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The Evaluation of Sinoatrial Node Function 1N Man*

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The Evaluation of Sinoatrial Node Function 1N Man* The Evaluation of Sinoatrial Node Function 1n Man* J. THOMAS BIGGER, JR, M.D.t Associate Professor of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York HAROLD C. STRAUSS, M.D., C.M.t Associate in Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York The function of the sinoatrial node is com­ ence with the extracellular fluid and often shows plex. In nearly all hearts, this small bit of tissue is some overshoot, that is, the inside of the cell may responsible for spontaneously generating the impulse become slightly positive relative to the extracellular which will be distributed to the remainder of the potential. After reaching this peak inside-positive heart, maintaining coordinated electrical and me­ value of transmembrane voltage (V111 ), the sinus chanical function. In recent years, it has become node cell slowly repolarizes to a maximum inside­ clear that S-A node dysfunction is not rare, can negative value-so-called maximum diastolic volt­ cause disabling symptoms, and often presents diffi­ age. Then, the transmembrane voltage spontaneously cult management problems. The challenges pre­ begins to decrease ( phase 4 depolarization) until sented by the "Sick Sinus Syndromes" have in­ a critical value of V 111 , threshold voltage, is reached creased our desire to know more about normal and self-excitation recurs. The rate of recurring S-A node function and about function in disease self-excitation could theoretically be altered by states. changes in: 1) maximum diastolic voltage, 2) The intimate mechanisms of sinus node func­ threshold voltage, and 3) rate of phase 4 depolari­ tion remain a mystery despite the "prying eye" of the zation. Changes in firing of a sinus node cell are microelectrode and modern anatomical and chem­ most often mediated by changes in rate of phase 4 ical methods. At least the time-voltage course of depolarization. We still do not know the precise spontaneous activity in the sinus node cells has been sequence of membrane permeabilities as a function elucidated. After self-excitation, a pacemaking sinus of time and voltage which are responsible for the node cell slowly depolarizes to zero potential differ- normal automatic behavior of the S-A node. Sinus node rate is sensitively adjusted to most * Supported in part by a Grant-in-Aid from the New suitably meet the needs of the body as a whole. York Heart Association and by United States Public Health These adjustments are usually mediated through Service Grants HL 12738 and HL 07541. autonomic reflexes which change the rate and pattern Presented by Dr. Bigger at the Symposium on Cardiac Arrhythmias, June I 0, 1972, at Virginia Beach, Virginia. of firing on sympathetic and/ or parasympathetic t Recipient of a Research Career Development Award nerves terminating at or near the sinus node. Re­ from the National Heart and Lung Institute (1 -K04-HL- lease of norepinephrine from sympathetic nerve 70204); this work was begun during his tenure as Senior terminals in the vicinity of a sinus node cell will Investigator, New York Heart Association. accelerate phase 4 depolarization and the sponta­ i Pharmaceutical Manufacturers Association Founda­ tion Faculty Development Awardee in Clinical Pharmacol­ neous firing rate of the S-A node while acetylcholine ogy; this work was begun during a National Heart and Lung released from cholinergic terminals has the opposite Institute Traineeship (USPHS Grant 5-Tl2-HL-05864). effect. MCV QUARTERLY 9(1): 77-85, 1973 77 78 BIGGER AND STRAUSS: SINOATRIAL NODE FUNCTION Once the normal automatic mechanism has abnormality was recorded electrocardiographically. generated an impulse in the S-A node itself, the Since that time there has been a great increase in impulse must be transmitted to the ordinary and our knowledge of the electrocardiographic features specialized atrial fibers in order to effect atrial and, of second degree S-A block. More recently, the ultimately, total cardiac excitation. The action poten­ use of electrical pacemakers as a therapeutic device tial of the S-A nodal cell is of a type associated has led to an increased interest in and understanding with slow conduction and vulnerability to block or of a variety of clinical patterns of S-A nodal dys­ fragmentation in transmission, that is, phase O is function . These clinical patterns include: small in amplitude and extremely slow rising. Also, 1. severe sinus bradycardia, not induced by the S-A nodal pacemaker cells are small, have drugs or inappropriately severe for the type multiple connections with their neighbors, and are and amount of drug administered. entangled in a dense connective tissue stroma. These 2. periods of second degree S-A block, in­ anatomical features undoubtedly contribute to slow appropriate for drug therapy. conduction in the sinus node. In addition, the sinus 3. long pauses in sinoatrial rhythm caused by node is surrounded by a group of cells which are sinus arrest, repetitive concealed sinus exit intermediate in time-voltage course between S-A block or third degree S-A exit block. nodal cells and atrial specialized cells. These cells, 4. chronic atrial fibrillation with a slow ven­ called "perinodal fibers" are not automatic under tricular rate in the absence of drugs which normal circumstances but do have electrophysiologic slow A-V conduction, and inability of the properties which promote slow conduction and heart to resume stable sinus rhythm after block; "perinodal cells" represent a barrier to con­ electrical cardioversion. duction into the S-A node and a region where 5. the tachycardia-bradycardia syndromes. "organization" and amplification of impulses leaving Several features of these syndromes deserve the S-A node might occur. comment. The first three listed have been recog­ All of the events discussed above-impulse nized for a long time and if accompanied by heart generation in the S-A node and its transmission to failure or central nervous system symptoms are the atrium-are invisible both on the body surface often treated, and successfully, with implanted elec­ electrocardiogram and in local extracellular atrial trical pacemakers. For a long time we recognized electrograms. Analysis of the behavior of the S-A that patients with atrial fibrillation who had a slow node in man is even more complicated than analysis ventricular rate without drug treatment were prone of the A-V node. We have been able to study the to develop very slow ventricular rates when treated A-V node in man by recording local electrograms with digitalis and often had severe sinus brady­ from the atrial margin of the A-V node and, on cardia, sinus pauses and other rhythms of sinus the other side, the nearby bundle of His. Pro­ dysfunction when cardioverted. Recently, we have grammed stimulation of the atria or ventricles and learned that this is due to the fact that many patients analysis of the electrical responses allow a rather with severe S-A node dysfunction also have im­ complete characterization of the A-V node. The paired A-V conduction and sluggish ventricular S-A node is somewhat analogous to the A-V node pacemakers. The tachycardia-bradycardia syndromes in that the impulse generated in the S-A node must (fig. l) have been recognized for about twenty pass through the "perinodal fiber" (analogous to years, but they presented difficult, often insurmount­ the A-V node) in order to reach specialized atrial able, management problems until combined treat­ fibers (analogous to the bundle of His). However, ment with drugs and an electrical pacemaker became this analogy is very incomplete in that the S-A available. node itself is an area of slow conduction and, in It is easy to recognize S-A nodal dysfunction addition, spontaneously generates impulses. when it presents as one of the five syndromes listed Experimental and clinical observations made above. However, it can be difficult to know whether in the first decade of the twentieth century estab­ S-A node dysfunction is present. Two examples lished that second degree S-A block could occur in which present clinical difficulty are: 1) moderate animal and human hearts. In fact, second degree sinus bradycardia which may or may not indicate sinoatrial block was well established clinically from intrinsic malfunction of the S-A node and portend analysis of the jugular venous pulse well before this a series of difficult rhythm problems and their BIGGER AND STRAUSS: SINOATRIAL NODE FUNCTION 79 ,., '1 1 : ! rr· ~ 1· : :i; I I 1l illi Jill4 l"lj,i ~ j i I. r \f o i.ttf 1~· 1----:.. I j -, . ·ft jJJ Tr; ~F ~~ ~ ! ll ;it I ! Iii ' t t - I . ,. 1 jj i 1 I : rr Ii :HJU+ ::: 111: :; i . : : :11 1 :, :i! 1;:: 1'1: -1 : : : i Iii l: '. : ; i ii : '.: l · l Iii - i '. '. '. i IJ 1+-1 : :1 : II1 1 : : : : ; '. / i:: : : 1::: : lj ; : . : !· p 11. : :~ : J I i: . : .. I .. : • ; ; : : ' : I I i ·- ,_, i l c .. ll . u '. : : : I : ; . :.a..· : : I ~ I ij fl ...,....,.r,-: · "l"Plfl ""1 · , , :.iii ! . : -, , I : : . : : . :·f t I ! '. : '. '. ! ' : ! ~: ·:::·: : ;II:: :: till j;; ;:;;i: i:1 i:i; ,ut m ! 'I 'II : .: !- I.,' :1:: ' " I : i1. ·· -++-- I ' I !I I III' II! .I Fig. I- The tachycardia-bradycardia syndrome. A 67-year-old man referred for evaluation of recurrent syncope, dizziness, and weakness. Lead ll of his admission electrocardiogram shows a repeated change in rhythm from atrial flutter to sinus bradycardia. He was treated with a permanent transvenous pacemaker and digitalis and has been symptom-free for more than a year. sequelae and 2) drug-induced sinus bradycardia or nating with periods of atrial tachyarrhythmias. In S-A block which improves to normal or near-normal these patients the sinus rate usually ranged between when the inducing drug is removed.
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