Well-being and cerebral oxygen saturation during acute heart failure in humans

Well-being and cerebral oxygen saturation during acuteheart failure in humans

P. L. Madsen, H. B. Nielsen and P. Christiansen

Department of Internal Medicine, Nñstved Community Hospital, Denmark

Received 16 August 1999; accepted 16 November 1999

Correspondence: Dr Per Lav Madsen, Department of Infectious Diseases, Rigshospitalet M 7721, Tagensvej 20, DK-2200 Copenhagen N, Denmark

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Summary

Cerebral symptoms and near-infrared spectrophoto-metry-determined cerebral oxygen saturation (ScO2)

were followed in patients treated for normotensive

acute congestive heart failure. The reproducibilityand normal range for ScO2 were established from 39

resting subjects without cardio-respiratory disease:

the ScO2 ranged from 55 to 78% with a coef®cient ofvariation for triple determination of 6%. Patients

rated cerebral symptoms on a scale with end-points of

0 (best) and 10 (worst). In eight patients with acuteheart failure, arterial oxygen tension increased during

decongestive treatment, from 9á1 (4á9±10) to 10á4 kPa

(7á3±17); median with range, as did arterial oxygensaturation, from 94 (48±97) to 97% (87±99) (P<0á02),

whereas the mean arterial pressure, heart rate andarterial carbon dioxide tension remained unchanged.

The cerebral symptom score improved from 8 (3±10)

to 1 (1±9) and the ScO2 increased from 34 (20±58) to50% (19±91) (P<0á02). A ninth patient presented with

a silent but massive myocardial infarction: she was

cerebrally obtunded with a ScO2 of 18% and soondied. In patients with normotensive acute heart failure

and cerebral symptoms, cerebral oxygen saturation is

low, and during successful treatment ScO2 increaseswith the well-being of the patient.

Keywords: cardiac failure, cerebral circulation,

cerebral oxygenation, near-infrared, spectroscopy.

Introduction

During acute heart failure, hypotension, a low

cardiac output and arterial gas tensions may affect

cerebral oxygenation and the well-being of the

patient. Cerebral hypoxia is evident in the hypo-

tensive and cerebrally obtunded patient, whereas asymptomatic patient is less readily suspected of

cerebral hypoxia if blood pressure is not affected.

However, during acute heart failure, adequateoxygenation of the brain cannot be safely assumed

despite near-normal arterial pressure and blood gas

variables. Pulmonary congestion may cause arterialhypoxaemia, and the patient may hyperventilate and

thereby lower cerebral blood ¯ow (Kety & Schmidt,

1948). If pulmonary oedema progresses, hypoxaemiaworsens and eventually metabolic acidosis shifts the

haemoglobin oxygen saturation curve to the right.

Hypercapnia1 is a late ®nding, and the cerebrovas-cular vasodilatatory response to hypercapnia is

abolished by hypoxaemia (Paulson & Waldemar,

1990). With such complex pathophysiology, bedsidemonitoring of cerebral oxygenation is likely to be of

help in management of the critically ill cardiac

patient.Cerebral haemoglobin oxygen saturation (ScO2)

may be non-invasively assessed by dual-wavelength

near-infrared spectrophotometry (NIRS), a tech-nique equivalent to pulse oximetry for arterial

oxygen saturation (Madsen & Secher, 1999). In the

present study, cerebral symptoms and ScO2 of thefrontal cerebral lobes were investigated in norm-

otensive patients admitted to hospital with acute

congestive heart failure. It was hypothesized thatScO2 would be low when symptoms of cerebral

discomfort were prevalent, and that ScO2 would

improve if treatment was successful and symptomsvanished.

............................................................................................................................................................................................................................................................................................................................

158 Clinical Physiology 20, 2, 158±164 · Ó 2000 Blackwell Science Ltd

Methods

Nine patients (®ve men, 73 years old (range 53±90))met the criteria for inclusion in the study (Table 1).

The patients presented with acute congestive heart

failure as indicated by dyspnoea, rales2 and a history ofheart disease (Braunwald et al., 1997), but they were

not in shock as their systolic (SAP) and mean (MAP)arterial pressures were higher than 100 and

70 mmHg, respectively. Criteria for exclusion from

this study were angina pectoris and the administrationof morphine, due to concern that such circumstances

would affect the mental state of the patients. Also,

patients were eligible for inclusion only when cerebraland muscle oxygen saturation could be measured

before treatment. All patients were treated as consid-

ered appropriate and were followed until they wereclinically stable. Patients were seated and given

oxygen via a nasal catheter (5±10 l min±1) and furose-

mide (n � 9; 60 mg (range 40±120) supplementedwith nitroglycerine intravenously (n � 3; 1 mg h±1).

Healthy subjects and patients with predominantly

rheumatism and skin diseases recruited from a generalpractitioner's of®ce served as controls (Table 2).

Reproducibility of ScO2 determination was assessed

during three separate measurements within 2 min.Since patients with heart failure were seated upright,

the ScO2 response to short-term orthostasis was

determined in eight healthy subjects in response totwo 10 min periods of passive 50° head-up tilts

separated by 30 min of recovery. Informed consent

was obtained from each patient and subject, and the

study was approved by the local ethics committee(98-1/23).

Systolic (SAP) and diastolic blood pressures (DAP)

were measured by sphygmomanometry, and heartrate (HR) was derived from a three-lead electrocar-

diogram. Mean arterial pressure (MAP) was DAP plus

1/3 of the pulse pressure. Arterial blood samples wereobtained anaerobically in heparinized syringes and

immediately analysed for arterial oxygen saturation

(SaO2) and tension (PaO2), carbon dioxide tension(PaCO2) and pH (OSM-3 and ABL-4, Radiometer,

Copenhagen, Denmark). Patients rated cerebral

symptoms (dizziness, drowsiness, tiredness, faintnessor light-headedness) on a scale with end-points of 0

(best) and 10 (worst). The patients were requested to

separate such symptoms from dyspnoea, anxiety andany chest discomfort. Patients were given values of `9'

and `10', respectively, if they were too weak to answer

adequately or if they were cerebrally obtunded.

Table 1 Demographic data for patients with acute heart failure.

Sex/age NYHA EF (%) Chronic diseases Previous medication Cause of acute heart failure

M/84 II ± CHF, IHD, COPD, atrial ®brillation Diuretics, digoxin, calcium antagonist Atrial ®brilliation

M/78 III ± CHF, aortic stenosis, pacemaker Diuretics, digoxin Aortic stenosis

F/89 III 40 CHF, IHD, MI, aortic stenosis Diuretics, digoxin Aortic stenosis

M/69 III 30 CHF, IHD, CABG facta10 , COPD Diuretics, ACE inhibitor, b1-blockade,

statin

Newly instituted b1-blockade

of ventricular tachycardia

F/76 II 55 IHD, hypertension, uraemia Diuretics, amlodipine Uncontrolled hypertension

M/62 III 30 CHF, IHD, COPD, atrial ®brillation Diuretics, digoxin, ACE inhibitor Lack of drug compliance

M/53 II 49 CHF, IHD, MI antea11 , CABG facta Diuretics, b1-blockade, statin Lack of drug compliance

F/81 III ± IHD, NIDDM, breast cancer Diuretics, digoxin, steroid Pneumonia

F/92 III 45 CHF, IHD, MI antea Diuretics, ACE inhibitor Silent anterior acute MI

New York Heart Association functional group (NYHA) before present incident; left ventricular ejection fraction (EF); chronic diseases, previous

medication, and cause of acute decompensation in nine patients. CABG, coronary artery by-pass grafting; CHF, chronic heart failure; COPD,

chronic obstructive pulmonary disease; IHD, ischaemic heart disease; MI, myocardial infarction.

Table 2 Demographic data for control subjects.

Ambulatory patients Normal subjects12

Total number/men 22/14 17/16

Age (range) (years) 51 (18±74) 25 (20±30)

SAP(mmHg) 133 (110±170) 115 (105±135)

DAP (mmHg) 70 (60±95) 70 (60±85)

Ambulatory patients were recruited from a general practitioner's of®ce

and suffered predominantly from rheumatism or diseases of the skin.

DAP, diastolic arterial pressure; SAP, systolic arterial pressure.

P. L. Madsen et al. � Cerebral oxygenation during heart failure............................................................................................................................................................................................................................................................................................................................

Ó 2000 Blackwell Science Ltd · Clinical Physiology 20, 2, 158±164 159

The ScO2 was measured by dual-wavelength NIRS

(INVOS 3100 Cerebral Oximeter, Somanetics,4 Troy,

MI, USA) with the light source and the sensor placedon the forehead immediately below the hairline. With

NIRS using continuous light, the absolute chromo-

phore content cannot be determined since the pathlength of the light in the tissue is not known. Using

dual-wavelength NIRS, an ScO2 proportional to the

`true' value is derived from the ratio of relativeabsorbencies of two near-infrared wavelengths

re¯ecting deoxygenated (732á50 nm) and the sum of

deoxygenated and oxygenated haemoglobin(808á75 nm). Contributions from extra-cranial tissues

are suppressed by measuring the ratios of twodetectors located 3á0 and 4á0 cm from the light

source. In ®ve heart failure patients, NIRS-deter-

mined muscle oxygen saturation (SmO2) was meas-ured over the right biceps muscle at the level of the

heart.

Variability of ScO2 determinations is reported asthe coef®cient of variation. Changes were evaluated

by the Wilcoxon rank sign test for matched pairs.

Co-variation was evaluated with Spearman's rankcorrelation coef®cient. Results are reported as medi-

ans with range unless otherwise stated, and a P value

£0á05 was considered signi®cant.

Results

Eight of nine heart failure patients had two determin-

ations of ScO2 made. Their PaO2 increased (from 9á1(4á9±10) to 10á4 (7á3±17) (kPa)) and SaO2 (from 94(48±97) to 97% (87±99)) (P<0á02; Fig. 1). Their

cerebral symptom score improved from 8 (3±10) to

1 (1±9), and their ScO2 increased from 34 (19±58) to50% (19±74) (P<0á02), with a tendency for co-varia-

tion of changes (Spearman's r � )0á58; P � 0á10;

Fig. 2). The SAP (130 mmHg, range 100±170),DAP (74 mmHg (60±95)), HR, PaCO2, pH and

SmO2 remained unchanged. The ninth patient, a 92-

year-old woman, presented with a silent but massiveleft ventricular anterior infarction and pulmonary

oedema (SaO2 56%, PaCO2 8á3 kPa, pH 7á02, blood

pressure 147/68 mmHg, ScO2 18% and was evalua-ted to have a cerebral score of `10'), and she soon died.

In the 22 control patients without cardiovascular

diseases, the ScO2 and SmO2 were 65% (range 55±78)

(mean � SD 66 � 8%; P<0á05 compared with the

heart failure patients) and 65% (45±90) (68 � 14%;

P<0á05 compared with the heart failure patients),respectively. During three separate measurements,

ScO2 and SmO2 varied maximally by 4% (2±6)

(coef®cient of variation 6%) and 7% (0±12) (coef®-cient of variation 10%), respectively. In the 17 normal

subjects, ScO2 was 75% (59±91) (P<0á05 versus the

control patients). In eight healthy subjects, the ScO2,MAP and HR were unchanged by repeated head-up

tilts, and in 48 patients and controls the cerebral

symptom score and the ScO2 co-varied (Spearman'sr � )0á72; P<0á002; Fig. 3).

Discussion

Cerebral oxygen saturation (ScO2) was 34% inpatients presenting with normotensive acute conges-

tive heart failure and cerebral symptoms. In addition

to improvements in the scores for the patients'cerebral symptoms, ScO2 recovered to 50% during

treatment and hence approached the ScO2 of the

control patients (65%) and normal subjects (75%).Patients with acute pulmonary congestion may be

unresponsive or agitated, and cerebral symptoms may

be misinterpreted as fatigue or anxiety. In this study,symptoms and signs of cerebral hypoperfusion (diz-

ziness, drowsiness, tiredness, faintness or light-head-

edness, somnolence and coma) were separated fromanxiety, dyspnoea, fatigue and chest pain, and co-

variation with ScO2 was demonstrated. Descriptions

of acute heart failure relate impaired cerebraloxygenation to arterial hypotension or severe hypo-

xaemia, but in these normotensive and only moder-

ately hypoxaemic patients, ScO2 was reduced to lessthan half of the normal value and cerebral symptoms

were prevalent.

In seven of nine patients, pulmonary congestionwas an exacerbation of a chronic condition associated

with impaired control of the cerebral perfusion. In

chronic heart failure patients, resting cerebral blood¯ow and the lower limit of its auto-regulation are

reduced even during treatment with diuretics, digoxin

and ACE inhibitors (Paulson & Waldemar, 1990;Kamishirado et al., 1997). In patients treated with

ACE inhibitors, regulation of cerebral perfusion

is also abnormal during dynamic exercise: as

Cerebral oxygenation during heart failure � P. L. Madsen et al.............................................................................................................................................................................................................................................................................................................................


Figure 1 Cerebral, circulatory and blood gas variables before and after decongestive treatment in eight patients withacute left heart failure. Each patient is represented by a line in the horizontal plane, and vertical bars indicate the medianwith range. A cerebral symptom score of 10 designates worst possible symptoms. Filled symbols indicate a signi®cantdifference (P£0á05) compared with the pre-treatment value.



demonstrated by transcranial Doppler, an insigni®-cant elevation in the middle cerebral artery mean

blood velocity of ~8% during one-legged exercise wasconverted into an ~9% decrease with both legs

involved, although MAP and PaCO2 were similar

(HellstroÈm et al., 1997). In patients with chronic atrial®brillation and a limited capability to increase cardiac

output during exercise, middle cerebral artery mean

blood velocity increases less during cycling (~10%)than in age-matched healthy subjects (~20%; Ide

et al., 1999). Also, cerebral perfusion is lowered

during paroxysms of atrial ®brillation (Totaro et al.,1993) and during tachycardia in patients with coro-nary artery disease (Hagendorff et al., 1994), and both

cerebral blood ¯ow and cognitive function increase

following pacemaker implantation in patients withbradycardia (Koide et al., 1994). Arterial hyperten-

sion, diabetes (Kastrup et al., 1990) and familial

hypercholesterolaemia (Rodriguez et al., 1994) in¯u-ence regulation of cerebral blood ¯ow, and cerebral

auto-regulation is impaired in patients resuscitated

after cardiac arrest (Nishizawa & Kudoh, 1996). Inthe heart failure patient with cerebral symptoms,

cerebral hypoxia can be expected even in the face ofnear normal blood pressure and blood gas variables,

and in this study, some patients presented with a

critically lowered ScO2 despite near-normal MAP,SaO2 and PaCO2. We suspect that these patients have

impaired capacity for cerebral vasodilation in

response to a low cardiac output.The NIRS technique has been evaluated by exper-

imentally altering cerebral perfusion. During head-up

tilt-induced hypotension and near-fainting (ortho-static hypotension), ScO2 mirrors changes in the

transcranial Doppler-determined middle cerebral

artery blood velocity, and conforms to cerebral auto-regulation of blood ¯ow (Madsen et al., 1995, 1998;

Colier et al., 1997). Also, ScO2 re¯ects cerebral

perfusion and oxygenation during ventilatorymanoeuvres changing arterial oxygen and carbon

dioxide tensions (Madsen et al., 1995; Smielewski

et al., 1995; Pollard et al., 1996). As determined byNIRS and invasively by arterial (~�6 of the ScO2 signal)

and internal jugular vein blood sampling (~3/4), ScO2

is correlated in subjects breathing different hypoxic gasmixtures (Pollard et al., 1996). As determined by

NIRS, cerebral oxygenation integrates cerebral blood

¯ow and arterial oxygen content (Madsen et al., 1995).With transcutaneous NIRS, part of the signal

re¯ects oxygenation of skin and subcutis, and the

proportion varies with the inter-optode distance. Tore¯ect cerebral oxygenation, the inter-optode distance

needs to be at least 2á5 cm (van der Zee et al., 1992),

and with the applied device using two receivingoptodes with distances to the emitter of 3á0 and

4á0 cm, respectively, the signal is weighted towards the

cerebrum although an in¯uence of scalp ischaemia bytourniquet is noted (Owen-Reece et al., 1996). In this

Figure 2 Changes during decongestive treatment in cere-bral oxygen saturation and cerebral symptom score for eightpatients with acute heart failure. A decrease in the cerebralsymptom score indicates improved cerebral symptoms.

Figure 3 Cerebral oxygen saturation and cerebral symptomscore (10 designates worst possible cerebral symptoms) innine patients with acute congestive heart failure (d) and in22 ambulatory patients (s) and 17 normal subjects ( � ).



study, contribution from extra-cranial tissue to the

ScO2 signal was small: thus, the ScO2 was stable during

repeated normotensive head-up tilts that do not affectcerebral perfusion but lower skin and subcutaneous

blood ¯ow (Larsen et al., 1996). In line with a more

stable cerebral perfusion than muscle perfusion, thecoef®cient of variation for ScO2 was smaller than that

for SmO2. Also, the SmO2 was low in the heart failure

patients when compared with the value obtained in thecontrols. In contrast to ScO2, SmO2 was unaffected by

treatment of acute heart failure, substantiating the fact

that NIRS re¯ects mainly deeper tissues than the skinand subcutis since ScO2 and SmO2 would otherwise

expect to change in parallel. The discrepancy betweenthe increase in ScO2 and the stable SmO2 suggests that

muscle blood ¯ow is low during acute heart failure and

that the applied decongestive medication did not affectmuscle blood ¯ow. Between control patients and

volunteers the difference in ScO2 was ~10%. Poten-

tially, this difference relates to age, skin blood ¯ow andarterial gas tension.

NIRS has been used to determine cerebral haemo-

globin oxygenation during cardiac surgery withpatients on extra-corporal circulation (Nollert et al.,1995a,b). In these patients, cerebral haemoglobin

oxygenation was in¯uenced mainly by PaCO2 andfound to detect patients with post-operative neuro-

psychological dysfunction due to peri-surgical cere-

bral hypoxia. Also, NIRS re¯ected the lack of cerebralperfusion in one patient with cardiac arrest (Pilkington

et al., 1995) and in patients during threshold setting of

an implantable cardioverter7 -de®brillator (de Vries,1997). A >5% change in ScO2 indicates a change in

cerebral oxygenation (Madsen & Secher, 1999).

In patients with acute heart failure, cerebral oxygensaturation was critically lowered and cerebral

symptoms were prevalent; both recovered during

decongestive treatment. With near-infrared spectro-photometry, the cardiorespiratory system can be

assessed with respect to its ability to oxygenate the

brain, in addition to the limited and possibly inade-quate goal of maintaining blood pressure and arterial

gas variables.

Acknowledgements

Erling Veje is thanked for the determination of

wavelengths employed by the INVOS-3100 device.

The study was supported by the Danish Heart

Foundation (97-2-4-53-22541) and the Laerdal

Foundation for Acute Medicine.

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Well-being and cerebral oxygen saturation during acute heart failure in humans

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