THE CIRCULATION IN ANAESTHESIA*

EMERSON A MOFFrrr, M D, AND ALAN D SESSLEB, M D

i

ALL-n~CLUSrV-v. REV~WS Of the effects of anaesthesia on the crrculatmn are gvall- able ~ 2 T h s presentaUon focuses on chmcally observed effects of anaesthesm and

: I

their slgmficance and management

BAsic CONSIDF_~'rIONS

The cn'eulataon of blood, and consequently the vimbfllty of body tassue, ~S con- trolled by three major factors myocar&al actmn vascular resmtance, and blood volume (Fig 1) C: one or more of these factors is altered wxthout s others For instance, ff peripheral remstance eve1 lowered by a lngh level of spinal anaesthema, the

Cardmc output

Perxphe ral reslstance

Blood volume

or cardmc output, peripheral reulatory failure occurs When ~ c m n t compensahon by the a large part of the body is

arcu]atmn may fall

Integral components of ~he c lrcuL~tmn

Blood pressure ..... '

Venous pressure

Pulse rate,,, , , , , , , , , , , , ,

I l l III1 i 1

It I1| I

Available clmxcal ffheasurements

Fmvm~ 1 Components and measurements

The parameters by wlnch ~we momtor the crrct~ sure, pulse rate and volume, capillary refill t~me pupils, and operative rote Another variable that pressure, wlnch reflects the integrated funetmn o the cmculatmn Momtormg venous pIessure can causes of a crrculatory problem and to its mtelhgen~

of the clrculataon

latmn are arterial blood pres- and appearance of thd skin, mrnple to measure is ~enous

the three factors that control gwe valuable clues as io the treatment

GENERAL EFFECTS OF ANAESTHETXC AGENT~ ON THE CIRCULATION

The effect of an anaesthetm agent on the myo~rdmmrl per se is of secondary interest to the effect on the whole cmculatmn More nnportant yet is tile net

~From the Section of Anesthemology, Mayo Chmc ,~d Mayo Foundahon, Rochester, Minnesota /

l%ad at the meeting of the Ontario D~wsmn of the Canal&an Anaesthetasts Socmty, I~ado~ Ontario, October 11 and 12, 1963

173

Car~. Anaes See J, vol 11, no 2, March, 1964

174 �9 I v l ]

CANADIAN ANAESTHETISTS [SOCIETY JOUR.~AL

effect of an anaesthetic agent on th~ enttre eardmvascular syste m and the response of the body s compensatory mr Factors influencing the circu- latory effects o{ an agent are rate of admmlstxahon of the agent, d e p t h and durahon of anaesthesm, ventllataon, and preopelatwe pathophysmlogac state o~ the heart and circulatory system

Agents that produce general anaesthesm decrq~ase myocardm] contrac~aty an d~rect relahonship to the concentrahon of the agent an the arterial blood (Fag 2) Reduced cardmc output, wath or wathout change ~n heart rate, ensues The exeep- hon to this ~s mtrous oxade, which has no demonstrable effect on the heart when oxygenatmn as normal

Cardlar output

Pempheral reslstanee

Blood volume

||go||o|g||g|6|OI

ii!llllll, l] 60009noi6g680$|O||onog6|

Falls

F a l l s

No change

Blood pressure Falls

Venous pressure Rmes

Pulse ra te Rises or f a l l s

Frcum~ 2 Effects of lanaesthesm

The peripheral vascular bed enlarges wath deepening anaesthesm 2% larger pro- porhon of the blood volume as accommodated peripherally Venous return ~s reduced and cardmc output decreases secoadanly Vessels an the skin, muscle, and subeutane~)us hssue beds ale ddated p~'amalnly at the expense of the renal and splanchmc vascular beds, which are constricted In addahon, after mduchon of anaesthesm, a large volume of blood magrates from the pulmonary vascular "'reservoar" to the peripheral vessels z

The basac pattern of myocardml depressl0n and peripheral vascular dfiatahon as modified an some instances In hght p]anes of anaesthesm, autonomac reflexes and release of hormones (epmephnne, 17-kydroxyeorhcosterolds) may parhally compensate for the detrimental effects of the agents on the clrculahon

EFFECTS OF INDIVIDUAL AGENTS

D~ethyl Ether Investigators disagree on the effects of ether on the clrculahon Jones and asso-

ciates 4 found that, without premedacahon, in surgical levels of anaeslhesla, heart rate and cardiac output increased, arterial pressure and perapheral resistance decreased, and venous pressure changes were vanabie Kubota and co-workers ~ found that, after hght premedlcatmn and surgical anaesthesm, there weae no "stahstacally amportant" changes m cardmc output, peripheral resistance, arterial pressure, or heart rate, but there was a defimte meaease m venous pressure Other reports 6-s also show lack of agreement, probably because of ~hght dafter- ences m the condahons of study

M O F F I T T & SESSI~_~R

Cardmc output

Perxpheral resistance

Blood volume

CmCVLATmN[ m AIN~XF.STHESU~

1 L I | | I | | I I I I I | I I | I I I I | | I | I I | I I I I I I I | ~1111|

11 .....

t75

Blood pressuz e ..... Unchanged

Venous pressure

Pulse rate

FxcuR~. 3

~ i s e s

Effects of ether

It appears hkely that ether does depress myocardml contractthty, as ewdenced by the increase m venous pressure generally found I (Fag 3) As a result of an increase m heart rate and stlmu]ataon by endogenous epinephrine and norepme- phrme, c~rdmc output and blood pressure are wdlmamtamed until deep anaes- thesia is reached The peripheral vasculm resistance 1Is lowered

Ether as still one of the safest agents because o~! its small detrimental effect on the carculataon, ats relatwe slowness m causing changes m levels of anaesthe- saa, and its stnnulataon of spontaneous resptrataon

Cyclopropane ~ones and associates 9 found that cardiac output, ~lLrterlal and venous pre~ul~,

and peripheral resistance all were increased during anaesthesia with cyclopro- pane In their study, the pataents were not premedlcatedll~ and were kept hg, htly anaesthetazed for 2 hours with steady alveolal concentrahons of cyclopropane Besp~ration was spontaneous but with normal arten,~ carbon dmxade tensions In deeper anaesthesia, with end-e~plred concentrahons of cyclopropane above 20 volumes per cent, carchac output decreased m dlre~t relataonshlp to the increase m concentration of anaesthetic agent These work~trs also found, as did L1 and Etsten, ~~ that, after preoperahve administration of morp]nne, cardiac output: and heart rate decreased even dunng hght anaesthesm hrte~ aal and venous pressures

! and peripheral resistance stall were increased (Fig 41)

1960000|g9|60000|696600|06866(0|006069w

Cardmc ,output

Pempheral resis tance

Blood volume

Falls

Rises

Falls

Blood pressure

Venous pressure

l~Ise r z t e

Fxc~u~E 4

R i s e s

R~ses

Fall8

Effects of cyclopropane

176 CANADIAN ANAESTI-IE

The increases m blood pressure and t lae stnnulatmn There also must be a p or slower, heart rate The mamtenanc~ thesm makes cyclopropane a popular ch

nsxsl' S ~ jov-ar~Ja~

enuheral tone are hkely due'to sympathe: tras~mpathetac response to gWe a normal, , or good haemodynamms an light anaes- )ace for the poor-risk pataent i

Arrhythrmas are common wath cyclo I ,ropane, ]?artmularly wath bagh concentra- tmns of st and increased tensions of ca "bonl dlo~ade ~ It must be co~cluded that eyclopropane has some spectfie effect oh the I myocardmm, whch causes chsplaee- ment of the pacemaker, anterference in t]ie bundle of Has, or increased local excatab~hty

Cyclopropane shock as probably rehted to carbon dmxade retentmn m Both cyclopropane and carbon dmxade are stamu [ants of the sympathetac system It as reasonable that, after elumnatmg either of them, hypotensmn occurs from cessa- tmn of the high sympathetic acttvaty

Halothane

Deutsch and assocmtes la report that, m n~rmal persons wathout premedmahon, carchac output, peripheral resastance, anc~ arterial pressure were sagnrflcant]y reduced after 30 to 60 mmutes of exposur~ to 1 5 per cent halothane (F~g 5)

i | | I i | w | |O| |6O

1 C a r d m c output Fa l l s '

P e m p h e r a l r e m s t a n c e

Blood volume

ppoit|OOOOgtBO|B61

I,t,1,1 ,,t,t,l,l,t,I,,l,,l,l,t /'/'iil,l'/'/'/'l"Hrllll

Fa l l s

Rlses

Blood p r e s s u r e Fa l l s

Venous pressure Rxses

Pu l se r a t e F a l l s

FmvaE 5 Effects cif halothane

After about 2 hours, the cardmc output retturned to normal wath aln increase an heart rate The increase m blood volume ~?ound dunng halothane ,anaesthesm 14 would aid this process

Many mvestagators have found, as chd Wenthe and co-workers, 15 that halo- thane causes reduced cardmc output, by venous pressure The decreased blood prr pheral resastance from artenolar ddatataoI response but the bradyeardla denotes paras7

The proponents of halothane contend th

nyocar&al depression, vcath increased ,sure is parhally due to I[owered peri-

Halothane cheats httle~ sympathehc mpathetae excatataon at, because of the peripheral vascular

&latatmn, body tassues are adequately peifused m spite of the decreased blood pressure There as no questmn but that hal othane can be used safely m low con- centrataons even an p~r-nsk cardiac patmnts 16,17

Barbiturates Lttle change m curculatory dynamms occurs when the intravenous admm~stra-

tmn of barbaturates as used prudently an eornbmatmn wath mtrous oxide and

MOFFITT & S E S S ~ CIRCULATION IN ANk4JgSTHESIA !77

C a r d m c output

P e m p h e r a l r e s i s t a n c e

Blood volume

Blood p r e s s u r e ....

Venous p re s sux e

Pu l se r a t e

l l l i l i l | I O I I I I I I I I I1111 l i l ] l | l l l l l l i l i l l

II"IIIIIII ' , Falls

' I N I ehaJ

I I I I I I I I I I I I I I I I I

I I I I I

Fal l s

c h a ~ e

Fa l l s

Rases

Fa l l s

FmunE 6 Effects of tluopental

relaxants However, rapid mductmn wRh a large causes a severe depressmn an cardmc output and al This may be due an part to a &rect effect on the hear blood because of venous dflatataon, 19 wRh lessened responsable

The patient wath abnormal ol unstable carcu]atmn, gloss haemorrhage, reacts poorly to barbaturates D given ]ess often

~ose of thmpental sodmm "tenal pressure is (Fag 6) ~, but peripheral pooling of

venous return, is largely

as m hypertensmn or after ~ses must be reduced and

Spinal Anaesthesia The cEculatory effects are primarily due to a decrease m peripheral remstance

because of preganghomc sympathetm block 20 Artenolar and venous tones are lessened The hypotensmn depends on the height of t[:he block and as not slgrdfi- cant untal sensory loss as above the costal margin

I l i i | l g l O O t i | i l l l

'///till/l/

| l | i | | t | | l l l l l | I | O l | l ~ l ~

Fa l l s

Fa l l s

No change

Blood p r e s s u r e ,

Venous p r e s s u r e

Pu l se r a t e

F x ~ 7

Fal l~

F a l l s

F a l l s

Effects of spinal anaesthesia

The perapheral p ~ l m g of blood wath less return to the heart secondardy decreases car&ae output and blood pressure Venou~ pressure as low (Fag !~'). Elevating the feet or giving a venoconstractor, suchl as mephentermme (Wlla- mine), wall increase venous return, cea~'al venous pressure, car&ac output, and arterial pressure

Bradycardla, often seen wath spinal anaesthesm, ls~ attributed to block of ~he

178 C.~AVmN aNAr_.saamlas~ 1 ~ JOtraNaL J preganghomc eardmc accelerator fibrea m the T1 to T4 reglon related to the seventy of the hypotenslor~

It I also seems

Methoxyflurane At hght levels of anaesthesm, metho~yflu~

exert effects smular to those of halotl~anel pressure, stroke volume, and peripheral va~ control values Heart rate increased sh-~htly be prmaardy due to the decrease m cardme decreased myocarchal contractahty

ane (Penthrane) has been found to Values for eardmc index, artenal

-'~ula, remstance all were lower than I The hypotenslon was ebneluded to

output, winch probably was due to

Halopropane Tins agent, also a fluorinated compound, has been reported to decrease arterial

pressure and peripheral resistance22 Pulse. rate and venous pressure were increased wlule cardiac output was unclaangect

OTHER FACTORS AFFECTIN~ THE CIRCULATION

State of Ventsla~on All agents commonly used for general ana~

orade and ether, depress the respiratory cc spontaneous respiration Tachycardm and a~

~sthesla, with the exceptaOn of nitrous .ntre Hypoventdatlon 1~ hkdy with gmented cardiac output and arterial

pressure result from todd hypoxaa and resplr~ttory acldos:s When thes~ conditions are severe, the heart becomes meffechve b~,cause of hypoxla and lt~ rate slows Carchac output and arterial pressure decrease, venous pressure mcreases, and the ctrculahon soon fads completely

With controlled resplrahon, hyperventtlatl0n is usual Oxygenataonlls adequate but the posltave-pressure breathmg has a deleterious effect on cardmc output 2z The Ingher mean pressure m the airway ~ninb,lts venous blood flow rote the thorax and through the lungs Less blood re,'Iches the left ventricle and its output falls

Relaxants No dtrect effect on the heart has been Shown 24 Gallamme (Flaxedd) does

increase heart rate and repeated doses of sucemyIchohne can decreas~ it severely, espeexally m ehddren Extreme alteration of ratte m eather dtreeta0n decreases cardiac output and blood pressure

In addmon, loss of external tone by vessels because of muscle paralysis allows them to oblate and causes more peripheral poohng Tubocurarme may produce ganghome blockade with vasodllahon ff a large dose is gwen rapidly

Acidosis A todd degree of metabohc acadosas, wit h a decrease of the standard blear-

bonate and buffer base, occur~ dunng g~neral anaesthesia and Surgery 2~ If pre-exastmg acidosis, as m diabetes mellttus, I has been present, or ff tissue perfu- s, on is inadequate, as m poor c,rculataon d~nng operatton, moderate to severe

~ o ~ a z ' r ~ s m s t ~ c~acv'~aaoN ~ ~l,~rar.st~

metabohe acidosis will occur The subnormal blood pH depresses the myoe~- chum and cardiac output d~munshes Venous pressure ts increased and arterial pressure ~s decreased

~ ~ . ~ - ~ c ~m~ C ~ s m OF L ~ A ~ q u ~ l C m c m ~ o N

When the avatlable data, prnvaardy arterial pressure values, mdacate that the carchovascular status ~s unsatas~actory, successful testo,rahon of c~rctdataon can be accomphshed ratmnaHy ff one first determines the Likely causes If the venous pressure also is low or as becoming low, the cause v The problem is either a low clreulahng blood voh~m, of the czardaovaseular system or peripheral vasodilatat be increased safely by g~vmg blood or plasma-vo] increase cardiac output __and arterial pressure m 'acec Stroke volume Is increased when the atrial pressures ~ h n g pressures are increased up to a central venou., of mercury Further increases an atrial pressure will ca

Venous pressure rs a helpful mcheator m the sltuat replacement When hypotenston persxsts, a lugh yen the problem has shifted from one of msuf~cmnt bloo~ chal meff~eaency resultmg h~m adm~rustratmn of h blood oontammg more than nognal amounts of potass~

Admamstratmn of a vasoconstnctmg drug ~s mdmat~

not primarily myocardml m relatmn to the capacity

ton The blood volume can ume expanders Thas wall rdance wath Starhng's law or end-daastohc ventncldar pressure of about 15 mm

ase the heart to fail ion of rapid blood loss a~d ous pressure mcheates that 1 volume to one of myocar- Fpotherrme, aeldotm ACD a m

when the cause of made- quate clrculaUon appears to be d~latataon of the vascular bed Tins type of eardlo- ,,ascular problem may occur wath high spinal anaesthesaa or overdosage wath ganghon-blocknng agents such as tnmethaphan (Arforlad)

The ,muse is primarily poor myocarchal contrachh]ty if the venous pressure is more th~n 15 mm of mercur~ or is increasing rapidly the heart is having d ~ - cultv pumping the volume of bk~3d being returned t~ it, regardless of the blood volume at that Orne In th~s case, several factors musilt be mveshgated Excess:we concen~z~ataon of anaesthehc agent is the first consl,tJlera|lon The posslbflaty of myocax~al fadure because of prevaous chsease ol of hypo~a from any cause also must be considered, the alveolar and arterial temmns of oxygen should be increased I:hsorders of carchac rate and rhythm may be present Atropine wtll abohsh sinus bradycardm Isoproterenol ~ I increase the ventncular rate m com- plete heart block Intravenous adm~ms~aUon of lalnatosade C (Cechlamd) or chgox~L (Lanoxm) is mdacated for a clr~ ulahon tha~ is fading because of atrial fibrillation or flutter and for myocarcha] ]mlure with Itachyeardm Admamstra~mn of sochum bmarbonate will help ff slgnrficant metabdhc a,cldosls is thought hkely to be present

.~o ther cause of h~gh venous pressuIe is overtratnsfusmn of blood or flultds Even during operahon, phlebotomy or hmb tourniquets are possable and effect~tve Vasopressors, gwen an the presence of high venous pressure, theoretmally Wdl force more blood centrally and wall further embarrass' heart action

Knowing the venous pressure is valuable an that ~]t allows one to &fferentiate between a problem necessatahng treatment of a poorly hmctmmng heart and a

problem m winch the blood volume p a n ~ z safely increased to maprove the crrculatmn It allows one to decade windi of u,, ~e three components that control tho crreulataon ~s the malor factor at fault

S~mple Means of Measuring Venous Pmssura A system snmlar to that ]?or measuring the pressure of cerebrospmal fired func-

taons satlsfactordy A glass or &sposable~pla, tic manometer and a three-way stop- cock are fixed to the intravenous stan d T]:m ~Lree outlets of the StOpcock are connected (1) to a veto, (2) to the ma~omr and (3) to an mtravlenous set so that the veto can be connected either tO the manometer or to the intravenous set by turning the stopcock Another method :ts to use an intravenous set with a bmlt-on sadearm tubing winch is used as a Imanometer Zero on the manometer must be placed at and-chest level at all tapes to obtain a meaningful reading Fluctuataon of the ~qmd m the manometer wvth resplratton mdmates a dear system

It as preferable to measure central ve!aous pressure by a small catheter advanced into the chest A needle m the extel~al jugular veto, however, will transmit accurately a pressure close to that m the right atrium

S U M M A B Ik ~

The lntegntyof the clrculaUon depends qn the summation of the effects of the cardmc output, the peripheral vascular resls}tancg~, and the blood volume Agents producing general anaesthesm affect the crrculatJon by decreasing cardmc output and peripheral resistance, t_has effect is m agents m the blood Other factors wluch m,,i are the status of venUlat~on, the degree of ants, and the occurrence of metabohc ac~ means of evaluatang the c~rculataon, veno~ These values permit drfferentaatlon between taon needs improvement and one an which to treat an inadequate carculat~on

proportion to the conCentratxon of" Ly alter the circulation m anaesthesm hypoxm, the admlmstratllon of relax- ~[osls Along with the usual chmcal as plessure values are helpful data a problem m w~ch myocardml func- ,lood volume can be safdqy increased

L'mt6grat6 de la clrculataon d6pend de la de la r6slstance p6raph6nque et du volume sent ranesth6s~e g6n6ra]e affectent la c~rcul, et la r6sastance p6nph6nque, ces effets sonl centratton de ces substances dans le sang

sormne des effets du d6blt cardmque, sangum Les substances qm prodm-

~taon en dnmnuant le d6b~t cardmque directement propo~onnels 5. la con-

~es autres facteurs qm peuvent modx- tier la clrculat~on, au cours de l'anesth6sle, son| le volume de la ,r le degr6 d'hyporae, l'admmlstratlon de myor&olutlfs et l'appantlon d'~e~dose m6ta- bohque En plus des slgnes chnlques usue]s sm lesquels nous nousl basons pour 6valuer la crrculataon, ]a presslon vemeuse~ peut fourmr de pr6cleux renselgne- ments Ses donn6es permettent de fmle le~ dmgnost~e entre une s~llaat~on 06 le myocarde a besom de support et une sltu~tlon o6 le volume sangum peut &re augrnent6 en toute s6curat6 pour eornger une carculatlon mad6quate ,

oFFrrr s sstam cmcOr TION 181

REFERENCES

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2 PmcE, H L General Anesthesm and Ctreulatory Home0stasls Physlol Rev 40 (suppl 4) 187 (1960)

3 JOrINSON, S R The Effect of Some Anaesthetac Agents o n the Clrculatlon m Man With Specaal Reference to the Slgmficance of Pulmonary Bl,i~od Volume for the Ctrculatory Regulataon Acta Chtr Scand Suppl 158 (1951), pp 1-J143

4 JoNEs, R E , LIND% H W , D~.UTSCH, S, Dml, PS, R D, & PrtlCE, H L Hemodynamm Actions of Dmthyl Ether m Normal Man Anestheslolog~, 23 299 (1962)

5 Kr, mOVA, Ytrmo, Scm~xlzra~, H J , & VAI~-DAM, L D Hemodynamm Effects of Dmthyl Ether m Man Anesthesiology 23 306 (1982)

6 Fxmwcm, G, P~.~roFm, J w , & WOOD, E H Hemodynamac F~ffects of Ether Anesthesm and Surgery m 11 Cases Anesth & Analg 35 18 (1956])

7 ETSTEN, B~.NJAMm & LI, T H Effects of Anesthesm ~pon the Heart Am J CarchoI 706 (1960)

8 PmME, F J & GRAY, T C The Effect of Certain Anaesthetic and Relaxant Agents on C~rculatory Dynalmcs Bnt J Anaesth 24 101 (1952~

9 JoNrs, R E, GULDMANN, N, LIN~E, H W, DmPFs, R D , & PRICE, H L Cyclopropane Clrcu]ataon m Aaaesthesla HI Effects of Cyclopropane on Resplrataonland Normal Man

Anesthesmlogy 21 380 (1960) /

10 Lr, 1 ~ H & ETSaXN, BENJAMIN Effect of Cyclopropan,~ Anesthesia on Carchac Output and Related Hemodynamms m Man Anesthesmlogy 18 ~5 (1957)

11 LumE, A A, JONES, R E~ LINDE, H W , PRICE, M L DRIPPS, R D, & PmcE, Ho L Cyclopropane Anesthesm I Cardaac Rate and Rhythm duralag Steady Levels of Cyclo- propane Anesthesm at Normal and Elevated End-Expl:rator~ Carbon Dmxade Tensmns .~mesthesmlogy 19 457 (1958) /

12 Dmlees, R D The Immech,,ate Decrease m Blood PreSsure Seen at the Conclusion of Cyclop pro ane Anesthesm Cyclopropane Shock Anes~hhesmlogy 8 15 (1947)

13 DEUTSCH, S, LINDE, H W , Dml, ws, R D, &PracE, H L Circulatory and Respiratory Actaons of Halothane m Normal Man Anesthesmlogy 2J 63]L (1962)

14 Gaa2LE, EaN~.ST, FINCh, A J , AB~MS, A L , & WILLL~MS, ] A The Effect of Cyclo- propane and Halothane on the Blood Volume m Man/Anesthesmlogy 23 828 (19{12)

15 WENTrm, F M, PATmCK, R T , & WOOD, E H Effects of Anesthesia wlth Halothane on the Human Clro_dataon Anesth & Analg 41 381 (1962)

16 DAwsoN, B ~ N , TrmvE, R A, & ~ , J W Halothane m Open Cardiac Operatmns A Techmc for Use With Extracorporeal Ctrculatton Anesth & Analg 39 59 (1980)

17 T~vE, R A, MOFFITT, E A, & KmKLIN, J W Anes~hetm Management during Open Intracarchac Surgery AneSthesiology 23 823 (1962)

18 DOBmN, A B & WVANT, G M The Physiological Effec!ts of Intravenous Anaesthesia on Man Canad Anaesth Soc J 4 295 (1957)

19 EC~.STEIN, J W, HAMILTON, W K, & McCAMMOND, ~ M The Effect of Tluopental on Peripheral Venous Tone Anesthesmlogy 22 525 (1981)

20 Grm~.NE, N M Physmlogy of Spinal Anesthesia Baltimbre ~Nxlhams & Wdkms (1958) 21 WALKER, J A, ECCERS, G W N, JR, & ALLEN, C R Cardmvascular Effects of Methoxy-

flurane Anesthesm m Man Anesthesiology 23 639 ( 1962 ) .22 V~rtm, R W , YOUNC, R V, LUND, L O, VOCEL, J H~K, & GRow.n, R F Halopro-

pane Anesthesia m Man Laboratory and Chmcal Stuch,~ Anesthesiology 24 217 ( 1983 )

23 COT~Am~, Arcom~, MOTLEY, H L, WEm~o, LA~s, & RICHAm~S, D W JR Phystolog~cal Studaes of the Effects of Intermittent Posxtxve Pressuret Breathing on Carchac OutpUt in Man Am J Physml 152 162 (1948)

24 ]?ATON, W D The Effects of Muscle Relaxants other than Muscular ReIaxataon /~zms- thesmlogy 20 453 (1959)

25 TAVLOa, L M, THEYE, R A, DEVLOO, R A, & ~(IRKLIN, J W Patterns of Acid-Base Changes during Surgical Convalescence Surg Gynec & Obst I14 97 (1962)