Question 12

College Answer

(a) A detailed description of the ionic events of the phases of the sino-atrial node AP was expected. A diagram of the sino-atrial node potential which included the phases and labelled x and y axis was helpful in this description. Some comparison with other cardiac action potentials added depth to answers, as did a brief description of the inflences on the action potential such as the autonomic nervous system.

(b) This section required a detailed explanation of impulse propagation both between cardiac myocytes and across the myocardium. Safety mechanisms to be mentioned included anatomical insulation, refractory periods and rate.

Discussion

The diagram the examiners refer to would probably look something like this:

And in words:
 

• The pacemaker cell slowly depolarises in Phase 4. In other words, there is no resting membrane potential - instead, there is a constant drift towards more positive values, mediated by the "funny current". 
• The depolarisation threshold is less negative. The pacemaker cells tend to depolarise when their membrane potential reaches -50 mV.
• The Phase 0 depolarisation is more gradual than the depolarisation of a ventricular myocyte. This is because the pacemaker cells lack functional voltage-gated sodium channels, and their depolarisation is mediated by L-type calcium channels, which open and close much more slowly.
• There is no Phase 1. 
• There is no Phase 2;  the peak positive membrane potential is sustained only for a very short period
• There is a steep rapid Phase 3, as the pacemaker cell repolarises. The final membrane potential at the end of Phase 3 is something like -60-65 mV, slightly less negative than the resting membrane potential of the normal working myocyte. 

b)

Propagation is, in order, 

• SA node: dominant pacemaker
• Internodal tracts conducts action potentials (velocity = 1.7 m/sec)
  • Atrial muscle can also slowly slowly able to conduct action potentials, ~ 0.4m/sec. This 
• AV node: main communication of action potential to the ventricles; responsible for introducing a delay between atrial and ventricular systole so that the atria may finish contracting.
• His-Purkinje system
• Ventricular muscle

Safety mechanisms:

• Fast conductive tissue: ensures that the SA node remains the dominant pacemaker
• Slow conduction of muscle tissue: slow, so that the SA node remains the dominant pacemaker
• Slow automaticity of other conductive tissue: as above, but still able to act as pacemaker in the absence of SA node function or AV conduction (eg. in complete heart block)
• Slow AV node conduction (0.05 m/sec): prevents 
• Cardiac fibrous skeleton: insulates atria from the ventricles

Antoni, H. "Electrophysiology of the heart at the single cell level and cardiac rhythmogenesis." Comprehensive Human Physiology. Springer, Berlin, Heidelberg, 1996. 1825-1842.

Pinnell, Jeremy, Simon Turner, and Simon Howell. "Cardiac muscle physiology." Continuing Education in Anaesthesia, Critical Care and Pain 7.3 (2007): 85-88.

Bers, Donald M. "Cardiac excitation–contraction coupling." Nature 415.6868 (2002): 198-205.

Scher, Allen M., et al. "The mechanism of atrioventricular conduction." Circulation Research 7.1 (1959): 54-61.

Antzelevitch, Charles, and Alexander Burashnikov. "Overview of basic mechanisms of cardiac arrhythmia." Cardiac electrophysiology clinics 3.1 (2011): 23-45.

Sedmera, D., and R. G. Gourdie. "Why do we have Purkinje fibers deep in our heart?." Physiological research 63 (2014).

Tawara, Sunao. Das reizleitungssystem des Säugetierherzens. Fischer, 1906.

Miyazaki, Hidekazu. "Anatomy and physiology of the atrioventricular node: what do we know today?." Cardiac Arrhythmias. Springer, London, 2014. 5-18.

Wang, Ke, et al. "Architecture of atrial musculature in humans." Heart 73.6 (1995): 559-565.