DEVTOME.COM HOSTING COSTS HAVE BEGUN TO EXCEED 115$ MONTHLY. THE ADMINISTRATION IS NO LONGER ABLE TO HANDLE THE COST WITHOUT ASSISTANCE DUE TO THE RISING COST. THIS HAS BEEN OCCURRING FOR ALMOST A YEAR, BUT WE HAVE BEEN HANDLING IT FROM OUR OWN POCKETS. HOWEVER, WITH LITERALLY NO DONATIONS FOR THE PAST 2+ YEARS IT HAS DEPLETED THE BUDGET IN SHORT ORDER WITH THE INCREASE IN ACTIVITY ON THE SITE IN THE PAST 6 MONTHS. OUR CPU USAGE HAS BECOME TOO HIGH TO REMAIN ON A REASONABLE COSTING PLAN THAT WE COULD MAINTAIN. IF YOU WOULD LIKE TO SUPPORT THE DEVTOME PROJECT AND KEEP THE SITE UP/ALIVE PLEASE DONATE (EVEN IF ITS A SATOSHI) TO OUR DEVCOIN 1M4PCuMXvpWX6LHPkBEf3LJ2z1boZv4EQa OR OUR BTC WALLET 16eqEcqfw4zHUh2znvMcmRzGVwCn7CJLxR TO ALLOW US TO AFFORD THE HOSTING.

THE DEVCOIN AND DEVTOME PROJECTS ARE BOTH VERY IMPORTANT TO THE COMMUNITY. PLEASE CONTRIBUTE TO ITS FURTHER SUCCESS FOR ANOTHER 5 OR MORE YEARS!

Atrial Fibrillation

Pathophysiology

On a general basis, cardiac arrhythmias are due to abnormal impulse generation or abnormal impulse conduction or both (1).

Abnormal Impulse Initiation

The abnormal generation of an electrical impulse is due to abnormal automaticity (1,2). If the automaticity of the SA node is increased, the result would be an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). Various cardiac fibres have the ability to have automaticity (1,2). This includes the Purkinje fibres, AV node, artrial tissue and ventricular tissue (1,2). Abnormal atrial automaticity may cause atrial fibrillation (1,2). The abnormal automaticity that originates from pulmonary veins can also precipitate atrial fibrillation (1,2).

The automaticity of the fibres from the heart are controlled partly by the sympathetic and parasympathetic nervous systems (1,2). Increased activity of the sympathetic nervous system may increase the automaticity of the SA node or other automatic cardiac fibres (1,2). Factors that can also lead to abnormal increases in automaticity of the extra SA nodal tissues include hypoxia, artrial or ventricular stretch, and electrolyte abnormalities such as hypokalemia or hypomagnesemia (1,2).

Abnormal Impulse Conduction

Abnormal impulse conduction is referred to as re-entry (1,2). This is often initiated due to abnormal premature electrical impulse and as a result the mechanism of athrymia is due to both abnormal impulse formation and abnormal impulse conduction (1,2). Reentry requires three conditions to be present (1,2). There has to be at least two pathways down which an electrical impulse may travel (1,2). There also has to be an unidirectional block in one of the conducting pathways (1,2). Lastly, there has to be a slowing of the velocity of the impulse conduction through the other pathway that is used for conducting (1,2).

In normal circumstances, if a premature impulse is conducted, it cannot be conducted in either direction down either pathway as the tissue is currently in the absolute refractory period from the previous beat (3). A premature impulse could be conducted down both pathways if the timing makes it slightly premature and it arrives after the tissue is no longer refractory (1,2). If refractoriness is prolonged down one of the pathways, a precisely well timed premature beat could be conducted down one pathway but cannot be conducted in either direction in the pathway with prolonged refractoriness due to the tissue still being in the absolute refractory period (1,2). If the third condition for reentry is present, which is if the velocity of the impulse conduction in another pathway is slowered, the impulse that travels forward down the other pathway still will not be conducted (1,2). Since the impulse in the other pathway is traveling at such a slow pace, when it circles around and travels upward down the other pathway, that pathway will no longer be in its absolute refractory period and now the impulse may travel upward in that pathway (1,2). The electrical impulse will reenter a previously stimulated pathway in the wrong direction and will cause a circular movement of electrical impulses (1,2). When the impulse travels in this circular fashion, it will excite each cell around it and if the impulse travels at a rate that is faster than the intrinsic rate of the SA node, a tachycardia will occur (1,2). A prolonged refractoriness or slow impulse conduction speed may be due to various regions that include myocardial ischemia, and past myocardial infarction (1,2).

Goals of Therapy

Goals include reducing the symptoms, reducing the morbidity which includes improved heart function, reduce incidence of strokes, reduce emergency department visits, reduce hospitalization rates and improve quality of life (3). There is limited data suggested to reduce mortality, but that is also a desired goal (3). Specific goals include controlling and cure precipating causes, controlling rapid ventricular rate, preventing thromboembolic complications, converting AF to NSR and reducing recurrences of AF by attempting to maintain NSR (3).

Symptoms

Symptoms of atrial fib include reduced exercise tolerance, weakness, fatigue, dizziness, lightheadedness, palpitations, chest pain, shortness of breath, syncope or may also be asymptomatic (up to 20% of patients) (1). In the EKG, there are no p waves, irregular and narrow QRS complexes (1). Complications can include heart failure, chest pain which also includes MI or angina (1). The pulse is irregularly irregular in rhythm, rate and volume because only occasional impulses will penetrate the AV node (1). Various factors can increase the risk of development of Afib (1). These include male gender, >50 years of age, obesity (greater than 30 kg/m2 BMI), hypertension, hypothyroidism, diabetes, family history of AF in a first degree relative, particularly a parent, clinically overt heart disease, and inflammatory process (1). This means that the adjusted stroke rate is 1.9% per year. Rate control is the preferred initial long term strategy (1). Diltiazem is an appropriate agent for rate control therapy (1). The major concern is the concurrent St. John’s wort therapy which may decrease the concentration of diltiazem due to St. John’s wort being an inducer for P-glycoprotein, which Diltiazem is a substrate of (2). Thus, St. John’s wort should be discontinued.

References

  1. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 7th ed. Toronto: McGraw-Hill; 2007. p. 288
  2. Van Norman GA, Quan KJ, Davoudi R. Atrial Fibrillation. MD Consult [online]. Maryland Heights MO: Elsevier Inc. 2011 [cited 2012 Mar 3]. Available from: www.mdconsult.com
  3. Pritchett EL. Management of atrial fibrillation. N Engl J Med 1992(19); 326:1264

Disclaimer

This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers


QR Code
QR Code atrial_fib (generated for current page)
 

Advertise with Anonymous Ads