Download Criteria for “making the cut” as an enduring concept: Used often

Criteria for “making the cut” as an enduring concept:
1.
2.
3.
4.
5.
Used often (daily or nearly so)
Is a foundational fact
Is an integral part of “guild membership”
Ignites curiosity
Contributes to lifelong learning strategies (per Dr. Roden)
So, in an effort to put this to use in a more real world kind of way, here’s how I might
teach something like tissue perfusion.
Basic Questions: Why do we need to breathe? Why do we have a blood pressure?
Most students will answer that we breathe because O2 needs to enter the body and
CO2 needs to leave. Why is that?
Leaving the discussion of CO2 for the moment (as this would get us into the morass
of acid-base balance, and we can talk about that some other time), we need O2
because:
Tissues are metabolically active and require energy. Energy, in the form of ATP, is
synthesized in each cell by several routes, the most efficient of which is oxidative
phosphorylation in the mitochondria. Electrons are supplied the food that is eaten,
digested, and absorbed; brought to the mitochondria by intermediates (that can be
discussed in greater detail); and passed in a stepwise fashion down the ETC to yield
ATP. Something has to pick up the electrons at the end, and that something is O2.
Stick a couple of protons in there, and you get water. If you follow the rest of the
chemistry, you see that there’s CO2 produced as an end product as well. So, in
summary, you take a compound and convert it to CO2, water, and energy. That’s
combustion. As we all know, combustion requires O2. All of the fancy biochemistry
is working to make sure that we don’t go up in flames. It amounts to a slow burn,
and to support that, you need O2. In a bit, we’ll talk about what happens when you
don’t have it.
Okay, so every cell needs oxygen. It gets into the body when we breathe. But it’s got
to get to every cell. Therefore, it needs a carrier. That, as you know, is blood, and
more specifically, hemoglobin. Now that we have a carrier, we need to move it
around to where it’s going. That’s what the heart and blood vessels are for. Let’s get
specific about this, because it turns out to be important. First, we need to know that
there’s adequate oxygen content in the blood. There’s an equation for that, and it is:
CaO2 = ([Hgb] x 1.36 x % saturation) + (0.0031 x PaO2)
So, how much oxygen is in the blood depends mainly on how much hemoglobin is in
the blood and how saturated it is with oxygen. The fraction of dissolved oxygen
(which is PaO2, or the partial pressure of oxygen in arterial blood) is, under most
sane circumstances, a miniscule contribution. However, things that can really
compromise tissue oxygenation are things that lower the Hgb concentration or that
lower the oxygen saturation. For fun, calculate the difference in O2 content if your
saturation drops from 98% (which is normal) to 80%. How about if your
hemoglobin concentration drops by half? How about if your PaO2 drops by half?
These relationships are more complex, because of course the saturation and the
amount of dissolved oxygen are fairly closely related.
So now you’ve got O2 in the blood and you need to move it around. Enter the heart
and blood vessels. It’s a pump connected to tubes for the purposes of this
discussion. The tubes get smaller and smaller until they’re small enough to allow O2
to move through the walls and into nearby cells. How the blood gets around is a
function of how much the pump is pumping. That’s cardiac output, or:
C.O. = HR x SV
How fast the heart pumps and how much it squeezes out each time it pumps. But
what you need is flow. Remember V = I x R from physics? Voltage is a potential
difference, current is flow, and resistance is… um, resistance. Rearrange it and you
see that flow, or current, is a function of potential difference and resistance, or I =
V/R. To put it into biological terms (here’s one of the reasons you had to take
physics to get into medical school):
MAP – CVP = CO x SVR, or solved for flow, CO = (MAP – CVP)/SVR
The potential difference is the mean arterial pressure minus the central venous
pressure (pressure in arteries minus pressure in veins). The flow is the cardiac
output. And the resistance is called systemic vascular resistance, which is simply a
summation of all of the resistances in all of the little vessels throughout the body.
Mean arterial pressure can be easily calculated from a blood pressure measurement
and is simply:
MAP = 1/3 SBP x 2/3 DBP
Systolic BP is the top number in the “120/80” and is the pressure when the heart
squeezes, and diastolic BP is the bottom number, the pressure when the heart
relaxes. Your heart spends more time relaxed, so DBP has a bigger impact on the
mean pressure. CVP is directly measured and is generally low.
Wasn’t the question “Why do we breathe?” Okay, let’s regroup. Tissues need
oxygen. We now know how oxygen gets in and gets around. So, tissues are in
trouble if any of the following happen:
-Too little oxygen getting to the lungs
-Too little oxygen getting to the blood from the lungs
-Too little Hgb to carry the oxygen
-Something wrong with the Hgb such that it can’t carry oxygen
-Too little blood flow to the tissues to meet their needs
All of these possibilities can happen. Too little oxygen to the lungs is really a
function of either being in a place with very little oxygen available (e.g., at altitude)
or of not moving enough air (e.g., respiratory depression from narcotic overdose).
Too little oxygen getting to the blood from the lungs can be a problem of some other
gas getting in the way, such as CO2… actually, let’s pause here for a brief digression.
If CO2 concentrations in the blood get high enough, the concentration in the lungs
goes up appreciably. Get it high enough, and it’ll start displacing oxygen, as there’s
only so much room for different gases in the alveoli. This, of course, can be
quantified, in the form of the alveolar gas equation:
PAO2 = FiO2(Patm – Pwater) – (PaCO2 (1-FiO2[1-RQ]))/RQ
Whoah! Let’s simplify. PAO2 is the pressure of oxygen in the alveoli. FiO2 is the
fraction of inspired oxygen. PaCO2 is the pressure of CO2 in arterial blood, a
directly measured value. RQ is the respiratory quotient, a ratio of the amount of
CO2 produced by the whole body divided by the amount of O2 consumed to produce
that CO2. It’s a summation of the processes discussed at the subcellular level above.
If a person is breathing regular ol’ air, the FiO2 is 21%. Atmospheric pressure at sea
level is 760 mmHg. The pressure of water vapor in the lungs of a person with a
normal body temperature is 47 mmHg. The RQ is estimated at 0.8 for most settings.
So, a more user-friendly version of the equation looks like this:
PAO2 = FiO2(Patm – 47) – 1.2(PaCO2)
What you can see from this is that as the CO2 in the blood goes up, the oxygen in the
alveoli will go down. Even more interesting, if you know how much oxygen is in the
alveoli, and you measure how much dissolved oxygen is in the arterial blood (PaO2),
you can calculate the so-called “A-a gradient.” The functional significance of this is
that if the difference is really big, oxygen isn’t moving into the blood for some
reason. Oh, yes! That’s where we left off. Too little oxygen getting to the blood from
the lungs. This can be another gas like CO2 getting in the way, a barrier to diffusion
of O2 (e.g., fluids like water, blood, or pus in and/or around the alveoli such as is
seen in ARDS, pulmonary edema, hemorrhage, pneumonia or other infection;
something like scar tissue or cells getting in the way such as is seen in pulmonary
fibrosis), or a problem with blood getting to where the oxygen is (e.g., a pulmonary
embolus).
There has to be a place for the oxygen to go in the blood. If there’s too little Hgb,
there’s nowhere for the oxygen to go. This, generally speaking, is called anemia. If
you lose the Hgb really fast along with the other components of blood, that’s called
hemorrhage. If you don’t make enough hemoglobin for whatever reason (e.g., iron
deficiency) or if you break down your red blood cells faster than you should (e.g.,
diseases like thalassemia, G6PD deficiency, paroxysmal nocturnal Hgburia, others),
you still have a low [Hgb] in the blood.
You’re also in trouble if you have enough Hgb, but for some reason it can’t pick up
oxygen. The classic inherited form of this is sickle cell anemia (which also involves
rapid red cell turnover). Sickle Hgb doesn’t bind oxygen very well once it’s in the
sickle conformation. The classic acquired forms of the Hgb oxygen binding problem
are CO poisoning and methemoglobinemia. CO binds tighter than O2 can, and
methemoglobin (which is Hgb with oxidized iron in the heme part of the molecule)
doesn’t bind O2 very effectively.
Finally, you can have all the oxygen in the world in the blood, but if you can’t move it
around and perfuse tissues, it doesn’t matter. Problems here can be pump problems
or pressure problems.
Pump problems are problems of cardiac output, and these can be either HR or SV
problems, or both. If your HR is 20, your cardiac output sucks even though your SV
is normal. If your HR is 300, you don’t have enough time to fill the heart between
beats, so your SV is teeny. If your heart doesn’t contract in a coordinated way, you
have no effective SV. This is what we call ventricular fibrillation, and this is why
people are forever getting shocked on TV with bozo TV docs shouting “CLEAR!” (As
you’ll see, it doesn’t really happen that way… or shouldn’t.) If your heart muscle is
too weak to generate a SV, we call that cardiomyopathy, and the functional outcome
is heart failure. If the heart failure is so profound that it cannot generate a blood
pressure because it cannot generate flow, we call that cardiogenic shock. (Small
digression: Shock is a medical term, a precise diagnosis that means inadequate
delivery of oxygen to tissues, mainly due to a dangerously low blood pressure.)
Problems with getting blood to tissues can also be pressure problems. If you simply
don’t have enough blood because, let’s say, some oh-so-helpful street thug has
stabbed you in the chest, your driving pressure will be dangerously low, because
there has to be something inside the blood vessels and the heart to transmit that
pressure. This is hemorrhagic (or hypovolemic) shock. If that same street thug
instead cuts your spinal cord with surgical precision, you can lose sympathetic
nerve input to your blood vessels, which normal tells them to constrict to some
degree. All of your blood vessels relax, your SVR and MAP drop precipitously, and
this is called spinal (or a type of distributive) shock. If you have a rip-roaring
infection, your immune system can explode and unleash an inflammatory storm.
Part of your body’s response to this, for reasons that are not at all clear even now, is
to dilate your blood vessels. (Perhaps the body’s way to try to ensure that blood can
get where it needs to go without any resistance? As I say, no one really knows.)
Your blood pressure falls, and this is called septic shock. It is in the top 10 causes of
death. The mortality rate is around 25-30%. Blood clots or other obstructions can
be thought of as pressure problems, mainly because the resistance approaches
infinity, and there is no way to generate the pressure needed to maintain flow. The
reason a heart attack happens is because the flow of blood is blocked, the heart
muscle is starved of oxygen, and ultimately dies. If it happens in the brain, it’s called
a stroke, but a similar deal. In the intestines, it’s ischemic bowel, and it can be a
surgical emergency or a fatal process.
What you do to fix a problem of oxygen delivery to tissues depends a great deal
upon what the problem is. So, the first things you need to do are make sure the
person is safe and then figure out which of the above processes are at work.
Sometimes it’s as simple as giving more oxygen to someone to breathe while you try
to figure out what’s going on and how to fix it. Sometimes it means putting a tube
into someone’s trachea to help him or her breathe and to deliver lots more oxygen.
Sometimes it means giving fluid or blood to support their blood pressure and give
back Hgb so that their oxygen carrying capacity is restored, while at the same time
working to stop their bleeding or to treat their overwhelming infection. Sometimes
it means supporting their heart’s ability to pump, with drugs (called inotropes,
examples include dobutamine and milrinone) or even with mechanical devices
(examples include intra-aortic balloon pumps and left ventricular assist devices).
So, we’ve talked about why we need to breathe and a bit about why we have a blood
pressure. What are the unanswered questions? Well…
-How do we breathe? This involves a more in-depth discussion of the structure and
function of the lungs themselves, with the associated blood vessels, nerves, and a
brief discussion of the right ventricle. More on this soon.
-What happens when there’s not enough oxygen in the tissues? This is a discussion
of the pathophysiology of tissue ischemia and can be nicely linked with…
-What about CO2? This is the other side of the respiratory coin. We’ll talk about
how it’s made normally, what the body does with it, and how it relates to acid-base
balance. Yes, really. In life outside the uterus, we primarily breathe in response to
CO2 and acid, not oxygen. The lungs get rid of thousands of millimoles of acid per
day in the form of CO2.
-What are the major controversies in medicine around this topic? Well, plenty.
There’s lots of ongoing discussion about the best way to take care of a deathly ill
patient whose lungs are so sick that you just can’t get oxygen in. Do you put them on
heart-lung bypass, so-called ECMO (ExtraCorporeal Membrane Oxygenation), while
their lungs heal (might look for the CESAR trial and its commentaries)? Do you flip
them onto their stomachs (yes, this is for real, and you might read some of
Gattinoni’s papers on prone ventilation)? Do you give them inhaled medicines to
dilate the blood vessels in the lungs (e.g., nitric oxide, prostacyclin)? An interesting
review of the recent data for just these very narrow questions can be found in
Critical Care Medicine, v38, no8, p1644.
Okay, so how does this serve the 5 criteria? Well, I’d argue that these are concepts
that underlie what many doctors do every day, so we all probably should know
them. Vital signs, as we say, are vital. Foundational facts? Check. Some of this is
stuff you need to know to be “in the guild.” I’d hope that this approach might ignite
curiosity. The intent would be to give enough information to feel like you’ve learned
something in a meaningful way, to identify where the gaps are, and to feel like you
know enough to go after those answers. That impetus, to my way of thinking, is
what lifelong learning is all about. There’s nothing on evaluating the CESAR trial, for
example, but I can’t do everything in one session. 