Heart as Electrical Pump

Question 1

What’s the structure of myocytes?

Answer 1

Intercalated discs allowing mechanical/electrical communication between them (=syncitium)
Bundle of myofibrils with thin actin and thick myosin myofilaments making up a sarcomere (repeating units).

Question 2

Explain the nature of action potentials in the SA node

Answer 2

Spontaneous - SA pacemaker cells have no true resting membrane potential but are influenced by external factors (autonomic nerves, hormones, drugs, ions)

SA node is primary pacemaker but any cardiac cell can take over this role if it’s damaged

Question 3

Explain the form of action potentials in the cardiac myocyte

Answer 3

Voltage gated Na+ channels open, rapid depolarisation
Channels close, K+ channels open and slow Ca2+ channels (plateau)
Ca2+ channels close, repolarisation and refactory period
K+ channels close to stop efflux of K+

Question 4

Explain the propagation of action potentials

Answer 4

Depolarisation spreads along syncytium in one direction (opposite to the refectory zone) by cytosolic ion flux through desmosomes

Refractory period longer in cardiac cells than skeletal muscle as tetanus would be dangerous

Question 5

Explain the functional anatomy of cardiac conduction system

Answer 5

Two myocardial syncytia separated by AV node which delays communication from SA node in atria to ventricles

Question 6

Explain the mechanism of excitation-contraction coupling

Answer 6

AP propagates along sarcolemma, depolarisation causes Ca2+ influx via T-tubules and bind to troponin, causing movement of tropomyosin to reveal binding site for myosin head

Question 7

Briefly explain the 4 phases of the cardiac cycle

Answer 7

1. Atrial pressure increases higher than ventricular so atria contract (systole) to eject blood into ventricles
2. Isovolumetric ventricular contraction, ventricular systole so aortic and pulmonary valves open to eject blood from ventricles to major vessels
3. End of ventricular contraction, ventricular repolarisation and dichrotic notch seen as semilunar valves shut
4. Isovolumic relaxation, atrial pressure increases, venous return, AV valves open so ventricles fill (both in diastole)

Question 8

Describe the pressure changes during the cardiac cycle

Answer 8

Pressure volume loop of ventricles explains this

Atrial pressure > ventricular pressure MV opens
Ventricular pressure > atrial pressure MV closes
Ventricular pressure > aortic pressure, aortic valve opens
Aortic pressure > ventricular pressure, aortic valve shuts

Question 9

What principles underlie valvular pathology?

Answer 9

Narrowing of valves = ventricular outflow obstruction

Hypertrophy of ventricles, sarcomeres increase, stroke volume increases until affected vessel will functionally dilate

Question 10

What’s the function of cardiac myocytes being arranged in a syncytium?

Answer 10

Allows low threshold all or nothing response with rapid propagation of electrical activity

Question 11

Outline excitation-coupling contraction in cardiac myocytes

Answer 11

Excitation: AP originates in pacemaker cells and propagates along sarcolemma to spread down T-tubules
Coupling: Ca2+ enters sarcoplasm from T-tubules, sarcoplasmic reticulum and cell membrane though voltage-gated Ca2+ channels
= intracellular Ca2+ rises

Ca2+ binds to Troponin C (4 binding sites) which exposes Myosin head binding site on Actin by moving Tropomyosin out the way
ATP also binds and is hydrolysed to provide energy for Myosin head to bind in higher energy state

Question 12

How does the Ca2+ concentration affect contraction?

Answer 12

Higher Ca2+ concentration the more Troponin C molecules will be activated (4 binding sites show cooperatively)

At the end of AP, Ca2+ pumped back into SR and T-tubules by Ca2+/Mg2+ ATPase pump

Low Ca2+ stops Myosin-Actin interaction = contraction stops