Week 2: Cardiac function Flashcards
What are the 2 main cardiac cells? What are their main function?
- Autorythmic: Generate heart beat
- Myocardial: Mechanical Pumping
What are the main components of cardiac myocytes? and breifly what do each of the components do?
Intercalated discs: Tightly connect cardiac myocytes together and keep them all in sync.
Desmosomes: Intercellular junctions that provide strong adhesion between cells
Gap Junctions: allow for depolarizing current to move quickly from cell to cell
Many Mitochondria: Required for high ammount of activity
Large T-Tubules: Allows for more Ca2+ from ECF to move into the cell.
What is the “drift” event of the AR cells due to?
- Cyclical decrease in normal passive K+ efflux from cells
- Special voltage-gated Na2+ channels (If Channels) open when the membrane becomes hyperpolarised resulting in Na2+ influx and continued K+ Efflux.
- Ca2+ moves through transient Ca2+ Channels (T-Type) which takes the membrane to threshold.
How does the autonomic Nervous system effect AR cells?
SympNS: Speeds heart rate by increase calcium influx and If channel flow.
ParasympNS: Slows heart rate by Increasing pottasium Efflux and decreasing calcium influx
This is all controlled by type of neurotransmitter that is released.
Why is the SA node the pacemaker of the heart?
Because it depolerizes the fastest.
How does the electrical signal travel through the heart? what is the pathway?
- AP originates from AR cells in SA node
- Spreads via gap junctions down internodal pathways across atrial myocardial cells = Biggining atrial contraction
- There is now an AV node delay (Pause)
- The signal then continues through from the AV node to the bundle of his -> bundle branches -> purkinje fibres
- As the signals transfer down through the ventricular walls, ventricular contraction will begin from the apex of the heart.
Why do we have an AV nodal delay?
this 0.1 second delay allows for completion of atrial contraction = squeezing remaining blood into ventrical.
Explain what happens during the excitation of contractile cardiac cells?
- AP is brought about by a sudden increase in membrane permeability to Na+ .
- Na+ Permeability then falls to a lower resting level
- The membrane decreases permeability to potassium and increases permeability to calcium causing a maintained depolerisation phase that lasts around 700 milliseconds.
Explain what is happening during steps 0-4? what charges are present at each step?
- Sodium channels open
- Sodium channels close (+20mv to +30mv)
- Slow calcium channels open and fast K+ channels close
- Calcium channels close and slow K+ channels open
- Return to resting membrane potential (-90mv)
why do we need a refractory period in contractile cardiac muscle but not skeletal muscle?
Contractile cardiac muscle acts as a pump for the heart and unlike skeletal muscle cannot go into tetatus. The reason for this is because the ‘pump” has to fill. The refractory period is the period that the heart refils itself (relaxing) and gets ready to pump blood back around the body (contraction).
Are T-Tubules larger in Skeletal muscle cells or Myocardial cells? explain?
- T-Tubules of myocardial cells are larger than those in skeletal muscle cells and they branch inside of the cell
- Due to cardiac muscle having a relatively less sarcoplasmic reticulum within the cell, it relies on the larger T-Tubules to get Ca2+ from the ECF into the cell.
What is happening in stages 1 through to 10?
- AP enters from adjacent cell
- Voltage gated Ca2+ channels open = Ca2+ enters cell
- Ca2+ induces Ca2+ release (CICR) through Ryanodine receptor-channels (RyR)
- Local release causes Ca2+ spark
- Ca2+ sparks create a Ca2+ signal
- Ca2+ ions bind to troponin to initiate contraction (Actin and Myosin complex)
- Relaxation occurs when Ca2+ unbinds from troponin
- Ca2+ is pumped back into the sarcoplasmic reticulum for storage.
- Ca2+ is exchanged with Na+ by the NCX antiporter
- Na+ gradient is maintained by the Na+-K+-ATPase
How is the plateau phase established?
The extra Ca2+ from the ECF is largely responsible.
What is the effect of phospholamban on Ca2+-ATPase activity when stimulated by Catecholamines (adrenalin)?
When phospholamaban is stimulated by adrenanlin it enhances Ca2+-ATPase activity on the SR membrane resulting in an increase to storage of Ca2+ so that when an AP comes, there will be a stronger contraction because of the greater ammount of Ca2+ that was stored.
What is an ECG?
A graphic recording of the hearts electrical activity. It indirectly measures the depolerisation and repolarisation of heart muscle cells.