Resuscitation 84 (2013) 16431644

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Resuscitation
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Editorial

Non-invasive monitoring during cardiac arrest: NIRS has potential but data remain limited

It is of no surprise there is on-going interest in near infrared spectrometry (NIRS) as a method of non-invasive hemodynamic monitoring during resuscitation of cardiac arrest. Other noninvasive measures of perfusion in shock include cerebral perfusion pressure, mixed venous oxygenation and partial pressure of end tidal carbon dioxide. They each have signicant limitations. Yet, the hope is that cerebral oximetry will ll a gap among these non-invasive tools and provide a real-time, reliable, and accurate method of assessing cerebral perfusion. Given the literature examining and describing its usefulness as a tool for monitoring tissue perfusion, and thus cardiac output, during cardiac surgery, shock, trauma, among others,1 NIRS is ripe for study in the cardiac arrest population. The application of NIRS has been shown to be feasible.24 The signicance of initial and peak values has been previously explored and remains uncertain.5,6 The trend in NIRS values has been suggested as an ominous sign, heralding initial or re-arrest.3,6 Yet, the time to recovery of NIRS values after return of spontaneous circulation (ROSC) may be signicantly delayed despite well-controlled resuscitative measures.7 Thus, while we read Ahn et al. with enthusiasm, it yields limited additional insight into the application of regional cerebral oxygen saturation monitoring (rSO2 ) in the peri-arrest period.8 The study by Ahn et al. has a straightforward design.8 It includes both out-of-hospital and in-hospital patients, although more were in-hospital and male. The prospective intervention was the use of a cerebral oximetry device, applied to the forehead of each patient as early as possible during resuscitation. Unfortunately, there was signicant variation in time to placement of the censor for patients in the study population, and no data on time from placement to ROSC or cessation of resuscitation are presented. By reporting the mean rSO2 values, the authors accomplish three goals. They conrm previous evidence that the mean rSO2 is higher among those who have ROSC and the physiologic basis for this technology as a measurement of cerebral perfusion has merit.2 The authors also provide more data to support the observation of a change in rSO2 among cardiac arrest patients undergoing CPR who obtain ROSC. There is, to date, conicting evidence on how substantial this difference is.2,6 Lastly, the authors investigate the question that makes their study novel: whether there is an rSO2 mean difference among patients presenting with different types of initial cardiac arrest rhythms. The evidence suggests a relationship between presenting rhythm and rSO2 . We agree with the limitations described by the authors: small subpopulations, no control over time to placement of device, lack of Utstein data, exclusion of patients with early ROSC, and the
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examination of both in-hospital and out-of-hospital populations.8 However, we suggest there is also a paucity of data provided on the dynamic nature of rSO2 as a measure of perfusion. It is well known that the trend in rSO2 is often more useful than the single mean value.2,3,6,9 While the study did nd that the patients with ROSC had a signicantly higher mean rSO2 [over the resuscitation period] than those without, we gain little insight into the value of peak rSO2 prior to ROSC; trends in rSO2 leading to ROSC; rate of rSO2 change leading to or following ROSC; or peak rSO2 after ROSC.8 Researchers with an interest in investigating cerebral oximetry as a tool for resuscitation might learn from the early experience with end-tidal CO2 . The relationships between ETCO2 , cardiac output,1012 and type of cardiac arrest13,14 have been extensively studied in both animals and humans. ETCO2 has also been wellstudied as a measure of quality resuscitation and a marker for predicting ROSC.15 A few early studies are particularly noteworthy. Garnett et al. evaluated continuous ETCO2 monitoring while holding both ventilation and automated CPR constant.16 They observed a signicant rise in ETCO2 in those patients who achieved ROSC. Gazmuri et al. demonstrated the changes in ETCO2 in a model incorporating extracorporeal circulation for refractory cardiac arrest.17 After initiation of support, ETCO2 slowly began to rise. All subjects were successfully weaned from the pump only after ETCO2 exceeded 15 mmHg. Future studies using cerebral oximetry can be similarly designed to investigate trends in rSO2 , its relationship to ROSC, and variation among presenting rhythms. The relationship between CPR quality and cerebral oximetry bears mention. This study proposes that it provides evidence of the relationship between CPR quality and cerebral oximetry.8 After close examination, there is no subjective or objective measure of CPR quality provided in the introduction, methods or results. Additionally, with the lack of dynamic data for rSO2 , it is difcult to conclude that rSO2 is an effective measure of CPR quality. Cerebral oximetry has been previously assessed during cardiac arrest while controlling the quality of cardiopulmonary resuscitation.9,18 Ultimately, having a better understanding of the dynamic nature of rSO2 , as well as what might inuence NIRS accuracy (i.e. hemoglobin level, mitochondrial dysfunction19,20 ), is necessary prior to concluding that rSO2 may be a viable treatment target or a marker of cardiac arrest resuscitation quality and/or futility. With these limitations, the study is quite intriguing and further advances the conversation on the utility of cerebral oximetry during cardiac arrest. At the bleeding edge of cerebral oximetry, ambiguities persist. We humbly submit the following inquiries:

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Editorial / Resuscitation 84 (2013) 16431644 9. Kamarainen A, Sainio M, Olkkola KT, et al. Quality controlled manual chest compressions and cerebral oxygenation during in-hospital cardiac arrest. Resuscitation 2012;83:13842. 10. Ornato JP, Garnett AR, Glauser FL. Relationship between cardiac output and the end-tidal carbon dioxide tension. Ann Emerg Med 1990;19:11046. 11. Weil MH, Bisera J, Trevino RP, Rackow EC. Cardiac output and end-tidal carbon dioxide. Crit Care Med 1985;13:9079. 12. Morimoto Y, Kemmotsu O, Murakami F, Yamamura T, Mayumi T. End-tidal CO2 changes under constant cardiac output during cardiopulmonary resuscitation 1993;21:15726. 13. Berg RA, Henry C, Ottow CW, et al. Initial end-tidal CO2 is markedly elevated during cardiopulmonary resuscitation after asphxial cardiac arrest. Pediatr Emerg Care 1996;12:2458. 14. Lah K, Krizmaric M, Grmec S. The dynamic pattern of end-tidal carbon dioxide during cardiopulmonary resuscitation: difference between asphyxial cardiac arrest and ventricular brillation/pulseless ventricular tachycardia cardiac arrest. Crit Care 2011;15:R13. 15. Sanders AB, Kern KB, Otto CW, Milander MM, Ewy GA. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation: a prognostic indicator for survival. JAMA 1989;262:134751. 16. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA 1987;257:5125. 17. Gazmuri RJ, Weil MH, Bisera J, Rackow EC. End-tidal carbon dioxide tension as a monitor of native blood ow during resuscitation by extracorporeal circulation. J Thoracic Cardiovasc Surg 1991;101:9848. 18. Koyama Y, Wada T, Lohman BD, et al. A new method to detect cerebral blood ow waveform in synchrony with chest compression by near-infrared spectroscopy during cardiopulmonary resuscitation. Am J Emerg Med 2013;19. 19. Kishi K, Kawaguchi M, Yoshitani K, et al. Inuence of patient variables and sensor location on regional cerebral oxygen saturation measured by INVOS 4100 near-infrared spectrophotometers. J Neurosurg Anesthesiol 2003;15: 3026. 20. Ward KR, Ivatury RR, Barbee RW, et al. Near infrared spectroscopy for evaluation of the trauma patient: a technology review. Resuscitation 2006;68: 2744.

- What is the relationship between NIRS and non-Utstein predictors of cardiac arrest outcome such as total ischemic time? - Can NIRS target specic areas of hypoperfusion, i.e. the hippocampus, which matters more than the frontal lobe? - How far away are we from cerebral oximetry to be used as a marker for futility of continued resuscitation efforts? - How do cerebral oximetry values for quality of resuscitation match end tidal carbon dioxide values? - If we identify that the best outcomes are associated with higher peak and early sustained rSO2 values, is this evidence for emergency cardiopulmonary bypass (ECPB) in the ED? As we search for a viable, real-time therapeutic target that is both easy to use and reliable, we must explore each of these technologies that hold promise. The next steps for elucidating the clinical importance of NIRS remain. Conict of interest statement No conicts of interest to declare. References
1. Cohn SM. Near-infrared spectroscopy: potential clinical benets in surgery. J Am Coll Surg 2007;205:32232. 2. Parnia S, Nasir A, Shah C, et al. A feasibility study evaluating the role of cerebral oximetry in predicting return of spontaneous circulation in cardiac arrest. Resuscitation 2012;83:9825. 3. Frisch A, Suffoletto BP, Frank R, et al. Potential utility of near-infrared spectroscopy in out-of-hospital cardiac arrest: an illustrative case series. Prehosp Emerg Care 2012;16:56470. 4. Newman DH, Callaway CW, Greenwald IB, et al. Cerebral oximetry in out-ofhospital cardiac arrest: standard CPR rarely provides detectable hemoglobinoxygen saturation to the frontal cortex. Resuscitation 2004;63:18994. 5. Ito N, Nanto S, Nagao K, Hatanaka T, Kai T. Regional cerebral oxygen saturation predicts poor neurological outcome in patients with out-of-hospital cardiac arrest. Resuscitation 2010;81:17367. 6. Meex I, De Deyne C, Dens J, et al. Feasibility of absolute cerebral tissue oxygen saturation during cardiopulmonary resuscitation. Crit Care 2013;17:R36. 7. Reynolds JC, Salcido D, Koller AC, et al. Tissue oximetry by near-infrared spectroscopy in a porcine model of out-of-hospital cardiac arrest and resuscitation. Resuscitation 2012;84:8437. 8. Ahn A, Nasir A, Malik H, et al. A pilot study examining the role of regional cerebral oxygen saturation monitoring as a marker of return of spontaneous circulation in shockable (VF/VT) and non-shockable (PEA/Asystole) causes of cardiac arrest. Resuscitation 2013;84:17136.

Teresa Camp-Rogers University of Texas at Houston, United States Kelly N. Sawyer (MD, MS) Oakland University William Beaumont School of Medicine, United States author. E-mail address: tcamprogers@gmail.com (T. Camp-Rogers) 16 September 2013
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