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An unusual electrocardiographic pattern of cardiac glycoside poisoning
International Journal of Cardiology 82 (2002) 79–81 www.elsevier.com / locate / ijcard
Letter to the Editor
An unusual electrocardiographic pattern of cardiac glycoside poisoning a, b c Luca Lanzarini *, Paolo Lanzarini , Alberto Casazza a
Department of Cardiology, IRCCS-Policlinico S. Matteo Hospital, Piazza Golgi 2, 27100 Pavia, Italy Division of Infectious Diseases, IRCCS-Policlinico S. Matteo Hospital, Piazza Golgi 2, 27100 Pavia, Italy c Second Department of Anesthesia and Intensive Care, IRCCS-Policlinico S. Matteo Hospital, Piazza Golgi 2, 27100 Pavia, Italy b
Received 20 September 2001; accepted 28 September 2001
Keywords: Digitalis intoxication; Electrocardiogram
The electrocardiogram (ECG) presented in Fig. 1 was registered about 24 h after the deliberate ingestion of a vague dose of digoxin (probably 5–10 mg) in a 46-year-old female affected by human immunodeficiency virus infection. No signs or symptoms related to cardiac involvement were documented before the event; the patient declared drug ingestion during the daily medical interview. By this time plasma digoxin level was .4 ng / ml (normal range 0.8–2 ng / ml). She was asymptomatic. No significant plasma electrolyte abnormalities were found. The patient was treated with digoxin-specific FAB antibody fragments. A control ECG obtained 24 h later, with a digoxin plasma level of 1.85 ng / ml, is illustrated in Fig. 2. The remaining hospital stay was uneventful. The initial ECG (Fig. 1) shows some peculiar and unusual abnormalities of ventricular repolarization characterized by an apparent QT-interval prolongation (not confirmed by the calculation of the QTc) and a QT-interval dispersion. Prominent U-waves,
probably linked to the development of late cardiac potentials, are also evident. The association of bradycardia and delayed afterdepolarizations due to digoxin-induced intracellular calcium overload, is probably responsible of this pattern of repolarization. The more pronounced abnormalities recorded in the index beat (*) compared with the following beat, were probably due to a longer R–R preceding interval. This patient without cardiac symptoms confirm that, in subjects with excessive serum digitalis concentrations, the likelihood of having clinical signs of intoxication is lesser if the electrocardiogram records a slow rhythm compared with signs of increased automaticity [1]. References [1] Abdad-Santos F, Carcas AJ, Ibanez C, Frias J. Digoxin level and clinical manifestations as determinants in the diagnosis of digoxin toxicity. Ther Drug Monit 2000;22:163–8.
*Corresponding author. Tel.: 139-038-250-3934; fax: 139-038-2503895. E-mail address: [email protected] (L. Lanzarini). 0167-5273 / 02 / $ – see front matter 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 01 )00592-7
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L. Lanzarini et al. / International Journal of Cardiology 82 (2002) 79 – 81
Fig. 1. Twelve-lead electrocardiogram obtained in basal condition 24 h after drug ingestion when digoxin plasma level was .4 ng / ml. The rhythm is probably a slow ectopic atrial rhythm (33 beats / min). R–R interval is 1840 ms. P–R interval is 120–130 ms. A peculiar change in cardiac repolarization is evident with apparent prolongation of the QT interval (640 ms in lead II, 680 ms in lead V5), polymorphism of T wave and prominent and prolonged U wave. However, QT corrected for heart rate (QTc) (500 ms in lead II, 470 ms in lead V5) exceeds the upper range of normality by a few milliseconds. Note that aVR is reported as 2aVR.
L. Lanzarini et al. / International Journal of Cardiology 82 (2002) 79 – 81
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Fig. 2. Twelve-lead electrocardiogram obtained 24 h after therapy with digoxin-specific FAB antibody fragments was administered and digoxin plasma level had fallen to 1.85 ng / ml. The rhythm is normal sinus rhythm (63 beats / min). R–R interval is 960 ms. P–R interval is 160 ms. A change in ST segment is present with diffuse mild ST depression and decreased T-wave amplitude, characteristic of digoxin treatment. QT interval measures 420 ms in lead II and QTc 431 ms.
Letter to the Editor
An unusual electrocardiographic pattern of cardiac glycoside poisoning a, b c Luca Lanzarini *, Paolo Lanzarini , Alberto Casazza a
Department of Cardiology, IRCCS-Policlinico S. Matteo Hospital, Piazza Golgi 2, 27100 Pavia, Italy Division of Infectious Diseases, IRCCS-Policlinico S. Matteo Hospital, Piazza Golgi 2, 27100 Pavia, Italy c Second Department of Anesthesia and Intensive Care, IRCCS-Policlinico S. Matteo Hospital, Piazza Golgi 2, 27100 Pavia, Italy b
Received 20 September 2001; accepted 28 September 2001
Keywords: Digitalis intoxication; Electrocardiogram
The electrocardiogram (ECG) presented in Fig. 1 was registered about 24 h after the deliberate ingestion of a vague dose of digoxin (probably 5–10 mg) in a 46-year-old female affected by human immunodeficiency virus infection. No signs or symptoms related to cardiac involvement were documented before the event; the patient declared drug ingestion during the daily medical interview. By this time plasma digoxin level was .4 ng / ml (normal range 0.8–2 ng / ml). She was asymptomatic. No significant plasma electrolyte abnormalities were found. The patient was treated with digoxin-specific FAB antibody fragments. A control ECG obtained 24 h later, with a digoxin plasma level of 1.85 ng / ml, is illustrated in Fig. 2. The remaining hospital stay was uneventful. The initial ECG (Fig. 1) shows some peculiar and unusual abnormalities of ventricular repolarization characterized by an apparent QT-interval prolongation (not confirmed by the calculation of the QTc) and a QT-interval dispersion. Prominent U-waves,
probably linked to the development of late cardiac potentials, are also evident. The association of bradycardia and delayed afterdepolarizations due to digoxin-induced intracellular calcium overload, is probably responsible of this pattern of repolarization. The more pronounced abnormalities recorded in the index beat (*) compared with the following beat, were probably due to a longer R–R preceding interval. This patient without cardiac symptoms confirm that, in subjects with excessive serum digitalis concentrations, the likelihood of having clinical signs of intoxication is lesser if the electrocardiogram records a slow rhythm compared with signs of increased automaticity [1]. References [1] Abdad-Santos F, Carcas AJ, Ibanez C, Frias J. Digoxin level and clinical manifestations as determinants in the diagnosis of digoxin toxicity. Ther Drug Monit 2000;22:163–8.
*Corresponding author. Tel.: 139-038-250-3934; fax: 139-038-2503895. E-mail address: [email protected] (L. Lanzarini). 0167-5273 / 02 / $ – see front matter 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 01 )00592-7
80
L. Lanzarini et al. / International Journal of Cardiology 82 (2002) 79 – 81
Fig. 1. Twelve-lead electrocardiogram obtained in basal condition 24 h after drug ingestion when digoxin plasma level was .4 ng / ml. The rhythm is probably a slow ectopic atrial rhythm (33 beats / min). R–R interval is 1840 ms. P–R interval is 120–130 ms. A peculiar change in cardiac repolarization is evident with apparent prolongation of the QT interval (640 ms in lead II, 680 ms in lead V5), polymorphism of T wave and prominent and prolonged U wave. However, QT corrected for heart rate (QTc) (500 ms in lead II, 470 ms in lead V5) exceeds the upper range of normality by a few milliseconds. Note that aVR is reported as 2aVR.
L. Lanzarini et al. / International Journal of Cardiology 82 (2002) 79 – 81
81
Fig. 2. Twelve-lead electrocardiogram obtained 24 h after therapy with digoxin-specific FAB antibody fragments was administered and digoxin plasma level had fallen to 1.85 ng / ml. The rhythm is normal sinus rhythm (63 beats / min). R–R interval is 960 ms. P–R interval is 160 ms. A change in ST segment is present with diffuse mild ST depression and decreased T-wave amplitude, characteristic of digoxin treatment. QT interval measures 420 ms in lead II and QTc 431 ms.