Cerebral oxygenation measured by near-infrared spectroscopy during circulatory arrest and cardiopulmonary resuscitation

N. Nagdyman*,1, T. P. K. Fleck1, P. Ewert1, H. Abdul-Khaliq1, M. Redlin2 and P. E. Lange1

1 Department of Congenital Heart Disease, Paediatric Cardiology and Paediatric Intensive Care Medicineand 2 Department of Anaesthesiology, Deutsches Herzzentrum Berlin, Augustenburger Platz 1,D-13353 Berlin, Germany

Corresponding author. E-mail: nagdyman@dhzb.de

Accepted for publication: April 12, 2003


    Abstract
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
We measured cerebral oxygenation by near-infrared spectroscopy (NIRS) during an unexpected cardiac arrest and successful cardiopulmonary resuscitation (CPR). A 4-yr-old girl with cyanotic congenital heart disease developed an arrhythmia during cardiac catheterization with subsequent circulatory arrest. Continuous monitoring of cerebral oxygenation showed marked changes in oxygen status immediately after the beginning of the tachyarrhythmia. After 1 min of circulatory arrest, a decrease in oxygenated haemoglobin concentration and cytochrome oxidase signal indicated a critical reduction of oxygen tension. With the beginning of CPR, a rapid increase in cytochrome oxidase oxygenation was observed. Previous values, however, were only restored when sinus rhythm was obtained after successful cardiac defibrillation. Our observations suggest that non-invasive cerebral NIRS measurement gives useful additional real-time information on cerebral oxygenation during cardiac arrest and CPR.

Br J Anaesth 2003; 91: 000–00

Keywords: brain, cerebral oxygenation; children; complications, circulatory arrest; heart, resuscitation; measurement techniques, near-infrared spectroscopy


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Near-infrared spectroscopy (NIRS) is a non-invasive method to measure oxygenation in a localized tissue field and measures the transmission of infrared light through biological tissue. This indicates changes in oxygenation and the concentration of tissue chromophores such as total haemoglobin concentration (tHb) with its constituent oxygenated haemoglobin (HbO2) and deoxygenated haemoglobin (HHb) and cytochrome oxidase (CytOx), which is the terminal enzyme in the mitochondrial respiratory chain. Changes in chromophore concentrations are quantified by using the modified Lambert–Beer law.1 NIRS is becoming used in paediatric intensive care medicine to obtain real-time information on tissue oxygenation, particularly in pre-term and term neonates to investigate brain, liver and splanchnic tissue oxygenation.24

The NIRO 300 (Hamamatsu Phototonics, Japan), which uses spatially resolved spectroscopy (SRS) as an algorithm,5 6 measures a tissue oxygenation index (TOI) and a tissue haemoglobin index (THI) as absolute values without the need to know a path-length factor. TOI reflects the ratio of k x HbO2/(k x HbO2 + k x HHb) and THI reflects the denominator k x HbO2 + k x HHb, where k is an unknown but constant tissue parameter.5 TOI represents the tissue saturation and is measured in percent, whereas THI is an absolute figure of the total haemoglobin but, due to the factor k, measured in arbitrary units. As it is an absolute value, its changes from one measuring point to another can be measured as a percentage. We describe our observations on cerebral NIRS monitoring in a patient who needed CPR during cardiac catheterization.


    Case report
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 4-yr-old girl (18 kg) with an Ebstein malformation was to have diagnostic cardiac catheterization. The child suffered from increasing exertional dyspnoea and cyanosis with a transcutaneous peripheral oxygen saturation of <90%. An episode of supraventricular tachycardia was suggestive of a pre-excitation syndrome. The initial aim of NIRS recording was to investigate the effect of deep conscious sedation on cerebral oxygenation. The study was approved by the Ethics Committee of the Medical Faculty, and written informed consent was given by the parents.

The NIRS probe was placed on the forehead in the supraorbital region receiving reflected light from the frontal neocortex. The patient was given midazolam and ketamine i.v. Monitoring was by ECG and pulse oximetry. Blood pressure was measured non-invasively at intervals of 5 min. During the examination a catheter was introduced into the right atrium and through the atrial septal defect into the left atrium. This triggered a supraventricular tachycardia (heart rate=230 beats min–1). A sudden decrease in HbO2, tHb, CytOx, TOI and THI was observed. Figure 1 shows how the NIRS values changed.



View larger version (20K):
[in this window]
[in a new window]
 
Fig 1 Measurements of cerebral oxygenation data. Oxygenated (HbO2), deoxygenated (HHb) and total haemoglobin (tHb), cytochrome oxidase (CytOx) and tissue oxygenation index (TOI). Display of the full measurement (numbered dotted lines show the different events): 1=baseline with sinus rhythm (SR); 2=beginning of supraventricular tachycardia (SVT) and cardioversion (CV); 3=beginning of cardiopulmonary resuscitation (CPR); 4=ventricular fibrillation (VF) and CPR; 5=defibrillation (SVT, end of CPR); 6=cardioversion (SVT was cardioverted into SR). When low cardiac output occurred (event 2) an immediate change of intravascular oxygen was shown by a decrease in tHb, HbO2, CytOx, TOI and THI. A decrease in CytOx indicated reduced oxygen in the cell, which was reversed by CPR (event 3). All values started to normalize when spontaneous circulation was restored.

 
The NIRS output showed desaturation of the TOI from 65% to 13%, and the THI decreased from 82 to 55 arbitrary units, indicating a decrease of 33% in the total haemoglobin content in the measured area. HbO2 decreased by 37 µmol litre–1 and the HHb signal increased by 24 µmol litre–1. CytOx signal showed a rapid decrease of 1 µmol litre–1 from baseline (Fig. 1, event 2). Mean arterial pressure decrease to <20 mm Hg and peripheral pulse oximetry did not show any valid signals because of the low pulse pressure. After two unsuccessful attempts at cardioversion, ventilation and cardiac compressions were started and with an increase in HbO2, tHb, THI and CytOx, TOI values started to increase with a short latency (Fig. 1, event 3). During this time ventricular fibrillation started (Fig. 1, event 4). After 24 min of CPR, the ventricular fibrillation was stopped by defibrillation and followed by a supraventricular tachycardia (heart rate=190 beats min–1) with a mean arterial pressure of 60 mm Hg. Values for HbO2, tHb and TOI started to decline again with the beginning of tachycardia, while HHb values increased once again (Figure, event 5). The CytOx signal demonstrated slight fluctuations at a greater value compared with the baseline values before the resuscitation ({Delta}0.8 µmol litre–1). Cardioversion led to sinus rhythm and blood pressure increased to 90 mm Hg. A slight increase in HbO2 and TOI and a decline in HHb were seen (Fig. 1, event 6). CytOx signal started to decline, but NIRS monitoring was interrupted because the patient was transferred to the intensive care unit. Under therapy with propafenon no further cardiac tachyarrhythmia occurred. Corrective surgery of the congenital heart defect was carried out and the child was discharged from intensive care with no neurological deficits.


    Discussion
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
In our patient, a decrease of the NIRS values (HbO2, CxtOx, THI, TOI) was noted before the circulatory situation became apparently severe. The pulse oximeter failed to provide data on arterial saturation during the resuscitation as would be expected because of the poor signal whereas the NIRS signal changes were immediately visible. Changes in CytOx redox state are only seen when the availability of oxygen at the cellular intramitochondrial level has decreased to critical values.7 8 A decrease of CytOx correlated with a decreased brain energy state and may indicate impending cellular injury.9 The immediate decrease of intravascular cerebral oxygen differs clearly from the slow changes following circulatory arrest in deep hypothermia during corrective cardiac surgery.2

The reason for an increase in CytOx to values greater than baseline after restoration of spontaneous circulation remains unclear. A possible explanation could be the compensatory reoxygenation following an ischaemic period or the influence of mechanical ventilation with oxygen 100%.

NIRS has been studied in cardiac arrest in 18 patients arriving in an emergency department with circulatory arrest or shortly after restoration of spontaneous circulation.10 The authors reported that if regional cerebral oxygen saturation (SrO2) is small after cardiac arrest, there is a greater mortality. Recently published data11 describe cerebral oximetry in a patient with cerebral infarction and circulatory arrest, with a difference between the NIRS signals obtained from the centre of the stroke compared with the non-stroke areas. The saturation in an ischaemic area that is metabolically inactive can be normal because oxygen extraction does not occur from cerebral venous blood, which can also be from other adjacent brain regions that are perfused. Thus, the interpretation of NIRS data may be difficult in patients with cerebral stroke without the use of other imaging methods.11 Our data support observations of another report where SrO2 decreased from 60% to 41% in a patient with circulatory arrest.12 Systemic perfusion was restored with cardiopulmonary bypass and the changes during hypoxaemia were reversed. The authors inferred that NIRS might be useful to determine the effectiveness of CPR. None of the reports1012 that measured cerebral oxygenation during cardiac arrest commented on CytOx changes because they used a different transcranial NIRS monitoring system (INVOS 3100, Somanetics Inc., Troy, MI, USA). A recent study compared two different near-infrared spectrophotometers (INVOS 4100 and the NIRO 300) measuring cerebral oxygen saturation during changes of cerebral blood flow induced by carbon dioxide challenge.13 The INVOS 4100 and the NIRO 300 showed a significant linear correlation for values of SrO2 and TOI during carbon dioxide alteration, but Bland–Altman analysis14 showed that the individual values and the relative changes displayed by the two devices were not equivalent.

Discrepancies between persisting bowel desaturation measured with NIRS and short episodes of systemic desaturation were reported in neonates.15 We could not measure the circulation and systemic saturation continuously to detect differences between cerebral and systemic saturations.

Studies of the relationship between cerebral measurements with other devices and regional cerebral oxygenation measured by spatially resolved NIRS give different results.16 17 Measurements of jugular bulb oxygen saturation (SjO2) measured by co-oximetry and TOI measured by NIRO 300, do not agree well despite a statistically significant correlation.16 The NIRS cerebral monitoring measures TOI in a small region of the cerebral microvasculature, whereas SjO2 reflects a more global measurement, so inhomogeneous distribution of blood or metabolic activity will reduce the agreement between the two methods.18 In addition, the TOI signal reflects an average of arterial (25%), capillary (5%) and venous (70%) blood. Cerebral cortex haemoglobin saturation, measured directly by the spatially resolved method, reflects predominantly the saturation of the intracranial venous compartment of circulation.17 Unfortunately, we did not have other measurements of brain oxygenation in our patient to verify that the decrease in TOI represented a change in cerebral oxygen saturation. SjO2 and TOI may measure different entities, so that although there is a significant correlation between SjO2 and TOI, the two measures are not interchangeable.16

Our observations show that non-invasive cerebral NIRS measurement gives useful real-time information on cerebral oxygenation during cardiac arrest and CPR and this deserves further investigation.


    Acknowledgement
 
We thank Anne M. Gale of the Deutsches Herzzentrum Berlin for editorial assistance.


    References
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
1 Owen-Reece H, Smith M, Elwell CE, Goldstone JC. Near infrared spectroscopy. Br J Anaesth 1999; 82: 418–26[Free Full Text]

2 Abdul-Khaliq H, Troitzsch D, Schubert S, et al. Cerebral oxygen monitoring during neonatal cardiopulmonary bypass and deep hypothermic circulatory arrest. Thorac Cardiovasc Surg 2002; 50: 77–81[CrossRef][ISI][Medline]

3 Fortune PM, Wagstaff M, Petros AJ. Cerebro-splanchnic oxygenation ratio (CSOR) using near infrared spectroscopy may be able to predict splanchnic ischaemia in neonates. Intensive Care Med 2001; 27: 1401–7[CrossRef][ISI][Medline]

4 Schulz G, Weiss M, Bauersfeld U, et al. Liver tissue oxygenation as measured by near-infrared spectroscopy in the critically ill child in correlation with central venous oxygen saturation. Intensive Care Med 2002; 28: 184–9[CrossRef][ISI][Medline]

5 Suzuki S, Takasaki S, Ozaki T, Kobayashi Y. A tissue oxygenation monitor using NIR spatially resolved spectroscopy. Proc SPIE 1999; 3579: 144–5

6 Matcher SJ, Kirkpatrick P, Nahid K, Cope M, Delpy DT. Absolute quantification methods in tissue near infrared spectroscopy. Proc SPIE 1995; 2389: 486–95

7 Hoshi Y, Hazeki O, Kakihana Y, Tamura M. Redox behavior of cytochrome oxidase in the rat brain measured by near-infrared spectroscopy. J Appl Physiol 1997; 83: 1842–8[Abstract/Free Full Text]

8 Ferrari M, Williams MA, Wilson DA, Thakor NV, Traystman RJ, Hanley DF. Cat brain cytochrome-c oxidase redox changes induced by hypoxia after blood-fluorocarbon exchange transfusion. Am J Physiol 1995; 269: H417–24[ISI][Medline]

9 Tsuji M, Naruse H, Volpe J, Holtzman D. Reduction of cytochrome aa3 measured by near-infrared spectroscopy predicts cerebral energy loss in hypoxic piglets. Pediatr Res 1995; 37: 253–9[Abstract]

10 Mullner M, Sterz F, Binder M, Hirschl MM, Janata K, Laggner AN. Near infrared spectroscopy during and after cardiac arrest—preliminary results. Clin Intensive Care 1995; 6: 107–11[Medline]

11 Nemoto EM, Yonas H, Kassam A. Clinical experience with cerebral oximetry in stroke and cardiac arrest. Crit Care Med 2000; 28: 1052–4[ISI][Medline]

12 Pilkington SN, Hett DA, Pierce JM, Smith DC. Auditory evoked responses and near infrared spectroscopy during cardiac arrest. Br J Anaesth 1995; 74: 717–19[Abstract/Free Full Text]

13 Yoshitani K, Kawaguchi M, Tatsumi K, Kitaguchi K, Furuya H. A comparison of the INVOS 4100 and the NIRO 300 near-infrared spectrophotometers. Anesth Analg 2002; 94: 586–90[Abstract/Free Full Text]

14 Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986; 1: 307–10[ISI][Medline]

15 Petros AJ, Heys R, Tasker RC, Fortune PM, Roberts I, Kiely E. Near infrared spectroscopy can detect changes in splanchnic oxygen delivery in neonates during apnoeic episodes. Eur J Pediatr 1999; 158: 173–4[CrossRef][ISI][Medline]

16 Ali MS, Harmer M, Vaughan RS, Dunne JA, Latto IP. Spatially resolved spectroscopy (NIRO-300) does not agree with jugular bulb oxygen saturation in patients undergoing warm bypass surgery. Can J Anaesth 2001; 48: 497–501[Abstract/Free Full Text]

17 Quaresima V, Sacco S, Totaro R, Ferrari M. Noninvasive measurement of cerebral hemoglobin oxygen saturation using two near infrared spectroscopy approaches. J Biomed Opt 2000; 5: 201–5[CrossRef][ISI][Medline]

18 Brown R, Wright G, Royston D. A comparison of two systems for assessing cerebral venous oxyhaemoglobin saturation during cardiopulmonary bypass in humans. Anaesthesia 1993; 48: 697–700[ISI][Medline]





This Article
Abstract
Full Text (PDF)
E-Letters: Submit a response to the article
Alert me when this article is cited
Alert me when E-letters are posted
Alert me if a correction is posted
Services
Email this article to a friend
Similar articles in this journal
Similar articles in ISI Web of Science
Similar articles in PubMed
Alert me to new issues of the journal
Add to My Personal Archive
Download to citation manager
Search for citing articles in:
ISI Web of Science (3)
Disclaimer
Request Permissions
Google Scholar
Articles by Nagdyman, N.
Articles by Lange, P. E.
PubMed
PubMed Citation
Articles by Nagdyman, N.
Articles by Lange, P. E.