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CPR cardiopulmonary resuscitation or cerebral perfusion restoration
Resuscitation 83 (2012) 925
Contents lists available at SciVerse ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Editorial
CPR cardiopulmonary resuscitation or cerebral perfusion restoration It has long been recognised that following cardiac arrest, cerebral oxygenation falls rapidly. The brain is a metabolically highly active organ and cell death begins after only a few minutes of anoxia.1 The main mode of death following resuscitation from cardiac arrest remains neurological death.2 Recent guidelines have stressed the importance of continuous chest compressions in order to maintain coronary perfusion pressure.3 This has led towards a greater emphasis on the use of supraglottic airway devices (SADs) to manage the airway in order to minimise interruptions in chest compressions. A paper in this edition of resuscitation shows that in a swine model, inflation of a SAD causes impairment in carotid artery blood flow.4 This has been shown with a number of different devices all of which have inflatable cuffs. There are obvious limitations in being a swine model, but it is already known that SADs reduce carotid blood flow in anaesthetised humans so the effects are probably translatable.5 In addition the use of epinephrine during CPR can further reduce carotid blood flow.6 This leads to the very real concern that recent changes in the management of cardiac arrest will lead to an increased number of survivors but those survivors will be in a poor neurological condition. Should the management of cardiac arrest then be aimed primarily at minimising neurological damage during resuscitation? Advances such as extracorporeal life support and prehospital cooling of patients would suggest that this may be the direction to go. The concept of CPR as cerebral perfusion restoration as opposed to trying to maximise coronary perfusion. So the pendulum may be swinging again in favour of brain focussed resuscitation potentially at the expense of coronary perfusion. The concept of focussing resuscitation on the brain is not new, we have attempted abdominal binding and leg raises to improve cerebral blood flow for over twenty years.7 These techniques however have never translated into an improved outcome for patients.8 Then if we were to utilise only level one evidence in cardiac arrest management then we would have little in our armoury. What is concerning considering the amount of healthcare resource that is used in the management of cardiac arrest, is how little is known regarding the incidence of carotid disease as either a cause or an incidental finding following cardiac arrest. Carotid disease has a high incidence in patients with coronary artery disease reported as high as 40% and in these patients there is a higher incidence of myocardial events even following revascularisation.9 It is highly likely therefore that patients following cardiac arrest are at high risk of impaired carotid blood flow even with adequate cardiac output. Further impairing that flow with SADs and epinephrine could have serious consequences. The reasons for the large variations in neurological outcome following cardiac arrest remain unclear, and it is entirely plausible that altered cerebral blood flow is a factor in this. 0300-9572/$ – see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.resuscitation.2012.05.002
Further research into the effects of SADs on carotid blood flow is required. It would be useful to know if devices with no inflatable cuffs such as the iGEL (Intersurgical, Wokingham, UK) have the same potential to cause alterations in blood flow. It is also important to understand if the reductions in carotid blood flow are associated with reduced cerebral blood flow or if there is compensation via the vertebral arteries. One of the most important issues that this paper points to is the ultimate outcomes we are aiming for in the management of cardiac arrest. Long term good neurological outcome has to be the ultimate focus of all clinicians involved in resuscitation, and it is reassuring that this has been recognised in the recommended outcomes of resuscitation trials.10 1. Conflict of interest We report no conflict of interest. References 1. Lipton P. Ischemic cell death in brain neurons. Physiol Rev 1999;79:1431–568. 2. Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med 2004;30:2126–8. 3. Lim SH, Shuster M, Deakin CD, et al. Part 7: CPR techniques and devices: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2010;81(Suppl. 1), e86–92. 4. Segal N, Yannopoulos D, Mahoney BD, et al. Impairment of carotid artery blood flow by supraglottic airway use in a swine model of cardiac arrest. Resuscitation 2012;83:1025–30. 5. Colbert SA, O’Hanlon DM, Flanagan F, Page R, Moriarty DC. The laryngeal mask airway reduces blood flow in the common carotid artery bulb. Can J Anaesth 1998;45:23–7. 6. Burnett AM, Segal N, Salzman JG, McKnite MS, Frascone RJ. Potential negative effects of epinephrine on carotid blood flow and ETCO(2) during active compression-decompression CPR utilizing an impedance threshold device. Resuscitation 2012;83:1021-4. 7. Koehler RC, Chandra N, Guerci AD, et al. Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs. Circulation 1983;67:266–75. 8. Koster RW, Sayre MR, Botha M, et al. Part 5: Adult basic life support: 2010 International consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation 2010;81(Suppl. 1), e48–70. 9. Komorovsky R, Desideri A. Carotid ultrasound assessment of patients with coronary artery disease: a useful index for risk stratification. Vasc Health Risk Manag 2005;1:131–6. 10. Becker LB, Aufderheide TP, Geocadin RG, et al. Primary outcomes for resuscitation science studies. Circulation 2011;124:2158–77.
Matt Thomas ∗ R. Jonathan Hadfield Intensive Care Unit, University Hospitals Bristol,UK ∗ Corresponding
author. E-mail address: [email protected] (M. Thomas) 8 May 2012
Contents lists available at SciVerse ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Editorial
CPR cardiopulmonary resuscitation or cerebral perfusion restoration It has long been recognised that following cardiac arrest, cerebral oxygenation falls rapidly. The brain is a metabolically highly active organ and cell death begins after only a few minutes of anoxia.1 The main mode of death following resuscitation from cardiac arrest remains neurological death.2 Recent guidelines have stressed the importance of continuous chest compressions in order to maintain coronary perfusion pressure.3 This has led towards a greater emphasis on the use of supraglottic airway devices (SADs) to manage the airway in order to minimise interruptions in chest compressions. A paper in this edition of resuscitation shows that in a swine model, inflation of a SAD causes impairment in carotid artery blood flow.4 This has been shown with a number of different devices all of which have inflatable cuffs. There are obvious limitations in being a swine model, but it is already known that SADs reduce carotid blood flow in anaesthetised humans so the effects are probably translatable.5 In addition the use of epinephrine during CPR can further reduce carotid blood flow.6 This leads to the very real concern that recent changes in the management of cardiac arrest will lead to an increased number of survivors but those survivors will be in a poor neurological condition. Should the management of cardiac arrest then be aimed primarily at minimising neurological damage during resuscitation? Advances such as extracorporeal life support and prehospital cooling of patients would suggest that this may be the direction to go. The concept of CPR as cerebral perfusion restoration as opposed to trying to maximise coronary perfusion. So the pendulum may be swinging again in favour of brain focussed resuscitation potentially at the expense of coronary perfusion. The concept of focussing resuscitation on the brain is not new, we have attempted abdominal binding and leg raises to improve cerebral blood flow for over twenty years.7 These techniques however have never translated into an improved outcome for patients.8 Then if we were to utilise only level one evidence in cardiac arrest management then we would have little in our armoury. What is concerning considering the amount of healthcare resource that is used in the management of cardiac arrest, is how little is known regarding the incidence of carotid disease as either a cause or an incidental finding following cardiac arrest. Carotid disease has a high incidence in patients with coronary artery disease reported as high as 40% and in these patients there is a higher incidence of myocardial events even following revascularisation.9 It is highly likely therefore that patients following cardiac arrest are at high risk of impaired carotid blood flow even with adequate cardiac output. Further impairing that flow with SADs and epinephrine could have serious consequences. The reasons for the large variations in neurological outcome following cardiac arrest remain unclear, and it is entirely plausible that altered cerebral blood flow is a factor in this. 0300-9572/$ – see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.resuscitation.2012.05.002
Further research into the effects of SADs on carotid blood flow is required. It would be useful to know if devices with no inflatable cuffs such as the iGEL (Intersurgical, Wokingham, UK) have the same potential to cause alterations in blood flow. It is also important to understand if the reductions in carotid blood flow are associated with reduced cerebral blood flow or if there is compensation via the vertebral arteries. One of the most important issues that this paper points to is the ultimate outcomes we are aiming for in the management of cardiac arrest. Long term good neurological outcome has to be the ultimate focus of all clinicians involved in resuscitation, and it is reassuring that this has been recognised in the recommended outcomes of resuscitation trials.10 1. Conflict of interest We report no conflict of interest. References 1. Lipton P. Ischemic cell death in brain neurons. Physiol Rev 1999;79:1431–568. 2. Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med 2004;30:2126–8. 3. Lim SH, Shuster M, Deakin CD, et al. Part 7: CPR techniques and devices: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2010;81(Suppl. 1), e86–92. 4. Segal N, Yannopoulos D, Mahoney BD, et al. Impairment of carotid artery blood flow by supraglottic airway use in a swine model of cardiac arrest. Resuscitation 2012;83:1025–30. 5. Colbert SA, O’Hanlon DM, Flanagan F, Page R, Moriarty DC. The laryngeal mask airway reduces blood flow in the common carotid artery bulb. Can J Anaesth 1998;45:23–7. 6. Burnett AM, Segal N, Salzman JG, McKnite MS, Frascone RJ. Potential negative effects of epinephrine on carotid blood flow and ETCO(2) during active compression-decompression CPR utilizing an impedance threshold device. Resuscitation 2012;83:1021-4. 7. Koehler RC, Chandra N, Guerci AD, et al. Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs. Circulation 1983;67:266–75. 8. Koster RW, Sayre MR, Botha M, et al. Part 5: Adult basic life support: 2010 International consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation 2010;81(Suppl. 1), e48–70. 9. Komorovsky R, Desideri A. Carotid ultrasound assessment of patients with coronary artery disease: a useful index for risk stratification. Vasc Health Risk Manag 2005;1:131–6. 10. Becker LB, Aufderheide TP, Geocadin RG, et al. Primary outcomes for resuscitation science studies. Circulation 2011;124:2158–77.
Matt Thomas ∗ R. Jonathan Hadfield Intensive Care Unit, University Hospitals Bristol,UK ∗ Corresponding
author. E-mail address: [email protected] (M. Thomas) 8 May 2012