Cardiac Muscle and Cardiac Action Potential Flashcards
1
Q
Describe cardiac muscle
A
- Striated and branched
- Intercalated discs
- Myogenic activity
- Resting potential of cardiac muscle cells is unstable, gradually increases
2
Q
Describe heart beat in cardiac muscle
A
- Every fibre contracts at each heart beat
- Not possible to alter strength of contraction via recruitment
- Rhythmic twitching- AP frequency not a control mech.
- Strength varied by Ca conc inside cardiac cell
- Ca enters from outside also intracellular stores
- When muscle activated- cytoplasmic Ca conc rises rapidly and initiates contraction of cardiac muscle
3
Q
How do positive inotropic drugs work?
A
- Increasing intracellular calcium concentration
4
Q
Describe calcium movement upon excitation
A
- Second inward current passes across membrane- causes Ca to enter cell
- AP in cell penetrates along transverse tubule- AP deep in muscle
- Ca from outside cell as a result of AP
5
Q
Describe the activation of calcium-induced calcium release
A
- AP also acts on cisterna Ca store- releases more Ca
- Ca also activates Ca-induced Ca release
- Ca conc in cytoplasm increases and causes cardiac contraction
- If muscle twitches, Ca has to go down again so that muscle can relax
- Small amount into mitochondria
6
Q
What channels are there and what do they do?
A
- ATP-dependent Ca pump- pumps Ca out of cytoplasm into extracellular fluid
- Na/K ATPase- generates Na gradient fo Na/Ca pump, primary active transport
- Second active pump Na/Ca- Na flows down normal gradient, secondary active transport
- Ca also actively pumped into SR using ATP- results in rapid drop of Ca conc in cytoplasm
7
Q
How does cardiac ischaemia affect calcium movement and contraction?
A
- Slowed, causing ventricle to relax- harder to fill- stiff
- ATP deficient cell
- Limits O2 supplying muscle cell- slow release/uptake of Ca back into SR
- So, ischaemic heart - stiff ventricle
- Blood from lungs down PV, LA, LV- normally rapid filling
- With ischaemia- stiff because Ca slow to leave cytoplasm, muscle slow to relax, impedes filling and leads to diastolic failure.
8
Q
What is diastolic failure?
A
- Inability of the heart to pump as much blood as it should due to failing in filling of heart, unlike normal (systolic) heart failure
9
Q
Describe calcium and muscle contraction
A
- Same as skeletal muscle
- Actin and myosin filaments pass over each other- cross bridges form and break
- Ca bind to troponin C
- Troponin C attached to tropomyosin
- Cross bridge formed and moves actin filament over myosin filament
- Myosin head disengages and process repeats
- ATP required to alter configuration head as part of process
10
Q
Describe the five phases of ventricular action potential
A
0- depolarisation by Na influx
1- initial repolarisation caused by K efflux
2- plateau phase resulting from Ca influx- second inward current maintained for a while
3- repolarisation caused by K= efflux
4- resting potential- Na channels reactivated
11
Q
What occurs in cardiac muscle if there is hyperkalaemia?
A
- High plasma potassium
- High ennough to lift the resting potential of the ventricular muscle
- Membrane potential may not return to its normal resting value
- Therefore, not all Na channels may fully rest- may lead to cardiac arrest
12
Q
Describe action potential at SAN
A
- Resting pot not resting
- Steep slow during resting potential- pacemaker property
- As SAN depolarises- eventually Na gates open and initiates AP normal way
- No significant plateau
- Frequency of SAN firing depends on slope of unstable resting potential
- If steep- faster firing and HR (SNS- noradrenaline)
- If flat- longer interval, slow firing and HR (PNS, ACh)
13
Q
Describe action potentials at atrial cells
A
- Activity through AVN
- Similar shape to SAN, but slope in phase 4 less because AVN lacks particular Na channel- slower depolarisation
- Contributes to AVN delay
- Takes a while for acitivty from atria through to ventricles
- Atrial systole can complete itself
- Blood can move in ventricles before ventricular systole
14
Q
Describe action potentials in Purkinje cells
A
- Similar to ventricular muscle cells
- Middle plateau phase due to Ca entry
- Long plateau phase means cardiac muscle cannot go into tetanic contraction
- repolarisation in cardiac AP occurs after muscle twitch
- individual twitches can’t add together
- long plateau means they’re individual, contraction over before muscle cell ready to depolarise again
15
Q
What do positive inotropes do and give examples?
A
- Increase Ca conc in muscle cell
- β-agonists (dopamine, Adr, NA), speed up Ca uptake into intracellular stores therefore increasing availability
- Cardiac glycosides (digitalis, digoxin), inhibit Na/K ATPase, increase Na conc in cell, decrease Na/Ca exchange and increase intracellular Ca conc.
