So picture this, it is 3:00 in the morning.
Oh, the classic ICU hour. Right, The ventilator is just
alarming incessantly. You've got a patient whose BO2
is dropping rapidly like through the 70s, and the arterial blood
gas you just pulled makes absolutely no logical sense.
Yeah. In the clinical world, that's
just a standard Tuesday night. Exactly, but you know in your MD
anesthesiology Viva voce this is the exact moment the examiner
decides your fate. Do you freeze or do you
completely deconstruct the Physiology and like, defend your
ventilator strategy right there under pressure?
And that's exactly why we do not accept surface level answers
from postgraduate candidates. I mean, when you step into that
hall or when you stand at the foot of that ICU bed, you are
the ultimate guardian of tissue oxygenation.
Right. So today, for everyone
listening, we are not just memorizing textbook definitions,
you are stepping into the examiner's mind with us.
We're going to dissect respiratory failure today, not
as a static disease, but as a dynamic, evolving physiological
collapse. If you can explain the why and
the how behind a falling PO2, you won't just pass, you'll
command the room. I mean, if you can trace that
oxygen molecule from the ventilator circuit all the way
down to the mitochondria, that's the gold standard.
So let's start at the foundation, but let's push past
the basic Med school stuff. Absolutely.
Respiratory failure is strictly defined as the inability of the
respiratory system to perform adequate intrapulmonary gas
exchange. But the numbers attached to this
like a PO2 of less than 60mm of mercury on room air and a PECO 2
greater than 49, they always felt, I don't know, somewhat
arbitrary to me when I was a junior resident.
Well, they're anything but arbitrary.
Right. Why?
It's a 60 for the oxygen, Why not 55?
This is exactly where a Viva examiner is going to start
probing you. The number 60 is chosen
specifically because of the sigmoidal shape of the
oxyhemoglobin dissociation curve.
The Cliff, Exactly the Cliff at APO 2 of 60.
You are standing precisely on the precipice of the steep
portion of that curve. So if a patient's PO2 drops from
a perfectly normal 100 down to 60, their hemoglobin saturation
really only falls from, say, 98% down to about 90%.
So they're still compensating pretty well there.
Right. But once you drop from 60 to 50,
you fall off the Cliff. The saturation just plummets
into the 70s or worse. The examiner wants to see that
you understand that 60 is the point of imminent catastrophic
failure. OK, that makes perfect sense.
And what about the Pad 2 threshold, the 49mm of mercury?
That's the point at which the carbon dioxide accumulation
definitively overcomes the body's normal buffering
capacity, assuming, you know there's no primary metabolic
alkalosis driving it, right? But more importantly for
anesthesia, you must articulate why these thresholds matter to
us uniquely. I mean, every single time you
induce general anesthesia, you are actively pushing the patient
toward respiratory failure. Because we're abolishing airway
tone and depressing the central drive.
Yes. And we are drastically reducing
their functional residual capacity or FRC.
Let's hover on FRC for a second, because the relationship between
FRC and closing capacity is just an absolute goldmine for written
answers. It really is.
When we paralyze a patient, you know, the diaphragm relaxes, it
gets pushed cephalid by the abdominal contents of the FRC
plummets and if that FRC falls below the closing capacity, the
small Airways in the dependent regions of the lung just they
collapse during normal tidal breathing.
They do, and blood continues to flow past those collapsed
alveoli, which it's a functional shunt.
And that hysiological cascade is exactly why the traditional
binary classification, you know, just Tye hyoxemic and Tye 2
hyercagnic, it's no longer sufficient for a modern exam.
Right. The examiners want more now.
They expect you to utilize the expanded classification system.
You absolutely have to bring type 3 and type 5 into your
written essays and your Viva discussions.
It proves you have a comprehensive understanding of
perioperative medicine. OK, so let's map out that
expanded system for the listener.
We have a patient crashing over that oxygenation Cliff.
If it's a pure oxygenation failure, the classic type I
we're defining it by APO 2 below 60 with a normal or even low
PO2. Correct.
So type I is primarily a parent chemical issue.
The lung tissue itself. Exactly.
The alveoli, the interstitium, the capillary interface, that's
what's diseased. And this is acute and life
threatening because, well, the brain and the heart simply
cannot survive prolonged hypoxemia.
Right. And then Type 2 conversely is
hypercapnic respiratory failure. So that's ventilatory
insufficiency. Yes, the PO2 is still below 60,
but the hallmark here is a PO2 greater than 45 or 50
accompanied by a respiratory acidosis.
This isn't the lung tissue, this is a failure of the pump.
So the central nervous system drive, the neuromuscular
junction, the chest wall mechanics precisely.
But then we get to type 3, which is honestly arguably our
specific domain as anaesthesiologists, the
perioperative or atelectatic respiratory failure.
We are essentially talking about the iatrogenic consequences of
our interventions, right? And surgical trauma.
Indeed, we are. Type 3 relates specifically to
post operative atelectasis and altered lung mechanics.
I mean, think about it, When a patient undergoes major
abdominal surgery, they experience significant pain.
Don't they splint their diaphragm?
Exactly. They simply will not take deep
breaths. Combine that with the residual
effects of volatile anesthetics, neuromuscular blockade, opioid
induced respiratory depression. And just being supine.
Right supine positioning, their FRC just collapses.
Secretions pool the Airways close.
Examiners want to see you classify this distinctly because
the management is entirely different from a classic Type I
pneumonia. Yeah, you're looking at early
mobilization, regional anesthesia for pain control,
incentive spirometry, maybe some CPAP, not antibiotics and
proning. Exactly.
OK. What about type 5?
Because I feel like this is the one that really trips candidates
up. Shock related respiratory
failure. That's a tricky 1.
If a patient is in profound hemorrhagic or cardiogenic
shock, their primary problem is hemodynamic collapse.
So why? Why on earth do we classify this
under a respiratory failure umbrella?
That is a phenomenal analytical question.
Let's look at the hemodynamics of the respiratory muscles
themselves. In a healthy resting individual,
the work of breathing consumes merely 2 to 3% of the total
cardiac output. It's negligible.
But in a state of profound shock, where there is systemic
hypoperfusion and severe metabolic acidosis, the
respiratory rate skyrockets. The body is desperately
attempting to blow off CO2 to compensate for the lactic
acidosis. So the diaphragm and intercostal
muscles are just working furiously.
Furiously, and in this state, the work of breathing can
consume up to 50% of total oxygen delivery.
Wait 50% just for breathing? Yes.
So the respiratory muscles are actively stealing blood flow
from the splash, neck, bed, the kidneys, the brain, just to keep
the chest wall moving. Exactly.
The cardiovascular system is already failing and it's simply
cannot supply enough oxygen to these vigorously working
muscles. Eventually those muscles
experience ischemia, day fatigue, day fatigue, and you
get sudden respiratory arrest. When we intubate a patient in
severe shock, we are not necessarily doing it just
because their PO2 is low. We're doing it to take over the
work of breathing. Wow.
So by paralyzing and mechanically ventilating them,
we instantly liberate that massive percentage of cardiac
output and give it back to the vital organs.
Precisely, if you explain that hemodynamic redistribution in
your exam, you prove that you understand the integrated path
of Physiology of a critically I'll patient.
Man, that is the kind of insight that turns a failing grade into
a distinction. All right, so we know the broad
classifications. Let's drill down into the
microscopic breakdown. Let's do it.
If the respiratory muscles are intact but oxygenation is still
failing, what is breaking down within the lung itself?
We need to thoroughly dissect the five mechanisms of
hypoxemia. This is exam gold.
It's non negotiable for the exam.
You have to be able to list, define and physiologically
explain all 5. The 1st and overwhelmingly the
most common is ventilation perfusion mismatch or VQ
mismatch. This occurs when alveoli are
under ventilated relative to their perfusion, so you get a
low VQ ratio. And to really understand VQ
mismatch at a postgraduate level, we have to bring up
West's zones of the lung, right? Absolutely.
Because gravity dictates both ventilation and perfusion, so
they're never perfectly matched. Even in a totally healthy
person, perfusion is heavily gravity dependent, so it pools
in the lung bases. Yes, and ventilation also
increases at the bases, but just not to the same degree as
perfusion. Right.
So the base of the lung naturally has a lower VQ ratio
than the apex. Precisely.
And any pathological state that exacerbates this normal
inequality causes hypoxemia. I mean, take it Asthma
exacerbation. Intense bronchoconstriction
limits ventilation to certain lung units, but blood continues
to flow past them. So the blood leaving those units
has a super low oxygen content. Right.
And when that mixes with the well oxygenated blood from the
healthy units, the overall arterial PO2 drops.
But the body has a defense mechanism against this, doesn't
it? Hypoxic pulmonary
vasoconstriction or HPV. Yes, and you must mention HPV in
your answers. It's critical.
When an alveosis becomes hypoxic, the mitochondria in the
adjacent pulmonary smooth muscle cells actually sense that drop
in oxygen. And that triggers a cascade.
It does. It changes potassium channel
activity leading to cellular depolarization, calcium influx,
and intense local vesoconstriction.
The body intelligently shunts blood away from the poorly
ventilated alveolus toward the better ventilated areas.
Trying to fix its own VQ mismatch?
Exactly. But what happens when that
mismatch is so severe that it just completely eliminates
ventilation? That brings us to mechanism #2
shunt, specifically right to left shunt, where the VQ ratio
equals absolute 0. A shunt occurs when mixed venous
blood from the right side of the heart passes to the left side
without ever participating in gas exchange.
So it completely bypasses the system.
Right. This could be intracardiac like
a VSD or tetralogy of phthalate, or more commonly for us it could
be inter pulmonary. Like when alveoli are totally
filled with fluid in ARDS or completely collapsed and severe
atelectasis. Let me push you on a critical
clinical scenario regarding shunt, because this comes up a
lot. If a true shunt means blood is
completely bypassing ventilated alveoli, then walking up to the
ventilator at 3:00 AM and cranking the FIO 2 up to 100%,
that's not just unhelpful, right?
It's potentially causing oxygen toxicity without actually fixing
the profound hypoxia. That right there is the ultimate
test of a candidate's understanding of oxygen
transport. What's the physiological reason
for that failure to respond? Remember the oxygen delivery
equation. The vast majority of oxygen is
bound to hemoglobin. Only a tiny tiny fraction is
dissolved in the plasma. In a severe shunt, the blood
perfusing the colast alveoli leaves completely deoxygenated.
If there's no air. There right?
Meanwhile the blood perfusing the healthy alveoli is already
100% saturated. Even at room air or moderate Fio
2, you physically cannot put more than 4 molecules of oxygen
on a single hemoglobin molecule. Right, it's maxed out.
So by increasing the Fio 2 to 100%, you were only slightly
increasing the dissolved oxygen in the plasma of those healthy
units when that tiny amount of extra dissolved oxygen mixes
with the massive volume of completely deoxygenated shunted
blood. It does nothing.
The PO2 barely moves. Exactly.
Oxygen is essentially useless for a true shunt.
So what's the actual physiological intervention then?
You must apply positive and expiratory pressure or PEEP.
PEEP physically splints the collapsed Airways open.
It forces alveolar fluid back into the interstitium and
recruits those collapsed units back into the functional lung
volume. Converting A0 VQ ratio back into
a viable ventilated unit Precisely.
OK, so we have VQ mismatch and shunt.
What is the third mechanism of hypoxemia?
Diffusion impairment. This relates directly to fixed
law of diffusion, which states that the rate of gas transfer is
directly proportional to the surface area and pressure
gradient and inversely proportional to the thickness of
the membrane. Right, so conditions like
pulmonary fibrosis or interstitial lung disease, where
the membrane gets severely thickened with scar tissue.
And the classic Viva trap here involves exercise, doesn't it?
Like a patient with early pulmonary fibrosis might have a
normal PO2 sitting on the exam table, but the moment they walk
down the hall they become profoundly desaturated.
Exactly, and you need to explain the timing.
At rest, a red blood cell spends about .75 seconds traversing the
pulmonary capillary. Even with a thickened membrane,
oxygen usually has enough time to equilibrate.
But during exercise, cardiac output massively increases.
Right, which drives the blood through the capillary much
faster. The transit time might drop to
.25 seconds. The oxygen simply cannot diffuse
across that thick fibrotic barrier fast enough before the
red blood cell is just swept away into the systemic
circulation. That makes perfect sense.
OK, 4th mechanism. Hypoventilation.
This is a global reduction in minute ventilation.
We'll explore this deeply when we look at the alveolar gas
equation, but essentially, if you aren't bringing fresh air
into the lungs, the partial pressure of carbon dioxide in
the alveolus rises steadily as metabolism continues.
And because the total pressure in the alveolus is fixed by
atmospheric pressure, that rising CO2 physically displaces
the oxygen molecules. Leading to hypoxemia, Yes.
Got it. And the 5th and final mechanism.
Reduced inspired oxygen tension or a low Fio 2.
The textbook example is ascending to high altitude where
the barometric pressure drops, thus dropping the partial
pressure of oxygen. But in the realm of anesthesia,
we need to talk about equipment, right?
Absolutely. You must mention the risk of a
hypoxic gas mixture due to a pipeline crossover and empty
oxygen cylinder or a flow meter failure.
Great. So let's apply these mechanisms
to real clinical pathologies. How does the examiner want us to
categorize the causes of Type I and Type 2 failure?
For type I, the parenchymal failure, you're looking at
diseases that fill or collapse the alveoli.
Pneumonia fills them with pus and inflammatory exudate.
Cardiogenic pulmonary edema fills them with transsudative
fluid due to elevated hydrostatic pressure from a
failing left ventricle. And ARDS fills them with protein
rich fluid because of overwhelming capillary leak.
Let's talk about pulmonary embolism because this is just a
fascinating pathological evolution.
If the examiner gives you a scenario day three post op from
major orthopedic surgery, sudden hypoxemia and tachycardia, we
suspect APE. Classy.
But wait. APE physically blocks blood flow
to a segment of the lung that creates ventilation without
perfusion, which is alveolar Dead Space or an infinitely high
VQ ratio. And Dead Space impairs CO2
clearance leading to hypercapnia.
So why is the hallmark of an acute PE profound hypoxemia?
That is the exact physiological paradox the examiner wants you
to solve out loud. You're correct, the initial
insult is pure Dead Space, but within minutes a complex
secondary cascade begins. The platelets.
Yes, the platelets. Adhering to the embolus and
degranulate, They release potent vasoactive and
bronchoconstrictive mediators like serotonin and thromboxane
A2. This causes intense localized
bronchospasm in the surrounding uninfarcted lung tissue.
Wow. And the lack of pulmonary blood
flow starves the type 2 pneumocytes too.
Right, exactly. They cease producing surfactant.
And without surfactant, alveolar surface tension skyrockets and
the alveoli collapse. Precisely.
So now you have severe adilectosis and
bronchoconstriction in the lung units surrounding the embolus.
As blood flow is diverted away from the blocked artery, it's
forced to perfuse these now collapsed, unventilated alveoli.
So the initial high VQ Dead Space has rapidly evolved into a
low VQ functional shunt. Yes, that secondary shunting is
the primary driver of the severe refractory hypoxemia seen in a
massive PE. That is a brilliant breakdown.
Now let's look at the pump failure, the causes of type 2
respiratory failure. For your exam structure, always
break type 2 down anatomically. Start at the brain and work your
way down. OK, so first CNS depression.
Yes, this includes drug overdoses like opioids,
benzodiazepines, or barbiturates that suppress the medullary
respiratory centers. It also includes brain stem
strokes or profound hypothyroidism leading to Myxima
coma. Second would be the wiring, the
neuromuscular disorders. Right conditions like Guillain
Barre syndrome, myasthenia gravis, ALS, or a high cervical
cord lesion. Take Guillain Barre for example.
You have an acute ascending demyelinating polyneuropathy.
As the demyelination reaches the phrenic nerves and intracostal
nerves, the motor units just fail.
They do. The patient's vital capacity
progressively drops. They physically cannot generate
the negative intrathoracic pressure required to pull air
into the lungs. Alveolar hypoventilation ensues
and CO2 begins to climb. 3rd the physical structure itself.
Chest wall and plural disorders. Yes, severe chyphoscoliosis
mechanically restricts expansion.
Morbid obesity causes massive chest wall loading, which
drastically reduces compliance, or a massive pleural effusion or
tension pneumothorax that physically compresses the lung
tissue. And finally, airway obstruction.
COPD is the most common chronic cause here, but severe acute
asthma exacerbations can also lead to type 2 failure when the
patient finally fatigues after hours of breathing against
immense airway resistance. OK, we know the definitions, the
classifications, the mechanisms, and the causes, but how do we
actually prove which mechanism is at play in the clinical
setting? We need to transition to
arterial blood gas interpretation because reading
an ABG in an OSCE under a strict time limit is terrifying.
It can be the math gets jumbled, the numbers blur together.
We need a rigid, bulletproof system.
You must approach every ABG like a mathematical proof.
Step one, look at the pay O2. Is the patient hypoxemic?
Step 2 look at the pay O2 is it low, normal or elevated?
This immediately differentiates type I from type 2.
Step three, look at the pH. Acidemia, alkalimia or normal?
Exactly and Step 4 assess compensation.
This is where you differentiate an acute respiratory acidosis
from a chronic 1. Let's demystify the math of
compensation. How much should the bicarbonate
rise in response to a climbing CO2?
You must memorize the one for 10 and four for 10 rules in acute
respiratory acidosis, say an acute opioid overdose.
The kidneys haven't had time to compensate.
The initial buffering is purely cellular.
So for every 10mm of mercury rise in pack O2 above the normal
baseline of 40, the serum bicarbonate will passively
increase by 1 mill equivalent per liter.
Correct, but if it's a chronic condition like severe COPD, the.
Kidneys have had days or weeks to adapt.
Right. They up regulate the retention
of bicarbonate and the excretion of hydrogen ions.
In this state. For every 10 milliliter of
mercury rise in pack O2 above 40, the bicarbonate will
increase by 4 mill equivalents per liter.
OK, so if a patient has a baseline pack O2 of 70, which is
30 above normal, their bicarbonate should be elevated
by roughly 12, putting them at a baseline bicarb of around 36.
Exactly. And if their bicarb is 36 and
their pH is near normal, you know this is a chronic
compensated state. You absolutely must not rapidly
ventilate their CO2 down to 40 or you'll cause a profound life
threatening metabolic alkalosis. That's such a crucial point, but
the absolute Holy Grail of ABG interpretation in an exam
setting is the alveolar arterial or a a ingredient if you fail to
calculate this in Aviva. You will likely fail the
station. Period.
Let's focus heavily on this. I've always struggled with the
abstract nature of the alveolar gas equation.
It's just a string of letters and numbers.
Can we conceptualize this? Like, let's think of the
alveolus not as a balloon, but as a rigid box with a fixed
volume. I like that.
That's an excellent framework. At a given atmospheric pressure
at sea level, that box can only hold a certain absolute number
of gas molecules. Right.
The pressure inside that rigid box is determined by atmospheric
pressure. Now the majority of the
molecules in the box are nitrogen, which is inert and
doesn't participate in gas exchange.
Water vapor takes up a fixed amount of pressure too.
So what is leftover? Is the space available for just
oxygen and carbon dioxide? Precisely so if a patient
develops Guillain Barre and stops ventilating, the metabolic
production of CO2 continues. CO2 molecules begin flooding
into that rigid box. Because the box cannot expand
and the pressure must remain constant, those accumulating CO2
molecules physically displace and push the oxygen molecules
out of the alveolus. Wow.
OK. So the partial pressure of
oxygen in the alveolus capital PAO 2 must fall as the Paco 2
rises? That physical displacement is
represented mathematically by the alveolar gas equation.
Listeners write this down carefully.
PAO 2 equals the Fio 2 multiplied by the atmospheric
pressure minus the vapor pressure of water.
OK, from that entire product you subtract the pay KO2 divided by
the respiratory quotient, which is typically .8.
Let's do the math live for a specific clinical case so they
can hear it in action. Patient is on room air which is
21% or .21 Fio 2. We're at sea level so
atmospheric pressure of 760. Water vapor is 47.
So 760 -, 47 is 713. Multiply that by .21 and you get
a approximately 150. 150 This is the partial pressure of oxygen
in the conducting Airways before gas exchange begins.
Correct. Now we must subtract the
alveolar CO2. Since alveolar CO2 rapidly
equilibrates with arterial CO2. We use the Peco 2 from our blood
gas divided by .8. OK, let's say our exam candidate
is handed an ABG. The patient is breathing room
air. Their PO2 is 50 and their PECO 2
is 70. The immediate reaction of a
panic student is to look at the low PO2 and say, oh, the patient
has lung disease, maybe pneumonia.
Which is immediately incorrect. Let's run your numbers through
the rigid box. We start with 150, then we
subtract the result of 70 / .8. 70 / .8 is 87.5.
Right, so 150 -, 87.5 leaves us with a PA O2, the oxygen
actually sitting in the alveolus of 62.5mm of mercury.
So the box only contains 62.5mm of mercury of oxygen, purely
because the CO2 took up all the space.
Exactly. Now we calculate the gradient.
The albeolar oxygen is 62.5. The ABG tells us the arterial
oxygen is 50. We subtract the 2. 62.5 - 50 is
an A a gradient of 12.5. An A gradient of 12.5 on room
air is entirely normal. A normal gradient generally
falls between 5 and 15, increasing slightly with age.
What this normal Grady definitively proves is that
there is absolutely no barrier to diffusion.
There is no shunt. There is no VQ mismatch.
The lung parent commit is pristine, the oxygen transferred
perfectly from the alveolus to the blood.
The only reason the arterial oxygen is low is because the
alveolar oxygen was displaced by hypoventilation.
That is the ultimate Viva trap right there.
If you see a Peyo 2 of 50 and a Peyco 2 of 70, you must
calculate the A gradient before you blurt out a diagnosis.
If it's normal, the lungs are fine.
You need to investigate the CNS, the spinal cord, or the
neuromuscular junction. Exactly.
And if you calculate it and the gradient is wide in say 40 or
50, then you know you have concurrent parenchymal disease.
That single calculation is the difference between passing and
failing. The mathematics dictates the
clinical management. Now let's move away from the
paper and look at the patient in the bed.
We need to discuss clinical features and diagnosis.
We're always taught to look for cyanosis as the cardinal sign of
hypoxia, but is it actually reliable?
It is notoriously unreliable depending on its critical error.
Central cyanosis, the bluish discoloration of the tongue and
mucous membranes, does not depend on the percentage of
oxygen saturation. What does it depend on?
It depends on the absolute concentration of deoxygenated
hemoglobin in the capillaries. Specifically, you need about 5g
per deciliter of deoxygenated hemoglobin to visually perceive
cyanosis. So if a patient has severe
anemia, let's say they had a massive intraoperative
hemorrhage and their total hemoglobin is now only 6.
If their total hemoglobin is 6, they could have an Spo 2 of 70%,
meaning they are profoundly hypoxic and suffering cellular
death, but they will only have roughly 1.8g of deoxygenated
hemoglobin. So they won't look blue at all.
They will look pale, perhaps ashen, but they will never turn
cyanotic because they simply do not possess enough hemoglobin to
cross that 5g visual threshold. Conversely, a patient with
severe polycythemia and a hemoglobin of 20 might look
completely blue while maintaining a perfectly adequate
oxygen delivery. Wow, so you must rely on your
ABG and your clinical signs of sympathetic activation.
Tachycardia, tachypnia, agitation, confusion.
Absolutely. What about the signs of
hypercapnia? Carbon dioxide is a potent
peripheral vasodilator and a CNS depressant.
Clinically, you'll see warm flushed extremities, a bounding
pulse, tremors, asterixis or flapping tremors, headache, and
progressively deepening drowsiness or coma.
The vasodilation aspect is a massive trap in neuroanesesis,
right? It is paramount.
CO2 doesn't just dilate peripheral vessels.
It is the primary regulator of cerebral blood flow.
For every 1mm of mercury rise in Paco 2, cerebral blood flow
increases by approximately 1 to 2 milliliters per 100 grams of
brain tissue per minute. So if you have a patient with a
traumatic brain injury who goes into type 2 respiratory failure.
That rising CO2 will massively engorge the cerebral vasculature
in a fixed cranial vault. That increased blood volume
causes a spike in intracranial pressure, potentially leading to
brain herniation and death. This is why strict Paco 2
control, often targeting low normal levels, is mandatory in
neuroanesthesia. OK, aside from the ABG, what
other investigations are examiners looking for?
The chest X-ray is fundamental primarily to differentiate the
causes of acute pulmonary edema. If the X-ray shows cardiomegaly,
curly B lines indicating intracellular fluid and pleural
effusions, you're likely dealing with cardiogenic failure.
But if the heart size is normal and you see diffuse bilateral
patchy alveolar infiltrates the classic whiteout lung, you
suspect non cardiogenic edema, specifically ARDS.
And what role do pulmonary function tests play?
Because we don't usually do them at 3:00 AM.
True, we don't, but for chronic causes of respiratory failure,
KFT's are vital for differentiating obstructive from
restrictive diseases. In obstructive disease like
COPD, the hallmark is a low FEV 1 FVC ratio, typically less than
.7. And in restrictive disease like
pulmonary fibrosis. The total lung capacity and FEC
are low, but the FEV one FEC ratio remains normal or even
high because the elastic recoil is preserved or increased.
You should be prepared to draw the flow volume loops on the
whiteboard too. Right, an obstructive loop will
show a classic scooped out or coved expiratory phase due to
dynamic airway collapse. Exactly.
You must be able to draw that. All right, we have classified
it, mapped the path of Physiology, calculated the
gradient and reviewed the imaging.
Now we must treat the patient. Management is absolutely
essential. Where do we begin?
You never ever skipped the basics in an exam.
You start with the rigid ABC framework airway assessed
patency. If the patient has an altered
sensorium and absent gag reflex where is unable to clear copious
secretions, you secure the airway immediately with
endotracheal intubation. Breathing, optimize oxygenation
and assess the need for mechanical ventilatory support.
Right and circulation. Establish large bore IV access,
commence fluid resuscitation if indicated, and manage shock with
vasopressors or inner tropes to ensure that once you oxygenate
the blood, it actually gets to the tissues.
Let's talk about oxygen therapy under breathing.
The junior reflex is often to just crank the flow meter up to
15 liters through a non rebreather mask for everyone who
looks breathless. But that's dangerous, isn't it?
Saying that in Aviva will immediately cost you marks.
Oxygen is a drug. It has specific indications,
toxicities and targets. In a patient with no chronic
lung disease presenting with acute hypoxemia, your target SO2
is generally 92 to 98%. But in a patient with chronic
COPD who is a known CO2 retainer, your target is
strictly 88 to 92%. We need to explain exactly why
oxygen can kill a COPD retainer. The old dogma was simply that
their brain is so used to high CO2 that their respiratory Dr.
switches entirely to a hypoxic Dr. and if you give them oxygen
they just stop breathing. But modern Physiology tells us
it's much more complex than that.
The hypoxic Dr. theory is a gross oversimplification.
Giving high flow oxygen to a COPD patient exacerbates
hypercapnia through 2 distinct physiological mechanisms that
you must articulate. The first is the Haldane effect.
Let's break that down. Deoxygenated hemoglobin has a
high affinity for binding carbon dioxide.
When you flood the blood with oxygen, the hemoglobin becomes
fully saturated with oxygen. This oxygenated hemoglobin
physically changes its confirmation and drastically
lowers its affinity for CO2. Forcing massive amounts of CO2
to be dumped from the red blood cells back into the plasma,
sharply spiking the PECO 2. Exactly.
That's the chemical mechanism. And the hemodynamic mechanism.
The second mechanism involves the reversal of hypoxic
pulmonary vasoconstriction. Remember, the COPD patient has
chronic poorly ventilated emphysemaidis boule.
Their body has intelligently constricted the blood vessels
around those useless Boulet to shunt blood to better areas.
Right. So when you give them high
concentrations of inspired oxygen, that oxygen diffuses
into those poorly ventilated spaces.
The local hypoxia is temporarily reversed and those constricted
pulmonary vessels suddenly dilate.
Now massive amounts of blood flow are rushing to lung units
that have terrible ventilation mechanics.
So you've massively worsened the global VQ mismatch and vastly
increased the alveolar Dead Space.
Leading to a further dangerous climb in pack O2.
That is a master class explanation.
Now, what devices are we using to deliver oxygen precisely?
Ventry masks are excellent for these patients because they
utilize the Bernoulli principle to entrain room air at a fixed
ratio, delivering a highly controlled, precise FIO 2 say
exactly 24% or 28%. And we also rely heavily on high
flow nasal cannula HFNC. Yes.
HFNC provides heated, humidified oxygen at flow rates up to 60
liters per per minute, which flushes out the anatomic Dead
Space in the knees or pharynx. Importantly, the high flow
generates A mild C pap effect of roughly 3 to 5 centimeters of
water, which helps splint the upper Airways open and recruit
alveoli. But if HF and C isn't enough, we
move up the escalation ladder to non invasive ventilation NIV.
Right NIV, specifically by PAPI, which provides both inspiratory
and expert ORY. Positive airway pressure is
strongly indicated for two main pathologies.
First, acute exacerbations of COPD complicated by hypercapnic
acidosis. Generally a pH between 7.25 and
7.35. And 2nd acute cardiogenic
pulmonary edema. Yes, for the positive pressure
literally pushes the hydrostatic fluid back out of the alveoli
and decreases left ventricular preload.
The advantages of NIV are obvious.
You avoid the morbidity of an endotracheal tube ventilator,
associated pneumonia and the need for deep sedation.
But when must we say no to NIV and proceed straight to
intubation? Absolute contraindications
include a patient in a coma or with an altered sensorium who
cannot protect their airway, hemodynamic instability or
severe shock, facial trauma or burns, precluding a mask seal,
and a high risk of aspiration such as active hemonesis.
So if those are present, or if the patient's pH drops below
7.25 despite NIV, you must proceed to invasive mechanical
ventilation. You have no other choice.
OK, the patient is intubated. They have severe ARDS.
What are the high yield examiner approved ventilator settings?
The examiner wants to hear you systematically describe lung
protective ventilation specifically based on the ARDS
NET protocol. You must drill these specific
parameters into your memory first.
You utilize low tidal volumes, specifically targeting 6
milliliters per kilogram of predicted body weight, not
actual body weight. Let's emphasize that why
predicted body weight. Because your lungs do not grow
larger when you gain adipose tissue, a 150 kilogram man of
average height has the exact same lung capacity as a 70
kilogram man of the same height. Right, so if you calculate 6
millilograms based on actual body weight for the obese
patient, you'll deliver a massive destructive tidal
volume. Exactly, we strictly use low
tidal volumes to prevent volume trauma, the physical over
distension and tearing of the fragile alveolar epithelium.
The second parameter is pressure.
We must maintain a plateau pressure, the static pressure in
the alveoli at the end of inspiration of less than 30
centimeters of water. This prevents Barrow trauma
which can cause macroscopic alveolar rupture leading to
pneumothorax or new immediate acidism.
And the third parameter is PEEP. We've mentioned it before, but
we need to discuss the hemodynamic trade-offs.
We crank up the PEEP to open the lung, recruit collapsed alveoli
and overcome the right to left shunt.
But the heart is sitting right in the middle of those lungs.
It's not a free lunch. Far from it.
This is a critical concept that bridges pulmonary Physiology
with cardiovascular intensive care.
PEEP is inherently unnatural. Humans breathe via negative
intrathoracic pressure, which sucks blood back into the right
atrium. When we apply significant PEEP,
we're transmitting positive pressure throughout the thoracic
cavity. Right.
And this positive pressure compresses the superior and
inferior vena cava, drastically impairing venous return or
preload to the right heart. And if the right heart doesn't
fill, it can't pump. Furthermore, high PEEP
compresses the delicate pulmonary capillaries running
between the distended alveoli. This increases pulmonary
vascular resistance, which is essentially an increase in right
ventricular afterload. So the right ventricle is
receiving less blood and it has to pump harder to push it
through the lungs. Consequently, right ventricular
stroke volume drops, which means left ventricular filling drops,
causing a severe reduction in cardiac output and systemic
blood pressure. So let's tie this back to the
ultimate goal, tissue oxygenation.
What does this mean for the patient mathematically?
We return to the oxygen delivery equation.
Oxygen delivery DO 2 is the product of cardiac output
multiplied by arterial oxygen content.
The oxygen content is mostly determined by hemoglobin
concentration and saturation. So if you increase the PEEP from
10 to 18, you might recruit alveoli, resolve the shunt and
see the PO2 and saturation on the monitor rise beautifully.
But if that high PEEP simultaneously drops your
cardiac output by 40% because of impaired venous return, the
total product of the equation, the actual molecules of oxygen
arriving at the brain and kidneys, might plummet.
You literally sacrificed cardiac output for a prettier blood gas
and the patient still dies of cellular hypoxia.
Exactly. The art of mechanical
ventilation is titrating PEEP to find the optimal point where
alveolar recruitment is maximized without severely
compromising cardiac output. That complex hemodynamic
interplay is exactly what a senior examiner is waiting to
hear. This transitions perfectly into
Part H complications and ICU care.
We've touched on Baritron and volley trauma under the umbrella
of ventilator induced lung injury or vilai, but what are
the other components? Aside from bear trauma, pressure
damage and volume trauma, volume tearing, you must define atelect
trauma. This is the sheer stress injury
caused by the repetitive opening and closing of unstable fluid
heavy alveoli with every single breath.
It's like constantly bending a paper clip until it snaps.
Exactly adequate P prevents this by keeping the alveoli splinted
open throughout the respiratory cycle.
Finally, there is bio trauma. Bio trauma is fascinating.
It's where physical physics turns into systemic biology.
Precisely, it is mechanotransduction.
The physical stretching and tearing of the alveolar
epithelium trigger a massive release of pro inflammatory
cytokines like interleukin 6 and TNF alpha into this systemic
circulation. So you're literally mechanically
generating a state of Systemic Inflammatory response syndrome
or SIRS. The lung trauma becomes a
systemic sepsis mimic leading to multi organ dysfunction
syndrome. Other complications include
ventilator associated pneumonia, which carries a high mortality,
and oxygen toxicity where prolonged exposure to 100% IO 2
generates reactive oxygen species that destroy the
pulmonary endothelium. So how are we monitoring these
intubated patients to prevent this?
Meticulous continuous monitoring Arterial lines are mandatory for
continuous blood pressure assessment, especially given the
hemodynamic effects of PEEP we just discussed, and for frequent
ADG sampling. We also rely heavily on
continuous capnography or ET. Because a sudden precipitous
drop in ETCO 2 could immediately indicate a massive pulmonary
embolism or a disconnect in the ventilator circuit.
Exactly, while a gradual rise indicates increasing Dead Space
or worsening hypoventilation. Let's look at the end game.
Getting them off the ventilator weaning.
You assess readiness with spontaneous breathing trials,
but examiners love to test the cardiovascular impact of
weaning, don't they? It's kind of the inverse of the
PP problem. It is the exact inverse.
We call it weaning induced pulmonary edema.
Think about the hemodynamics. Patient's been on positive
pressure ventilation for a week. The positive pressure has been
suppressing their venous return and artificially assisting their
left ventricle by reducing its transmural pressure gradient,
essentially reducing LV after load.
Now we suddenly turn off the positive pressure and make them
breathe on their own through an endotracheal tube which acts
like a narrow straw. Right.
To pull air through that narrow resistance, the patient must
generate a massive negative intrathoracic pressure.
This sudden violent vacuum effect has two catastrophic
consequences. Oh wow.
First, it sucks a massive volume of venous blood back into the
right heart, flooding the pulmonary circulation.
Exactly. Second, the extreme negative
pressure surrounding the heart vastly increases the after load
on the left ventricle. It is like the left ventricle is
trying to pump blood out of a black hole.
The sudden volume overload combined with immense after load
can cause acute left ventricular failure.
Yes, the fluid backs up and they develop flash pulmonary edema.
If they aren't failing to breathe, their heart is failing
from the sudden work of breathing.
That is an incredible physiological narrative.
Let's pull everything together into Part 1 exam integration.
We need to build a mental comparison table that our
listeners can write down for Type I versus Type 2.
Listeners visualize a table with type I in the first column and
type 2 in the 2nd row. One pathophysiology, type I is
fundamentally AVQ mismatch or a right to left shunt.
Type 2 is fundamentally alveolar hypoventilation.
Row 2 ABG findings Type I shows a pay O2 less than 60 with a
normal or low pack O2. Type 2 shows a pay O2 less than
60 but with a pack O2 greater than 45 and respiratory
acidosis. Row 3 causes Type 1 is caused by
alveolar filling or collapse, AR, DS, pneumonia, pulmonary
edema. Type 2 is caused by pump
failure, COPD, neuromuscular blockade aid, opioid overdose.
And row 4 management focus. Type I requires PEEP to recruit
alveoli and carefully titrated Fio 2.
Type 2 requires ventilatory support, either NIV or invasive
ventilation to physically increase minute ventilation and
clear the CO2. Exactly what are the specific
Viva traps that trip up candidates?
The most common mistakes include failing to calculate the A
gradient before diagnosing a mixed ABG, confusing the causes
of Dead Space versus shunt. And as we discussed, believing
that administering 100% oxygen will cure a severe true shunt,
examiners will also explicitly ask you to define permissive
hypercapnia in the context of ARD's.
How should they phrase that definition to secure full marks?
The examiner approved answer is permissive Hypocapnia is an
intentional lung protective strategy where elevated packet 2
is tolerated in order to minimize tidal volumes and keep
plateau pressures below 30 centimeters of water.
The goal is to prevent ventilator induced lung injury,
provide that the arterial pH does not fall below 7.20 and
there are no contraindications such as elevated intracranial
pressure. Boom, perfect.
And regarding visual aids in a written exam, a good diagram is
worth an entire page of text. You must be able to confidently
draw 3 diagrams. First the VQ mismatch spectrum.
Draw a horizontal line. On the far left, show Dead Space
where VQ equals Infinity because perfusion is 0.
In the middle, show normal matching where VQ is roughly .8.
On the far right show shunt where VQ equals 0 because
ventilation is 0. Second, draw the oxygen
dissociation curve, explicitly detailing the bore effect and
the metabolic factors like temperature 2-3 DPZ P and pH
that shift it left or right. And third, provide a clean
branching flow chart for your ABG interpretation.
Let's do a rapid fire summary of the absolute high yield take
homes. Number one, define failure
rigorously. PAO 2 under 60, PICO 2 / 49.
Know why those numbers matter on the dissociation curve #2
classify completely Use types before particularly emphasizing
the FRC collapse in perioperative type 3 and the
massive hemodynamic theft by the respiratory muscles in shock
related type 4. #3 Understand the five mechanisms of
hypoxemia, specifically how PE evolves from Dead Space to shunt
due to lack of surfactant and bronchoconstriction #4 Always,
always calculate the A gradient using the rigid box of the
alveolar gas equation to isolate peranchymal disease from
hypoventilation. #5 Execute lung protective ventilation, 6 Miller
kilogram predicted body weight, plateau pressure under 30, and
titrated PEEP and #6 master the hemodynamics.
Articulate how PEEP drops cardiac output and how sudden
negative pressure during weaning triggers acute left ventricular
failure. If a candidate reaches the end
of a 20 mark written essay on this topic, they need a strong
closing statement. Could you dictate a model
conclusion paragraph? Absolutely.
In conclusion, respiratory failure represents a critical
collapse of oxygenation, ventilation, or both,
fundamentally disrupting tissue oxygen delivery.
Management mandates a rapid systematic approach centered on
robust ABG interpretation to identify the underlying
physiological mechanism, whether it be intrapulmonary shunt,
severe VQ mismatch, or alveolar hypoventilation.
Definitive therapy requires A delicate balancing act,
restoring adequate gas exchange via targeted oxygenation and
lung protective mechanical ventilation, while vigilantly
mitigating the severe hemodynamic compromises and bio
trauma inherent to positive pressure support.
That is authoritative. If you write that, you have
proved you belong in the specialty.
Before we conclude, I want to leave you with one final
advanced physiological concept to ponder.
We've said this entire session rigorously discepting macro
circulatory parameters. We have balanced PO2PO2, cardiac
output and oxygen delivery equations.
But remember, the ultimate frontier in modern intensive
care is the microcirculation. All right, the capillaries.
Yes, you can perfectly recruit the lungs.
You can achieve A flawless ABG, you can utilize inner tropes to
generate a completely normal cardiac output and blood
pressure. But in severe sepsis the
microcirculation fails. Endothelial swelling and
microthrombie physically shunt blood flow past the capillary
beds directly into the venules, bypassing the mitochondria
completely. So the oxygen is right there,
but it can't cross. Exactly.
Furthermore, the mitochondria themselves become poisoned and
unable to utilize whatever oxygen does arrive, a state
known as cytopathic dysoxia. The cells starve in a sea of
plenty. The next time you were standing
at the bedside of a septic patient staring at a perfect ABG
and a normal blood pressure, but the lactate continues to rise
and the patient is still dying, ask yourself what is happening
at the microscopic mitochondrial level.
And realizing how much we still have to control at that
microscopic level is exactly what keeps the specialty so
humbling and so fascinating. Thank you for an incredibly
rigorous, exhausting, but ultimately exam crushing master
class. It was my pleasure.
And to you listening, remember that while this deep dive equips
you to dominate your exams, the true final goal is saving the
physiological life of the patient in that ICU bed.
The diagnostic landscape might be muddy, but your physiological
reasoning is now crystal clear. Keep studying the mechanisms,
keep questioning the numbers, and keep diving deep.