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36 Cards in this Set

  • Front
  • Back
describe the T-tubules of ventricular and atrial muscle cells?
Ventricular = Very large (much larger than skeletal muscle T-tubules) and filled with glycocalyx

Atrial = virtually non-existent
what sepperates muscle fibers end-to-end?
intercalated disks
while cardiac muscle cells are not a true syncytium what allows them to function as such?
gap junctions between all the cells allow electrical signals to rapidly pass from cell to cell
aside from cardiac muscle cells, what other type of cells can be found in the heart?
non-contractile cells also which serve as conduction cells

characterized by absence of myofibrils
depolarization in fast action potentials is created by what ion flux and in what direction?
Na+ influx
depolarization in slow action potentials is created by what ion flux and in what direction?
Ca+ influx
what is responsible for the slight return to negative membrane potentials during phase 1 of fast action potentials?
K+ efflux
during phase 2, what causes the action potential repolarization to slow?
the efflux of K+ is somewhat offset by the influx of Ca++
what occurs during phase 3 of a heart cell action potential?
rapid efflux of K+ leads to repolarization
describe what happens in all heart cells except the pacemaker cells during phase 4?
a equal efflux of Na+ and influx of K+ keeps the cells interior at a steady negative state while replacing intracellular Na+ with K+
describe what happens in the pacemaker cells during phase 4?
efflux of K+ is reduced and a slow influx of Na+ causes slow membrane depolarization until the threshold is reached
what are the fibers which carry electricle impulses tot he ventricles?
Perkinje fibers
do Perkinje fibers have fast or slow response action potentials?
fast
where are heart cells with slow response action potentials found?
SA and AV nodes
describe the two factors which determine action potential speed?
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)
what is the threshold for activation of Na+ channels?
-70 mV
what is the threshold for activation of Ca++ channels?
-40 mV
where are the pacemaker cells located?
in the SA node usually
what is the primary pacemaker should the SA node be damaged?
the AV node
what is the beat rate of the SA node?
70-80 beats/min
what is the beat rate of the AV node?
40-60 beats/min
if you see the ventricles contracting before the atria what has happened?
the AV node has taken over pacemaking
what is the last and final resort after both the AV and SA nodes no longer function as pacemakers?
the Perkinje fibers take over and cause 30-40 beats/min... usually will not see atrial contractions, only ventricular
how do the pacemaker cells in all of the different locations know when to take over pacemaking?
the fastest firing pacemakers take take precedence thus when they fail the next fastest pacemaker takes over
describe the conduction of the electrical impulse generated in the SA node to the whole heart?
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
what is the conduction speed in the AV node?
.05 m/s
what is the conduction rate in the bundle of His?
1-4 m/s
what normally determines whether an impulse will pass throught the AV node?
sympathetic (increases conduction) and parasympathetic (decreases conduction) stimulation
what abnormal process can block electrical impulses through the AV node?
infarct or other cellular damage
describe the pathology of reentry arrythmias?
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.
what is the major cause of reentry arrythmias?
ischemia in heart tissue leading to a high extracellular K+ concentration which causes depolarized membrane potentials and conduction block (slow heart beat)
how do you fix the reentry arrythmias seen in tissue necrosis?
you give lidocain which blocks Na+ channels which helps to repolarize the heart cells
what is the result of a pH of 6.5 on the heart?
it blocks calcium induced calcium release causing a reduction in cardiac muscle contraction
what type of receptor does calcium bind to on the endoplasmic reticulum?
a ryanodine receptor
what are the 3 ways in which calcium can be removed from the cardiac muscle cells?
1. sarcoplasmic reticulum calcium pump (ATP dependent)
2. sarcolemma calcium pump (ATP dependent)
3. sarcolemma 1 calcium / 3 Na+ exchanger (ATP independent)
explain how the Ca++/Na+ exchanger pump can be used to treat congestive heart failure?
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