L8 - Electrical Heart and Vasculature

Question 1

What is the resting membrane potential of

a) a ventricular myocyte
b) the SA mode

Answer 1

a) -90mV

b) -60mV

Question 2

Recognise the SA mode and ventricular potentials (see lecture)

Answer 2

See lecture

Question 3

Is the length of the action potential longer or shorter than cardiac cells in skeletal muscle and neurons?

Answer 3

Shorter

Question 4

Describe the following four stages of the ventricular action potential

a) upstroke
b) transient downstroke
c) plateau phase
d) downstroke

Answer 4

a) opening of voltage gates sodium channels
b) transient outward current of k, due to some channels opening and NCX reversing
c) opening of L type voltage gated calcium channels (influx) and k effluent balancing each other out
d) inactivation of voltage gated calcium channels and opening of voltage gated potassium channels

Question 5

What channels are responsible for the funny current? What ion do they let through? And when are they activated?

Answer 5

HCN channel
Sodium
Hyperpolarisation

Question 6

Describe the three phases of the SA mode action potential

a) pacemaker potential
b) upstroke
c) downstroke

Answer 6

a) result of funny current from opening of HCN channels that slowly depolarise toward threshold (-50)
b) opening of voltage gated calcium channels
c) opening of voltage gated potassium channels

Question 7

What is the medical name for if action potentials fail altogether?

Answer 7

Asystole (No electrical conduction or pulse)

Question 8

What is the safe range for plasma potassium levels?

Answer 8

3.5-5.5mmol/L - above is hyperkalaemia and below is hypokalaemia

Question 9

What effects does hyperkalaemia have on the cardiac action potential?

Answer 9

Shallow upstroke of action potential - explanation - Ek is now less negative, the extra potassium movement inactivated some Nav channels meaning we get a shallower/slower upstroke (more gradient)

Shorter depolarisation and repolarisation - explanation -because Ek is not as negative

increases risk of fibrilation and then asystole

Question 10

What is the major risk of hyperkalaemia

Answer 10

Asystole - may get an initial increase in excitability

Question 11

What are the treatments for hyperkalaemia if caught before asystole?

Answer 11

Calcium gluconate

Insulin and glucose together

Question 12

What are the effects of hypokalaemia on the cardiac AP

Answer 12

Longer action potential as the result of an extended repolarisation phase - explanation - reduced EC potassium means takes longer to repolarise- just know at this level no more

Question 13

Hypokalaemia leads to longer action potentials, why is this dangerous?

Answer 13

Longer action potentials can lead to early after depolarisations, which means some cells start to depolarise whilst the other is still going. This can cause oscillations in the membrane potentials and ventricular fibrillation in turn

Question 14

Which layer of blood vessels controls the tone by contracting or relaxing it’s muscle

Answer 14

Tunica media

Question 15

See flow chart and know smooth muscle versus cardiac excitation-contraction coupling

Answer 15

Yep

Question 16

Explain the steps involved in excitation-contraction coupling in cardiac myocytes

Answer 16

Depolarisation of T tubules opens L type calcioum channels -> calcium spark -> calcium bings ryanodine receptors on ER -> CICR -> Calcium binds troponin C -> tropomyosin moves revealing mysoin binding site on actin -> Cross-bridge formation and power stroke -> SERCA, NCX and Ca ATPases re-establish resting IC calcium levels

Question 17

Depolarisation of VOCC’s and noradrenaline binding arenoceptors cause increase in IC calcium in smooth muscle contraction. Explain the rest

Answer 17

Calcium binds calmodulin in the cytosol -> complex activates MLCK -> complex phosphorylates a myosin light chain -> myosin head can now bind to actin -> Cross bridges and power stroke. -> as calcium levels decrease MLCP which is constituively active dephosphorylates the myosin light chain

Question 18

Explain the mechanism of calcium release through the acitvation of alpha 1 adrenoceptors

Answer 18

Galphaq activation -> activation of PLC -> Cleaves PIP2 to DAG and IP3 -> IP3 binds its receptor on the SR -> CICR