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Relationships between delayed ischemic dysfunctions and intracranial hemodynamics following subarachnoid hemorrhage
JOURNALOFTHE
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143 V ( 1996) 72–78 SJournal of the Nearcdogictr]Sciences E
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Relationships between delayed ischemic dysfunctions and intracranial hemodynamics following subarachnoid hemorrhage J
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L.kpurmreru@ NWW1OAIY, TechnicalUniuer~ifyq/”Munich, Mdll>lr@e28. D-81675Jfurfick GerrrIwI.I
Received10Octobel-1995:revised22March 1996;accepted8 April 1996
Abstract
Delayed ischemic dysfunctions (DID) arc rmc of the main cmnplicatirms following subarachnoid hemorrhage. It was the aim of our study to amrlyse the possible prognostic value d’ different transcrauial Doppler ultrasonogmphy parameters and to elucidate the risk of developing DID with particular reference to the intracranial pressure. The relative change 0[’ mean blood flow velocity and of corresponding ccrcbral circulatory resistance index as well as the intracranial pressure were cletermincd in 44 patients with spontaneous snbarachuoirl hemorrhage. No relationship was found between the occurrence and extent of DID and the relative change of mcwr flow velocity during the clinical cm.nse. In contrast, there was a significant correlation between the relative change of the cerehml circulatory resistance index and the occurrence of’DID. While patients without or with reversible DID showed a decreased resistance index compared to the initial value (without DID: – IT~o+ 15%; reversible DID: –3% f 1470),patients with irreversible DID had a significant increase of the resistance index ( + 1470+ 970). Accordingly, patients with irreversible DID showed a significant increase of intracranial pressure compared to the patients with reversible D W c t t eo o rv I n c ao et h c c hl c l erl uiDh a index by bedside monitoring is a useful tool to predict the occurrence of subarachrwid hemorrhage-associated DID and has therapeutic impact. Kejwords: Subarachnoid hemorrhage; Vasospasm; Intracranial pressure; Delayed ischemic dysfunction; Transcranial Doppler ukrasonography
I ou s c ud t e o pIi ae i oe d h . nc r t b r e t t em e n ao cl c is ti wo d u D i de s y ( lfs c sf o ah pD u l p n ee y ( cl Or urt I mto eoh Ceift a h r (e a a amc c o ow S hm tr a p n rh plhA p oht r bi t mp aci rs iHa g t dru i m f r n e e d v e u e i c b o i a b1 o o a ps (b0 aue K – tr o a l iv 3l s eue m rt edsp 0 t ( a F i W 1 o t i o Lo e a j 1a 9 T tr gs 8 n gu a B 1 r n 9 me i8l 5 h i rl4ee . h 9 d i ,et e esici qi r i siabp n e d au p e r ro o ife ta l ve cio d ern g f rc r erat i t uwlblp l r u a n T n c t h e a t l d e u c b fe ( c brr l b Cepe l obes e B r ta f o o r ao F o l ribmi n i o n T df c e y aa o vs h c r fb ca pu u n weetn r ar rc i i e tr t at oi t svss i wt i w ni i r i r w n b e o g f v c a v o e c b c a v e d a tu S r h s b s e ou e bs eu p r s A a a a , ispal d r w c t ob t m ni f s m( i G ep ao ( d r o e ha e S1 a c r I or nth est e9 t oe a 1 H e a 1 V 9 l1e T om 9 l 8t9 f r l t o . a 8 8o cd D0 t o. poc h b 8j v3 r u , o ; et a tf f vec r i c i i p fi c esm eh e t hp o et m s r i s i aa c i s p nb s o c eid i lt une hi i tm cn it d h r pb t i a ha u pT tr n l i aio C a ota nm e o t n nv t a d o nm i im n ma o ii no s ic t ea aa s c1t P mcS i ol ( r r e to9ra au e c v a b v ou c i o i l sl o n l nP nu ono(r (PaCOq). p ( a r a c ed r I t as ti e 1 C s e a orn X n u r( xe9 MbP sr i e1 n hii be iaox 9 u t d e t i e fs sia S o A t s ci bog o rn ae iri uC ef ( e a 1 G w f M e C 9 o o c l r x Corresponding author. Tel.: (+49-89) 4140-4668; Fax: (+49-89) v a a n e s w r t t d e o e e l 4140-4867. 1 I
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0022-510X\ 96/$15.00 Copyright 0 1996 Elsevier Science B.V. All rights reserved. PII S0022-5 10X(96)O0138 -4
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Tablec hI9 e ea 1 HD t t w9o nl c a l w ve l i 2 .ve t i a e e )s s e Essential u all o C ce f i da h n mi a cp l dictaof Bt patients e n r io n u o gv d l e e io Group A t Group B GI-oupC Group Dl . d e f i a c i s S s u en t oa bv sntu i ee Number r dofnpatients i a dr v13 i n15an sa 9 ns se 7 i il c age 46 n D u l o (t dr i pa e a c s m T oMean p o n(years) o aon l43 C g s 45 r r te51 a r p Dl hrar Range 18-65 32-64 l b f va e a t e d tt o tl l i w (years) i oa e cnm19–73 oo h e i e 21-65 h n tn t Male/Female 7/6 7/8 4/5 6/1 m c a ( ie ( e rar 1 d AHM e t aad 9b lC e sr r l 8 aldrA e. l a G 1 i T fl h 9v she b e n r8bLocation of laneurysm: l e a 7 f o ec o cha ) o r d , i c a oi dn m p i s pi e aa i o v gICA rd ra n ea u a1se e I a t dn t t 1 l t o r 3m ACA/ACoA 2 v b aT H s d t ot ov Cowa s r pe i 5 a v ua 5D h s5 b e im r MCA T f v a e w s lD ( l s oe a C o A c ic i oa2— i t 4 l I a 2is t2 t eD lw e — PCA/PCoA 1 1 1 S e a 1 C 9e e a 1 o 9H i l 8 Nom a 9 l l 8 p 6 r . e 8 t 6 d ; . ro — verified aneurysm 5 2 2 a G 1 iK l le a 1 i 9 Gs n e n bg r 9 8e l a lo c h 9 7 osh . df , s ACA, anterior a 1 t v o t p9 f l ta a p 9 or r hICA, internal h ae l carotid 2 . artery; dm o icerebral ) h eiu artery; cACOA,t ante, , t q e u D e m s is ( i A i fo artery; u MCA, n amiddle en cerebral a d artery; r b PCA, es posterior D h r It a tfrior a communicating Dl ei s de cerebral artery; PCOA, posterior communicating artery. e a 1 S e a 1 H 9e l a G a 9 i li 8 r l . l 8 sd 6 n. be e 6t , a ; 1 K l e a i19 L n e a g 1 98a e l l h9u l97 o . f m 9 e 1; r . s t p wh v a h f v oth r e i i e wl i l e o a e cn t r i g et od t t eilA l lio i l dytt m m a s ya w m o pw m t i o e th m p i a n w t t iha fi n i7 dc lae i at S f , pr v f s ar s ebu t i q eDnf t i u w fr pf e va oi 6 e enor t a p rnect rw r ut4fal sihe a riia ey o a t s i o m oc v u ca la i ut h s ns a r a co cn r t A oe s tr iec o nn ps eo nou S df enba sac I ( e a H 1 H e a a 1 G 9 yel C 7 a ll Cs hst 8o t . hPno i e o a n. 7 c m b ea 9oa x l a 1 V a E 9on1 l t em f l v9 7p la9dn Cr h tb s 2 2t mr e e, n ;ha ai ( o p n . d l 8i e oic yet t i )a v ( ie o i l i nM o d f fo pa i lm F c p f ur t 7 to 1i ooe em Vdd t n d cse pnv rt mg i oar a be Tota T w h d e i p m r o(ra Kn e e e l si i ptnfv o l rilt e ce nhe ud a 1 1 S a K la 1 l i S i n h n 99gu t e fi nc. d l 9 i i h h nn o ne 3 tat fiama o, 9era m ; b d t e i t c vf es l if ao t g di lo n2 m ec ni huhw a f ub i oa io Tg l f chc n t I taai M vb s o s aT pe t va r rF eC (e r tu ud a e vS h t adm sei ah sF d eWta t V o e h la fel t n t ec 9d i o 1 e wl Ip e ih a s T e c n9 t t g r am l e D b c wo t o ro D e S r e t nai e a i fa ss H ( a t s 1n i v oagd 9 rn li aci 9 fl fyhe o H l 3 c ( s e awei e rn)f uu1i d iv di r eTI dh t i o t i n ca an ( d aa f t nr oot cS orac o a e C neCetn sd ui a et ag m s i l a e or hIt a p t n c w o t o r o cr D I aecr i l cu rs a t l i cosa he r oi f snotfD n e i s G e a ( t re ts r1 ouo vt at s e9 d v b l aow l sla d 9 y hi ousem e t s c 3t o c, o ht a t e i a au n p t pc a s t o rr r o c e Fa e ec ea ( m auf f i d eC r G h1s o I (ut r s il e l ee9 so C v iG Dt a1 m( 0e il ia hi yt t r r o t et e t . ea,l D H a o p 3 po Iwt p r woe a l x b oioa i o oeal m sl r v i e f an t d l cn a eeo p r s u icue v cr s rt uop c l ad e ebag y c m i as ai t cc l est a t oa Cusre iG d N pe v r fw o e i f t dbav c o h I u ra( rv. v o ti h lt l n i esCa tf C s hae m i iu f x s i d o a t r eo nsM t I ff pa d d S i w a t c yr ) p v ( ee a 1G l r 9 o ol c c 9 o s o i ti m c s 3p .o t a aa em t T o o t bs w t ja t p e t n h h so c a ut t u a re i l i h fn v d y e at e p vr o d o T i pg a f af n t r of l as e C mt r u ei oe h tc n p o rS a e Ds w d p s ir a o 2 c Outcome r A c ei grading t t i I i i a f . o c t t n u ee e t I B o t f wn dai C ha en vsd c ed ePi len sd o ge o . Argen e tuer t cr d i v r a ssec a e d h ivi o or Di lfo e bsn a re t c d iri r s if t e oi i vtr n li nd v S ti pan os ta nsdC a o iii i f w A r gt vD s D u n oa b sn T m ie o nI g id G A n c s o rnl e d i idu oe a onr s o i e o un n a i t c o t C e(n Dh 2 P a m a te i t n o tI d . s G B d eo a r r v n e e e d v l ou f w 1c u c or n l a enmi cs . i d 2 Patient population . I o i o nC ( f D r ae rv rr el ron F po s r a f us t t p fS y o i Gf- rC nd fee t e o a po r r anv i eu noeA i r nt ge tfo enC (ye i u dti fi w e i t ns T e er d t os t oh s l u ld re h a oya hls dn ois i ver oi D rt I r a l ssa p a s a i T 1 At a h n wi a p g boen eg w e f o a p fo d a p i r St ua o i gGru ml D p n eop w r a do ae ro n bi sg dt s sdt dt t ioneis c 7af i ira a eo (b n o p w p nr ei 2 e oie t r r m fu av ea ey ’sr r fdl h ds ma es ee
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and CXpI-eSSedas a pe!-cent value. T s p w r c mean ha + s e a t mdT A v o aaI-e given as d l e p w et c ro P r fo r i(u oe r s sc ra hrt ep w l camo tn oo nC t e d ut o aa i a di i R s T m t i i o vn np of ta t i l , o v rmh uI t a o , i yc Fl v r i vzn hCi is n o t ce et p T as w ot ti t v p u e eda Cn rdi s l J f pnu ui f a rbs ohewla Cp ens r , st 3 m a t t a o 0r w i t r a e umh tn Sc – i t s m fo m sch cgr H 4 u o A hd c m eni S a p r an i e ii t m c am n i lml oed ee od iP f <0.05 i cd w a inf c i v p ft otbat s e ei e t t d o Si w c a To m g n e h nc af s Aso ii a u g rsa Cr n m i e i eem s w o i a pb d nate t i u ta m h ii olr r e end ri i ne pae E a s n w ap u e i 2e o t ru r r r fg a l oy e r7 s h r ym p I t a p T t ma h ie w t pa e eCer et e e s ns s m . et 3 sR i e n u f i t c po o rv a ar ia h s tn hm f o aie s e cu t p s ar d a c l i p p N r i e w fn l b atg o te o .a c e o D a t mx M m a td te 2 ICP and additional measurements . 4bl c c t o o io D e ( 1n u . u n p P o aa g a r n n t reM v i I 3 p t Ia w m t s eii m b a e 8u h al C ncs a t i e0 at uv l nn a s ee rc1 cn l u a e t p s( r D iaG I uo n i ad c nsI ce u tdv nowl s m ar s u e nt ii ca h g o getg c o R f r g r A t D (P e < 0 s F r 1r p l p A t a ao l r nivt e b w t g A a B a w wr a b C a D w oe e Table 2 o s d l ( < i0 w ino f a h. gb f Relationship between delayed ischemic dysfunctions during clinical course s di ( Pgi < 0 bn f t ia f . e R and severity of the SAH in inital CT according to the criteria of Fisher et o g B ( D r a r C e ( i v D tF al. ( I980) for all 44 patients 1 l p a o n Group B Group C Group D CT-Score Grouo A A c bo r m r e I pa D C ot 3 (207.) 5 (38.5’%) I t d o t p h a M l d i t t t hi 6 (40%) 3 (33.3%) 7 (53.8%) 11 p w I a m e t b D i t 3 e f 6 (40%) 6 (66,7%) 7 (100%) I (7.7%) 111 t i x vCoh i a cn s t t r he
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2 upper p r Ht o t a woo u J n w200 ,hu u i ee p ve lg ar 40 r e s ) bog t rin e o rri ~ nv a ef t c li wac r h ta e c in r n ot a e ac e o Dc W p xu o g r ah h t Ir nt rc e i iu Dce o n c c l n 100: 1 ph ar e o 1 7 vl groups C B-D e showed a l ~ o ,’ t [% e , d -1 ~ so ( B 8 ~ 9 g C r 2 P o9 7 u smaller increase o r ~ 6 ~ 6 D 7 ~4 g A v2 B u 6 g C r 8 >IA 0. 0. 7r %o s %s o ou ; v D i I c a s on ri n e bg s ls t n ir . t f m ta i i o) s w c n .t a: s . g ae -50 the occurrence and extcut o D a t c o r r e I sn h p o.10 n ! r ~w o ( 2 hu p P s Fw a poa tc a i -1oo nt ri p t i ev ghe c l -20e 2 s n do w r De s a dv i r heec tr c o o s Ir tm i ew bp C r—–l a rCMW l a e hs e -150 ]1 -30 rCR v ( A ga B i – ~ 1 l 4 u -a u1 t i n – 17% i 15%; h tr i3 o e lY e -200 i a r a Ln . t s ’ i F<0 w i t p. h w e0r DID tr r eJ 1i i h v e ee ) , A B c D ( C a D tg a v r r dv a i o ae sn ohu btr l i p a n o s s u cg Group t i v ( n C 1 + 9 ag Di 2 + 7 h t r 4l i o % u a 6 7 u% e l P <0 A s di . (gPi < 0 wn 0f a i f . f 1 e i r l c ) 0 e a n n . 40 f b g B (e o D r r a tC e( u vi o w re1 I rreu n es n eT vi p D d be n ,.b D I l D ~ 30 ) e . ,.-’ ! g oo ‘ a I i v fl n g A te gc D ’ r rZ r C re a h a o ,., s e e ue ~ 20 ( 2 l p T I F i la op o g na A i w tr e h C ig hl ioe e ) ,u n , r , s a B w s I wirhin normal range (group A v B n ) n aL t d s 4“’’’’’’” 10~ P o g aC d i p t oa r g Dil d e o tr e k. ---i n c vu ot u l s e af o d i i I ln s w p s ct die i r g n01 i e inv e C c ia f t fe s l fi t de ycl c A B D f g s ~ o Ad
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Fig. 2. Average values of the re[arive change of mean flow velocity (rC ~~v ). the correspondingrcladvc chimge III cwehml cimulntoty resis tance index (rc ~), and the intracranial pressure (ICP) on the day with [hc highest MFVlevelof the patientduringthe time of otrscrvalion(groupA,) and during lime before DID (groups B–D). The average pC03 was not significantly different between the formgroups.
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Fig. 1. Relationship between maximal mean flow velocity (MFV, upper panel), corresponding resistance index (R, lower panel) and the development of delayed ischemic dysfunction (DID, groups A–D) in 44 patients. Each point indicates the maximal MFV achieved and the corresponding R of each patient during the time of observation (group A) and during the time before DID (groups B–D). The horizontal Iine shows the average The average pC02 was r not significantly different value of each g between the four groups.
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W r t l p eo t ri o n ogo c g D i t m c o o S (m a pBa K I l 1 L e aj 1 9 I uo s 19 n( 8l p d a i e rn t v r de ieHe ce v i i o g c v t le r e spi a rt s ie e p f rt d e eo D O dv r p f rt t iM a ea s pn vh nah d r e go nt v a p vr o t ed g a n s fb di d W oe i s big c fn e t a m Mv v a o t f e D gax h r t T c o so p d n n da d de ot h M v e 2 xc a O t oc h lD emF w o i o b w o s s t e lM e al c m v oee h r l ( a 1 c e T r o b d se t em M v ro a vn s o cD v cc o iu i a n r h w t o i u c ( e ua 1 AA a e a p1 aS 9a e al s H a G a 19 i K rl el a i 98 a 1 l
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t h M v9 w n n h a i 9e n c le Fe 1 a sg u o s r )a e 9i e b n o e d l (u ee r a l 1 L o f ol a 9 io w lg uc ci m d a 3 G o e a ( rrf n s e 1 o ci oo g s 9 v on l iesu 9 rf r e i , 3n rc b t i a e o Dn a t mt t c T i aw i h d xe I e on h i e n C n cm R e D e e al ( cc o av e 1o c e n mi v9 tl lt p l o 9y ai y c. nrC r Te C mh b S e a a t o a nP o c s gB c E u ue rh s e , i S p M ao t o t o c h ifI o c A e u nt r ih MCA normal st r sD e n diameterof diameterofarteriolesnormal w ea wl s f h os y H c op o oi c a p t i e c ior a f et t u s sea ICPnormal i o p w hv a M t v ht p l e o r F e un p t g e t ,e n eay i i hi a t s du ei ob D wv s n e n eh l o e u p I e m o n ne d oq e ro t r hnp l l e 200 se o i ad cu r . sti T ba s t u c xe h e vhf 150 t e o sx c ii oe m ms e v ph t c e t ee nh s na r a nc th a e 100 i a u c net a o a o sr vt bpe . g a suam e l c g ae csi t a o nt . r st a aa C s dw mo p e tPs h rq n p u eP a 50i aa s v h ) mt c e o D i vt p e O aC l f h ot i t p i I+’ men e 0 : eIlw h d nB n s itt t e o eh x y d i p o p so s p u h l te o r einr f rMFV t =n156g cmkt i R = 0.41 sc th i T vl a ew e a t l o v ooc aCc ce ‘~v? i ut ciiameterofMC.reducecl t rh e i rl d ee diameterofarteriolesdilatated s aa n s gw i C o ho e i g sy r pa ptL. p ~ o aICPnormal h e h pi B s c e ao m lr ( e a 1 G i 9e l r 8 o a 4 . u ) n d U a c s o siP a mA ( uu ip l 1 u ca u n t t 9 n ih e o g8 p o t t o M v a ti s d h o an u e h t Fa l a ghe ud r m M v a s w ho dc o u e i nt C s p t gr e a i p c n ht i d h oA a t t a sos l r g e n u n t ln ch a i p o a r o a bue e e ce c v t ue o v f I p o c rs l w l ld et i o vu ue n id m m i w o i c f e u o e MFV = 104 cm/s R = 0.7 s t t I ti t nm r M hf ve al ah u\“;\\, C a- t R eas h enl u F c d r u ]), diameterof MCA reduced a t a i I nc l t f c nh r r ne a eee . I&_~ g C a~ a diameterofarteriolesdilat.ated s a l s a tu e d t e w t a o st s so vh e ei s a s h 4i!$ vs oh em s l e n(A) p n n \\ s o . e Q !~~~!~~~%!~~compressed b o M ( Ka e a l 1 Si an s gR, =9FaR, t + l E2J e + Rst = tl e nh 9 o n. f d te h c n l 9 hr)s a K l 1 iT i ni c 9 g ot ch oeu h 3 f io e v a , Fig. hemodynamics, p h e c fm Shl o o a t sd la y 3. Regulation l un enof the cerebral oa Agm b wn (A) h Middle i cerebral i xe cs ar~ery(MC-A)and sequential arterioles in different functional states, (B) q d eo D wuv u en w dl t e e Envelope o e r curve pof’the e IDopplerm snifrequencyt spectrum e iofr the MCA. nhm Top; t s c o o t nM s o i d e F r l h a t i V o e normal state. The MCA territory is normally characterized by a relatively n T o f i b nua t cf hr t o ob low rtotal flow t resistance a m em ( F,) resulting hao p t circulatory me resistance i oul inh a ilow (/?). ~{ equals the sum of the flow resistance of the vessel sections d f y S o w u n R rl e aa m l A p index m o s r e w i s e i H c e e n n s — — — (R,, o t p ce e e iea a b sprhMCA stem; o i R2, v s R3,aebridging tsveins),r Centre: c a t:asospasm uea fn s ur r rh arterioles; of the MCA .srem with normal ICP, The reduction of the MCA stem ( o s ai K r l i n g e l h p i oo a n u s c dt e c i p g a b u a l t l a c o t e o i lumen caused by vasospasm leads to an increase in flow velocity and an 1 S a K 9al 1l i P n n RI 9rise. 9ag This XIe increase n. t ddoes l 9not noticeably 1h i influence o e R, 3which fet is, e a g e eA ht ua n f I r rh i o determined o cl the peripheral o o rflow i resistance au g (~z t + ~2C) idistal m ut to s w . ndi oby mainly the the u g r~ insonated h i i artery segment. When o autoregulation u n isa intact,d w a ar s t p oi C aB b s m at n e l o~the increased El s i l rg i n a rn i o d f d e o C ii i c aw l duec ato vasospasm a cn isa compensated ~ t efor t tby la reactive a idilatay i tion of the arterioles and precapillary sphincters, lowering the ~z. This t i na (t r 3 I r a t a w gD F e ch r r a ei a i i n) o e i l mav g e e l mechanism keeps R, constant and consequently the CBF in a sufficient e a ( w b 1t t pe w 9 a a t l h l range. h9 The t decreased i e 2 i e b e e a ) v t s n. ~z produces an increase in diastolic tlow velocity c fo t h m e e p o mv ef oI a nd soin af hreduction ys ofo R downn to ae 0.5swhile aEt is t stillp within cm normal e a resulting ICP,t Vaar P s a e s S t py dc m a u eprange. E Bottom: e tt L1asospasmof v do thei M~’A eA mnstem with increased aley to a i o C n i a nd c o dia r lir sospasm ewith caBat concomitant ICP ate increase results atr insa compression iti ofn thee bridging veins with a consequential increase of F3. The F3 increase ( e Ka 1 Iac t w 9oo s l a n cannot l9 be compensated mt in because u r 2 the. arterioles h g rarea aheady maximally ) ah s for, l a r i p v o w r a en e t w e vdilated r as ia consequence C ic e r evasospasm re g n stem. t lHence i r the ofa the in othes MCA d ( Bes t gt f ud r i cg ri eelevated hc g fi~ results la o in ans iincrease e h of aF, and p atudecrease es a of thet CBF. s tA ra i w n e s x et n h d e a t a ahigh c ue~, is hreflected u r rby anf increased so R of the iTCD l lt ccurves.aThe MFV oyc e s o o t c ed ct m d o n cpu e o decreases er cdespite r unchanged r a vasospasm, lr h iindicating r e ea diminished i dCBF. b ln a This decline of MFV is proportional to the ICP increase. p e ed t l br p fl ( r. u le e seP u i o s o o vg o s nw e o u, a 1 T t h p9 h e l a ia rh8 r n t e c a5 f i . e r o i e ) er s n v e a, . ci e l p t o d ne d ev d c ee o te a r l f p oo noc i ghnd i f i g iu f eg innt s VC ub M l P w i ea r D ( tr Cva eF i gih v a e re r I i c vr nI tolsw o ( m K D s a a i h o vM nc o t oet c rw e ap l1 e1 aiFa te i n ra i g9h9 n) al d e I s nTn u sn i ut ci o tita mp ro cv Cn u si ec p o g a A a B b i tar h a d id o i i ed
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and between cerebral I n v l c t a d ar r i ei c n e l aHopper, s C d J. (1992)s Correladons a tu e ci tarterial e dvelucid t nl t ea o D m v BA p oe w a Iru tics, bloodhtlow,Fgtr aad delayed ischemia D ei i tdkrl subartichrruidalhemorn eh , cgs rhage. Stroke, 23: 492-497, an e Re o 0 vl v . e a ei r D v showed r e o r I p s i e b d l Fisher, C.M., Kistler, J.P. and Daves, J,M, (1980) Relation of cerebral oi r nD w r nv o e e i pv br e evasospasm s stor subamchnoid eI s hemorrhage a e vl i visualizedy bybr computed a , tol ev w a R b i0 d t p ieoe e u l hn rl eNeurtrsurgery, .t th6: 1–9, aiv o as nh mogrtcphicscanning, (ielmers, H.J., Beks, v e l l o c i t o J.W.F’.and i Joume6, H.L. e (1979) Regional s ccrcbrtd w . blood I c t o so S en ta t( ce t i u1 flow r uin patients n o with asubarachnoid d9m l hemorrhage, es u Actuy9 Neuin t rochir., 47: 245–251. n d ea s m ci obog t n rnf o e Geraud, s ri t ef t i r li a wac ht tar t e e in G,, Tremmrlet, M,, Guell, A. and Bes. A. (1984)The prognostic F p i ou o t lI a u t s i n ao nr t c n d i i h C l c e h i e l t t r value ol”mminvasivti(:13P’memrrtenmnt in srrhatmchnoidhemorrhage, c y DID after S T c Io c hnbA d- t f e lo15: 301-305. e i s H c uu st u i l Swokc, Snyth. t d l i o r o f i e m cf se I h aeaiGranowsktc, n s M.,sBritton. r tu K.E., Afshal, t r e d F.,i Wright, e a C,W,, n m o nR,R.J,, e et e cereblal i l t i t s i t v i tha h k c s n I,ee, u T,Y.e hand eo Nimorr, d C.C, ha (1980) s d Globsslund l a u regional pi y blood s aycn t flow, Noninvasive quantitation in patients with suhsrrachrmidhcmrrro f r i e w a s t dm l i d T es s i a t t e o h i a a s o l n u n e c a r f f w e l rhage. J. Ncurrxurg,, 53: 153–159. c m h m h t e oa a a uf a o nt Grosser, s ao f [).G., Straitrm, rg hc du keTrcvcrrr, v g M. e rrnduBullock, c eR.l (1992) s a y .1., I f l w uu i c p s nht v e uC f u Prediction ra lof ai symptomatic ti a ui p after s osubarachnoid l ec h nhemorrhage P ne lsc vasospasm by l r i et r sa t b i rv ( r s3t a e ti rapidly e increasing h rF a transcranial d n i L)opplcrvelocity n goi and c i cerebral l) blood ri e e W r t f t e hus i o e t f g r r r Iluw changes, a atStl-eke, a t i 23:674-679. p t he re u u n ge ht d Grosset, D.G., Straiton, J., McDonald, I., Cuckbom, M. and Bullock, R. i s t d u a i np h g f p frg (1993)r Usco ofegtranscnuritd e a Doppler r sumrgraphy c e s toe prrxlict h develops net ( A R< d t p o m u e 0 ha1 lr of a delayedx ischemic e h deficit ai . trfler subtrrtrchncrid iv n am s) n ment hcmorrhrrge,J, M i as n h u d e c f im o of F omc Neurrrsrrrg.,78: i dp a183-187. c ey t in n s ea V a mn s J.M. (1987) without elevated Is T e A.G. C hand a tTime o courses ot’ blood m P velocity t v a oo c r h s Harders, p Gilshach, a e mi e changes measured i t a d o nm ii n m i ohs t d rehdedr to virsosprism i a in the p t circle of Willis ii o snby e n transcranial Doppler crltrsrsound,J. Neurosurg., 66: 7 18–728. da t pr . m hFenskc, urA. and Schtirmann, h aieIntracranial 6 ( N R v ( d t p o m u e 0a h 3 r608. l x ei h ai . mv na as ) n risk as M i a in I nod a d c ri i F rHunt, c s W.E, e and Hess, e ta R.M. (1968) Cd iaSurgical t n related s ue to time Vc of’e s intervention in the repair of intracranial aneurysms. J. Neurosurg., 28: C T p h a v a h h r P f tt d a i e e14–20. e i i Pe v s n veo h r g t sl . e t aneurysm: h l st m o i rD I tr c eei a v t t ha Id e Kassell, N,F.r anddBoarini, n s s D.J.e (1985)iiPatients D withberuptured f ei p mr a oe a a c nt g be s t r g d pre- and i re postoperative u o oemanagement. a r u In:sR.H. n t Wilkins e vs S.S. e msRen- i and Neurosurgery, Bd e l McGraw-Hill, w m s pp. e i a a h y h p y t e p( r ee ha t r gachary e Av(Eds.), n o s r 2., i e NewavYork, 1367-1371. 1 S e a 1 o 9a s I l pC9 l8 P o e d 8 mc n7e c. i o r 8 e ;f na Kawamura, S., Sayama, I., Yasui, N. and Uemura, K. (1992) Sequential w I e m i owa na i s ir t C r o a t r n i t n e h m u r e s changes in cerebral blood flow and metabolism in patients with
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Relationships between delayed ischemic dysfunctions and intracranial hemodynamics following subarachnoid hemorrhage J
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L.kpurmreru@ NWW1OAIY, TechnicalUniuer~ifyq/”Munich, Mdll>lr@e28. D-81675Jfurfick GerrrIwI.I
Received10Octobel-1995:revised22March 1996;accepted8 April 1996
Abstract
Delayed ischemic dysfunctions (DID) arc rmc of the main cmnplicatirms following subarachnoid hemorrhage. It was the aim of our study to amrlyse the possible prognostic value d’ different transcrauial Doppler ultrasonogmphy parameters and to elucidate the risk of developing DID with particular reference to the intracranial pressure. The relative change 0[’ mean blood flow velocity and of corresponding ccrcbral circulatory resistance index as well as the intracranial pressure were cletermincd in 44 patients with spontaneous snbarachuoirl hemorrhage. No relationship was found between the occurrence and extent of DID and the relative change of mcwr flow velocity during the clinical cm.nse. In contrast, there was a significant correlation between the relative change of the cerehml circulatory resistance index and the occurrence of’DID. While patients without or with reversible DID showed a decreased resistance index compared to the initial value (without DID: – IT~o+ 15%; reversible DID: –3% f 1470),patients with irreversible DID had a significant increase of the resistance index ( + 1470+ 970). Accordingly, patients with irreversible DID showed a significant increase of intracranial pressure compared to the patients with reversible D W c t t eo o rv I n c ao et h c c hl c l erl uiDh a index by bedside monitoring is a useful tool to predict the occurrence of subarachrwid hemorrhage-associated DID and has therapeutic impact. Kejwords: Subarachnoid hemorrhage; Vasospasm; Intracranial pressure; Delayed ischemic dysfunction; Transcranial Doppler ukrasonography
I ou s c ud t e o pIi ae i oe d h . nc r t b r e t t em e n ao cl c is ti wo d u D i de s y ( lfs c sf o ah pD u l p n ee y ( cl Or urt I mto eoh Ceift a h r (e a a amc c o ow S hm tr a p n rh plhA p oht r bi t mp aci rs iHa g t dru i m f r n e e d v e u e i c b o i a b1 o o a ps (b0 aue K – tr o a l iv 3l s eue m rt edsp 0 t ( a F i W 1 o t i o Lo e a j 1a 9 T tr gs 8 n gu a B 1 r n 9 me i8l 5 h i rl4ee . h 9 d i ,et e esici qi r i siabp n e d au p e r ro o ife ta l ve cio d ern g f rc r erat i t uwlblp l r u a n T n c t h e a t l d e u c b fe ( c brr l b Cepe l obes e B r ta f o o r ao F o l ribmi n i o n T df c e y aa o vs h c r fb ca pu u n weetn r ar rc i i e tr t at oi t svss i wt i w ni i r i r w n b e o g f v c a v o e c b c a v e d a tu S r h s b s e ou e bs eu p r s A a a a , ispal d r w c t ob t m ni f s m( i G ep ao ( d r o e ha e S1 a c r I or nth est e9 t oe a 1 H e a 1 V 9 l1e T om 9 l 8t9 f r l t o . a 8 8o cd D0 t o. poc h b 8j v3 r u , o ; et a tf f vec r i c i i p fi c esm eh e t hp o et m s r i s i aa c i s p nb s o c eid i lt une hi i tm cn it d h r pb t i a ha u pT tr n l i aio C a ota nm e o t n nv t a d o nm i im n ma o ii no s ic t ea aa s c1t P mcS i ol ( r r e to9ra au e c v a b v ou c i o i l sl o n l nP nu ono(r (PaCOq). p ( a r a c ed r I t as ti e 1 C s e a orn X n u r( xe9 MbP sr i e1 n hii be iaox 9 u t d e t i e fs sia S o A t s ci bog o rn ae iri uC ef ( e a 1 G w f M e C 9 o o c l r x Corresponding author. Tel.: (+49-89) 4140-4668; Fax: (+49-89) v a a n e s w r t t d e o e e l 4140-4867. 1 I
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Tablec hI9 e ea 1 HD t t w9o nl c a l w ve l i 2 .ve t i a e e )s s e Essential u all o C ce f i da h n mi a cp l dictaof Bt patients e n r io n u o gv d l e e io Group A t Group B GI-oupC Group Dl . d e f i a c i s S s u en t oa bv sntu i ee Number r dofnpatients i a dr v13 i n15an sa 9 ns se 7 i il c age 46 n D u l o (t dr i pa e a c s m T oMean p o n(years) o aon l43 C g s 45 r r te51 a r p Dl hrar Range 18-65 32-64 l b f va e a t e d tt o tl l i w (years) i oa e cnm19–73 oo h e i e 21-65 h n tn t Male/Female 7/6 7/8 4/5 6/1 m c a ( ie ( e rar 1 d AHM e t aad 9b lC e sr r l 8 aldrA e. l a G 1 i T fl h 9v she b e n r8bLocation of laneurysm: l e a 7 f o ec o cha ) o r d , i c a oi dn m p i s pi e aa i o v gICA rd ra n ea u a1se e I a t dn t t 1 l t o r 3m ACA/ACoA 2 v b aT H s d t ot ov Cowa s r pe i 5 a v ua 5D h s5 b e im r MCA T f v a e w s lD ( l s oe a C o A c ic i oa2— i t 4 l I a 2is t2 t eD lw e — PCA/PCoA 1 1 1 S e a 1 C 9e e a 1 o 9H i l 8 Nom a 9 l l 8 p 6 r . e 8 t 6 d ; . ro — verified aneurysm 5 2 2 a G 1 iK l le a 1 i 9 Gs n e n bg r 9 8e l a lo c h 9 7 osh . df , s ACA, anterior a 1 t v o t p9 f l ta a p 9 or r hICA, internal h ae l carotid 2 . artery; dm o icerebral ) h eiu artery; cACOA,t ante, , t q e u D e m s is ( i A i fo artery; u MCA, n amiddle en cerebral a d artery; r b PCA, es posterior D h r It a tfrior a communicating Dl ei s de cerebral artery; PCOA, posterior communicating artery. e a 1 S e a 1 H 9e l a G a 9 i li 8 r l . l 8 sd 6 n. be e 6t , a ; 1 K l e a i19 L n e a g 1 98a e l l h9u l97 o . f m 9 e 1; r . s t p wh v a h f v oth r e i i e wl i l e o a e cn t r i g et od t t eilA l lio i l dytt m m a s ya w m o pw m t i o e th m p i a n w t t iha fi n i7 dc lae i at S f , pr v f s ar s ebu t i q eDnf t i u w fr pf e va oi 6 e enor t a p rnect rw r ut4fal sihe a riia ey o a t s i o m oc v u ca la i ut h s ns a r a co cn r t A oe s tr iec o nn ps eo nou S df enba sac I ( e a H 1 H e a a 1 G 9 yel C 7 a ll Cs hst 8o t . hPno i e o a n. 7 c m b ea 9oa x l a 1 V a E 9on1 l t em f l v9 7p la9dn Cr h tb s 2 2t mr e e, n ;ha ai ( o p n . d l 8i e oic yet t i )a v ( ie o i l i nM o d f fo pa i lm F c p f ur t 7 to 1i ooe em Vdd t n d cse pnv rt mg i oar a be Tota T w h d e i p m r o(ra Kn e e e l si i ptnfv o l rilt e ce nhe ud a 1 1 S a K la 1 l i S i n h n 99gu t e fi nc. d l 9 i i h h nn o ne 3 tat fiama o, 9era m ; b d t e i t c vf es l if ao t g di lo n2 m ec ni huhw a f ub i oa io Tg l f chc n t I taai M vb s o s aT pe t va r rF eC (e r tu ud a e vS h t adm sei ah sF d eWta t V o e h la fel t n t ec 9d i o 1 e wl Ip e ih a s T e c n9 t t g r am l e D b c wo t o ro D e S r e t nai e a i fa ss H ( a t s 1n i v oagd 9 rn li aci 9 fl fyhe o H l 3 c ( s e awei e rn)f uu1i d iv di r eTI dh t i o t i n ca an ( d aa f t nr oot cS orac o a e C neCetn sd ui a et ag m s i l a e or hIt a p t n c w o t o r o cr D I aecr i l cu rs a t l i cosa he r oi f snotfD n e i s G e a ( t re ts r1 ouo vt at s e9 d v b l aow l sla d 9 y hi ousem e t s c 3t o c, o ht a t e i a au n p t pc a s t o rr r o c e Fa e ec ea ( m auf f i d eC r G h1s o I (ut r s il e l ee9 so C v iG Dt a1 m( 0e il ia hi yt t r r o t et e t . ea,l D H a o p 3 po Iwt p r woe a l x b oioa i o oeal m sl r v i e f an t d l cn a eeo p r s u icue v cr s rt uop c l ad e ebag y c m i as ai t cc l est a t oa Cusre iG d N pe v r fw o e i f t dbav c o h I u ra( rv. v o ti h lt l n i esCa tf C s hae m i iu f x s i d o a t r eo nsM t I ff pa d d S i w a t c yr ) p v ( ee a 1G l r 9 o ol c c 9 o s o i ti m c s 3p .o t a aa em t T o o t bs w t ja t p e t n h h so c a ut t u a re i l i h fn v d y e at e p vr o d o T i pg a f af n t r of l as e C mt r u ei oe h tc n p o rS a e Ds w d p s ir a o 2 c Outcome r A c ei grading t t i I i i a f . o c t t n u ee e t I B o t f wn dai C ha en vsd c ed ePi len sd o ge o . Argen e tuer t cr d i v r a ssec a e d h ivi o or Di lfo e bsn a re t c d iri r s if t e oi i vtr n li nd v S ti pan os ta nsdC a o iii i f w A r gt vD s D u n oa b sn T m ie o nI g id G A n c s o rnl e d i idu oe a onr s o i e o un n a i t c o t C e(n Dh 2 P a m a te i t n o tI d . s G B d eo a r r v n e e e d v l ou f w 1c u c or n l a enmi cs . i d 2 Patient population . I o i o nC ( f D r ae rv rr el ron F po s r a f us t t p fS y o i Gf- rC nd fee t e o a po r r anv i eu noeA i r nt ge tfo enC (ye i u dti fi w e i t ns T e er d t os t oh s l u ld re h a oya hls dn ois i ver oi D rt I r a l ssa p a s a i T 1 At a h n wi a p g boen eg w e f o a p fo d a p i r St ua o i gGru ml D p n eop w r a do ae ro n bi sg dt s sdt dt t ioneis c 7af i ira a eo (b n o p w p nr ei 2 e oie t r r m fu av ea ey ’sr r fdl h ds ma es ee
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al lc o n o ec i r 7 (loo%) A b de we s m t ur r t e n ee eat s r b sr ie r u i or y a TH - d zT M e6 p v u C 4 li h sn E o ra ps id p ep eo e a x l s c a b eii e a gnr n d ice t t r a e l i e lt o o e eb t o e r r r rr h de n m e o ( tn cn n t S la Ut i I t a dn i ckiulo bs n i svoh K tou yiiC y w ao gt o a r t s n e ia n p y tr pt o em o me pe r wcr pnid mea d t r t Aa i i or 1uc c r de 9 n t i co t r si 7 wr e i h m de b n l6cw p bo h oa igut ) e f a o t ir l po n w h a e s c r o I tmvbiy e l f s e cp t rRo uactra ia lr M ewo a r m t a sw f i n d t s s pi f e s ep t l t l h e t o t M w e o t ve s o t ai e m e s l t a o o c x lo i i . p e d l pA c e a idr t vand - e d l i l ( a o w sm pc t b b o o ogi a. l n Tt i mn lCi b o po r ( r l ot c l m e s l t aa c xw i a eai eM
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and CXpI-eSSedas a pe!-cent value. T s p w r c mean ha + s e a t mdT A v o aaI-e given as d l e p w et c ro P r fo r i(u oe r s sc ra hrt ep w l camo tn oo nC t e d ut o aa i a di i R s T m t i i o vn np of ta t i l , o v rmh uI t a o , i yc Fl v r i vzn hCi is n o t ce et p T as w ot ti t v p u e eda Cn rdi s l J f pnu ui f a rbs ohewla Cp ens r , st 3 m a t t a o 0r w i t r a e umh tn Sc – i t s m fo m sch cgr H 4 u o A hd c m eni S a p r an i e ii t m c am n i lml oed ee od iP f <0.05 i cd w a inf c i v p ft otbat s e ei e t t d o Si w c a To m g n e h nc af s Aso ii a u g rsa Cr n m i e i eem s w o i a pb d nate t i u ta m h ii olr r e end ri i ne pae E a s n w ap u e i 2e o t ru r r r fg a l oy e r7 s h r ym p I t a p T t ma h ie w t pa e eCer et e e s ns s m . et 3 sR i e n u f i t c po o rv a ar ia h s tn hm f o aie s e cu t p s ar d a c l i p p N r i e w fn l b atg o te o .a c e o D a t mx M m a td te 2 ICP and additional measurements . 4bl c c t o o io D e ( 1n u . u n p P o aa g a r n n t reM v i I 3 p t Ia w m t s eii m b a e 8u h al C ncs a t i e0 at uv l nn a s ee rc1 cn l u a e t p s( r D iaG I uo n i ad c nsI ce u tdv nowl s m ar s u e nt ii ca h g o getg c o R f r g r A t D (P e < 0 s F r 1r p l p A t a ao l r nivt e b w t g A a B a w wr a b C a D w oe e Table 2 o s d l ( < i0 w ino f a h. gb f Relationship between delayed ischemic dysfunctions during clinical course s di ( Pgi < 0 bn f t ia f . e R and severity of the SAH in inital CT according to the criteria of Fisher et o g B ( D r a r C e ( i v D tF al. ( I980) for all 44 patients 1 l p a o n Group B Group C Group D CT-Score Grouo A A c bo r m r e I pa D C ot 3 (207.) 5 (38.5’%) I t d o t p h a M l d i t t t hi 6 (40%) 3 (33.3%) 7 (53.8%) 11 p w I a m e t b D i t 3 e f 6 (40%) 6 (66,7%) 7 (100%) I (7.7%) 111 t i x vCoh i a cn s t t r he
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2 upper p r Ht o t a woo u J n w200 ,hu u i ee p ve lg ar 40 r e s ) bog t rin e o rri ~ nv a ef t c li wac r h ta e c in r n ot a e ac e o Dc W p xu o g r ah h t Ir nt rc e i iu Dce o n c c l n 100: 1 ph ar e o 1 7 vl groups C B-D e showed a l ~ o ,’ t [% e , d -1 ~ so ( B 8 ~ 9 g C r 2 P o9 7 u smaller increase o r ~ 6 ~ 6 D 7 ~4 g A v2 B u 6 g C r 8 >IA 0. 0. 7r %o s %s o ou ; v D i I c a s on ri n e bg s ls t n ir . t f m ta i i o) s w c n .t a: s . g ae -50 the occurrence and extcut o D a t c o r r e I sn h p o.10 n ! r ~w o ( 2 hu p P s Fw a poa tc a i -1oo nt ri p t i ev ghe c l -20e 2 s n do w r De s a dv i r heec tr c o o s Ir tm i ew bp C r—–l a rCMW l a e hs e -150 ]1 -30 rCR v ( A ga B i – ~ 1 l 4 u -a u1 t i n – 17% i 15%; h tr i3 o e lY e -200 i a r a Ln . t s ’ i F<0 w i t p. h w e0r DID tr r eJ 1i i h v e ee ) , A B c D ( C a D tg a v r r dv a i o ae sn ohu btr l i p a n o s s u cg Group t i v ( n C 1 + 9 ag Di 2 + 7 h t r 4l i o % u a 6 7 u% e l P <0 A s di . (gPi < 0 wn 0f a i f . f 1 e i r l c ) 0 e a n n . 40 f b g B (e o D r r a tC e( u vi o w re1 I rreu n es n eT vi p D d be n ,.b D I l D ~ 30 ) e . ,.-’ ! g oo ‘ a I i v fl n g A te gc D ’ r rZ r C re a h a o ,., s e e ue ~ 20 ( 2 l p T I F i la op o g na A i w tr e h C ig hl ioe e ) ,u n , r , s a B w s I wirhin normal range (group A v B n ) n aL t d s 4“’’’’’’” 10~ P o g aC d i p t oa r g Dil d e o tr e k. ---i n c vu ot u l s e af o d i i I ln s w p s ct die i r g n01 i e inv e C c ia f t fe s l fi t de ycl c A B D f g s ~ o Ad
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Fig. 2. Average values of the re[arive change of mean flow velocity (rC ~~v ). the correspondingrcladvc chimge III cwehml cimulntoty resis tance index (rc ~), and the intracranial pressure (ICP) on the day with [hc highest MFVlevelof the patientduringthe time of otrscrvalion(groupA,) and during lime before DID (groups B–D). The average pC03 was not significantly different between the formgroups.
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Fig. 1. Relationship between maximal mean flow velocity (MFV, upper panel), corresponding resistance index (R, lower panel) and the development of delayed ischemic dysfunction (DID, groups A–D) in 44 patients. Each point indicates the maximal MFV achieved and the corresponding R of each patient during the time of observation (group A) and during the time before DID (groups B–D). The horizontal Iine shows the average The average pC02 was r not significantly different value of each g between the four groups.
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W r t l p eo t ri o n ogo c g D i t m c o o S (m a pBa K I l 1 L e aj 1 9 I uo s 19 n( 8l p d a i e rn t v r de ieHe ce v i i o g c v t le r e spi a rt s ie e p f rt d e eo D O dv r p f rt t iM a ea s pn vh nah d r e go nt v a p vr o t ed g a n s fb di d W oe i s big c fn e t a m Mv v a o t f e D gax h r t T c o so p d n n da d de ot h M v e 2 xc a O t oc h lD emF w o i o b w o s s t e lM e al c m v oee h r l ( a 1 c e T r o b d se t em M v ro a vn s o cD v cc o iu i a n r h w t o i u c ( e ua 1 AA a e a p1 aS 9a e al s H a G a 19 i K rl el a i 98 a 1 l
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t h M v9 w n n h a i 9e n c le Fe 1 a sg u o s r )a e 9i e b n o e d l (u ee r a l 1 L o f ol a 9 io w lg uc ci m d a 3 G o e a ( rrf n s e 1 o ci oo g s 9 v on l iesu 9 rf r e i , 3n rc b t i a e o Dn a t mt t c T i aw i h d xe I e on h i e n C n cm R e D e e al ( cc o av e 1o c e n mi v9 tl lt p l o 9y ai y c. nrC r Te C mh b S e a a t o a nP o c s gB c E u ue rh s e , i S p M ao t o t o c h ifI o c A e u nt r ih MCA normal st r sD e n diameterof diameterofarteriolesnormal w ea wl s f h os y H c op o oi c a p t i e c ior a f et t u s sea ICPnormal i o p w hv a M t v ht p l e o r F e un p t g e t ,e n eay i i hi a t s du ei ob D wv s n e n eh l o e u p I e m o n ne d oq e ro t r hnp l l e 200 se o i ad cu r . sti T ba s t u c xe h e vhf 150 t e o sx c ii oe m ms e v ph t c e t ee nh s na r a nc th a e 100 i a u c net a o a o sr vt bpe . g a suam e l c g ae csi t a o nt . r st a aa C s dw mo p e tPs h rq n p u eP a 50i aa s v h ) mt c e o D i vt p e O aC l f h ot i t p i I+’ men e 0 : eIlw h d nB n s itt t e o eh x y d i p o p so s p u h l te o r einr f rMFV t =n156g cmkt i R = 0.41 sc th i T vl a ew e a t l o v ooc aCc ce ‘~v? i ut ciiameterofMC.reducecl t rh e i rl d ee diameterofarteriolesdilatated s aa n s gw i C o ho e i g sy r pa ptL. p ~ o aICPnormal h e h pi B s c e ao m lr ( e a 1 G i 9e l r 8 o a 4 . u ) n d U a c s o siP a mA ( uu ip l 1 u ca u n t t 9 n ih e o g8 p o t t o M v a ti s d h o an u e h t Fa l a ghe ud r m M v a s w ho dc o u e i nt C s p t gr e a i p c n ht i d h oA a t t a sos l r g e n u n t ln ch a i p o a r o a bue e e ce c v t ue o v f I p o c rs l w l ld et i o vu ue n id m m i w o i c f e u o e MFV = 104 cm/s R = 0.7 s t t I ti t nm r M hf ve al ah u\“;\\, C a- t R eas h enl u F c d r u ]), diameterof MCA reduced a t a i I nc l t f c nh r r ne a eee . I&_~ g C a~ a diameterofarteriolesdilat.ated s a l s a tu e d t e w t a o st s so vh e ei s a s h 4i!$ vs oh em s l e n(A) p n n \\ s o . e Q !~~~!~~~%!~~compressed b o M ( Ka e a l 1 Si an s gR, =9FaR, t + l E2J e + Rst = tl e nh 9 o n. f d te h c n l 9 hr)s a K l 1 iT i ni c 9 g ot ch oeu h 3 f io e v a , Fig. hemodynamics, p h e c fm Shl o o a t sd la y 3. Regulation l un enof the cerebral oa Agm b wn (A) h Middle i cerebral i xe cs ar~ery(MC-A)and sequential arterioles in different functional states, (B) q d eo D wuv u en w dl t e e Envelope o e r curve pof’the e IDopplerm snifrequencyt spectrum e iofr the MCA. nhm Top; t s c o o t nM s o i d e F r l h a t i V o e normal state. The MCA territory is normally characterized by a relatively n T o f i b nua t cf hr t o ob low rtotal flow t resistance a m em ( F,) resulting hao p t circulatory me resistance i oul inh a ilow (/?). ~{ equals the sum of the flow resistance of the vessel sections d f y S o w u n R rl e aa m l A p index m o s r e w i s e i H c e e n n s — — — (R,, o t p ce e e iea a b sprhMCA stem; o i R2, v s R3,aebridging tsveins),r Centre: c a t:asospasm uea fn s ur r rh arterioles; of the MCA .srem with normal ICP, The reduction of the MCA stem ( o s ai K r l i n g e l h p i oo a n u s c dt e c i p g a b u a l t l a c o t e o i lumen caused by vasospasm leads to an increase in flow velocity and an 1 S a K 9al 1l i P n n RI 9rise. 9ag This XIe increase n. t ddoes l 9not noticeably 1h i influence o e R, 3which fet is, e a g e eA ht ua n f I r rh i o determined o cl the peripheral o o rflow i resistance au g (~z t + ~2C) idistal m ut to s w . ndi oby mainly the the u g r~ insonated h i i artery segment. When o autoregulation u n isa intact,d w a ar s t p oi C aB b s m at n e l o~the increased El s i l rg i n a rn i o d f d e o C ii i c aw l duec ato vasospasm a cn isa compensated ~ t efor t tby la reactive a idilatay i tion of the arterioles and precapillary sphincters, lowering the ~z. This t i na (t r 3 I r a t a w gD F e ch r r a ei a i i n) o e i l mav g e e l mechanism keeps R, constant and consequently the CBF in a sufficient e a ( w b 1t t pe w 9 a a t l h l range. h9 The t decreased i e 2 i e b e e a ) v t s n. ~z produces an increase in diastolic tlow velocity c fo t h m e e p o mv ef oI a nd soin af hreduction ys ofo R downn to ae 0.5swhile aEt is t stillp within cm normal e a resulting ICP,t Vaar P s a e s S t py dc m a u eprange. E Bottom: e tt L1asospasmof v do thei M~’A eA mnstem with increased aley to a i o C n i a nd c o dia r lir sospasm ewith caBat concomitant ICP ate increase results atr insa compression iti ofn thee bridging veins with a consequential increase of F3. The F3 increase ( e Ka 1 Iac t w 9oo s l a n cannot l9 be compensated mt in because u r 2 the. arterioles h g rarea aheady maximally ) ah s for, l a r i p v o w r a en e t w e vdilated r as ia consequence C ic e r evasospasm re g n stem. t lHence i r the ofa the in othes MCA d ( Bes t gt f ud r i cg ri eelevated hc g fi~ results la o in ans iincrease e h of aF, and p atudecrease es a of thet CBF. s tA ra i w n e s x et n h d e a t a ahigh c ue~, is hreflected u r rby anf increased so R of the iTCD l lt ccurves.aThe MFV oyc e s o o t c ed ct m d o n cpu e o decreases er cdespite r unchanged r a vasospasm, lr h iindicating r e ea diminished i dCBF. b ln a This decline of MFV is proportional to the ICP increase. p e ed t l br p fl ( r. u le e seP u i o s o o vg o s nw e o u, a 1 T t h p9 h e l a ia rh8 r n t e c a5 f i . e r o i e ) er s n v e a, . ci e l p t o d ne d ev d c ee o te a r l f p oo noc i ghnd i f i g iu f eg innt s VC ub M l P w i ea r D ( tr Cva eF i gih v a e re r I i c vr nI tolsw o ( m K D s a a i h o vM nc o t oet c rw e ap l1 e1 aiFa te i n ra i g9h9 n) al d e I s nTn u sn i ut ci o tita mp ro cv Cn u si ec p o g a A a B b i tar h a d id o i i ed
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J. Klirrgelhij”eret al, \Jourrral ofjhr NeurologicrrlSciences 14.{(1496) 72–7X
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