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BRADYARRHYTHMIAS
75
improve temporarily, there is a high probability for the
patient to need further intervention, as well as for him
to deteriorate while he is awaiting that intervention.
PR: I think that observation units within the ED are
variable in their staffi ng and in their capabilities.
Some don’t have a nurse whose sole obligation is the
patients in the observation unit; I wouldn’t put any
patient with a risk of deterioration in such a unit. But
there are some heart units and observation units that
do have good equipment and good nurses assigned,
and in that case I don’t know that there is much less
observation than in the CCU. In the ED, you also have
to worry about what kind of manpower you have to
respond to the observation unit. Many EDs have a
single physician responsible for both the patients in
the main department and the patients in the observa-
tion unit, and that can stretch medical response time
to an unacceptable length.
PR: Are there other conditions here that could be
contributing to this problem and would need further
workup or management? Are we looking at subtle
sepsis, for example? What additional workup would
you include in the management of this patient?
SG: You may want to tease out his initial complaints;
he is lightheaded with exertion, short of breath, and
weak. All of these are nonspecifi c complaints, but all
of them are complaints that someone could develop
with a concomitant infectious process. The complaint
that we are not told about is whether the patient has
been febrile; we are also not told if the patient has
been coughing, having chest discomfort, or other
symptoms that would be concerning for infection
such as dysuria, changes in frequency of urination,
rashes, etc. I think you have to take the pieces of his-
tory that you do know and say, what is the likelihood
that this is going to be something else?
Given these known symptoms, how much do I have
to pursue further workup? I would say, if the patient
doesn’t have a fever, and doesn’t have any signs of
infection on physical examination, then it’s unlikely
that the patient’s going to have an infection. It’s rea-
sonable to do some very basic testing, such as a chest
X-ray study and a urinalysis to make sure that we are
not missing a very common but, in this case occult,
infection, but I probably would stop there so long as
the patient is afebrile, and doesn’t have a profound
leukocytosis or leukopenia.
SG: Traditionally, we would place alligator clips on
the pacer wire and on an EKG V lead, then look for
a current of injury (ST elevation) on EKG. As soon as
we saw this, we would pull back ever so slightly away
from what must have been the right ventricular wall,
and know that the wire was in place. This can be done
from any ED bedside.
PR: I still suspect beta-blockade to be the cause of
his symptoms. It’s not clear to me why this suddenly
became too much for the man. I would still hope that
after admitting him to the hospital he would turn
around with relief from the beta-blockade, and not
require permanent pacemaker placement. Clearly,
what was done in this case was precisely that: to not
rush to pace him, but to admit him, and to see what
happens over a little time. When he continued to be
bradycardic, a pacemaker was inserted. Of course,
part of our problem is that we don’t always have beds
to admit such a patient to, and then one becomes a
little bit more concerned about what to do in the ED.
Do you believe that a patient like this would progress
all right in an observation bed in the ED?
SG: Were telemetry to be the same in the ED as it is
in the coronary care unit (CCU), then I would say
yes. Unfortunately, most EDs, that I know, don’t have
someone watching the monitor 24 hours a day, 7 days
a week. Even with all of the bells and whistles that
we have in the modern ED, it’s hard to closely moni-
tor a dangerous dysrhythmia, even when only admit-
ted to the ED for the short term. I would not keep
this patient in an observation unit. I think the patient
would benefi t from being in a unit that has very close
telemetry monitoring. Should the patient’s rhythm
deteriorate over the course of the observation process
before the decision is made whether to place a perma-
nent pacemaker, it could be appropriately recognized
and dealt with quickly. Unfortunately, the reality of
emergency medicine is that we don’t have that kind
of monitoring.
RH: When we make the decision of who to put in the
observation unit in the ED, we have to decide whether
there is a high, medium, or low likelihood to develop
a problem. We are better off putting people with a
low likelihood to have a problem, like those with
low-risk chest pain, in the observation units. Here we
have a 75-year-old man with low blood pressure, low
heart rate, and third-degree heart block; even if it does
CHAPTER 5
76
do get some ischemia, it is not likely to be sustained.
Although isoproterenol can be shut off, it may take a
little longer to clear from the system.
PR: If you got a call about this patient from the fi eld
from an ambulance that was coming a fairly long dis-
tance, which is typical for our more rural EDs, would
you be inclined to start pharmacological therapy in
the ambulance?
SG: This is one of those cases where you say “primo
non nocere” or “fi rst do no harm.” You take a patient,
who is relatively stable in an ambulance, and you start
administering drugs; if they become far sicker and far
more ill, they are still in an ambulance. For this rea-
son I would say, “Wait until he gets here unless the
blood pressure or heart rate deteriorates further, and
then we can better assess him in an institution where
we have more options available.”
PR: This case fortunately has a good outcome. I wish
all heart blocks looked this good when they arrive in
the ED. Frequently they do not.
SG: I would suspect that this is likely related to a slow
deterioration of his conduction system. He likely tol-
erated a relatively low heart rate for a while and that
is why he had a good outcome.
Case resolution
The patient was admitted to the CCU with concern for
third-degree block. Metoprolol was held for several
days to identify whether this medication was the cause
of the patient’s bradycardia. However, bradycardic epi-
sodes persisted, and on hospital day three, a pacemaker
was placed without complications. The patient was
discharged the next day and on one month follow-up
he had no complaints.
Section III: Concepts
Background/epidemiology
Bradycardia, defi ned as a heart rate of less than
60 beats per minute, is a relatively common fi nding
during routine evaluation of patients in the ED. With
a vast array of etiologies and related electrocardio-
graphic manifestations, the clinical implications of
bradycardias range from negligible incidental fi ndings
to life-threatening bradyarrhythmias. The fi rst task is
The next thing I might consider is: does this patient
actually have concomitant cardiac ischemia? Given
his presentation, that is a reasonable thought. The
EKG doesn’t suggest cardiac ischemia. The EKG is
the best test that we have, but unfortunately is not
particularly sensitive for acute myocardial infarction;
at best, it’s in the 50% range. Serial cardiac enzymes
in this patient would be reasonable to make sure this
event is not a manifestation of a concomitant infarc-
tion. Then you get to more and more remote diagno-
ses, such as thyroid disease and so forth. The more
remote the possibility, the less likely the diagnosis,
especially when you have more likely diagnoses such
as conduction diseases or beta-blocker toxicity.
PR: Are there medications that you would especially
want to avoid should the patient deteriorate further?
If his blood pressure drops and you want to intubate
him, are there any respiratory management drugs that
would make the bradycardia and heart block worse?
RH: Most of us are using succinylcholine preceded by
etomidate, and I think we should be okay with these
medications here.
SG: Intubation increases your vagal tone, and if you
do need to intubate the patient, this patient may need
pre-intubation atropine.
RH: That is written in every book, but do you really
fi nd that in practice your patients increase vagal tone
and drop their heart rates when you intubate them?
PR: Only when they are hypoxic.
RH: Just because I am expected to see a drop in
heart rate when the patient is instrumented, I don’t
know that I would reach for atropine now if I haven’t
already given atropine for the persistently low blood
pressure and heart rate.
PR: Would you use isoproterenol to support the blood
pressure while you were doing other things in this
patient, as perhaps this might solve some of the con-
cerns about atropine?
SG: Isoproterenol has fallen off the ACLS guidelines.
PR: Why did it fall out of favor?
SG: I suspect that it fell out of favor because there
are better therapies. External pacing, as uncomfort-
able though it may be, is a better choice because it is
more effective. Atropine is short lived so that if you
BRADYARRHYTHMIAS
77
Initial workup history and physical
Similar to any emergency patient, the initial evalua-
tion entails a rapid assessment of the patient’s airway,
breathing, and circulation. Also, for all critical patients,
it involves promptly gaining intravenous access, pro-
viding supplemental oxygen, and cardiac monitoring.
Unique to bradycardic patients, pacer pads should be
applied to all patients until defi nitive management has
been provided. Early preparation is necessary so that
transcutaneous pacing can be initiated rapidly when
necessary, as studies show decreased effectiveness of
pacing after loss of spontaneous circulation.
3
After immediate stabilizing interventions, a focused
history and physical examination can be performed.
Current symptoms that may indicate cerebral hypop-
erfusion in the setting of bradycardia, such as diz-
ziness, presyncope, or syncope, must be elicited.
Additionally, the clinician should identify symptoms
of cardiac ischemia, including chest pain, shortness of
breath, or nausea. Recent infectious illnesses should
be noted as well as any travel history, as certain ill-
nesses endemic to Central and South America may
cause bradycardia. Given the wide range of etiologies
in bradycardia, a thorough review of a patient’s past
medical history should be undertaken, with special
attention paid to any history of structural heart dis-
ease, neoplastic disease, connective tissue disorders,
or rheumatologic disorders. The patient’s medication
list should be reviewed, and any nodal blocking agents
or cholinergic agents should be noted. The physical
examination should focus on the overall appearance
of the patient, as well as any abnormalities on car-
diovascular examination, including those related to
rhythm, murmurs, rubs, or an abnormal pulse rate.
Etiologies/differential diagnosis
The function of the cardiac conduction system is an
integral step in creating the differential diagnosis. The
sino-atrial (SA) node, located at the junction of the
superior vena cava and the right atrium, consists of
a group of specialized cells that spontaneously depo-
larize. Impulse is then conducted via the internodal
pathway to the AV node, which is located in the lower
septum of the right atrium. Electrical activation con-
tinues through the AV node, with a slight delay to
ensure complete atrial contraction prior to ventricular
contraction. Conduction continues via the Bundle of
to determine whether the patient exhibits any signs
or symptoms related to the bradycardia, and to treat
accordingly.
Identifying the association between a slow heart
rate and a patient’s presentation proves challenging at
times. The cardiac output is the product of left ven-
tricular stroke volume and the heart rate. For exam-
ple, in cases of an asymptomatic sinus bradycardia,
often seen in seasoned athletes, increased stroke vol-
ume compensates for a slower heart rate; the result
is a normal cardiac output and suffi cient cerebral
perfusion to leave the patient entirely asymptomatic.
One study fi nds an incidence of sinus bradycardia in
conditioned athletes to be as high as 50–80%, with a
prevalence of 23% in the general population.
1
In other cases, a bradyarrhythmias seems to be clearly
temporally related to an episode of cerebral hypoper-
fusion, such as syncope, or obvious documented sys-
temic hypotension. In one retrospective cohort study
of 247 patients with bradycardia, 21% of patients
with a hemodynamically signifi cant bradycardia died
within 30 days of presentation, with 41% of the
deaths attributable to cardiovascular causes.
2
Thus,
further diagnostic studies and interventions are clearly
indicated in the case of hemodynamically signifi cant
bradycardia.
In the third category, a person presents with vague
persistent complaints such as dizziness or weakness,
and is found to have a bradycardia. In this case, the
emergency physician must better describe the brady-
cardia in terms of the electrocardiographic rhythm
and likely etiology; this information would be used
to determine whether this slow heart rate could be
the cause of the patient’s symptoms, and therefore
requires intervention. The fi rst important responsi-
bility, then, is to determine whether the bradycardia
is the cause of the symptoms. Secondly, it must be
determined whether or not a patient is symptom-
atic from a bradycardia. A rhythm strip should be
obtained in order to further delineate the conduc-
tion abnormality causing the slow heart rate. Some
bradycardias have the potential to deteriorate into
an unstable rhythm even in the setting of a well-
appearing patient, and these must be identifi ed by
EKG. Third, once the need to intervene is identifi ed,
a clinician must consider the risks and benefi ts of
the available emergency therapies, including phar-
macologic intervention, transcutaneous pacing, or
transvenous pacing.
CHAPTER 5
78
with bradyarrhythmias. The resulting bradycardias in
these cases are often due to ischemia at the AV node or
increased parasympathetic tone in the setting of a right
coronary artery- related infarction. They are often
responsive to atropine or other pharmacologic inter-
vention. The AV blocks that develop in the setting of
an anterior myocardial infarction, on the other hand,
often result from occlusion of the left anterior descend-
ing artery and lead to septal infarction and dysfunction
of the Bundle of His and bundle branches, while often
sparing the AV node. In these cases, complete heart
block involves a wider QRS complex on electrocardi-
ography, and confers a poorer prognosis with a more
limited response to pharmacologic interventions.
6
Other extrinsic causes of bradycardia include non-
ischemic cardiac diseases such as cardiac amyloidosis,
neoplasm, cardiomyopathy, collagen vascular disease,
and pericarditis.
4
In particular, infi ltrative sarcoidosis
should be considered as a potential etiology of bra-
dycardia, as up to 25% of patients with this disease
demonstrate cardiac involvement on pathology. A
highly unstable complete heart block is the most com-
mon presenting cardiac manifestation of infi ltrative
sarcoidosis.
6,10
Rheumatologic diseases that have been
shown to cause AV conduction disturbances include
Sjogren’s syndrome, Wegener’s granulomatosis and
Behçet’s syndrome.
6
Infectious diseases can cause bradyarrhythmias
whether in acute or chronic forms. Viral illnesses
known to cause bradycardia or heart block include
mononucleosis, hepatitis, varicella, respiratory syn-
cytial virus, mumps, rubella, rubeola, and varicella,
although infl uenza rarely involves the heart.
6
Bacterial
endocarditis can also cause various degrees of heart
block when the infection invades the conduction
system.
6,11
Chagas disease, caused by protozoan infec-
tion of Trypanosoma cruzi, should be considered in
the evaluation of any bradycardic patient who lives in
Central or South America. While the disease has prom-
inent gastrointestinal and cardiac manifestations, sud-
den cardiac death accounts for the death of 55–65%
of people with this disease.
12
The cardiac arrest is
usually precipitated by exercise, and results from ven-
tricular tachycardia, ventricular fi brillation, asystole,
or complete heart block.
13
Lyme disease, caused by
the spirochete Borrelia burgdorferi, has cardiac mani-
festations during the early-disseminated phase of the
disease, which usually occurs within weeks to months
after infection. The primary manifestations of Lyme
His into the interventricular septum, where it trav-
els for one to two centimeters before dividing into
the right and left bundles. These bundles divide into
branches as they run along the interventricular sep-
tum before terminating in Purkinje fi bers that form
interweaving networks on the endocardial surface of
both the right and left ventricles. Rapid conduction of
impulses across this network allows for nearly simul-
taneous contraction of both ventricles.
4
In terms of perfusion, the sinus node is supplied by
the right coronary artery in 65% of patients, the cir-
cumfl ex artery in 25% of patients, and both in 10%
of patients. The AV node receives its blood supply
from the posterior descending artery, which arises
from the right coronary artery in 80% of patients, the
circumfl ex artery in 10%, and both in 10%.
5
The con-
duction system is densely innervated by both the sym-
pathetic and parasympathetic nervous systems. While
increased adrenergic input increases SA automaticity
during exercise and emotion, parasympathetic input
predominates at rest in most healthy individuals,
leading to an increased AV-nodal conduction time and
refractoriness.
4
Disorders of impulse formation or conduction
through the cardiac conduction system can be caused
by intrinsic or extrinsic factors. Intrinsic factors, those
that involve some structural or functional abnormal-
ity of the SA node or conducting tissue itself, account
for only 15% of bradyarrhythmias encountered in the
ED.
6
The sick sinus syndrome encompasses the major-
ity of these intrinsic abnormalities. Its characteristics
include severe chronic and inappropriate bradycar-
dia, sinus pauses, sinus arrest and exit blocks (with
and without appropriate escape rhythms), alternating
bradycardia and atrial tachydysrhythmias, and con-
current AV conduction disturbances in over 50% of
patients.
7,8
This broadly-defi ned syndrome has a num-
ber of documented etiologies including vascular dis-
ease of the SA nodal artery, congenital and acquired
cardiac disease, and genetic mutations, but its most
common cause is the replacement of the sinus node
with fi brous tissue, with or without degeneration and
fi brosis of other conduction pathways (including the
AV node).
9
Extrinsic causes of bradycardia account for the
majority of cases seen in the ED, and have a wide vari-
ety of etiologies. While any distribution of ischemia
may be associated with bradycardia, inferior wall acute
myocardial infarctions are most commonly associated
BRADYARRHYTHMIAS
79
radiation therapy for malignancy. Neurologic causes
include increased intracranial pressure and Cushing’s
syndrome, as well as an ictal-bradycardia syndrome.
6
Lastly, vagal events, such as vomiting or urination,
may cause transient bradycardia, and are often impli-
cated in cases of neurocardiogenic or “vaso-vagal”
syncope.
Testing
The cornerstone for emergency testing in bradycardia
is electrocardiography. The EKG will often identify
the disorder of impulse formation or conduction. In
sinus bradycardia, a disorder of impulse formation,
the ventricular rate is less than 60 beats per minute.
Importantly, each P wave is followed by a narrow QRS
complex, the P-wave morphology does not change,
and the PR interval remains consistent (Figure 5-2).
In an AV junctional rhythm, the rhythm is initiated
by the AV node either due to lack of stimulation from
the SA node or from an abnormally rapid AV node
automaticity. Generally, the AV node has an intrinsic
rate of 45–60, so it should not fi re until sinus automa-
ticity falls below this rate.
16
The QRS complex mor-
phology should appear the same as in sinus rhythm,
with the P waves falling before, during, or after the
QRS complex (Figure 5-3).
A ventricular escape rhythm, also known as an
idioventricular rhythm, occurs at a rate of less than
disease carditis include conduction system dysfunc-
tion and decreased cardiac output due to myoperi-
carditis. The conduction abnormalities range from
fi rst-degree AV block to complete heart block. One
review of 52 patients with Lyme disease carditis fi nds
that 87% of new Lyme disease patients have some
degree of AV block, with the majority being symp-
tomatic from this block.
14
Another important extrinsic cause of bradycardia is
medication, regardless of therapeutic or toxic doses.
Nodal blocking agents such as beta-blockers, calcium
channel blockers, or digitalis are extremely common
causes. Alpha-2-agonists such as clonidine, as well as
cholinergic agents and other antidysrhythmia agents,
can also produce bradycardia.
5
In terms of toxicologic
ingestions, botanicals such as foxglove, oleander, and
lily of the valley contain cardiac-glycosides that can
create a digitalis like toxicity.
6
Additionally, multiple
medications, when taken in overdose (such as tricyclic
antidepressants, carbamazepine, quinine, amantadine,
cyclobenzaprine, thiordiazine, and chloroquine) act
like class Ia antidysrhythmics and can produce seri-
ous heart block in addition to their more well-known
sinus tachycardia.
6,15
Other potential extrinsic causes of bradycardia
include electrolyte abnormalities such as hyper-
kalemia, hypercalcemia, and hypermagnesemia. It
is rarely associated with hypoglycemia. Iatrogenic
causes exist, including post-heart transplantation or
Figure 5.2 Sinus bradycardia.
CHAPTER 5
80
more than 0.20 seconds. Importantly, all P waves are
conducted with consistent PP and RR intervals. This
is usually caused by a delay in the AV node, thus dem-
onstrating a narrow QRS (Figure 5-5).
Mobitz type I (Wenckebach) second-degree AV block
is a disorder of atrioventricular conduction character-
ized by progressive prolongation of the PR interval
until a P wave is not conducted, resulting in a “dropped
50 beats per minute. It acts as a safety net, demon-
strating ventricular automaticity in the absence of
proper conduction from above (i.e, sinus arrest, AV
block). It produces a wide QRS, and should not be
treated with lidocaine given the potential for cardiac
standstill
16
(Figure 5-4).
First-degree AV block is a disorder of atrioventric-
ular conduction, and is defi ned by a PR interval of
Figure 5.3 Atrioventricular junctional rhythm.
V1
V4
V5
V6
V2
V3
aVR
aVL
aVF
I
II
II
III
Figure 5.4 Idioventricular rhythm.
BRADYARRHYTHMIAS
81
a dropped beat. The RR interval decreases the same
amount that the PR interval lengthens. This disorder
is usually caused by slowed conduction at or above
the AV node, resulting in a narrow QRS (Figure 5-6).
beat.” After the dropped beat, the cycle repeats itself,
starting again with a normal PR interval. The rhythm
strip often shows the appearance of “grouped beat-
ing” as the RR interval shortens progressively after
Figure 5.5 First-degree atrioventricular block.
10
l
ll
lll
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
V
Figure 5.6 Mobitz type 1 block.
CHAPTER 5
82
except for a 2:1 block are easy to distinguish from a
Mobitz type I block by lack of prolonging PR seg-
ments (Figure 5-8). A 2:1 block may be either form of
Mobitz block, and the patient should be monitored to
see whether a higher degree of heart block develops.
Third-degree AV block is a disorder of atrioven-
tricular conduction in which no atrial impulses reach
the ventricles, and an escape pacemaker must emerge.
There is no relationship between the P waves and the
QRS complexes. The PP intervals and RR intervals
are regular throughout. The block in this case may
occur anywhere from the AV node to the Purkinje
system, with the more severe symptoms occurring in
lower blocks (Figure 5-9).
In addition to obtaining an EKG with a rhythm
strip, serum electrolytes and chest radiography are
useful tests to obtain in the ED for all patients with
clinically signifi cant bradycardia (Figure 5-10).
While this rhythm is often seen during acute myocardial
infarction, it is usually a stable rhythm providing ade-
quate perfusion, and is usually responsive to atropine.
Mobitz type II second-degree AV block is a dis-
order of atrioventricular conduction character-
ized by consistent PR intervals throughout (which
may be normal or prolonged) and with intermittent
nonconducted P waves. Thus, this rhythm does not
have progressive PR prolongation demonstrated in
Wenckebach. Since the conduction block usually
occurs in the His Purkinje system, a wide QRS is usu-
ally seen (Figure 5-7). This rhythm has the potential
to deteriorate into a third-degree block, and usually
requires permanent cardiac pacing. Emergent phar-
macologic interventions are often ineffective, and
emergent pacing may be required. The magnitude of
the AV block is described by the ratio of P waves to
QRS complexes (i.e; 2:1 v. 3:2 conduction.) All ratios
Figure 5.7 Mobitz type 2 block.
V1
V4
V5
V6
V2
V3
aVR
aVL
aVF
I
II
II II II II
III
Figure 5.8 Mobiz type 2 (2:1) block.
BRADYARRHYTHMIAS
83
aVR
aVL
aVF
V1
V2
V3
I
II
II
III
V4
V5
V6
Figure 5.9 Third-Degree atrioventricular block.
Bradycardia Algorithm
Heart Rate <60 bpm
Heart rate improves?
Signs of poor perfusion (hypotension, altered mental status, chest pain)?
Yes No
Yes No
• Prepare for transcutaneous pacing
• Give atropine while awaiting pacing
• Attempt transcutaneous pacing ASAP for
unstable rhythm OR if atropine fails
• Consider giving epinephrine or dopamine
• Continue close monitoring
• Treat the primary problem
• Continue close monitoring
• Attempt transvenous pacing
• Treat the primary problem
Figure 5.10 Management of bradycardia.
Disposition
In cases of symptomatic bradycardia due to an extrin-
sic cause, patients require admission for treatment
of that specifi c cause. In one study, a retrospective
analysis of a bradycardia registry, it is reported that
51% of patients with compromising bradycardia
have an inciting cause that requires specifi c treatment.
These causes include: adverse drug effect (21%),
CHAPTER 5
84
Asymptomatic unstable bradycardia (Mobitz type •
II second-degree AV block or third-degree AV
block) should be admitted on telemetry monitoring
for an EP evaluation.
In symptomatic or compromising bradycardia, •
pacer pads should be placed on the patient while
an EKG is obtained. See Table 5-1 for complete
management.
If reversible causes of bradycardia are identifi ed, •
interventions such as potassium for hypokalemia,
activation of the catheter laboratory in STEMI,
antibiotics and aggressive fl uid management in
sepsis, active rewarming in hypothermia, glucagon
in beta-blocker ingestion, or digi-bind in digitalis
toxicity should be initiated emergently.
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Barthell E, Troiano P, Olson D, Stueven HA, Hendley 3
G. Prehospital external cardiac pacing: A prospective,
controlled clinical trial. Ann Emerg Med. 1988:17:
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www.accessmedicine.com/content.aspx?aID=3051157&
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Mangrum, JM, DiMarco JP. The evaluation and 5
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acute MI (14%), pacer dysfunction (6%), intoxica-
tion (6%), and electrolyte disorder (4%).
17
In cases of idiopathic bradycardia, those who expe-
rience compromising symptoms from the bradycardia,
and those whose rhythm on electrocardiography has
the known predisposition to deteriorate into a more
unstable rhythm (i.e; Mobitz type II) require admission
to the hospital for further evaluation and treatment.
Regardless of the cause, hemodynamically unstable
bradycardia should be treated medically with atropine,
which is considered the fi rst line treatment.
18
If unsuc-
cessful, epinephrine or dopamine are second line agents
that may be used as temporizing measures until pacing
can be implemented or if pacing fails.
18
Glucagon may
also be considered in the setting of a known or presumed
beta-blocker or calcium channel blocker ingestion, and
has been shown to improve heart rate and symptoms in
such patients when atropine is ineffective.
18,19
In the setting of an unstable patient and failure of
medical management, transcutaneous pacing should
be started with stimulation of the left ventricle (LV)
through electrodes placed on the chest wall. Pain with
impulse, skeletal muscle contraction, and diffi culty
with LV capture remain limitations to this intervention,
but it can serve as a lifesaving bridge to transvenous or
permanent pacing.
20
Transvenous pacing requires catheter placement by
central line (usually right internal jugular or left subcla-
vian vein) into the heart with direct stimulation of the
right ventricle. Complications of this procedure include
myocardial perforation, pneumothorax, infection,
ectopy, nonsustained ventricular tachycardia, or throm-
boembolism leading to a pulmonary embolism.
20
While patients with isolated asymptomatic sinus
bradycardia or asymptomatic stable AV blocks (fi rst-
degree AV block or Mobitz Type I second-degree AV
block) require only electrocardiographic monitoring
while in the ED; patients with higher grade block or
new symptomatology require admission to the hospi-
tal. One study shows that 50% of patients presenting
to the ED with compromising bradycardia ultimately
require permanent pacing.
17
Section IV: Decision making
To establish the diagnosis of a benign bradycardia, •
an EKG should be obtained and the patient can be
discharged home with routine follow up.
Table 5-1. Pharmacologic doses in symptomatic
bradycardia.
18
Drug Dose
Atropine 0.5–1 mg IV q3-5 min (max 3 mg)
Epinephrine
2–10 g/min
Dopamine
2–10 g/kg/min
Glucagon 3 mg IV (followed by infusion at
3 mg/h if necessary)