71635
| Question | Answer |
| Disadvantages of digoxin | Narrow therapeutic index Glycosides can cause rhythm disturbances within or slightly above therapeutic index. AV block; ectopic beats, vent. tachycardia, ventricular fibrillation, death |
| Benzimidazole derivatives eg. Pimobendan activity | Two actions contribute to inotropic activity. Inhibits type 3 cAMP PDE Increases Ca sensitivity of cardiac myofibrils (02 sparing effect) Long duration 8-12 hours Inodilator |
| Negative inotropes 1) 2) 3) | 1) Beta adrenoceptor antagonists- Inhibits catecholamines, negative inotropic effect and chronotropic action. Used in hearts driven by high sympathetic tone. Prevent heart failure. 2) Na channel blockers. Decreased Na entry so Ca efflux, depleting internal calcium stores and reducing force of contration 3) Calcium channel blockers Decreased calcium entry and force of contration |
| Action of cardiac glycosides eg. digoxin? | Effects on cardiac muscle Positive inotropic- binds K+ binding site on NA/K-ATPase Negative chronotropic- centrally: slows HR and AV conduction by increasing vagal tone Direct: sensitise cardiac muscle to Ach Reflex: increase in SV stimulates baroreceptors, reflexly increase vagal tone and decrease smypathetic to heart |
| What is the action 1) milrinone 2) Methylxanthines | 1)inhibits PDE 3; increases contraction without HR; vasodilator 2)weak +ve inotropes, vasodilators, mild diuretics, CNS stimulants. Inhibits PDE; release of Ca from intracellular sources eg. Theophylline, Etamiphylline camsylate, propentofylline. |
| Drugs that increase HR 1) Name a muscarinic antagonist and describe when its used 2) Name a beta adrenoreceptor agonist and describe when its used | 1) atropine- non-selective, Premed for surgery when vagal stimulation and slowing is a problem. Treatment for bradycardia (incomplete heart block) 2) isoprenaline- non-selective, agonist to increase HR more than beta 1 selective drugs; vasodilation in skeletal muscle, beta 2 effect; emergency treatment to complete 3rd degree heart block |
| what is a side effect of drugs that increase contractility by increasing cAMP? | arryhythmias |
| Antidysrhythmic drugs 1) Of the 4 types, what are the only ones not to interact directly with ion channels? | 1) Class 2 |
| antidysrhythmic drugs 1) Class 1 | 1) Block voltage dependent Na channels (decrease rate and magnitude of depolarisation, reduce conduction velocity in non-node tissue) a) procainamide b) lidocaine |
| antidysrhythmic drugs Class 2 | Antagonise beta adrenoreceptors, propranolol; sotalol- some class 3 activity (Reduce excessive sympathetic tone may cause arrhythmias) |
| antidysrhythmic drugs Class 3 | Action not fully understood but involves blockage of K channels involved in cardiac repolarisation, amiodarone |
| antidysrhythmic drugs Class 4 | Block Ca channels, verapamil, diltiazem. Reduce plateau current, shorten ap, negative inotropic effect reducing work; slow av node conduction |
| Targets for drugs acting on cardiac muscle | 1) Receptors on the cell membrane: Muscarinic M2; Beta 1 adrenoreceptors 2) Ion channels in the cell membranes: fast Na; slow Ca; K 3) Cardiac muscle cell enzymes: Na/K ATPase; Phosphodiesterase |
| Positive inotropes 1) 2) 3) 4) | 1) Sympathomimetics (agonist) b-adrenoreceptors; dobutamine and dopamine 2) Phosphodiesterase inhibitors- milrinone and methylxanthines 3) Cardiac glycosides- digoxin; also negative chronotropic effects 4) Benzimidazole derivatives- pimobendan (inodilator) Ca sensitisation and PDE3 inhibition |
| In what circumstances are 1) dobutamine used 2) dopamine | 1) acute low output heart failure 2) shock and low output heart failure |
| Drugs that slow HR 1) Name muscarinic agonists 2) Name drugs that increase vagal tone 3) Beta adrenoreceptor antagonists | 1) Pilocarpine, Bethanechol (not used clinically, side effect) 2) Cardiac glycosides (also target Na/k; ATPase increasing force of contraction) 3) Propranolol, sotatol: non-selective Atenolol: Beta 1 selective Pindolol- partial agonist (useful in sinus tachycardia hyperthyroidism (cats), reduce sympathetic tone |
| How is heart failure of long standing characterised? | 1) Down-regulation of cardiac adrenoreceptors 2) Inability of receptors to couple effectively to cAMP generation |
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