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Cardiovascular System > Electrical activity of the heart > Flashcards

Electrical activity of the heart Flashcards

1
Q

Why is electrical property of the heart important?

A

It stimulates the physical activity/contraction of the heart

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2
Q

What is the sarcoplasmic reticulum?

A

A big calcium store

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3
Q

What are cardiac muscle cells electrically joined by?

A

Gap junctions

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4
Q

What are cardiac muscles physically connected by?

A

Desmosomes

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5
Q

What does the electrical connecton and physicall connection form?

A

Intercalated discs.

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6
Q

What is the resting membrane potential of the cardiac cll due to?

A

The high resting membrane permeability to leaky Potassium channels.
Potassium continually leaks out of the cell at rest until it reachs -90mV (rmp)

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7
Q

Explain the non pacemaker action potential.

A
  1. RESTING MEMBRANE POTENTIAL
    - high resting permeability to Potassium which conitnually leaks out until -90mv, resting membrane potential.
  2. RAPID DEPOLARISATION
    - caused by voltage gated sodium channels. Na flows into cells and depolarises the cell and channel quickly closes.
  3. PLATEAU
    - Increase in Voltage gated Ca channels (L type)
    - Open slower but stay open for longer.
    - Decrease in permeability to Potassium.
  4. -REPOLARISATION
    - Decrease in permeability to Ca channels
    - Increase in permeability to K channels
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8
Q

Explain the pacemaker action potential.

A
  1. ACTION POTENTIAL
    - Increase in permeability to voltage gated Ca channels (L type)
  2. PACEMAKER/PRE-POTENTIAL
    - Gradual decrease in permeability to K
    - Early increase in permeability to Na
    - Late increase n permeability to Ca (T type)
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9
Q

Explain the pacemaker action potential.

A
  1. ACTION POTENTIAL
    - Increase in permeability to voltage gated Ca channels (L type)
  2. PACEMAKER/PRE-POTENTIAL
    - Gradual decrease in Potassium
    - Early increase in permeability to Sodium
    - Late increase in permeability to Calcium (T type)
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10
Q

What does pacemaker explain?

A
  1. Autorhythmicity.
    - Heart has its OWN rhythm.
  2. Basis for unders tanding the Modulation the activity of the heart
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11
Q

What does the ECG tell you?

A

Disorders of conduction or disorders f rhythym

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12
Q

What part of the heart does the ECG usually tell you about?

A

An issue with the Atrioventricular node

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13
Q

What are the disorders of conduction?

A
  • 1st degree heart block
  • 2nd Degree heart block
  • 3rd degree heart block
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14
Q

What is 1st degree heart block? How does it show on an ECG?

A
  • Atrioventricular node is taking a long time for depolarisation from atria -> VENTRICLES.
  • Long interval between P and QRS
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15
Q

What is 2nd degree heart block?

How does it show on an ECG?

A
  • Sometimes the action potential does not get through. Only some atrial deplarisation gets through to the ventricles.
  • Longer intervals between P and QRS and then QRS completely disappears
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16
Q

What is 3rd degree heart block?

How does it show on an ECG?

A
  • No transmission between Atria and ventricles.
  • NO correct sequence of p + qrs
  • Total heart block
17
Q

What does P, QRS, T show on an ECG?

A

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

18
Q

How do we make the whole of the heart repolarise and contract at the right place and time?

A

Via the special conducting system.

  1. Sino atrial node (pacemkaer)
  2. Atriventricular Node (delay box- conducts really slowly)
  3. Bundle of hIS + pURKINJE fibres
19
Q

Why does the atrioventircular node conduct slowly?

A
  • Delay box to allow the whole of the atria to contract and relax before the ventricles do their job.
20
Q

Describe what the Bundle of His + Purkinje fibres do.

A

The cardaic muscle conducts VERY quickly- rapid conduction system.
- Depolarisation is spread throghout the whole heart which contrats at the same time.

21
Q

What are modulators of electrical activity?

A
  • Sympathetic and parasympathetic system
  • Drugs (Ca channel blockers which decrease the amount of calcium coming in, less bind to troponin, decreasing the amount of cross bridges being formed and ddecreasing the strength of contraction) (Cardiac glycosides which increase the amount of calcium being released, more cross bridges, the bigger the strength of contraction)
  • Temperature
  • Changes in ion concentration
22
Q

Describe how ion concentraton changes affect the eleectrical activty of the heart.

A
  • Hyperkalemia (high plasma K).
    Depolarises cells, reduces potassium concentration gradient. Fibrillation and heart block
  • Hypocalcaemia
  • Decreased crossbridges therefore strength of contraction and heart rate
  • Hypercalcaemia
  • Increased cross bridges and therefore strength of contraction, increasing heart rate
23
Q

Explain the basis of excitation- contraction coupling

A
  1. Action potential enters the contractile cell and moves across the sarcolemma and into the t tubules.
  2. T tubules opens voltage gated L Type Ca channels in the cell membrane.
  3. Ca enters the cell and opens ryanodine receptor Ca release channels in the sarcoplasmic reticulum.
  4. When the ryanodine receptor Ca channels open, stored Ca flows out of the sarcoplasmic reticulum and into the cytosol.
  5. Ca-> cytosol. This creates a Ca spark. mULTIPLE SPARKS FROM DIFFERENT rYr CHANNELS SUMMATE TO CREATE A cA SINGAL.
  6. Ca ions bind to Troponin and initate the cycle of crossbridge formation and movement and contraction takes place.
  7. CaTroponin complex moves Tropomyosin away from actin’s myosin binding site and myosin binds to actin cross bridge, releasing ADP.
24
Q

What is the process of excitation contraction coupling in cardiac muscle cells known as?

A

Ca induced Ca release.

- The myocardial RyR channels open in response to Ca binding to them .

25
Q

What does muscle contraction mainly rely on?

A

internal Ca stores from the sarcoplasmic reticulum (90%) and extracellular Ca (!0%)

26
Q

Outline what excitation-contraction coupling is.

A

The process where muscle action potentials initiate calcium signals that in turn activates a contraction relaxation cycle.

27
Q

Explain the difference in action potentials of skeletal and cardiac muscle.

A
  • Skeletal muscle have short action potentials, meaning it can repeatedly fire action potentials which can formed a sustained contraction/tetanus.
  • Cardiac muscle have very long action potentials, meaning it cannot repeatedly fire action potentials therefore cannot form sustained contraction/tetanus.
28
Q

What is the significance of cardiac muscle having long action potentials?

A
  1. Cells have a long refractory period
  2. Can regulate how much Ca comes into the cell from outside, therefore regulate the strength of contraction.
    a) i.e. Ca is part of excitation-contraction couplin. and the Ca thats released normally doesnt bind to all of the troponin sites. But more CA= more cross bridges=bigger strength of contraction, stronger heart beat.
29
Q

Explain the difference in resting membrane potentials of skeletal muscle and cardiac muscle.

A
  • Skeletal muscle has RMP of -90mV, as do cardiac muscle HOWEVER some cardiac muscle has an unstable resting membrane potential which will continually depolarise towards threshold- pacemaker cells. Its fires its own action potentials making the heart contract.
30
Q

What are the disorders of rhyth,m?

A
  1. Supraventricular tachycardia/ Atrial flutter
  2. Atrial fibrillation
  3. Ventricular fibrillation
31
Q

What is supraventricular tachycardia?

What does it show on an ECG?

A
  • High heart rate originating in the atria.

- Conduction is fine- just very fast. P wave sitting on the back of the T wave.

32
Q

What is atrial fibrillation?

What does it show on an ECG?

A
  • Atria not doing any co-ordinated contraction AT ALL.
  • increased risk of stroke.
  • No P waves
33
Q

What is ventricular fibrillation?

What does it show on an ECG?

A
  • NO QRS

- Medical emergeny- defibrillator treatment to restart the heart.

34
Q

What is the signal for contraction?

A

Depolarisation in a (cardiac) muscle cell

Cardiovascular System (10 decks)

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