Origin And Conduction Of Cardiac Impulse / Force Generation By The Heart / The Cardiac Cycle

Question 1

Where does the excitation of the heart originate and what is its role?

Answer 1

Sino-atrial (SA) node:
- Cluster of specialised pacemaker cells
- Controls sinus rhythm
- Have no stable resting membrane potential, they generate spontaneous pacemaker potentials
- Spreads excitation via gap junctions to both atria or AV node

Question 2

Pacemaker potential:

Answer 2

1. T-type low voltage channels open
2. Funny current causes hyperpolarisation via slow influx of Na+
3. Decreased K+ effux, Ca2+ influx
4. Depolarisation via opening of long lasting Ca2+ channels causing Ca2+ influx
5. Repolarisation via inactivation of Ca2+ channels
6. Activation of K+ channels causing K+ effux

Question 3

AV node:

Answer 3

Only point of electrical contact between atria and ventricles
Delays conduction
Bundle of his and network of purkinje fibres carry impulse from AV node to myocardium

Question 4

Action potential in myocytes:

Answer 4

Phase 0: Na+ influx
Phase 1: Na+ channels close, K+ effux
Phase 2: Ca2+ influx
Phase 3: Closure of Ca2+ channels, K+ effux
Phase 4: Resting membrane potential reached

Phases 0,3,4: Generation of action potential in pacemaker cells

Phase 2: Allows muscle cells to contract and depolarise, switches on systole

Question 5

Bradycardia and tachycardia:

Answer 5

Bradycardia: Resting HR below 60
Tachycardia: Resting HR above 100

Question 6

What is an ECG and what do the leads detect?

Answer 6

Surface electrodes detect waves of depolarisation and repolarisation

Lead 1: Right arm - left arm
Lead 2: Right arm - left leg
Lead 3: Left arm - left leg

Question 7

ECG waves

Answer 7

P-wave: Arterial depolarisation
QRS complex: Ventricular depolarisation
T-wave: Ventricular repolarisation
PR interval: AV node delay
ST segments: Ventricular systole
TP interval: Diastole

Question 8

How ANS effects HR

Answer 8

Vagus nerve (parasympathetic):
- Exerts continuous influence on SA node under rest
- Vagal tone: slows intrinsic HR from high HR to normal resting HR

Vagal stimulation (parasympathetic):
- Slows HR from SA node
- Increases AV node delay
- Acetylcholine on M2 receptors

Sympathetic stimulation:
- Increases HR from SA node
- Decreases AV node delay
- Noradrenaline on B1 adrenoreceptors

Question 9

Cardiac muscle structure:

Answer 9

Striated (due to regular arrangement of contractile protein)

Myocytes coupled by gap junctions

Desmosomes: In intercalated discs, mechanical adhesion between adjacent cells

Myofibrils: Contractile muscles that makes up muscle fibre

Actin - causes lighter appearance
Myocyin - causes darker appearance
Sacomeres - actin and myocyin arranged

Question 10

Sliding filaments mechanism:

Answer 10

ATP-dependent interaction between sliding actin (thin) and myocyin (thick) filaments
ATP and Ca2+ required

Question 11

How excitation of cardiac muscle results in contraction:

Answer 11

Ca2+ released from sacroplasmic reticulum (SR), depends on presence of extracellular Ca+

Power up: Myocin hydrolyses ATP before binding
Power stroke: Myocin releases ATP once blinded

Question 12

Diastolic and Systolic AP:

Answer 12

Diastole:
- Ventricular muscle relaxes

Systole:
- Ventricular muscle contracts
- Ca2+ sourced from Phase 2 of AP
- Causes more Ca2+ release

Question 13

Importance of a long refractory period:

Answer 13

Prevents generation of tetanic contraction

Plateau phase, Na+ channels are in depolarised closed state
Descending phase: K+ channels open, membrane can’t depolarise

Absolute RP: No stimulus can depolarise cell
Relative RP: Large stimulus can generate AP

Question 14

Stroke volume:

Answer 14

Volume of blood pumped out by left ventricle per heart beat

SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)

EDV = Volume of blood in each ventricle at end of diastole

After load: Resistance when heart is pumping causes extra load imposed after heart contracts
- Heart can’t eject full volume so EDV increases

Question 15

Intrinsic control of SV

Answer 15

Intrinsic: SV changed due to change in diastolic length / stretch of myocardial fibres

Starlings law (intrinsic): Matches SV of RV and LV
- Low EDV = Weak contraction, low SV
- High EDV = Strong contraction, high SV

Question 16

Extrinsic control of SV

Answer 16

Via nerves and hormones

Inotropic effect: Stimulation of sympathetic nerves increases force contraction
- Positive: Increased SV
- Negative: Decreased SV

Sympathetic stimulation:
- Increased force of contraction increases Ca2+ influx
- BP and ventricular relation increases

Question 17

Cardiac cycle definition

Answer 17

All events that occur from the beginning of one heartbeat to the beginning of the next

Question 18

Different phases of the cardiac cycle

Answer 18

Passive filling
- Atria and ventricles relaxed
- Blood flows into right and left atria and then into ventricles

Atrial contraction
- Atrial depolarisation causes atria to contract, forcing blood into ventricles and completing EDV

Isovolumetric ventricular contraction - systole
- Atrial pressure falls after contraction
- This causes AV valves to close (S1 sound)
- Ventricle depolarisation os halfway through, rapidly building pressure in ventricles
- No blood is ejected, ventricular volume unchanged

Ejection
- Aorta and pulmonary valves open when pressure in ventricles is greater than in aorta/pulmonary trunk
- Blood pumped into aorta and pulmonary artery
- Ventricles relax, decreasing pressure in ventricles
- This causes aortic and pulmonary valves to close (S2 sound)

Isovolumetric relaxation - diastole
- All valves are closed
- Ventricles relax causing AV valves to open
- Ventricles bill with blood and cycle repeats

Question 19

Changes in ventricular pressure and volume throughout the cardiac cycle

Answer 19

Systole - Ventricular pressure increases
Diastole - Ventricular pressure decreases

Systole - Ventricular volume decreases
Diastole - Ventricular volume increases

Question 20

Status of the heart valves during different stages of cardiac cycle

Answer 20

Filling phase:
- AV valves open
- Aortic/pulmonary valves closed

Isovolumentric contraction - systole:
- AV valves close (S1 sound)
- Aortic/pulmonary valves closed

Ejection:
- AV valves closed
- Aortic/pulmonary valves open at start then close (S2 sound)

Isovolumetric relaxation - diastole:
- AV valves closed at start then open
- Aortic/pulmonary valves closed

Question 21

Origin of normal heart sounds S1 and S2

Answer 21

S1 (lub):
- Caused by closure of mitral (left AV) and tricuspid (right AV) valves
- Marks beginning of systole

S2 (dub):
- Caused by closure of aortic and pulmonary valves
- Marks end of systole and beginning of diastole

Mitral location: 5th left intercostal space
Tricuspid location: 4th left intercostal space

Question 22

How is arterial pressure maintained during ventricular diastole

Answer 22

Ventricles relax, reducing pressure in ventricles which cause AV valves to open

Question 23

Clinical significance of the estimation of Jugular Venous Pressure (JVP) and outline JVP waveforms

Answer 23

Stretch and recoil of arteries keeps blood moving during diastole despite arterial pressure falling to nearly 0

JVP occurs right after arterial pressure waves