ANESTHESIOLOGY

HISTORY of ANESTHESIA

ANESTHESIA is one of
America’s greatest
contribution to the field of
Medicine and to mankind.
 Try to imagine today's health care
without surgery.

It's almost impossible

Now try to imagine surgery without anesthesia

Equally impossible.

Without anesthesia,
many of modern medicine's greatest benefits
simply would not exist
 Pain, a Burden to be Borne
•  In the early days, most people expected to
experience pain in their lives
•  Pain was one of God's punishments for
the wicked and purifying trials for the
good;
•  For the woman in labor, pain was the
spiritual experience that would transform
her into a self-sacrificing mother.
•  Before anesthesia, the best surgeons
were the fastest.
•  Four Herculean men would hold a patient
on a gurney and surgery would proceed.
(“PIGIL ANESTHESIA”)
•  Quick and simple procedures such as
amputations were the majority of surgeries
and most patients would just faint from the
unbearable pain.
 HISTORY of ANESTHESIA
Most commonly used substances to kill pain:
•  opium derived from the poppy flower,
Papaver somniferum.
•  alcohol or wine,
•  mandragora or mandrake from the plant
Atropa mandragora,
•  belladonna from the deadly nightshade,
•  marijuana or Cannabis indica.
 •  From: René Descartes.
From: René Descartes. L'homme de Rene Descartes.
Renatus Des Cartes de homine. Lvgdvni Paris:
Batavorvm: Charles Angot, 1664
Petrvm Leffen & Fransciscvm Moyardvm,
Rene Descartes was the one who first
1662
Described the pain pathway
 HISTORY of ANESTHESIA

In the 1800s the enigma of pain,

has yielded slowly to determined
investigators and clinicians
 Anesthesia History Files

What eventually evolved

into anesthesia
as we know it today
was ushered in with
the chance observation that
the inhalation of nitrous oxide
("laughing gas")
produced a state •  1800 June 25: Humphry Davy
completes the introduction to his
of intoxication during classic work, Researches,
which people became highly Chemical and Philosophical;
amused Chiefly Concerning Nitrous Oxide,
or Dephlogisticated Nitrous Air,
and insensitive to pain.
and its Respiration.
 Anesthesia History Files

Horace Wells (1815-1848), a New England dentist, experimented

with anesthetics in the early 1840s. He attempted at a public
demonstration of nitrous oxide anesthesia failed, humiliating him.
 Anesthesia History Files

Charles Thomas Jackson (Massachusetts)

In 1846, Jackson suggested to Morton (his

student) that he use sulfuric ether
 Anesthesia History Files

Ether was used :

•  as a sedative in the treatment of tuberculosis,

asthma and whooping cough, and as a remedy
for toothache.
•  Its anesthetic potential had never been
exploited.
 Anesthesia History Files
On March 30, 1842,
Crawford Long
made the first use of
ether as a surgical
anesthetic when he
removed a tumor
from the neck of
patient James
Venable.
In 1846, Morton made his famous demonstration of surgical anesthesia at the
Massachusetts General Hospital, using a hastily rigged apparatus to deliver ether to the
patient.
 Anesthesia History Files
In the subsequent bitter debate over
who "discovered" anesthesia,
Charles Thomas Jackson attempted
to claim the achievement for
himself. By 1873, however,
Jackson had been admitted to an
insane asylum where he died in
1880
 Anesthesia History Files

•  In late 1847 Simpson

discovered the
anesthetic
properties of
chloroform
 Anesthesia History Files
•  In 1847 he began to
administer ether at St.
George's Hospital in
London and published a
book on ether anesthesia.
•  In 1853 and 1857 he
administered chloroform to
Queen Victoria for the
births of Prince Leopold
and Princess Beatrice
Dr John Snow
•  Cocaine was first used to achieve topical
anesthesia in 1884.
•  Spinal and epidural anesthesia were
discovered soon after and a combination
of drugs was being used to allow optimal
conditions for physicians to perform
surgery.
By the 1880s
anesthesia,
with aseptic
technique, was
standard
practice in
American and
European
surgical
theaters
 Anesthesia History Files
•  While the surgeon's
prestige and power
soared, the anesthetist
was a mere assistant--a
nurse, intern or medical
student.
•  The development of the
independent medical
specialty of
anesthesiology would
not occur until the early
20th century
Anesthesia History Files
•  After World War II ended in 1945,
major developments in the field of
anesthesiology opened new
avenues of medical and surgical
care that were previously
unthinkable. Thus began the
modern era of anesthesia
 ROLE OF AN
ANESTHESIOLOGIST
à  Constantly changing and its unique role
expanding à to include but not limit itself to :
1.  Provision of insensibility to pain
2.  Monitoring and restoration of homeostasis
3.  Diagnosis & treatment of painful syndromes
4.  Clinical Management of Cardiac and
Pulmonary Resuscitation
5.  Evaluation of Respiratory function and
application of Respiratory Therapy
 The Anesthesiologists’ Role

1.  Deliver pain management and provide life

sustaining care for the pts during surgery
2.  Treat acute and chronic pain via
multidisciplinary approach
3.  Perioperative Physician
4.  Supervise post-operative care
5.  Intensivists
ANESTHESIOLOGISTS’ ROLE
During surgery

1.The Operating theater is still their domain

2.Provide utmost stability of the different vital

organ systems during surgery by vigilant
monitoring and interventions if necessary due
onslaught of the stresses of surgery per se.

3.Provide adequate analgesia during surgery

4. Provide adequate sedation with the objective

of negative recall or awareness
 The Anesthesiologist’s Role

1.  Deliver pain management and provide life

sustaining care for the pts during surgery
2.  TREAT ACUTE AND CHRONIC PAIN VIA MULTI-
DISCIPLINARY APPROACH
3.  Perioperative Physician
4.  Supervise post-operative care
5.  Intensivists
ANESTHESIOLOGISTS’ ROLE
In Pain Managment

“ NO PAIN : PATIENTS GAIN”

•  Acute pain management- caused by
trauma or other acute illnesses but more
so in postoperative analgesia
•  Chronic pain- alleviates patients sufferings
due to nagging and debilitating pain
utilizing multi modal therapy approach
•  Participate in the multidisciplinary
management of cancer
 The Anesthesiologists’ Role

1.  Deliver pain management and provide life

sustaining care for the pts during surgery
2.  Treat acute and chronic pain via
multidisciplinary approach
3.  PERIOPERATIVE PHYSICIAN
4.  Supervise post-operative care
5.  Intensivists
 PERIOPERATIVE PHYSICIAN:

•  PREOP EVALUATION
•  INTRAOP MX
•  POSTOP PREPARATIONS AND MX
 Ultimate Goals of Preanesthetic
& Preoperative Assessment

•  Reduce the morbidity of surgery

•  Increase the quality but reduce the cost of
preoperative care
•  To return the patient to desirable
functioning as quickly as possible
Michael Roizen,ASA Refresher Course 2005
 PREOPERATIVE EVALUATION,
PREPARATION & PREMEDICATION
à Consists of doing a good HX of the patient
•  present & past history
•  Presence of coexisting diseases
•  General survey of the patient (anticipate
technical difficulties à spinal deformity, facial
abnormalities & degree of hydration
•  Preoperative orders – fasting prior to OR,
preoperative medications & IV fluid
maintenance à ordered during the visit
 ASA PHYSICAL STATUS
•  CLASS I – no organic, physiologic, biochemical
or psychologic disturbance
Example: Hemorhoidectomy
•  CLASS II – mild to moderate systemic
disturbance caused by the condition to be treated
or concomitant disease
Example: Px with DM or HPN
•  CLASS III – severe systemic disturbance that
limits activity
Example: recent MI
 ASA PHYSICAL STATUS
•  CLASS IV – severe systemic disturbance
that is life threatening
Example: Cardiac Insufficiency or
Advance Pulmonary disease
•  CLASS V – Moribund subjected to surgery
in desperation
IMPORTANCE OF PRE-MEDICATION

1.  To alleviate apprehension and fear

2.  To lower BMR
3.  To diminish secretions
4.  To decrease reflex excitability
5.  To counteract undesirable effects of
anesthesia
6.  To produce amnesia
 DRUGS USED for PRE-
MEDICATIONS
May consist of any 2 or 3 of
the following drugs
DRUGS USED for PRE-MEDICATIONS
A.  Tranquilizers – Sedative
1.  Barbiturates – short acting
(phenobarbital)
2.  Phenothiazines
3.  Benzodiazepines
B.  Opiates – Analgesics
1.  Meperidine 3. Butorphanol
2.  Nalbuphine 4. Morphine SO
4
C.  Belladona alkaloids – Anticholinergic
1.  AT SO4
2.  Scopolamine SO4
 TYPES OF ANESTHESIA

A.  GENERAL ANESTHESIA

B.  REGIONAL ANESTHESIA
GENERAL ANESTHESIA
•  Anesthetic agents introduced either of
the following routes, producing a
depression of the brain
1.  Oral
2.  Rectal
3.  Intramuscular
4.  Intravenous Mask Inhalational
5.  Inhalational Nasal Insufflation
Endotracheal Intubation
 GENERAL ANESTHESIA

•  Definition: reversible state of

unconsciousness produced by
anesthetic agents, with loss of the
sensation of pain over the whole body
 GENERAL ANESTHESIA
•  MOA- results of reversible changes in
neurologic function caused by drugs that
inhibits synaptic transmission
– In Inhalational Anesthesia (volatile
anesthetics) à inhibition of synapses in
the NEURO-BASAL THALAMUS
– In IV anesthesia à drug receptor
interactions
 INDICATIONS FOR GENERAL
ANESTHESIA
•  Infants and children
•  Adults who prefer GA
•  Extensive surgical procedures
•  Patients with mental disease
•  Long duration of surgery
•  Surgery for which LA is impractical or
unsatisfactory
•  Hx of toxic or allergic reactions to LA drugs
•  Anticoagulant treatment
Order of Descending
Depression
Cortical and Psychic Centers
↓
Basal Ganglia and Cerebellum
↓
Spinal cord
↓
Medullary centers
 COMPONENTS of GENERAL
ANESTHESIA
1.  Sensory Block – loss of sensation
2.  Motor Block – loss of muscle tone
3.  Reflex Block – loss of reflexes
4.  Mental Block – loss of
consciousness
Clinical Signs of General Anesthesia
a.  Insufficient Depth – breath holding, delirium,
involuntary movement, retching and increase
mucus secretion
b.  Sufficient Depth – stable Cardiovascular
response, adequate muscle relaxation,
amnesia and absence of troublesome reflexes
c.  Excessive Depth – no response, nor ability to
resume normal ventilatory function at the end of
the operation with decrease blood pressure
and obtundation
 Maintenance of AIRWAY in GA
1.  Chin lift or jaw thrust maneuver
2.  Pharyngeal Airway
3.  Tracheal Intubation
 ADVANTAGES of
ENDOTRACHEAL INTUBATION
1.  Airway patency is assured

2.  Protection from aspiration

3.  Gastric distention is prevented

 Disadvantage
•  Not being adept to the technique
 Complications of GENERAL
ENDOTRACHEAL ANESTHESIA
1.  Trauma during intubation

2.  Endobronchial intubation

3.  Esophageal intubation

4.  Endotracheal tube obstruction

5.  Laryngospasm
 Complications of General
Anesthesia
A.  Intra-operative Complications
1.  Respiratory Difficulties – hypoventilation due
to respiratory depression
2.  Airway Obstruction
a.  Upper Airway Obstruction
1)  Falling back of the tongue
2)  Foreign bodies above glottis
3)  Endobronchial intubation
4)  Larryngeal spasm & hiccups
 b.  Lower Airway Obstruction
1)  Aspiration
2)  bronchospasm
3.  Cardiovascular Complications
a.  Hypotension
b.  Hypertension
c.  Arrythmias
4.  Occular Complications
5.  Malignant Hyperthermia
B.  Post-operative Complications
1.  Respiratory Complications
a.  Atelectasis
b.  Pneumothorax
2.  Post Anesthesia Shivering
 Prevention of Post-operative
Complications in GA
1.  Continuous monitoring – post-op, BP,
PR, RR, T
2.  Avoid excessive sedation
3.  O2 inhalation
4.  Turn from side to side
5.  Deep breathing
6.  Steam Inhalation to liquefy sputum
secretions
INHALATIONAL
ANESTHETICS
•  Anesthetic potency of volatile anesthetic
is measured by MAC (Minimum Alveolar
Concentration)
•  Value represents alveolar concentration of
an anesthetic (at one atmosphere) that
prevents movement in 50% of the
subjects response to pain
 Commonly used Inhalational
Anesthetics
A.  Halothane
•  Halogenated alkane
•  Sensitize the myocardium to the action of
Epinephrine
•  May cause cardiac dysrhytmias
•  Maybe toxic to the liver causing necrosis
– “HALOTHANE HEPATITIS”
B.  Enflurane
•  Nonflammable fluorinated ethyl methyl
ether
•  Bio-transformation releases Fluoride but
not nephrotoxic levels
•  Increases ICP, increase risk of seizure
activity
•  May cause Tonic-CLonic Twitching of the
muscles of the face & limbs at high
concentrations
C.  Isoflurane
•  Methyl ethyl ether isomer of enflurane
•  Can cause coronary artery vasodilatation
which might lead to CORONARY ARTERY
STEAL SYNDROME

D.  Desflurane
•  Fluorinated methyl ethyl ether
•  Cannot be delivered by standard
vaporizers. Requires USE OF
ELECTRICALLY HEATED VAPORIZERS
•  Low tissue solubility à rapid elimination
and awakening. (ULTRA SHORT
DURATION of ACTION)
E.  Sevoflurane
•  Fluorinated isopropyl ether
•  Reacts with CO2 absorbents to form a
special halokene (COMPOUND A) à
metabolized to nephrotoxins which can
lead to Kidney damage
•  Potential nephrotoxicity due to organic
fluoride avoided in pre-existing Renal
disease
F.  Nitrous Oxide
•  Laughing gas
•  Only INORGANIC gas in clinical use
•  At room tempreture à Gas BUT is Liquid
under pressure in the tank
•  Weak Anesthetic BUT Potent Analgesic
•  Causes DIFFUSION HYPOXIA
•  SHOULD NOT be used in doses higher
than 70 % and combined with 30% O2
INTRAVENOUS AGENTS
 Drugs
1.  Barbiturates

2.  Non-Barbiturates
•  Benzodiazepines •  Analgesic- Hypnotic Combinations

•  Ketamine •  Balanced Anesthesia

•  Propofol •  muscle relaxant
•  Neuroleptanalgesia • N2O
Barbiturates
MOA: enhances and mimic action of GABA
by binding to the receptor

Thiopental
•  Ultra short acting barbiturates
•  Blocks central brain core (RAS) à
unconsciousness
•  rapid onset short duration of action
Indications
•  Induction of anesthesia
•  As a sole anesthetic agent
•  Supplementation to other drugs
•  Conjunction with regional anesthesia
•  Treatment of Status Epilepticus
•  Cerebral protection with raised ICP
Contraindications
•  Severe shock or hypovolemia
•  Status asthmaticus
•  Porphyria
•  Absence of IV access, or general
anesthetic equipment
Non-Barbiturates
1.  Benzodiazepenes
•  MOA: potentiation of neural inhibition
mediated by GABA-aminobutyric acid
•  Pharmacologic effect
Ø  Anxiolytic
Ø  Sedative
Ø  Hypnotic
Ø  Muscle relaxant
Ø  Amnesic (ANTEROGRADE AMNESIA)
Ø  Anticonvulsant
Benzodiazepenes
a.  Diazepam
•  Insoluble in water
•  Relieves muscle spasm and spasticity via central
effect
b.  Lorazepam
•  Insoluble in water
•  5 to 10 X potent as diazepam
•  Used as premedication
•  PROFOUND ANTEROGRADE ANESTHESIA
c.  Midazolam
•  Same as diazepam
•  Water soluble & has an imidazole ring
•  Anterograde amnesia is shorter than Lorazepam
•  Short elimination half life (t1/2): 2hrs
•  Useful drug for sedation in
1)  Outpatient anesthesia
2)  Minor procedures and regional anesthesia
3)  Intensive care
Non-Barbiturates
3.  Propofol
•  rapid loss of consciousness with rapid recovery
•  Bolus dose of 2mg/kg is ~4-5 minutes
•  Minimal accumulation due to rapid metabolism
•  Advantages:
»  Rapid clearance and few residual effects on
awakening
»  Decrease ICP, reduced IOP, arterial BP
»  Effective in treating nausea and vomitting
Non-Barbiturates
4.  Neuroleptanalgesia
•  Combination of a potent analgesic and a
neuroleptic tranquilizer (fentanyl +
droperidol = Innovar)
•  Produces state of mental detachment and
indifference to pain
•  MOA: competitive antagonism at
Dopaminergic receptors
»  DROPERIDOL

»  FENTANYL
 NEUROLEPTANESTHESIA
addition of nitrous oxide, oxygen
and muscle relaxants
IV DRUGS used as ADJUNCTS to
ANESTHESIA
1.  Opiods
•  Classification
Ø  AGONISTS

Ø  AGONIST/ANTAGONIST

Ø  ANTAGONIST
Morphine
–  Central actions and side effects
•  DEPRESSANT EFFECT à analgesia, sedation,
depresses respiration & cough reflex, decreases
GI motility
•  EXCITATORY EFFECT à euphoria, miosis,
nausea & vomiting, bradycardia, release of ADH
•  Increases smooth muscle tone
•  HISTAMINE RELEASE à broncospasm,
erythema
Meperidine
–  Actions similar to morphine
–  Shorter duration of respiratory depression
–  Not as marked euphoria
–  More pronounced nausea & vomiting
–  Mild quinidine like effect
–  Less histamine release
–  Less or no GIT actions
Naloxone (Pure opioid Antagonist)
–  Competitive antagonists at the opioid
receptor sites
2.  Muscle Relaxants – Neuromuscular
blockers
•  Types of Neuromuscular Blockers (NMB)
a.  Depolarizer

b.  Non-depolarizer
a.  Depolarizers
MOA: prolongs depolarization/ mimic Ach action
reduces sensitivity of the post-junctional
membrane to Ach
SUCCINYLCHOLINE
–  Depolarization of the membrane w/c persists
until the drug diffuses away
–  Manifest 1st muscle twitching and
fasciculation
–  ONLY DEPOLARIZING AGENT IN
CLINICAL USE
–  Elimination: enzymatic destruction by
PSEUDOCHOLINESTERASE
–  Onset of action: 30 secs Duration: 5 mins
–  Recovery within 5 to 10 mins
b.  Non-Depolarizers
MOA: acts by competitive inhibition
•  Reversed by Anticholinesterases (prostigmine,
neostigmine)
•  Do not cause muscular contractions
(fasciculations)
Types of non-depolarizers
a)  Long acting (45 mins)
Pancuronium – eliminated via kidney
b)  Intermediate acting (20-30 mins)
1)  Atracurium – eliminated vai HOFFMAN elimination
pathway
2)  Vecuronium – eliminated thru the biliary
3)  Rocuronium – eliminated thru the kidney
c)  Short Acting (15- 20 minutes)
Mivacurium – eliminated by pseudocholinesterases
Clinical Uses
•  Facilitate tracheal intubation
•  Provide skeletal muscle relaxation during
surgery (adjunct to GA)
•  Used in intensive care units
Regional Anesthesia
 PHYSIOLOGY OF NERVE
CONDUCTION
•  Nerve Fiber – impulse – transmitting
unit
•  Membrane
–  90% of lipids
–  10% protein
•  Channels guarded by “gates”
–  K+ pass freely in and out
–  Na+ barred outside
•  Negative resting potential -70 to -90 mV
 PHYSIOLOGY OF NERVE
CONDUCTION
•  Nerve Stimulation
–  Gates open
–  Na+ rushing in
–  Shifting of polarity
–  Depolarization
 Classification of
Regional Anesthesia
(according to SITE of application)

I. TOPICAL – skin or mucous membrane

spray – refrigeration (e.g. boils / abcess)
ointment – insect bites
instillation – urethral meatus
contact – cotton pledgets in nasal mucosa
II. INFILTRATION – incision site / tissue to be
cut (e.g. sebaceous cyst)
III. FIELD BLOCK – around tissue to be cut
(e.g. breast mass)
IV. INTRAVENOUS REGIONAL (Bier Block)

§ Peripheral vein of
upper / lower extremity

§ I.V. catheter inserted

§ Desanguinated
extremity

§ Esmarch elastic
bandage
§ 2 tourniquets (BP cuffs)

§ bandage removed
§ LA injected over 2-3
minutes

§ Distal tourniquet inflated

after 20-30 minutes

§ Proximal tourniquet
deflated

§ Slow release of
tourniquet after at least
15-20 minutes

§ Use: short surgical

procedure
< 45 minutes in upper /
lower extremity
V. CONDUCTION BLOCK – along nerve
or course of nerves

A. Peripheral Nerve Blocks

B. Central Blocks
Peripheral Nerve Blocks

1. RETROBULBAR NERVE
BLOCK
(ciliary ganglion)
•  Indications
–  Cataract surgery
–  Corneal transplant
–  Enucleation
•  Complications
–  Retrobulbar hemorrhage
–  Globe perforation
•  Contraindications
–  Bleeding disorders
–  Extreme myopia
–  Open-eye injury
 Peripheral Nerve Blocks
2. GASSERIAN GANGLION BLOCK
Branches of trigeminal nerve
(ophthalmic, maxillary, mandibular)

Indications
•  Trigeminal neuralgia
•  Cancer pain in face
•  Operations in face teeth, gum, mandible, etc.
•  Technique: LA injected into respective
foramen of nerve branches
Peripheral Nerve Blocks
3. CERVICAL PLEXUS BLOCK

•  Anterior rami of C1-C4 spinal nerve roots

•  Sensory supply to jaw, a neck, occiput, chest-
shoulders, clavicle, upper border of scapula
•  Indications
–  Operations in the neck
–  Cervical lymph node biopsy
–  Carotid endarterectomy
–  Thyroid operations
Peripheral Nerve Blocks
4. BRACHIAL PLEXUS BLOCK

•  Anterior rami of C4-T2 spinal nerve roots

•  Entire motor supply of upper extremity
•  Almost entire sensory supply – except over
shoulder and medial arm
Major Peripheral Branches
a. Axiliary N – shoulder
abduction
b. Musculocutaneous –
elbow flexion
c. Radial – elbow, wrist,
and finger extensions
d. Median – wrist and
finger flexion
e. Ulnar – wrist and
finger flexion
Peripheral Nerve Blocks
4. BRACHIAL PLEXUS BLOCK

•  Indication:
operations of upper extremity

•  Approaches to Brachial Plexus Block

1. interscalene approach
2. supraclavicular
3. axillary
BRACHIAL PLEXUS BLOCK
Interscalene approach
 BRACHIAL PLEXUS BLOCK
Supraclavicular approach
BRACHIAL PLEXUS BLOCK

Axillary approach
Peripheral Nerve Blocks
5. INTERCOSTAL NERVE BLOCK
•  Anterior rami of 1st eleven spinal nerves
•  At inferior surface of ribs

•  Indications
–  Post-op analgesia of thoracic and upper abdomen
surgeries
–  Relief of pain from rib fractures, herpes zoster,
pleurisy, CA

•  Complications: pneumothorax
INTERCOSTAL NERVE BLOCK
INTERCOSTAL NERVE BLOCK
INTERCOSTAL NERVE BLOCK
Peripheral Nerve Blocks

6. WRIST BLOCK
•  Ulnar nerve
•  Median
•  Radial

•  Indications:
–  surgery or analgesia
distal to
metacarpophalangeal
joints
–  suture of lacerations
–  paronychia, abcess
 Peripheral Nerve Blocks
7. DIGITAL NERVE BLOCK

•  Digital branches of
ulnar, median, radial

•  Indications:
–  minor procedure in
fingers

•  Reminder:
–  avoid using large volume
of LA
–  do not add
vasoconstrictors
Peripheral Nerve Blocks
8. ANKLE BLOCK

•  Blocks five nerves supplying foot

a. Deep peroneal
b. Superficial peroneal
c. Saphenous
d. Posterior tibial
e. Sural

•  Indications
–  Surgery of foot and toes in frail patients
who cannot tolerate hemodynamic effects
of GA or neuraxial block
Peripheral Nerve Blocks

8. ANKLE BLOCK

•  Precaution
–  Avoid epinephrine to
reduce risk of
ischemia

•  Complication
–  Intravascular
injection
Peripheral Nerve Blocks
9. PUDENDAL
NERVE BLOCK

•  sacral plexus (S2 – S3 –

S4)

•  Indications
–  perineal surgery
o  hemorrhoids
o  lacerations
–  obstetric vaginal delivery

•  Complications
–  puncture of fetal head
–  inadvertent IV infection
Peripheral Nerve Blocks
10. DORSAL PENILE BLOCK

•  Base of penis at symphysis pubis

•  Blocks dorsal nerve
•  Fan-shaped injection at the base blocks
dorsal and ventral branches

•  Indications
–  Penile surgery
–  Post-op pain relief
Peripheral Nerve Blocks
10. DORSAL PENILE BLOCK

•  Precautions
–  Avoid big volume of solution
–  Avoid epinephrine or any vasoconstrictor

•  Complication
–  Artery spasm – ischemic injury to penis
Central Blocks
A. SPINAL ANESTHESIA
Sub Arachnoid Block, Intrathecal Block

•  Local anesthestic deposited at sub arachnoid

space
•  Acts on spinal nerve roots, dorsal ganglia, not
on substance of spinal cord
•  Redistributed via vascular absorption
•  Produces sympathetic block, sensory
analgesia and motor block
Indications
•  Surgery involving lower half of body
–  Upper abdomen
–  Lower abdomen
–  Perineum
–  Lower Extremity
•  Obstetrics – vaginal delivery
Caesarian section
•  Painful diagnostic and therapeutic
procedures below diaphragm
Contraindications
•  Absolute
–  Bleeding disorders
–  Septicemia
–  Inc. intracranial pressure
–  Chronic dermatitis or infection near puncture site
–  Pre-existing spinal cord disease
–  Hypotension
–  Patient refusal
–  Systemic disease with neurologic sequelae

•  Relative
–  Hemorrhage
–  Back problem due to muscle strain, arthritis
–  Extremely tense / psychotics
–  Children
–  Respiratory disease
Drugs Used
•  Tetracaine
•  Lidocaine
•  Bupivacaine

Factors Determining Level of Anesthesia

•  volume of solution
•  concentration
•  barbotage
•  speed of injection
•  patient position
•  specific gravity of solution
•  site of injection
•  height of patient
•  increased intra-abdominal pressure
Technique

A. Position
–  Lateral decubitus – knees flexed to chest
hin put down on chest (nose-to-knee)
–  Sitting – when lateral approach is difficult (e.g.
obese patients)

B. Puncture Sites
– Interspaces between L2-L3, L3-:4, L4-L5
– Line joining highest points of iliac crests
crosses either body of L4 or interspace
between L4-L5
Structures Traversed By Spinal Needle

a. Skin
b. Subcutaneous Tissue
c. Supraspinous ligament
d. Interspinuous ligament
e. ligamentum flavum
f. Dura
PHYSIOLOGIC EFFECTS (Immediate
Complications)
A. Cardiovascular
Sympathectomy ⇒ vasodilation ⇒ ⇓ BP, ⇓ CR
B. Respiratory
Difficulty of breathing
Apnea (high level)
C. Gastrointestinal
Nausea / vomiting in 20%

DELAYED COMPLICATIONS
–  Headache – leak of CSF
–  Backache
–  Urinary retention
–  Hemiplegia – hematoma
Levels of Spinal Anesthesia –
Dermatomes Involved

1.  Saddle Block – sensory loss involves lowers

lumbar and sacral segments.
Area that “sits on the saddle”.
2.  Low Spinal – level of umbilicus (T10) lower
thoracic lumbars and sacrals.
3.  Mid-Spinal – costal margin (T6) lower thoracic
lumbars and sacrals
4.  High Spinal – nipple line (T4) thoracic segments
(T4 – T12) lumbars and sacrals
 Central Blocks
B. EPIDURAL ANESTHESIA
•  Anatomy
–  Epidural space – base of skull (foramen magnum) to the coccyx
(sacrococcygeal membrane)
–  Distance from skin to epidural space – 4-5 cm
–  Epidural space contains loose areolar tissue, fat, arterial and
venous networks, lymphatics, spinal nerve roots

•  LA deposited in epidural space

•  Block spinal nerve roots that traverse peridural space
•  Blocks sympathetic nerves traveling with the anterior roots
•  Applications range from sensory analgesia, minimal motor block,
or dense anesthesia and full motor block – controlled by drug
choice, concentration, dosage
Types – selective blockade possible
because it can be performed at any
level of spine
•  Cervical epidural
•  Thoracic epidural
•  Lumbar epidural
•  Caudal epidural

Factors Influencing Spread of Solution

•  Height of patient
•  Drugs used
•  Volume
•  Concentration
•  Level of catheter insertion
Technique
•  Method
–  Single dose injection
–  Fractional – continuous epidural – repeated
injections of LA through catheter inserted into
epidural space
•  Position
–  Cervical epidural – sitting (C7)
–  Thoracic epidural (T7) Lateral
–  Lumbar epidural Decubitus, full
(L1-L2, L2-L3, L3-L4, L4-L5) flexion
Method of Identifying Epidural Space

Principle: negative pressure in space

•  Loss of resistance
–  Plunger of syringe pushed without resistance
once epidural needle is in
•  Hanging Drop
–  Drop of saline at hub of epidural needle is
sucked in once it enters space
Indications
•  All operations below diaphragm
•  May be used in
–  Poor risk patients
–  Cardiac diseases
–  Pulmonary diseases
–  Metabolic disturbances
–  When GA is contraindicated
–  When spinal anesthesia is contraindicated
–  Painful conditions including post-op pain relief
 Contraindications – similar to spinal
•  Severe hemorrhage
•  Coagulation defects
•  Previous laminectomy
•  Uncooperative / apprehensive
•  Local inflammation at site
•  Patient refusal

Advantages
•  Well-defined area of anesthesia
•  Longer duration
•  More severe disturbances of spinal anesthesia
minimized
•  GI complaints minimized
•  Catheterization minimized
•  Less respiratory effects
Disadvantages
•  Technically more difficult
•  Muscle relaxation not complete
•  Large volume necessary
•  Danger of dural puncture
•  Incomplete / patchy block

Physiologic Effects
•  Similar to those observed in spinal anesthesia
•  Slower onset
•  Less intensity of motor and sensory block

Drugs: opiods, opiates, low-dose LA

Central Blocks
C. CAUDAL ANESTHESIA
•  LA injected into the epidural space in the sacral
canal through sacral hiatus
•  Blocks lumbosacral plexus (T12, L1-5, S1-3) and
coccygeal plexus (S4-5, coccygeal nerves)
•  Indications
–  OB – vaginal deliveries
–  Surgery involving lower abdomen, perineum
–  Post-op pain control following these surgeries
especially pediatric patients
Technique
•  Patient prone or lateral
•  Needle inserted into sacral hiatus
•  15-20 ml Lidocaine

Physiologic Effects
•  Similar to lumbar epidural
•  Related to level achieved – volume of
drug
Complications
•  Accidental Dural puncture
•  General systemic reactions
•  Infection at site of injection

Disadvantages
•  Difficult to obtain high level
•  Needs big amount – systemic reactions
possible
•  Infection possible
•  5-10% failure – anatomic anomalies or
incorrect method
ANESTHETIC AGENTS
&
LOCAL TOXICITY

(addendum by dr. b.)

 Local Anesthetics
•  Reversible inhibition of sensory nerve
impulse conduction

•  Prevent transmission of information to the

CNS

•  No loss of consciousness
Clinical Usefulness
Depends on:
•  Inherent Anesthetic potency
•  Rate of onset
•  Duration of effect

Which in turn is dependent on:

•  Physiochemical properties
•  Inherent vasodilator activity
 Physiochemical Properties
1.  Lipid Solubility

2.  Protein Binding - duration

3.  pKA – determines onset of anesthesia

 Pharmacokinetics of Common
Local Anesthetics

Molecular Protein Maximum

pKa
weight binding dose (mg)
300
Lidocaine 234 7.9 65 %
500 w/ Epi
Racemic 175
288 8.01 95 %
bupivacaine 225 w/ Epi
Ropivacaine 328.89 8.07 94 % 150

L-bupivacaine 324.9 8.09 > 97 % 150-375

 Vasodilator Properties
•  All except cocaine exhibit biphasic effect
on vascular smooth muscle
•  Extreme low concentration
vasoconstriction
•  Concentration for regional anesthesia
vasodilators
NON PHARMACOLOGIC FACTORS
INFLUENCING ACTIVITY
1.  Dosage

2.  Addition of vasoconstrictor

3.  Site of injection

4.  Additives

5.  Mixture of LA
1.  Dosage
•  Primary qualities of regional anesthesia
(onset, duration, depth) are related to the
mass of the drug à volume x concentration
2.  Site on Injection
•  Due to the particular anatomy of the area of
the injection, variation in the rate of
absorption & amount of drug used
•  In Spinal anesthesia, lack of nerve sheath
around spinal cord are responsible for the
rapid onset
3.  Additives
a.  CO2
b.  NaHCO3 – increase pH near pKA more ionized à
faster entry faster onset
c.  KCl
d.  Dextran

4.  Mixture of Local Anesthesia

à basis is for the mixture of local anesthesia to
compensate for the short duration of action and
the long latency of others
Clinically Useful Local Anesthesia
1.  AMINO-ESTERS
•  Ester link between aromatic and main portion of
the molecule

2.  AMINO-AMIDES
•  Amide linkages
Local Anesthetics Classification
1) Amides CH3
O CH2 CH3
NH C CH2 N
CH2 CH3
CH3
Lidocaine, Bupivacaine,
Ropivacaine, Levobupivacaine
2) Esters CH3
O CH3
CH2
C C CH2 CH2 N
CH2 CH3
CH3
Procaine, Chloroprocaine,
Cocaine, Tetracaine
 Mechanism of Action

Ø  Prevent generation and conduction of

nerve impulses by decreasing or
preventing the large transient increase in
permeability of excitable membranes to
Na+
 Local Anesthetics
Mechanism of Action

blocks voltage-sensitive Na+ ion channels

in neuronal membrane

prevent Na+ influx (Depolarization)

prevent transmission
of nerve impulses
a.  Low anesthetic potency & short duration of
action à procaine & chloroprocaine

b.  Intermediate anesthetic potency & duration

of action à lidocaine, mepivacaine &
prilocaine

c.  High anesthetic potency and prolonged

duration of action à tetracaine,
bupivacaine : racemic and
levobupivacaine, ropivacaine,
ethidocaine
 TOXICITY
Local Anesthetic Toxicity
A.  Systemic – CNS, CVS

B.  Local – neural & skeletal muscle irritation

C.  Specific – addiction, allergy,

methemoglobinemia
 Systemic Toxicity
1.  CNS Toxicity
•  Related to intrinsic anesthetic potency
•  LOW DOSE – excitatory
§  Mechanism: selective blockade of inhibitory Pathway in
the cerebral cortex à allows facilitatory neurons to
function unopposed

•  LARGE DOSES – CNS depression

§  Mechanism: inhibition of both facilitatory & inhibitory
Pathway
§  Sign: convulsion ceases, respiratory depression, arrest
 Subjective CNS Symptoms
Ø  light headedness

Ø  Dizziness

Ø  Visual & Auditory disturbances – difficulty in

focusing & tinnitus

Ø  disorientation

Ø  drowsiness
 Objective CNS Signs
(at low dose)
Ø  shivering

Ø Muscular twitching

Ø Tremors – muscles of face and distal parts of

the extremities

Ø  convulsions – tonic, clonic

 Relationship of LA Toxicity to
Lidocaine Plasma Concentration
Ø  CVS depression - higher conc
Ø  respiratory depression - higher conc
Ø  coma
Ø  convulsion
Ø  unconsciousness
Ø  muscular twitching
Ø  visual & auditory disturbances
Ø  lightheadedness
Ø Numbness of tongue – low concentration
note: CNS is more susceptible to the effect of LA,
hence CNS ssx preceed CV ssx of depression
Factors that Affect CNS Toxicity
•  Potency

•  Rate of Injection

•  Rate at which a particular blood level is

attained
 Effects of Increase pCO2 on CNS
Toxicity
•  pCO2 level is inversely related to
convulsive threshold
•  Enhances cerebral blood flow so more
local anesthesia is delivered to the brain
•  Decrease plasma protein binding of local
anesthesia, more local anesthesia
available to the brain
2.  CVS Toxicity – Cardiac, Vascular
a.  Cardiac Effect
•  Dose dependent negative inotropic
action – depends on potency of LA
•  Inhibit Na conductance in fast channels
•  High concentration of lidocaine,
procaine & tetracaine can block slow
calcium channels
•  Increase LV EDP, direct pulmonary
vasoconstriction effect
 Cardiotoxicity

1)  INDIRECT EFFECTS

a) block sympathetic  innervation

b) other CNS-mediated mechanisms

2)  DIRECT EFFECTS
a) Block  Na+ channels
conduction delay & QRS prolongation

b) Block K+ & Ca++ channels

LIDOCAINE
–  decreases max rate of depolarization w/o
altering RMP
–  Action potential duration and effective
refractory period decreases
–  Ratio of effective refractory period to AP is
incresed in Purkinjie fibers and ventricular
muscles
Lidocaine- (INCREASED DOSE)
–  prolongation of conduction time, increase PR
interval and QRS duration
–  Decrease pacemaker activity in SA node –
sinus bradycardia & sinus arrest
–  Decrease AV node – increases PR interval,
partial, complete AV dissociation
 BUPIVACAINE

v  local anesthetic used in regional

anesthesia for over 3 decades
⇒ good motor/sensory block
⇒ less associated with tachyphylaxis
⇒ potential for cardiotoxicity and
CNS toxicity
BUPIVACAINE
•  Causes ventricular arrhythmia
– Mechanism: depresses the rapid phase of
Depolarization (V max)
» Slow rate of recovery resulting in incomplete
restoration of V max between action
potentials when heart rate exceeds 100/min
» Unidirectional block and re-entry type of
arrythmia
 LEVOBUPIVACAINE
Cardiotoxic potential in animal studies

v  less affinity for myocardial Na channels

than D-bupivacaine in isolated guinea pig
ventricular myocytes
Stereoselective block of cardiac sodium channels by
bupivacaine in guinea pig ventricular myocytes.
Valenzuela, et. al. 1995
Stereoisomers – compounds made up of
same atoms connected by the same
sequence of bonds with different 3D
structure

Enantiomers – pairs of stereoisomers

that, in their 3D projection, are related to
each other as an object to its mirror
image, and thus are not superimposable
 RACEMIC BUPIVACAINE
ENANTIOMERS:
1. Dextrorotation = (+)
enantiomer that rotates
polarized light to the
right
2. Levorotation = CH3 CH3 CH3 CH3
(-) enantiomer that NH NH
rotates polarized light
to the left O O

+ +

RACEMIC MIXTURES N N
equal amounts of C4H9 C4H9
enantiomers in a
chiral compound R (+) enantiomer
S (-) enantiomer
LEVOBUPIVACAINE DEXTROBUPIVACAINE
 Clinical Relevance of Stereoisomers

Toxicological & local anesthetic effects of optically

active isomers of 2 local anesthetic compounds.
Aberg, 1972
Optical isomers of mepivacaine & bupivacaine.
Laduena, 1972

v dose required to produce LD50 is less for R(+)

than the S(-) enantiomer of bupivacaine
 LEVOBUPIVACAINE
Cardiotoxic potential in animal studies

v 3-4x less toxic than equivalent

concentrations of bupivacaine in
isolated perfused rabbit heart
v QRS widening/ occurrence of
arrhythmia less marked in heart
perfused with Levobupivacaine vs
D-Bupivacaine
Comparative effect of racemic bupivacaine, levobupivacaine &
ropivacaine on isolated rabbit heart. Mazoit, et. al. 1999
 Difference between Bupivacaine
and Lidocaine Toxicity
•  Ratio of dosage required for irreversible cardiovascular
collapse: the dosage that will produce CNS toxicity
(convulsion) à lower for Bupivacaine

•  Ventricular Arrhythmia and fatal ventricular fibrillation

with bupivacaine, not with lidocaine

•  Pregnant patients more sensitive to cardiotoxic effects of

Bupivacaine

•  Resuscitation more difficult with bupivacaine

•  Acidosis and hypoxia potentiate cardiotoxicity of

bupivacaine
 CVS Toxicity
b.  Peripheral Vascular Effects (BIPHASIC)
LOW DOSE – stimulates myogenic contraction and
augments basal tone leading to higher pressure

HIGH DOSE – inhibits myogenic activity àvasodilation

COCAINE – initial effect is vsaodilatation followed by

vasoconstriction at low and high doses
Mechanism of Action – inhibits re-uptake of NE by tissue
binding site, therefore no re-uptake leading to increase
free NE, potentiating the effects of adrenergic
stimulation.(hypertension and ventricular ectopia)
 Local Toxicity
•  The more potent longer acting local
anesthesia (e.g. Bupivacaine,
ethidocaine): > degree of localized skeletal
muscle damage than less potent shorter
acting agents like Lidocaine and Prilocaine
•  Reversible
•  No clinical signs of local irritation
 Specific Toxicity
1.  Methemoglobinemia – PRILOCAINE
–  Mechanism: degraded in the liver to
otoluidine which causes oxidation of Hgb
à requires 600mg Prilocaine to produce
clinical level of Methemoglobenemia
àReversed with Methylene blue
2.  Allergy
–  AMINO ESTERS à derivatives of para-
amino-benzoic-acid (allergenic)
 LOCAL ANESTHESIA
TOXICITY
•  Depend on blood level of local anesthesia
delivered to the brain and heart
•  Appropriate dose and technique rarely
causes adverse reaction
•  Toxic levels – usually due to intravascular
injection or excess dose in extravascular
administration
 EXTRAVASCULAR INJECTION BLOOD
CONCENTRATION
Depends on:
•  Absorption

•  Tissue Redistribution

•  Metabolism

•  Excretion
 Factors Affecting Absorption
•  Site of injection – more blood supply >
absorption

•  Choice of Drugs – characteristics of the drug

may affect absorption

•  Dosage

•  Addition of Epinephrine – depends on the

sensitivity of the vessels at the site of injection
and local anesthesia itself
DAGHAN SALAMAT!!