Tachycardia in a 61-Year-Old Woman

Jeffrey Siegelman, MD; Daniel M. Lindberg, MD

Disclosures

June 24, 2015

Management of thyrotoxicosis consists of a five-pronged, ordered approach, targeting each step in the biosynthetic pathway of thyroid hormone and its activity on target tissues.

Treatment begins with administration of propylthiouracil (PTU) or methimazole, both of which act by inhibiting new hormone synthesis. PTU has the added effect of decreasing peripheral T4 to T3 conversion. Beta-blockers are then used to inhibit target activity of thyroid hormone. Propranolol is the preferred agent because it also blocks peripheral conversion of T4. When cardioselective agents are preferred, atenolol or metoprolol may be used. At least 1 hour after administration of PTU or methimazole, the patient may be given iodide to inhibit further thyroid hormone release.

Iodine must be given only after synthesis of new hormone is blocked because iodide administration can have the undesired effect of increasing new hormone synthesis. Potassium iodide or Lugol solution of iodine is recommended. Peripheral conversion of T4 to T3 is blocked, as noted above, and dexamethasone may be used as well. Further treatment is supportive and may include acetaminophen for fever and hydrocortisone if the patient is hypotensive as a result of adrenal insufficiency. Salicylates are contraindicated because they displace bound thyroid hormone in the blood.[2,3]

Of note, PTU, methimazole, and iodide solutions are all classified as pregnancy class D and, as such, should not be used in pregnancy.

With regard to the management of cardiac symptoms related to thyrotoxicosis, treatment is focused on reducing adrenergic drive to the heart and restoring normal cardiac rhythm. As mentioned above, beta-blockers are very effective for rapid hemodynamic improvement. Either propranolol or metoprolol given intravenously can be used to improve heart rate control in either sinus tachycardia or atrial fibrillation. In severe cases, a continuous infusion of esmolol may be required for rate control. Amiodarone should be avoided when treating atrial fibrillation from thyrotoxicosis because of its high iodine content, which may induce or exacerbate thyroid storm.

If a patient is hemodynamically unstable from atrial fibrillation, direct current cardioversion should be used. If symptoms of pulmonary congestion appear, diuretics may be used. Other drugs for heart failure (angiotensin-converting inhibitors, angiotensin receptor blockers, or aldosterone receptor antagonists) are reasonable agents in patients who have depressed left ventricular systolic function.

Anticoagulation is recommended for patients in atrial fibrillation secondary to thyrotoxicosis. The American College of Cardiology/American Heart Association/European Society of Cardiology guidelines recommend anticoagulation with warfarin to an international normalized ratio of 2-3 until the patient is euthyroid, after which recommendations and risk stratification are the same as those for atrial fibrillation without thyrotoxicosis.[3]

This patient's clinical presentation bordered between thyrotoxicosis and thyroid storm, and she was hemodynamically stable. She was treated immediately with propranolol and PTU and was admitted to a monitored bed in the medical service. Because her clinical condition improved and she remained stable, the admitting team chose to forgo further therapy with iodine and steroids. Her atrial fibrillation resolved within 12 hours, but an echocardiogram revealed cardiomyopathy with a left ventricular ejection fraction of 45% that was attributed to her long-standing hyperthyroidism.

A diagnosis of Graves disease was made. Treatment with methimazole and metoprolol was continued, and anticoagulation was initiated. Five months later, the patient was still taking methimazole. Her thyroid function had normalized, her cardiomyopathy had reversed, and her anticoagulation was discontinued, because atrial fibrillation did not recur. Incidentally, tuberculosis was ruled during her admission with three induced sputum samples.

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