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LOCAL ANESTHETICS,IV

SEDATION AND PAIN


MANAGEMENT
MORAYA ALQAHTANI,MD

Local Anesthetic
history

Cocaine-1800
Niemann-1859
1884-1st use in clinical practice
1904-procaine
1925-dibucaine
1932-tetracaine
1942-Licocaine
Mepivicaine,prilocaine,bupivicaine,etidocaine.
ropivicaine

neurophysiology

Nerve structure

pharmacokinetics

Weak bases
Lipid soluble
Pka:8-9 at physiological pH
Lipophilic portion-hydrophilic portion
and intermediate link

pharmacokinetics

Degree of ionization.
Both are involved in the blockage of the nerve
They act by blocking Na channel
Duration of esters are shorter

pharmacokinetics
Vasoconstrictor activity at low doses
Vasodilatation at higher doses
Metabolism:Esters by plasma cholinesterase
PAMA
Amides metabolized in the liver

pharmacokinetics
Vasoconstrictor activity at low doses
Vasodilatation at higher doses
Metabolism:Esters by plasma cholinesterase
PAMA
Amides metabolized in the liver

pharmacokinetics
Clearance:amide mainly hepatic,
widely distributed compared to esters
More stable
Minimal allergic reaction

Pharmacological factors
Lipid solubility
Absorption and distribution:
pharmacological factors
Physical factors:age,hepatic,renal,inflammation

pharmacological factors
*injection site
*dosage
*presence of epinephrine ,carbonation
*protein binding
*chemical properties

Classification of LA
Short acting
Intermediate
acting
Long acting

Procaine

60-90 min

Chloroprocaine

30-60 min

Mepivicaine
Prilocaine
Lidocaine
Tetracaine
Bupivicaine

20-24
20-24
90-200
80-600

Etidocaine

DRUG

Maximum
Plain(mg)

Maximum
Epinephrine(mg)

Chloroprocaine

800

1000

Lidocaine

300

500

Mepivacaine

300

500

Prilocaine

500

600

Bupivacaine

175

225

Etidocaine

300

400

LA
Preparation:
- topical :ointments,cream,lotion,spray
-Injection
EMLA:Eutotic Mixture of Local Anesthetics
2.5% prilocaine
2.5% lidocaine

TOXICITY

Toxicity
Allergic reaction
Local toxicity
Systemic toxicity

Allergic reaction
Rare condused with adverse effects
More with esters-PABA
Delayed type
No cross sensitivity
prevention: *proper Hx & PE
*skin test- 20%-30% false positive

Local toxicity
Direct trauma
Intraneuronal injection
Rare
preventable

Systemic toxicity
CNS
CVS
Methemoglobinemia

CVS
Conduction
Contractility
Peripheral effect

CVS more resistant than CNS


Bupivicaine more cardiac toxicity
Ropivicaine less cardiac toxicity
Lidocaine :anti arrhythmic drug

CNS

Concentration dependant
Low concentration
CNS:increases with hypoxia,acidosis ,pregnancy
Adverse effect:
drowsiness,light headiness
slurred speech,restlessness,
vertigo,tinnitus, muscle twitching,
tremors,convulsion, coma,

IV Sedation

Practical consideration
Quite environment
Repeated cuff blood pressure measurement should
be avoided
Monitors should be muted apart from alarm.

Requirements of analgesia
1.Continuous IV access.
2.Continuous monitoring with both ECG and
pulse oximeter.
3.Both the practitioner and the assistant should
have recently certified in CPR.
4.Resuscitation equipments should be available
(crash cart).
5.Possibility to transfer for full critical care
facilities e.g. Other hospital, ICU, OR.

Steps to Sedoanalgesia
1.Premedication with BDZ
2.Adequate local or regional anesthesia
3.IV sedation e.g. Midazolam
4.Adjuvant analgesia with narcotics only if
local/regional anesthetic is ineffective.

IV Anesthetics
Neuroleptanesthesia
Neuroleptic drugs :
Phenothiazines e.g. Chlorpromazine.

Butyrophenones e.g. Haloperidol, Droperidol.


Rarely used in anesthesia because of hypotension
droperidol fentanyl (Innovar )

IV Anesthetics
Butyrophenones result in significant:

Sedation.

Tranquility.

Immobility

Antiemesis

IV Anesthetics
Their side effects include:
An extrapyramidal syndrome with
face and neck dyskinesia.
Oculogyric crises.
Torticollis.
Agitation
Hallucination

IV Anesthetics
Droperidol (like other Butyrophenones) affect
GABA receptors and alters the balance of
dopamine and acetylcholine in certain brain sites.

Neuroleptanesthesia is contraindicated in patients


receiving Mono Amine Oxidase Inhibitors,
abusing drugs or alcohol and those with
Parkinsons disease.

Benzodiazepines
Diazepam (valium)

1959

Lorazepam (ativan)

1971

Midazolam (versed)

1976

pharmacokinetics
Small molecule
Lipid soluble
Metabolized in the liver
Habitual use of alcohol
Lorazepam has higher
affinity to receptors

Benzodiazepines

Action mediated through GABA


Mainly on CNS ,minimal action on PNS
Cells become hyperpolarized resistant to exitation
Function is blood level dependant
20%
:anxiolytic
30%-50% :sedation
60%
:loss of consciousness
Tolerance

Short acting

Midazolam

6-11ml/kg/min

Intermediate
acting

Lorazepam

0.8-1.8ml/kg/min

Long acting

Diazepam

0.2-0.5ml/kg/min

Benzodiazepines

Hypnotic
Sedative
Anxiolytic
Amnestic
Anticonvulsant:increases seizure threshold
Muscle relaxant

Benzodiazepines
Uses Sedation,Induction,maintainance
Contraindication:

Hypersensitivity, myasthenia gravis, COPD,


acute narrow angle glaucoma.
Safety has not been established in children and
pregnant females

Benzodiazepines
Side effects
*high safety margin
*free allergic reaction
*inactive non toxic metabolite
*respiratory problem
*venous irritation,thrombophlebitis
*unpredictable interval of amnesia
Rx: Flumazenil (Anexate) 0.2 mg IV over 15 sec. Then
0.1mg IV q60 sec. To effect (max. 1mg).

Benzodiazepines
Dosage:
midazolam:
IM 0.07 mg/kg (5mg) 30 60 min.prior (50% of
dose if >60 years)
I.V. sedation: titrate with small doses (2mg
initial followed by 1mg q2 min to effect)
(max.dose 0.1mg/kg) (reduce dose by 30% if
premedicated and by 50% if >60yo).

Diazepam (Valium ) : IM/PO premedication: 5-10


mg. 1 to 2 h prior (reduce dose by 50% if >60yo).

IV sedation: 5 - 10 mg IV q3h. (Reduce by 50%


if >60yo).

Lorazepam (ativan):
PO/SL premedication: 50mcg/kg (maximum
4mg) 1-2 hour prior (50% of dose if more than 60
yo)

OPOIDS

Classification
Natural
Semisynthetics
synthetics

Natural opoids
Morphine
Codeine
Papaverine
Semisynthetic
Heroin
-dihydromorphone

Synthetic opoids
Levorphenols:
-Methadone
-pentazocine
Phenypiperidine
-meperidine
-fentanyl

opoids
Inhibit the action of opoid neurotransmitters

Analgesic effect differences:


-access to the receptor
-binding affinity
-lipophility,ionization
-distribution,clearance

OPOIDS
In general most of them
*respiratory depression
*bradycardia except demerol
*anti tussive
*sleep
*nausea,vomiting,constipation
*hypersensitivity
Overdose :naloxone 0.4 mg IV q 2min

opoids
Morphine:
Pharmacology: Onset of action 2 to 5 min.
Duration of action 4-5 hrs.
Indication:Analgesia, induction of anesthesia.
Contraindication:
Hypersensitivity, MAO inhibitors within 14 days
(hpertensive crises, tachyarrethmias).
Dosage: 0.1-0.2 mg/kg IV/IM/SC q3h.

opoids
Hydromorphone :
-7-8 times stronger than morphine
-rapid distribution
-good in renal failure patient
-dose:2-4 mg po

Demerol
Pharmacology: Onset of action 2 to 5 min. via IV

duration of action 2-4 hrs.


absorbed slowly
7 to 10 times less potent than morphine
60% bound to protien
Dosage:up to 1.8 mg/kg IM/SC/IV q2h.

Fentanyl
Demorol family
-100x morphine
High lipid solubility
Metabolized in the liver , excreted by bile or
kidney
Poor hypnotic and sedative activity at low doses
No histamine release

katamine
Cataleptic, analgesic, and dissociative anesthetic
agent.
Onset of action 30 sec. For IV ,12-25 min for IM
dosing.
Dosage:induction 2.0 mg/kg IV over 60 sec or 10
mg/kg IM (adults and children).
Maintenance of anesthesia: 50% of induction dose
IV or IM, as anesthesia is lost.

katamine
Contraindication:Hypersensitivity,
pregnancy,uncontrolled HTN

Adverse effect:HR,BP,RR, pleasant dreams 5%,


unpleasant dreams 2%, hallucinations 1%,
confusion 3% (give BDZ with it to prevent bad
trips).

Other IV anesthetics
propofol

Most resent 1977


High lipid solubility
Alkylphenols
Viscous milky white substance
1% of propofol
*1%soy bean oil
*2.25% glycerol
*1.2% pure egg

Propofol

Metabolized in the liver


Iactive metabolite ,98% protein bound
Hypnotic,analgesic,induction
Titratable level of sedation
Dose: sedation 10-50 micgm/kg/min
induction 0.1-1 mg/kg over 3 min
Side effects:respiratory depression

PAIN MANAGEMENT

Definition
Effect of pain
-Neuroendocrine system
-CVS
-Resp
-GIT
-GUT
-immunity

NSAIDs
Limited use for acute PO pain

Mechanism of action

Prostaglandins -fever ,pain,vasodilatation

Classification

Mechanism of action

pharmacokinetics
Rapidly absorped
Metabolized in the liver,inactive metabolites
High protein bound
Action dose dependent

Side effects
Gastropathy
Hemostasis
nephrotoxocity

Ketorolactromethaminne
(Toradol)
Pyrolle acetic acid
High analgesic potency

2mg of toradol = 1mg og morphine = 6-10mg of demerol

Dose 60mg IM followed by 30 mg IM q 6h


50% in renal problem

Toradol
Most sufficient for sever pain
0.3% incidence of PU
Bleeding with long term use
Increases bleeding time

Nausea and Vomiting

History of PO emesis
Female
Obesity
Pain
Type of surgery
Anesthetic drugs
Gastric distension

Treatment
Prophylactic antiemetic droperidol 10 to 20
micgm/kg
Ondansetron 4 to 8 mg IV
Metoclopramide (10 to 20 mg IV)
Transdermal scopolamine

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