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Related Concept Videos

Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...

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Related Experiment Video

Updated: Jul 13, 2026

Mouse Cardiac Arrest Model for Brain Imaging and Brain Physiology Monitoring During Ischemia and Resuscitation
07:18

Mouse Cardiac Arrest Model for Brain Imaging and Brain Physiology Monitoring During Ischemia and Resuscitation

Published on: April 14, 2023

Cardiovascular collapse associated with beta blockade in thyroid storm.

R Dalan1, Melvin K Leow, Melvin C Leow

  • 1Department of Endocrinology, Tan Tock Seng Hospital, Singapore. rinkoo99@yahoo.com

Experimental and Clinical Endocrinology & Diabetes : Official Journal, German Society of Endocrinology [And] German Diabetes Association
|August 19, 2007
PubMed
Summary
This summary is machine-generated.

Oral propranolol use in thyroid storm patients with low cardiac output may precipitate cardiorespiratory arrest. Consider ultra-short-acting beta-blockers like esmolol cautiously as a safer alternative.

Related Experiment Videos

Last Updated: Jul 13, 2026

Mouse Cardiac Arrest Model for Brain Imaging and Brain Physiology Monitoring During Ischemia and Resuscitation
07:18

Mouse Cardiac Arrest Model for Brain Imaging and Brain Physiology Monitoring During Ischemia and Resuscitation

Published on: April 14, 2023

Area of Science:

  • Cardiology
  • Endocrinology
  • Pharmacology

Background:

  • Thyroid storm is a life-threatening condition characterized by exaggerated hyperthyroid symptoms.
  • Management often involves beta-blockers to control adrenergic symptoms.

Observation:

  • Three cases of thyroid storm patients experienced sudden cardiorespiratory arrest shortly after oral propranolol administration.
  • These events occurred within hours to 12 hours of initiating propranolol therapy.

Findings:

  • Oral propranolol may pose a risk for cardiorespiratory arrest in select thyroid storm patients, particularly those with low-output cardiac failure.
  • The timing of arrest suggests a potential adverse reaction to oral beta-blocker therapy in this critical state.

Implications:

  • Clinicians should exercise caution when prescribing oral propranolol to thyroid storm patients with compromised cardiac function.
  • Intravenous esmolol, an ultra-short-acting beta-blocker, may be a safer alternative when beta-blockade is necessary, with careful monitoring.