anesthesiology lectures- edited

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ANESTHESIOLOGY



HISTORY of ANESTHESIA

ANESTHESIA is one of America’s greatest

contribution to the field ofMedicine 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 toexperience pain in their lives

• Pain was one of God's punishments forthe wicked and purifying trials for thegood;

• For the woman in labor, pain was thespiritual experience that would transformher into a self-sacrificing mother.



• Before anesthesia, the best surgeonswere the fastest.

• Four Herculean men would hold a patienton a gurney and surgery would proceed.(“PIGIL ANESTHESIA”)

• Quick and simple procedures such asamputations were the majority of surgeries

and most patients would just faint from theunbearable pain.




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.L'homme de Rene Descartes .Paris:Charles Angot, 1664

From: René Descartes.Renatus Des Cartes de homine . LvgdvniBatavorvm:Petrvm Leffen & Fransciscvm Moyardvm,

1662Rene Descartes was the one who firstDescribed the pain pathway



In the 1800s the enigma of pain,has yielded slowly to determined

investigators and clinicians




Anesthesia History Files

• 1800 June 25: Humphry Davycompletes the introduction to hisclassic work, Researches,Chemical and Philosophical;Chiefly Concerning Nitrous Oxide,or Dephlogisticated Nitrous Air,

and its Respiration.

What eventually evolvedinto anesthesia

as we know it today

was ushered in withthe chance observation that

the inhalation of nitrous oxide("laughing gas")

produced a stateof intoxication duringwhich people became highly

amusedand insensitive to pain.



Horace Wells (1815-1848), a New England dentist, experimentedwith anesthetics in the early 1840s. He attempted at a public

demonstration of nitrous oxide anesthesia failed, humiliating him.


http://www.library.ucla.edu/libraries/biomed/his/painexhibit/images/wells_l.jpg



Charles Thomas Jackson (Massachusetts)

In 1846, Jackson suggested to Morton (hisstudent) that he use sulfuric ether




Ether was used :

• as a sedative in the treatment of tuberculosis,asthma and whooping cough, and as a remedyfor toothache.

• Its anesthetic potential had never been

exploited.




On March 30, 1842,Crawford Longmade the first use of

ether as a surgicalanesthetic when heremoved a tumorfrom the neck of

patient JamesVenable.




In 1846, Morton made his famous demonstration of surgical anesthesia at the

Massachusetts General Hospital, using a hastily rigged apparatus to deliver ether to thepatient.



In the subsequent bitter debate overwho "discovered" anesthesia,

Charles Thomas Jackson attemptedto claim the achievement forhimself. By 1873, however,

Jackson had been admitted to aninsane asylum where he died in1880




• In late 1847Simpson discovered

the anestheticproperties ofchloroform




• In 1847 he began toadminister ether at St.George's Hospital inLondon and published a

book on ether anesthesia.

• In 1853 and 1857 headministered chloroform to

Queen Victoria for thebirths of Prince Leopoldand Princess Beatrice

Dr John Snow




• Cocaine was first used to achieve topicalanesthesia in 1884.

• Spinal and epidural anesthesia werediscovered soon after and a combinationof drugs was being used to allow optimalconditions for physicians to perform

surgery.



By the 1880sanesthesia,with aseptictechnique, was

standardpractice inAmerican andEuropeansurgicaltheaters



• While the surgeon'sprestige and powersoared, the anesthetistwas a mere assistant--anurse, intern or medical

student.

• The development of theindependent medicalspecialty ofanesthesiology would

not occur until the early20th century




• After World War II ended in 1945,major developments in the field ofanesthesiology opened new

avenues of medical and surgicalcare that were previouslyunthinkable. Thus began themodern era of anesthesia




ROLE OF ANANESTHESIOLOGIST

Constantly changing and its unique roleexpanding 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 Resuscitation5. Evaluation of Respiratory function and

application of Respiratory Therapy



The Anesthesiologists’ Role

1. Deliver pain management and provide lifesustaining care for the pts during surgery

2. Treat acute and chronic pain viamultidisciplinary 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 vitalorgan systems during surgery by vigilantmonitoring and interventions if necessary dueonslaught of the stresses of surgery per se.

3.Provide adequate analgesia during surgery

4. Provide adequate sedation with the objectiveof negative recall or awareness



The Anesthesiologist’s Role


2. TREAT ACUTE AND CHRONIC PAIN VIA MULTI-

DISCIPLINARY APPROACH 3. Perioperative Physician


5. Intensivists



ANESTHESIOLOGISTS’ ROLE In Pain Managment

“ NO PAIN : PATIENTS GAIN”

• Acute pain management- caused bytrauma 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 multidisciplinarymanagement of cancer



The Anesthesiologists’ Role


2. Treat acute and chronic pain viamultidisciplinary approach

3. PERIOPERATIVE PHYSICIAN


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 ofpreoperative care

• To return the patient to desirable

functioning as quickly as possibleMichael Roizen,ASA Refresher Course 2005



PREOPERATIVE EVALUATION,

PREPARATION & PREMEDICATION

• present & past history

• Presence of coexisting diseases• General survey of the patient (anticipate

technical difficulties spinal deformity, facialabnormalities & degree of hydration

• Preoperative orders – fasting prior to OR,preoperative medications & IV fluidmaintenance ordered during the visit

Consists of doing a good HX of the patient



ASA PHYSICAL STATUS

• CLASS I – no organic, physiologic, biochemicalor psychologic disturbance

Example: Hemorhoidectomy

• CLASS II – mild to moderate systemicdisturbance caused by the condition to betreated 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 disturbancethat is life threatening

Example: Cardiac Insufficiency or

Advance Pulmonary disease

• CLASS V – Moribund subjected to surgeryin desperation



IMPORTANCE OF PRE-MEDICATION

1. To alleviate apprehension and fear

2. To lower BMR

3. To diminish secretions4. To decrease reflex excitability

5. To counteract undesirable effects of

anesthesia6. To produce amnesia



DRUGS USED for PRE-

MEDICATIONSMay consist of any 2 or 3 of

the following drugs



A. Tranquilizers – Sedative

1. Barbiturates – short acting(phenobarbital)

2. Phenothiazines

3. BenzodiazepinesB. Opiates – Analgesics

1. Meperidine

2. NalbuphineC. Belladona alkaloids – Anticholinergic

1. AT SO4

2. Scopolamine SO4

3.Butorphanol

4.Morphine SO4

DRUGS USED for PRE-MEDICATIONS



TYPES OF ANESTHESIA

A. GENERAL ANESTHESIA

B. REGIONAL ANESTHESIA



GENERAL ANESTHESIA



• Anesthetic agents introduced either ofthe following routes, producing adepression of the brain

1. Oral

2. Rectal

3. Intramuscular

4. Intravenous5. Inhalational

Mask Inhalational

Nasal Insufflation

Endotracheal Intubation



GENERAL ANESTHESIA

• Definition: reversible state of

unconsciousness produced byanesthetic agents, with loss of thesensation of pain over the whole body



GENERAL ANESTHESIA

• MOA- results of reversible changes inneurologic function caused by drugs thatinhibits synaptic transmission

– In Inhalational Anesthesia (volatileanesthetics) inhibition of synapses inthe NEURO-BASAL THALAMUS

– In IV anesthesia

drug receptorinteractions



INDICATIONS FOR GENERALANESTHESIA

• Infants and children

• Adults who prefer GA

• Extensive surgical procedures

• Patients with mental disease• Long duration of surgery

• Surgery for which LA is impractical orunsatisfactory

• Hx of toxic or allergic reactions to LA drugs

• Anticoagulant treatment

O d f D di



Order of DescendingDepression

Cortical and Psychic Centers↓

Basal Ganglia and Cerebellum↓

Spinal cord↓

Medullary centers



COMPONENTS of GENERALANESTHESIA

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 increasemucus 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 endof the operation with decrease blood pressureand obtundation



Maintenance of AIRWAY in GA

1. Chin lift or jaw thrust maneuver



2. Pharyngeal Airway



3. Tracheal Intubation

ADVANTAGES f



ADVANTAGES ofENDOTRACHEAL INTUBATION

1. Airway patency is assured

2. Protection from aspiration

3. Gastric distention is prevented



Disadvantage

• Not being adept to the technique

C li ti f GENERAL



Complications of GENERALENDOTRACHEAL ANESTHESIA

1. Trauma during intubation

2. Endobronchial intubation

3. Esophageal intubation

4. Endotracheal tube obstruction

5. Laryngospasm

C li ti f G l



Complications of GeneralAnesthesia

A. Intra-operative Complications

1. Respiratory Difficulties – hypoventilation dueto respiratory depression

2. Airway Obstructiona. 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. Hypertensionc. Arrythmias

4. Occular Complications

5. Malignant Hyperthermia



B. Post-operative Complications

1. Respiratory Complications

a. Atelectasis

b. Pneumothorax2. Post Anesthesia Shivering

P ti f P t ti



Prevention of Post-operativeComplications 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 breathing6. Steam Inhalation to liquefy sputum

secretions



INHALATIONAL

ANESTHETICS



• Anesthetic potency of volatile anesthetic is

measured by MAC (Minimum AlveolarConcentration)

• Value represents alveolar concentration of

an anesthetic (at one atmosphere) thatprevents movement in 50% of thesubjects response to pain

Commonly used Inhalational



Commonly used InhalationalAnesthetics

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 butnot nephrotoxic levels

• Increases ICP, increase risk of seizureactivity

• May cause Tonic-CLonic Twitching of the

muscles of the face & limbs at highconcentrations



C. Isoflurane• Methyl ethyl ether isomer of enflurane

• Can cause coronary artery vasodilatationwhich might lead to CORONARY ARTERYSTEAL SYNDROME

D. Desflurane• Fluorinated methyl ethyl ether• Cannot be delivered by standard

vaporizers. Requires USE OFELECTRICALLY HEATED VAPORIZERS

• Low tissue solubility rapid eliminationand awakening. (ULTRA SHORTDURATION of ACTION)



E. Sevoflurane• Fluorinated isopropyl ether

• Reacts with CO2 absorbents to form aspecial halokene (COMPOUND A) metabolized to nephrotoxins which can

lead to Kidney damage• Potential nephrotoxicity due to organic

fluoride avoided in pre-existing Renaldisease



F. Nitrous Oxide• Laughing gas

• Only INORGANIC gas in clinical use

• At room tempreture Gas BUT is Liquidunder pressure in the tank

• Weak Anesthetic BUT Potent Analgesic• Causes DIFFUSION HYPOXIA

• SHOULD NOT be used in doses higherthan 70 % and combined with 30% O

2



INTRAVENOUS

AGENTS



Drugs

1. Barbiturates

2. Non-Barbiturates• Benzodiazepines

• Ketamine

• Propofol• Neuroleptanalgesia

• Analgesic- Hypnotic Combinations

• Balanced Anesthesia

• muscle relaxant•N2O



Barbiturates

MOA: enhances and mimic action of GABAby 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 generalanesthetic equipment



1. Benzodiazepenes • MOA: potentiation of neural inhibition

mediated by GABA-aminobutyric acid

• Pharmacologic effect Anxiolytic

Sedative

Hypnotic

Muscle relaxant Amnesic (ANTEROGRADE AMNESIA)

Anticonvulsant

Non-Barbiturates



Benzodiazepenes

a. Diazepam

• Insoluble in water

• Relieves muscle spasm and spasticity via centraleffect

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 onawakening

» Decrease ICP, reduced IOP, arterial BP

» Effective in treating nausea and vomitting



Non-Barbiturates4. Neuroleptanalgesia

• Combination of a potent analgesic and aneuroleptic tranquilizer (fentanyl +droperidol = Innovar)

• Produces state of mental detachment andindifference to pain

• MOA: competitive antagonism atDopaminergic receptors

» DROPERIDOL

» FENTANYL



NEUROLEPTANESTHESIA

addition of nitrous oxide, oxygenand muscle relaxants

IV DRUGS used as ADJUNCTS to



IV DRUGS used as ADJUNCTS toANESTHESIA

1. Opiods

• Classification

AGONISTS

AGONIST/ANTAGONIST

ANTAGONIST



Morphine

– Central actions and side effects• DEPRESSANT EFFECT analgesia, sedation,

depresses respiration & cough reflex, decreasesGI 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 opioidreceptor sites



2. Muscle Relaxants – Neuromuscularblockers

• Types of Neuromuscular Blockers (NMB)

a. Depolarizer

a. Non-depolarizer



a. Depolarizers

MOA: prolongs depolarization/ mimic Ach action

reduces sensitivity of the post-junctionalmembrane to Ach



SUCCINYLCHOLINE – Depolarization of the membrane w/c persists

until the drug diffuses away – Manifest 1st muscle twitching and

fasciculation

– ONLY DEPOLARIZING AGENT INCLINICAL USE

– Elimination: enzymatic destruction byPSEUDOCHOLINESTERASE

– 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-depolarizersa) Long acting (45 mins)

Pancuronium – eliminated via kidney

b) Intermediate acting (20-30 mins)

1) Atracurium – eliminated vai HOFFMAN elimination

pathway2) Vecuronium – eliminated thru the biliary

3) Rocuronium – eliminated thru the kidney

c) Short Acting (15- 20 minutes)

Mivacurium – eliminated by pseudocholinesterases

Cli i l U



Clinical Uses

• Facilitate tracheal intubation

• Provide skeletal muscle relaxation duringsurgery (adjunct to GA)

• Used in intensive care units



Regional Anesthesia

PHYSIOLOGY OF NERVE



PHYSIOLOGY OF NERVECONDUCTION

• Nerve Fiber – impulse – transmittingunit

• 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



PHYSIOLOGY OF NERVECONDUCTION

• Nerve Stimulation – Gates open

– Na+ rushing in

– Shifting of polarity

– Depolarization

Classification of



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 becut (e.g. sebaceous cyst)

III. FIELD BLOCK – around tissue to be cut(e.g. breast mass)

Classification ofRegional Anesthesia

(according to SITE of application)

IV. INTRAVENOUS REGIONAL (Bier Block)



(

Peripheral vein ofupper / lower extremity

I.V. catheter inserted

Desanguinatedextremity

Esmarch elasticbandage



2 tourniquets (BP cuffs)

bandage removedLA injected over 2-3minutes

Distal tourniquet inflatedafter 20-30 minutes

Proximal tourniquetdeflated

Slow release oftourniquet after at least 15-20 minutes

Use: short surgicalprocedure< 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



p

1. RETROBULBAR NERVEBLOCK(ciliary ganglion)

• Indications – Cataract surgery

– Corneal transplant – Enucleation

• Complications – Retrobulbar hemorrhage – Globe perforation

• Contraindications – Bleeding disorders – Extreme myopia – Open-eye injury



2. GASSERIAN GANGLION BLOCKBranches of trigeminal nerve(ophthalmic, maxillary, mandibular)

Indications• Trigeminal neuralgia

• Cancer pain in face

• Operations in face teeth, gum, mandible, etc.• Technique: LA injected into respectiveforamen of nerve branches




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

p



4. BRACHIAL PLEXUS BLOCK

• Anterior rami of C4-T2 spinal nerve roots

• Entire motor supply of upper extremity

• Almost entire sensory supply – except overshoulder and medial arm

p



Major Peripheral Branchesa. Axiliary N – shoulderabductionb. Musculocutaneous –

elbow flexionc. Radial – elbow, wrist,and finger extensionsd. Median – wrist andfinger flexion

e. Ulnar – wrist andfinger flexion




4. BRACHIAL PLEXUS BLOCK

• Indication:operations of upper extremity

• Approaches to Brachial Plexus Block1. interscalene approach2. supraclavicular3. axillary

BRACHIAL PLEXUS BLOCK



Interscalene approach

Supraclavicular approach




Supraclavicular approach




Axillary approach




5. INTERCOSTAL NERVE BLOCK• Anterior rami of 1st eleven spinal nerves

• At inferior surface of ribs

• Indications

– Post-op analgesia of thoracic and upper abdomensurgeries

– Relief of pain from rib fractures, herpes zoster,pleurisy, CA

• Complications: pneumothorax

INTERCOSTAL NERVE BLOCK



6. WRIST BLOCK

• Ulnar nerve• Median

• Radial

• Indications: – surgery or analgesia

distal to

metacarpophalangealjoints – suture of lacerations – paronychia, abcess




• Digital branches of

ulnar, median, radial

• Indications: – minor procedure infingers

• Reminder:

– avoid using large volumeof LA – do not add

vasoconstrictors

7. DIGITAL NERVE BLOCK




8. ANKLE BLOCK

• Blocks five nerves supplying foota. Deep peronealb. Superficial peronealc. Saphenousd. Posterior tibiale. Sural

• Indications – Surgery of foot and toes in frail patients

who cannot tolerate hemodynamic effects

of GA or neuraxial block




8. ANKLE BLOCK

• Precaution – Avoid epinephrine to

reduce risk ofischemia

• Complication

– Intravascularinjection



Peripheral Nerve Blocks9



9. PUDENDALNERVE BLOCK

• sacral plexus (S2 – S3 – S4)

• Indications – perineal surgery

o hemorrhoidso lacerations

– obstetric vaginal delivery

• Complications – puncture of fetal head – inadvertent IV infection




10. DORSAL PENILE BLOCK

• Base of penis at symphysis pubis• Blocks dorsal nerve

• Fan-shaped injection at the base blocksdorsal and ventral branches

• Indications – Penile surgery – Post-op pain relief



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 arachnoidspace

• Acts on spinal nerve roots, dorsal ganglia, noton 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 UsedT t i



• 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



q

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 crestscrosses either body of L4 or interspacebetween 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



PHYSIOLOGIC EFFECTS (ImmediateComplications)

A. CardiovascularSympathectomy vasodilation BP, CR

B. RespiratoryDifficulty of breathing

Apnea (high level)C. GastrointestinalNausea / vomiting in 20%

DELAYED COMPLICATIONS – Headache – leak of CSF – Backache – Urinary retention – Hemiplegia – hematoma

Levels of Spinal Anesthesia



Levels of Spinal Anesthesia – Dermatomes Involved

1. Saddle Block – sensory loss involves lowerslumbar and sacral segments.

Area that “sits on the saddle”.

2. Low Spinal – level of umbilicus (T10) lowerthoracic 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 drugchoice, concentration, dosage

Types – selective blockade possiblebecause it can be performed at any



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



Technique

• Method

– Single dose injection

– Fractional – continuous epidural – repeatedinjections of LA through catheter inserted into

epidural space

• Position

– Cervical epidural – sitting (C7)

– Thoracic epidural (T7)

– Lumbar epidural

(L1-L2, L2-L3, L3-L4, L4-L5)

Lateral Decubitus, full flexion



Method of Identifying Epidural Space



y g p p

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



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



g

• 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 anesthesiaminimized

• GI complaints minimized

• Catheterization minimized

• Less respiratory effects

Disadvantages• Technically more difficult



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) andcoccygeal plexus (S4-5, coccygeal nerves)

• Indications

– OB – vaginal deliveries

– Surgery involving lower abdomen, perineum

– Post-op pain control following these surgeriesespecially pediatric patients

Technique



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 ofdrug



Complications

• Accidental Dural puncture



• Accidental Dural puncture

• General systemic reactions• Infection at site of injection

Disadvantages

• Difficult to obtain high level

• Needs big amount – systemic reactionspossible

• Infection possible

• 5-10% failure – anatomic anomalies orincorrect method



ANESTHETIC AGENTS&LOCAL TOXICITY

(addendum by dr. b .)

Local Anesthetics



• Reversible inhibition of sensory nerveimpulse conduction

• Prevent transmission of information to theCNS

• 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



Molecularweight

pKaProteinbinding

Maximumdose (mg)

Lidocaine 234 7.9 65 %

300

500 w/ Epi

Racemicbupivacaine

288 8.01 95 %175

225 w/ Epi

Ropivacaine 328.89 8.07 94 % 150

L-bupivacaine 324.9 8.09 > 97 % 150-375

Local Anesthetics

Vasodilator Properties



• All except cocaine exhibit biphasic effecton vascular smooth muscle

• Extreme low concentration

vasoconstriction• Concentration for regional anesthesia

vasodilators

NON PHARMACOLOGIC FACTORSINFLUENCING ACTIVITY



INFLUENCING ACTIVITY

1. Dosage

2. Addition of vasoconstrictor

3. Site of injection

4. Additives

5. Mixture of LA

1. Dosage

P i liti f i l th i



• Primary qualities of regional anesthesia

(onset, duration, depth) are related to themass of the drug volume x concentration

2. Site on Injection

• Due to the particular anatomy of the area ofthe injection, variation in the rate ofabsorption & amount of drug used

• In Spinal anesthesia, lack of nerve sheath

around spinal cord are responsible for therapid onset

3 Additives



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 tocompensate for the short duration of action andthe 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



CH2 N

CH2

CH2

CH3

CH3

CH2 CH2 N

CH2

CH2

CH3

CH3

CH3

CH3

CH3

CH3

NH C

O1) Amides

Lidocaine, Bupivacaine,Ropivacaine, Levobupivacaine

Procaine, Chloroprocaine,

Cocaine, Tetracaine

C

O

C

2) Esters

Mechanism of Action



Prevent generation and conduction ofnerve impulses by decreasing or

preventing the large transient increase inpermeability of excitable membranes toNa+

Local Anesthetics Mechanism of Action



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 ofti i & hl i



action procaine & chloroprocaine

b. Intermediate anesthetic potency & durationof action lidocaine, mepivacaine & prilocaine

c. High anesthetic potency and prolongedduration of action tetracaine,bupivacaine : racemic andlevobupivacaine, ropivacaine,ethidocaine

TOXICITY



Local Anesthetic ToxicityA. 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 infocusing & tinnitus

disorientation

drowsiness

Objective CNS Signs(at low dose)



( )

shivering

Muscular twitching

Tremors – muscles of face and distal parts ofthe extremities

convulsions – tonic, clonic

Relationship of LA Toxicity toLidocaine 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 isattained

Effects of Increase pCO2 on CNSToxicity



y

• pCO2 level is inversely related toconvulsive 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

C di Eff



a. Cardiac Effect

• Dose dependent negative inotropicaction – depends on potency of LA

• Inhibit Na conductance in fast channels

• High concentration of lidocaine,procaine & tetracaine can block slowcalcium channels

• Increase LV EDP, direct pulmonary

vasoconstriction effect

Cardiotoxicity



1) INDIRECT EFFECTS

2) DIRECT EFFECTS

a) block sympathetic innervation

b) other CNS-mediated mechanisms

a) Block Na+ channels

conduction delay & QRS prolongation

b) Block K+ & Ca++ channels

LIDOCAINE



LIDOCAINE

– decreases max rate of depolarization w/oaltering RMP

– Action potential duration and effective

refractory period decreases – Ratio of effective refractory period to AP is

incresed in Purkinjie fibers and ventricularmuscles

Lidocaine- (INCREASED DOSE)



Lidocaine (INCREASED DOSE)

– prolongation of conduction time, increase PRinterval 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 ofDepolarization (V max)

» Slow rate of recovery resulting in incompleterestoration of V max between actionpotentials when heart rate exceeds 100/min

» Unidirectional block and re-entry type of

arrythmia

LEVOBUPIVACAINE

Cardiotoxic potential in animal studies



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



Enantiomers – pairs of stereoisomersthat, in their 3D projection, are related toeach other as an object to its mirror

image, and thus are not superimposable

same atoms connected by the samesequence of bonds with different 3Dstructure

ENANTIOMERS:

1 Dextrorotation = (+)

RACEMIC BUPIVACAINE



1. Dextrorotation = (+) enantiomer that rotates

polarized light to theright2. Levorotation =

(-) enantiomer thatrotates polarized lightto the left

CH3

NH

CH3

O

+

N

C4H9

S (-) enantiomerLEVOBUPIVACAINE

CH3

NH

CH3

O

+

N

C4H9

R (+) enantiomerDEXTROBUPIVACAINE

RACEMIC MIXTURES equal amounts of enantiomers in achiral compound

Clinical Relevance of Stereoisomers



Toxicological & local anesthetic effects of opticallyactive 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 equivalentconcentrations of bupivacaine inisolated perfused rabbit heart

QRS widening/ occurrence ofarrhythmia less marked in heartperfused with Levobupivacaine vs

D-BupivacaineComparative effect of racemic bupivacaine, levobupivacaine &ropivacaine on isolated rabbit heart. Mazoit, et. al. 1999

Difference between Bupivacaineand Lidocaine Toxicity



• Ratio of dosage required for irreversible cardiovascularcollapse: the dosage that will produce CNS toxicity(convulsion) lower for Bupivacaine

• Ventricular Arrhythmia and fatal ventricular fibrillationwith bupivacaine, not with lidocaine

• Pregnant patients more sensitive to cardiotoxic effects ofBupivacaine

• Resuscitation more difficult with bupivacaine

• Acidosis and hypoxia potentiate cardiotoxicity ofbupivacaine

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 byvasoconstriction at low and high doses

Mechanism of Action – inhibits re-uptake of NE by tissue

binding site, therefore no re-uptake leading to increasefree NE, potentiating the effects of adrenergicstimulation.(hypertension and ventricular ectopia)

Local Toxicity



• The more potent longer acting localanesthesia (e.g. Bupivacaine,ethidocaine): > degree of localized skeletal

muscle damage than less potent shorteracting 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 produceclinical level of Methemoglobenemia

Reversed with Methylene blue

2. Allergy

– AMINO ESTERS derivatives of para-amino-benzoic-acid (allergenic)

LOCAL ANESTHESIATOXICITY



• Depend on blood level of local anesthesiadelivered 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 BLOODCONCENTRATION



Depends on:• Absorption

• Tissue Redistribution

• Metabolism

• Excretion

Factors Affecting Absorption



• Site of injection – more blood supply >absorption

• Choice of Drugs – characteristics of the drugmay affect absorption

• Dosage

• Addition of Epinephrine – depends on thesensitivity of the vessels at the site of injectionand local anesthesia itself

DAGHAN SALAMAT!!

anesthesiology lectures- edited

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