Notes on Anesthesia


* · General Anesthesia · 4. Anaesthesia

* Anesthesia – is a reversible condition of comfort, quiescence and physiological stability in a patient before, during and after performance of a procedure.

* General anesthesia – for surgical procedure to render the patient unaware / unresponsive to the painful stimuli.

* Drugs producing G. Anaesthesia – are called general anaesthetics

* Local anesthesia – reversible inhibition impulse generation and propagation in nerves. In sensory nerves, such an effect is desired when painful procedures must be performed, e.g., surgical or dental operations.

mage Source:

* Drugs producing L. Anaesthesia – are called local anaesthetics · 5. Local anaesthesia

* Some terms related to Local anaesthesia:

o Surface anaesthesia : Ointment / jelly / solutions applied on mucous membrane.

o Infiltration anaesthesia : Injection of the LA to produce analgesia over an area.

o Regional anaesthesia : spinal, epidural and IV regional anaesthesia.

o Spinal – sub-arachnoid space.

o Epidural – between spinal bone and dura matter.

o IV Regional – limited to limbs and practically upper limbs. · 6. What are General anaesthetics ?

* General Anaesthetics are the drugs which produce reversible loss of all sensation and consciousness, or simply, a drug that brings about a reversible loss of consciousness.

* These drugs are generally administered by an anesthesiologist in order to induce or maintain general anesthesia to facilitate surgery.

* General anaesthetics are – mainly inhalation or intravenous · 7. What are the Drugs used as GA ? (Classification)

* Inhalation:

* Gase: Nitrous Oxide

* Volatile liquids:

o Ether

o Halothane

o Enflurane

o Isoflurane

o Desflurane

o Sevoflurane

* Intravenous:

* Inducing agents:

* Thiopentone, Methohexitone sodium, propofol and etomidate

* Benzodiazepines (slower acting):

* Diazepam, Lorazepam, Midazolam

* Dissociative anaesthesia:

* Ketamine

* Neurolept analgesia:

* Fentanyl · 8. Essential components of GA:

* Triad of General Anesthesia:

o need for unconsciousness

o need for analgesia

o need for muscle relaxation

* Essential components of GA:

o Loss of all sensations – pain

o Unconsciousness

o Amnesia

o Immobility and muscle relaxation

o Loss of somatic and autonomic reflexes · 9. History – The Primitive techniques

* Club

* Strangulation

* Alcohol

* Mesmerism

* Plants · 13. Mechanism of GA(Potency)

* For inhalation anesthetics – Minimum Alveolar Concentration (MAC) – 1 (one) MAC is defined as the minimum alveolar concentration that prevents movement in response to surgical stimulation in 50% of subjects.

* Practically –

* Alveolar concentrations can be monitored continuously by measuring end-tidal anesthetic concentration using spectrometry

* End point (immobilization) – can me measured.

* Other end points – Verbal commands or memory etc.

* For Intravenous agents – Potency of IV agent is defined as the free plasma concentration (at equilibrium) that produces loss of response to surgical incision in 50% of subjects.

* Difficult to measure :

o no available method to measure blood or plasma concentration continuously

o Free concentration at site of action cannot be determined · 14. Mechanism – contd.

* The unitary theory of anesthesia – Meyer-Overton rule (1901)

* Lipid : water partition coefficient (fluidization)

* Potency of a gas correlated with its solubility in olive oil (olive oil : water) – lipid bilayer as the only target for anesthetic action.

* Clear exceptions have been found out now.

* The unitary theory has been discarded now. · 15. Modern theory on Mechanism of general anesthesia

* Major targets – ligand gated ion channels.

* Important one – GABA A receptor gated Cl ¯ channel.

o Examples – Many inhalation anesthetics, barbiturates, benzodiazepines and propofol

o Potentiate the GABA to open the Cl ¯ channels · 16. Molecular Actions: GABA A Receptor

* Ligand-gated ion channels

o Chloride channels gated by the inhibitory GABA A receptor

* GABA A receptor mediates the effects of gamma-amino butyric acid (GABA), the major inhibitory neurotransmitter in the brain

* GABA A receptor found throughout the CNS

* Most abundant, fast inhibitory, ligand-gated ion channel in the mammalian brain

* Located in the post-synaptic membrane · 17. GABA A receptor – contd.

* GABA A receptor is a 4-transmembrane (4-TM) ion channel

o 5 subunits arranged around a central pore: 2 alpha, 2 beta, 1 gamma

* Each subunit has N-terminal extracellular chain which contains the ligand-binding site

* 4 hydrophobic sections cross the membrane 4 times: one extracellular and two intracellular loops connecting these regions, plus an extracellular C-terminal chain · 18. GABA A receptor – contd. · 19. GABA A receptor – contd.

* Receptor sits in the membrane of its neuron at the synapse

* GABA , endogenous compound, causes GABA to open

* Receptor capable of binding 2 GABA molecules, between an alpha and beta subunit

o Binding of GABA causes a conformational change in receptor

* Opens central pore

* Chloride ions pass down electrochemical gradient

o Net inhibitory effect, reducing activity of the neuron · 20. Mechanism of GA – contd.

* Other Mechanisms:

* Glycine – Barbiturates, propofol and others can activate in spinal cord and medulla

* N – methyl D- aspartate (NMDA) type of glutamate receptors – Nitrous oxide and ketamine selectively inhibit · 21. Signs and stages of GA

* Guedel in 1920 described with ether – Guedel`s stages of GA.

* Descending depression of CNS.

* Higher to lower areas of brain are involved.

* Vital centers located in medulla are paralyzed last.

* But, in spinal chord lower segments are affected earlier than the higher segments. · 22. signs & stages of GA – contd. · 23. stages of GA – contd.

* Stage I: Stage of Analgesia

* Starts from beginning of anaesthetic inhalation and lasts upto the loss of consciousness.

* Pain is progressively abolished during this stage.

* Patient remains conscious, can hear and see, and feels a dream like state.

* Reflexes and respiration remain normal.

* It is difficult to maintain – use is limited to short procedures only. · 24. stages of GA – contd.

* Stage II: Stage of Delirium and Excitement:

* From loss of consciousness to beginning of regular respiration.

* Excitement – patient may shout, struggle and hold his breath

* Muscle tone increases, jaws are tightly closed.

* breathing is jerky; vomiting, involuntary micturition or defecation may occur.

* Heart rate and BP may rise and pupils dilate due to sympathetic stimulation.

* No stimulus or operative procedure carried out during this stage.

* Breatholding are commonly seen. Potentially dangerous responses can occur during this stage including vomiting, laryngospasm and uncontrolled movement.

* This stage is not found with modern anaesthesia – preanaesthetic medication, rapid induction etc. · 25. stages of GA – contd.

* Stage III: Stage of Surgical anaesthesia

* Extends from onset of regular respiration to cessation of spontaneous breathing. This has been divided into 4 planes:

* Plane 1: Roving eye balls. This plane ends when eyes become fixed.

* Plane 2: Loss of corneal and laryngeal reflexes.

* Plane 3: Pupil starts dilating and light reflex is lost.

* Plane 4: Intercostal paralysis, shallow abdominal respiration, dilated pupil. · 26. stages of GA – contd.

* Stage IV: Medullary / respiratory paralysis

* Cessation of breathing failure of circulation death.

* Pupils: widely dilated.

* Muscles are totally flabby.

* Pulse is imperceptible

* BP is very low. · 27. Phases of GA

* There are 3 (three) phases:

* Induction

* Maintenance

* Recovery · 28. Phases of GA – contd.

* Induction: It is the period of time which begins with the beginning of administration of anaesthesia to the development of surgical anaesthesia (Induction time). Induction is generally done with IV anaesthetics like Thiopentone Sodium

* Maintenance: Sustaining the state of anaesthesia. Usually done with an admixture of Nitrous oxide and halogenated hydrocarbons

* Recovery: At the end of surgical procedure administration of anaesthetic is stopped and consciousness regains (recovery time) · 29. Pharmacokinetics of inhalation anaesthetics: Pathway for anaesthetics: · 30. Pharmacokinetic of inhalation GA – contd.

* Depth of anaesthesia depends on Potency of the agent (MAC) and Partial Pressure (PP) attained in the brain.

* Induction and recovery depends on rate of change of PP in brain. · 31. Pharmacokinetic of inhalation GA – contd.

* Factors affecting PP of anaesthetics in Brain:

* PP of anaesthetic in the inspired gas

* Pulmonary ventilation

* Alveolar exchange

* Solubility of anaesthetic in blood – Blood: gas partition coefficient

* Solubility in tissues

* Cerebral blood flow · 32. Blood : gas partition coefficient

* Solubility of an anesthetic agent in blood is quantified as the blood : gas partition coefficient.

* It is the ratio of the concentration of an anesthetic in the blood phase to the concentration of the anesthetic in the gas phase when the anesthetic is in equilibrium between the two phases.

* Lower the blood : gas co-efficient – faster the induction and recovery – Nitrous oxide.

* Higher the blood : gas co-efficient – slower induction and recovery – Halothane . · 33. Rate of Entry into the Brain: Influence of Blood and Lipid Solubility · 34. BLOOD GAS PARTITION CO-EFFICIENT · 35. Agents with low solubility in blood quickly saturate the blood. The additional anesthetic molecules are then readily transferred to the brain. BLOOD GAS PARTITION COEFFICIENT · 36. Elimination of GA

* Mostly through lungs in unchanged form.

* Channel of absorption (lungs) become channel of elimination

* Enter and persists in adipose tissue for long periods – high lipid solubility and low blood flow.

* They are not metabolized except Halothane

* Second gas effect

* Diffusion hypoxia · 37. Techniques of inhalation GA

* Open drop method

* Through anaesthetic machines

* – Open system

* – Closed system

* – Semi-closed system · 38. Continuous flow (Boyle’s) anaesthetic machine

* Anaesthetic Machine (Boyle’s equipment)

* The anaesthetic machine

* Gas source- either piped gas or supplied in cylinders

* Flow meter

* Vaporisers

* Delivery System or circuit · 39. Properties of an Ideal anaesthetic agent:

* For Patient:

o Pleasant, non-irritating and should not cause nausea or vomiting

o Induction and recovery should be fast

* For Surgeon:

* – analgesia, immobility and muscle relaxation

* – nonexplosive and noninflammable · 40. Properties of GA – contd.

* For the anaesthetist:

* – Margin of safety

* – Heart, liver and other organs

* – Potent

* – Cheap, stable and easily stored

* – Rubber tubing or soda lime

* – Rapid adjustment of depth of anaesthesia · 41. Individual Inhalation anaesthetic agents · 42. 1. Diethyl ether ( C 2 H 5 – O – C 2 H 5 )

* Colourless, highly volatile liquid with a pungent odour. Boiling point – 35 ºC

* Produces irritating vapours and are inflammable and explosive.

* Pharmacokinetics:

* – 85 to 90 percent is eliminated through lung and remainder through skin, urine, milk and sweat.

* – Can cross the placental barrier. · 43. Ether – contd.

* Advantages

* – Can be used without complicated apparatus.

* – Potent anaesthetic and good analgesic.

* – Muscle relaxation.

* – Wide safety of margin.

* – Respiratory stimulation and bronchodilatation.

* – Does not sensitize the heart to adrenaline

* – No cardiac arrythmias.

* – Can be used in delivery.

* – Less likely hepato or nephrotoxicity.

* Disadvantages

* – Inflammable and explosive.

* – Slow induction and unpleasant -atropine.

* – Slow recovery – nausea & vomiting

* – Cardiac arrest.

* – Convulsion in children.

* – Cross tolerance – ethyl alcohol. · 44. 2. Nitrous oxide / laughing gas (N 2 O):

* NH 4 NO 3 (s) -> 2 H 2 O (g) + N 2 O (g)

* Colourless, odourless inorganic gas with sweet taste.

* Noninflammable and nonirritating, but of low potency.

* Very potent analgesic

* Carrier and adjuvant to other anesthetics – 70% + 25-30% + 0.2-2% · 45. Nitrous oxide – contd.

* Advantages:

* – Non-inflammable and nonirritant.

* – Rapid induction and recovery

* – Very potent analgesic (low concentration)

* – No nausea and vomiting.

* – Nontoxic to liver, kidney and brain.

* Disadvantages:

* – Not potent alone (supplementation)

* – Hypoxia.

* – Inhibits methionine synthetase (precursor to DNA synthesis).

* – Inhibits vitamin B-12 metabolism.

* – Dentists, OR personnel, abusers at risk.

* – Gas filled spaces – dangerous · 46. 3. Halothane:

* Fluorinated volatile liquid with sweet odor, non-irritant non-inflammable and supplied in amber colored bottle.

* Potent anaesthetic, 2-4% for induction and 0.5-1% for maintenance.

* Boiling point – 50 ºC

* Pharmacokinetics: 60 to 80% eliminated unchanged. 20% retained in body for 24 hours and metabolized. · 47. Halothane – contd.

* Advantages:

* Non-inflammable and non-irritant

* Pharyngeal and laryngeal reflexes – bronchodilatation

* Potent and speedy induction & recovery

* Controlled hypotension

* Inhibits intestinal and uterine contractions

* Disadvantages:

* Special apparatus

* Poor analgesic and muscle relaxation

* Respiratory depression

* Hypotension and arrythmia

* Decreased urine formation

* Hepatitis: 1 in 10,000

* Malignant hyperthermia: Ryanodine receptor · 48. 4. Enflurane:

* Non-inflammable, with mild sweet odour and boils at 57 ºC

* Similar to halothane in action, except better muscular relaxation.

* Depresses myocardial force of contraction and sensitize heart to adrenaline.

* Induces seizure in deep anaesthesia and therefore not used now – Epileptiform EEG

* Metabolism one-tenth that of halothane– does not release quantity of hepatotoxic metabolites

* Metabolism releases fluoride ion– renal toxicity · 49. 5. Isoflurane:

* Isomer of enflurane and have simmilar properties but slightly more potent.

* Induction dose is 1.5 – 3% and maintenance dose is 1 – 2%.

* By special vapourizer. · 50. Isoflurane – contd.

* Advantages:

* Rapid induction and recovery

* Good muscle relaxation

* Good coronary vasodilatation

* Less Myocardial depression than no myocardial sensitization to adrenaline

* No renal or hepatotoxicity

* Low nausea and vomiting

* No dilatation of pupil and no loss of light reflex in deep anaesthesia

* No seizure and preferred in neurosurgery

* Uterine muscle relaxation

* Disadvantages:

* Pungent and respiratory irritant

* Special apparatus required

* Respiratory depression

* Maintenance only, no induction

* ß adrenergic receptor stimulation

* Costly · 51. Intravenous Anaesthetics:

* For induction only

* Rapid induction (one arm-brain circulation time

* For maintenance not used

* Alone – analgesic and muscle relaxants

* Intravenous:

* Inducing agents:

* Thiopentone, Methohexitone sodium, propofol and etomidate

* Benzodiazepines (slower acting):

* Diazepam, Lorazepam, Midazolam

* Dissociative anaesthesia:

* Ketamine

* Neurolept analgesia:

* Fentanyl · 52. 1 Thiopentone sodium:

* Barbiturate

* Water soluble

* Alkaline

* Dose-dependent suppression of CNS activity

* Dose: 3-5mg/kg iv (2.5%) solution – 15 to 20 seconds · 53. Thiopentone sodium – contd.

* Pharmacokinetics:

* Redistribution

* Hepatic metabolism (elimination half-life 7-12 hrs)

* CNS depression persists for long (>12 hr) · 54. Tiopentone – contd,.

* Redistribution:

Blood Brain Muscle Body fat conc. of thiopentoone Time · 55. Side effects of Thiopentone:

* Pre-anaesthetic course – laryngospasm

* Noncompatibility – succinylcholine

* Tissue necrosis–gangrene

* Post-anaesthetic course – analgesic · 56. Thiopentone – contd.

* Advantages:

* Rapid induction

* Does not sensitize myocardium to adrenaline

* No nausea and vomiting

* Non-explosive and non-irritant

* Short operations (alone)

* Other uses: convulsion, psychiatric patients and narcoanalysis of criminals

* Disadvantages:

* Depth of anaesthesia difficult to judge

* Pharyngeal and laryngeal reflexes persists – apnoea – controlled ventilation

* Respiratory depression

* Hypotension (rapid) – shock and hypovolemia

* Poor analgesic and muscle relaxant

* Gangrene and necrosis

* Shivering and delirium · 57. 2. Propofol

* Replacing thiopentone

* Oily liquid used as 1% emulsion

* Rapid induction (one arm-brain circulation time): 15 – 45 seconds and lasts for 5–10 minutes

* Rapid distribution – distribution half-life (2-4 min)

* Short elimination half-life (100 min)

* Dose: Induction – 2mg/kg bolus i.v.

* Maintenance – 9 mg/kg/hr i.v.

* Propofol is extensively metabolized

o 88% of an administered dose appears in the urine

* Metabolized by hepatic conjugation of the inactive glucuronide metabolites · 58. Propofol – contd.

* Advantages:

* Rapid induction

* Does not sensitize myocardium to adrenaline

* No nausea and vomiting

* Non-explosive and non-irritant

* Total i.v. anaesthesia

* Short operations (alone)

* Disadvantages:

* Induction apnoea

* Hypotension

* Braddycardia

* Dose dependent respiratory depression

* Pain during injection: local anaesthetic combination · 59. 3. Ketamine:

* Phencyclidine derivative

* Dissociative anaesthesia: a state characterized by immobility, amnesia and analgesia with light sleep and feeling of dissociation from ones own body and mind and the surroundings.

* Site of action – cortex and subcortical areas – NMDA receptors

* Dose: 5-10mg/kg im or 1-2mg i.v. · 60. Ketamine – contd.

* Disadvantages:

* Limb movements and nystagmus

* Emergence phenomenon – 50% patients

* Hypertensives

* Increase in IOT and ICP

* Uterine stimulation

* Psychosis and shizophrenia

* Rare laryngospasm

* Poor muscle relaxation · 61. Ketamine – contd.

* Uses:

* Characteristics of sympathetic nervous system stimulation (increase HR, BP & CO) – hypovolumic shock

* In head and neck surgery

* In asthmatics

* Short surgical procedures – burn dressing, forceps delivery, breech extraction manual removal of placenta and dentistry

* Combination with diazepam – angiography, cardiac catheterization

* OPD surgical procedures · 62. 4. Fentanyl

* Neurolept analgesia: droperidol

* 4-acylanilino derivative

* Opioid analgesic

* Duration of action: 30-50 min.

* Uses:

* in combination with diazepam used in diagnostic, endoscopic and angiographic procedures

* Adjunct to spinal and nerve block anaesthesia · 63. Fentanyl – contd.

* Advantages:

* Smooth onset and rapid recovery

* Suppression of vomiting and coughing

* Commanded operation

* Less fall in BP and no sensitization to adrenaline

* Disadvantages:

* Respiratory depression

* Increase tone of chest muscle

* Nausea, vomiting and itching during recovery · 64. Complications of anaesthesia:

* During anaesthesia:

* Respiratory depression

* Salivation, respiratory secretions


* Cardiac arrhythmias

* Fall in BP

* Aspiration

* Laryngospasm and asphyxia

* Awareness

* Delirium and convulsion

* Fire and explosion

* After anaesthesia:

* Nausea and vomiting

* Persisting sedation

* Pneumonia

* Organ damage – liver, kidney

* Nerve palsies

* Emergence delirium

* Cognitive defects · 65. Preanesthetic medication:

* Definition:

* It is the term applied to the use of drugs prior to the administration of an anaesthetic agent to make anaesthesia safer and more agreeable to the patient.

* Aim:

* Relief of anxiety

* Amnesia for pre and post operative events

* Analgesia

* Decrease secretions

* Antiemetic effects

* Decrease acidity and volume of gastric juice · 66. Preanaesthetic medication – contd.

* Drugs used:

* Sedative-anxiolytics – diazepam or lorazepam, midazolam, promethazine etc.

* Opioids – Morphine and its congeners

* Anticholinergics – Atropine

* H 2 blockers – ranitidine, famotidine etc.

* Antiemetics – Metoclopramide, domperidone etc. · 67. The Practical approach: Protocol

* Preoperative assesment Preanaesthetic medication Induction by thiopentone or Propofol Muscle relaxants Intubation Nitrous oxide + halogenated hydrocarbon Withdraw and recovery.

Spinal Anesthesia The Subarachnoid Block


Anesthesia for any surgical procedure below the level of T4 requiring sensory loss with or without motor blockade not requiring a secured airway or mechanical ventilation

Anesthesia for a vaginal or cesarean delivery

Physiology of Spinal Anesthesia

Local anesthetic solution injected into the subarachnoid space blocks conduction of impulses along all nerves with which it comes in contact, although some nerves are more easily blocked than others.

There are three classes of nerve: motor, sensory and autonomic. The motor convey messages for muscles to contract and when they are blocked, muscle paralysis results. Sensory nerves transmit sensations such as touch and pain to the spinal cord and from there to the brain, whilst autonomic nerves control the caliber of blood vessels, heart rate, gut contraction and other functions not under conscious control.

Generally, autonomic and pain fibers are blocked first and motor fibers last. This has several important consequences. For example, vasodilation and a drop in blood pressure may occur when the autonomic fibers are blocked and the patient may be aware of touch and yet feel no pain when surgery starts.



Supraspinous/Interspinous Ligaments

Connect adjacent spinous processes

Ligamentum flavum

Connects the lamina of the adjacent vertebrae

Anterior/Posterior Longitudinal Ligaments

The primary supportive ligaments of the vertebral column

Binds vertebral bodies and provides stability

Blood Supply

Arterial Supply

The two posterior spinal arteries arise from the vertebrals and supply the posterior 1/3 of the cord.

The anterior spinal artery arises from the vertebrals and supplies the anterior 2/3 of the cord.

The radicular arteries enter every intervertebral foramen and supply the spinal nerve roots

The radiculospinal branches arise from the vertebral arteries and the aorta. Of these, the largest is the Artery of Adamkiewicz. It supplies much of blood flow to anterior spinal artery.

Venous drainage

Anterior spinal vein

Posterior spinal vein


Sitting Position

No torque

Chin on chest

Arms resting on knees

Footstool/Table to support feet

Lateral Position

Shoulders perpendicular to bed

Positioned with hips on edge of bed

Hugging pillow/knee chest position

Approaches for Spinal Anesthesia

Median Approach. The most common approach, the needle or introducer is placed midline, perpendicular to spinous processes, aiming slightly cephalad.

Paramedian Approach. Indicated in patients who cannot adequately flex because of pain or whose ligaments are ossified, the spinal needle is placed 1.5 cm laterally and slightly caudad to the center of the selected interspace. The needle is aimed medially and slightly cephalad and passed lateral to the supraspinous ligament. If the lamina is contacted, the needle is redirected and “walked off” in a medial and cephalad direction.

Taylor or Lumbosacral Approach. This approach is useful in patients with calcified or fusion of higher intervertebral spaces. The injection site is 1cm medial and 1cm caudad of the posterior iliac spine. The needle is directed 45 degrees medial and 45 degrees caudad, after contacting the lamina the needle is walked upward and medially to enter the L5-S1 interspace.


Anatomic landmarks for the desired level of the block are first identified.

Superior Iliac crests palpated and L4 is identified.

The spine is palpated to ensure spine position with relation to the plane of the floor.

A sterile field is established with povidone-iodine applied with three basic sponges, the solution is applied starting from the injection site moving outward in a circular fashion.

A fenestrated drape is applied, and using a sterile gauze, wipe the iodine from the injection site to avoid initiation into the subarachnoid space.

A skin wheal is raised with 2cc of 1% lidocaine using a 25G needle to the selected space.

A 17G introducer is passed through the skin wheal, angled slightly cephalad through the epidermis, dermis, sub Q, supraspinous ligament, interspinous ligament, stopping in the ligamentum flavum.

A 25G choice needle is inserted into the introducer, passing through the epidural space, dura, and arachnoid to the sub arachnoid space stopping when the presence of CSF is determined.

CSF is aspirated and mixing lines are identified as a change in baricity and temperature as the local anesthetic and CSF mix in the syringe.

The dose is slowly injected, aspirating after instillation.

All needles are removed intact and the patient is positioned.

Monitoring It is essential to monitor the respiration, pulse and blood pressure closely. The blood pressure can fall precipitously following induction of spinal anesthesia, particularly in the elderly and those who have not been adequately preloaded with fluid. Warning signs of falling blood pressure include pallor, sweating or complaining of nausea or feeling generally unwell.

For example, a moderate fall in systolic blood pressure to 80mmHg in a young fit patient or 100mmHg in an older patient is acceptable, provided the patient looks and feels well and is adequately oxygenated.

Bradycardia is quite common during spinal anesthesia particularly if the surgeon is manipulating the bowel or uterus. If the patient feels well, and the blood pressure is

maintained, then it is not necessary to give atropine. If, however, the heart rate drops below 50 beats per minute or there is hypotension, then atropine 300-600mcg should be given intravenously.

It is generally considered good practice for all patients undergoing surgery under spinal anesthesia to be given supplemental oxygen by face mask at a rate of 2-4 liters/minute, especially if sedation has also been given.

Spinal Needles

Pencil Point Needles (Sprotte)

Designed to spread the dural fibers and help reduce the occurrence of post dural puncture headache

Yields a distinct “pop” as the pencil point penetrates the dura

Offers increased “tip strength” to minimize bending or breakage

Precision-formed side hole enables directional flow of anesthetic and reduces the possibility of straddling the dura

Tracks straight when advancing through ligaments toward the dura

Cutting Needle (Quincke)

Dural “pop” is less likely to be appreciated due to the sharper tip

Increased risk of Postdural Puncture Headache due to increased trauma to the dura

Introducer may not be necessary depending on patient size

Common Local Anesthetics

Local Anesthetic +/- Fentanyl 0.25mcg/kg or 0.25-0.5mg Duramorph Concentration T10 level Lower Abdomen T4 level Upper Abdomen Duration Plain Duration With Epinephrine

Procaine 10% 125mg 200mg 45min 60min

Bupivicaine 0.75% in 8.25% dextrose 12-14mg 12-18mg 90-120min 100-150min

Tetracaine 1% in 10% glucose 10-12mg 10-16mg 90-120min 120-240min

Lidocaine 5% in 7.5% glucose 50-75mg 75-100mg 60-75min 60-90min

Ropivicaine 0.2-1% 12-16mg 16-18mg 90-120min 90-120

Factors Affecting the Spread of the Local Anesthetic Solution

A number of factors affect the spread of the injected local anesthetic solution within the CSF and the ultimate extent of the block obtained. Among these are:

the baricity of the local anesthetic solution

the position of the patient

the concentration and volume injected

the level of injection

the speed of injection

The specific gravity of the local anesthetic solution can be altered by the addition of dextrose. Concentrations of 7.5% dextrose make the local anesthetic hyperbaric (heavy) relative to CSF and also reduce the rate at which it diffuses and mixes with the CSF. Isobaric and hyperbaric solutions both produce reliable blocks. The most controllable blocks are probably produced by injecting hyperbaric solutions and then altering the patient’s position.

Assessing the Block

Some patients are very poor at describing what they do or do not feel; therefore, objective signs are valuable. If, for example, the patient is unable to lift his legs from the bed, the block is at least up to the mid-lumbar region.

Sensory loss can best be assessed by testing temperature sensation using an alcohol swab. First touching the patient with the damp swab on the chest or arm (where sensation is normal), so that they appreciate that the swab feels cold. Then work up from the legs and

lower abdomen until the patient again appreciates that the swab feels cold. The level of sympathectomy can be best assessed with light pin pricks moving from nipple line down.

Practical Problems

The spinal needle feels as if it is in the right position but no CSF flows.

Wait at least 30 seconds, then try rotating the needle 90 degrees and wait again. If there is still no CSF, attach an empty 2ml syringe and inject 0.5-1ml of air to ensure the needle is not blocked then use the syringe to aspirate while slowly withdrawing the spinal needle. Stop as soon as CSF appears in the syringe.

Blood flows from the spinal needle.

Wait a short time. If the blood becomes pinkish and finally clear, proceed with the spinal. If blood only continues to drip, then it is likely that the needle tip is in an epidural vein and it should be advanced a little further or angled more medially to pierce the dura.

The patient complains of sharp, stabbing leg pain.

The needle has hit a nerve root because it has deviated laterally. Withdraw the needle and redirect it more medially away from the affected side.

Wherever the needle is directed, it seems to strike bone.

Make sure the patient is still properly positioned with as much lumbar flexion as possible and that the needle is still in the mid-line. If you think that you are not in the midline check with the patient which side they feel the needle. Alternatively, if the patient is elderly and cannot bend very much or has heavily calcified interspinous ligaments, it might be better to attempt a lateral approach to the dura.

Common Complications

Postdural Puncture Headache � incidence related to use of larger needles (22G), cutting needles. Occurrence can also be reduced by rotating the needle so that the bevel is pointed to the side, this decreases trauma to the dura.

Transient Radicular Syndrome/Transient Neurological Syndrome � self resolving pain related to the use of Lidocaine, lithotomy position, and early ambulation post-op.




Less Common Complications

Cauda Equina Syndrome

Total Spinal

Urinary Retention

Cardiac Arrest

Spinal/Epidural Hematoma

Aseptic Meningitis

Bacterial Meningitis

Cranial Nerve Palsies

Cranial Subdural Hematoma


Please enter your comment!
Please enter your name here