2016B Question 02
Compare and contrast the action potentials from the sino-atrial node and a ventricular myocyte.
61% of candidates achieved a pass in this question.
A detailed comparison of the ionic fluxes responsible for the generation of action potentials in these cells was expected. The duration of these ion fluxes and voltages at which they occurred along with a discussion of the conventional physiological phases of action potential were expected as part of the answer. An understanding of the physiology behind these changes was also rewarded. These changes could be described in prose, tabular format or diagrammatically. Better answers often included more than one of these formats and this increased the extent of the detail they were able to provide.
Additional marks were awarded for a discussion of the effects of parasympathetic and sympathetic innervation and concepts such as refractory periods of action potentials and their basis and variability.
Common difficulties encountered appeared to be in the production of legible and accurate diagrams, and confusion arising as to the primary ions responsible for the depolarisation of the two cells in cells in question.
No marks were awarded for discussing the effects of antiarrhythmic agents in depth on the myocardial tissues, or the detailed anatomy of the conducting system.
- Pacemaker action potential
- Ventricular myocyte action potential
- Allows rapid, co-ordinated signalling
- Rapid depolarisation followed by repolarization
- Ion channels cycle through resting → Activated → Inactivated states
|Determinants of ion flux||
- Channel permeability: Voltage dependent
- Electrochemical gradients
- Na+ and Ca2+ into cell, K+ out of cell
- Mainly due to Na+K+ATPase
Pacemaker Action Potential
- i.e. Intrinsic, rhythmic, frequent depolaristion and contraction
- HCN channel produces ‘funny current’ – i.e. Mixed Na+ and K+ influx
- [cAMP] ∝ If ∝ slope of phase 4 ∝ heart rate
- Note depth of repolarisation ∝ IK ∝ 1/(heart rate)
- Post-repolarisation refractoriness
- RRP extends into phase 4
- ERP: Insufficient HCN and Ca2+ channels resting; action potential (AP) impossible
- RRP: Enough HCN and Ca2+ channels resting but fewer than normal; AP possible with higher than normal stimulus
|Factors increasing rate||
- ↑ SNS → ↑ If = ↑ ICa2+ > IK+ → ↑ Steepness all slopes, especially phase 4
- ↑ Temp → ↑ Cell metabolic rate (enzymes, pumps)
- ↓ K+ → Less hyperpolarisation
- Neonate: ↑ resting HR (fixed stroke volume)
|Factors decreasing rate||
- ↑ PSNS: → ↓ If, ↑ IK → ↓ Steepness phase 4, increased hyperpolarisation
- ↓ Temp → ↓ Cell metabolic rate (enzymes, pumps)
- Hypoxia → Failure of Na+K+ATPase, unable to repolarize cell, HCN not reactivated
- Elderly: Fibrous/fatty change in conduction system, ↓ β1 adrenoceptors
Ventricular Myocyte Action Potential
- Plateau → Time for systolic ejection and prevention of tetany
- Variable timing → Co-ordinated contraction
- e.g. Endocardial cells start earlier, finish later
- Absolute (ARP): No Na+ channels resting; AP impossible
- Effective (ERP): Insufficient Na+ channels resting; AP impossible
- Relative (RRP): Enough Na+ channels resting, but fewer than normal; AP possible with higher than normal stimulus
- Supranormal period (SNP): AP possible with lower than normal stimulus
- SNS: Shortens duration of action potential
- Hypoxia: Failure of Na+K+ATPase → Depolarisation to -50mV → Inactivation of fast-Na+ channel and activation of L-Ca2+ channel → Behaves like pacemaker cell → Arrhythmia