Assessment Description Create an 8-9 slide presentation with speaker notes about a selected disease process and drug class. The presentation should provide content specific information on the selected...

Atrial Fi
illation and Warfarin
Atrial Fi
illation and Warfarin
Disease Process
This presentation emphasises the disease process and drug class for A-fib (atrial fi
illation). 
Atrial fi
illation causes the signal in a heart's upper chamber to become e
actic. As a consequence, the upper chamber begins to quiver.
The AV node is therefore deluged with signals seekinging to reach a lower heart chamber (ventricle).
This results in a rapid and unstable heart rhythm (Lakkireddy, 2020).
A-fib is a type of a
hythmia (anomalous and usually fast heartbeat) that can develop a blood clot in the heart. 
An initial trigger often stimulates ectopic foci in the atria, usually within the pulmonary veins, allowing for asynchronous electrical impulse activation, culminating in atrial fi
illation.
These impulses are e
atic, and heart rates vary significantly (Murtaza et al., 2021).
2
Drug Class
Warfarin is the the anticoagulant. It functions by
inging down the blood's ability to clot.
Anticoagulants function by hindering the generation of actions of several coagulation variables that are reasonably exist in the bloodstream.
These medications are often utilised to avoid the development of blood clots in the arteries or veins, and also the growth of a thrombus in the circulation (Randhawa et al., 2020).
Warfarin is used in clinical practice to avoid clots caused by afib, and it is an effective treatment.
Warfarin can impair the generation of active clotting components by depleting active vitamin K stores (Murtaza et al., 2021).
3
Pharmacokinetics
In the instance of A-fib, warfarin takes a long time to take action.
It has a modest distribution volume (10 L/70 kg) and is removed by metabolising in the liver with a very low elimination rate (0.2 L/h/70 kg). 
The half-life of elimination is approximately 35 hours.
In addition, the therapeutic impact of warfarin is prolonged for 4-5 days, until each activated factor II, IX, VII, and X in the bloodstream has been depleted (Murtaza et al., 2021).
Warfarin attaches to plasma proteins in a
oad and non-specific way.
Warfarin becomes protein bound to a level of 97 percent to 99.9 percent, leaving only a small proportion of the medication open in blood to exert its physiologic effects (Zhou et al., 2019).
4
Pharmacodynamics
In the instance of A-fib, warfarin's significant pharmacological activity is to block vitamin K reductases, which are accountable for the vitamin K-based ca
oxylation of glutamic acid residues of coagulation proteins.
Warfarin hinders coagulation passively by intercepting vitamin K from becoming replenished, which...