Flashcards in Physiology - Excitation of the Heart Deck (23)
Excitatory System = ?
NOT = ?
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
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
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
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)
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