ARTICLE Evaluation of Relationship Between Arterial and Venous Blood Gas Values in the Patients with Tricyclic Antidepressant Poisoning Nastaran Eizadi-Mood Anesthesiology and Intensive Care Department, Isfahan University of Medical Sciences, Isfahan, Iran Neda Moein Department of Poisoning Emergency, Noor Hospital, Isfahan, Iran Mahmood Saghaei Anesthesiology and Intensive Care Department, Isfahan University of Medical Sciences, Isfahan, Iran Introduction. Determination of arterial blood gas (ABG) values is essential in the evaluation of patients with TCA poisoning. The relationship between arterial and venous blood gas pH has not been established in TCA poisoning. In TCA poisoning, blood vessels vasodilatation due to antidepressant- induced a-blockade and also metabolic acidosis may lead to arterialization of venous blood, which in turn enhances the relationship between ABG and VBG parameters. Therefore this study was designed to evaluate the relationship between ABG and VBG pH values in TCA poisoned patients. Methods. This prospective study was performed in the Poisoning Emergency Department of Noor Hospital, Isfahan, Iran. Samples for arterial and venous blood gas analysis were obtained during initial evaluation of TCA-poisoned patients and 30 min after treatment with sodium bicarbonate. The venous blood gas samples were collected with samples for other blood tests at the time of intravenous line insertion. Laboratory data were recorded on a database form initiated in the emergency department and analyzed by paired student t-test. The degree of agreement between the arterial and venous pH measurements was evaluated by Bland and Altman method. Results. Data from 50 TCA- poisoned patients were analyzed. There were significant differ- ences between mean differences of ABG and VBG parameter values on the initial evaluation. There was also a relationship between arterial and venous pH on the initial evaluation. Conclusion. In TCA poisoning, the peripheral venous pH measurement is a valid and reliable substitute for arterial pH. Keywords Tricyclic antidepressant poisoning; Arterial blood gas; Venous blood gas INTRODUCTION The tricyclic antidepressants (TCA) are one of the frequently prescribed pharmacological agents for the treat- ment of both endogenous and reactive depression. Overdoses of these drugs continue to be a cause of serious morbidity and mortality worldwide. The distinctive characteristics of these drugs are significant central nervous system and cardiovascu- lar toxicity, the latter being responsible for the mortality as a result of these drugs. Cardiac manifestations range from mild conduction abnormality and sinus tachycardia to wide complex tachycardia, hypotension, and arrhythmia. Central nervous system toxicity may include delirium, lethargy, seizures, and coma (1). Sodium bicarbonate is the most effective agent for treatment of complications associated with TCA toxicity. Blood pH has been suggested as a safety end point for sodium bicarbonate therapy. Close repetitive monitoring of the blood pH to maintain the pH between 7.45 to 7.55 is indicated (2). Therefore determination of arterial blood gas (ABG) values is essential in the evaluation of patients with TCA poisoning (1). Sampling of arterial blood is a painful, sometimes technically difficult procedure. The most common complica- tions associated with arterial puncture are pain, arterial injury, thrombosis with distal ischemia, hemorrhage, and aneurysm formation (3). The risks increase with repeated arterial punc- tures. Venous (VBG) blood gas samplings may be a useful alternative to arterial blood gas sampling. The relationship between arterial and venous blood gas is well established (4–8); however, this relationship has not been established in TCA poisoning. In TCA poisoning blood vessels vasodilata- tion due to antidepressant-induced a-blockade and also metabolic acidosis may lead to arterialization of venous blood which in turn enhances the relationship between ABG and Received 27 June 2004; accepted 14 March 2005. Address correspondence to Nastaran Eizadi-Mood, Dean, Depart- ment of Poisoning Emergency, Noor Hospital, Isfahan University of Medical Sciences and Health Services, Isfahan, Iran; E-mail: izadi@med.mui.ac.ir 357 Clinical Toxicology, 43:357–360, 2005 Copyright D Taylor & Francis Inc. ISSN: 0731-3810 print / 1097-9875 online DOI: 10.1081/CLT-200066071 Order reprints of this article at www.copyright.rightslink.com