EC Coupling Flashcards

1
Q

What would happen if cells didn’t contract in a synchronised fashion?

A

Parts of the ventricle would contract at different times meaning blood wasn’t properly ejected-this is called VENTRICULAR FIBRILLATION and would be fatal

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2
Q

What are the intra and extra cellular concentrations of ions in cardiac myocytes?

A
  • Sodium and calcium are high extracellularly and low intracellularly - think of it as always moving in, and the threshold closes the channels meaning movement stops
  • Potassium is low extracellularly and high intracellularly,-think of it as always moving out and the threshold closes the channel meaning movement stops
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3
Q

What happens in hyperpolarisation?

A

There is excessive Potassium conductance and the potassium gradient moves close to its equilibrium (-96mV) so the cells becomes hyperpolarised

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4
Q

What is an absolute refractory period?

A

Period of time in which it is impossible to evoke another action potential

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5
Q

What is a relative refractory period?

A

Period in which an action potential can be produced so long as the stimulus is of sufficient strength (must be overtly stronger than usual)

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6
Q

What does automaticity mean?

A

It is a pacemaker cells ability to depolarise spontaneously without stimulus-it is able to do so because of its unstable resting potential as a result of funny sodium channels (slow)

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7
Q

How are the refractory periods of skeletal and cardiac muscle different? why is this important?

A

The refractory period of cardiac muscle is MUCH longer than skeletal muscle
This is important because it prevents cardiac muscle from undergoing summation and tetanus as a result of repetitive stimulation-if this was to occur cardiac output would disappear and it would be fatal

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8
Q

How do refractory periods differ throughout the heart?

A

The epicardial tissue becomes depolarised LATER than the endocardial tissue, so the epicardial tissue has a shorter action potential to stop any re-entry mechanisms affecting the endocardial tissue

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9
Q

Explain the differing action potential lengths between epicardial and endocardial tissues:

A

The epicardial tissues are depolarised later than the endocardial tissues because the impulses have to travel further to reach them.
If the epicardial action potential was the same length as the endocardial, the endocardial would be finished but the epicardial only just repolarising, which would RE-ACTIVATE the endocardial tissue producing a RE-ENTRY mechanism and thus an arrhythmia

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10
Q

What causes the differing lengths of action potentials and refractory periods in different cardiac tissues?

A

Each tissue expresses different amounts of Sodium, Calcium and Potassium ion channels meaning the action potentials occur at different rates because it takes a longer or shorter amount of time to reach the threshold

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11
Q

How do you measure voltage across cell membranes?

A

Patch clamping

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12
Q

Which ion channel is most important in explaining differing lengths of action potential/refractory period?

A

The Potassium Channel.
There are rapid and slow potassium channels. Tissues with short action potentials/refractory periods such as the epicardial tissue have a higher proportion of rapid channels, whereas tissues such as the endocardium with longer action potential/refractory period have a higher proportion of slow potassium channels.
These channels control how quick or slow the cell is able to repolarise and therefore determines the refractory length of the cell

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13
Q

What is an arrhythmia?

A

a cardiac contraction of abnormal origin, rate, rhythm, conduction velocity, and sequence of heart activation

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14
Q

What are the main causes of arrhythmias?

A
  1. Pathological heart diseases e.g channelopathies, HF and congenital structural defects
  2. other system disease
  3. electrolyte disturbance and acid/base imbalance
  4. physical/chemical factors and toxicosis
  5. unknown
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15
Q

What are the two mechanisms of arrhythmia?

A
  1. Abnormal Formation
    - Sinus pulse
    - Ectopic pulse
  2. Abnormal Conduction
    - Re-entry
    - Conduction block
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16
Q

What are the classifications of arrhythmia?

A
  1. Abnormal formation
    - Sinus Arrhythmia
    - Atrial Arrhythmia
    - AV junctional Arrhythmia
    - Ventricular Arrhythmia
  2. Abnormal Conduction
    - Sinus Atrial Block
    - Intra Atrial Block
    - Atrio-ventricular Block
    - Intra-ventricular Block
17
Q

Who developed the ECG?

A

William Einthoven

18
Q

How does an ECG work?

A

It detects waves of depolarisation using skin electrodes.
If the impulse travels towards the positive electrode it is a positive deflection
If the impulse travels away from a positive electrode it is a negative deflection

19
Q

What does each part of the ECG mean?

A

P wave= Atrial Depolarisation
QRS= Ventricular Depolarisation
-Q=Depolarisation of interventricular septum
-R=Depolarisation of main mass of ventricles
-S=Final depolarisation of base of the heart
T wave= Ventricular Repolarisation

20
Q

An example of a Sodium Channelopathy:

A

Long QT Syndrome:

  • Mutation to Alpha Subunit of Na channel
  • Mutation prevents inactivation of the channel so there is a maintained sodium current
  • This causes delayed repolarisation of the cell
  • Delayed repolarisation increases the risk of irregular rhythms called Torsades De Pointes which causes VF

Brugada Syndrome:

  • Mutation to alpha subunit prevents full activation of the Na channel (opposite to long QT)
  • Means that the Na current amplitude is reduced and the upstroke of depolarisation is slowed
  • There are regional differences in this slowing and so an opportunity for re-entrant mechanisms arises
  • VF can occur
21
Q

Example of Calcium Channelopathies:

A

-Affects the L-type VGCCs
Brugada Syndrome
-Reduced calcium current means slowed impulse conduction and thus re-entry
Timothy Syndrome
-mutant channels are slow to inactivate so repolarisation is delayed
-Calcium becomes overloaded and re-entry mechanisms can occur

22
Q

Examples of Potassium Channelopathies:

A

-Affects the hERG channel
Short QT Syndrome
-Mutant channels gain function so the cell repolarises too quickly
Long QT Syndrome
-Mutant channel loses function so takes too long to repolarise