intermittent and specific as: syncope.
the establishment of the correlation between symptoms and simultaneous changes
in rhythm is the key to diagnosis and management.
often chronic & nonspecific as: dizziness, fatigue, weakness, or heart
In such cases, the relation between symptoms and bradycardia is less certain.
I. Sinus Node Dysfunction (Sick Sinus Syndrome)
It is a common cause of bradycardia. The prevalence of sinus-node dysfunction
has been estimated to be as high as 1 in 600 patients over the age of 65
years, and the syndrome accounts for approximately 50 percent of pacemaker
implantations in the United States. It may be manifested as sinus bradycardia,
sinus pauses or arrest, sinus tachycardia, sinus brady-tachycardia synd,
atrial fibrillation or flutter.
Intrinsic cause: pathologic sinus node, or
Extrinsic causes: include the use of pharmacologic agents (e.g.,
(beta)-adrenergic blockers, calcium-channel blockers, digoxin, some
antihypertensive agents, and antiarrhythmic drugs), electrolyte imbalance,
hypothermia, hypothyroidism, increased intracranial pressure, and excessive
II. Atrioventricular-Conduction Disturbances
Unlike the sinus node, however, the atrioventricular node and bundle of His
provide a discrete connection between the atria and ventricles, so focal
injury from infarction, infection, or catheter-related trauma is a common
cause of problems.
First-degree atrioventricular block (PR Interval values over 0.2 second
with a retained 1:1 atrioventricular relation constitute first-degree
Second-degree atrioventricular block occurs when an organized atrial
rhythm fails to conduct to the ventricle in a 1:1 ratio but some
atrial-ventricular relation is maintained.
Mobitz type I second-degree AV block (Wenckebach block) is diagnosed
when the electrocardiogram shows a stable PP interval and a progressive increase
in the PR interval until a P wave fails to conduct. The PR increment usually
decreases with each beat in the cycle, so that the RR intervals actually
shorten. After the blocked P wave, the next PR interval returns to the initial
Mobitz type II second-degree AV block is most often associated
with disease of the His-Purkinje system. In 2:1 block, a narrow QRS complex
and associated periods of Wenckebach block, or simultaneous sinus slowing
("vagotonic block"), suggest that atrioventricular nodal block is present,
whereas a wide QRS complex suggests the presence of infranodal block.
Third-degree atrioventricular block is often referred to as "complete
heart block." In such cases, atrial activity and ventricular activity are
independent of each other. The location of the block is implied by the escape
rhythm. A narrow QRS complex, typically with a rate between 40 and 60 beats
per minute, implies the presence of atrioventricular nodal block. Wide QRS
escape rhythms at slower rates imply that the block is located in the
History and physical examination, esp. medication history, precipitating
factors and associated symptoms or signs. Severe nocturnal bradycardia should
raise a strong suspicion of obstructive sleep apnea. The diagnosis of
neurocardiogenic syncope, also commonly called vasovagal syncope, can usually
be made on clinical grounds. If the diagnosis is uncertain, testing while
the patient is lying in a head-up position on a tilt table may be used to
provoke an episode of syncope and confirm changes in heart rate and blood
pressure during such episodes.
His-bundle electrocardiography accurately measures atrioventricular
nodal and His-Purkinje conduction times and identifies the site of the block.
Its ability to assess the risk of future atrioventricular block is limited,
however, except at extreme HV intervals (the conduction intervals between
the His bundle and the ventricular myocardium). Programmed stimulation
test can be used to assess refractory periods and responses to changes
in atrial rate. Sinus-node function can be assessed both by measurement of
the magnitude of overdrive suppression (sinus-node recovery times) and by
direct and indirect measures of sinoatrial conduction.
The management of bradycardia is determined by the severity of symptoms,
the degree of correlation between symptoms and confirmed bradycardia, and
the presence of potentially reversible causes. When bradycardia, even
if extreme, is present only during sleep, pacing is usually not indicated.
Temporary Rx for Bradycardic cardiac arrest or symptomatic bradycardia:
Atropine 0.5 mg IV, may repeat q 3-5 min up to about 2 mg ( 0.03 - 0.04 mg/kg)
Pacemaker external (transcutaneous) or transthoracic, or transvenous (permanent
Dopamine 5-20 ug/kg/min infusion (Class IIb)
Epinephrine 2-10 ug/min infusion (Class IIb)
Isoproterenol 2- 20 ug/min infusion titrated to BP & Heart rate - use
with extreme caution.
There are few indications for intervention in patients with bradycardia who
are truly asymptomatic. The American College of Cardiology and American Heart
Association guidelines for the implantation of pacemakers (15) list only
the following as universally accepted (class I) indications
In asymptomatic patients:
Third-degree atrioventricular block with documented asystole lasting three
or more seconds (in sinus rhythm) or escape rates below 40 beats per minute
in patients while awake;
Third-degree atrioventricular block or second-degree atrioventricular Mobitz
type II block in patients with chronic bifascicular and trifascicular block;
Congenital third-degree atrioventricular block with a wide QRS escape rhythm,
Ventricular dysfunction, or bradycardia markedly inappropriate for age.
Potential (class II) indications for pacing in asymptomatic patients include
third-degree atrioventricular block with faster escape rates in patients
who are awake,
second-degree atrioventricular Mobitz type II block in patients without
bifascicular or trifascicular block, and
the incidental finding on electrophysiologic study of block below or withinthe
bundle of His or an HV interval of 100 msec or longer.
For symptomatic patients:
the correlation between symptoms and confirmed bradycardia and the potential
reversibility of causative factors are the keys to appropriate decision making.
Symptoms definitely related to simultaneous, confirmed bradycardia that is
caused by intrinsic sinus-node dysfunction or atrioventricular block should
be treated with permanent pacing.
The sinus bradycardia or atrioventricular nodal block in the settings of
myocardial infarctio or infection rarely requires permanent pacing.
Permanent damage occurs more readily to the bundle of His than to the sinus
and atrioventricular nodes, and even transient complete atrioventricular
block in the His-Purkinje system due to infarction or infection justifies
the insertion of a pacemaker.
In cases in which only nonspecific symptoms, such as fatigue, dizziness,
or heart failure, are present and the associated bradycardia is not extreme,
pacing is rarely indicated. Among patients with recurrent unconfirmed syncope
and chronic bifascicular or trifascicular block, pacing is indicated if other
likely causes (e.g., ventricular tachycardia) have been ruled out.
When symptomatic bradycardia is due to extrinsic causes, clinical judgment
is required. Although a change in therapy should be considered if drug-induced
bradycardia is suspected, pacing may be an acceptable approach if no agent
with equivalent efficacy is available. Occasionally, use of pindolol, a
(beta)-adrenergic blocker with intrinsic sympathomimetic activity, may prevent
bradycardia while the patient is at rest.
Pacing is also appropriate in patients with the bradycardia-tachycardia syndrome
if the agents required for control of the ventricular rate during atrial
arrhythmias cause bradycardia during sinus rhythm. Atrium-based pacing is
preferred in patients with sinus-node dysfunction because it reduces the
incidence of atrial fibrillation, pacemaker syndrome, and thromboembolism.
(45) Dual-chamber pacing is needed if atrioventricular block is also present.
When bradycardia occurs only in specific situations, patient education and
prevention strategies should be tried first.
The role of pacing in patients with neurocardiac syncope and confirmed
bradycardia is controversial. Many of these patients also have a prominent
vasodepressor component to their syndrome, and standard pacing techniques
may not completely relieve symptoms. New algorithms that include short periods
of high-rate pacing when bradycardia is detected may be more effective. (46)
Patient education and pharmacologic trials are indicated before pacing in
most patients with neurocardiac syncope.
Bradycardia is a common clinical finding. The clinician must determine the
relation between bradycardia and symptoms and differentiate between physiologic
and pathologic conditions. In cases in which bradycardia is symptomatic and
irreversible, pacemaker therapy is highly effective for the relief of symptoms.
Heart Rate in Normal Subjects
Spodick and others estimated that the "normal" range of heart rates in the
afternoon was 46 to 93 beats per minute for men and 51 to 95 beats per minute
for women. Nocturnal rates are slower, decreasing during sleep by an
average of 24 beats per minute in young adults and by 14 beats per minute
in those over 80 years of age. Ambulatory electrocardiography in healthy,
asymptomatic persons has shown that transient bradyarrhythmias are common
during sleep. Heart rates between 30 and 35 beats per minute, sinus pauses
of 2.5 seconds or less, sinoatrial block, junctional rhythms, and first-degree
and second-degree atrioventricular nodal block are common enough during sleep
to be considered normal variants. Trained athletes are particularly prone
to bradycardia, with heart rates below 40 beats per minute common at rest
. In one series, sinus pauses lasting between two and three seconds were
found in 37 percent of athletes during sleep. In view of these findings,
the current guidelines of the American College of Cardiology and the American
Heart Association for pacemaker implantation suggest that asymptomatic episodes
of sinus bradycardia (with the heart rate as low as 30 beats per minute),
sinus pauses of up to three seconds, and atrioventricular nodal Wenckebach
block should be considered to be within the normal range. (15) Even if more
pronounced bradycardia is documented, reversible causes may be responsible.
For example, profound bradycardia often develops in patients with obstructive
sleep apnea and hypoxia but may be eliminated if the sleep apnea is appropriately
Pitcher et al. reviewed Holter-monitor tracings from 66 asymptomatic patients
with chronic atrial fibrillation and found that two thirds of them had pauses
longer than two seconds and 20 percent had pauses longer than three seconds.
Therefore, they concluded that daytime pauses of up to 2.8 seconds and nighttime
pauses of up to 4.0 seconds during atrial fibrillation should be considered
to be within expected limits. On the basis of these data, it is wise to interpret
isolated, asymptomatic pauses during atrial fibrillation conservatively.