Heart 5: Mechanisms of Dyshythmias Flashcards Preview

FHB I - Cardiac Unit > Heart 5: Mechanisms of Dyshythmias > Flashcards

Flashcards in Heart 5: Mechanisms of Dyshythmias Deck (41):

What do all cardiac dysrhythmias result from?
What are the 3 main types?

alterations in impulse formation (ectopic pacemaker that fires off inappropriately) or impulse conduction or both.
(caused by change in rate, rhythm, or output)

1)automaticity (inappropriate formation of AP)
2)re-entry of excitation (conduction problem)
3) triggered activity (inappropriate formation of AP)


Describe automaticity as it relates to dysrhythmias. What tissues does it affect? What would phase 4 look like?
What is tachycardia? Bradycardia?

automaticity mechanism anything that alters the existing mechanisms that drive pacemakers in specialized conduction system primarily. where automatic fibers located sinus node. around AV, HisPurkinje system. not atrial or ventricular muscle these fibers are never automatic. can be drive to generate inappropriate AP but don't have normal automatic mechanisms-phase 4 is flat.

same mechanisms to generate normal mechanisms but go array. mechanism of impulse formation, forming AP inappropriately. fire at inappropriate rate
(ex: ionic channels- if firing inappropriately then arrhythmia. may or may not be pathological. premature beat occasionally- benign but arrhythmia.

Alterations in pacemaker rate that are mediated through changes in the pacemaker mechanisms that normally exist in pacemaker cells, i.e. the pacemaker cells located within the specialized conduction system.
tachycardia is defined as a heart rate > 100 beats/min.
bradycardia is defined as a heart rate less than 60 beats/min


What is given to help premature beats?

beta blockers-
premature beats prob bc of high sympathetic tone... benign arrhythmias.

beta blockers- blocking action of adrenaline. ischemia or infarct…


What are possible causes of tachy-dysrhythmias?

Possible causes of TACHY-dysrhythmias:

a) norepinephrine (sympathetic nervous activity)
b) stimulants - amphetamines
c) stretching - ventricular aneurysm
d) electrolytes - hypokalemia
e) sick sinus syndrome, fever, hyperthyroidism


What are possible EKG manifestations of enhanced automaticity?

a) sinus tachycardia
b) premature atrial contraction (PAC)
c) premature ventricular contraction (PVC)
d) atrial or ventricular tachycardia (AT; VT)
e) supraventricular tachycardia (SVT)


If a coronary vessel is blocked and an infarct occurs the heart will beat more slowly as a result. Why?

/Why is slowing down HR if patient is in heart failure a good idea?

reflex. as heart contracting fast it generates metabolites and gets tired.. muscle gets tired and doesn't want to push too far and gets ischemic. heart v aerobic muscle and not tolerant to ischemia. if it senses ischemia then reflex to tell vagus to slow things down.

slowing down HR if heart failure is good idea… (heart is a muscle and generating force and doing it all the time.. it needs ATP to do that… needs constant flow. ATP comes from oxygen. heart v aerobic and needs constant flow of oxygen…coronary disease limits amount of O…so benefit of slowing down HR is use less O and thats good for a sick heart… heart is muscle that works continuously so need continuous O and that means continuous blood flow. manage O consumption of heart…most therapies go toward this.


What happens when NE dumped on ventricle inappropriately?

inappropriate sympathetic nerve stimulation... premature beats bc of high sympathetic tone


What effect can caffeine have on pacemaker activity? Describe the mechanism.

causes enhanced pacemaker activity in latent pacemakers and induces premature beat.

caffeine to enhance pacemaker activity- phosphodiesterase inhibitor. inhibits breakdown of cAMP (2nd messenger of sympathetic nerve stimulation) so enhancing the effect of nerve stimulation. when NE acts on beta receptor to increase cAMP through adenyl cyclase it doesn’t get broken down. cAMP doesn’t get degraded as fast w caffeine and enhanced sympathetic activity. cocaine blocks uptake or degradation of NE and enhances effects of NE -causes same type of fatal arrhythmia's.


With a premature beat, even though it's an extra beat, one might feel a pause in HR instead. Why?

bc that premature beat doesn't generate enough pressure to open the aortic valve so you don’t feel a regular pulse but next beat is stronger than normal - and that’s the thumping you feel in chest… beat that follows premature beat is stronger than normal and thats the thumping patients feel in chest

-early beat not enough Ca in SR to get a good contraction...so compensatory pause... but with next beat you've have extra time to fill Ca in SR.


Explain how stretching/ventricular aneurysm can cause tachy-dysrhythmias.

weakening in wall of either heart or artery and causes wall to bulge out. (arterial aneurysms more common) sometimes congenital.

after MI wall becomes weak bc cell dead then pressure in heart pushes out free wall of ventricle and causes budge and thats an aneurysm that must be repaired w patch. if ruptures it bleeds off. along endocardial surface there are Purkinje fibers w pacemaker capability and they get stretched from this aneurysm normally at site of junction between the normal and abnormal tissue…stretching cardiac cell opens stretch activated channels (SAC channels) allows inward current into cell and enhances slope of diastolic depolariztion and hit threshold and get ventricular tachycardias


Explain how hypokalemia /electrolytes affect automaticity.

electrolytes- hypokalemia (bc of analomous rectification…doesn't change RMP as much. as result of decrease of K permeability can lengthen AP through IK1 and can cause arrhythmias as a result of prolonged QT syndrome. can enhance latent pacemaker activity..doesn't affect sinus node. changes in K concentration never affect sinus node.. what happens is inward Na current. little bit of outward K current. more inward current than outward current. net inward current causing depolarization. if have K going out and put cell on low K and decrease K permeability less K will go out and now you tip balance so now net inward current is now larger… affect balance of currents by reducing K permeability- that's what low K does to automaticity- as a result of net inward current will enhance diastolic depolarization… hit threshold and start firing premature beats…can go into runs of tachycardia. occurs primarily in latent pacemakers in atria or ventricle. that's what see in pt with low K.


Describe sick sinus syndrome.

usually due to inflammation or fibrosis. tachy. then brachy. fast then slow.
ablate sinus node and put in pacemaker

in sick sinus node get rapid and slow beats mixed together. aging - sinus node more fibrotic and lose pacemaker cells and sinus rate slows down. older people do have pathological bradycardia and get pacemaker


How will fever, or hyperthyroidism affect automaticity?

fever will always raise HR. and hyperthyroidism always causes enhanced pacemaker activity and also predisposes atrial

high thyroid- thyroid hyper secreted then bc high thyroid circulating level already..then do exam on gland, just palpating gland can stimulate release of more thyroid. thyroid storm. increase body temp.. high level of aderegenic receptors in heart.. give beta blockers to protect heart so they don't go into thyroid storm. fibrillation.


Why might a patient experience shortness of breath as a result of atrial fibrillation?

lose atrial contribution when go into a-fib. heart starts to fail as get older. cardiac output- atrial input more important as ventricle weakens, need extra blood from atria. go into atrial fibrillation and lose that amount of blood from atria into ventricle and now ventricle having harder time generating cardiac output so not perfusing through lungs appropriately and get shortness of breath.


What are possible causes of brady-dysrhythmias?

a) drugs - anti-arrhythmics, β-blockers, Ca2+ antagonists, digitalis, barbiturates, anesthetics.
b) ischemia or infarct
c) sick sinus syndrome
d) aging – fibrosis

premature beats with bradycardia- bc of loss of overdrive suppression..if sinus rate goes really low no longer suppressing those latent pacemakers in atria and ventricle and can wind up seeing premature beats.


What are some EKG manifestations of brady-dysrhythmias?

a) sinus bradycardia
b) atrial or ventricular premature beats - these may occur in the setting of pathological bradycardia because of the loss of overdrive suppression.


How do Ca antagonists work? What effect do they have?

slow sinus rate. most people take for hypertension but a side effect is that is slows HR a lot and can lower BP so get dizzy when stand. bc you block Ca into sinus node, reduce SR component and wind up slowing sinus rate


What is the effect of digitalis?

direct effect is slow down sinus rate by enhancing CNS stimulation of Vagus. more vagal activity to sinus node and considered a benefit for heart failure- main thing is increases strength of contraction of ventricle but it also slows down sinus node through vagal mechanism.


What are the 3 general requirements for re-entry of excitation?

a) geometry for a conduction loop
b) slow or delayed conduction
c) unidirectional conduction block


Why is slow conduction one of the risk factors for re-entry?

if loop is very fast, then by the time it comes back the patch of tissue hit the first time is still refractory. when things fast it's not an issue bc you're hitting absolute refractory periods. problem is when its slow bc you can hit repolarized tissue and reactivated tissue so loop back again


What is the arrhythmia that often kills someone after an MI? How is it caused?

re-entry (can occur anywhere in heart)
this is what kills you as a result of MI, not lack of muscle...its the abnormal tissue generated as a result of MI

Possible causes:
a) ischemia
b) infarction
c) congenital bypass tracts-
Ex. Wolf-Parkinson-White (WPW)


What is the effect of ischemia?

RMP can determine the speed and conduction ...ischemia always depolarizes the RMP and lose Na channels.


Normally when an impulse comes down and encounters loop tissue describe what happens. What about after an MI? Describe what happens.

normal tissue- impulse comes down both ways and extinguishes e/o
heart beat stops at end of one cycle bc whole heart is refractory... which stops heart from beating (so extinguish e/o bc of refractoriness) get MI and damage through a branch - no arrhythmia. could have a block in both antegrade and retrograde direction
in MI the electrical signal can't conduct in antegrade direction but can in retrograde direction and enters the damaged tissue... but conduction through the damaged region is slow or delayed (may be partially inactivated Na channel or no Na channels and Ca channel carrying current)


Describe the process of how an impulse through damaged tissue loops back again.

impulse that first came down has an AP and has finale refractory period. impulse comes down and causes refractoriness of 300 milliseconds(duration of AP that occurred) impulse conducts through slow area and takes say 400 milliseconds to conduct through damaged region. when it comes out it will see excitable tissue bc refractory period of previous excitation is over and now tissue is excitable again. and bc this conduction took longer than refractory period it will conduct back into heart and go around and around and it will be ventricular tachycardia and stimulate whole heart.

say refractory period only took 200 milliseconds it would have encountered refractory period when it came out and would have died. so its a timing situation. how long does it take for impulse to conduct through damaged region in relation to normal refractory period of the ventricle?


How is re-entry of excitation treated?

class 3 makes refractory period of normal tissue longer so when impulse comes out of damaged tissue it encounters refractory tissue not excitable tissue. now we don't use as much bc v dangerous. non specific effects and other issues. now try to map and find damaged region and ablate or burn that damaged tissue so no conduction through so create situation like in C. better to have dead tissue than tissue that is damaged and can still have some conduction through it.


What might you see on an EKG when someone has re-entry of excitation?

Some EKG manifestations:
a) premature atrial or ventricular beats
b) atrial or ventricular tachycardia
c) supraventricular tachycardia
d) atrial flutter
e) atrial or ventricular fibrillation


Describe WPW. What is it?

congenital bypass tract- type of re-entry that does not involve infarct.
impulse from sinus node to piece of tissue that's connecting right atrium to right ventricle (bypass tracts that bypass AV node)...tissue not supposed to be there and has functional characteristics of a Purkinje fiber. so has rapid conduction and long refractory period.


Describe what happens in WPW. What do you see on an EKG?

in resting sinus node conditions an impulse comes down through bypass tract first and stimulates a portion of the rt ventricle and also travels down through AV node. (conduction through AV node is slow as usual) and that enters ventricles normally and causes the rest of QRS. So QRS complex is prolonged because it has a delta wave and then a QRS.. delta wave (upward deflection) is due to impulse coming through early through bypass tract bc there's no delay then rest of QRS is typical bc coming through conduction system and have prolonged QRS as a result... at this point its pre-excitation syndrome...


What happens if you get a premature beat in WPW?

but if you get premature beat in atria which often happens then its unable to conduct through bypass tract
-unidirectional block bc long refractory period.
cant get through bc has long refractory period. is able to conduct through AV node and by the time it gets through AV node (AV node is slow conducting pathway in reentry. not damaged tissue…its actual AV node delaying activation to ventricle) by time gets through AV node the bypass tract has recovered its excitability and impulse gets into ventricle and goes retrograde through bypass tract and goes around and around and sets up ventricular tachycardia and is called supra…bc involves structures above ventricle …not being driven by sinus node. not sinus arrhythmia its a real arrhythmia. antegrade thru AV node and retrograde through bypass tract


Describe atrial fluttler/ fibrillation.

Re-entry can cause premature atrial or ventricular beats - atrial flutter is 300-4000 beats around atria. ventricle is going at a rapid rate but not nearly as high as atria. in EKG see ppppp then one gets through ... atrial flutter

A-fib - only see under reentry.

flutter-regular rhythm going around and around one pathway
fibrillation- chaotic multiple reentry loops making tissue occurring in completely asynchronous way


Describe triggered activity.

can occur in atrial or ventricular tissues

-delayed after depolarizations (DAD)
...due to abnomally elevated intracellular Ca. dysrhythmias resulting from digitalis toxicity

-early after-depolarizations (EAD)
-relayed to prolongated of AP duration
-mechanism prob due to abnormal reactivation of slow inward L-type Ca current
-also may contribute to prolonged QT syndrome by extending duration of AP

triggered activity is impulse formation completely abnormal doesn't rely on any normal mechanisms that exist. de-noval mechanism which creates its own mechanism. DADs or E(early) ADs. DADs used to intracellular Ca elevation. usually occurs with ischemia or infarct where SR dumps Ca into cytosol. most of Ca is bound to SR. cant be floating around in cytosol. transient release of Ca from SR and causes activation of channel movement you don't want to see.


What are some possible causes of DADs? What are some possible EKG manifestations? What would it look like on an EKG

Possible causes:
a) digitalis toxicity
b) elevated catecholamines (increase slow inward Ca current, rapid HR)
c) rapid heart rate (more Ca coming in per minute)
d) all in combination

Possible EKG manifestations:
a) premature atrial (PAC) or ventricular contractions (PVC)
b) atrial or ventricular tachycardia

See slide 9.


Discuss digitalis toxicity and how by inhibiting pump you get stronger contraction. What is the downside?

digitalis-raises intracellular Ca. used for congestive heart failure to strengthen contraction of heart by raising intracellular Ca but has v low therapeutic index (concentration that causes therapeutic effect is close to concentration that causes arrhythmias) dangerous drug. digitalis toxicity can overload SR with Ca and wind up releasing Ca inappropriately.

Na/K pump pumping Na out of cell and K into cell... important for extrusion of Ca during diastole when you want the muscle relaxed. stronger heart contraction bc by inhibiting Na/K get buildup of Na inside the cell - so the gradient is not as strong as before. if less strong gradient then not as strong of a force to bring Na in and not as much force to bring Ca out. so Ca will be picked up and pumped into SR Ca stores... that will give stronger contraction in next heartbeat.

problem: when you overload the SR with Ca it can be arrhythmogenic...high levels of Ca in SR can leak out and when it leaks out it gets picked up by Na/Ca exchanger which would bring in more Na which would have a depolarizing effect- if get to threshold can fire off AP. if you get whole patches of cells that are hyper-excitable then you can get arrhythmia.

(someone on digitalis goes to play tennis and get HR up and all things conspire to get Ca too high and get DADs. )


What would a DAD vs EAD look like on an EKG?

Slide 9, slide 12


What are possible causes of EAD? What would it look like on an EKG?

Possible causes:
1. acidosis (as in ischemia)
2. hypokalemia
3. quinidine
4. slow heart rates (bradycardia)
(all cause lengthened AP duration and lead to triggered activity)

Possible EKG manifestations:
1. premature atrial (PAC) or ventricular contractions (PVC)
2. atrial or ventricular tachycardia (torsade de pointes)

EAD is more lethal. result of QT syndrome. related to prolongation of AP…anything that prolongs AP duration abnormally can trigger EADs. similar to DAD but don't know mechanism as well. not related to intracellular Ca. occurs early in AP when it should be refractory.

ischemia causes them… hypokalemia lengthens AP duration and can promote EADs … quinidine prolongs AP. and slow HR will promote longer AP. get premature atrial beats…this tachycardia can result in serious arrhythmia.


Between EAD and DAD which manifests at slow HR and which at fast HR?

EAD can manifest these at slower heart rates. these manifest at slower HR bc slower HR lengthen AP… Leads to coupled beats (regular irregularity)
anything that lengthens AP can precipitate EAD.
So the next AP comes in during the relative refractory period- very dangerous.

(DAD caused by higher HR bc brings in more Ca)


What would EAD look like on an EKG?

Slide 12. R on T. Spontaneous beat (R wave) on the repolarization wave of the previous beat.

on EKG- see QRS (AP around heart), QRS on relative refractory period…this is R on T..spontaneous beat R wave occurring on relative refractory period of previous beat. v dangerous. parasystole… regular irregular. fixed.. coupled beats. v dangerous kind of arrhythmia bc hitting rel. ref. period can throw heart into VF.


What are some anti-arrhythmic therapies?

drugs (Na channel blockers, K channel blockers, Ca channel blockers, beta blockers)
radio-frequency ablation
DC cardioversion
implantable cardioverter-defibrillation (ICD)

beta blockers. nonspecific drugs can cause all types of other problems …some lupus,
so in reponsone develop radiofreq. ablation. put catheter and figure out where arrhythmia coming from and burn it… try to do for a-fib. disrupt pathway that reentry coming from

DC cardio-defibrillatior. large current through heart which depolarizes all cells. …cells were out of whack and hopefully now depolarize all cells to plateau so all synchronize and REpolarize together then sinus node takes over again. sinus node never into arrhythmia …unless issue with sinus node itself. no overdrive suppression of sinus node. always there beating unless disease of sinus node itself. these arrhythmias do not affect sinus node.


Describe the implantable ICD.

if have EADS like congenital abnormality in Na or K channel causing prolonged QT syndrome predisposes to atrial/Ventricular fib. put in ICD. large electrode connected to battery pack.. senses electrical activity of heart and when it goes into VF it shocks heart. implantable defibrillator.

putting in a ICD. battery pack in subclavian. electrode to sense in atria. stimulating electrode in Rt ventricle.


What are the following EKG reference values?


P-R interval: 0.12 – 0.20 sec (120-200 msec)

QRS complex: 0.07 - 0.10 sec (70-100 msec)

Q-T interval: 0.25 – 0.43 (250 – 430 msec)

Tachycardia: cycle length less than 0.6 sec (600 msec) (>100 beats/min)

Bradycardia: cycle length greater than 1.0 sec (1000 msec) (less than 60 beats/min)


How does hypokalemia cause tachycardia?

inward rectifier K channel decreases its permeability in response to hypokalemia. RMP doesn’t change as much as you might expect

bc of the decrease in outward current, the inward currents become more effective. So T type channels (Ca coming in phase 4 depolarization) IF (Na coming in so diastolic depolarization) so depolarize cell toward threshold. so phase 4 diastolic depolarization goes faster and latent pacemakers start generating runs of tachycardia. Not from the AV or sinus node cells, they’re relatively resistant bc of low inward rectifier K channel expression. but cells around them start to fire, leading to tachycardia.

hypokalemia can also lengthen the AP, this is a complex effect but a similar mechanism- decreased K efflux results in a relatively more effective Na and Ca influx (during upstroke of AP they come in quicker and get longer AP and relative refractory period) and arrhythmias