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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
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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 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
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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
• 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
• Benzodiazepine: Midazolam, diazepam
• Propofol
• Etomidate
• Thiopental
• Ketamine
• Opioids: Fentanyl, Sufentanil, Remifentanil
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Benzodiazepines
• 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
• 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
• 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
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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
• 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
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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
• 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– 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– 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
– 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
• 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– 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 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
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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
73
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
• Nondepolarizing
• Rapid onset
• Dose-dependent duration
• No side-effects
• Elimination independent of organ function
• No active or toxic metabolites
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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
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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
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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
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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
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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
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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
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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
82
Muscle Relaxants
Vecuronium
• No effects on HR, BP
• Requires reconstitution
• Reliable and controllable duration of action
• Slower onset
• Stable hemodynamics/no histamine release
83
Cisatracurium• Organ-independent Hofmann elimination.
• Good for renal and liver dysfunction patients
• No effect on hemodynamics
Muscle Relaxants
84
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
85
Effects of Rocuronium on Heart Rate
Time (minutes)Time (minutes)
100100
9090
8080
7070
6060
5050
40400.00.0 1.01.0 2.02.0 3.03.0 4.04.0 5.05.0 6.06.0
Heart
Rate
(b
eats
/min
)H
eart
Rate
(b
eats
/min
)
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
86
Effects of Rocuronium on Mean Arterial Pressure
Time (minutes)Time (minutes)
100100
9090
8080
7070
6060
50500.00.0 1.01.0 2.02.0 3.03.0 4.04.0 5.05.0 6.06.0M
ean
Art
eri
al Pre
ssu
re (
mm
Hg
)M
ean
Art
eri
al Pre
ssu
re (
mm
Hg
)
600 mcg/kg600 mcg/kg900 mcg/kg900 mcg/kg1200 mcg/kg1200 mcg/kg
Levy et al. Levy et al. Anesth AnalgAnesth Analg 1994;78,318-321. 1994;78,318-321.
87
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
Pla
sma H
ista
min
e (
ng
/ml)
Pla
sma H
ista
min
e (
ng
/ml)
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
3.03.0
2.52.5
2.02.0
1.51.5
1.01.0
0.50.5
0.00.0
88
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
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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:
90
Local Anesthetics
91
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.
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Amides and Esters
• Chloroprocaine (Nesacaine)
• Cocaine (crack)
• Procaine
• Tetracaine (Pontocaine)
• Lidocaine (Xylocaine)
• Bupivacaine (Marcaine)
• Etidocaine (Duranest)
• Mepivacaine (Carbocaine)
• Prilocaine (Citanest)
• Ropivacaine
93
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
94
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)
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Mechanism of action
• Local anesthetics bind directly to the intracellular voltage-dependent sodium channels
• Inactivates sodium channels at specific sites within the channel
96
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
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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
98
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
99
Factors affect LA action
• Protein binding - increased binding increases duration of action
• Diffusibility - increased diffusibility decreases time of onset
100
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
101
Order of sensory function block
• 1. pain
• 2. cold
• 3. warmth
• 4. touch
• 5. deep pressure
• 6. motor
Recovery in reverse order
102
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
103
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
104
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).
105
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.
106
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.
107
Types of Local Anesthesia
Epidural Anesthesia
• This type of anesthesia is accomplished by injecting a local anesthetic into the Epidural space.
108
Types of Local Anesthesia
Spinal Anesthesia
• Local anesthetic is injected into the subarachnoid space of the spinal cord
109
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
110
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
111
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
112
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
113
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
114
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
115
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