Biomedical Engineering 403

More Autonomic Control of the Heart

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3
Autonomic Control of the Heart

Heart rate is controlled by the brain

Many HR responses are based on feedback from the periphery telling the
brain what is going on downstairs.
The NTS integrates sensory feedback with influences from higher brain
areas sends coordinated action plans to   Nucleus Ambiguus and Dorsal
Motor Nuc of Vagus, and spinal cord.

Most important to heart rate are baroreceptors

Baroreflexes
        Baroreceptors in aortic arch and carotid sinuses; relay info to
brain via 9th and 10th cranial nerves
        Actually respond to stretch rather than pressure, so burst with
each systole
        Increased BP slows HR and reduces BP

Chemoreflexes
        Chemoreceptors respond to hypoxia, hypercapnia, and acidosis of
blood.
        Located in carotid and aortic bodies (adjacent to carotid sinus
and aorta), relay info via 9th and 10th
        Excited by hypoxia or hypercapnia
        stimulate vagal centers, slowing HR, unless input from lung
stretch receptors shows enhanced respiration,               which
increases HR.

Lung Stretch Receptors cause tachycardia
        Important in asphyxia and respiratory sinus arrhythmia

Muscle receptors--muscle activity causes tachycardia (forebrain also
involved in exercise response)

Somatic Pain causes tachycardia
Visceral Pain causes bradycardia
Distention of the bladder causes reflex tachycardia

Respiratory sinus arrhythmia
        HR accelerates during inspiration, decelerates during expiration
        Increased vagal activity during expiration
        Symp activity is increased during inspiration, but released NE is
removed slowly damping out rhythmic           effects--So RSA is due
almost entirely to oscillations in vagal activity and proportionate to
vagal             tone
        Caused by central input from respiratory centers and baroreflexes
due to change in thoracic pressure

Slower HRV--largely sympathetic, thermoregulatory

Diving Response--caused by cold water touching trigeminal receptors of
face.  Heart rate falls due to vagal inhibition  of pacemakers.  More
pronounced in diving animals, and in combination with peripheral
vasoconstriction,         allow diving mammals to stay submerged up to 2
hours.


Medulla--
NTS contains first synapse for all afferents (baroreceptors,
chemoreceptors, lung stretch receptors, muscle work        receptors).
Relays info to Nuc Ambig and Dorsal Motor nuleus to slow heart, and to
ventrolateral medulla,      which contains symp preganglionic neurons.
Cortex--
Motor areas relay exercise info, which contributes to exercise-dependent
tachycardia
Emotional states, sexual stimulation, attention, etc. affect heart rate
via forebrain

Hypothalamus--
Is responsible for organized autonomic responses to emotional states
Depressor Area recieves input from NTS activates cardial vagal fibers
causing HR slowing
Defence Area stimulated by amygdala causes tachycardia by inhibiting
baroreceptor traffic to NTS

Cardiac muscle contracts in basically the same way as skeletal muscle.

Control of myocardial performance--Sympathetic
        NE interacts with beta-adrenergic receptors on cardiac cell
membranes;  this reaction activates adenylyl                cyclase, which
raises intracellular levels of cAMP, activating protein kinases that
phosphorylate               proteins  that activate calcium channels in
myocardial cell membranes--This increases Ca++ influx               during
action potential plateau and more calcium is released from sarcoplasmic
reticulum in             response to each cardiac excitation, increasing
contractile strength
        Sympathetic activity enhances atrial and ventricular contractility
(particularly via left stellate nerves)

Control of myocardial performance--Parasympathetic
        Vagus inhibits atrial myocardium (and to a lesser extent
ventricular myocardium) and, AV conduction tissue
        ACh  from vagal endings interacts with muscarinic receptors in
cardiac cell membranes, inhibiting adenylyl              cyclase, hence
decreasing myocardial contractility
        ACh from vagal endings also inhibits release of NE from
neighboring sympathetic terminals
        Conversely sympathetic nerves inhibit release of ACh from
neighboring vagal fibers (via activity of NE and              neuropeptide
Y)

No!
Please don't make me go to any of those pages!
I want to go somewhere completely different!