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Electrocardiographic changes associated with ritodrine-induced maternal tachycardia and hypokalemia

  • Susan K. Hendricks
    Affiliations
    Department of Obstetrics, Gynecology, Reproductive Sciences, Children's Hospital San Francisco, California, USA

    Department of Cardiology, Children's Hospital San Francisco, California, USA

    the University of California, San Francisco, California, USA
    Search for articles by this author
  • Jonathan Keroes
    Affiliations
    Department of Obstetrics, Gynecology, Reproductive Sciences, Children's Hospital San Francisco, California, USA

    Department of Cardiology, Children's Hospital San Francisco, California, USA

    the University of California, San Francisco, California, USA
    Search for articles by this author
  • Michael Katz
    Correspondence
    Reprint requests: Michael Katz, M.D., Department of Obstetrics and Gynecology, M-1489, University of California, San Francisco, CA 94143.
    Affiliations
    Department of Obstetrics, Gynecology, Reproductive Sciences, Children's Hospital San Francisco, California, USA

    Department of Cardiology, Children's Hospital San Francisco, California, USA

    the University of California, San Francisco, California, USA
    Search for articles by this author
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      Abstract

      One hundred twelve patients in preterm labor were followed prospectively, with electrocardiograms taken before ritodrine therapy and at 6 and 24 hours of treatment. Ninety-six percent of patients developed sinus tachycardia. Other changes were seen in 79% of the study group. These changes included ST segment depression in 70%, T wave flattening or inversion in 55%, and prolongation of the QT interval in 35% of our sample. None of the electrocardiograms showed the presence of significant axis deviation, a change in QRS interval, or arrhythmia. No correlation was seen between symptoms of ischemia and electrocardiographic changes. A drop in potassium concentration was noted initially, but a direct correlation between potassium concentrations and frequency of electrocardiographic changes was not present. We conclude that the electrocardiographic changes that are often observed during myocardial ischemia may be frequent in asymptomatic patients treated with ritodrine and that these changes may be a physiologic expression of ritodrine-induced tachycardia or hypokalemia. The validity of the use of the presence of electrocardiographic changes as the only criterion for discontinuation of ritodrine therapy is questioned.

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