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CVS Physiology > Electrical Activity of the Heart > Flashcards

Electrical Activity of the Heart Flashcards

1
Q

How does skeletal muscle contract?

A

Sarcoplasmic reticulum big calcium store and the calcium causes coupling
Calcium binds to triponomyosin which is bound to troponin. When calcium binds it breaks that bond
Calcium release causes skeletal muscle to contract
This is caused by an AP due to a motor neurone releasing ACh for the nicotinic receptors

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2
Q

How does cardiac muscle contract?

A

Cells connected by gap junctions
Desmosomes do the physical joining together
If one cell depolarises then fires an AP then it is more likely that the next cell will also
Allows calcium to come in from the outside
Cardiac muscle produces a sub maximal contraction so can regulate how much can come from the outside which regulates the strength of contraction

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3
Q

What are a gap junction and a desmosome together known as?

A

Intercalated disc

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4
Q

Site of AP cardiac muscle (CM) vs skeletal muscle (SM)

A

CM - 200 miliseconds (longer)

SM - 2 miliseconds

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5
Q

Calcium CM vs SM

A

CM - calcium comes from outside

SM - calcium comes from inside

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6
Q

Types of contraction CM vs SM

A

CM - Sub maximal contraction

SM - Maximum contraction

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7
Q

Refractory period CM vs SM

A

CM - Very long due to stimulation on different parts of the graph
SM - very short due to twitch contractions summing to make a sustained contraction

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8
Q

What does the very long refractory period in cardiac muscle result in?

A

The muscle has to relax before it can contract again

This stops it doing a tetanus

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9
Q

Describe the cardiac muscle functional syncytium

A

Electrically connected by GAP JUNCTIONS
Physically connected by desmosomes
Forming intercalated discs

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10
Q

Action potential length of cardiac muscle

A

Long

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11
Q

What makes sure that cardiac muscle cannot exhibit tetanic contraction?

A

Long refractory period

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12
Q

What kind of muscle has an unstable resting potential? What do these act as?

A

Cardiac muscle

Act as pacemakers

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13
Q

Features of non pacemaker cells

A

Sit at a certain voltage until told to depolarise by the gap junctions

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14
Q

Features of pacemaker cells

A

Will spontaneously depolarise to threshold and fire an AP

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15
Q

Permeability of non pacemaker cells at resting membrane potential

A

Sodium and calcium low

High potassium

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16
Q

Non pacemaker action potential

A
  1. Resting membrane potential
    - High resting Pk+
  2. Initial depolarisation
    - increase in PNa
    - voltage gated sodium channels opening when there is depolarisation from neighbouring cells leads to an increase in sodium permeability and massive depolarisation
    - this DOES NOT repolarise - it stays in plateu phase
  3. Plateau
    - increase in PCa2+ (L-type) and decrease in PK+
    - stays in plateau phase because of voltage gated calcium channels slowly letting calcium flow in, therefore the plateau is due to calcium constantly flowing in and also a decrease in permeability to potassium by blocking the channels
  4. Repolarising
    - reverse
    - decrease in PCa2+ and increase PK+ so sodium and calcium channels shut and leaky potassium opens
17
Q

What causes the pacemaker AP?

A

Just calcium channels

18
Q

Pacemaker action potential

A
  1. AP
    - increase in PCa2+ (L-type)
  2. Pacemaker potential (pre potential)
    - gradual decrease in PK+ by closing the leaky potassium channels
    - early increase in PNa+ (=PF) - if a bit of sodium is let in at the early bit of pacemaker
    - late increase in PCa2+ (T-type) as they are tiny calcium channels so only a wee bit of Ca is let in but pushes the cell the last wee bit towards threshold
19
Q

Modulators of electrical activity

A 
Sympathetic and parasympathetic systems 
Drugs 
- Ca2+ channel blockers 
- cardiac glycosides 
Temperature
Hyperkalaemia 
Hypokalamia 
Hypercalcaemia
Hypocalcaemia
20
Q

Effects of CCBs on contraction

A

Decreases

21
Q

Effects of cardiac glycosides on contraction

A

Increases

22
Q

Effects of temp on contraction

A

Increases approx. 10 beats / min / degree centigrade

23
Q

Effects of hyperkalaemia

A

Fibrillation and heart block

High K outside the cell decreases the concentration gradient for K and so depolarises the cell

24
Q

Definition of fibrillation

A

APs are spontaneously fired in an uncoordinated fashion

25
Q

Effects of hypokalaemia

A

Fibrillation and heart block (anomalous)

Lose K and then cells start to hyperpolarise and then loads of channels open and the cells depolarises

26
Q

Effects of hypercalcaemia

A

Increased HR and force of contraction

27
Q

Effects of hypocalcaemia

A

Decreased HR and force of contraction

28
Q

Features of the sinoatrial node

A

Pacemaker
Approx 0.5m/sec
Where the fastest pacemakers are

29
Q

Where is the sinoatrial node found?

A

Right atrium

30
Q

Features of the annulus fibrosis

A

Non conducting
AP gets stuck here and does not pass into the ventricle
Only way AP can pass through is the AV node

31
Q

Where is the annulus fibrosis found?

A

Between atrium and ventricles

32
Q

Features of atrioventricular node

A

Delay box
Approx. 0.05m/sec
Atrium has time to get the blood to the ventricle before the ventricle starts pumping, because the node slows it down

33
Q

What is the nerve fibres at the ventricles which makes them contract?

A

Bundle of His

34
Q

What does the Bundle of His break down into?

A

Purkinje fibres

35
Q

Features of purkinje fibres

A

Rapid conduction system

Approx. 5m/sec

36
Q

Does an ECG tell you about how the heart pumps?

A

No

37
Q

What kind of disorders does an ECG tell you about?

A

Disorders of rhythm

Disorders of conduction

38
Q

Examples of disorders of conduction

A

Degree blocks

39
Q

How does a defibrillator work?

A

Depolarises all of the cells to their refractory cells and so this stops the heart, so they are ready to receive action potentials again

CVS Physiology (12 decks)

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