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20 Cards in this Set
- Front
- Back
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Sinus nodal fiber resting membrane potential |
from -55 to -60 mV (compared to -85 to -90 of ventricular muscle fiber)
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SA node AP
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Fast Na channels blocked due to high resting potential; AP caused by slow Ca channels (causes more gradual slope for AP when compared to ventricular fibers)
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What causes self-excitation
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leakiness to sodium and calcium ions
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Total delay in AV nodal and bundle system
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0.13 seconds (0.16 second delay from SA node to ventricles total)
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Why is there slower conduction in penetrating AV bundle fibers
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mainly due to diminished numbers of gap junctions (causes greater resistance)
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Special characteristic of AV bundle
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AP can't travel backwards into the atria (normally)
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Direction of cadiac impulse
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endocardial to epicardial surface via spiraling layers
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Intrinsic rate of AV nodal fibers
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40-60 beats per minute
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Intrinsic rate of purkinje fibers
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15-40 beats per minute
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Intrinsic rate of SA nodal fibers
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70-80 times per minute
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ectopic pacemeker
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any place other than SA node (cells have faster intrinsic rate than SA node) - causes abnormal sequence of contration
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blockageof transmission
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new pacemaker generally AV node or bundle
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AV block
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signal can't travel from atria to ventricles (atria beat with SA node)
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Stokes-Adams syndrome
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delayed heartbeat after AV block (5-20 seconds after)
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Parasympathetic neurotransmitter in heart (from vagus nerve)
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acetylcholine (decreases SA rhythm rate and excitability of AV junctional fibers)
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Ventricular escape
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Parasympathetic stimulation stops heart - rate then controled by AV bundle
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acetylcholine affect on permeability
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increases K permeability (hyperpolarization = decreased excitability)
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safety factor
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transmission of cardiac impulse through transitional fibers into AV nodal fibers
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sympathetic affects
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Increases force of contration of ALL cardiac muscle; increases rate of SA node discharge; increases rate of conduction and excitability
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sympathetic neurotransmitter
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norepinephrine (increase permeabilty of Na and Ca ions)
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