Flashcards in Heart 4: Cardiac Pacemaker Mechanisms Deck (24):
What is the hierarchy of pacemaker activity?
SA node is primary pacemaker and has fastest inherent beating rate.
SA node > latent atrial pacemakers > AV nodal/His bundle (junctional) > bundle branches > Purkinje fibers (sinus node controls heart in normal conditions and suppresses the activity of other pacemakers. if other pacemakers pop up they'll be slower)
What are the mechanisms that underlie the SA node pacemaker activity and are responsible for its diastolic slope?
T-type Ca current
hyperpolarization-activated inward current (iF)
deactivation of K current (IK)
inward Na/Ca exchange current activated by intracellular SR Ca release.
after the membrane repolarizes, all these mechanisms contribute to diastolic depolarization. hits threshold and forms another AP so slope of diastolic depolarization det. HR
What is a special type of tissue found in all pacemaker tissue in the body?
Explain the mechanism.
pacemaker channel, in heart it's iF and is activated by hyperpolarization (only channel in heart that is activated by hyperpolarization
When the cell repolarizes, it turns on this channel, leaks some Na in, causing some of the depolarization.
(has nothing to do with Na channel that causes upstroke of AP, just carried by Na)
when cell REpolarizes during phase 3, goes through the voltage that turns on iF channel and when turns on inward current that contributes to this depolariztion. when cell REpolarizes, instead of depolarizing to turn on channel, REpolarization opens up channel and allows Na to flow in which causes some depolarization.
(if you block it with a drug you reduce pacemaker activity about 30 percent)
Describe the T type Ca current and L type channel.
T type- activated at negative voltages. contributes to diastolic depolarization. at negative voltages when cell depolarizes, turns on the inward Ca current. (leaks in positive charge, makes cell less negative)
L-type- causes upstroke (when inhibited brings in less Ca and less Ca for SR release)
T type- involved with pacemaker activity
How does SR Ca release relate to pacemaker activity?
when Ca released from inside the cell, it stimulates the Na/Ca exchanger... so Na flows in and Ca flows out.
if you release Ca intracellularly this exchanger will pick it up inside the cell and bring it out of cell in exchange for Na and that net inward current contributes to depolarization of the membrane
How do Purkinje fibers differ from SA node?
don't have all the same mechanisms. it's a latent pacemaker in the ventricles and can generate pacemaker activity in abnormal conditions. at such a negative voltage though that they don't have all the mechanisms that SA does. only has iF channels and deactivation of K current
How do the IK channels contribute to SA/Purkinje pacemaker activity?
they deactivate. less K leaving means less positive charge leaving so cell becomes less negative.
normally iK channels turn on and cause repolarization. Outward current of K repolarizes the membrane. in order for channel to recover, must turn off. decrease in K conductance means less K leaving cell and inside of cell is more positive and contributes to pacemaker activity
What mechanisms are responsible for changes in HR?
change in slope of diastolic depolarization
change in maximum diastolic potential
change in threshold
pacemaker shifts- changes in pacemaker site can cause abrupt changes in HR because of the hierarchy of pacemaker activities (pathological)
What does increasing the maximum diastolic potential result in?
if you increase the maximum that means its more polarized, more negative, at a more negative value have farther to come back before hit threshold again. if you raise threshold it'll take longer to hit and will slow SR...
What happens if you go into 3rd degree heart block?
What happens in sick sinus syndrome?
AV node infarcts and pacemaker picks up in ventricle in Purkinje network (about 30 beats per minute) so HR changes in a hurry. atria may be at 70 beats per minute.
sick sinus syndrome. sinus node not stable then pacemaker shifts to atria pacemaker and slows down and shift to junction then shifts back up to sinus node and need artificial pacemaker. so shift in pacemaker location will change HR dep. on where pacemaker generating impulses from.
How does Ach affect pacemaker rate? Draw a graph.
changes the slope and increases the maximum negative potential- slower to threshold and farther to go
Ach -vagal stimulation and slow HR. increases K permeability more leaves, cell more negative, depresses diastolic depolarization, gets to threshold later, therefore cycle length is longer, slowed HR
no resting membrane potential so maximum negative point is called maximum diastolic potential. by increasing K permeability you can shift that down also…. by shifting to more negative voltages get to threshold later which slows HR. Ach. does both. Ach. will decrease slope of diastolic depolarization and depress max diastolic voltage -both drive membrane potential away from threshold to slow down HR. vagal slows HR and slows conduction at AV node
What would happen if you didn't have sympathetic stimulation to AV node when HR goes up?
need sympathetic nerve stimulation to AV node when HR goes up they go together in order to facilitation conduction from atria to ventricle at short cycle lengths.
if no sympathetic stimulation to AV node when HR goes up you’d have heart block. if you inject a beta blocker into AV nodal region..so NE has no effect on AV node but stimulate sinus node its presenting impulses to AV node at much shorter intervals. AV node has long refractory period without NE affecting AV node those impulses can’t go through… long refractory period. would only increase HR to about 130 before you’d go into AV block and doesn't go through AV node anymore.
What is overdrive suppression?
What are 3 clinical applications of this?
its not like sinus node going faster than latent pacemaker..sinus node is actually suppressing electrical activity of other pacemakers in heart. clinical implications. def of overdrive suppression. latent pacemaker act. in Purkinje network… so intrinsic freq. is 30 beats per minute and always being stimulated faster by sinus node..so sinus node is always stimulating latent pacemakers at faster rate than they want to go. if stop sinus node these latent pacemakers don't take over instantly. heart goes into pause for 10 -12 seconds. heart beating then induce AV nodal block, would your ventricular pacemaker pick up instantly? no. if SA pacemaker stops stimulating pacemakers in ventricle by conduction then latent pacemakers take time to warm back up bc they’ve been suppressed by electrical activity of SA node. if you do go into block you’ll pass out… ventricular pacemaker won't save life. decrease in arterial pressure will stimulate sympathetics and hopefully that will drive ventricular pacemakers to pick up activity
1) SA nodal or AV nodal block (2nd or 3rd degree heart block- infarcted AV node)
2) stopping artifical pacemakers (wean pt off slowly to allow ectopic pacemaker to pick up while you change batteries)
3) sick sinus syndrome- site of pacemaker keeps shifting around
when latent pacemakers are competing with SA.
Describe autonomic control of heart rate (Ach).
Ach (vagal nerve stimulation)
primarily inhibits pacemakers within SA node, atria and AV nodal regions ( does NOT affect pacemaker in Purkinje fibers)
increases K permeability, inhibits cAMP-dependent slow inward L-type Ca current and IF current
(decreases slope of diastolic depolarization and hyperpolarizes maximum diastolic potential)
Describe the basic effects of L type Ca current and IF current.
Ach inhibits cAMP slow inward L type Ca current - doesn't affect pacemaker rate but does decrease conduction through AV node.
iF current inhibited by Ach.
Ach. is released from vagus, muscarine receptors, inhibits cAMP and that will inhibit L type Ca current. brings in less Ca and less Ca for SR release. will inhibit IF bc IF modulated by cAMP so decrease diastolic slope and hyper polarizes diastolic potential.
Why is vagal nerve stimulation a better treatment for heart failure than beta blockers?
What is sinus arrhythmia?
Normal (non-pathological) variability in pacemaker cycle length (heart rate) caused primarily by respiratory changes in parasympathetic (vagal) nerve activity to the SA node.
misnomer bc not arrhythmia just rhythm of heart changes. normal variability of pacemaker cycle length. NORMAL. caused by respiratory changes in parasympathetic nerve activity in sinus node.
What happens during inspiration and expiration? What would it look like on EKG?
inspiration causes decrease in cycle length (increase in heart rate) by inhibition of parasympathetic nerve activity. Stretch receptors in the lung feed back and decrease HR.
expiration causes increase in cycle length (decrease in heart rate) caused by stimulation of parasympathetic nerve activity.
inhale, stretch receptors in lung send signals to brainstem that inhibit efferents of vagus. bc you have less vagal activity during inspiration your sinus rate goes up a little bit and cycle length shortens. opposite during expiration… feedback to brainstem increases vagal activity and HR slows and cycle lengthens. EKG shows variability …not due to sympathetics but vagal modulation of sinus node.
Describe the EKG you would see in a normal sedentary person vs a normal aerobically trained person.
sinus arrhythmia is more pronounced in aerobically trained individuals. low base rate HR (means high vagal tone) sedentary people have high basal HR and weak vagal tone. wouldn't see this type of EKG (slide 10) on sedentary person. Vagal stimulation is anti-arryhthmic. higher vagal tone are less prone to arrhythmia's.
Describe the autonomic control of the heart (NE).
sympathetic nerve stimulation
-sympathetic nerves stimulate ALL cardiac pacemakers
-increase cAMP dependent slow inward L type Ca current and iF current (increases diastolic slope). (L type Ca current- doesn't affect the pacemaker rate, but does increase conduction through AV node..more Ca in SR)
-no effect on K or on the maximum diastolic potential
-increase slope of diastolic depolarization
Does sympathetic stimulation affect the maximum diastolic potential?
-no effect on K or on the maximum diastolic potential
does increase slope of diastolic depolarization through increase of iF current
What would a sinus tachycardia look like on EKG? sinus bradycardia? Draw.
sinus tachycardia happens when exercise... is a supra VT...impulse coming from AV and stimulating QRS normally. depends on clinical context.
sinus (means P wave) bradycardia- v slow HR. systole and long diastole. can see QT interval changing though no T wave on this recording.