Warfarin

How it works

Warfarin inhibits vitamin K epoxide reductase, reducing hepatic synthesis of the vitamin K–dependent clotting factors II, VII, IX and X (and proteins C and S). Because circulating factors must first be cleared, full anticoagulation is delayed by several days.

Prescribing in practice

• The dose is individualised to a target INR (commonly 2.0–3.0 for AF and most VTE); the structured dose field is indicative only and must be titrated to the patient's INR.
• Onset is delayed — where immediate anticoagulation is needed, a parenteral anticoagulant is used to bridge until the INR is therapeutic.
• Many drugs and foods alter the INR; review interactions at every medication change and counsel on consistent dietary vitamin K.
• High INR or bleeding is managed per local protocol (e.g. vitamin K, prothrombin complex concentrate).

Monitoring

INR guides dosing — frequent during initiation and after any change, then at stable intervals. Re-check the INR after starting or stopping any interacting drug.

Counselling the patient

• Take it at the same time each day; do not double up after a missed dose without advice.
• Keep dietary vitamin K (green leafy vegetables) consistent rather than avoiding it.
• Report unusual bruising or bleeding, dark stools, or blood in the urine.
• Tell any prescriber, pharmacist or dentist that you take warfarin before new medicines or procedures.

Evidence & guidelines

Anticoagulation in AF is guided by stroke-risk assessment (e.g. CHA₂DS₂-VASc) per NICE NG196. DOACs are generally preferred first-line, with warfarin retained where DOACs are unsuitable (e.g. mechanical heart valves, antiphospholipid syndrome).