Professional Documents
Culture Documents
5ACCSAP - Sinus Node Dysfunction and AV Conduction Disease
5ACCSAP - Sinus Node Dysfunction and AV Conduction Disease
ACCSAP
Table of Contents
Sinus Node Dysfunction and Atrioventricular Conduction Disease ...............................................................1
Sinus Node Dysfunction and Atrioventricular Conduction Disease ................................................................... 2
Introduction ....................................................................................................................................................... 3
Sinus Node Dysfunction ..................................................................................................................................... 4
Diagnosis and Treatment of Sinus and AV Conduction Disease ...................................................................... 17
Indications for Pacing ....................................................................................................................................... 19
Future Directions ............................................................................................................................................. 21
References ....................................................................................................................................................... 22
Sinus Node Dysfunction and Atrioventricular Conduction Disease
1
Sinus Node Dysfunction and Atrioventricular Conduction Disease
Author
Nazem Akoum, MD, MS, FACC
Disclosures
This author has nothing to disclose.
Learner Objectives
Upon completion of this module, the reader will be able to:
1. Classify causes of bradycardia as impulse generation in sinus node dysfunction (SND) or impulse
propagation in atrioventricular (AV) conduction disease.
2. Recognize that, in AV conduction disease, the site of block can be in the AV node or further
downstream in the His-Purkinje system.
3. Distinguish AV dissociation, in which the ventricular rate is faster than the atrial rate, from AV block,
in which the atrial rate is faster than the ventricular rate.
4. Match the appropriate workup, including exercise testing, ambulatory monitoring, and invasive
electrophysiology testing, with the suspected cause of bradycardia.
Introduction
Introduction
Under normal physiologic function, SA node depolarization propagates to the ventricles with high fidelity so
that the sinus rate is the same as the ventricular rate, ranging from 60-100 bpm at rest. Electromechanical
coupling allows for sequential AV contraction, which ensures normal blood flow between the cardiac
chambers and out to the great vessels.
Normal physiologic function also includes input from the autonomic nervous system, which influences the
heart rate and AV conduction by exerting its effects on the SA and AV nodes. Nervous system input is
delivered through the vagus nerves, which provide the parasympathetic arm, and postganglionic
sympathetic nerves originating in the sympathetic trunk. Variations in the heart rate and AV conduction are
therefore expected, with shifts in the autonomic balance. The sinus rate is expected to increase with stress
or activity (vagal withdrawal and sympathetic stimulation) and to decrease with rest (increased vagal tone
and sympathetic withdrawal). The vagal tone is normally higher than the sympathetic tone. When both are
withdrawn (e.g., pharmacologically using simultaneous atropine and beta-blockers or in a denervated
transplanted heart), the intrinsic sinus rate is about 100 bpm.
In the remainder of this module, abnormalities in the sinus node function and AV electrical conduction will
be discussed, including their clinical presentations, workup, and treatment interventions.
3
Sinus Node Dysfunction and Atrioventricular Conduction Disease
The etiology of SND is not clear and is • Age-related sinus node dysfunction also may be
likely multifactorial. Fibrotic infiltration associated with atrial fibrillation (AF), the so-called
of the sinus node region has been tachy-brady syndrome. This may be associated
reported and may slow the rate of with prolonged pauses, which can be symptomatic
after termination of AF. A common scenario would
spontaneous depolarization. Advanced
be an elderly patient with persistent AF who
age, atrial fibrillation (AF), hypertension, develops a prolonged pause on termination of AF.
valvular heart disease, ischemic heart This can be exacerbated by drugs, especially those
disease, and other conditions are that block sodium channels such as flecainide.
associated with SND. Aside from these
intrinsic problems with the sinus node,
SND can be extrinsic and caused by drugs, carotid sinus hypersensitivity or hypervagotonia, or metabolic
derangements (Table 1) .
In patients with AF or other tachyarrhythmias, sinus node disease manifests with the so-called tachy-brady
syndrome. The overdrive of atrial tachyarrhythmias suppresses SA nodal depolarization. Upon termination
of a tachyarrhythmia episode, a diseased SA node takes a long time to recover and initiate spontaneous
depolarization. The resulting pause and bradycardia may cause symptoms of lightheadedness, presyncope,
or syncope. Often, patients are treated with sodium channel blockers, beta-blockers, or calcium channel
blockers to suppress atrial tachyarrhythmias. These drugs exacerbate SND with more severe bradycardia and
prolonged pauses. Figure 2 shows an example of AF terminating with a prolonged pause and ensuing sinus
bradycardia.
Figure 1
Figure 1
5
Sinus Node Dysfunction and Atrioventricular Conduction Disease
Table 1
Table 1
AV = atroventricular.
Figure 2
Figure 2
Disorders of AV Conduction
Disorders of AV Conduction
Key Point
7
Sinus Node Dysfunction and Atrioventricular Conduction Disease
Recognizable ECG patterns of abnormal AV conduction include five different types of block: 1) first-degree
AV block; 2) Mobitz type I second-degree or Wenckebach block; 3) Mobitz type II second-degree block; 4)
third-degree AV block; and 5) advanced second-degree AV block.
Table 1
AV = atroventricular
First-Degree AV Block
First-Degree AV Block
In this pattern, the timing between the onset of the P wave and the onset of the QRS complex is longer than
the upper limit of normal conduction time of 200 msec. This is not truly a block in the conduction, as all
atrial depolarization waves traverse to the ventricles. First-degree AV block is commonly seen during periods
of high vagal tone (e.g., during sleep or treatment with beta-blockers or calcium channel blockers).
9
Sinus Node Dysfunction and Atrioventricular Conduction Disease
type I second-degree AV block is usually in the AV node. Like first-degree AV block, this pattern is seen
frequently during sleep or periods of high vagal tone and with drug treatment.
Figure 3
Figure 3
AV = atrioventricular.
Key Point
11
Sinus Node Dysfunction and Atrioventricular Conduction Disease
Figure 4
Figure 4
AV = atrioventricular.
Third-Degree AV Block
Third-Degree AV Block
In third-degree or complete heart block,
the electrical depolarizations of the Key Point
atrium are completely blocked from
• Atrioventricular (AV) block should be
conducting to the ventricles. Ventricular distinguished from AV dissociation, in which the
depolarization is provided through ventricular rate is faster than the atrial rate. In AV
backup or escape pacemakers found in block, the atrial rate is faster than the ventricular
the AV junction (junctional escape rate.
rhythm) or lower in the conduction
system or myocardial cells (ventricular
escape rhythm). The rate of the escape rhythm is slower than the sinus node and its morphology suggests its
13
Sinus Node Dysfunction and Atrioventricular Conduction Disease
site of origin (Figure 5). This form of AV dissociation observed in complete heart block is to be distinguished
from that present in ventricular tachycardia, in which the ventricular rate is faster than the atrial rate.
Figure 5
Figure 5
Note the presence of AV dissociation with no conduction from the atrium to the ventricle.
AV = atrioventricular.
15
Sinus Node Dysfunction and Atrioventricular Conduction Disease
Figure 6
Figure 6
Note that AV conduction is present for the first two beats, followed by loss of conduction for the following
two consecutive p waves, followed by resumption of conduction.
AV = atrioventricular.
17
Sinus Node Dysfunction and Atrioventricular Conduction Disease
chronotropic incompetence, in which they typically fail to achieve the expected heart rate with exercise.
When presyncope or syncope occurs without documented bradycardia or heart block on ambulatory
monitoring, yet suspicion for SND or AV conduction disease remains high, invasive electrophysiologic testing
is performed. SA node function is studied by measuring the sinoatrial node recovery time (SNRT), corrected
to different pacing rates. Corrected SNRT >525 msec is considered abnormal.
Intracardiac His bundle recording is occasionally used for assessing AV conduction disease. Findings such as a
split His bundle recording or eliciting infra-Hisian conduction block through rapid pacing or programmed
stimulation constitute evidence of a diseased AV conduction system. This invasive approach is reserved for
patients with unexplained and worrisome syncope.
19
Sinus Node Dysfunction and Atrioventricular Conduction Disease
Recommendations for pacing following myocardial infarction should include an assessment of the extent of
myocardial damage as well as the location of the obstruction and territory affected.
Table 2
AV = atrioventricular; CHB = complete heart block; ASDB = advanced second-degree block; HR = heart rate;
bpm = beats per minute; EPS = electrophysiology study; LV = left ventricular; SND = sinus node dysfunction.
References
1. Epstein AE, DiMarco JP, Ellenbogen KA, et al.; American College of Cardiology Foundation, American Heart
Association Task Force on Practice Guidelines, Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update
incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm
abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task
Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2013;61:e6-75.
2. Park DS, Fishman GI. The cardiac conduction system. Circulation 2011;123:904-15.
Future Directions
Future Directions
Certain genetic mutations have been linked to sinus node and conduction system disease. Sodium voltage-
gated channel alpha subunit 5 (SCN5A), hyperpolarization activated cyclic nucleotide gated potassium
channel 4 (HCN4), ryanodine receptor 2 (RYR2), calsequestrin 2 (CASQ2), and ankyrin-B mutations are
associated with SND, whereas mutations of SCN5A, sodium voltage-gated channel beta subunit 1 (SCN1B),
potassium inwardly rectifying channel subfamily J member 2 (KCNJ2), T-box transcription factor 5 (TBX5),
and NK2 homeobox 5 (NKX2-5) are associated with conduction system disease. Neuromuscular genetic
disorders including emerin, lamin A/C, and myotonic dystrophy type 1 are also associated with AV
conduction disease.2 Gene- and stem cell–based therapies are currently being investigated as therapeutic
options for patients with either genetic or degenerative abnormalities of the cardiac electrical conduction
system.
21
Sinus Node Dysfunction and Atrioventricular Conduction Disease
References
References
1. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS guideline on the evaluation and
management of patients with bradycardia and cardiac conduction delay: a report of the American
College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the
Heart Rhythm Society. J Am Coll Cardiol 2019;74:e51-e156.
2. Park DS, Fishman GI. Development and function of the cardiac conduction system in health and
disease. J Cardiovasc Dev Dis 2017;4:7.
23