Normal sinus node
Normal sinus rhythm (NSR) is an atrial rhythm caused by electrical activation that originates from the sinus node, a structure located in the area of the junction of the right atrium and superior vena cava. NSR P waves, representing atrial depolarization (but not sinus node activity itself), are upright in leads I and aVL and the inferior leads (II, III, aVF), indicating the high to low atrial activation pattern ( Fig. 1.1 ). The P wave in leads V 1 -V 2 may be upright, biphasic, or slightly inverted, whereas the P waves in leads V 3 -V 6 tend to be upright, indicating right to left atrial activation. The P-wave morphology may change with alterations in autonomic tone, heart rate, and atrial abnormalities such as hypertrophy. High vagal tone can be associated with a more inferior exit of the impulse from the sinus node, whereas high sympathetic tone can be associated with a more superior exit from the node.
Clinical Symptoms and Presentations
NSR is generally considered to have a rate of 60 to 100 beats per minute (bpm), although 50 bpm is still normal. Rate changes with alterations in autonomic tone; at rest, most individuals have their heart rate regulated by the vagus nerve.
Individuals with high vagal tone (such as those who are in excellent physical condition) may exhibit sinus arrhythmia, a normal rhythm in which the rate varies with respiration ( Fig. 1.2 ). In sinus arrhythmia, inspiration increases the rate and expiration decreases the rate. Sinus arrhythmia is common during sleep and in patients with obstructive sleep apnea, in which the decrease in rate can be substantial.
Various forms of sinus arrhythmia exist, including a non–respiration-dependent form that may indicate sinus node dysfunction (SND).
Ventriculophasic sinus arrhythmia is present when alterations in the sinus rate are due to atrioventricular (AV) block: The P-P intervals enclosing a QRS complex are shorter than P-P intervals not enclosing a QRS complex.
A change in sinus rate can be gradual or abrupt and can occur with change in body position and exercise. Patients who are in good physical condition generally have more gradual acceleration in sinus rate with exercise and a rapid slowing of the sinus rate at the end of exercise, compared with less physically fit individuals or individuals with heart disease. Higher resting sinus rates have been associated with increased risk for overall mortality.
Wandering atrial pacemaker (WAP) ( Fig. 1.3 ) occurs in association with high vagal tone and is a benign rhythm. In WAP, there are varying exit points of the sinus impulse from the sinus node or impulses that originate from the sinus node and wander from the node to the low atrium and back. WAP is often seen in patients with sinus arrhythmia. WAP should not be confused with “multifocal atrial rhythm” (see Fig. 3.13 ).
Approach to Management
Although sinus rhythm generally does not require any treatment, an inability to increase the sinus rate appropriately in response to increases in metabolic needs (“chronotropic incompetence”) may require permanent rate responsive cardiac pacing when it is documented to cause symptoms. Definitions of chronotropic incompetence are many and varied, and there is no general agreement as to its parameters.
Sinus node dysfunction, including sinus bradycardia and tachycardia-bradycardia syndrome
Sinus bradycardia (SB) ( Fig. 1.4 ) is generally defined as sinus rates of less than 60 bpm, although 50 bpm is likely within the normal range of rate. SB is often a normal finding in young, healthy adults, especially in athletes with high vagal tone. SB frequently occurs at rest and during sleep. In trained athletes or individuals with high vagal tone, sinus rates in the 40s and even at times in the 30s, especially during sleep, are not uncommon. SB may be associated with a narrow QRS complex or, in the presence of bundle branch block (BBB) or intraventricular conduction delay, with a wide QRS complex ( Fig. 1.5 ).
The sinus rate normally slows with age. SND from sinus node degeneration is more frequent in older persons. SND, sometimes termed “sick sinus syndrome,” is a very common arrhythmia and includes sinus pauses, sinus arrest, inappropriate SB, chronotropic incompetence, sinoatrial (SA) exit block, combinations of SA and AV conduction abnormalities, and tachycardia-bradycardia (tachy-brady) syndrome (e.g., paroxysmal or persistent atrial tachyarrhythmias with periods of bradycardia or postconversion sinus pauses) ( Fig. 1.6 ).
SB is often associated with sinus arrhythmia, escape rhythms (junctional and ventricular), accelerated rhythms (junctional and ventricular), atrial arrhythmias, WAP, or SA or AV Wenckebach-like periods. SB is usually benign but can be associated with certain conditions and diseases, including hypothyroidism, vagal stimulation, carotid sinus hypersensitivity, increased intracranial pressure, myocardial infarction (MI), and drugs such as β-adrenergic blockers (including those used for glaucoma), calcium channel blockers, amiodarone, sotalol, clonidine, lithium, and parasympathomimetic drugs. SB occurs in 14% to 36% of MIs and can be associated with AV block. The bradycardia usually resolves without the need for chronic therapy. SB is usually associated with inferior-posterior infarction (caused by increased vagal tone from stimulation of vagal afferents, the Bezold-Jarisch reflex). Clinical syndromes, such as neurocardiogenic syncope and some specific rhythm disorders such as tachy-brady syndrome, can be associated with symptomatic bradycardia as well as symptoms caused by rapid ventricular rates during atrial fibrillation or flutter; severe SB or sinus arrest can occur after spontaneous conversion prior to recovery of the sinus node. SB can be exacerbated by drugs that are used to slow AV node conduction during atrial arrhythmias.
Clinical Symptoms and Presentation
SB is asymptomatic in the vast majority of patients. When present, symptoms may include fatigue, effort intolerance, palpitations, dizziness, lightheadedness, near syncope, syncope, dyspnea, and angina. SND, including chronotropic incompetence, can impair cardiac output or exacerbate heart failure and can be associated with or trigger atrial arrhythmias (e.g., atrial fibrillation) and ventricular arrhythmias (e.g., torsades de pointes). Hemodynamic tolerance of SB is a function of heart rate (a rate of < 30 bpm is usually not well tolerated), underlying disease (less tolerated with poor ventricular function), and age (better tolerated in those < 50 years old). Tachy-brady syndrome may present with rapid palpitations during atrial arrhythmias and lightheadedness, dizziness, near syncope, and/or syncope during postconversion pauses. SND and/or tachy-brady syndrome can result from cardiac surgery, particularly associated with right atriotomy. SND is relatively common after heart transplantation, as the donor atria can be damaged by ischemia and by atrial anastomoses. The sinus node of the native heart rarely interacts with or affects the transplanted sinus rate. Other causes of SB and/or pauses in heart transplant patients include drugs (rare), trauma, and rejection.
Approach to Management
Evaluation or treatment often is unnecessary if the patient is asymptomatic. Treatment depends on the nature of the rhythm disturbance and is usually directed toward prevention of symptoms. Asystole can be life-threatening, but more often it causes symptoms and is due to vagal surges or SND. Asystolic pauses in a young, otherwise healthy person are generally due to vagal surges related to a neurocardiogenic response. An asystolic response after cardioversion, after a tachycardia, and in a patient who is older or has heart disease is often due to SND. Because SND can be subclinical but exacerbated by medical therapy, rate-slowing drugs should be avoided if possible.
A heart rate less than 30 bpm is an indication to evaluate further for treatment. Symptoms caused by SND can be difficult to assess. Exercise testing (if feasible with a temporary pacemaker if a previous exercise test showed inappropriate heart rate response) can help distinguish the cause of symptoms. If severe SND (i.e., SB associated with sinus exit block, sinus pauses, and sinus arrest) is suspected but cannot be documented by physical examination, telemetry monitor strip, or electrocardiogram (ECG), it can be evaluated further with a Holter monitor (low sensitivity), event monitor, implantable loop recorder, or electrophysiology test (low sensitivity and specificity).
The timing of the pauses or the bradycardia is important. It is not uncommon for a patient to develop SB or asystolic episodes during sleep. Although often caused by enhanced vagal tone, this may in some patients be related to sleep apnea. If pauses are seen during sleep on telemetry or Holter monitoring, sleep apnea should be considered and ruled out.
Short-term monitoring is used for the acute setting in the hospital. Such monitoring is capable of detecting all rhythm disturbances over a period of time. Admitting a patient with symptoms suggestive of bradycardia and then placing the patient on a monitor are usually unproductive steps unless the patient is having frequent and severe episodes. Thus, the first-line approach is long-term monitoring, as long as this approach is considered safe. External event recorders can document episodes of symptomatic SB, but their yield will depend on the frequency of the episodes. In some instances, these events can be difficult to capture because of their episodic nature; in these cases, an implantable loop recorder that continuously records and erases the cardiac rhythm (but has memory) may be optimal. This leadless implant can record and save episodes automatically or can be triggered manually.
The Holter monitor, a continuous 24-hour ambulatory monitor, has the advantage of determining all heart rhythms, symptomatic or asymptomatic, during the recording period and therefore helps determine the presence or absence of SND; however, correlative information relating rhythm and symptoms is often lacking.
Electrophysiology testing can be used to determine SND. The test includes a measurement for SA conduction time and sinus node recovery time. Both of these measurements have a low degree of sensitivity, and the specificity is essentially unknown. Thus, the utility of the electrophysiology test is relatively uncertain, and it is not routinely used to diagnose or exclude the arrhythmia.
Autonomic testing is generally not performed to determine the effect of parasympathetic and sympathetic activation as a cause for changes in heart rate. In patients with syncope in whom a neurocardiogenic reflex is suspected but not diagnosed with certainty, the tilt table test may be helpful in determining its presence. The tilt table test has an unclear specificity and sensitivity, and there is no gold standard to determine the presence or absence of the neurocardiogenic reflex and the relationship of this reflex to SB or asystole. The accuracy with which this test predicts the cause of syncope is dependent on both the protocol and the patient. In a patient with apparent asystolic episodes caused by suspected SND, the tilt table test may be helpful in distinguishing an autonomic reflex from SND.
For the patient with recent syncope or severe symptoms thought to be due to SND, hospital admission is required, especially for those with multiple medical problems, those who have been injured, and those who are older. Acute treatment is needed if there are severe symptoms or serious sequelae of bradycardia ( Tables 1.1 and 1.2 ).