EMT Pharmacology

Introduction
It was the middle of the night, and I was alone in the back of the ambulance with my patient. I

don't really remember much about the call other than the patient being a trauma and they were

in pain. It was a thirty-minute transport to the trauma center. I knew this meant that I would be

administering multiple interventions along the way, one of which was analgesia. When the time

came to address the patient's pain, I reached into the medication bag and pulled out one of the

sealed medication boxes. Next, I gathered a syringe and needle, ripped open the seal, picked

up the vial of fentanyl, and drew up the appropriate dose. Finally, I attached the syringe to the

IV and watched the second hand on my watch as I planned to push the fentanyl over two

minutes slowly. I pushed the plunger a little to ush the saline through the port and

administered a small amount of volume.

Fifteen seconds passed, and I looked at the plunger and pushed again.

At thirty seconds, the same procedure.

(…)

At one minute and thirty seconds, I looked at the syringe and stopped.

I distinctly remember feeling like my heart was about to bust through my ribs. My stomach

sank. My brain had just told me:

"You never read the vial.”

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The next few moments were a whirlwind of actions, emotions, and racing thoughts.

Where the hell is that vial? I just have to nd the vial. Did I already throw it away? How much of

that actually went in? I have to hit the blood pressure and print the ETCO2 waveform. The

SPO2 is still good. I'm going to turn up their oxygen, just in case. I need to tell my partner. Is

the fentanyl next to the rocuronium? Isn't the Vasopressin vial just like the Fentanyl one? Shit.

What color was the vial? Why can't I remember? I should ask the patient to tell me a story so

they keep talking. Where the fuck is that fucking vial?

It was in my pocket. Turns out, it was Fentanyl like I intended. The patient was ne, but I

wasn’t. A very long thirty seconds ago, I was convinced I was going to be a story on the news.

Up until that point, I had no idea how people made medication errors. It was so simple, I

thought.

Right patient? I only have one patient at a time, so I'm pretty sure I won't be mixing them up.

Right drug? Well, I can read, so that shouldn't be too di cult.

Right dose? I have all my medication doses memorized, plus I can check my phone if I can't

remember.

Right time? I know all about onset times and how long medications last, and I'm always super

careful about pushing them over time.

Right route? I'm not going to stick a needle into an albuterol vial or anything.

Right reason? I know my indications, and if it ends up being something weird, I can just look it

up.

Right documentation? I don't do anything stupid, like throw away gloves with notes on them.

I always write out my medications on a medication tracking sheet.

Everything I thought was wrong.

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 A patient is completely vulnerable when they’re in your care. They put trust in you as a

healthcare provider to have a system in place to make sure they’re getting the medication they

need. It’s not about looking at the ‘rights’ and thinking to yourself that you have everything

gured out; it’s about being thoughtful, present, and methodical each time you prepare a

medication, regardless of which medication it is.

Let’s rewrite the ‘rights’ into action items that actually mean something:

Right patient? I will check that what I know about this patient is actually true before I

administer a medication.

Right drug? I will read the name and concentration of the vial out loud and con rm it with

someone else before I pop the top.

Right dose? I will not rely on my memory but will check a reference to ensure proper dosing.

Right time? I will think carefully about the situation surrounding this procedure and make sure

the timing of each dose is correct.

Right route? I will make sure that I am using the route appropriately and that it is the correct

route for the given situation.

Right reason? I will double-check my indications and make sure the medication is not

contraindicated for some reason.

Right documentation? I will keep track of the medications I gave, when I gave them, and how.

As you start learning how to administer your rst medications as an EMT, it’s the perfect time to

form a habit of going through these ‘rights’ - you’ll thank yourself for the rest of your career.

Enjoy the book! We’re con dent that it will help you become more knowledgeable and skilled in

pharmacology and help you keep your patients safe as well!

- The FOAMfrat Team

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 Table of Contents

Oxygen 6
Albuterol and Atrovent 22
Epinephrine 34
Aspirin 49
Nitroglycerin 56
Naloxone 66
Oral Glucose Gel and Glucagon 80
Flashcards 94

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 Oxygen
For a more detailed look at oxygenation as a whole, check out the ~40-page FOAMfrat

Oxygenation Workbook available for free at: https://www.foamfrat.com/oxygenation

In this pharmacology workbook, we’ll focus on the administration of oxygen through various

devices. This might seem a little out of place, but oxygen is a medication just like any other,

and getting good at oxygen administration means becoming pro cient with the devices we use

to administer oxygen and understanding the nuances of your patient’s needs.

The rst key to understanding oxygen administration is that oxygen is a volume that we’re

administering to the patient at a certain rate - the volume and rate that we’re working with is

how many liters are administered over one minute (L/min). If this is di cult to imagine with gas,

try picturing it with water.

In the illustration above, we have a bucket that will leak at a rate of 10 L/min. If you want to ll

up the bucket to the point that it over ows, you’ll have to put water in at a rate that is higher

than the leak. If we’re aiming to give oxygen at a ‘high ow,’ we need to overcome the rate

(L/min) the patient is breathing in (inspiratory ow rate). Examples:

1. You’re giving oxygen at 6 L/min, and the patient is inhaling at 25 L/min (not high- ow ❌ )

2. You’re giving oxygen at 15 L/min, and the patient is inhaling at 25 L/min (not high- ow❌ )

3. You’re giving oxygen at 30 L/min, and the patient is inhaling at 25 L/min (high- ow✓)
4. You’re giving oxygen at 60 L/min, and the patient is inhaling at 50 L/min (high- ow✓)

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 Usually, when you’re taught about oxygen administration, you’re only taught about the oxygen

administration ow rates and what percent of oxygen the patient receives from that ow rate. (1)

Device Flow FiO2 Range

(Extremely variable with patient IFR)

Nasal Cannula Typical: 0.25 - 6 L/min 22 - 40%

[PreOx / ApOx*: 15 - ?]
Simple Mask Typical: 5 - 10 L/min 35 - 50%
[PreOx: 15 - ?]

Partial Rebreather Mask Minimum 10 L/min 40 - 70%

[PreOx: 15 - ?]

Oxygen-Driven CPAP/BIPAP Typically 10-15 L/min 31-100%

[PreOx: 15 - ?]

High-Flow Nasal Cannula Typical top end of ~60 L/min 35 - 90%

Bag Valve Mask Variable by operator (squeeze) 21 - 100%

Typically supplied with 15 L/min

Ventilator Low ow - High ow 21 - 100%

(~100 L/min or more) (Not variable)

“PreOx” = Pre-oxygenation before a procedure like intubation.

“ApOx” = Apneic oxygenation (keeping a nasal cannula owing during intubation).
“FiO2” = Fraction (percent) of oxygen delivered.

However, you’ll see that the far right column notes these percents are variable depending on

the rate that the patient is breathing in. If you have a patient breathing in at 15 L/min and you

have a CPAP device owing at 15 L/min, that patient should be receiving 100% oxygen.

However, if the patient breaths in at 30 L/min, they would only be receiving 47% oxygen. Here

is a chart from Flow-Safe II CPAP systems that those percents are based on (2):

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 While they don’t note the inspiratory ow rate (instead represented by respiratory rate and time
spent on inhalation vs. exhalation), we can still gure out the ow rate by doing some math:

1. 20 breaths a minute (once every 3 seconds)

2. I:E is 1:1 (equal time inhaling and exhaling)
3. 1.5 seconds in, 1.5 seconds out
4. Breathing in 750 mL over 1.5 seconds
5. 750 / 1.5 = 500mL
6. Breathing in 500mL every 1 second
7. 500mL x 60 seconds is 30,000mL
8. 30,000mL (30 L/min IFR)

You can only claim that you’re giving “high- ow oxygen” if you are meeting or exceeding the

inspiratory ow rate of your patient (3). It’s worth noting that the normal inspiratory ow rate for

someone quietly breathing while at rest (no respiratory distress) is ~25 L/min. During respiratory

distress, the inspiratory ow rate may exceed 100 L/min (4).

You might be thinking: Do I have to do all of this math? How would I know their tidal volume

and, therefore, their IFR?

Unless you’re using a mechanical ventilator or non-invasive machine, you won’t. Instead, you’ll

take a few normal measurements and give it your best guess. What would be the important

items to observe?

• Respiratory Rate - this is one of the best indicators of respiratory status (5) (the ETCO2 RR).

• Respiratory e ort - do they seem like they’re really hungry for air ow?

• SPO2 - if it’s below your target, they need more oxygen.

• ETCO2 - is it high or low? Is that because they need more support?

Again, more on oxygenation as a general topic in the FOAMfrat Oxygenation Workbook noted

above. Let’s get back to logistics. So far, we know that ow rate is very important, and the

quoted levels of FiO2 are variable depending on the inspiratory ow rate (IFR). The more severe

respiratory distress or failure becomes, the more likely the patient is to need higher ow rates

and support from devices that apply positive pressure.

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Next, let’s talk about devices - there are many to choose from in EMS. There are nasal

cannulas, ETCO2 nasal cannulas, simple masks, partial non-rebreather masks, CPAP devices,

and bag-valve masks (we’ll leave advanced airways out of this since they’re just a path for

oxygen).

Nasal Cannulas

Nasal cannulas are very versatile and can be applied at higher or lower ow rates.

(6) Wettstein, Richard & Shelledy, David & Peters, Jay. (2005).
Delivered oxygen concentrations using low- ow and high- ow
nasal cannulas. Respiratory care. 50. 604-9.

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 The chart on the previous page shows an approximate FiO2 based on our liter ow (keep in

mind the IFR) and a di erence between closed and open-mouth breathing. Standard nasal

cannulas can also be used under devices such as non-rebreather masks and simple masks to

increase ow and FiO2 (always follow your local guidelines for using these devices).

It’s also worth mentioning that there are some clinicians who use very high rates of ow on

regular nasal cannulas during severe dyspnea, pre-oxygenation, and intubation. These ow

rates exceed what is generally recommended for standard nasal cannulas, usually exceeding

15 L/min and sometimes greatly surpassing that rate (follow your local guidelines). To add a

little context to this point, the reason for limiting most cannulas to a ow rate of 6 L/min is to

limit dry gas exposure to the nares (since this could cause epistaxis) and for patient comfort. In

emergency settings, these are not our biggest concerns - our biggest concern is brain death

due to hypoxia. We need to weigh the risk vs. bene t of ow rates when compared to the

severity of the patient.

The ETCO2 NC is similar to the regular nasal cannula, with the additional ability to sample

ETCO2. These cannulas are not ideal for the purpose of giving a lot of ow to the patient due

to their design. Depending on the manufacturer, only one nasal prong may give oxygen while

the other samples ETCO2, and high ow rates may interfere with how it samples ETCO2. For

these reasons, ow rates of 1-6 L/min are typically adhered to, and the devices are not used

for pre-oxygenation or apneic oxygenation.

Standard NC ETCO2 NC
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 Oxygen Masks

There are a few di erent types of oxygen delivery masks that can get a little confusing to tell

the di erence between.

1. Simple mask - 2 open ports, no reservoir.

2. Oxy-Mask - Open mask.

3. Partial non-rebreather - 1 open port, reservoir.

4. Non-rebreathers - zero open ports, reservoir.

Open
1 2

3 4
Open One-way valves
One-way valve

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 Most commonly, clinicians refer to the Simple Mask and Oxy-Mask as “Simple Masks,” while

both Partial Non-Rebreathers and Non-Rebreathers are called “Non-Rebreathers” (even though

there are di erences between all of these, as noted on the previous page).

Most commonly, services will carry a simple mask and a partial non-rebreather. Why not a non-

rebreather with two one-way valves? If oxygen runs out, or the patient has a very high IFR, the

non-rebreather will not allow enough air to enter the mask from the atmosphere, and the

patient can su ocate (this has happened and is the reason why many services and hospitals

only carry partial non-rebreathers). This is true even if oxygen is owing. If you’re owing at 10

L/min with a non-rebreather, but the patient is breathing in at 100 L/min, the gaps around the

mask will not allow enough air entry, and the patient will want to rip the mask o of their face

due to the feeling of ow starvation. The reservoir bag can help with this, but perhaps not

enough when the patient has a high IFR. If your patient won’t keep their mask on that’s

supposed to be helping them, it might be because they’re not getting enough ow.

The ow rate for most of these devices is 10-15 L/min (never less than that with non-

rebreathers so that the patient doesn’t su ocate). However, the same points apply to the

masks as the nasal cannula - they’re frequently used at high ow rates to match respiratory

distress (7). You know what’s coming next. Follow your local guidelines.

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 CPAP Devices

There are a few popular CPAP devices - the Flow-Safe II CPAP and two versions of the

Pulmodyne CPAP (O2-MAX and GO-PAP).

The Flow-Safe II CPAP is ow-driven, meaning that as you increase the L/min, you get more

continuous positive pressure (CPAP). The O2 hose that comes with the device will have a label

attached to it, indicating what ow rate should approximate which corresponding pressure.

It looks like this:

FLOW-SAFE
FLOW (LPM CPAP/PEEP (approx. cmH20)

8-9 5

10-12 7.5

13-14 10

Flush 13 (Max.)

The chart we were using for FiO2 calculations on page 7 is also from Flow-Safe.

The Flow-Safe II CPAP will allow the patient to breathe in (entrain) room air if the patient has an

IFR that exceeds the ow rate of the device (keep in mind that entraining room air decreases

the FiO2).

The Flow-Safe II:

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The Pulmodyne CPAP functions a little di erently. Instead of solely relying on oxygen ow to

create pressure, there is a mechanical valve that can be adjusted to set pressure. There is

another very important point to consider with the Pulmodyne CPAP - it uses the Venturi e ect

to create extra ow (L/min). The Venturi e ect causes room air to get sucked into the device,

which dilutes the FiO2. This is great for ow rates but doesn’t provide as high of a percentage

of oxygen as you might think. Check out the di erences in FiO2 and ow rates in the

screenshots below from the Pulmodyne website:

https://www.pulmodyne.com/product/go-pap

https://www.pulmodyne.com/product/o2-max

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Both the Flow-Safe and Pulmodyne CPAP devices are great, but there are key di erences in

the way they work. No matter what device you carry, grab one from your training department

and get really familiar with it - these devices can turn a respiratory distress patient around

when used appropriately! Practice putting the device on your partner, how the nebulizer

attaches to it, how the mechanics of the device work, etc. The more familiar you are with the

device, the more con dent you’ll be in applying it to patients.

CPAP key points:

• If the patient is altered, be cautious. They might vomit and aspirate without warning you.

• Any positive pressure ventilation can lower BP - be aware of hypotensive patients.

• First-time CPAP patients may need a lot of coaching due to anxiety.

• Watch your portable oxygen tanks - CPAP can burn through oxygen quickly, like a NRB.

• Practice, practice, practice applying and securing the device.

Bag-Valve Mask

Anesthesiologists will tell you that learning to manually ventilate a patient with a BVM is an art,

and it’s not easy to master. All providers are prone to squeezing the bag too often, too hard,

too fast, or all of the above. On top of that, it can be di cult to get a good seal on the patient’s

face.

https://quadmed.com/mercury-medical-small-adult-cpr-2-bag/ 15
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Typically the seal with a BVM is held with a C-E Grip, but it’s much easier to hold a good seal

with two hands (utilizing two clinicians) (8). Once you have a good seal, it’s time to start thinking

about squeezing the bag. It’s usually said to squeeze the bag over one second and watch for

visual chest rise. This isn’t bad advice, but it can be di cult to appreciate the motion of the

chest rise. This brings us back to knowing a little bit about how much to squeeze the bag.

There was a very interesting study where researchers measured the tidal volume delivered with

either a standard adult BVM or a pediatric BVM. They measured 50 di erent EMS clinicians to

evaluate the volume they delivered. The adult BVM usually resulted in a tidal volume of

>900mL, while the pediatric BVM resulted in average tidal volumes of around 600mL. This

meant that the clinicians ventilated appropriately with an adult BVM 5.1% of the time and a

pediatric BVM 17.5% of the time. Even the 625mL average with the pediatric BVM is the

appropriate tidal volume for a 6’5” male (tidal volume is based on height and sex).

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 What does this tell us? We’re giving too much tidal volume. Ventilating too frequently or giving

a tidal volume that’s too large reduces blood coming back to the chest because it’s di cult for

blood to enter the chest when positive pressure ventilation is applied. Not over-ventilating a

patient is especially important during cardiac arrest. There is a clear relationship between

excessive BVM use and poor outcomes in cardiac arrest.

It would take an entire workbook to explain the intricacies of a BVM and proper technique, but

here are some key points:

• Ensure oxygen is owing and keep the reservoir in ated.

• Get a good seal - use two hands if needed and get help from another clinician.
• Monitor the tidal volume - a one-hand squeeze will reduce the risk of over-in ation.

• Use a manometer to ensure you’re not using excessive pressure (try to stay in the green).

• Monitor the frequency - use ETCO2 to get a real-time rate.

• PEEP valves can improve oxygenation and reduce lung injury.

Here is a simpli ed view of oxygenation:

This is the same strategy clinicians apply when using a mechanical ventilator. PEEP is

increased, the tidal volume is optimized (using appropriate pressures on the manometer), and

nally, the time spent on inhalation increases (9).

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 Oxygen Tanks

Whenever you’re giving oxygen from a tank, your time is limited. Obviously, the lower the ow,

the longer the tank will last. However, high ow rates can eat through your oxygen rather

quickly. So, how long will a tank last at certain ow rates? We’ll use a formula for this, but we’ll

also include some round numbers to remember.

PSI x Tank Conversion Factor

Formula: Minutes remaining =
Flow Rate

PSI and Flow Rate are obvious, but what is a “Tank Conversion Factor”? Tank conversion

factors are di erent for each tank. The common ones are:

E Tank: 0.28
D Tank: 0.16
H Tank: 3.14
M Tank: 1.56

To avoid the math, use this calculator: https://respiratorycram.com/oxygen-tank-duration-

calculator/ (or just Google “oxygen tank duration calculator”).

Here are some round numbers for common tanks and ow rates:

D Tank at 2000 PSI, owing 6 L/min: 53 minutes

D Tank at 2000 PSI, owing 15 L/min: 21 minutes
M Tank at 2000 PSI, owing 15 L/min: 208 minutes

Here’s an interesting one:

D Tank at 500 PSI, owing 15 L/min: 5 minutes

Just like we would be concerned about how much medication is left in a bag going into an IV,

we need to be aware of how long our oxygen tanks will last. If you’re going into a respiratory

distress call with 500 PSI in your portable tank, you only have 5 minutes at 15 L/min. Is that

really enough? It’s not likely. Keep your tanks full, and be aware of how bene cial your main

tank can be for respiratory calls. Prioritizing moving the patient to the ambulance gives you

plenty of oxygen as well as multiple sources to attach devices.

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 Oxygenation

When a patient is having a hypoxic emergency, think about it as issues involving ow

(ventilation), di usion, and perfusion (10).

Flow (ventilation) refers to how much ow you’re giving the patient. If your patient has a high

IFR, they may need more ow and even stacked devices such as a nasal cannula and an

oxygen mask at high ow rates.

Di usion is getting oxygen through the wall of the alveoli and into the pulmonary capillary.

There may be pulmonary edema, mucus, or atelectasis (closed alveoli) that would bene t from

positive pressure like CPAP or a BVM with a PEEP valve. The positive pressure helps to thin

the mucus or pulmonary edema and recruit (open) alveoli, allowing them to participate in gas

exchange again. Also, keep in mind that the supine patient will be more di cult to ventilate. If

possible, sitting the patient up may improve lung function by reducing chest and abdominal

pressure on the lungs.

Perfusion means that the patient has adequate blood pressure and hemoglobin to carry that

oxygenation. There is also a component of perfusion that has to deal with acidosis as well

(having a very high CO2, for example). If the CO2 is too high, oxygen has trouble attaching to

hemoglobin and, therefore, cannot be transported to tissues very e ciently. We usually

consider oxygenation and ventilation as separate processes, but in this regard, they are related

(it’s important to maintain an appropriate CO2 as well).

You can turn these into action items by asking yourself:

• Does this patient need more ow because they’re entraining room air, diluting the FiO2?

• Does this patient have a lung issue making it too di cult for oxygen to ow through into the

bloodstream? Like mucus, pulmonary edema, atelectasis, or bronchospasm?

• Is this a perfusion issue where acidosis or hypotension is causing an oxygenation issue?

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 Oxygen Pro le

Description: Oxygen is a colorless, odorless gas that is essential for human life. As a

medication, it is used to increase the concentration of oxygen in the patient's blood and

tissues, thereby enhancing cellular function and recovery.

Mechanism of Action: Oxygen therapy increases the amount of oxygen in the blood, thereby

improving the oxygen supply to the body's cells. This supports cellular metabolism, particularly

in situations where the body's oxygen demand is high, or the supply is compromised.

Indications: Oxygen is indicated in conditions causing hypoxia or hypoxemia, such as chronic

obstructive pulmonary disease (COPD), pneumonia, asthma, and trauma. It is also used in

acute settings such as cardiac arrest, shock, and severe bleeding.

Contraindications: While never contraindicated if the patient has hypoxia/hypoxemia, use

caution in patients with acute stroke or acute coronary syndrome. Follow AHA

recommendations or your local guidelines for SPO2 ranges (usually the minimal ow to

maintain saturations in a normal range).

Dosage: The dosage ( ow) of oxygen varies based on the patient's condition and oxygen

saturation levels. Flow rates will be based on the device used and your local guidelines.

Route: Blow-by, nasal cannula, oxygen masks, pressurized masks (CPAP and BiPAP),

Bag-valve mask, or through mechanical ventilation.

Duration: The duration of oxygen will be based on the patient’s condition. Things that will

cause rapid desaturation include high metabolism/oxygen requirement, hyperthermia, acidosis

(high CO2), low SPO2 (the lower the SPO2, the faster the desaturation), high BMI, and

mismatches between ventilation and perfusion, such as pulmonary edema or pulmonary

embolism.

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Oxygen Tips and Tricks:

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 Albuterol and Atrovent
If you want to keep a door open, you push it open, and then you place a doorstop to prevent it

from closing. You can think of albuterol and atrovent (ipratropium bromide) the same way -

albuterol opens the bronchi, and Atrovent keeps them open (11, 12).

Albuterol
Opens the door

Atrovent
Keeps it open

While both medications are typically thought of as ‘bronchodilators,’ albuterol truly is a

bronchodilator, and Atrovent is more of an ‘anti-broncho-constrictor.’

There are, of course, more technical terms for these two medications. Albuterol is a

sympathomimetic (it mimics the actions of the sympathetic nervous system). Atrovent is a

parasympatholytic (it lyses the action of the parasympathetic nervous system).

Every organ in the body is under dual innervation from both sides of the autonomic nervous

system. You’ll recall that the sympathetic side is the ‘ ght/ ight/freeze’ portion of the

autonomic nervous system, while the parasympathetic side is the ‘rest/digest’ portion. How

would each of these in uence the lungs?

Autonomic Bronchi Mucus

Sympathetic Dilation Decreased

Parasympathetic Constriction Increased

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 When we give a medication like albuterol, it strengthens the sympathetic side. Meanwhile,

giving medication like atrovent will weaken the parasympathetic side.

It’s like a tug-of-war for the lungs:

Sympathetic Parasympathetic
Bronchodilation Bronchoconstriction
Decreased Mucus Production Normal Increased Mucus Production

Asthma / COPD / Anaphylaxis

Sympathetic Parasympathetic
Bronchodilation Bronchoconstriction
Decreased Mucus Production Normal Increased Mucus Production

Albuterol and Atrovent

Speci cally, albuterol is stimulating the sympathetic nervous system through a beta-2

adrenergic receptor. Atrovent, on the other hand, is blocking the stimulation of the

parasympathetic side via blockade of the muscarinic acetylcholine receptor M3 (“M3

receptor”). On the next page, I’m going to quote the Wikipedia articles for both of these

receptors. It’s a little dense, for sure. However, we wanted to include these pathways in this

book for those of you that are interested in a deeper understanding of the pharmacology

behind these two synergistic medications.

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The Beta-2 Article (albuterol):
“The beta-2 adrenergic receptor (β2 adrenoreceptor), also known as ADRB2, is a cell membrane-spanning beta-
adrenergic receptor that binds epinephrine (adrenaline), a hormone and neurotransmitter whose signaling, via
adenylate cyclase stimulation through trimeric Gs proteins, increased cAMP, and downstream L-type calcium
channel interaction, mediates physiologic responses such as smooth muscle relaxation and bronchodilation.”

The M3 article (Atrovent):

“The M3 muscarinic receptors… are located in the smooth muscles of the blood vessels, as well as in the lungs.
Because the M3 receptor is Gq-coupled and mediates an increase in intracellular calcium, it typically causes
contraction of smooth muscle, such as that observed during bronchoconstriction and bladder voiding.”

Here’s a graphic outlining those pathways:

As you can see from this incredibly simple and easy-to-understand graph… -_- …it’s all about

increasing or decreasing the action of MLCK (myosin light chain kinase). MLCK is what causes

muscles to constrict. MLCK causes myosin heads to slide along Actin laments to shorten the

muscle, resulting in contraction or shortening:

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 In some disease processes, there is the added complication of in ammation, as well. This

compounds the issues of bronchoconstriction and mucus production. In ammation,

bronchoconstriction, and mucus production all reduce the size of the airways and make it very

di cult for air to enter the lungs and even more di cult for air to leave the lungs (which leads

to air-trapping / auto-PEEP / breath stacking).

The ow reduction from the decreased diameter of the airways is more severe than one might

think. Poiseuille's Equation tells us about resistance to ow (13). It states that halving the

diameter increases resistance 16-fold! However, that also means doubling the diameter of the

airways will result in a 16-fold decrease in resistance (less resistance to ow is a good thing).

Increasing the diameter, and therefore reducing the resistance, is the goal with albuterol and

atrovent.

So far, we know:
• Albuterol is a sympathomimetic medication (beta-2 adrenergic agonist) that increases the
strength of the sympathetic nervous system, resulting in bronchodilation and reduced
mucus production.
• Atrovent is a parasympatholytic medication (M3 cholinergic antagonist) that decreases the
strength of the parasympathetic nervous system, resulting in a reduction of
bronchoconstriction and mucus production.
• Smaller airways reduce ow dramatically, and our goal is to dilate airways to decrease the
amount of work the patient needs to exert in order to move air into, and especially, out of
the lungs to prevent air trapping / auto-PEEP / breath stacking.

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 Nebulizers

The method of administration of albuterol and atrovent is by nebulization. Nebulization is

simply the process of breaking down uid into such ne particles that they suspend in the air.

Nebulizer devices accomplish this through a very simple process utilizing gas ow and a ba e.

Using gas ow and a ba e is just like breaking rocks by throwing them against the concrete.

The speed you throw the rock is like the gas ow, and the concrete is like the ba e.

Patient inhalation

Suspended particles

Ba e

Oxygen Flow

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 Here’s an assembled nebulizer:

voir!
eser
et the r
t forg
Don’

Don’t forget to monitor the ETCO2 waveform!

“Shark n” appearance means uneven
alveolar emptying due to various levels of
bronchiole constriction in the airways!

It takes very little practice to become pro cient at assembling a nebulizer (most actually cannot

be assembled incorrectly because of the size of the ttings). Typically, the skill goes like this:

1. Decide between a nebulizer with a mask or a hand-held nebulizer.

2. Fully assemble the nebulizer.

3. Attach to oxygen.

4. Unscrew the cap, place desired medication inside, and screw the cap closed.

5. Start oxygen ow (usually 8 L/min).

6. Administer to the patient and coach breathing (in through the mouth, out through the nose if they can*).

*The blue corrugated ex tubing at the end of the nebulizer above is an oxygen and medication reservoir.
Suspended medication and oxygen build up in the reservoir when the patient isn’t breathing. But, if they
exhale through the device, it will wash the medication and oxygen out with their breath. This is where the
recommendation to have them exhale through their nose comes from (if they can).

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Keep in mind that you can also add nebulizers to non-invasive (CPAP/BiPAP) masks, BVMs,

and ventilators. And when using the nebulizer mask, you can leave things like an ETCO2 NC on

the patient to monitor their respiratory status or a regular NC to maintain more FiO2.

Nebulizer Bias

There are a couple of biases to be aware of when you’re giving a patient a nebulizer. When we

place a nebulizer on a patient, you will likely see the SPO2 and work of breathing improve

almost immediately (within the rst minute or so). This can lead us to believe that we’ve

administered the correct treatment - and maybe you have. However, it takes albuterol and

atrovent approximately 5 minutes to have a meaningful impact, and the medications don’t peak

until around 30 minutes after the treatment has begun. So, why would the SPO2 improve so

rapidly when we administer a nebulizer?

Obviously, it’s the increased oxygen ow. If the nebulizer is your rst treatment, the patient just

went from room air with no supplemental oxygen to 8 L/min of oxygen (especially if you placed

them on a nebulizer mask). The oxygen will show its bene t rst, and then a few minutes later,

you will start to see the bene ts of the nebulized medications. This is important to note

because we could trick ourselves into thinking that the nebulized medication was the right

choice. Again, maybe it was, but we want to be aware of this bias. There is a saying that goes:

‘not everything that wheezes is asthma’ (or COPD, for that matter).

Cardiac wheezes, for example, can be di cult to distinguish from wheezes from asthma or

COPD. Cardiac wheezes occur when a patient has such bad pulmonary edema that they not

only have rales ( uid in the alveoli that ‘pop' open when they inhale) but also have edematous

bronchi that are pu ed up with uid. Bronchodilators would not be bene cial in this patient

population.

The pediatric population with bronchiolitis may also have wheezing, but their wheezing is far

down in the small airways where they don’t have enough smooth muscle to relax in order for

the medication to have a bene t (bronchodilators can be tried but have no proven bene t).

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 The other bias to be aware of is the thought that a nebulizer is much more bene cial than a

metered dose inhaler (MDI). At a glance, there seems to be a huge dose discrepancy between

these two modalities. Comparing the dosages of nebulization versus MDI pu s, it’s easy to see

why this bias exists. Even a small dose of nebulized albuterol is 2.5mg (2,500 mcg). Meanwhile,

the MDI only supplied 90mcg per pu . If we were to compare these two doses simplistically, it

would seem like the nebulizer treatment is 28 times larger than the MDI pu (2,500 / 90 = ~28).

However, this isn’t an accurate comparison. Much of our nebulizer is lost to the room air. The

nebulizer continuously runs even when the patient is exhaling and while the patient is between

breaths. The MDI is only active during inhalation (and a spacer should always be used to

maximize deposition in the lungs). These factors change our comparison quite drastically (14).

Small Volume Nebulizer (SVN) Dose Equivalent MDI Dose (with spacer)

2.5 mg 4 pu s

5.0 mg 8 pu s

Of course, there is also the oxygen to account for. A patient taking only an MDI is getting the

medication, but no supplemental oxygen, which some patients will need.

The e cacy of nebulization can be increased by mimicking the inhalation-only timing of the

MDI through the use of a BAN (breath-actuated nebulizer), which only allows the medication to

ow to the patient when they inhale, or through the use of a vibrating mesh nebulizer.

Breath Actuated Nebulizer (BAN) Vibrating Mesh Nebulizer MDI with Spacer

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 Slightly Selective

At the outset of this chapter, we reviewed the e ects of the sympathetic and parasympathetic

nervous systems. Both albuterol and atrovent allow the sympathetic nervous system to have a

stronger in uence on the lungs to allow the airways to dilate. However, there is some crossover

that occurs with the rest of the body as well - these medications do not have a perfectly

selective action in the lungs. What happens when there is a crossover to the rest of the body?

One of the most common crossover e ects of albuterol and atrovent is tachycardia - an

increased heart rate.

(15) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018588/

The graph above was measuring young and healthy volunteers with no dyspnea. Their heart

rates climbed ~10 beats per minute on average (blood pressure did not show the same

increase). This isn’t profound, but the e ects on an actual patient in respiratory distress might

be more pronounced. Some institutions have ‘relative contraindications’ for breathing

treatments and tachycardia, but there is often little choice but to treat the underline cause of

the tachycardia - dyspnea (follow your local guidelines). Patients may experience tremors and

anxiety as well, which they will often refer to as ‘jitters’ following breathing treatments.

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 Albuterol Pro le

Description: Albuterol (also known as salbutamol) is a SABA (short-acting beta agonist).

Albuterol is a bronchodilator medication that is commonly used to treat conditions that cause

bronchospasm. Asthma, chronic obstructive pulmonary disease (COPD), and anaphylaxis are

common reasons for a patient to receive albuterol.

Mechanism of Action: Albuterol works by stimulating beta-2 adrenergic receptors in the lungs,

which leads to the relaxation of the smooth muscles in the airways. This causes the airways to

dilate, making it easier for air to ow in and out of the lungs and reduce air trapping.

Indications: Bronchospasm due to asthma, COPD, or anaphylaxis. Hyperkalemia (albuterol

temporarily lowers serum potassium levels).

Contraindications: Known history of hypersensitivity. Known severe hypokalemia (low serum

potassium).

Dosage: Typically 2.5 - 5.0 mg as needed or tolerated. Doses start at 1.25mg for small

pediatrics. Continuous nebulization may be indicated in severe bronchospasm.

Route: Nebulization/inhalation.

Onset: ~5 minutes.

Peak: ~30 minutes.

Duration: 3-6 hours.

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 Ipratropium Pro le

Description: Atrovent (also known as ipratropium bromide) is an anticholinergic bronchodilator

(helps prevent constriction). It is primarily used for the treatment of respiratory conditions such

as chronic obstructive pulmonary disease (COPD) and asthma. EMS services and hospitals

typically carry “ipratropium bromide” and not the brand name “Atrovent” - this is important for

the contraindications section below.

Mechanism of Action: Ipratropium acts by blocking the action of acetylcholine, a

neurotransmitter involved in bronchoconstriction. By inhibiting the e ects of acetylcholine,

ipratropium helps to relax the airways, allowing for increased air ow through the lungs. It works

by selectively binding to the muscarinic receptors (M3) in the airway smooth muscles, leading

to prolonged bronchodilation (stopping bronchoconstriction).

Indications: Bronchospasm due to asthma, COPD, or anaphylaxis.

Contraindications: Known hypersensitivity to ipratropium bromide. Allergy to peanuts (soy

lecithin) is a contraindication to brand names “Atrovent” and “Combivent” MDI products, not

the generic “ipratropium bromide” typically supplied for nebulizers in EMS. To con rm, check

the package insert that comes with your ipratropium bromide - it will speci cally note these

details if soy lecithin is present in the product.

Dosage: 0.5 mg, which most guidelines will state can be repeated up to 3 times at 20-minute

intervals / as needed. The dose may be decreased to 0.25 mg in the pediatric population.

Route: Nebulization / Inhalation.

Onset: ~15 minutes.

Peak: 1-2 hours.

Duration: 4-8 hours.

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Albuterol and Atrovent Tips and Tricks:

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 Epinephrine
Epinephrine is a sympathomimetic, just like albuterol. However, it has a wider spectrum of

mimicking e ects than albuterol. We found out that albuterol is a Beta-2 agonist, which mostly

had an impact on the lungs when given via nebulization. However, there is also Beta-1 and

Beta-2 in the cardiovascular system, and Alpha-1 e ects as well (16). We’ll need this broad

spectrum of e ects if we want to help patients with anaphylaxis, croup, and severe asthma.

Receptor Subtype Location E ect

Alpha-1 Adrenergic Vascular Wall Vasoconstriction

Increased duration of contraction without

Heart
increased chronotropy

Beta Adrenergic Beta-1 Heart Increased inotropy and chronotropy

Lungs Bronchodilation
Beta-2
Blood Vessels Vasodilation

Let’s break those down.

Alpha-1 provides vasoconstriction. This is useful in distributive (vasodilatory) forms of shock,

such as anaphylaxis, sepsis, and neurogenic shock. That vasoconstriction can also reduce

swelling in the airway, which is very useful in anaphylaxis and croup.

Beta-1 provides inotropy (increased strength of contraction) and increased chronotropy

(increased rate of contraction). This means we’ll see a larger increase in heart rate with

epinephrine than most other medications (which we may or may not want).

Beta-2 provides bronchodilation and vasodilation. We’ve covered the Beta-2 actions in the

lungs in the albuterol section, but what about the vasodilation in the cardiovascular system?

This might seem counterintuitive to the Alpha-1 action, but these actions take place in di erent

locations. Beta-2 will vasodilate large veins and arteries in skeletal muscle and vital organs,

while Alpha-1 constricts smaller veins and arteries in non-vital organs (vital for the ght-or- ight

response).

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 All of this makes sense for the ght-or- ight response. If you’re ghting or running for your life,

you would rst want an increased heart rate and blood pressure for more oxygen delivery to

your muscles, brain, heart, and lungs (beta-1). Next, you would want your airways to dilate in

order to move more air and dilate your large veins and arteries to get more blood to vital organs

and muscles (Beta-2). Finally, you would also want vasoconstriction to reduce any airway

swelling further and limit blood ow to your skin (so you don’t bleed out if injured) and other

non-vital organs so that blood and oxygen can ow to areas where you need it to survive

(Alpha-1).

While albuterol was selective to the lungs, epinephrine is causing all of these actions, which lls

in some areas that albuterol can’t cover. This is where the indications for albuterol and

epinephrine start to di er.

Asthma

Imagine you’re caring for a patient experiencing a severe asthma exacerbation. They’re on

numerous medications for daily control of their symptoms, and you note a history of needing

intubation due to the severity of their asthma attacks (which is never what you want to hear).

You immediately apply a nebulizer mask to the patient and start with a larger-than-usual dose

of albuterol, along with some ipratropium. The patient’s oxygen saturation increases slightly,

but their chest is silent, they’re moving incredibly small tidal volumes, and it doesn’t seem like

the medication you’re providing through the nebulizer is making it very far into the lungs. You

start to worry that nebulizers alone will not x this patient. So, what’s next?

If nebulizer treatments alone are not working, there are other interventions to try, but we’ll focus

on the pharmacology here. In a case like the one presented above, intramuscular epinephrine

might be the right move (17). This will allow Beta-2 stimulation to enter the body in a way that

bypasses the lungs (muscle -> bloodstream -> lungs).

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Here is a graphic from the FOAMfrat Pediatric Respiratory Distress - Part One Class:

(Follow your local protocols)

There are some medications on that chart that are outside of the EMT scope, but it’s useful to

see the whole treatment algorithm. You’ll notice down the right side that epinephrine might be

given at any time - it’s something to consider at any point during treatment if conventional

therapy is not working.

With epinephrine administration for asthma, the mechanism is exactly the same as albuterol -

we’re looking for Beta-2 stimulation that bypasses the lungs. It is worth noting that because

epinephrine is not as speci c as albuterol when it comes to stimulating the sympathetic

nervous system, you will likely see a more widespread mimic of the ght-or- ight response.

This means you’re likely to see a higher increase in heart rate, blood pressure, peripheral

vasoconstriction, etc.

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 Croup

Croup is also known as laryngotracheobronchitis. That name tells us a little about where this

viral infection primarily has its e ect - the upper airway (particularly the larynx and trachea). It

typically a ects children between the ages of six months and three years, and most of these

cases occur in the fall and winter months. The parain uenza virus causes most cases of croup,

although other respiratory viruses can also be responsible.

You might suspect croup if the patient has a fever, stridor, and a high-pitch ‘barking’ cough.

Hoarseness, respiratory distress, and nasal congestion are also common ndings. Of note,

croup has more upper airway symptoms than lower airway symptoms. This is an important

di erentiation since medications like albuterol only relieve lower airway symptoms like

wheezing due to bronchospasm (we need epinephrine for upper airway issues like stridor, but

beta dilation helps move more air as well) (18).

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 Wheezes and stridor are often confused. Here’s a table that compares and contrasts the two:

Stridor
High-pitched, harsh sound heard during
inspiration.
Usually associated with upper airway
obstruction, such as croup, epiglottitis, or
foreign body aspiration.
Results from partial or complete blockage of
the upper airway, leading to turbulent air ow.
Typically heard in the upper respiratory tract
and is more localized to the neck and
tracheal area.
Will not respond to bronchodilator
medications, as the obstruction is
anatomically located in the upper airway.
Epinephrine is needed in cases of croup.
Wheezing
High-pitched, musical sound heard during
expiration (and inhalation when severe).
Typically associated with obstructive lung
diseases, such as asthma, chronic
obstructive pulmonary disease (COPD), and
bronchiolitis.
Caused by narrowed or constricted airways,
leading to air ow obstruction and turbulent
air ow.
Commonly heard in the lower respiratory
tract and may be bilateral.
Often responds well to bronchodilator
medications, such as inhaled beta-agonists.

As epinephrine comes into contact with swollen tissue, it causes the vasculature around that

tissue to constrict, which reduces edema and swelling. As edema and swelling subside, air ow

improves, and so should the patient’s condition.

Swelling

Trachea

“Steeple Sign” 38
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 Because nebulized epinephrine doesn’t have to travel far to get to this airway obstruction, this

route should work very well in cases of croup. However, it’s not every day that you come

across a patient with croup. This might leave some clinicians wondering how sick the patient

needs to be to receive nebulized epinephrine. Let’s reference a system called the Westley

Croup Severity Score to see the usual treatment for this patient population.

Step 1: Score
Clinical Feature Assigned Score

Normal, Including sleep = 0

Level of consciousness
Disoriented = 5

None = 0
Cyanosis With agitation = 4
At rest = 5

None = 0
Stridor With agitation = 1
At rest = 2

None = 0
Air Entry Decreased = 1
Markedly decreased = 2

None = 0
Mild = 1
Retractions
Moderate = 2
Severe = 3

Step 2: Management
Score Severity Description Management

Occasional barky cough

Home treatment (antipyretics, uids, mist)
≤2 Mild No stridor at rest
Outpatient: Single dose PO dexamethasone
Mild or no retractions

Frequent barky cough

Single dose PO dexamethasone
Stridor at rest
3-7 Moderate Nebulized epinephrine
Mild to moderate retractions
Hospitalization not generally required
No or little distress or agitation

Frequent barky cough Single dose PO / IM / IV dexamethasone

Stridor at rest Repeated doses of nebulized epinephrine PRN
8-11 Severe
Marked retractions Inpatient admission usually required
Signi cant distress and agitation Improved after corticosteroid and nebulized EPI

Depresses LOC Single dose PO / IM / IV dexamethasone

Impending
Stridor at rest Repeated doses of nebulized epinephrine PRN
≥12 Respiratory
Severe retractions / Poor air entry ICU admission usually required
Failure
Cyanosis or pallor May require intubation

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Scoring tools like this have limited use in the prehospital setting, where you’re normally not

being so formal about your assessment and are usually treating the patient based on their

signs and symptoms. With that in mind, draw your attention speci cally to this box on the chart

from the previous page:

Score Severity Description Management

Frequent barky cough

Single dose PO dexamethasone
Stridor at rest
3-7 Moderate Nebulized epinephrine
Mild to moderate retractions
Hospitalization not generally required
No or little distress or agitation

We can simply match this description with the management and understand that if the patient

is at least this bad or worse, they’re indicated for nebulized epinephrine. It’s interesting to note

that even though the patient may have only mild retractions and no distress, as long as they

have a frequent ‘barky cough’ and stridor at rest, nebulized epinephrine is indeed indicated,

and treatment should not be delayed.

Racemic Nebulized Epinephrine

A croup patient may receive either epinephrine from a standard glass ampule (page 46) or

racemic epinephrine from the same type of plastic vial albuterol and ipratropium come in.

Regardless of which type is used, you’ll need to add 3.0 mL of saline to the nebulizer after you

place whichever type of epinephrine you use into it (to dilute the medication for prolonged

nebulization).

Racemic epinephrine is a mixture of two mirror-image forms of epinephrine, L-epinephrine, and

D-epinephrine (L-epinephrine is the ‘regular' form). Both are e ective in treating croup, so don’t

feel left out if you use the same kind as you would for asthma or anaphylaxis (18).

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 Anaphylaxis

Anaphylaxis causes airway swelling in both the upper and lower airways, but the problems

don’t stop there. Anaphylaxis is a distributive form of shock, meaning it causes systemic

vasodilation (and therefore results in hypotension). When giving a patient with anaphylaxis

epinephrine, we’ll be giving it via the intramuscular route as we would for asthma. This is

because we don’t only want epinephrine’s action to be exerted on the airway. We want

epinephrine to act on the entire body (especially the vascular system). In anaphylaxis, we’re

utilizing all of the actions of epinephrine to bene t the patient (19).

The Alpha-1 properties of the epinephrine are what causes the squeeze on the vasculature that

will raise the blood pressure, as well as decrease the upper airway swelling. Beta-1 properties

will increase cardiac output. Beta-2 properties will reduce bronchoconstriction. Epinephrine

also has properties that stabilize mast cells and histamine to help control the release of

mediators contributing to the anaphylaxis response. This is why epinephrine is the cornerstone

treatment of anaphylaxis - all of its properties contribute to xing the numerous issues

occurring.

Hives, Itching, pallor.

Wheezing, Stridor, obstruction.

Hypotension, tachycardia.

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You’ll likely encounter anaphylaxis during its initial symptom onset, shortly after the patient has

exposure to whichever agent caused their symptoms. Medication causes of anaphylaxis may

appear within ~5 minutes of exposure, venom may take ~15 minutes, and food may take up to

~30 minutes to cause symptoms. However, it may not be over after the initial episode. There

can be a biphasic nature to anaphylaxis as well (some reports claim this happens in 5-25% of

cases).

Schematic representation of a biphasic anaphylactic reaction. The second-phase reaction has

been described as occurring between 1 and 8 hours after the initial reaction, but new evidence
suggests that this second phase may occur up to 38 hours (mean 10 hours) after the initial
reaction. About one-third of the second-phase reactions are more severe, one-third are as severe
and one-third are less severe (20) Anne K. Ellis and James H. Day CMAJ 169 (4) 307-312).

42
 Intramuscular Epinephrine

Intramuscular administration of epinephrine might mean drawing the medication up from an

ampule or using an auto-injector. Let’s discuss a little bit about IM injections before we jump to

those speci c types.

Muscles have more vasculature (better blood supply) than the subcutaneous layer used for SQ

injections. This means the medication we inject into muscles will get into the bloodstream

faster and be delivered to its target in the body more rapidly. Some clinicians consider an IM

injection similar to a slow intravenous push (for practical purposes - there are key di erences).

Z-Tracking
Pulling traction on the skin during injection

90º to the surface of the skin

Through the SQ layer

Into the muscle

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 We must pick the right muscle when we want the body to absorb an IM medication quickly.

What should be on our wish list?

• Safe (not close to anything that would pop if punctured with a needle).
• Large (the larger the muscle, the more volume it can take)
• Easy to nd (obvious landmarks)
• Lots of blood supply (faster absorption)

Typically, this means the Vastus Lateralis (the lateral thigh). It’s safe, large, easy to nd, and has

lots of blood supply. There are, of course, considerations with each site that is chosen.

Below is a chart of the needle sizes and max volumes (for any medication given) for di erent

anatomical locations, as well as what length of needle you’ll need for di erent age groups:

Valeriote, T. (2016). The right route: The site of injection matters: Emergency physicians monthly. Emergency Physicians Monthly | Independent news and analysis in emergency medicine. Retrieved from https://epmonthly.com/article/the-right-route/

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 Epinephrine Auto-Injectors

The rst thing to know about auto-injectors is that they’re not meant to be held with your

thumb over the end…

Image from Koh et al, 2019

This is because, in a stressful situation, you might not realize you’re holding it backward.

Rather than rewriting all of the instructions, just check out the actual EpiPen (Jr) instructions.

This is the same thing a patient prescribed would receive. The only thing you may want to

change is exposing and cleaning the site of injection (rather than giving it through clothing)

[EpiPen = 0.3mg, EpiPen Jr = 0.15mg]

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 Epinephrine in Glass Ampule

Glass ampules are much less convenient than vials. When using a vial, we simply have to

remove the top, clean it, and pierce the top with a needle. Glass ampules, on the other hand,

require breaking glass, lter needles, changing needles, and doing away with sharps. However,

there are bene ts to an ampule. Sterility, stability, and the ability to examine the medication are

all improved with ampules, even though they’re not as convenient. Either way, you’re likely

using a glass ampule when administering epinephrine (some patients use ampules as well).

The process to use ampules goes like this:

1. Tap the ampule until all of the liquid falls into the wide part.
2. Wrap a 2x2 around the top, and then another one around the bottom.
3. Slowly apply pressure away from you - keep your ngers clear of the break site.
4. Dispose of the top in sharps.
5. Draw up the medication with a lter needle or lter straw.
6. Discard the body of the ampule into sharps.
7. Swap the lter needle / straw for the needle you intend to use for injection.
8. Administer the medication.

These ampules are supplied in a 1mg/mL concentration. We used to call this 1:1,000

concentration, but this has led to some confusion with the 1:10,000 concentration. Now, we

refer to it in the normal terms of how many milligrams are contained in each milliliter (mg/mL).

Since this medication is 1mg in 1mL, this means that whatever amount of mL you draw up,

you’re getting the same amount of mg. For example, drawing up 0.3mL is also 0.3mg.

mg mg mg mg mg mg mg mg mg mg

mL mL mL mL mL mL mL mL mL mL

0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0

Typical Pediatric and Adult Epinephrine Dose

Always calculate exact dose according to your protocol) 46
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 Epinephrine Pro le

Description: Epinephrine belongs to the class of drugs known as sympathomimetic amines. It

is a hormone and neurotransmitter naturally produced and synthesized for medical use.

Mechanism of Action: Epinephrine acts on adrenergic receptors in the body, speci cally alpha

and beta receptors (Alpha-1, Beta-1, Beta-2). It stimulates these receptors, which causes

vasoconstriction, bronchodilation, and positive inotropy (meaning it constricts blood vessels,

relaxes the smooth muscles in the airways, and increases cardiac contractility).

Indications: Anaphylactic shock, asthma, croup. IV epinephrine (not covered here) is used for

a variety of indications, such as bradycardia, shock, and cardiac arrest.

Contraindications: None in life-threatening emergencies.

Dosage: Adult IM for Anaphylaxis and Asthma: 0.3 - 0.5mg.

Pediatric IM for Anaphylaxis and Asthma:
• 7.5 to <15 kg: 0.1 m
• 15 to <30 kg: 0.15 mg
• ≥30 kg: 0.3 mg

Route: Intramuscular, intravenous, subcutaneous, and nebulization.

Onset: Intramuscular: ~3-5 minutes.

Peak: <10 minutes

Duration: Variable. Repeat doses are usually spaced 15 minutes apart.

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Epinephrine Tips and Tricks:

48
 Aspirin
You’re dispatched for a patient experiencing crushing chest pain. It’s a 75-year-old male with a

history of congestive heart failure and has had stent placement in the past. Upon arrival at the

patient, he’s pale and diaphoretic - your impression of the patient is that he is experiencing

acute coronary syndrome. To save the patient’s life, you reach into the medication bag and pull

out… the same medication the patient has in their medicine cabinet. 😅

Admittedly, aspirin is not the most exciting medication that we carry, but it’s incredibly

important. Aspirin has been proven to have bene ts in acute coronary syndrome, but it takes

time to work (21, 22). This means it’s important to get this medication administered to the patient

as soon as appropriate (‘time is [heart] muscle’). So, how does aspirin work to bene t a patient

with myocardial ischemia or infarction?

Aspirin is an anti-platelet medication that di ers from a blood thinner (even though it’s

commonly referred to as a ‘blood thinner’ by laypeople).

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Aspirin inhibits a process called primary hemostasis, which happens before the clotting

cascade. That’s the main di erence - aspirin inhibits the formation of the primary hemostatic

plug, while blood thinners inhibit the clotting cascade that follows (23). Don’t worry, we won’t be

hitting the clotting cascade here. But let’s talk about the formation of the primary hemostatic

plug for a moment so we can understand the mechanism of aspirin.

This process starts with some type of injury (from inside or out). Then, collagen is exposed,

which activated VFW (von-Willebrand factor). A glycoprotein attaches to VFW, which is

glycoprotein Ib (GpIb). A very interesting lipid called Thromboxane A2 attracts other platelets to

the platelets that are already attached to VWF. Once the platelets get close to each other,

another glycoprotein called glycoprotein IIb, IIIa combined with some brinogen locks those

platelets together so that they can start to form a clot (the primary hemostatic plug).

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Aspirin inhibits a precursor of TXA2 called Cyclooxygenase 1 (COX-1), which inhibits the

formation of TXA2, and therefore stops platelets from being attracted to one another. This is

why people will say that aspirin makes platelets ‘slippery’ - because it allows them to oat by

one another without being attracted (and therefore attaching) to each other.

Contraindications to aspirin therapy include documented aspirin allergy (if it causes the patient

to experience asthma or anaphylaxis), active bleeding, or a known platelet disorder. Active

bleeding or a known platelet disorder are obvious contraindications since inhibiting the

formation of the primary hemostatic plug would worsen these conditions (the bene ts would

not outweigh the risk). Allergy is also an obvious contraindication that doesn’t need any

explanation. However, asthma is added to this list as well. Why?

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COX-1 and TXA2 are part of a forked pathway in the body. When the body forms arachidonic

acid, it can either form COX-1 or LOX (lipoxygenase). If you administer aspirin, you’re limiting

the amount of arachidonic acid that will turn into COX-1, which means more of it will turn into

LOX. LOX creates leukotrienes, which cause bronchospasm. A patient will not be at much risk

for bronchospasm unless they have asthma (hence the contraindication) (24).

Acute Coronary Syndrome

In acute coronary syndrome (ASC), the patient may have a clot that is blocking one or more

coronary arteries (or a severe narrowing). If a clot is causing the problem, you don’t want that

clot to get even larger. This is why aspirin is so important - it can help prevent the problem from

becoming worse.

As a quick refresher, patients with ACS typically present with these signs/symptoms:

• Chest pain or discomfort.

• Shortness of breath (dyspnea).
• Palpitations.
• Nausea or vomiting.
• Diaphoresis.
• Light-headedness, dizziness, or fainting (syncope).
• Fatigue or weakness.

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 Aspirin PO Administration

Aspirin will either be supplied as enteric-coated or non-enteric-coated. “Enteric” refers to the

intestinal system - the enteric coating is an intestinal coating that protects the pill from

stomach acid. The purpose of this is to let the pill break down later on in the intestinal tract,

hopefully reducing the amount of stomach upset that patients typically experience when taking

aspirin. The downside of the enteric coating is that it takes longer for the aspirin to start

working (which is not ideal in the emergency setting). You can have a patient chew an enteric-

coated aspirin (325mg), but it’s not ideal. Rather, non-enteric coated 81mg chewable tablets

are used (usually 4 to total a dose of 324mg).

Enteric Coated Non-Enteric Coated

(Chewable)

The process is rather simple for administering PO (per oral) aspirin:

• Ensure the patient is conscious and oriented enough not to choke on or aspirate the

medication.

• Give them instructions for chewing the medication and ensuring they swallow all of it.

• It’s up to you whether you choose to hand the patient the pills or place them in their mouth

directly. Keep in mind that patients often drop pills or miss their own mouths.

• *Watch patient chew and swallow*

• If appropriate, the patient can have just enough water to help ensure all the aspirin enters

their stomach.

• Check mouth.

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 Aspirin Pro le

Description: Aspirin, also known as acetylsalicylic acid, is a salicylate drug commonly used as

an analgesic, antipyretic, anti-in ammatory, and anti-platelet agent.

Mechanism of Action: Aspirin exerts its anti-platelet e ect through irreversible inhibition of

cyclooxygenase-1 (COX-1) enzymes in platelets. This prevents the synthesis of thromboxane

A2, a potent vasoconstrictor and promoter of platelet aggregation, thereby inhibiting platelet

function.

Indications: Aspirin is indicated in a variety of conditions. In an emergency setting, it is

particularly crucial for the management of acute coronary syndromes (ACS), including unstable

angina and myocardial infarction.

Contraindications: Contraindications include hypersensitivity or allergy to aspirin or other

salicylates, active gastrointestinal bleeding, other bleeding disorders (e.g., hemophilia), and the

third trimester of pregnancy. Additionally, it should be used with caution in patients with a

history of gastrointestinal ulcers or other bleeding risks, renal or hepatic impairment, asthma,

and in those on concurrent anticoagulant therapy.

Dosage: In the setting of ACS, a loading dose of 162-324 mg of non-enteric-coated chewable

aspirin is recommended (325 mg if they chew an enteric-coated aspirin).

Route: PO

Onset: The anti-platelet e ect occurs within 30 minutes to an hour.

Peak: The peak plasma concentrations occur 1 to 2 hours following oral administration of non-

enteric coated chewable or soluble aspirin.

Duration: The anti-platelet e ect lasts for the lifespan of the platelet (7-10 days) due to the

irreversible binding of aspirin to the cyclooxygenase enzyme.

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Aspirin Tips and Tricks:

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 Nitroglycerin
Nitroglycerin causes vasodilation, which is why it lowers blood pressure (25). When we make the

container (the vascular system) larger, the pressure decreases because we have the same

amount of blood in a bigger container. This is the same concept we see in distributive/

vasodilatory forms of shock like sepsis, anaphylaxis, and neurogenic shock - they all lower the

blood pressure by making the container much too large. With administration of nitroglycerin,

we’re purposefully lowering the blood pressure. Why?

There are a few theories as to why nitroglycerin may help perfuse the heart, but the main

mechanism of action might not be what you’ve been taught. The traditional explanation of why

nitroglycerin is administered is to dilate the coronary arteries. However, this is debated not only

in the mechanism of action but also whether or not this would even be bene cial. Dilating the

coronary arteries would lower their ability to push perfusion through them since dilating vessels

lowers their pressure. Some may say that the dilation would allow a clot to ow further down

the artery, thus allowing it to travel into smaller arteries and occlude a smaller portion of the

heart’s perfusion. This may be true, but there isn’t much evidence to support it. So, if dilating

coronary arteries is questionable, what is the actual mechanism of nitroglycerin in acute

coronary syndrome?

A view looking up from the base of the heart, showing a closed aortic valve and the coronary arteries.
Notice how the coronary arteries originate at the base of the aorta.
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 Perfusion through the coronary arteries is all about the pressure di erence between the

diastolic blood pressure and the pressure left inside of the left ventricle during diastole. The

heart is mainly perfused during diastole when blood comes back towards a closed aortic valve,

which diverts blood into the right and left coronary ostium (the holes in the aortic root that feed

into the coronary arteries). To visualize that, here is a view of the aortic valve as if you’re trying

to look back into the left ventricle.

Systole Diastole
Blood leaves the LV through the Diastolic blood pressure cannot
aortic valve into systemic return to the LV, so it is diverted into
circulation. the coronary arteries.

Since the ow of blood into the coronary arteries is mainly happening during diastole, this is

the reason why we’ll also look at the left ventricle during diastole - we need to look at opposing

pressures during the same time period to gain an understanding of why we might want to lower

this patients blood pressure while treating acute coronary syndrome.

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Now that we understand that the diastolic blood pressure is entering the coronary arteries, we

can add another value - the LVEDP (left ventricular end-diastolic pressure), which is the

pressure inside of the left ventricle at the end of diastole.

The DBP and the LVEDP essentially ghting over what’s in between them, which is the

ventricular wall. Whatever pressure is left over between these two is called our coronary

perfusion pressure (CoPP) (25). Here is the formula for CoPP:

Diastolic blood pressure - Left Ventricular End Diastolic Pressure = Coronary Perfusion Pressure

When we administer nitroglycerin, we’re hoping to lower the LVEDP more than the DBP,

resulting in higher coronary perfusion pressure. Nitroglycerin has stronger vasodilatory actions

on the veins than arteries, so vasodilation in the veins reduces the blood coming back to the

heart (the LVEDP) while not having as much impact on the arterial constriction of the arterial

system (DBP). Here’s an example that might drive this point home:

Before Nitro: 70 (DBP) - 20 (LVEDP) = 50 (CoPP)

After Nitro: 65 (DBP) - 5 (LVEDP) = 60 (CoPP)

The DBP was reduced by 5 mmHg, but the LVEDP was reduced by 15, resulting in a higher

CoPP.

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To illustrate this, imagine holding a heavy sphere in your palm. Initially, your hand can handle

the weight. However, leaving the weight there for long enough would form a pressure ulcer, and

the tissue under the sphere would become necrotic. How would you solve this problem?

Would dilating the veins and arteries in your hand be the correct intervention? Not likely - that

would only lower the pressure attempting to perfuse that tissue. Instead, you would remove the

sphere so that perfusion could return to the tissue. This is the same principle that nitroglycerin

acts under to improve perfusion to the ventricular wall.

How does nitroglycerine actually accomplish this vasodilation? Nitroglycerin is a nitrate

medication that is primarily metabolized in smooth muscle cells and uses an enzyme called

mitochondrial aldehyde dehydrogenase (ALDH2). The metabolism process results in the

production of nitric oxide (NO), which is a substance that causes dilation of blood vessels

(mostly on the venous side at usual doses). Basically, nitroglycerin is a nitric oxide donor that

relaxes blood vessels and therefore reduces blood pressure.

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 Does it Work?

Nitroglycerin does work in the mechanisms that we discussed in the previous section.

However, a better question to ask would be: Does it make a di erence? Whenever we’re

administering a medication, we want to know if the result of giving that medication actually

bene ts the patient in the end. With all of the other medications in this guide, the bene t is

clear and appreciable. However, nitroglycerin is not as straightforward. Some services have

even removed nitroglycerin from their STEMI guidelines because medical directors have not

been convinced by current evidence that the bene ts outweigh the risks. Nitro can cause

hypotension. Hypotension results in hypoperfusion, and any episode of hypoperfusion

(especially to the heart) will worsen outcomes. This is for each medical director to decide on -

always follow your local guidelines.

It’s too much to cover here, but if you’re interested in the e cacy of nitroglycerin, check out

this page, as well as the blogs and video podcasts and the references that go along with it.

https://www.foamfrat.com/post/we-removed-nitro-from-our-stemi-guideline-w-matt-schneider
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 Sublingual Nitroglycerin Administration

Sublingual nitroglycerin administration is pretty simple - just spray it under the patient’s tongue

(or place a tablet). Technically, you can give nitroglycerin through the buccal route as well (in

between the cheek and gum). However, sublingual administration is still preferred since it

provides a more rapid and reliable absorption.

Typically, sublingual administration is used for a medication we want to absorb and start

working right away, while the buccal route of administration is usually used for a more

sustained release. However, they both bypass the liver's rst-pass metabolism since the veins

surrounding the mouth (under the tongue and in the cheek/gum) empty straight into the

superior vena cava.

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 As we discussed with aspirin, the patient requires a certain level of consciousness to receive

nitro tablets, even if they’re not trying to swallow them (they should ideally dissolve under the

tongue). Spray shouldn’t cause any issues, but it’s hard to imagine a scenario in which you

would be spraying nitroglycerin into a patient’s mouth that has a very low level of

consciousness. To be safe, reserve anything being administered PO, SL, or BU to a patient

with an appropriate level of consciousness that can follow commands.

Phosphodiesterase-5 Inhibitors

Phosphodiesterase-5 Inhibitors are used for erectile dysfunction and sometimes for pulmonary

hypertension and are taken by millions of Americans. Phosphodiesterase-5 Inhibitors

medications include:

• Sildena l (Viagra)

• Tadala l (Cialis)

• Vardena l (Levitra)

These drugs work by blocking the enzyme phosphodiesterase type 5, which increases the

cyclic guanosine monophosphate (cGMP) level in the smooth muscle cells (26). Elevated cGMP

levels cause relaxation and dilation of blood vessels. When nitroglycerin is used, it increases

the level of nitric oxide (NO) in the body, increasing cGMP levels (as NO stimulates the enzyme

that produces cGMP). This also results in vasodilation.

If a patient takes both a PDE5 inhibitor and nitroglycerin, the combined e ect can cause a

signi cant and potentially dangerous increase in vasodilation. This can result in a severe drop

in blood pressure, leading to symptoms like dizziness, fainting, or even more serious

cardiovascular events.

This is the reason why nitrates like nitroglycerin are contraindicated in patients who are taking

PDE5 inhibitors. Usually, there should be a gap of at least 24-48 hours (depending on the

speci c PDE5 inhibitor) between the use of a PDE5 inhibitor and nitroglycerin to avoid

potentially disastrous hypotension.

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 Nitro, the ECG, and IV

There is some thought that a patient needs an ECG and an IV prior to the administration of

nitroglycerin. This is understandable since clinicians have long been taught that if the patient

has a myocardial infarction involving the right ventricle (the inferior portion of the heart),

nitroglycerin could cause severe hypotension. Given this warning, it’s often been said that

nitroglycerin should be withheld until an IV is placed because the risk of hypotension involved

with RV infarction is so real (because the patient would need IV uids to correct the

hypotension). Is there any truth to this?

One thorn in the side of this line of thinking is self-administered nitroglycerin. Patients with

recurrent chest pain are often prescribed nitroglycerin and self-administer it frequently when

they have episodes of angina pectoris. No one expects the patient to run their own ECG and

place their own IV prior to administration. It’s also worth noting that the dose the patient self-

administers is the same dose we would administer (0.4mg). Is there any truth to the claim that

inferior myocardial infarction is more strongly associated with hypotension (27)?

What’s the take-home point? Hypotension associated with nitroglycerin is a real concern.

However, myocardial infarction location does not exacerbate hypotension - all patients are at

equal risk. Should the patient always have an IV prior to administration? That’s another

decision for your medical director. Either way, beware of board-line low blood pressures.

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 Nitroglycerin Pro le

Description: Nitroglycerin, also known as glyceryl trinitrate (GTN), is an organic nitrate

compound with the chemical formula C3H5N3O9. It is a potent vasodilator primarily used for

the prophylaxis and treatment of angina pectoris and acute coronary syndrome.

Mechanism of Action: Nitroglycerin is metabolized by mitochondrial aldehyde dehydrogenase

(ALDH2) to produce nitric oxide (NO) in smooth muscle cells. The resulting NO activates

guanylate cyclase, leading to increased production of cyclic guanosine monophosphate

(cGMP). The elevated cGMP activates a protein kinase that phosphorylates certain proteins,

ultimately causing relaxation of the smooth muscle and vasodilation. This mechanism of action

primarily reduces myocardial oxygen demand by decreasing preload (via venodilation) but can

also modestly reduce afterload and improve coronary blood ow.

Indications: Angina pectoris / Acute coronary syndrome, congestive heart failure exacerbation.

Contraindications: Nitroglycerin is contraindicated in patients with severe anemia, closed-

angle glaucoma, hypotension, or with hypersensitivity to nitroglycerin. It is also contraindicated

in patients who have taken phosphodiesterase-5 inhibitors within the last 24-48 hours due to

the risk of severe hypotension. It should be used with caution in patients with severe aortic

stenosis or hypertrophic cardiomyopathy.

Dosage: 0.4 mg sublingually spray or tablet, usually repeated every 5 min for up to 3 doses.

Route: Sublingual, buccal, transdermal, and intravenous.

Onset: The onset of action for nitroglycerin is rapid. Sublingual or spray formulations have an

onset of action within 1-3 minutes.

Peak: For sublingual spray/tab formulations, the peak e ect typically occurs within 5-10 min.

Duration: Typically 30-60 minutes.

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Nitroglycerin Tips and Tricks:

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 Naloxone
Are opioids poison? The answer to that question certainly depends on the context. Heroin

laced with fentanyl will almost certainly result in a ‘poisoning.’ However, pain relief after a

traumatic injury would be therapeutic and much appreciated by the patient. This calls to mind

the old saying:

“The di erence between a medicine and a poison is the dose.”

Opioid deaths have reached epidemic proportions, and death rates keep climbing yearly.

(28) https://nida.nih.gov/research-topics/trends-statistics/overdose-death-rates

In the media, a lot of attention has been placed on making naloxone available for everyone,

from laypersons to law enforcement. This is expected. When someone has received a (near)

lethal dose of an opioid, naloxone (usually) provides an almost magical return of consciousness

by displacing opioid agonists from their receptor sites.

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Opioids work by binding to speci c proteins called opioid receptors, which are found in the

brain, spinal cord, and gastrointestinal tract. When these drugs bind to the opioid receptors in

the brain and spinal cord, they can e ectively block the transmission of pain signals to the

brain (29). There are three main types of opioid receptors:

• Mu (µ)

• Delta (δ)

• Kappa (κ)

When discussing drugs like heroin and fentanyl, the Mu receptors are the most relevant. When

opioids bind to these receptors, they reduce neuronal excitability, which means they slow down

or inhibit the function of the nervous system.

In the context of an overdose, high levels of opioids can ood the system and excessively

activate these receptors. The over-activation of the Mu receptors suppresses the body's

respiratory center in the medulla oblongata in the brainstem, causing respiratory depression.

This can lead to decreased oxygen levels in the blood (hypoxia), a ecting the functioning of

vital organs, including the brain. Essentially, death is caused by:

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 Ideally, naloxone helps to reverse these signs and symptoms by displacing opioids from the

Mu receptors, which should restore normal neuronal function (neurological functions get back

up to speed). This is why naloxone is known as an opioid antagonist. This means that it has a

high a nity for opioid receptors but does not activate them. Instead, it competes with opioids

for these receptor sites and can displace opioids from these receptors because of its higher

a nity (30).

Activated Mu Receptor Inactivated Mu Receptor

with opioid stimulation with Naloxone in place

Naloxone works to reverse these symptoms by binding to these same mu receptors, displacing

the opioids from the receptors due to their higher a nity, and thereby inhibiting the opioids

from continuing to exert their e ects. Unlike opioids, naloxone doesn't activate the receptors to

a signi cant degree, meaning it won't produce the analgesic or euphoric e ects of opioids.

A very important point to note is that naloxone's e ect is temporary, typically only lasting

between 30 minutes to an hour, and it might need to be administered multiple times in the case

of potent synthetic opioids like fentanyl. This is because naloxone is metabolized and excreted

from the body faster than most opioids, so once the naloxone has been eliminated, if there are

still opioids present in the body, they can reattach to the receptors and cause symptoms to

return. This is especially important to note if your patient wishes to refuse transport after

naloxone is administered (a common problem).

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 Scene Safety

Scene safety should come to mind when administering naloxone. A patient who is a regular

opioid user may immediately go into withdrawal symptoms upon waking from their coma.

Usually, we think about withdrawal in terms of vital signs, such as the patient experiencing

tachycardia, hypertension, diaphoresis, tachypnea, nausea/vomiting, and even seizures (as well

as the pain associated with general withdrawal). This can lead to the patient being generally

overstimulated since the patient is used to having some level of depressant in their system to

keep them at what they would consider a ‘normal' baseline.

This state of overstimulation post naloxone administration can lead to the patient becoming

combative and violent. The saying ‘hope for the best, plan for the worst’ should come to mind

when administering this medication. Will every patient become combative and cause a scene

safety issue? No - the patient may wake up peacefully. However, clinicians should have a

guideline in place in case the patient does wake up and start swinging (or worse: (31) https://

www.cdc.gov/niosh/ re/pdfs/face201913.pdf).

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 Multiple Agents

The full case report from the previous page noted that the patient had multiple types of drugs

in their system, including methamphetamine. In other words, the patient was on 'uppers and

downers.’ A patient presenting with coma may (not always) have a downer outweighing their

upper.

In cases of mixed drug use, the patient is likely aiming for a balance:

Too much of a downer will disturb this balance and cause coma:

Once we treat the overdose of downers, the uppers are unmasked:

There is usually no way to know for sure if a stimulant like methamphetamine is hiding behind

an opioid overdose. Again, this is why it’s important to have a plan in place for handling cases

in which the patient becomes combative.

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 Diagnostic momentum

Whenever we respond to a patient su ering from a coma of unknown origin, we tend to

suspect opioid overdose above all other pathologies. Given the statistics we saw about opioid

overdose at the outset of this chapter, suspecting an opioid as the cause of coma certainly

isn’t unreasonable. A clinician might be more suspicious of an opioid overdose if the patient is

young, has no other known medical history that would cause coma, etc. This is where a

concept called ‘diagnostic momentum’ comes into play.

Diagnostic momentum refers to a situation in which a clinician gets tunnel vision and doesn’t

consider other causes for a speci c sign/symptom set (in this case, other causes of coma).

This becomes a very important point to consider when relying on one treatment (naloxone) to

x the problem of coma. Why?

Consider the example of a young patient with a history of drug use and no other medical

history. Today, the patient took a small dose of recreational opioids (not enough to cause a

coma), which caused them to be less coordinated. The patient trips, falls, and hits their head

on the concrete, causing a brain bleed. EMS arrives on the scene, suspects an overdose, and

starts giving naloxone immediately. The SPO2 continues to drop, and the patient is breathing

slowly with low tidal volume and is not protecting their airway. The clinicians sit and wait for

naloxone to work. Then they give more naloxone. Then more… until the patient su ers cardiac

arrest. What went wrong? Diagnostic momentum put the clinicians into a sunken-cost fallacy.

Sunken-cost fallacy:
• the phenomenon whereby a person is reluctant to abandon a strategy or
course of action because they have invested heavily in it, even when it is
clear that abandonment would be more bene cial."the sunk-cost fallacy
creeps into a lot of major decisions"

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Instead of getting caught in a sunken-cost fallacy and betting the patient’s life on an opioid

overdose, we want to consider all possibilities.

There are more causes of coma than we could possibly cover here, and naloxone only works

for one of them - opioid overdose. This brings to mind the question we opened this chapter

with: “Are opioids poison?”

An overdose of opioids essentially puts the patient into a state of general anesthesia. In fact,

high doses of sedatives and opioids are used by anesthesiologists to facilitate surgery. Since

these patients receive this coma-inducing amount of opioids, why don’t they go into cardiac

arrest?

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 These patients survive because the patient is oxygenated and ventilated during their opioid-

induced coma (32). This xes all of the problems that could cause your comatose patient to go

into cardiac arrest.

Protecting the airway and providing oxygenation and ventilation will accomplish the same

goals that the anesthesiologist provides to prevent their patients from arresting. These patients

do not arrest because opioids are some type of poison - they arrest because of hypoxia. If we

x the hypoxia (regardless of the cause of the coma), we can protect the patient. This does not

always need to be an advanced airway, such as a supra-glottic airway or endotracheal tube,

but be aware of gastric in ation and vomiting if you’re using a bag-valve mask on an

unprotected airway (be prepared to clear the airway)

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When we rely solely on naloxone, we’re putting all of our eggs in one basket - an opioid

overdose. These patients are in need of the same basic steps that any patient with a low level

of conscious needs: Strong BLS.

It may seem as though we’re beating this point to death, but the importance of addressing

airway, breathing, and circulation before assuming a diagnosis cannot be overstated.

This can all probably be summed up with a meme - avoid becoming this provider:

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 Intranasal Naloxone Administration

Naloxone is most commonly given via the intranasal route, but it can be given IM, IV, or IO as

well. We covered the IM route in the epinephrine section, so we’ll focus on intranasal here.

When administering medication via the IN route, here are a few pointers:

• Determine the desired dose (usually double IV dose because you lose some down the

throat), and leave 0.1mL of air in the end of the syringe.

• Attach the MAD (mucosal atomization device) to the syringe, and place the MAD snugly at

the opening of the nostril.

• Point the syringe towards the top of the ear and push rapidly.

• Repeat as needed - space doses 5 minutes apart per nostril.

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 Choosing a Dose

The goal with naloxone is to return the patient to a calm state in which their respiratory drive is

adequate without sending them into acute withdrawals. Since acute withdrawal symptoms,

agitation, and combativeness are real concerns when administering naloxone, choosing a dose

can be a little tricky. Actually, it can be nearly impossible to pick exactly the right dose. Think of

all the unknowns that go into naloxone administration:

• Does the patient have any other drugs in their system (uppers or more downers)?

• What type of opioid did the patient ingest?

• What dose of that opioid did the patient ingest?

• How much tolerance does the patient have to opioids?

• How do they individually respond to naloxone?

Considering all of that, how much naloxone will you give to the 25-year-old male patient who is

currently unresponsive? How do you get them to that perfect point where they have adequate

respiratory drive but no agitation? One thing that can help is the Richmond Agitation Sedation

Scale.

Goal

l
Usua
ta r t ing
S
Point

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 As long as you’re supporting the patient’s airway, breathing, and circulation, you have some

time to gure out how to attempt to reverse their overdose properly.

To illustrate this, don’t worry about keeping your golf score low. Instead of trying to take a long

putt in one swing, just tap the ball until you get to the hole. Giving a large dose and

overshooting a little bit (or a lot) could end up causing a whole di erent problem.

Before we close this chapter and look at our medication pro le and tips and tricks, we should

add one more important point of the waking-up phase of naloxone. There is a phenomenon

called negative pressure pulmonary edema that is caused by the patient taking in a large

breath before their airway is open. The vacuum that is created in their lungs can draw in uid

from their lungs and cause pulmonary edema, which will cause yet another respiratory issue.

Another theory about this pulmonary edema is catecholamine surge post naloxone

administration. Again, the airway, breathing, and circulation always come rst (33, 34).

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 Naloxone Pro le

Description: Naloxone Hydrochloride is a pure opioid antagonist that competes with opioids

for binding at opioid receptors.

Mechanism of Action: Naloxone acts as a competitive antagonist at Mu opioid receptors. It

has a higher a nity for these receptors than many opioids, allowing it to displace opioids from

these receptors and reverse their e ects, including respiratory depression caused by opioid

overdose.

Indications: Complete or partial reversal of opioid drug e ects, including respiratory

depression resulting from natural and synthetic opioids or opioid analogs. It is also indicated in

the diagnosis of suspected acute opioid overdose.

Contraindications: Naloxone is contraindicated in patients known to have hypersensitivity to

naloxone or any of the other ingredients in the formulations.

Dosage: Typically 0.4 to 2 mg. May be repeated at 2-3 minute intervals.

Route: IV, IM, and IN routes.

Onset: For IV administration, onset is typically within 1-2 minutes. For IM administration, onset

is usually within 2-5 minutes. Intranasal administration may have a slightly slower onset.

Peak: Usually observed within 20-60 minutes after administration, depending on the route of

administration and individual patient characteristics.

Duration: The duration of action of naloxone is typically 30-120 minutes, though this may be

shorter or longer depending on the half-life of the opioid being counteracted, the dose of

naloxone given, and the individual patient's metabolism. This is important to note because

many opioids, particularly synthetic opioids, have a longer duration of action than naloxone,

and symptoms of opioid overdose may return after the e ects of naloxone wear o .

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Naloxone Tips and Tricks:

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 Oral Glucose And Glucagon
Hypoglycemia is a true emergency. Glucose is needed for metabolism; without it, cardiac arrest

and active brain death will occur. This seems obvious, but it is debated. The thought that

hypoglycemia does not cause cardiac arrest is discussed in detail in our blog entitled

“Hypoglycemia in Cardiac Arrest,” which you can check out if you have any doubts

surrounding this topic (lots of references there). We’ll also bring out some salient points from

that blog in this chapter.

https://www.foamfrat.com/post/hypoglycemia-in-cardiac-arrest

Before we address the issue of hypoglycemia, let’s rst discuss what glucose is and why we

need adequate blood glucose levels.

“Glucose, also called dextrose, one of a group of carbohydrates known as simple sugars
(monosaccharides). Glucose (from Greek glykys; “sweet”) has the molecular formula C6H12O6. It
is found in fruits and honey and is the major free sugar circulating in the blood of higher animals.”

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Glucose is a simple sugar (monosaccharide) that serves as the primary source of energy for the

body and is the starting material for cellular respiration. Glucose is either used immediately for

energy, stored in the liver or muscles for later use, or converted into fat. Here are some

important points to understand about glucose:

Cellular Respiration: Within cells, glucose is broken down through a process called cellular

respiration. This involves three stages: glycolysis, the Krebs cycle, and the electron transport

chain. The end result of this process is the production of ATP (adenosine triphosphate), which

is the energy currency of cells.

Glycogenesis: When the body has an excess of glucose, it can store this for later use through

a process called glycogenesis (using insulin to store the glucose). During glycogenesis, glucose

molecules are combined to form glycogen, which is stored in the liver and muscle cells. When

the body needs energy and no glucose is available in the bloodstream, glycogen is converted

back into glucose by the hormone glucagon (which is why it’s administered - to turn stored

glycogen into glucose in the blood).

Lipogenesis: If the body has a substantial surplus of glucose, it may convert this glucose into

fat for long-term storage. This process is called lipogenesis. Of note, insulin is used in this

process of using and storing glucose. The pancreas releases insulin to use and store glucose

and uses glucagon to release those stores back into the blood.

Blood Glucose Regulation: The body also works hard to ensure blood glucose levels stay

within a narrow range, typically between 80-100 mg/dl. This is managed primarily by the

hormones insulin and glucagon. When blood glucose levels rise, the pancreas releases insulin,

which allows cells to take in glucose for energy use or storage. When blood glucose levels fall,

the pancreas releases glucagon, which signals the liver to release stored glucose back into the

bloodstream.

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If all of that seemed rather dense, you can take some comfort in the fact that energy

metabolism is not a simple subject, and everyone struggles to understand it. Your pancreas is

constantly balancing blood glucose through the use of insulin and glucagon, and when this

organ fails to do its job correctly (resulting in either hyperglycemia or hypoglycemia), correcting

the blood glucose level is not an easy task (35). Here is a graphic that might make this process a

little easier to understand. Start with the pile of fruit, follow the red, then the blue.

Beta cells in your pancreas sense the increased glucose levels in the blood and respond by

producing insulin. That insulin moves the glucose into cells, which includes storing it in the liver

(in the form of glycogen) and in fat cells. This causes the blood glucose to lower. As time goes

on and the body is in need of glucose, alpha cells in the pancreas sense this low level of sugar.

Alpha cells then respond by excreting glucagon, which breaks down glycogen (packed

together glucose molecules), which allows glucose to exit storage sites and enter the blood,

where it can be used by cells for energy.

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 In this guide, we’ll focus solely on hypoglycemia since managing hyperglycemia in the

emergency setting requires the administration of insulin, which could be an entire workbook on

its own. So, how do patients end up in a hypoglycemic state, and how is it corrected? There

are two main ways that a patient may develop hypoglycemia (36).

Mechanisms of Hypoglycemia

The rst mechanism by which a patient may develop hypoglycemia is that metabolism

outpaces glucose availability. This is more di cult than it seems unless the patient has some

type of metabolic disorder. For a healthy person, when glucose becomes low, glycogen will be

broken down in the liver, which will increase blood glucose. What if we exhaust those stores?

The body will begin breaking down fat stores into ketones to take the place of glucose in

cellular metabolism. Also, protein will be broken down into glucose in a process called

gluconeogenesis to maintain blood glucose levels. This is why people who start a ketogenic or

‘carnivore’ (only meat) diet do not typically experience episodes of hypoglycemia - dietary

protein is made into glucose, or their muscles will break down into glucose to maintain normal

levels. Fat and protein and necessary for life, but carbohydrates (sugar) can be substituted as

long as normal pancreatic function is present (in the absence of disease). However, in a patient

with metabolic disease, decreased blood glucose can occur due to decreased energy intake

(the L in SAMPLE). Basically, the patient needs to take in enough energy to match their energy

output.

80-100

Input must be proportional to output to maintain balance.

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The second way in which a patient may become hypoglycemic is too much storage of glucose,

leaving the bloodstream depleted. The most common mechanism for too much glucose

storage is when a patient takes too much insulin or metformin (especially if these medications

are taken at the wrong time - when the patient hasn’t eaten). It’s not uncommon for a patient to

get into the habit of taking their insulin or metformin (or both) at a certain time of day but forget

to maintain their diet surrounding that time period. In your career, you’ll encounter many

patients who inform you that they forgot to eat but remembered to take their diabetic

medication. To understand these episodes of hypoglycemia, you’ll want to be familiar with

insulin and anti-hyperglycemic agents like metformin (Glucophage) that the diabetic population

regularly take.

There are various types of insulin, classi ed according to their onset, peak time, and duration

of action. T1DM patients always need insulin, while T2DM might be prescribed insulin.

• Rapid-acting insulin begins to work shortly after injection and peaks after 1 hour, lasting
for 2 to 4 hours.
• Short-acting insulin takes about 30 minutes to start working and peaks at 2 to 3 hours,
with a duration of 3 to 6 hours.
• Intermediate-acting insulin has an onset of 2 to 4 hours, peaks at 4 to 12 hours, and lasts
for 12 to 18 hours.
• Long-acting insulin takes several hours to start working but has a minimal peak e ect and
can last over 24 hours.

Hours

Of note, there are other insulin-involved mechanisms of hypoglycemia, such as errors of metabolism and
insulin-secreting tumors, but we’ll stick to the more commonly occurring mechanisms here.

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 A patient may still take their insulin by using a vial and syringe, but this is becoming less

common. Insulin pens are a little easier to use and dose but are might expensive and might not

o er the dosing exibility that the regular syringe does.

There are now insulin pumps that pair with continuous glucose monitors (CGMs), which sample

the blood glucose and immediately communicate that data to the insulin pump. This takes

much of the guesswork out of insulin administration, and it’s getting pretty close to the level of

having pancreatic function back. These are very useful for T1DM patients. Here are a couple of

examples of CGMs that are paired with insulin pumps:

As you can see, there are a variety of ways a patient may take their insulin. While none of these

systems are completely error-free, the more automated systems can provide some bene ts.

The dose of insulin that the patient takes is usually dependent on their blood sugar, which is

called a “sliding scale” - here is an example of what the patient might follow if they inject dose-

by-dose:

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What about anti-hyperglycemic agents? The following list of medications is mainly taken by

T2DM patients (some T1DM patients may take them in special circumstances). The

medications are roughly listed from most commonly prescribed to least (37).

• Biguanides: Metformin is the most widely used medication in this class. It works by
decreasing glucose production by the liver and improving insulin sensitivity in peripheral
tissues.

• Sulfonylureas: Medications like glipizide, glyburide, and glimepiride stimulate the beta cells
of the pancreas to produce more insulin.

• Thiazolidinediones (TZDs): Medications like pioglitazone and rosiglitazone help make the
body's cells more sensitive to insulin, allowing more glucose to enter cells.

• DPP-4 inhibitors: Drugs such as sitagliptin, linagliptin, saxagliptin, and alogliptin work by
blocking the action of an enzyme called DPP-4, which leads to an increase in insulin
production and a decrease in glucose production.

• SGLT2 inhibitors: Medications like canagli ozin, dapagli ozin, and empagli ozin work by
blocking a protein called sodium-glucose co-transporter 2 (SGLT2), which causes the
kidneys to excrete more glucose in the urine.

• GLP-1 receptor agonists: Drugs like liraglutide, exenatide, and dulaglutide mimic the
action of a hormone called GLP-1, which stimulates insulin secretion, slows gastric
emptying, and reduces appetite.

• Alpha-glucosidase inhibitors: Acarbose and miglitol are medications that delay the
absorption of carbohydrates in the gut, leading to a slower and lower rise in blood glucose
throughout the day, particularly after meals.

Don’t worry, it’s not required to memorize all of these medications. As you look at more and

more lists of medications that patients take, you’ll become familiar over time with what these

medications are and what they do.

Now that we’re familiar with the common mechanisms in which a patient may develop

hypoglycemia let’s brie y delineate T1DM from T2DM before we jump into the speci cs of oral

glucose and glucagon.

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 T1DM vs. T2DM

Type 1 Diabetes Mellitus (T1DM) used to be referred to as juvenile-onset diabetes or insulin-

dependent diabetes. T1DM represents ~5-10% of diagnosed diabetes cases. The underlying

cause is the autoimmune destruction of the beta cells in the pancreas, which leads to absolute

insulin de ciency (they don’t make enough insulin to keep up with their metabolism). The lack

of insulin leads to increased blood and urine glucose. Type 1 diabetes commonly presents in

childhood or adolescence but can develop at any age. Patients with Type 1 diabetes require

lifelong insulin therapy and are at risk for other autoimmune disorders (38).

Here is a graph describing how T1DM will progress to diabetic ketoacidosis (DKA). Start at the

pile of fruit, and keep going.

This graphic explains why glucose stays in the bloodstream - there is no insulin to let the

glucose into cells. These patients also have di culty storing fat and maintaining any sort of

liver glycogen stores for the same reason - low insulin levels (you need insulin to be anabolic).

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Type 2 Diabetes Mellitus (T2DM), on the other hand, is characterized by insulin resistance, a

condition in which cells fail to respond to insulin e ciently, and a relative insulin de ciency.

Unlike T1DM, where the cause is the autoimmune destruction of beta cells, T2DM is a disease

of lifestyle (obesity, lack of exercise, diet, etc.) The insulin resistance in T2DM leads to an initial

overproduction of insulin by the pancreatic beta cells. Over time, this overproduction can lead

to the exhaustion of the beta cells, leading to a relative insulin de ciency. While patients with

T2DM may manage their disease through diet, exercise, and oral medication, some may

eventually accept insulin therapy as the disease progresses. Unlike T1DM, T2DM is often

associated with comorbidities like heart disease, stroke, and kidney disease (39).

One point about T1DM and T2DM that is often misunderstood is that they both initially present

with hyperglycemia, not hypoglycemia. Hypoglycemia comes later, once blood sugar is

regulated - usually iatrogenic (hypoglycemia caused by healthcare/medications).

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 Administering Oral Glucose Gel

Oral glucose gel contains 15 grams of simple carbohydrates. You can think of it as similar to

honey, jelly, fruit juice, or various types of candy of similar consistency. In fact, many patients

who su er from hypoglycemia will substitute oral glucose gel for these items. Oral glucose,

however, is ideal for raising blood sugar rapidly due to ease of digestion.

Check your own local guidelines about what is considered “hypoglycemia” for your service, but

a blood glucose level<60 mg/dl is typically indicated for treatment.

Here is a package of oral glucose gel and the directions for use on the back:

While an adult will typically receive the entire tube of glucose gel, pediatric dosing is usually 0.3

grams per kilogram (a 15kg pediatric would receive ~5 grams). Oral glucose gel usually works

within ~15 minutes or less.

As the name suggests, oral glucose gel is administered orally. As you can see from the

directions, the patient should swallow the medication. It can be administered via sublingual or

buccal routes, but the onset may not be as rapid. Oral glucose gel comes with the same

warning as aspirin - don’t give it to a patient who could choke on it. If the patient is too altered

to follow commands and protect their airway (swallow), they’ll need dextrose through their

bloodstream, not their GI tract.

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 Administering Glucagon

Glucagon is the counter-regulatory hormone to insulin. As we discussed earlier, glucagon goes

to glycogen stores in the liver and converts them to glucose (glycogenolysis) which is released

into the bloodstream to raise blood glucose. Since this hormone works when released from the

pancreas, glucagon should work when we add it to the system exogenously. However, the

patient needs glycogen stores. If the patient is fasting, is a chronic alcoholic, or has T1DM (low

insulin, thus low glycogen stores), glucagon results may vary.

Glucagon (1 mg) must be reconstituted since the medication comes in powder form.

Glucagon is typically administered intramuscularly, although it can also be given via the

subcutaneous, intravenous, and intranasal routes. One important point to consider surrounding

glucagon administration is that it doesn’t work immediately like giving someone intravenous

dextrose - it may take up to 15 minutes to raise the blood glucose to an appreciable degree

(assuming the patient has glycogen stores to break down).

Glucagon is typically reserved for patients who are not eligible for PO nutrition due to their level

of consciousness. Following oral glucose gel or glucagon administration, it is usually indicated

to give the patient complex carbohydrates and some protein, like a ham sandwich or

something with similar nutritional value. Food will maintain their BGL while these medications

wane over their short duration.

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 Oral Glucose Pro le

Description: Oral glucose gel is a concentrated, carbohydrate-based gel preparation that is

typically composed of dextrose, water, and sometimes added avorings. It is designed to

quickly absorb through the mucosa and rapidly increase blood glucose levels.

Mechanism of Action: Oral glucose gel acts by quickly delivering dextrose to the

bloodstream. Once in the bloodstream, dextrose is transported into cells with the aid of insulin,

where it is metabolized to produce energy.

Indications: Oral glucose gel is indicated for the treatment of hypoglycemia.

Contraindications: Patients with altered consciousness may also not be able to safely ingest

oral glucose gel due to the risk of aspiration.

Dosage: The typical dose for adults is 15-20 grams of glucose and 0.3 grams/kg for children.

Route: P.O., sublingual, buccal.

Onset: Within ~10-15 minutes.

Peak: Within ~30 minutes to 1 hour after administration.

Duration: The duration of action can vary depending on individual factors such as the patient's

insulin levels and metabolic rate, but the e ects of a single dose are typically noticeable for 1-2

hours. However, glucose levels should be re-checked after 15 minutes, and if they're still low,

another dose may be needed. Ongoing monitoring is critical until the patient is stabilized.

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 Glucagon Pro le

Description: Glucagon is a peptide hormone produced by the alpha cells of the pancreas. It is

a hyperglycemic agent commercially available in injectable forms, both as a powder for

reconstitution and a pre- lled auto-injector or nasal powder.

Mechanism of Action: Glucagon increases blood glucose levels by stimulating the hepatic

conversion of glycogen to glucose (glycogenolysis) and enhancing the synthesis of glucose

(gluconeogenesis). It also reduces glycogen synthesis and decreases glucose utilization in the

liver.

Indications: Glucagon is indicated for treating severe hypoglycemia in patients with diabetes

mellitus when diminished consciousness precludes oral carbohydrates. It's also used as a

diagnostic aid in radiologic examinations to inhibit gastrointestinal tract movement temporarily.

Contraindications: Pheochromocytoma or insulinoma due to the risk of a substantial increase

in blood pressure and hypoglycemia. In prolonged fasting, starvation, or chronic hypoglycemia,

glucagon response may be blunted or absent in such cases.

Dosage: For adults and pediatrics >20 kg or older than 6 years, the dose is typically 1 mg. For

pediatric patients weighing <20 kg or younger than 6 years, a typical dose is 0.5 mg.

Route: Intramuscular, subcutaneous, intranasal, or intravenous.

Onset: Typically between 10 to 20 minutes.

Peak: Within 30 minutes to an hour.

Duration: The hyperglycemic e ect of glucagon is typically noticeable for 60 to 90 minutes. It's

important to note that once blood glucose levels have been corrected, the administration of

carbohydrates is advised to replenish hepatic glycogen stores.

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Oral Glucose and Glucagon Tips and Tricks:

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 Conclusion
And that’s about it… only ~100 pages of information to consider before you administer the

medications within your scope of practice. 😅

But seriously, let’s pause for a second to acknowledge your critical role as an EMT. Your ability

to administer medications is more than a checkmark on your PCR - it’s a trust given to you by

your patients that your choice is the right choice during their emergency. With each drug and

dose, you walk a delicate line between bene t and risk. For that reason, constantly update your

knowledge, use your resources, and never stop learning.

Thank you for downloading and reading this guide! We hope this made you feel more con dent

and comfortable with the medications we discussed!

- The FOAMfrat Team

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 Flashcards
The following 9 pages are taken from the medication pro les at the end of each chapter but in

ashcard form. Feel free to print these pages out, fold them in half, and use them to test your

knowledge!

Anyone can use rote memorization to make it seem like they know a lot about a subject -

repeating facts is an unimpressive display of knowledge. However, if you really understand the

information from the medication pro le pages, testing your memory will help cement those

points into your brain. Don’t just memorize the answers; ask yourself why that answer is

correct.

When you’re rst learning medications within your scope of practice, it’s common to confuse

details like the dose of one medication versus another. You may think of epinephrine at

0.3-0.5mg for an adult, but recall the dose for glucagon at 1mg instead. This never really stops

happening. You’ll get better at it over time, and usually, looking at a medication vial will jog your

memory. However, never rely on your memory. Always use a reference to ensure your

practicing safe patient care. There is no taking a medication back once you’ve administered it.

Happy studying!

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 Oxygen
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Duration

Description: Oxygen is a colorless, odorless gas that is essential for human life. As a
medication, it is used to increase the concentration of oxygen in the patient's blood and
tissues, thereby enhancing cellular function and recovery.
Mechanism of Action: Oxygen therapy increases the amount of oxygen in the blood, thereby
improving the oxygen supply to the body's cells. This supports cellular metabolism,
particularly in situations where the body's oxygen demand is high or the supply is
compromised.
Indications: Oxygen is indicated in conditions causing hypoxia or hypoxemia, such as
chronic obstructive pulmonary disease (COPD), pneumonia, asthma, and trauma. It is also
used in acute settings such as cardiac arrest, shock, and severe bleeding.
Contraindications: While never contraindicated if the patient has hypoxia / hypoxemia, use
caution in patients with acute stroke or acute coronary syndrome. Follow AHA
recommendations or your local guidelines for SPO2 ranges (usually the minimal ow to
maintain saturations in a normal range).
Dosage: The dosage ( ow) of oxygen varies based on the patient's condition and oxygen
saturation levels. Flow rates will be based on the device used and your local guidelines.
Route: Blow-by, nasal cannula, oxygen masks, pressurized masks (CPAP and BiPAP),
Bag-valve mask, or through mechanical ventilation.
Duration: The duration of oxygen will be based on the patient’s condition. Things that will
cause rapid desaturation include: High metabolism / oxygen requirement, hyperthermia,
acidosis (high CO2), low SPO2 (the lower the SPO2 the faster the desaturation), high BMI,
and mismatches between ventilation and perfusion such as pulmonary edema or pulmonary
embolism

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 Albuterol
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Albuterol (also known as salbutamol) is a SABA (short acting beta agonist).
Albuterol is a bronchodilator medication that is commonly used to treat conditions that cause
bronchospasm. Asthma, chronic obstructive pulmonary disease (COPD), and anaphylaxis are
common reasons for a patient to receive albuterol.

Mechanism of Action: Albuterol works by stimulating beta-2 adrenergic receptors in the

lungs, which leads to relaxation of the smooth muscles in the airways. This causes the
airways to dilate, making it easier for air to ow in and out of the lungs, and reduce air
trapping.

Indications: Bronchospasm due asthma, COPD, or anaphylaxis. Hyperkalemia (albuterol

temporarily lowers serum potassium levels).

Contraindications: Known history of hypersensitivity. Known severe hypokalemia (low serum

potassium).

Dosage: Typically 2.5 - 5.0 mg as needed or tolerated. Doses starting at 1.25mg for small
pediatrics. Continuous nebulization may be indicated in severe bronchospasm.

Route: Nebulization / inhalation.

Onset: ~5 minutes.

Peak: ~30 minutes.

Duration: 3-6 hours.

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 Ipratropium
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Atrovent (also known as ipratropium bromide) is an anticholinergic

bronchodilator. It is primarily used for the treatment of respiratory conditions such as chronic
obstructive pulmonary disease (COPD) and asthma. Typically, EMS services and hospitals
carry “ipratropium bromide” and not brand name “Atrovent” - this is important for the
contraindications section below.
Mechanism of Action: Atrovent acts by blocking the action of acetylcholine, a
neurotransmitter involved in bronchoconstriction. By inhibiting the e ects of acetylcholine,
Atrovent helps to relax the airways, allowing for increased air ow through the lungs. It works
by selectively binding to the muscarinic receptors (M3) in the airway smooth muscles, leading
to prolonged bronchodilation (stopping bronchoconstriction).
Indications: Bronchospasm due asthma, COPD, or anaphylaxis.
Contraindications: Known hypersensitivity to ipratropium bromide. Allergy to peanuts (soy
lecithin) is a contraindication to brand names “Atrovent” and “Combivent” MDI products, not
the generic “ipratropium bromide” typically supplied for nebulizers in EMS. To con rm, check
the package insert that comes with your ipratropium bromide - it will speci cally note these
details if soy lecithin is present in the product.
Dosage: 0.5 mg, which most guidelines will state can be repeated up to 3 times at 20 minute
intervals / as needed. The dose may be decreased to 0.25 mg in the pediatric population.
Route: Nebulization / Inhalation.
Onset: ~15 minutes.
Peak: 1-2 hours.
Duration: 4-8 hours.
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 Epinephrine
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Epinephrine belongs to the class of drugs known as sympathomimetic amines.

It is a hormone and neurotransmitter that is naturally produced, and is synthesized for
medical use.
Mechanism of Action: Epinephrine acts on adrenergic receptors in the body, speci cally
alpha and beta receptors (Alpha-1, Beta-1, Beta-2). It stimulates these receptors, which
causes vasoconstriction, bronchodilation, and positive inotropy (meaning it constricts blood
vessels, relaxes the smooth muscles in the airways, and increases cardiac contractility).
Indications: Anaphylactic shock, asthma, croup. IV epinephrine (not covered here) is used for
a variety of indications such as bradycardia, shock, and cardiac arrest.
Contraindications: None in life-threatening emergencies.
Dosage: Adult IM for Anaphylaxis and Asthma: 0.3 - 0.5mg.
Pediatric IM for Anaphylaxis and Asthma:
• 7.5 to <15 kg: 0.1 m
• 15 to <30 kg: 0.15 mg
• ≥30 kg: 0.3 mg
Route: Intramuscular, intravenous, subcutaneous, and nebulization.
Onset: Intramuscular: ~3-5 minutes.
Peak: <10 minutes
Duration: Variable. Repeat doses are usually spaced 15 minutes apart.

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 Aspirin
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Aspirin, also known as acetylsalicylic acid, is a salicylate drug commonly used
as an analgesic, antipyretic, anti-in ammatory, and anti-platelet agent.
Mechanism of Action: Aspirin exerts its anti-platelet e ect through irreversible inhibition of
cyclooxygenase-1 (COX-1) enzymes in platelets. This prevents the synthesis of thromboxane
A2, a potent vasoconstrictor and promoter of platelet aggregation, thereby inhibiting platelet
function.
Indications: Aspirin is indicated in a variety of conditions. In an emergency setting, it is
particularly crucial for the management of acute coronary syndromes (ACS) including
unstable angina and myocardial infarction.
Contraindications: Contraindications include hypersensitivity or allergy to aspirin or other
salicylates, active gastrointestinal bleeding, other bleeding disorders (e.g., hemophilia), and
third trimester of pregnancy. Additionally, it should be used with caution in patients with a
history of gastrointestinal ulcers or other bleeding risks, renal or hepatic impairment, asthma,
and in those on concurrent anticoagulant therapy.
Dosage: In the setting of ACS, a loading dose of 160-325 mg of non-enteric coated
chewable aspirin is recommended
Route: PO
Onset: The anti-platelet e ect occurs within 30 minutes to an hour.
Peak: The peak plasma concentrations occur 1 to 2 hours following oral administration of
non-enteric coated chewable or soluble aspirin.
Duration: The anti-platelet e ect lasts for the lifespan of the platelet (7-10 days) due to the
irreversible binding of aspirin to the cyclooxygenase enzyme.

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 Nitroglycerin
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Nitroglycerin, also known as glyceryl trinitrate (GTN), is an organic nitrate

compound with the chemical formula C3H5N3O9. It is a potent vasodilator primarily used for
the prophylaxis and treatment of angina pectoris and acute coronary syndrome.
Mechanism of Action: Nitroglycerin is metabolized by mitochondrial aldehyde
dehydrogenase (ALDH2) to produce nitric oxide (NO) in smooth muscle cells. The resulting
NO activates guanylate cyclase, leading to increased production of cyclic guanosine
monophosphate (cGMP). The elevated cGMP activates a protein kinase that phosphorylates
certain proteins, ultimately causing relaxation of the smooth muscle and vasodilation. This
mechanism of action primarily reduces myocardial oxygen demand by decreasing preload
(via venodilation) but can also modestly reduce afterload and improve coronary blood ow.
Indications: Angina pectoris / Acute coronary syndrome, congestive heart failure
exacerbation.
Contraindications: Nitroglycerin is contraindicated in patients with severe anemia, closed-
angle glaucoma, hypotension, or those with hypersensitivity to nitroglycerin. It is also
contraindicated in patients who have taken phosphodiesterase-5 inhibitors within the last
24-48 hours due to the risk of severe hypotension. It should be used with caution in patients
with severe aortic stenosis or hypertrophic cardiomyopathy.
Dosage: 0.4 mg sublingually spray or tablet, usually repeated every 5 min for up to 3 doses.
Route: Sublingual, buccal, transdermal, and intravenous.
Onset: The onset of action for nitroglycerin is rapid. Sublingual or spray formulations have an
onset of action within 1-3 minutes.
Peak: For sublingual spray/tab formulations, the peak e ect typically occurs within 5-10 min.
Duration: Typically 30-60 minutes.
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 Naloxone
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Naloxone Hydrochloride is a pure opioid antagonist that competes with opioids
for binding at opioid receptors.
Mechanism of Action: Naloxone acts as a competitive antagonist at Mu opioid receptors. It
has a higher a nity for these receptors than many opioids, allowing it to displace opioids
from these receptors and reverse their e ects, including respiratory depression caused by
opioid overdose.
Indications: Complete or partial reversal of opioid drug e ects, including respiratory
depression resulting from natural and synthetic opioids or opioid analogues. It is also
indicated in the diagnosis of suspected acute opioid overdose.
Contraindications: Naloxone is contraindicated in patients known to have hypersensitivity to
naloxone or any of the other ingredients in the formulations.
Dosage: Typically 0.4 to 2 mg. May be repeated at 2-3 minute intervals.
Route: IV, IM, and IN routes.
Onset: For IV administration, onset is typically within 1-2 minutes. For IM administration,
onset is usually within 2-5 minutes. Intranasal administration may have a slightly slower
onset.
Peak: Usually observed within 20-60 minutes after administration, depending on the route of
administration and individual patient characteristics.
Duration: The duration of action of naloxone is typically 30-120 minutes, though this may be
shorter or longer depending on the half-life of the opioid being counteracted, the dose of
naloxone given, and the individual patient's metabolism. This is important to note because
many opioids, particularly synthetic opioids, have a longer duration of action than naloxone,
and symptoms of opioid overdose may return after the e ects of naloxone wear o .
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 Oral Glucose
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Oral glucose gel is a concentrated, carbohydrate-based gel preparation that is

typically composed of dextrose, water, and sometimes added avorings. It is designed to be
quickly absorbed through the oral mucosa and rapidly increase blood glucose levels.

Mechanism of Action: Oral glucose gel acts by quickly delivering dextrose to the
bloodstream. Once in the bloodstream, dextrose is transported into cells with the aid of
insulin, where it is metabolized to produce energy.

Indications: Oral glucose gel is indicated for the treatment of hypoglycemia.

Contraindications: Patients with altered consciousness may also not be able to safely ingest
oral glucose gel due to the risk of aspiration.

Dosage: The typical dose for adults is 15-20 grams of glucose, and 0.3 grams/kg in children.

Route: P.O., sublingual, buccal.

Onset: Within ~10-15 minutes.

Peak: Within ~30 minutes to 1 hour after administration.

Duration: The duration of action can vary depending on individual factors such as the
patient's insulin levels and metabolic rate, but the e ects of a single dose are typically
noticeable for 1-2 hours. However, glucose levels should be re-checked after 15 minutes and
if they're still low, another dose may be needed. Ongoing monitoring is critical until the
patient is stabilized.

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 Glucagon
Description
Mechanism of action
Indications
Contraindications
Dosage
Route
Onset
Peak
Duration

Description: Glucagon is a peptide hormone produced by the alpha cells of the pancreas. It
is a hyperglycemic agent that is commercially available in injectable forms, both as a powder
for reconstitution and pre- lled autoinjector or nasal powder.
Mechanism of Action: Glucagon works to increase blood glucose levels by stimulating
hepatic conversion of glycogen to glucose (glycogenolysis) and enhancing the synthesis of
glucose (gluconeogenesis). It also reduces glycogen synthesis and decreases glucose
utilization in the liver.
Indications: Glucagon is indicated for the treatment of severe hypoglycemia in patients with
diabetes mellitus when diminished consciousness precludes oral carbohydrates. It's also
used as a diagnostic aid in radiologic examinations to temporarily inhibit movement of the
gastrointestinal tract.
Contraindications: Pheochromocytoma or insulinoma due to the risk of substantial increase
in blood pressure and hypoglycemia. Caution in prolonged fasting, starvation, or chronic
hypoglycemia, as glucagon response may be blunted or absent in such cases.
Dosage: For adults and pediatrics >20 kg or older than 6 years, the dose is typically 1 mg.
For pediatric patients weighing <20 kg or younger than 6 years, a typical dose is 0.5 mg.
Route: Intramuscular, subcutaneous, intranasal, or intravenous.
Onset: Typically between 10 to 20 minutes.
Peak: Within 30 minutes to an hour.
Duration: The hyperglycemic e ect of glucagon is typically noticeable for 60 to 90 minutes.
It's important to note that once blood glucose levels have been corrected, administration of
carbohydrate is advised to replenish hepatic glycogen stores.
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 References
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