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CARDIO SPECIALTY EXAM MY OWN > Electrophysiology and arrythmias > Flashcards

Electrophysiology and arrythmias Flashcards

1
Q

what is the nernst equation ;

A

Em=-61.5logKi/Ko

Ki; K inside the cell
Ko; K outside the cell

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2
Q

When Na is pumped out of the cell, it accumolates along the membrane wall. Why?
And why does it just not re-enter the cell

A

The Na is +, but the inside of the cell is - due to all the potassium (remember K is + but it leaves a - charge due to the nernst equation). However, the sarcolemma is poorly positive to Na and diffusion of this back into the cell takes a long time. This is why Na does not contribute significantly to repolarisation

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3
Q

IS the Sacolemma more permeable to Na or K? and why is this important ?

A

Singificantly more to K. If 400,000 Na ions are pumped out, 4 diffuse back in. IF 400,000 K are pumped out 200 diffuse back in. This is why K is the main ion involved in repolarisation

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4
Q

What is the resting membrane potential?

A

voltage difference across the cell membrane.

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5
Q

What determines ion flow through an ion channel ?

A

Ions which move through passive channels will only do so when the channel is open, and the flow is governed by;

1) The potential (electrical driving force) across the membrane
2) The concentration gradient across the membrane for the respective ion (from high -> low)

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6
Q

What is the Net driving force?

A

I=N x I x p
It is given by;
1) The potential (electrical driving force) across the membrane
2) The concentration gradient across the membrane for the respective ion (from high -> low)

I= total current, N= number of open channels, i= current through each of the channels, p=probability of channel opening.

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7
Q

what is the Hodgkin-huxley hypothesis ?

A

The channels exist in 3 states; resting, active and inactive
- Resting state; activation gate is shut and the inactivation gate is open
- Inactive;
- Active state; activation gate is open and the inactivation gate is open and the current flows.

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8
Q

what is voltage gating?

A

each channel is protected by two-pore gates that determine the open and closed state. The ions can only pass when the pore is in the open position – this is otherwise known as voltage gating.

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9
Q

Why are Ca channels considered time dependent?

A

Because they will only open once the majority of Na channels are closed.

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10
Q

What is the role of the Na:K ATPase ?

A

1) Ensures a large resting negative potential (pumps + Na out of the cell, while K, due to the Nerst equation is K and rests on the inside of the cell) and guarantees a large internal K gradient

2) Ensures exitability; Exitability is given by a large influx of Na into the cell and these pumps guarantee that the cytoplasm is Na poor compared to the extracellular fluid. If Na were already in the cell the influx could not happen during depolarization

3) Generates an electrochemical gradient with the inside of the cell more negative than the outside

4) Produces a Na current that provides energy for the removal of free Ca and hydrogen ions (H+) (indirect function)

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11
Q

What is the role of the ATP dependent Ca pump and how important is this?

A

The sarcollemic Ca2+ transported transports free intracellular Ca2+ out of the cel. However, this process actually only removes a small fraction of the Ca that enters into the cell during depolarization. Almost all of the Ca2+ that enters the heart is remoced by the Na-Ca exchanger.

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11
Q

what are the two subunits of the Na:K ATPase?

A
  • alpha - spans the sarcolemma and is found on the extracellular side of the sarcolemma
  • ß- This is on the cytoplasmic side, and is where ATP binds to
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12
Q

What are the 4 major time dependent and voltage gated membrane channels?

A

1) Ina
2) Ica
3) Ik
4) If

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13
Q

What are the roles of the 4 major time dependent and voltage gated membrane channels?

A

1) INa; The ionic Na current Responsible for rapid depolarization in atrial and ventricular muscle and Purkinje fibers
2) ICa The ionic calcium current is responsible for depolarizing the SA and AV node and, thus, triggering the action potential in all cardiomyocytes
3) Ik The ionic repolarizing potassium current responsible for the repolarization of all cardiomyocytes
4) If the ionic pacemaker current is partly responsible for pacemaker activity in the SA and AV nodal cells and Purkinje fibres.

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14
Q

What are the SA and AV nodess main time and voltage gated channels ?

A

by ICa, Ik and If .

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15
Q

What are the atria and ventricle myofibres main time and voltage gated channels ?

A

INa, ICa and Ik

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16
Q

What are the main ion channels which control the purkinje cells ?

A

1) Ina
2) Ica
3) Ik
4) If

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17
Q

what are the components of membrane ion channels?

A

a channel protein, a selectivity filter and gating proteins

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18
Q

What is the role of Ina channels?

A

These carry a LARGE current across the membrane to produce rapid depolarization.

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19
Q

what are key features of INa

A
  • Large number (Up to 200 channels per square micron )
  • Voltage dependent gating
  • Ability to open quickly
  • Binding spot between the selectivity filter and the gates where certain dugs can bind to; eg Lidocaine
  • Have a resting, open and inactive state (H and M configuration)
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20
Q

Describe the M and H states of Ina;

A

Two gates with an m and h configuration;
1) Resting configuration; Closed in the “m” and “h” is open. In the resting configuration, the channel is closed but excitable and actually exists in h state.
2) Open state; The channel is open for a few hundredths of a microsecond when the ‘m’ gate opens. The wave of depolarisation moves the channel into the ‘open’ position once the threshold potential of ~70mV. This allows a rapid influx of Na into the cell down a concentration gradient
3) Inactivated state; As the ‘h’ gate is voltage dependent, the rapid influx of Na causes a massive potential change which causes the Na channel to change back into the ‘m’ state. This channel will remain inactivated until the cell has repolarisd to ~ -60 to -70mV. When this occurs, the “m” gate closes, and the “h” gate opens to return the cell to its resting state (closed but excitable).

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21
Q

Ica carry current into the cell or out?

A

In

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22
Q

What are the functions of Ica

A

1) To activate release of Ca from the sarcoplastic reticulum in atrial and ventricular muscle cells by the process know as Ca2+ -induced Ca2+ release (CICR)
2) To contribute to pacemaker activity of the SA node
3) To provide regenerative action potential in the SA and AV nodes
4) To prolong the refractory period by maintain small ICa during phase 2 of the action potential
5) To provide delay between atrial and ventricular contractions, with smaller current during phase 0 of the action potential in the AV node and thus a slower conduction and slower discharge of membrane capacitance of neighboring cells.
6) To contribute to phase 0 of the action potential (along with Ina) in atrial, ventricular and purkinje fibers, this increasing conduction velocity in these fibers

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23
Q

At what potentals do Ca channels close?

A

at very negative potentials

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24
Q

What are the two types of iCa?

A

L- type
T- type

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25
Q

what drugs block L type Ica?

A

Veramapil, diltiazem, and nifedipine

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26
Q

By blocking L-type Ca channels, what effect is seen on the action potential?

What about by increasing the current?

A

blocking these prolongs AV conduction, and shorten the action potential duration.

Increasing the Ca current through these receptors, prolongs the action potential by increasing the height and the plateau of the depolarisation wave.

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27
Q

How does sympathetic modulation affect Ca channels ?

A

Modulates the activity of L-type Ica

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28
Q

How does magnesium affect ICa?

A

Mg phosphorylates Ica allowing prolongation of the action potential by increasing the height of the plateau

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29
Q

what is the role of T-type channels?

A

These are the channels that allow for continuous rhythmic bursts that control the SA node of the heart

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30
Q

what are the main Ca channels which are found on the sarcoplasm?

A

Ryanodine (RyR); Dominant Ca release channel in heart muscle.
Inositol tryphosphate (IP3R);

31
Q

what is the Ca spark?

A

The Ryr channels and L-type are in close proximity. As a result, Ca that flows through the L-type triggers the RyR (calcium spark). This allows for a rapid and large Ca release from the sarcoplastic reticulum amplifying the signal. The massive calcium influx into the cytoplasm can then bind to Troponin C initiating contraction.

32
Q

Post contraction, how is the Ca removed from the cytoplasm?

A

Post contraction, most of the calcium is pumped back into the sarcoplastic reticulum with aid of the Ca2+ ATPase and some is extruded by the cell using the Na Ca exchanger.

33
Q

what are the 4 outcomes for the Ca that has detached from the contractile apparatus

A

1)It is pumped back into the sarcoplastic reticulum by an ATPase dependent pump
2)It is extruded by the cell by Na and Ca exchange
3)Pumped out of the cell by an ATPase dependent pump
4)It binds to intracellular calcium buffers.

34
Q

How does digoxin provide therapeutic (or toxic) effect?

A

Digitalis is a Na channel and reduces the effect of the NaCa exchanger causing the accumulation of Ca intracellularly resulting in prolongation of the plateu and causing + ionotropy.But it also causes eads by spiking up the plateu

35
Q

what are the roles of the NaCa exchanger?

A

Moves 3Na ions into the cell and extrudes 1Ca ion.

1) Contribute to inward depolarizing currents
2) Prolong the plateau phase of the action potential
3) Contribute to depolarisation during diastole

This transporter is the chief means of Ca transport out of the cell.

36
Q

Why is K complementary to Na?

A

K currents are complimentary to Na currents, ie Na depolarize, K repolarize.

37
Q

What direction do K rectifier channels pump potassium in?

A

The rectifying channels can transport potassium across the membrane both directions but they are generally more effective at doing it one direction compared to another.

thesre then called inward or outward rectifier currents

38
Q

How do Outward K rectifier channels affect refractory period ?

A

can both prolong or shorten the refractory period according to the heart rate. They may also be under the influence of physiological reactions.

39
Q

what are the 5 main K rectifiers ?

A

1) Delayed rectifier (Ik)
2) Inward K rectifier (Ik1)
3) Transient outward K current (Ito)
4) Acetylcholine- activated inward K rectifier (Ik(ACH))
5) ATP- activated K+current (Katp)

40
Q

Which rectifier has the largest effect on ventricular REPOLARISATION ?

A

DELAYED RECTIFIER (IK)

41
Q

what is the activity profile of the IK?

A

Activates long after phase 0
- this protects the heart from premature excitation during the supervulnearble period, yet short enough during tachycardia to allow for a repolarisation and a resting diastolic phase between beats

42
Q

What are the two components of IK ?

A

o Rapidly activated (Ikr)
o Slow activated (Iks)

43
Q

give examples of drugs that target rapidly activated and slow activated IK’s

A

IKr; D-Sotalol
IKs; amiodarone, quinidine, clofilium and dofetilide and tedisamil

44
Q

What is blockade of Iks dependent on ?
What augments Iks?

A

 Blockade of Iks prolongs action potential duration according to the density of channels, the heart rate, the neurohormonal status of the heart
 ß-stimulation may augment IKs and its effect on repolarisaiton
 An increase in HR may enhance the abikity of Iks to prolong a tion potential duration.

45
Q

Why are Ikr blockers rate dependent ?

A

Increased Blocking with Faster Heart Rates: Many IKr blockers exhibit reverse use-dependence, meaning they are more effective at slower heart rates. However, some IKr blockers may show rate-dependence in specific scenarios or formulations, causing more pronounced effects at faster heart rates.

Reverse Use-Dependence and Proarrhythmia: Reverse use-dependence, a characteristic of many IKr blockers (like dofetilide and sotalol), means that the QT prolongation effect is more substantial at slower heart rates. This can increase the risk of early afterdepolarizations (EADs) and torsades de pointes, a type of ventricular arrhythmia, especially if the heart rate is slow.

46
Q

Where are IK1 found?

A

Seen in the atrial, AV node, his Purkinje and ventricular cells.

47
Q

what is the role of IK1

A

This IK1 is critical to the maintenance of the resting membrane potential and maintains it near the K equilibrium potential.

An important feature is that it allows inward current to flow more readily than outward. Additionally the function of the channel is confined to a narrow voltage rage between the resting potential and -30mv. Therefore, this contributes to the terminal part of phase 3.

48
Q

What occurs if IK1 are blocked?

A

Blockage prolongs action potential duration slightly. Inhibition may induce membrane depolarization, and cause arrythmias.

49
Q

When does IKto activate and deactivate?

A

After depolarisation, Ito rapidly activates and inactivates.

50
Q

Where are IKto found?

A

Present sub-epicardial and not sub-endocardial, Ito contributed to the heterogeneity of repolarization.

51
Q

what does blockage of IKto cause?

A

Blockage decreases rate of repolarization during plateau and elevates the early plateus voltage. Pharmacological suppression will prolong the action potential duration .

52
Q

Where are IK/ach found and what are they influenced by?

A

Found in the SA and AV nodal cells, where stimulation of the parasympathetic nervous system results in the release of acetylcholine.
ACH release stimulates an OUTWARD K current (Ik(ach) ruing phase 3 and 4 of the action potential

53
Q

When do you see activation and inhibition of Katp channels

A

ATP- sensitive potassium channels (Katp) are inhibited by physiologic levels of intracellular ATP and are activated during ischemia or anoxia. Activation of these may explain why the action potential duration is shortened during ischaemia.

54
Q

what are the phases of the action potential ?

A

0) Phase 0; depolarisation
a. Rapid in the atrial, ventricular, his purkinje system
b. Slow in the SA and AV node
1) Phase 1: initial rapid repolarisation
2) Phase 2: plataeu
3) Phase 3: rapid repolariatation
4) Phase 4: resting membrane potential

55
Q

what are fast and slow rate

A
  • Fast-response; these are cells capable of a high rate of depolarisation and due to a high concentration of Na channels. These have the property of conducting the depolarisation wave from point A to point B quickly and are not the main contraction cells. These are the Purkinje fibres for example
  • Slow-reponse; these cells have few Na channels and depend on ICa for depolarisation. As a result they have slow confuction and automaticity. These are cells of the AV and SA node.
    o These can be found anywhere in the heart and are often upregulated with diseases such as ischaemia, injury and electrolyte imbalance
56
Q

what is the difference between the effective and relative refractory period?

A
  • Effective refractory period (ERP); cell will not respond
  • Relative refractory period (RRP); cell does not respond appropriately
57
Q

what determines the effective and relative refractory period?

A

Refractory period is determined by the cells transmembrane potential.
- During ERP; from phase 0 to -60mV in phase 3), no stimulus can evoke a response
- During RRP; from -60mV in phase 3 to -70mV, only a strong stimulus can evoke a propagated response.

58
Q

what is overdrive supression?

A

This is the inhibitory effect of a faster pacemaker on a slower one.

59
Q

what is the mechanism behind overdrive supression?

A

The mechanism of overdrive suppression is hyoperpolarisation. Rapid pacing causes an increase in extracellular K and increased influx of Na into the cells. The increase in intracellular Na is, in turn, a stimulus for the Na-K pump, which empties the cell of Na and eventually renders it more negative than normal (hyperpolarization), depressing its activity – this means it takes cells longer to reach the threshold through phase 4

60
Q

what are the modulators for ß receptors? examples?

A

ß-andrenergic receptors are modulated by cAMP-dependent protein kinease, such as L-type Ca current, the If and the Ik current

61
Q

what receptors are activated with vagal stimualtion?

A

M2

62
Q

Clinically, how does vagal upregulation result in an antiarrythmic effect?

A

terminates AV reentry mechanisms (paroxysmal supraventricular tachycardia) because it slows AV conduction

63
Q

what are the 3 mechanisms that result in inhibition of automaticity in the SA node?

A

1) Activation of acetylcolinne-activated inward K rectifying currents - Ik(ACH)
2) Inhibition of the inward positive If current
3) Inhibition of the inward Ca current.

These hyperpolarise the membrane. As a result it takes longer to reach threshold potential, this sloweing SA and Av node potentials.

64
Q

what are use dependent antiarrythmics?

A

These drugs are more effective at faster rates. These antiarrythmics bind at specific locations on the ion channels, and access to the channels is determined by how many times per minute they are open. Hence use dependent drugs such as lidocaine are more effective at faster rates since. Other variable influences include voltage, ph, molecular weight and so on.

65
Q

what are voltage dependent antiarrythmics?

A

When the resting voltage of cardiac cells is reduced by depolarising currents, such as ischaemia, certain channels become more accessible; e.g. Na channels become more accessible to blocking action of lidocaine

66
Q

what is the mechanism of rate dependent drugs?

A

Mediated by the action of the drug on K channels in a rate-dependent fashion. The degree of rate dependency varies amongst different drugs and the prolongation of refractoriness is more marked at slow heart rats rather than fast ones.

67
Q

The magnitude of the potential recorded on the ECG at any one site is dependent on;

A

1) directly proportional to the average rate of change of intracellular potential as determined by the action potential shape
2) directly proportional to the size of the wavefront
3) inversely proportional to the square of the distance from the activation front to the recording site
4) directly proportional to the cosine of the angle between the direction of activation spread and a line drawn from the site of activation to the recording site

68
Q

Lead I, II and III of an ECG measure the electrical potential between which limbs, respectively?

A
  • Lead I register the potential difference between the left arm (positive electrode) and right arm (negative)
  • lead II displays the potential difference between the left leg (positive electrode) and right arm (negative electrode)
  • lead III records the potential difference between the left leg (positive electrode) and left arm (negative electrode).
68
Q

If a lead is placed on the right leg, this measures the potential between which limbs

A

None. The electrode on the right leg serves as an electronic reference that reduces noise and is not included in these lead configurations.

69
Q

What is Einthoven’s triangle

A

The vectors form a triangle, known as the Einthoven triangle, in which the potential in lead II equals the sum of potentials sensed in leads I and III, that is:

I=III=II.

70
Q

What is the wilson central terminal ?

A

An exploring electrode is placed at each of six specific precordial sites and connected to the positive input of the recording system.
The potential in each V lead can be expressed as:
Vi=Ei−WCTVi=Ei-WCT
where
WCT=(LA=LL=RA)/3
and V i is the potential recorded in precordial lead i, E i is the voltage sensed at the exploring electrode for lead V i , and WCT is the potential in the composite Wilson central terminal, and LA, LL, and RA are the potentials in the left arm, left leg, and right arm, respectively.

71
Q

what are the 3 augmented leads

A

aVF, aVR, and aVL

72
Q

The exploring electrode that forms the positive input for each aurmented lead are;

A
  • aVR it is the right arm electrode
  • aVL it is the left arm electrode
  • aVF it is the left leg electrode
73
Q

How can you calculate aVR, aVL, and aVF if you know the the precordial leads?

A

aVR=RA−(LA+LL)/2
aVL=LA−(RA+LL)/2
aVF=LL−(RA+LA)/2

74
Q

The amplitude of a wavefront in lead VL depends on what and how this is calculated. How is this affected when the activation direction is parallel or perpendicular to the lead?

A

The amplitude of the recorded waveform in a lead equals the length the projection of the heart vector onto the lead vector.

VL=Hcos𝜃

V L is the recorded voltage in lead L, H is the strength (length) of the heart vector, and Ɵ is the angle between the heart vector H and the lead vector.
Thus, when the direction of activation (i.e., the direction of the heart vector) and that of the lead vector are parallel (Ɵ = 0 degrees and cosine Ɵ = 1), the recorded voltage is maximal; when the activation is perpendicular to the lead axis, the recorded potential equals zero (Ɵ = 90 degrees and cosine Ɵ = 0).

75
Q
A

CARDIO SPECIALTY EXAM MY OWN (14 decks)

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