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Excitatory System = ?
NOT = ?

Conducts impulses
Doesn't cause muscles to contract nor does it add to pressure


Sinus Node (SA Node)

Located in the superior posterolateral wall of the right atrium below the vena cava

Pacemaker of the heart - b/c it fires the fastest (does NOT need nerve cells to generate action potential)

Directly attach to atrial muscles causing an immediate spread of the signal

Sodium Leak Channels
Voltage-Gated L Type Calcium Channels
Voltage-Gated Potassium Channels

Cells fire at heart rate

Depolarization lasts longer than that of skeletal muscles (due to calcium) = no twitch BUT more continuous impulse

Moderate amount of gap junctions (comparatively)


SA Node Action Potential

1) RMP = -55 to -65 mV = unstable b/c leaks sodium (and to a lesser extent calcium) through open channels

Self-excitation due to leakage

2) Depolarization (Threshold of -40 mV reached) -
Voltage-gated L Type Calcium channels open and calcium rushes in

3) Repolarization - Voltage-gated L type calcium channels close and Voltage-gated potassium channels open and sodium rushes out of cell

4) Hyperpolarization - Potassium channels remain open past resting membrane potential = membrane potential becomes more negative; Potassium channels eventually close

5) Sodium (and to a lesser extent calcium) leak channels bring the RMP back to -55 to -65 mV


The Ends of the SA Nodal Cells fuse with...

Right Atrial Muscle - causing depolarization

Anterior Interatrial Band (Bachmann's Bundle) - Transmit the impulse to the left atrial muscle fibers

Internodal Pathways - Brings the signal to the AV Node


What controls the speed of cardial signal transduction?

Gap Junctions = increase the speed = no insulation between fibers of the same type

There is insulation between atrial and ventricular muscle = pauses at AV Node


What is caused by atrial contraction?



Atrio-Ventricular Node (AV Node)

Located in the posterior wall of the right atrium behind the tricuspid valve

Causes a delay of the passage of the impulse from atria to ventricles = allows for atria to contract (empty rest of blood) into ventricles before the ventricles contract

The signal is slowed down due to a decrease in the presence of gap junctions in the AV Node and the AV Bundle

Action potential is similar to that of the SA Node


AV Bundle

Only muscular connection between the atria and the ventricles

One way conduction = prevents reentry of cardiac impulses into the atria from the ventricles

Low amount of gap junctions = helps to slow down signal from the atria


What is the delay of cardiac impulse from the atria to the ventricles and why is it necessary?

0.16 seconds (time of travel to the AV Node, time of AV Node depolarization, and time of AV Bundle depolarization

It is necessary for the atria to contract to finish filling the ventricles with blood before the ventricles can contract


Purkinje Fibers

Lead from the AV Node to the AV Bundle to the Ventricles

The AV Bundle splits into the right and left bundle branches and then branches into smaller and smaller terminal fibers and loop up ventricle walls

Allows for almost immediate transmission of cardiac impulse through the ventricles (conduction velocity of 1.5-4 m/sec)

Lots of gap junctions

Also have few myofibrils = lots of signal transmission BUT very little contraction

Fibers fuse with Ventricular muscle fibers = conducted impulse from endocardium to epicardium


What does the ventricle action potential cause?



What would happen if the Atria and Ventricles were connected any where else besides the AV Bundle allowing for the impulse to go back to the atria from the ventricles?

Cardiac Arrhythmias, Atrial Fibrilation


Intrinsic Pacemaker Rate of Adult Canine Heart Tissue

How fast the parts of the heart fire on their own

SA Node the fastest (allows determination that it is the pacemaker of the heart)
AV Node after that
Then the Bundle Branches and the Purkinje Fibers
The Atrial and Ventricular Myocardium have not intrinsic heart rate

This tells us that if the SA Node becomes nonfunctional, other areas can cause contraction of heart muscles


Why is the SA Node vs the AV Node or the Purkinje Fibers the pacemaker of the heart?

The SA Node self-excites the fastest

The signal transmitted from the SA Node to the AV Node and eventually the Purkinje Fibers is faster than the speed of self-excitation of either of these structures...


What occurs if the SA Node becomes nonfunctional?

Sinus Arrest (dog) = the AV Node paces the heart = lower heart rate and disruption in the normal rhythms of the atria and the ventricles


What happens if the AV Node becomes nonfunctional?

3rd Degree Heartblock (dog) = the SA Node paces the atria and the Purkinje Fibers pace the ventricles = no coordination of contraction = need an artificial pacemaker


What happens if both the SA Node and the AV Node become nonfunctional?

Bundle Branches pace the heart = VERY low heart rate


What happens if the Purkinje Fibers become nonfunctional?

Non Synchronous ventricle muscle contraction = the overall pumping effect would be greatly decreased (decrease as much as 20-30%)

Can lead to fainting and death


Ectopic Pacemaker

A pacemaker other than the SA Node

Causes abnormal sequence of contraction of different areas of the heart causing significant debility of heart pumping

Can be caused by:
1) An abnormality in either the AV Node or the Purkinje Fibers causing an intrinsic heart rate faster than the SA Node = whichever has the faster rate takes over as the pacemeker
2) Rare situation = a place in the atrial or ventricle muscle develops excessive excitability and becomes the pace maker
3) Blockage of signal from the SA Node to the rest of the heart = AV Node usually becomes the pacemaker

If AV block occurs = SA Node controls atria contraction at a normal rate BUT ventricle contraction rate is abnormal and controlled by the Purkinje Fibers = new pacemaker
Slower Purkinje fiber signal transmission rate can cause fainting and death due to debilitated ventricle punping


The heart is supplied with both....

...Sympathetic and Parasympathetic Nerves


Parasympathetic Nerves in the Heart

Distributed mainly to the SA Node and the AV Node and to a lesser extent the muscle of the 2 atria (very little to ventricualr muscles)

Parasympathetic (Vagal) Stimulation:
Vagus nerve releases Acetylcholine (ACh) to activate muscarinic receptors (G-Protein Coupled Receptors = protein cascade) =
1) Slows the rate of contraction by increasing the permeability of potassium at the SA Node = hyperpolarization = takes a lot longer for the SA Node to self-excite and depolarize
2) Decrease the excitability of the AV Nodal Fibers (btwn the atrial musculature and the AV Node) = slows transmission of cardiac impulse

Slowing impulse to ventricular muscle too much = Purkinje Fibers = own pacemaker = Ventricular Escape


Sympathetic Nerves in the Heart

Distributed to all parts of the heart (strong in ventricle muscle)

Sympathetic Stimulation:
Opposite effects of vagal stimulation = Release of Norepinephrine = stimulate beta-adrenegic receptors = increase of permeability to to sodium and calcium ions:
1) Increases the rate of SA Node discharge through increased leakage = moves potential closer to threshold = increases heart rate
2) Increases the rate of conduction through the AV Node and AV Bundle = decreases conduction time between atria and ventricles
3) Increases the force of contraction of atria and ventricles = extracellular calcium ions play a role in the contraction of smooth muscles of the heart


Signal Transmission from SA Node to the Ventricles

The action potential from the SA Node spreads at a moderate speed through all of the right atrial muscle fibers and left atrial muscle fibers (through the interatrial band) immediately

Then to the AV Node through the Internodal Pathways = slows down the signal allowing for the ventricles to fill with blood from the atria before they contract

Then the signal travels to the AV Bundle = also slow transduction of the impulse

The signal is then transmitted through the Purkinje Fibers greatly speeding up the transmission.

The Purkinje fibers then fuse to the ventricular muscle fiber and the signal spreads from the endocardium to the epicardium

The ventricle muscles contract pushing blood out the pulmonary artery or the aorta
The conduction speed slows to moderate as the signal is transmitted through the ventricle muscle to the epicardium