The pitfalls of bedside regional cerebral oxygen saturation in the early stage of post cardiac arrest

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1 Kinoshit et l. Sndinvin Journl of Trum, Resusittion nd Emergeny Mediine (2015) 23:95 DOI /s COMMENTARY The pitflls of edside regionl ererl oxygen sturtion in the erly stge of post rdi rrest Kosku Kinoshit *, Atsushi Skuri nd Shingo Ihr Open Aess Astrt It remins unertin whether neuromonitoring relily predits outome in dult post-rdi rrest ptients in the erly stge treted with therpeuti hypothermi. Reent reports demonstrted regionl ererl oxygen sturtion of rdi rrest ptients on hospitl rrivl ould predit their neurologil outome. There hs een little disussion out the signifine of regionl ererl oxygen sturtion in ptients with post-rdi rrest syndrome. Amplitudeintegrted eletroenephlogrphy monitoring my lso provide erly prognosti informtion for post-rdi rrest syndrome. However, even when the initil eletroenephlogrphy is flt fter the return of spontneous irultion, good neurologil outome my still e otinle if the eletroenephlogrphy shifts to ontinuous pttern. The eletroenephlogrphy vried from flt to vrious ptterns, suh s flt, epilepti, or ontinuous during the first 24 h, while regionl ererl oxygen sturtion levels vried even when the eletroenephlogrphy ws flt. It is therefore diffiult to estimte whether regionl ererl oxygen sturtion urtely indites the oupling of ererl lood flow nd metolism in the erly stge fter rdi rrest. Creful ssessment of prognosis is neessry when relying solely on regionl ererl oxygen sturtion s single monitoring modlity. Keywords: Crdi rrest, Post-rdi rrest ptients, Regionl ererl oxygen sturtion, Amplitude-integrted eletroenephlogrphy Bkground Reent reports demonstrte reltionship etween regionl ererl oxygen sturtion (rso 2 ) of rdi rrest ptients on hospitl rrivl nd their neurologil outome [1, 2]. Dt re insuffiient to support the utility of neuromonitoring for the predition of outome of postrdi rrest syndrome (PCAS) ptients [3] treted with therpeuti hypothermi. Few reports hve disussed the sequentil hnges or physiologil signifine of rso 2 during therpeuti hypothermi immeditely fter the return of spontneous irultion (ROSC). Monitoring with eletroenephlogrphy (EEG) my e le to provide erly prognosti informtion fter ROSC in ptients with therpeuti hypothermi [4, 5]. Even when EEG indites flt pttern in the erly stge of ROSC, good neurologil outome my still e otinle fter * Correspondene: kinoshit.kosku@nihon-u..jp Division of Emergeny nd Critil Cre Mediine, Deprtment of Aute Mediine, Nihon University Shool of Mediine, 30-1 Oyguhi Kmimhi Itshi-ku, Tokyo , Jpn rdi rrest if the EEG shifts to ontinuous pttern during hypothermi [6]. Yet rso 2 vlues tend to vry widely even when EEG ptterns re flt in the erly stge, whih mkes it diffiult to estimte the neurologil outome using only single modlity for monitoring y rso 2. In this pper we will disuss the linil pitflls of rso 2 performed in onjuntion with EEG for omtose ptients fter ROSC. Clinil issues of rso 2 in ptients with PCAS Theoretilly, rso 2 n estimte the lne etween the ererl metoli rte of oxygen (CMRO 2 ) nd ererl lood flow (CBF), whih linerly orreltes with ererl venous oxygen sturtion nd with CBF [7]. A host of ftors suh s lood pressure, lood volume, lood visosity, oxygen delivery/metolism, nd hypo/hyperpni led to the vsodiltion or onstrition of the rin vessels when the ererl utoregultory mehnism responds normlly, [8] nd ererl utoregultion keeps 2015 Kinoshit et l. Open Aess This rtile is distriuted under the terms of the Cretive Commons Attriution 4.0 Interntionl Liense ( whih permits unrestrited use, distriution, nd reprodution in ny medium, provided you give pproprite redit to the originl uthor(s) nd the soure, provide link to the Cretive Commons liense, nd indite if hnges were mde. The Cretive Commons Puli Domin Dedition wiver ( pplies to the dt mde ville in this rtile, unless otherwise stted.

2 Kinoshit et l. Sndinvin Journl of Trum, Resusittion nd Emergeny Mediine (2015) 23:95 Pge 2 of 7 the CBF onstnt in response to hnges in these ftors. However, the onditions of PCAS hve mny ftors for dysutoregultion suh s hypotension nd inrese or derese in PCO 2, wherey CBF would e ffeted y these dysutoregultory ftors. Physiins therefore hve to onsider mny ftors when estimting rso 2 vlues Fig. 1 Chnges in rso 2 nd flt EEG pttern in PCAS. A femle in her 70s ws trnsferred to the hospitl y mulne with n irwy ostrution suffered during mel. Her initil rdi rhythm indited pulseless eletril tivity. The time from rdi rrest to ROSC ws 31 min. The initil rso 2 vlue ws % (-) one hour fter ROSC nd the EEG pttern ws flt. Her rso 2 deresed with deline in lood pressure nd rose following dopmine infusion (-). However, her rso 2 grdully deresed (-) nd she experiened nother rdi rrest (-d) with steep deline in rso 2. Throughout the ourse of tretment in the ICU, the EEG mintined flt pttern regrdless of rso 2 vlue ( nd ). A: rso 2 (%); B: EEG, 1 h fter ROSC. C: EEG, 5 h fter ROSC. Arrows: (): BP 112/58 mmhg, rteril gses: PCO mmhg, ph 7.189; (): sbp 88 mmhg, strt dopmine dministrtion, PCO mmhg, ph 7.232; (): sbp 92 mmhg, rteril gses: PCO mmhg, ph 7.353; d: rdi rrest, strt hest ompression. sbp: systoli lood pressure; ROSC: return of spontneous irultion; rso 2 : regionl ererl oxygen sturtion; EEG: mplitude-integrted eletroenephlogrphy (NioletOne TM IMI, Jpn)

3 Kinoshit et l. Sndinvin Journl of Trum, Resusittion nd Emergeny Mediine (2015) 23:95 Pge 3 of 7 Fig. 2 High rso 2 nd epilepti EEG pttern in PCAS. A mle in his 50s ollpsed suddenly with hest pin. His initil rdi rhythm indited ventriulr firilltion. The time from rdi rrest to ROSC ws 24 min. The dignosis for this ptient ws ute myordil infrtion. The rso 2 monitoring nd onurrent EEG monitoring ws ommened n hour fter his ollpse. His initil rso 2 reding ws 80 % (-) nd the EEG pttern () ws flt regrdless of rso 2 vlue. Therpeuti hypothermi ws ommened fter the ptient s ICU dmission nd his rso 2 grdully deresed s his systemi rteril pressure fell. The ptient s rso 2 returned to its initil level one he reeived dopmine infusion (-). The EEG pttern hnged to epilepti pproximtely 24 h fter ROSC (). The outome for this ptient ws persistent vegettive stte. rso 2 (%); B: EEG, 1 h fter ROSC; C: EEG, 25 h fter ROSC. Arrows: : BP 168/100 mmhg, rteril gses: PCO mmhg, ph 7.441; : BP 85/40 mmhg, strt of dopmine dministrtion, rteril gses: PCO mmhg, ph 7.429; : BP 136/88 mmhg, rteril gses: PCO mmhg, ph BP: lood pressure; ROSC: return of spontneous irultion; rso 2 : regionl ererl oxygen sturtion; EEG: mplitude-integrted eletroenephlogrphy

4 Kinoshit et l. Sndinvin Journl of Trum, Resusittion nd Emergeny Mediine (2015) 23:95 Pge 4 of 7 rso2 (%) Fig. 3 (See legend on next pge.)

5 Kinoshit et l. Sndinvin Journl of Trum, Resusittion nd Emergeny Mediine (2015) 23:95 Pge 5 of 7 (See figure on previous pge.) Fig. 3 High rso 2 nd suppression-urst EEG pttern in PCAS. A femle in her 30s experiened rdi rrest used y severe ronhil sthm. Her initil rdi rhythm indited pulseless eletril tivity. The time from rdi rrest to ROSC ws 45 min. The initil rso 2 vlue ws 85 % (Fig. 4-). The EEG pttern indited suppression-urst pttern 3 h fter ROSC. She reeived dopmine infusion fter fll in lood pressure (Fig. 4-). Therefter, her rso 2 grdully returned round % nd kept onstnt (Fig. 1-) for 24 h. The outome for this ptient ws rin deth. EEG mesurements were tken for only 3 h fter ROSC (not for 24 h) in this ptient. (): rso 2 (%); (): EEG, 3 h fter ROSC. Arrows: : BP 155/94 mmhg, rteril gses: PCO mmhg, ph 7.125; : BP 90/48 mmhg, rteril gses: PCO mmhg, ph 7.430; : BP 124/54 mmhg, rteril gses: PCO mmhg, ph BP: lood pressure; ROSC: return of spontneous irultion; rso 2 : regionl ererl oxygen sturtion; EEG: mplitude-integrted eletroenephlogrphy fter rdi rrest. The rso 2 dt of rin-ded ptients lso demonstrtes tht rso 2 vlues do not lwys indite the ererl oxygen metolism [9]. As seen in Fig. 1, for exmple, n EEG pttern n remin flt regrdless of the rso 2 vlue. The rso 2 vlue my depend on the lood pressure, euse CMRO 2 is thought e extremely suppressed when the EEG pttern is flt (Fig. 1, ). In the experimentl model, the EEG ws flt fter trnsient olusion of oth ommon rotid rteries nd grdully hnged from flt to ontinuous pttern fter the relese of the olusion [10]. In the linil setting, the EEG is lso flt fter rdi rrest nd hnged from flt to vrious ptterns fter ROSC [6]. CMRO 2 ws lso initilly depressed fter ROSC [11, 12]. The lne of CBF nd metolism is signifintly ltered fter ROSC [13] while CBF might e norml [14] or deresed [11] in the resusitted rin during the 24 h following rdi rrest. A previous study reports tht CMRO 2 is not le to predit neurologil outome in the erly stge of ROSC [15]. Therefore, the estimtion of injured rin or outome using for rso 2 might need to e refully ssessed in the erly stge fter PCAS. Higher rso 2 in the erly stge in PCAS Higher rso 2 vlues n generlly e ssumed to hve the following pthophysiologil signifine: hyperemi, inluding retive hyperemi (e.g., n inresed level of PCO 2 ), or hyperperfusion (lower CMRO 2 nd higher CBF). They n lso reflet hyperemi used y severe metoli depression due to severe rin dmge in PCAS. Cererl oxygen extrtion frtion, however, n e expeted to derese in omtose ptients immeditely fter ROSC s onsequene of the primry ererl metoli suppression [11]. This ppers to e the se even if higher rso 2 levels re deteted when the EEG is flt, given tht the CMRO 2 my e drstilly suppressed. Figures 2 nd 3 demonstrte n rso 2 level tht strts t round 80 % nd remins onstntly high therefter. Finlly, the EEG indited epilepti or suppression-urst EEG ptterns of type thought to portend poor outome. It ws diffiult to determine the linil signifine of the high rso 2 vlues in the erly post-resusittion phse [4 6]. We therefore suspet tht high rso 2 vlues with epilepti or suppression-urst EEG ptterns indite more severe rin dmge fter rdi rrest. Lower rso 2 in the erly stge in PCAS Menwhile, other ftors use lower rso 2 vlues in PCAS. The min uses of low rso 2 stem from too little oxygen supply to meet the ererl oxygen demnd, sign of ererl ishemi used y unstle hemodynmis, hypoxi, or deresed PCO 2 rther thn ererl metoli suppression. Physiins will e le glen hints for the next steps in their tretment strtegies for onditions of these types. Good neurologil outome my e otinle fter PCAS if two onditions re met: first, the ptient shows no drsti elevtion of rso 2 ompnying n extremely low voltge on the initil EEG; seond, the ptient shows nd no sign of eletrogrphi sttus epileptius (Fig. 2) or suppression-urst pttern (Fig. 3), espeilly in the erly post-resusittion phse [6]. A seond use of lower rso 2 vlues is the ontinution of no-reflow phenomenon suffered y the rin, whih is hrterized y lk of reperfusion fter ererl ishemi [16] used y post-ishemi hypoperfusion, n inrese in lood visosity, redution in the lier of smll vessels, or impired mirovsulr perfusion [16, 17]. In the results, CBF might e redued even if lood pressure is within norml rnge. Interestingly, no-reflow res mnifested s spotty res of persistently distured reirultion were found to spred from the deep site to the rin surfe ortex s the durtion of the rdi rrest inresed [16]. This ws point of onern, euse the rso 2 proes re pled over the ptient s forehed. We suspet tht the presene of spotty no-reflow re on the rin surfe my impede the ssessment of the ererl oxygen metolism for rso 2 euse it mesures the hemogloin oxygen sturtion in the regionl forerin ortex. Continuous monitoring for rso 2 performed in onjuntion with EEG for PCAS ptient undergoing therpeuti hypothermi There hs een little disussion out the signifine of rso 2 in ptients with PCAS who re undergoing therpeuti hypothermi. The norml rnge of rso 2 in dult PCAS ptients treted with therpeuti hypothermi lso

6 Kinoshit et l. Sndinvin Journl of Trum, Resusittion nd Emergeny Mediine (2015) 23:95 Pge 6 of 7 Fig. 4 Chnges in rso 2 nd ontinuous EEG pttern in PCAS. A mle in his 50s ollpsed suddenly while running. He reeived y-stnder CPR nd his initil rdi rhythm indited ventriulr firilltion. Defirilltion ws performed y prmedis (34 min fter ollpse) nd the ptient ws trnsferred to our hospitl. ROSC ws otined nd therpeuti hypothermi initited immeditely following his dmission. The initil rso 2 vlue ws round 45 % fter ROSC. The EEG pttern ws flt t 3 h fter ROSC () nd shifted to ontinuous pttern over the next 21 h (). His finl neurologil outome ws fvorle. rso 2 (%); B: EEG, 3 h fter ROSC; (): EEG, 24 h fter ROSC. Arrows; (): BP 100/54 mmhg, rteril gses: PCO mmhg, ph 7.338; (): BP 182/112 mmhg, rteril gses: PCO mmhg, ph 7.437; (): BP 174/120 mmhg rteril gses: PCO mmhg, ph BP: lood pressure; ROSC: return of spontneous irultion; rso 2 : regionl ererl oxygen sturtion; EEG: mplitude-integrted eletroenephlogrphy

7 Kinoshit et l. Sndinvin Journl of Trum, Resusittion nd Emergeny Mediine (2015) 23:95 Pge 7 of 7 remins unertin euse of the hypothermi redution of CMRO 2. The mplitude-integrted eletroenephlogrphy (EEG) in PCAS during therpeuti hypothermi ws reently lssified into four tegories: extremely low voltge (flt; mximum voltge < 5 μv); suppressionurst pttern; eletrogrphi sttus epileptius with reurrent epilepti form tivity; nd ontinuous EEG [6]. Sttus epileptius (Fig. 2) nd suppression-urst ptterns (Fig. 3) on EEG re suggested to hve poor outomes [4 6]. Ptterns of these types ould e used to predit extensive rin injury fter rdi rrest [4, 5]. Although the initil ontinuous EEG pttern ws flt (extremely low voltge), we were interested to oserve ses in whih the EEG susequently shifted to ontinuous pttern over the following 24 h of therpeuti hypothermi (Fig. 4) nd lter went on to otin good neurologil outome [6]. During the time EEG is flt in the erly stge fter ROSC, the rso 2 vlues might e refleted y the influenes from ftors suh s lood pressure, CBF, PCO 2 or no-reflow phenomenon. These result demonstrte tht rso 2 lone is insuffiient for prediting neurologil outome fter PCAS nd tht rso 2 nnot e onfirmed to relily indite whether CBF nd metolism re oupling or unoupling in the erly stge fter ROSC. Conlusion The EEG is extremely suppressed fter ROSC nd grdully hnges to vrious ptterns. CMRO 2 might lso e initilly depressed while the EEG is suppressed. Given the possile therpeuti implitions of ontinuous rso 2 monitoring in ptients with rin injury, the vritions of rso 2 nd potentil influenes of mny ftors t this stge mde it diffiult to determine the linil signifine of rso 2 in PCAS. Creful ssessment of prognosis is neessry when relying solely on rso 2 s single monitoring modlity. Ptients onsent Informed onsent ws otined from ll individul prtiipnts inluded in the study. This study ws pproved y the Clinil Reserh Institutionl Review Bord (IRB: RK ) of this hospitl. Authors ontriutions K.K. designed, wrote this rtile. K.K., A.S., nd S.I. disussed this omments. K.K. red nd pproved the finl mnusript. Reeived: 23 My 2015 Aepted: 28 Otoer 2015 Referenes 1. Ito N, Nishiym K, Cllwy CW, Orit T, Hyshid K, Arimoto H, et l. Noninvsive regionl ererl oxygen sturtion for neurologil prognostition of ptients with out-of-hospitl rdi rrest: prospetive multienter oservtionl study. Resusittion. 2014;85: Hyshid K, Nishiym K, Suzuki M, Ae T, Orit T, Ito N, et l. Estimted ererl oxyhemogloin s useful inditor of neuroprotetion in ptients with post-rdi rrest syndrome: prospetive, multienter oservtionl study. Crit Cre. 2014;18: Noln JP, Neumr RW, Adrie C, Aiiki M, Berg RA, Böttiger BW, et l. Post-rdi rrest syndrome: epidemiology, pthophysiology, tretment, nd prognostition. 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A pthophysiologi nd prognosti positron emission tomogrphy pilot study. Resusittion. 2003;57: Fisher M, Hossmnn KA. No-reflow fter rdi rrest. Intensive Cre Med. 1995;21: Ginserg MD, Myers RE. The topogrphy of impired mirovsulr perfusion in the primte rin following totl irultory rrest. Neurology. 1972;22: Arevitions PCAS: Post-rdi rrest syndrome; rso 2 : Regionl ererl oxygen sturtion; ROSC: Return of spontneous irultion; EEG: Eletroenephlogrphy; CMRO 2 : Cererl metoli rte of oxygen; CBF: Cererl lood flow; EEG: Amplitude-integrted eletroenephlogrphy. Competing interests The uthors stte tht they hve no onflit of interest (COI).