Near-infrared spectrophotometry determined brain oxygenation during fainting

Near-infrared spectrophotometry determined brain

oxygenation during fainting

P . M A D S E N , F . P O T T , S . B . O L S E N , H . B A Y N I E L S E N , I . B U R C E V

and N . H . S E C H E R

The Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Denmark

ABSTRACT

During orthostatic hypotension we evaluated whether presyncopal symptoms relate to a reduced

brain oxygenation. Nine subjects performed 50° head-up tilt for 1 h and eight subjects were followed

during 2 h of supine rest and during 1 h of 10° head-down tilt. Cerebral perfusion was assessed by

transcranial Doppler determined middle cerebral artery blood velocity (MCA vmean), while brain blood

oxygenation was assessed by near-infrared spectrophotometry determined concentration changes

for oxygenated (DHbO2) and deoxygenated haemoglobin and brain cell oxygenation by the oxidized

cytochrome c concentration (DCytO2). During head-up tilt, six volunteers developed presyncopal

symptoms and mean arterial pressure (88 (78±103) to 68 (57±79) mmHg; median and range), heart

rate (96 (72±111) to 65 (50±107) beats min)1), MCA vmean (59 (51±82) to 41 (29±56) cm s)1), DHbO2

(by )5.3 ()3.0 to )14.8) lmol l)1) and DCytO2 were reduced (by )0.2 ()0.1 to )0.4) lmol l)1;

P < 0.05). During tilt down the cardiovascular variables recovered immediately and DHbO2 increased

to 2.2 ()0.9±12.0) mmol L)1 above the resting value and also DCytO2 recovered. In the nonsyncopal

head-up tilted subjects as in the controls, blood pressure, heart rate, MCA vmean and brain

oxygenation indices remained stable. The results suggest that during orthostasis, presyncopal

symptoms relate not only to cerebral hypoperfusion but also to reduced brain oxygenation.

Keywords blood pressure, central venous pressure, cerebral blood ¯ow, electrical impedance,

hypotension, near-infrared spectroscopy, transcranial Doppler, vaso-vagal syncope,

venous oxygen saturation.

Received 4 November 1996, accepted 13 October 1997

Head-up tilt related presyncopal symptoms are associ-

ated with a reduction in the transcranial Doppler de-

termined middle cerebral artery mean blood velocity

(MCA vmean) (Brooks et al. 1989, Grubb et al. 1991,

Jùrgensen et al. 1993) and also with a reduced level of

cerebral oxygen saturation as detected by near-infrared

spectrophotometry (NIR) over the forehead (Madsen

et al. 1995). In support, this NIR-determined saturation

decreases also in response to hyperventilation and it is

only to a small extent in¯uenced by skin blood ¯ow

(Madsen et al. 1995, Smielewski et al. 1995). However, it

is not known if such cerebral desaturation relates to a

reduced brain oxygenation or only to a lower blood

¯ow. A more detailed evaluation of the cerebral oxy-

genation is made possible with the assessment of ab-

sorbance at different wave lengths in the near infrared

spectrum. Thus, oxidized mitochondrial cytochrome c

has an absorbance peak in the 780±870 nm range that

disappears with reduction, while oxygenated and de-

oxygenated haemoglobin also absorb light at higher and

lower wave lengths (Wray et al. 1988).

We evaluated the NIR-determined absorbance at

different wavelengths during head-up tilt induced hy-

potension in order to assess if presyncopal symptoms

relate to a reduced brain oxygenation. Cerebral perfu-

sion was followed by MCA vmean and changes were

compared with those obtained during head-down tilt

(the Trendelenburg position) and supine rest.

METHODS

Following written informed consent six men and three

women [age 28 (range 21±40) years, height 1.76 (1.71±

1.87) m and weight 70 (64±79) kg; median and range]

with normal orthostatic tolerance participated in the

head-up tilt study. Five men and three women [age 28

Correspondence: P. Madsen, Department of Anaesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK-2100 Copenhagen é, Denmark

Acta Physiol Scand 1998, 162, 501±507

Ó 1998 Scandinavian Physiological Society 501

(22±60) years, height 1.76 (1.58±1.90) m and height 74

(59±84) kg] were subjected to head-down tilt followed

by supine rest. The protocol was approved by the

Ethics Committee of Copenhagen (01±105/95).

Experimental procedure

For the head-up tilt study, subjects arrived in the lab-

oratory at 09.00 h following an overnight fast. The

room temperature was maintained at 23 (21±24) °C.

After instrumentation, the subjects were kept supine for

60 min on a tilt table provided with a bicycle saddle but

with no support for the feet. Passive head-up tilt to 50°was performed over 10 min interrupted at each 10°increment to allow time for measurements. In order to

reduce venous return and to avoid a movement related

increase in pulmonal oxygen uptake (VO2), the subjects

were requested to abstain from any movement. They

remained in the 50° head-up position for 1 h or until

presyncopal symptoms (nausea, lightheadedness and a

feeling of heat) or signs (pallor, relative bradycardia,

and hypotension) appeared. If such symptoms or signs

became manifest, they were returned immediately to the

supine position and measurements were continued for

an additional 30 min of recovery.

A catheter (1.0 mm i.d.; 20-gauge) was inserted in

the brachial artery of the non-dominant arm for mean

arterial pressure (MAP), oxygen saturation (Sa,O2) and

carbon dioxide tension (PaCO2). Another catheter

(1.7 mm i.d.; 16-gauge) was placed in the superior caval

vein through the basilic vein for central venous pres-

sure (CVP) and oxygen saturation (Sv,O2), (Madsen

et al. 1993). MAP and CVP were measured by trans-

ducers (Bentley, Uden, Holland) fastened to the subject

in the mid-axillary line at the level of the heart.

Transducers were connected to a monitor (8041, Si-

monsen & Weel, Copenhagen, Denmark) that inte-

grated pressures and heart rate (HR) over 6 s. The HR

was derived from a two-lead electrocardiogram. Chan-

ges in the central blood volume were indicated by

thoracic electrical impedance (TI) at 90 kHz (CN Inc.,

Copenhagen, Denmark; Matzen et al. 1991, Hanel et al.

1994, Pawelczyk et al. 1994). Electrical impedance also

re¯ects volume changes during venous stasis of an arm

(Nyboer 1959) and in the lower extremities during

head-up tilt (Matzen et al. 1991). The coef®cient of

variation for TI was 0.6% during supine rest, and

changes in response to two 10 min 50° head-up tilts

separated by 30 min were not signi®cantly different.

VO2 and ventilation (VE) were measured breath-by-

breath by a MedGraphics apparatus and associated

software (Cardiopulmonary Exercise System CPX/D,

St. Paul, MN., USA).

Muscle oxygen saturation (Sm,O2) was followed by

continuous light NIR (INVOS 3100 Cerebral Oxime-

ter, Somanetics, Troy, USA; Madsen et al. 1995). The

sensor was placed on the biceps muscle of the domi-

nant arm at the level of the heart. Oxygen saturation

was estimated from the ratio of relative absorbances of

two wave lengths re¯ecting deoxygenated (732.50 nm)

and the sum of deoxygenated and oxygenated haemo-

globin (808.75 nm). Fluid volume changes in the right

upper arm were assessed by electrical impedance

(Minnesota Impedance Cardiograph 304, Greenwich,

USA). Two electrodes were spaced 5 cm apart and

placed on the lateral aspect of the deltoid muscle. Two

other electrodes were placed above the medial condyle

also at a distance of 5 cm.

Cerebral oxygenation was determined by continuous

light NIR (NIRO-500, Hamamatsu Phototonics KK,

Japan). The emitter and the sensor were spaced 3±5 cm

apart and placed on the forehead above the right frontal

sinus. The pulsed laser diodes produce light at four

wave lengths (779, 821, 855, and 908 nm) and a pho-

tomultiplier tube detects the transmitted light. The

optodes were held in position with adhesive tape, and

the forehead was wrapped in dark cloth to avoid

background light. Concentration changes of oxygenated

(DHbO2) and deoxygenated haemoglobin (DHb) and of

oxidized cytochrome c (DCytO2) were calculated by the

algorithm of Wray et al. (1988) and signals were inte-

grated over 0.5 s. For the pathlength factor in the adult

head, we employed a value of 5.93 (van der Zee et al.

1992, also to be consulted for a discussion of the

technique). The chromophore concentrations were set

to `zero' before tilt-up and the relative concentration

changes reported. No signi®cant differences in DHbO2,

DHb and DCytO2 changes were found between two

10 min 50° head-up tilts separated by 30 min.

Right middle cerebral artery vmean was monitored

beat-to-beat with the use of a 2 MHz pulsed Doppler

(Multidop X, DWL, Sipplingen, Germany). The prox-

imal segment of the artery was insonated by the

transtemporal approach at a depth of approximately

50 mm (Aaslid et al. 1982) and the probe was secured

with a head band. MCA vmean was computed from the

envelope of the maximum frequencies by the equip-

ment, and the pulsatility index (PI) was the difference

between the systolic (vsys) and diastolic velocities (vdia)

divided by vmean.

Blood samples were obtained anaerobically in hep-

arinized syringes (QS50, Radiometer, Copenhagen,

Denmark) every 5 min starting 30 min before the head-

up tilt, at each 10° increment and every 5 min during

the sustained tilt. Samples were also obtained when

presyncopal symptoms or signs appeared, immediately

after tilt-down, and every 5 min for 30 min after the

subjects were returned supine. Oxygen saturations and

Paco2 were determined immediately on OSM-3 and

ABL-4 apparatus (Radiometer).

Brain blood oxygenation and near-infrared spectrometry á P Madsen et al. Acta Physiol Scand 1998, 162, 501±507

502 Ó 1998 Scandinavian Physiological Society

During the control protocol the subjects rested su-

pine for 30 min and were tilted 10° head-down for 1 h.

After return to the supine position, they rested for 2 h.

Every 5 min, MAP, HR, MCA vmean and brain oxy-

genation were determined.

Statistical methods

Results are presented as medians with range. Changes

during tilt were related to the mean value of the last

15 min of supine rest and to the preceding value during

the hypotensive incidence. Presyncopal symptoms ap-

peared at different times, and graphs are constructed

from the median tilt time. Changes with time were

evaluated by the Friedman test and if proven signi®-

cant, such deviations were located with the Wilcoxon

test by rank. A value of P £ 0.05 was considered sig-

ni®cant.

RESULTS

Control

During supine rest and 10° head-down tilt, MAP [84

(69±100) mmHg], HR [54 (44±70) beats min)1],

MCA vmean [62 (44±84) cm s)1], vdia [42 (26±56) cm

s)1], vsys [93 (68±131) cm s)1] and thereby PI [0.86

(0.71±1.35)] all remained stable. Also, DHbO2 [0.0 (0.0±

0.2) mmol L)1], DHb [0.0 (0.0±0.5) mmol L)1] and

DCytO2 [0.0 (0.0±0.5) mmol L)1] did not change.

Head-up tilt

Head-up tilt resulted in appearance of presyncopal

symptoms and signs after 26 (8±44) min in six subjects.

Two subjects were tilted down due to discomfort other

than faintness after 25 and 35 min, respectively, and

one subject sustained the full 60 min head-up tilt pe-

riod. In these three subjects, cardiovascular variables

and brain oxygenation remained stable. In the six

subjects who developed presyncopal symptoms, all

variables but Sa,O2 [98 (97±98%)] and DHb [)0.1

()1.1±0.5) mmol L)1] changed signi®cantly. The sub-

jects who experienced the presyncopal symptoms were

relieved immediately after return to the supine position,

but they remained pale for several minutes.

During the 50° head-up tilt, MAP [88 (78±103) to

103 (93±118) mmHg] and HR increased [62 (55±94) to

96 (72±111) beats min)1], but with the development of

the presyncopal symptoms, they decreased abruptly to

68 (57±79) mmHg and 65 (50±107) beats min)1, re-

spectively (Figure 1). While CVP decreased during

tilting [8 (2±9) to 1 (0±5) mmHg], it remained stable

during the sustained tilt. Sv,O2 decreased from 77 (77±

78) to 60 (54±67)% and returned to the baseline level

immediately after the subjects were tilted down. The TI

increased by 4.7 (2.8±6.0) W.

The Sm,O2 decreased from 70 (58±85) to 58 (53±

75%) during the tilt but recovered to 61 (54±79%) at

the onset of the presyncope. The electrical impedance

across the upper arm was reduced by 1.1 (0.2±3.6) W.

VO2 and VE were stable at 0.23 (0.20±0.27) l min)1 and

8 (5±9) l min)1 for as long as subjects were comfort-

able, but increased slightly (to 0.37 (0.30±0.61) l min)1

and 12 (10±30) l min)1, respectively) when the presyn-

copal symptoms appeared. Thus, PaCO2 decreased from

5.3 (4.9 to 5.7) to 4.6 (4.1±5.4) kPa.

During the tilt, MCA vmean increased from 59 (51 to

82) to 63 (54±83) cm s)1, but it was reduced to 49 (38±

79) cm s)1 during the maintained tilt (Figure 2). When

the presyncopal symptoms appeared, it decreased fur-

ther to 41 (29±56) cm s)1, and after tilt-down it re-

turned to the resting value. The vsys and vdia decreased

from 86 (74±118) and 70 (58±86) to 41 (34±59) and 25

(15±40) cm s)1, respectively. Thus, PI was 0.74 (0.59±

0.82) at rest and during head-up tilt but increased to

0.84 (0.64±0.93) when the presyncopal symptoms ap-

peared.

During supine rest, the DHbO2 and DCytO2 were

stable, but during the tilt, DHbO2 decreased by )2.6

(0.0 to )6.8) mmol L)1 and subsequently recovered to

the resting level. In association with the development of

presyncopal symptoms DHbO2 again decreased by )5.3

()3.0 to )14.8) mmol L)1. After tilt-down, it recovered

to a maximum of 2.2 ()0.9 to 12.5) mmol L)1 above

the resting value before this value was re-established.

During the tilt, DCytO2 remained stable, but with ap-

pearance of the presyncopal symptoms it decreased by

)0.2 ()0.1 to )0.4) mmol L)1 and recovered when the

subject was tilted down.

DISCUSSION

In six of nine subjects, head-up tilt was associated with

arterial hypotension and appearance of presyncopal

symptoms. Although care was taken to return near-

fainting subjects supine as quickly as possible, the

middle cerebral artery mean blood velocity was reduced

together with the NIR determined oxygenated hae-

moglobin concentration. In addition, the oxidized cy-

tochrome c concentration was reduced, and, as for the

oxygenated haemoglobin concentrations, it recovered

after the subjects were tilted back to the supine position

supporting prior hypo-oxygenation. Conversely, during

supine rest, head-down tilt and head-up tilt in non-

syncopal subjects, the NIR-determined brain oxygen-

ation and MCA vmean remained stable.

The cardiovascular response to head-up tilt included

a tachycardic-normotensive phase followed by a bra-


Acta Physiol Scand 1998, 162, 501±507 P Madsen et al. � Brain blood oxygenation and near-infrared spectrometry

dycardic-hypotensive episode related to sympathetic

and parasympathetic activity, respectively (Pedersen

et al. 1995). The responses were related to central hy-

povolaemia as re¯ected in Sv,O2 (Madsen et al. 1993),

Sm,O2 (Madsen et al. 1995), and TI (Matzen et al. 1991).

In contrast, the CVP decreased only during the tilt; this

may be related to a repositioning of both the transducer

and the heart. The Sm,O2 decreased for as long as blood

pressure was maintained and increased when the pre-

syncopal symptoms appeared (Madsen et al. 1995). This

pattern corresponds to muscle blood ¯ow which is

reduced during normotensive central hypovolaemia and

elevated when blood pressure decreases (Barcroft et al.

1944). Yet, Sm,O2 could be in¯uenced by local ¯uid

Figure 1 Median values with range for heart rate, mean arterial and central venous pressures, arterial, central venous and muscle oxygen

saturations and thoracic impedance at rest ()30±0 min), during tilt-up (0±10 min), during 50° head-up tilt (10±36 min) and recovery (36±60 min)

for six subjects who experienced presyncopal symptoms. Data are related to the median head-up tilt time. Filled symbols different from rest,

P < 0.05; * different from preceeding value, P < 0.05.



accumulation and venous stasis independent of muscle

blood ¯ow, and electrical impedance across the upper

arm decreased. But the impedance signal was stable

when hypotension developed and a reduction in Sm,O2

was converted to an increase.

Brain perfusion was evaluated by the MCA vmean

and haemoglobin oxygenation. MCA vmean re¯ects ce-

rebral blood ¯ow for as long as the arterial diameter

remains stable, and the DHbO2 re¯ects oxygenated

haemoglobin supply if utilization and blood volume do

not change. Oxygen utilization as re¯ected by VO2 was

near constant during the head-up tilt, and central hy-

povolaemia must be severe before `supply dependency'

is noted and VO2 (Shoemaker et al. 1993) and cerebral

Figure 2 Median values with range for the middle cerebral artery blood mean, systolic and diastolic velocities and changes in oxidized

cytochrome c and oxygenated haemoglobin concentrations and in the transcranial Doppler determined pulsatility index at rest, during 50° head-up

tilt and recovery for six subjects who experienced presyncopal symptoms. Filled symbols different from rest, P < 0.05; * different from

preceeding value, P < 0.05.



metabolism for oxygen is affected (Grubb & Raichle

1982).

During the tilt, MAP and MCA vmean increased and

DHbO2 decreased, but they returned to the resting

values during the sustained tilt. The transient elevation

of MAP and MCA vmean may be attributed to vascular

constriction by elevated sympathetic tone. For example,

during tilting, the radial artery constricts for several

minutes until it, as MAP, returns to the pre-tilt level

(Iversen et al. 1995). The recovery of MCA vmean and

DHbO2 may be explained by cerebral vasodilatation

(Fog 1937, Kontos et al. 1978). If so, the process re-

quired minutes while the autoregulatory response as

re¯ected by transcranial Doppler has a duration of only

�5 s (Aaslid et al. 1989).

During the sustained tilt, the preserved DHbO2 and

MCA vmean support that the NIR signal was dominated

by tissue supplied by the internal carotid artery, as the

external carotid ¯ow is poorly autoregulated (Paulson

et al. 1990) and skin blood ¯ow decreases during

normotensive head-up tilt (Skagen & Bonde-Petersen

1982). Also, with the appearance of the presyncopal

symptoms both DHbO2 and MCA vmean decreased, and

DHbO2 displayed an overshoot during tilt-down al-

though the subjects remained pale.

During the presyncopal attack, the decrease in ox-

ygenated haemoglobin was secondary to the decrease in

blood pressure and PaCO2. Cerebral artery sympathetic

tone is not known, but impaired perfusion may be

explained by arterial collapse when the critical closing

pressure is reached (Jùrgensen et al. 1993). `Paradox'

small vessel constriction has been proposed on the

ground of an increase in PI (Grubb et al. 1991). How-

ever, the increase in PI re¯ects that both Vsys and

Vdia decreased �16 cm s)1, while vmean decreased

�18 cm s)1; a combination that may equally well be

ascribed to poor ®lling as to vasoconstriction.

The DCytO2 was taken to relate to the brain mi-

tochondrial cytochrome c oxidation. It was maintained

during head-up tilt in accordance with a preserved

oxygenated haemoglobin supply and was not affected

until MCA vmean and DHbO2 decreased markedly.

When subjects were relieved of symptoms, both

DHbO2 and DCytO2 recovered indicative of prior hy-

po-oxygenation. Since the changes in the DCytO2-signal

were small, other chromophore changes may have had

an in¯uence, but the DCytO2-signal could be separated

from the haemoglobin signals. Thus, the DCytO2 re-

mained unchanged during the tilt when DHbO2 de-

creased and it increased during tilt-down when DHb did

not change.

In conclusion, brain oxygenation remained stable

during orthostatic manipulations that did not induce

presyncopal symptoms. However, when such symp-

toms appeared they were related to a reduction not only

in the cerebral perfusion, but also to a lowered level of

brain oxygenation.

We thank Heidi Hansen and Anette Uhlmann for expert technical

assistance, Erling Veje for determination of the wavelengths

employed by the INVOS-3100 device, and Ludwig Schleinkofer

from the Hamamatsu Corporation for introducing us to the NIRO-

500 machine. Per Madsen and Henning Bay Nielsen were supported

by the Danish Medical Research Council, and the study was

supported by the Laerdal Foundation for Acute Medicine.

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