ANS applied physiology Flashcards
Where do the preganglionic SNS neurons arise from?
Lateral horn of the spinal cord
Describe the course of these pre-ganglionic SNS fibres
Descend 1 - 2 sebments within the spinal cord before emerge along with the posterior segmental roots. They then synapse in the ganglia of the paravertebral sympathetic chain to give rise to LONG post-ganglionic neurons
As the SNS is ‘thoracolumbar’ how is the head and neck supplied with
The cervical (stellate) ganglia:
Superior
Middle
Inferior
Formed from preganglionic fibers emerging from the first 3 thoracic segments
What anatomical course do sympathetic fibres usually follow
the arterial blood supply to these organs
Describe the structure and function of the Adrenal medulla
It is a specialized sympathetic ganglion in which post-ganglionic cells are modified into secretory cells rather than nerve fibres –> consequently the output of this gland is neuronal rather than neural:
Noradrenalin ± 70 %
Adrenalin ± 29 %
Dopamine ± 1 %
From which cranial nerves does parasympathetic cranial (craniosacral) outflow occur
3, 7, 9, 10
Where are PSNS ganglia found and how does the length of preganglionic PSNS fibers compare to postganglionic PSNS fibres
Ganglia are near target organs and as such pre-ganglionic neurons are significantly longer than PSNS postganglionic neurons
Where is ACh the neurotransmitter in the ANS and PNS
- All ANS ganglia (including adrenal medulla)
- All PSNS post ganglionic nerve endings
- At 2 places in the SNS
- –> Apocrine sweat glands
- –> Vasodilation in blood vessels of skeletal muscle
PNS –> Dominant neurotransmitter in the motor system including the neuromuscular junction
Summarize basic function, distribution of the adrenergic receptors
alpha 1 - arteriolar smooth muscle + –> VC
alpha 2 - Pre-synaptic + –> - SNS
beta 1 - heart + inotropy and chronotropy
beta 2 - lungs + bronchodilation and reduce secretions
Describe the redistribution of blood flow consequent to the ‘fight or flight response’
Redistribution of blood flow to “fight or flight” organs with sustained perfusion of the brain.
Blood diverted away from skin/liver/GIT/kidney via alpha adrenergic vasoconstriction
Blood diverted toward heart, muscle, lungs, brain via Beta beta adrenergic and vasodilation (muscarinic in muscle)
Describe the overall organization of the ANS
PSNS (Craniosacral)
- CN 3,7,9,10 innervate 4 PSNS ganlgia in the head and neck. Ciliary (Eye), Sphenopalatine (lacrimal), Submandibular (Submaxillary and sublingual glands), Otic (parotid glands)
- The Vagus nerve then supplies the vocal chords to the colon
- The pelvic nerve supplies the colon/rectum/bladder/sex organs
SNS
The sympathetic chain runs paravertebrally
T1 - T4
Supply head and neck:
3 cervical ganglion (Supplied from T1 - T#3): Superior/middle and inferior supply SNS to head and neck. These nerves follow the course of the carotid artery and its branches.
Also supply heart/lungs
T5 - T12 via the Greater and small splanchnic nerves –> supplies stomach to sex organs via three ganglia: Celiac, Superior mesenteric, inferior mesenteric ganglion
Summarize the organization of the ANS
PSNS
- 4 ganglia in the head
- CN 3,7,9,
- Vagus: Subglottic to colon
- Pelvic: Colon to sex organs
SNS
- 3 ganglia in the neck
- 3 ganglia in the abdomen: greater/small splanchnic nerves also here
- No ganglion for thoracic structures
- T1 - T4: Head to Lungs
- T4 - T12: Stomach to sex organs
SNS effects on pulmonary vasculature
pulmonary vessel constriction
Does the PSNS effect force of contraction in the heart
Yes
What is the heart rate of transplant patients and why?
± 110
Vagal nerve transected
Explanation
Adults: PSNS dominates –> Resting heart rate 70 - 80 bpm
Kids: SNS dominates –> HR ± 100
What pharmacological strategies are available to stimulate parasympathetic activity - name the agents and their clinical use
Muscarinic agonists - Ophthalmology: Constrict pupil, opening flow to aqueous humor and decreasing IOP.
- Pilocarpine
- Carbacol
- Methacholine
Anticholinesterase - Anaesthetics and myasthenia gravis
- Increase Ach available at M receptors and at NMJ
- Neostigmine
- Pyridostigmine (myasthenia)
- Organophosphates
What pharmacological strategies are available to inhibit parasympathetic activity. Name the drugs and differentiate between them
Muscarinic antagonists - from the plant Atropa belladonna (Deadly nightshade)
- Atropine - crosses BBB with central effects (confusion in elderly)
- Glycopyrrolate - does not cross BBB
- Hyoscine - used for GI and HPB colic
- Homatropine
Describe the effects of antimuscarinic drugs on the CNS, CVS, RSP and GIT
CNS - atropine is a mild stimulant and can cause confusion in the elderly
CVS - Tachycardia - vagus blocked allowing unopposed SNS. IF brady due to hypoxia - no tachycardia
RSP - Bronchodilatation and reduces secretions
GIT - Anti-sialogogue. Reduced gastrin secretion. Reduced secretions. GI motility is reduced not abolished.
Describe the mechanism of action of adrenalin and noradrenalin at different doses
Adrenalin
Low doses: beta effects (initial decrease SVR)
High doses: alpha effects increase with increasing dose
Noradrenalin
Predominant alpha 1 effects with some beta effects all doses
Describe the mechanism of action of dopamine and dobutamine at different doses
Dopamine and dobutamine
Low doses: Stimulate dopamine receptors
High doses: Stimulate adrenergic receptors
Dopamine (similar to adrenalin)
Low dose: Beta 2
High dose: Alpha 1
Dobutamine
Beta 1 (minimal beta 2 and alpha 1 with slight decrease SVR)
–> shift of perfusion from GIT to heart and skeletal muscle but with overall improved splanchnic perfusion
What is the mechanism of action, dose, onset and duration of Ephedrine?
Dual mechanism of action
- Release NA of endogenous noradrenaline from sympathetic terminals
- Direct effect on alpha and beta receptors
Dose: 2.5 - 10 mg titrated to BP
Onset: 1 minute
Duration: 1 hour
What are the receptor specific adrenegic receptor agonists? What is their mechanism dose, onset, duration of action
Phenylephrine
Alpha 1 agonist –> increase SVR
Dose: 50 - 100ug per dose titrated to BP
Explain how to use a paediatric infusion set to estimate infusion rate
Dimensional analysis
60 drops/ml
_________
1 drop/second
= 60 s/ml
= 60s/ml x 1 min/60s
= 1 min/ml
AND
60 drops/ml
_________
2 drop/s
= 30s/ml
= 30s/ml x 1min/60s
= 1min/2ml
= 2ml/min
SO NUMBER OF DROPS PER SECOND = NUMBER of MLS PER MINUTE
What is the mechanism of action of clonidine and dexmedetomidine?
Clonidine
- alpha 2 predominant
- also alpha 1
Dexmedetomidine (more specific for alpha 2)
- alpha 2 (8 x more selective than clonidine)
Stimulation of alpha 2 receptors
- -> Sedation (central alpha 2 effects)
- -> Anxiolytic
- -> Analgaesia without respiratory depression
- -> Decrease SVR
What is the Richmond Agitation Sedation Score
+4 Violent
+3 Aggressive (pulls tubes/catheters)
+2 Agitated (frequent movements/fights vent)
+1 Restless (anxious but movement not vigorous)
0 Alert and calm
- 1 Drowsy: eyes open with contact to voice >10s
- 2 Light sedation: eye open with contact to voice < 10s
- 3 Mod sedation: eye open to voice
- 4 Deep sedation: eye open to physical stimulation
-5 Unarousable: No response to voice or physical
Give examples of selective beta 2 receptor agonist and their use
Asthma
Salbutamol
Terbutaline
Fenoterol
Give examples of the selective alpha 1 blockers and their use
Phenoxybenzamine
- Great for phaeochromocytoma as the drugs binds covalently to alpha receptor which destroys the receptor
- Non-competitive alpha 1 antagonist
Prazosin
- alpha 1 antagonist - t1/2 short –> requires QID dosing
Doxazosin
- Longer half life
- Used as antihypertensive and preop in phaeo.
What is the only available parenteral beta blocker readily available in RSA
Labetalol
What is the mechanism of action of labetalol
10 X greater affinity for beta receptors than alpha receptors but does block both types of receptor
How does the dosing of beta blockers differ depending on oral vs intravenous administration and why is this the case
Beta blockers have high first pass metabolism
IV doses are therefore significantly lower than oral doses
What is the major disadvantage of non-selective Beta antagonists
Beta antagonism in the lungs –> increasing airway resistance in asthmatics
Describe the metabolic effects of beta bolckers
- Inhibit lipolysis
2. Inhibit gluconeogenesis (risk of hypoglycaemia)
