Supraventricular Tachycardia

Etiology and Pathogenesis

Categorization of SVTs may be based on the site of origin, their mechanism, or their appearance on surface ECGs. Sites of origin include the sinus node, the atrium, the AV node, and the proximal His bundle. Some wide complex tachycardias are also supraventricular in origin and recognizing and differentiating them from ventricular tachycardias (VTs) are important. Fig. 37.1 details a stepwise algorithm to approaching a tachycardia based on the surface ECG appearance and response to clinical maneuvers.

Reentry is the most common mechanism of SVTs. Reentry requires two roughly parallel conducting pathways, shown as pathways A and B in Fig. 37.2 , that must be connected proximally and distally by conducting tissue, thus forming a potential electrical circuit. Second, one of the pathways (pathway B in our example) must have a refractory period that is substantially longer than the refractory period of the other pathway. Third, the pathway with the shorter refractory period (pathway A) must conduct electrical impulses more slowly than the other pathway. If all these seemingly implausible prerequisites are met, reentry can be initiated when an appropriately timed premature impulse is introduced to the circuit. The premature impulse must enter the circuit at a time when pathway B (the one with the long refractory period) is still refractory from the previous depolarization and at a time when pathway A (the one with the shorter refractory period) has already recovered and is able to accept the premature impulse.

The other main mechanism is abnormal automaticity of tissue that may arise in any of the previously described sites for SVTs. Tachycardias due to abnormal automaticity may be unifocal or multifocal. The least common mechanism of tachycardia is triggered reentry.

History

Most SVTs present with palpitations as a common sign; however, more ominous presentations such as shortness of breath, obtunded consciousness, chest discomfort, or severe chest pain may also be presenting signs. Sudden cardiac death (SCD) is an extremely rare form of presentation and occurs in <0.3% of patients per year. SCD occurs almost exclusively in patients with Wolf-Parkinson-White (WPW) syndrome with rapid AF that degenerates to ventricular fibrillation (VF).

Abrupt onset and termination suggests a pathological tachycardia, and the response to vagal maneuvers indicates that the AV node may be an integral part of the circuit, such as AV reentrant tachycardia (AVRT) or AV nodal reentrant tachycardia (AVNRT). Statistically, these account for >90% of SVTs. However, abrupt termination with vagal maneuvers may also be seen more uncommonly in focal atrial tachycardia (FAT) and some types of VTs. A described irregularity could predict AF, AFl, or AT with variable block, although the awareness of regularity versus irregularity may vary widely.

Palpitations in patients with SVT are usually characterized by sudden onset and termination, which are hallmarks in differentiating them from sinus tachycardia. Episodes may last for seconds or minutes, but in rare cases, episodes can last several hours and sometimes for days. The frequency is also variable, and although some patients may present with several episodes per day, the usual presentation is more commonly a few a year. The frequency and duration of episodes, and severity of symptoms often help guide how aggressively a provider must pursue a diagnosis or treatment plan. However, patients may be instructed in how to count their pulse rate manually, and there are currently numerous smart phone applications that can reliably record a heart rate.

SVTs are usually triggered by ectopic beats in most people. Substances like asthma medications, cold supplements, herbal remedies, and dietary supplements, especially those containing sympathomimetic compounds, alcohol, caffeine, or tobacco may predispose people to increased ectopy and trigger an episode of SVT. Tiredness, emotional upheavals, or stress can also lead to an adrenergic surge, precipitating SVT.

A medical history such as hyperthyroidism or catecholamine-producing tumors may predispose patients to episodic palpitations.

Examination

Examination is an important and essential tool because it can differentiate the patient who needs an emergent treatment from one who does not.

A physical examination should include the general appearance of the patient, heart rate, blood pressure, and jugular venous pressure (JVP). Physical maneuvers, using methods such as ice to the face, a carotid sinus massage, Valsalva, or coughing may be both diagnostic and therapeutic if the AV node is an integral part of the circuit, as described earlier. A slowing of the tachycardia with a vagal maneuver can uncover 1:1 AV conduction or help a bundle branch aberrancy recover and change a wide complex tachycardia to a narrow complex tachycardia. Presence of a murmur, displaced apical impulse, or a gallop can portend associated heart disease.

Diagnostic Tools

The ECG is the principal tool in diagnosis, especially during tachycardia. Many patients with SVTs may have normal resting ECGs, and longer term ECG monitoring may require a continuous ambulatory recorder, such as a 24-hour to 14-day Holter monitor. Event monitors may be useful in patients with infrequent symptoms. There are two types of event recording devices, one that has a capability of recording only when activated, and a second type, which is a looping recorder that continuously records the rhythm in addition to tracing several minutes before the recording and tracking the activation. Upper and lower rate parameters can also be programmed to record automatically on these devices. Again, these monitors are only useful if symptoms occur while the monitor is being worn; implantable loop recorders may be considered in patients with infrequent symptoms. These are especially useful for determining the presence or absence of an arrhythmia during symptoms of syncope or palpitations when conventional testing has proven inconclusive.

Other ambulatory tests such as an exercise stress to diagnose arrhythmias that occur during increased catecholamine surges may be useful.

Finally, an invasive electrophysiology (EP) study in which intracardiac catheters are used to record activity from several regions of the heart is useful for a definitive diagnosis and permanent treatment.

Electrocardiography

Most narrow complex tachycardias (QRS <120 ms) are SVTs, and wide complex tachycardias (QRS >120 ms) are VTs with some overlap ( Box 37.1 ). Regardless of the QRS width, noting the P waves and the relationship of the P waves to the QRS is extremely helpful. More P waves than QRS complexes suggest a tachycardia of atrial origin. When there is a 1:1 relationship between the two, it is important to determine if the rates are identical and if not, if there is a predictable relationship between the PP and RR intervals. The P-wave axis is useful in determining the origin of atrial activation. One method for subdividing a narrow complex tachycardia is to examine the relationship between the QRS complex and the P wave on the ECG. A line is drawn halfway between two successive QRS complexes, and if the P waves are buried in the tail end of the QRS or before the line, these are considered short RP tachycardias. If the P wave is noted after the line, these are considered to be long RP tachycardias. A description of these tachycardias is listed in Table 37.1 . Fig. 37.3 shows typical ECG recordings of the most common forms of SVT.

Box 37.1

Features to Support Ventricular Tachycardia in Wide Complex Tachycardia

• Supports ventricular tachycardia

• Atrioventricular dissociation

• Fusion beats

• Capture beats

• P and QRS rate and rhythm linked to suggest atrial activation, depends on ventricular activation

TABLE 37.1

Characteristics of Narrow Complex Tachycardia

Type	Ventricular Rate	Rhythm	Presentation	Prevalence	P-wave Contour	RP Relationship	Ventricular Response to Vagal Maneuvers	Mechanism
FAT	75–200	Regular May be irregular	Paroxysmal May be incessant	Rare	Abnormal (depends on site of origin)	Long (May Wenckebach)	Abrupt slowing with return to normal rate	Automatic
Atrial flutter	75–175	Regular May be regularly irregular	Paroxysmal	Common	Saw tooth	Long (May Wenckebach)	Abrupt slowing with return to normal rate	Reentrant
AF	120–160	Grossly irregular	Paroxysmal May be incessant	Common	Baseline undulation	—	Slowing, irregularity remains
AVNRT (typical)	120–250	Regular	Paroxysmal	Common	Retrograde Buried in terminal QRS	Short	Terminates	Reentrant
AVNRT (atypical)	100–250	Regular	Paroxysmal	Rare	Retrograde	Long	Terminates	Reentrant
ORT	130–280	Regular	Paroxysmal	Common	Retrograde	Short	Terminates	Reentrant
ART	130–280	Regular	Paroxysmal	Rare	Retrograde		Terminates	Reentrant
Preexcited AF	120–250	Irregular	Paroxysmal	Common	P waves difficult to see		May degenerate to VF
PJRT	120–200	Regular May be irregular	Incessant	Rare	Retrograde	Long	Terminates	Reentrant
Mahaim	130–250	Regular	Paroxysmal	Rare	Retrograde	Short	Terminates	Reentrant
JET	120–280	Regular	Paroxysmal	Rare	Retrograde (may be AV dissociation)	Short	None or slowing down	Automatic

AF , Atrial fibrillation; ART , antidromic reentry tachycardia; AV , atrioventricular; AVNRT , AV nodal reentrant tachycardia; FAT , focal atrial tachycardia; JET, junctional ectopic tachycardia; ORT , orthodromic reentry tachycardia; PJRT , persistent junctional reciprocating tachycardia; VF , ventricular fibrillation.

In some cases, P waves may not be discernable on the surface ECG and repeating an ECG at double standard or placing the arm leads in various chest positions to discern P waves (Lewis leads) may help. Esophageal recording, or intracavitary or epicardial recording may also be used. This is especially useful in postoperative patients who are often sedated and sometimes have temporary epicardial wires in place. Long rhythm strips and review of telemetry may be useful to look for perturbations and their resulting effects during the tachycardia.

Differential Diagnosis