Cardiac Electrophys Flashcards

1
Q

Membrane potential

A

difference in movement of ions creating a charge separation across cell membrane

  • measured on inside of cell
  • electrical force
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2
Q

forces that drive ion movement

A

electrical force- membrane potential

and chemical force- due to difference in concentration of intra and extracellular fluid

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3
Q

nernst potential

A

ion’s individual chemical force depending on

  • ratio of intra and extra concentrations
  • valence of ion
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4
Q

magnitude of ion’s current depends on

A

forces during ion movement- nernst potential and membrane potential

and

conductance- how easily ion can move across membrane

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5
Q

conductance

A

ability of ion to cross cell membrane and related to:

  • # of open ion channels
  • leak channels
  • ion concentration
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6
Q

Current

A

Iion= gion x (V - Eion)

g is conduction
I is current
V-E is electrochemical potential driving ion movement
V=E, no force driving movement and net current is 0

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7
Q

Larger V-Eion becomes

A

increases the force driving movement of ion

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8
Q

Fractional conductace

A

fgk= gk/ (gk+gNa)

Value of 0 if cell is impermeable, 1 is cell is only permeable to that ion

fgNa + fgK=1

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9
Q

Maximal limits for membrane potential set by

A

Ek and Ena

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10
Q

sequence of excitation in heart

A

SA node–> atrial muscle–> AV node–> common bundle–> bundle branches–> purkinje fibers–> ventricular muscle

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11
Q

Calcium dependent action potentials in

A

SA node and AV node

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12
Q

Intrinsic pacemaker

A

SA node

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13
Q

Sodium dependent action potential

A

atrial myocytes, bundle of his, purkinje fibers, ventricular myocytes

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14
Q

magnitude of depolarizing current during upstroke of AP will determine

A
  • threshold potential
  • amplitude of AP
  • rate of rise of AP
  • conduction velocity (propagation of AP down tissue)
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15
Q

ECG

A
P wave- atrial depol (sodium current) 
PR interval
QRS complex- ventricular depol
ST segment- phase 2 of ventricular AP 
T wave- vent repol 
QT interval
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16
Q

SA and AV node AP phases

A

Phase 4- funny sodium current is > Ik– depolarzing
Phase 0- upstroke of AP due to Ical
Phase 3- repolarizing phase where Ik is > depolarizing currents (delayed rectifier potassium current)

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17
Q

Maximum diastolic potential

A

most neg potential in SA node- normally -50 mV

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18
Q

Atrial and ventricular AP

A

Phase 4- stable resting potential (inward rectifier K channels)
Phase 0- upstroke due to Ina
Phase 1- transient repol due to K current
Phase 2- plateau due to balance between Ical and Ik (delayed rectifier channels)
Phase 3- repol due to Ik (delayed rectifier)

19
Q

What phases determine duration of ventricular AP

A

phase 2 and phase 3

20
Q

Effect of NE on SA and AV node

A

Released by SYM
Increase If (funny sodium channel)
Increase Ical
Increase heart rate primarily by increasing If in SA node - MDP less neg and phase 4 more steep
Increased SYM will increase IcaL and increase conduction velocity in AV node (dec PR interval)

21
Q

Effect of ACh on SA and AV node

A

Released by PARA
Dec If
Dec IcaL

22
Q

Effect of SYM on atrial and ventricular myocytes

A
  • does not change Ina- no change in amp or width of QRS complex and P wave
  • Inc IcaL and Inc Ik
23
Q

Duration of vent AP determined by

A

Phase 2 and phase 3-

Ik inc- AP duration decreased as the rate of repol is increased- spiked T wave

24
Q

Inc SYM firing will

A

increase inotropic state by increasing IcaL- make phase 2 more positive

25
Q

common mediator of SYM and PARA that influences major cardiac ionic currents

A

adenylate cycase

  • SYM acts via beta 1 to activate adenylate cyclase- enhances L type calcium, delayed rectifier potassium, and funny sodium currents
  • PARA via vagus (ACh) acts via muscarinic receptor to inhibit adenylate cyclase and inhibits activation of above currents
26
Q

Normal extracellular K concentration

A

3.5-5 mEq/L

27
Q

Hypo and hyperkalemia cause

A

depolarization of resting membrane potential in cardiac muscle

  • less negative than normal
  • opp effects on K currents
28
Q

Voltage gated Na channel

A
activation gate (rapid)
inactivation gate (slow)
-normal resting potential activation gate is closed and inactivation gate is opened 
-depolarization decreases # of resting Na channels in atria and ventricle--> decrease Ina during upstroke of AP
29
Q

When Ina is decreased

A
  • threshold potential is less negative (dec excitability)
  • rate of rise of AP will be decreased
  • amp of AP decerased (diminished height of P and QRS wave)
  • dec conduction velocity (wider P and QRS)
30
Q

Hypokalemia

A

-decreased gk–> decreased Ik–> longer AP duration (because phase 3 has gradual repol)- T wave is flat

decreased gk will increase fgNa- more neg Ek than normal

U wave may occur- delayed repolarizing wave

31
Q

Hyperkalemia

A

inc gk–> inc Ik–> shorter AP duration (spiked T wave)

inc gk– less negative Ek than normal (more positive)
-less negative resting potential- fewer resting Na channels

32
Q

Potassium effects on SA node- hypokalemia

A

MDP less negative
Phase 4 more steep
Tachycardia

33
Q

Potassium effects on SA node- hyperkalemia

A

MDP more negative
Phase 4 less steep
Dec rate of firing of SA node (baroreflex may inc SYM firing)

34
Q

Tx of hypokalemia

A

IV infusion of potassium

35
Q

Tx of hyperkalemia

A
  • inc plasma calcium to recover resting Na channels by shifting inactivation curve towards more positive potentials
  • Sodium bicarb indirectly enhances Na K pump by inc Na influx via Na H exchanger
  • Insulin stimulates Na-K pump, moving K into cell
  • Lasix enhances K excretion by kidney
36
Q

Absolute refractory period

A

During phase 2 and early phase 3- the time when Na channels are in inactive state

37
Q

Relative refractory period

A

Later in phase 3 when membrane potential mecomes negative enough to allow convertion of inactive Na channels back to resting state

38
Q

Functional refractory period

A

ARP + RRP

Decreases when duration of AP decreases- SYM activity

39
Q

Reentrant loops

A

conduction velocity decreased (dec in voltage gated sodium current), duration of AP is decreased (inc potassium or dec calcium current), or both (high risk), inc size of tissue due to hypertrophy or dilatation (inc loop length, can’t depolarize simultaneously)

Length of loop occupied by AP= CV x Duration

Distance = rate x time

40
Q

Conduction velocity reduced in conditions where

A

Ina is decreased
Ik increased
IcaL decreased

41
Q

Early after depolarizations

A

If K+ current is suppressed, EAD can occur in late phase 2 or early phase 3 due to Ca++ window

  • decreased rate of repol caused by hypokalemia or cocaine
  • calcium window current due to opening of inactivation gates before activation gates have closed
42
Q

Delayed after depolarizations

A

Can occur during phase 4

  • high HR causes accumulation of Ca within myocytes (not enough time to pump ca out of cell)
  • inc cystolic Ca levels activate- Na/Ca exchanger which causes net depolarizing current, or non specific cation channel which causes depolarizing current
43
Q

Vfib

A

disorganized, chaotic ventricular rhythm due to multiple reentrant loops causing depol

  • no effective cardiac contraction
  • markedly reduced cardiac output
  • requires defibrillation which will cause entire mass of myocardial cells to depolarize at same time and will be followed by spontaneous resumption of supraventricular rhythm
44
Q

Afib

A

Multiple reentrant loops in atria (no P waves)
CO slightly reduced from normal
Results in stasis of blood in atria- inc risk of coagulation