Arrhytmia

DIAGNOSTIC OF ARRHYTMIA
History
Begins with a careful history addressing specific questions regarding the presence of palpitations, syncope, spells of lightheadedness, chest pain, or symptoms of congestive heart failure. Palpitations,[1] an awareness of one’s heartbeat (see Chap. 3 ), may result from irregularities in cardiac rate or rhythm or a change in contractility of the heart. Some patients are able to reproduce this sensation by tapping their hand on their chest, knee, or a table top in a fashion similar to the perceived palpitation or may recognize a cadence tapped out by a physician. Such a maneuver can help establish the rate and rhythm of the arrhythmia by narrowing it to a particular rate range, a regular or irregular arrhythmia, or one in which a regular rhythm is interrupted by premature beats. The latter are often perceived only upon the contraction that ends the pause following the premature beat. The patient may feel as though the heart has stopped for a moment. Rapid, irregular tapping can suggest the ventricular response to atrial fibrillation, whereas rapid, regular tapping can suggest an atrioventricular (AV) nodal reentrant supraventricular tachycardia, particularly in a young person, or ventricular tachycardia (VT) in an older person. Information regarding the nature of the onset and termination of the rhythm disturbance is particularly important. Knowing the rate of the arrhythmia is crucial, and a brief demonstration by the physician of how to determine the heart rate can yield important dividends. The patient, and sometimes a close relative, should be instructed in how to count the pulse.
Answers by the patient to key questions can provide clues to the type of rhythm disturbance, particularly if the physician has additional information, such as physical findings and a 12-lead electrocardiogram (ECG). For example, a young adult with presyncope, normal physical findings, and ECG changes indicating Wolff-Parkinson-White (WPW) syndrome should be asked whether the palpitations are regular or irregular, how fast they are, and how they start and stop. If the tachycardia is regular, with a rate of approximately 200 beats/min, and of sudden onset and termination, it is likely that the patient is experiencing an AV reciprocating tachycardia; on the other hand, if the rhythm is irregular, the patient may have atrial fibrillation, a potentially more serious arrhythmia in the presence of WPW syndrome. In an older patient with presyncope, especially with a history of myocardial infarction, the physician should suspect VT if the ventricular rate is rapid and suspect AV heart block or sinus nodal disease if the rate is slow. The ventricular rhythm can be regular or irregular. Premature atrial or ventricular beats, perceived as dropped or skipped beats by the patient, are probably the most common cause of palpitations.
The physician should inquire about circumstances that can trigger the arrhythmia, such as emotionally upsetting events, ingestion of caffeine-containing beverages, cigarette smoking, exercise, excessive alcohol intake, or gastrointestinal problems (Fig. 25-1) . A careful diet and drug history can be useful, for example, in revealing that palpitations develop only after the use of a nasal decongestant that contains a sympathomimetic vasoconstrictor or in revealing that the patient has been exposed to "street" drugs such as cocaine. States conducive to the genesis of arrhythmias should be considered, such as thyrotoxicosis, pericarditis, mitral valve prolapse, hypokalemia secondary to diuretics, and so forth. The family history can be helpful. In addition to the congenital long QT syndrome, a variety of other familial disorders can result in arrhythmias, including myotonic dystrophy, Duchenne muscular dystrophy (see Chap. 71 ), and dilated cardiomyopathy (see Chap. 48 ). Congenital conduction system disorders can result in sudden death.
Physical Examination
In addition to recording the cardiac rate and rhythm, a number of physical findings can be helpful. For example, findings accompanying AV dissociation include variable peak systolic blood pressure as the atria alter their contribution to ventricular filling, variable intensity of the first heart sound as the PR interval changes despite a regular ventricular rhythm, intermittent cannon a waves in the jugular venous pulse as atrial contraction occurs against closed AV valves, and apparent "intermittent" gallop sounds when atrial systole occurs at various times of the cardiac cycle. The venous pulse provides a window through which to judge atrial and ventricular rates and relative timing relationships. It is of interest that Wenckebach first noted the two types of second-degree AV block that bear his name by recording the jugular phlebogram before the ECG was available.
to ventricular filling, variable intensity of the first heart sound as the PR interval changes despite a regular ventricular rhythm, intermittent cannon a waves in the jugular venous pulse as atrial contraction occurs against closed AV valves, and apparent "intermittent" gallop sounds when atrial systole occurs at various times of the cardiac cycle. The venous pulse provides a window through which to judge atrial and ventricular rates and relative timing relationships. It is of interest that Wenckebach first noted the two types of second-degree AV block that bear his name by recording the jugular phlebogram before the ECG was available.

Examining the second heart sound can be helpful (see Chap. 4 ). A paradoxically split second heart sound can occur during a QRS complex with a left bundle branch block contour that results from VT or supraventricular tachycardia with aberration. A widely split second heart sound that does not become single during expiration can accompany a right bundle branch block. Unfortunately, similar physical findings occur with different cardiac arrhythmias. For example, progressive diminution of the intensity of the first heart sound results as the PR interval lengthens, which can occur during AV dissociation when the atrial rate exceeds the ventricular rate or during a Wenckebach second-degree AV block. Similarly, constant cannon a waves can occur with 1:1 AV relationships during ventricular or supraventricular tachycardia. Since AV dissociation can occur (uncommonly) during supraventricular tachycardia and VA association can occur during VT, the clues provided by physical findings can be only suggestive.
Carotid Sinus Massage
The response to carotid sinus massage or the Valsalva maneuver provides important diagnostic information by increasing vagal tone and primarily slowing the rate of sinus nodal discharge and prolonging AV nodal conduction time and refractoriness. Sinus tachycardia slows gradually during carotid massage and then returns to the previous rate when the massage is discontinued; AV nodal reentry and AV reciprocating tachycardias that involve the AV node in one of its pathways can slow slightly, terminate abruptly, or not change, and the ventricular response to atrial flutter, atrial fibrillation, and some atrial tachycardias usually decreases (Table 25-1) . Rarely, carotid sinus massage terminates a VT.
To perform carotid massage, the patient is placed in a supine position with the neck hyperextended and the head turned away from the side being tested, the sternocleidomastoid muscles relaxed or gently pushed out of the way, and the carotid impulse felt at the angle of the jaw. The carotid bifurcation is touched gently initially with the palmar portion of the fingertips to detect hypersensitive responses. Then, if no change in cardiac rhythm occurs, pressure is applied more firmly for approximately 5 seconds, first on one side and then on the other (never on both sides simultaneously) with a gentle rotating massaging motion. External pressure stimulates baroreceptors in the carotid sinus to trigger a reflex increase in vagal activity and sympathetic withdrawal. Responses can occur with right-sided massage and not left, or vice versa, so each side should be tested separately. Generally, the maximal response occurs with the first massage if repeated attempts are performed at short intervals. Some risk is associated with carotid sinus massage, particularly in older patients, and cerebral emboli can occur.[2] Before massage, the carotid artery should be auscultated so that massage is not performed in patients who have carotid bruits indicative of carotid arterial disease.
Electrocardiography
The ECG remains the most important and definitive single noninvasive diagnostic test. Figure 25-2 depicts an algorithm for diagnosing specific tachyarrhythmias from the 12-lead ECG. Initially, a 12-lead ECG is recorded, and a long recording using the lead that shows distinct P waves is obtained for proper analysis. If P waves are not clearly visible, atrial activity can be recorded by placing the right and left arm leads in various chest positions to discern P waves (so-called Lewis leads) and applying esophageal electrodes or by using intracavitary right atrial leads. An echocardiogram showing atrial contraction can be helpful.
Each arrhythmia must be approached in a systematic manner to answer the following questions: Are P waves present? What are the atrial and ventricular rates? Are they identical? Are the P-P and R-R intervals regular or irregular? If irregular, is it a consistent, repeating irregularity? Is there a P wave related to each ventricular complex? Does the P wave precede or follow the QRS complex? Is the resultant PR or RP interval constant? Is the RP interval long and the PR interval short, or vice versa? Are all P waves and QRS complexes identical and normal in contour? To determine the significance of changes in P wave or QRS contour or amplitude, one must know the lead being recorded. Are P, PR, QRS, and QT durations normal? In view of the clinical setting, what is the significance of the arrhythmia? Should it be treated and, if so, how? For supraventricular tachycardias with a normal QRS complex, a branching decision tree may be useful.
The Ladder Diagram
The ladder diagram is used to depict depolarization and conduction schematically. Straight or slightly slanting lines drawn on a tiered framework beneath an ECG trace represent electrical events occurring in the various cardiac structures (Fig. 25-3 A and B). Since the ECG and therefore the ladder diagram represent electrical activity against a time base, conduction is indicated by the lines of the ladder diagram sloping in a left-to-right direction. A less steep line depicts slower conduction. A short bar drawn perpendicular to a sloping line represents blocked conduction (Fig. 25-3 C). Activity originating in an ectopic site such as the ventricle is indicated in another tier drawn beneath the ventricular tier. In general, atrial, AV junctional, or ventricular activity is diagrammed to begin in that particular tier. It is important to remember that sinus nodal discharge and conduction and, under certain circumstances, AV junctional discharge and conduction can only be assumed; their activity is not recorded on scalar ECG.
Electrophysiological Study
When an electrophysiological study is indicated, it is performed by introducing multipolar catheter electrodes into the vascular system and positioning them in various parts of the heart. The catheters are used to record local electrical activity and to stimulate the heart. Multiple leads are recorded simultaneously, usually at a paper speed of 50 to 200 mm/sec. (Standard ECGs are generally recorded at a paper speed of 25 mm/sec.) Because of the rapid recording speed, intervals or complexes of normal duration may appear prolonged. An electrode positioned across the septal leaflet of the tricuspid valve records His bundle activity, as well as low right atrial activity and high ventricular septal depolarization. Occasionally, a right bundle branch deflection
can also be recorded. Three basic measurements are made by using the ECG and the His bundle catheter recording: the PA, A-H, and H-V intervals (Fig. 25-3 D). The PA interval is the time between the onset of the P wave in the surface tracing (which generally slightly precedes the onset of the high right atrial recording) and the low right atrial deflection and is recorded in the His lead. This interval reflects intraatrial conduction and has not proved to be of much clinical value.
THE A-H INTERVAL.
The A-H interval is timed from the onset of the first rapid deflection recorded in the atrial electrogram (A) in the His bundle lead to the beginning of the His (H) deflection. Since the low right part of the atrium and the His bundle anatomically delineate the boundaries of the AV node, the A-H interval closely approximates AV nodal conduction time. The A-H interval is affected by various interventions: Atropine and isoproterenol shorten the A-H interval, whereas vagal maneuvers, digitalis, propranolol, verapamil, adenosine, and rapid or premature atrial pacing lengthen it. The normal range for the A-H interval is 55 to 130 milliseconds, depending on the heart rate, autonomic tone, and other factors.
THE H-V INTERVAL.
The H-V interval is the time from the beginning of the H deflection to the earliest onset of ventricular depolarization recorded in any lead. This interval represents conduction from the His bundle through the bundle branch-Purkinje system to the point of ventricular muscle activation and is usually constant--between 30 and 55 milliseconds--regardless of the heart rate or autonomic tone. Other intervals are discussed under the individual tachycardias.