So let’s start off with sympathomimetics.
This is a pretty one to understand.
All the sympathomimetics do
is up regulate the sympathetic nervous system.
So basically, they increase the heart rate,
increase the blood pressure,
generally produce sinus tachycardia.
Although in high doses,
they can also precipitate tachyarrhythmias.
They don’t do a whole lot to respiration,
although some patients may present with tachypnea
And many patients will present with hyperthermia,
largely due to the motor activity
and agitation associated with sympathomimetic ingestions.
When you examine the pupils on these patients,
they’ll be mydriatic.
So their pupils will be very large.
Their skin maybe normal
but diaphoresis is quite common
and their secretions are generally gonna be normal.
So again, this is a pretty easy toxidrome to understand.
It basically involves up regulation
on the sympathetic nervous system,
fast heart rate, high blood pressure, mydriasis,
but generally not a lot of effects on skin or secretions.
By contrast, we have the anticholinergic toxidrome.
So as you can imagine,
when you block the parasympathetic nervous system,
you’re going to have unopposed sympathetic innervation.
So a lot of the features of the anticholinergic toxidrome
are similar to sympathomimetics.
You’re gonna have a fast heart rate,
a high blood pressure,
a rapid cardiac rhythm,
and in some cases,
you may have tachyarrhythmias.
Generally, not a lot of effect on respiration
but very commonly an elevated temperature.
This is actually an important feature of anticholinergic toxicity.
Much like patients with sympathomimetic exposure,
you’re gonna have mydriasis,
so large pupils.
However, this is where it gets different.
So these patients lose cholinergic innervation to the skin
and the mucosa.
So they’re gonna have dry skin and more importantly,
they’re gonna have almost no secretion.
So they’re gonna have dry mouth,
they’re gonna have no tears,
they’re gonna appear clinically to be very dehydrated.
So there’s a Mnemonic for the anticholinergic toxidrome.
It’s mad as a hatter,
cause these patients will all have altered mental status
Blind as a bat,
which refers to the very dilated pupils.
Red as a beet,
which refers to the skin flushing
that you commonly see in patients
with anticholinergic ingestions.
Hot as a hare
and I’m not really sure why hares are so hot,
but this refers to the dry skin and elevated body temperature.
And then lastly, dry as a bone.
So these patients will have dry mucous membranes
and a lack of oral and ocular secretions.
Now, it might not surprise you to hear
that the cholinergic toxidrome
is pretty much the opposite of the anticholinergic toxidrome.
So these patients will have a slow heart rate,
a normal to low blood pressure.
They’ll typically be in sinus brady tachycardia,
arrhythmias are very unusual with this toxidrome.
They’re gonna have some degree of respiratory depression.
Typically, a pretty normal temperature
although they might be on the low side.
And their pupils are gonna be miotics.
So their pupils will be constricted, small.
So this is a really important differentiating feature
of the cholinergic toxidromes.
These patients will be wet.
So their skin will be profusely diaphoretic
and their secretions will be copious.
You’ll see lots and lots of secretions in the mouth,
you’ll see lots of tearing.
And that’s because that’s what
the parasympathetic nervous system does.
It basically innervates
all of the parts of the body that produce secretions.
And you can easily remember the cholinergic toxidrome
by thinking about fluids pouring out of every orifice.
So there’s a Mnemonic for the cholinergic toxidrome
that includes salivation,
copious oral secretions.
Lacrimation, copious tearing.
these patients will commonly be incontinent of urine.
Defecation or diarrhea
that’s an area where they’re often incontinent as well.
GI dysmotility and emesis.
So basically you can imagine,
there’s something rather pouring out
of every orifice in this patient.
There’s another Mnemonic which some people prefer
that is includes diarrhea, urination,
miosis or muscle weakness,
emesis, lacrimation, and salivation.
Now, whether or not you use these Mnemonics
or however you think of the anticholinergic toxidrome,
an easy way to remember it again,
is if they have copious secretions,
if there’s fluid pouring out of every orifice,
you wanna be thinking about the cholinergics.
The sedative-hypnotics are pretty easy to understand
because what they do is cause sedation.
So somnolence is gonna be the primary hallmark.
These patients sometimes can be so deeply sedated
that they lose their airway protective reflexes
so you do need to consider the possibility
of intubation in some cases
and respiratory depression might also occur.
these patients require mechanical ventilation.
There’s not a lot of autonomic effects
associated with this sedative hypnotics.
patients often take multiple drugs at the same time,
so they may have autonomic effects related to co-ingestions
or other things that they took along
with their sedative ingestion.
Opioids are very similar to the sedative-hypnotics
in that they produce somnolence.
However, they universally produce miosis.
So opioids are very powerful pupillary constrictor.
And when you see pinpoint or very constricted pupils,
you should always think about opioids.
The other thing to remember about opioids
is that they very commonly cause respiratory depression.
So patients can come in apnea
or with respiratory rates that are significantly low a
nd this can be a fatal event.
So for these patients,
we need to be pretty aggressive about treating them
and restoring their normal respiration
in order to save their lives.
So here’s the review of the toxidromes
and I’m gonna highlight some of the things
that differentiate them so you can remember.
these patients will present hypertensive and tachycardic,
and typically, their mental status will be agitated.
will look alike a lot like sympathomimetic patients,
except they will have very dry skin, very dry secretions.
our cholinergic patients will be copiously wet.
They'll have diaphoretic skin,
they’ll have increased secretions,
and typically they will be somnolent rather than agitated.
Our sedative hypnotic patients will of course be sedated,
and our opioid patients will also be sedated.
they’ll present with miosis and respiratory depression.
this will help you keep different clinical syndromes
associated with different classes of drugs straight
and allow you to rapidly narrow your toxic logic differential
when you’re faced with a patient who has an exposure.