Exactly.#yes you have guessed it very right. let me add a bit more to it. actually, both Quinidine and Procainamide are Class 1A anti-dysrrythmic drugs. their main cardiac effect is depressant via blockage of Na channels and all that you know. besides that, both drugs have mild intrinsic anti-muscarinic effects(mainly increased SA nodal rate and increased heart rate),this definitely counter-acts their primary depressant effect,so the drug that has lesser anti-muscarinic effect will be more efficacious in manifesting its primary anti-depressant effect i.e Procainamide. okay. thats it!
Quinidine vs. Procainamide
This sentence has been confusing me for some time now:
"Perhaps the most important difference between quinidine and procainamide is the less prominent antimuscurinic action of procainamide. Therefore, the directly depressant actions of procainamide on sinoatrial and atrioventricular nodes are not as effectively counterbalanced by drug-induced vagal block as in the case of quinidine."
So, how exactly does drug-induced vagal block counterbalance the effects of quinidine?
If quinidine has antimuscurinic action, that means it inhibits the parasympathetic control to the heart. If it inhibits the parasympathetic influence, and parasympathetic control is dominant out of the two systems, that makes the sympathetic effects more pronounced, i.e. increased. If sympathetic effects on the heart are 'increased,' that means that quinidine's action of depressing the SA/AV nodes are being opposed, or 'counterbalanced,' since sympathetic stimulation will obviously be excitatory.
So, quinidine would induce better counterbalancing of its depressant effects through its antimuscurinic action which leads to sympathetic dominance, than would procainamide.
That's my best guess.
I've been up too long to figure this out, but I really needed to write it down somewhere to get to the bottom of it.
"Perhaps the most important difference between quinidine and procainamide is the less prominent antimuscurinic action of procainamide. Therefore, the directly depressant actions of procainamide on sinoatrial and atrioventricular nodes are not as effectively counterbalanced by drug-induced vagal block as in the case of quinidine."
So, how exactly does drug-induced vagal block counterbalance the effects of quinidine?
If quinidine has antimuscurinic action, that means it inhibits the parasympathetic control to the heart. If it inhibits the parasympathetic influence, and parasympathetic control is dominant out of the two systems, that makes the sympathetic effects more pronounced, i.e. increased. If sympathetic effects on the heart are 'increased,' that means that quinidine's action of depressing the SA/AV nodes are being opposed, or 'counterbalanced,' since sympathetic stimulation will obviously be excitatory.
So, quinidine would induce better counterbalancing of its depressant effects through its antimuscurinic action which leads to sympathetic dominance, than would procainamide.
That's my best guess.
I've been up too long to figure this out, but I really needed to write it down somewhere to get to the bottom of it.
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Does somebody knows how augmentin works? I was prescribed and have to take it a while =_=
Augmentin is bactericidal and works by inhibiting the synthesis of bacterial cell walls.Does somebody knows how augmentin works? I was prescribed and have to take it a while =_=
Amoxicillin inhibits bacterial cell wall mucopeptide synthesis. Clavulanic acid inactivates a wide range of beta-lactam enzymes found in bacteria resistant to beta-lactam antibiotics:thumbsup:
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