• Sinus arrhythmia. Sinus arrhythmia is characterized by phasic variation in sinus cycle length.¹⁴ In the respiratory type, heart rate increases with inhalation and decreases with exhalation. It is seen predominantly in the young and reflects variations in parasympathetic and sympathetic signals to the heart and is considered a normal event. Nonrespiratory sinus arrhythmia is unrelated to respiratory effort and is seen in digitalis intoxication.

• Sinus tachycardia. Tachycardia in an adult is defined as a heart rate greater than 100 beats per minute, with otherwise normal findings on the ECG.¹⁴ The rate usually is between 100 and 180 beats per minute. This condition most often is a physiologic response to exercise, anxiety, stress, or emotion. Pathophysiologic causes include fever, hypotension, hypoxia, infection, anemia, hyperthyroidism, and heart failure. Drugs that may cause sinus tachycardia include atropine, epinephrine, alcohol, nicotine, and caffeine.

• Sinus bradycardia. Bradycardia is defined as a heart rate less than 60 beats per minute, with an otherwise normal ECG tracing.¹⁴ It often coexists with a sinus arrhythmia. It is relatively common among well-conditioned athletes and healthy young adults and decreases in prevalence with advancing age. Pathophysiologic causes of bradycardia include intracranial tumor, increased intracranial pressure, myxedema, hypothermia, and gram-negative sepsis. Bradycardia may occur during vomiting and vasovagal syncope and as the result of carotid sinus stimulation. Drugs that may cause bradycardia include lithium, amiodarone, beta blockers, clonidine, and calcium channel blockers.

• Premature atrial complexes. Impulses arising from ectopic foci anywhere in the atrium may result in premature atrial beats. Premature atrial complexes, or contractions, occur frequently in otherwise healthy people but often occur during infection, inflammation, or myocardial ischemia.¹⁴ They may be provoked by smoking, lack of sleep, excessive caffeine, or alcohol.¹³ They are common in conditions associated with dysfunction of the atria such as congestive heart failure.

• Atrial flutter. Atrial flutter is characterized by a rapid, regular atrial rate of 250 to 350 beats per minute. It is rare in healthy persons and most often occurs in association with septal defects, pulmonary emboli, mitral or tricuspid valve stenosis or regurgitation, or chronic ventricular failure.¹⁴ It ialso may be noted in patients with hyperthyroidism, alcoholism, or pericarditis.

• Atrial fibrillation. AF is the most common sustained arrhythmia in adults.¹⁹ It is characterized by rapid, disorganized, and ineffective atrial contractions that occur at a rate of 350 to 600 beats per minute. The ventricular response is highly irregular. The atria do not contract effectively, thereby promoting the formation of intraarterial clots, along with consequent embolism and stroke. Thus, patients with AF who are at risk for stroke (e.g., history of previous stroke, systemic emboli, valvular heart disease, hypertension, diabetes, coronary heart disease, heart failure) should be placed on a regimen of warfarin for antithrombotic therapy, with a target international normalized ratio (INR)²⁰ of 2.0 to 3.0.^14,21 Patients who cannot take warfarin, as well as those who do not have risk factors for stroke, may be managed with dabigatran or aspirin therapy. AF is associated with a history of congestive heart failure, valvular heart disease and stroke, left atrial enlargement, abnormal mitral or aortic valve function, or treated systemic hypertension, as well as with advanced age.^12,22 It may occur intermittently or may be chronic. Symptoms are variable and depend on underlying cardiac status, ventricular rate, and loss of atrial contraction. Treatment consists of medication or cardioversion.

• Atrial tachycardias. Any tachycardia arising above the AV junction for which the ECG shows a P wave configuration different from that for sinus rhythm is called atrial tachycardia.¹⁹ Atrial tachycardia is characterized by an atrial rate between 150 and 200 beats per minute¹⁴ and may result from enhanced normal automaticity, abnormal automaticity, triggered activity, or reentry. It commonly is seen in patients with coronary artery disease, myocardial infarction (MI), cor pulmonale (right ventricular hypertrophy and pulmonary hypertension), or digitalis intoxication.

• Preexcitation syndrome (e.g., Wolff-Parkinson-White syndrome). The atria and ventricles are electrically insulated from each other by fibrous tissue that forms the anatomic AV junction. Normally, impulses are transmitted from atria to ventricles across this electrical bridge; however, in some persons, additional electrical bridges connect the atria and ventricles, bypassing the normal pathways and forming the basis for preexcitation syndromes such as Wolff-Parkinson-White syndrome.¹⁹ The basic defect in this disorder involves premature activation (preexcitation) of the ventricles by way of an accessory AV pathway that allows the normal SA-AV pathway to be bypassed. This accessory pathway allows rapid conduction and short refractoriness, with impulses passed rapidly between atria and ventricles, and it provides a route for reentrant (backflow) tachyarrhythmias. Resultant paroxysmal tachycardia is characterized by a normal QRS complex, a regular rhythm, and ventricular rates of 150 to 250 beats per minute, along with sudden onset and termination.¹⁴ Wolff-Parkinson-White syndrome is found in all age groups but is more prevalent among men and decreases with age. For most patients with recurrent tachycardia, the prognosis is good, but sudden death occurs rarely, at a frequency of 0.1%.¹⁴

• AV block. Heart block is a disturbance of impulse conduction that may be permanent or transient, depending on the underlying anatomic or functional impairment. Conduction impairment in heart block is classified by severity, with the various forms divided into three categories.¹⁴ During first-degree heart block, conduction time is prolonged, but all impulses are conducted. Second-degree heart block occurs in two forms: Mobitz type I (Wenckebach) and type II. Type I heart block is characterized by progressive lengthening of conduction time until an impulse is not conducted. Type II heart block denotes occasional or repetitive sudden block of conduction of an impulse without previous lengthening of conduction time. When no impulses are conducted, complete or third-degree block is present. AV block occurs when the atrial impulse is conducted with delay or is not conducted at all to the ventricles at a time when the AV junction is not physiologically refractory.¹⁴ Conduction delay may occur at the AV node, within the His-Purkinje system (bundle branches), or at both sites. AV block may be first-degree or second-degree block, or it may be complete. AV block may be caused by a multitude of conditions such as surgery, electrolyte disturbance, myoendocarditis, tumor, myxedema, rheumatoid nodules, Chagas’ disease,* calcific aortic stenosis, polymyositis, and amyloidosis. In children, the most common cause is congenital. Drugs (e.g., digitalis, propranolol, potassium, quinidine) also may cause AV heart block. Symptoms increase in severity with increasing degree of block.