Pattern Recognition of Arrhythmias Atrial Rhythms

Key Points

• Treatment of asymptomatic or minimally symptomatic, non-life-threatening atrial rhythms should be less risky than no treatment at all.

• The proarrhythmic side effects of drug therapy, including ventricular fibrillation, should be carefully weighed before initiation of drug therapy.

Sinus rhythm is a regular, organized atrial rhythm between 60 and 100 beats/min at rest in healthy individuals. Slower rates as low as 40 to 50 beats/min may be normal in some individuals. Originating high in the right atrium, sinus P waves should be positive in limb leads I and II. Sinus bra-dycardia originates in the sinus node with a P wave indistinguishable from the normal sinus beat, but at a rate slower than the established lower limit of 60 beats/min. This is physiologically normal in patients during sleep, in athletic individuals, and as a consequence of many adrenergic blocking drugs (e.g., p-blockers). Excessive bradycardia may come as a consequence of changes in vagal tone in sleep apnea, during painful stimuli, or mesenteric stretch. There are typically no significant changes in the P-QRS-T intervals with resting sinus bradycardias. During vagal-mediated sinus slowing, associated prolongation in the P-R interval may give a clue as to the etiology. Typically, no treatment is necessary in this benign condition. If the heart rate slowing is excessive or symptomatic, acute atropine administration, epinephrine and dopamine may be used acutely. Over the long term, pacemaker implantation may be necessary.

Sinus arrhythmia is the normal variation of heart rate, likely caused by changes in volume and vagal tone as a consequence of respiration. Occasional slowing below 60 beats/ min at rest is considered acceptable. Patients with high adrenergic tone such as heart failure often lose normal variations in heart rate and a reduction in the degree of sinus arrhythmia. A wandering atrial pacemaker occurs if, at normal heart rates, there is significant variation in the P wave morphology and regularity. Associated P-R and R-R intervals are variable because of the different atrial origin and variations in the prematurity of the atrial beat. It is more frequent in young persons and as a result of changes in vagal tone. The origin of the impulse may arise from within the sinus node complex but at distant sites within the right atrium, giving rise to the changes in P-wave morphology.

A sinus pause and the more extreme case of sinus arrest are demonstrated as a sudden change in the heart rate, often proceeded by mild slowing in the general sinus rate. A sinus pause is typically caused by changes in vagal tone such as gagging, carotid sinus stimulation, pain, and as a consequence of neurocardiogenic activation (Fig. 27-34). Very long episodes of no surface atrial activity are considered to have sinus arrest. This may result from atrial tissue disease, drug therapy, metabolic derangements, and significant vagal activation. Figure 27-35 demonstrates a long pause noted during neurocardiogenic reflex activation during a tilt-table test in the evaluation of syncope. The pause was approximately 50 seconds and resulted in loss of consciousness. Typically, withdrawal of the offending agent, improvement in cardiac

Figure 27-34 Sinus rhythm is followed by sinus arrest and motion artifact during a seizure. Sinus rhythm then resumes.

Figure 27-34 Sinus rhythm is followed by sinus arrest and motion artifact during a seizure. Sinus rhythm then resumes.

twice the shortest P-P interval. The return cycle length is longer than the cycle length before the pause.

function, and elimination of stimuli causing reflex vagal activation help ameliorate symptoms. In difficult symptomatic cases and in patients without a reversible cause, pacemakers may be necessary. Demonstration of sinus pauses and sinus arrest as a cause of dizziness or syncope may be difficult and requires prolonged ambulatory monitoring.

A pause may also result from sinus node disease. In patients with atrial disease, myofibrosis, and atrial pressure overload, changes in the automaticity and rhythmic depolarization of the SA node may be affected. Regular impulses may fail to exit the sinus node complex and depolarize the atrium, resulting in no P wave on the surface ECG and no atrial mechanical contraction. This may occur in regular patterns, such as in type I SA block, characterized by sequential shortening of the P-P interval and then absence of a P wave. The return cycle length is less than twice the shortest cycle length, and the next cycle is longer than the cycle length just before the dropped P wave (Fig. 27-36). Type II SA block is characterized by constant P-P intervals followed by a missing P wave. The pause is twice the cycle length of the P-P interval, and the return cycle length is the same as the sinus rate (Fig. 27-37).

Premature atrial contractions (PACs) or depolarizations may occur frequently in normal patients. The ECG finding is that of an abrupt early P wave that may or may not be followed by a QRS complex. PACs may occur as isolated events, couplets, or as sequential events. Most individuals are minimally symptomatic if at all. Benign causes include exogenous stimulants such as tobacco, caffeine, alcohol excess, and sympa-thomimetic drugs. Digitalis toxicity should be considered in patients receiving digitalis treatment. Patients with underlying heart or lung disease or ectopy from extrinsic compression on the atrium and adjacent abnormal structures may become symptomatic. Reducing automaticity or triggered activity through antiarrhythmic therapy and treating hypoxia and ischemic heart disease may reduce patient symptoms. In asymptomatic patients, no specific therapy is necessary. Beta blockers and calcium channel blockers may reduce ectopy rates and slow or block the ventricular response to the PACs, thus reducing symptoms. Potent antiarrhythmic medications (class Ia, Ic, or III) may occasionally be necessary.

An ectopic atrial rhythm is said to occur when the P wave does not have the normal upright morphology in limb leads

Figure 27-37 Sinus rhythm with type II second-degree sinoatrial block. Note the almost constant P-P interval before loss of P-wave activity. The pause is twice the cycle length of sinus rhythm. The return cycle length is the same as before the pause.
returns at the end of the rhythm strip. A dual-chamber pacemaker senses and tracks both types of P waves and paces the ventricle accordingly.

Figure 27-39 Ectopic atrial tachycardia is initiated by a premature atrial complex. Note the P-wave morphology change of the faster ectopic atrial rhythm.

Figure 27-39 Ectopic atrial tachycardia is initiated by a premature atrial complex. Note the P-wave morphology change of the faster ectopic atrial rhythm.

I, II, and III. Heart rate during the rhythm can be slower than, equal to, or greater than normal sinus rhythm. Ectopic rates greater than 100 beats/min are termed ectopic atrial tachycardia (Figs. 27-38 and 27-39). The morphology of the ectopic P wave should be consistent and the P-P intervals approximately equal. This helps to distinguish this from sequential PACs. Asymptomatic ectopic atrial rhythms are usually benign and do not require therapy. Patients with incessant, rapid tachycardias may eventually develop rate-related car-diomyopathy. Treatment for or prophylaxis against this type of cardiomyopathy is warranted.

Several additional atrial tachyarrhythmias deserve attention. Sinus tachycardia, or sinus rhythm at a rate greater than expected for the physiologic state, may be seen. Atrial wave morphology is normal. However, sustained increased rates may be related to failure of autonomic regulation, metabolic stress, drug use (prescribed or illicit), or idio-pathic causes. Inappropriate sinus tachycardia syndrome is usually a self-limited problem of young people and may be caused by a variety of factors. Positional orthostatic tachycardia syndrome (POTS) is a condition of marked increases in heart rate with upright posture, not always associated with a fall in blood pressure. Volume status is usually normal and differentiates this from simple orthostatic hypotension with reflexive tachycardia. Treatment of these disorders using beta blockers and serotonin antagonists has been helpful in some individuals. Expansion of plasma volume may also be helpful ( POTS.html).

Multifocal atrial tachycardia is characterized as irregular atrial activity at rates greater than 100 beats/min. Three or more P waves are present as the driving force of the tachycardia. Patients in metabolic stress and with hypoxia are prone to this arrhythmia. Treatment is usually supportive, but verapamil helps some patients. Treatment with digoxin is rarely helpful, and upward titration may result in toxicity indistinguishable from the original rhythm disorder (Hazard and Burnett, 1987).

The ECG findings of atrial fibrillation (AF) are the absence of organized atrial activity with an irregular, usually rapid ventricular response (Fig. 27-40). Atria are depolarized from widespread regions of both the left and right atrium and result in chaotic activation at rates exceeding several hundred beats per minute. AF may be asymptomatic or highly symptomatic, ranging from simple palpitations to MI and heart failure. Recognition of the arrhythmia is the first step in good care. Treatment using an appropriate anticoagulation strategy, ventricular rate control, and consideration of sinus rhythm restoration is necessary even in asymptomatic patients (see later discussion).

Atrial flutter (AFL) is also a rapid rhythm of the atrium, usually at a rate near 300 beats/min. The ventricular response may be fixed or variable. Sawtooth flutter waves are usually noted in the inferior limb leads (Fig. 27-41). Misidentifica-tion of atrial flutter with 2:1 conduction as sinus tachycardia is common and should be considered in all regular tachy-cardic rhythms. Similar to AF, treatment strategies should include anticoagulation with warfarin (Coumadin). In contrast to AF, atrial activation in flutter is organized and frequently caused by macroreentry. The wave front ascends the right atrial septum, crosses the roof of the right atrium, and extends down the lateral wall along the cristae. The wave front then extends between the inferior vena cava and the tricuspid annulus along the isthmus and proceeds to the atrial septum. Targeting the isthmus is often done with linear radiofrequency (RF) lesions to effect cure (Fig. 27-42).

Junctional Rhythms

Similar to PACs, earlier-than-expected depolarization arising from the AV node complex results in a QRS without a preceding P wave, termed a premature junctional complex (PJC).

atrioventricular node is variable, resulting in the irregular ventricular response.
Figure 27-41 Atrial flutter is more organized, resulting in a sawtooth appearance in the limb leads and precordial leads. Atrial rates of almost 300 beats/min are noted, with variations in the ventricular response.
(From Feld GK, Fleck P, Chen PS, et al. Radiofrequency catheter ablation for the treatment of human type I atrial flutter: identification of a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation i992;86:i233-i240.)

fifth QRS complex and resets the junctional rhythm. Excessive bradycardia and the associated junctional rhythm may be associated with digoxin toxicity.

fifth QRS complex and resets the junctional rhythm. Excessive bradycardia and the associated junctional rhythm may be associated with digoxin toxicity.

Retrograde, inverted P waves may be seen within the early portion of the QRS or following the QRS complex. These are usually benign but may be an early sign of occult cardiac disease. Drugs, adrenergic stimulants, and metabolic stress may be associated with PJCs. In the absence of heart disease or underlying medical condition, these usually asymptomatic beats do not require treatment.

When the AV junction has rhythmic spontaneous depolarization, a junctional or nodal rhythm occurs (Fig. 27-43). The normal pacemaker function of the AV node cells occurs at a rate of 35 to 50 beats/min. In sinus node failure, the junctional pacemaker rate may be higher than the sinus rate, resulting in junctional bradycardia. Abnormal reentry within the AV node results in junctional tachycardia, usually at a rate between 120 and 190 beats/min, and is considered a form of supraventricular tachycardia. Differentiation of accelerated junctional tachycardia from more typical supraventricular tachycardias is not possible by surface ECG. Because of simultaneous activation of the ventricle and retrograde activation of the atrium, junctional rhythms may be more symptomatic than their rate would predict.

Disorders of Atrioventricular Node Conduction

Key Points

• Atropine may worsen AV block if block occurs at the level of the Purkinje system. Increased sinus rates conducting through the AV node will be blocked from the refractory His-Purkinje tissue.

• In contrast, epinephrine may enhance both AV conduction and shorten Purkinje refractoriness, resulting in decreased block. Atropine delivery thus may help distinguish the level of AV block and determine the urgency of permanent pacing.

• The atrial rate must be faster than the escape rate to confirm complete heart block.

• Digoxin toxicity and ischemia may cause accelerated junctional rhythm and should be considered when this rhythm is seen.

First-degree AV block is demonstrated as a P-R interval of greater than 200 milliseconds (Fig. 27-44). Persistent AV delay is usually noted, but variations may be seen depending on heart rate. Adrenergic tone shortens the AV delay, whereas drugs such as beta blockers and calcium channel blockers may worsen AV conduction, leading to more progressive types of AV block. First-degree AV block is almost always at the level of the AV node. Except for very long AV intervals resulting in atrial contraction while the prior ventricular beat is maintaining AV valve closure, first-degree AV block typically does not require treatment. Advanced age is often associated with this conduction disorder.

Second-degree AV block is separated into type I (Wenckebach), type II, 2:1, and high-grade AV block. Type I second-degree AV block is characterized by a progressive prolongation of the P-R interval followed by failure to conduct and depolarize the ventricle. The P-R interval on the return beat will be shorter than the P-R just before the block

Figure 27-44 Sinus rhythm with first-degree atrioventricular block and bundle branch block.

(Fig. 27-45). Similar to first-degree AV block, this typically does not require treatment with a pacemaker and does not predict life-threatening complete heart block. In patients with concomitant BBB, the clinician should question if block is actually occurring at the level of the His-Purkinje system. Withdrawal of drugs indicated in AV block is indicated. Dual-chamber pacing in symptomatic patients may be necessary.

Type II second-degree AV block is the abrupt failure of conduction through the AV node and absence of a QRS complex. The P-R intervals should be similar before and after block. Atrioventricular block may occur both at the level of the AV node and His-bundle complex and is indistinguishable without invasive electrophysiology study. Pacing is usually indicated to avoid unpredictable progression to complete heart block. Withdrawal of AV conduction blocking drugs is indicated. Two-to-one (2:1) AV block can result in very low heart rates and considerable symptoms, including syncope and low-output heart failure. Loss of ventricular activation every other beat typifies this rhythm. Block at the level of the AV node is suggested by preexistent PR prolongation, but block at the level of the His-Purkinje system cannot be excluded by surface ECG.

High-grade AV block or intermittent complete AV block is similar to type II second-degree AV block. However, more than one consecutive QRS complex is absent with the block. This degree of AV block strongly suggests significant AV nodal disease or distal Purkinje disease, and the physician should strongly consider permanent pacemaker implantation. The one exception may be high-grade AV block occurring at night in the setting of sleep apnea.

Third-degree AV block results from failure of atrial impulses from the sinus node to conduct down to the ventricle (Fig. 27-46). The finding on a rhythm strip or ECG indicates serious cardiac disease and may be related to significant valvular or coronary disease. An escape rhythm that is narrow suggests that the level of block is above the His-bundle complex and may be more stable. Adrenergic stimulation or atropine may result in an accelerated junctional escape. A slow, wide QRS escape suggests the level is below the His-bundle system, and atropine is unlikely to help. Adrenergic stimulation may help increase the escape rate. Urgent temporary or permanent pacing is indicated. Transcutaneous pacing may be used temporarily but is unreliable and poorly tolerated by the patient.

Figure 27-45 Sinus rhythm with type I (Wenckebach) second-degree atrioventricular block. There is prolongation of the P-R interval, then a dropped QRS.

Figure 27-45 Sinus rhythm with type I (Wenckebach) second-degree atrioventricular block. There is prolongation of the P-R interval, then a dropped QRS.

Figure 27-46 Sinus rhythm with third-degree (complete) atrioventricular block. There is complete dissociation of atrial and ventricular activity. The escape rate is less than 30 beats/min, and QRS complex is wide, suggesting a ventricular escape.

Ventricular Rhythms Key Points

• Determination of the site of pacing is important.

• A bundle branch block pattern on surface ECG contralateral to the site of pacing should occur.

• Inappropriate left ventricular endocardial lead placement delivered across a patent foramen ovale can be detected before serious consequences of embolic stroke.

• Appropriate left ventricle epicardial pacing can be confirmed through paced right BBB morphology. Right ventricular endocardial pacing results in a left BBB pattern on surface ECG.

The presence of a wide QRS is usually caused by (1) normal AV conduction with bundle branch block (BBB) aberrancy, (2) presence of preexcitation, or (3) origin of the beat within the ventricle as a premature ventricular contraction (PVC) or consecutive ventricular activation, as seen in ventricular tachycardia (VT). A PVC is noted as an early beat, arising before normal atrial activation through the AV node can activate the His-bundle system and depolarize the ventricle. PVCs occur as single beats and couplets but may consecutively appear much like VT. Unifocal PVCs are typically seen as more benign than multifocal PVCs. The origin of the abnormal beats is usually enhanced automaticity or triggered activity. Cardiac literature has demonstrated higher mortality rates in patients with ischemic heart disease with decreased ejection fraction and increased rates of ventricular ectopy. Suppression of these ectopic beats with Class I or Class III antiarrhythmic medicines, however, has not significantly improved mortality (Cardiac Arrhythmia Suppression Trial, 1992; Echt et al., 1991).

Ventricular ectopy in patients with a normal heart is not correlated with significant increases in mortality. Patients are usually asymptomatic, although even low-frequency ectopy may bother some individuals. Beta-blocker therapy for these patients often results in symptomatic improvement. In highly symptomatic patients, membrane-active drugs (Class I or III) may occasionally be required. Electrophysiologist referral should be made if antiarrhythmics are used. Some symptomatic patients may also be treated with RF ablation of the arrhythmic focus.

Ventricular tachycardia is clinically divided into two main categories: In monomorphic VT, QRS complexes are nearly identical, and the R-R interval is typically regular. Slight variations at the beginning and end of a run of VT tend to show greater fluctuations in rate. This tends to occur more frequently in scar-related reentry in patients with prior MI and in patients with "normal heart" VT, such as right ventricular outflow tract tachycardia and idiopathic left ventricular tachycardia (Fig. 27-47). In polymorphic VT (PMVT), QRS morphology is constantly changing, and the R-R intervals are often inconsistent. Torsades de pointes is a specific clinical PMVT and is characterized by a long QT interval in the first beat of the tachycardia and a twisting about the axis on a rhythm strip (Fig. 27-48). In almost all cases, referral to a cardiologist or electrophysiolo-gist is indicated. Frequently, inpatient evaluation is necessary.

Ventricular fibrillation (VF) is a disorganized electrical rhythm of the ventricle and leads to no meaningful ventricular contraction. Without cardiac resuscitation and electrical cardioversion, the individual will die. Figure 27-49 demonstrates a patient hospitalized with a myocardial infarction. Immediate hospitalization is recommended in patients who have had prior episodes of near syncope or syncope in which VT is suspected due to known underlying isch-emic or nonischemic heart disease. Patients suspected of long QT syndrome or VT associated with clinically significant hypertrophic obstructive cardiomyopathy (HOCM) should be considered for inpatient or invasive evaluation. Patients who are resuscitated from an out-of-hospital VF arrest must be referred to a cardiac specialist for further evaluation and treatment because of the high rate of recurrence (Huikuri et al., 2001). Inpatient evaluation may include invasive coronary angiography or electrophysiology testing.

Paced Rhythms

Temporary or permanent pacemaker implantation is now performed at almost all hospitals in which a cardiologist practices. Activation of myocardium results in a nearly

Figure 27-47 Nonsustained monomorphic tachycardia is seen in the setting of underlying atrial fibrillation with increased ventricular response. This terminates spontaneously.

Figure 27-48 Torsades de pointes polymorphic ventricular tachycardia is initiated by sequential premature ventricular contractions (PVCs) that prolong the Q-T interval in a rate-dependent manner. An early PVC landing in the long Q-T interval results in the characteristic twisting about the axis. Spontaneous termination is seen.

Figure 27-48 Torsades de pointes polymorphic ventricular tachycardia is initiated by sequential premature ventricular contractions (PVCs) that prolong the Q-T interval in a rate-dependent manner. An early PVC landing in the long Q-T interval results in the characteristic twisting about the axis. Spontaneous termination is seen.

normal P wave but with a notable BBB pattern of ventricular capture on the surface ECG. The ECG recorder may amplify the energy from the pacemaker pulse, resulting in a pacing artifact on the surface 12-lead or rhythm strip to aid in interpretation. Knowledge of the type of pacemaker and the current programming may be necessary for complete analysis. The pacing morphology can be reviewed to confirm consistent and appropriate lead placement. Sensed cardiac events may result in pacemaker inhibition and masking of its presence. Evaluation of unexpected events on the ECG may identify abnormal pacemaker operation (Fig. 27-50). Detailed pacemaker ECG interpretation is beyond the scope of this chapter.

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