we’re gonna switch gears a little bit now
and talk about pulseless electrical activity.
And this is one of my favorite rhythms to think about
because it’s physiologically much more complex
and interesting than V-fib and V-tach
and there’s a broad differential that you’ll gonna learn about.
So what is PEA?
PEA again, stands for Pulseless Electrical Activity.
And what that means is that there’s organized
electrical conduction on the monitor.
Normal looking QRS complexes with P waves and T waves
and all the things you expect from a cardiac rhythm.
However, there is clinically no pulse.
So normal looking activity on the monitor
but no pulse when you actually palpate the neck.
What is the single most important intervention for PEA?
It’s a little bit of a trick question.
The most important intervention
is to figure out what caused it and fix that.
So unlike V-fib and V-tach
where we do the same thing for everybody across the board
regardless of the cause.
In the case of PEA,
we’re only gonna be able to make our patient better
if we can figure out the cause and treat it.
Now of course,
we’re gonna provide support and care in the meantime
but ultimately, our goal is gonna be to make a diagnosis.
There’s two major mechanisms of PEA
that I’d like you to be aware of.
One is the empty heart and the other is EMD
or Electromechanical Dissociation.
We’re gonna compare and contrast these a little bit.
So in the case of an empty heart,
the heart is conducting normally.
There’s nothing wrong with the heart’s conduction system.
You know, if I were to get shot right now in the aorta
and all of my blood volume were to pour out on the floor,
there’s nothing wrong with my heart,
it’s gonna conduct perfectly normally.
In the case of electromechanical dissociation
the heart is also conducting normally.
Electrical activity in the heart is preserved.
However, when the heart is empty,
again, if I got shot in the aorta
and all of my blood's on the floor,
there’s nothing wrong with my heart itself.
So at least in the short term,
it’s gonna keep contracting just as hard and fast as it can
to try to profuse my body.
So contraction occurs and it’s normal.
However, that contraction ultimately is ineffective, right?
Because no matter how hard the heart squeezes
if there’s nothing inside of it,
if my blood is on the floor and not inside the heart,
the hearts not gonna fill,
it’s not gonna send blood out to the body.
in electromechanical dissociation,
there are normal cardiac action potentials
that yield the pretty spikes that we see on the cardiac monitor.
However, these action potentials
do not yield cardiac contraction.
So the heart's conduction is normal
but the contraction is either absent or so impaired
that it doesn’t produce a pulse.
empty heart PEA
is caused either by hypovolemia as I mentioned
with the example of all my blood volume being on the floor,
or can be caused by some kind of an obstructive process
that prevents the heart from filling.
So examples of those are things like cardiac tamponade.
You’ve got a big collection of blood around the heart.
It physically compresses the heart.
The heart can’t fill normally,
so it can’t send blood out to the body normally.
Same with tension pneumothorax, right?
You have a huge high pressure air collection in the chest,
it’s gonna mechanically squish the heart
and prevent normal filling.
These are all empty heart forms of PEA.
By contrast, electromechanical dissociation
is gonna be caused by systemic derangements in the body.
So these are gonna be things that affect energy metabolism
such that the heart is able to produce the energy
to maintain normal conduction
but it’s not able to maintain the energy
to enable mechanical contraction.
And as you can imagine,
contraction requires a lot more metabolic energy than conduction.
So it’s gonna be the thing to go in the setting
of severe derangements of metabolism in the body.
So what’s your differential diagnosis of PEA?
There’s a common mnemonic that’s used
which is the H’s and the T’s.
And I’m gonna tell you a secret,
I don’t love this
because it doesn’t force you to think about it physiologically
but a lot of students find it useful
so we'll go through them.
Like we already mentioned,
if you don’t have any blood volume,
your heart's gonna be empty.
Your heart's not gonna have a good output.
Well, how do we make energy in the body?
We make it out of oxygen and glucose.
So if you’re hypoxic,
your aerobic metabolism is gonna be ineffective
and you’re not gonna be able to produce
a normal amount of energy to drive cardiac contraction.
So it’s potentially a cause of PEA.
Acidosis or hydrogen ion,
'cause you know, we had to make it start with an H.
In that kind of a situation, you know,
there’s a different optima for every process in the body.
There’s PH optimum, temperature optimum,
and physiologic processes just don’t work right
when you have extreme derangements of those optima.
So in the case of profound acidosis,
the heart actually can’t squeeze normally.
So even though conduction is intact
the cardiac contraction is not.
Hyper or hypokalemia,
it has to be pretty profound,
but severe derangements of potassium
can actually precipitate PEA.
Hypothermia, like I mentioned,
for the same reason as acidosis.
If the body is really, really cold
the heart's not gonna be able to contract normally.
We talked about tension pneumothorax,
as a cause of empty heart PEA and the same for tamponade.
There’s a number of toxins that can potentially produce PEA
by uncoupling energy metabolism from normal cardiac contraction.
Massive MIs can cause such profound reduction
in cardiac squeeze that you can’t actually clinically detect a pulse.
And massive PEs can cause such severe obstruction
of normal pulmonary blood flow
that they basically cause empty heart PEA
the same way any other obstructive cause would.
So with PEA, it’s even more important
than with other types of cardiac arrest
to understand the underlying cause
and to identify what’s going on.
So you wanna get as much information as you can
about the circumstances that led up to the arrest.
What was the patient doing when it happened?
Did the patient have any symptoms beforehand?
Did they suddenly clutch their chest and complain of pain
or were they grasping for breath?
Did they turn blue?
Did they attempt suicide?
Was there some type of trauma?
All of these things will help you narrow the differential for PEA
and treat the patient accordingly.
For physical exam,
it’s especially important if you don’t have a good history,
which in many cases of cardiac arrest you won’t.
But if the patient has any signs of physical trauma
when you look at them,
maybe you’re gonna think about more hemorrhage
as a potential cause of PEA or tension pneumothorax.
If the patient's pregnant
that should make you think about pulmonary embolism.
If they have a dialysis catheter hanging out of the chest,
that’s gonna make you think about hyperkalemia, etc.
So physical findings can potentially give you clues
that will help narrow your differential
and prioritize your treatments
so that you can help the patient with PEA.
Another nice adjunct we have nowadays is bedside ultrasound.
So ultrasound is a great extension of physical exam.
It allows us to look inside the body
in ways that we couldn’t before
and identify in real time,
is there a pericardial effusion present or signs of tamponade?
Is there evidence of a pneumothorax
which is seen by absence of lungs sliding on ultrasound?
Is there an abnormal cardiac ejection fraction,
maybe the heart's just barely beating.
Maybe the IVCs really distended
suggesting the patient is volume overloaded.
Or maybe it’s really collapsible and tiny
suggesting that they're dehydrated.
So ultrasound is especially good for cardiac tamponade
and pericardial effusion.
This is an example of a cardiac ultrasound
where you can see some of the chamber’s labeled.
But most importantly,
you see a large pericardial effusion
which is outlined here on the screen.
And that’s big enough that you would certainly
want to perform a pericardial synthesis and get rid of that
to see if that helps the heart beat more effectively
and improves your cardiac output.
There's also the inferior vena cava
which is a great overall indicator
of your patient’s volume status.
So like I mentioned before,
patients who are really volume depleted
either from dehydration maybe from a diarrhoeal illness,
or hemorrhage, blood loss.
These patients will have very, very skinny,
collapsible inferior vena cavas.
So if your vena cava's tiny
or if collapses down to nothing when you breath in deeply.
That suggests the patient in need of volume.
Whereas you IVC is normal in caliber
and it doesn’t collapse down to nothing
or maybe it’s even distended,
that suggests that you’re euvolemic
or potentially even volume overloaded.
So these can help kind of guide your thinking a little bit
about the patient
and particularly for patients
who have evidence of intervascular volume depletion,
by giving them fluids or blood,
you can potentially reverse their PEA.
I didn’t have an image to show you here
but I’ll also just mention,
ultrasound is very commonly used to evaluate
for tension pneumothoraces.
There’s a number of test that you can do that'll help you
quickly identify that at the bedside without moving the patient.