Ecg Desordenes Metabolicos

Emerg Med Clin N Am 24 (2006) 145–157

ECG Manifestations of Selected Metabolic and Endocrine Disorders
David A. Wald, DO
Department of Emergency Medicine, Temple University Hospital, 3401 North Broad Street, Jones Hall, 10th Floor, Philadelphia, PA 19140, USA

Hypercalcemia Hypercalcemia shortens the plateau phase (phase 2) of the cardiac action potential and decreases the effectiverefractory period, resulting in shortening of the ST segment [1–3]. Classically this is manifested on the ECG as a shortened QT interval. The QT interval is the distance measured from the beginning of the QRS complex to the end of the T wave [4]. This interval approximates the duration of ventricular systole. The correlation between the duration of the QT interval and the serum calcium level, however, isnot linear. It may be unpredictable because of the many factors that affect the QT interval, including: patient age, heart rate, gender, antidysrhythmic medication, and other electrolytes [3]. Because the QT interval varies with cycle length, the rate corrected QT interval (QTc) often is measured to correct for heart rate. The QTc interval is determined by the formula: QT interval/ORR. The upperlimit of the QTc is, conservatively, roughly 0.44 seconds for both genders, although the normal QTc range in women is slightly longer than in men. Shortening of the QaT interval also is noted in patients who have hypercalcemia. The QaT interval is measured from the beginning of the QRS complex to the apex of the T wave. This occurs because hypercalcemia commonly is associated with early peaking anda gradual down slope of the descending limb of the T wave [4]. The QaT interval correlates best with the serum calcium level [3]. In cases of severe hypercalcemia (serum calcium O16 mg/dL), the duration of the T wave can increase. When this occurs, the QT interval may seem normal even though the ST segment remains shortened [5–7]. Other ECG abnormalities that may occur in patients who have severehypercalcemia

E-mail address: waldda@tuhs.temple.edu 0733-8627/06/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.emc.2005.08.010 emed.theclinics.com

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include an increased amplitude of the QRS complex, ST segment elevation, diphasic T waves, prominent U waves, and J (Osborn) waves (Fig. 1) [3,4,8]. Hypocalcemia Hypocalcemia prolongs the durationof the plateau phase (phase 2) of the cardiac action potential [1,4]. Characteristic ECG manifestations of hypocalcemia are prolongation of the QT interval as a result of lengthening of the ST segment (Fig. 2) [7]. Although variable, QT interval prolongation is proportional to the degree of hypocalcemia. When prolonged, the QTc rarely exceeds 140% of normal [9]. When the QTc seems to be prolongedgreater than 140% of normal, it suggests that the U wave has been incorporated into the T wave and that the QU interval is being measured. T-wave changes are not common, because hypocalcemia does not affect phase 3 of the action potential. Decreased T-wave voltage, T-wave flattening, terminal T-wave inversion, or deeply inverted T waves, however, have been described in cases of severe hypocalcemia[4,9,10]. Although rarely reported, hypocalcemia also can be associated with ST segment elevation, mimicking an acute myocardial infarction or T-wave abnormalities simulating myocardial ischemia [9,11]. Coronary artery spasm in the presence of hypocalcemia may play a role in manifesting these ECG abnormalities. Concomitant hypomagnesemia can exacerbate the ECG manifestations of hypocalcemia.

Fig.1. (A) Hypercalcemia. This ECG is from a patient with a serum calcium level of 14.7 mg/dL, demonstrating a shortened QT interval. In addition, prominent U waves (arrows) are seen best in the right precordial leads. (B) Normocalcemia. This is baseline ECG from the same patient as in (A) when her serum calcium level was normalized (7.8 mg/dL). The QT interval is no longer shortened and the U...