3 High-Yield Paradoxes: COPD, warfarin, carbon monoxide

Here are a few counterintuitive fun facts that almost always come up on the USMLE:

• Oxygen can worsen respiratory failure in COPD
• COPD → chronically high CO₂ → desensitizes chemoreceptors → patients rely on hypoxic respiratory drive (low O₂ triggers breathing).
• Over-oxygenation → removes hypoxic drive → causes hypoventilation and further CO₂ retention.
• Takeaway: In COPD, aim for O₂ saturation of 88%-92%. Any higher, and patients may stop breathing!
• Warfarin increases clotting risk before preventing clots
• Warfarin inhibits vitamin K-dependent clotting factors (II, VII, IX, X) AND natural anticoagulants (Proteins C & S).
• Proteins C & S have shorter half-lives → depleted first → transient hypercoagulable state initially.
• Takeaway: Always bridge warfarin therapy with fast-acting heparin until INR is ≥2.0. Otherwise, clotting risk increases!
• Carbon monoxide (CO) poisoning causes hypoxia but increases SpO₂
• CO binds hemoglobin with over 200 times the affinity of oxygen → oxygen delivery to tissues is severely reduced.
• Pulse oximetry can't distinguish between oxyhemoglobin and carboxyhemoglobin (COHb), so SpO₂ looks reassuring.
• Takeaway: Diagnose CO poisoning clinically. Confirm with ABG (carboxyhemoglobin levels), not pulse ox!

These topics trip a lot of students up, but once you remember they're the opposite of what they seem, they'll be easy points on your exam.