Electrical And Molecular Mechanism In Heart And Vasculature. Flashcards
How does K+ permeability set the RMP.
Cardiac monocytes are permeable to K+ ions at rest. K+ ions move down a concentration gradient, out of the cell. Small movement of ions makes the inside negative, with respect to the outside. As charge builds up, an electrical gradient is established.
Describe the equilibrium potential for K+ ions.
Net outflow of K+ until Ek is reached. Me,brand potential is close to Ek, but RMP is not equal to Ek. RMP has a very small permeability to other ion species, but K+ is the main determinant.
How does a rise in calcium come about and why is it required?
Cardiac monocytes are electrically active, and are electrically coupled to each other. Action potential triggers an increase in cytosolic [Ca2+], a rise in calcium is required to allow actin and myosin interaction (generates tension- contraction).
Summarise the cardiac action potential.
RMP due to background K+ channels open at rest. Upstroke due to opening of voltage-gated Na+ channel (influx of Na+). Initial repolarisation due to transient outward K+ channels. Plateau due to opening of voltage-gated Ca2+ channels (influx of Ca2+). Repolarisation due to efflux of K+ through voltage-gated K+ channels.
What are the pacemaker cells of SA and AV nodes?
They are specialised myocytes that can spontaneously depolarise and fire action potentials.
Describe SA node action potential.
Initial depolarisation to threshold is pacemaker potential (funny current). Upstroke is due to opening of V-gated Ca2+ channels, the downstroke is due to the opening of V-gated K+ channels.
Describe different consequences caused by faulty action potentials.
If action potentials fire too slowly -> bradycardia. If action potentials fail -> systole. If action potentials fire too quickly -> tachycardia. If electrical activity becomes random -> fibrillation.
Hyperkalaemia vs hypokalaemia.
Hyperkalaemia- plasma K+ concentration is too high >5.5 mmol/L. Hypokalaemia- plasma concentration is too low < 3.5 mmol/L.
Why are cardiac myocytes so sensitive to changes in K+?
As K+ permeability dominates the resting membrane potential, the heart has many different kinds of K+ channels.
What’s the effect of hyperkalaemia?
Depolarises the myocytes and allows the upstroke of the action potentials. Ek gets less negative, inactivating some of the V-gated Na+ channels.
Risks/treatment of hyperkalaemia?
Risks: heart can stop (asystole), mild: 5.5-5.9 mmol/L, moderate: 6-6.4 mmol/L, severe >6.5mmol/L. Treatment: calcium gluconate, insulin + glucose (won’t work if the heart is already stopped).
What’s the effect of hypokalaemia?
Lengthens the action potential -> delays repolarisation.
What’s the problem with hypokalaemia?
Longer action potentials can lead to EADs, this can lead to oscillations in membrane potentials -> can result in ventricular fibrillation.
Describe excitation-contraction coupling.
Depolarisation opens L-type Ca2+ channels in T-tubule system. Localised Ca2+ entry opens Calcium-Induced Calcium Release channels in the SR. Close link between L-type channels and Ca2+ release channels.
How is cardiac myocytes contraction regulated?
Ca2+ binds to troponin C, conformational change shifts tropomyosin to reveal myosin binding site on actin filament.
