A 42-year-old woman with a history of provoked pulmonary embolism 8 months ago presents to the emergency department with acute onset dyspnea and hemoptysis. She has been on warfarin maintenance therapy since her prior PE. Vital signs: temperature 37.2°C, heart rate 118/min, blood pressure 128/82 mmHg, respiratory rate 22/min, oxygen saturation 88% on room air. Physical examination reveals tachypnea and decreased breath sounds at the right lung base. Laboratory studies show INR 6.8, troponin 0.02 ng/mL (normal <0.04), and D-dimer >500 ng/mL. CT pulmonary angiography confirms acute pulmonary embolism with a right lower lobe subsegmental filling defect. The patient is started on intravenous unfractionated heparin, and warfarin is held. Which of the following best explains the clinical rationale for initiating heparin rather than increasing the warfarin dose in the acute management of this PE?

1. A)Heparin has superior bioavailability compared to warfarin due to its ability to cross the blood-brain barrier
2. B)Heparin can be rapidly reversed with protamine sulfate, whereas warfarin reversal requires fresh frozen plasma and vitamin K
3. C)Heparin achieves therapeutic anticoagulation within hours by potentiating antithrombin III, whereas warfarin requires 5-7 days to achieve full therapeutic effect by depleting vitamin K-dependent factorsGABARITO
4. D)Heparin directly lyses existing thrombi through activation of plasminogen, while warfarin only prevents new clot formation
5. E)Warfarin is contraindicated in patients with elevated INR values above 6.0 due to increased risk of spontaneous bleeding