A 55-year-old man with dilated cardiomyopathy has an ejection fraction of 28%. His cardiac output is 3.2 L/min with a heart rate of 90 bpm. His arteriovenous oxygen difference is 7.5 mL/dL. Which of the following compensatory mechanisms is MOST responsible for maintaining tissue oxygenation despite the low cardiac output?
- A Increased myocardial oxygen extraction
- B Right shift of the oxyhemoglobin dissociation curve due to elevated 2,3-BPG ✓
- C Activation of the renin-angiotensin-aldosterone system increasing preload
- D Increased respiratory rate compensating for reduced perfusion
Explanation
In chronic low-output heart failure, tissues compensate by increasing 2,3-bisphosphoglycerate (2,3-BPG) in red blood cells, which right-shifts the oxyhemoglobin dissociation curve (decreases oxygen affinity), facilitating greater oxygen unloading at the tissue level. The elevated A-V O2 difference of 7.5 mL/dL (normal ~5 mL/dL) reflects this enhanced peripheral extraction. While RAAS activation increases preload, it does not directly enhance tissue oxygen delivery efficiency; increased 2,3-BPG is the primary metabolic adaptation to maintain tissue oxygenation when cardiac output is chronically reduced.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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