CLINICAL PROGRESS

Acid-Base Management for Open-Heart SurgeryBy S. A. ALLAN CARSON, L.R.C.P.&S.(I), LUCIEN E. MORRIS, M.D., K. WILLIAMEDMARK, M.D., THOMAS WV. JONES, M.D., GORDON A. LOGAN, M.D., LESTER R.

SAUVAGE, M.D., AND GEORGE I. THOMAS, M.D.

THE occurrence of serious acid-base dis-turbance is not only more likely during

open-heart procedures than with other formsof surgery, but its correction and the con-tinued maintenance of good acid-base statusis often critical. The operation, including sur-gery on the heart itself, offers considerablecardiovascular stress to the debilitated patientwho has a limited cardiac reserve. The addedinsult of acid-base imbalance may be morethan the heart can tolerate, and careful man-agement, including correction of any imbal-ance, may prevent an adverse outcome to anotherwise successful operation.

Definition of Acid-Base StatusIt is generally accepted that at 37C., the

pH of arterial blood has a normal value of7.40. Acid-base imbalance may occur as eitheracidosis (pH below normal) or alkalosis (pHabove normal). Acidosis is further defined asrespiratory, which is due to retention of car-bon dioxide producing an arterial pCO2 abovethe normal value of 40 mm. Hg, or metabolic,which is due either to excess of acid metabo-lites or to decrease in available base. Similarly,alkalosis may be respiratory (pCO2 below40 mm. Hg) or metabolic (due to excess baseor loss of acid). Respiratory and metabolicacidosis or alkalosis may be combined, thus

From the Heart Center and Anesthesia ResearchLaboratories, Providence Hospital, Seattle, Washing-ton.

Supported in part by funds from The NationalInstitutes of Health Grant H-5959 (Cl), Washing-ton State Heart Association, and the John A. HartfordFoundation.

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creating the need for more definitive termsto describe fully the acid-base status. Henceacidosis or alkalosis may be mixed, uncom-pensated, partially compensated, or fully com-pensated. If it is the last, the choice as towhether it be described as fully compensatedacidosis or fully compensated alkalosis de-pends on the apparent initial cause of the im-balance. Because of the confusion sometimescreated by these terms, acid-base managementis often considered to be a complicated matter.Primary consideration of the respiratory andmetabolic components as separate entities,lhowever, helps to clarify understanding of thesituation, and the management of an im-balance becomes more straightforward. Thesetwo components may have an additive effector a compensatory effect on one another btittlhe treatment of each component must beconsidered in every instance. In some situa-tions, treatment of one component may resultin spontaneous correction of the other, where-as, in other cases, active treatment will henecessary for both.The clinical picture resulting from acid-

base imbalance is unreliable, as it varies withthe types of acidosis or alkalosis and the de-gree of compensation. It may also be con-fused by the presence of other factors; forexample, from their clinical appearance it isdifficult to differentiate between the effects ofmetabolic acidosis and residual curarization.1The aim of good management is primarily toprevent acid-base disturbance, and secondlyto correct any imbalance and to maintain goodacid-base balance with continued treatment ifnecessary. To attain this goal, accurate meas-

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urements must be made of the acid-base statusas frequently as necessary to prevent majordeviation from the normal.

Measurement of Acid-Base Status

There are many methods of determiningacid-base status but certain requirements mustbe fulfilled if the method is to provide goodcontrol and allow good management. Theacid-base status may change quickly leadingto rapid deterioration in the patient's condi-tion or, equally rapidly, as a result of vigoroustreatment, and information regarding suchchanges must be readily obtained. Informa-tion of the acid-base status from a blood sam-ple taken an hour previously is not onlypresently inapplicable but, if acted upon, re-sults in little better than blind treatment.Worse, during the time of awaiting the re-sults upon which treatment is to be decided,the patient may have succumbed from grossacid-base imbalance. Therefore, any methodused must be not only accurate and compre-hensive but also rapid and capable of produc-ing almost immediate results.These requirements of a good, rapid, ac-

curate method of ascertaining the acid-basestatus in our opinion appears to be best ful-filled by the thermostatically controlled tripleelectrode system, with use of a pH electrode,Severinghaus pCO2 electrode, and modifiedClark P02 electrode. Once this equipment iscalibrated, it is possible to obtain values forpH, pC02, P02, and oxygen saturation (bycalculation from pH and PO2).2 Base excessor deficit is quantitated by a special appli-cation of the Siggaard-Andersen nomogram,3' 4

as previously described.5 This value of baseexcess or deficit, in milliequivalents per literas bicarbonate, is valid irrespective of tem-perature. Should the patient's temperature beother than normothermic, appropriate correc-tions for pH, pCO2, and P02 are applied.6 8Thus a comprehensive quantitative assessmentof the acid-base status is obtained within afew minutes of obtaining a 2- to 3-ml. sampleof arterial blood.The Astrup method of measuring pH, pCO2,

and base deficit or excess by equilibratingsamples of blood with known tensions of car-

Circulation, Volume XXIX, March 1964

bon dioxide 3 is also rapid and requires evenless blood but this alone does not give ameasure of the state of oxygenation and thevalues are only applicable under conditions ofnormothermia.

It is best to use arterial blood samples todetermine the acid-base status, since venousor capillary blood values vary greatly de-pending on the degree of blood pooling andstasis that may occur in shock conditions. Ar-terial blood gas analysis may not give anaccurate indication of the intracellular status;nevertheless, it would appear to give the bestmeasure of the efficacy of the cardiovascularand respiratory systems. Samples are with-drawn, either from an arterial catheter or byarterial puncture, into a syringe previouslywetted with heparin (1,000 units per ml. con-centration).

Phase before Cardiopulmonary BypassFrom the time of administration of pre-

anesthetic drugs until the commencement ofcardiopulmonary bypass, acid-base imbalanceis a potential hazard although in most casesit does not occur to any great extent.

Respiratory AcidosisRespiratory acidosis may occur as a result

of inadequate elimination of carbon dioxidefrom the lungs due to inadequate ventilation.It may also be the result of right-sided heartfailure, since insufficient blood is beingbrought into contact with the alveolar mem-brane where diffusion of carbon dioxide intothe alveoli occurs. Atelectasis results in per-fusion of alveoli in which no gaseous exchangetakes place and this, too, produces respiratoryacidosis.

Respiratory acidosis consequent upon anes-thesia and the open-chest procedure can usual-ly be avoided during the phase of the opera-tion before bypass if the anesthesiologist aug-ments ventilation to insure adequate elimina-tion of carbon dioxide from the lungs. Moder-ate hyperventilation, as provided by manyanesthesiologists, is usually satisfactory at thistime but gross hyperventilation, producingrespiratory alkalosis, is to be avoided. Ifrespiratory alkalosis occurs as the result of

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overventilation during anesthesia, the body,in an effort to maintain a normal pH, mayproduce a compensatory base deficit. Thisbase deficit is revealed as a metabolic acidosiswhen the arterial pCO2 is allowed to returnto a normal value.

Metabolic Acidosis

Metabolic acidosis is not usually a problemprior to bypass but may occur and on occasionbecomes quite severe by the time bypass iscommenced. The causes may be similar tothose to be described in phases after bypassand after operation. Occasionally a progres-sive metabolic acidosis is encountered priorto bypass, even in the presence of adequatearterial pressure and pO2, presumably due toa low cardiac output incident to anesthesiaand thoracotomy.

Prevention and treatment of metabolic aci-dosis are important prior to bypass, just as inthe other phases of the operation. Maintenanceof good oxygenation and a reasonable ar-terial pressure should be ensured and in somecases vasopressor agents may be necessary. If,before the beginning of bypass, there is abase deficit of more than a few milliequiva-lents per liter as bicarbonate in the patient'sarterial blood, it should be corrected withsodium bicarbonate solution intravenously insufficient amount to reduce the base deficit tozero. It is easier to maintain good acid-basestatus throughout the bypass period if thepatient is not in base deficit when bypass isstarted.

Bypass PhaseGross acid-base changes may occur during

bypass. If considerable imbalance does de-velop and remain uncorrected at the end ofthe bypass period, this may add markedly tothe stress of the phase after bypass and resultin increased postoperative morbidity. Dis-turbances occurring during bypass have beengreatly lessened since the introduction of high-flow perfusion technics. Nevertheless, goodacid-base maintenance still requires constantattention. If gross respiratory alkalosis is per-mitted during bypass, it may result in aprogressive base deficit. There is evidence thatrespiratory alkalosis produces a shift in the

hemoglobin oxygen dissociation curve to theleft,9 leading to tissue anoxia, since underthese conditions oxygen is not liberated bythe hemoglobin so readily. It may be alsothat under conditions of respiratory alkalosisthere is decreased peripheral tissue perfusion.When the temperature is kept relatively un-

changed at 37C., it is only necessary to main-tain a pH of 7.40 and a pCO2 of about 40mm. Hg by adding a low percentage of carbondioxide to the pump oxygenator gas mixture.Then, if the perfusion is satisfactory, acid-baseimbalance is not usually a problem. Shouldthe tissue perfusion be inadequate, it may benecessary to correct any base deficit withsodium bicarbonate, which may be added tothe blood on the venous side of the oxygenatorprior to discontinuation of bypass.

If hypothermia is to be employed, thenacid-base management becomes more im-important and more involved, since gross im-balance may result under these conditions.Throughout the operation optimal pH shouldbe maintained but it is important to realizethat a pI1 of 7.40 is not the optimal pH at areduced temperature. Edmark 10 suggestedthat the pH should be reduced during hy-pothermia; to achieve this he advocated theuse of 0.3 N hydrochloric acid. When carbondioxide is used instead of a hydrochloric aciddrip to control the pH of the blood in. thepump oxygenator and with a pH-temperaturescale similar to that suggested by Edmark(fig. 1), it has been possible to avoid the oc-currence of base deficit or metabolic acidosisduring hypothermic bypass.) The pH is re-duced by 0.0147 of a pH unit for each degreeCentigrade below 37. Using this technic, wehave been able to prevent other phenomenausually associated with hypothermia. For ex-ample, ventricular fibrillation and cessation ofspontaneous respiratory effort have been com-monly observed when the temperature is low-ered below about 30C.; with pH control,however, spontaneous respiratory effort con-tinues at temperatures below 25C., andventricular fibrillation usually does not occurunless there is interference with coronaryblood flow or severe cardiac manipulation bythe surgeon. If ventricular fibrillation is re-

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GCID-BASE M1ANAGEMEN 45NT

optimalPR

7 50

7.40

7 *30

7.20

7.10

7.00

6.90 4

6.60

6.70

6.40

6.30

6.200 5 10 15 20 25 30 35 40

Trprature * C

Figure 1

mperacture opstimal zp1l relationshlp *siniilar to tha(itl iginailfllh suggested l) LEd1iark ( ippei. line ); op1ti.nialpH reading whoera iincorreeterl for tem7iperatuire wEithlthe electrode maiairntained at 37C. (lowser line). Foreximple, at a temperature of 20C. the optimcal pHwvould be 7.15 blat withl the electrode mtaintaitned at370. the inistrumt7enit reading weould be 6.90.

quired fo3r the surgery it mtist be induticedelectrically, sometimes repeatedly or- coni-tinuolol sly.The esseence of muaniageimenit is still mnain -

ten-ianice of optimal p11 but, sinice optimal p11i.s clhaniging as the temperatiure is altered, itis niecessary to vary the pereei)tage of carbonclioxide iIn tle p'III"p oxygeniator gas mixture tomiiaitaini thle desired pl1. For this reasoni, pHmeasuiremenits are o0)taimed fronm samples of1)10(o1 takeni frequteniitly fromii the arterial sideof the oxygenator. Since it is dififhclt to mnain-tail) the electro(le bath at the changingr ten)-peratuire of the 1)l00(d in] the oxygenator, it isnlore conveinient to maintitiii the electrodles at

37C. and to apply corr-ectioin factors for thetemperatuire clifference between 37C. anid thatof the blood.', ` One of is ( S.A.A.C. ) las de-sigined a ciretlar slide rule for applicationi ofthe Rosenthali pl-l-temperatuire correction fae-tor, wihichi eliminiates the necessity for cal-culation anid tlihus speeds the results uiponwhich the carbon dioxide percentage of thepuinp respiratory imixtuir.e is altered.

Thlroighouit the bypass procedutre it is jin-portanit to miaintaini optimal pH at all timesineluiding the rewarming period whien thecarbon dioxiide pereentage nmay have to begreatly reduced. Since the perceentage miustvary according to the temperature and es-pecially xvith tlec raite of cialige of tempera-ttire, it is niot possil)le to miaintaini g,ood aci(l-base 1balance ly adminiisterii g a predeter-mined fixed pereenitage of carbon dioxide intothe ptimp oxygenator throughout bypass.

If the priminig fluid of the ptiimip oxygeniatorsystemil is niot enitirelv whlole blood, the buffercapacity of this mixttire mu>st be considered.In order to ensiuirie acioe1iate buffer capacity,soditium bicarlo)nate mul;st l)e a(dde(1 to the ex-tent of 45 mEq. per liter of diluienit fluiids. Thisprovides ani over-all )uffer capacity approxi-nating that of whiole 1l)10(d. Freshly drawvnhiepariniized 1l)0( is preferable for primingpurposes as older 1lood(or acid-citrate-dex-trose blood may be quite acidotic. Neverthie-less, after the pump is primed and followingrecircullation with ani oxygeni-low CO2 mix-tiire in the oxygeniator, it is advisable to meas-uire the degree of base deficit and correct thisby adding more sodiunm 1)icarl)onate. [Basecleficit (mEq./L.) x primirng volulme (liters)=amlount of sodiuim l)icarbonate (mEq.)necessary to correct the base deficit.

Metabolic acidosis m-ay occuir during bypassin spite of cacreflii managemenit. Usuially thismulst be asstumed to hlave been the resuilt ofinadequiate tissuie perftusion, provided goodoxygenatioln wsas mail)tail)ed in the oxygenator.If a l)ase deficit of mor-e than a fev milli-equivalents per liter as licarl)onate existstoward the ncid of the bypass period, itslhould be cor-rected 1)efore discontinuilg theperftusion. Additioni of suifficient sodiuim bi-carbonate to r-eduice the base deficit to zero

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Table 1

Cardiopulmonary Bypass with Hypothermia. Examples of Cases during Which 2 percent CO2 Was Administered Throughouit Bypass with No Attenmpt to Control pH

Operatioin

I.V.S.D. repair

I.V.S.D. repair and

modif. pul. stenosis

Atrial septalconstruction

Plul. valvulotomy

Aortic valvecommissurotomy

Oxygenator bloo1(tenmperature (C.)

31.0 Cooling28.0 Stable36.0 Rewarming25.0 Cooling22.5 Stable32.0 Rewarminm

3 1.5 Cooling27.5 Stable34.5 Rewarm'ngf

28.6 Stable28.6 Stable35.7 Rewarming

28.0 Stable33.0 Rewarming35.0 Rewx arming

This does not include the CO,, reaching the oxygenator via the coronarysurgical field is being flooded with 100 per cent CO, to prevent air embolism.

is advisable, for it ensures that the heart willnot be depressed by metabolic acidosis upon

resumption of the normal circulation.

Phases after Bypass and OperationEven if the acid-base status is good at the

end of bypass, a serious acid-base imbalancemay subsequently develop after bypass or

operation. Alkalosis is to be avoided at thesetimes just as earlier. It seldom occurs spon-

taneously but rather as the result of overlyvigorous treatment. The usual problem is al-most invariably one of either respiratory or

metabolic acidosis.

Respiratory Acidosis

During the post-bypass period the anes-

thesiologist can usually avoid respiratory aci-dosis just as in the period before bypass byadequately eliminating carbon dioxide fromthe lungs. Hyperventilation producing respira-tory alkalosis should be similarly avoided.

In the immediate postoperative phase, res-

piratory acidosis from inadequate ventilationis common. Pain from the large incision may

cause gross limitation of chest movement so

that the ventilatory effort is mostly diaphrag-

suction when tie

matic. Diaphragmatic breathing exercises be-fore operation may greatly contribute to theadequacy of the respiration in the recovery

ward but relief of the chest pain often cor-

rects the situation most dramatically. A long-acting intercostal nerve block, performed atthe conclusion of the operation, may be allthat is required. Sometimes moderate dosesof analgesics given intermittently are alsonecessary, but respiratory depression due tooverdosage of these drugs in combination withresidual effects of anesthesia is to be an-

ticipated and avoided if possible. In addition,among other effects, severe metabolic acidosiscauses depression of respiration, and correc-

tion of metabolic acidosis may resuilt in a

marked increase in ventilation.Postoperative atelectasis is a common se-

quel to open-heart surgery although in mostcases it may be localized. Diffuse and gross

atelectasis occuirring after bypass has beendescribed.11 This condition resembles lyalinememlbrane disease of the neonate and hasbeen attributed to absorption duiring bypassof the surface active material that normallylines the alveoli.1' Since carbon dioxide dif-

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CO-- ill pumprespiratorymiixture *

2.92

2

2

2

2

2

22

29

Elapsed tinmeon bypass,

lir. ,nn.

945-

1,472152

1,189

452,311848

1, 3

91,151,50

Base deficit(mEq./liter asbicarbonate )

-6.5-8.5-8.0-8.7-1.0-10.0-5.0-6.0-1.(_ 2.0-11.0-10.(-5.0-9.5- 9.0

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fuses much more readily across the alveolarmembrane than does oxygen, this condition ofdiffuse atelectasis may be revealed by a lowor falling arterial P02 in the presence of anearly normal arterial pCO2.

Gases may be absorbed from the alveoli bythe bronchial circulation during bypass andthis may predispose to alveolar collapse andatelectasis. For this reason, it may be usefulduring bypass to maintain expansion of thelungs with air rather than anesthetic gas mix-tures of high oxygen content. The incidenceof atelectasis after bypass might then be less,since the nitrogen of air is not so readilyabsorbed from the collapsed lung. At anyrate, it is essential for the anesthesiologist to

inflate the lungs fully at the end of bypassand during these efforts the lungs should befree in the chest and unrestrained by surgicalretractors or packing.

Treatment of Respiratory Acidosis

The treatment of respiratory acidosis is toensure adequate elimination of carbon dioxidethrough the lungs. If adequate ventilation can-not be promoted by pain relief and counter-action of depressive effects, then respirationmust be augmented mechanically. The use ofa mechanical ventilator must not be under-taken lightly as this of itself can cause com-plications. Ventilation should be sufficient toreduce the pCO2 to a normal value but gross

Table 2Cardiopulmonary Bypass with Hypothermia. Examples of Cases during Which Suf-ficient CO2 Was Administered in Pump Oxygenator to Maintain pH Optimal withTemperature According to Edmark's Scale

Operation

Part. repl.mitral valve

Total repl.aortic valve

Total repl.aortic valve

Mitralcommissurotomy

Mitralcommissurotomyt

Mitral annulo-plasty andcommissurotomyt

Repair of tornmitral chordae andmitral annulo-plastyt

Oxygenator bloodtemperature ('C.)

34.5 Cooling27.8 Stable33.5 Rewarming28.5 Cooling25.5 Stable35.2 Rewarming

31.0 Cooling28.5 Stable33.0 Rewarming34.5 Cooling27.0 Stable35.2 Rewarming

30.0 Cooling27.5 Stable34.8 Rewarming29.0 Cooling26.7 Stable34.6 Rewarming28.8 Cooling27.0 Stable33.0 Rewarming

* This does not include the CO2 reaching the oxygenator via the coronary suction when the

surgical field is being flooded with 100 per cent CO2 to prevent air embolism.t In these cases sufficient sodium bicarbonate was added to the pump priming mixture and

intravenously to the patient to correct any base deficit prior to bypass. In the previous cases

some sodium bicarbonate was added to the pump priming mixture but no attempt was madeto correct accurately for base deficit in either the pump or the patient prior to bypass.

Circulation, Volume XXIX, March 1964

C02 in pumprespiratorymixture *

851

752

842

442.5

1064

10102

1282

Elapsed timeon bypass,hr. ,min.

61, 42,1719

1, 63,20

122,263,54

751

1,511045

1,36112450

1335

1,16

Base deficit(mEq./liter asbicarbonate)

-2.5-5.0-5.7

0-3.0-2.5

0-3.0-5.3

-4.5-2.5-2.5

0-2.0-1.8

00

-3.00

-2.5-1.2

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hyperventilation should be avoided in therecovery room just as during the other phasesand for the same reasons. Some means ofhumidification must be provided or plugs ofaccumulated mucus may inspissate and lead tofurther atelectasis.

If atelectasis is not widespread, the periodicuse of a respirator for a few minutes of in-termittent positive-pressure breathing may besufficient. In some cases, it may be necessaryto use the respirator continuously to avoidrespiratory acidosis. Tracheotomy is oftennecessary in these patients. If such trouble isespecially anticipated, it may be advisable toperform the tracheotomy several days priorto the major surgery, to avoid problems of in-fection or bleeding or the necessity of thisprocedure as an emergency under adverse con-ditions.Even in the absence of respiratory acidosis,

mechanical ventilation may be indicated insome cases. It is sometimes possible for apatient spontaneously to maintain a nearlynormal pCO2 but at great cost in oxygenconsumption, due to the work of respiration.In the presence of low cardiac output andarterial oxygen desaturation, removing thework of respiration may be beneficial in lessen-ing the demand on an overworked heart."3Augmentation of spontaneous respiration,

rather than controlled artificial respiration isthe technic of choice, although, in a minorityof cases, controlled ventilation may be neces-sary to maintain a satisfactory pCO2. A ven-tilator triggered by the patient's own effortusually ensures that gross respiratory alkalosiswill not occur. Gaining control of respiration,however, or initial synchronization of thespontaneous respiratory effort with the ven-tilator may be difficult and require a period ofgross hyperventilation. To avoid this, admin-istration of a relaxant may occasionally benecessary at first.

Metabolic AcidosisIn the presence of normal urinary excretion

of acid metabolites, metabolic acidosis occursprimarily under conditions of anerobic tissuemetabolism, which releases excess acid metab-olites into the blood. Hence anything that

interferes with oxygenation of the tissue cellsmay cause metabolic acidosis.

Poor oxygenation of the blood in the lungswill result in arterial oxygen desaturation andconsequently there will be less oxygen avail-able to the tissues. The cellular hypoxia soproduced results in some degree of anerobicmetabolism, which causes metabolic acidosis.This poor oxygenation may arise from severalcauses. There may be a low oxygen concentra-tion in the respired gases or ventilation maybe insufficient. Atelectasis hinders oxygenationof the blood, since blood perfusing unven-tilated areas of lung cannot be oxygenated.

Shift in the hemoglobin oxygen dissociationcurve to the left, known to occur withrespiratory alkalosisj9 may lead to tissue an-oxia, since under these conditions oxygen isnot liberated as readily by the hemoglobin.This is another reason for avoidance of grosshyperventilation following bypass.

If the blood is being adequately oxygenatedin the lungs and the oxygen is readily suppliedby the blood to the tissue cells, the occurrenceof metabolic acidosis must then be due tocellular hypoxia from poor perfusion of tissue,resulting from peripheral vasoconstriction orlow cardiac output. If the cardiac output isinadequate, this, in itself, will result in pe-ripheral vasoconstriction and usually the twvofactors go hand in hand.

Prevention of Metabolic Acidosis

Good oxygenation of the blood must beachieved by adequate ventilation. The patientis usually placed in an oxygen-enriched atmos-phere postoperatively, by use of an oxygentent, and it may be necessary to administeroxygen instead of air when a ventilator isemployed, especially if atelectasis is present.In the presence of severe atelectasis hyper-ventilation with oxygen may be necessary toprovide adequate oxygenation of the blood.Under these circumstances some form of iso-capneic hyperventilation technic may be nec-essary in an attempt to achieve adequatearterial oxygen saturation without incurringgross respiratory alkalosis. Cold may causemarked vasoconstriction; for this reason theuse of thermal blankets to maintain a normal

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temperature is advocated postoperatively.Shivering should be avoided, as this can ac-count for considerable oxygen consumption.Retention of acid metabolites in the bloodmust be avoided and thus good urinary outputshould be maintained. Osmotic diuretics suchas mannitol are often given prophylacticallyfor this purpose.

Following a bypass procedure, there maybe several reasons for a low cardiac output.Often the heart is grossly debilitated, even be-fore surgery, and does not have much reserve.The corrective surgery in the heart itself, insome cases including elimination of a shunt,may present considerable increase in work tothe myocardium, which may be unable tocope with this load for a time after resump-tion of the normal circulation. Inadequateblood volume may be the cause of both lowcardiac output and peripheral vasoconstric-tion and thus blood replacement should bemade on the basis of blood volume studies orcentral venous pressures. If the patient waspreviously maintained on digitalis, this shouldbe continued throughout surgery and post-operatively. Following multiple blood trans-fusions, accumulation of citrate may result inlow cardiac output which may improve afterintravenous administration of calcium glu-conate or calcium chloride.

Correction of Metabolic Acidosis

It has been well established that metabolicacidosis will cause depression of cardiac func-tion.14 Since a low cardiac output results infurther metabolic acidosis, a vicious circlemay be established that must be broken if thepatient is to survive. "Flogging" the alreadyfailing heart with cardiac stimulants and ad-ministering large amounts of vasopressors areill advised and may actually cause the demiseof the patient because of further vasoconstric-tion and thus more metabolic acidosis. Fur-thermore, vasopressors are less effective in thepresence of acidosis,l4 15 and ultimately mayfail to maintain adequate arterial pressure.

It is more rational to correct the metabolicacidosis and continue to maintain good acid-base status by the administration of drugs thatwill buffer the acid metabolites in thle blood

Circulation, Volurme XXIX, March 1964

and eventually correct the environment of thetissues. In addition to the use of buffers it maystill be necessary to support blood pressurewith vasopressors but, if so, much smalleramounts of these drugs will be required. Cor-rection of metabolic acidosis itself should notbe considered as sufficient treatment butrather an expedient method of "buying time"during which the cause of the circulatoryinadequacy may be treated, e.g., by bloodtransfusion, improved ventilation and oxygena-tion, and intravenous administration of car-diac glycosides.Sodium bicarbonate and THAM (trishy-

droxymethyl aminomethane ) -are the two buf-fers most commonly used. In cases of moderateacidosis sodium bicarbonate would appearto be satisfactory. The use of sodium bicar-bonate alone in combating severe metabolicacidosis may result in a large amount of sodi-um being given. Furthermore, bicarbonate be-comes totally ionized when introduced into theblood stream and does not enter the cellswhere the metabolic acidosis originates,whereas THAM has been shown to remainabout 30 per cent un-ionized, and it is thoughtthat this portion enters the cells 16 where itmay act as an intracellular buffer. THAM alsohas an osmotic diuretic action that helps tomaintain good urinary output.When correcting metabolic acidosis, we

give sodium bicarbonate at first up to a totaldosage of about 2 mEq./Kg. If this is notsufficient to establish and maintain good acid-base status, buffer administration is continuedwith 0.3-molar THAM. If possible, the THAMis given through a catheter placed into acentral venous stream, as this substance hasbeen shown to cause local tissue necrosis if itextravasates into the subcutaneous tissue.The correction of metabolic acidosis with

intravenous buffers should not be undertakenin haphazard fashion. Administration of afixed amount of sodium bicarbonate in a

dosage according to the weight of the patientmay produce some temporary improvementbut is usually inadequate if the cause of the

* Talatrol-Abbott Laboratories.

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metabolic acidosis is still active. On the otherhand, when acid-base status is rapidly and re-peatedly assessed through blood-gas analyses,it is then possible to titrate the buffers intra-venously according to their effect and by thismeans not only to correct the metabolic aci-dosis but also to maintain good acid-basestatus as long as is necessary with buffers; i.e.,until the cardiac output is sufficient to main-tain good circulation. In this way, the heart nolonger has to cope with the depressant effectof the metabolic acidosis and has a betterchance to recover. The blood gas analyses aremade as often as necessary to maintain goodcontrol. The buffer is infused by intravenousdrip in sufficient amount to reduce the basedeficit to zero, and administration is thencontinued at a rate that will hold the arterialblood at about zero base deficit, the dripbeing slowed if there is a tendency towardbase excess and increased if base deficit shouldrecur. It may be necessary to continue ad-ministration in this way for several hours andthe total dosage of buffer may be quite large.So far no ill effects have been seen by us withthis titration method of administration. Com-plications previously attributed to administra-tion of buffers may have been, in some cases,due to overdosage producing alkalosis. How-ever, it seems more likely that in most in-stances inadequate amounts of buffer havebeen given and the effects of the continuingmetabolic acidosis have been mistaken forside effects of buffer.

Mixed AcidosisThe occurrence of a mixed acidosis may be

due to a combination of separate causes forthe respiratory and metabolic components.Accordingly, the mixed acidosis may be man-aged usually by improving ventilation, cor-recting the metabolic acidosis, and treatingthe original causes of the imbalance.

In the period after bypass a mixed acidosismay occur, the cause of which is uinresponsiveto medical treatment. T-ui.s may happen ifprior to surgery there was a higlh pulmonaryvascular resistance combined with a shunt thatallowed some of the output of blood from theright heart to bypass the lungs. Such cases are

really considered inoperable but occasionallyin a borderline situation surgery is under-taken. After the corrective surgery with elim-ination of the shunt, the load of forcing itstotal output through the lungs in the face ofthe high pulmonary vascular resistance mayprove to be too much for the right ventricle.This results in right heart failure and respira-tory acidosis. Consequent low output from theleft side of the heart results in poor tissueperfusion and metabolic acidosis. If the pul-monary vascular resistance is not too high,then "buying of time" through correction- ofthe acidosis with buffers plus medical treat-ment of the heart failure, e.g., by rapid dig-italization, may be sufficient. If this is to noavail then surgical re-establishment of theshunt may be necessary to ease the load onthe right heart. Even though this is a retro-grade step in the operation, it may be theonly way to prevent early death of the patientfrom acute right heart failure. Here, oncemore, repeated blood gas analysis providesrapid assessment of developing changes andallows interpretations and decisions that facili-tate management.

DiscussionAmong the commonest problems in open-

heart surgery are those of cerebral complica-tions resulting sometimes in irreversible braindamage. Prevention of respiratory alkalosismay help to maintain better cerebral circula-tion throughout an open-heart operation sothat the brain is well nourished at all times.Clemmesen, Juul-Christensen, and Wandall '"

have demonstrated in dogs that if the pul-monary circulation is perfused on bypass,pulmonary edema develops when severe al-kalosis due to carbon dioxide deficiency ispresent. Although the pulmonary circulationis not perfused during open-heart operations,the bronchial circulation is intact and conse-quently perfused; if perfutsion is with alkaloticb1)O1h, this may be responsible for some lulngdlamage.

Bindslev, Juul-Christensen, and Wandall 1!have demonstrated an increased fragility ofred cells with alkalosis and report that in

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ACID-BASE MANAGEMENT

hyperventilation studies on dogs, intravascularhemolysis was produced.

During the past year, using the technic here-in described, we have noticed a decided im-provement in morbidity following open-heartsurgery with very few unexplained cerebral,pulmonary, and hemolytic problems. Withcareful acid-base management throughout theoperation we have found that (1) the pa-tient regains consciousness rapidly at theconclusion of the anesthesia, (2) there is sel-dom any respiratory depression or subsequentabnormal respiratory pattern, (3) there isseldom any obvious vasoconstriction or cya-nosis of extremities, (4) the blood pressure isusually good and is easily obtained by thecuff method, and (5) intensive supportivemeasures, such as the use of vasopressors andcontinuous artificial augmentation of ventila-tion, are rarely necessary.The occurrence of metabolic acidosis after

bypass may be prevented in large part byavoidance of respiratory alkalosis during by-pass. One of the most important realizations isthat during hypothermia an arterial blood pHof 7.40 and pCO2 of 40 mm. Hg is not optimalbut may in fact represent a relative respira-tory alkalosis. Because of all these considera-tions, we believe that severe respiratory al-kalosis should not be permitted at any timeduring the operation. If acidosis occurs for anyreason, it should be corrected forthwith. More-over, the longer the bypass period, the moreimportant this becomes. With only a shorttime on bypass at normothermia, such as inrepair of an atrial septal defect, it is relativelyunimportant; with prolonged bypass proce-dures and especially under hypothermic con-ditions it becomes very important indeed.Eradication of the severe insult which acidosisexerts on the debilitated cardiovascular systemmay produce great improvement in the pa-tient's condition.Much has yet to be learned regarding acid-

base metabolism and heart surgery. It is hopedthat further data related to these changingconcepts will be forthcoming in the near

future.Circulation, Volume XXIX, March 1964

SummaryAn important part of managing patients

during open-heart surgery is continuous moni-toring of the acid-base status prior to, during,and following cardiopulmonary bypass. Theuse of a thermostatically controlled triple elec-trode system whereby arterial pH, pCO2, andP02 can be measured and base excess or basedeficit quantitated by special application ofthe Astrup-Andersen nomogram is enthusias-tically endorsed.

In the opinion of the authors, respiratoryalkalosis is to be avoided throughout the en-tire operation and postoperatively, as this ap-pears to result in a base deficit, which is sub-sequently revealed as a metabolic acidosis.Particular consideration is given to the bypassphase when hypothermia is employed, since"optimal" pH appears to vary with tempera-ture.Continued maintenance of good acid-base

status with buffers is advocated. It is con-sidered that buffer administration should beon a "titration" principle with frequent arterialblood gas analyses.

Possible reasons are presented for the im-proved postoperative morbidity wlhen optimalacid-base status is maintained throughout theoperation and postoperatively.

References1. BROOKS, D. K., AND FELDMAN, S. A.: Metabolic

acidosis. A new approach to "'neostigmineresistant curarization."- Anesthesia 17: 161,1962.

2. SEVERINGHAUS, J. W.: Blood 02 dissociation linecharts. In Handbook of Respiration. NationalAcademy of Sciences, National Research Coun-cil. Philadelphia, W. B. Saunders Company,1958, pp. 72 and 73.

3. ASTRUP, P., JORGENSEN, K., SIGGAARD-ANDERSEN,0., AND ENGEL, K.: The acid-base metabolism.A new approach. Lancet 1: 1035, 1960.

4. SIGGAARD-ANDERSEN, 0.: The pH log PCO eacid-base nomogram revised. Scandinav. J.Clin. & Lab. Invest. 14: 598, 1962.

5. CARSON, S. A. A., AND MoRRis, L. E.: Controlledacid-base status with cardiopulmonary bypassand hypothermia. Anesthesiology 23: 618,1962.

6. BRADLEY, A. F., STUPFEL, M., AND SEVERING-HAUS, J. W.: Effect of temperature on PCO2and PO of blood in vitro. J. Appl. Physiol. 9:201, 1956.

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7. MARSHALL, R., AND GUNNING, A. J.: The meas-urement of blood gas tensions during pro-found hypothermia. J. Surg. Res. 2: 351, 1962.

8. ROSENTHAL, T. B.: Effect of temperature on thepH of blood and plasma in vitro. J. Biol.Chem. 173: 25, 1948.

9. CALLAGHAN, P. B., LISTER, J., PATON, B. C., ANDSWAN, H.: Effect of varying carbon dioxidetensions on the oxyhemoglobin dissociationcurves under hypothermic conditions. Ann.Surg. 154: 903, 1961.

10. EDMARK, K. WV.: Continuous blood pH measure-ment with extracorporeal cooling. Surg., Gynec.& Obst. 109: 743, 1959.

1 1. OSBORN, J. J., POPPER, R. WV., KERTH, W. J.,AND GERBODE, F.: Respiratory insufficiencyfollowing open heart surgery. Ann. Surg. 156:638, 1962.

12. GARDNER, R. E., FINLEY, T. N., AND TOOLEY,W. H.: The effect of cardiopulmonary bypasson surface activity of lung extracts. Bull. Soc.internat. Chir. 5: 542, 1962.

13. NORLANDER, 0. P.: Symposium: Postoperativecare of patients after open heart operations.First European Congress of Anaesthesiologists,Vienna, 1962. (To be published.)

14. DARBY, T. D., ALDINGER, E. E., GADSDEN, R. H.,AND THROWER, W. B.: Effects of metabolicacidosis on ventricular isometric systolic ten-sion and the response to epincphrine and levalr-terenol. Circulation Research 8: 1242, 1960.

15. CAMPBELL, G. S., HOULE, D. B., CRISP, N. W.,WEIL, M. H., AND BROWN, E. B.: Depressedresponse to intravenous sympathicomimeticagents in humans during acidosis. Dis. Chest33: 18, 1958.

16. HOLMDAHL, M. H., AND NAHAS, G. G.: Volumeof distribution of C14 tagged 2-amino-2-hy-droxymethyl-l, 3-propanediol (THAM). Fed-eration Proc. 20: 75, 1961.

17. PAYNE, \V. S., THEYE, R. A., AND KIRKLIN, J. WV.:Effect of carbon dioxide on rate of brain cool-ing during induction of hypothermia by directblood cooling. J. Surg. Res. 3: 54, 1963.

18. CLEMMESEN, T., JUUL-CHRISTENSEN, E., ANDWANDALL, H. H.: Acid-base balance and pul-monary circulation. Perfusion experiments.Acta chir. scandinav., Suppl. 283, 17, 1961.

19. BINDSLEV, A., JUUL-CHRISTENSEN, E., ANDWANDALL, H. H.: Hemolysis in dog blood: Invitro experiments. J. Thoracic & Cardiovas.Stirg. 42: 55, 1961.

Articles should be so written that not only intelligent people but specialists infields other than those of the writer may read them with pleasure and profit. Noarticle, even the most learned, needs be so written as to rebuff all readers exceptthose strengthened to their task by animus or malice. An author too great or toolazy to consider and labor for the comfort of his readers, is either too grand forthe condescension, or too low for the privilege, of print.-WILLIAMI MILLS IVINS,JR., 1881-1961. Late Curator of Prints, Metropolitan Museum of Art, New YorkCity. Bulletin of the Metropolitan Museum of Art, February 1963. Submitted byMiss Dorothy Vickery, American Heart Association, New York.

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LOGAN, LESTER R. SAUVAGE and GEORGE I. THOMASLUCIEN E. MORRIS, K. WILLIAM EDMARK, THOMAS W. JONES, GORDON A.

Acid-Base Management for Open-Heart Surgery

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1964 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.29.3.456

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