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29 Cards in this Set
- Front
- Back
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auto-rhythmi-city
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contraction wo stimuli from nervous system
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Cardiac AP
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reduce K permeability out -- allow Na, Ca slowly leak in -- reach thread hold -- L-type Ca open -- depolarized AP -- K open repolarized -- (K like to go out -- Na like to go in -- Ca open when like to go in)
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Mem pol in cardiac AP 0-4
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K close -- Na-Ca leak in to threadhold -- 0: Na open dep (upshoot) --1: Na slowly chose - Ca open - K still close (fall slightly-still high) -- 2: L type Ca (long lasting) open - Na close (Na-Ca compensate --> plate-au-still high 200 ms) -- 3: K Open - Ca close (falling fast - very low) -- 4: same as 3 until Na-Ca leak to threadhold ----- total 300 ms
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Wave summation and absolute refractory period
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many stimuli adding up (high frequency) cause FUSED tetanus with short ARP (can't contract)
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ARP - RRP in cardiac muscle
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no wave summation - long refractory period (200-250 ms) - abs (0-half3- no response to any stimuli at all)- rel (after 4 - no response to norm stimulus)
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Normal ventrical contraction number
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60 bpm - small wave is atrial contract - large wave is ventrical contract (phase 1)
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Extrasystole only happens when
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relaxation or after half of phase 3 ---> to create an extra ventricular contraction
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Sympathetic vs Parasympathetic
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fight (more sym - more contraction force) vs relax (para more active than sym -- low HR same force)
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Vagal escape (after bi hu` dung' tim)
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resumption of heartbeat caused by sympathetic reflexes or initiation of a rhythm by the Purkinje fibers
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SA node (sinoatrial) - pace maker
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autorhythmic cardiac cells in right atrial wall
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Heart stop beating cause by (hu` dung' tim)
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excessive stimulation of vagus nerve
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Vagus nerve carries
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parasympathetic (slow down HR same force) thus excessive vagus stimulation cause the heart to stop beating
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like pilocarpine, it decreases heart rate
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muscarine is a poison found in poisonous mushrooms. muscarine binds to acetylcholine receptors and mimics its action. what does it do to heart rate?
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Homeothermic (35.8-38.2oC) - hyper-thermia and hypo-thermia in human vs
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poi-kilo-thermic in frog
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Ringer's solution Room - Body temp in C
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Cl-Na-K-P-Ca-Mg ---- physiological solution -- keep heart viable and effects on temperature --------------- 25oC vs 37oC
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Extrinsic control - nor-epi-nephrine - adrenaline
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b1 ANDREGENIC receptor (SA) - G-pro - AC - cAMP - open Na-Ca channels ---> inc rate of depo and shorten repol ---> inc HR
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Parasym - Acetylcholine
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Muscarinic cholinergic receptor - open K and close Na-Ca channels --> dec rate of depo
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Andrenergic - Cholinergic -
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chemical inhibit - mimic - enhance EPI-nephrine - NORepi (andernaline) vs Achetylcholine
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Epinephrine Digitalis (digoxin-fox glove) ------------ Pilocarpine Atropine
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Andrenergic: agonist - antagonist ---------- Cholinergic: Agonist - Anta
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Agosist vs Antagonist
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Agonist works same as Ep-Ach-Nor vs opposite to them Antagonist
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Epi-Atropine
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inc HR: adrenergic agonist vs cholonergic antagonist
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Digoxin-Pilorcarpine
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decrease HR ---> inc Force and dec HR (frequency) vs Chlonergic Ant
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More K leak channels (ezer to get out) than
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Ca - Na to get in
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Phase 0
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Na rush in K close (shoot up depol big time)
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Phase 1
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Na in slowly K still close (small dip - small repol)
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Phase 2
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Na close - Ca open (plateau) -- 0 to 3 1/2 asb ref per
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Phase 3
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K open Ca slowly close (repol big time) -- half 3 (rel ref per)
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Phase 4
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K open Ca Na close (resting pot) ---- wait for Na-Ca leak in to reach threadhold
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Digoxin
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binds to a site on the extracellular aspect of the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes) and decreases its function
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