So let’s talk about the path of physiology of hemorrhagic shock.
Very simply, hemorrhage means blood loss.
Shock means tissue level hypoxia.
So hemorrhagic shock refers to inadequate blood flow
in order to oxygenate tissues.
The tissues aren’t getting enough blood supply
to get the oxygen supply that they need
to meet their metabolic demands.
Physiologic compensation can mask the effects of blood loss.
So especially early in the course of blood loss,
patients are very good at increasing their cardiac output,
increasing their heart rate,
increasing their vascular resistance
in order to maintain tissue level perfusion.
And this can make it difficult to identify shock
in the early stages.
So we have to really be vigilant
in looking for signs of hemorrhagic shock in our patients.
The hemorrhagic shock is divided up into different classes.
And it’s not so much important to memorize
all of the features of every class of shock.
But it is important to understand
how shock progresses clinically
and to note that it’s a non-linear progression.
So different classes of shock
are divided up according to how much blood you lose.
You’ll note that in class 1 shock,
you’re losing under 15% of your blood supply.
In class 2 shock,
you’re losing up to 30% of your blood supply
which is quite a lot.
In class 3 up to 40%
and in class 4 more than 40%.
But here’s a really interesting stuff.
So in class 1 shock,
you typically are not even gonna be tachycardic.
You’re gonna have a normal blood pressure,
normal urine output and a normal mental status.
So you can loss 750 CCs of blood
which if you saw that strewn around the room
would be quite impressive to you.
That is a lot of blood loss.
Yet you’re gonna have almost no physiologic derangement from that.
Now, when you get up into class two shock,
you’re gonna start to see,
maybe development of a little bit of tachycardia
and maybe some narrowing of the pulse pressure.
So now, our sympathetic nervous system has started to kick in.
We’re responding to blood loss by raising the heart rate,
raising the vascular tone which is gonna increase our pulse
and increase our diastolic blood pressure
to narrow our overall pulse pressure.
we’re still really not gonna have not much in the way
of tachypnea, maybe a little bit.
We should have reasonably normal urine output.
And while the patient might feel anxious,
they’re not necessarily gonna be confused or altered.
However, when you get up over 1.500 CCs
we begin to really significantly decompensate.
So this is where we begin to see significant tachycardia.
And this is the first place where we see the hypotension.
Patients also will be uniformly tachypnic.
They’re gonna begin to lose their urine output.
And they’re gonna be confused or lethargic
in terms of their mental status
'cause they’re not getting great cerebral perfusion.
So as we lose more and more blood,
our physiologic derangements get worse.
But it’s important to recognize
that it happens in a non-linear fashion.
So when we lose 500 to 1.000 CCs of blood,
our overall clinical status is really pretty good.
But we start to sort of deteriorate a little bit around 1.500 CCs,
but then when we get over that level,
we actually deteriorate quite rapidly.
So you can see this is a non-linear progression
and up at the higher ends of the blood loss curve,
you’ll have more significant clinical manifestations
with relatively less blood loss.
This is all the product of compensation.
So small amounts of blood loss
or really moderate amounts of blood loss,
we compensate for very well.
But once we exceed our ability to physiologically compensate,
really, everything starts to deteriorate
and we start to see these life threatening signs and symptoms
that we are all familiar with.
So one of the things to remember about hemorrhagic shock
is that the clinical signs,
at least up until the bitter end are relatively unreliable.
Now, vital signs correlate pretty well
with how much acute blood loss the patient has,
but other kinds of things
like capillary refill and skin turgor,
and pallor and those kind of things.
They’re not necessarily terribly reliable, especially in adults.
Vital signs are more useful
but there are exceptions to these rules.
So at extremes of age,
you’ll see differences in how patients physiologically compensate.
Kids are notorious for compensating extremely well
up until the very bitter end
at which point they will begin to deteriorate extremely rapidly.
Older people might not have much capacity
to compensate at all
and might show signs of shock
with relatively less blood loss.
There is also the consideration of medications.
So patients who are on beta blockers,
calcium channel blockers,
other kinds of drugs that blunt
the physiologic response to blood loss
can make it more difficult to assess
the clinical degree of blood loss the patient has.
And lastly, healthy young people
will often have low resting heart rates.
It’s not uncommon for young people,
especially trained athletes to have heart rates in the 40s or 50s.
So they might have significant blood loss
with the heart rate of 80.
That’s not technically tachycardic for the overall population
but it is for that person.
So you always wanna interpret vital signs
in the context of the patient’s baseline physiologic state,
especially in as much as you know what it is.
So really important thing to remember on hemorrhagic shock
is that any vital sign abnormality should be taken seriously.
Remember, when we looked at the classes of shock,
the first vital sign to change is gonna be the heart rate.
So tachycardia is gonna occur
once the patient has lost between 750 and 1.500 CCs of blood.
We don’t wanna wait until the patient becomes grossly tachycardic
or hypotensive to start considering the possibility of blood loss,
because you don’t develop those findings
until very late in the process of hemorrhagic shock.
You have to lose more than 1.500 or 2.000 CCs
to clinically appear frankly shocky.
So the bottom line
is if your patient is tachycardic,
if their pulse pressure is narrowing,
if they have any early finding suggestive of hemorrhagic shock,
you wanna take it seriously,
you wanna identify the source of bleeding
and you wanna reverse it.
Because if you wait until your patient is hypotensive,
they would have already loss a significant amount of blood
and their outcomes are gonna be bad.