Cardiac physiology 2- Electrical activity of the heart

define:

Polarised 

Depolarised 

Re-polarised 

Polarised : intracellular is MORE NEGATIVE  

Depolarised : intracellular becomes MORE POSITIVE  

Re-polarised : becoming more negative following depolarisation  

define:

Voltage

Current

Voltage = the difference in + charge from each side of the membrane  

Current = the flow of charged particles  

define:

Influx: 

Efflux: 

Influx: the flow of ions into the cell  

Efflux: the flow of ions out of the cell  

name the 5 phases in the electrical cardiac cycle in order

PHASE 4 – RESTING MEMBRANE POTENTIAL

PHASE 0 – RAPID DEPOLARISATION

PHASE 1 – INITAL REPOLARISATION 

PHASE 2 – PLATEAU  

PHASE 3 – REPOLARISATION 

what happens during PHASE 4 – RESTING MEMBRANE POTENTIAL

• which channels open

• what is the mV

1. Voltage independent (VI) K+ channels open  

2. K+ tends to diffuse out (leaving negatively charged proteins behind) 

3. Resting potential = -80mV  

what happens during PHASE 0 – RAPID DEPOLARISATION 

• what is reached

• what ion enters the cell

• what happens to the cell

1. Upon reaching threshold, voltage gated Na+ channels open  

2. Na+ influx along electrochemical gradient  

3. Intracellular gains +ve charge -> DEPOLARISATION  

what happens during PHASE 1 – INITAL REPOLARISATION  

• what ion channel inactivates

• what channel opens

• what happens to the cell

1. VG Na+ channels quickly inactivate  

2. Fast VG K+ channels open  

3. K+ efflux -> intracellular loses positive charge -> short REPOLARISATION  

4. Fast VG K+ channels quickly inactivate  

what happens during PHASE 2 – PLATEAU  

• what channel opens

• what part of the graph is this

• what ion channel inactivates

1. VG L-type Ca2+channels open  

2. Ca2+ influx (slow) -> PLATEAU  

3. Initiating step leading to myocyte contraction  

4. L-type Ca2+ inactivate slowly  

what happens during PHASE 3 – REPOLARISATION 

• what channel slowly opens

• what leaves the cell

• what happens to the cell

1. Slow VG K+ channels open  

2. K+ efflux -> intracellular loses +ve charge -> REPOLARISATION  

3. VI K+ channels contribute  

4. Absolute refractoy period throughout (until -50mV) 

what are the two types of junctions in cardiac muscles

1. Desmosome – mechanical coupling  

2. Gap junction – electrical coupling  

this is how myocytes relay depolarisation in a mexican wave type motion

what does cardiac AP trigger

cardiac AP triggers Ca2+ induced Ca2+ release  

explain Ca2+ induced Ca2+ release  

• what channel depolarisation open

• what ion enters, where does it bind

• what does this cause, what opens

• what does this opening induce, triggering what

• Depolarization from the action potential opens voltage-gated L-type calcium channels (LCC) in the T-tubules. 

• Calcium ions enter the cell through these channels and bind to ryanodine receptors (RyRs) on the sarcoplasmic reticulum (SR). 

• This small influx of calcium is enough to open the RyRs, which are located very close to the LCCs in a specialized junction called a dyad. 

• The opening of RyRs causes a much larger release of calcium from the SR into the cytosol, amplifying the signal and triggering muscle contraction.  

what happens to the length of sarcomere during contraction

• Ca2+ binding to myofilaments causes sarcomere shortening  

myocyte relaxation

• where do Ca2+ go to

• what assists their entry to this magical place

• how else are Ca ions removed (2)

• Ca2+ needs to go back into the sarcoplasmic reticulum for myocyte relaxation  

• They hop off of the myofilaments and enter SR through SERCA 

• SERCA = sarcoplasmic reticulum calcium transporting ATPase 

• Pumps back the Ca2+ into SR  

• The removal of Ca2+ from sarcomere happens also by: 

• NCX = sodium/calcium exchanger  

• PMCA = plasma membrane calcium ATPase 

• These pump ions out of the cell  

 

what is automacity

• Cardiac muscle exhibits AUTOMATICITY  

• Sinoatrial nodal myocyte – pacemaker – APs are self generated  

• Automatic nervous system regulates the intrinsic rate set by the pacemaker (60-100bpm) 

what are the three phases of the SAN action potential

PHASE 4 – PACEMAKER POTENTIAL  

PHASE 0 – DEPOLARISATION 

PHASE 3 – REPOLARISATION  

explain what happens in PHASE 4 – PACEMAKER POTENTIAL  

• which ion channel is leaky

• which ion slowly influx

• what does this lead to

• what is there a fast influx of

• No fast Na+ channels  

• No VG K+ channels  

• No true resting membrane potential  

1. Following repolarisation (60mV), HCN channels open – leaky  

2. Slow influx of Na+ - SPONTANEOUS depolarisation 

3. VG T-type Ca2+open, influx of Ca2+  contributes to decay of pacemaker potential  

explain what happens in PHASE 0 – DEPOLARISATION 

• which ion channels are open

• what does this do to the cell

1. Decay of pacemaker potential reaches threshold (40mV), L-type Ca2+ channels open 

2. Further influx of Ca2+ along electrochemical gradient -> DEPOLARISATION  

explain what happens in PHASE 3 – REPOLARISATION  

• which channel closes and which opens

• what happens to the cell (2)

• which channel is activated

1. l-type Ca2+ channels inactivate and VG K+ channels open  

2. K+ efflux along electrochemical gradient -> REPOLARISATION  

3. VG K+ channels remain open -> HYPERPOLARISATION  

4. This activates HCN channels  

why do APs propagate faster through myocytes than nodal cells (4)

1. Myocytes have greater potential difference  

2. Increased density of gap junctions  

3. Increased length 

4. Increased diameter  

describe the wave of excitations journey that causes atrial → ventricular depolarisation

ATRIAL DEPOLARISATION 

1. AP generated by SAN  

2. Wave of excitation spreads across both atria -> ATRIAL DEPOLARISATION -> CONTRACTION 

3. Wave of excitation travels slowly through AV node  

AV node delay : allows ventricles to fully fill before contraction  

VENTRICULAR DEPOLARISATION 

4. AP travels to the atrioventricular bundle/ bundle of His 

5. AP propagates along R+L bundle branches  

6. Excites purkinje fibre network -> apex to base  

7. VENTRICULAR DEPOLARISATION initiates ventricular contraction during systole  

As the wave of excitation spreads, endocardial myocytes are depolarised before epicardial myocytes  

what happens to ventricles after depolarisation

• direction

VENTRICULAR REPOLARISATION: 

8. After depolarisation, ventricles slowly repolarise in opposite direction to depolarisation  

9. Repolarisation initiates ventricular relaxation  

DEpolarisation: down and left 

describe ventricular AP that leads to myocyte contraction - brief

1. Action potential of the SA node  

2. Cardiac conduction system  

3. Ventricular AP  

4. Ca2+ induced Ca2+ release  

5. Myocyte contraction