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EDITORIAL Table of Contents   
Year : 2009  |  Volume : 12  |  Issue : 2  |  Page : 101-103
Therapeutic hypothermia after cardiac arrest in cardiac surgery: A meaningful pursuit?

Department of Anesthesia, Critical Care and Pain Relief, Wockhardt Hospitals, Bannerghatta Road, Bangalore-560 076, India

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Date of Web Publication21-Jul-2009

How to cite this article:
Chakravarthy M. Therapeutic hypothermia after cardiac arrest in cardiac surgery: A meaningful pursuit?. Ann Card Anaesth 2009;12:101-3

How to cite this URL:
Chakravarthy M. Therapeutic hypothermia after cardiac arrest in cardiac surgery: A meaningful pursuit?. Ann Card Anaesth [serial online] 2009 [cited 2021 Sep 28];12:101-3. Available from:

The return of spontaneous circulation (ROSC) following resuscitation of cardiac arrest may not assure a successful cerebral resuscitation. Anxiety about the cerebral status after ROSC is common as current investigative modalities do not aid clinicians in predicting cerebral outcome. Despite inadequate evidence regarding outcome, clinicians try 'neuroprotective' treatment in a desperate attempt to 'do something'. To combat the above, therapeutic hypothermia (TH) seems to be a step in the right direction. Oddly, despite the short term benefits of TH, the practice does not seem to have caught on in cardiac surgical units.

The American Heart Association has set up an advanced life support task force of the international liaison committee on resuscitation (ILCOR) to issue a statement on TH after ROSC. The advisory statement on TH published by ILCOR seems to have (re)kindled interest among clinicians. [1] In the early 1950s, mild to moderate hypothermia was commonly used to protect the brain against global ischemia that occurred as a consequence of some open-heart surgeries. However, it was subsequently abandoned due to uncertainty of the benefits and difficulties with its use. [2],[3],[4] Following these practices, Hicks reported beneficial effects of hypothermia after cardiac arrest due to asphyxia. [5] The period from early 1990s to recent years saw several promising human studies providing lucid evidence of the utility of TH after ROSC. [6],[7],[8],[9] The results of a prospective randomized study by an Australian group in 2002, seemed to provide clinicians with more answers and an enhanced acceptance of this technique. [10] In this study, 49 percent of patients who received TH survived in comparison to 26 percent who did not. These numbers are significant keeping in mind that the hypothermia group had a greater chance of developing complications such as arrhythmias, infection, and coagulopathy.[10] Mechanisms causing benefits during TH are unknown; however, hypothermia per se reduces the cerebral oxygen requirement by six percent for every 1°C reduction in brain temperature.[11] Such a reduction in oxygen requirement might obviously encourage brain function recovery. The ILCOR statement further states that, "mild hypothermia is thought to suppress many of the chemical reactions associated with reperfusion injury. These reactions include free radical production, excitatory amino acid release, and calcium shifts, which can in turn lead to mitochondrial damage and apoptosis". [1] Mild hypothermia may also diminish oxidative deoxyribonucleic acid (DNA) damage and pro-death signaling events after cerebral ischemia and this may be yet another mechanism of cerebral protection. [12]

There seems to be a level 1 evidence for use of TH in ROSC following out-of-hospital cardiac arrest due to ventricular fibrillation, while there is weaker evidence (level 2) about patients who had cardiac arrest due to other reasons.[6] The outcome of using this technique is superior in cardiac arrest due to ventricular fibrillation (implying normal neurovascular tree and brain prior to cardiac arrest) than ROSC after either traumatic brain injury or cerebrovascular accidents. Since most post operative cardiac arrests in cardiac surgical units are due to ventricular fibrillation or cardiac asystole, benefits from the use of TH in hemodynamically stable patients appear realistic. However, the literature on this topic

(in cardiac surgical patients) is sketchy and a conclusion that hypothermia is not commonly practiced by the cardiac surgical units may be drawn without much prejudice. A case report of favourable outcome in a patient after ROSC after a cardiac arrest resulting from pulmonary embolism, adds value to the thought that cardiac surgical units should be practicing TH more often.[13] On the other hand, it has been suggested that until further evidence is available, TH should not be used in patients with severe cardiogenic shock or life-threatening arrhythmias, pregnant patients, or patients with primary coagulopathy even though thrombolytic therapy itself may not preclude patients from receiving this therapy. [1]

The outcome in pediatric patients is also not clear; however, Gunn et al. , are of the opinion that only a sub-sect of babies benefit from this procedure. [14] According to most authors, cooling should be instituted as early as possible after ROSC, but a delay of four to six hours has not been found to alter the outcome significantly. [10] Topical and core cooling by various techniques (such as application of ice packs, cold towels, infusion of cold intravenous fluids, instillation of cold solutions in the peritoneum and pleura) have been tried, but none seem to be ideal. It is important that further in-vivo studies be conducted to define the therapeutic window within which prolonged hypothermia is optimally neuro-protective after cardiac arrest. [15] Techniques to cool patients rapidly are not available to clinicians yet; and their availability may notably alter the outcome and it is reasonable to believe that such methods would be for the better than trying therapies of dubious outcomes. Profound neuromuscular block is necessary to prevent shivering, which might cause rewarming of the patient. Currently esophageal and middle ear temperatures are used as surrogates to brain temperature for want of more appropriate sites. Commonly, temperatures of 34 to 35° C are acceptable in cardiac surgical patients, while temperatures below those could potentiate an environment conducive for arrhythmogenecity. There are still several questions regarding TH - the site to accurately monitor the brain temperature, the degree and duration of cooling, time and speed of rewarming, and metabolic management of patients during hypothermia, which can only be answered by frequent use after ROSC.

As stated before, short term beneficial effects of TH have been shown by many authors but long term benefits may be known only after further work. [16] Despite lack of knowledge of long term benefits, the use of TH can be encouraged after ROSC in cardiac surgical settings considering that there are no other more advantageous treatment options available. Despite the conspicuous absence of publications from cardiac surgical units, it would be simple for the cardiac surgical teams to produce TH after ROSC, as they are already familiar with various aspects of hypothermia and rewarming. Additionally, the easy availability of the heating-cooling machine will make it easier to institute hypothermia and rewarming. It would be best if cardiac surgical teams set up protocols to engage their teams in providing TH for patients who have reasonable hemodynamics after ROSC. There is a recent trend among a few cardiac anesthesiologists to terminate cardiopulmonary bypass at a slightly hypothermic temperature with a view to decrease the neurological complications. [17] The other editorial in this issue touches upon those issues. [18] This may be a nascent step towards TH. In conclusion, it seems that TH may not only improve the outcome but also contribute to the global data on the subject.

   References Top

1.Nolan JP, Morley PT, Vanden Hoek TL. Therapeutic hypothermia after cardiac arrest: An advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation. Circulation 2003;108:118-21.  Back to cited text no. 1    
2.Williams GR, Spencer FC. The clinical use of hypothermia following cardiac arrest. Ann Surg 1958;148:462-8.  Back to cited text no. 2    
3.Ravitch MM, Lane RR, Safar P, Steichen FM, Knowles P. Lightning strike: Report of a case with recovery after cardiac massage and prolonged artificial respiration. N Engl J Med 1961;264:36-8.  Back to cited text no. 3    
4.Marion DW, Leonov Y, Ginsberg M, Katz LM, Kochanek PM, Lechleuthner A, et al . Resuscitative hypothermia. Crit Care Med 1996;24:81S-9S.  Back to cited text no. 4    
5.Hicks SD, DeFranco DB, Callaway CW. Hypothermia during reperfusion after asphyxial cardiac arrest improves functional recovery and selectively alters stress-induced protein expression. J Cereb Blood Flow Metab 2000; 20:520-30.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Bernard SA, Jones BM, Horne MK. Clinical trial of induced hypothermia in comatose survivors of out-of-hospital cardiac arrest. Ann Emerg Med 1997;30:146-53.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Zeiner A, Holzer M, Sterz F, Behringer W, Schφrkhuber W, Müllner M, et al . Mild resuscitative hypothermia to improve neurological outcome after cardiac arrest: A clinical feasibility trial. Hypothermia after Cardiac Arrest (HACA) Study Group. Stroke 2000;31:86-94.  Back to cited text no. 7    
8.Felberg RA, Krieger DW, Chuang R, Persse DE, Burgin WS, Hickenbottom SL, et al . Hypothermia after cardiac arrest: Feasibility and safety of an external cooling protocol. Circulation 2001;104:1799-804.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Callaway CW, Tadler SC, Katz LM, Lipinski CL, Brader E. Feasibility of external cranial cooling during out-of-hospital cardiac arrest. Resuscitation 2002;52:159-65.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549-56.  Back to cited text no. 10    
11.Keller E, Steiner T, Fandino J, Schwab S, Hacke W. Changes in cerebral blood flow and oxygen metabolism during moderate hypothermia in patients with severe middle cerebral artery infarction. Neurosurg Focus 2000;8:e4.  Back to cited text no. 11    
12.Ji X, Luo Y, Ling F, Stetler RA, Lan J, Cao G, et al . Mild hypothermia diminishes oxidative DNA damage and pro-death signaling events after cerebral ischemia: A mechanism for neuroprotection. Front Biosci 2007;12:1737-47.  Back to cited text no. 12  [PUBMED]  
13.Bartels M, Tjan DH, Reussen EM, van Zanten AR. Therapeutic hypothermia after prolonged cardiopulmonary resuscitation for pulseless electrical activity. Neth J Med 2007;65:38-41.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Gunn AJ, Thoresen M. Hypothermic neuroprotection. NeuroRx 2006;3:154-69.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Lawrence EJ, Dentcheva E, Curtis KM, Roberts VL, Siman R, Neumar RW. Neuroprotection with delayed initiation of prolonged hypothermia after in vitro transient global brain ischemia. Resuscitation 2005;64:383-8.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]
16.Holzer M, Bernard SA, Hachimi-Idrissi S, Roine RO, Sterz F, Müllner M; et al . Hypothermia for neuroprotection after cardiac arrest: Systematic review and individual patient data meta-analysis. Crit Care Med 2005;33:414-8.  Back to cited text no. 16    
17.Sahu B, Chauhan S, Kiran U, Bisoi A, Ramakrishnan L, Nehra A. Neuropsychological function in children with cyanotic heart disease undergoing corrective cardiac surgery: Effect of two different rewarming strategies. Eur J Cardiothorac Surg 2009;35:505-10.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]
18.Chauhan S. Brain, cardiopulmonary bypass and temperature: What should we be doing?. Ann Card Anaesth 2009;12:104-6.  Back to cited text no. 18    

Correspondence Address:
Murali Chakravarthy
Department of Anesthesia, Critical Care and Pain Relief, Wockhardt Hospital, Bangalore
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.53426

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