| Home | E-Submission | Sitemap | Contact us |  
International Journal of Arrhythmia 2014;15(4): 4-13.
Electrocardiographic Features of
Therapeutic Hypothermia


   Therapeutic hypothermia (TH) has emerged as an important adjunctive therapy of cardiac arrest victims recommended by the international resuscitation guidelines.1,2 The positive effects on improvement in neurologic function and survival have been proved in two recent trials.3,4 Characteristic electrocardiographic (ECG) changes occur in patients with hypothermia. The J wave, also known as the Osborn wave, is the most characteristic ECG feature in hypothermia.5 The J wave is also noted in certain non-hypothermic conditions such as Brugada syndrome and early repolarization syndromes (ERS). The presence of J waves in such syndromes is related to the occurrence of ventricular fibrillation (VF), leading to sudden death. However, whether hypothermic patients with J waves are susceptible to fatal ventricular arrhythmia remains undetermined. Previous reports have shown that the incidence of ventricular arrhythmia is unexpectedly low in hypothermic patients with J waves, varying from 0% to 2%.6-8
   In the present study, we investigated electrocardiographic changes induced by TH and the possible arrhythmogenic potential of the TH-induced J waves.


Study Design

   During the study period from August 2010 to August 2013, 68 patients underwent TH after return of spontaneous circulation. The patients' medical records were reviewed to evaluate clinical characteristics such as age, sex, vital signs, cause of arrest, initial rhythm, and ECG findings on admission. To achieve the assigned temperature as rapidly as possible, ice-cold fluids and surface temperature-management devices (ARCTIC SUN®Temperature Management System, BARD Medical, CO) were utilized. The following recommendations were made: cool unconscious patients to 33℃ within 12 hours post-restoration of spontaneous circulation; achieve the desired patient temperature as rapidly as possible; maintain the target temperature for 24 hours; rewarm gradually to 36.5℃ in hourly increments of 0.1-0.25℃/h; and maintain normothermia of ~37.5℃ after rewarming. We compared the clinical characteristics and basic ECG parameters of patients with and without J waves. The study protocol was reviewed and approved by the Ethics Committee of the College of Medicine, Ulsan University.

ECG Analysis

   The following ECG parameters were analyzed: heart rate, PR interval, duration of the QRS complex, and QT and QTc intervals. J wave was defined as notches or slurs in the terminal part of the QRS complex with an amplitude ≥0.1 mV above the isoelectric line in at least 2 contiguous leads.9 The J-wave amplitude was measured as the difference between the top of the J wave and the isoelectric line using Cardio Calipers (On-Screen Electrocardiogram Measurement) from Iconico.com. For the comparison of the distribution of J wave, ECG lead areas were grouped as right precordial (V1-3), left precordial (V4-6), high lateral (I, aVL), and inferior (II, III, and aVF).

Statistical Analysis

   All statistical analyses were performed with SPSS software (SPSS Inc., Chicago, IL). Categorical variables were analyzed by the χ2 test. Continuous variables were analyzed by the t-test. A P value <0.05 was regarded as significant.


Clinical Characteristics

   A total of 68 patients (mean age, 59.8±1.7 years; 42 male) who underwent TH were analyzed. The mean body temperature on TH was 33.3±0.1℃. J waves were observed in 40 patients during TH. J waves were newly developed in 37 patients and preexisting J waves were augmented in three patients. Two patients with ERS and a patient with alcoholic ketoacidosis displayed preexisting J waves on 12 lead ECG prior to TH. Figure 1 displays representative examples of J waves recorded during TH. A patient with ERS had prominent J waves compared to a patient with non-cardiogenic arrest.
   Clinical and ECG characteristics are presented in Table 1. There were no significant differences between patients with and without J waves in terms of age, sex, temperature achieved during TH and ECG parameters.

ECG Changes Observed during TH

   ECG tracings were assessed for the presence of TH-induced electrocardiographic changes. A consistent reduction in heart rate from 102±29 to 86±23 beats/min (15.4% reduction, p<0.0001) was observed. QRS duration showed a significant (10.7%) increase from 94.3±17.5 ms before TH to 104.4±25.4 ms during TH (p=0.001). The QT and QTc intervals displayed significant 18.5% and 8.7% increases, respectively (371.1±63.3 ms before TH to 439±86.9 ms during TH, p<0.0001, and 468.0±44.2 ms before TH to 512.7±74.6 ms during TH, p<0.0001).

Causes of Cardiac Arrest and Initial Rhythm

   The causes of cardiac arrests were highly variable. Cardiac causes were responsible in 16.2% of the study subjects, while non-cardiac etiology was present in 75.0% of the patients (Table 2). In cardiac etiology, acute myocardial ischemia caused by myocardial infarction or coronary artery spasm predominated.
   Initial rhythm determined by ECGs at the emergency room is shown in Table 3. VF was present in 10/11 (90.1%) of patients, and pulseless electrical activity/asystole was recorded in 1/11 (9.1%) of the patients in the cardiac etiology group. However, VF was present in only 4/47 (7.8%) of the non-cardiac cause patients.

Distribution and Mean Amplitude of J Wave during TH

   As shown in Table 4, J waves were common in the inferior and left precordial leads, followed by the high lateral and right precordial leads. Although the frequency of J waves was low in the right precordial leads, the mean amplitudes of J waves (when observable) were higher in the right precordial leads than in other ECG leads. This resulted in prominent right precordial J wave augmentation in two patients with primary arrhythmic disorders. In these patients, J waves were markedly augmented during TH compared with the remainder (0.450±0.095 vs. 0.173±0.012 mV).

Patients who Developed VF during TH

   VF occurred in two patients during TH. The two patients were later diagnosed with Brugada syndrome and ERS, respectively. A 56-year-old male patient who was diagnosed with Brugada syndrome displayed newly developed J wave in the left precordial leads during TH (at 32.8℃). However, the J-ST segment elevation in V1 and V2 became diminished during TH. J waves in the left precordial leads occurred immediately post DC cardioversion for VF (Figure 2). A 70-year-old male patient, who was diagnosed with ERS, had marked augmentation of J wave in the left precordial leads (V3-4) during TH (at 33.2℃) (Figure 3). Prominent J waves were observed after DC cardioversion for VF. The two patients underwent cardioverter/defibrillator implantation prior to discharge.


   The main findings of this study are as follows: (1) J waves were induced or augmented in 58.8% of the patients undergoing mild TH (target temperature 33℃); (2) J waves appeared more commonly in the inferior and lateral leads than in the right precordial leads; and (3) it was hypothesized that patients with primary arrhythmic disorders displayed a higher prevalence and amplitude of J waves and were more vulnerable to develop VF during TH than those without primary arrhythmic disorders.
   Recent population-based studies have established an association between the early repolarization pattern and VF, whether idiopathic in nature or secondary to ischemia.10-12 The tendency for hypothermia to induce similar electrocardiographic changes is well established.5,13 Consequently, TH post cardiac arrest can provide an opportunity to examine the impact of J wave-associated hypothermia on malignant arrhythmic potential.14 This retrospective cohort study assessed the impact of TH on the prevalence, distribution, and magnitude of J waves, and their association with malignant arrhythmia.
   During the cooling phase, 58.8% of our study population displayed J wave above 0.1 mV. It is well documented that the prevalence of J wave varies with core temperature.15,16 Reports on patients with accidental hypothermia suggest that the prevalence of J wave would be minimal during mild hypothermia (temperature 33℃).15-17 However, Rolfast et al reported a 30% prevalence of J waves during TH18 and the most recent study by Williams et al discovered a prevalence of J wave (51.2%) similar to our study findings.19 According to these results and our observations, the prevalence of J wave during TH appears higher than previously reported.
   Similar to results of previous reports, the J wave was most frequently recorded in the leads facing the left ventricle and in the inferior limb leads.20 Recent data show that the inferolateral J wave is occasionally malignant and therefore strongly associated with sudden cardiac death.10,21 In addition, the inferolateral J wave in Brugada syndrome is significantly associated with a poor prognosis.22-25 In this study, VF occurred in two patients with primary arrhythmia disorder (Brugada syndrome and ERS). The small number of subjects in this study made it difficult to estimate the incidence of VF during TH. From our results alone, we cannot determine the relationship between the presence of J waves and the incidence of VF in the general population. Nontheless, considering the temporal relationship between the J wave and VF occurrence, TH may serve as a trigger for VF in certain susceptible patients. Incidence of VF in patients with primary arrhythmic disorder in comparison with the general population needs to be determined in future prospective studies. Recently, a Target Temperature Management trial26 showed that hypothermia, at a targeted temperature of 33℃, did not confer a benefit as compared with a targeted temperature of 36℃. After consideration of this finding, a targeted temperature of 36℃ may be a safe alternative to avoid potential TH complications while treating abnormal patient groups (e.g., primary arrhythmia disorder patients).


   J waves were present in the majority of patients undergoing TH after cardiac arrest. TH-related J waves were most frequently recorded in the inferior and lateral precordial leads. VF was rarely observed (2.7%) and was confined to patients with Brugada syndrome or ERS. Although this study cannot prove causality between the VF and the J wave during TH, it illustrates a temporal relationship between hypothermia and increased frequency of malignant arrhythmias in patients with primary arrhythmic disorders. Application of TH may require careful attention in this susceptible, high-risk population.


  1. Peberdy MA, Callaway CW, Neumar RW, Geocadin RG, Zimmerman JL, Donnino M, Gabrielli A, Silvers SM, Zaritsky AL, Merchant R, Vanden Hoek TL, Kronick SL and American Heart A. Part 9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:S768-786.
  2. Deakin CD, Nolan JP, Soar J, Sunde K, Koster RW, Smith GB and Perkins GD. European Resuscitation Council Guidelines for Resuscitation 2010 Section 4. Adult advanced life support. Resuscitation. 2010;81:1305-1352.
  3. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G and Smith K. Treatment of comatose survivors of out-ofhospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557-563.
  4. Hypothermia after Cardiac Arrest Study G. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346:549-556.
  5. Osborn JJ. Experimental hypothermia; respiratory and blood pH changes in relation to cardiac function. Am J Physiol. 1953;175:389-398.
  6. Delaney KA, Vassallo SU, Larkin GL and Goldfrank LR. Rewarming rates in urban patients with hypothermia: prediction of underlying infection. Acad Emerg Med. 2006;13:913-921.
  7. Rankin AC and Rae AP. Cardiac arrhythmias during rewarming of patients with accidental hypothermia. Br Med J (Clin Res Ed). 1984;289:874-877.
  8. Vassal T, Benoit-Gonin B, Carrat F, Guidet B, Maury E and Offenstadt G. Severe accidental hypothermia treated in an ICU: prognosis and outcome. Chest. 2001;120:1998-2003.
  9. Antzelevitch C. Genetic, molecular and cellular mechanisms underlying the J wave syndromes. Circ J. 2012;76:1054-1065.
  10. Haissaguerre M, Derval N, Sacher F, Jesel L, Deisenhofer I, de Roy L, Pasquie JL, Nogami A, Babuty D, Yli-Mayry S, De Chillou C, Scanu P, Mabo P, Matsuo S, Probst V, Le Scouarnec S, Defaye P, Schlaepfer J, Rostock T, Lacroix D, Lamaison D, Lavergne T, Aizawa Y, Englund A, Anselme F, O'Neill M, Hocini M, Lim KT, Knecht S, Veenhuyzen GD, Bordachar P, Chauvin M, Jais P, Coureau G, Chene G, Klein GJ and Clementy J. Sudden cardiac arrest associated with early repolarization. N Engl J Med. 2008;358:2016-2023.
  11. Patel RB, Ng J, Reddy V, Chokshi M, Parikh K, Subacius H, Alsheikh-Ali AA, Nguyen T, Link MS, Goldberger JJ, Ilkhanoff L and Kadish AH. Early repolarization associated with ventricular arrhythmias in patients with chronic coronary artery disease. Circ Arrhythm Electrophysiol. 2010;3:489-495.
  12. Rosso R, Kogan E, Belhassen B, Rozovski U, Scheinman MM, Zeltser D, Halkin A, Steinvil A, Heller K, Glikson M, Katz A and Viskin S. J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance. J Am Coll Cardiol. 2008;52:1231-1238.
  13. Emslie-Smith D, Sladden GE and Stirling GR. The significance of changes in the electrocardiogram in hypothermia. Br Heart J. 1959;21:343-351.
  14. Bastiaenen R, Hedley PL, Christiansen M and Behr ER. Therapeutic hypothermia and ventricular fibrillation storm in early repolarization syndrome. Heart rhythm. 2010;7:832-834.
  15. Vassallo SU, Delaney KA, Hoffman RS, Slater W and Goldfrank LR. A prospective evaluation of the electrocardiographic manifestations of hypothermia. Acad Emerg Med. 1999;6:1121-1126.
  16. Higuchi S, Takahashi T, Kabeya Y, Hasegawa T, Nakagawa S and Mitamura H. J waves in accidental hypothermia. Circ J. 2013;78:128-134.
  17. Mattu A, Brady WJ and Perron AD. Electrocardiographic manifestations of hypothermia. Am J Emerg Med. 2002;20:314-326.
  18. Rolfast CL, Lust EJ and de Cock CC. Electrocardiographic changes in therapeutic hypothermia. Crit Care. 2012;16:R100.
  19. Williams SE, Sabir I, Nimmo C, Linton N, Sebag FA, Harrison JL, Wright M, Barrett NA, Shankar-Hari M and O'Neill MD. Quantitative assessment of the effects of therapeutic hypothermia on early repolarization in idiopathic ventricular fibrillation survivors: a 7-year cohort study. Circ Arrhythm Electrophysiol. 2014;7:120-126.
  20. Gussak I, Bjerregaard P, Egan TM and Chaitman BR. ECG phenomenon called the J wave. History, pathophysiology, and clinical significance. J Electrocardiol. 1995;28:49-58.
  21. Haissaguerre M, Sacher F, Nogami A, Komiya N, Bernard A, Probst V, Yli-Mayry S, Defaye P, Aizawa Y, Frank R, Mantovan R, Cappato R, Wolpert C, Leenhardt A, de Roy L, Heidbuchel H, Deisenhofer I, Arentz T, Pasquie JL, Weerasooriya R, Hocini M, Jais P, Derval N, Bordachar P and Clementy J. Characteristics of recurrent ventricular fibrillation associated with inferolateral early repolarization role of drug therapy. J Am Coll Cardiol. 2009;53:612-619.
  22. Kamakura S, Ohe T, Nakazawa K, Aizawa Y, Shimizu A, Horie M, Ogawa S, Okumura K, Tsuchihashi K, Sugi K, Makita N, Hagiwara N, Inoue H, Atarashi H, Aihara N, Shimizu W, Kurita T, Suyama K, Noda T, Satomi K, Okamura H, Tomoike H and Brugada Syndrome Investigators in J. Long-term prognosis of probands with Brugada-pattern ST-elevation in leads V1-V3. Circ Arrhythm Electrophysiol. 2009;2:495-503.
  23. Kawata H, Morita H, Yamada Y, Noda T, Satomi K, Aiba T, Isobe M, Nagase S, Nakamura K, Fukushima Kusano K, Ito H, Kamakura S and Shimizu W. Prognostic significance of early repolarization in inferolateral leads in Brugada patients with documented ventricular fibrillation: a novel risk factor for Brugada syndrome with ventricular fibrillation. Heart rhythm. 2013;10:1161-1168.
  24. Sarkozy A, Chierchia GB, Paparella G, Boussy T, De Asmundis C, Roos M, Henkens S, Kaufman L, Buyl R, Brugada R, Brugada J and Brugada P. Inferior and lateral electrocardiographic repolarization abnormalities in Brugada syndrome. Circ Arrhythm Electrophysiol. 2009;2:154-161.
  25. Takagi M, Aonuma K, Sekiguchi Y, Yokoyama Y, Aihara N, Hiraoka M and Japan Idiopathic Ventricular Fibrillation Study I. The prognostic value of early repolarization (J wave) and ST-segment morphology after J wave in Brugada syndrome: multicenter study in Japan. Heart rhythm. 2013;10:533-539.
  26. Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, Horn J, Hovdenes J, Kjaergaard J, Kuiper M, Pellis T, Stammet P, Wanscher M, Wise MP, Aneman A, Al-Subaie N, Boesgaard S, Bro-Jeppesen J, Brunetti I, Bugge JF, Hingston CD, Juffermans NP, Koopmans M, Kober L, Langorgen J, Lilja G, Moller JE, Rundgren M, Rylander C, Smid O, Werer C, Winkel P, Friberg H and Investigators TTMT. Targeted temperature management at 33 degrees C versus 36 degrees C after cardiac arrest. N Engl J Med. 2013;369:2197-2206.
PDF Links  PDF Links
Full text via DOI  Full text via DOI
Download Citation  Download Citation
Electrocardiography Changes after Stroke  2014 ;15(2)