So just to break down a couple of these interventions
a little bit more.
Epinephrine is a vasoconstrictor,
that's why we use it in cardiac arrest.
As you probably remember from pharmacology,
it's a nonselective adrenergic drug.
Meaning, it acts on the alpha
and beta adrenergic receptors all equally.
The great thing about epinephrine
is it increases systemic vascular resistance.
So it clamps down all the blood vessels below the diaphragm
and it cuts off blood flow to organs
we don't care about in cardiac arrest
like the liver and the kidney.
What we care about in cardiac arrest
is the heart itself and the brain
because those are the two organs
that are gonna determine
our ultimate outcome in the setting of arrest.
even though it makes a lot of sense to give a medication
that would optimize cardiac and cerebral blood flow,
there’s not really great scientific evidence
supporting the use of epinephrine
and we'll talk a little bit more what there is.
So there’s only one randomized controlled trial
on epinephrine that’s ever been done
in the history of medicine
and it was just done a year or two ago
by a group down in Australia
and basically what they found
is that when epinephrine was given in place of placebo
for patients with out of hospital cardiac arrest,
these patients were much more likely to survive
the resuscitation itself
or to get a pulse back during the resuscitation
and they were much more likely to survive
their hospital transport
and actually get admitted to the hospital.
So they would live through their ambulance ride,
live through their time in the ED
and make it up into an ICU setting.
Unfortunately, there's no evidence
that the group that received epinephrine
was more likely to survive to hospital discharge.
So while their short term outcomes were a lot better,
their long term outcomes were comparable.
One of the reasons for this is that unfortunately,
the sample size of the study ended up being smaller
than the investigators intended
and they weren’t able to demonstrate
a less likely outcome like survival to hospital discharge
'cause they just didn't have the sample size to do it.
So the bottom line is we still don't really know
if epinephrine changes long-term outcomes in cardiac arrest
and if it makes you any more likely to survive
to the end of your hospitalization
or to survive with a neurologically good outcome.
Now EPI is a bit double-edged sword.
So on the pro side for EPI,
we know that it increases vascular tone,
optimizes perfusion of the heart and the brain
and it improves short term survival
which clearly is an absolute prerequisite
for a long-term survival.
So it seems like it would be a pretty good idea.
However, remember what I told you causes cardiac arrest?
It's mostly myocardial infarctions
and other forms of ischemic coronary disease.
So when you give EPI,
what does it do to the heart?
It increases rate,
it increases contractility,
it increases myocardial oxygen demand which can worsen ischemia.
EPI also does reduce perfusion to other organs
which is problematic
and we don't know what effect,
if any, it has on long-term survival
it might do no good,
it might even be harmful in the long run,
we truly don't know.
So hopefully, we'll get more scientific evidence
regarding epinephrine as time goes on.
But for right now,
experts in the field believe
that the pros outweigh the cons
it’s considered the standard of care in cardiac arrest.
So according to current protocols,
EPI is a mandatory intervention.
You give one milligram of it in 1 to 10.000 dilution
every 3 to 5 minutes throughout the cardiac arrest.
Now, there aren’t many drugs doses you need to know cold,
but this is one that you really should know
both for your exams and for your life.
One milligram of EPI,
1 to 10.000 formulation
repeated every 3 to 5 minutes
throughout the cardiac arrest.
The other drug that was mentioned
in our arrest algorithm is amiodarone.
Amio as you may know
is a class three antiarrhythmic drug and it is indicated
for all cases of shock refractory V-fib and V-tach
But the current heart association guidelines don't say,
"You definitely should give this drug
'cause its awesome and saves lives."
They say, "You can think about it."
So it’s not actually a mandatory intervention and that's because
there are two large-scale studies of amiodarone
that have shown evidence of short term survival
compared to placebo.
However, there's no evidence that amiodarone
is superior to other anti-arrhythmics
such as lidocaine which was traditionally used in cardiac arrest
and there's no evidence that it offers any benefit whatsoever
for long term survival outcomes.
That means, that your patients
will have had their cardiac arrest detected quickly,
they will have received rapid CPR that’s high in quality,
they will have had their rhythm detected quickly
and had a shock administered.
So they’ve got a pretty good chance of intact survival
if we can just get their heart restarted.
Contrast to the patients we see in the ED,
who arrest at home or out in public places,
who may or may not have a witnessed arrest,
who may or may not receive rapid CPR and rapid defibrillation.
These patients often have
a much higher degree of cerebral injury,
a much higher degree cardiac injury
from their cardiac arrest event
and they’re less likely to benefit from amiodarone.
So we have to be a little bit circumspect in whether or not
we’re gonna use it in this population of patients.
So the bottom line with the amiodarone
is it’s used very commonly
for refractory V-fib and V-tach
that’s not responsive to epinephrine and electricity.
The dose is 300 milligrams
which is double the normal loading dose
you would use for other indications
and you really should think about it in cases where you suspect
that the patient might have a positive outcome
if you can reorganize their cardiac rhythm
but maybe not useful to give it in patients
who are likely to have severe cerebral anoxia
and go on to have a bad outcome no matter what you do.
So let's review the algorithm one more time.
We're gonna call for help and we're gonna start CPR
as quickly as we can.
We're gonna go ahead and perform defibrillation,
and fortunately for us,
we’re very likely to be able to get our hands on a defibrillator
out in public
because they’ve become so readily available in public settings.
If the patient's in V-fib or V-tach,
we're gonna shock them.
After the first shock,
we're gonna perform five cycles of CPR
or two minutes by the clock
at which point we’re gonna give one milligram of epinephrine.
After giving epinephrine,
we're gonna again, resume CPR
for five cycles or two full minutes
at which point once again, we’ll recheck the rhythm.
If it's still shockable, we’ll perform another defibrillation,
and then we will consider the use of amiodarone
because at this point,
we would consider the patient
to be in shock refractory V-fib or V-tach.