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Flashcards in electical activity long Deck (37):
1

What are the Ionic concentrations in and outside of resting myocytes

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2

Nernst potential for K+

[K+]i = [K+] inside cell 150mv

[K+]o = [K+] outisde cell 4mv

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3

Formular for the membrane potential 

If the equilibrium potential for each ion remains unchanged (ie the concentration gradient doesn't change) the membrane potential depends on permability and conductance of the ions. So if only 1 ion is conducting (eg K+) the membrane potential will be that ion's equilibrium potential

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4

simplified membrane potential

the resting membrane potential is near the equilibrium potential for K+ as it has high conductance compared to the other ions.

The permeability/conductance of the cell membrane to ions is due to negatively cahrged protein in the cell

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5

how are concentration gradients maintained

Energey dependant ionic pumps

1. ATP dependent Ca++ pump (if Ca++ accumulates inside get cellular dysfunction

2. Na+/Ca+ exchanger (3:1) in either direction

3. Na+/K+ ATPase pump 3:2 (3 Na+ out for every 2 K+ in)

ATP (therfore O2) dependant, in the sarolemma in the membrane

Note: ability to maintain ionic concentration gradients means that Em chagnes are due to changes in ionic conductance

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6

The 2 types of ion channels

1. voltage gated - open and close in response to changes in membrane potential. Na, K, Ca voltage gated channels exist and are involved int he action potential

2. Receptor gated channels. Eg acetylcholine released by the vagus nerve innervating the heart binds to a sarcolemmal receptors that causes special type of K channel to open

7

Fast Na channels - how they work normally and what happens if cell is hypoxic

- at resting membrane potential it is closed

- m gate opens with depolarization

- h gate closes after a few milliseconds stopping Na so get repolarization

- at end negative membrane potential causes m to close and then h to open

This channel responds differently if the resting membrane potential is partially depolarized or the cell slowly depolarizes. EG hypoxic cell means cell is partially deploarized which inactivates the Na cheannel by closing H gates

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8

3 factors that determine the amount of ion that passes through membrane

1. number of channels

2. duration they are open

3. The electrochemical gradient drving them

9

types of cardiac action potentials

non pacemaker cells - triggered by depolarzing currents from adjacent cells. Em -90mV

pacemaker cells - cabable of spontaneous ap generation. Em - 60mV

o Diff concentrations of Na, K and Ca in and outside cell ? correct
• K 135 in 5 out, Nernst -94
• Na+ 10 in 140 out, Nernst 70
• Ca++ <0.1 in, 2 out, Nernst 134  

NOTE: both are different from ap's of neural and skeletal muscle cells

10

what are the differences in action potentials between cells types

duration (due to different ionic conductance)

nerve 1 milisecond

skeletal muscle 2-5milisecond

ventricular 200-400milisecond

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11

PO 1.43

ionic basis of normal cardiac excitation

non pacemaker action potential (atrial and ventricular myoctyes, purkinje cells)

250ms

phase 4 - resting membrane potential (near Ek),  -90mV, due to inward rectifier K channel (Ik1), due to [K] as this is most permeable. regained by Na+/K+ ATPase and Na+/Ca+
 
phase 0 - cell rapidly depolarizes from -90mV to threshold voltage of -70mV due to ap conducted by adjacent cell because of fast Na+ channel conductance. gK falls because potassium inward rectifier channel becomes non conducting at positive potentials
 
phase 1 - initial repolarization when transient outward K+ (lto) channel opens and fast Na+ channel inactivates
 
phase 2 - plateau phase, large increase in slow inward gCa++ through long lasting ltype Ca+ channels delays repolarization(maintains depol). This happens with membrane potential is -40mV. Blocked by verapamil, diltiazema nd nifedipine. Balanced by K+ outflow through transient outward (lto) and rapid delayd rectifier (lKr) channels

phase 3 - repolarzation when gK+ increases (through IKr, Lto and inward rectifier (Ik1) channels) and gCa++ decreases.
Na channel inactive until half was through phase 3 (absolute refractive period 250ms), then more H gates open so Na permeability increses Na+ reopens at -50 and an appropriate stimulus can cause another action potential (relative refractory period 50ms)

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12

what happens if fast Na chennels are blocked or inactivated by slow deplarization

phase 0 less steep and ap has lower amplitude, depolarization happens through slow inward Ca+ chennels (Ltype) - slow response ap's

13

PO 1.43 ionic basis of automaticity and normal cardiac excitation

Pacemaker action potentials

DIfferente because:

• no true resting potential but regular spontaneous ap's
• depolarzation due to slow inward Ca++ through L type Ca channels instead of fast Na+ (Na+ inactivate as cell more depolarized which closes the h gate)
• no inward K rectifiers so less stable resting membrane potential RMP
• HCN channels responsible for funny current
• Less negative RMP (-60mV) and threshold (-40mv)
• No plateau in phase 2

SA node ap 150ms. myocyte is 250ms

o pacemaker cells are in sinoatrial node (SAN), atrioventricular node (AVN) and purkinje cells (PC)
o rate of automaticity faster in SAN so its primary, others secondary

3 phases:

phase 0 - rapid depolarzaion due to increased gCa++ through L type Ca channels that open at threshold -40mV. gK decreases, funny channel and transient Ca++ channel closes

phase 3 - repolarzation, voltage operated delayed rectifer inward K+ channels open so gK+ increases, Ca++ channels close. Ends at -65mV when K+ channels closes again

phase 4 – spontaneous, diastolic, depolarization leading to subsequent generation of new action potential. Due to
• gK declining
• a 'pacemaker/funny' current (If, slow inward movement of Na)
• increase in gCa++ through transient t type channels which open briefly at -50mV, not blocked by verap/diltia,
• Long L type Ca++ opens and soon threshold reached

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PO 1.43

ionic basis of abnormal cardiac excitation

1. if SA node becomes depressed or its ap doesn't reach secondary pacemakers, overdrive suprrsion ceases and new pacemaker is the ectopic foci but his is slow and get decreased HR and CO

2. afterdepolarization - Non pacemaker cells may undergo spontaneous depolariztion in phase 3 or early phase 4 triggering abnormal action potential, if large enough can trigger self sustaining ap's - tachycardia

early - in phase 3, from slow inward Ca++, happens if ap's prolonged

delayed - in last phase 3 or phase 4, happens if high intracelluar Ca++ like in ischaemia, dig tox, xs catecholamine stimulation4

3.damaged/dysfunctional conduction system (card 19) damages the pathway so ventricles can't generate pressure and can get arrhythmia (eg if AV node doesn't slow ap's from SA node get af of AF, or if ischaemic or receives XS vagal stimulation vent wont contract  and rely on latent pm in the ventricle as above)

4. ventricular ectopic outside of fast conducting system means ventricular depol relies on slow cell to cell condction between myocytes (0.5m/sec)

5. accessory conduction pathways between atria and ventricle alters the sequenc of ventricular depol can can cause SVT

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15

PO 1.43 normal intrinsic automaticity of SA node

o intrinsic automaticity of SA node - regulation


100-110/min but HR 60-200 due to autonomic nerves acting on SA node and other factors like hormones, serum K and Ca, hypoxia, temp and stretch


- Autonomic regulation


o Sympathetic via adrenergic increases cAMP which increases depolarization and HR (pos chronotropy)
• Stimulates funny channel so increases slope of phase 4
• Also lowers phase 0 threshold


o Parasympathetic via cholinergic decreases cAMP hyperpolarizes  resting Em, slow HR (neg chronotropy)
• Increases threshold potential
• Decreases phase 4 slope
• Decreases resting Em


- Hormones
o Adrenergic stimulation through Gq
o Thyroxine increases concentration of adrenergic receptors and rate of Ca++ uptake so increased HR and CO for increase basal metabolic rate


- Temperature
o Increases the rate of enzymatic processes so increased O2 requirements so increased CO and HR


- Serum ion concentration need to add to this
o Serum K+ modulates K channels
o Hypokalaemia – increased excitability, VT, Vf
o Hyperkaleamia – decreased excitability, brady, asystole


- Hypoxia leads to bradycardia

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16

types of cardiac ion channels

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17

PO 1.43  factors that may influence cardiac electical activity

 

how does sympathetic and vagal tone affect SA node

(see also card 5 and 6 of structure and function)

Sympathetic (see also cell structure and function card 6)

- norephinephrine binds to B1 adrenoceptors couple to stimulatory G protein (Gs-protein), this activates adenylyl cyclase and increases cyclic adenosin monophosphate (cAMP) so get increased opening L-type Ca++ channel and increased If (slow Na+ channels) so rate of depol increases

Vagal (see also cell structure and function card 7)

- Acetylcholine released at Sa node binds to M2 and decreases cAMP via inhibiotry G protein (Gi-protein)

- Acetylcholine may also increase cyclic guanosine monophosphate (cGMP) through nitric oxide (NO - cGMP) pathway which inactivates L-type Ca chennels

- Acetylcholine also activates KaCh - special type of K channel that hyperpolarizes the cell by increasing K conductance

18

PO 1.43 factors that may influence electrical cardiac activty

 

mechanisms that affect SA node firing rate

 

- catecholamines epinphrine  work like norepinephrine

- hypokaleamia increases rate of phase 4 depol because decreased K conductance

- hypoxia causes depolarization abolishing pacemaker activity

- digitalis increases parasympathetic activity and inhibits the sarcolemmal Na+/K+ ATPase so get deoplarization and brady

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19

PO 1.43 normal cardiac excitation, correlation of mechanical with ionic/electric

electrical conduction in the heart - describe the pathway that allows rapid, organized, near synchornous depolarization and contraaction of ventricular myocytes to generate ventricular pressure

SA node ap propagates cell to cell.

Cardiac cells connected by low resistance gap junctions at the intercalated disks, so when one depolarizes the positive ionic current spreads to the next

As it depolarizes the atrial muscle it commences excitation-contraction coupling (PO 1.44)

ap spreads between myocytes AND through internodal tracts of atria(specialised conducting pathways)

atria separated from ventricle by non conducting tissue, ap enters ventricle through Atrioventricular node in inferior posterior interatrial septem which slows the impulse (allows complete atrial depol, contraction and emptying and limits frequency of impulse)

then to bundle of HIS, left and right bundle branches - very fast

then purkinje fibers which connect with ventricular myocytes even faster

ventricular myocytes depolarize and contract

20

PO 1.43 normal cardiac excitation - speed of conducting pathways

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21

PO 1.43 factors that may influence electrical cardiac activity

 

regulation of conduction velocity

intrinsic and extrinsic factors

Intrinsic

- electrical resistance between cells and nature of the ap. if increased fast Na+ channels, depol happens faster eg. hypoxia decreases these channels so decreased conduction

- in AV nodal cells change in Ca conduction changes rate

Extrinsic

- sympathetic, norephinephrine binds to B1 adrenoceptors and increases conduction velocity - BB blocks this

-parasympathetic, decreases conduction by acetylcholine on M2

 

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22

PO 1.43 physiological basis of the ECG in normal and abnormal state

P wave - atrial depolarization, .08 to .1 second (repol happens in ventricular depol)

Flat after P - impulse travelling in AV node (slow conduction)

PR interval - from onset of P to beginning of QRS, .12 - .2 secs, time between onset of atrial depol and ventric depol. > .2 seconds means conduction defect in AV node (1st degree HB)

QRS - ventricular depol, .06 - .1 (happens rapidly), > .1 is impaired ventricular conduction (BBB, aberrant conduction, ectopic)

ST - entire ventricle depolarized, = plateau phase of ventricular ap. if up or down its due to non unifrm membrane potentials in ventricular cells

t wave - ventricular repolarization (phase 3 of ap)

QT - ventricular depol and repol, lasts the duration of ventricular ap's, .2 - .4 (shorter if high heart rate). long QT can make susceptible to arrhythmia. QTc assesses this independant of HR, normal is < .44

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23

PO 1.43

ecg pic and interpretation of pathological ecg

rythem strip II - sinus rythem, SA node controls rythem, 60-100bpm

brady - normal resting high vagal tone, depressed SA node function

tachy - normal is exercise/excitment

AF - high atrial rate, not all conducted through AV

af - depol arises from site other than SA  node so no p wave, AV node limits ventricular rate so still have time for filling

AV nodal block - depressed impulse conduction

1st degree - delayed conduction through AV node, > .2sec

2nd degree - AV node doesn't conduct every impulse

3rd degree - none conducted, ventricle depolarizes from an ectopic junction so its slow (AV node and bundle of HIs 50-60bpm, purkinje 30-40bpm), QRS will be abnormal and wide

VT - usually due to  reentry cicuits from abnormal impulse conduction in the ventricle or a rapid ectopic pacemaker site

VF - can happen from VT as can't fill, unco-ordinated depolarization, can't see QRS

premature depolarizations - early p or QRS that is odd shape

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24

how ecg records p wave

 

p wave is atrial depolarizing, peak is when left side has but right side hasn't yet, back to isoelectric line is when whole thing has (so no potential difference exists between the electrodes). repolarization starts where depol started so if could see atrial repol ud get a negative deflection

In reality many depol waves emerge from SA node and go in many directions, the mean electrical vector is the summation of all of them, pos if towards pos electrode, neg if away and no change if perpendicular

 

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25

how ecg records QRS

Ventricle begins to repolarize where the last cells depolarized, so repol goes in other direction and t wave positive

for ventricle, diff vectors happen at diff points in time, size of vector is related to mass of tissue undergoing depol (bigger is more voltage)

mean electrical axis is the summation of 1-4 (the average depol vector over time), use to identify left and righ axis deviations (BBB, ventricular hypertrophy)

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26

ECG interpretation rules

depolarization heading toward postive electrode or repolarization heading away is a positive voltage

repolarziation moving towards positive electrode or depolarization heading away is a negative voltage

depol or repol perpendicular is no deflection

Amplitude depends on mass of tissue

instantaneous amplitude of measrued potentials depends on orientation of the pos electrode relative to the mean vector (because at any 1 time there are many separate waves of depol)

27

6  limb leads

 look at electrical activity along frontal plane

limb leads are bipolar (have pos and neg electrodes)

lead 1 - pos on left arm and neg on right arm

lead 2 - pos left leg, neg right arm

lead 3 - pos left leg, neg left arm

triangle is einthoven's triangle

Right leg electrode is the ground

Augmented leads aVR (pos electrode r arm), aVF (pos electrode left left) , aVL (pos electrode left arm):

-derived from the same electrodes used to give I, II, III

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28

PO 1.43 common pathological states of ECG

how do u determine the mean electrical axis?

practically - wave of depol from right to left along 0 degree axis, lead I is most positive

mean electrical axis - look at 6 limb leads, axis is perpendicular to smallest net QRS (pos minus neg). eg lead III has smallest net amplitude, axis is +30 because aVR is the most negative

normal axis is -30 - +90. Abnormalities occur with conduction defects

< -30 is left axis deviation

>+90 is Right axis deviation

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29

Chest leads

chest leads unipolar - all pos (neg is a combo of the others being the neg)

record electrical activity in horizontal plane

V1 over right ventricle free wall

V6 over left ventricle lateral wall

normal electricle activation of the ventricle makes V1 neg and V 6 pos (depol travels away from V1 and towards V6)

30

how does ischaemia disrupt rythem and conduction

see slide 31 effect of hypoxia on cell (cause depolarization so disrupts conduction)

altered conduction can:

- exagerate Q wave

- cause arrhytmia

-change QRS shape

-Ischaemia makes injury current flow from depolarized ischaemic area to normal regions, this moves the isoelectric regions and puts the ST up or down

- reentry current

- tachycardia

- alter pacemaker activity, can get latent pacemaker and ectopic beats

- accumulation intracellular calcium causing after depol and tachycardia

 

 

31

effect of hypoxia on cell

loss of ATP so K+ leaks out of cells through K ATP channels (no longer inhibited by ATP) and because ATP pump not working, so cell depolarized, so fast Na+ channel inactivated, so decreased conduction velocity

32

what determines the resting membrane potential

Resting membrane potential determined by:
o Na+/K+ ATPase pump
o Difference in ion conductance – depends on electrochemical gradient and channels for the ions
o Presence of non permeable charged proteins

33

34

Types of ion channels

o Sodium

• Fast Na+ (Ina), voltage gated, open in phase 0 when Em reaces threshold -70mV to let Na in. reopen at -50mV in phase 3
• Slow Na+ (If), voltage and receptor gated, open in phase 4 pacemaker cells for funny current to let Na+ in


o Calcium
• Long L type, voltage gated, open in phase 2 of myocytes to let long lasting current in, open in phase 4 and 0 of pacemaker cells to let long lasting current in at -40mV
• Transient T type, voltage gated, open in phase 4 of pacemaker cells at -50mV to let Ca in


o Potassium
• Inward rectifier Ik1, voltage gated, maintains neg potential in phase 4, closes at positive potentials with depol, decay contributes to pacemaker currents. Maintains stability of resting membrane potential, K goes out
• Transient outward Ito, voltage gated, phase 1, 2 and 3 in myocytes, K goes out
• Delayed rectifier, IKr, volatage gated, phase 3 repol, K+ goes out, close at -65mV
• ATP sensitive (IkATP), receptor gated, inhibited by ATP, open when ATP decreases
• Acetylcholine activated (IkACh), receptor gated, Activated by acetylholine, Gi-protein coupled

35

explain threshold of ap's

o Electrical point at which action potential is self propagating
o Determined by sensitivity of ion channel responsible for depol (fast Na in myocytes, -70mv, Ltype Ca in pacemakers, -40mV) and the concentration of ion outside the cell
o SA node threshold reached by stead depol – automaticity rather than needing a sudden change in electrical potential as for fast Na channels

36

explain excitability

o Slope of phase 0, increased the further in phase 3 you get
o The steeper the upstroke the higher the condction velocity
o After the absolute refractor period, halfway through phase 3, at -50mV fast a channel recover from inactive state so can cause another ap if greater than normal stimulus in the relative refractory period
o Refractoriness is longer in pacemaker cells

37

explain irritability

o Irritability
o Ease of stimulating an arrhythmia at time between RMP and threshold when cell is hyperexcitable
o Weaker stimuli can get cell to threshold and cause an ap but the upstroke is less excitable (flatter) causing decreased conduction velocity