The Cardiovascular System, Rhythmic Excitation of the Heart

The atria contract 1/6th of a second before the ventricles.

Specialised excitatory and conductive system of the Heart.
SA node - Sinus node or sinoatrial node, initiates the cardiac impulse
Internodal pathway - SA to AV node
AV node - delays impulse from the atria to the ventricles
AV bundle - conducts from AV node to the ventricles
Purkinje Fibers - conducts impulses to all parts of the ventricles.

The Sinus Node controls the heart rate: The membrane potential of sinus node is -55 to -60 mV
The heart rate is caused by:

• The fast sodium channels are inactivated at the normal resting potential, but there is slow leakage of sodium in the fiber.
• Between action potentials the resting potential gradually increases because of slow leakage sodium until the potential reaches -40mV
• At this time, the calcium-sodium channels become activated, allowing rapid entry of sodium and calcium and thus causing the action potential. 
• Greatly increased numbers of potassium channels open, allowing potassium to escape from the cells, within about 100 to 150 ms after the calcium-sodium open. This returns the membrane potential to its resting potential, and the self excitation cycle starts again with sodium leaking slowly into the sinus node fibers.

The Internodal and interatrial pathways transmit impulses in the atrium. 

There are three internodal pathways - the anterior, the middle and the posterior internodal pathway - that carry impulses from the SA node to the AV node. Small bundles of atrial muscle fibers transmit impulses more rapidly than the normal atrial muscle -like the anterior interatrial band, conducts impulses from the right atrium to the anterior part of the left atrium.

The AV node delays impulses from the atria to the ventricles.  This delayed time allows the atria to empty into the ventricles before ventricular contraction. The delay in the AV node is achieved by slow conduction: (1) membrane potential is much less negative in the AV node and the bundle than in the normal cardiac muscle. (2) few gap junctions exist between the cells in the AV node and the bundle, so that resistance to ion flow is great.

The transmission of impulses through the Purkinje system and the cardiac muscle is rapid. 

The action potentials travel at a velocity of 1,5 to 4,0 m/s, which is 6x the velocity of cardiac muscle.

The high permeability of the gap junctions at the intercalated discs between the Purkinje fiber cells likely causes the high velocity of transmission. 

The atrial and ventricular syncytia are separate and insulated from one another. 

Separated by a fibrous barrier that acts as an insulator - forcing atrial impulses to enter through the AV bundle.

The transmission of impulses through cardiac muscle travel at a velocity of 0.3 to 0.5 m/s. Travel from the endocardium to the epicardium in 0.03ms. 

Control of excitation and conduction in the Heart.

The sinus node is the normal pacemaker of the heart. The intrinsic discharge rate for the SA node, 70-80bpm, AV-node 40-60bpm, Purkinje system 15-40bpm.

An ectopic pacemaker may  develop a rhythmic rate faster than the SA node - the most common location would be in the AV node or the AV bundle.

  

AV block occurs when impulses fail to pass from the aorta to the ventricles.  After a sudden block, the purkinje fibers do not emit rhythmic impulses for 5 to 30 seconds because it has been overidden by the sinus rhythm. During this time the ventricles fail to contract, and person may faint because of the lack of cerebral perfusion. This is known as the STOKES-ADAMS SYNDROME.

Control of Heart Rhythmicity and Conduction by the Cardiac Nerves: Sympathetic and Parasympathetic. 

Parasympathetic (vagal) stimulation slows the cardiac rhythm - through acetylcholine release causes:

1. The rate of sinus node discharge decrease
2. The excitability of the fibers between the atrial muscle and the AV node to decrease.

The heart rate can decrease to half normal, but strong vagal stimulation can temporarily stop the heartbeat. The purkinje fibers then develop their own rhythmicity at 15 to 40 bpm. This is called ventricular escape. 

The mechanism of vagal effects on the heart are as follows:

1. Acetylcholine increases the permeability of the sinus node and the AV fibers to potassium; this causes hyperpolarization of these tissues and makes them less excitable.
2. The membrane potential of the Sinus Node fibers decrease from -55 to 60mV to -65 to -75mV.

The normal upward drift in the membrane potential is caused by sodium leakage in these tissues requires a much longer time to reach self-excitation.

Sympathetic Stimulation increases cardiac rhythm.

The rate of Sinus Node discharge increases

The cardiac impulse conductance rate increases in all parts of the heart

The force of contraction increases in both atrial and ventricular muscle.

Sympathetic stimulation releases norepinephrine - increasing the permeability to sodium and calcium, increasing the resting membrane potential and makes the heart more excitable, and therefore increasing the heart rate.

The greater calcium permeability increases the force of contraction of cardiac muscle.