Techniques for Supraventricular Tachycardias

Introduction

Patients in the emergency department frequently complain of palpitations, heart fluttering, or a rapid heart beat, and this is often coupled with weakness, chest pain, or dizziness. The physician must determine the exact rate, rhythm, origin, and cause of the tachycardia and then “gain control” of the heart rate (HR) by slowing or normalizing it or by treating the underlying cause. Determining the cause, origin, and rhythm of the tachycardia is often complicated by the fact that the underlying rate may be very fast (in excess of 150 to 300 beats/min), which makes interpretation of the electrocardiogram more difficult. Furthermore, the sources or pacemakers producing or facilitating the tachyarrhythmia may be from one or multiple locations: in the sinoatrial (SA) node, in one or more ectopic atrial foci, in the atrioventricular (AV) node, or in the ventricular free walls or septum. There may also be an abnormal conduction pathway between the atria and the ventricles. In some conditions, one or more “pacemakers” can be discharging simultaneously. To facilitate the diagnostic process, discrimination between atrial and ventricular electromechanical activity must be attempted. This chapter provides a framework to facilitate the decision-making process with a focus on emergency interventions for various tachydysrhythmias.

Techniques for unmasking, identifying, and treating the various forms of tachyarrhythmias are presented in Box 11-1. This chapter addresses the utility of the vagal reflex in treating and managing various pathophysiologic conditions and the use of medications and cardioversion as they apply to the treatment of various supraventricular tachycardias (SVTs). The major focus is on the evaluation and treatment of SVTs. A more comprehensive discussion regarding the treatment of ventricular tachycardia (VT) is provided in Chapter 12.

Overview and Significance: Anatomy and Physiology of Supraventricular Tachycardia

Normally, the human heart beats at approximately 80 beats/min (±20 beats/min). If the HR exceeds 100 beats/min, it is called tachycardia. If it drops below 60 beats/min, it is called bradycardia. The heart’s ability to increase the rate of a normal sinus rhythm is primarily related to age: the maximum HR possible with a sinus tachycardia is approximately 220 beats/min minus age, with normal variations as high as 10 to 20 beats/min. As an example, a 60-year-old man cannot usually mount a sinus tachycardia higher than 160 beats/min in response to sepsis, exercise, fever, anxiety, or adrenergic stimulation. Faster rates would indicate a pathologic cardiac rhythm, not a physiologic response.

There are two general categories or types of tachycardias: SVT and VT. The term supraventricular tachycardia describes a rapid HR that has its electrochemical origin either in the atria or in the upper portions of the AV node. Ventricular tachycardias originate in the ventricular free walls or interventricular septum (or both). VTs can quickly become unstable and require special consideration (Fig. 11-1F).

Figure 11-1 Tachydysrhythmias. A, Sinus tachycardia. B, Supraventricular tachycardia (SVT). C, Atrial fibrillation. D, Atrial flutter. E, SVT with aberrancy. F, Ventricular tachycardia.

SVTs can be further classified as narrow-complex (QRS duration <0.12 second) and wide-complex tachycardias (QRS duration >0.12 second). The rhythms of these dysrhythmias can be regular or irregular. Examples of narrow-complex SVTs are sinus tachycardia (Fig. 11-1A); atrial fibrillation (AF) (Fig. 11-1C); atrial flutter (Fig. 11-1D); AV nodal reentry; atrial tachycardia (Fig. 11-1B), both ectopic and reentrant; multifocal atrial tachycardia (MAT); junctional tachycardia; and accessory pathway-mediated tachycardia. The term wide-complex tachycardia describes rhythms such as VT (Fig. 11-1F), SVT with aberrancy (Fig. 11-1E), or a preexcitation tachycardia facilitated by an accessory pathway between the atria and ventricles.

Tachycardias may be benign or can have significant physical effects on the patient. When the HR is 60 beats/min, approximately one cardiac cycle of contraction (systole) and relaxation (diastole) occurs per second. The excitation for cardiac contraction typically originates in the SA node, the intrinsic “pacemaker” of the heart. The pacemaker impulse traverses across and depolarizes the atria, which causes atrial contraction or systole. Subsequently, the depolarization reaches the AV node. On initiating depolarization of the AV node, the conduction velocity of this depolarizing impulse transiently decreases (i.e., undergoes “decremental conduction”) so that the ventricles can fill with blood from the antecedent atrial contraction. (Remember: The duration of diastole must be roughly twice the duration of systole to allow adequate ventricular filling.) The AV node also serves as a gate or selective block to prevent an excessive number of depolarizing impulses from reaching the ventricles when the atrial rate is accelerated.

Immediately thereafter, this depolarizing wave accelerates as it travels down the bundle of His to the Purkinje fibers and causes ventricular depolarization leading to contraction. Subsequently, the ventricles begin to relax (i.e., enter diastole and begin to fill with blood before the next depolarization). This describes the events of one cardiac cycle or heartbeat. The changes in electrochemical voltage during these events are depicted on the electrocardiogram in the usual sequential PQRST (the P wave indicates SA nodal depolarization, the PR interval denotes atrial depolarization followed by activation of the AV node, and the QRS complex summarizes electrical activity during ventricular depolarization) (Fig. 11-2).

Figure 11-2 Electrocardiographic and membrane potential of ventricular cells.

The discharge rate of the SA node is usually modulated by a balance of input from the sympathetic and parasympathetic nerves (i.e., the autonomic nervous system). Sympathetic input to the heart is provided by the adrenergic nerves, which innervate the atria and ventricles, and by circulating hormones such as epinephrine and norepinephrine, which are released from the adrenal gland and cause the HR to increase. Parasympathetic input to the heart is provided by the vagus nerve (cranial nerve [CN] X) fibers. These nerve fibers innervate the SA and AV nodes. Vagal output to the SA node causes slowing of the HR by decreasing the depolarization rate of the “intrinsic pacemaker,” whereas vagal output to the AV node enhances nodal blockade of atrial depolarization impulses to the ventricles. Hence, vagal stimulation results in slowing of electrical activity, examples being termination of an SVT, slowing of the ventricular rate of AF (via the AV node), or simply producing a sinus bradycardia (via the SA node). Under normal physiologic circumstances, the HR is modulated to meet the metabolic needs of the body’s peripheral circulation. Changes in AV electrochemical events (i.e., rates and rhythms) are manifested as changes in the electrocardiographic intervals and waveforms.

As noted earlier, SVT rhythms can be either sinus (i.e., originating in the SA node: sinus tachycardia) or ectopic (i.e., originating in atrial myocytes above the ventricles). The rate of discharge of the SA node often varies as a result of various physiologic and pharmacologic stimuli, including fever, hypovolemia, shock, anemia, hypoxia, anxiety, pain, cocaine, and amphetamines. These conditions often require or precipitate increased blood flow and hence cardiac output (CO) to peripheral tissues. This increase in peripheral blood flow or CO is accomplished by an increase in HR (Remember: CO = HR × SV [stroke volume]). These are usually normal, benign physiologic responses to various stimuli or triggers. Direct treatment of these rhythms is not generally necessary; however, determining and treating the cause of the sinus tachycardia usually eliminates the fast HR. Nonetheless, when single or multiple ectopic, spontaneously discharging foci develop in the atria or upper portions of the AV node, they can begin to “take over” or “override” the normal pacemaker activity in the heart (i.e., the SA node) and produce a rapid HR exceeding 100 beats/min. These foci may develop as a result of increased irritability or automaticity of atrial myocytes secondary to electrolyte abnormalities, hypoxia, pharmacologic agents, or atrial stretch caused by volumetric overload. If these foci are not treated or suppressed and the atrial depolarization rate proceeds to accelerate to rates greater than 150 beats/min (i.e., the heart is beating in excess of 2 beats/sec) and the impulses get through the AV node to the ventricles, the time for diastolic filling of the ventricles will be compromised and result in a precipitous drop in SV. This will ultimately cause a drop in CO regardless of the increase in HR. Furthermore, as CO begins to drop, mean arterial blood pressure (MABP) will decrease and cause hypoperfusion of the brain and other peripheral tissue (Remember: MABP is the product of CO times total peripheral resistance [TPR]—MABP = CO × TRP). Treatment of this tachycardia can be achieved pharmacologically by suppressing the automaticity of myocytes with medications (e.g., calcium channel blockers or β-blockers) and subsequently treating the underlying cause or causes—hypoxia, electrolytes, and the like. Decreasing the hemodynamic consequences of this arrhythmia requires increasing the “blocking” of these impulses from reaching the ventricles via the AV node. This can be done by enhancing vagal input to the AV node or by pharmacologic enhancement of AV blockade. Multiple rapid depolarizations of the atria, which are conducted to the ventricles, can ultimately have a bimodal type of response: a modest increase in HR will cause an increase in CO, whereas a massive increase in the atrial rate with a concomitant increase in the ventricular rate will cause a drop in CO. This can lead to an unstable patient with signs and symptoms such as confusion, altered mental status, or persistent chest pain. When the patient becomes unstable, immediate treatment is indicated.

In addition to areas of increased automaticity that can precipitate SVTs, a condition described as reentry can also cause SVTs. Reentry describes a condition whereby a depolarization impulse is being propagated down a pathway in which some of the myocytes are still in the effective refractory period and a “unidirectional block” is present and preventing the impulse from traveling normally down this pathway. However, as the impulse travels around the area of the “unidirectional block,” the tissue allows the depolarization front to travel in the opposite (antidromic) direction, back to the initial point of entry into this pathway. This allows the depolarization wavefront to restimulate the myocytes and initiate another propagated depolarization through the same tract (Fig. 11-3). If this condition persists and these impulses stimulate the atria effectively and traverse the AV node, an SVT may develop as a result of reentry. Suppression of this dysrhythmia can be achieved by terminating the conditions favoring reentry, and the hemodynamic consequences may be attenuated by enhancing AV nodal blockade of the ventricles (e.g., through vagal stimulation, medication), thus slowing the ventricular response to this condition. Termination of reentry can be accomplished by either pharmacologic modification of the myocytes to render them refractory to depolarization impulses for a longer period in a stable patient or by synchronized cardioversion to uniformly depolarize the myocytes and terminate the conditions favoring the SVT.

Figure 11-3 Cardiac conduction with supraventricular tachycardia. A, Normal depolarization down paths 1 and 2 that will “extinguish” or “cancel out” normal depolarization/repolarization and conductance at point 3. B, Abnormal. 1, Normal conduction; 2, delayed/slowed conduction with a unidirectional block; 3, normal conduction pathway.

Another situation to consider in the development and propagation of SVTs is the presence of preexcitation or an accessory pathway between the atria and the ventricles. Arrhythmias secondary to these causes can be managed with the use of appropriate pharmacologic agents to either suppress conduction through the accessory pathway or block AV nodal transmission without enhancing conduction through the accessory pathway.

To complete this discussion, we must also consider that there may be the possibility of an interventricular conduction delay being present before the development of an SVT. If this is the case, the SVT may appear as a wide-complex tachycardia and can be confused with other dysrhythmias. However, an even more dangerous situation can occur if a wide-complex tachycardia of ventricular origin (VT) is present and is misdiagnosed as an SVT with aberrancy. As a result, the patient could be treated inappropriately, with the intervention causing suppression of ventricular activity and ultimately cardiac arrest. VT with a pulse is considered an unstable rhythm that often requires synchronized cardioversion (discussed in more detail in Chapter 12).

The clinician must have a means of slowing down and sorting out these physiologic events so that appropriate diagnosis and treatment or intervention decisions can be made. With the application of vagal maneuvers, in some cases the activity of the atria and ventricles may be isolated enough to facilitate a correct diagnosis. An understanding of the underlying pathophysiology will guide appropriate treatment.

Vagal Maneuvers

Background Anatomy and Physiology

The physiologic effects of pressure on the carotid sinus have been known for centuries. They were first described in the medical literature in 1799, when Parry wrote a treatise titled “An Inquiry into Symptoms and Causes of Syncope Anginosa, Commonly Called Angina Pectoris.”¹ He noted that pressure on the bifurcation of the carotid artery produced dizziness and slowing of the heart. The term carotid is derived from the Greek karos, which means heavy sleep.

The bifurcation of the common carotid artery possesses an abundant supply of sensory nerve endings located within the adventitia of the vessel wall (Figs. 11-e1 and 11-e2). These nerves have a characteristic spiral configuration; they continually intertwine along their course and eventually unite to form the carotid sinus nerve. The afferent impulses travel from the carotid sinus via Herring’s nerve or the carotid sinus nerve to the glossopharyngeal nerve (CN IX) and then to the vasomotor center in the medullary area (nucleus tractus solitarius) of the brainstem (Fig. 11-e3). The vasomotor center is composed of three distinct areas, each with a distinctive function. The vasomotor center is located bilaterally in the reticular substance of the medulla and in the lower third of the pons. The center transmits efferent impulses downward through the spinal cord and the vagus nerve. The efferent impulses, which originate in the medial portion of the vasomotor center, travel along the vagus nerve (CN X) to the sinus node and the AV node of the heart. The vasomotor center’s medial portion lies in immediate apposition to the dorsal motor nucleus of the vagus nerve (CN X). These impulses in the medial portion of the vasomotor center decrease HRs. Efferent impulses originating in the lateral areas of the vasomotor center travel along the sympathetic chain to the heart and to the peripheral vasculature. These sympathetic impulses control either vasoconstriction or vasodilation of the vascular system. A balance between vasoconstriction and the vasodilation maintains proper vasomotor tone.^2,3

Figure 11-e1 The carotid sinus.

Figure 11-e2 Stretch receptors of the carotid sinus

Figure 11-e3 Schematic depicting the arterial baroreceptor reflex. CVLM, caudal ventrolateral medulla; NTS, nucleus tractus solitarius; RVLM, rostral ventrolateral medulla; SNS, sympathetic nervous system; vaginal nuclei, dorsal motor nuclei, nucleus ambiguous.

The afferent nerve endings in the carotid sinus are sensitive to MABP and to the rate of change in pressure. Research indicates that pulsatile stimuli are more effective than sustained pressure in evoking a response. Elevated blood pressure stretches the baroreceptors, which leads to increased firing of the afferent nerve endings.² As for low–blood pressure states, the carotid sinus baroreceptors are exquisitely sensitive to low blood pressure. Hypotension causes a drop in afferent firing.²

The parasympathetic and sympathetic nervous systems play independent but coordinated roles in the carotid sinus reflex. Increased firing of the carotid sinus results in reflex stimulation of vagal activity and reflex inhibition of sympathetic output. The parasympathetic effect is almost immediate; it occurs within the first second and causes a drop in HR. The sympathetic effect, which causes a drop in blood pressure through vasodilation, becomes manifested only after several seconds.⁴ The changes in blood pressure may not take full effect until a minute has elapsed.⁵ The changes in blood pressure and HR are independent phenomena. Epinephrine blocks the reduction in blood pressure, whereas a fall in HR is blocked by the administration of atropine.

A cerebral effect, characterized by loss of consciousness, was once thought to be due to stimulation of the carotid sinus. However, it is seen only when sufficient pressure is exerted to occlude the more distal temporal artery pulsation and when contralateral carotid disease is present. This cerebral effect is now believed to be a result of decreased bilateral cortical perfusion.

The parasympathetic branch of the carotid sinus reflex supplies the sinus node and the AV node. The effect of parasympathetic stimulation is to slow the HR. The SA pacemaker is more likely to be affected than the AV node, except when digitalis has been administered.2,5,6

Indications for Vagal Maneuvers

Vagal maneuvers are potentially useful in attempting to slow down or break an SVT. They are also indicated in settings in which slowing conduction in the SA or AV node could provide useful information (Box 11-2 and Figs. 11-4A-E and 11-5A-D). Such settings include patients with wide-complex tachycardia, in whom carotid sinus massage (CSM) aids in the distinction between SVT and VT. CSM can elucidate narrow-complex tachycardia in which the P waves are not visible or aid in detection of suspected rate-related bundle branch block or pacemaker malfunction. After CSM, a wide-complex SVT may be converted to normal sinus rhythm, P waves may be revealed after increased AV node inhibition, or ventricular complexes may narrow as the ventricular rate slows. Because CSM slows atrial and not ventricular activity, AV dissociation may be seen more easily and is indicative of VT (see Fig. 11-4). In rapid AF or atrial flutter with a 2 : 1 block, either P waves or irregular ventricular activity with absent P waves may be revealed (Figs. 11-5A and B). Sinus tachycardia may also be more apparent once P waves are unmasked by slowing the SA node (see Figs. 11-4C and D). Adenosine may be used for the same diagnostic purpose in these situations as well.⁷ In order of decreasing frequency, the electrocardiographic changes seen with CSM and vagal maneuvers are presented in Box 11-3.

Box 11-2 Potential Observations with Vagal Maneuvers in the Management of Tachydysrhythmias

1. Vagal maneuvers may slow the atrial rate in VT or complete heart block and may therefore demonstrate previously hidden P waves or obvious (AV) dissociation.

2. Abrupt changes in the heart rate without conversion are a result of increasing AV block.

3. Gradual slowing of the ventricular rate suggests the presence of sinus rhythm. Only rarely do vagal maneuvers decrease AV conduction in the presence of a sinus mechanism.

4. The dysrhythmias most likely to convert to sinus rhythm are PAT and paroxysmal nodal tachycardia.

5. Dysrhythmias that are associated with AV conduction defects (PAT with block, atrial flutter, and atrial fibrillation) infrequently convert to a sinus rhythm, but the ventricular rate slows. Rarely, atrial slowing will be sufficient to allow 1 : 1 AV conduction, which may actually increase the ventricular rate (see Fig. 11-6).

AV, atrioventricular; PAT, paroxysmal atrial tachycardia; VT, ventricular tachycardia.

Figure 11-4 A, Ventricular tachycardia. Carotid sinus massage (CSM) slows the atria but not the ventricles, thus establishing the presence of atrioventricular (AV) dissociation and supporting the diagnosis of ventricular tachycardia. The QRS interval measures 0.16 sec. Note the atrial rate slowing from 102 to 88 beats/min while the ventricular rate is unaffected. B, Paroxysmal atrial tachycardia with variable block. CSM uncovers P waves hidden in the ventricular complex. The upper strip resembles atrial flutter or atrial fibrillation with ventricular ectopic beats. The lower strip shows paroxysmal atrial tachycardia with variable block at an atrial rate of 166 beats/min. C, Sinus tachycardia. The sinus P wave is obscured within the descending limb of the T wave. CSM transiently slows the sinus rate and exposes the P wave. The rate then increases. The strips are continuous. D, Sinus tachycardia with a high-level block. Arrows indicate sinus P waves. Strips are continuous. The basic rhythm is sinus, but a marked first-degree AV block is present. A high-degree (advanced) AV block associated with transient slowing of the sinus rate is produced by CSM. E, Paroxysmal atrial tachycardia. CSM abolishes the dysrhythmia and results in a period of sinus suppression with a junctional (J) escape beat. Prolonged periods of asystole may produce anxiety in physicians waiting for the resumption of a sinus pacemaker. (A and B, From Lown B, Levine SA. Carotid sinus—clinical value of its stimulation. Circulation. 1961;23:766. Reproduced by permission; C, from Silverman ME. Recognition and treatment of arrhythmias. In: Schwartz GR, Safar P, Stone JH, et al, eds. Principles and Practice of Emergency Medicine. Vol 2. Philadelphia: Saunders; 1978. Reproduced by permission; D, from Chung EK. Electrocardiography. 2nd ed. New York: Harper & Row; 1980. Reproduced by permission; E, from Silverman ME. Recognition and treatment of arrhythmias. In: Schwartz GR, Safar P, Stone JH, et al, eds. Principles and Practice of Emergency Medicine. Vol 2. Philadelphia: Saunders; 1978. Reproduced by permission.)

Figure 11-5 A, Atrial flutter. Carotid sinus massage (CSM) (downward arrow) produces marked slowing of the ventricular rate in atrial flutter. Note the obvious flutter waves with an atrial rate of 300 and a long period of ventricular standstill. The strips are continuous. B, Atrial fibrillation. CSM slows the ventricular response transiently, and thus the fibrillating baseline is revealed. The ventricular rate subsequently accelerates. C, Occult premature ventricular contractions. CSM reveals ventricular extrasystoles, thereby explaining the cause of palpitations in this case. D, A run of ventricular tachycardia is seen immediately after a supraventricular dysrhythmia is terminated by CSM. The patient remained asymptomatic, and a normal sinus rhythm was established spontaneously within a few seconds. If asystole is prolonged, ask the patient to cough vigorously (cough-induced cardiopulmonary resuscitation) or apply a precordial thump. (A, From Chung EK. Electrocardiography. 2nd ed. New York: Harper & Row; 1980. Reproduced by permission; B, from Silverman ME. Recognition and treatment of arrhythmias. In: Schwartz GR, Safar P, Stone JH, et al, eds. Principles and Practice of Emergency Medicine. Vol 2. Philadelphia: Saunders; 1978. Reproduced by permission; C, from Lown B, Levine SA. Carotid sinus—clinical value of its stimulation. Circulation. 1961;23:766. Reproduced by permission.)

Vagal maneuvers, CSM in particular, may also be a useful aid to the diagnosis of syncope in the elderly. Some 14% to 45% of elderly patients referred for syncope are thought to have carotid sinus syndrome (CSS).6,8,9 CSS is defined as an asystolic pause longer than 3 seconds or a reduction in systolic blood pressure greater than 50 mm Hg in response to CSM (Fig. 11-6). Because it shares many characteristics with sick sinus syndrome, it has been suggested that both are manifestations of the same disease. CSS causes cerebral hypoperfusion, which can lead to dizziness and syncope. Analysis of patients with CSS indicates that it results from baroreflex-mediated bradycardia in 29%, hypotension in 37%, or both in 34%.^10,11 Therefore, syncope, chronic near-syncope, or a fall of unclear etiology in the elderly is an important indication for diagnostic CSM.^12,13

Figure 11-6 Hyperreactive carotid sinus reflex. Gentle pressure was applied to the carotid sinus for 3 seconds, which resulted in a pause of approximately 7 seconds in sinus rhythm. This syndrome may be the cause of syncope. (From Bigger JT Jr. Mechanisms and diagnosis of arrhythmias. In: Braunwald E, ed. Heart Disease. Vol 1. Philadelphia: Saunders; 1980. Reproduced by permission.)

Although the use of digoxin has been overshadowed by the use of other potentially less toxic agents such as calcium channel blockers and β-blockers, the clinician can still prospectively simulate the cardioinhibitory effects of digoxin on a patient by performing vagal maneuvers. This can guide use and dosage of the medication before initiating treatment with digoxin. Significant slowing or block with CSM suggests a similar sensitivity to digoxin, and a smaller loading dose should be considered (Table 11-1).

TABLE 11-1

Ventricular Response to Carotid Sinus Massage and Other Vagal Maneuvers

TYPE OF ARRHYTHMIA	ATRIAL RATE (bpm)	RESPONSE TO CAROTID SINUS MASSAGE AND RELEASE
Normal sinus rhythm	60-100	Slowing with return to the former rate on release
Normal sinus bradycardia	<60	Slowing with return to the former rate on release
Normal sinus tachycardia	>100-180	Slowing with return to the former rate on release; appearance of diagnostic P waves
AV nodal reentry	150-250	Termination or no effect
Atrial flutter	250-350	Slowing with return to the former rate on release; increasing AV block; flutter persists
Atrial fibrillation	400-600	Slowing with persistence of a gross irregular rate on release; increasing AV block
Atrial tachycardia with block	150-250	Abrupt slowing with return to a normal sinus rhythm on release; tachycardia often persists
AV junctional rhythm	40-100	None; ± slowing
Reciprocal tachycardia using accessory (WPW) pathways	150-250	Abrupt slowing; termination or no effect; may unmask WPW
Nonparoxysmal AV junctional tachycardia	60-100	None; ± slowing
Ventricular tachycardia	60-100	None; may unmask AV dissociation
Atrial idioventricular rhythm	60-100	None
Ventricular flutter	60-100	None
Ventricular fibrillation	60-100	None
First-degree AV block	60-100	Gradual slowing caused by sinus slowing; return to the former rate on release
Second-degree AV block (I)	60-100	Sinus slows with an increase in block; return to the former rate on release
Second-degree AV block (II)	60-100	Slowing
Third-degree AV block	60-100	None
Right bundle branch block	60-100	Slowing with return to the former rate on release
Left bundle branch block	60-100	Slowing with return to the former rate on release
Digitalis toxicity–induced arrhythmias	Variable	Do not attempt CSM