The aim of this study was to evaluate HRV in children requiring intensive care unit stays due to TCA poisoning between March 2009 and July 2010. In the time-domain nonspectral evaluation, the SDNN ( ), SDNNi ( ), RMSDD ( ), and pNN50 ( ) were found to be significantly lower in the TCA intoxication group. The spectral analysis of the data recorded during the first 5 minutes after intensive care unit admission showed that the values of the nLF ( ) and the LF/HF ratio ( ) were significantly higher in the TCA intoxication group, while the nHF ( ) values were significantly lower. The frequency-domain spectral analysis of the data recorded during the last 5 minutes showed a lower nHF ( ) in the TCA intoxication group than in the controls, and the LF/HF ratio was significantly higher ( ) in the intoxication group. The LF/HF ratio was higher in the seven children with seizures ( ). These findings provided us with a starting point for the value of HRV analysis in determining the risk of arrhythmia and convulsion in TCA poisoning patients. HRV can be used as a noninvasive testing method in determining the treatment and prognosis of TCA poisoning patients. 1. Introduction Poisoning is a common and important cause of morbidity and mortality worldwide, especially during childhood. More than 50% of patients reported to poison control centers are adolescents or less than five years of age [1]. Among the substances that cause poisoning, drugs have been reported as the most common factor. In Turkey, tricyclic antidepressants (TCA) occupy an important place among the causes of poisoning, and the incidence of such events has increased over the last decade [2]. TCAs (amitriptyline, nortriptyline, clomipramine, desipramine, imipramine, doxepinm, and protriptyline) are frequently used for the treatment of depression, chronic pain syndrome, school phobia, hyperkinesias, nocturnal enuresis, and attention deficit-hyperactivity disorder [3]. TCA-related poisoning influences the autonomic nervous system, central nervous system (CNS), and cardiovascular system (CVS), and clinical signs appear within 6–8 hours. There is no laboratory test to precisely diagnose TCA-related poisoning, and it is impossible to predict the prognosis. The semiquantitative enzyme immunoassay technique may be useful for measuring TCA levels; however, there is no correlation between drug levels and clinical findings [4]. The most severe life-threatening condition in TCA-related poisoning is the dysrhythmias that occur due to the quinidine-like effects on the myocardial tissue. Electrocardiogram (ECG)
References
[1]
T. L. Litovitz, W. Klein-Schwartz, E. M. Caravati, J. Youniss, B. Crouch, and S. Lee, “1998 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System,” American Journal of Emergency Medicine, vol. 17, no. 5, pp. 435–487, 1999.
[2]
N. And？ran and F. Sar？kayalar, “Pattern of acute poisonings in children in Ankara: what has changed in twenty years?” The Turkish Journal of Pediatrics, vol. 46, pp. 147–152, 2004.
[3]
P. K. Gillman, “Tricyclic antidepressant pharmacology and therapeutic drug interactions updated,” British Journal of Pharmacology, vol. 151, no. 6, pp. 737–748, 2007.
[4]
G. W. Kerr, A. C. McGuffie, and S. Wilkie, “Tricyclic antidepressant overdose: a review,” Emergency Medicine Journal, vol. 18, no. 4, pp. 236–241, 2001.
[5]
E. M. Caravati, “The electrocardiogram as a diagnostic discriminator for acute tricyclic antidepressant poisoning,” Journal of Toxicologyy, vol. 37, no. 1, pp. 113–115, 1999.
[6]
M. T. Boehnert and F. H. Lovejoy, “Value of the QRS duration versus the serum drug level in predicting seizures and ventricular arrhythmias after an acute overdose of tricyclic antidepressants,” The New England Journal of Medicine, vol. 313, no. 8, pp. 474–479, 1985.
[7]
Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology, “Heart rate variability: standards of measurement, physiological interpretation, and clinical use,” European Heart Journal, vol. 17, pp. 354–381, 1996.
[8]
L. C. M. Vanderlei, C. M. Pastre, R. A. Hoshi, T. D. de Carvalho, and M. F. de Godoy, “Basic notions of heart rate variability and its clinical applicability,” Brazilian Journal of Cardiovascular Surgery, vol. 24, no. 2, pp. 205–217, 2009.
[9]
C. L. Kaufman, D. R. Kaiser, J. Steinberger, A. S. Kelly, and D. R. Dengel, “Relationships of cardiac autonomie function with metabolic abnormalities in childhood obesity,” Obesity, vol. 15, no. 5, pp. 1164–1171, 2007.
[10]
S. M. Rodríguez-Colón, E. O. Bixler, X. Li, A. N. Vgontzas, and D. Liao, “Obesity is associated with impaired cardiac autonomic modulation in children,” International Journal of Pediatric Obesity, vol. 6, no. 2, pp. 128–134, 2011.
[11]
W. Rutjanaprom, N. Kanlop, P. Charoenkwan et al., “Heart rate variability in beta-thalassemia patients,” European Journal of Haematology, vol. 83, no. 5, pp. 483–489, 2009.
[12]
F. Kardelen, G. Tezcan, G. Akcurin, H. Ertug, and A. Yesilipek, “Heart rate variability in patients with thalassemia major,” Pediatric Cardiology, vol. 29, no. 5, pp. 935–939, 2008.
[13]
O. Hallioglu, C. Okuyaz, E. Mert, and K. Makharoblidze, “Effects of antiepileptic drug therapy on heart rate variability in children with epilepsy,” Epilepsy Research, vol. 79, no. 1, pp. 49–54, 2008.
[14]
M. Ak？aboy, S. Atalay, T. U？ar, and E. Tutar, “Heart rate variability during asymptomatic periods in children with recurrent neurocardiogenic syncope,” The Turkish Journal of Pediatrics, vol. 53, no. 1, pp. 59–66, 2011.
[15]
K. L. Kwok, T. C. Yung, D. K. Ng, C. H. Chan, W. F. Lau, and Y. M. Fu, “Heart rate variability in childhood obstructive sleep apnea,” Pediatric Pulmonology, vol. 46, no. 3, pp. 205–210, 2011.
[16]
H. V. Muzumdar, S. Sin, M. Nikova, G. Gates, D. Kim, and R. Arens, “Changes in heart rate variability after adenotonsillectomy in children with obstructive sleep apnea,” Chest, vol. 139, no. 5, pp. 1050–1059, 2011.
[17]
H. V. Huikuri, M. J. P. Raatikainen, R. Moerch-Joergensen et al., “Prediction of fatal or near-fatal cardiac arrhythmia events in patients with depressed left ventricular function after an acute myocardial infarction,” European Heart Journal, vol. 30, no. 6, pp. 689–698, 2009.
[18]
M. T. La Rovere, G. D. Pinna, R. Maestri et al., “Short-term heart rate variability strongly predicts sudden cadiac death in chronic heart failure patients,” Circulation, vol. 107, no. 4, pp. 565–570, 2003.
[19]
A. H. Kemp, D. S. Quintana, M. A. Gray, K. L. Felmingham, K. Brown, and J. M. Gatt, “Impact of depression and antidepressant treatment on heart rate variability: a review and meta-analysis,” Biological Psychiatry, vol. 67, no. 11, pp. 1067–1074, 2010.
[20]
W. S. Waring, J. Y. Rhee, D. N. Bateman, G. E. Leggett, and H. Jamie, “Impaired heart rate variability and altered cardiac sympathovagal balance after antidepressant overdose,” European Journal of Clinical Pharmacology, vol. 64, no. 11, pp. 1037–1041, 2008.
[21]
I. Djonlagic, H. Djonlagic, T. Kibbel, S. Suefke, and C. Dodt, “Heart rate variability reveals risk of arrhythmias after intoxication with antidepressants,” Intensive Care Medicine, vol. 33, no. 1, pp. 200–202, 2007.
[22]
P. Manikoth, R. Subramanyan, S. Menon, and S. M. Al Khusaiby, “A child with cardiac arrhythmia and convulsions,” The Lancet, vol. 354, no. 9195, p. 2046, 1999.
[23]
T. G. Rosenbaum, M. Kou, and J. N. Love, “Are one or two dangerous? Tricyclic antidepressant exposure in toddlers,” Journal of Emergency Medicine, vol. 28, no. 2, pp. 169–174, 2005.
[24]
H. L. Leonard, M. C. Meyer, S. E. Swedo et al., “Electrocardiographic changes during desipramine and clomipramine treatment in children and adolescents,” Journal of the American Academy of Child and Adolescent Psychiatry, vol. 34, no. 11, pp. 1460–1468, 1995.
[25]
J. Sarko, “Antidepressants, old and new: a review of their adverse effects and toxicity in overdose,” Emergency Medicine Clinics of North America, vol. 18, no. 4, pp. 637–654, 2000.
[26]
A. ？itak, D. D. Soysal, R. ü？sel, M. Karab？cüoglu, and N. Uzel, “Seizures associated with poisoning in children: tricyclic antidepressant intoxication,” Pediatrics International, vol. 48, no. 6, pp. 582–585, 2006.
[27]
L. P. James and G. L. Kearns, “Cyclic antidepressant toxicity in children and adolescents,” Journal of Clinical Pharmacology, vol. 35, no. 4, pp. 343–350, 1995.
[28]
P. Palatini and S. Julius, “The role of cardiac autonomic function in hypertension and cardiovascular disease,” Current Hypertension Reports, vol. 11, no. 3, pp. 199–205, 2009.
[29]
A. Haensel, P. J. Mills, R. A. Nelesen, M. G. Ziegler, and J. E. Dimsdale, “The relationship between heart rate variability and inflammatory markers in cardiovascular diseases,” Psychoneuroendocrinology, vol. 33, no. 10, pp. 1305–1312, 2008.
[30]
K. P. Anderson, “Sympathetic nervous system activity and ventricular tachyarrhythmias: recent advances,” Annals of Noninvasive Electrocardiology, vol. 8, no. 1, pp. 75–89, 2003.
[31]
A. Algra, J. G. P. Tijssen, J. R. T. C. Roelandt, J. Pool, and J. Lubsen, “Heart rate variability from 24-hour electrocardiography and the 2-year risk for sudden death,” Circulation, vol. 88, no. 1, pp. 180–185, 1993.
[32]
A. F. Folino, G. Russo, B. Bauce, E. Mazzotti, and L. Daliento, “Autonomic profile and arrhythmic risk stratification after surgical repair of tetralogy of Fallot,” American Heart Journal, vol. 148, no. 6, pp. 985–989, 2004.
[33]
B. Bjelakovic, S. Ilic, K. Chouliaras et al., “Heart rate variability in children with exercise-induced idiopathic ventricular arrhythmias,” Pediatric Cardiology, vol. 31, no. 2, pp. 188–194, 2010.
[34]
G. Eisenhofer, T. Saigusa, M. D. Esler, H. S. Cox, J. A. Angus, and P. K. Dorward, “Central sympathoinhibition and peripheral neuronal uptake blockade after desipramine in rabbits,” American Journal of Physiology, vol. 260, no. 4, part 2, pp. R824–R832, 1991.
[35]
M. D. Esler, G. Wallin, P. K. Dorward et al., “Effects of desipramine on sympathetic nerve firing and norepinephrine spillover to plasma in humans,” American Journal of Physiology, vol. 260, no. 4, part 2, pp. R817–R823, 1991.
[36]
K. Udupa, T. N. Sathyaprabha, J. Thirthalli et al., “Alteration of cardiac autonomic functions in patients with major depression: a study using heart rate variability measures,” Journal of Affective Disorders, vol. 100, no. 1–3, pp. 137–141, 2007.
[37]
F. Lederbogen, C. Gernoth, B. Weber et al., “Antidepressive treatment with amitriptyline and paroxetine: comparable effects on heart rate variability,” Journal of Clinical Psychopharmacology, vol. 21, no. 2, pp. 238–239, 2001.
[38]
C. A. Arranto, C. Mueller, P. R. Hunziker, S. C. Maysch, and U. Eriksson, “Adverse cardiac events in ICU patients with presumptive antidepressant overdose,” Swiss Medical Weekly, vol. 133, no. 35-36, pp. 479–483, 2003.
[39]
K. Srinivasan, M. V. Ashok, M. Vaz, and V. K. Yeragani, “Effect of imipramine on linear and nonlinear measures of heart rate variability in children,” Pediatric Cardiology, vol. 25, no. 1, pp. 20–25, 2004.
[40]
D. S. Goldstein, O. Bentho, M. Y. Park, and Y. Sharabi, “Low-frequency power of heart rate variability is not a measure of cardiac sympathetic tone but may be a measure of modulation of cardiac autonomic outflows by baroreflexes,” Experimental Physiology, vol. 96, pp. 1255–1261, 2011.
[41]
A. M. D. Watson, S. G. Hood, R. Ramchandra, R. M. McAllen, and C. N. May, “Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex,” American Journal of Physiology, vol. 293, no. 1, pp. H798–H804, 2007.
[42]
B. A. Kingwell, J. M. Thompson, D. M. Kaye, G. A. McPherson, G. L. Jennings, and M. D. Esler, “Heart rate spectral analysis, cardiac norepinephrine spillover, and muscle sympathetic nerve activity during human sympathetic nervous activation and failure,” Circulation, vol. 90, no. 1, pp. 234–240, 1994.
