Excitable heart

Question 1

what sets up the resting membrane potential of the heart?

Answer 1

• cardiac myocytes are permeable to K+ at rest so K+ diffused down concentration gradient leaving inside of cell comparatively negative.
• net outflow until Ek reached.

Question 2

why is the resting membrane potential not equal to Ek of K+ at -95mv?

Answer 2

• due to very small permeability to other ion species at rest.

Question 3

how does excitation lead to contraction? (brief)

Answer 3

• cardiac myocytes are electrically active, firing action potentials which trigger cytosolic release of Ca2+ from sarcoplasmic reticulum.
• this calcium required for actin myosin interaction which eventually generates contraction.

Question 4

describe a ventricular action potential.

Answer 4

• resting potential maintained until threshold reached due to SAN excitation.
• Upstroke as V-gated sodium channels open ( and K+ close) causing rapid depolarisation.
• special K+ channel opens briefly for slight repolaristion alongside V-gated calcium channels. this balance delays repolarisation to allow for contraction to end.
• then calcium channels inactivated and V-gated K+ channels open causing repolarisation.

Question 5

Describe pacemaker action potential.

Answer 5

• pacemaker potential also knows as the funny current which flows through HCN channels allowing Na+ influx depolarising cell slowly.
• in turn opens V-gated Ca2+ channels causing increased upstroke depolarisation.
• opening of K+ channels causes repolarisation.
• no true resting potential.

Question 6

what are some issues caused by changes to action potential intervals?

Answer 6

• AP fired too slowly = bradychardia <60bpm
• AP fails = asystole
• AP fired too quickly = tachycardia >100bpm
• Ap too random = fibrillation

Question 7

what effect does hyperkalaemia have?

>5.5mmol.L^-1

Answer 7

• Ek less negative as plasma K+ raised so membrane depolarises a bit.
• inactivates some Na+ channels causing shorter AP and slows upstroke.

Question 8

what are some risks of hyperkalaemia?

Answer 8

• asystole.
• initial increase in excitability as resting potential closer to threshold.

*treated with insulin+glucose, calcium gluconate.

Question 9

what is the affect of hypokalaemia?

<3.5mmol.L^-1

Answer 9

• lengthens action potential and delays repolarisation as K+ opening suppressed.
• Ek more negative so larger than normal stimulus needed to generate action potential so less excitable.

Question 10

what are the risks of hypokalaemia?

Answer 10

• longer AP can lead to early after depolarisations and oscillations in membrane potentials resulting in ventricular fibrillation.