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Volume 1, Number 33
Weekly EMS Drill
Pharmacology Discussion - Atropine
OBJECTIVE: This drill will continue a series of discussions regarding the drugs that we carry in the CCFD.
This week, we will be discussing Atropine Sulfate. We are most familiar with its indications as a
“cardiac” drug, and it is the first injectable drug of choice for bradycardia in most circumstances, as well as
being indicated for the PEA and Asystole protocols. Atropine has some other medical uses, including treatment
of irritable bowel syndrome, certain biliary tract and genitourinary disorders, as well as being the initial drug of
choice for organophosphate poisoning.
Let us begin our discussion of Atropine’s effects with a review of the nervous system. Several weeks
ago, in the discussion regarding epinephrine administration, we reviewed autonomic sympathetic nervous
system receptor sites, namely the alpha and beta sites. Now we will review the autonomic parasympathetic
receptor sites.
We should remember that the neurotransmitter for parasympathetic post-ganglionic receptor sites is
acetylcholine, or Ach. Receptor sites which are affected by acetylcholine are the muscarinic receptor sites, and
nicotinic receptor sites. Primary sites for muscarinic receptor stimulation are the muscle tissues of the heart, the
smooth muscles of the lungs and digestive tract, as well as the glands.
The primary focus of this discussion regards the muscarinic receptors located in the heart. Primarily,
these affect the cardiac electrical, or conduction, system. The vast majority of this effect is distributed in the
atrial area, affecting the Sino-atrial node, the Bachmann’s bundle, and the Atrio-ventricular node. Very little
parasympathetic influence is rendered to the ventricular conduction system. We will remember that beta
receptor sympathetic stimulation will cause an increase in heart rate, force of contraction, and electrical
conduction velocity. Parasympathetic stimulation works against these effects.
Recall the five phases of cardiac depolarization, and that depolarization of the heart is initiated by
sodium influx to the cell during phase 0. Re-polarization of the cardiac tissue is accomplished primarily by
potassium being returned to the inside of the cell in appropriate amounts during the terminal portion of phase 3
and initial portion of phase 4. Parasympathetic stimulation to the heart is provided by the cardiac branch of the
vagus nerve (CN X, or the tenth cranial nerve). Specifically, the activity of the vagus nerve influencing
muscarinic receptor sites in the myocardium leads to increased permeability of the cardiac cells to potassium
ions. This allows increased potassium to enter the cell, in effect “hyperpolarizing” the cell. Assuming normal
leaky sodium channel activity causing prepotential drift, it will then take a longer time for the cell membrane to
reach threshold potential and initiate depolarization.
This is the very reason that the initial treatment option for an SVT is vagal stimulation, in one of the
various forms, due to the intrinsic slowing of the heart rate as an effect. A paramedic utilizing an overly
aggressive intubation technique could stimulate bradycardia in the patient, especially in pediatrics, which are
very susceptible to this phenomenon due to their smaller airways. In any patient, a very strong vagal stimulus
could hyperpolarize the cell membrane to such an extent that it could abolish depolarization completely.
This brings us full circle back to our drug Atropine. Ask most providers “What is the effect of
atropine?” Most, (especially nurses) will say, “It speeds up the heart rate.” Technically, that is not the case.
Most of us learned in paramedic school that atropine is a parasympathetic blocker, and it is, but going further, it
is more accurately a parasympathetic muscarinic receptor site antagonist, meaning it blocks the action of the
muscarinic receptor sites in the cardiac arena, reducing cell permeability to potassium ions, therefore not
allowing the cell to hyperpolarize. So, again, technically it does NOT “speed up the heart rate”; more accurately
the effect of atropine is to block the action of the muscarinic receptor sites that are trying to slow the heart rate
down. In the absence of this muscarinic activity, the beta cells would be unencumbered in their efforts to
increase the heart rate, and thus, the side effect of an increase in heart rate. Atropine does not directly stimulate
the heart to “go faster”.
This concept is very important to remember in certain care situations which come up in our everyday
practice. If the patient is showing, say, a sinus bradycardia, or a junctional bradycardia, (both of which originate
supraventricularly) or a lower degree atrioventricular block, then atropine will likely be effective in increasing
the heart rate because these conditions . However, a very common initial rhythm in a post-defibrillation patient
is a ventricular bradycardia, or “ventricular escape”. Recall that there are few, if any parasympathetic nerve
fibers innervating the ventricular muscle mass or conduction system. Therefore, administering atropine will
likely have little effect on the heart rate in a patient with ventricular escape, because, again, atropine has no
direct stimulatory effect on the heart such as beta receptors would have. High degree heart blocks present a
similar situation. Atropine is not contraindicated for a third degree heart block with a ventricular (wide
complex) response, it likely would just have no effect on the heart rate, since the target tissue (the AV junction)
is likely severely ischemic or infarcted, and cannot respond. These patients would likely gain more therapeutic
benefit from the paramedic initiating transcutaneous pacing in an expeditious manner.
Atropine is also indicated in the setting of pulseless electrical activity, IF the electrical activity showing
on the monitor indicates an absolute bradycardia. The pulseless nature of the activity could have been triggered
by strong parasympathetic stimulation. Since atropine shakes out to be a “rate drug” after all, atropine is also
indicated if the patient is in a ventricular Asystole. In both of these cases, we would try the direct stimulatory
effect of epinephrine prior to administering atropine.
With the next pharmacology discussion, we will delve into the effects of atropine for other patient case
presentations.