1. AUTONOMIC NERVOUS SYSTEM
(PHYSIOLOGY)
- Anatomy
- Physiology
- Tests for autonomic integrity.
- Anaesthesia and ANS physiology
1. General 2. Regional.
- Autonomic reflexes during anaesthesia and surgery
- Autonomic nervous system dysfunction
- Anaesthesia in Patients with ANS dysfunction
- Autonomic nervous system in intensive care
- Autonomic nervous system and chronic pain.
3. 1. The ANS is organized on the basis of the reflex arc
impulses initiated in visceral receptors are relayed via
afferent autonomic pathways to the CNS, integrated with in
it at various levels of and transmitted via efferent pathways
to visceral effectors.
2. The ANS is activated mainly by centers located in spinal
cord, hypothalamus, brainstem and portion of cerebral
cortex (limbic cortex)
3. ANS includes
- Sympathetic nervous system
- Parasympathetic nervous system
- Enteric nervous system.
4.
5. SYMPATHETIC NERVOUS SYSTEM
It orginates from spinal cord in the thoracolumbar region
(T1 to L3). It Composed of two neurons – pre ganglionic and post
ganglionic.
The preganglionic fibres originate from the intermediolateral
horn of the spinal cord and its fibres pases through the anterior root
of the cord into the corresponding spinal nerve. Immediately after the
spinal nerve leaves the spinal cord the preganglionis sympathetic
fibres leaves the nerve and pass through the white ramus into three
types of ganglia –
I. Paired sympathetic chains having 22 paired ganglia
which lie along either side of vertebral column. The segmental
distribution - T1 – head region
T2 – neck
T3 – T6 – in the thorax
T7 – T11 – in the abdomen
T12 – L2 – in the legs
6. II. Unpaired prevertebral ganglia reside in the aldomen and
pelns antirior to vertebral column and they are
a. Celiac – innervated by T5 – T12 and innervates liver,
spleen, kidney pancreas, small bowel and proximal colon.
b. Superior mesentric ganglia – innervates distal colon
c. Inferior mesentric ganglia – innervates rectum, bladder
and genitals.
III. Terminal or collateral ganglia – present near target organ, are
small and few in number. Adrenal medulla and other
chromaffin tissue are of these type. The preganglionic fibres
without synapsing pass directly into adrenal medulla and end
on modified neuronal cells that secrete epinephrine and
norepinephrine.
7. PARASYMPATHETIC NERVOUS SYSTEM
It arises from III, VII, IX and X cranial nerves; second and
third sacral segments and occasionally first and fourth
sacral segment. Almost 75% of parasympathetic flow is
from vagus.
Preganglionic fibres arising from
1. Edinger – westphal nucleus of oculomotor nerve
2. Medulla oblongata – i. Facial nerve
ii. Glassophargngeal nerve
iii. Vagus nerve
3. Sacral segments – Pelvic nerve
8. ENTERIC NERVOUS SYSTEM
Found within the walls of G.I.T., pancreas and gall
bladder this system is having high degree of local autonomy in
digestion and peristalsis.
Contain
The submucous plexus – Control of exocrince and
endocrine secretion by cells on G.I.T.
Myentric plexus – Control of peristaltic activity
9. PHYSIOLOGY
1. Most of the organs exhibit dual innervations with
sympathetic and parasympathetic system frequently
mediating opposing effects.
2. One of the two systems normally dominates the organs
function providing the resting tone.
3. In a few organs the sympathetic system alone provides
innervations to certain, blood vessel, spleen, piloerector
muscles adrenal medulla and uterus while glands of
stomach and pancreas receive only parasympathetic nerve
supply.
10. Sympathetic nervous system is concerned with often wide
spread fight or flight response to the stress
The parasympathetic deals with more discrete
adjustments of relaxed homeostasis.
11. NEUROTRANSMITTERS
Acetylcholine, nor epinephrine, epinephrine
All preganglionic neurons and post ganglionic parasympathetic
neurons secrete acetylcholine
2% of post ganglionic sympatnetic secreted acetylcholine
These neurons are termed cholingeric
98% of post ganglionic sympathetic neurons secrete
noepinephrine
These neurons are termed adrenergic
12. RECEPTORS
Receptors are structures with receive neuro transmitter from
the axonal terminals of neurons
a. Cholinergic receptors
1. Muscarinic 2. Nicotinic
M1 – Gastric secretion Nm – Neuro muscolar junction
relaxation of LES
M2 – Cardiac muscarinic Nn – Autonomic ganglia
receptor (brady cardia) adrenal medulla catecolamine -
M3 – Visceral smooth muscle release
contraction glandular CNS – Excitation and inhibition
secretion vaso dilatation
If the efflux of k+ ions is Na+ Ion Influx produce
reduced de polarization depolarization of the
results and the effect is membarane therefore excitation
13. b. ADRENERGIC RECEPTORS
α1 – Constricts blood vessels, viceral organ sphincters
Dilation of pupil
α2 – Blood platelets, Exocrine glands of the Pancreas and Liver
Hyperpolarization, Therefore, they are Inhibitory
Inhibit insulin and enzyme secretion from the pancreas and
Inhibit gall bladder contractions
β1 – Heart, Kidney
Depolarization, Therefore, They are excitatory
Increases heart rate and strength of contraction, secretion of
renin from, JG cells of the kidney
β2 – lungs both blood vessels and bronchioles, coronary blood
vessels, smooth muscle of the digestive and urinary systems.
This receptor binds only epinephrine which is produced by
the adrenal medulla
Dilation of the bronchioles of the lungs, blood vessels of the
lungs and heart, decreased motility and tone of the digestive
system, relaxation of urinary bladder
β – Adipose tissue
17. TESTS FOR AUTONOMIC INTEGRITY
Autonomic functions can be evaluated by
1. History
2. Non invasive tests
3. Invasive tests
1. HISTORY – One can have suspicion of ANS involvement
from the history itself.
I. CVS – Postural hypotension or orthostatic hypotension is
having typical history of fainting episodes, dizziness,
headache, dimmission of vision.
II. CNS – Night blindness due to involvement of autonomic
fibres supplying the muscles of iris.
III. Genitourinary – Impotence, frequency incontinence
and retention of urine
18. IV. Glandular or secretory function – difficulty in eating due
to decreased salivation, dureased laerimation causing eye
irritation, impaired sweating causing temperature elevation.
V. H/o chronic diseases like DM, CRF and hypertension.
VI. Family history of any autonomic disorders.
VII. Personnel history – history of antihypertensives,
antidepressants, tranquillisers and diuretics. History of
chronic alcohol intake.
2. NON INVASIVE TESTS
I. Test of cardiac vagal function
1. Respiratory sinus arrhythmia
2. Valsalva ratio
3. Bradycardia during phenylephrine challenge
4. Absence of tachycardia with atropine.
19. II. Test of sympathetic function
1. Cardiac
a. Tachycardia during standing or head up tilt
b. Tachycardia during valsalva strain (phase II)
2. Peripheral
a. Blood pressure overshoot after valsalva release
b. Blood pressure increase with cold pressor test
c. Diastolic BP increase with isometric hand grip exercise
d. Systolic and diastolic BP response to upright position
20. 1. Respiratory sinus arrhythmia
Tests the parasympathetic function it determines the
max to minimum heart rate variation that occurs during
forceful breathing.
Method : Seated or lying subject should breathe in at 6
breaths / min (5 sec. Inspiration and 5 sec. Expiration)
maximum and minimum heart rate and resp. rate interval
variation are recorded.
The average minimum to maximum heart rate variation
during 3 consecutive breaths should be greater than 10 beats
/ min. the ratio of longest RR interval during expiration to
shortest RR interval during inspiration constitutes expiration
and inspiration ratio. (E:I ratio less than 1.2 is abnormal in
pts. upto 40 years of age.)
21. 2. Postural stress : (Supine to standing)
It test the sympathetic function it is the most commonly
performed bedside test to know ANS. Involvement. Changes in
heart rate and BP in response to assumption of standing
position.
Heart rate and BP should be recorded in pts. in supine
position after a resting period of 10 min. then the pt. is asked to
stand up unaided and after 50 sec. pulse rate and BP are to be
measured.
A decline in systolic BP of greater than 20 mmHg and or
diastolic BP of 10mmHg in standing is abnormal absence of
tachy cardiac during standing has also been interpreted as an
impairment of sympathetic drive to heart.
22. 3. Cold pressor test
This test is to evaluate the peripheral sympathetic
vasoconstrictor mechanism. Blood pressure is recorded after 1
min immersion of hand in ice cold water. Both systolic and
diastolic BP at the end of 1 min of immersion should increase
atleast by 10 mmHg.
4. Isometric handgrip exercise
The tests the sympathetic function. Blood pressure
response to a sustained isometric contraction at 30% of the
patients maximum strength is recorded. Blood pressure
should increase at least by 10-15 mmHg at the end of
contraction. The failure to rise of BP more than 10 mmHg is
suggestive of deficient efferent sympathetic mechanisms.
23. 5. Valsalva Maneuver
It tests both sympathetic and parasympathetic function
procedure: the subject sits quietly or lies supine and blows into
a mouth piece with an open glottis and holds an airway
pressure of 40 mmHg for 15 sec (Phase II) and is asked to
release the strain (phase IV).
Result
Heart rate normally increases during phase II of the
maneuver i.e. 10 to 15 sec after initiating the blowing but prior
to release of strain. This tachycardia is due to baroreflex
stimulation to the fall in blood pressure seen as a result of
raised intrathoracic pressure (decreased venous return) on
release of strain (phase IV) preload and cardiac output are
restored and these is blood pressure overshoot. This
hypertension stimulates baroreceptors initiating rapid reflex
bradycardia.
24. The ratio of longest RR interval (minimum HR) during
phase IV to the shortest RR(maximum HR) during Phase II
has been used as an index of cardiac nagal function known as
valsalva Ratio. A ratio of less than 1.2 is abnormal. Failure of
heart rate increase during positive intrathoracic pressure
phase points to sympathetic dysfunction and during of the
heart rate to slow during the period of BP overshoot points to
a parasympathetic dysfunction.
Failure to observe a BP overshoot following release of
strain suggests that peripheral sympathetic vasoconstriction
has not occurred.
25. 6. Power spectral analysis of heart rate variability
There are slower periodic oscillations in heart period which
can be decomposed into a series of sine waves with different
amplitudes and frequencies.
This frequencies domain approach reveals a consistent
peak or power at the breathing frequency between 0.2 to 0.3
Hz (due to intact parasympathetic innervation of SA node) and
another peak at low frequencies between 0.05 to 0.15 Hz. (due
to changing levels of cardiac sympathetic activity).
Low frequency component is augmented by increased
sympathetic drive e.g. head up tilt, mental arithmetic and
reduced in quadriplegics with interrupted sympathetic
pathways.
26. INVASIVE TEST
Theses are done to locate the pressure site of pathology
and for research purposes. They are done by:
i) Intraneural recording of postganglionic sympathetic activity.
ii) Response of ANS to infusion of pressor drugs.
iii) Eliciting axon reflex by intradermal injection of acetycholine.
Epinephrine test
3 drop at 1 minute interval for 3 times check pupil size at 15,
30 and 45 minute. No effect on normal pupil sympathetically
denervated pupil will dilate
Ephidrine test
25 mg IM ephidrine – N response – HR increases
sympathetically denervated –
No change in heart rate.
27. Atropine test
0.8 mg IM Atropine – N response heart rate increases
sympathetically denervated –
No change in heart rate.
Neostigmine test
1 mg IM Neostigmine – N response – heart rate decreases
Parasympathetically denervated –
No change
OTHER TESTS
i) Measurement of skin temperature
ii) Tests of sudomotor function.
a) Wight of sweat.
b) Galvanic skin resistance test
iii) Tests of lacrimal function.
iv) Tests of ladder and gastrointenstinal dysfunction
28. LABORATORY TESTS
a) Measurement of plasma levels of catecholamines and
other vasoactive hormones such as renin, angiotensin
and vasopressin. Levels of these hormones are reduced
in autonomic dysfunction.
b) Measurement of forearm blood flow with
plethysmography.
c) Cerebral elecroencephalography and blood flow studies.
SELECTION OF TEST
Five simple non-invasive tests of cardiovascular reflexes are
adequate for assessment of autonomic involvement.
Definite abnormalities are indicated by two or more tests.
29. ANAESTHESIA AND AUTONOMIC NERVOUS SYSTEM:
1. GENERAL ANAESTHESIA:
Various drugs used during the act of anaesthesia have their
effects on autonomic nervous system.
Premedicants :
I) Agents used to decrease secretions eg. atropine are
anticholinergics
ii) Metoclopramide an antiemetic is a dopaminergic antagonist
iii) Opioids – Opioids induced respiratory depression is due to
inhibition of acetylcholine release from central nervous
system. (Morphine causes decrease peripheral vascular
resistance leading to venous pooling due to histamine
release).
Pentazocine causes increase in plasma catecholamine
levels. Brady cardia caused by fentanyl is vagal in origin.
30. iv) β antagonists are used to reduce the stress response seen
during intubation.
Induction agents
Intravenous agents except ketamine causes reduced
sympathetic activity. There is reduction in arterial pressure
associated with baroreceptor mediated tachycardia.
Ketamine produces sympathetic stimulation.
Etomidate is a potent inhibitor of adrenal steridogenesis.
Volatile anaesthesics
Halothane, enflurane and isoflurance causes resulting in
decrease in plasma catecholomines.
Cyclopropane and diethyl ether increase sympathetic
activity by central action or an effect on vasomotor neurons in
spinal cord.
31. Muscle relaxants
Pancruronium stimulates sympathetic system
releasing adrenaline causing increase in heart rate and blood
pressure.
Autonomic changes under anaesthesia can serve as
valuable indices to measure awareness and depth of
anaesthesia. Decreasing arterial BP, pulse rate, plasma
Catecholamine levels and cortisol levels indicates increasing
depth of anasthesia.
32. 2. CENTRAL NEURAXIAL BLOCKADE
Spinal anaesthesia
Cardiovascular changes are seen following spinal
anaesthesia due to sympathetic blockade. Hypotension and
bradycardia are the most common finding.
Incidence of haemodynamic changes depends on the level
of blockade. In low spinal anaesthesia sacral parasympathetic
lumbar and lower side thoracic sympathetic are blocked the
consequences are secondary to parasympathetic vagal effect
on splanchnic bed and viscera. In high spinal almost all
sympathetic fibers are blocked and the parasympathetic to
thoracic and abdominal viscera via vagus remains active and
causes severe bradycardia or even asystole.
33. In saddle block. The sacral parasympathetic outflow and
lower portion of lumber outflow are blocked.
Most of the thoracolumbar sympathetic outflow is intact
and physiologic disturbances are minimal
CONSEQUENCES OF AUTONOMIC IMBALANCE AFTER
SPINAL ANAESTHESIA
CVS
Hypotension due to venodilatation and arterial dilatation
thus causing reduction in after load, cardiac output or both
Bradycardia occurs due to blocked of sympathetic
cardioaccelator fibers T1 - T2 when the cardiac vagal innervation
is intact and decreased filling pressure (Bainbridge reflex)
Gastrointestinal effects
Unopposed parasympathetic activity causes gut to be
contracted, peristalsis is present and intestines are usually
active.
34. Bronchial effects
Sympathetic fibers to the bronchial muscles is derived
from upper 5 or 6 thoracic segments. Blocked of these
fibers in high spinal anaesthesia leads to some bronchial
spasm secondary to vagal activity.
Epidual anaesthesia
Degree of hypotension is low as compared to the spinal
anaesthesia as the onset of anaesthesia is slow the
compensatory mechanisms could be initiated more
segmental type of anaesthesia is possible.
35. AUTONOMIC REFLEXES DURING ANAESTHESIA
AND SURGERY
Activation of some of the important autonomic reflexes
during anaesthersia and surgery can at times create
haemodynamic disturbance. Hence it is imperative to
review few of the autonomic reflex that are of clinical
relevance.
i) OCULOCARDIAC REFLEX
Pressure over the eyeballs and traction of the external
ocular muscles causes this reflex which results in
bredycardia, asystole, cardiac dysrhythmias and ventricular
fibrillation. Hypoxic, hypercarbia and light plane of
anaesthesia aggravates this reflex.
36. ii) ABDOMINAL REFLEX
These are generally during operations within the
abdominal cavity from stimulation of autonomic nervous
system by traction and pressure. Response usually
consists of bradycardia and hypotension as circulatory
effect and aponea, tachypnoea and larvngospasm as
respiratory feature.
a) Peritoneal and mesentric reflex: Pulling or stretching of
the peritonium and mesentry and traction on the ovaries
elicit this reflex.
b) Coeliac plexus reflex: Traction on the stomach,gall
bladder hilum of liver or retraction of duodenum elicits
this reflex.
c) Brewer Luckhardt reflex: Also k| as diaphragmatic
traction reflex. Manipulation or traction in the diaphragm
results in reflex.
37. iv) REFLEXES ASSOCIATED WITH PELVIC NERVE:
a) Recto laryngeal reflex :
Dilation of anal sphincter especially under general
anesthesia elicits the reflex. Usual responses are
laryngeal spasm and apnea (afferent arc is via pelvic
nervous and sacral spinal used to the vagal motor nucleus
and efferent is through the recurrent laryngeal nerve).
b) Recto – cardiac reflex :
Cardiovascular response during anal sphincter
dilatation in the form of bradycardia and hypotension.
Prevention of autonomic reflexes can be done by
maintaining adequate depth of anaesthesia. Atropine can
be given as a prophylaxis. Ask the surgeon to stop
manipulation and proceed gently and slowly.
38. AUTONOMIC NERVOUS SYSTEM DYSFUNCTION
They can be primary, familial, idiopathic or due to
secondary systemic diseases.
PRIMARY
i) Idiopathic orthostatic hypotension
ii) Shy drager type of othostatic hypotension (ANS
dysfunction associated with widespread parenchymatous
degeneration is CNS and spinal cord. Primary defect is
loss of neuronal cells an element of sympathetic nervous
system dysfunction which can result from the depletion of
norephinephrine from peripheral efferent nerve endings.
S/s orthostatic hypotension urinary retention, bowel
dysfunction, diminished sweating, sluggish pupillary
reaction, abnormal control of breathing and sexual
impotence)
39. FAMILIAL
i) Riley Day Syndrome
(Rare AR disorder of ANS seen as Vasomotor instability,
depressed ventilatory responses to arterial hypoxaemia and
hypercarbia, hypertension, decreased or absent pain
perception, defective test and thermal dyscrimination;
kyphoscolosis, impaired gag reflex and oesophageal
motility).
ii) Lesch – Nyhan syndrome
(genetically ditermined disorder of purine metabolism
occuring in males. Sympathetic nervous system response
to stress is enhanced).
iii) Gill familia dysautonomia
41. 1. Aging
Approximately 20% of people over 65 years of age
have postural hypotension. At least one half of these
patients experience dizziness, faintness or loss of
consciousness. There will be a selective or earlier
impairment of parasympathetic function with aging with a
minimum or a more gradual involvement of sympathetic
nerves system. Heart rate changes in response to changes
in blood pressure, valsalva maneure and respiratory cycle
are blunted with aging. Resting and exercise induced
norepineprine response is blunted with aging.
42. 2. Chronic alcoholism
Orthostatic intolerance occurs in chronic alcoholism
and also after acute alcohol intoxication withdrawal of
alcohol.
Alcohol has direct effect on baroreceptor and poor
nutrition associated with alcoholism impairs the sympathetic
nervous system at both central and peripheral levels.
Valsalva ratio and cardiac acceleration following iv atropine
are shown to be diminished in alcoholics with neurological
deficits.
43. 3. Diabetes mellitus
It may result from neuronal degeneration or
metabolically related neuronal dysfunction. The afferent
central and efferent reflex pathways each can be involved.
Vagal neuropathy occurs earlier than sympathetic
neuropathy. Presence of symptomatic postural hypotension is
associated with poor prognosis. Patients may have
esophageal dysfunction, gastric hypotonia, bradycardia,
hypotension, abnormal blood pressure falls, painless
myocardial infarction and unexplained cardio respiratory
arrest and impaired ventilatory control.
44. 4. Tetanus
Sympatho-adrenal hyperactivity is a feature of tetanus
as well as chief cause of death. A direct effect on tetanus tonic
on the sympathetic nervous system produces high plasma
catecholamine levels.
5. Phaeochromocytoma
It is a catecholamine secreting tumour associated with
hypertension, hypermetabolism and hyperglycaemia.
Preoperatively patients are managed on alpha blockers to
restore blood volume, assess end organ damage and to treat
cardiac arrhythmia
45. 6. Gullien Bairre syndrome
Autonomic nervous system involvement is secondary to
axonal degeneration marked liability of blood pressure,
perristent facial flashing, urinary retention, tachy and brady
arrhythmia are often seen. Neuropathic lesions in afferent limb
of baroreceptor may lead to SAIDH and resulting
hyponatremia.
46. 7. Autonomic changes in spinal cord transection
Spinal cord transection not only affects motor sensory
function but also exhibit profound alterations in autonomic
nervous system. The involvement depends on the level of
transaction.
The acute effects of spinal cord transaction I.e., spinal
shock includes flaccid paralysis, total absence of sensation, loss
of temperature regulation and spinal cord reflexes below the
level of injury. Decreased systemic BP, bradycardia,
abnormalities in ECG – ST-T changes and ventricular
premature beats.
Anaesthesia management concentrates on airway,
management, avoidance of hypovolumia. Anaesthesia is given
so that the pt. should tolerate tube and muscle relaxant is used
as per the need for surgery.
47. Several weeks later patients goes into chronic stage
where the spinal reflexes are regained but there is over
activity of sympathetic nervous system, involuntary skeletal
muscle spasm and autonomic hyperreflexia is seen when
there is spinal cord transaction above T6 and rarely below
T10.
Stimulus below the level of transection initiates
afferent reflexes which initiates reflex sympathetic activity
over the splanchnic outflow tract in the from of generalised
vasoconstriction. Vasoconstriction leads to increase BP
which stimulates baroreceptors to cause bradycardia
48. ANAESTHESIA IN PATIENTS WITH ANS DYSFUNCTION
Management of anaesthesia is based on understanding
the impact of reduced autonomic nervous system activity on the
cardiovascular responses to such events like change in body
position, positive airway pressure, acute blood loss and effects
produced by admistration of negative inotrophic anesthetic
agents and cutaneous vasodilation above the level of
transection.
Pt may have nasal stuffiness, cardiac dysrhythmias,
cerebral, retinal or subarachnoid haemorrhage, loss of
consciousness seizures and intra operatively excessive blood
loss. T/t includes ganglianic blocking drugs, trimethaphan,
pentolinium, adrenergic antagonists phentolamine;
phenoxybenzamine direct acting vasodilates like nitropusside.
Goal of anaesthesia is to prevent the stimulus leading to
autonomic hyperreflexia.
49. Spinal, epidural or general Anaesthesia can be given but
it may be difficult to give position. Avoidance of succinylscoline
and presence of drugs like nitroprusside to avoid precepitus
hypertension is important.
Posture
Shifting of patient to OT. Preferably in supine position.
Induction also to be done in supine position.
Premedication
Preloading should be done properly as there are
chances of sudden fall in BP.
Atropine may fail to produce tachycardia.
Metoclopramide and ranitidine to avoid regurgitation and
aspiration.
Narcotic analgesia and other drugs causing respiratory
depression are avoided.
50. Monitoring
Pulseoximeter,
Continuous arterial BP monitoring
ECG,CVP,
Temp and urinary output.
Etco2
Induction
Thiopentone sodium if used to be given slowly with
proper intravascular fluid replacement. Diazepam and fentanyl
may also be used.
Ketamine produces accentuated blood pressure
response.
Rapid sequence intubation as pts have gastroparesis.
51. Maintenance
Spontaneous breathing with nitrous oxide and oxygen
with minimal concentration of halothane is advised. Muscle
relaxants if needed cardio stable drugs like vecuronium is to be
used.
IPPV produces exaggerated reduction in blood pressure
since compensatory mechanisms are not functioning. Blood
loss, should be meticulously assessed and replaced promptly.
Tachycardia as a compensatory response to blood loss is
absent.
Volatile anesthetics produce exaggerated myocardial
depression and hypotension hence to be used meticulously.
Fluid balance is to be maintained. Hypothermia should be
avoided as these pts. Tend to become poikilothermic because
of sympathetic dysfunction. Vasopressors if needed should be
used safely clue to chances of exaggerated response.
52. REGIONAL ANAESTHESIA
The risk of hypotension after administration of spinal or
epidural detracts from the use.
Post spinal urinary retension may occur.
The preoperative pressure of impotence must be
brought into notice before administering regional
anaesthesia to avoid medicolegal problems.
53. AUTONOMIC NERVOUS SYSTEM (PHYSIOLOGY)
IN INTENSIVE CARE
Mechanical intermittent positive pressure ventilation
causes increase intrathoracic pressure during all phases of
respiratory which causes decrease of cardiac output.
On critically ill patients with significant autonomic
dysfunction the reflex mechanism fails and so cardiac output
falls drastically.
54. AUTONOMIC NERVOUS SYSTEM AND CHRONIC PAIN
1. Phantom limb Pain
Decreased blood flow causes this phantom limb pain
ectopic discharge of epinephrine from a stump neuroma has
been postulated as an imp. Peripheral mechanism.
Sympathetic block or sympathetomics or β blockers
increase the blood flow and reduce the intensity of burning
pain.
55. 2. Lumber sympathetic block
Used mainly to alleviate the rest pain of chronic
peripheral obliterative vascular disease. These ganglia receive
preganglionic sympathetic fibers from ower thoracic
sympathetic chain and preganglionic somatic fibre from 1st
and
2nd
lumber nerves.
The postganglionic fibres are vasoconstrictor to the
arterioles and pilomotor and sudomotor to the skin within the
distribution of nerves. Block of lumber sympathetic fibres
cause absence of sweating and warm dry skin.
3. Coeliac plexus block
Used to provide analgesia from intractable pain caused
by cancer of pancreas, stomach, gall bladder and liver
56. 4. Superior hypogastric plexus block
It is the main sympathetic plexus mediating pain from
the pelvic organs. It is useful for producing analgesia in cancer
pain secondary to cervical, prostate, testicular cancers and
radiation injury.
5. Complex regional pain syndrome
Complex painful disorders as a consequence of trauma
affecting the limbs may or may not be associated with obvious
nerve lesion. These disorders are now called complex Regional
Pain Syndrome. The clinical picture is characterized by a trial of
autonomic (sensory) motor and sensory symptoms. The
autonomic features are abnormal skin blood flow,temperature
and sweating.
