Transcript Anatomy, physiology and pharmacology of the autonomic

Anatomy, physiology and
pharmacology of the
autonomic supply of the
heart
The Medulla control centre
• The medulla is the primary site in the brain for regulating
sympathetic and parasympathetic (vagal) outflow to the
heart and blood vessels.
• The nucleus tractus solitarius of the medulla
receives sensory input from different baroreceptors and
chemoreceptors in the circulation.
• The medulla also receives information from other brain
regions (e.g., hypothalamus). The hypothalamus and
higher centres modify the activity of the medullary
centres and are particularly important in stimulating
cardiovascular responses to emotion and stress (e.g.,
exercise, thermal stress).
The flow of Autonomic cardiac Qi
SNS innervation of the heart
• Preganglionic neurons of the sympathetic
division of the heart originate in the spinal
cord and emerge in the spinal nerves at
the levels of T-1 through to T-5, then
leave the sympathetic chain as post
ganglionic neurons travelling to the
cardiac plexus.
SNS innervation of the heart
• Sympathetic efferents are more diffuse
their parasympathetic counterparts,
being present throughout the atria
(especially in the SA node, but also the AV
node) and ventricles, including the
conduction system of the heart.
Sympathetic nerve endings release Noradrenaline.
SNS innervation of the heart
Obviously, the SNS is stimulated in flight, fight and
fright, but cardiac function is also altered by SNS
affects on neural activation. When you’re awake:
• HR increases (positive chronotropy)
• Force of contraction increases (positive
inotropy)
• AV nodal conduction velocity increases increased PR interval (positive dromotropy)
• Increased rate of myocyte relaxation
(positive lusitropy)
PNS innervation of the heart
PNS innervation of the heart
• Supplied by the right (primarily innervates the SA
node) and left vagus (left vagus innervates the AV
node) nerves (CN X) which provide cervical cardiac
nerves to the cardiac plexus.
• Unlike the sympathetic innervation, which must first
synapse within chain ganglia to supply the heart with
postsynaptic (postganglionic) fibres, the
parasympathetic fibres synapse at ganglia located
directly on the heart and short postsynaptic fibres
then supply the target organ.
• Atrial muscle is more innervated by vagal efferents
than the ventricular myocardium
PNS innervation of the heart
ACh released by vagus nerve binds to M2
muscarinic receptors producing:
• negative chronotropy
• Negative dromotropy
• negative inotropy
• Negative lusitropy
in the atria (the negative inotropic and lusitropic
effects of vagal stimulation are relatively weak in
the ventricles – since not much PNS
representation there).
Balance of Qi
Messing with autonomic
receptors
• Β-blockers (especially type 1 selective) will
antagonise β-adrenoceptors leading to slower
HR, negative inotropy, longer PR intervals etc (eg.
Metoprolol, Atenolol, Bisoprolol etc)  Used in
treatment of Angina, HTN, Heart failure, acute MI,
arrhythmias etc.
• Muscarinic anticholinergics (eg. Atropine) will
antagonise the muscarinic receptors responsible
for parasympathetic stimulation of the heart leading
to the brakes being removed from the heart,
resulting in an increase in HR, shorter PR interval
etc  used in severe bradycardia and conduction
block.
Something quirky
The autonomic nerve presynaptic terminals also
possess adrenergic and cholinergic receptors
that function to regulate the release of
Noradrenaline:
• Prejunctional α2-adrenoceptors inhibit
Noradrenaline release
• Prejunctional β2-adrenoceptors facilitate
noradrenaline release
• Prejunctional M2 receptors inhibit noradrenalin
release, which is one mechanism by which vagal
stimulation overrides sympathetic stimulation in
the heart.