1 Clinical Anesthesia Part I JUNYI LI, MD lijunyiutmb@yahoo.com April 1, 2009.

transcript

Clinical Anesthesia

Part I

JUNYI LI, MD

lijunyiutmb@yahoo.com

April 1, 2009

Practice of anesthesiology

• Practice of anesthesiology is the practice medicine

• Preoperative evaluation• Intraoperative management • Postoperative care• Anesthesiology is perioperative medicine• Subspecialty of anesthesiology: Critical care medicine Pain management

Practice of anesthesiology

• Anesthetic equipment: - Breathing system - Anesthetic machine• Patients monitors• Clinical pharmacology for anesthesia - Induction agents - Inhalation anesthetics - Neuromuscular blocking agents & reversal agents - Local anesthetics

Medical gas

Gas E-cyl(L) H-cyl(L) Pressure(psi) Color Form O2 625-700 6000-8000 1800-2200 White Gas

Air 625-700 6000-8000 1800-2200 ? Gas

N2O 1590 15900 745 Blue Liquid

N2 625-700 6000-8000 1800-2200 Black Gas

Anesthesia machine

Diagram of a generic two-gas anesthesia machine

Components of the circle system

Standard monitors• Oxygenation Inspired gas: oxygen analyzer Blood oxygenation: pulse oximetry• Ventilation Continual end-tidal CO2 by capnography• Circulation Continual ECG Arterial blood pressure: invasive or noninvasive Pulse or heart sounds by auscultation or a-line• Body temperaure

Monitor

End-tidal CO2 monitor - capnography

Relationship between O2 saturation & PO2

Special monitors

• CVP – volume status

• PA – PAP, CO, mixed venous oximetry

• TEE – volume, contractility, ischemia

• CNS – ICP, EEG, evoked potential

CVP wave form and ECG

Pressure wave form during PAC insertion

TEE Monitor

Induction agents

• Benzodiazepine: Midazolam, diazepam

• Propofol

• Etomidate

• Thiopental

• Ketamine

• Opioids: Fentanyl, Sufentanil, Remifentanil

Benzodiazepines

• Use for premedication, sedation and induction

• Minimal CV depression• Depress ventilatory response to CO2

• Reduce cerebral oxygen consumption, cerebral blood flow and ICP

Propofol

• Use for induction, maintenance infusion and sedation infusion

• Decrease SVR, BP, cardiac contractility, preload and cause significant hypotension

• Profound respiratory depression

• Decrease cerebral blood flow and ICP

• Low rate of postoperative nausea and vomiting

Etomidate

• Use for induction

• Minimal effect on CV system

• Less ventilation depression than thiopental or benzodiazepines

• Decrease cerebral metabolic rate, CBF & ICP

• Long-term infusions lead to adrenocortical suppression

Thiopental

• Use for induction and sedation

• Decrease BP due to vasodilation and decrease of preload

• Increase HR due to central vagolytic effect

• Decrease ventilatory response to hypocapnia and hypoxia

• Decrease cerebral O2 consumption, CBF & ICP

Ketamine

• Use for induction• Increase ABP, HR, CO, PAP and myocardial work. • Avoid in CAD, uncontrolled HTN and arterial aneurysm• Benefit for acute hypovolemic shock• Minimal ventilatory drive depression• Potent bronchodilator• Increase salivation• Increase cerebral O2 consumption, CBF and ICP• May has myoclonic activity• Undesirable psychotomimetic side effect

Opioids

• Fentanyl, sufentanil and remifentanil • Minimal CV effect• Depress ventilation, decrease RR• Induce chest wall rigidity to prevent adequate

ventilation• Decrease cerebral O2 consumption, CBF &

ICP• GI effect: slow gastric emptying time, cause

biliary colic

Inhalation anesthetics

• Nitrous oxide, chloroform and ether were the first universally accepted general anesthetics

• Methoxyflurane and enflurane are no longer used because of toxicity and efficacy

• Current inhalation agents: nitrous oxide, halothane, isoflurane, desflurane, seveflurane

Pharmacokinetics

• Uptake

• Distribution

• Metabolism

• Elimination

Factors affecting inspiratory concentration (FI)

• Fresh gas flow rate

• Volume of breathing circuit

• Absorption by machine or breathing circuit

Factors affecting alveolar concentration (FA)

• Uptake

• Ventilation

• Concentration

Uptake

• Anesthetic agents are taken up by pulmonary circulation during induction (FA/FI < 1)

• The greater the uptake - The greater the difference between FA and

FI (lower FA/FI) - The slower the rate of rise of the alveolar concentration - The slower rate of induction

Factors affecting anesthetic uptake

• Solubility in the blood

• Alveolar blood flow

• The difference in partial pressure between gas and venous blood

Anesthetic Uptake

Solubility in blood

• Partition coefficients: the ratio of the concentration of anesthetic gas in each of two phases at equilibrium (equal partial pressures)

• The higher the blood/gas coefficient

- The greater the solubility

- The greater its uptake by pulmonary

circulation

- Alveolar partial pressure rises more slowly• Induction is prolonged

Alveolar Blood Flow

• Equal to cardiac output (in the absence of pulmonary shunting)

• Cardiac output increases

- Anesthetic uptake increases

- The rise in alveolar partial pressure slows

- Induction is delayed• Low-output states overdosage with soluble agents• Myocardial depressant (halothane) lowering

cardiac output positive feedback loop

Cardiac output and uptake

The Partial Pressure Difference between Alveolar Gas and Venous Blood

• Depends on tissue uptake

• Factors affecting transfer of anesthetic from blood to tissue:1. Tissue solubility (tissue/blood partition

coefficient)

2. Tissue blood flow

3. The difference in partial pressure between arterial

blood and tissue

• Uptake

• Ventilation

• Concentration

Ventilation

• Increasing alveolar ventilation

- Constantly replacing anesthetic taken up by

bloodstream

- Better maintenance of alveolar concentration

• Ventilation depressant (halothane)

- Decrease the rate of rise in alveolar

concentration

Ventilation and FA/FI ratio

• Uptake

• Ventilation

• Concentration

Concentration

Factors Affecting Arterial Concentration (Fa)

• Ventilation/perfusion mismatch increase the alveolar-arterial difference

• An increase in alveolar partial pressure

• A decrease in arterial partial pressure

Factors Affecting Elimination

• Elimination1. Biotransformation: cytochrome P-4502. Transcutaneous loss: insignificant3. Exhalation: most important

• Factors speed recovery– Elimination of rebreathing, high fresh gas flows, low

anesthetic-circuit volume, low absorption by anesthetic circuit, decreased solubility, high cerebral blood flow, increased ventilation, length of time

• Diffusion hypoxia: elimination of nitrous oxide is so rapid that alveolar O2 and CO2 are diluted

Pharmacodynamics

• General anesthesia:

- reversible loss of consciousness,

- analgesia,

- amnesia,

- some degree of muscle relaxation• All inhalation agents share a common machanism of

action at molecular level• The anesthetic potency correlates with their lipid

solubility

Pharmacodynamics

• Anesthetic binding might significantly modify membrane structure

• Alternations in any one of several cellular systems: ligand-gated ion channels, second messenger functions, neurotransmitter receptors

• GABA receptor, glycine receptor α1-subunit, nicotinic acetylcholine receptors, NMDA receptors…

Minimum Alveolar Concentration

• MAC: the alveolar concentration that prevents movement in response to a standardized stimulus in 50% of patients

• 1.3 MAC prevent movement in 95% of patients

• 0.3-0.4 MAC is associated with awakening

• 6% decrease in MAC per decade of age

MAC of inhaled anesthetics

• Nitrous oxide: 104%

• Halothane: 0.74%

• Isoflurane: 1.5%

• Desflurane: 6.3%

• Sevoflurane: 2.0%

Nitrous Oxide

• The only inorganic anesthetic gas in clinical use• Colorless and odorless• Cardiovascular

– Depress myocardial contractility

– Arterial BP, CO, HR: unchanged or slightly↑ due to stimulation of catecholamines

– Constriction of pulmonary vascular smooth muscle increase pulmonary vascular resistance

– Peripheral vascular resistance: not altered

– Higher incidence of epinephrine-induced arrhythmia

Nitrous Oxide

• Respiratory– Respiratory rate: ↑

– Tidal volume: ↓

– Minute ventilation, resting arterial CO2: minimal change

– Hypoxic drive (ventilatory response to arterial hypoxia): depressed

• Cerebral– CBF, cerebral blood volume, ICP: ↑

– Cerebral oxygen consumption (CMRO2): ↑

Nitrous Oxide

• Neuromuscular– Not provide significant muscle relaxation– Not a triggering agent of malignant hyperthermia

• Renal– Increase renal vascular resistance– Renal blood flow, glomerular filtration rate, U/O: ↓

• Hepatic– Hepatic blood flow: ↓

• Gastrointestinal– Postoperative nausea and vomiting

Nitrous Oxide

• Biotransformation & toxicity– Almost all eliminated by exhalation– Biotransformation < 0.01%– Irreversibly oxidize Co in vit.B12 inhibit

vit.B12-dependent enzymes interfere myelin formation, DNA synthesis

– Prolonged exposure bone marrow suppression, neurological deficiencies

– Avoided in pregnant patients

Nitrous Oxide

• Contraindications– N2O diffuse into the cavity more rapidly than air

(principally N2) diffuse out– Pneumothorax, air embolism, acute intestinal obstruction,

intracranial air, pulmonary air cysts, intraocular air bubbles, tympanic membrane grafting

– Avoided in pulmonary hypertension

• Drug interactions– Due to high MAC, combination with more potent agents

decrease the requirement of other agents– Potentiates neuromuscular blockade

Halothane

• Halogenated alkane• Cardiovascular

– Direct myocardial depression dose-dependent reduction of arterial BP

– Coronary artery vasodilator, but coronary blood flow↓ due to systemic BP↓

– Blunt the reflex: hypotension inhibits baroreceptors in aortic arch and carotid bifurcation vagal stimulation↓ compensatory rise in HR

– Sensitzes the heart to the arrhythmogenic effects of epinephrine (<1.5μg/kg)

– Systemic vascular resistance: unchanged

Halothane

• Respiratory– Rapid, shallow breathing– Alveolar ventilation: ↓– Resting PaCO2: ↑– Hypoxic drive: severely depressed– A potent bronchodilator, reverses asthma-induced

bronchospasm– Depress clearance of mucus promoting

postoperative hypoxia and atelectasis

Halothane

• Cerebral– Dilating cerebral vessels cerebral vascular resistance↓

CBF↑– Blunt autoregulation (the maintenance of constant CBF

during changes in arterial BP)– ICP: ↑, prevented by hyperventilation prior to

administration of halothane– Metabolic oxygen requirement: ↓

• Neuromuscular– Relaxes skeletal muscle– A triggering agent of malignant hyperthermia

Halothane

• Renal– Renal blood flow, GFR, U/O: ↓– Part of this can be explained by a fall in arterial BP and

CO, preoperative hydration limits these changes

• Hepatic– Hepatic blood flow: ↓

• Biotransformation & toxicity– Oxidized in liver by cytochrome P-450– In the absence of O2 hepatotoxic end products– Halothane hepatitis is extremely rare (1/35,000)

Halothane

• Contraindications– Unexplained liver dysfunction following previous exposure

– No evidence associating halothane with worsening of preexisting liver disease

– Intracranial mass lesion, hypovolemic, severe cardiac disease…

• Drug interactions– Myocardial depression is exacerbation by β-blockers and

– With aminophylline serious ventricular arrhythmia

Isoflurane

• Pungent ethereal odor• A chemical isomer of enflurane• Cardiovascular

– Minimal cardiac depression

– HR: ↑ due to partial preservation of carotid baroreflex

– Systemic vascular resistance: ↓ BP: ↓

– Dilates coronary arteries coronary steal syndrome or drop in perfusion pressure regional myocardial ischemia avoided in patients with CAD

Isoflurane

• Respiratory– Respiratory depression, minute ventilation: ↓– Blunt the normal ventilatory response to hypoxia and

hypercapnia– Irritate upper airway reflex– A good bronchodilator

• Cerebral– CBF, ICP: ↑, reversed by hyperventilation– Cerebral metabolic oxygen requirement: ↓

• Neuromuscular– Relaxes skeletal muscle

Isoflurane

• Renal– Renal blood flow, GFR, U/O: ↓

• Hepatic– Total hepatic blood flow: ↓

• Biotransformation & toxicity– Limited metabolism

Desflurane

• Structure is similar to isoflurane• High vapor pressure• Low solubility ultrashort duration of action• Moderate potency• Cardiovascular

– Systemic vascular resistance: ↓ BP: ↓– CO: unchanged or slightly depressed– Rapid increases in concentration lead to transient elevation

in HR, BP, catecholamine levels– Not increase coronary artery blood flow

Desflurane

• Respiratory– Tidal volume: ↓, respiratory rate: ↑

– Alveolar ventilation: ↓, resting PaCO2: ↑

– Depress the ventilatory response to ↑PaCO2

– Pungency and airway irritation

• Cerebral– Vasodilate cerebral vasculature CBF, ICP: ↑, lowered

by hyperventilation

– Cerebral metabolic rate of oxygen: ↓ vasoconstriction moderate the increase in CBF

Desflurane

• Neuromuscular– Dose-dependent decrease in the response to train-of-four

and tetanic peripheral nerve stimulation

• Renal– No evidence of any nephrotoxic effects

• Hepatic– No evidence of hepatic injury

• Biotransformations & toxicity– Minimal metabolism– Degraded by desiccated CO2 absorbent into CO

Desflurane

• Contraindications– Severe hypovolemia, malignant hyperthermia,

intracranial hypertension

Sevoflurane

• Nonpungency and rapid increase in alveolar anesthetic concentration smooth and rapid inhalation inductions in pediatric and adult patients

• Faster emergence associated with greater incidence of delirium in pediatric populations

• Cardiovascular– Mildly depress myocardial contractility– Systemic vascular resistance, arterial BP: ↓– CO: not maintained well due to little rise in HR– Prolong QT interval

Sevoflurane

• Respiratory– Depress respiration– Reverse bronchospasm

• Cerebral– CBF, ICP: slight ↑– Cerebral metabolic oxygen requirement: ↓

• Neuromuscular– Adequate muscle relaxation for intubation of children

• Renal– Renal blood flow: slightly ↓– Associated with impaired renal tubule function

Sevoflurane

• Hepatic– Portal vein blood flow: ↓

– Hepatic artery blood flow: ↑

• Biotransformation & toxicity– Liver microsomal enzyme P-450

– Degraded by alkali (barium hydroxide lime, soda lime), producing nephrotoxic end products (compound A)

– Fresh gas flows be at least 2 L/min

– Not be used in patients with preexisting renal dysfunction

Muscle Relaxants

Introduction 0f Muscle relaxant1494 - 1942 Curare1947 - 1951 Succinylcholine chloride, Gallamine, Metocurine, Decamethonium1960’s Alcuronium1970’s Pancuronium bromide, Fazadinium1980’s Vecuronium bromide, Atracurium besylate1990 Pipecuronium bromide1991 Doxacurium chloride1992 Mivacurium chloride1994 Rocuronium bromide1999 Rapacuronium bromide

Depolarizing & Nondepolarizing Blockade

• Depolarizing muscle relaxants acts as Ach receptor agonists, but not metabolized by acetylcholinesterase, resulting in a prolonged depolarization of the muscle end-plate

• Nondepolarizing muscle relaxants function as competitive antagonists of Ach

Structural Classes of Nondepolarizing Muscle relaxant

• Steroids: Rocuronium bromide,

Vecuronium bromide,

Pancuronium bromide,

Pipecuronium bromide• Naturally occurring benzylisoquinolines:

curare, metocurine• Benzylisoquinoliniums:

Atracurium besylate,

Mivacurium chloride,

Doxacurium chloride

The Ideal Relaxant

• Nondepolarizing

• Rapid onset

• Dose-dependent duration

• No side-effects

• Elimination independent of organ function

• No active or toxic metabolites

Sustained 5-second head lift Ability to appose incisors (clench teeth) Negative inspiratory force > – 40 cm H2O Ability to open eyes wide for 5 seconds Hand-grip strength Sustained arm/leg lift Quality of speaking voice Tongue protrusion

Assessing Postoperative Neuromuscular Function

1. VagolyticPartially block cardiac muscarinic receptorinvolved in heart rate slowing, resulting in increased heart rate:

rapacuronium > pancuronium > rocuronium > vecuronium

2. Generally do not promote histamine release Exception: rapacuronium

3. Organ-dependent elimination Kidneys and liver

Neuromuscular BlockersSteroids

1. Histamine release dTc > atracurium > mivacurium > cisatracurium can cause rare bronchospasm, decreased blood

pressure, increase of heart rate2. Generally organ-independent elimination1

esp: atracurium, cisatracurium, mivacurium3. Noncumulative2

4. Absence of vagolytic effect these drugs do not block cardiac-vagal (muscarinic)

receptors

Neuromuscular Blockers:Benzolisoquinolines

Ultra- Ultra- ShortShort ShortShort

6 - 86 - 86 - 86 - 8 12 - 2012 - 2012 - 2012 - 20 30 - 4530 - 4530 - 4530 - 45 >60>60>60>60

<15<15<15<15 25 - 3025 - 3025 - 3025 - 30 50 - 7050 - 7050 - 7050 - 70 90 -18090 -18090 -18090 -180

Classification of Neuromuscular Classification of Neuromuscular Blockers by Duration of Action (Minutes)Blockers by Duration of Action (Minutes)

LongLongIntermediateIntermediate

Clinical duration (min)

Recovery time (min)

Exsamples succiylcholine mivacurium cisatracurium doxacurium

DURATION OF ACTION • Ultra-Short: Succinylcholine chloride• Short: Mivacurium chloride• Intermediate: Rocuronium bromide,

Vecuronium bromide,

Atracurium besylate

Cisatracurium• Long: Pancuronium bromide,

curare,

metocurine,

Pipecuronium bromide,

Doxacurium chloride

Succinylcholine• Depolarizing muscle ralaxant• Rapid onset of action (30-60 s) and short duration of

action (less than 10 min)• Metabolized by blood pseudocholinesterase• Side effect & clinical consideration: Bradycardia

Hyperkalemia

Muscle pain

Increased intraocular, intragastric and intracranial pressure

Malignant hyperthermia

Muscle Relaxants

Muscle RelaxantsPancuronium

• Vagolytic: increases heart rate, may require beta blockade

• Easy to use

• Long duration of action

• Slower onset

• Not easily reversed at end of case

Muscle Relaxants

Vecuronium

• No effects on HR, BP

• Requires reconstitution

• Reliable and controllable duration of action

• Slower onset

• Stable hemodynamics/no histamine release

Cisatracurium• Organ-independent Hofmann elimination.

• Good for renal and liver dysfunction patients

• No effect on hemodynamics

Muscle Relaxants

Rocuronium• No effects on HR, BP

• Easy to use, liquid, no refrigeration

• Reliable and controllable duration of action

• Fast onset

• Stable hemodynamics/no histamine release

Effects of Rocuronium on Heart Rate

Time (minutes)Time (minutes)

100100

40400.00.0 1.01.0 2.02.0 3.03.0 4.04.0 5.05.0 6.06.0

Levy et al. Levy et al. Anesth AnalgAnesth Analg 1994;78,318-321. 1994;78,318-321.

600 mcg/kg600 mcg/kg900 mcg/kg900 mcg/kg1200 mcg/kg1200 mcg/kg

Effects of Rocuronium on Mean Arterial Pressure

Time (minutes)Time (minutes)

100100

50500.00.0 1.01.0 2.02.0 3.03.0 4.04.0 5.05.0 6.06.0M

al Pre

Effects of Rocuronium on Histamine Release

Time (minutes)Time (minutes)0.00.0 1.01.0 2.02.0 3.03.0 4.04.0 5.05.0

3.03.0

2.52.5

2.02.0

1.51.5

1.01.0

0.50.5

0.00.0

Muscle RelaxantsRapacuronium

• Minimal effects on HR, BP

• Controllable duration of action

• Fast onset

• Stable hemodynamics/minimal histamine release

• Potential for bronchospasm led to its removal in 2001

Cardiovascular stability Nondepolarizing vs depolarizing Organ-independent elimination Clinically significant active or toxic metabolites Predictability of duration Cumulative effects Reversibility Time to onset Stability of solution Cost

Rationale for Selection of NMBAs:Rationale for Selection of NMBAs:

Local Anesthetics

Local Anesthetic

1. Interrupts pain impulses without a loss of patient consciousness

2. The process is completely reversible

3. Does not produce any residual effect on the nerve fiber.

Amides and Esters

• Chloroprocaine (Nesacaine)

• Cocaine (crack)

• Procaine

• Tetracaine (Pontocaine)

• Lidocaine (Xylocaine)

• Bupivacaine (Marcaine)

• Etidocaine (Duranest)

• Mepivacaine (Carbocaine)

• Prilocaine (Citanest)

• Ropivacaine

Local Anesthetics

Esters: • These include cocaine, procaine, tetracaine,

and chloroprocaine. • They are hydrolyzed in plasma by pseudo-

cholinesterase. • Paraaminobenzoic acid (PABA) is by-product

of metabolism • PABA is the cause of allergic reactions seen

with these agents

Local Anesthetics

Amides:

• Include lidocaine, mepivicaine, prilocaine, bupivacaine, and etidocaine

• Metabolized in the liver to inactive agents

• True allergic reactions are rare (especially with lidocaine)

Mechanism of action

• Local anesthetics bind directly to the intracellular voltage-dependent sodium channels

• Inactivates sodium channels at specific sites within the channel

Mechanism of action

• slow rate of depolarization• reduce height of action potential• reduce rate of rise of action potential• slow axonal conduction • ultimately prevent propagation of action potential• do not alter resting membrane potential• increase threshold potential

Block sodium channel of never fiber

Factors affecting LA action

Effect of pH • Charged (cationic) form binds to receptor site

inside the cells• Uncharged form penetrates membrane which

determine the onset time• Efficacy of drug can be changed by altering

extracellular or intracellular pH • LA are weak base

Lipid solubility• Most lipid soluble:

– Tetracaine– Bupivicaine– Ropivacaine– Etidocaine

• Increased lipid solubility has greater potency and longer duration of action.

• Decreased lipid solubility means a faster onset of action.

Factors affect LA action

• Protein binding - increased binding increases duration of action

• Diffusibility - increased diffusibility decreases time of onset

Vasoconstrictors

• Vasoconstrictors decrease the rate of vascular absorption which

• Allows more anesthetic to reach the nerve membrane and

• Improves the depth of anesthesia.

Factors affect LA action

Order of sensory function block

• 1. pain

• 2. cold

• 3. warmth

• 4. touch

• 5. deep pressure

• 6. motor

Recovery in reverse order

LA Absorption

• Mucous membranes easily absorb LA

• Skin is a different story…

• Which LAs can we use for this?

– EMLA cream- 5% lidocaine and 5% prilocaine in an oil-water emulsion

– An occlusive dressing placed for 1 hour will penetrate 3-5mm and last about 1-2 hours.

– Typically 1-2 grams of drug per 10cm2 of skin

Rate of systemic absorption

• Intravenous > tracheal > intercostal > caudal > paracervical > epidural> brachial plexus > sciatic > subcutaneous

• Any vasoconstrictor present??

• High tissue binding also decreases the rate of absorption

Types of Local Anesthesia

Local Infiltration (Local Anesthesia):

• Use for skin and subcutaneous tissue infiltrating block

• Local infiltration is used primarily for surgical procedures involving a small area of tissue (for example, suturing a cut).

Topical Block:

• Applying to mucous membrane surfaces and blocking the nerve terminals in the mucosa.

• Used during examination procedures involving the respiratory tract.

• Local anesthetic is always used without epinephrine.

Nerve Block

• Local anesthetic is injected around a nerve that leads to the operative site.

• Usually more concentrated forms of local anesthetic solutions are used for this type of anesthesia.

Epidural Anesthesia

• This type of anesthesia is accomplished by injecting a local anesthetic into the Epidural space.

Spinal Anesthesia

• Local anesthetic is injected into the subarachnoid space of the spinal cord

Clinical Uses• Esters

– Benzocaine- Topical, duration of 30 minutes to 1 hour

– Chloroprocaine- Epidural, infiltration and peripheral nerve block, max dose 12mg/kg, duration 30minutes to 1 hour

– Cocaine- Topical, 3mg/kg max., 30 minutes to one hour

– Tetracaine- Spinal, topical, 3mg/kg max., 1.5-6 hours duration

Clinical Uses

• Bupivacaine- Epidural, spinal, infiltration, peripheral nerve block, 3mg/kg max., 1.5-8 hours duration

• Lidocaine- Epidural, spinal, infiltration, peripheral nerve block, intravenous regional, topical, 4.5mg/kg or 7mg/kg with epi, 0.75-2 hours duration

• Mepivacaine- Epidural, infiltration, peripheral nerve block, 4.5mg/kg or 7mg/kg with epi, 1-2 hours

• Prilocaine- Peripheral nerve block (dental), 8mg/kg, 30 minutes to 1 hour duration

• Ropivacaine- Epidural, spinal, infiltration, peripheral nerve block, 3mg/kg, 1.5-8 hours duration

Amides

Local Anesthetic Toxicity

• Neurological– Symptoms include perioral numbness, tongue

paresthesia, dizziness, tinnitus, blurred vision, restlessness, agitation, nervousness, paranoia, slurred speech, drowsiness, unconsciousness.

– Muscle twitching heralds the onset of tonic-clonic seizures with respiratory arrest to follow.

– Cauda equina syndrome by repeated doses of 5% lidocaine and 5% tetracaine

Local anesthestic toxicity

• Respiratory center may be depressed (medullary)…postretrobulbar apnea syndrome

• Lidocaine depresses hypoxic respiratory drive (PaO2)

• Direct paralysis of phrenic or intercostal nerves

Respiratory system

Local Anesthetic toxicity

• Depress spontaneous Phase IV depolarization and reduce the duration of the refractory period

• Depress myocardial contractility and conduction velocity at higher concentrations

• Smooth muscle relaxation and vasodilation• May lead to bradycardia, heart block,

hypotension and cardiac arrest

True Allergic Reactions to LA’s

• Very uncommon

• Esters more likely because of p-aminobenzoic acid (allergen)

• Methylparaben preservative present in amides is also a known allergen

Local Anesthetic Toxicity

• Cause myonecrosis when injected directly into the muscle

• When steroid or epi added the myonecrosis is worsened

• Regeneration usually takes 3-4 weeks

• Ropivacaine produces less sereve muscle injury than bupivacaine

Muscle

1 Clinical Anesthesia Part I JUNYI LI, MD lijunyiutmb@yahoo.com April 1, 2009.

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