NR567 Final Exam Study Guide latest update 2023

Therapeutic dosing and monitoring of warfarin (Coumadin) Treatment with warfarin should be initiated with standard doses of 5–10 mg. The initial adjustment of the prothrombin time takes about 1 week, which usually results in a maintenance dosage of 5–7 mg/d. The prothrombin time (PT) should be increased to a level representing a reduction of prothrombin activity to 25% of normal and maintained there for long-term therapy. When the activity is less than 20%, the warfarin dosage should be reduced or omitted until the activity rises above 20%. Inherited polymorphisms in 2CYP2C9 and VKORC1 have significant effects on warfarin dosing; however, algorithms incorporating genomic information to predict initial warfarin dosing were no better than standard clinical algorithms in two of three large randomized trials examining this issue. The recommended INR for prophylaxis and treatment of thrombotic disease is 2–3. Patients with some types of artificial heart valves (eg, tilting disk) or other medical conditions increasing thrombotic risk have a recommended range of 2.5–3.5. Types of anticoagulants- mechanisms of action and indications for use • Vitamin K antagonists. • Direct Oral Anticoagulants (DOACs) • Low molecular weight heparins (LMWH) What is the mechanism of action for anticoagulants? • Anticoagulants achieve their effect by suppressing the synthesis or function of various clotting factors that are normally present in the blood. Such drugs are often used to prevent the formation of blood clots (thrombi) in the veins or arteries or the enlargement of a clot that is circulating in the bloodstream. What are the indications for anticoagulants? • Anticoagulation is an important component of the management strategy for several common medical conditions. It is indicated for the prevention of recurrent thrombosis in patients with venous thromboembolism (VTE), which includes deep venous thrombosis and pulmonary embolism, and ischemic stroke. Understand Starling’s law The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction. This assumes that other factors remain constant. The Frank–Starling law of the heart (also known as Starling's law and the Frank–Starling mechanism) represents the relationship between stroke volume and end diastolic volume.[1] The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant. [1] As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length,[2] without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality. Medications which increase and decrease preload and afterload For heart failure, ACE inhibitors and ARBs reduce workload on the myocardium by reducing both preload and afterload.