Cardiac + Electromechanical Coupling
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Created by:
chaiteapaddy on November 10, 2011
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19 terms
Terms | Definitions |
|---|---|
 sinoatrial node, atrioventricular node and purkinje fibers | What cardiac tissues have automaticity? |
| sinoatrial node, sinus rhythm | What tissue depolarizes first generally and is referred to as the pacemaker? What is its rhythm called? |
| ectopic focus or ectopic pacemaker | What is the term for an improper generator of cardiac APs? |
| intercalated disks, gap junctions | What allows the cardiac AP to spread so well? |
| norepinephrine increases depolarization (during phase 4) and pacemaker rates | What transmitter does the sympathetic NS use on the heart and what does it do? |
| positive chronotropic effect, Beta-1 receptors, increases Ca++ conductance | What type of effect does norepinephrine have? What receptors does it use? What is its mechanism of action? |
| Acetylcholine increases membrane potential and decreases the depolarization rate during phase 4 | What type of effect does the parasym NS have on the heart? What transmitter does it use? |
| negative chronotropic effect, muscarinic, increases K+ conductance | What type of effect does ACh have? What receptors does it use? What is the mech of action? |
| Reentry | Normally a cardiac AP ends when it meets itself on the opposite side of the heart from the sinoatria node. What is the term for when it does not and gets caught in a continuing cycle? |
| AV node. Small cell size, low amplitude, slow depolarization rate | Where does the AP slow down? What causes it to do this? |
| Purkinje Fibers | What specialized fibers rapidly distribute the AP across the ventricles? |
| Ca++ enters the cell via T-tubules which triggers further release from the SR, Ca++ binds troponin and contraction occurs | Describe the behavior of Ca++ in cardiac action potentials |
| dihydropyridine (DHPR) | What compound acts as a voltage gated channel, allowing Ca++ into the cell in an AP? |
| Ryanodine receptors | What compounds acts as a Ca++ ligand-gated channel, releasing Ca++ from the SR? |
| +inotropic effect, increases intracell Ca++ thus greater force of contraction. Also faster uptake makes phase 2 and contractile phase (systole) shorter. | What effect does sympathetic stimulation have on contractile myocytes? |
| cardiac glycosides / digoxin | What compounds increase the force of contractin by inhibiting Na+/K+ pumps and thus increasing cellular Ca++? |
| Low K+ interfers w/ Na+/K+ pump, causing arrhythmias | What problem can hypkalemia cause? |
| too much K+ reduces amplitude, slowing the AP and altering phase 3 | What problem can hyperkalemia cause? |
| hypo decreases contractility while hyper increases it | Both hyper/hypokalemia can cause membrane potential disturbances which affect contractility how? |
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