Physiology 3120 Lecture Notes - Lecture 34: Atrioventricular Node, Vagus Nerve, Sinoatrial Node
2 May 2018
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Human Physiology Lecture 34
Mechanical Performance of the Heart
Mechanical performance of the heart: Cardiac Output
- Note: CO IS MATCHED TO THE OXYGEN DEMANDS OF THE BODY
o The more active you are, the more oxygen you need = increased CO
Mechanical performance of the heart: Control CO by changing HR
- Changing HR is all about the input from the ANS
- HR primarily controlled by ANS
o PNS (vagus) nerves are distributed mainly to SA and AV nodes and have an small (indirect?)
effect on ventricular muscle.
▪ Decrease HR, SV
▪ Little input to cardiac contractile cells (slight impact on ventricular muscles)
o SNS nerves are distributed to SA and AV node with a strong input to ventricular muscle
▪ Increase HR
▪ Strong input to ventricular muscle – CHANGE IN FORCE OF CONTRACTION
- Note: all about changing the pre-potential of the SA nodal action potential
Changing Heart Rate:
Effects of PNS (Vagal) stimulation
1. Decreases HR (negative chronotropic response)
– By decreasing SA node activity
– Chronotropic = heart rate
2. Decreases AP conduction through AV node
o Need to slow down the propagation of the AP through the AV node
o Function of the AV node is to slow down the AP so that the atria finish contracting before the
ventricles do (prevent them from contracting at the same time)
o Slowing it down even FURTHER
3. Decreases force of contraction slightly (negative inotropic effect)
Mechanisms of PNS effects:
- Ach (released by the cholinergic binds to muscarinic (M2) receptors
o Increases K+ permeability of the SA nodal cells hyperpolarizes cells
▪ Potassium is going to leave the cell, taking positive charge with it
▪ Instead of repolarizing back to -60mV, it will repolarize to -70mV
▪ Starting at a more hyperpolarized level
o Decrease in Ca++ permeability (and possibly Na+)
▪ Slow opening of the L-type Ca++ channels
▪ Instead of having a lot of Ca++ come in, and slow build of K+, you have less Ca++
coming in and more K+ allowed to leave the cell
▪ Slower build up of positive charge inside the cell during the pacemaker potential
traversal may be decreased by closing some funny Na+ channels
▪ Impact on Na+ conductance is con
o With more K+ leaving and less Ca++ entering SA node cells decreases slope of pre-
potential
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o = HYPERPOLARIZATION OF MEMBRANE + DECREASE SLOPE OF PRE POTENTIAL
▪ Take longer to reach threshold, decreasing HR
- Starting at a lower level (hyperpolarizing membrane) & the slope of pre-potential is decreased
- Once you hit threshold, you fire a normal AP
o T type channels close
o L type channels open
- But the whole idea is that you’re taking longer to reach threshold, causing (R to slow down
- The above changes also decrease AP conduction through AV node
o Similar changes
o )f you’re slowing down (R, you have to slow down AP propogation through the AV node
- Remember:
o Threshold = -40mV
o Membrane potential repolarize to -60mV
o Slow spontaneous depolarization is caused by increased permeability of SA nodal cell to
sodium & calcium
▪ Leaking in through leak channel – sodium through funny, calcium through T type,
some through L-type
▪ Building up the slow positive charge
▪ Have decrease of permeability to potassium
Effects of sympathetic stimulation:
1. Increase in heart rate (positive chronotropic response)
2. Increases AP conduction rate through AV node
3. Increase force of cardiac contraction (positive inotropic response)
- NOTE: maximal stimulation of the SNS can triple heart rate and double the force of contraction
Mechanism of sympathetic effects:
- Norepinephrine (released by sympathetic nerve endings) binds to β1 adrenergic receptors
o Na+ (funny channels) permeability
▪ Opening more of the funny channels
▪ Funny channels allow sodium to come through & are partially responsible for
creating the pre-potential
o Ca++ permeability
▪ Opening up T-type (transient) AND L-type calcium channels during pre-potential
▪ Increase the opening of the slow L-type Ca++ channels
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- Increase the rate of depolarization of the pre potential– faster build up of positive charge, increasing
the slope of the pre-potential
o Reach threshold faster, and fire AP faster = increased HR
- In the AV node, increase in sodium and calcium permeability would make it easier for each fiber to
excite the succeeding fiber thereby decreasing conduction time between atria and ventricles
- In atrial and ventricular contractile cells, the increase in calcium permeability would increase
calcium influx and consequently increase the force of contraction
- The rest of the AP once you have reached threshold is the same
- NOT changing the level of repolarization
o Will repolarize back to -60mV
o This is because you have NOT changed the membranes permeability to potassium
o Repolarization is all about potassium leaving the cell
- S-A node: Na+ and Ca++ permeability increases slope of pre-potential
- A-V node: Na+ and Ca++ permeability
o Decreasing conduction time between atria and ventricles
o Increase the conduction speed!
- Want to INCREASE the slope of the pre-potential
Overall Control of Heart Rate
- CO output is matched to the O2 demands of the body
- For heart rates < 100 bpm activate PNS
o At rest (70 bpm), there is always PNS activity: Vagal Tone
▪ PNS activity is ALWAYS going to the heart
▪ Always tonic activity in the vagus nerve keeping the HR low when at rest
o The more you activate PNS, the lower the HR
o Low oxygen demands, you will have low HR
- For heart rates = 100 bpm no PNS, no SNS
o (eart’s own intrinsic rate (set by SA node)
▪ Rate at which the SA node wants to fire at
o NO ACTIVITY GOING TO HEART – removed all autonomic activity to the heart
▪ HR automatically goes to 100 beats per minute
- For heart rates > 100 bpm activate SNS
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find more resources at oneclass.com
Document Summary
Note: co is matched to the oxygen demands of the body: the more active you are, the more oxygen you need = increased co. Mechanical performance of the heart: control co by changing hr. Changing hr is all about the input from the ans. Strong input to ventricular muscle change in force of contraction. Note: all about changing the pre-potential of the sa nodal action potential. Effects of pns (vagal) stimulation: decreases hr (negative chronotropic response) Ach (released by the cholinergic binds to muscarinic (m2) receptors. Increases k+ permeability of the sa nodal cells hyperpolarizes cells: potassium is going to leave the cell, taking positive charge with it. Instead of repolarizing back to -60mv, it will repolarize to -70mv. Starting at a more hyperpolarized level: decrease in ca++ permeability (and possibly na+) Instead of having a lot of ca++ come in, and slow build of k+, you have less ca++ coming in and more k+ allowed to leave the cell.
