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.

ANATOMY ANS is part of the motor division

of PNS

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.

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

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.

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

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

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.

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.

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

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 excitation

b. ADRENERGIC RECEPTORSα1 – Constricts blood vessels, viceral organ sphincters

Dilation of pupil α2 – Blood platelets, Exocrine glands of the Pancreas and Liver

Hyperpolarization, Therefore, they are InhibitoryInhibit insulin and enzyme secretion from the pancreas and Inhibit gall bladder contractions

β1 – Heart, Kidney

Depolarization, Therefore, They are excitatoryIncreases 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

β3 – Adipose tissue

NEURAL CONTROL OF A.N.S.

AUTONOMIC REFLEX ARC

ACTIONS OF SYMPATHETIC AND PARASYMPATHETIC

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

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.

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

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.)

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.

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.

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.

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.

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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)

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

SECONDARY TO SYSTEMIC DISEASES

1. Aging 2. Diabetes mellitus

3. Chronic alcoholism 4. Chronic renal failure

5. Hypertension 6. Carcinomatosis

7. Chagas diseases 8. Tetanus

9. Pheochromocytoma 10. Spinal cord injury

11. Neurological diseases 12. Gullein Barrie syndrome.

i) Tabes Dorsalis

ii) Syringomyelia

iii) Amyloidosis.

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.

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.

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.

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

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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

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.