A 30-year-old woman with hemoglobin of 5 g/dL develops resting tachycardia, a soft flow murmur, and a cardiac output measured at 8 L/min. The main mechanisms sustaining this high output state are:
- A Reduced blood viscosity lowering vascular resistance plus tissue hypoxia causing generalized vasodilation ✓
- B Sympathetic stimulation increasing contractility with unchanged total peripheral resistance
- C Expansion of plasma volume raising preload above normal levels
- D Increased 2,3-BPG shifting the oxygen dissociation curve leftward to improve loading
Explanation
Anemia lowers viscosity directly, reducing resistance, and reduced oxygen delivery triggers local tissue vasodilation; both effects cut afterload and permit a large rise in stroke volume. Sympathetic activation contributes tachycardia but cannot alone double output if resistance were unchanged. Plasma volume actually falls relative to red cell mass in severe anemia. Reduced 2,3-BPG effect is wrong in direction: anemia raises 2,3-BPG, shifting the curve rightward to ease unloading.
Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.
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