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Cardiac Arrhythmias is written for the physician with an advanced interest in electrocardiography. The text is based on the extensive experimental and clinical observations of the two authors and endeavors to correlate abnormal electrophysiological mechanisms with specific cardiac arrhythmias. Each chapter begins with basic physiological principles and proceeds to practical clinical application. The current knowledge of membrane potentials, excitability, cardiac cell refractoriness, automaticity, excitation conduction, slow and fast currents, early and delayed afterpotentials, and the gap phenomenon is presented and discussed. Enhanced automaticity in the atrioventricular conducting system, repetitive reentry or circus movements, and delayed or after depolarizations in Purkinje fibers are described as mechanisms responsible for the genesis of ectopic tachycardias. Sinus arrest, sinoatrial block with decremental conduction, and the sick sinus syndrome is explained by examining alterations in the automaticity of the sinus node. The classification of upper, middle, and lower nodal rhythm is abandoned because most of

To the Editor.— Tizes recently described (236:1846-1847, 1976) "cardiac arrest" in a patient following venipuncture. The arrest was assumed by the absence of heart sounds and pulses, cessation of breathing, and other symptoms, but without ECG recording; the patient recovered after cardiopulmonary resuscitation. We recently had a very similar case, which supplies ECG evidence of what may happen during a routine venipuncture. Report of a Case.— A 54-year-old man who five years earlier had a coronary bypass operation was admitted with chest pain to our Coronary Care Unit. Here a routine venipuncture was done while his ECG was constantly monitored. Immediately after the needle puncture, the patient complained of weakness and within two seconds lost consciousness. The ECG showed extremely slow sinus rhythm with possible sinoatrial block, prolonged sinus pauses, and nodal escape rhythm (Figure 1). Atropine, 1.0 mg, was immediately administered through an open intravenous (IV) route in his

Cardiac pacing has enjoyed rapid growth since it became technically available about 25 years ago. Its indications since then have broadened to include virtually every known arrhythmia. Criteria for pacing, published by the American College of Cardiology and the American Heart Association in 1983, and since then adapted with modification by Medicare, divide indications for implantation of pacemakers into the following three classes: (1) pacing clearly required, (2) some disagreement about necessity, and (3) contraindicated.Guidelines for Cardiac Pacing is a videotape moderated by William C. Roberts, MD, editor in chief, American Journal of Cardiology. Panel members are Drs Leonard S. Dreifus, Seymour Furman, Paul C. Gillette, Jerry C. Griffin, David L. Hayes, and Paul A. Levine. Intermedics has produced Guidelines for Cardiac Pacing to clarify certain controversial gray areas concerning the use of pacemakers in patients with congenital heart block, acquired heart block, sinoatrial block, and hypersensitive carotid sinus

Much praise should be given to Ferrer 1 who has popularized the sick sinus syndrome. As a result of her endeavors, many lives have been prolonged and numerous patients have been freed from disturbing neurological and/or cardiac symptoms. It is estimated that sinus node disorders currently account for 50% of the pacemakers implanted. Ferrer's contributions also have stimulated fundamental investigations of sinus node anatomy and electrophysiology, as emphasized in Bower's excellent review in this issue (p 133). Despite our better understanding of the sick sinus syndrome through clinical observations and research, there remain many unanswered problems and questions. The sick sinus syndrome is not a single entity, but is characterized by a spectrum of cardiac rhythm disturbances that include marked sinus bradycardia, sinus arrest, sinus standstill, sinoatrial block, the tachycardiabradycardia syndrome, sinus bradycardia with conducted or nonconducted atrial premature systoles, atrial fibrillation with a slow ventricular response not due to

The literature concerning possible cardiotoxic effects of lithium therapy in man is reviewed. Reports indicate a high frequency of electrocardiographic T wave morphology changes with lithium therapy. Therapeutic and toxic levels of lithium have infrequently been associated with serious cardiac dysfunction. Of particular concern are cases of sinus mode dysfunction or sinoatrial block and the appearance or aggravation of ventricular irritability. The incidence of cardiac complications may increase with age. The necessity or cardiac screening and monitoring of patients receiving lithium is discussed.

The sick sinus syndrome describes a rather heterogeneous group of patients whose presenting symptoms are primarily cerebrovascular in nature (Stokes-Adams attacks, dizziness, and cerebrovascular accidents). The principal pathophysiological disturbance is "sinus node" dysfunction characterized by bradyarrhythmias (sinus bradycardia, sinoatrial block, sinus arrest) with or without associated tachyarrhythmias (tachycardia-bradycardia syndrome).1An interest in and an awareness of this syndrome is mandated by the frequency of these complaints. Historically, the first causal relationship delineated was between Stokes-Adams attacks and sinus bradycardia and sinoatrial block.2-4Later in 1954 Short5described syncope in patients with alternating bradyarrhythmias and tachyarrhythmias. Lown6actually coined the term "sick sinus" syndrome to describe a group of patients in whom, after electrical cardioversion, chaotic atrial activity, bradycardia, ectopic beats, and atrial and nodal tachycardia developed. Ferrer7ultimately grouped these patients with diverse symptoms and dysrhythmias together under the general heading "sick sinus syndrome" in

"THE SICK sinus syndrome" is a term coined by Ferrer1referring to a constellation of signs, symptoms, and ECG criteria defining sinus node dysfunction in a clinical setting. These criteria, which have been described by many investigators,2-7include sinus bradycardia, sinus arrest, sinoatrial block, alternating bradyarrhythmias and tachyarrhythmias, and carotid hypersensitivity. Any one or combination of these features may be seen in the typical sick sinus patient who has syncope or other evidence of cerebral dysfunction. Symptoms, nevertheless, are a manifestation of failure of escape pacemaker function and not truly a feature of sinus node malfunction. SINUS NODE AS PACEMAKER The sinus node is a highly organized cluster of specialized cells located in the area of the junction between the superior vena cava and the right atrium. Microscopically, three cell types have been described in the sinus node: P cells, transitional cells, and working cells.8The P

Acute accidental digoxin ingestion in two children was associated with cardiac conduction abnormalities including atrioventricular (AV) block, AV dissociation, and sinoatrial block. Normal sinus rhythm or tachycardia was restored with atropine sulfate, thus implicating the vagal effects of the cardiac glycoside as the cause of the conduction disturbances. Elevated blood serum digoxin levels were correlated with the conduction abnormalities in these patients. Serial serum digoxin levels are suggested as an aid in the management of these problems.

For some authors, positive head-up tilt-test (HUT) and/or ATP-test could identify patients with vaso-vagal syncope. It has been shown that endogenous adenosine plays a role in the mechanism of syncope in patients with positive HUT. Indeed, patients with positive HUT have higher adenosine plasma levels (APL) than patients with negative HUT. Moreover, APL increase during HUT, only in patients with positive HUT. Adenosine triphosphate injection can induce in some patients with unexplained syncope a cardio-inhibitory but the role of endogenous adenosine in those patients is unknown. Methods In this prospective study we studied APL before and during ATP-test. Twenty consecutive patients with syncope of unexplained origin were included (56.0 □ 23.1 y., 13 females). They underwent baseline APL measurement followed by ATP-test. Then APL was measured 1, 5 and 15 minutes after ATP injection. APL were determined by High Performance Liquid Chromatography method on venous blood samples obtained in resting patients. ATP-test consisted of the intravenous bolus injection of 20 mg ATP during continuous recording of the surface ECG. The test was considered positive when a ventricular pause of ≥ 6 sec. occurred, due either to complete atrioventricular block or sinoatrial block. Results Nine patients had positive ATP-test. There was no statistical difference between patients with positive and negative ATP-test at baseline, 1, 5 and 15 minutes after ATP injection: 0.32 □ 0.16 μmol/L vs 0.49 □ 0.61 μmol/L, 0.32 □ 0.16 μmol/L vs 0.37 □ 0.21 μmol/L, 0.29 □ 0.23 μmol/L vs 0.41 □ 0.26 μmol/L, 0.34 □ 0.20 μmol/L vs 0.28 □ 0.13 μmol/L, respectively. There was no variation of APL during ATP-test in patients with positive and negative ATP-test. Conclusion Endogenous adenosine is not involved in the mechanism of ATP-test. These results suggest that ATP-test and HUT have different mechanism and could identify different groups of patients with syncope of unexplained origin.