Abstract
Thyroid hormones have an integral role in cardiac homeostasis, and hypothyroidism may be associated with impaired myocardial contractility, altered endothelial function, and blunted response to catecholamines. Herein, the case of a patient with undiagnosed severe hypothyroidism, who developed an acute myocardial infarction and cardiac arrest during sedation for bronchoscopy, is described. He required prolonged resuscitation, which included coronary catheterization and placement of an intra-aortic balloon pump. The resuscitation was noteworthy for blunted physiologic responses to large doses of epinephrine; in particular, persistent bradycardia without evidence of conduction abnormalities. On admission to the intensive care unit, he was hypothermic (31.4°C), bradycardic, and hypotensive. Laboratory investigations revealed profound hypothyroidism, and thyroid hormone replacement was initiated. Within hours of initiation of thyroid hormone replacement, the need for vasopressor support was reduced. He had a complete recovery and was discharged home neurologically intact. The authors of the present report believe that this favorable neurologic outcome could be attributed to efficient resuscitation, prompt coronary revascularization, and profound hypothermia likely related to a hypothyroidism-associated hypometabolic state.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1410-1414 |
| Number of pages | 5 |
| Journal | Journal of Cardiothoracic and Vascular Anesthesia |
| Volume | 36 |
| Issue number | 5 |
| DOIs | |
| State | Published - May 2022 |
Keywords
- amiodarone
- cardiac arrest
- hypothyroidism
- myocardial infarction
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Anesthesiology and Pain Medicine
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