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36 Cards in this Set
- Front
- Back
describe the T-tubules of ventricular and atrial muscle cells?
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Ventricular = Very large (much larger than skeletal muscle T-tubules) and filled with glycocalyx
Atrial = virtually non-existent |
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what sepperates muscle fibers end-to-end?
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intercalated disks
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while cardiac muscle cells are not a true syncytium what allows them to function as such?
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gap junctions between all the cells allow electrical signals to rapidly pass from cell to cell
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aside from cardiac muscle cells, what other type of cells can be found in the heart?
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non-contractile cells also which serve as conduction cells
characterized by absence of myofibrils |
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depolarization in fast action potentials is created by what ion flux and in what direction?
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Na+ influx
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depolarization in slow action potentials is created by what ion flux and in what direction?
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Ca+ influx
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what is responsible for the slight return to negative membrane potentials during phase 1 of fast action potentials?
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K+ efflux
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during phase 2, what causes the action potential repolarization to slow?
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the efflux of K+ is somewhat offset by the influx of Ca++
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what occurs during phase 3 of a heart cell action potential?
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rapid efflux of K+ leads to repolarization
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describe what happens in all heart cells except the pacemaker cells during phase 4?
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a equal efflux of Na+ and influx of K+ keeps the cells interior at a steady negative state while replacing intracellular Na+ with K+
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describe what happens in the pacemaker cells during phase 4?
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efflux of K+ is reduced and a slow influx of Na+ causes slow membrane depolarization until the threshold is reached
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what are the fibers which carry electricle impulses tot he ventricles?
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Perkinje fibers
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do Perkinje fibers have fast or slow response action potentials?
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fast
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where are heart cells with slow response action potentials found?
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SA and AV nodes
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describe the two factors which determine action potential speed?
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amplitude of action potential (the lower the membrane potential the easier to create a action potential) and the rate of potential change (more channels open at once)
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what is the threshold for activation of Na+ channels?
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-70 mV
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what is the threshold for activation of Ca++ channels?
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-40 mV
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where are the pacemaker cells located?
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in the SA node usually
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what is the primary pacemaker should the SA node be damaged?
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the AV node
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what is the beat rate of the SA node?
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70-80 beats/min
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what is the beat rate of the AV node?
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40-60 beats/min
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if you see the ventricles contracting before the atria what has happened?
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the AV node has taken over pacemaking
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what is the last and final resort after both the AV and SA nodes no longer function as pacemakers?
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the Perkinje fibers take over and cause 30-40 beats/min... usually will not see atrial contractions, only ventricular
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how do the pacemaker cells in all of the different locations know when to take over pacemaking?
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the fastest firing pacemakers take take precedence thus when they fail the next fastest pacemaker takes over
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describe the conduction of the electrical impulse generated in the SA node to the whole heart?
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goes to the atrial muscle cells via the bachmann's bundle
travels to the AV node via 3 internodal fibers, from AV node it travels through the bundle of His to Perkinje fibers, Perkinje fibers distribute signal from central (intraventricular septum) to lateral and from endocardium to epicardium |
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what is the conduction speed in the AV node?
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.05 m/s
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what is the conduction rate in the bundle of His?
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1-4 m/s
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what normally determines whether an impulse will pass throught the AV node?
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sympathetic (increases conduction) and parasympathetic (decreases conduction) stimulation
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what abnormal process can block electrical impulses through the AV node?
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infarct or other cellular damage
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describe the pathology of reentry arrythmias?
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impulses cannot travel in a anterograde direction in the heart, but still can loop back around in a slow retrograde fashion. For this to happen the heart must either be beating very slowly or the heart muscle cells must have an abnormally fast repolarization.
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what is the major cause of reentry arrythmias?
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ischemia in heart tissue leading to a high extracellular K+ concentration which causes depolarized membrane potentials and conduction block (slow heart beat)
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how do you fix the reentry arrythmias seen in tissue necrosis?
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you give lidocain which blocks Na+ channels which helps to repolarize the heart cells
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what is the result of a pH of 6.5 on the heart?
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it blocks calcium induced calcium release causing a reduction in cardiac muscle contraction
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what type of receptor does calcium bind to on the endoplasmic reticulum?
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a ryanodine receptor
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what are the 3 ways in which calcium can be removed from the cardiac muscle cells?
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1. sarcoplasmic reticulum calcium pump (ATP dependent)
2. sarcolemma calcium pump (ATP dependent) 3. sarcolemma 1 calcium / 3 Na+ exchanger (ATP independent) |
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explain how the Ca++/Na+ exchanger pump can be used to treat congestive heart failure?
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drugs such as digitalis block Na+/K+ exchangers thus increase intracellular Na+ concentrations which reverses the direction of the Ca+/Na+ exchanger bringing more Ca+ into the cell causing muscle contraction
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