Techniques for Supraventricular Tachycardias

Introduction

Patients in the emergency department frequently complain of palpitations, heart fluttering, or a rapid heartbeat, which 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 (ECG) 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/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. SVT describes a rapid HR that has its electrochemical origin either in the atria or in the upper portions of the AV node. VTs originate in the ventricular free walls or interventricular septum (or both). VTs can quickly become unstable and require special consideration ( Fig. 11.1 F ).

SVTs can be further classified as narrow-complex (QRS duration < 0.12 second; or three small boxes on the ECG) 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 (see Fig. 11.1 A ); atrial fibrillation (AF) (see Fig. 11.1 C ); atrial flutter (see Fig. 11.1 D ); AV nodal reentry; atrial tachycardia (see Fig. 11.1 B ), 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 (see Fig. 11.1 F ), SVT with aberrancy (see Fig. 11.1 E ), or a preexcitation tachycardia facilitated by an accessory pathway between the atria and ventricles.

Tachycardias can 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 and contraction systole. 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 ECG 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 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 (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 (MAP) will decrease and cause hypoperfusion of the brain and other peripheral tissue (MAP is the product of CO times total peripheral resistance [TPR]: MAP = CO × TPR). 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, such as 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, 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 wave front 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 in an unstable patient.

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 (“aberrant conduction”) 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 calcium channel blockers or β-blockers, resulting in vasodilation, loss of inotropy, and ultimately cardiac arrest. The safest course of action is to always assume that a regular wide-complex tachycardia is VT and treat with ventricular antiarrhythmia medications or electrical cardioversion. These therapies will generally result in successful cardioversion of the rhythm, regardless of whether the rhythm is actually VT or SVT with aberrancy.

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.

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. 11.4 A–E and 11.5 A–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 (see Figs. 11.5 A and B ). Sinus tachycardia may also be more apparent once P waves are unmasked by slowing the SA node (see Figs. 11.4 C and D ). Adenosine may be used for the same diagnostic purpose in these situations as well. 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 Electrocardiogram Changes With Vagal Maneuvers

• 1.

  Sinoatrial slowing, which occurs in approximately 75% of cases and leads to sinus arrest approximately 3% of the time.

• 2.

  Atrial conduction defects, as manifested by an increase in width of the P wave on the electrocardiogram.

• 3.

  Prolongation of the PR interval and higher degrees of atrioventricular block, which are seen in approximately 10% of cases.

• 4.

  Nodal escape rhythms.

• 5.

  Complete asystole, defined as sinus arrest without ventricular escape lasting longer than 3 seconds, which occurs in 4% of cases.

• 6.

  Premature ventricular contractions.

Vagal maneuvers, CSM in particular, may also be a useful aid in 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). 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%. Therefore syncope, chronic near-syncope, or a fall of unclear etiology in the elderly is an important indication for diagnostic CSM. 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

Adapted from Braunwald E, editor: Heart disease: a textbook of cardiovascular medicine , ed 6, Philadelphia, 2001, Saunders, p 642.

TYPE OF ARRHYTHMIA	ATRIAL RATE (beats/min)	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; CSM, carotid sinus massage; WPW, Wolff-Parkinson-White (syndrome).

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 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.

CSM

CSM is a bedside vagal maneuver involving digital pressure on the richly innervated carotid sinus ( Fig. 11.7 ). The procedure is likely underused by clinicians but should be routinely considered as an initial intervention. 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.

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.

Contraindications

CSM is likely underused by clinicians but 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 theoretical 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 coworkers 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.

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. Passively raising the supine patient's legs is an additional maneuver to be used with the Valsalva maneuver ( Fig. 11.8 ). The use of both a Valsalva maneuver and supine position/leg raise are suggested as routine techniques. Begin CSM on the patient's right carotid bulb because some investigators have found a greater cardioinhibitory effect on this side. 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. 11.9 , 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 supine patient's head backward and slightly to the opposite side. Passively raise the legs. 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 11.9 , step 3 ). Once the pulsation is identified, use the tips of the index and middle 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. 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. If not already performed, use simultaneous Valsalva maneuvers with the patient in the head-down position/leg raise to enhance carotid sinus sensitivity before the technique is abandoned (see Fig. 11.9 , 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 associates found seven complications in a total of 5000 massage episodes, 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 Levine 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. 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. 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. It is easily done by having the patient take a deep breath, put their thumb in their mouth with closed lips, and attempt to exhale without expelling any air. 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. There is no reason not to routinely perform a Valsalva maneuver/leg raise with CSM.

Contraindications

Patients must be able to cooperate with the clinician's commands. Dyspneic or tachypneic patients may not be able to hold their breath for the period needed to complete the maneuver.

Technique

The patient should be supine, with a cardiac monitor in place, IV access secured, antiarrhythmics available, and defibrillation available. Ask the patient to take a deep breath and hold it, or attempt to blow it out against their thumb in their mouth encircled by closed lips. Instruct the patient to bear down and try to exhale without allowing air to leave the lungs. Passively raise the patient's legs (see Fig. 11.8 ). Ask the patient to try and hold this position for 10 to 20 seconds. An adjunctive method is to have the patient take and hold a deep breath and try to push against the clinician's hand with the abdomen while the clinician gently pushes on the anterior wall of the abdomen. Then perform CSM, first on the right side for 5 seconds. Perform CSM on the left side if this is not successful.

Apneic Facial Exposure to Cold (Diving Reflex, or 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 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 ECG 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.

Berk and colleagues demonstrated in healthy volunteers that immersion of the face in cold water and the Valsalva maneuver can produce a greater vagal response than CSM. Lim and associates in 1998 and Mehta and coworkers in 1988 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 ( Fig. 11.10 and Box 11.4 )

After unsuccessful CSM, 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.

Box 11.4

Electric and Chemical Cardioversion

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