Supraventricular Tachycardias: Recognition and Management in the Intensive Care Setting

Ammar Habib

Joseph J. Gard

Traci L. Buescher

Samuel J. Asirvatham

Overview and Classification

Supraventricular tachycardias (SVTs) are frequently encountered in the intensive care unit (ICU) setting [1]. Although generally considered benign, in the context of the critically ill patient, SVTs can be particularly problematic, complicating care and at times, contributing to patient morbidity and mortality.

Atrial fibrillation (AF) and macroreentrant atrial tachycardias are the most common SVTs observed in ICU practice. However, regular reentrant tachycardias such as atrioventricular node reentry (AVNRT) may be initiated or exacerbated by the stress of critical illness or the use of adrenergic agents.

The intensive care provider should be familiar with the common varieties of SVTs and have an approach developed to quickly diagnose the exact arrhythmia (Fig. 42.1). Such diagnosis is essential in the formulation of a management plan for the treatment of acute events as well as prevention of recurrence.

Although several approaches for the diagnosis of SVT have been described, in the context of the critically ill patient, the use of easily recognized parameters aids quick diagnosis and thus prompt institution of a management plan. In most situations, three criteria—regularity of the tachycardia (regular or irregular), QRS width (narrow complex or wide complex), and, when relevant, measurement of the RP interval (interval between the preceding QRS complex and a recognized P wave during tachycardia) provide sufficient data for accurate diagnosis.

In this chapter, regular narrow complex tachycardia is addressed first, followed by the more common irregular tachycardias. Each category includes a description of the pathogenesis, electrocardiographic recognition, and general principles of management of the common varieties. Because of the frequency of occurrence of AF, this arrhythmia is discussed in relatively more depth. For each section, emphasis is placed on points of interest designed to specifically assist the caregiver for critically ill patients.

Regular Narrow Complex Tachycardia

When a regular narrow complex tachycardia (QRS duration < 120 milliseconds) is observed, several important arrhythmias should be considered in the differential diagnosis. These include sinus tachycardia, AVNRT, atrioventricular reentrant tachycardia (AVRT) using an accessory pathway (AP), and automatic atrial tachycardia. Each of these arrhythmias is discussed in more detail in the text to follow. Atrial flutter may present as a regular tachycardia, but often because of variable atrioventricular (AV) conduction block, it manifests as an irregular tachycardia and may be confused with AF. Junctional tachycardia is also a rare regular narrow complex tachycardia that is typically self limited and very unusual in the adult intensive care patient population.

These tachycardias may be of sudden onset and abrupt termination (AVNRT, AVRT) or may occur and dissipate gradually (sinus tachycardia, automatic atrial tachycardia). A useful further distinguishing electrocardiographic feature within this subset of SVTs is the RP interval. First, a careful search for the P wave should take place. If the P wave is recognized, it should be determined whether it occurs closer to the preceding QRS or to the succeeding QRS complex. If the P wave occurs closer to the succeeding QRS (long R–P tachycardia), sinus tachycardia and atrial tachycardia should be considered (Fig. 42.2). When the P wave is closer to the preceding QRS (short R–P tachycardia), AVNRT or AVRT are likely although important exceptions exist [2,3,4].

The P wave morphology may also be useful in determining the mechanism of arrhythmia. The P wave in sinus rhythm (upright in leads II, III, and aVF and biphasic in lead V₁) is easily recognized. When an abrupt change in the P wave morphology occurs regardless of the heart rate, a nonsinus mechanism including atrial tachycardia should be suspected (Fig. 42.3).

Sinus Tachycardia

Metabolic stress commonly encountered in the critically ill patient often causes increased automaticity of the sinus node, producing a regular narrow complex tachycardia. Other causes of sinus tachycardia in the critical care setting include administration of adrenergic medications, hypovolemia, and inflammation. Sinus tachycardia is characterized on ECG by regular PR interval and a uniform P wave morphology that is upright in leads II, III, and aVF. Ventricular rate typically ranges from 100 to 140 beats per minute with gradual variation in response to the underlying clinical condition or therapeutic intervention.

Sinus tachycardia is often a normal physiologic response to underlying systemic illness. Treatment of the underlying cause usually helps slow down the heart rate. At times, however, the increased heart rate (albeit a physiologic response to some other stress) may itself be detrimental. For example, in patients with critical coronary disease, rapid sinus rates may give rise to an acute ischemic syndrome and possible ventricular arrhythmia. Similarly, in conditions such as critical mitral stenosis and severe diastolic dysfunction, rapid rates are detrimental as diastolic filling times need to be maximized. In these circumstances, temporary use of beta-blockers or calcium channel blockers
can decrease heart rates while the primary cause of the sinus tachycardia is being investigated.

Figure 42.1. Narrow complex tachycardias in the intensive care unit. The most common regular narrow QRS tachycardias are atrioventricular node reentry, accessory-pathway related tachycardia, and automatic tachycardias such as sinus tachycardia and atrial tachycardia. These arrhythmias can be readily differentiated in most cases with careful analysis of the electrocardiogram. A long RP tachycardia (right panel) where each P wave is closer to the succeeding rather than the preceding QRS is characteristic of sinus tachycardia and atrial tachycardia. In tachycardias where an extranodal accessory pathway is used for retrograde conduction (orthodromic reciprocating tachycardia, ORT), a short RP interval is seen with an easily discernible retrograde P wave. With AV node reentry (left panel), because AV activation proceeds from a common turnaround point in or near the AV node, the R wave and P wave may be nearly simultaneous producing a very short RP interval and difficult to discern P wave (see text for details).

Figure 42.2. Patient with initially regular SVT than with a change in ventricular response rate. The underlying supraventricular arrhythmia is an atrial tachycardia (automatic or macroreentrant). Note the differences in P wave morphology to sinus rhythm with negative P waves in the inferior leads and all positive P wave (not biphasic) in lead V₁. The abrupt changes in ventricular responses may exacerbate symptoms especially in patients already compromised with critical illness.

Automatic atrial tachycardias are very similar in occurrence to sinus tachycardia in the intensive care setting. They are frequently seen in patients in shock, under stress, or on high doses of beta-adrenergic agents (epinephrine, high-dose dopamine). They can be readily distinguished from sinus tachycardia by close analysis of the P wave morphology. Unlike sinus tachycardia, however, these arrhythmias are not always a result of a persistent underlying abnormality (blood loss, hypoxia, etc.) and may be a primary cause of functional deterioration in a given patient [5,6]. Sodium channel blockers (class I antiarrhythmic agents) can be used for both acute termination and prevention of recurrences [7,8,9]. Typically, however, treatment of the underlying problem and decreasing the use of intravenous sympathomimetics is sufficient to prevent recurrence in patients who have developed atrial tachycardia in the setting of critical illness.

Specific Considerations in the Intensive Care Unit

In patients who are continuously monitored, sinus tachycardia can often be diagnosed by looking at the transition from normal heart rates to the present rate of tachycardia. For example, if the patient has a regular long R–P tachycardia at 170 beats per minute, all intervening rates from the baseline rate (100, 110, 130, 150 bpm, etc.) will be seen and demonstrate gradual onset of the tachycardia with progressively faster rates and a reverse pattern of resolution.

If an abrupt increase in heart rate is noted, a non-sinus mechanism should be suspected. However, some critically ill
patients develop inappropriate sinus tachycardia—a disorder of the autonomic control of the sinus node that results in P wave morphology identical to sinus rhythm but with abrupt and frequent increases in the heart rate for no apparent or definable reason [10,11,12]. Inappropriate sinus tachycardia may also be associated with other features of autonomic dysfunction and contribute to hypotension. Persistent tachycardia can be a feature of this condition, especially when patients recover from catastrophic illness.

Figure 42.3. 12-Lead electrocardiogram of typical atrioventricular node reentry (AVNRT). The P waves are readily recognized just following the QRS complex. The regular tachycardia with short RP interval should raise suspicion for this arrhythmia. The P waves are typically very narrow in AVNRT as a result of the early septal activation during this tachycardia. AV nodal blockade will terminate the arrhythmia and likely prevent recurrence. This arrhythmia may be hemodynamically poorly tolerated even when relatively slow because of the near simultaneous atrioventricular activation. This results in atrial contraction against a closed atrioventricular valve producing increased back pressure in the venous beds (systemic and pulmonary).

Atrioventricular Nodal Reentry Tachycardia

AVNRT is a common arrhythmia in the ICU and the most common form of regular SVT, accounting for approximately 60% of cases [1,13]. It is more common in female patients between the ages of 20 and 40 years. Patients may complain of palpitations that occur with sudden onset and resolve spontaneously [14]. In addition, some patients may experience the urge to micturate either during or after termination of the rhythm. Older and debilitated patients may have severe symptoms in addition to the palpitations including angina and syncope.

AVNRT is a reentrant tachycardia that has a complex circuit. The atrial myocardial inputs to the AV node are discrete, involving an anterior input called the fast pathway and a posterior input in the region of the coronary sinus (CS) called the slow pathway. Because of these discrete inputs, in some patients, there is sufficient disparity in the conduction times and refractory periods of the two pathways, allowing initiation and maintenance of a reentrant tachycardia (AVNRT) [15,16,17].

In sinus rhythm, there is near simultaneous antegrade conduction through both the fast and slow pathway. Conduction proceeds more rapidly in the fast pathway and is responsible for the normal PR interval and conduction to the ventricle. Retrograde penetration of the slow pathway occurs and prevents the antegrade wave front through the slow pathway from reaching the AV node. Consequently, slow pathway activation remains electrically silent. When a premature atrial beat occurs, block in conduction down the fast pathway (relatively shorter refractory period) allows antegrade conduction with a long PR interval down the slow pathway. From this site, retrograde activation of the fast pathway may now occur and the reentrant arrhythmia ensues. Accordingly, the typical electrocardiographic feature of initiation of AVNRT is a premature atrial contraction with a long PR interval followed by the sudden onset of a regular narrow complex tachycardia with a very short RP interval.

AVNRT is characterized on ECG by a regular narrow complex tachycardia with P waves buried within or appearing either just before or after the QRS complex. The P wave is often closer to the preceding QRS complex, giving rise to a short RP tachycardia. The RP interval reflects the time from ventricular activation to atrial activation and is short in AVNRT because of the rapid conduction of the impulse retrograde to the atrium via the fast pathway. “Short RP” tachycardias signify fast retrograde activation that is characteristic of AVNRT. Ventricular rate is often noted to be between 150 and 250 beats per minute.

Acute management of symptomatic AVNRT often begins with attempts at Valsalva-like maneuvers which increase vagal tone and influence pathway refractoriness. If these are effective, no further therapy is usually required [18]. Medical therapy is indicated in patients with continued symptoms. Adenosine may be used as a first-line treatment and invariably terminates the
tachycardia. Other agents that may be used in the acute setting include intravenous (non-dihydropyridine) calcium channel blockers like verapamil or diltiazem. Beta-blockers and digoxin, like calcium channel blockers, may be used to slow conduction within the AV nodal system to interrupt reentry.

Specific Considerations in the Intensive Care Unit

Patients will typically have a history of AVNRT with symptomatic episodes in the setting of critical illness resulting from catecholamine stress and frequent premature atrial beats that initiate reentry. Repeated episodes may occur that result in hemodynamic instability. Once the diagnosis is established, it is important that cardioversion not be considered as primary management of this arrhythmia since recurrence is likely and simpler measures to terminate the arrhythmia exist. Any AV nodal blocking agent will terminate the arrhythmia (adenosine, esmolol, metoprolol, verapamil, etc.). A short-acting agent like adenosine may be tried first. If immediate reappearance is observed, intravenous infusion of an AV nodal blocking agent can be initiated and titrated both for blood pressure control as well as prevention of recurrence. Rarely, patients will have incessant AVNRT compromising their care. Anti-arrhythmic agents or urgent radiofrequency ablation can be considered in those situations.

Atrioventricular Reentry Tachycardia

AVRT is caused by a reentrant circuit that involves both the AV node and an extranodal AP. APs are typically muscular connections that traverse the AV annulus connecting atrial and ventricular myocardium directly, thus bypassing the AV node [19,20,21].

There are several manifestations with APs that may result in electrocardiographic changes and arrhythmia in the intensive care setting. In sinus rhythm, when the AP conducts in an antegrade direction, a typical constellation of electrocardiogram (ECG) findings result. The early part of the QRS is abnormal (δ wave) because of preexcitation of the ventricular myocardium rather than depolarization via the usual infrahisian conduction system. The combination of a short PR interval in addition to the δ wave enables ECG diagnosis of preexcitation. Wolff–Parkinson–White (WPW) syndrome results when reentrant tachycardia occurs in the presence of this pattern of preexcitation.

Reentrant tachycardias include those with antegrade conduction down the AV node and up the AP (orthodromic-reciprocating tachycardia) and the inverse circuit with antegrade conduction down the AP and retrograde conduction up the AV node (antidromic tachycardia). Finally, preexcited atrial fibrillation is a potentially life-threatening arrhythmia, the recognition and management of which is discussed in the text to follow (Figs. 42.4–42.6).

AVRT is a reentrant narrow complex tachycardia like AVNRT. Patients with AVRT have an AP that allows conduction to bypass the AV node. An impulse, either a premature atrial contraction or a premature ventricular contraction, travels to the AV node through the bundle of His, activating the ventricular system. Subsequently, the propagation travels up the AP causing retrograde conduction back to the atrium. This circuit is known as orthodromic AVRT because the antegrade pathway conducts the impulse to the ventricles via the normal AV node and His–Purkinje system. Orthodromic AVRT generally has a narrow QRS complex but may have a wide QRS complex when there is an underlying bundle-branch block. The ventricular rate continues to be controlled by the AV node during orthodromic AVRT. Because it is a regular narrow complex tachycardia, it may be difficult to distinguish this rhythm from AVNRT or atrial tachycardia (discussed later). Termination of this rhythm usually transpires secondary to AV nodal conduction fatigue, increased vagal tone, or a premature extrasystolic beat.

Figure 42.4. When an extranodal accessory pathway is present, the most common arrhythmia is ORT (orthodromic reciprocating tachycardia). Conduction occurs down the normal AV conduction system and up the accessory pathway producing a short RP tachycardia with an RP interval typically more than 100 ms.

Antidromic tachycardia manifests as a regular wide complex tachycardia and can occur in patients with antegrade conducting APs [22,23] (Fig. 42.7). This variant is less common but important to recognize since it may be confused with ventricular tachycardia. Initiation typically occurs with a premature atrial contraction that blocks in the AV node. Antegrade conduction proceeds via the AP to the ventricle with the return
limb of the circuit through retrograde AV nodal conduction. Both orthodromic and antidromic AVRT are dependent on AV nodal conduction, and thus, AV nodal blockade (adenosine, beta-blockers, etc.) will terminate the arrhythmia and prevent recurrence. In contrast, a preexcited tachycardia occurs when another SVT (independent of the pathway) such as sinus tachycardia, AF, atrial flutter, etc., arises, but because of the presence of the antegrade conducting AP, rapid conduction to the ventricle takes place, bypassing the AV node. For these arrhythmias, AV nodal blockade would be contraindicated as there would be promotion of rapid aberrant conduction via the AP predisposing to ventricular arrhythmias. This is particularly problematic during AF when direct conduction through the antegrade AP may lead to ventricular fibrillation. The 2003 American College of Cardiology/American Heart Association (ACC/AHA) SVT management guidelines indicated that the incidence of sudden death with WPW is increased in patients with a minimum R-R interval < 250 milliseconds during AF (regardless of whether AF is spontaneous or induced), a history of symptomatic tachycardia, multiple APs, and Ebstein’s anomaly [24].

Figure 42.5. When an extranodal accessory pathway is present, a regular wide complex tachycardia may also result. Here, the tachycardia circuit proceeds antegrade down the accessory pathway and up through the AV nodal conduction system producing a regular wide QRS tachycardia with the QRS morphology dependent on the site of the accessory pathway. ART, antidromic-reciprocating tachycardia.

Figure 42.6. Potential life-threatening arrhythmia seen in patients when extranodal accessory pathway is preexcited atrial fibrillation. The AV node normally protects the ventricle from rapid ventricular rates during atrial fibrillation. However, when an accessory pathway is present, conduction may proceed down the accessory pathway as well as the AV node producing extremely rapid ventricular rates. The characteristics of a preexcited AF electrocardiogram include irregularly irregular R-R intervals along with rapid rates and importantly, irregular QRS duration and morphology as well (see text for details).

Figure 42.7. Regular wide complex tachycardia. When a regular wide complex tachycardia is seen in the critical care setting, ventricular tachycardia should always be considered. However, if the baseline electrocardiogram shows preexcitation, an antidromic tachycardia can be diagnosed and easily terminated with any AV nodal blocking agent. If the baseline electrocardiogram is not available, wide QRS tachycardia with consistent 1:1 R–P association in the absence of structural heart disease should raise suspicion for an accessory pathway-mediated mechanism.

The acute management of regular tachycardia in patients with APs (orthodromic or antidromic AVRT) is similar and consists of AV nodal blockade to terminate the arrhythmia and the use of longer-term beta-blockers or calcium channel blockers to prevent recurrence. AV nodal blocking therapy is often sufficient as a temporizing maneuver until the patient’s critical illness subsides and definitive ablation therapy can be offered [25,26].

Acute Management of Hemodynamically Significant AVRT

Valsalva-like maneuvers that increase vagal tone may be attempted initially. As with acute treatment of AVNRT, adenosine may be used as a first-line agent for medical management. Because of its very short half-life, a trial of adenosine may be attempted in patients with tenuous hemodynamics prior to emergent cardioversion. However, adenosine may potentially cause increased atrial vulnerability, a serious proarrhythmic side affect [27,28]. An alternative category of drugs often administered in the acute setting for treatment of orthodromic AVRT includes intravenous calcium channel blockers. Intravenous verapamil may be used and repeated every 2 to 3 minutes for acute termination of orthodromic AVRT but may be relatively contraindicated in patients with significant hypotension or depressed ventricular function or heart failure. Additional agents that may be used and often considered second-line treatment include intravenous beta-blockers (like metoprolol and propranolol) and procainamide. Rather than having a direct effect on AV nodal conduction, procainamide acts on the atrial and ventricular myocardium, causing decreased conduction and increase refractoriness of APs and the His–Purkinje system.

In contrast, when an irregular wide complex tachycardia is noted in a patient with known WPW, urgent intervention is required [29,30,31]. Preexcited AF once recognized, should be immediately terminated (Fig. 42.8). If the patient is hemodynamically unstable, urgent cardioversion is required. If not, an antiarrhythmic agent such as procainamide can be used. Procainamide may chemically convert the patient from AF to sinus rhythm and in addition, suppress conduction via the AP.

Figure 42.8. Preexcited atrial fibrillation. All caregivers for critically ill patients should be familiar with this pattern. An irregular wide complex tachycardia is noted. Importantly, the ventricular rates are fast, and each QRS morphology is slightly different. Especially if the baseline electrocardiogram had shown preexcitation (WPW) pattern, this urgent condition of preexcited atrial fibrillation should be immediately recognized. Regardless of present symptoms, cardioversion should be considered if the patient is relatively unstable; chemical cardioversion with an agent such as procainamide that may convert the atrial fibrillation to sinus rhythm and simultaneously slow conduction to the accessory pathway can be tried.

Patients with AVRT should be referred to a cardiac electrophysiologist for possible radiofrequency catheter ablation. Catheter ablation is highly successful, is associated with low risk, and eliminates the need for long-term drug therapy [32]. Ablation is often considered first-line therapy in young patients who prefer a curative approach.

Specific Considerations for the Intensive Care Setting

Preexcited AF should be immediately recognized and treated when observed but is an unusual presentation in critically ill patients. More commonly, repeated episodes of reentrant AVRT (usually orthodromic) arise in patients with known APs. Frequent and sometimes incessant episodes can result from the stress of critical illness combined with possible discontinuation of previously used AV nodal blocking agents for medical management. Judicious use of short-acting intravenous beta-blockers will help prevent recurrences of arrhythmia without major untoward hemodynamic consequences.

Caregivers of the critically ill patient must also be aware that the presence of a WPW pattern on the EKG by itself is not a contraindication to use beta-blockers or other AV nodal blocking agents if clinically required for comorbid illnesses such as coronary disease. If, however, a patient with WPW has AF, AV nodal blocking agents should be avoided or used in conjunction with antiarrhythmic agents like procainamide to suppress AP conduction (Fig. 42.9).

Figure 42.9. Characteristic electrocardiogram in patient with antegrade preexcitation. Note the short PR interval and the δ wave clearly seen in the lateral precordial leads and lead II. The R wave seen in lead V₁ and negative δ wave in lead I is consistent with the left-sided accessory pathway. If a patient with this baseline electrocardiogram develops atrial fibrillation, this should be treated as a medical emergency because of risk of ventricular fibrillation from the atrial fibrillatory waves conducting to the ventricle via this pathway without the intervening protective effects of the AV node.

Irregular Narrow Complex Tachycardia

Several of the regular narrow complex tachycardias already discussed may occasionally present with irregular R-R intervals. However, by far, the most common irregular narrow complex tachycardia occurring in an ICU setting is AF. In this section, we discuss this common arrhythmia in detail, presenting information on pathogenesis, recognition of variants, and acute management in the critically ill patient. Although less common, atrial flutter with variable conduction block and multifocal atrial tachycardia should be distinguished from AF since management differs significantly.

Atrial Fibrillation

AF is the most common type of arrhythmia, and the most common SVT seen in the ICU. Incidence increases with age; it is found in less than 0.1% of adults younger than 55 years but in more than 9% of the population age 80 years or older [33,34]. AF is characterized by the presence of chaotic appearing multiple shifting reentrant atrial wavelets that may appear flat or irregular. Classification of AF usually depends on the duration and frequency of occurrence. Paroxysmal AF makes up about 40% of cases and may last up to 7 days, terminating spontaneously. Nonparoxysmal AF lasts more than 7 days and requires cardioversion for termination. Identification of AF is important clinically because of the increased risk of hemodynamic instability and mortality associated with this arrhythmia in the intensive care setting. AF is characterized by irregular atrial contractions, as demonstrated on ECG by irregularly irregular f waves that may manifest as continuous irregular variation in the baseline (Fig. 42.10).

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