1 Electrical events of the cardiac cycle

Question 1

Which ions carry the current in the Sinoatrial node

and through which channels

Answer 1

Sinoatrial node

Na+ and Ca2+
Slow channels

Question 2

Which ions carry the current in the ventricular myocytes

and through which channel?

Answer 2

Ventricular myocytes

Na+ (fast channels) - depol.
Ca+ (slow channels) - repol.

Question 3

Describe the changes in the cardiac myocyte action potentials, and it’s relation to the cardiac cycle

Answer 3

Various parts of the heart are being excited to contract at different stages of the cardiac cell (atrial or ventricular contraction)

• Shape of AP in pacemaker areas:
  > SAN and AVN are very different from AP in other areas (rapid upstroke Na+, plateau from K+)
• Whereas in ventricular muscle, the plateau phase is when Ca2+ enters cells, causing Ca2+ induced Ca2+ release, producing contraction of muscle
  > contractile phase = plateau phase of ventricular muscle

Question 4

Describe how cardiac muscle cells are adapted for synchronous electrical activity

Answer 4

• Junctions between cardiac muscle cells (intercalated discs) = gap junction = where there are connexon pores between 2 cells
• So electrical status of one cell rapidly stimulates the electrical status of other cells it’s in contact with

(cardiac cells = branched, unlike smooth or skeletal)

Question 5

What is the intrinsic spontaneous beating rate of SA node cells?

hence, what is its purpose?

Answer 5

105 bpm (approx.)

So, its activity drives that of all the other parts of the heart

Question 6

What is the beating rate of atrial and ventricular cardiac cells?

Answer 6

30-40 bpm

Question 7

Describe the SA node’s pacemaker role, in relation to its’s resting membrane potential

Answer 7

As a pacemaker area, the SA node cells have a much less stable resting membrane potential than other parts of the heart
- (there is creeping depolarisation)
- called PACEMAKER POTENTIAL -
> (this steepness is in all cardiac cells - not as steep though)

Question 8

What are the consequences to the intrinsic resting heart rate if the SA node is damaged

Answer 8

If the SA node is damaged, then the intrinsic resting heart rate decreases (60-100bpm)

Question 9

Describe the ionic basis for action potentials in SA nodes

Answer 9

• There is creeping depolarisation = where there is an opening of a specific cation channel - ‘FUNNY CHANNELS’
  > This is only expressed in SA node, but not in atrial or ventricular myocytes
• When funny channels open, the membrane permeability to Na+ and K+ increases
• But as the cell has a relatively -ve membrane potential
  > there is a low K+ efflux, but there is a Na+ influx
• This results in the PACEMAKER POTENTIAL
• When Vm reaches the threshold for AP (in SA node cells), the ion channels which open are L-type Ca2+ ion channels which open, causing depolarisation
• As membrane potential moves to the equilibrium potential for Ca2+, they come into the cells
• At the peak of SA node AP, Ca2+ channels close, K+ channels open (efflux)
• Membrane potential starts to come back to the equilibrium potential of K+ (more electronegative than resting)
• Back to resting potential
• K+ channels close, the start of pacemaker potential (funny channels)

Question 10

Describe the normal path of conduction of electrical activity through the heart

Answer 10

• Cells of SA node undergo spontaneous discharge
  > So, the frequency with which the heart beats is driven by SAN discharge rate
• Electrical activity spreads across atria (depolarisation) - from left to right atria, and down the R atria
  > causing contraction of atria
• There is insulating tissue between atria and ventricles - forcing signals to go via the AV node
• There is a slight pause in charge at the AV node
• When the AV node discharges, this activates the BUNDLE OF HIS and PURKINJE FIBRE system, ensuring near-simultaneous depolarisation of the muscle mass in both ventricles
  > producing contraction of the ventricular muscles, squeezing blood:
  = From R ventricle to the pulmonary artery to lung (deO2 blood)
  = From L ventricle to aorta - to rest of body (O2 blood)

Question 11

What are the consequences of SA node damage to the path of conduction and/or cardiac cycle

Answer 11

If SAN was damaged, or path of conduction was affected, there may be a spontaneous discharge of ventricular muscle cells - contraction

• (but, not in the same way, less frequent - 30-40bpm)
• and contraction is not coordinated

This all results in a decrease in cardiac output

Question 12

Describe the ionic basis of action potentials for ventricular myocytes

Answer 12

The shape of the AP curve is different:

• VG fast Na+ channels open, resulting in Na+ influx - causing rapid depolarisation
• VG slow Ca2+ channels open (some K+ channels close), causing Ca2+ influx, resulting in a plateau in Vm - maintained depolarisation
• Then, VG K+ channels open, causing repolarisation

This all lasts 300ms

Question 13

Describe the difference in AP length between ventricular myocytes and nerve cells

Answer 13

Ventricular myocyte AP (300ms) is significantly longer than nerve cells (3-5ms)

Question 14

Describe the nervous system influence on cardiac activity

Answer 14

There is no requirement for neural input for the heart to beat
- The SA node controls the frequency of the heartbeat

But, there is neural heart input:
- In the medulla of the brainstem, there is the cardiovascular centre (CV), which are a collection of neurons

Question 15

Describe the inputs the cardiovascular centre receives in the medulla of the brainstem

Answer 15

The CV center (neurons) receive input from around the nervous system:
- the higher center of the brain: cerebral cortex, limbic system, hypothalamus
- sensory receptors:
> proprioceptors - monitor movement
> chemoreceptors - monitoring blood chemistry (CO2, pCO2, pH)
> baroreceptors - in the wall of blood vessels - monitor BP

Question 16

Describe the sympathetic outputs the cardiovascular centre sends in the medulla of the brainstem

Answer 16

Output to the heart via:

• Cardiac accelerator nerves (sympathetic)
  > increase rate of spontaneous depolarization in SAN and (AVN) - INCREASE HEART RATE
  > increase contractility of atria and ventricles - INCREASE STROKE VOLUME
• Can increase cardiac output (CO)
  CO = heart rate x stroke volume
  > +ve chronotropic (increase in heart rate)
  > -ve ionotropic

These effects are controlled by the release of NORADRENALINE - B1 adrenoceptor

Question 17

Describe the parasympathetic outputs the cardiovascular centre sends in the medulla of the brainstem

Answer 17

• Vagus nerves (CNX - parasympathetic) - not as powerful (not as many)
  > they decrease the rate of spontaneous depolarization in SAN and (AVN) - DECREASES HEART RATE
• They affect pacemaker areas, and not atria and ventricular, and don’t affect the force of contraction of the heart
  > they only have -ve chronotropic effects (decrease in heart rate)

These effects are controlled by the release of ACETYL CHOLINE - Muscarinic receptors (M2)

Question 18

Describe the differences in the sympathetic and parasympathetic controls of the heart by the cardiovascular centre in the medulla

Answer 18

• Sympathetic uses cardiac accelerator nerves, whereas parasympathetic uses Vagus nerve
• Sympathetic = increase in spontaneous depolarization in SAN (and AVN) AND contractility in atria and ventricles,
  WHEREAS
• parasympathetic decreases only spontaneous depolarization in SAN (and AVN)

So, sympathetic affects heart rate and stroke volume, whereas parasympathetic only decrease heart rate

Sympathetic effects are controlled by the release of Noradrenaline - at B1 adrenoceptors
WHEREAS
Parasympathetic effects are controlled by the release of Acetyl Choline - at Muscarinic receptors (M2)

Question 19

Describe the autonomic effects on SA node AP by sympathetic activation

Answer 19

• Sympathetic activation increases the slope of the pacemaker potential (prepotential)
• This is mediated by increased opening of ‘funny channels’ - open for longer;

> This means that SA node action potentials arise more frequently, as threshold potential for AP is reached much more quickly

Question 20

Describe the autonomic effects on SA node AP by parasympathetic activation

Answer 20

• Parasympathetic activation:
  > both hyperpolarises the SA node cells
  > + decreases the slope of the pacemaker potential (reaches threshold potential slower)

These effects are mediated by increased opening of K+ channels

Question 21

Explain how the resting heart rate is kept in check

Answer 21

SAN intrinsic activity is around 105 bpm

So, the balance between effects keeps resting heart rate in check:

• VAGAL TONE damps down resting heart rate
  > by HYPERPOLARISING SAN, and by decreasing slope of pacemaker potential
• SYMPATHETIC TONE keeps the heart rate up
  > by increasing slope of pacemaker potential

When both divisions of the autonomic NS are blocked, the intrinsic heart rate is 105bpm

Question 22

Describe how K+ disturbances and heart rhythms are closely linked, and how problems may arise

Answer 22

K+ ion channels (and [K+]) are very important in determining the ability of cardiac myocytes to repolarise + setting the resting membrane potential

• If plasma K+ levels increase (HYPERKALAEMIA), this can have catastrophic effects on cardiac excitability
  > This will push membrane potential to less negative values + may allow cells to reach threshold more easily

Question 23

Give some effects of HYPERKALAEMIA (in relation to ECG)

Answer 23

• The PR and QRS interval are within normal limits

- Very tall peaked + slender T waves present

Question 24

Give some effects of HYPOKALAEMIA (in relation to ECG)

Answer 24

Hypokalaemia is also dangerous but not as rapidly fatal as hyperkalemia
- Cardiac arrhythmia: T wave is not noticeable (K+ conc. is wrong)