A 35-year-old woman with severe iron deficiency anaemia (haemoglobin 5 g/dL) presents with exertional dyspnoea and a wide pulse pressure. Her echocardiogram shows a hyperdynamic left ventricle with ejection fraction 70%. The primary mechanism of her high-output state is:

• A Increased blood viscosity forcing the heart to generate higher pressures
• B Expansion of plasma volume secondary to sodium retention alone
• C Direct chronotropic stimulation of the sinoatrial node by erythropoietin
• D Tissue hypoxia causing peripheral vasodilation, which reduces afterload and reflexly raises cardiac output ✓

Explanation

Anaemia produces high-output failure through two linked mechanisms: reduced blood viscosity lowers peripheral resistance, and impaired oxygen delivery triggers local tissue vasodilation. The resulting fall in total peripheral resistance is countered by baroreceptor-mediated increases in heart rate and stroke volume, raising cardiac output. Viscosity is decreased, not increased, which eliminates option A. If prolonged, this state leads to eccentric hypertrophy and biventricular failure.

Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.

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