RMP and AP Flashcards by Amanda Beach

What 3 properties give us consistency of the heart

automaticity, conduction system, functional syncytium

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What structures are apart of conductions system

SA note, inter-atrial pathway, AV node, common AV bundle, R and L bundle fibers and the purkinje fibers

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What cells are usually in charge of driving heart rate

SA nodes because reach threshold first

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What would you expect to see if SA node fails

bradycardia

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How does SA spread to AV node? left atrium?

AV node- internodal pathway

left atrium- brachmanns bundle or known as anterior interarterial myocardial band

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3 functional regions of AV node

AN
N- nodal
NH

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What paths slow conduction

AN and N

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how does AN slow conduction

longer path

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how does N region slow conduction

slower velocity

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Why is there a delay between atria and ventricles

so we have time for filling of the heart during diastole

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What is decremental conduction

effect dies out over time

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Which node is common to have conduction blocks

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Once AV nodes fail what fibers take over

purkinje. 20-40 bpm

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What do patients with Wolff-Parkinson-White Syndrome have

alternate path around AV node(bundle of kent). conducts directly atria to ventricle and is faster. but the ventricle depolarization is slower

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Where does the right and left bundle branches go

R- down right IV septum

L- splits anterior and posterior

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How are purkinje fibers arranged

linear like sarcomeres.

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Which part of conduction system has fastest conduction velocity and how?

purkinje because they have a huge diameter

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in which direction are purkinje fibers activated

endocardium- epicardium

apex- base

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In ventricular m how are APs conducted

cell to cell

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Which cells repolarize after depolarization

base- apex

epicardium- endocardium

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What events are significant for ventricular depolarization

early contraction of IV septum(anchor)
early contraction of papillary m (prevent backflowto atria)
depolarization apex to base

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Where is the slowest conduction velocity in the heart? and why?

AV and SA nodes

small diameter

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how many nuceli are in cardiac m

mononucleated

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Where is Ca stored in Cardiac m

ECF and SR

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what is faster. rate of contraction of skel m or cardiac

skel m. cardiac is 1.5x slower

What are markers of myocardial injury

Troponin T and I markers and CK-MB

What accounts for the electrical syncitium of the heart

all cardiac m cells contract in syncrony

What allows for cell to cell communication

intercalated disks

If cell to cell communication is not working properly what do you see on the EKG

widened QRS complex

What is the all or none of the heart

either all cardiac cells contract or none

how do we alter contractility of cardiac m

increase Ca. sympathetic input

Why do we need Ca from ECF

to trigger release of Ca from SR

What do we need for relaxation of cardiac cells

Sarcolemmal 3Na/1Ca antiporter and Sarcolemmal Ca pump using ATP SERCA

Can cardiac m increase force of contraction through tetanus

Why can cardiac m not go under tetanus

AP is long (plateau)

How do we have a long AP in cardiac cells

VG L type Ca channels | and delayed K channel

Do pacemaker cells have RMP

no- maximum diastolic potential

What do we have instead of RMP in pacemakers

slow depolarizaiton phase

What is the RMP of fast conducting cells

-80 - -90

Ion distribution for RMP

Na and Ca high extracell | K high intracell

What is the RMP permeable to

effect of hyperkalemia

increase depolarization

Are AP constant thorughout all areas of cardiac cell conduction

no, initiation time shape and duration of APS changes depending on what cells.

2 main types of cardiac AP

fast response fibers and slow response fibers

Which RMP is more negative, fast or slow response AP

fast is more negative.

What is the threshold potential in slow and fast AP

slow is -40 | fast is -70

Which type of cardiac AP has faster upstroke

fast

Rank conduction veolocities of slow response, fast response in ventricles and fast response in purkinje

purkinje fastest then fast response ventricle slow response are the slowest

which fibers respond to greater AP firing rate

fast response fibers because recover fast from refractory period

What are the 4 main ion currents in cardiac AP

NA, Ca, K, and funny current

What phase is Ca responsible for in slow response fibers

slow depolarization- AV SA nodes

What phase is Ca responsible for in fast response fibers

plateau phase

What phase is the funny current responsible for in slow response AP

"pacemaker current" partialy helps the slow depolarization phase

What type of ion current is the funny current

If the upstroke of a cardiac AP is solely due to Ca influx what type fiber is it

slow response AP

What two ions contribute to the rapid spike at the begining of a fast response cardiac AP

Na and Ca

Which type cardiac AP has a transient K current

fast response

What ions are still moving during the plateau phase in fast cardiac AP

K and Ca and tiny bit of Na

what ions are moving during the electrical diastolic phase of slow response cardiac AP

K Ca and the funny current

what ion impacts the conduction velocity

what are the types of Ca channels in cardiac myocytes

L type Ca and T type Ca

When does Ca activate and inactivate in fast response AP

activate at more positive and inactivate slower than Na

What are the two K channels that contribute to respolarization

rapid and slow

describe K movement in SA and AV node

decreases efflux to promote depolarization

What would be the effect of a K channel blocker on AP in fast response

lose that little dip of repolarization after upstroke. Also prolonged AP

What AP is shorter, atrial AP or ventricl

AP because faster K efflux to repolarize

What are the 4 dependent currents in Purkinje fibers

Na Ca K and funny

What are the 2 factors that affect conduction velocity

AP amplitude | Rate or slope of the depolarization

When is there the greatest number of inactivation gates on Na channels

right after depolarization

How does hyperkalemia slow conduction velocity

decreases amplitude and slope depolarization because many of Na channels will be inactivated.

When do we see hyperkalemic states in cardio clinically

Ischemia- affects ATPase so ion [ ] not normal | Infarcted cells- cells release intracell K

When is the effective refractory period

after initiation of fast AP, locked Na gates

When is the relative refractory period

not fully excitable. before repolarization is complete

What does AP look like when happens during relative refractory

depends when it takes place/ if right before reached depolarization- looks normal. if right when refractory begins, small amplitude

What is the purpose of refractory periods

avoid tetanus and gives time for adequate filling (diastole) | also can limit ectopic beats

What is an Ectopic foci

AP that do not follow normal conduction pathway

What does an EKG look like with ventricular ectopic foci? why?

wide QRS because takes longer for cells to communicate cell - cell

What are proarrhytmias

increased inward currents or decreased outward currents for repolarization

What do afterdepolarizations result in clinically

tachycardia

What will an early afterdepolarization look like

lower slope, lower amplitude, so slow conduction detrimental. Long QT syndrome-- Torsades de pointes

What can cause a delayed afterdepolarization

elevated Ca

What is reentry of cardio

abnormal impulse that takes on own path. own pacemaker rhythm

What is a global rentry pathway

own curcuit

what is needed for reentry to occur

partial depolarization, unidirectional block, effective refractory period is shorter than necessary time (so new one during relative refractory)

Where does global reentry happen

between atria and ventricle

what can result clinically from global reentry

supraventricular tachycardia

where does local reentry occur

within atria. or within ventricles

What can result clinically from local reentry

atrial or ventricular tachycardia

What can cause reentry

autonomic input. sympathetic decreases ERP, vagal increases ERP

3 main factors promotin reentry

lengthened conduction pathway decreased conduction velocity reduced refractory period

What can cause lengthened conduction pathway

dilated heart chamber

What can cause decreased conduction velocity

hyperkalmeia, ischemia, purkinje system block

what drugs reduce refractory period

Epinephrine

What is the purpose of an external automated defibrillator EAD

alternating current promoting a reset by putting all cells into refractoriness at once- stopping fibrillation

How do we change HR in slow response

how quickly threshold reached, starting point RMP, or changing threshold itself

When is the inward funny current increased

the more negative membrane gets. hyperpolarization

What is moving through funny channel

Na influx, non specific

What results if decrease ECF Ca

small upstroke and amplitude of fast

Will hyperkalemia increase or decrease HR

decrease because changes driving form for K and slowing dow repolarization

Tetrodotoxin block

transitions from fast response to slow response fibers