This is one of the posts where I remind you that I am not your
medical director, boss, paycheck signer, protocol author, or decision-maker
regarding your continued EMS employment. So take the opinions laid out here
with a grain of salt, huh? But see if I can convince you to come over to my
side.
Here’s a scenario for you. You and your partner respond to a cardiac
arrest, with dispatch giving CPR instructions over the phone. You arrive to find a 25-year-old male
pulseless and apneic, and asystolic on the monitor. First responders report
that their AED delivered one shock prior to your arrival.
Digging into the patient’s pre-arrest history, you discover the
patient is a brittle asthmatic and had been struggling to control his breathing
all day. His friend reports that he had been hitting his metered dose inhaler (with
the spacer attached) much more than usual. There is no other recent illness,
trauma, drug use, or significant information. The scene is safe to hang out and
work the arrest.
What are your treatment priorities for this patient?
Continuing high-quality CPR in 2 minute rounds, of course. Harder! Faster! Intravenous or
intraosseous access. Epinephrine every three to five minutes. Ensure
ventilation, whether through an OPA initially or through a King or an ETT as needed.
My plan would be to work the patient on scene until I pronounced him or got
pulses back. I think asystole is confirmation of death, in most cases, so I
would probably be looking at a round or two and calling it if things didn't
turn around.
Here is what brought this rant up: In this case I found online, the scenario includes “…bagging in a duoneb
treatment…” Click the link and read the case. Would you give the patient a duoneb treatment via in-line neb into
an endotracheal tube? I mean, he is an asthmatic who was having trouble
breathing before he arrested. Albuterol
and atrovent could improve his breathing, right?
Nope. I wouldn’t. As a matter of fact, hell-no I wouldn’t give an in-line albuterol treatment to a patient
in cardiac arrest.
Why waste your time, attention, and efforts delivering
albuterol? Simplify your task list!
I attempted to research the use of albuterol or atrovent in the
setting of cardiac arrest. I didn’t find anything pertinent. I suspect that it
is too silly a question for research to have been done on it. I tried to find
information on the absorption of nebulized albuterol in cardiac arrest. Nothing.
I searched ACLS algorhythms and other guidelines for albuterol administration in
cardiac arrest patients. Nope. Is albuterol efficacious to reverse asthmatic
cardiac arrest? Dunno, but probably not. I did find that an MDI with a spacer is as effective as a nebulizer in
treating an acute asthma exacerbation. So it isn’t as though your neb will be
more effective than the MDI that the patient had been hitting all day. I also
found that the amount of nebulized medication absorbed is related to tidal
volume (duh), which is decreased when you’re bagging a patient. It is even
worse when you consider the deadspacing resulting from all the extra in-line
neb tubing.
Here is my thought: In a cardiac arrest, you are already pouring
a β-2 agonist into the patient’s body. Epinephrine. Have you ever given
intramuscular (or subcutaneous, if you’re old enough) epi to an asthmatic? It
hits like a hammer and starts to open the lungs quickly. In a cardiac arrest,
you aren’t giving a half-milligram into the deltoid. You are blasting a whole
milligram into the venous circulation. And then repeating it after three
minutes. And then potentially repeating it again and again.
Think of IV epi like the water in a swimming pool. Albuterol is
like adding another drinking cup of water. Yeah, the dumping the little cup into the pool added
more water, but not any amount that it significant compared to the water that is in the whole
pool.
Part 12.1 of the AHA
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Science* deals with an asthmatic arrest, specifically. “When cardiac arrest
occurs in the patient with acute asthma, standard ACLS guidelines should be
followed.” Standard ACLS guidelines never mention albuterol or atrovent in
cardiac arrest algorhythms. Respiratory arrest is treated by opening and
securing an airway. V-Fib and V-Tach get defibrillated every two minutes, get
IV epi every 3-5 minutes, and may get amiodarone. PEA or asystolic arrests get epi. Hypoxia is treated by securing an airway and
ventilating the patient. Acidosis is treated by ventilation (not bicarb).
Tension pneumo is treated by a big-ass needle between the ribs. My prehospital
protocols are similar. No albuterol. No atrovent.
The
AHA Guidelines continue: “Complications of severe asthma, such as tension pneumothorax,
lobar atelectasis, pneumonia, and pulmonary edema, can contribute to
fatalities. Severe asthma exacerbations are commonly associated with
hypercarbia and acidemia, hypotension due to decreased venous return, and
depressed mental status, but the most common cause of death is asphyxia.”
Albuterol doesn’t reverse asphyxia; ventilation does. Ventilation also helps
reverse hypercarbia and academia.
But giving it doesn’t hurt…
Yes it does. It is one more task you have to perform. It
requires endotracheal intubation, or at least a supraglottic airway. You can’t
deliver albuterol via BVM and mask. When you have an intubated patient, most of
your time should be spent thinking about whether or not the distal tip of the
tube is where you intend it to be. You
don’t need to be distracted by an in-line neb.
This is the Rube Goldberg puzzle you want to assemble during a cardiac arrest, huh? |
In-line nebs are a hassle to assemble. They are like friggin’
puzzles. An in-line neb interferes with
monitoring an intubated patient’s end-tidal CO2 level – the best way to monitor
the distal end of your tube.
The list of actions you should perform during a cardiac arrest
is long. I wouldn’t make the mistake of prioritizing a nebulizer treatment
higher than CPR, IV access, IV epinephrine, airway management, intubation
confirmation… The list of more-important tasks is long and illustrious.
Managing a cardiac arrest in the field is a difficult task to do
well. Why would you complicate a difficult task for marginal or theoretical (if
any) benefit? Don’t waste your time with the neb.
1 comment:
Why not just consider dumping 5mg of albuterol straight down the ET tube and continuing on about your business and reassessing? There is not a lot of evidence for this, but the one AJEM article I found showed remarkable results. Granted, these were non-arrested patients, but their blood gases prior to receiving the albuterol were bad enough that it wouldn't surprise me had they have.
http://www.ajemjournal.com/article/S0735-6757(04)00184-6/pdf
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