1. Sinus Arrhythmia, Bradycardia, & Tachycardia

Sinus arrhythmia is a cyclic increase in normal heart rate with inspiration and decrease with expiration. It results from reflex changes in vagal influence on the normal pacemaker and disappears with breath holding or increase of heart rate due to any cause. It has no clinical significance. It is common in both the young and the elderly.

Sinus bradycardia is a heart rate slower than 50/min due to increased vagal influence on the normal pacemaker or organic disease of the sinus node. The rate usually increases during exercise or administration of atropine. In healthy individuals, and especially in patients who are in excellent physical condition, sinus bradycardia to a rate of 50 or even lower is a normal finding.

However, severe sinus bradycardia may be an indication of sinus node pathology (see below), especially in elderly patients and individuals with heart disease. It may cause weakness, confusion, or syncope if cerebral perfusion is impaired. Atrial and ventricular ectopic rhythms are more apt to occur with slow sinus rates. Pacing may be required if symptoms correlate with the bradycardia.

Sinus tachycardia is defined as a heart rate faster than 100 beats/min that is caused by rapid impulse formation from the normal pacemaker; it occurs with fever, exercise, emotion, pain, anemia, heart failure, shock, thyrotoxicosis, or in response to many drugs. Alcohol and alcohol withdrawal are common causes of sinus tachycardia and other supraventricular arrhythmias. The onset and termination are usually gradual, in contrast to paroxysmal supraventricular tachycardia due to reentry. The rate infrequently exceeds 160/min but may reach 180/min in young persons. The rhythm is basically regular, but serial 1-minute counts of the heart rate indicate that it varies five or more beats per minute with changes in position, with breath holding, or with sedation. Rare individuals have persistent or episodic “inappropriate” sinus tachycardia that may be very symptomatic or may lead to left ventricular contractile dysfunction. Radiofrequency modification of the sinus node has mitigated this problem.

Preferences:
_{Mangrum JM et al: The evaluation and management of bradycardia. N Engl J Med 2000;342:703.}

2. Atrial Premature Beats (Atrial Extrasystoles)

Atrial premature beats occur when an ectopic focus in the atria fires before the next sinus node impulse or a reentry circuit is established. The contour of the P wave usually differs from the patient’s normal complex. The subsequent R-R cycle length is usually unchanged or only slightly prolonged. Such premature beats occur frequently in normal hearts and are never a sufficient basis for a diagnosis of heart disease. Speeding of the heart rate by any means usually abolishes most premature beats. Early atrial premature beats may cause aberrant QRS complexes (wide and bizarre) or may be nonconducted to the ventricles because the latter are still refractory.

3. Differentiation of Aberrantly Conducted Supraventricular Beats from Ventricular Beats

This distinction can be very difficult in patients with a wide QRS complex; it is important because of the differing prognostic and therapeutic implications of each type. Findings favoring a ventricular origin include (1) atrioventricular dissociation, (2) a QRS duration exceeding 0.14 s, (3) capture or fusion beats (infrequent), (4) left axis deviation with right bundle branch block morphology, (5) monophasic (R) or biphasic (qR, QR, or RS) complexes in V1, and (6) a qR or QS complex in V6. Supraventricular origin is favored by (1) a triphasic QRS complex, especially if there was initial negativity in leads I and V6, (2) ventricular rates exceeding 170/min, (3) QRS duration longer than 0.12 s but not longer than 0.14 s, and (4) the presence of preexcitation syndrome.

The relationship of the P waves to the tachycardia complex is helpful. A 1:1 relationship usually means a supraventricular origin, except in the case of ventricular tachycardia with retrograde P waves. If the P waves are not clearly seen, Lewis leads (in which the right arm electrode is placed in the V1 position two interspaces higher than usual and the left arm electrode is placed in the usual V1 position) may be employed. This accentuates the size of the P waves. Esophageal leads, in which the electrode is placed directly posterior to the left atrium, achieve the same effect even more clearly. Right atrial electrograms may also help to clarify the diagnosis by accentuating the P waves.

4. Paroxysmal Supraventricular Tachycardia

This is the commonest paroxysmal tachycardia and often occurs in patients without structural heart disease. Attacks begin and end abruptly and may last a few seconds to several hours or longer. The heart rate may be 140-240/min (usually 160-220/min) and is perfectly regular (despite exercise or change in position). The P wave usually differs in contour from sinus beats. Patients may be asymptomatic except for awareness of rapid heart action, but some experience mild chest pain or shortness of breath, especially when episodes are prolonged, even in the absence of associated cardiac abnormalities. Paroxysmal supraventricular tachycardia may result from digitalis toxicity and then is commonly associated with atrioventricular block.

The most common mechanism for paroxysmal supraventricular tachycardia is reentry, which may be initiated or terminated by a fortuitously timed atrial or ventricular premature beat. The reentry circuit most commonly involves dual pathways (a slow and a fast pathway) within the atrioventricular node. This is referred to as AV nodal reentry tachycardia (AVNRT). Less commonly, reentry is due to an accessory pathway between the atria and ventricles (AVRT). Approximately one-third of patients with supraventricular tachycardia have aberrant pathways to the ventricles. The pathophysiology and management of arrhythmias due to accessory pathways differs in important ways and is discussed separately below.

Treatment of the Acute Attack

In the absence of heart disease, serious effects are rare, and most attacks break spontaneously. Particular effort should be made to terminate the attack quickly if cardiac failure, syncope, or anginal pain develops or if there is underlying cardiac or (particularly) coronary disease. Because reentry is the most common mechanism for paroxysmal atrial tachycardia, effective therapy requires that conduction be interrupted at some point in the reentry circuit.

A. Mechanical Measures
A variety of methods have been used to interrupt attacks, and patients may learn to perform these themselves. These include Valsalva’s maneuver, stretching the arms and body, lowering the head between the knees, coughing, and breath holding. Carotid sinus massage is often performed by physicians but should be avoided if the patient has carotid bruits or a history of transient cerebral ischemic attacks. Firm but gentle pressure and massage are applied first over the right carotid sinus for 10-20 seconds and, if unsuccessful, then over the left carotid sinus. Pressure should not be exerted on both sides at the same time! Continuous electrocardiographic or auscultatory monitoring of the heart rate is essential so that pressure can be relieved as soon as the rhythm is broken or if excessive bradycardia occurs. Carotid sinus pressure will interrupt up to half of the attacks, especially if the patient has received a digitalis glycoside or other agent (such as adenosine or a calcium channel blocker) that delays atrioventricular conduction. These maneuvers stimulate the vagus nerve, delay atrioventricular conduction, and block the reentry mechanism, terminating the arrhythmia.

B. Drug Therapy
If mechanical measures fail, two rapidly acting intravenous agents will terminate more than 90% of episodes. Intravenous adenosine has a very brief duration of action and minimal negative inotropic activity. A 6-mg bolus is administered. If no response is observed after 1-2 minutes, a second 12-mg bolus should be given, followed by a third if necessary. Since the half-life of adenosine is less than 10 seconds, the drug must be given rapidly (in 1-2 seconds from a peripheral intravenous line); use half the dose if given through a central line. Adenosine is very well tolerated, but nearly 20% of patients will experience transient flushing, and some patients experience severe chest discomfort.

Calcium channel blockers also rapidly induce atrioventricular block and break most episodes of reentry supraventricular tachycardia. Intravenous verapamil may be given as a 2.5-mg bolus, followed by additional doses of 2.5-5 mg every 1-3 minutes up to a total of 20 mg if blood pressure and rhythm are stable. If the rhythm recurs, further doses can be given. Oral verapamil, 80-120 mg every 4-6 hours, can be used as well in stable patients who are tolerating the rhythm without difficulty, but avoid it if there is any concern that the arrhythmia may be ventricular in origin. Intravenous diltiazem (0.25 mg/kg over 2 minutes, followed by a second bolus of 0.35 mg/kg if necessary and then an infusion of 5-15 mg/h) may cause less hypotension and myocardial depression.

Esmolol, a short-acting beta-blocker, may also be effective; the initial dose is 500 ug/kg intravenously over 1 minute followed by an infusion of 25-200 ug/min. Parasympathetic stimulating drugs such as edrophonium, 5-10 mg intravenously, which delay atrioventricular conduction, may break the reentry mechanism. Because it frequently causes nausea and vomiting, it should be used only if the previously discussed agents fail. Metaraminol or phenylephrine, alpha-adrenergic stimulants that activate the baroreceptors by raising the blood pressure and causing vagal stimulation, can break attacks but should be used cautiously because they may provoke excessive hypertension. Digoxin is effective, but it often requires several hours to safely administer an adequate dose. An initial dose of 0.5-0.75 mg intravenously over 20 minutes, followed by 0.25-mg or 0.125-mg increments every 2-4 hours up to a total of 1-1.25 mg, is used. Intravenous procainamide may terminate supraventricular tachycardia; however, since it facilitates atrioventricular conduction and an initial increase in rate may occur, it is usually not given until after digoxin, verapamil, or a beta-blocker has been administered.

C. Cardioversion
If the patient is hemodynamically stable or if adenosine and verapamil are contraindicated or ineffective, synchronized electrical cardioversion (beginning at 100 J) is almost universally successful. If digitalis toxicity is present or strongly suspected, as in the case of paroxysmal tachycardia with block, electrical cardioversion should be avoided.

Prevention of Attacks

A. Radiofrequency Ablation
Because of concerns about the safety and the intolerability of antiarrhythmic medications, radiofrequency ablation is the preferred approach to patients with recurrent symptomatic reentry supraventricular tachycardia, whether it is due to dual pathways within the atrial ventricular node or to accessory pathways.

B. Drugs
Digoxin orally is the usual drug of first choice because of its convenience and efficacy. Verapamil, alone or in combination with digitalis, is a second choice. (Note: Verapamil increases digoxin serum levels.) Beta-blockers are also effective. Patients who do not respond to agents that increase refractoriness of the atrioventricular node may be treated with class Ia (disopyramide, quinidine, procainamide), class Ic (propafenone), or class III (sotalol, amiodarone) drugs. In patients with evidence of structural heart disease, either sotalol or amiodarone is probably a better choice because of the lower incidence of ventricular proarrhythmia during chronic therapy.

Preferences:
_{Chauhan VS et al: Supraventricular tachycardia. Med Clin North Am 2001;85:193.}

Hebbar AK et al: Management of common arrhythmias: Part I. Supraventricular arrhythmias. Am Fam Physician 2002;65: 2479.