Electrical Activity of the Heart Flashcards

1
Q

How are cardiac muscle cells physically linked?

What direction is this in?

A

Desmosomes

Horizontal

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2
Q

What is the function of gap junctions in intercalated discs?
What direction to they go in?

A

Bridge for proteins and electrical currents to travel between cells.
Vertical

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3
Q

What neurotransmitter causes APs to be fired in cardiac muscle cells?
What receptor type does it act upon?

A

Noradrenaline (and the hormone adrenaline)

Beta 1 receptors

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4
Q

Describe the process of cardiac muscle contraction-excitation coupling

A

NA and adrenaline act on Beta 1 receptors leading to cell depolarisation along the sarcolemma.
Calcium ions enter the cell via L type calcium channels.
This stimulates the release of calcium from the sarcolemma.
Ca2+ binds to troponin, pushing tropomyosin out the way.
This enables the power stroke to be fired and the myosin filament to slide along the actin filament.
Making the muscle contract

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5
Q

List the differences between cardiac and skeletal muscle

A

Cardiac vs skeletal =
NT: NA vs AC
Contraction-excitation coupling: no tetanus vs tetanus
Entry flow from Ca2+: can regulate contraction vs ca’t regulate contraction
Pacemaker cells: yes vs no

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6
Q

Explain the difference between cardiac and skeletal muscle in terms of contraction-excitation coupling

A

Refractory period in Cardiac muscle lasts 250msec ensuring that that summation is not allowed - the muscle must relax before another AP is fired and the next coupling occurs.
Refractory period in skeletal muscle is only 2msec which allowed more APs to quickly be fired and summated contraction or tetanus.

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7
Q

In cardiac muscle, how is contraction strength regulated by calcium ions?

A

Entry flow of Ca2+ from outside the cell regulates contraction strength by not fully saturating the troponin.

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8
Q

What is the hallmark feature of pacemaker cells?

A

Unstable RMP (resting membrane potential)

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9
Q

Describe how RMP is created

A

Normally, RMP is created by leaky potassium ion channels.

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10
Q

Describe how a cell becomes depolarised in basic terms

A

Normally, RMP is created by leaky potassium ion channels.

The cell is depolarised by the opening of calcium and sodium ion channels leading to the depolarisation of the cells.

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11
Q

Describe the firing of an AP in non pacemaker cells

A

Initial depolarisation to threshold occurs by increased PNa+ into the cell
Once the AP has been fired, there is a plateau, triggered by increased PCa2+ ions (L-type) and decreased PK+.
Repolarisation is triggered by increased PK+ ions and reduced PCa2+.

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12
Q

Describe the firing of an AP in pacemaker cells and how this explains the autorythmicity of the heart

A

The pacemaker potential is a gradual prepotential triggered by
- gradual reducing PK+
- early increase in PNa+ (PF) - these channels are opened by the repolarisation of the previous AP, explaining the autorythmicity of the heart
- late increase PCa2+ (T-type)
The AP is caused by increased PCa2+
Repolarisation is caused by reduced PCa2+ and increased PK+

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13
Q

List the modulators of electrical activity of the heart

A
Sympathetic and parasympathetic systems
Drugs
Temperature
Hyper and hypokalaemia
Hyper and hypocalcaemia
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14
Q

Describe the effect of calcium channel blockers on heart contractility

A

Reduce the amount of Ca2+ ions into cells thus reducing contractility

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15
Q

Describe the effect of cardiac glycosides on heart contractility

A

Increase amount of Ca2+ ions into cells so increase contractile force

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16
Q

Describe the effect of temperature on contractility

A

Increased by 10bpm per increase in 1 degree celcius

17
Q

Describe the effect of hyperkalcaemia on contractility

A

Reduced concentration gradient between cell and plasma leads to cells being unable to repolarise leading to heart block and fibrillation

18
Q

Describe the effect of hypokalcaemia on contractility

A

Heart block and fibrillation

19
Q

Describe the effect of hypercalcaemia on contractility

A

Increased HR and contractility

20
Q

Describe the effect of hypocalcaemia on contractility

A

Decreased HR and contractility

21
Q

What is the function of the sinoatrial node?

A

Pacemaker cells

22
Q

What is the conduction velocity of the sinoatrial node?

A

0.5m/sec

23
Q

What is the annulus fibrosis?

A

Non-conducting rings around a heart chambers

24
Q

What is the function of the AV node?

A

Delay box

25
Q

What is the conduction velocity of the AV node?

A

0.05m/sec

26
Q

What is the function of pujinke fibres?

A

Rapid conduction of depolarisation upwards from apex

27
Q

What is the conduction velocity of pujinke fibres?

A

5m/sec

28
Q

Describe the step by step process which occurs in the special conduction system

A
  1. Depolarisation at sinoatrial node
  2. Depolarisation continues through specialised conducting system of non-contractile autorythmic fibres causing atrial contraction in contractile cells with depolarisation spreading out through gap junctions
  3. Continues through branched intermodal pathway
  4. Atrial contraction ends and depolarisation goes through AV node
  5. Goes through bundle of His
  6. Goes through left and right bundle branches
  7. Goes up through Purjinke fibres causing ventricular contraction by contractile cells with depolarisation spreading out through gap junctions
29
Q

Describe how extracellular APs are seen peripherally in an ECG

A

Each AP in a myocyte produces a small extracellular (cf transmembrane) electrical potential. When the many myocytes are depolarising and repolarising at the same time the summate to create large extracellular extracellular waves which can be seen on the ECG in the periphery

30
Q

Describe the what the basic waves in an ECG correspond to.

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation