S4 Electrical and Molecular Events Flashcards
What sets up the resting membrane potential in cardiac myocytes?
- The cells are permeable to K+ at rest
- K+ moves out of cell down concentration gradient
- This small movement in ions makes the inside negative to the outside
- As charge builds up, an electrical gradient is established
How does excitation cause contraction in cardiac myocytes?
Cardiac myocytes are electrically active (fire action potentials)
An action potential triggers an increase in cytosolic Ca2+
A rise in calcium is required to allow actin and myosin interactions (generates a contraction (tension))
What are the RMP in an axon, skeletal muscle, SAN and cardiac ventricle?
Axon - -70mV
Skeletal muscle - -90mV
SAN - -60mV
Cardiac ventricle - -90mV
What are the stages in a ventricular (cardiac) action potential?
- Opening of voltage-gated Na+ channels (Na+ influx)
- Transient outward K+ current
- Opening of voltage gated Ca2+ channels (some K+ channels also open) - plateau (Ca2+ influx and K+ efflux)
- Ca2+ channels inactivate, K+ voltage gated channels open (K+ efflux)
What are the stages in a SA node action potential?
- Pacemaker potential (funny current) - influx of Na+
- Opening of voltage-gated Ca2+ channels (upstroke)
- Opening to voltage-gated K+ channels - K+ efflux (down stroke)
When is the pacemaker potential activated?
When the membrane potentials are more negative than -50mV
The more negative, the more it activates
What are the HCN channels?
Hyperpolarisation-activated, Cyclic Nucleotide-gated channels e.g. cAMP
Present in pacemaker potential stage
Allow influx of Na+ which depolarises the cells
What are the channel types involved in the pacemaker potential?
- HCN channels
* Transient (T-type) and L-type Ca2+ channels
What does the natural automaticity mean about the SA node action potential?
You don’t need any nervous input to get the action potential started, it is just due to depolarisation of itself
Does the SA node have an unstable or stable membrane potential?
Unstable
What does nervous input into the SA node do?
Modulates the rate of heart contraction
But the SA node produces an action potential without the nervous input
What is the clinical condition if action potential fire too slowly?
Bradycardia (if heart rate is below 60bpm)
What is the clinical condition if action potential fire too quickly?
Tachycardia (if heart rate is above 100bpm)
What is the clinical condition if action potentials fail?
Asystole
What is the clinical condition if electrical activity becomes random?
Fibrillation
When is a plasma K+ concentration considered too high (hyperkalaemia)?
If the concentration is above 5.5mmol/L-1
When is a plasma K+ concentration considered too low (hypokalaemia)?
If the concentration is below 3.5mmol/L-1
What are cardiac myocytes so sensitive to changes in the K+ concentration?
Because the K+ permeability dominates the resting membrane potential
What is the ideal plasma K+ concentration range?
3.5 - 5.5mmol/L-1
What is the effect of hyperkalaemia on cardiac myocytes?
The K+ equilibrium potential gets less negative so the membrane potential DEPOLARISES a bit leading to inactivation of some of the voltage-gates Na+ channels which SLOWS THE UPSTROKE
Ek = 61.5mV (rather than -90mV)
What are the risks of hyperkalaemia in terms of cardiac myocytes?
- the heart can stop - asystole
- may initially increase excitability
Can be mild, moderate or severe (dependent on the concentration)
How do you treat hyperkalaemia in terms of cardiac myocytes?
- calcium gluconate (makes the membrane a little less excitable)
- insulin and glucose - insulin drives K+ into cells and lowers the extracellular K+ level, give with glucose to avoid hypoglycaemia
Treatment only works if the heart hasn’t already stopped
What are the effects of hypokalaemia on cardiac myocytes?
- lengthens the action potential
* delays depolarisation
What are the problems with hypokalaemia in terms of cardiac myocytes?
A longer action potential can lead to early after depolarisations which can lead to oscillations in the membrane potential resulting in ventricular fibrillation
