Transcript Clinical Anesthesia - Shantou University

Clinical Anesthesia
Part I
JUNYI LI, MD
April 1, 2009
[email protected]
1
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
2
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
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Medical gas
Gas E-cyl(L) H-cyl(L) Pressure(psi) Color Form
O2
Air
N2O
N2
625-700
625-700
1590
625-700
6000-8000
6000-8000
15900
6000-8000
1800-2200
1800-2200
745
1800-2200
White
?
Blue
Black
Gas
Gas
Liquid
Gas
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Anesthesia machine
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Diagram of a generic two-gas anesthesia machine
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Components of the circle system
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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
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Monitor
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End-tidal CO2 monitor - capnography
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Relationship between O2 saturation & PO2
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Special monitors
•
•
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•
CVP – volume status
PA – PAP, CO, mixed venous oximetry
TEE – volume, contractility, ischemia
CNS – ICP, EEG, evoked potential
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CVP wave form and ECG
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Pressure wave form during PAC insertion
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TEE Monitor
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Induction agents
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•
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Benzodiazepine: Midazolam, diazepam
Propofol
Etomidate
Thiopental
Ketamine
Opioids: Fentanyl, Sufentanil, Remifentanil
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Benzodiazepines
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•
•
•
Use for premedication, sedation and induction
Minimal CV depression
Depress ventilatory response to CO2
Reduce cerebral oxygen consumption, cerebral
blood flow and ICP
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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
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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
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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
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Ketamine
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•
•
•
•
•
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•
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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
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Opioids
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•
•
•
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
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Inhalation anesthetics
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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
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Pharmacokinetics
•
•
•
•
Uptake
Distribution
Metabolism
Elimination
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Factors affecting inspiratory
concentration (FI)
• Fresh gas flow rate
• Volume of breathing circuit
• Absorption by machine or breathing circuit
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Factors affecting alveolar
concentration (FA)
• Uptake
• Ventilation
• Concentration
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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
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Factors affecting anesthetic uptake
• Solubility in the blood
• Alveolar blood flow
• The difference in partial pressure between gas
and venous blood
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Anesthetic Uptake
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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
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Factors affecting anesthetic uptake
• Solubility in the blood
• Alveolar blood flow
• The difference in partial pressure between gas
and venous blood
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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
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Cardiac output and uptake
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Factors affecting anesthetic uptake
• Solubility in the blood
• Alveolar blood flow
• The difference in partial pressure between gas
and venous blood
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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
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Factors affecting anesthetic uptake
• Solubility in the blood
• Alveolar blood flow
• The difference in partial pressure between gas
and venous blood
38
Factors affecting alveolar
concentration (FA)
• Uptake
• Ventilation
• Concentration
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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
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Ventilation and FA/FI ratio
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Factors affecting alveolar
concentration (FA)
• Uptake
• Ventilation
• Concentration
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Concentration
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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
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Factors Affecting Elimination
• Elimination
1. Biotransformation: cytochrome P-450
2. Transcutaneous loss: insignificant
3. 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
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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
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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…
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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
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MAC of inhaled anesthetics
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Nitrous oxide: 104%
Halothane: 0.74%
Isoflurane: 1.5%
Desflurane: 6.3%
Sevoflurane: 2.0%
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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
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Nitrous Oxide
• Respiratory
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–
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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): ↑
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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
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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
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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
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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
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Halothane
• Respiratory
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–
–
–
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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
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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
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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)
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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
CCB
– With aminophylline  serious ventricular arrhythmia
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Isoflurane
• Pungent ethereal odor
• A chemical isomer of enflurane
• Cardiovascular
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–
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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
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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
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Isoflurane
• Renal
– Renal blood flow, GFR, U/O: ↓
• Hepatic
– Total hepatic blood flow: ↓
• Biotransformation & toxicity
– Limited metabolism
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Desflurane
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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
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Desflurane
• Respiratory
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–
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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
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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
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Desflurane
• Contraindications
– Severe hypovolemia, malignant hyperthermia,
intracranial hypertension
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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
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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
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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
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Muscle Relaxants
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Introduction 0f Muscle relaxant
1494 - 1942 Curare
1947 - 1951 Succinylcholine chloride,
Gallamine, Metocurine, Decamethonium
1960’s
Alcuronium
1970’s
Pancuronium bromide, Fazadinium
1980’s
Vecuronium bromide, Atracurium besylate
1990
Pipecuronium bromide
1991
Doxacurium chloride
1992
Mivacurium chloride
1994
Rocuronium bromide
1999
Rapacuronium bromide
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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
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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
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The Ideal Relaxant
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Nondepolarizing
Rapid onset
Dose-dependent duration
No side-effects
Elimination independent of organ function
No active or toxic metabolites
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Assessing Postoperative
Neuromuscular Function
 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
75
Neuromuscular Blockers
Steroids
1. Vagolytic
Partially block cardiac muscarinic receptor
involved 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
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Neuromuscular Blockers:
Benzolisoquinolines
1. Histamine release
dTc > atracurium > mivacurium > cisatracurium
can cause rare bronchospasm, decreased blood
pressure, increase of heart rate
2. Generally organ-independent elimination1
esp: atracurium, cisatracurium, mivacurium
3. Noncumulative2
4. Absence of vagolytic effect
these drugs do not block cardiac-vagal (muscarinic)
receptors
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Classification of Neuromuscular
Blockers by Duration of Action (Minutes)
UltraShort
Short
Intermediate
Long
Clinical duration
(min)
6-8
12 - 20
30 - 45
>60
Recovery time
(min)
<15
25 - 30
50 - 70
90 -180
Exsamples
succiylcholine mivacurium
cisatracurium doxacurium
78
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
79
Muscle Relaxants
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
80
Muscle Relaxants
Pancuronium
• Vagolytic: increases heart rate,
may require beta blockade
• Easy to use
• Long duration of action
• Slower onset
• Not easily reversed at end of
case
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Muscle Relaxants
Vecuronium
• No effects on HR, BP
• Requires reconstitution
• Reliable and controllable duration of
action
• Slower onset
• Stable hemodynamics/no histamine
release
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Muscle Relaxants
Cisatracurium
• Organ-independent Hofmann elimination.
• Good for renal and liver dysfunction patients
• No effect on hemodynamics
83
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
84
Effects of Rocuronium on Heart Rate
600 mcg/kg
900 mcg/kg
1200 mcg/kg
Heart Rate (beats/min)
100
90
80
70
60
50
40
0.0 1.0 2.0 3.0 4.0 5.0 6.0
Time (minutes)
Levy et al. Anesth Analg 1994;78,318-321.
85
Mean Arterial Pressure (mmHg)
Effects of Rocuronium on Mean Arterial Pressure
600 mcg/kg
900 mcg/kg
1200 mcg/kg
100
90
80
70
60
50
0.0 1.0 2.0 3.0 4.0 5.0 6.0
Time (minutes)
Levy et al. Anesth Analg 1994;78,318-321.
86
Plasma Histamine (ng/ml)
Effects of Rocuronium on Histamine Release
3.0
2.5
600 mcg/kg
900 mcg/kg
1200 mcg/kg
2.0
1.5
1.0
0.5
0.0
0.0
1.0 2.0 3.0 4.0
Time (minutes)
Levy et al. Anesth Analg 1994;78,318-321.
5.0
87
Muscle Relaxants
Rapacuronium
• 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
88
Rationale for Selection of NMBAs:
 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
89
Local Anesthetics
90
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.
91
Amides and Esters
•
•
•
•
Lidocaine (Xylocaine) •
Bupivacaine (Marcaine)
Etidocaine (Duranest) •
•
Mepivacaine
(Carbocaine)
•
• Prilocaine (Citanest)
• Ropivacaine
Chloroprocaine
(Nesacaine)
Cocaine (crack)
Procaine
Tetracaine
(Pontocaine)
92
Local Anesthetics
Esters:
• These include cocaine, procaine, tetracaine,
and chloroprocaine.
• They are hydrolyzed in plasma by pseudocholinesterase.
• Paraaminobenzoic acid (PABA) is by-product
of metabolism
• PABA is the cause of allergic reactions seen
with these agents
93
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)
94
Mechanism of action
• Local anesthetics bind directly to the
intracellular voltage-dependent sodium
channels
• Inactivates sodium channels at specific sites
within the channel
95
Mechanism of action
Block sodium channel of never fiber
•
•
•
•
•
•
•
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
96
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
97
Factors affect LA action
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.
98
Factors affect LA action
• Protein binding - increased binding increases
duration of action
• Diffusibility - increased diffusibility decreases
time of onset
99
Factors affect LA action
Vasoconstrictors
• Vasoconstrictors decrease the rate of vascular
absorption which
• Allows more anesthetic to reach the nerve
membrane and
• Improves the depth of anesthesia.
100
Order of sensory function block
•
•
•
•
•
•
1. pain
2. cold
3. warmth
4. touch
5. deep pressure
6. motor
Recovery in reverse order
101
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
102
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
103
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).
104
Types of Local Anesthesia
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.
105
Types of Local Anesthesia
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.
106
Types of Local Anesthesia
Epidural Anesthesia
• This type of anesthesia is accomplished by
injecting a local anesthetic into the Epidural
space.
107
Types of Local Anesthesia
Spinal Anesthesia
• Local anesthetic is injected into the
subarachnoid space of the spinal cord
108
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
109
Clinical Uses
Amides
• 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
110
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
111
Local anesthestic toxicity
Respiratory system
• Respiratory center may be depressed
(medullary)…postretrobulbar apnea syndrome
• Lidocaine depresses hypoxic respiratory drive
(PaO2)
• Direct paralysis of phrenic or intercostal
nerves
112
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
113
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
114
Local Anesthetic Toxicity
Muscle
• 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
115