Sinus Bradycardia/Tachycardia Including Respiratory Variablity

Scott Goldston

Sinus Tachycardia

Clinical Highlights

Normal adult heart rates are 60 to 100 beats per minute (bpm). See Chap. 8, section on Normal ECG at Age Intervals for discussion of childhood norms. Sinus tachycardia is a rapid heart rate that originates from the sinus node. Diagnostic criteria include normal P-wave morphology (normal for the patient), normal PR intervals (0.12–0.2 s), and a 1-to-1 P wave to QRS relationship. Rate is usually less than 160 except in critically ill patients. Occasionally, sinus tachycardia cannot be confirmed and other rhythm diagnoses must be considered. There are numerous causes, including fever, dehydration, hypoxia, stimulants (ie, coffee, nicotine, and illicit drugs), pulmonary embolism, anemia, anxiety, hyperthyroidism, hypotension/shock, sepsis, and many more.

ED Care and Disposition

Sinus tachycardia may be perceived as a fast or “pounding” heartbeat. Usually symptoms are felt if there is underlying cardiac disease. Treating the underlying disorder will typically resolve the tachycardia and success can be gauged by the trend toward a normal rate. Consider airway, breathing, and circulation first; oxygen, fluids, airway intervention, or specific therapy are often required.

Pearls and Pitfalls

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  Sinus tachycardia is always 1:1 P wave to QRS conduction.

  
  
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  There is no specific treatment for sinus tachycardia, treat the underlying cause.

  
  
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  If you have trouble identifying P waves in rhythms over 120/minute, consider running the electrocardiogram (ECG) at double speed.

  
  
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  If workup and treatment of suspected sinus tachycardia fail to prove useful, pursue other rhythm diagnoses.

Sinus Bradycardia

Clinical Highlights

Sinus bradycardia is a heart rate that is below 60 bpm originating from the sinus node. In addition to rate, diagnostic criteria include normal P-wave morphology (normal for the patient), normal PR intervals (0.12–0.2 s), and a 1-to-1 P wave to QRS relationship. There are multiple causes including normal physiology (athletes, sleep, etc.), increased vagal activity (cough, vomiting, Valsalva, etc.), or sudden exposure to cold. Several medications cause sinus bradycardia, including beta-blockers, digoxin, calcium channel blockers, amiodarone (and many other antiarrhythmic drugs), and clonidine. There are also many pathologic causes, such as increased intracranial pressure, acute myocardial infarction (AMI), hypothyroidism, and carotid sinus hypersensitivity. Although frequently asymptomatic, the patient may have fatigue or symptoms of presyncope or syncope.

ED Care and Disposition

If asymptomatic, no treatment is indicated. Treatment is usually aimed at finding and correcting the source. If required, first-line treatment is almost always atropine. Temporary transcutaneous or transvenous pacing may be required.

Pearls and Pitfalls

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  Sinus bradycardia is the most common presenting arrhythmia in an AMI (up to 15%–25%).

  
  
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  Sinus bradycardia is usually a response to an underlying disease process from medication use or pathology.

Sinus Arrhythmia

Clinical Highlights

Sinus arrhythmia is a normal variant of sinus rhythm, most commonly due to respiratory effect. The criterion is variation in sinus node discharge larger than 0.12 seconds between the shortest and longest intervals (measured by the R-to-R interval). During normal respiration there are changes in the autonomic tone. Inspiring causes a decrease in vagal tone, thus increasing a sinus rate. The opposite is true with expiration, causing the sinus rate to decrease.

Pearls and Pitfalls

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  Sinus arrhythmia is a normal variant of sinus rhythm, and no treatment is required.

Premature Atrial Contractions (PAC)

Jackson Henley

Clinical Highlights

A premature atrial complex (PAC) is an atrial depolarization that originates from an ectopic focus anywhere in the atria outside of the sinoatrial (SA) node. They occur earlier in the cardiac cycle than those originating from the SA node. The patient may present with a chief complaint of palpitations, or they may incidentally be found to have PACs on an ECG or on telemetry monitoring while in the emergency department (ED). PACs are generally benign heart arrhythmias that rarely lead to clinically significant arrhythmias unless the patient has a history of significant arrhythmia such as atrial fibrillation. PACs may be caused by abnormal automaticity within the atria or from a reentry phenomenon. PACs can occur in isolation or may occur as frequently as every other beat, as in atrial bigemeny.

On ECG interpretation, an ectopic P wave will occur in a shorter interval after the prior T wave, indicating that it is premature. It will also have a different morphology than a regular P wave. The P wave of the ectopic focus may have different polarity PR interval compared to the normal P wave. Depending on when the PAC occurs, it may not lead to ventricular depolarization. If the PAC occurs early enough during the cardiac cycle, the atrioventricular (AV) node being in its refractory period may not conduct the signal.

ED Care and Disposition

As PACs rarely lead to clinically significant arrhythmias, PACs usually do not require further workup or intervention. If PACs are accompanied by concerning symptoms such as chest pain or shortness of breath in a patient with underlying cardiopulmonary disease, further testing may be warranted such as cardiac biomarkers, serum electrolytes, or a toxicology screen. Because PACs may be related to a toxin, such as caffeine, alcohol, or tobacco, the patient should be encouraged to stop the potential offending agent. Beta-blockers may improve symptoms associated with PACs by reducing their frequency. These medications can be considered if the symptoms are bothersome to the patient and are interfering with daily activities.

Pearls and Pitfalls

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  PACs are generally considered a benign arrhythmia.

  
  
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  PACs are observed on an ECG as an early atrial depolarization after a preceding T wave with a different morphology than other P waves.

  
  
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  If there is a suspected underlying cause of PACs, especially if it is easily reversible (toxin), this should be addressed. If symptoms persist and interfere with the patient’s life significantly, the use of a beta-blocker may be considered.

Cedric Lefebvre

Clinical Highlights

Wandering atrial pacemaker (WAP) is an electrophysiological phenomenon in which multiple areas, or ectopic foci, within the atria initiate action potentials and temporarily serve as the dominant pacemaker. The constantly shifting location of impulse origin gives the impression of “wandering” foci. Each electrical impulse is transmitted from the atria to the ventricles. This signal conduction leads to ventricular depolarization, and the resulting QRS complexes are narrow and uniform. The overall rhythm is usually irregularly irregular. Each QRS complex will be preceded by a P wave but because the origin of the atrial impulses varies from beat to beat, P-wave morphology will not be uniform. P waves can differ in size, shape, and vector. Typically, WAP will demonstrate at least three different P-wave morphologies on the ECG. The PR interval is generally normal (0.12–0.20 milliseconds) but may vary from beat to beat. The heart rate will be less than 100 bpm. If the heart rate exceeds 100 bpm, the term “multifocal atrial tachycardia” applies.

The causes of WAP include increased vagal tone, digoxin toxicity, chronic lung disease, valvular disease, and coronary disease or ischemia. Certain sympathomimetic medications can induce arrhythmias including WAP. WAP can also occur in normal, healthy patients and during sleep. Patients with WAP may experience palpitations. If the overall heart rate is slow, WAP may cause fatigue or dizziness. At times, WAP is identified incidentally on an ECG.

ED Care and Disposition

WAP is generally a benign condition, is usually transient, and rarely requires treatment. However, the etiology of WAP includes serious underlying medical diseases (ie, lung disease); therefore, an investigation into such conditions should be pursued when indicated. The significance of WAP is most likely related to the condition of the patient in which it is noted. In an asymptomatic young athlete, WAP may stem from increased vagal tone, whereas in a patient with lung disease, WAP may suggest acute illness. In an elderly patient, WAP may be an indication of sinus node malfunction or disease. In rare instances, if the symptoms associated with WAP are persistent or severe, atrial pacing may be necessary.

Pearls and Pitfalls

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  Unlike PACs, a dominant P wave is not identified in WAP and periods of RR interval regularity are not seen.

  
  
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  WAP should not be confused with atrial pauses, atrial arrest, or a junctional escape rhythm with reemergence of sinus beats. Unlike WAP, these arrhythmias are clinically significant and require immediate attention or intervention.

  
  
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  For a patient with a history of respiratory disease found to have WAP, the patient should be assessed for an acute respiratory illness or an exacerbation of chronic respiratory disease and treated accordingly.

David M. Cline

Supraventricular tachycardia (SVT) is a broad category of rapid cardiac rhythms that originate above the bifurcation of the bundle of His or that have mechanisms dependent on the bundle of His (see also Chap. 2, Electrocardiography: Normal Heart, Acute Ischemia, and Chronic Disease, section on Normal Cardiac Conduction). Therefore, SVT can be used to describe sinus tachycardia and atrial tachycardias (AT) including atrial flutter and fibrillation. However, clinicians generally use the term “SVT” to describe paroxysmal, narrow complex tachycardias that start abruptly and end abruptly. Over the last 30 years, the classification of SVT has advanced with the advent of diagnostic and therapeutic cardiac electrophysiology. The two major mechanisms of SVT are reentry and increased automaticity, with reentry accounting for the majority of SVT rhythms.

Clinical Highlights

Patients most commonly complain of sudden onset of palpitations, but may experience anxiety, fatigue, chest pain, near-syncope, or syncope. The most common cause of SVT is AV nodal reentrant tachycardia (AVNRT), the second most common cause of SVT is AV reciprocating, or reentrant tachycardia (AVRT). Table 5.1 lists the major AV node–dependent causes of SVT. Table 5.2 lists the causes of SVT that are not dependent on the AV node for perpetuation of the abnormal rhythm.

ED Care and Disposition

Detailed management of these tachycardias is described in the individual chapters named for each of the different rhythms. In general, for stable patients with narrow complextachycardias where sinus tachycardia can be excluded, a step-wise approach is used in an attempt to abort the tachycardia: vagal maneuvers, adenosine, calcium channel blockers, beta-blockers, and then amiodarone. If at any point the patientbecomes unstable, direct current (DC) cardioversion is recommended; sedate the patient if the clinical circumstances allow time for drug administration. See specific chapters below for treatment recommendations corresponding to the rhythms listed in Table 5.2. The exception is sinus node reentry tachycardia (SNRT), which is treated with vagal maneuvers; adenosine can also be used.

Pearls and Pitfalls

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  Wide complex tachycardia should always be first treated as ventricular tachycardia (VT) unless the diagnosis of SVT with aberrant conduction is 100% certain.

  
  
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  Palpitations secondary to SVT are frequently misdiagnosed as anxiety.

  
  
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  Patients should be warned that adenosine transiently pauses their heartbeat and yields a brief but uncomfortable feeling in many patients.

AV Nodal Reentry Tachycardia Slow-Fast Conduction, Fast-Slow Conduction

David M. Cline

Clinical Highlights

Patients with AV nodal reentrant tachycardia (AVNRT) most commonly complain of sudden onset of palpitations, but may experience anxiety, fatigue, near-syncope, or syncope. AVNRT is the most common cause of SVT. The section earlier, Classification and Mechanisms of SVT, illustrates the AVNRT reentry mechanism. The AVNRT reentry circuit includes the AV node (AV node is in one arm of the circuit); there is a fast arm usually situated along the septal portion of the tricuspid annulus with a longer refractory period, and a slow arm situated posteriorly, close to the coronary sinus ostium, with a short refractory period. The typical mechanism (80%–90% of cases) involves slow–fast conduction, an ectopic beat initiates the reentry circuit, and the impulse finds the fast arm refractory from the last normal sinus node impulse; therefore, it travels down the slow arm but then is able to arc back up the fast arm (which has now completed its refractory period), creating the circus movement of the propagated conduction and resulting tachycardia. Most commonly the P wave is hidden in the QRS, but may be found at the end of the QRS complex as a pseudo r’ wave most commonly in lead I, or a pseudo S wave in leads II and III.

The atypical mechanism (10% of cases) of AVNRT involves fast–slow conduction, an ectopic beat initiates the reentry circuit, the impulse travels down the fast arm, and arcs back up the slow pathway to create the circus movement of the propagated conduction and resulting tachycardia. The QRS is narrow, and the retrograde P wave appears after the corresponding QRS, often in the ST segment. A retrograde P wave following the QRS is also common in AVRT with a concealed pathway (see section AV Reciprocating Tachycardia).

Slow–slow AVNRT is the least common form, accounting for 1% to 5% of cases. In this form of AVNRT, the impulse is first conducted antegrade down the slow AV nodal pathway and then retrograde up the slow left atrial fibers approaching the AV node. The P wave may appear just before the QRS complex, and this makes it hard to distinguish the rhythm from sinus tachycardia.

ED Care and Disposition

For stable patients with AVNRT, a step-wise approach is recommended in an attempt to abort the tachycardia: vagal maneuvers, adenosine, calcium channel blockers, beta-blockers, and then amiodarone. If at any point the patient becomes unstable, DC cardioversion is recommended; sedate the patient if the clinical circumstances allow time for drug administration.

Pearls and Pitfalls

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  Palpitations secondary to AVNRT (the most common cause of SVT) are frequently misdiagnosed as anxiety.

  
  
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  Patients should be warned that adenosine transiently stops their heartbeat and yields a brief but uncomfortable feeling in many patients.

John D. Wofford

Cedric Lefebvre

Clinical Highlights

AV reciprocating (or reentrant) tachycardia (AVRT) is the second most common type of SVT, accounting for 20% to 30% of SVT cases. It is more likely to affect younger male patients in whom sudden onset of palpitations, chest pain, anxiety, dyspnea, and dizziness may be experienced. AVRT involves an accessory pathway outside of the AV node that enables an electrical signal to bypass the AV node from atria to ventricle. A bypass tract may conduct impulses in both directions, whereas a concealed accessory pathway conducts signals exclusively in a retrograde direction from ventricle to atria. See section Classification and Mechanisms of Supraventricular Tachycardia for a discussion of the mechanism of the reentry in AVRT. When the reentry circuit conducts anterograde though the AV node to the ventricle and retrograde through the accessory pathway back to the atrium, orthodromic AVRT is established, yielding a narrow complex tachycardia, which is the most common pattern (85% of AVRT). Conversely, if the activation signal follows the accessory pathway in an anterograde direction to the ventricle and returns to the atrium via the AV node, antidromic AVRT occurs (15% of AVRT), yielding a wide complex tachycardia.

Anterograde conduction through the accessory pathway is typically more rapid than AV nodal transmission; therefore, the ventricles may be activated early (varies with location of the pathway). Such ventricular preexcitation can generate a delta wave on ECG. A symptomatic patient with an accessory pathway that manifests as a delta wave on ECG has Wolf–Parkinson–White (WPW) syndrome (discussed in section WPW Syndrome). Accessory pathways that conduct anterograde may permit unrestricted conduction of rapid atrial impulses, as in atrial fibrillation, resulting in ventricular rates exceeding 300 bpm. This may mimic ventricular tachycardia (VT) or ventricular fibrillation (VF).

ED Care and Disposition

In most cases of AVRT, the ECG reveals a narrow complex tachycardia at a rate of 160 to 300 bpm. P waves may be “buried” in the QRS complex or retrograde P waves can appear after each QRS complex. In orthodromic AVRT, inverted P waves can be seen with a RP interval of less than one half the RR Interval. In antidromic AVRT, a wide complex tachycardia is noted with inverted P waves and a RP interval greater than one half the RR interval.

In general, for stable patients with narrow complex tachycardias, a step-wise approach is used in an attempt to abort the tachycardia: vagal maneuvers, adenosine, calcium channel blockers, beta-blockers, and then amiodarone. If at any point the patient becomes unstable, DC cardioversion is recommended; sedate the patient if the clinical circumstances allow time for drug administration.

Patients with ventricular preexcitation physiology require special consideration because they are at risk for VF induced by rapidly conducted atrial impulses. Adenosine can be considered for SVT in the presence of WPW syndrome if the QRS complexes are narrow. For wide complex tachycardias, adenosine and especially other AV nodal–blocking agents should be avoided. Amiodarone, or procainamide, can be used for hemodynamically stable patients; these drugs are typically successful for either VT or SVT with aberrancy. Use DC cardioversion for unstable patients.

After appropriate measures have been employed to stabilize the patient, cardiology consultation should be obtained for reentry tachycardias. For patients with an easily terminated tachyarrhythmias, mild symptoms, and no comorbidities, close outpatient cardiology follow-up may be reasonable. Long-term management of these conditions can be achieved with medication (often beta-blockers) or potentially with radiofrequency ablation.

Pearls and Pitfalls

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  SVT with a heart rate ≥250 bpm should prompt consideration of the presence of a preexcitation syndrome.

  
  
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  AVRT with widened QRS complexes should not be treated with adenosine or other AV nodal–blocking medications as this could provoke VF in a patient with an accessory pathway.

  
  
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  If there is a doubt concerning the possibility of VT versus SVT with aberrancy in a stable patient, the treatment algorithm for VT should be followed.

  
  
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  Unstable patients with suspected SVT (or VT) should receive DC cardioversion.

J. Stephan Stapczynski

Clinical Highlights

Preexcitation occurs when the ventricular myocardium is depolarized via an alternative electrical connection between the atria and ventricles that bypasses part or all of the normal AV conduction system. The anatomic basis for the WPW syndrome are bundles of myogenic tissue that transverse the AV annulus (termed Kent bundles), directly linking the atria to the ventricles. During sinus rhythm, the atrial depolarization can be conducted down to the ventricles by both the accessory tract and the normal conducting system. In manifest (visible delta wave) WPW syndrome, ventricular activation is produced by a fusion of both pathways and appears on the surface ECG as a short PR interval and a slurred initial portion of the QRS complex (termed the delta wave). The delta wave represents anterograde conduction through the accessory pathway; the remainder of the QRS represents normal conduction through the AV node to His-Purkinje fibers.

SVT are common in patients with WPW syndrome. The most common arrhythmia is paroxysmal reentrant SVT sustained when electrical depolarization is conducted around a loop composed of the bypass tract and the AV conducting system, with the impulse traveling down one and up the other. If reentrant impulses conduct down (anterograde) the AV node His-Purkinje system and back up the accessory pathway, the SVT is narrow and is termed orthodromic AVRT. If the reentrant impulses conduct down the accessory pathway and back up the His-Purkinje system to AV node, the SVT is wide complex and is termed antidromic AVRT (see Classification and Mechanisms of SVT section earlier).

About 5% to 10% of patients with WPW syndrome develop atrial fibrillation or flutter. In these arrhythmias, the predominant pathway for ventricular activation depends on the refractory period of Kent bundle and AV node; the path with the shorter refractory period conducts. New-onset atrial fibrillation in most patients with the WPW syndrome is conducted through the AV node yielding narrow QRS complexes; however, if the accessory pathway conducts primarily, the QRS complexes will be wide and the rate may be excessively rapid. With atrial flutter, 1:1 AV conduction is possible, with ventricular rates of 300 bpm. With atrial fibrillation, very rapid and irregular ventricular rates are possible and excessive stimulation of the ventricles may precipitate ventricular fibrillation (VF).

ED Care and Disposition

Unstable patients with WPW syndrome tachyarrhythmias should be treated with urgent synchronized cardioversion, starting at 100 J, with pharmacologic sedation if time permits.

Stable patients with WPW syndrome and narrow complex SVT can be treated with vagal maneuvers or drugs (adenosine, verapamil, diltiazem, or beta-blockers) that slow conduction through the AV node and break the reentry cycle.

Wide complex tachycardias in patients with WPW syndrome are at risk for rapid ventricular rates and degeneration into VF. Avoid beta-blocking agents, calcium channel blockers, and adenosine that can shorten the refractory period of the Kent bundle and accelerate the ventricular rate. Therefore, wide complex tachycardias in patients with WPW syndrome—antidromic SVT, atrial flutter, or atrial fibrillation with a rapid ventricular response—are best treated with cardioversion. Alternatively, agents that prolong the refractory period of the accessory tract, such as intravenous (IV) procainamide or amiodarone, can be used.

Patients with WPW syndrome and tachyarrhythmias should be referred to a cardiologist with electrophysiology capability; admission to the hospital is required for unstable patients and persistently tachycardic or symptomatic patients. Asymptomatic patients with a new WPW pattern on ECG testing need routine follow-up.

Pearls and Pitfalls

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  The ECG in patients with WPW syndrome may mimic the QRS complex, ST segment, and T wave changes of myocardial ischemia and the delta wave may be difficult to appreciate amid such abnormalities.

  
  
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  A ventricular rate >250 bpm should raise the suspicion of preexcitation syndrome.

  
  
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  Avoid beta-blocking agents, calcium channel blockers, and adenosine in WPW syndrome patients with wide complex tachycardias.

Laura Yoder

Clinical Highlights

The Lown–Ganong–Levine (LGL) syndrome is now believed to be due to enhanced AV nodal conduction. The proposed mechanism is an intranodal bypass tract or atrionodal tracts formerly known as James fibers. This diagnosis has been largely abandoned in the era of electrophysiology. Syndrome diagnostic criteria classically have been: a short PR interval (less than 0.12 s) and a normal QRS complex on ECG, and the clinical history of intermittent palpitations or episodes of paroxysmal SVT, atrial flutter, or atrial fibrillation.

The most important differential diagnosis is that of the WPW syndrome that has a specific treatment. The ECG finding that differs is the delta wave leading into the QRS complex seen with WPW; this is not found in LGL.

ED Care and Disposition

If a patient carries this historical diagnosis, their tachycardia should be treated as other tachycardias, differentiating narrow complex tachycardias from wide complex tachycardias. Unstable patients should undergo emergent synchronized cardioversion. For stable patients with narrow-complex tachycardias, adenosine can be used diagnostically, as well as attempted therapeutically. Wide complex tachycardias should first be treated as VT until proven otherwise.

Pearls and Pitfalls

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  The LGL syndrome is largely a historical diagnosis; patients who have undergone prior electrophysiology testing may carry the diagnosis of enhanced AV nodal conduction that may yield the ECG findings formerly used in the diagnosis of LGL syndrome.

  
  
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  An abnormal QRS pattern or the presence of delta wave should trigger concern for WPW, and should be managed as WPW.

Multifocal Atrial Tachycardia

Jennifer Mitzman

Clinical Highlights

Multifocal atrial tachycardia (AT) occurs when three or more nonsinus atrial foci conduct though the AV node. On an ECG, this presents as more than three distinct P-wave morphologies preceding the QRS complex. The QRS complex is narrow as ventricular conduction through the AV node His-Purkinje system is normal. It is differentiated from Wandering Atrial Pacemaker based on the rate; the rate must be over 100 bpm to meet criteria for Multifocal AT.

Multifocal AT is most commonly seen in patients with chronic lung disease with worsening dyspnea as the chief complaint. However, as a result of the excessive heart rates, patients may present with palpitations, dizziness, or syncope. In patients with other risk factors for myocardial ischemia, MI or acute congestive heart failure can also occur. It has also been documented with metabolic disturbances, septic shock, and historically with theophylline toxicity.

ED Care and Disposition

Treatment of multifocal AT relies foremost on identifying and addressing the underlying condition. Hypoxia associated with chronic comorbidities is the single most frequent cause and should always be addressed first. Verapamil 5 mg IV is considered the first-line therapy when a specific cause is unknown, but should be used with caution in hypotensive patients. Metoprolol is also effective though can cause undesirable bronchospasm.