CVPP Week 5: Autonomic Nervous System

What spine levels are sympathetic fibers

T1-L2/L3

What spine levels are parasympathetics fibers

CN 3 7 9 10 and sacral plexus

Ultimate control of ANS is

Medulla oblongata

Sympathetic NS pre and post ganglionic axon lengths

Short pre-ganglionic

Long post-ganglionic

"Far from effector organ"

Parasympathetic NS pre and post ganglionic axon lengths

Long pre-ganglionic

Short post-ganglionic

"Close to effector"

Central control controlled by

CNS and PNS nerves

Local control is ____ and give 3 examples

Independent of nerves

1. Pacemaker potentials (SA node)

2. Heterometric autogeneration (starling's law)

3. Chemical secretions (NO, histamine, K+)

Two primary factors influencing local control

1. Hypoxia of tissues

2. Accumulation of cellular waste products (H+)

Other than central and local control, what is the last thing that controls circulation?

Hormones (epi/norepinephrine)

Where does sympathetic NS arise from

Reticular formation in brainstem

Sensory input and efferent output of sympathetic NS

Sensory input: goes to cerebral cortex and activates reticular formation

Efferent output: goes through thoraco-lumbar region and synapses

Parasympathetic NS arises from...

Dorsal medulla —> dorsal vagal nucleus

(Majority of parasymp activity is carried out by vagus nerve)

Autonomic NS controls what involuntary muscles and glands (3)

Cardiac muscle —> controls heart

Smooth muscle —> controls tunica media of vessels

Adrenal medulla—> release NT

T/F: generally, pattern of ANS is equal but opposite

True (but not in CV system!)

Does sympathetic or parasympathetic nerves control most of the blood vessels

Sympathetic

Where do blood vessels receive both symp and parasymp innervation from

Face, GI tract and external genitals

T/F: sympathetic nerves control the heart most of the time

False, its parasympathetic

Does parasympathetic nerves have direct influence over stroke volume?

No, only heart rate

What NT does somatic nervous system release

Acetylcholine

What NT does sympathetic nerve secrete

Norepinephrine

What NT does adrenal medulla secrete for sympathetic division

Epinephrine

What NT does parasympathetic divison secrete

Acetylcholine

Parasympathetic Right vagus nerve goes to....

SA node

Parasympathetic Left vague nerve goes to...

AV node

What does acetylcholine do when it's released from parasymp nerves

Increase K+ permeability —> decrease HR

What receptors do Ach act on in parasympathetic division

Muscarinic receptors

Where does sympathetic innervation go to

Both nodes and regular cardiac myocytes

What do sympathetic nerves release in the heart

Norepinephrine and epinephrine

What does Nor/epinephrine do to the heart when it is released

Increase Na and Ca permeability —> increase HR and SV

What receptors does Nor/epinephrine act on

Adrenergic receptors (sympathetic)

Sympathetic nerve release ______ to do what to blood vessels

Norepinephrine, Vasoconstriction

Adrenal medulla release _____ to do what do blood vessels

Epinephrine, Vasoconstriction

Parasympathetic nerves release ____ to activate _____ to do what to blood vessels

Release Ach to activate muscarinic receptors to cause vasodilation

Parasympathetic innervation of blood vessels to where they vasodilate happens where (3)

face, GI tract and external genitals

What're the two types of adrenergic receptors

Alpha

Beta

Where do we find alpha receptors

Blood vessels (vasoconstriction)

-mainly from norepinephrine

Where do we find beta receptors

Heart

Where to find Beta-1 receptors

Nodes —> increase HR

Myocardium —> increase in SV

Where to find Beta-2 receptors

Found in smooth muscle (coronary arteries and bronchioles)

When Beta-2 receptors are activated, what do they do to the smooth muscle?

Vasodilation from epinephrine

Norepinephrine bind to....

Alpha (tunica media) and Beta-1 (nodes and cardiac myocytes) receptors

Chronotropic effect =

Increase in HR (Beta-1)

Inotrophic effect

Contractility = increase in SV (Beta-1)

Epinephrine binds to...

Alpha (tunica media) and both Beta-1 (heart) and Beta-2 (coronary artery and bronchiole) receptors

Beta blockers are specific to which Beta receptor

Beta-1

What do beta blockers do

Block receptors so NT can't act on it

Slows down heart and reduce workload

For people with hypertention

Intrinsic rate of SA nose

60-100 BPM

Where is SA node located

Right atrium

AKA for SA node

Pacemaker

AV node is also known as...

SA node back up

Where is AV node located

Between atria and ventricles

Why is AV node slowest rate of conduction?

Give time for atria to fully contract to squeeze all of the blood into ventricle (but is second fastest at depolarizing!)

When threshold voltage is reached, cell depolarizes and what ions flow through voltage gated pores

Na flows in and K flows out of cell

T/F: Cardiac myocytes need a stimulus

False because SA node is pacemaker

Where is fastest leak of Na "funny" current

Fastest leak of Na is at SA node through hyperpolarization-activated cyclic nucleotide gated channels (HCN) = Na channels

Pacemaker potential AKA

Spontaneous diastolic depolarization

What is spontaneous diastolic depolarization

Leaky membranes that constantly leak Na and Ca into cell (funny current)

-mainly at SA node

Does spontaneous diastolic depolarization ever reach a stable membrane potential

No, spontaneous and slow decline in membrane potential during diastole causes it to not

What comes first in pacemaker potential: T-type or L-type Ca channels? And which one causes the upstroke

T-type opens first then L-type

-L-type causes upstroke (hella Ca in)

Do HCN channels open before Ca channels in pacemaker potentials?

Yes

HCN = hyper-polarization cyclic nucleotide gated channels

What happens in repolarization of pacemaker potential

HCN and Ca channels close and voltage gated K channels open so K goes out of cell

For regular cardiac muscle action potential look at graph on slide 22, better to study that then me trying to explain it

Where do you find pace maker potentials?

SA and AV node

Fast response myocytes AKA

Cardiac cells (not SA and AV node)

What does plateau phase and what does it do for myocytes

Caused by slow Ca channels and helps prevent fatigues (absolute refractory period)

What're the resting potentials for pacemaker potentials and myocytes

Pacemaker potentials = -60mV

Myocytes = -90mV

Where does stimulus start in our cardiac myocytes

SA node

EKG of heart

Av node is second fastest rate of depolarization but....

Slowest at conduction

-allows atria to squeeze all the blood into ventricle

Intercalated discs are also known as

Low resistance junctions

Conduction velocity def

The speed at which a cardiac action potential moves from one part of the heart to another

Based on size, the ____ the ____

Based on size, the bigger the faster

-Ex: AV node is the smallest so its the slowest

Norepinephrine (_____) and Epinephrine (______) = Increases permeability to _____ and _____ (FILL IN THE BLANK)

Norepinephrine (nerves) and Epinephrine (adrenal medulla) = Increases permeability to Na and Ca

-gets to threshold faster

Acetylcholine = _____ permeability to ______ (FILL IN THE BLANK)

Acetylcholine = Increases permeability to K

Adrenergic effect =

Increased HR and SV (sympathetic)

Cholinergic effect =

Decreased HR, no effect on SV (parasympathetic)

Length tension relationship

The more a muscle is stretched - to a point - the more tension it develops

Starling's law of the heart AKA (2)

Heterometric autoregulation and Frank/Starling mechanism

Ejection fraction equation

Stroke volume / EDV

- % of blood that leaves ventricles with each contraction

Normal EF vs Heart failure EF

Normal = 55-70%

Heart failure = less than 40%

Things that would increase EJ in normal heart (2)

1. Sympathetic activation = increase in SV

2. Increase in venous return —> increase EDV —> greater stretch (starling's) —> greater contraction (increase in SV)

In heart failure, the ____ in venous return ____ejection fraction

In heart failure, the increase in venous return decreases ejection fraction (heart too weak to create greater contraction)