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21 Cards in this Set
- Front
- Back
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Whats the different phases in cardiac action potential |
Phase 0, phase2 (plateau phase) , phase 3 and phase 4 |
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What happens in phase 0 |
Sodium channels detect a change in membrane potential and they open and flow sodium in and more sodium flows in due to the positive feedback loop. Peak then sodium channels get shut down |
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What is phase 1 |
Partial repolarization of the membrane thanks to a rapid decrease in sodium ion passage as the fast sodium ions close |
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Whats phase 2 |
Plateau phase Movement of calcium ions out of the cell maintains depolarisation. It gets its name because the electrical charge across the membrane changes very little |
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What is phase 3 |
Repolarisation as sodium and calcium channels close and membrane potential returns to baseline level |
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Phase 4 |
Starting to depolarise again and much slower |
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What are sinoatrial(SA) And antrioventricular (AV) node cells |
Slow conductors that use calcium channels mainly in their action potential upstroke, thus blocked by calcium channel blockers such as verapamil |
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What are atrium, bundle of his and ventricle cells |
Fast conducting cdlks rhat use sodium channels mainly in their action potential upstroke, thus blocked by sodium channel blockers |
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Give example of sodium channel blockers |
Quinidine, lidocaine and propafenone |
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What are the two stages of refractory period |
Absolute refractory period Relative refractory period |
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What happens in absolute refractory period |
Na channels are inactivated and no matter what stimulus is applied they will not reopen to allow na+ in and depolarise the membrane to the threshold of action potential |
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What is relative refractory period |
Some if the Na+ channels have re opened from inactivation but the threshold is higher than normal making it more difficult for the activated Na+ channels to raise the membrane potential to the threshold of excitation |
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What type of drugs can be used in membrane potential for each stage |
Phase 0- class1 na channelblockers Phase 2- classIV Ca channel blockers and class II beta blockers Phaee 3- class III k channel blockers Phase 4 action potential- beta blockers |
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What do effective anti-arrhythmic drugs do |
Increase the refractory period or slow upstroke of action potential Or both |
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What do beta blockers do |
Decrease cardiac automaticity and contractility, partly by blocking beta adrenergic receptors. Antagonise the effects of catecholamines on Ca channels |
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What does class III amiodarone do |
A ‘dirty drug’ inhibits k channels (delays repolarisation) Na channels and Ca channels (slight), blocks beta-receptors non competitively, blocks alpha receptors, potent suppressor of ectopic automaticity |
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What does class IV verapamil and diltiazem do |
Blocks mainly L type calcium channels Decreases SA and purkinje fibre automaticity, slows conduction through and increases refractory period if av node |
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For cardiac arrhythmias whats a good mediacation |
Digoxin- slows conduction in the AV node Digitoxin- same -more powerful |
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What is inotropic drug and whats an example |
Digoxin Increases contraction Inhibits na/k-ATPase which is responsible for na/k exchange across the muscle cell membrane do increases na in cell and ca in the cell so increase force if myocardial contraction |
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Why does calcium and sodium build up in the cell with digoxin? |
Sodium/calcium exchanger removes calcium from inside cells which stops contraction Digoxin hinds to na/k pump and inhibits so cant take sodium out the cell. Because the build up of na ions on the inside, the na/ca pump can bring na in but not sodium ions out so theres an increase of calcium inside cells |
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What are the indurect effects of inotropic drugs |
digoxin increases vagal activity and facilitates muscarinic transmission to the heart Slows hr Slows AV conductance Prolongs refractory period of the AC node |
