Techniques for Supraventricular Tachycardias

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Chapter 11

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.

Box 11-1   Diagnostic and Therapeutic Approaches to Supraventricular Tachycardias

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).

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).

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.

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

image

Figure 11-e1 The carotid sinus.

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.

Box 11-3   Order of Decreasing Frequency of ECG Changes with Vagal Maneuvers

image

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.)

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

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

AV, atrioventricular; bpm, beats per minute; CSM, carotid sinus massage; WPW, Wolff-Parkinson-White (syndrome).

Adapted from Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 6th ed. Philadelphia: Saunders; 2001:642.

Equipment and Setup

Before the initiation of any clinical intervention such as vagal maneuvers, administration of medication, or cardioversion for SVT, place the patient on a cardiac monitor, establish intravenous (IV) access, and infuse a slow, keep-vein-open (KVO; 60 mL/hr saline IV) solution through the IV line. Monitor the patient with a pulse oximeter and blood pressure monitor. Keep numerous antiarrhythmic medications readily available at the bedside. Keep a defibrillator/pacemaker at the bedside in anticipation of a worsening dysrhythmia. Administer oxygen for the procedure, especially if conscious sedation is anticipated. Place the patient in the Trendelenburg position if tolerated. Merely placing the patient in this position may terminate the SVT as a result of increased pressure on the carotids and maximum carotid bulb stimulation. This position may also prevent syncope if there is a significant decrease in blood pressure or HR.

Carotid Sinus Massage

CSM is a bedside vagal maneuver involving digital pressure on the richly innervated carotid sinus (Fig. 11-7). It takes advantage of the accessible position of this baroreceptor for diagnostic and therapeutic purposes. Its main therapeutic application is for termination of SVTs caused by sudden paroxysmal atrial tachycardia. It also has diagnostic utility in the assessment of tachydysrhythmias and rate-related bundle branch blocks. In addition, it can provide clues to latent digoxin toxicity, as described previously, by potentiating manifestations of the toxicity. It can also be used to sort out the differential diagnosis of syncope. Further information can be found on Expert Consult.

Returning to the use of CSM as a diagnostic technique for assessing digoxin toxicity, the adverse effects and toxicity from digoxin depend more on the response of the host than on the actual digoxin level. In cases of suspected digoxin toxicity, before the digoxin level is available or when it is in the “normal range,” CSM may be a useful diagnostic adjunct. Significant inhibition of AV node conduction associated with ventricular ectopy, especially ventricular bigeminy, should lead to suspicion of digoxin toxicity.1

Contraindications

CSM is contraindicated in the very rare patient likely to suffer neurologic or cardiovascular complications from the procedure. Patients with a carotid bruit should not undergo CSM because of the risk for carotid embolization or occlusion. A recent cerebral infarction is another contraindication because even a marginal reduction in cerebral blood flow may produce further infarction. Age, by itself, is not a contraindication to CSM. However, the elderly are more likely to have carotid artery disease and may experience transient and, very rarely, permanent neurologic or visual symptoms after CSM. Complications are thought to be due to transient cerebral ischemia or embolization of plaque, similar to a transient ischemic attack.

The presence of diffuse, advanced coronary atherosclerosis is associated with increased sensitivity of the carotid sinus reflex. This hypersensitivity is further augmented during an anginal attack or acute myocardial infarction. Brown and coworkers14 found that the degree of carotid sinus hypersensitivity was directly proportional to the severity of coronary artery disease as documented by cardiac catheterization. Patients with acute myocardial ischemia or with recent myocardial infarction are already at higher risk for VT or ventricular fibrillation (VF). A CSM-induced prolonged asystole may further predispose them to these dysrhythmias. Therefore, CSM should be avoided in these patients.

Both digoxin and CSM act through a vagal mechanism to inhibit the AV node. Patients taking digoxin may experience greater inhibition of the AV node with a longer AV block as a result. Patients with apparent manifestations of digoxin toxicity or known digoxin toxicity should not undergo CSM because the AV inhibition may be profound.15

Technique

This technique can be performed with or without a concomitant Valsalva maneuver. Alternatively, pressure can be applied to the abdomen by an assistant. Some clinicians prefer to place the patient supine or with the head of the bed tilted downward. Begin CSM on the patient’s right carotid bulb because some investigators have found a greater cardioinhibitory effect on this side.12,16,17 However, scientific agreement on this issue is not unanimous. Simultaneous bilateral CSM is absolutely contraindicated because the cerebral circulation may be severely compromised. Before attempting CSM, first auscultate for carotid bruits on both sides of the neck (Fig. 11-8, step 2). The presence of a bruit is a contraindication to massage.

Keep the patient relaxed for two reasons. A tense platysma muscle makes palpation of the carotid sinus difficult, and an anxious patient will be less sensitive to CSM as a result of heightened sympathetic tone.

Tilt the patient’s head backward and slightly to the opposite side. Palpate the carotid artery just below the angle of the mandible at the upper level of the thyroid cartilage and anterior to the sternocleidomastoid muscle (see Figs. 11-7 and 11-8, step 3). Once the pulsation is identified, use the tips of the fingers to administer CSM for 5 seconds in a posteromedial direction, aiming toward the vertebral column. Although earlier practitioners used a longer duration of massage, a shorter period minimizes the risk for complications and is adequate for diagnostic purposes in the majority of patients.18 Pressure on the carotid sinus may be steady or undulating in intensity; the force, however, must not occlude the carotid artery. The temporal artery may be simultaneously palpated to ensure that the carotid remains patent throughout the procedure.

If unsuccessful, repeat CSM after 1 minute. If the procedure is still unsuccessful, massage the opposite carotid sinus in a similar fashion. Perform simultaneous Valsalva maneuvers with the patient in the head-down position to enhance carotid sinus sensitivity before the technique is abandoned (Fig. 11-8, step 4). CSM may be repeated once antiarrhythmic medications (e.g., calcium channel blockers and β-blockers) have been given, and often the combination is more effective. However, repetition of CSM after the administration of adenosine is not thought to have any utility.

Complications

Neurologic complications of CSM are rare and usually transient. In a review of neurologic complications in elderly patients undergoing the procedure, Munro and associates19 found seven complications in a total of 5000 massage episodes, for an incidence of 0.14%. Reported deficits included weakness in five cases and visual field loss in two others. In one case the visual field loss was permanent. Patients in this study were excluded from CSM if they had a carotid bruit, recent cerebral infarction, recent myocardial infarction, or a history of VT or VF. The duration of massage was 5 seconds. Lown and Levine1 described one patient with brief facial weakness during several thousand tests. Carotid emboli and hypotension have both been implicated as possible causes of the neurologic deficits. Unintentional occlusion of the carotid artery may also be responsible for some neurologic complications.

Cardiac complications include asystole, VT, or VF. A normal pause of less than 3 seconds is part of the physiologic response to CSM; a longer pause may be diagnostic of CSS (see Fig. 11-6). In a review of reported cases of ventricular tachydysrhythmia, five cases were described.20 All five patients were receiving digoxin, and in several cases VT or VF followed AV block. Digoxin is associated with more prolonged AV block from CSM, which perhaps leaves these patients more vulnerable.

Valsalva Maneuver

In general, mean changes in bradycardia are greatest with the Valsalva maneuver and the diving response.2,21,22 During the Valsalva maneuver (i.e., exhaling against a closed glottis or bearing down as though to defecate), intrathoracic pressure increases and leads to increased arterial pressure as a result of increased afterload. This increased pressure is transferred to the peripheral vascular system. Venous return to the heart is decreased, which results in a decrease in the SVT. This is followed by increased venous pressure. All these changes in pressure lead to an initial increase in HR and carotid sinus pressure. As the maneuver is sustained, vagal tone is increased, thereby leading to a compensatory decrease in SA and AV conduction. This is the expected or desired diagnostic or therapeutic response.

Apneic Facial Exposure to Cold (“Diving Response,” Diving Bradycardia): Technique

This technique can be viewed as a variation on the simple Valsalva maneuver. It has been found to be useful in children who may be unable to cooperate with or may be incapable of performing a Valsalva maneuver. Classically, the technique consists of covering the face with a bag of crushed ice and cold water (0°C to 15°C) for 15 to 30 seconds and then observing the electrocardiogram for a break in the tachycardia. Another variation of this technique is to drip ice water into the nostril of a small child. The procedure is based on the classic diving reflex of bradycardia. Slowing the SVT to unmask the hidden, underlying rhythm is similar to the effects of CSM. Conversion of sudden atrial tachycardia to sinus rhythm should be observed in 15 to 35 seconds. The procedure is convenient and noninvasive and can be self-administered.25–30

Berk and colleagues16 demonstrated in healthy volunteers that immersion of the face in cold water and the Valsalva maneuver can produce a greater vagal response than CSM can. Lim and associates in 199831 and Mehta and coworkers in 198817 also found that the Valsalva maneuver was more effective than CSM for conversion of induced SVT.

Another technique that was used but has fallen out of favor is direct ocular pressure. There are many contraindications to this technique, such as retinal or lens surgery, glaucoma, thrombotic-related eye conditions, and penetrating or recent blunt trauma to the eye. This procedure is no longer recommended.

Selected Pharmacologic Agents

A pharmacologic approach to SVT is preferred in stable patients. In the presence of severe hypotension, chest pain, or other evidence of extremis, cardioversion is the preferred intervention. In unusual circumstances, such as rapid AF in patients with known Wolf-Parkinson-White (WPW) syndrome, certain medications should be used with caution, and cardioversion may be considered the first-line intervention.

Adenosine

The use of vagal maneuvers has been eclipsed in recent years by the use of adenosine, an endogenous, ultrashort-acting, vagal-stimulating purine nucleoside that is ubiquitous in body cells. Its action is to slow conduction time through the AV node and depress the AV node. If vagal maneuvers have been attempted and failed to produce the desired response, use of adenosine is an appropriate subsequent intervention.

Extracellular adenosine is cleared rapidly from the circulation by the erythrocyte and vascular endothelium system that transports adenosine intracellularly. Here, rapid metabolism via a phosphorylation or deamination cycle produces inosine or adenosine monophosphate. Adenosine produces a short-lived pharmaceutical response because it is metabolized rapidly by the described enzymatic degradation. The half-life of adenosine is less than 10 seconds, with the metabolites becoming incorporated into the high-energy phosphate pool.32–35

Indications and Contraindications: Most forms of paroxysmal supraventricular tachycardia (PSVT) affect a reentry pathway involving the AV node, and adenosine depresses the AV node and sinus node activity. Adenosine is indicated for the conversion of PSVT associated with or without accessory tract bypass conduction (WPW, Lown-Ganong-Levine [LGL]). The other use of adenosine is for diagnostic slowing of SVT to unmask AF, atrial flutter, or VT. The diagnostic and therapeutic effects of adenosine on tachydysrhythmias are similar to those elicited by vagal maneuvers. Adenosine’s safety is derived from its short duration of action—usually about 10 to 12 seconds.

Adenosine should not be used in patients with a known history of second- or third-degree AV block or sick sinus syndrome unless there is a functioning internal pacer. Also, if the patient has a known hypersensitivity to adenosine or a history of severe reactive airway disease or active wheezing, the drug should not be used. In addition, adenosine should not be used in patients with an underlying accessory pathway (WPW, LGL) in the setting of AF. In this circumstance, the HR may increase because the enhanced AV node blockade permits conduction through the bypass tract.

Dosage: The initial dose recommended is a 6-mg rapid bolus administered over a period of 1 to 3 seconds. The dose should be followed by a 20-mL saline flush (Fig. 11-9). If no response occurs within 1 to 2 minutes, a 12-mg dose should be administered in the same manner as the initial dose. This second dose should also be followed by a 20-mL saline bolus.

Side effects of adenosine are common and transient. Many patients experience an unsettling feeling, and this should be explained to the patient before administering the drug. Common sensations include flushing, dyspnea, and chest pain. Important drug interactions include theophylline or related methylxanthines (caffeine and theobromine), which can block adenosine receptor sites. If these medications are being taken by the patient, administer a larger dose of adenosine. If the patient is taking dipyridamole or carbamazepine, these drugs may block uptake of adenosine and potentiate its effects, so contemplate administering a smaller IV dose of adenosine (e.g., 3 mg).36 Adenosine is safe and effective in pregnancy.37 Also, if the patient has a central line or a transplanted heart, try an initial 3-mg dose.

Calcium Channel Blockers

Diltiazem

Diltiazem is a nondihydropyridine calcium channel blocker. It controls the rate of influx of calcium into myocytes during depolarization. This calcium channel blocker slows conduction of impulses through the AV node and prolongs the refractory period of the AV node. As a result, this drug is capable of terminating reentry-based tachycardias that have not converted with the use of adenosine or vagal maneuvers, and it can be used to control the ventricular response rate in a variety of SVTs (AF, atrial flutter). In addition, diltiazem can be used for the treatment of stable, narrow-complex tachycardias that are driven by automaticity (e.g., ectopic, multifocal, or junctional tachycardias).

Its effects on AV nodal tissue are selective in that it reduces AV conduction in tissue responsible for the tachydysrhythmia but spares normal conduction tissue.34,38–40

Verapamil

Verapamil is also a calcium channel blocker. This medication blocks the slow channel for entry of calcium into myocytes. Verapamil blocks not only the calcium channels in the specialized conduction tissue of the myocardium but also the contracting cells of the heart. As a result, verapamil prolongs the effective refractory period within the AV node and slows conduction.2,39 It also has a modest effect on myocardial contractility.2

Indications and Contraindications: Verapamil is effective in (1) converting narrow-complex PSVT to normal sinus rhythm and (2) controlling the ventricular response in AF or atrial flutter if the AF or atrial flutter is not complicated by the presence of an accessory bypass tract (WPW, LGL). With specific regard to WPW syndrome and rapid AF, caution is advised with the use of verapamil. However, verapamil has been reported to be safe in those with overt or concealed accessory conduction pathways.42

Verapamil should not be used or be used with caution in the following settings: (1) PSVT with accessory bypass tract conduction, (2) AF or atrial flutter with accessory bypass tract conduction (WPW syndrome), (3) coexistence of sick sinus syndrome or second- or third-degree AV block unless an internal pacer is present, (4) severe left ventricular dysfunction (systolic blood pressure <90 mm Hg) or cardiogenic shock, and (5) patients with known verapamil hypersensitivity.7,33,34,38–40 Because of its prolonged activity, verapamil should used with caution in patients with congestive heart failure.

In the presence of SVT, hypotension may be caused by the negative inotropic and vasodilating effects of verapamil. Administration of calcium before IV verapamil results in a decreased incidence of hypotension without compromising the effectiveness of channel blockers. The most common adverse effect of IV calcium is flushing. Use of digoxin does not contraindicate calcium pretreatment. A dose of calcium gluconate, 1 g (ionized calcium, 90 mg) administered over a period of 3 minutes, is recommended for preventing or lessening the hypotensive effect of verapamil without affecting its antiarrhythmic effects.43

β-Adrenergic Blockade

β-Blockers are very useful agents for control of the ventricular response in patients with PSVT, AF or atrial flutter, and atrial tachycardia. No β-blocker offers a distinctive advantage over another because when used clinically, they can all be titrated to a desired effect on dysrhythmias and hypertension. Examples of β-blockers are atenolol, metoprolol, propranolol, and esmolol. What separates the different drugs and their use is the various pharmacologic characteristics that control adverse reactions, speed of onset, dosage regimens, contraindications, and drug interactions.

The electrophysiologic effect of β-blockers results from inhibition of binding of catecholamine at β-receptor sites. These medications reduce the effects of circulating catecholamines, and this is manifested as a decrease in HR, blood pressure, and myocardial contractility. The PR interval may be prolonged, but the QRS and QT intervals are not affected. Their actions are most noted on cells that are most stimulated by adrenergic actions. Typically, these sites are the sinus node, the Purkinje fibers, and ventricular tissue when it is stimulated by catecholamines.2,33,34,39 These medications also have various cardioprotective effects in patients suffering from acute coronary syndromes. They exert their cardioprotective effects by decreasing myocardial workload, and hence they decrease myocardial oxygen consumption and demand.2 β-Blockers are useful in the treatment of narrow-complex tachycardias that originate secondary to a reentry phenomenon or an automatic focus (MAT, an ectopic pacemaker, or a junctional rhythm). These drugs can also be used to control rates in patients suffering from AF or atrial flutter, as long as ventricular function is nominal. Some representative doses of these β-blockers are (1) atenolol (β1), 5 mg IV slowly over a period of 5 minutes; if no effect, repeat in 10 minutes; (2) metoprolol (β1), 5 mg IV slowly, may repeat up to 15 mg total; and (3) propranolol, 0.1 mg/kg IV by slow push and divided into three equal doses at 2- to 3-minute intervals; the total dose may be repeated in 2 minutes. The administration rate of the drug should not exceed 1 mg/min.

In general, β-blockers should not be used in patients with a history that includes diabetes, lung disease, bradycardia, or heart block; use of a calcium channel blocker; hypotension; or the presence of a vasospastic condition. β-Blockers should also not be used in patients with AF in the presence of bypass tracts, as is true for the calcium channel blockers adenosine and amiodarone.

Esmolol

Esmolol is a rapid-, short-acting, β1-selective (cardioselective) β-blocker. At therapeutic doses it inhibits β1 receptors in cardiac muscle. At higher doses its selectivity is lost and it affects β2 receptors in the lung and vascular system. Esmolol is rapidly metabolized in erythrocytes and has a half-life of about 2 to 9 minutes. Its elimination half-life is approximately 9 minutes.34,38

Procainamide

A time-honored antiarrhythmic, procainamide slows conduction and decreases the automaticity and excitability of atrial, ventricular, and Purkinje tissue. It also increases refractoriness in atrial and ventricular tissue. Procainamide prolongs the QT interval without having much effect on Purkinje fibers or ventricular tissue.36

Indications and Contraindications: A long-established clinical application is for management of the rate of SVT, SVT with aberrant conduction (wide-complex SVT), AF or atrial flutter associated with WPW conduction, and VT. The advantage of using procainamide is the ability to convert to the oral form when rate control is achieved.

The dose of procainamide recommended by advanced cardiac life support is usually 15 to 18 mg/min, although in urgent situations up to 50 mg/min can be used. Procainamide is generally used in clinical situations in which time is not a factor in patient care. Long-term management in the emergency department necessitates monitoring of the plasma concentrations of procainamide and its N-acetylprocainamide metabolite. Hypotension and conduction disturbances (torsades de pointes, heart block, and sinus node dysfunction) are often signs of high plasma levels. Use caution in patients with a history of hypokalemia, long QT intervals, and torsades de pointes. Hematologic and rheumatologic disturbances are factors in long-term use. The end point of administration of the drug is when the arrhythmia is suppressed, hypotension occurs, the QT duration increases by 50% over baseline, or a maximum of 17 mg/kg of the drug has been administered (1.2 g in a 70-kg adult).32

Digoxin

Digoxin is a time-honored drug used for the treatment of AF and atrial flutter. It is the only antidysrhythmic with inotropic characteristics. Digoxin is less useful for the emergency clinician because of its long delay of onset.

Digoxin is a cardiac glycoside found in a number of plants. It is extracted from the leaves of Digitalis lanata. Digoxin increases intracellular Na+ and K+ by inhibiting sodium-potassium adenosine triphosphatase, the enzyme that regulates the quantity of Na+ and K+ inside the cell. An intracellular increase in Na+ stimulates Na+-Ca+ exchange, which leads to increased intracellular Ca+. The effects of digoxin are both direct action on cardiac muscle and indirect action on the cardiovascular system. The indirect effects are mediated by the autonomic nervous system. The results of these actions are vagomimetic effects on the SA node and the AV node.

The consequences of these actions are (1) increased force and velocity of myocardial contraction (positive inotropic effect), (2) slowing of HR and AV nodal conduction (vagomimetic effect), and (3) a decrease in symptomatic nervous system effects (neurohormonal-deactivating effect).32,33,45–48

Indications and Contraindications: Although its use in controlling the ventricular response rate in chronic AF is well established, it is no longer the mainstay of therapy for narrow-complex tachycardias, for which newer agents have replaced digoxin. Its inotropic character is still widely used in the setting of heart failure.

Use of digoxin should be avoided in the clinical settings of sinus node disease and AV blockade. It may cause complete heart block or severe sinus bradycardia. Do not use digoxin in patients with accessory bypass tract rhythms (WPW or LGL). It may cause a rapid ventricular response or VF. Patients with idiopathic hypertrophic subaortic stenosis, restrictive cardiomyopathy, constrictive pericarditis, or amyloid heart disease are particularly susceptible to digoxin toxicity.49

Amiodarone

Amiodarone has become one of the workhorses of treatment of dysrhythmia in the emergency department. It is often considered a Vaughan-Williams class III drug because it is a potassium channel blocker. However, this medication also blocks sodium and calcium channels and α- and β-adrenergic receptors. As a result of its potassium-blocking properties, amiodarone prolongs the action potential duration and increases refractoriness of the atria and ventricular tissue, the sinus and AV nodal tissue, and Purkinje fibers. Amiodarone also blocks sodium channels in depolarized tissue. It slows depolarization in the SA node and slows conduction through the AV node. Its calcium antagonist effect is minimal.15,33,34,38

Indications and Contraindications: Amiodarone is used for the control of narrow-complex supraventricular and ventricular dysrhythmias. It is useful in the management of narrow-complex tachycardias that originate from a reentry rhythm (SVT). It is effective in the conversion of stable wide-complex tachycardias, and it is useful in managing polymorphic VT with a normal QT interval. Amiodarone can be used for wide-complex tachycardias of undetermined origin. This drug can also be used for the management of AF and atrial flutter with aberrancy, SVT with accessory pathway conduction, and the rare adult junctional tachycardia. Another use for this medication is control of the rapid ventricular rate as a result of accessory pathway conduction in preexcited atrial arrhythmias. It is a strong second-line choice with procainamide for hemodynamically stable VT.

Its use can precipitate heart failure, hypotension, and severe bradycardia. When used with β-blockers and calcium channel blockers, amiodarone can have the added risk of hypotension and bradycardia. Torsades de pointes has been reported after the use of amiodarone in conjunction with drugs that have increased the QT interval. Also, amiodarone should be used with great caution, if at all, in the presence of AF with accessory pathways; there are several case reports of patients decompensating after receiving IV amiodarone when it was used for rapid AF plus WPW syndrome.54–59 In the setting of possible AF with an accessory pathway, procainamide is safer. Finally, note that amiodarone will also prolong the QT interval, so it is best to avoid this drug in patients with a preexistent long QT interval, just like procainamide.

Electrical Cardioversion

In life-threatening or unstable situations, patients in AF are to be immediately cardioverted because the risk for continued AF outweighs the risk for thromboembolism.38,60–68 Cardioversion is specifically indicated when the patient is unstable; that is, a change in mental status occurs, the patient becomes hypotensive, ischemic chest pain develops, heart failure develops, or the ventricular rate exceeds 140 to 150 beats/min.39 Urgent restoration of normal rhythm in patients with symptomatic new-onset AF is best achieved by direct cardioversion with either a monophasic or a biphasic defibrillator. Success rates with biphasic defibrillators are reported to be approximately 94% to 95%.69–71 The cardioversion procedure is discussed in greater detail in Chapter 12.

Current guidelines for the treatment of symptomatic new-onset AF focus on the length of time that the patient has been in AF or atrial flutter. This is the determining factor for the initiation of anticoagulation when confronted by the need for cardioversion to sinus rhythm. Accordingly, onset within 48 hours or less has been determined to be the time limit that a patient with new-onset AF can undergo cardioversion without the need for anticoagulation. Studies have shown that staying under the 48-hour limit allows cardioversion to occur with the lowest risk for thromboembolism.38,61,66,72 Patients who have been in AF for longer than 48 hours and are not in need of urgent care need to undergo anticoagulation to an international normalized ratio (INR) of 2.0 to 3.0 for a 3-week duration before cardioversion.44 If this approach is not clinically acceptable, transesophageal echocardiography (TEE) should be performed in addition to heparinization.

If no clot in the left atrial appendage is visualized on TEE, the heparinized patient should immediately undergo cardioversion and take anticoagulants for the next 4 weeks. If a clot is visualized in left atrial appendage, the patient should first be anticoagulated to an INR or 2.0 to 3.0 for 3 weeks’ duration before cardioversion73–77 (see Box 11-4).

Box 11-4   Recommendations for Cardioversion

Recommendations for Antithrombotic Therapy to Prevent Ischemic Stroke and Systemic Embolism in Patients with Atrial Fibrillation Undergoing Cardioversion†

1. For patients with AF lasting 48 hours or longer or of unknown duration for whom pharmacologic or electrical cardioversion is planned, we recommend anticoagulation with an oral vitamin K antagonist (VKA), such as warfarin,‡ to a target INR of 2.5 (range, 2.0 to 3.0) for 3 weeks before elective cardioversion and for at least 4 weeks after sinus rhythm has been maintained.

2. For patients with AF lasting 48 hours or longer or of unknown duration who are undergoing pharmacologic or electrical cardioversion, we recommend either immediate anticoagulation with IV unfractionated heparin (target PTT, 60 seconds; range, 50 to 70 seconds) or LMWH (at full DVT treatment doses) or at least 5 days of warfarin (target INR, 2.5; range, 2.0 to 3.0) at the time of cardioversion and performance of screening multiplane TEE). If no thrombus is seen, cardioversion is successful, and sinus rhythm is maintained, we recommend anticoagulation (target INR, 2.5; range, 2.0 to 3.0) for at least 4 weeks. If a thrombus is seen on TEE, cardioversion should be postponed and anticoagulation should be continued indefinitely. We recommend performing TEE again before attempting later cardioversion (all grade 1B addressing the equivalence of TEE-guided versus non–TEE-guided cardioversion).

3. For patients with AF of known duration and shorter than 48 hours, we suggest that cardioversion be performed without prolonged anticoagulation. However, in patients without contraindications to anticoagulation, we suggest beginning IV heparin (target PTT, 60 seconds; range, 50 to 70 seconds) or LMWH (at full DVT treatment doses) at initial encounter.

4. For emergency cardioversion in a hemodynamically unstable patient, we suggest that IV unfractionated heparin (target PTT, 60 seconds; range, 50 to 70 seconds) or LMWH (at full DVT treatment doses) be started as soon as possible, followed by at least 4 weeks of anticoagulation with an oral VKA, such as warfarin‡ (target INR, 2.5; range, 2.0 to 3.0), if cardioversion is successful and sinus rhythm is maintained.

5. For cardioversion of patients with atrial flutter, we suggest the use of anticoagulants in the same way as for cardioversion of patients with AF (grade 2C).

*From Fuster V, Ryden LE, Asinger RE, et al. ACC/AHA/ESC guidelines for the management of atrial fibrillation. Circulation. 2001;104:2118.

†From Singer DE, Albers GW, Dalen JE, et al. Antithrombotic therapy in atrial fibrillation: American College of Chest Physicians evidence based guidelines (8th edition). Chest. 2008;133(6 suppl):5465.

‡Dabigatran is useful as an alternative to warfarin for the prevention of stroke and systemic thromboembolism in patients with paroxysmal to permanent AF and risk factors for stroke or systemic embolization who do not have a prosthetic heart valve or hemodynamically significant valve disease, severe renal failure (creatinine clearance <15 mL/min), or advanced liver disease (impaired baseline clotting function). (Wann S, Curtis AB, Ellenbogen KA et al. 2011 ACCF/AHA/HRS focused update on the management of atrial fibrillation: update of dabigatran. J Am Coll Cardiol. 2011;57:1330.)

§From Wann LS, Curtis AB, January CT, et al. Focused update on the management of atrial fibrillation. Circulation. 2011;123:104.

An alternative treatment strategy with a reported success rate of 50% to 70% is ibutilide in a bolus IV infusion. Be cautious when using ibutilide in patients with prolonged QT intervals or severe left ventricular dysfunction. Ibutilide has a 4% risk for ventricular arrhythmia. Pretreatment with ibutilide before electrical cardioversion can increase the chance for successful conversion to nearly 100%.32,33,39,78–81

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