly, you'll see hypoxic pulmonary vasoconstriction or
double lumen tubes or Physiology of the lateral decubitus
position as standalone 5 mark questions.
They're testing specific pockets of your knowledge.
And the Viva, that's where the nerves really kick in.
In the Viva they will physically hand you a double lumen tube and
say identity. Identify this, tell me about it
or they'll give you a scenario. The dreaded scenario.
The classic 1 you are doing a lobectomy.
The patient is on one lung ventilation and the saturation
drops to 85%. What do you do?
And you need a stepwise answer. You need an algorithm, a calm,
logical, stepwise answer. If you stumble on the management
of hypoxia, you fail the station.
Period. Safety is paramount.
OK, that definitely says the stakes.
Let's move to Part B indications.
This seems like it could be a rote memory section, but I know
examiners are picky about the order and classification.
How do we present this to impress them?
Presentation is everything. Do not just vomit a list of
surgeries onto the page. You must classify them
logically. The standard text Morgan, Yao,
Miller, they all classify indications into absolute and
relative. Absolute and relative and the
order matters. The order matters tremendously.
If you list a lobectomy, which is a relative indication, before
you list a massive lung Abscess, which is absolute.
You show the examiner you don't understand clinical priority.
You put the life saving indications first.
OK, so let's start with the absolute indications.
These are the must knows the non negotiables.
The first category of absolute indications is isolation for
contamination control. The goal here is to prevent
spillage from a diseased lung to a healthy.
Lung. So protecting the good lung.
Protecting the good lung at all costs.
Think about infection. Imagine a patient with a massive
lung Abscess or severe Bronchiectasis.
We're talking about a lung cavity filled with liters of
pus. If that pus spills into the
healthy lung when you turn the patient lateral, you've
essentially caused bilateral pneumonia.
You've destroyed the patient's only means of oxygenation.
It's catastrophic. And hemorrhage fits in here too,
I assume. Yes, massive hemoptysis.
If a patient is bleeding heavily from a tumor or a vessel in one
lung, you must isolate that side.
You have to stop the healthy lung from literally drowning in
blood. OK.
So infection and hemorrhage, that's category one for absolute
indications. Yeah.
What's the second absolute category?
The second is called differential lung ventilation.
This is a bit more of a physiological concept.
It's for situations where the two lungs have such a different
mechanical properties that they simply cannot be ventilated
together effectively via a single tube.
The classic example being the a bronchopleural fistula.
Exactly a bronchopleural fistula or BPF.
Let's walk through that. A fistula is an abnormal
connection between the bronchus and the pleural space.
So air is leaking out. Air is leaking out.
If you try to ventilate that patient with a standard tube,
all the positive pressure you apply follows the path of least
resistance. It goes straight out the fistula
and into the chest drain. The lung doesn't inflate the air
just bypasses it entirely. And the patient becomes hypoxic
and hypercarbic. Very quickly.
So to ventilate that patient at all, you must isolate the good
lung and ventilate it alone while the fistula side is left
open. I also have giant unilateral
bulla on my list here under differential ventilation.
Correct. A bulla is a large thin walled
air SAC. If you apply positive pressure
ventilation to a patient with a giant bulla without isolation,
one of two bad things can happen.
The bullet can expand and rupture, causing attention.
Pneumothorax. Which is an emergency.
A life threatening emergency or the bullet can act like a
compliance sink. It's so floppy that it steals
all the tidal volume from the healthy parts of the lung,
leading to poorer gas exchange. So isolation is absolute.
And there's one more rare one that always seems to pop up in
exams. Unilateral bronchopulmonary
lavage. Yes, specifically for a
condition called pulmonary alveolar proteinosis.
It's a rare disease where the alveoli fill up with a thick,
proteinaceous Milky fluid. Right.
And the treatment is basically to wash it out.
Literally, the treatment is to wash the lung out with liters
and liters of warmed saline. Obviously you cannot drown one
lung with saline while the other is trying to breathe unless they
are perfectly absolutely isolated from each other.
So to summarize for an exam answer, absolute indications are
one, protection from contamination like infection or
hemorrhage, and two, situations requiring differential
ventilation, like a BPF or a giant Bola.
Perfect. Now let's talk about relative
indications. In the real world.
This is actually 95% of what we do, isn't it?
It is this category is broadly termed surgical exposure.
We collapse the lung to make the surgeon's life easier, the
surgery faster and often safer. How do we break this down?
We can subdivide this into high priority and lower priority,
though the lines are blurring. High priority would include
major procedures like a thoracic aortic aneurysm repair, a
pneumonectomy, removal of the entire lung, or an upper
lobectomy. Why is an upper lobectomy
considered high priority compared to say, a middle or
lower lobectomy? It's purely about anatomical
access. The upper lobes are harder for
the surgeon to get to and manipulate.
But let's be honest, in the modern era of minimally invasive
surgery, this distinction is becoming a bit academic.
You mean because of UTS? Exactly, if you are doing video
assisted thoracoscopic surgery VATS where the surgeon is
working through tiny keyhole ports with a camera, OLV is
effectively mandatory. They cannot see a thing if the
lung is inflating and deflating. So for any VATS procedure, you
can consider it a very strong, relative, almost absolute
indication. So for the exam, I should list
isolation for protection first as the absolute indications,
then list surgical exposure as the relative category.
But be sure to mention that in modern practice, especially with
VATS, it's essentially required. Exactly.
That nuance shows you understand both the textbook theory and the
reality of the modern operating theater.
It's a high scoring approach. All right, let's dive into Part
C Physiology. This is what you call exam gold.
If I can explain this clearly, I passed the Physiology stage and
we talked about the shunt earlier.
Let's really unpack the ventilation perfusion or VQ
changes. OK, let's visualize the switch.
The patient is anesthetized in the lateral position and you're
ventilating both lungs. VQ is mismatched as we'll
discuss, but it's relatively stable.
Then you tell your assistant to clamp the lumen to the non
dependent lung. Let's say the left lung is up
and you clamp it's tube. So ventilation to that lung
instantly stops v = 0. Instantly V is 0.
But the heart doesn't know you've done this.
It keeps pumping blood. The right ventricle keeps
sending unoxygenated blood to the pulmonary artery, which
splits and sends blood to both the right and the left lung.
So perfusion Q continues to that collapsed left.
Lung, it continues, and so that blood goes through the
capillaries of the collapsed lung, picks up 0 oxygen and then
returns via the pulmonary veins to the left atrium.
That is the definition of a right to left shunt.
Now let's look at the math, because the textbooks like Yao
and Artuzio love the math. What kind of numbers are we
talking about here? In a normal healthy person, the
physiologic shunt, the small amount of blood that bypasses
the lungs, is less than 5%. It's negligible.
OK. When you start OLV, assuming the
patient is on their side, roughly 40 to 50% of the cardiac
output is still directed to that non dependent lung, at least
initially. So theoretically, if I just
clamp the tube without any compensatory mechanisms, I
should have a 40 to 50% shunt? Theoretically, yes, and a 50%
shunt is incompatible with life. Your PO2 would plummet
instantly. You would be profoundly cyanotic
within minutes, but that's not what happens.
Why not? Because the body has a powerful
intrinsic defense mechanism, and in reality the shunt usually
settles around 20 to 30%. Still significant, but
manageable. And that defense mechanism is
hypoxic pulmonary vasoconstriction.
This brings us to .4. I see this ass as a short note
all the time. Write short notes on HPV.
How do I structure that answer to get full marks?
OK for a short note on HPV you need 4 parts.
Definition, mechanism, role in OLV and factors that inhibit it.
Let's start with the definition. Start with a precise definition.
HPV is a protective local physiologic reflex where
pulmonary arterioles constrict in response to low alveolar
oxygen tension. The emphasis is on alveolar
oxygen. Crucial distinction.
It is not the oxygen in the blood, the PO2, that triggers
it. Primarily it's the lack of
oxygen in the air SAC. The Pio 2 itself itself.
The lung senses hypoxia locally and reacts locally.
OK, that's the definition. Now the mechanism.
The examiner wants to know the cellular level stuff.
How does the lung know to constrict?
It's incredibly complex and not fully understood, but here are
the keywords for your answer paper.
It involves an oxygen sensor in the smooth muscle cells of the
pulmonary arteries. Under hypoxic conditions, this
sensor leads to an inhibition of voltage gated potassium
channels. OK, stick with me.
Potassium channels are inhibited.
What happens next? Normally, potassium leaks out of
the cell, keeping the inside of the cell negatively charged.
When you inhibit these channels, potassium is trapped inside the
cell. Positive charges build up.
This causes the cell membrane to depolarize.
And that depolarization is the trigger.
That's the trigger. That change in voltage opens up
L type voltage gated calcium channels.
Calcium then floods into the cell from the outside.
And calcium causes contraction and smooth muscle.
Calcium binds to comodulin, which activates myosin light
chain kinase, the actin, myosin filament slide and boom
vasoconstriction. Is there any other pathway
involved? I seem to remember something
about nitric oxide. Yes, that's another important
piece of the puzzle. Normally healthy oxygenated lung
tissue constantly produces vasodilators like nitric oxide
or NO and prostacyclin. They keep the vessels relaxed.
So when the alveolus becomes hypoxic.
Nanosynthesis drops, so you're getting a double whammy.
You have an active vasoconstriction process
happening due to the calcium influx, and at the same time
you're losing the background vasodilation.
The balance tips heavily toward construction.
So the vessel effectively strangles the blood flow to the
useless collapsed lung. Exactly.
It's an elegant auto regulation system.
It diverts blood away from the hypoxic lung towards the
ventilated oxygen rich lung. This is what reduces the shunt
fraction by about 50%. So instead of that catastrophic
50% shunt, you get a more manageable 20 to 25% shunt.
Is this response instant? Does it happen the second I
clamp the tube? That's a great question, and
it's the detail that will get you extra marks.
It's biphasic. Biphasic.
Yes, phase one is rapid. It starts within the seconds of
the onset of hypoxia and reaches about half its maximal effect at
around 20 to 30 minutes. But then there's a bit of a
lull. In Phase 2.
Phase 2 is a slower, more sustained response that kicks in
after about 40 minutes and continues to increase for up to
two hours. Which implies that the most
dangerous time for hypoxia might actually be in that first 20 to
30 minutes right at the start, before that phase two
reinforcement really kicks in. 100% that first half hour of one
lung ventilation is when you are most physiologically vulnerable
and need to be most vigilant. Now here is the classic Viva
trap. The examiner asks what factors
inhibit HPV? Basically, what can we as
anaesthetists do to accidentally kill this life saving reflex and
cause hypoxia? This is a huge topic.
If you inhibit HPV, you increase the shunt and the patient
saturation will fall. You need to know this list cold.
What's at the top of the list? The biggest culprit is our own
drugs, Volatile anaesthetics, halothane, isafluorane,
sevafluorane, dysfluorane. They are all directed
vasodilators and they inhibit HPV in a dose dependent manner.
So the more gas I give, the worse the inhibition.
Precisely the general rule of thumb, the one to quote in the
exam, is keep the volatile concentration below 1 Ms. At
concentrations greater than one MAS, they significantly blunt
the HPV response. So if I'm struggling with
oxygenation during OLV, turning up the civil thorium is the
absolute wrong move. The worst thing you can do?
It might deepen the anesthesia and stop the patient from
moving, but it will worsen the and make the hypoxia more
profound. This is a major reason why TIVA,
or total intravenous anesthesia with propofol is so popular for
thoracic cases. Cropofol does not inhibit HPV.
What about other drugs? Any direct vasodilator?
Think about drugs we might use for blood pressure control.
Nitroglycerin, Sodium nitroproside, Hydrolazine.
They'll dilate everything, including the vessels in the
collapsed lung, which overrides HPV.
Beta agonists like salbutamol can also inhibit it.
What about physiological factors?
Things not related to drugs. Alkalosis is a big one, both
respiratory and metabolic. Hypocapnia, a low CO2 from
overventilating the patient, causes pulmonary vasodilation
and blunts HPV. So if you're hyperventilating
the patient thinking you're helping by blowing off CF2, you
might actually be worsening their oxygenation.
That's a key clinical point. It is also extreme changes in
volume status. Hypervolemia can mechanically
force vessels open. Hypothermia inhibits the
response and finally infection. A septic or infected lung often
doesn't vasoconstrict well because of all the inflammatory
mediators which are potent vasodilators.
OK, let's move to .5, the effect of anesthesia and positioning.
We almost always do these cases in the lateral decubitus
position. The patient is lying on their
side. How does that by itself mess
with VQ matching? This is a fantastic Viva
question. You have to explain it as a tale
of two states, the awake patient versus the anesthetized and
paralyzed patient. Let's start with the awake
patient lying on their side. What's happening?
In the awake patient, gravity pulls blood down, so the
dependent lung, the bottom lung, gets more blood flow.
More perfusion. OK, perfusion goes down.
What about ventilation? You'd think ventilation might go
to the top lung because it's less squashed, but the opposite
is true. In the awake, spontaneously
breathing patient, the dependent part of the diaphragm is pushed
up into the chest by the abdominal contents.
It's more curved. And a more curved muscle is a
stronger muscle. By the law of la place, being
more curved gives it a mechanical advantage.
On contraction. It acts like a stronger piston,
so in the await patient the bottom lung gets more blood and
more ventilation. V&Q are pretty well matched.
So awake lateral is actually quite efficient.
Now, what happens when we induce anesthesia and paralysis?
Everything falls apart. First you paralyze the
diaphragm. It turns from an active piston
into a floppy passive sheet. Now the weight of the abdominal
contents, the liver on the right, the stomach and spleen on
the left pushes up and crushes the dependent lung.
It loses compliance. So ventilation shifts.
Yes, air is lazy. It follows the path of least
resistance. So with positive pressure
ventilation the air preferentially goes to the non
dependent or upper lung which is less compressed and more
compliant. But gravity hasn't changed.
Blood still goes down. Exactly.
Gravity still pulls blood to the dependent or bottom lung.
So now you have a massive VQ mismatch.
The blood is going down, but the air is going.
Up. Blood goes down, the air goes
up. It's the worst case scenario for
gas exchange. We call this the 4060 rule.
As a rough guide, in the lateral position under anaesthesia,
about 60% of blood flow goes to the dependent lung and 40% goes
to the non dependent lung. But most of your ventilation is
going to that non dependent lung with less blood flow.
This is why the dependent lung is so prone to atelectasis even
before you start OLV. That Physiology really sets the
stage for the challenge. Now let's talk about the tools
we use to manage this Part D techniques and devices for OLV
.6 lung isolation techniques. You have three main weapons in
your arsenal. Number one and the most common
is the Double lumen Endotracheal Tube or DLT.
That's the gold standard. What are the other options?
#2 is the bronchial blocker and #3, which is usually reserved
for emergencies or very small pediatric patients, is
endobronchial intubation with a standard single lumen tube
basically just intentionally main stemming a regular tube?
Let's focus on the exam favorite .7, the double lumen tube.
Describe it for the listener who can't see one right now.
DLT is essentially 2 tubes of different lengths bonded
together side by side. They're usually D shaped in
cross section to save space. One tube is shorter and ends in
the trachea. That's the tracheal lumen.
The other tube is longer and is designed designed to extend into
a main stem bronchus. That's the bronchial lumen.
And they have two cuffs. It has two cuffs and two pilot
balloons. There's a large tracheal cuff,
usually white, which is a high volume, low pressure cuff just
like a standard ETT. It sits in the trachea and seals
the entire airway. And the second cuff.
The second cuff is the bronchial cuff, which is usually blue.
It's smaller and sits inside the bronchus to seal just that one
lung. Traditionally these were low
volume, high pressure cuffs which carried a risk of ischemic
damage, but modern ones are much better.
OK, the eternal question, left versus right DLT, the patient is
having a right sided thoracotomy.
Which tube do I choose? This is a classic trick
question. In 90 to 95% of all cases, the
answer is you choose a left DLT. Even if you are operating on the
right lung. Even if you are operating on the
right lung, you place a tube in the left main stem bronchus and
ventilate the left lung while the right lung, the surgical
lung collapses. Why?
Why not match the tube to the bronchus?
On the non operative side it seems more logical.
It's all about the anatomy and the margin of safety.
The left main bronchus in an adult is relatively long, About
5, 5 centimeters before the 1st branch, the left upper lobe
takes off. It's like a long safe landing
strip. It's easy to park a tube there
without blocking anything. And the right side is different.
Dramatically different. The right main bronchus is
extremely short, sometimes only 1 1/2 to 2cm before the right
upper lobe bronchus originates. It comes off at a very sharp
angle. So if I try to place a right
DLTI risk blocking the right upper lobe?
Almost guaranteed, if the tube is just a little too deep, the
bronchial cuff will cover the RUL orifice and you'll collapse
the entire right lung when you only meant to ventilate it.
If it's too shallow, the cuff will herniate back into the
trachea and you won't get good isolation.
I've seen right DLTS have a special slot in the cuff.
They do to solve this problem right?
DLTS have a special ventilated slot, like a Mufi's eye on the
side of the bronchial cuff that you must align perfectly with
the RUL orifice using a bronchoscope.
It is technically very difficult and the tube can easily get
dislodged. It's a last resort.
So when do we use a right DLT? What are the specific
indications? Only when you absolutely cannot
use the left bronchus. For example, if there's a large
tumor inside the left main bronchus that you can't get
past, or if there's been a trauma, a left sided bronchial
rupture, or sometimes a descending thoracic aortic
aneurysm can compress the left bronchus so much you simply
can't pass a tube. Only then do you reach for the
right sided tube. Got it now .8 bronchial
blockers. These seem to be gaining
popularity. When should I be thinking about
using a blocker instead of DLT? The number one reason to think
blocker is difficult? Airway.
Why is that? DLT's are bulky, they're stiff,
they're large, and they have an aggressive curve.
If you have a patient with a known difficult airway, a
Malampotti 4, limited mouth opening, poor neck extension,
you do not want to be wrestling with the DLT.
The risk of trauma or a failed intubation is too high.
So what's the strategy? The strategy is you secure the
airway first with a normal familiar single lumen tube,
maybe over a fiber optic scope, confirm you're in, and then once
the airway is safe, you pass the bronchial blocker through the
single lumen tube and guide it into position.
Or if the patient already has a tracheostomy.
A perfect indication you can't easily put a long curved DLT
through a short straight tracheostomy stoma.
A blocker pass through a single lumen tract tube works great.
Another key indication is if you anticipate the patient will need
post operative ventilation. Right, because you can't leave a
DLT in for long. You can't, it's uncomfortable
and traumatic. So if you use a DLT, you have to
exchange it for a single lumen tube at the end of the case,
which is a high risk procedure. In a post thoracotomy patient
with a blocker, you just deflate the balloon and pull the blocker
out, leaving the standard ETT in place.
What are the downsides then? Why don't we just use blockers
for everyone? The two main problems are slow
lung deflation and easy dislodgement.
ADLT has a huge lumen to let air out, and for suctioning a
blocker's central channel is tiny, maybe 2mm.
It can take forever for the lung to collapse, which frustrates
the surgeon. And the dislodgement issue?
They're just not as secure as a DLT.
A little bit of coughing or even just the surgeon manipulating
the bronchus can easily push the blockers balloon back into the
trachea and suddenly you lose isolation and you're ventilating
both lungs again right in the middle of a critical part of the
surgery. That brings us to .9
confirmation. This is absolutely critical.
You've placed your device, whether it's a DLT or a blocker,
how do you know for sure that it's in the right spot?
There are clinical methods and then there's the gold standard.
Clinically, we use auscultation. You follow a sequence, inflate
the tracheal cuff, confirm bilateral air entry, then
inflate the bronchial cuff, clamp the trachealumen and
listen. You should hear breath sounds
only on the ventilated side and silence on the clamped side.
But how reliable is that? Honestly, for the exam and for
real life, clinical signs are unreliable.
Sound can be transmitted across the media.
Steinm the gold standard. The only acceptable answer for
ensuring safety is fiber optic bronchoscopy FoB.
Describe the view for a correctly placed lefty Lt.
The examiner hands you the scope.
What are you looking for? It's a 2 step check.
First I pass the scope down the tracheal lumen.
I should be able to clearly see the Karina to the right.
I see the entrance to the right. Main bronchus is wide open and
unobstructed to the left. I should see the top of the blue
bronchial cuff of the DLT sitting just inside the left
main bronchus just below the Carina.
What are you checking for specifically with that cuff?
I'm making sure it's not herniating out into the trachea,
which would risk slipping, and that it's not so deep that it
might be blocking the left upper lobe.
You want to see just a sliver of blue?
OK, that's step one. What's Step 2?
Step 2 is I pull the scope out and pass it down the bronchial
lumen. Looking through the tube, I
should see a clear, unobstructed view down the left bronchus.
I should be able to identify the orifices of the left upper and
lower lobes. This confirms my tube isn't too
deep. And when do you perform this
check? You check immediately after
intubation while the patient is still supine, and this is the
Viva trap that catches everyone. You must check it again after
you have turned the patient into the lateral decubitous position.
Because the tube moves during positioning.
Almost always, turning a patient from supine to lateral can move
the Carina relative to the tube tip by a centimeter or more.
What was a perfect position supine can become a disaster in
the lateral position. You must reconfirm with the
scope before the surgeon makes an incision.
Moving on to part E Anaesthetic management .10 Preoperative
assessment. What am I looking for?
We use the three legged stool approach described in Miller.
It's a framework for assessing risk.
The first leg is respiratory mechanics.
So PFTS, pulmonary function tests.
Exactly. You're looking at the FEV one
and the FTC. The key number to remember is an
FEV one of less than two liters or less than 40% of predicted.
If the patient is below that, they are at high risk for post
operative complications. We also calculate a predicted
post operative FEV one or POOFE V1 to see what they'll be left
with. OK, that's leg one.
What's the second leg? The second leg is gas exchange.
You're assessing the lung parenchyma itself.
The main test here is the DLCO, the diffusing capacity for
carbon monoxide. ADLCO less than 40% predicted is
another major red flag and you'll look at the baseline
arterial blood gas. Are they retaining CO2 at rest?
Is their PO2 low on room air? And the third leg of the stool.
The third leg is cardio pulmonary reserve.
This assesses the patient's overall fitness.
It's one thing to have good lungs, but can the heart and
muscles handle the stress of surgery?
This is where we look at things like stair climbing.
Can they climb two flights of stairs without stopping?
Or more formally, A cardio pulmonary exercise test to
measure their VO2 Max. What's the critical value for
VO2 Max? AVO. 2 Max of less than 10 to 15
milliliters per kilogram per minute is associated with a very
high risk of morbidity and mortality.
Let's talk about predictors of desaturation.
If I'm looking at a patient's chart pre op, what tells me this
particular patient is going to be difficult and will likely
turn blue during OLV? There are three classic
predictors. First right sided surgery.
Why right sided? Because the right lung is
bigger. The right lung has three lobes
and accounts for about 55% of total lung function.
The left has two lobes and accounts for 45%.
If you collapse the bigger lung, you're creating a bigger initial
shunt. Makes sense.
What's the second predictor? Low preoperative pay O.
If the patient is already struggling to oxygenate on 2
lungs while breathing room air, they have very little
physiological reserve. When you take one lung away,
they are very likely to become significantly hypoxemic.
And the third one is a bit of a paradox, isn't it?
The VQ scan. Yes, this is a great one to
mention in an exam. A normal VQ scan is a risk
factor for desaturation. That sounds completely
counterintuitive. It does, but think about it.
A VQ scan tells you how much perfusion is going to the lung
that you are about to operate on.
If that lung has normal perfusion, it means you are
about to create a huge shunt when you collapse.
It as opposed to a patient with a big tumor.
Exactly, if a patient has a massive tumor that has already
destroyed the blood supply to that lung, it's perfusion on the
VQ scan will be very low. In that case, collapsing it
doesn't really change the Physiology much.
The shunt is already present. So paradoxically, a healthy,
well perfused lung is more dangerous to collapse. .11
Induction in airway management. Any special considerations here?
The induction itself is usually a standard 4 induction.
The key is you need profound muscle relaxation.
You cannot have the patient coughing or straining while you
are trying to position a bulky DLT.
That's a recipe for airway trauma.
OK, what about tube sizing? It's important.
Too small a tube gives you high resistance and makes suctioning
difficult. Too large a tube risks trauma to
the larynx or bronchus. As a rough guide, for adult
females we use a 35 or 37 French tube and for males a 39 or 41
French. You mentioned a key tip earlier,
nitrogen washout. Can you expand on that?
Yes, before you initiate OLV, you should ventilate the patient
with 100% oxygen for a few minutes.
The goal is to wash out all the nitrogen from the lung that
you're about to collapse and replace it with oxygen.
Why does that help? Because nitrogen is an inert
gas, it has very low blood solubility.
If you leave a lung full of nitrogen and air, the nitrogen
acts like a splint holding the alveoli open, and the lung
collapses very slowly. Whereas oxygen gets absorbed.
Oxygen is rapidly absorbed by the blood flowing through the
pulmonary capillaries. So if the lung is full of pure
oxygen, this process of absorption atelectasis helps the
lung collapse much much faster. The surgeon will thank you. .12
Intra operative ventilation strategy.
I said this is very high yield and that practice has changed
significantly. It has.
If you read an old textbook it might say use high tidal
volumes, 10 to 12 milliliters per kilogram to prevent
atelectasis and keep the sats up.
Do not say this in the exam. Why not?
Because we now know that causes volley trauma and Barrow trauma.
You're forcing all that volume into just one lung.
You're over distending the healthy alveoli causing
inflammation and setting the patient up for post operative
acute lung injury, or Ali. So what is the modern standard?
What should I say in the Viva? You should say you will use a
protective lung ventilation strategy.
This has several key components. OK, what's the first one?
First, tidal volume. We use low tidal volumes, around
5 to 6 milliliters per kilogram of predicted body weight, not
actual body weight. We are gentle with that one
working lung. 2nd component. Heap positive and expiratory
pressure. We advocate for the routine
application of about 5 centimeters of water of PEEP to
the dependent ventilated lung. And why is that so important?
Remember our discussion about positioning That dependent lung
is being crushed by the media Steinem and the abdomen.
It is desperate to collapse. Applying a little bit of PEEP
acts as a pneumatic splint to keep those alveoli open and
participating in gas exchange. So low volume?
Add peep. What about the respiratory rate?
You adjust the respiratory rate to maintain a reasonable Paso
two. It will likely need to be higher
than normal, maybe 16 to 18 breaths per minute, to
compensate for the low tidal volume.
And what if the CO2 still climb? This is where the concept of
permissive hypercapnia comes in. We're often willing to tolerate
a slightly higher Paso two, say up to 50 or 60mm of mercury, as
long as the pH is above 7.25. The priority is protecting the
lung from high pressures, even if it means accepting a little
bit of respiratory acidosis. OK, we are now in the thick of
it. Part F Management of hypoxia.
This is the big 20 mark question.
The surgeon is working, you're on OLV and the pulse oximeter
starts that dreaded downward alarm tone.
De Tone De Tone 88 percent 85. First rule is don't panic.
Panic paralyzes your thinking and kills the patient.
You need to have a calm pre rehearsed drill.
But first let's talk about .13 causes.
Why is this happening? What's the most common reason?
By far the most common cause is tube Mal position.
The DLT has slipped, the bronchial cuff has herniated
back into the trachea, or the tube is advanced too far and is
now obstructing an upper lobe. Before you think of anything
else, you think about the tube. What are some other causes?
It could be a simple obstruction like a thick sputum plug in the
airway, it could be bronchospasm, or it could be
curely physiological. You have a massive shunt because
the patient's HPV is poor, maybe because your volatile agent is
too high, or your patient has low cardiac output leading to
low mixed venous oxygen saturation, which makes any
shunt much more impactful. So .14 the stepwise management
of hypoxia. Walk me through the algorithm,
the drill. OK, stats are falling.
Immediately turn your Fio 2 to 100%.
If you're using their oxygen mix, this eliminates that as a
variable. OK, 100% oxygen, what's Step 2?
Step 2. Check tube position.
Announce to the surgeon that you have a problem.
Quickly auscultate. But most importantly you must
confirm the tubes position with your fiber optic bronchoscope.
This is not optional. So I have to pause everything
and get the scope out. You do pass it down the tracheal
lumen first. Is the branchial cuff still in
the bronchus or has it herniated out?
If it has, fix it. That will solve 90% of your
problems right there. What's step three if the two
position is perfect? Step 3.
Suction both lumens. A thick mucus plug can
completely obstruct A lumen and cause a massive shunt.
Clear the airway. Step.
Four Step 4. Check and optimize hemodynamics.
Is the patient hypotensive? Is the cardiac output low?
If it is, the blood returning to the lungs is already very
desaturated, which magnifies the effect of the shunt.
Treat the hypotension with fluids or vasopressors.
OK, so I've done all the basic checks.
Tube is fine, airway is clear, blood pressure is good, but I'm
still saturating at 85%. What's next?
Now we have to start manipulating the Physiology.
Correct Step 5. Perform a recruitment maneuver
on the dependent lung. That bottom lung is squashed and
likely has significant atelectasis.
Give a sustained breath. For example, hold a pressure of
30 to 40 centimeters of water for 20 to 30 seconds to pop open
those collapsed alveoli. And after recruiting?
Step 6. Apply or increase PEEP to the
dependent lung. If you started with five, try
increasing it to 8 or 10. This will help keep those newly
recruited Ovioli open, but be careful.
Why be careful? Peep is usually good for
oxygenation. It's a delicate balance.
If you apply too much PEEP to the pendant lung, you can over
distend it. This increases the pulmonary
vascular resistance in that good lung.
And that diverts. Blood, it diverts blood flow
away from the good ventilated lung and forces it back into the
collapsed non ventilated lung which actually increases your
shun fraction and makes hypoxia worse.
You have to find the sweet spot. OK so I've tried recruitment and
optimal peep and it didn't work. We are getting desperate.
Sats are critically low. What's the big gun?
Step 7 Apply C pap to the non dependent collapsed lung.
This is probably the single most effective physiological maneuver
you can perform. Explain that I'm applying
pressure to the lung the surgeon is operating on.
Yes, you connect a special circuit and apply a small amount
of continuous positive airway pressure, just two to five,
maybe up to 10 centimeters of water and some oxygen flow to
the lung that is supposed to be collapsed.
But won't that inflate the lung and completely obscure the
surgical field? At 2:00 to 5:00 centimeters, it
usually just puffs it up a tiny bit.
It often doesn't interfere with the surgeon too much, but what
it does physiologically is provide oxygen to those alveoli
in the collapsed lung. So the blood that is inevitably
shunting through that lung now has a chance to pick up some
oxygen. So it converts a pure shunt into
an area of low VQ. Precisely, it can raise the
saturation from 80% to 95% almost instantly.
It's a hugely powerful technique.
And if even that fails. If that fails you have two
options left. Step 8 is to tell the surgeon
stop. I need to re expand the lung.
You abandoned OLV temporarily. Go back to two lung ventilation,
bring the sats up to 100% and then try again once the patient
is stable. And the final ultimate step.
Step 9, which is really a surgical maneuver, clamp the
pulmonary artery. If the surgeon is doing a
pneumonectomy or low the bectomy, they can temporarily or
permanently clamp the pulmonary artery branch going to the
collapsed lung. This mechanically eliminates the
shunt entirely. That is the ultimate fix.
That is a life saving algorithm. So to recap the order Fio 2
check tube suction hemodynamics, recruit dependent lung, PEEP to
dependent lung, CPAP to non dependent lung, then
intermittent to lung ventilation.
Correct. Memorize that order.
It's logical, it's safe, and it shows the examiner you
understand the underlying Physiology.
Let's wrap up with Part G post operative and ICU
considerations. Now that the surgery is over,
what are we most worried about? .15 Post operative
complications, the biggest fear after major lung resection is
acute lung injury or Ali in the remaining lung.
This is from the ventilation strategy we used.
It can be it presents like ARDS, you see pulmonary edema,
hypoxia. It can be caused by the volume
trauma from over distending the dependent lung or from
reperfusion injury when the collapsed lung is re inflated.
This is. Exactly why we are now so
obsessed with the protective lung ventilation strategy.
What about other complications? Nerve injuries are common,
brachial plexus injury from poor arm positioning during the lung
surgery and lateral or phrenic nerve damage from the surgery
itself, leading to a paralyzed humidiophrine which can be
devastating after endominectomy. And .16 post operative
management. What is the most critical
element here? Without a doubt, pain control.
A thoracotomy is one of the most painful incisions in all of
surgery. If the patient is in agony, they
won't take deep breaths, they won't cough effectively, and
they will develop atelectasis and pneumonia.
So what's the gold standard for analgesia?
The thoracic epidural is the gold standard.
A catheter placed in the epidural space, providing A
continuous infusion of local anesthetic and opioid, provides
excellent dynamic analgesia without sedation.
And if an epidural is contraindicated or fails?
A para vertebral block is a fantastic alternative.
It involves injecting local anesthetic next to the spine
where the intercostal nerves exit, effectively blocking the
entire half of the chest wall. Finally, Part H Exam
integration. Let's create some quick
reference comparison tables and highlight the traps.
A good idea. Table 1.
DLT versus bronchial blocker key pros and cons.
OK DLT pros fast and definitive isolation.
Lung deflation is quick and you have large lumens for easy
suctioning. DLT cons more difficult to
place, higher risk of airway trauma and you must exchange it
at the end of the case if post op ventilation is needed.
And the blocker? Blocker Pros Excellent for known
difficult airway, can be used in patients with a tracheostomy and
no need to change the tube for post op ventilation.
Blocker Cons Lung deflation is very slow.
The narrow channel makes suctioning pour and it dislodges
very easily. Table 2.
Awake a lateral versus anesthetized lateral position.
Simple awake lateral ventilation matches perfusion.
Both are preferentially directed to the dependent lung.
VQ matching is good. Anesthetized lateral A massive
VQ mismatch. Ventilation preferentially goes
to the non dependent upper lung, while perfusion preferentially
goes to the dependent lower lung.
And the Viva traps, we've mentioned a few, the need to
recheck the tube after positioning, the danger of high
volatile agent concentrations inhibiting HPV.
What about nitrogen? Right.
An examiner might ask why did you use 100% oxygen for
induction instead of inter oxygen mix?
The answer is not just about pre oxygenation you say I use 100%
oxygen to facilitate a nitrogen washout as nitrogen has low
blood solubility and acts as a splint delaying the collapse of
the non dependent lung. Pure oxygen promotes rapid
absorption atelectasis. That's a very slick answer.
And if they ask you to draw a diagram in the exam.
Be prepared. Practice drawing a simple
diagram of the Karina with a left DLT in position.
Practice drawing the shunt diagram showing mixed venous
blood in a capillary bypassing an unventilated alveolus, and
practice drawing the hypoxia management algorithm as a flow
chart. Visuals break up text and score
points. So let's structure a long answer
introduction. Introduction then indications
classified as absolute and relative.
Then Physiology with a big section on HPV, then techniques
comparing DLTS and blockers, then a detailed section on the
stepwise management of hypoxia. Finished with post op
complications and management. Let's summarize .20.
What are the key high yield take home points for the student
heading into that exam hall? OK, here's the rapid fire recap.
OLV is the deliberate separation of the lungs for surgical
exposure or protection from contamination.
It creates a massive physiological shunt.
Your body's primary defense against this shunt is hypoxic.
Pulmonary vasoconstriction do not inhibit HPV with high
concentrations of volatile agents. 4 The left DLT is the
standard choice for lung isolation due to the anatomical
margin of safety of the left main bronchus.
The gold standard for confirming placement is fiber optic
bronchoscopy, and you must recheck position after turning
the patient lateral. Ventilate the single lung using
a protective strategy. Low tidal volume of 5 to 6mm per
kilodrama and add five of PEEP. Seven, if hypoxia occurs, follow
the algorithm. First check and fix the tube.
Last, apply CPAP to the non dependent lung or ask the
surgeon to pause. Excellent post operative pain
control, preferably with a thoracic epidural, is critical
to prevent pulmonary complications.
Fantastic to the student listening.
You have the knowledge now. The key is structure.
Structure your answers clearly use headings, bullet points and
diagrams. Don't ramble.
Be the safe, calm, knowledgeable consultant they want to hire.
Exactly. Go draw that hypoxia algorithm
right now. Burn it into your memory.
Good luck. That's it for this deep dive.
We'll see you next time.