## Pathophysiology of Hyperthyroidism **Key Point:** Thyroid hormones (T3 and T4) increase cellular metabolic rate, oxygen consumption, and heat production. They enhance cardiac contractility and heart rate through β-adrenergic sensitization. ### Characteristic Cardiovascular Features | Feature | Mechanism | Clinical Significance | |---------|-----------|----------------------| | Tachycardia (resting and sleeping) | Direct β-adrenergic effect on myocardium | Persistent, even at rest | | Increased cardiac output | ↑ Heart rate + ↑ Contractility | High-output state | | Widened pulse pressure | ↑ Systolic BP, ↓ Diastolic BP | Bounding pulse | | Decreased peripheral resistance | Vasodilation from thyroid hormones | Warm extremities | **High-Yield:** In hyperthyroidism, cardiac output is **increased** (not decreased). The heart works harder and faster, leading to a hyperkinetic circulation. Stroke volume may be normal or slightly increased due to enhanced contractility. ### Metabolic Features **Key Point:** - Weight loss despite increased appetite (increased caloric demand) - Heat intolerance and excessive sweating (↑ thermogenesis) - Increased metabolic rate by 20–40% ### Why Option 3 is Wrong Decreased cardiac output is the hallmark of **hypothyroidism** (low-output state), not hyperthyroidism. In hyperthyroidism, the cardiac output is elevated due to: 1. Increased heart rate 2. Enhanced myocardial contractility (thyroid hormones increase β-receptor sensitivity) 3. Reduced peripheral vascular resistance This high-output state can precipitate or worsen atrial fibrillation, especially in older patients. **Clinical Pearl:** A sleeping heart rate >90 bpm in a young patient should raise suspicion for hyperthyroidism. The tachycardia does not normalize with rest or sleep — this is a key discriminator from anxiety-driven tachycardia.
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