Cardiac Function

Question 1

What is the function of the SA node + what type of cells is it made up of ?

Answer 1

• pacemaker
• generates spontaneous action potentials
• action potentials pass to atrial muscle cells and AV nose
• made of specialised cardiac muscle cells, continuous with atrial syncytium

Question 2

Why are action potentials conducted more slowly in the AV node ?

Answer 2

• ensures ventricles contract after atrial has contracted fully and have emptied blood into ventricle

Question 3

What is the function AV bundle ?

Answer 3

• passes through hole in cardiac skeleton to reach inter ventricular septum

Question 4

Where so the right and left bundle branches extend ?

Answer 4

• beneath endocardium to apices of right and left ventricles

Question 5

What is the role of purkinje fibres ?

Answer 5

• has many gap junctions
• large diameter cardiac muscle with few myofibrils
• conduct action potential to ventricular muscle cells (myocardium)

Question 6

Stages of conduction through the heart ?

Answer 6

• SA node initiates impulse
• stimulates artia to contract
• impulse is delayed in the AV node so that atria can empty blood into ventricles before ventricular contraction
• impulse at AV bundle and divides into left and right branches which carry impulse along septum
• impulse reaches purkinje fibres which distribute impulse to ventricular myocardium
• this triggers ventricular contraction

Question 7

Structure of cardiac muscle ?

Answer 7

• mononucleated
• faintly striated
• connected by intercalated discs

Question 8

Why is action potentials conducted propagation slower in cardiac muscle compared to skeletal ?

Answer 8

• slower because of gap junctions + smaller diameter of fibres in cardiac cells
• faster is skeletal cause of larger diameter fibres

Question 9

Sliding Filament Theory of Cardiomyocyte contraction ?

Answer 9

• Ca2+ binds to troponin C (TN-C) on thin filaments
• exposes binding site on actin for myosin head
• ATP hydrolysis provides energy for actin-myosin conformational change
• ‘ratcheting’ of actin-myosin and shortening of the sarcomere occurs
  • Ca2+ dissociates from TN-C and myosin unbinds from actin with energy from ATP
  • Cycle ends when ATP binds to myosin and the sarcomere returns to original length.

Question 10

Stages of cardiomyocyte contraction ?

Answer 10

• Ca2+ enters the cardiomyocyte through L-type channels.
• CICR (Calcium-Induced Calcium Release) = Ca2+ triggers the release of more Ca2+ from the sarcoplasmic reticulum (SR).
• Intracellular Ca2+ Rise: Intracellular Ca2+ rises to ~0.5-2 µM.
• Ca2+ binds to troponin-C, freeing the myosin binding site on actin.
• Actin moves over myosin, leading to myocyte contraction.
• Ca2+ is reabsorbed into the SR by the SERCA pump and removed from the cell via the Na+/Ca2+ exchanger and an ATP-dependent Ca2+ pump.
• Ca2+ dissociates from troponin-C, inhibiting the binding site on actin.
• ATP is required to unbind myosin from actin and reset the sarcomere to its normal length.

Question 11

What are the 5 phases of cardiac action potential in contractile cells ?

Answer 11

• phase 0 - rapid depolarisation = rapid influx of Na+ through fast Na+ channels
• phase 1 - initial repolarisation = K+ begins to leave the cell causing slight dip in potential
• phase 2 - plateau phase = Ca2+ enters via L-type channels, balances K+ leaving so plateaus also generates contraction
• phase 3 - repolarisation phase = k + efflux through delayed rectifier, decreased membrane potential
• phase 4 = resting potential

Question 12

What are the K+ channels in ventricular cardiac cells + what’s their role in action potential ?

Answer 12

1. Inward Rectifier (IK1):
   • maintains phase 4 resting membrane potential by allowing K+ to flow into the cell, helping to stabilize the negative potential.
2. Transient Outward (Ito):
   • contributes to phase 1 (initial repolarization) by allowing a brief efflux of K+ from the cell, causing a small dip in the action potential.
3. Delayed Rectifier (IKr, IKs):
   • important for phase 3 (repolarization) by facilitating K+ efflux, which helps return the membrane potential to its resting state.

Question 13

What is pacemaker tissue + pacemaker potential ?

Answer 13

• areas of the heart where ‘resting potential is unstable
• after action potential, membrane becomes more positive until threshold potential reached, triggers new AP
• pacemaker potential = slow depolarisation of membrane between 2 successive AP

Question 14

What is automaticity in pacemaker tissue ?

Answer 14

• Ability to spontaneous depolarise and trigger Action potential without external stimulation

Question 15

Where is packemaker tissue found + not found ?

Answer 15

• active in SA node
• AV node
• bundle of His
• not in ventricular muscle cardiomyocytes

Question 16

What are the phases of action potential in SA node ?

Answer 16

Pacemaker Cells: No true resting potential, generate regular, spontaneous action potentials.

Phase 4: Spontaneous Depolarization
• Mechanism: Inward movement of Na+, outward movement of K+.
• K+ movement decays over time.
• Pacemaker potential depolarizes to -55 mV.
• Ca2+ inward current accelerates from -55 to -40 mV (threshold potential).

Phase 0: Depolarisation
• Ca2+ influx increases due to L-type Ca2+ channels.

Phase 3: Repolarisation
• Voltage-controlled K+ channels open, K+ efflux, repolarizing the cell.
• Ca2+ channels inactivate during this phase.

Question 17

How does the parasympathetic nervous system regulate the cardiac cycle?

Answer 17

• The cardioinhibitory centre in the medulla oblongata controls the vagus nerve, which branches to the SA and AV nodes.
• Ach is released, causing hyperpolarization of the heart.
• This results in a decreased heart rate (dominant effect).

Question 18

How does the sympathetic nervous system regulate the cardiac cycle?

Answer 18

• The cardioaccelerator centre activates sympathetic neurons (cardiac nerves).
• These neuron’s release norepinephrine, which has a minor effect on heart rate
- but increases the force of contraction and contractility.

Question 19

How does parasympathetic + sympathetic nervous system affect action potential ?

Answer 19

• refer to graph
• parasympathetic = increases hyperpolarisation
• sympathetic = rapid depolarisation

Question 20

What is a P wave ?

Answer 20

• atrial depolarisation / contraction

Question 21

What is QRS complex ?

Answer 21

• ventricular depolarisation

Question 22

What is T wave ?

Answer 22

• repolarisation of ventricles

Question 23

What is the PR interval ?

Answer 23

• Start of atrial depolarisation to start of ventricular depolarisation

Question 24

What is the Q-T interval ?

Answer 24

• time required for ventricles to undergo single cycle of depolarisation and repolarisation

Question 25

What is Ischaemic heart disease ?

Answer 25

• Deprivation of blood supply to cardiac tissue • Angina Symptoms (chest pain) • can cause HEART ATTACK - eg. Coronary heart disease

Question 26

What are Cardiac dysrhythmias ?

Answer 26

- Disruption of contraction control • an cause CARDIAC ARREST

Question 27

What is cardiac failure ?

Answer 27

- Inability of heart to distribute blood • can cause HEART FAILURE

Question 28

What are beta blockers ?

Answer 28

- block β1 receptors which adrenaline/ noradrenaline binds to - so slows down SA-node which initiates heartbeat - slows down heart rate + lowers blood pressure

Question 29

What are calcium channel blockers ?

Answer 29

- block L-type Ca2+ channel - no influx of Ca2+ ions - so slows SA-node - so lowers heart rate + blood pressure