Electrical Activity of the Heart Flashcards
How does skeletal muscle contract?
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
How does cardiac muscle contract?
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
What are a gap junction and a desmosome together known as?
Intercalated disc
Site of AP cardiac muscle (CM) vs skeletal muscle (SM)
CM - 200 miliseconds (longer)
SM - 2 miliseconds
Calcium CM vs SM
CM - calcium comes from outside
SM - calcium comes from inside
Types of contraction CM vs SM
CM - Sub maximal contraction
SM - Maximum contraction
Refractory period CM vs SM
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
What does the very long refractory period in cardiac muscle result in?
The muscle has to relax before it can contract again
This stops it doing a tetanus
Describe the cardiac muscle functional syncytium
Electrically connected by GAP JUNCTIONS
Physically connected by desmosomes
Forming intercalated discs
Action potential length of cardiac muscle
Long
What makes sure that cardiac muscle cannot exhibit tetanic contraction?
Long refractory period
What kind of muscle has an unstable resting potential? What do these act as?
Cardiac muscle
Act as pacemakers
Features of non pacemaker cells
Sit at a certain voltage until told to depolarise by the gap junctions
Features of pacemaker cells
Will spontaneously depolarise to threshold and fire an AP
Permeability of non pacemaker cells at resting membrane potential
Sodium and calcium low
High potassium
Non pacemaker action potential
- Resting membrane potential
- High resting Pk+ - 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 - 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 - Repolarising
- reverse
- decrease in PCa2+ and increase PK+ so sodium and calcium channels shut and leaky potassium opens
What causes the pacemaker AP?
Just calcium channels
Pacemaker action potential
- AP
- increase in PCa2+ (L-type) - 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
Modulators of electrical activity
Sympathetic and parasympathetic systems Drugs - Ca2+ channel blockers - cardiac glycosides Temperature Hyperkalaemia Hypokalamia Hypercalcaemia Hypocalcaemia
Effects of CCBs on contraction
Decreases
Effects of cardiac glycosides on contraction
Increases
Effects of temp on contraction
Increases approx. 10 beats / min / degree centigrade
Effects of hyperkalaemia
Fibrillation and heart block
High K outside the cell decreases the concentration gradient for K and so depolarises the cell
Definition of fibrillation
APs are spontaneously fired in an uncoordinated fashion
