Question 7(p.2)

Outline normal impulse generation and conduction in the heart. Describe the features present in a normal heart that prevent generation and conduction of arrhythmias.

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College Answer

This question required description of the SA node, its primary role and generation of the
pacemaker potential and the influence of the autonomic nervous system. A diagram of the
conducting pathways, highlighting specialized tissues with fast or slow conduction velocities
would have been appropriate. The importance of the AV node in preventing retrograde
conduction and high rates conducted to the ventricles (>220 / min) was often neglected in
answers. A discussion of the Purkinje Fibres with particular reference to the absolute and
relative refractory periods was essential.
Additional marks were awarded for mention of the atrial internodal pathways, conduction
within the ventricles from the endocardial to epicardial surfaces and the significance of the
compensatory pause in response to ectopic beats.
Syllabus C1b 2.a, b;
Reference: Cardiovascular Physiology, “Electrical Activity of the Heart” (Chapter 2), Berne
and Levy.

Discussion

This question expected a lot, judging from the examiner's comments. How to roll this answer into a compact form, readily expelled over ten minutes of frantic scribbling? Here, an attempt is made to concentrate all the relevant features mentioned in the college answer, with the greatest economy of words.

Normal conduction in the heart (in order of conduction)

  • SA node:
    • Small bundle of cells in the superior right atrium; the dominant pacemaker
    • Pacemaker function facilitated by If "funny" potassium current which automatically depolarises the cell membrane during Phase 4
    • This potassium channel is cAMP-gated, and this allows autonomic control over the SA nodal rate
  • Internodal tracts 
    • Tracks of minimally modified myocytes arranged in parallel along the atrial wall; capable of automaticity under extreme conditions
    • High velocity conduction (velocity = 1.7 m/sec, vs atrial muscle = 0.4m/sec)
  • AV node
    • Small bundle of cells at the septal part of the right atrial base
    • Capable of automaticity; rate ~ 40-70 bpm
    • Responsible for introducing a delay between atrial and ventricular systole so that the atria may finish contracting. Slow conduction: 0.05 m/sec
    • Long refractory period:
      • prevents retrograde conduction
      • limits conducted rate to a maximum of ~ 220
  • His-Purkinje system
    • Operates at high velocity,  up to 4m/sec
    • Long absolute refractory period prevents depolarisation and therefore protects from "circus" action potentials (prevents VT)
    • Relative refractory period permits depolarisation (early afterdepolarisations)
  • Ventricular muscle
    • Depolarises from endocardium outwards to the epicardium
  • Compensatory pause
    • The refractory period of ventricular myocytes after a VEB prevents the propagation of the next SA nodal action potential, introducing a delay before the next QRS complex following a VEB.

References

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.

Stanton, M. G. "Origin and magnitude of transmembrane resting potential in living cells." Philosophical Transactions of the Royal Society of London. B, Biological Sciences 301.1104 (1983): 85-141.

Baczkó, István, Wayne R. Giles, and Peter E. Light. "Resting Membrane Potential Regulates Na+–Ca2+ Exchange‐Mediated Ca2+ Overload during Hypoxia–Reoxygenation in Rat Ventricular Myocytes." The Journal of physiology 550.3 (2003): 889-898.

Cooper, Patricia J., Christian Soeller, and Mark B. Cannell. "Excitation–contraction coupling in human heart failure examined by action potential clamp in rat cardiac myocytes." Journal of molecular and cellular cardiology 49.6 (2010): 911-917.

Santana, Luis F., Edward P. Cheng, and W. Jonathan Lederer. "How does the shape of the cardiac action potential control calcium signaling and contraction in the heart?." Journal of molecular and cellular cardiology 49.6 (2010): 901.

Hund, Thomas J., and Yoram Rudy. "Determinants of excitability in cardiac myocytes: mechanistic investigation of memory effect." Biophysical journal 79.6 (2000): 3095-3104.

Carmeliet, E. D. W. A. R. D. "Cardiac transmembrane potentials and metabolism." Circulation research 42.5 (1978): 577-587.