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Case Report: Cardiotoxic Calcemia
Case Report: Cardiotoxic Calcemia CHACE CARPENTER, MO,
MICHAEL E. MAY, MO, PHD
ABSTRACT: The effects of hypercalcemia on the heart and the resulting alterations of the electrocardiogram are well established. However, there are only rare reports of arrhythmias caused by hypercalcemia in primary hyperparathyroidism. This article describes a case of severe hypercalcemia secondary to hyperparathyroidism causing tachy-brady syndrome. KEY INDEXING TERMS: Arrythmia; Hypercalcemia. [Am J Med Sci 1994;307(1):43-44.]
Case Report An 84-year-old female was admitted to our facility on July 6, 1992, because of hypercalcemia and disorientation. Three weeks before this admission, she was admitted to another hospital with an episode of congestive heart failure. Cardiac monitoring during that admission revealed tachy-brady syndrome, with ventricular rates as low as 15 beats/minute. Apermanent pacemaker was provided. Serum calcium level at that time was 13.6 mg/dL. No treatment was given for hypercalcemia. Her past medical history included right nephrectomy secondary to renal calculi 50 years before and history of intermittent flank pain. Physical examination revealed an elderly, well-nourished, female who was disoriented but in no apparent distress. Her heart rate was 80 beats/min and her blood pressure was 92/70 mm Hg. A neck examination was normal. The lungs were clear to auscultation and her heart rhythm was regular, without murmur or gallop. An abdominal exam was unremarkable. Neurologic examination was notable for hyperreflexia and orientation to person only.
Pertinent Laboratory Data
Her serum chemistries included: 89 mg/dL urea nitrogen, 6.9 mg/dL creatinine, 18.2 mg/dL total calcium, 9.31 mg/dL ionized calcium, 4.8 mg/dL phosphorous, 0.9 ng/mL digoxin, and 25.6 ~g/mL procainamide (normal, 4 to 10 ~g/mL). A chest radiograph showed a normal cardiac silhouette with a permanent pacemaker. An electrocardiogram revealed a dual-chamberpaced rhythm with a rate of 85 beats/min and QRS duration of 280 msec. An electrocardiogram from June 18, 1992, (before pacing) showed sinus tachycardia with a rate of 100 beats/min, QRS duration of 90 msec, QT interval of 320 msec, and Q-aT interval of 230 msec. From the Vanderbilt University School of Medicine, Nashville, Tennessee. Correspondence: Michael E . May, MD, PhD, B3307 MCN, Vanderbilt University, Nashville, TN 37232-2230. THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
Hospital Course
On admission, a pulmonary artery catheter showed a pulmonary capillary wedge pressure of 7 mm Hg. Initial treatment consisted of hydration with normal saline to a wedge pressure of 15 mm Hg and subcutaneous injection of 100 units of calcitonin every 12 hours. Mental status improved, creatinine level decreased to 4.6 mg/dL, and calcium level fell to 13.3 mg/dL. The intact parathyroid hormone level was 1,102 pg/mL (normal, 10 to 65 pg/mL) and the parathyroid hormone mid-molecule level was 1,085 pmoljL (normal, 30 to 90 pmoljL). A neck ultrasound revealed a 2 .2 X 1.5 cm mass near the lower pole of the right thyroid lobe. A computed tomography scan confirmed the presence of a mass inferior to the right lobe of the thyroid. On the fifth hospital day, the patient underwent neck exploration with resection of a 4.06 g parathyroid adenoma. The histologic diagnosis was atypical parathyroid adenoma. Digitalis and procainamide were discontinued upon admission, but the patient continued to require artificial pacing. Just before the operation, an electrocardiogram showed underlying sinus rhythm with fusion complexes. Her calcium level then was 12.5 mg/dL. Postoperatively, the heart was in normal sinus rhythm. First-degree atrioventricular block persisted, but pacing was unnecessary. Her calcium level was 8.8 mg/dL and her creatinine level was 2.8 mg/dL on discharge. Discussion
The characteristic electrocardiographic changes found in association with hyperparathyroidism are prolongation of the P-R interval, shortening of the ST segment, and consequent shortening of the Q-T interval. 1 However, elevation of the serum calcium level secondary to hyperparathyroidism usually does not induce cardiac arrhythmias. Recently, Rosenqvist et aP have suggested that conduction disturbances may occur in patients with severe hypercalcemia. They noted an apparent correlation between severity of hypercalcemia and degree of atrioventricular block. Our patient had severe hypercalcemia by Rosenqvist's standards, with calcium levels ranging between 13.6 mg/dL (at the time of diagnosis of cardiac arrhythmias) and 18.2 mg/dL. Sinus arrest with slow ventricular rates and bouts of paroxysmal supraventricular tachycardia were present before pacing during hypercalcemia. No bradycardia 43
Cardiotoxic Calcemia
or supraventricular tachycardia requiring pacing occurred after resection of the parathyroid adenoma. The toxic effects of hypercalcemia on the myocardium are similar to those seen with digitalis intoxication. Our patient had received digitalis. Digoxin levels were not excessive and her conduction disturbance persisted after digitalis was discontinued. Previously, there have been 11 reports of serious arrhythmias and only 4 reports of high-degree atrioventricular block with sinus arrest attributed to hyperparathyroidism. 2-4 The serum calcium level in these cases ranged from 12.5 to 20.0 mg/dL. Our patient represents a fifth case of severe hypercalcemia with the latter conduction disturbance. In conclusion, this case demonstrates that hyperparathyroidism can present as clinically significant
44
cardiac arrhythmias. The arrhythmias are reversible with treatment of the hyperparathyroidism by resection of the parathyroid adenoma.
References
1. Beck GH, Marriott HJL: The electrocardiogram in hyperparathyroidism. Am J Cardiol 3:411-413, 1959. 2. Rosenqvist M, Nordenstrom J, Andersson M; Edhag 0 : Cardiac conduction in patients with hypercalcemia due to primary hyperparathyroidism. Clin Endocrinol 37:29-33, 1992. 3. Dubois F, Charlier P, Solal AC, Passa P, Gourgon R: Hyperparathyroide primitive revelee par des troubles du rhthyme cardiaque. Arch Mal Coeur 82:2071-2074, 1989. 4. Chadli M, Chaieb L, Jemni L, Chatti N, Allegue M, Zebidi A, Djaidane A: Bigeminal arrhythmia associated with hyperparathyroid crisis. Can Med Assoc J 138:1115-1116,1988.
January 1994 Volume 307 Number 1
MICHAEL E. MAY, MO, PHD
ABSTRACT: The effects of hypercalcemia on the heart and the resulting alterations of the electrocardiogram are well established. However, there are only rare reports of arrhythmias caused by hypercalcemia in primary hyperparathyroidism. This article describes a case of severe hypercalcemia secondary to hyperparathyroidism causing tachy-brady syndrome. KEY INDEXING TERMS: Arrythmia; Hypercalcemia. [Am J Med Sci 1994;307(1):43-44.]
Case Report An 84-year-old female was admitted to our facility on July 6, 1992, because of hypercalcemia and disorientation. Three weeks before this admission, she was admitted to another hospital with an episode of congestive heart failure. Cardiac monitoring during that admission revealed tachy-brady syndrome, with ventricular rates as low as 15 beats/minute. Apermanent pacemaker was provided. Serum calcium level at that time was 13.6 mg/dL. No treatment was given for hypercalcemia. Her past medical history included right nephrectomy secondary to renal calculi 50 years before and history of intermittent flank pain. Physical examination revealed an elderly, well-nourished, female who was disoriented but in no apparent distress. Her heart rate was 80 beats/min and her blood pressure was 92/70 mm Hg. A neck examination was normal. The lungs were clear to auscultation and her heart rhythm was regular, without murmur or gallop. An abdominal exam was unremarkable. Neurologic examination was notable for hyperreflexia and orientation to person only.
Pertinent Laboratory Data
Her serum chemistries included: 89 mg/dL urea nitrogen, 6.9 mg/dL creatinine, 18.2 mg/dL total calcium, 9.31 mg/dL ionized calcium, 4.8 mg/dL phosphorous, 0.9 ng/mL digoxin, and 25.6 ~g/mL procainamide (normal, 4 to 10 ~g/mL). A chest radiograph showed a normal cardiac silhouette with a permanent pacemaker. An electrocardiogram revealed a dual-chamberpaced rhythm with a rate of 85 beats/min and QRS duration of 280 msec. An electrocardiogram from June 18, 1992, (before pacing) showed sinus tachycardia with a rate of 100 beats/min, QRS duration of 90 msec, QT interval of 320 msec, and Q-aT interval of 230 msec. From the Vanderbilt University School of Medicine, Nashville, Tennessee. Correspondence: Michael E . May, MD, PhD, B3307 MCN, Vanderbilt University, Nashville, TN 37232-2230. THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
Hospital Course
On admission, a pulmonary artery catheter showed a pulmonary capillary wedge pressure of 7 mm Hg. Initial treatment consisted of hydration with normal saline to a wedge pressure of 15 mm Hg and subcutaneous injection of 100 units of calcitonin every 12 hours. Mental status improved, creatinine level decreased to 4.6 mg/dL, and calcium level fell to 13.3 mg/dL. The intact parathyroid hormone level was 1,102 pg/mL (normal, 10 to 65 pg/mL) and the parathyroid hormone mid-molecule level was 1,085 pmoljL (normal, 30 to 90 pmoljL). A neck ultrasound revealed a 2 .2 X 1.5 cm mass near the lower pole of the right thyroid lobe. A computed tomography scan confirmed the presence of a mass inferior to the right lobe of the thyroid. On the fifth hospital day, the patient underwent neck exploration with resection of a 4.06 g parathyroid adenoma. The histologic diagnosis was atypical parathyroid adenoma. Digitalis and procainamide were discontinued upon admission, but the patient continued to require artificial pacing. Just before the operation, an electrocardiogram showed underlying sinus rhythm with fusion complexes. Her calcium level then was 12.5 mg/dL. Postoperatively, the heart was in normal sinus rhythm. First-degree atrioventricular block persisted, but pacing was unnecessary. Her calcium level was 8.8 mg/dL and her creatinine level was 2.8 mg/dL on discharge. Discussion
The characteristic electrocardiographic changes found in association with hyperparathyroidism are prolongation of the P-R interval, shortening of the ST segment, and consequent shortening of the Q-T interval. 1 However, elevation of the serum calcium level secondary to hyperparathyroidism usually does not induce cardiac arrhythmias. Recently, Rosenqvist et aP have suggested that conduction disturbances may occur in patients with severe hypercalcemia. They noted an apparent correlation between severity of hypercalcemia and degree of atrioventricular block. Our patient had severe hypercalcemia by Rosenqvist's standards, with calcium levels ranging between 13.6 mg/dL (at the time of diagnosis of cardiac arrhythmias) and 18.2 mg/dL. Sinus arrest with slow ventricular rates and bouts of paroxysmal supraventricular tachycardia were present before pacing during hypercalcemia. No bradycardia 43
Cardiotoxic Calcemia
or supraventricular tachycardia requiring pacing occurred after resection of the parathyroid adenoma. The toxic effects of hypercalcemia on the myocardium are similar to those seen with digitalis intoxication. Our patient had received digitalis. Digoxin levels were not excessive and her conduction disturbance persisted after digitalis was discontinued. Previously, there have been 11 reports of serious arrhythmias and only 4 reports of high-degree atrioventricular block with sinus arrest attributed to hyperparathyroidism. 2-4 The serum calcium level in these cases ranged from 12.5 to 20.0 mg/dL. Our patient represents a fifth case of severe hypercalcemia with the latter conduction disturbance. In conclusion, this case demonstrates that hyperparathyroidism can present as clinically significant
44
cardiac arrhythmias. The arrhythmias are reversible with treatment of the hyperparathyroidism by resection of the parathyroid adenoma.
References
1. Beck GH, Marriott HJL: The electrocardiogram in hyperparathyroidism. Am J Cardiol 3:411-413, 1959. 2. Rosenqvist M, Nordenstrom J, Andersson M; Edhag 0 : Cardiac conduction in patients with hypercalcemia due to primary hyperparathyroidism. Clin Endocrinol 37:29-33, 1992. 3. Dubois F, Charlier P, Solal AC, Passa P, Gourgon R: Hyperparathyroide primitive revelee par des troubles du rhthyme cardiaque. Arch Mal Coeur 82:2071-2074, 1989. 4. Chadli M, Chaieb L, Jemni L, Chatti N, Allegue M, Zebidi A, Djaidane A: Bigeminal arrhythmia associated with hyperparathyroid crisis. Can Med Assoc J 138:1115-1116,1988.
January 1994 Volume 307 Number 1