Sinus Node Dysfunction (“Sick Sinus Syndrome”)
- Sinus bradycardia: Sinus rate of less than 60 bpm.
- Sinoatrial exit block, type I: Progressively shorter P-P intervals,
followed by failure of occurrence of a P wave.
- Sinoatrial exit block, type II: Pauses in sinus rhythm that
are multiples of basic sinus rate.
- Sinus arrest, sinus pauses: Failure of occurrence of P waves
at expected times.
Atrioventricular (AV) Block
- First degree: Prolonged PR interval more than 0.2 seconds.
- Second degree
- • Type I: Progressive increase in PR interval, followed by failure
of AV conduction and nonoccurrence of a QRS complex
- • Type II: Abrupt failure of AV conduction not preceded by increasing
- High degree: AV conduction ratio 3:1 or greater.
- Complete: Independent atrial and ventricular rhythms, with
failure of AV conduction despite temporal opportunity for it to
The clinical presentation of patients with conduction system disease is determined by the existence of three underlying abnormal conditions:
bradycardia, inability to increase the heart rate in response to increases in metabolic needs, and atrioventricular (AV) dyssynchrony (inappropriately timed atrial and ventricular depolarization and
Pathophysiology & Etiology
Sinus node dysfunction (“sick sinus syndrome”) is usually due to a degenerative process that involves the sinus
node and sinoatrial (SA) area (Table 22–1).
Often, the degenerative process and associated fibrosis also involve
the AV node and its approaches as well as the intraventricular conduction
system; as many as 25–30% of patients with sinus node
dysfunction have evidence of AV and bundle branch conduction delay
Table 22–1. Causes of Sinus Node
| Save Table
Table 22–1. Causes of Sinus Node
|Acute myocardial ischemia or infarction|
Rate-sparing calcium channel blockers
Digitalis (with high prevailing vagal tone)
Class I antiarrhythmic agents
Class III antiarrhythmic agents (amiodarone, sotalol)
Respiratory sinus arrhythmia, in which the sinus rate increases with inspiration and decreases with expiration, is not an abnormal
rhythm and is most commonly seen in young healthy persons. Nonrespiratory
sinus arrhythmia, in which phasic changes in sinus rate are not
due to respiration, may be accentuated by the use of vagal agents,
such as digitalis and morphine, and is more likely to be observed
in patients who are older and who have underlying cardiac disease, although
the arrhythmia is not itself a marker for structural heart disease;
its mechanism is unknown. Ventriculophasic sinus arrhythmia is an
unusual rhythm that occurs during high-grade or complete AV block;
it is characterized by shorter P-P intervals when they enclose QRS
complexes. The mechanism is not known with certainty but may be
related to the effects of the mechanical ventricular systole: the
ventricular contraction increases the blood supply to the sinus node,
thereby transiently increasing its firing rate; the resulting increase
in intra-atrial pressure causes inhibition of the sinus rate. Ventriculophasic
sinus arrhythmia is not a pathologic arrhythmia and should not be
confused with premature atrial depolarizations or SA block. None
of the sinus arrhythmias indicates sinus node dysfunction.
Sinus node dysfunction is present when marked sinus bradycardia, pauses in sinus rhythm (sinus arrest), SA block, or a combination
of these exist (Figures 22-1, 22-2, 22-3, 22-4, and 22-5). Some clinically normal individuals without structural heart disease can experience significant sinus bradycardia
and prolonged sinus pauses under conditions of high vagal tone such
as sleep. In some patients a trigger, such as vomiting or coughing,
can be identified; in other patients, high levels of acetylcholine
may be responsible. Vagal stimulation, often from an identifiable
trigger (Table 22–2), is commonly
responsible for significant sinus bradyarrhythmias occurring in patients
in an intensive care setting.
Ladder diagrams illustrating sinus bradycardia and sinoatrial block, types I and II. ECG, electrocardiogram; SA, sinoatrial; SAA,
sinoatrial area; SN, sinoatrial node.
This 83-year-old woman was being treated for congestive heart failure and was receiving 200 mg/day of amiodarone for episodes of nonsustained ventricular tachycardia. She complained of profound effort fatigue but no symptoms of heart failure. Electrocardiogram reveals an atrial bradycardia at a rate of about 38/min. The P waves vary in morphology, suggesting some wandering of the atrial pacemaker. Left axis deviation and a left intraventricular conduction delay with ST and T wave abnormalities are present. The atrial bradycardia was presumed to be due to the amiodarone, which was discontinued, resulting in appreciable increase in a stable sinus rhythm, with amelioration of the patient’s effort
Continuous modified lead-II ambulatory electrocardiographic recording in a patient with recurrent presyncopal spells. Sinus
rhythm is present in the top strip; the second strip shows marked sinus slowing, followed by a 17-second period of sinus arrest without the appearance of a QRS escape rhythm. Sinus rhythm reappears in the fourth strip, gradually increasing its rate until stable rhythm is restored in the bottom strip. The absence of an escape rhythm raises the possibility of diffuse disease of the conduction system and impulse-generating tissue.
Progressive decrease in P wave cycle lengths followed by a pause in P wave rate, indicating type I second-degree sinoatrial block. The pauses in sinus rate are less than twice the preceding sinus cycle lengths, satisfying the criteria for Wenckebach periodicity. MCL, modified chest ...
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