16 Cardiac AP

Myocyte AP

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• at rest, pumps maintain ion distribution

• connected via gap junction

• if 1 depolarizes with positive ions inside, some positive go to 2, 2 depolarizes

• phase 4: myocyte at rest, -85

• phase 0: voltage begins to rise from positive ions entering via gap junction, Na channels open, further rise positive charges, positive loop

• phase 1: voltage become positive, Na channels close, K open and leak out, lower voltage

• phase 2: competing Ca in and K out, cancelling one another = plateau

• phase 3: Ca close, only K

• -85 maintained by inward rectifier channels: K out

• Soloist: class I antiarrhythmics

• Soloist holding peanut butter jar: class I antiarrhythmics block sodium channels (phase 0)

• Soloist tipping mic stand: class I antiarrhythmics decrease the slope of the phase 0 upstroke (slows conduction of the cardiac AP)

• Ca ion trigger mechanical contraction of myocyte

• excitation-contraction coupling: Ca connects electrical activity and mechanical activity of myocytes

• Pushing away the curtain: class III antiarrhythmics block K+ channels prolonging phase 2 and 3 of the cardiac action potential -> prolonged refractory period

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• No Ca involvement

• each cell individually depolarized by neuron

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Pacemaker AP

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• slightly higher resting voltage > -85

• no plateau

• phase 4: slowly drifts upward, funny current allow Na in

• phase 0: - 40 threshold, Ca open, inward Ca

• phase 3: above 0, Ca close, K open

• AV node, same shape, phase 4 slower, longer to reach threshold, usually depolarized by SA signal before threshold

• fast Na need -85 to function: fewer inward rectifier K (-85 resting membrane) > resting always above -60 > fast Na does not work

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• slow AV: delay conduction from atrium to ventricle

• slow phase 0

• block activated and inactivated Ca channels, not resting channels. Work more on tissues fire more frequently and exclusively activated by Ca current

• Notes: non-dihydropyridines (e.g. diltiazem, verapamil) treat arrhythmias by blocking Ca2+ current in the SA and AV nodes

• Disconnected bottom: non-dihydropyridine CCBs decrease atrioventricular conduction

• Duet: Class 2 antiarrhythmics

• Muted beta bugle: beta blockers (class 2 antiarrhythmics)

• notes: beta blockers treat arrhythmias by blocking sympathetic input to the SA and AV nodes

• Torn band camp: beta blockers decrease cAMP

• Crushed calci-YUM ice cream cartons: decreased cAMP leads to closure of membrane calcium channels

• Sliding up the keys: beta blockers prolong phase 4 of the nodal action potential -> decreased pacemaker activity, prolonged conduction time and refractory period.

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• Swing dancing: adenosine (a purine nucleoside with antiarrhythmic properties)

• Purine shaped gate: adenosine is a purine nucleotide

• A1 Swing: adenosine activates inhibitory A1 receptors on the myocardium and at the SA and AV nodes

• Falling calci-yum ice cream: activation of A1 receptors suppresses inward Ca2+ current (hyperpolarization, suppressed Ca2+ dependent AP

• Banana flying out of cup: activation of A1 receptors increases outward K+ current (hyperpolarization, suppressed Ca2+ dependent AP)