Chapter 100. Tachyarrthymias

1. How do you initially manage a patient with a hemodynamically unstable wide complex tachyarrhythmia?

2. What are the electrocardiographic features that suggest that a wide complex tachyarrhythmia is of ventricular origin?

3. What are the electrocardiographic features that suggest that a wide complex tachyarrhythmia is of supraventricular origin?

4. What is the differential diagnosis for short RP tachycardia? What is the differential diagnosis for long RP tachycardia?

5. Radiofrequency ablation often cures which tachycardias?

This chapter will review the initial bedside approach to a hospitalized patient with a new, potentially life-threatening tachycardia, defined as a heart rate ≥ 100 beats per minute (bpm). The reader is then referred to the cardiology chapters for definitive management of specific arrhythmias.

Normally, the sinoatrial node spontaneously activates the right atrium, then the interatrial septum, and then the left atrium. The initial portion of the P wave represents depolarization of the right atrium and the last portion depolarization of the left atrium. Normally, the atrioventricular (AV) node, His bundle, and bundle branches transmit impulses anterogradely from the atria to the ventricles. The QRS complex represents ventricular depolarization and the ST-T-U complex represents repolarization (Figure 100-1).

Unlike the normal AV conducting pathway, anomalous bands of tissue—accessory pathways—may be able to conduct in both directions between the atria and ventricles in a retrograde and antegrade fashion. Some anomalous bands of tissue, concealed bypass tracts, can conduct in a retrograde direction only from the ventricles to the atria.

Supraventricular tachycardias (SVTs) include all tachycardias that arise above the bifurcation of the bundle of His or that have mechanisms depending on the bundle of His.

Paroxysmal supraventricular tachycardias usually have narrow complexes with a normal QRS duration of < 90 ms; some, however, may have aberrant conduction notable for a different QRS configuration from the baseline ECG. Intraventricular conduction disturbances may be incomplete (100–120 ms) or complete bundle branch blocks (QRS ≥ 120 ms in duration) and may be rate related. A right bundle branch block (RBBB) configuration is more common than a left bundle branch block (LBBB) aberrant pattern. The altered depolarization causes secondary repolarization ST-T abnormalities, discordance of QRS-T wave vectors. Ischemia, electrolyte disturbances, and digitalis cause primary depolarization ST-T abnormalities independent of the QRS vector. Sudden death from SVT is rare.

Ventricular tachycardia (VT) arises from the ventricles and is more likely to cause cardiac compromise and sudden death.

Is This Patient Hemodynamically Stable?

Critical assessment of a tachyarrhythmia requires a determination of whether the patient has a potentially life-threatening arrhythmia. The first step always begins with reviewing the patient's vital signs and identifying any artifacts that may have produced ECG findings mimicking cardiac arrhythmias. For example, motion artifact from muscle tremors or rigors may produce ECG changes that simulate cardiac tachyarrhythmias on a cardiac monitor tracing. When hemodynamic instability exists, VT is assumed as the cause of the wide-complex tachycardia, and clinicians should proceed promptly to direct-current cardioversion according to ACLS protocols (Figure 100-3).

In hemodynamically stable patients with sustained SVT, clinicians should try to determine the mechanism of the tachycardia before initiating treatment.

ECG Interpretation

The goal of ECG interpretation is to identify the location of the ectopic impulse formation and to look for evidence of myocardial ischemia. (See Chapter 102: The Resting Electrocardiogram).

Are the QRS Complexes Narrow or Wide?

During the assessment of hemodynamic stability, clinicians examine the monitor strip to determine whether the QRS complex is narrow (<90 ms) or wide (> 90 ms). A SVT with intraventricular aberrant conduction, a SVT conducting to the ventricles over an accessory pathway, and a VT can all produce wide complex regular tachycardia. Distinguishing VT from SVT with aberrancy or SVT over an accessory pathway has important management implications.

Until proven otherwise, patients who have a wide QRS complex tachycardia and a history of structural heart disease (coronary artery disease or cardiomyopathy) are assumed to have VT. Application of the Brugada criteria may help differentiate VT from SVT with aberrant conduction, but requires interpretation of a 12-lead ECG.

The presence of atrioventricular (AV) dissociation, fusion beats, and capture complexes generally favor the diagnosis of VT. AV dissociation, when the atrial and ventricular rhythms are independent of each other, is present when the P waves “march” through the tachycardic sequence and surface at the appropriate time interval after the last QRS complex of the tachycardia. The ventricular rate is greater than or equal to the atrial rate. The absence of P waves in up to 70% of the VT cases, should not, therefore, reassure the examiner that the arrhythmia is supraventricular in origin. In addition, AV dissociation may occur in the presence of an accelerated junctional rhythm that is faster than sinus rhythm and hence is not specific for VT (Figure 100-4).

Fusion beats, arising from simultaneous activation of the ventricle from two sources, have a QRS configuration that is intermediate between supraventricular and ventricular complexes, and arise when the ventricle is depolarized simultaneously via the normal conduction system and a ventricular focus (Figure 100-5).

A markedly widened QRS > 140 ms supports the diagnosis of VT, especially if associated with a left axis of the QRS complex in the frontal plane. Activation of the ventricles over an accessory pathway generally proceeds from the base toward the apex resulting in predominantly positive QRS complexes in the precordial leads V4 to V6. The finding of negative QRS complexes in leads V4 to V6 makes VT more likely, since an LBBB conduction pattern has negative QRS complexes in these leads (Table 100-1).

What Is the Rate of the Tachycardia Based on the R-R Interval?

In patients with SVT, the heart rate must be ≥ 100 bpm but ventricular rates can be lower due to the presence of AV block. Sinus tachycardia is a regular narrow complex rhythm with a rate > 100 bpm. P waves are usually visible unless the rate is so rapid that they are buried in the T waves. Physiologic stress commonly causes sinus tachycardia, which should lessen with treatment of the underlying problem (such as postoperative pain, hypovolemia from blood loss or insufficient oral intake, sepsis, or withdrawal states).

Most patients with atrial flutter (AFl) have an atrial rate around 300 beats per minute, so with 2:1 conduction, the ventricular rate will be about 150 bpm and characteristic negatively directed “sawtooth” atrial waveforms are present in the inferior leads. The mechanism of this common form of Type I classic AFl is a macro reentrant circuit around the entire right atrium in a counterclockwise direction. A less common form of classic AFl occurs when a macro reentrant circuit proceeds around the right atrium in a clockwise direction, producing positive atrial waveforms in the inferior leads. Type II AFl has faster atrial rates in the range of 340 to 440 bpm. Sometimes the P wave can get buried in the T wave and be missed unless multiple leads from the ECG are examined. Carotid sinus pressure or adenosine administration may transiently slow the ventricular rate so that atrial waveforms can be appreciated (Figure 100-6).

Unlike sinus tachycardia, AFl, and other types of tachycardias that originate in the atrium, the mechanism of atrioventricular nodal reentry (AVNRT) involves a reentrant circuit within the AV node. The ventricular rate of AVNRT is typically in the range of 150–250 bpm with narrow QRS complexes. If visible, the P wave appears at the terminal portion of the QRS complex, reflecting retrograde atrial depolarization. In atrioventricular reentrant tachycardia (AVRT) atrial depolarization occurs later than in AVNRT so that the P waves may appear superimposed on the ST segment or T wave. Atrial tachycardia or AVRT is much less common than AVNRT (Figure 100-7).

Is the Rhythm Regular or Irregular Based on the R-R Interval?

Sinus tachycardia, AFl with consistent AV conduction such as 2:1 block, AVNRT, AVRT, and atrial tachycardia cause regular tachyarrythmias. Atrial fibrillation (AF), multifocal atrial tachycardia (MAT), and tachyarrythmias due to multiple anterograde AV nodal pathways cause irregularly irregular rhythms (Figures 100-8 to 100-10). MAT may be distinguished from sinus tachycardia with frequent multifocal atrial premature complexes because it does not have one dominant atrial pacemaker. MAT may be identified by ectopic P waves of at least three morphologies best seen in leads II, III, and V1, a ventricular rate of > 100 bpm, isoelectric baseline between P waves, and varying PP, PR, and RR intervals. Some P waves may be blocked due to their rapid rate. Atrial tachycardias with variable AV block may also appear irregular. It is sometimes helpful to look for discrete RR intervals that have a common divisor, as for example, a rate of 150 bpm for some sequences and 100 bpm for others consistent with AFl with variable block (2:1 and 3:1 with a stable atrial rate of 300 bpm) (Table 100-2).

Are P Waves Present during the Tachyarrhythmia? If Yes, What Is the Morphology of the P Waves and How Do the P Waves Compare to the Baseline ECG When the Patient Is in Sinus Rhythm?

The next step is to identify the presence of atrial activity and to examine the relationship between the P wave and the QRS complex. The P waves may be embedded at the end of the QRS complexes or within the T wave; therefore, it is important to compare the tracing to prior ECGs to examine for changes in the QRS and T wave morphology. The normal P wave is 0.08 to 0.11 seconds in duration and is always upright in leads I and II and always negative in lead aVR. It is usually upright in lead aVF. In lead III the normal P wave may be positive, negative, or biphasic and in lead aVL the normal P wave is usually negative or biphasic. In leads V1 and V2 the normal P wave is often biphasic and is always positive in leads V3 to V6.

Inferior leads, especially lead II and lead V1 are most helpful places to start although all leads should be examined for P waves. Ectopic atrial rhythms may have upright P waves arising from an atrial focus near the sinus node or inverted arising from an ectopic focus in the lower atrium. The location of the ectopic focus relative to the AV conduction system and the presence or absence of delay in this system determines the duration of the PR interval (whether short, normal, or prolonged). The QT interval (representing the duration of ventricular depolarization and repolarization) is typically normal in ectopic rhythms. Ectopic P waves will have a different morphology from sinus P waves and may be easier to identify if there is an earlier ECG tracing of sinus rhythm used as a reference. If the right atrium is activated first, as in sinus rhythm, the P wave is positive or biphasic in lead aVL and negative or biphasic in lead V1. If the left atrium is activated first, the P wave is negative or isoelectric in lead aVL and lead V1. Negative P waves in the inferior leads are seen in AVNRT and AVRT and atrial tachycardias that originate in the lower atrium.

When ectopic P waves precede the QRS complex, even if the QRS complex is wide, the tachycardia is supraventricular. If retrograde P waves (inverted in lead II and upright in lead aVR) precede the QRS complex, even if the QRS complex is wide, the tachycardia is also supraventricular in origin. When ectopic P waves follow the QRS complexes, the origin of the tachyarrhythmia may be either supraventricular from the AV junction or ventricular. Tachycardia arising from the AV node more commonly has narrow QRS complexes. However, AV junctional tachycardia may be associated with aberrant conduction causing a wide QRS complex tachycardia.

If P Waves Are Present, What Is the R-P Interval?

This requires examination of the ECG waveform and intervals to identify the presence of P waves that may be superimposed on the QRS complex or on the ST segment. If the rhythm strip is V1, for example, it may show both P waves and R waves and is therefore sufficient to determine the R-P interval. If retrograde P waves are located farther from the preceding QRS complex than the following QRS complex, then the tachycardia is a long R-P tachycardia. Sinus tachycardia is a long R-P tachycardia. Sinus tachycardia can be difficult to identify when the P wave fuses with the T wave of the preceding QRS complex. This situation usually occurs in critically ill patients with heart rates greater than 180 bpm, patients receiving pressors, or when there has been significant volume loss. Visible P waves would be expected to be upright in ECG leads I, II, III, and aVF (Table 100-3).

Sinus nodal reentrant tachycardia appears identical to sinus tachycardia with the exception that the initiation and termination of the rapid rhythm is abrupt. The mean heart rate is typically 130–140 bpm. Carotid sinus massage or valsalva may terminate sinus nodal reentrant tachycardia and gradual slowing may precede termination.

Other than sinus tachycardia, atrial tachycardia is the most common long R-P tachycardia. AV block may occur without interrupting the tachycardia because the AV node is not an integral part of the arrhythmia circuit. An ectopic atrial tachycardia with 2:1 block may be identified by finding a second P wave buried in the terminal portion of the QRS complex in the inferior leads. In this case measurement of the timing of deflections will demonstrate that they occur exactly halfway between the more visible P waves (Figure 100-11).

Suspect digitalis intoxication if paroxysmal tachycardia is associated with AV block.

Is the Mode of Onset and Termination of the Tachycardia Captured on the ECG?

Premature atrial complexes (PAC) trigger most paroxysmal supraventricular tachycardias. Ventricular premature complexes (VPC) usually trigger AV node-dependent tachycardias.

Is There a Baseline ECG?

If the patient is stable, obtain a 12-lead ECG to look for any changes from the baseline ECG that might suggest cardiac ischemia and for the presence of preexisting bundle block (Figure 100-12). Is there evidence of a prolonged QT interval, AV dissociation, capture and fusion beats, extreme axis deviation, atypical bundle branch block that might suggest preexisting structural heart disease increasing the likelihood of a ventricular origin to the tachycardia? Although uncommon, ECG changes suggestive of Wolf-Parkinson-White (WPW), prolonged or shortened QT interval, R precordial ST abnormalities characteristic of the Brugada syndrome, and epsilon waves seen in arrhythmogenic RV dysplasia in the baseline ECG have important management implications.

A baseline ECG may allow for comparison of the QRS complexes during the tachycardia with the configuration of isolated ectopic beats preceding the tachycardia. If preexcitation is apparent during normal sinus rhythm, the tachycardia is preexcited. Isolated atrial premature beats may lead to atrial group beats, atrial tachycardia, atrial fibrillation (AF), or atrial flutter (AFl). When the atrial tachyarrhythmias terminate, isolated atrial premature contractions may follow. Likewise, when the QRS configuration during isolated ventricular premature contractions before and after the tachycardia is identical to that present during the tachycardia, the origin of the tachycardia is ventricular.

Additional Data

For hemodynamically stable patients, physicians should perform a targeted history and physical examination specifically looking for signs and symptoms of significant heart and lung disease as well as vascular disease. Symptoms are more common in patients with structural heart disease. The neck veins should be examined for the presence of cannon A-waves that match the rate of tachycardia due to atrial contraction during ventricular systole when the tricuspid valve is closed. Canon A-waves would not occur in sinus tachycardia, ectopic atrial tachycardia, or atrial flutter. Their presence does not differentiate the two principal types of AV reentrant tachycardia. Less commonly, cannon A-waves may occur in VT when retrograde AV conduction depolarizes the atria during ventricular systole.

For the postoperative patient, electrolytes, cardiac enzymes, and complete blood count should be obtained in addition to a resting ECG. Oxygen should be administered as necessary and continuous ECG monitoring should be provided (Figure 100-13).

Attempt to Elucidate the Underlying Mechanism by Slowing or Terminating the Tachycardia

The treatment options for tachycardia depend on identification of the underlying mechanism. An acutely ill patient may have difficulty performing the Valsalva maneuver, a maintained forced expiratory effort against a closed glottis, correctly. The examiner may give the patient simple instructions to insert his index finger in his mouth, close his mouth around his finger, and exhale into a closed space. Ausculation for carotid bruits prior to performing carotid massage is a reasonable but very imprecise way to determine whether cerebrovascular disease is present, but most experts would avoid carotid massage if they identified a cervical bruit. The Valsalva maneuver, carotid sinus massage, and facial immersion in cold water did not slow down or terminate the tachycardia in this patient.

Adenosine potently blocks AV conduction transiently and would be expected to terminate AVNRT but not sinus tachycardia, atrial tachycardia, atrial flutter, or nonparoxysmal junctional tachycardia. Before administering adenosine, physicians should specifically inquire about a history of asthma or reversible COPD and whether the patient is receiving dipyridamole. Adenosine can trigger acute bronchospasm in vulnerable patients and dipyridamole can potentiate AV block. At the time of administration, they should also warn the patient about transient sensations of chest tightness, nausea, and flushing.

Intravenous administration of nodal blockers may reduce the ventricular rate and alleviate distressing symptoms despite persistence of the tachycardia. Nondihydropyridine calcium-channel blockers are preferable to adenosine in patients with atrial tachycardia. However, adenosine and calcium-channel blockers should be avoided in patients who have AF with an anterogradely conducting accessory pathway since slowing the native pathway may precipitate conduction down the accessory pathway, thereby increasing the ventricular rate. For surgical patients already taking a beta-blocker, the negative inotropic effects of calcium channel blockers may be accentuated.

In a postoperative patient, sinus tachycardia is common due to the adrenergic drive that develops as a result of hypotension, volume shifts, acute blood loss, pain and/or anxiety.

AVNRT typically occurs in otherwise healthy patients without valvular heart disease or organic heart disease. However, it may occur slightly more often in patients when underlying structural heart disease is present, possibly because these patients are more likely to have atrial or ventricular premature beats that can precipitate individual episodes of tachycardia.

In this patient, the tachycardia was mostly regular although at times appeared slightly irregular as well. The cycle length in most cases of paroxysmal SVT is regular although it may vary in a patient with more than one anterograde AV nodal pathway. Variable block in the AV node can produce a notably irregular ventricular rate in patients with atrial tachycardias.

Tachycardia-contingent bundle branch block may occur if either the right- or left-sided bundle branch reaches its effective refractory period and cannot conduct impulses to match the rapid rate of the tachycardia. In a patient with paroxysmal SVT-related wide complex tachycardia and a structurally normal heart, the bundle branch pattern will usually have a typical appearance, identical to conventional bundle branch morphology.

A change in AV rate with the development of bundle branch block aberration can only mean that the bundle branch block is part of the tachycardia circuit. This feature excludes every SVT mechanism except AV reentry. If there is no change in the AV rate with the development of bundle branch block aberration, AVNRT or atrial tachycardia is suggested because the bundle branches are not integral parts of these tachycardia mechanisms.

The presence of P-waves eliminated the possibility of atrial fibrillation in this postoperative patient, and no flutter waves were appreciated with slowing of the rhythm in response to vagal maneuvers. In addition to atrial fibrillation, preexcitation or conduction over an accessory pathway may cause the QRS morphology to be wide during SVT. Although this patient may have had some subtle slurring of the QRS in the precordial leads (ie, delta waves) on her baseline ECG, she did not have a short PR or wide QRS complex so WPW with a reentrant circuit seemed unlikely. She was also taking bupropion, which can cause tachycardia and arrhythmia. Her magnesium level was low and this may have contributed. Rheumatoid arthritis has been associated with conduction system disease. Comparison of P-wave morphology during sinus rhythm and during the tachycardia helped differentiate sinus tachycardia from atrial tachycardia.

In summary, the most likely etiology of the SVT was postoperative stress and hypoxia. Postoperative ischemia is also possible but less likely.

A stepwise approach to a hospitalized patient with a tachyarrhythmia should begin with asking the following questions:

1. Is this patient hemodynamically stable?

2. Are the QRS complexes narrow or wide?

3. Is the rhythm more likely to be ventricular in origin?

4. If the origin of the rhythm is likely supraventricular, what is the rate of the tachycardia based on the R-R interval? Is the rhythm regular? Are P waves present and if so, is their morphology the same as the baseline ECG when the patient is in NSR? What is the R-P interval?

Treatment of the rhythm will hinge on whether the patient has underlying structural heart disease, is hemodynamically unstable or in distress, and the likely mechanism. For all patients, electrolytes, cardiac enzymes, and a complete blood count should be obtained in addition to a resting ECG if possible. Oxygen should be administered as necessary and continuous ECG monitoring should be provided. Serum K+ and Mg+++ should be repleted, hypoxia corrected, underlying precipitants such as failure to administer home medications, pain and withdrawal states identified and treated. Persistent tachycardias unresponsive to the usual measures or clinical deterioration should prompt emergent specialty consultation.