ANESTHESIOLOGY

HISTORY of ANESTHESIA

ANESTHESIA is one of Americas 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: Ren Descartes. Renatus Des Cartes de homine. Lvgdvni Batavorvm: Petrvm Leffen & Fransciscvm Moyardvm, 1662

From: Ren Descartes. L'homme de Rene Descartes. Paris: Charles Angot, 1664
Rene Descartes was the one who first 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 of intoxication during which people became highly amused and insensitive to pain.

1800 June 25: Humphry Davy completes the introduction to his classic work, Researches, Chemical and Philosophical; Chiefly Concerning Nitrous Oxide, or Dephlogisticated Nitrous Air, 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
Constantly changing and its unique role expanding 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 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
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

Consists of doing a good HX of the patient
present & past history Presence of coexisting diseases General survey of the patient (anticipate technical difficulties spinal deformity, facial abnormalities & degree of hydration Preoperative orders fasting prior to OR, preoperative medications & IV fluid maintenance 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. 2. 3. 4. 5. To alleviate apprehension and fear To lower BMR To diminish secretions To decrease reflex excitability To counteract undesirable effects of anesthesia 6. To produce amnesia

DRUGS USED for PREMEDICATIONS 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

1. 2. 3. 4. 5.

Anesthetic agents introduced either of the following routes, producing a depression of the brain Oral Rectal Intramuscular Intravenous Mask Inhalational 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) inhibition of synapses in the NEURO-BASAL THALAMUS In IV anesthesia 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. 2. 3. 4. Sensory Block loss of sensation Motor Block loss of muscle tone Reflex Block loss of reflexes 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) 2) 3) 4) Falling back of the tongue Foreign bodies above glottis Endobronchial intubation 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 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) 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 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
Ketamine Propofol
Analgesic- Hypnotic Combinations

Balanced Anesthesia 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) 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

Anxiolytic Sedative Hypnotic Muscle relaxant Amnesic (ANTEROGRADE AMNESIA) Anticonvulsant

Benzodiazepenes
a. Diazepam
Insoluble in water Relieves muscle spasm and spasticity via central effect
Insoluble in water 5 to 10 X potent as diazepam Used as premedication PROFOUND ANTEROGRADE ANESTHESIA

b. Lorazepam

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
AGONISTS

AGONIST/ANTAGONIST
ANTAGONIST

Morphine
Central actions and side effects
DEPRESSANT EFFECT analgesia, sedation, depresses respiration & cough reflex, decreases GI motility EXCITATORY EFFECT euphoria, miosis, nausea & vomiting, bradycardia, release of ADH Increases smooth muscle tone HISTAMINE RELEASE 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

a. 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 1520 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 Retrobulbar hemorrhage Globe perforation Bleeding disorders Extreme myopia Open-eye injury

Complications

Contraindications

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, chestshoulders, 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 weight Lidocaine Racemic bupivacaine Ropivacaine L-bupivacaine 234 288 328.89 324.9

pKa
7.9 8.01 8.07 8.09

Protein binding 65 % 95 % 94 % > 97 %

Maximum dose (mg) 300 500 w/ Epi 175 225 w/ Epi 150 150-375

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 volume x concentration 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

2. Site on Injection

3. Additives
a. CO2 b. NaHCO3 increase pH near pKA more ionized faster entry faster onset c. KCl d. Dextran

4. Mixture of Local Anesthesia 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 NH CH3 O CH2 CH2 N CH2 CH3

CH3

Lidocaine, Bupivacaine, Ropivacaine, Levobupivacaine

2) Esters

CH3 O C CH3 C CH2 CH2 N

CH2 CH2

CH3

CH3

Procaine, Chloroprocaine, Cocaine, Tetracaine

Mechanism of Action
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 procaine & chloroprocaine

b. Intermediate anesthetic potency & duration of action lidocaine, mepivacaine & prilocaine
c. High anesthetic potency and prolonged duration of action 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 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

light headedness Dizziness Visual & Auditory disturbances difficulty in focusing & tinnitus disorientation drowsiness

Objective CNS Signs (at low dose)

shivering Muscular twitching Tremors muscles of face and distal parts of the extremities convulsions tonic, clonic

Relationship of LA Toxicity to Lidocaine Plasma Concentration

CVS depression - higher conc respiratory depression - higher conc coma convulsion unconsciousness muscular twitching visual & auditory disturbances lightheadedness 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
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 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

ENANTIOMERS: 1. Dextrorotation = (+) enantiomer that rotates polarized light to the right 2. Levorotation = (-) enantiomer that rotates polarized light to the left

RACEMIC BUPIVACAINE

CH3 NH

CH3 CH3 NH O + O +

CH3

RACEMIC MIXTURES equal amounts of enantiomers in a chiral compound

N C4H9
S (-) enantiomer LEVOBUPIVACAINE

N
C4H9
R (+) enantiomer 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 dose required to produce LD50 is less for R(+) than the S(-) enantiomer of bupivacaine

LEVOBUPIVACAINE
Cardiotoxic potential in animal studies

3-4x less toxic than equivalent concentrations of bupivacaine in isolated perfused rabbit heart 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) 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 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 requires 600mg Prilocaine to produce clinical level of Methemoglobenemia Reversed with Methylene blue

2. Allergy
AMINO ESTERS derivatives of paraamino-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!!