Chaotic atrial mechanism: characteristics and treatment

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arrhythmia occurring in elderly patients with ad- vanced heart ... CAM may progress to atrial fibrillation, just as .... confused with ventricular tachycardia, but ec-.
CRITICAL CARE MEDICINE

Vol. 2, No. 5, September-October, 1974

Chaotic atrial mechanism: characteristics and treatment RICHARD J. KONES, MD*; JOHN H. PHILLIPS, MD**

awarenes!. of this arrhythmia has re~ulted in its greater identification. 1 The criteria usually given for the diagnosis of chaotic atrial mechanism include: 1) three or more P wave morphologie!. in any single ECG lead; 2) absence of one predominant atrial focus; 3) varying PR, PP. and RR intervals; and 4) isoelectric PP intervals (Table 1 and Fig. I) . While there have been several recent studies characterizing the clinical associations of chaotic atrial mechanism, no definition of therapy has emerged. For example, it is unclear whether CAM is more likely to occur after cardioversion, or whether cardioversion is indeed the treatment of choice. Since the mortality of patients with CAM is uniformly high, the etiologies and management of CAM is of considerable interest. Accordingly, this prospective study was undertaken in order to determine the clinical, laboratory and pathologic associations of CAM and the mode of treatment best able to arrest the arrhythmia, and possibly improve survival.

Chaotic atrial mechanism (CAM) is a serious arrhythmia occurring in elderly patients with advanced heart disease, and appears to be related to multi focal atrial activit). The properties of CAM suggest it is an automatic ectopic rhythm, and rna) be produced under different combinations of conditions. CAM may progress to atrial fibrillation, just as ventricular tachycardia may lead to ventricular fibrillation. Drug-enhanced automaticity, distension of atrial walls, ischemic heart disease, or space-occup)ing lesions accounted for our cases. These appear to be similar to the currently accepted responsible events for pathologic ventricular automaticity. Both CAM and the ectopic automatic ventricular rh)thms are as~ociated with a high mortality, 1.ince both occur in patients with advanced heart disease. The additive antiarrhythmic action of combined propranolol and quinidine therapy rna} be helpful in managing CAM.

Chaotic atrial mechanism (CAM) is now recognized as a unique atrial arrhythmia with its own clinicopathologic associations. 1 ~ A greater

METHODS From the Cardiolog) Scctaon>. Flo"cr & F1fth A~cnue Ho>pllal,, New Vorl. 100~9. and Tulane Un1ver-11y 'X:hool of Medicine, New Orlean,, La. 70112

The diagnosis of CAM was made in 37 patients using the criteria outlined in Table 1 in a medicalschool affi iated hospital. A complete evaluation,

0 A,,;,tant Profe"or of Med1cine (Cardiology), New Vorl. Med1cal College, l'.e" York, ° Ch1ef of Cardiology. Tulane Un1~er~ity School of Mcdl\.lne, l"cw Orlean'>, I.a.

including history, physical examination, complete 243

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.. r

Fig. I A-Chaotic atrial mechanism mduced by excess use of isoproterenol

Fig. /8-Chaouc atnal mechanism found after pulmonary embolbm.

blood count, SMA-12, serum electrolytes, arterial and pH, spirometry, glucose tolerance test, serial electrocardiograms and continuous lead II electrocardiographic oscilloscope monitoring, and chest roentgenograms was performed for each patient. After appropriate treatment of the basic disease process, pharmacologic agents associated with the production of CAM were discontinued. Sequential therapy was then instituted as follows : diphenylhydantoin was given intravenously, digitalis was given either orally or intra>,~enously, quinidine orally or intramuscularly, cardioversion was attempted and propranolol and quinidine were combined in daily doses of 40 mg and 0.8-1.6 gm respectively. The route, dose and duration of administration of each agent was altered according to the patient's condition at the time, and therapy was discontinued when criteria for the diagnosis of CAM were no longer present. Other techniques, as listed in Table 5 were not considered in this study. Po~, Pco~,

RESULTS

Incidence. The incidence of chaotic tachycardia was 0.32~ of the total number of random electro-

cardiograms examined. Our patients were elderly; the mean age was slightly over 71 years. On occasion, CAM recurred in the same patient after conversion to another rhythm (not reflected in the incidence figure no ted above ). In general, CAM was found in seriously ill patients whose hospital mortality we found to be 5 I % . Clinical associations. Over 80% of the patients haJ chro nic lung disease (COPD ) and the majority of these used a nebulized isoproterenol for relief. The diagnosis of COPD was made by history, physical and x-ray findings, and confirmed by spirometry. Slightly under two-thirds of all patients had clinical evidence of congestive heart failure, half wtth acute o nsets. Five patients ( 16 %) suffered recent pulmonary emboli. Eleven patients ( 30% ) had abnormal glucose tolerance curves. Space-occupying lesions of the atria ( tumors, tuberculoma ) were reported in 5/ 17 ( 16 %) subjects at necropsy (Table 2). Pharmacologic agents. Although many patients were using isoproterenol as a bronchodilator, CAM disappeared in only six patients when the isoproterenol was discontinued. Of nineteen patients using digitalis, in o nly three did CAM revert when digitalis wa.~ removed from the regimen. Two of these patients had digoxin levels in the

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Kones & Phi/lip:, -

CHAOTIC ATRIAL MECHANIS~I

Table 1: Electrocardiographic criteria for the diagnosis of chaotic atrial mechanism (CAM). Discrete P waves of at least three forms in a single lead. Variable P-P intervals. R-R intervals and P-R mtervals. lsoelectric base line between P waves. Ab~ence

of a

~mgle

predominant supraventricular focus.

··toxic" range at levels of 3.6 and 4.2 ng/ ml respectively. However, as these patients were among the most critically ill, the question arises whether CAM was ameliorated by discontinuance of digoxin or by treatment of the basic disease processes. Laboratory correlations. Arterial hypoxia was common in patients with CAM (Table 3). No particular relation of CAM prevalence with serum potassium level!. was noted. Low-timed-forced expiratory volumes and forced expiratory flow rates were common. Therapeutic responses. Three patients responded to discontinuance of digitalis and six patients responded to removal of isoproterenol. In no case did diphenylhydantoin or quinidine abolish CAM. Digitalis administration in one patient with CAM probably caused atrial fibrillation , Cardioversion was unsuccessful in all patients. Combined propranolol and quinidine therapy was most efficacious since ten to 20 patients benefited from its use. DISCUSSION

Chaotic atrial mechanism had probably been described many years ago." and isolated cases have been reported since that time. 6 10 Recently, five series characterizing the clinical and electrocardiographic features of CAM more fully have

245

appeared. 1 1 ~ In certain respects our data agree with those of other authors (Table 4 ). The response to sequential antiarrhythmic maneuvers in the present series, however, has permitted certain conclusions regarding the mechanisms responsible for CAM (Table 2). It must be stressed that the high mortality of CAM is primarily due to the underlying disease in most patients, rather than a result of the arrhythmia per se. Pulmonary embolism and COPD. There JS general agreement that the incidence of acute and chronic lung disease in patients with CAM is high. The precise reason for this remains unproved. Systemic hypoxia, acidosis, atrial ischemia, use of both sympathomimetic and methylxanthine bronchodilators, increased vagal tone, and distension of the great vessels and/ or atrial walls have been mentioned as possible contributors. That atrial stretch is capable of producing atrial ectopic activity has been known for some time. 1 u· 17 In addition, mechanical or chemical stimulation of the tracheobronchial tree, or even increased transthoracic pressure may initiate ectopic atrial activity. Diabetes mellitus is common among patients with CAM. Since CAM is a disease of elderly and critically ill patients, the extent to which diabetes mellitus is peculiarly associated with CAM rather than with advancing age remains unclear. In our series, no patients had diabetic acidosis. Digitalis toxicity hac; been cited as a frequent cause of CAM! ·•• Our data agree with those of other investigators•~ t :c in that CAM may occur in association with digitalis toxicity on occasion, but by no means is digitalis the offender in the majority of patients. Although digitalis was used by most of the patients, and digitalis toxicity was more common in patients with advanced COPD and coexisting heart disease, these factors com-

Table 2: Summary of the characteristics of chaotic atrial mechanism (CAM). Often initiated by multifocal atrial premature complexes. Preceded and followed atrial fibrillation frequently. Appeared as a transitional rhythm during spontaneous conversion and DC cardtoversion. Unassociated with atrial tachycardia or PAT with block, but occas1onally with digitalis toxicity. Occurred in nonparoxysmal and paroxysmal forms. Ameliorated with quinidine and propranolol. Associated with acute disease capable of producing atrial distens1on or a Found in the severely ill elderly patient, producing a high mortality.

~pace-occupying

atnal lesion.

High mcidence of chronic pulmonary disease and relatively htgh incidence of dtabetes mellitus.

Table 3: Laboratory associations of chaotic atrial mechanism (CAM). No. of patients Po~

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= 65-90 torr

% 84 16 2.7

32

5

Po~ 5.5 mEq/ L KP· < 3.5 mEq/ L FEV 1 = 50-85 % pred1cted FEY 1 < 50% predicted FEFR = 50-85% predicted FEFR < 50% predicted

5.5

2 16 14 22

43 38 61 22

8

Po,= arterial O)()'gen 1eru.ion at lime of arrhythmia, K0 • =plasma

potassium concentration, FEV1 - forced expiratory volume/ ! ~ec, midrange ('25-75%) forced expiratory flow rate. All patients had arterial oxygen tension; and electrolyte determinations Thirty pauent> had spirometriel. performed. FEFR =

bined do not establish a causal relation between digitalis toxicity and CAM. However, there is little question that the net effect of digitalis may increase atrial myocardial automaticity under given circumstances in high doses. Hence the precise role of digitalis requires further investigation.

Differential diagnosis and relationship to other supraventricular arrhythmias. CAM was more frequent in patients who were acutely ill. It is important to recognize, however, that both paroxys-

mal and nonparoxysmal varieties occurred in both acutely and chronically-ill patients, although the nonparoxysmal form was by far more common. Differentiation of CAM from atrial flutter and atrial fibrillation usually poses little difficulty. Atrial tachycardia is urufocal and paroxysmal in its common presentation. Atrial parasystole may be dil>tinguished by the presence of a conduction sequence. CAM with aberrant conduction may be confused with ventricular tachycardia, but ectopic P waves precede each QRS in the former. CAM was clearly associated with multifocal atrial activity and atrial fibrillation in our patients, in agreement with Lipson and Naimi. 1 a In one patient post-cardioversion, a transition from chao tic atrial mechanism to atrial fibrillation was witnessed in a single electrocardiographic tracing. Atrial tachycardia and atrial flutter did not appear to be related arrhythmias. The relationship of CAM to wandering atrial pacemaker requires special comment. "Wandermg pacemaker" usually refers to mu1tifocal supraventricular escape complexes in the presence of sinus bradycardia. t:.l For this reason, Shine and assoc1ates 11 did not consider a wandering pacemaker related to CAM. However, their series was constlluted only by patients with chaotic atrial tachycardia. Phillips, Spano, and Burch 1 ~ mention that the PR interval seen with a wandering at rial pacemaker is more fixed than that usually present in CAM, and occasionally a pattern of "wandering" is present. These workers suggested that diffuse atrial disease and sinus node injury

Table 4: Comparison of the findings in six series of patient!:. with chaotic atrial mechanism (CAM) . Shine"

Phillips"

Lipson u

Chung '~

32 0.27

31 0.25

31 0.2

NR

34 NR

84 74

39 NR

NR

Number of patients Incidence (%) Chronic obstructive lung disease (%) Diabetes mellitus (%) Space occupying atrial lesions (% ) Pulmonary embolism (%) Advanced heart disease ''Related" atrial rhythms Special features Mortality (%) NR- not reported;

AF

NR NR high low

38 :urial fibnllauon

NR 16 high high diabetes 74 % 58

NR NR high very high progressed to AF 55% NR

65

92

NR II

high high digitalis toxicity 65% 50-60

Berlinerbfau " K oneJ and Phillips

31 0.4

0.32

48 26

81 30

16 NR 96 high no therapy advised > 50%

37

16 16 high high qumidine& propranolol 51

Kones & Phil/ips-

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Table 5: The proposed management of chaotic atrial mechanism (CAM). I. TREAT BASIC DISEASE

- - - -- ---- - A. Reduce atrial distention. B. Improve myocardial oxygenation and metabolic status.

C. Remove agents which increase automaticity. II. PHARMACOLOGIC Quinidine and propranolol. Ill. OTHER TECHNIQUES A. B. C. D.

Atrial overdrive. Carotid sinus nerve sumulatton. Permanent mduced atrial fibrillation- utgitalb and patred atrial pacing. Surgical mterruption of sympathetics or conducting system.

Those techn1ques '" categor)' 111 -.ere not '1ud1ed here and are not

resulted in ··competition for pacemaker control by other foci of atrial pacemaker tissue." Since multifocal atrial escape beats would be more likely to occur in the presence of a sinus bradycardia, enhanced automaticity of extra-sinus atrial pacemakers would necessarily be a requirement for the formation of CAM. The distinction between .. escape" multifocal atrial activity and enhanced atrial automaticity is important, but may in part be clouded by incorrect terminology. For instance, Berlinerblau and Feder';; conclude that CAM is an "accelerated and extreme form of a wandering pacemaker" but in fact the terms ··acceleration" and ··wandering pacemaker" are strictly mutually exclusive. Nevertheless, a wandering atrial pacemaker has been observed in patients before and after CAM. It is entirely possible that both true wandering pacemaker rhythm and CAM both correlate with diffuse disease of the sinoauricular node and atrium.

or

proven value 111 1rea11ng CAM.

All authors agree that control of the underlying disease is likely to be most rewarding in patients with CAM. While most antiarrhythmic agents used alone have not been successful in terminating CAM, many investigators have attempted to treat this arrhyth mia. Berlinerblau and Feder';; do not recommend treatment, terming the arrhythmia ''relatively benign," although they reported over 50% mortality in their patients. Our data suggest that the combination of propranolol and quinidine is most effective in abol-

··synergism" has been used to advantage in converting chronic atrial fibrillation. ~ ~ .. ~ ;• Quinidineresistant arrhythmias, whether they be paroxysmal or nonparoxysmal, or originate in the atrium, A-V node, or ventricle, respond to combined quinidine and propranolol therapy.~~ In a large series of 221 patients, Stern:!:. reported an improvement m patients with a variety of arrhythmias using quinidine and propranolol. The side effects of combined propranolol and quinidine therapy were few in our patients. The contraindications for the use of quinidine ( eg, sensitivity, bundle-branch block, atrioventricular block) and propranolol (severe aortic valve disease, severe mitral insufficiency, and severe bronchospasm) were taken into account during their use. Minimal bronchospasm and congestive heart failure were considered relative contraindications and judgment was exercised before the combined therapy was instituted. In part, the use of the two agents together appeared to allow arrhythmia control at tolerable doses of propranolol. Propranolol and quinidine share many electrophysiological properties which may explain their observed additive antiarrhythmic effects. 26 •27 Both agents depress resting membrane potential, membrane excitability, rate of rise of phase 0 of the action potential, conduction velocity, and spontaneous diastolic depolarization (Table 6). While quinidine prolongs the effective refractory period and action potential duration, propranolol shortens both. In therapeutic doses, propranolol has relatively less effect on ventricular muscle than

ishing CAM (Table 5). The use of this particular

on Purkinje fibers. 28 In addition, propranolol

TREATMENT OF CAM

combination of agents is not

0

new. ~ ~

2

and their

does not prolong intraventricular conduction, 2 n

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Table 6: The electrophysiological actions of quinidine and propranolol. Quinidine

Propranolol

J. OVERALL (eg, in atrial flutter)

t t

Atrial rate A-V conduction time II. PURKINJE FIBER ELECTROPHYSIOLOGY Resting membrane potential ( RMP) J. Excitability J. Membrane responstveness J. Rate of rise phase 0 ( dV I dt) J. Conduction velocity J. Slope phase 4 J. Automaticity J. Effective refractory period (ERP) t Action potential duration ( ADP) f 6 ERP/6 APD t

J. J,

J. J. J. J. J. l

J. t

Lll.lNTRAVENTRICULAR CONDUCTION TIME

t

-+

IV. EXCITATION-CONTRACTION COUPLING Intracellular cyclic AMP Calcium uptake by sarcoplasmic reticulum (SR) Contractility• V. CELLULAR DISTRIBUTION

0

-+

J.

J.

l

l

J.

Cell Z Line!> & Membrane Microsomal (SR) Fraction

Negauve inotropic effect lowered when combmed.

and hence the likelihood of reentry is not as great as with quinidine administration. However, the prolongation of the effective refractory period (ERP) produced by quinidine is decreased when beta-blocking agents are simultaneously employed. 'w In fact, competition for the receptor sites for ERP-lengthening by beta-blockers and quinidine has been proposed. Both quinidine and propranolol are negative inotropic agents. When combined, however, myocardial contractility is depressed to a les~er extent than the sum of the negative inotropic effects of each agent used alone. ~·J .:ct This interesting interaction has not been 1.atisfactorily explained. Further, the negative inotropic effect of quinidine is greatest during tachycardia and at slow heart rates may even become a positive inotropism . '~

September-October, 1974

Intracellular activator calcium available to the actomyosin filaments is reduced by both propranolol and quinidine. 27 ·a 3 The effect of both quinidine and propranolol on spontaneous depolarizations of the heart membrane, probably caused by transient inward calcium currents, are unknown. These fluctuations produce action potentia .s with a slow upstroke and low amplitude and a re more likely to initiate reentrant arrhythmias. 3',5'-adenosine monophosphate (cyclic AMP) concentrations are not altered by quinidine, but are appreciably reduced by propranolol. The different intracellular sites of action may explain the additive antiarrhythmic actions. However, the relationships among cyclic AMP, calcium concentrations, contractility, and the combined effect of propranolol and quinidine remains unclar ified to date. MECHA..NISM

Arrhythmias are currently thought to result from abnormalities of impulse formation and/ or conduction. :• ~ :I;, We propose that CAM is an ectopic automatic rhythm involving several foci, resulting not from a single process, but perhaps from a combination or constellation of biochemical and mechanical factors. Sympathetic drive and vagal tone normally regulate the automaticity of cardiac pacemakers. :lr. Both ·'pathologic a natomic" and pharmacologic alterations of normal and ectopic pacemakers may contribute to the formation of abnormal rhythms, including CAM. The particular characteristics of CAM (Table 2) are consistent with this view. Pharmacologic. Excess sympathetic stimulation \\as noted by Geesbreght and RandalP 7 to accelerate atrial pacemaker automaticity as well as shift the site of the pacemaker. Catecholamine cardiac responses are most likely mediated by increa~es in adenyl cyclase activity, resulting in augmented intracellular concentrations of cyclic AMP.:!' The methylxanthines are also cardiotonic, partly due to secondary catecholamine release, and possibly due to phosphodiesterase inhibition (the enzyme responsible for cyclic AMP degredation), thus also raising cyclic AMP levels within the cell. The methylxanthines may also directly influence intracellular calcium kinetics to effect changes in contractility. 27 2 h Excess use of agents in both classes ( ie, isoproterenol and aminophylline) is associated with the formation of CAM. Indeed, this observation led Lipson and Naimi 1 :1 to consider excess sympathetic activity

responsible for the pathogenesis of chaotic atrial tachycardia. As mentioned, reflex cardiac stimu-

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O l AOTI C ATRI AL MEC HAN I SM

lation may be media ted by both sympathetic and vagal pathway~, and may contribute to C AM fo rmatio n. PathoLOgic anatom ic. Anatomic changes commonly associated with C AM include atrial distention, diffuse fibrosis, and space-occupying lesions of the atria. The experimental evidence supporting atrial distention as an etio logy of atrial arrhythmias has been reviewed elsewhere.10· 1 ' The high incidence of acute p ulmonary embolism, C OPD, and acute congesti ve heart failure in patients with C AM has been generally explained on this basis. Reduction in atrial size during treatment of the underlying lung disease is considered impo rtant. H Diffuse atrial fibrosis, noted by Phillips, Spano, and Burch, 12 may also contribute significantl y to the genesis of CAM. Space-occ upying atrial lesions, as noted in o ur patients, were also reported by Berlinerblau and Feder. 11; Ischemia of the s inus node and atrial muscle may be responsible for the fo rmation of CAM in some patients. Altho ugh atrial infarction is quoted as a likely source for C AM origination, 1 ~ none of our patients had evidence of this process. Sinus node slowing due to ischemia, however, may remove the inhibition of lower pacemaker auto maticity normally accom panying the sinus mechanism .'1" Failure of such "endogeno us overdrive suppression ," probably mediated by a frequency-dependent electrogenic mechanism, may play a role in the formation of C AM. T his thesis is supported by the fact that those patients with C AM at slower rates tend to have mo re extensive and diffuse atrial disease tha n those patients with chaotic atrial tac hycardia, in whom drug-induced automaticity occurs mo re f requently. R EFE R ENCES

I. Chung SK: Pn11ctp/eJ of Cardtac Atrlrl'lhmws. Bahimorc. T he W illiam, and Wilkins Company, 1971, pp IIS-12 1. 1. F riedman IIH : (Jtagno.wc Electrocardiography and Vector· cardiOgraph)·. New York, McGraw Hill Book Company, 1971, pp 364-365. 3. Bellet S: C/111ical DISa11 J 78:171- 179, 1969. IJ. Lip-;on MJ. Na1mi S: Multifocal utnal tachycardia (chaouc atnal tachycardia). Crrc11/ariun 42:397-407, 1970. 14. Chung EK · Appra1sal of multi foca l atrial tach ycardia. 8111 Heat/ 1 33:500-504, 1971. 15. Be rline rblau R, Feder W: Chaotic atrial rhythm. J Elecrrocartlw/ 5 135-144, 1972. 16. Scherf 0 , Scharf MM. Goklcn MF Ellect oi stretch and pre~sure on stimulu., formation in dog.·, ~uncle. Proc Soc E~p Bw/ M ct/10:108-111, 1949. 17. Weber O M , Phillips JH: A Re-evaluation of electrocardiographic changes accompanying acute pulmonary emholism. A mer J Med Sci 251:381-398, 1966. 18. H onman B : Effects of digualis on electrical activity of card iac membranes, in Bnsic nnd Clin ical Phamracnlogy oj Digaa/s, edited by M arks BH. Weissler AM, Springfield, Illinois. Charles Thomas, 1972, p 113. 19. Shamrotl- L The Otsnrdet.f of Cardwc Rh)•llrlll, O).ford, Bl ackwel P ublbhers Ltd, 1971, p 117. 10. Stern S. Conver,ion of chronic atrial fibrillation to ~i n us rh ythm with combined propranolol and quinidine treatment. Amet Ht'ar/ 1 12:170- 172, 1966. 21. Stern e o f quinidine and propranolol. Circulariou 36: 11-22 1, 1967. ~3. Levi GF. P roto C: Combined trentment o f atrial fib1illaLion wit h quinidine and beta-blocker,. B rit 1/enrr J 34:911·914, 1972. 24. For- W J VanderArk CR, Reynolds EW J : Evaluation of propranolol and quinidine in the treat ment of quin idinere'"t:llll a rrh ythmias. Amn J Ca1dio/ 27· 190- 194, 1971. 15. Stern S · Treatmen t :tnd prevention of card iac arrh yth mias with propranolol and quinidine. Brit !/!'art 1 33:521-525, 197 1. 26. Drc1fus LS. Watanabe Y. Pamu11an J, et at· Propranolol hydrochloride and combined therapy in cardiac arrhythmias. Scientrfic Exhibit, American College of Cardiology 2 ht An· nual Se"ion. March 1-5, 1972, Chicago. 17 Kone., RJ : The iomc and molecular ba,is for ahered myocardial contract ility. Re.1 C'"""""' Cht'm Parlrnl Pharmacn/ 5 (suppl I ): 1-86, 1973. 28. Oavi, L O, Temle JV : Fftcct, vf p1opranolol on the transmembrane potentials of 'cntncular muscle and P urkin)e fiber, of the dog. Circ Re.r 22:Ml-o77, 1968. 29. Berkowitz W O, Wit AL. Stemcr C. et al : The effects of proprano lol on atrioventricular and intra,entricular conduction. Allt on some cardiodynamic and hemodynamic parameter, of normal individuals. Amer fl~atl J 78:217-223, 1969. :12. Kennedy R L, We't TC : Factor~ influencin g quinidinemduced changes in excitability and coni ractility. J Plwrm Exp Therap 168:47-59. 1969. 33. Kane' RJ : The equivalent electrical circuit of the myocardial cell membrane. J Mol Ct>/1 Cardiol: submiued for pubhcauon. 34. Bas