, Jeremy N. Ruskin2 and Jeremy N. Ruskin3
(1)
Harvard Medical School Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
(2)
Harvard Medical School, Boston, USA
(3)
Cardiac Arrhythmia Service, Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
Abstract
Supraventricular arrhythmias are relatively common, can occur in people of all ages, and may be associated with symptoms, morbidity, and mortality. In this chapter, we review the diagnosis and treatment of this class of arrhythmias.
Abbreviations
AF
Atrial fibrillation
AFL
Atrial flutter
AT
Atrial tachycardia
AV
Atrioventricular
AVNRT
Atrioventricular nodal reentrant tachycardia
AVRT
Atrioventricular reentrant tachycardia
BB
Beta blockers
BBB
Bundle branch block
BPM
Beats per minute
CCB
Calcium channel blockers
CHD
Coronary heart disease
EKG
Electrocardiogram
EPS
Electrophysiologic study
HF
Heart failure
ICD
Implantable cardioverter defibrillator
IST
Inappropriate sinus tachycardia
LBB(B)
Left bundle branch (block)
LGL
Lown-Ganong-Levine syndrome
MAT
Multifocal atrial tachycardia
NCT
Narrow complex tachycardia(s)
NPJT
Non-paroxysmal junctional tachycardia
PJRT
Permanent junctional reciprocating tachycardia
POTS
Postural Orthostatic Tachycardia Syndrome
PV
Pulmonary vein
RBB(B)
Right bundle branch (block)
SA
Sinoatrial
SACT
Sinoatrial conduction time
SCD
Sudden cardiac death
SNRT
Sinoatrial nodal reentrant tachycardia
ST
Sinus tachycardia
SVT
Supraventricular tachycardia(s)
TTE
Transthoracic echocardiography
VF
Ventricular fibrillation
WCT
Wide complex tachycardia(s)
WPW
Wolff-Parkinson-White syndrome
Introduction
Supraventricular arrhythmias are relatively common, can occur in people of all ages, and may be associated with symptoms, morbidity, and mortality. In this chapter, we review the diagnosis and treatment of this class of arrhythmias.
Basics
Supraventricular arrhythmias are abnormal heart rhythms that originate in the atria or in the conduction system proximal to or within the Bundle of His
Atrial arrhythmias
Junctional arrhythmias
May be broadly divided into
Bradyarrhythmias (rate < 60 [or 50] beats per minute (bpm))
Tachyarrhythmias (rate > 100 bpm)
Ectopic rhythms at physiologic heart rates – originating at a non-sinus site of impulse formation
Many, but not all supraventricular arrhythmias can be diagnosed on the 12-lead surface electrocardiogram (ECG)
Bradyarrhythmias (Also See Chap. 25)
May be due to sinus arrest or marked decrease (transient or permanent) of automaticity of the sinus node pacemaker cells or to impaired impulse conduction
Sinus Bradycardia
Etiologies include
Vagotonia, including that observed in athletes
Acute myocardial infarction
Medication-induced (e.g. β blockers [BB], calcium channel blockers [CCB])
Atrial disease (cardiomyopathy, fibrosis)
Treatment of symptomatic sinus bradycardia includes
Withdrawal of medication(s) inducing bradycardia
Vagolytic agents (e.g. atropine) and/or sympathomimetic amines, in acute setting
Temporary or permanent cardiac pacing
Sinus Arrest
Sinus arrest or marked sinus bradycardia may be due
Atrial disease
Metabolic abnormalities (e.g. hyperkalemia)
Pharmacologic agents (e.g. BB, non-dihydropyridine CCB)
Severe hypervagotonia
Sinoatrial (SA) Exit Block
Classified in a fashion similar to atrioventricular (AV) block; may be first-, second-, or third-degree (high-degree) sinoatrial exit block
The time interval between SA nodal activation and that of the atria ranges from 50 to 120 ms
For examples, see Chap. 33, ECG #21
First-Degree SA Block
Difficult to diagnose on the surface ECG, diagnosis may require invasive testing
One protocol uses regular atrial pacing at 10 beats per minute higher than the spontaneous sinus rhythm rate for 8 beats and measures the post atrial pacing pauses
The sinoatrial conduction time (SACT) is then calculated as half of the difference between the post atrial pacing interval and the spontaneous sinus rate
Second-Degree SA Block
Second-Degree SA Wenckebach Block
May be suspected when there is a pattern of decreasing P-P interval leading to a pause (which is longer than the longest P-P interval and shorter than double the shortest P-P interval), though this pattern is not always present
The block occurs at the level of the SA node or within the perinodal tissue
Second-Degree SA Type II Block
In Type II second-degree SA block, constant P-P intervals are followed by a single missing P wave
The block is typically within the perinodal tissue
It may be challenging to distinguish Type I versus Type II SA block
Third-Degree (High-degree) SA Block
Manifest by absence of P waves of sinus origin (configuration), with an escape rhythm, which may originate in or near the Bundle of His (narrow complex) or lower in the His-Purkinje system (wide complex)
Sinoventricular Conduction
There is no atrial activity on the surface ECG, similar to sinus arrest
The electrical impulse travels from the sinus node through specialized atrial pathways to the AV node without exiting into the rest of the atrial myocardium
May be observed in severe hyperkalemia
Sick Sinus Syndrome (SSS; Tachy-Brady Syndrome)
Due to SA nodal and atrial electrical dysfunction
In the brady-tachy variant of SSS, atrial bradyarrhythmias may alternate with tachyarrhythmias including
Atrial fibrillation (AF)
Atrial flutter (AFL)
Other supraventricular/atrial tachycardias (SVT)
Although coronary heart disease (CHD) is commonly present in patients with SSS, the SA nodal artery may be normal in coronary arteriograms
AV nodal disease and increased risk for thromboembolism may be present
Over time (years), the patient may develop paroxysmal, then persistent AF
Long pauses may be observed after conversion of tachyarrhythmias (post-conversion pause)
Such pauses may be accompanied by syncope (Stokes-Adams attacks, as well as pause-potentiated lengthening of the QT interval, with attendant risk for ventricular arrhythmia)
Bradyarrhythmias may facilitate the occurrence of reentrant tachycardias by magnifying discrepancies in the duration of refractoriness as occurs with longer cycle lengths
Atrioventricular (AV) Block
Transient or persistent delay or interruption of conduction between the atria and ventricles
Etiologies include
Hypervagotonia
Medication-induced (e.g. BB, CCB, many antiarrhythmic drugs)
Fibrosis and calcification of the conduction system (Lev’s disease and Lenègre’s disease)
Endocarditis or myocarditis
Acute myocardial infarction (Type I in inferior, Type II in anterior) or chronic ischemic heart disease
Iatrogenic (following intracardiac procedures)
Congenital (e.g. complete heart block with narrow QRS)
Classified as first-, second-, or third-degree (complete) AV block
Symptomatic AV block without a reversible cause is a common indication for permanent pacemaker implantation
For examples, see Chap. 33, ECG #22–26
First-Degree AV Block
Not true block, but increased delay of atrioventricular conduction
Manifest on surface ECG as PR interval greater than 200 ms
There remains a 1:1 correspondence between P waves and QRS complexes
In the absence of other conduction system disease, has good prognosis
The presence of first-degree AV block, however, indicates increased risk for progression to higher degrees of AV block
In the presence of wide QRS (especially LBBB), the prolongation of the PR interval may be due to delay in the AV node, delay in the His-Purkinje system, or both
His bundle recordings usually clarify the diagnosis
Second-Degree AV Block
Second-Degree AV Wenckebach Block (Mobitz I)
Demonstrates a pattern of increasing PR interval leading to a pause (prolonged RR interval) in which there is a P wave that is not followed by a QRS complex
In typical Wenckebach periodicity, as the PR interval increases, each increment is progressively smaller, each RR interval is progressively smaller, and the RR “pause” is longer than the longest P-P interval and shorter than double the shortest P-P interval
Atypical cases are not infrequent
The block occurs at the level of the AV node
Second-Degree AV Type II Block (Mobitz II)
In Type II second-degree AV block, constant PR intervals are followed by P waves (with essentially constant P-P intervals) with one or more missing R waves
The block is typically below the level of the AV node and within the His Purkinje System
High-grade AV block refers to a low ventricular rate in the absence of third-degree (complete) heart block; in these situations, there is some relationship between the P waves and the QRS complexes (e.g. when there are periods of multiple P waves not followed by R waves)
2:1 AV Block
When there is a 2:1 relationship between P waves and R waves (and therefore only one PR interval), it is impossible to determine whether this represents Type I or Type II AV block on a single ECG
Factors supporting Type II (distal) AV block include Q waves and a wide QRS complex on the ECG as well as a normal or minimally prolonged PR interval on the conducted beats
Maneuvers that increase vagal tone and cause conduction delay at the level of the AV node (e.g. carotid sinus massage, Valsalva maneuver, coughing) may be helpful in distinguishing Type I from Type II AV block
If these maneuvers precipitate prolongation in the PR interval or increase in the degree of block, Type I AV block is suggested
Type II AV block is suggested by shortening of the PR interval or decrease in the degree of block with these maneuvers
Maneuvers that increase sympathetic tone and decrease delay at the level of the AV node (e.g. standing, arm exercise) will have the opposite effects
Decrease in the PR interval or the degree of block suggests Type I AV block
Increase in the PR interval or the degree of block suggests Type II AV block
Third-Degree (Complete) AV Block
Manifest by absence of atrioventricular conduction (AV dissociation)
P waves are present but demonstrate no direct relationship to R waves by one of the mechanisms listed above
The block is typically below the level of the AV node and within the His Purkinje System
There may be R waves with regular RR intervals if a stable escape rhythm is present below the level of the AV node, which may have narrow QRS configuration (if the escape rhythm originates in or near the Bundle of His) or wide QRS configuration (originating lower in the His-Purkinje system)
The rate of a stable escape rhythm may correlate with the location of block (slower escape rhythms imply block that is more distal in the His Purkinje System)
Pauses may precede the establishment of stable escape rhythm due to overdrive suppression at the onset of the complete block
In complete heart block, the P-P interval containing a QRS complex may be shorter than those that do not (ventriculophasic sinus arrhythmia)
When the sinus (or other supraventricular) rhythm has a rate similar to that of the escape rhythm, there may be isorhythmic AV dissociation
Typically demonstrates short, variable PR intervals, with P waves that may move in and out of the QRS complex
Tachyarrhythmias
Supraventricular tachyarrhythmias (SVT) may be due to reentry, enhanced automaticity or triggered activity
Demonstrate a narrow (<120 ms) QRS unless there is aberrant intraventricular conduction, preexisting BBB, or accessory pathway
Narrow QRS tachyarrhythmias:
Sinus tachycardia (ST)
Inappropriate sinus tachycardia (IST)
Sinoatrial nodal reentrant tachycardia (SNRT)
Atrial tachycardia (AT)
Atrioventricular nodal reentrant tachycardia (AVNRT)
Atrioventricular reentrant tachycardia (AVRT)
Non-paroxysmal junctional tachycardia (NPJT)
Atrial fibrillation (AF)
Atrial flutter (AFL)
Multifocal atrial tachycardia (MAT)
Narrow QRS tachyarrhythmias may be divided into three categories depending on the structures needed for their maintenance (and initiation):
ST, IST, and SNRT require the SA node
AVNRT and AVRT require the AV node
AT, AF, AFL, and MAT require only atrial tissue
Sinus Tachycardia (ST)
Sinus rhythm with a heart rate > 100 bpm at rest is usually due to normal sympathetic activation such as in exercise, anxiety, fever, etc.
ST may also be due to hyperthyroidism, chronic pulmonary disease, pulmonary embolism, severe anemia, hypovolemia and many other causes (sepsis, pheochromocytoma, stimulant drugs)
Elimination or amelioration of the underlying cause is only treatment needed in the great majority of cases
BB are indicated in rare instances (e.g. in angina, acute myocardial infarction)
Inappropriate Sinus Tachycardia (IST)
IST is ST occurring in persons with structurally normal hearts in the absence of a physiologic or pharmacologic stimulus for tachycardia such as hyperthyroidism, severe anemia, or other causes of ST mentioned above
Autonomic imbalance, increased beta-adrenergic sensitivity, abnormal sinus node automaticity are present in these patients
Most patients have both high resting heat rates and marked increase in rate with mild exercise
Slow exercise conditioning, BB, ivabradine, and sinus node modification (catheter ablation) have been used for therapy, although catheter ablation is rarely recommended
Postural Orthostatic Tachycardia Syndrome (POTS) is a related condition characterized by marked increase (>30 bpm or to 120 bpm) of the sinus rate with or without orthostatic hypotension upon assuming the standing position
Can be observed with dehydration, hypovolemia after prolonged bed rest
In idiopathic forms, distal (lower extremity) denervation, increased sympathetic activity, hypovolemia, and abnormal baroreflex function may be present
Treatment includes increased salt and water intake, mineralocorticoids (e.g. fludrocortisone), or adrenoreceptor agonists (e.g. midodrine)
SA Nodal Reentrant Tachycardia (SNRT)
An uncommon supraventricular tachyarrhythmia with abrupt onset and offset where reentry occurs within the SAN or between the SAN and the surrounding perinodal tissue
The configuration of the P waves is normal
Heart rates between 100 and 150 bpm are typical
Therapy is usually not necessary
In severe cases, vagal maneuvers, adenosine, BB, or CCB can terminate the arrhythmia
BB and CCB may used for prevention
When both the arrhythmia and the medications are not tolerated, SAN ablation or modification may be used, although this is rarely recommended
Atrial Tachycardia (AT)
Focal AT are usually paroxysmal, though incessant forms exist
May be due to reentry or triggered activity [1]
Commonly originate in the RA (frequently from the crista terminalis) or in the pulmonary veins or other areas within the LA
Rates vary between 130 and 250 bpm and the P wave configuration depends on the site of origin of the arrhythmia
Treatment includes correction of precipitating abnormalities (hypokalemia, digoxin), vagal maneuvers, and adenosine (usually not effective), BB, non-dihydropyridine CCB in stable patients, and class I and III membrane-active antiarrhythmic drugs
Example: Chap. 33, ECG #35
Multifocal Atrial Tachycardia (MAT)
Typically occurs in older patients with pulmonary disease [2]
There must be distinct P waves of at least 3 configurations (may include the sinus configuration) associated with varying (at least 3) PP intervals, PR intervals, and RR intervals
Treatment includes correction of electrolyte abnormalities, therapy for the underlying precipitating disease
BB and CCB and antiarrhythmic drugs may be helpful in some cases
Multifocal atrial rhythm (60–100 bpm) and multifocal atrial bradycardia (<60 bpm) may also occur
Example: Chap. 33, ECG #36< div class='tao-gold-member'>Only gold members can continue reading. Log In or Register to continue
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