| drug | mechanism | route | use | ADR |
| ttt of CHF | ||||
| cardiac glycosides | inhibit Na/K ATPase >large + in sod intracelullar >expel Na to extra and + Ca by electrogenic Na/Ca exchanger > + free Ca intra >w react e contractile pr >contr (N.B therapeutic effect by inhibition of 30% of enz) ** indirect effects : a) cholenergic > + baroreceptors sensitivity >reflex stim of vagal centers >inhibit SA node stim ectopic atrial beat formation b)adrenergic system (clear at high doses .in therapeutic doses >reflex reductn in sym act due to + baroreceptor sensitivity and ! sensitivity to peri adrenergic receptors ,, toxic dose >centrally induced stim of sym act >induce cardiac arrythmia | digitoxin ,digoxin from GIT ,, ouabain >IV | 1-ttt of CHF (symptomatic) 2-ttt of supraventricular arrythmia to protect ventricle from it | 1-CNS symptoms 2-other side effects as (abdominal cramps ,diarrhea ,vomiting) 3-cardiac toxicity may range from bradycardia to AV block ,atrial fibrillation ,ventricular tachycardia ,ventricular fibrillation ,cardiac arrest ***ttt of toxicity 1-stopping the use of cardiac GS then readjustment of dose 2-oral or IV K is used as K inhibit binding of GS to Na/K ATPase 3-antiarrythmiac drugs as lidocaine (for ventricular arryth) 4-B blocker (for arryht due to sym over stim) 5-Ca channel blocker (for supraventriculat arryth) 6-atropine (for parasym stim) |
| anti-arrythmiac drugs | ||||
| Quinidine (class 1A) | bind to Na channels prevent sod influx thus slow phase 0 depolarization and also inhibit phase 4 spontaneous depolarizatn | quinidine sulphate orally | atrial and ventricular arrythmias | high doses can induce arrythmia ,it can cause AV block ,hyperkalemia + quinidine toxicity ,quinidine can + digitalis plasma level so + toxicity of DGS |
| Procainamide (class 1A) | similar to quinidine | orally and rarely IV | reversible lupus erythematosus -like syndrome ,toxic dose cause arryth ,cnd depression ,hallucination | |
| Disopyramide (class 1A) | similar to quinidine | orally | anticholenergic activity eg dry mouth ,urinary retention ,blurred vision ,constipation | |
| Lidocaine (class 1B) | reduction in the phase 0 of action potential . Unlike quinidine >it supress abnormal automaticity . Like quinidine >it abolish ventricular re-entry | IV because of rapid metab in liver if given orally | used for ventricular arrythmia ,it has little effect on atrial arryth or AV junction arryth | CNS effects (drowsiness ,slurred speech ,agitation ,cardiac arryth may also occur) |
| Phenytoin | similar to lidocaine | ,it + conduction at AV node so it is useful in digitalis induced arryth | ||
| Flecainide (class 1 c) | supress phase 0 action potential and causes inhibition of conductn and reductn of automaticity | premature ventricular contractn | dizziness ,blurred vision ,headache and nausea ,cardiac arryth may occur | |
| B adrenergic antagonists (class 2) | diminish phase 4 depolarization thus depress automaticity ,they prolong AV conductn and ! HR and contractility | ventricular arrythmia due to + sym act ,it is also useful for atrial arryth | ||
| Bretylium | class 3 block potassium channels thus inhibit depolarization of cardiac cell by inhibit inward pot current ,they prolong duratn of action eout alter phase 0 .instead they prolong effective refractory period | parentrally due to its poor abs | restricted to life threatening ventricular arryth | postural hypotension |
| Aminodarone | sever supraventricular and ventricular tachyarryth | clinical use is limited due to toxicity | ||
| class 4 | Ca channel blocker w + inward Ca current result in ! In the phase 4 spontaneos depolarization | |||