The Conduction System Flashcards
describe the electrical activity of the heart
inherent and rhythmical (heart beat)
describe the heart’s network of specialized cardiac muscle fibers (3)
- autorhythmic fibers
- self-excitable
- repeatedly generate AP’s that trigger heart contractions
what percentage of cardiac muscle fibers become autorhythmic?
about 1%
what are the 2 functions of autorhythmic cardiac muscle fibers? describe these functions
- act as a pacemaker: the set rhythm of electrical excitation causes contraction of the heart
- form conduction system: the network of specialized cardiac muscle fibers provide a path for each cycel of cardiac excitation and ensures that the cardiac chambers become stimulated to contract in a coordinated manner
where does cardiac excitation begin?
SA node
where is the SA node located?
in the right atrial wall just inferior to the opening of the superior vena cava
what do SA node cells do?
repeatedly depolarize to threshold spontaneously
what is the pacemaker potential due to?
spontaneous depolarization
what is the SA node also called?
the pacemaker of the heart
what happens when the pacemaker potential of the SA node reaches threshold?
triggers an action potential
what do sinus nodal fibers connect directly with?
atrial muscle fibers
what happens to each action potential from the SA node? what is the result of this?
propogates directly through both atria via gap junctions in intercalated disks of atrial muscle fibers; result in atrial contraction
give the conduction system sequence(6)
- action potential (AP) initiated in SA node and travels through internodal pathays to make atria contract
- AP reaches AV node
- AP enters the AV bundle/bundle of His
- after propogating along AV bundle, AP enters R and L bundle branches
- AP then travels to purkinjie fibers, which rapidly conduct AP from apex of heart upward to remainder of ventricular myocardium
- ventricles contract
where is the AV node located?
in the septum between the 2 atria, just anterior to the opening of the coronary sinus
what is the only site where APs can conduct from atria to ventricles?
the AV bundle/bundle of His
why is the AV bundle the only site where APs can conduct fron atria to ventricles?
everywhere else, the fibrous skeleton of the heart electrically insulates from atria to ventricles
where do the L and R bundle branches extend?
through the interventricular septum toward the apex of the heart
how often do the autorhythmic fibers in the SA node node initiate an AP?
every 0.6 seconds (100x/min)
describe how nerve impulses from the ANS and hormones like epinephrine influend the heart beat
they modify timing and strength of the heartbeat but DO NOT establish the fundamental rhythm
what happens if the SA node is damaged?
the slower AV node can pick up pacemaking tasks
what happens if both the SA node and the AV node are suppressed?
the distal fibers can maintain the heartbeat but their pace is too slow to maintain adequate blood flow to the brain
what are automaticity foci? (2)
focal areas of automaticity in the heart; potential pacemakers capable of pacing in emergency situations
describe automaticity foci under normal circumstances; what does this mean in terms of what they are referred to as?
electrically silent; is why they are referred to as “potential pacemakers”
what are the 3 ion channels that are important in causing action potential in cardiac muscle? which is the leaky one?
- fast sodium channels
- slow sodium-calcium channels (leaky)
- potassium channels
describe the resting potential of sinus nodal fibers and what this results in
high resting potential, results in inactivation of fast sodium channe;s
what kind of cell membranes do sinus fibers have and what does this result in?
have cell membranes that naturally leak Na+ and Ca2+ that results in the slow rise in membrane potential between heartbeats
what channels become activated when the SAnodepotential reaches threshold voltage?
sodium-calcium (slow and leaky)
what does the inherent leakiness of sinus nodal fibers to sodium and calcium result in?
self-excitation of the sinus nodal fibers
why doesn’t leakiness result in permanent depolarization of sinus nodal fibers? (2)
- sodium-calcium channels become inactivated
- potassium channels move K+ out of the cell, resulting in hyperpolarization of the cell which carries the membrane potential to “resting” potential
what is the resting membrane potential?
-55 to -60mV
what happens when the membrane potential reaches 0mV? (3)
- Na+/Ca2+ channels inactivate/close so ions are not flowing in anymore
- K+ channels open to move K+ out of the cell, againt concentration gradient
- this results in hyperpolarization and the membrane resturns to resting potential
when are artificial pacemakers needed?
when there is an issue with the conduction system of the heart (arrythmia); usually bradychardia
how are artifical pacemakers implanted? what are they? what do they consist of?
implanted surgically; devices that send out small electrical currents to ST heart to contract; consist of a battery and an impulse generator
where are artifical pacemakers usually implanted? what are they connected to?
implanted beneath skin just inferior to the clavicle; connected to 1 or 2 flexible leads that are threaded through the superior vena cava, then pass into the right atrium and right ventricle
whata re activity adjusted pacemakers?
a new upgrade that automatically speeds up the heartbeat during exercise
describe the anatomy that allows for transmission of the cardia impulse through the atria
sinus nodal fibers connect directly with atrial muscle fibers; small bands of atrial fibers also carry the impulse at a more rapid rate
how is the cardia impulse transmitted through the atria?
- anterior interatrial band passes through anterior walls of the R atrium to the L atrium
- anterior, middle, and posterior internodal pathways curve through the anterior, lateral, and posterior atrial walls and terminate in the AV node
- Bachman’s bundle (an extension of the internodal fibers) carries the signal to the L atrium
what causes the delay of impulse conduction from atria to ventricles?
AV node and adjacent conductive fibers due to fewer gap junctions increases resistance to conduction of excitatory ions from on conducting fiber to the next (fewer conduits for AP to move)
why is there a delay of impulse conduction from atria to ventricles?
atria have to contract and blood has to move into ventricles before the ventricles can contract and shoot that blood out
how long does it take the impulse to reach the AV node?
0.03 seconds
how long does it take the impulse to pass through the AV node and bundle? how long is this from initiation in the SA node?
0.13, for a total of 0.16 seconds from inital impulse in the SA node to reach the contracting muscles of the atria
what is the AV bundle/ bundle of His?
there is a continuous fiber barrier between the atrial muscle and ventricular muscle, the AV bundle/ bundle of His is the only exception/ entry through this barrier
can action potentials travel backwards through the AV bundle from the ventricles to the atria?
fuck no; would be so bad
what are the purkinjie fibers?
large fibers that transmit action potential rapidly (1.5-4ms); the last point of conduction system
where do the purkinjie fibers lead?
from the AV nod through the AV bundle and into the ventricles
what do the purkinjie fibers do?
transmit signal to contractile fibers
describe the permeability of the gap junctions at the intercalated disks in the purkinjie fibers?
very high; lots of ion flow and transmission
do the purkinjie fibers have myofibrils?
very few
describe rapid transmission anatomy and order in the ventricle
- the AV bundle passes downward into the ventricular septum and divides into L and R bundle branches
- the branches spread and progressively divide into smaller branches
- ends of purkinjie fibers penetrate about 1/3 of the way into the muscle mass and become continuous with the muscle fibers
- from the end of the purkinjie fibers, the cardiac impulse travels through ventricular muscle fibers themselves, which wraps around the heart in a double spiral with a fibrous septa between layers
how long does it take from the time the impulse enters the bundle branches until the impulse reaches the terminations of the purkinjie fibers?
about 0.03 seconds
how long does it take for the impulse to travel from the endochadial surface to the epicardial surface?
0.03 seconds
how long does it take for the cardiac impulse to travel from the initial bundle brances to the last ventricular muscle fiber?
0.06 seconds
how long does the initiation and transmission of an entire action potential take in the heart? say when slows down and speeds up
0.22 seconds, slows down between atria and ventricles, speeds back up when enters ventricles
describe the general path of an action potential through the conduction system
AP generated in SA node, travels along conduction system and spreads out to excite contractile fibers in atrial and ventricular muscle fibers
what is the resting membrane potential of the contractile fibers?
-90mV
what happens when the contractile fibers reach thrit threshold by the action potential of neighboring fibers?
voltage-gated fast Na+ channels open, allowing Na+ to flow in because the cytosol of contractile fibers is electrically more negative than intersititial fluid (Na+ concentration is high in intersititial fluid), Na+ moves down both electrical and concentration gradients into the cells of contractile fibers
what does the inflow of Na+ ions into contractile fiber cells cause?
reapid depolarization
what happens within a few seconds of the rapid depolarization of contractile fiber cells?
fast Na+ channels inactivate and Na+ inflow decreases
what is a plateau?
a period of maintained depolarization (0 to +10mV)
what is the plateau between depolarization and repolarization of contractile fibers caused by?
Ca2+ inflow balancing K+ outflow
how is the calcium inflow accomplished in the plateau period of contractile fibers
voltage-gated slow Ca2+ channels open in sarcolemma and Ca2+ moves in from intersititial fluid to the cytosol (down its concentration gradient),
what does the in flow of Ca2+ from sarcolemma to cytosol ultimately cause during the plateau period?
the increase of Ca2+ ultimately triggers contraction
just before the plateau period, at the same time that voltage-gated slow Ca2+ channels are open and pouring Ca2+ into the cytosol of contractile fibers, what else is happening?
SOME voltage-gated K+ channels open, allowing some K+ to leave the contractile fibers
wheere are voltage-gated K+ channels found?
also in the sarcolemma, just like slow voltage-gated Ca2+ channels
how long does the plateau phase last and what is the membrane potential of contractile fibers during this period?
lasts about 0.25 seconds and membrane potential is close to 0 (0 to +10 mV)
why is depolarization in skeletal muscle much briefer than depolarization in cardiac muscle?
skeletal muscle does not have the plateau phase that cardiac muscle has
describe repolarization of contractile fibers (3)
- after a delay, additional K+ voltage-gated channels open
- outflow of K+ restores negative resting potential of contractile fibers (-90mV)
- at same time, Ca2+ channels in saarcolemma and SR are closing, also contributing to repolarization (no more positive flowing in, allowing to return to negative)
what is the refractory period?
the time interval during which a second contraction cannot be triggered by ANY stimuli
how long does the refractory period last, comparatively? why? (2)
lasts longer than the contraction itself so
1. another contraction cannot begin until relaxation is well under way
2. tetanus cannot occur in cardiac muscle (also hella bad)
what would happen if tetanus occurs in cardiac muscle?
blood flow would cease, bad news bears
describe the general mechanism of contraction (3)
- similar in cardiac and skeletal muscle
- electrical activity (AP) leads to mechanical response (contraction)
- Ca2+ binds to troponin, which exposes binding sites for interactionn of actin and myosin
what kind of substances can influence the STRENGTH of heart contractions? give an example
substances that alter movement of Ca2+ through slow Ca2+ channels; example is epinephrine enhancing Ca2+ flow into cytosol strengthens contraciton force by providing more opportunities for actin and myosin to interact
where is parasympathetic (vagal) control of the heart rhythmicity distributed to? (2)
mainly to SA and AV nodes
what does stimulation of parasympathetic nerves to the heart cause a release of and what is the result? (2 results)
causes release of acetylcholine which
1. decreases the rate of rhythm or sinus node (slows SA node)
2. decreases excitability of AV junctional fibers between atrial musculature and AV node
what does weak to moderate stimulation of the paarasympathetic nervous system on the heart cause?
slows rate of heart pumping
whar does strong stimulation of the parasympathetic nervous system on the heart cause?
can completely stop heart beat for a few seconds
what is ventricular escape?
tissue in the ventricles can pick up the responsibility of stimulating the heart to beat (the purkinjie fibers) in response to strong stimulation of the parasympathetic nervous system
describe the mechanism of the parasympathetic (vagal) control of heart rhythmicity
- acetylcholine increases permeability of fiber membranes to potassium ions
- this causes hyperpolarization of the cell
- this reduces the resting membrane potential of sinus nodal fibers
- it now requires longer for sodium and calcium leakage to raise the membrane potential to threshold voltage and slows the heart rate
what 2 aspects of the nervous system are in play to control the heart rate
sympathetic and parasympathetic
describe sympathetic stimulation of cardiac rhythm (describe anatomy and list 3)
innervates all parts of the heart
1. increases the rate of sinus nodal discharge
2. increases rate of conduction
3. increases the force of contraction
describe the mechanism of sympathetic stimulation of cardiac rhythm
- stimulation of sympathetic nerves causes release of norepinephrine
- norepinephrine stimulate beta-1 adrenergic receptors
- believe to increase permeability of fiber membrane to sodium and calcium ions
where does cardiac muscle NOT REALLY get energy from?
produces little to none of the ATP it needs from anaerobic metabolism
how does cardiac muscle get energy?
relies almost exclusively on aerobic cellular respiration in its numerous mitochondria
how does necessary O2 get into cardiac muscle fibers
diffuses from blood in coronary circulation and is released from myoglobin inside cardiac muscle fibers
list 6 of the many fuels that power cardiac mitochondrial ATP production
- fatty acids (60% at rest)
- glucose (35% at rest)
- lactic acid (converted to pyruvate)
- amino acids
- ketone bodies
- creatine phosphate
what happens regarding fuel source for mitochondrial ATP in the heart during exercise?
the heart’s use of lactic acid from skeletal muscle rises
why does the heart have so many fuel sources for mitochondrial ATP production?
it MUST keep beating, or death duh
describe the role of creatine kinase
creatine kinase catalyzes the conversion of creatine phosphate + ADP to creatine + ATP
where is creatine kinase supposed to stay?
within skeletal or heart muscle cells
what happens to creatine kinase when skeletal or cardiac muscle cells are injured or dying?
CK is released into the blood
what is elevated levels of CK in the blood a marker for?
a sign that a myocardial infarction (MI, heart attack) has occured
