Electrical Activation Of Heart

Question 1

Describe features of the membrane of heart muscle cell?

Answer 1

Normally only permeable to K+
Potential determined only by ions that can cross membrane

Question 2

Explain negative membrane potential in the heart

Answer 2

K+ ions diffuse outwards (high to low conc)
Anions cannot follow
Excess of anions inside the cell
Generates negative potential inside the cell

Question 3

What does the myocyte membrane pump?

Answer 3

IN – K+
OUT – Na+ and Ca2+
Against electrical and concentration gradients
Therefore requires active transport (Na+-K+ pump)
Requires ATP for energy

Question 4

What happens in Phase 0 of action potential?

Answer 4

Rapid Depolarisation
Due to Na+ inflow

Question 5

What happens in Phase 1 of action potential?

Answer 5

Partial repolarisation
Due to K+ outflow and Inflow of Na+ stops

Question 6

What happens in Phase 2 of action potential?

Answer 6

Plateaus
Due to Ca2+ slow inflow

Question 7

What happens in Phase 3 of action potential?

Answer 7

Repolarisation
Due to K+ outflow
Inflow of Ca2+ stops

Question 8

What happens in Phase 4 of action potential?

Answer 8

Pacemaker potential
Due to Na+ inflow
Slowing of K+ outflow

Question 9

What are antiarrhythmic drugs?

Answer 9

Medications that prevent and treat a heart rhythm that’s too fast or irregular.

Question 10

What is a Ia antiarrythmic drug?

Answer 10

Na+ channel blocker
(Prolong conduction + repolarisation)

E.g. Quinidine,Procainamide,Disopyramide

Question 11

What is a Ib antiarrythmic drug?

Answer 11

Na+ channel blocker
(No effect on conduction + repolarisation)

E.g. Lignocaine

Question 12

What is a Ic antiarrythmic drug?

Answer 12

Na+ channel blocker
(Prolong conduction)

E.g. Flecainide

Question 13

What is a II antiarrythmic drug?

Answer 13

Beta blocker

E.g. Atenolol, Sotalol

Question 14

What is a III antiarrythmic drug?

Answer 14

K+ channel blocker
Prolong repolarisation

E.g. Amiodarone, Sotalol

Question 15

What is a IV antiarrythmic drug?

Answer 15

Ca2+ channel blocker

E.g. Verapamil

Question 16

Compare the contraction of skeletal muscle to cardiac muscle

Answer 16

Contraction of cardiac muscle lasts longer than skeletal muscle

Up to 15 times longer duration
Due to slow calcium channels
Decreased permeability of membrane to potassium after action potential

Question 17

What happens in propagation of action potential?

Answer 17

Action potential spreads over cell membrane
Positive charge from Na+ affects adjacent cells
Causes depolarisation
Newly depolarised cells also cause depolarisation
Ions can travel directly via gap junctions

Question 18

Explain the speed in conduction in the heart

Answer 18

Velocity of conduction faster in specialised fibres
Atrial and ventricular muscle fibres: 0.3 to 0.5 m/s
Purkinje Fibers: 4m/s

Question 19

What is the Sinus Node?

Answer 19

Normally determines the rate the heart beats
Resting membrane potential of -55 to -60 mV
Related to slow Na+ inflow
Gradually drifts towards threshold for discharge
Fast Na+ channels closed (inactivating gate closed)
Action potential driven by slow Ca2+ channels

Question 20

Explain Automaticity

Answer 20

Sinus node potential drifts towards threshold for discharge
Steeper the drift, faster the pacemaker
Spontaneous discharge rate of heart muscle cells decreases down the heart

Question 21

What is the AV Node?

Answer 21

• Transmits cardiac impulse between atria and ventricles
• Delays impulse
  Allows atria to empty blood into ventricles
  Fewer gap junctions
  AV fibres are smaller than atrial fibres

Question 22

What is His-Purkinje System?

Answer 22

• AV node - ventricles
• Rapid conduction
  To allow coordinated ventricular contraction
  Very large fibres
  High permeability at gap junctions

Question 23

What is the Refractory Period?

Answer 23

• Heart muscle
  Refractory to further stimulation during the action potential
  Fast Na+ +/- slow Ca2+ channels closed (inactivating gates)
• Normal refractory period of ventricle approx 0.25s
  Less for atria than for ventricles
• Prevents excessively frequent contraction
• Allows adequate time for heart to fill

Question 24

What is the Relative Refractory Period?

Answer 24

• After absolute refractory period
  Some Na+ channels still inactivated
  K+ channels still open
• Only strong stimuli can cause action potentials
• Affected by heart rate

Question 25

What is Sympathetic Stimulation?

Answer 25

Increases heart rate (positively chronotropic)
Increases force of contraction (positively inotropic)
Increases cardiac output

Controlled by
Adrenaline and noradrenaline + type 1 beta adrenoreceptors
Increases adenyl cyclase  increases cAMP

Increased sympathetic stimulation
Increases heart rate (up to 180-250 bpm)
Increases force of contraction
Large increase in cardiac output (by up to 200%)

Decreased sympathetic stimulation
Decreases heart rate and force of contraction
Decreases cardiac output (by up to 30%)

Question 26

What is Parasympathetic Stimulation?

Answer 26

Decreases heart rate (negatively chronotropic)
Decreases force of contraction (negatively inotropic)
Increases cardiac output

Controlled by:
Acetylcholine
M2 receptors – inhibit adenyl cyclase  reduced cAMP

Increased parasympathetic stimulation
Decreased heart rate (temporary pause or as low as 30-40 bpm)
Decreased force of contraction
Decreased cardiac output (by up to 50%)

Decreased parasympathetic stimulation
Increased heart rate

Question 27

When do Ryanodine receptors (RyR) open?

Answer 27

When they detect high calcium levels

Question 28

What effect do drugs have on action potential?

Answer 28

Calcium channel blockers (E.g. Verapamil) prolong the refractory period of cardiac tissues (AV Node)

Other classes of drugs
Potassium channel-blockers (E.g. Amiodarone)
Beta-blockers (E.g. Bisoprolol)
Sodium channel-blockers (E.g. Lignocaine)

Question 29

What is Long QT Syndrome?

Answer 29

Abnormality of (usually) K+ channel causes loss of function
Slower outward K+ current delays repolarization (hence prolongation of the QT interval)
Delayed repolarization increases the risk of Early Afterdepolarizations (EADs).

Question 30

What can Long QT Syndrome cause?

Answer 30

Risk of syncope / sudden cardiac death