Cardiac Ion Channels and the Heart Beat

Tying in with my PHYL3001 post about ion channels, now you're going to get a bit more context and see how these ion channels operate in the heart!

Normal electrical conduction

See previous post: The Heartbeat.

Morphological/functional classification of cells

There are three main types of cells that you should know about. I'm going to use this as an excuse to make another table, because tables are great (despite Blogger's tendency to want to put around 20 lines of space before tables :P).

Name	Shape	Diameter (μm)	No. of myofibrils	Location	Other
Pacemaker cells	Round or oval	3-9	Reduced no.	SA node and AV node
Conducting cells	Cylindrical	50	Reduced no.	Bundle of His, bundle branches, Purkinje fibres	Many intercellular connections
Contractile cells	Cylindrical	10-15	Abundant	Atria and ventricles	Many intercellular connections, extensive T-tubule system

Characteristics of fast and slow action potentials

There are two kinds of action potentials in the heart: a fast and a slow action potential. The slow action potential is responsible for the pacemaker activity of the pacemaker cells, whereas the fast action potential is responsible for the actual contraction that takes place in the atria and ventricles.

Ionic composition of the fast action potential

Behold, a crudely drawn graph of the fast action potential!

Let's break this down into the different phases (labelled with the different numbers)!

Phase 0: Upstroke and Overshoot

This phase is due to a sharp increase in Na⁺ conductance. A large influx of Na⁺ increases the membrane potential from around -80 to around +20. At the end of this phase, Na⁺ conductance decreases rapidly as the channels close.

Phase 1: Initial Repolarisation

This phase is due to the activation and inactivation of a transient outward K⁺ channel (I *think* this is due to the transient outward rectifiers mentioned in my previous post, though unlike what I've said in my previous post, this is happening at a positive, not at a negative, membrane potential). This transient outward current is also known as I_to. As positive charges are let out of the cell, the membrane potential drops slightly, but this is short-lived due to the rapid inactivation of the channels.

Phase 2: Plateau Phase

This phase is due to L-type (long-acting type) Ca²⁺ channels. These open slowly and close slowly, allowing Ca²⁺ to enter the cell briefly and maintain the positive membrane potential.

Phase 3: Final Repolarisation

This phase is due to delayed rectifier K⁺ channels, which, as I mentioned in my last post, are delayed in opening and allow K⁺ to exit (thus lowering the membrane potential).

Phase 4: Resting Membrane Potential

Finally, we have the action of inward rectifier K⁺ channels, which, as also mentioned in my last post, prevent excessive loss of K⁺. This current is also known as I_KI.

Ionic composition of the slow action potential

I'm going to go through this like I did for the fast action potential: first a graph, and then an explanation of each phase. This will be quicker, however, as the slow AP doesn't have phase 1 or 2.

Phase 0: Upstroke

Unlike in fast APs, Na⁺ is not involved in the slow AP. Instead, this phase is due to slow opening of L-type Ca²⁺ channels.

Phase 3: Repolarisation

Ca²⁺ channels close during this phase. Additionally, the outward potassium current increases during this time.

Phase 4: Max Diastolic Potential

During this phase, the cell has a lower conductance to K⁺ and a higher conductance to Na⁺. This results in a reduction in potassium current and/or a steady inward current of Na⁺. This inward current is also called I_h for some reason. Later on, Ca²⁺ conductance increases. This current is also known as I_Ca(T).

Refractory Periods

Just like other action potentials, the fast and slow action potentials of the heart also have refractory periods. There are two main types of refractory period: the early refractory period (ERP) and relative refractory period (RRP). During the early refractory period, between phase 0 and 3, another stimulus will not be able to set off another action potential. If, however, another stimulus comes along during the RRP, which immediately follows the ERP, early firing of the action potential may result.

Extrinsic influences on fast and slow action potentials

The autonomic system is one of the main extrinsic influences on action potentials. Sympathetic activity increases automaticity in pacemaker cells and contractility in contractile cells, whereas parasympathetic control decreases the rate of firing and conduction velocity. The sympathetic and parasympathetic systems also antagonise each other.

Whew! I find the fast and slow APs a little bit confusing, so hopefully I haven't confused you too much!