myocardial - heart · than72 hours) myocardial infarction. therewere ii8 menand 24 womenwhose ages...

British Heart Journal, I971 33, 526-532.

Acid-base imbalance and arrhythmias aftermyocardial infarction

J. Pilcher and R. E. NagleFrom Royal Infirmary, Sheffield S6 3DA; and Selly Oak Hospital, Birmingham

Studies have been made of 142 episodes of myocardial infarction to determine whether there is anyrelation between admission acid-base status and the incidence of ventricular arrhythmias. No suchrelation exists in uncomplicated infarction or in infarction complicated by heart failure. Experi-mental and clinical evidence suggests thatfor arrhythmias to be provoked by acid-base imbalancethis must be gross. Such degrees of imbalance are not attained in myocardial infarction withoutcardiac arrest or cardiogenic shock. There was an association between cardiogenic shock, agonalarrhythmias, and metabolic acidosis in this study. It seems likely that this association is largelymediated by an inadequate cardiac output provoking both acidosis and arrhythmias, but it isalso probable that acidosis, when gross, acts as a secondary agent in arrhythmic production.

Measurement of acid-base balance is of value in assessing probable mortality from myocardialinfarction - metabolic acidosis carrying a poor prognosis. It is of no value as a guide to thedevelopment offuture ventricular arrhythmias.

Metabolic acidosis may occur after myocardialinfarction (Neaverson, I966) and is particu-larly common in cardiogenic shock (Mac-Kenzie et al., I964). Experimental evidencesuggests that severe acidosis predisposes theheart to arrhythmias (Karis, Harmel, andHoffman, I960; Hecht and Hutter, I964;Gerst, Fleming, and Malm, I966) and pre-vents successful treatment of ventricularfibrillation (Ledingham and Norman, I962).Clinical evidence also suggests that sucharrhythmias may be caused by alkalosis(Flemma and Young, I964; Ayres and Grace,I969).The purpose of this study has been to corre-

late acid-base status found after myocardialinfarction with the presence or absence ofventricular arrhythmias over the subsequent24 hours and to determine the effect of severityof infarction upon any such relation. It shouldthen be possible to determine whether acid-base imbalance has any prognostic guide asto the likelihood of development of thesearrhythmias.

Patients and methodsStudies were made on I42 episodes of recent (lessthan 72 hours) myocardial infarction. There wereII8 men and 24 women whose ages ranged be-tween 33 and 82 (mean age 57 with a standard

Received I9 October 1970.

deviation of IO I years). All had been admitted toa coronary care unit and their live stay within thisunit varied between 36 hours and 24 days (mean5-5 days). A diagnosis of myocardial infarctionwas confirmed in all patients by a typical history,diagnostic changes in the electrocardiogram, anda transient rise in the relevant enzyme tests.

All patients except 5 were in sinus rhythm with-out significant ventricular premature beats at thetime of onset to the study. Of these 5, 2 were inatrial fibrillation of long standing and 3 were beingtransvenously paced for complete heart block.During their stay within the coronary care unit

all patients were oscilloscopically monitored withrespect to heart rate and rhythm. Nursing staffwere trained to recognize and where possible torecord any arrhythmia seen on either the indi-vidual single channel or central multichanneloscilloscopes.

Arterial samples were taken as soon as possibleafter admission to the unit and in all cases withingo hours ofthe probable onset ofinfarction. Directbrachial or radial artery punctures were well toler-ated without local anaesthetic. At least 5 ml bloodwere collected into heparinized glass syringes andarterial pressure used in driving back the syringeplunger. These blood samples were estimatedpersonally forpH and Pco2 using standard Radio-meter micro-electrodes at 370C. In general,estimation was done immediately after collectionand in no case did more than two hours elapsebetween collection and estimation: such sampleswere stored on ice pending estimation. Electrodecalibration followed the makers' instructions usingbuffer ampoules for pH and saturated reference

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Acid-base imbalance and arrhythmias after myocardial infarction 527

gases (Haldane) for Pco2. All samples were estim-ated in duplicate. These duplicate readings wereaccepted if they agreed to within o-oI pH unit orI mmHg for Pco2. Mean readings were thenrounded. Base excess or deficit has been calculatedfrom pH, Pco2, and haemoglobin, and approxim-ated to the nearest whole number.

All arrhythmias considered in this study oc-curred within the 24 hours subsequent to arterialsampling, and later arrhythmias have not beenincluded. Studied arrhythmias were: (i) ventricu-lar tachycardia; and (2) ventricular prematurebeats, provided and only if they fulfilled at leastone of the following criteria: (a) a frequencygreater than 5 a minute, (b) multifocal in origin,(c) arose from a single focus but occurred in pairsor runs; and (d) exhibited the R on T phenome-non.

Sinus, and atrial arrhythmias, escape rhythms,heart block, and bundle-branch block have notbeen included. Ventricular fibrillation only oc-curred once, in the absence of cardiogenic shock,during the period of study. This fibrillation waspacemaker induced and has not been included.The I42 episodes of myocardial infarction have

been divided into three severity groups. The firstgroup consists of those patients in whom there wasno clinical or radiological sign of heart failureover the period of study. This group is considereduncomplicated. Should there have been suchsigns, patients were allocated to the second orheart failure group. The third group consists ofpatients with cardiogenic shock. Only four patientssuffered this complication over the period ofstudy and six others subsequently. All died.The relation between acid-base status and the

incidence of arrhythmias has then been assessed.This has been done both overall and within eachseverity group using unpaired t-tests or x2 todetermine statistical significance.

ResultsThese are displayed by histogram in Fig.i and 2.

Overall results 104 patients (87 men andI7 women - mean age 56-o) did not sustainany ventricular arrhythmia over the period ofstudy immediately after infarction. Theirmean pH was 7.4I7 (standard deviation o os)and base-excess + i'o (SD 31i). Arrhyth-mias were sustained by 38 patients (31 menand 7 women - mean age 58'o) - there being24 patients with ventricular premature beatsof the types mentioned, IO patients with ven-tricular tachycardia, and 4 shocked patientswith agonal arrhythmias. The mean pH ofthese 38 patients was 7-414 (SD oo65) andtheir base-excess +o0os (SD 3 8). t testing ofthese results indicates no difference in pH be-tween the two groups (P > o i) but gives anequivocal result for base-deficit/excess(P < 0-I > 0oo5). Accordingly the results have

been broken down into severity groups inorder to obtain a definite answer.

Uncomplicated patients 54 patients werefree of complications and there were nodeaths in this group. No patient had a meta-bolic acidosis (as defined by a base-deficitgreater than - 3), while IO patients had ametabolic alkalosis (as defined by a base-excess greater than + 3). 46 of these patientsdid not sustain arrhythmias; their mean pHwas 7-4I9 (SD 0.036) and base-excess + 1.4(SD 2 4). Eight patients did undergo arrhyth-mias - all of whom were in normal acid-basebalance; their mean pH was 7.4I3 (SD 0o036)and base-excess + i o (SD i 8). t testing indi-cates that pH and base-excess are essentiallysimilar between the two groups (P> o-i).

Patients with heart failure There were84 patients with evidence of heart failureduring the 24 hours after acid-base measure-ments and of whom I4 died during theirhospital stay. Eight patients had a metabolicacidosis - 2 of these sustaining arrhythmias -while i6 had a metabolic alkalosis, arrhyth-mias occurring in 4. The remaining 20arrhythmic patients were in normal acid-basebalance. Testing by x2 suggests no relationbetween acidosis, alkalosis, and normal acid-base balance on the one hand and the presenceor absence or arrhythmias on the other. Thislack of relation is confirmed by t testing - 58non-arrhythmic patients having a mean pH of7'4I5 (SD o0o6) and base-excess of +0-7(SD 3 5) while 26 arrhythmic patients had amean pH of 7-429 (SD o0o55) and base-excessof +o 9 (SD 2.7).

Patients with cardiogenic shock Fourpatients showed evidence of severe cardio-genic shock during the 24-hour period ofstudy immediately after admission. Arterialsamples were obtained from these patients(= early onset shock) and from 4 of the 6patients who became shocked after the 24-hour period of study (= late onset shock). Allthese patients died - thereby sustaining agonalarrhythmias - within 24 hours of sampling.Of these 8 patients, 5 had a metabolic acidosis(2 of them showing the greatest base deficitof the whole series) and none was alkalotic.Their mean pH was 7-349 (SD o-o85) andbase deficit - s.I (SD 5o). Since there wasno shocked patient in whom arrhythmias didnot develop, no direct comparisons can bemade.

However, it does appear that cardiogenicshock per se has a significant association withacidosis (pH P <oo,5 base-deficit/excess



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528 Pilcher and Nagle

UNCOMPLICATED GROUParrhythmia present

V-ventricular tachycardia+hospital death

FIG I pH and ventricular arrhythnias.

P < Ooi - as compared with acid-base statusin non-shocked patients) and that shockcarries an increased risk of arrhythmia(P < ooI on these figures). Evidently there isan association between acidosis, arrhythmias,and cardiogenic shock, but one cannot saywhether the acidosis itself is the cause ofsuch arrhythmias.These findings suggest that the overall

equivocal results obtained for comparisonbetween base-deficit or excess and arrhyth-mias may be caused by the values obtained incardiogenic shock. Indeed this is the case andif shock be excluded mean base-excess for 34arrhythmic patients becomes + 0o95 (SD 2.5)- clearly indicating that there is no relationbetween acid-base status and arrhythmias in

myocardial infarction without cardiogenicshock.

Relation between death and acid-basebalance Eighteen patients died; 4 of thesesuccumbed to early onset cardiogenic shockand 6 to shock of late onset. The remainderall died after the 24-hour periods of study,death being caused by congestive cardiacfailure in 4 patients, cardiac rupture, certainlyin one and probably in another, and as adirect consequence of arrhythmia in the 2remaing patients.There is no association between alkalosis

and death; indeed no patient with a metabolicalkalosis died. However, there is a very signifi-cant association between both lowpH (< 7.36)

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UNCOMPLICATED GROUParrhythmia present

JNC aPLICaTED GROUP.arrhythmia absent

HEART FAILURE GROUParrhythmia present

HEART FAILURE GROUParrhythmia absent

SHOCK GROUP

=early onset=late onset

arrhythmia present

_+......_.i>-9 -9 -8 '-7 -6 '-5 -4 -3 -2 -V O +1I

ACIDOTIC NORMAL

V.ventricular tachycardia+-hospital death

+2 .3 1 +4 +5 - +6 7 .8 >+8ALKALOTIC

FIG 2 Base excess or deficit and ventricular arrhythmias

and metabolic acidosis and death (P < o-ooi).Almost certainly this is the result of inade-quate tissue perfusion via poor cardiac output.

DiscussionThis study categorically shows that there isno relation between acid-base status and ven-

tricular arrhythmias in myocardial infarctionwithout cardiogenic shock. However, it standsor falls on two assumptions. Firstly, either allarrhythmias must have been correctly recog-nized and detected, or alternatively non-

recognition must have been random over theobserved range of pH and base-deficit orexcess. Secondly, either acid-base statusremained constant over the period ofmeasure-ment or alternatively movement in acid-basestatus over this time was random between the

two groups of arrhythmic and non-arrhythmicpatients.

This study indicates an incidence of 27 percent ventricular arrhythmias over the timestudied. This incidence is certainly muchlower than the usually accepted incidences ofbetween 73 per cent (Imperial, Carballo, andZimmerman, I960) and 95 per cent (Julian,Valentine, and Miller, I964). These highfigures do of course cover all types of arrhyth-mia observed after infarction and, also unlikethis series, are not limited by time. Twenty-eight patients in this study sustained poten-tially dangerous ventricular premature beats(being isolated in 24 cases and proceeding toventricular tachycardia in 4) - an incidence of20 per cent. It is difficult to state comparablefigures, but the findings of Julian et al. (I964)and of Lown, Kosowsky, and Klein (I969)

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suggest an incidence of about 30 per cent forthese types of premature beats over the courseof infarction.

Comparisons with these figures certainlysuggest that arrhythmias have been missed inthis series. Indeed it would be surprising hadthey not been missed. However, nursingstaff, on whom arrhythmia detection largelydepended, though in general terms aware ofthe objects of the study were not informedabout acid-base status in any individualpatient, thus avoiding bias towards keenerobservations in acidotic or alkalotic patients.By this means it is felt that non-recognitionproblems do remain random.pH is the sum of metabolic and respiratory

acid-base status and rapidly affected byrespiratory change. In a study such as thisit is certainly affected by the often necessaryprior analgesia and perhaps by arterial punc-ture itself despite careful technique. Fluctua-tions of pH over short periods of time mustoccur, and there is no guarantee or even likeli-hood that the value obtained represents theirmean. Base-deficit or excess represents meta-bolic acid-base status only, and is free fromrapid swings due to respiratory change.Nevertheless, a 24-hour period of observationafter arterial puncture is a long enough timefor almost certain changes in this measure-ment to occur - and particularly in an unstablestate, such as after myocardial infarction.Short of on-line monitoring ofpH and Pco2,there is no means of knowing whether move-ment in acid-base status was indeed randombetween the groups of arrhythmic and non-arrhythmic patients. It does seem empiricallylikely, but this assumption must remainunproven.

In general terms cardiac tachyarrhythmiasare caused by an alteration in the firingrate of normally automatic specialized cells.Any factor that increases the automaticityof a group of cells outside the sinusnode to a level above that of the sinus nodewill result in an arrhythmia. Many factorscan do this and include acid-base imbalance.An increase in Pco2 causes an increase in therate of automatic diastolic depolarization(Karis et al., I960; HofEman and Cranefield,1964), while changes in pH not caused bychanges in Pco2 may also reduce the maxi-mum level of depolarization and therebyapproximate it to the threshold firing value(Karis et al., I960; Hecht and Hutter, I964).At a more clinical level metabolic acidosisreduces thethresholdforventricularfibrillation(Gerst et al., I966), and if it is not correctedafter cardiac arrest, post-arrest arrhythmiasare provoked (Ledingham and Norman, I962).

Alkalosis probably exerts an effect on thefiring rate of automatic cells by changing thedistribution of ions between intracellular andextracellular fluids. Experimental respiratoryalkalosis is known to shift both potassium andsodium into cells (Giebisch, Berger, and Pitts,I955), and it is likely that metabolic alkalosishas a similar effect (Adler, Roy, and Relman,I965). A decrease in extracellular potassiumcauses an increase in the rate of diastolicdepolarization (Hoffman and Cranefield,I964), and arrhythmias may ensue. Surpris-ingly, respiratory alkalosis was not found toalter the threshold for ventricular fibrillationin one study while metabolic alkalosis actuallyprotected the heart from this arrhythmia(Gerst et al., I966). However, the dangers ofarrhythmias being provoked by mechanicalhyperventilation are now well known (Flem-ma and Young, I964), and recently twopatients have been reported in whom recur-rent ventricular fibrillation after myocardialinfarction was associated with a respiratoryalkalosis, and in whom the arrhythmia couldnot be corrected until ventilation was de-pressed (Ayres and Grace, I969).The production of arrhythmias after myo-

cardial infarction is complex and certainlymultifactorial. They are certainly related tothe catecholamine release known to occur inmyocardial infarction (Valori, Thomas, andShillingford, I967). The rate of diastolicdepolarization is also increased by the passageof weak depolarizing currents across auto-matic cells (Trautwein and Kassebaum, I96I),and it has been suggested that the current ofinjury produced in dying or injured myocar-dium may enhance the automaticity of adja-cent cells and thereby initiate arrhythmias(Hoffman, Cranefield, and Wallace, I966).Localized myocardial ischaemia - such as ispresent in a peri-infarction zone - sensitizesthese adjacent automatic cells to the influenceof catecholamines (Hoffman and Cranefield,I964). Generalized arterial hypoxaemia iscommon after myocardial infarction (Valenciaand Burgess, I969), and hypoxaemia has beenshown to accelerate diastolic depolarizationwith possible arrhythmia production (Hoff-man et al., I966). Stretch is also known tohave a similar effect (Hoffman et al., I966),and may be a factor in the provocation ofarrhythmias affecting those hearts dilatedfrom heart failure.The situation becomes more complex in

view not only of the interrelationships of thevarious factors that may provoke arrhythmiasbut of their relation with cardiac contractility.Catecholamines certainly increase contrac-tility but may do this at the expense of further



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myocardial anoxia (Yurchak et al., I964),since the slight increase in coronary flow doesnot keep pace with augmented oxygen require-ments. Acidosis is a cardiac depressant (Ng,Levy, and Zieske, I967) but a stimulant tocatecholamine release in its own right (Malmet al., I966). Catecholamine release protectsthe heart from acidotic depression (Rocamoraand Downing, I969), but below a certain pHlevel this protection probably fails. This pro-tection failure was shown in dogs in whom thecritical pH level was 71I (Wildenthal et al.,I968). In myocardial infarction acidosis andhypoxaemia are usually coexistent, andhypoxaemia has been shown to enhancegreatly the myocardial depression of acidosis(Gelet, Altschuld, and Weissler, I969).At a clinical level, there seems likely to be

a vicious circle mechanism set in action bysevere infarction. With regard to cardiac out-put this is immediately reduced by the infarc-tion. The ensuing poor tissue perfusion leadsto metabolic acidosis. The heart is initiallyprotected against this by the associated cate-cholamine release, but abetted by hypoxaemiathis protection soon fails. The cardiac outputthen worsens - acidosis increases and cardiacoutput is yet further depressed, etc.A somewhat similar situation can be en-

visaged with regard to arrhythmias. They maybe provoked by the initial catecholamine re-lease after infarction and probably are initi-ated from those ischaemic automatic cellsadjacent to the infarct. Injury currents maybe important at this site. More severe infarc-tions are likely to be complicated by therespiratory alkalosis and cardiac dilatation ofleft ventricular failure. Hypoxaemia may beproduced by left ventricular failure or byother ventilation-perfusion abnormalities(Valencia and Burgess, I969) and may be pro-voked at myocardial level by catecholaminerelease. Each of these factors may initiatearrhythmias in their own right or potentiateeach other until arrhythmias are provoked.It seems likely that acid-base imbalance haslittle part to play in the initial production ofarrhythmias. Metabolic acidosis may laterplay an important, but secondary role.Abetted by hypoxaemia it may become suffici-ently severe to depress further cardiac output.This reduction in output will then aggravatemost of those other factors concerned inarrhythmia production while the furtheracidosis produced by this fall in output willtend to provoke further arrhythmias, etc.Whether acidosis can directly provoke

arrhythmias in this situation is obscured bythe other factors involved and by its probablesecondary action in their production. It seems

likely that acid-base imbalance must be grossbefore it plays a primary role. In experimentalstudies on isolated guinea-pig hearts very fewarrhythmias were provoked over thepH range6-95 tO 7-48 (McElroy, Gerdes, and Brown,I958), while in intact dogs there was no signifi-cant change in heart rate or rhythm over thepH range 7-23 to 7.39 (Goodyer et al., I96I).What little clinical evidence there is confirmsthis. The two patients described by Ayres andGrace (I969) with recurrent ventricular fibril-lation due to respiratory alkalosis were bothseverely alkalotic - the pH in each being inexcess of 7.7, while two postoperative patientsdescribed by Brooks and Feldman (I962)with alkali-responsive ventricular fibrillationwere quite grossly acidotic, their base-deficitsbeing in excess of - 20.

Despite the considerable volume of clinicaland experimental evidence detailed abovesuggesting that acid-base imbalance doescause arrhythmias, the findings of this studyare not in disagreement. To cause arrhythmiasacid-base imbalance must be gross. Gross im-balance is not observed in myocardial infarc-tion without prior cardiac arrest or cardio-genic shock. Consequently acid-base imbal-ance can play no more than the most trivialpart in arrhythmia production under mostcircumstances. This study has shown anassociation between cardiogenic shock, acido-sis, and arrhythmias. There is insufficientevidence from the study to determine whetherthere is any primary association betweengross acidosis and arrhythmias or whether itbe mediated via the inadequate cardiac outputof shock. The evidence detailed above suggeststhat both factors are operative - the secondprobably being more important than the first- and that they are cumulative.The results of this study confirm and ampli-

fy the conclusions of Anderson et al. (I968).They found that a metabolic acidosis ofgreater than - 2-5 on admission was associ-ated with an increased tendency to arrhyth-mias over the next three days. This acidosiswas accompanied by the signs ofan inadequatecardiac output (as shown by hypotension andcold extremities), and it was considered thatthe apparent association between acidosis andarrhythmias was probably related to the grea-ter severity of infarction in these patients.Their findings are essentially similar to thoseof this study.

Little work has been done on the effects ofalkali administration to patients with arrhyth-mias in myocardial infarction. Anderson et al.(I968) did give alkali to three acidotic hypo-tensive patients with arrhythmias. It did notcorrect these arrhythmias, though their



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general condition did improve. It certainlydoes seem logical to give alkahli to acidoticpatients and has been previously recom-mended by Neaverson (I966). Such alkaliadministration might be expected to act asa brake in the vicious circle mechanism ofacidosis causing a further fall in cardiac out-put, etc., but would not be expected to exertmuch influence on arrhythmias whose genesisis multifactorial.

This study would not have been possible with-out the skill and enthusiasm of the nursing staff,Ward A4, Selly Oak Hospital, Birmingham. J. P.was in receipt of a Sheldon Research Fellowshipfrom the Birmingham Regional Hospital Board.Retrospective statistical assistance was given byMr. R. A. Dixon of the Department ofPreventiveMedicine, University of Sheffield.

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cellular acid-base regulation. I. The response ofmuscle cells to changes in Co2 tension or extra-cellular bicarbonate concentration. Journal of Clini-cal Investigation, 44, 8.

Anderson, R., Gardner, F. V., Honey, H., Noble,I. M., and Woodgate, D. W. (I968). Relation be-tween metabolic acidosis and cardiac dysrhythmiasin acute myocardial infarction. British Heart Jour-nal, 30, 493.

Ayres, S. M., and Grace, W. J. (I969). Inappropriateventilation and hypoxemia as causes of cardiacarrhythmias. American Journal of Medicine, 46,495.

Brooks, D. K., and Feldman, S. A. (I962). Metabolicacidosis, a new approach to neostigmine resistantcurarisation. Anaesthesia, 17, i6I.

Flemma, R. J., and Young, W. G., Jr. (I964). Themetabolic effects of mechanical ventilation andrespiratory alkalosis in postoperative patients.Surgery, 56, 36.

Gelet, T. R., Altschuld, R. A., and Weissler, A. M.(I969). Effects of acidosis on the performance andmetabolism of the anoxic heart. Circulation, 40,Suppl. 4, 6o.

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Goodyer, A. V. N., Eckhardt, W. F., Ostberg, R. H.,and Goodkind, M. J. (I96I). Effects of metabolicacidosis and alkalosis on coronary blood flow andmyocardial metabolism in the intact dog. AmericanJournal of Physiology, 2oo, 628.

Hecht, H. H., and Hutter, 0. F. (I964). Action of pHon cardiac Purkinje fibers. Federation Proceedings,23, I57.

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physiological basis of cardiac arrhythmias. Ameri-can J'ournal of Medicine, 37, 670.

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Imperial, E. S., Carballo, R., and Zimmerman, H. A.(I960). Disturbance of rate, rhythm and conductionin acute myocardial infarction: a statistical study of153 cases. American Journal of Cardiology, 5, 24.

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Malm, J. R., Manger, W. M., Sullivan, S. F., Papper,E. M., and Nahas, G. G. (I966). The effect ofacidosis on sympatho-adrenal stimulation; particu-lar reference to cardiovascular bypass. J7ournal ofthe American Medical Association, 197, 12I.

Neaverson, M. A. (I966). Metabolic acidosis in acutemyocardial infarction. British Medical Journal, 2,383.

Ng, M. L., Levy, M. N., and Zieske, H. A. (I967).Effects of changes of pH and of carbon dioxidetension on left ventricular performance. AmericanJournal of Physiology, 213, II5.

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