Pharmacology of Cardiovascular System. Pharmacology. Pharmacotherapy. Pharmacy

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31.3.2014 31,3.2014 Risk Factors of Cardiovascular Classification of Antiarrhythmics Class la Antiashythmics Diseases, “Regn eaten ene Pharmacology of “lon potest (AP) cna the h logy eae Eats e-em duration of Apo sow Cardiovascular System ‘rent mes ees ‘eontonenion on eees ee cend conduction in at, n Purkinje Mbers ond ventrices + Meatatestsctemts gro —- | + Rotated mate cea Quinidine Ck iarhythmi ‘+ Chrical use i phormacological Block of Na channel, do ntact ‘ARRHYTHMIAS ‘*Qsgin: based on disturbances of caroverden woe fteton ad spond ot AP hcenee teeth +H (ischemic heart disease) sped, rear, formation an one ‘ute forms: unstable angina pectoris ana e snap ‘Cause: damage to the heart mascle, SE - GT, olersie stom, ‘Shorten the AP duration and (4); myocar iforcton (Mt) ‘aused by eo hypoxemia, schema, condcton abnormalities, the risk of refractory perio irene ferns amon. HD; Frpotalems or Bs erect ‘entreulr frtaton exertional AP, mixed), varont; ater ‘Goal of Theraay: restore norm 7 ineract St dysreytmie for of IHD Fit, prevartarytimiaretum, ‘Numerous cru interactions “+HYPERTENSION reduc ik of he mo srl Antianhythmics Antythmia treatment Lidocaine, timecaine Mexietne +e ot atts nde automat, || eign eceney een 9.0 imo entre roe venice’ sytney Tl urate of AP ttre and poses Soar ne || aetna pacanaes Saw linsable AP depolarization Fdotrequency ablation : administration long-term ater ML gl] + surge treatment a ne ee | aj 31.3.2014 Class Io Antiarthythmics ‘Blockade of Nav channel, reduces: the steepness of the onset of AP ‘Slow conduction, only a small effect ‘on the repolarization Propafenone ‘+Recuction of heart rate and BP ‘1: Paroxysmal SV arrhythmias, lfe- threatening ventricular arrhythmias; ater Mt ‘Regular ECG monitoring is needed, the sk of errythmiae ‘After v. application: effect immediatly, fasts ford h Class Il Antiarrhythmics spices {Prevesti of stachoamines on «They ea ryt sade, Esra os mee ites nasa fy {Egor acenein alll Sotalol ‘+Extends the duration of AP, and slows repolarization ‘Reduces myocardial O; consumption ‘and leeds to a decine in cording swore ‘01: snus and SV arrhythmia, ata ‘and extraventricuar extrasystoles =e Class Ill Antiarrhythmics ‘Amniodarone, bretyum ‘Block K* channels extend AP and reiuces sympathese sctvity ‘#1: SV and ventreular tachycardia, — | 313.2014 ‘Exteely Betiy +E pera ‘Nesemectve Aa supcesing cyt dont SE," thoi disorders, nepaotoiy, ence ot rene ‘Amiodarone EM moray nd ute Mat ih Hk of Class IV Antiarrhythmics #Ca™* channel blockers Verapamil itiazem ‘Prolong the reractary phase ‘+Recluce the frequency of impulses in the SA node — | application ‘Decreases eutomatcty of sinus node ‘and siows conduction inthe SA node, Sow responce of vertriclar armythima dusng SV arehythmia sfiseehoice drug — of Adenosine encaen ‘+ Alaicform of IHD (chest pain) Imbalance between myocardial MTB demands and possibes of ts Supply by 0, ‘*Recuction in coronary pertusion, arterial stenosis, coronary artery Spasm ‘Goals of PT: adjustment of Imbalances, improve bleed fom, infuence of atherogenesis ‘sntrates +08 ‘Blockers SAS Pharmacotherapy of Angina Pectoris oF CaP channels _ | Nitrates (Nitrodilators) ‘beter acon, decreased venous retin ‘Redcat vente ttng ond ‘npropiyacteadmiisyation, they edu he reqncy ofa + Senin. NGL 9 rapid ent of. ees fc 313.2014 Beta-blockers ‘Slow heart ate ‘Reduce penpheral vascular Fesistance and myocardial fontractity ‘Improve coronary fow and reduce myocardial O; demands ‘seduce the indgence of anginal ‘attacks and CV complications | Calcium channel blockers ‘Reduce Ca inthe cytoplasm of smooth muse cas ‘bitiazem (oscar), verapamil (etn, tata), ifledipine (Cx), ‘inyarepyrans of. gen ‘sVasodaton, decreased blood pressure, decreased heart rate, towing of fonducton inthe myoearium ‘Administration only in stow-rl *4/ Ste hptteton =a, 88 + Zs econo rng wosprt- eee oe Senge hry Sh +5 nieaeee 2708 amas ‘+41 Drugs with» postive Inotropic tet iota avcosides ‘+87 Diuretics #C/ Vosodlatatos: FACE, Inhibitors of AT I _aaelill Cardiac Giycosides +Digoxin ‘Causes fonie changes, the rise of (Cat increases myocardial antfacity, impulse formation slows ‘Chronic heart ale, impaired left ‘Ventre atrial foniaton ‘Reduce moridty, do not reduce mortality ‘Small therapeutic with High rsk of ntoxcation, |!

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