Cardiac Muscle

This post will be discussing our next topic in the Muscle section of Veterinary Physiology 1- cardiac muscle.

Structure: 

There are 3 types of cardiac muscle cells:

1. Pacemaker Cells: Found mainly in the Sinoatrial (SA) and Atrioventricular (AV) nodes. They initiate Action Potentials (APs) by generating pacemaker potentials.  They initiate contraction and set the heart rate.
2.   Conduction Fibres: this includes the Bundle of His and Purkinje fibres. They are large diameter muscle fibres and are specialised for rapid AP conduction. (4 m/sec vs. 0.5m/sec in myocardial cells).
3. Myocardial Cells: These cells generate force and are the majority of muscle cells.

Myocardial cells have a single nucleus and have a striated appearance. The cells branch out from each other and are coupled by gap junctions at intercalated disks. They also have a specialised T-tubule and Sarcoplasmic Reticulum (SR) system.

Spread of Electrical Activity in the Heart

 This involves several steps as outlined below:

1. Depolarisation initiated at SA node
2. Depolarisation spreads through atria
3. AV nodal delay (0.1sec)
4. Depolarisation travels down bundle of His
5. Depolarisation spreads through septum
6. Depolarisation spreads through bulk of ventricles (inside out)
7. Depolarisation spreads through base of left ventricle
8. Depolarisation spreads through ventricles (outside-in)

This website has a really cool animation which shows this process, it also has a useful diagram about the anatomy of the heart. 

Excitation

The trigger for contraction of the heart is myocardial cell AP firing. The trigger for myocardial AP firing is pacemaker cell AP firing. The control of cardiac muscle is myogenic, that is the signal for contraction arises within the heart muscle. This is in contrast with skeletal muscle which is neurogenic, contraction of the muscle is controlled by motor neurons.  


Pacemaker Cells:
 
Pacemaker cells generate APs spontaneously without external stimulation. This is because the resting membrane potential (RMP) slowly depolarises to threshold which then triggers an AP. This slow, spontaneous depolarisation to threshold is known as the pacemaker potential.Four steps occur during the firing of a pacemaker AP:

1. 'Funny" Na+ channels open causing Na+ influx. K+ channels close
2. Funny channels close. Voltage gated T-Type (transient type) Ca 2+ channels open causing a Ca 2+ influx. 
3. Voltage-gated L-Type (long lasting type) Ca 2+ channels open causing Ca 2+ influx. 
4.  Voltage gated K+ channels open causing a K+ efflux. L-type Ca2+ channels close. 

Below is an excellent video which explains this process really well.

Myocardial Cells:


Myocardial cells exhibit no pacemaker activity and depolarisation spreads from pacemaker cells or other myocardial cells. Myocardial cells have a very long AP with a very long refractory period. This is important because it prevents tetanus of the heart muscle (prolonged contraction caused by rapidly repeated stimuli). 5 events occur during the firing of an AP by a myocardial cell:

1.  Voltage gated Na+ channels open, leading to a Na+ influx
2. Na+ channels inactivate, stopping the Na+ influx, this causes a slight repolarisation
3. L-type Ca2+ channels open, this causes Ca2+ influx to occur which results in sustained depolarisation. 
4.  Voltage gated K+ channels open (this is triggered in step 3 but they open slowly), causing K+ efflux leading to repolarisation.

Below is another video which explains this process well. 

Excitation-Contraction Coupling


Cardiac muscle cells exhibit slower contraction than skeletal muscle but contraction which is faster than smooth muscle. Like in smooth muscle, excitation spreads from adjacent cells via gap junctions, extracellular Ca2+ entry is also required. Cardiac muscle requires action potential firing, contraction also involves Ca2+ binding to troponin to expose myosin binding sites on actin molecules, like skeletal muscle. 6 steps are involved in excitation contraction coupling in cardiac muscle cells:

1. current spreads to myocardial cells via gap junctions
2. AP travels along plasma membrane and down T-tubules
3. Voltage gated Ca2+ channels open causing Ca2+ entry
4. Ca2+-induced Ca2+ release from SR via ryanodine receptors
5. Ca2+ binds to troponin which exposes myosin binding sites on actin
6. Crossbridge cycling (contraction) occurs. 

Relaxation

 Relaxation requires the removal of Ca2+ from the cytosol (this is like skeletal and smooth muscle). Ca2+ is actively transported back into the SR, this occurs through active transport and Na+/Ca2+ exchange mechanisms. Relaxation can be summarised as follows:

1. Ca2+ dissociates from troponin
2. Ca2+ pumped into SR and Ca2+ transported out of cell by Ca2+/Na+ exchanger. This is driven by the Na+ concentration gradient maintained by the Na/K ATPase pump. 

The Effect of Digitalis on Cardiac Muscle Cells 

Digitalis is a poison which blocks the Na/K ATPase pump in muscle cells. This causes the intracellular build up of Na+ which reduces the activity of the Na/Ca exchanger. This results in intracellular build up of Ca2+ which leads to an increased force in heart muscle contraction.  



That's it for this post, if you have any questions please feel free to ask in the comments section below :)