The mechanism of action of rivaroxaban involves the competitive inhibition of factor Xa. Factor Xa, a crucial component of the common pathway of the clotting cascade, normally binds with prothrombin on the surface of activated platelets and catalyzes the hydrolysis of prothrombin into its active form, thrombin (Pratt & Cornely, 2014, pp. 177-178). Since factor Xa is the first synthesized component of the common pathway of the clotting cascade, the inhibition of this clotting factor results in the disruption of both the intrinsic and extrinsic pathways of the blood clotting cascade. Because activated thrombin can no longer be produced, the blood clotting cascade is halted and thrombi formation ceases. It is in this way that Apixaban indirectly inhibits platelet aggregation caused by thrombin formation. Due to this mechanism of action, rivaroxaban does not dissolve preexisting clots since it has no effect on fibrin or platelets. It is also important to note that the action of rivaroxaban can be reversed with the use of an antidote. Two potential antidotes, andexanet alfa and ciraparantag, are currently in development (Connors, 2015, p. 2471).
Side Effects. The use of rivaroxaban is associated with a number of side effects. Common side effects of rivaroxaban can include bruising, hemorrhage from gums, epistaxis, hematuria, black stool, and faintness. More serious adverse side effects associated with the use of this medication can include, but are not limited to hypotension, hemorrhage, spinal epidural hematoma, hemorrhagic stroke, and retroperitoneal