Week 10 Physiology - Cardiac Cycle

Question 1

Briefly, what is the electrophysiological basis for ECG?

Answer 1

Dipole = separation of charge, utilised by ECG leads to record positive deflection when net wave of depolarisation TOWARDS the lead, and NEGATIVE when away

Question 2

What is an interval vs a segment?

Answer 2

Interval includes waves (i.e PR interval, from start of P wave through to commencement of R wave)

A segment is the isoelectric line between waves (i.e. ST segment)

Question 3

What are the normal ranges for:
- PR interval (AV conductance)
- QRS (ventricular depolarisation and atrial repolarisation)
- QT interval (ventricular depolarisation and repolarisation
- ST segment (interval between ventricular depolarization and repolarization)

Answer 3

PR interval = 0.12 - 0.2s
QRS = 0.08-0.12s
QT = 0.4 - 0.43
ST = 0.32

Question 4

What is the resting membrane potential of myocardial fibres?

Answer 4

-90mv

Question 5

By what route does depolarisation spread from myocyte to myocyte?

Answer 5

Gap junctions (trans cellular route)

Question 6

Describe phases of cardiac cycle in myocardial cells?

Answer 6

Phase 0: Rapid depolarisation (opening of Na+ channels)
Phase 1: Initial rapid repolarisation (closure of Na+ channels)
Phase 2: Plateau phase (slow opening of Ca2+ channels)
Phase 3: Slow repolarisation (opening of delayed K+ channels)
Phase 4: Return to resting membrane potential

Question 7

What is the pacemaker potential? What electrolytes are at work? (Phase 4 of pacemaker cell cardiac cycle)

Answer 7

Slow depolarisation of the pacemaker cells (SA node) towards the membrane potential threshold.

Na+ influx at steady rate from channels activated by membrane potential <-50mV

When sufficient +ve current enters cell, depolarisation occurs at threshold

Question 8

What is phase 0 pacemaker phase?

What channels are inactivated at the end?

Answer 8

Threshold of -40mV has been reached by funny current, causing opening of voltage gated Ca2+ channels

Calcium influx rapidly depolarises cell, and hyper polarisation activated Na+ channels are inactivated, along with closure of Ca2+ channels, and opening of K+ channels

Question 9

What is phase 3 pacemaker potential?

Answer 9

Repolarisation - efflux of K+ out via open channels, leading to membrane repolarisation

N.B. there isn’t sustained opening of Ca2+ channels, and so the shape of the membrane potential is triangular, and returns to negative membrane potential to reactivate the ‘hyper polarisation activated cyclic nucleotide gated channels)

Question 10

What is the major difference between pacemaker potential and ventricular potential?

Answer 10

Pacemaker potential doesn’t have a ‘resting membrane potential’ - repolarisation activates the Phase 4 component of the cycle and facilitates next depolarisation

Question 11

How does the ANS alter heart rate?

Answer 11

Altering the slope of the pacemaker potential

Question 12

What is the effect of acetylcholine on SA node cells?

Answer 12

Increased K+ conductance via special K+ channels activated by GPCR signalling –> slows the depolarising effect of funny current (K+ and Na+ influx)

Question 13

What is the effect of SNS on nodal tissue?

Answer 13

Noradrenaline binds to beta-1 receptors, increased cAMP facilitates opening of L calcium channels, increasing rapidity of depolarisation phase

Question 14

Describe spread of cardiac conduction:

Answer 14

SA node –>intenodal pathways x3 –> AV node –> Bundle of His –> RBB –> LBB –> Purkinje fibres –> ventricular myocardium

Question 15

What conductive tissue connects the atria and ventricles?

Answer 15

Bundle of His

Question 16

What is the difference in location of vagal and sympathetic fibres?

Answer 16

Vagal/parasympathetic = endocardial
Sympathetic = epicardial

Question 17

What direction does depolarisation occur of ventricular muscle?

Answer 17

From left side of inter ventricular septum and moves first to the right across the mid potion of the septum.

Wave of depolarisation spreads down the septum to the apex, proceeding from endocardial to epicardial surface

Question 18

What is cardiac output, and what are its 2 major determinants?

Answer 18

mL of blood pumped from the heart per minute

CO = HR x SV

Question 19

Specifically with stroke volume, what are the 3 underlying factors which contribute to it?

Answer 19

Preload
Contractility
Afterload

Question 20

What is preload?

Answer 20

End-diastolic volume, filling of ventricles prior to systole (i.e. how much blood available in ventricles to be pumped out)

Question 21

Regarding contractility, what factors affect it?

Answer 21

Positive and negative inotropy, also related to preload with Frank-Starling forces

Question 22

What effect does after load have on cardiac output?

Answer 22

Afterload = amount of pressure that needs to be generated to overcome for blood to be pumped from the ventricles into systemic circulation.

If increased after load, this will reduce cardiac output

Question 23

What is phase 1 of the cardiac cycle?

Answer 23

Atrial systole - Additional blood propelled into ventricles (70% of ventricular filling is passive).
Closure mitral and tricuspid valves

Question 24

What is phase 2 of the cardiac cycle?

Answer 24

Isovolumetric contraction of ventricles – lasts about 0.05s – until pressures exceed aortic/pulmonary artery pressures and aortic and pulmonary valves open. AV valves bulge, causing rise in atrial pressure.

Question 25

What is phase 3 of the cardiac cycle?

Answer 25

Ventricular ejection - rapid initially then slows.
Peak left ventricular pressure 120mmHg.
Peak right ventricular pressure 25mmHg.
Eventually momentum of propelled blood overcome and aortic and pulmonary valves close

Question 26

What is phase 4 of the cardiac cycle?

Answer 26

Isovolumetric ventricular relaxation.
- ends when ventricular pressure falls below atrial pressure and AV valves open permitting ventricles to fill.

Question 27

What is phase 5 of the cardiac cycle?

Answer 27

Late diastole
Ventricular filling.
Blood passively fills atria and ventricles.
Filling is rapid initially.
Rate of filling declines as chambers fill and cusps of AV valves drift closed.

Question 28

What is the relationship of the stroke volume to ejection fraction?

Answer 28

Ejection fraction = stroke volume/end diastolic volume

i.e. 70/120mL
= 0.58 or 58%

Question 29

What is the cause of the 1st heart sound? The second?

Answer 29

Closure of the mitral and tricuspid valves
Closure of the aortic and pulmonic valves

Question 30

What is the cellular explanation for why increased preload increases cardiac output?

Answer 30

The sarcomere is stretched, allowing more potential contractility and therefore CO (up until a certain limit)

Question 31

What 2 factors influence the starling curve?

Answer 31

Inotropy
Afterload

Question 32

Summarise Poiseulle’s law:

Answer 32

Poiseulle’s law says that the flow rate depends on radius of vessel, fluid viscosity, vessel length, and the pressure difference between the ends

i.e. The theory behind why small increased in diameter lead to large increases in flow (significant of wide bore cannulas)

Question 33

What is laminar flow?

Answer 33

Concentric layers of blood moving in parallel down the length of a blood vessel. The highest velocity (Vmax) is found in the center of the vessel. The lowest velocity (V=0) is found along the vessel wall.

Question 34

What is turbulent flow?

Answer 34

Where normal linear blood flow is disrupted and becomes chaotic, increasing amount of energy required to push it along due to friction forces`

Question 35

What is Laplace’s law, and its application to aneurysms?

Answer 35

wall tension = intraluminal pressure × radius

Therefore, the more dilated the vessel, the greater the wall tension and the risk of perforation/rupture

Question 36

What are the reasons for ST elevation in transmural ACS?

Answer 36

1. Abnormally rapid repolarisation (due to accelerated opening of potassium channels)
2. Decline in resting membrane potential (loss of intracellular potassium
3. Slow repolarisation (due to delayed depolarisation relative to healthy adjacent tissue)

Question 37

What direction does current flow (regarding ischaemic vs non ischaemic areas of myocardium)?

Answer 37

Ischaemic —> non ischaemic

Question 37

What are the particularly important channels responsible for the generation of ‘injury currents’ in cardiac ischaemia?

Answer 37

K+ ATP pump (requires ATP to remain closed, which it is at RMP

Na+ K+ ATPase, which usually generates a hyperpolarising current (but doesn’t function when there is no ATP in the cell, therefore there is a decline in RMP and more rapid depolarisation)