2. SITE OF ACTION-
Target binding sites are the superficial and deep portions of spinal cord spinal
nerve roots in subarachnoid and epidural space and dorsal root ganglia.
• Speed of neural blockade depends on size, surface area, degree of
myelination of nerve fibres.(S1 and L5 posterior roots are largest and most
resistant to blockade)
• Differential blockade
„ Autonomic>sensory>motor
(For eg the level of anesthesia to cold sensation most cephalad and is one to
two segments higher than the level of pinprick anesthesia which in turn is one
to two segments higher than the level of touch anesthesia)
• „Sympathetic blockade may be two dermatomes higher than sensory block
(pain, light touch)
• Drug penetration and uptake is directly propotional to drug mass,CSF drug
concentration, contact surface area, lipid content and local tissue vascular
supply and inversely related to nerve root size
• Concentration of drug is highest at site of injection.
• Time for block regression is inversely propotional to to the CSF volume
Mechanism of Action
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3. PHYSIOLOGICAL EFFECTS OF SPINAL ANAESTHESIA
1.CARDIOVASCULAR SYSTEM
Combined α+β blocking effect on heart
Venodilatation and fall in venous return lead to low cardiac output and hypotension
during
onset (Bain-bridge reflex)
Decreased stroke volume and heart rate
Cardiac output shows a biphasic response
*i.e. early transient increase followed by eventual decrease.
In old age with cardiac disease SVR tend to fall by 25% whereas CO falls by only
10-15%
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4. Block of cardio acclerator sympathetic fibers from T1-T4 leads to
subsequent bradycardia
Extensive peripheral sympathectomy(T5-L2) also leads to
bradycardia and pooling in lower extremities
Hypotension triggers compensatory baroreceptor response leading
to vasoconstriction and tachycardia above block level, reduction in
venous return/RA filling which decreases signal output of intrinsic
chronotropic receptors of RA leading to increase in parasympathetic
tone.
BEZOLD JARISCH REFLEX- Bradycardia and subsequent
cardiac arrest due to profound hypotension via activation of 5HT3
mediated receptors of vagus and the ventricular myocardium.
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5. 2.GASTROINTESTINAL FUNCTIONS
• Nausea and vomiting due to GI hyper peristalsis due to
unopposed vagal activity. Contracted bowel and relaxed
sphincters due to sympathetic blockade.
• Spleen enlarges 2-3 times in high blocks when its
sympathetic efferent fibers (splanchnic nerves) are blocked.
• Bladder and urogenital dysfunction
• Colonic blood supply and oxygen availability is increased.
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6. 3.RESPIRATORY SYSTEM
• High spinal may cause paralysis of intercostal muscles,
diaphragm and accessory respiratory muscles.
• Cautiously given in patients with limited respiratory
reserve
• Tidal volume remain unchanged.
• Vital capacity decreases minimally d/t loss of abdominal
muscle contribution in forced expiration
• Apnea due to hypotension which causes medullary
ischemia in high/total spinal cases
4. THERMOREGULATION
• Vasodilatation causes heat loss which is compensated by
vasoconstriction and shivering above the level of block.
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7. 5.ENDOCRINE
-Stress response is inhibited
-response to insulin is augmented
-usual increase in ADH during surgery is inhibited
Spinal anesthesia in pregnacy
Decreased dose requirement due to
Mechanical factor : compression of IVC causes
shunting of blood to the venous plexus in the vertebral
canal leading to decreased vertebral canal space and CSF
volume
Hormonal factor – higher progesterone levels
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8. SPINAL NEEDLES
Standard spinal needle consist of three parts:-
-Hub
-Cannula
-Removable stylet
Sizes available- 16 to 30 gauge.
Length of spinal needle – 90mm
Needles are either
-Sharp or blunt at tip.
-Pencil point needle.
-Sharp or round bevel edge.
Dura cutting needle: QUINCKE-BABCOCK and
GREENE
Dura seprating: WHITCRE,SPORTE AND
PITKIN
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9. Spinal needle
Gauge(mm)
• 16(1.6mm)
• 18(1.2mm)
• 19(1.1mm)
• 20(0.9mm)
• 21(0.8mm)
• 22(0.7mm)
• 23(0.6mm)
• 25(0.5mm)
• 26(0.5mm)
• 27(0.40mm)
Colour code
• White
• Pink
• Cream
• Yellow
• Deep green
• Black
• Deep blue
• Orange
• Brown
• Grey
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10. DRUG
• Lidocaine is 5% and hyperbaric by addition of
7.5%dextrose
• Rapid onset of action and low toxicity
• Bupivacaine is 0.5%and made hyperbaric by addition
of 8%dextrose
Dose
• <5kg—0.5mg/kg body wt
• 5-15kg—0.4mg/kg body wt
• >15kg—0.3mg/kg body wt
• Ropivacaine (0.5% in dextrose)
• Levobupivacaine
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11. PHARMACOLOGY
• pKa, lipid solubility, and protein binding of the local anesthetic solution
• Short-acting : Procaine, Chloroprocaine, Articaine
• Intermediate-acting : Lidocaine, Prilocaine, Mepivacaine
• Long-acting : Tetracaine, Bupivacaine, Levobupivacaine, Ropivacaine
12. Procaine.
One of the oldest spinal anesthetics, drug of choice for spinal anesthesia
in the early 20th century.
High failure rate, more nausea, slower time to recovery.
Hyperbaric drug 50 to 200 mg in a 10% concentration.
Chloroprocaine.
Ultra–short-acting ester LA .
Rapid metabolism by pseudocholinesterase, minimal systemic or fetal effects in the
setting of epidural labor analgesia.
Spinal anesthesia for ambulatory surgery.
Preservative-free preparations of chloroprocaine available
Short-duration & faster recovery time than procaine, lidocaine, and bupivacaine.
TNS can occur with modern preparations but very few (0.6%)
Doses 30-60 mg
13. Lidocaine.
Rapid onset & Intermediate duration for shorter procedures that can be completed in 1.5
hours or less.
• Doses of 50 to 100 mg
• traditionally prepared as a 5% solution in 7.5% dextrose; associated with both permanent
nerve injury and TNS
Doses 30-60 mg
Prilocaine. Prilocaine is an amide local anesthetic based
• on the structure of lidocaine. Prilocaine was introduced in
• 1965 and has an intermediate duration of action that may
• lend itself to use in the ambulatory surgery setting.152 A
• dose of 40 to 60 mg of 2% hyperbaric prilocaine can provide
• a block to T10 for 100 to 130 minutes, whereas as little as
• 20 mg combined with fentanyl has been successfully used
• for ambulatory arthroscopic knee surgery.153 Prilocaine is
• rarely associated with TNS.152,154,155 In large doses (>600
• mg), prilocaine can result in methemoglobinemia. This
• should not be an issue with doses used for spinal anesthesia,
• but it has been reported after epidural infusions.
Editor's Notes
Decreased stroke volume and heart rate due to blockade of peripheral
(T1-L2) and cardiac (T1-T4) fibres and decreased adrenal medullary secretion
(Initial increase is due to greater decline in SVR than the venous return) especially
Procaine is a short-acting ester local anesthetic
and one of the oldest spinal anesthetics, having originally
replaced cocaine as the drug of choice for spinal anesthesia
in the early 20th century. Procaine itself was then
replaced by lidocaine, but with concerns about lidocaine
Procaine is a short-acting ester local anesthetic
and one of the oldest spinal anesthetics, having originally
replaced cocaine as the drug of choice for spinal anesthesia
in the early 20th century. Procaine itself was then
replaced by lidocaine, but with concerns about lidocaine