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Showing posts with label Anesthetics. Show all posts
Showing posts with label Anesthetics. Show all posts
General Anesthetics
By Piscean | Friday, March 9, 2012 | Posted in , , | With 0 comments

General anesthetics are drugs that immediately produce unconsciousnes and complete analgesia. These agents are generally administered by intravenous or inhalation routes. Preanesthetic and adjunct drugs are given before, during, and aft er surgery.

Mainly two classes are there
  1. Inhalation Anesthetics
  2. Injectable Anesthetics

Injectable General Anesthetics
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Injectable General Anesthetics
Intravenous anesthetics are often administered with inhaled general anesthetics. Administration of intravenous and inhaled anesthetics together allows the dose of the inhaled drug to be reduced, resulting in a decreased probability of serious side effects. They also provide more analgesia and muscle relaxation than is provided by an inhaled anesthetic alone. Drugs used as intravenous anesthetics include opioids, barbiturates, and benzodiazepines
Stages and Planes of Anesthesia
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Stages and Planes of Anesthesia
Before patients reach surgical anesthesia, they go through several stages. Th e use of these stages and planes of anesthesia helps to describe the levels and progression of anesthesia produced by anesthetics. Th ere are four stages of general anesthesia:

Stage I: Th is stage begins when the agent is administered and lasts until loss of consciousness. Stage I is characterized by:
  • Analgesia
  • Euphoria
  • Perceptual distortions
  • Amnesia
Stage II: Delirium begins with loss of consciousness and extends to the beginning of surgical anesthesia. Th ere may be excitement and involuntary muscular activity. Th e skeletal muscle tone increases and breathing is irregular. At this stage, hypertension and tachycardia may occur. It is important that the passage from Stage I to Stage III be attained as quickly as possible. Sudden death can occur during Stage II.

Stage III: Surgical anesthesia lasts until spontaneous respiration ceases. It is further divided into four planes based on:
  • Respiration
  • Th e size of the pupils
  • Refl ex characteristics
  • Eyeball movements
Th is stage is characterized by progressive muscular relaxation. Muscle relaxation is important during many surgical procedures as refl ex movements can occur when a scalpel slices through the tissues.

Stage IV: Medullary paralysis begins with respiratory failure and can lead to circulatory collapse. Th rough careful monitoring, this stage is avoided.
Preanesthetic medications
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Preanesthetic medications are used prior to the administration of an anesthetic to facilitate induction of anesthesia and to relieve anxiety and pain. They may also be used to minimize some of the undesirable effects of anesthetics, such as excessive salivation, bradycardia, and vomiting.

To accomplish these objectives, several drugs are often used at the same time. Th e following medications are commonly used as preoperative drugs:
  • Sedative-hypnotics such as hydroxyzine, promethazine
  • Antianxiety agents such as diazepam, droperidol
  • Opioid analgesics such as morphine, meperidine, fentanyl
  • Anticholinergics such as atropine, scopolamine
Anesthetics Introduction
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For several centuries, opiates and alcohol were the mainstays of anesthetics (substances used to reduce sensation of pain) in the control of pain. Th ese substances had limited success, but were probably better than nothing. It was not until the 1840s that surgical anesthesia (reduction or elimination of pain) became possible, with the introduction of three agents: chloroform, ether, and nitrous oxide. Th ese three substances, upon inhalation, quickly lead to a state of unconsciousness in which pain is not felt. Nitrous oxide is still one of the most widely used gaseous anesthetics, and diethyl ether is still occasionally used. Chloroform is rarely used today because of its toxicity, but other, newer halogenated hydrocarbons, such as halothane, are extremely common.

Gaseous anesthetics are the principal agents used in the maintenance of anesthesia, but agents given by other routes are still used in the induction of anesthesia. Anesthesia is basically characterized by four reversible actions: unconsciousness, analgesia, immobility, and amnesia. Th e critical factor is that there should be no signifi cant impairment of cardiovascular or respiratory functions, especially those supplying the brain and other vital organs with adequate blood, nutrients, and gases.

General anesthetics are used to produce loss of consciousness before and during surgery. Local anesthetics numb small areas of the body tissue where a minor procedure is to be done, and are commonly used in dentistry for minor surgery. Regional anesthesia aff ects a larger (but still limited) part of the body, but does not make the person unconscious. Spinal and epidural anesthesia are examples of regional anesthesia.
Local anaesthetics (local analgesics): use in dentistry
By Piscean | Monday, October 3, 2011 | Posted in , , | With 0 comments

Local anaesthetics (local analgesics): use in dentistry
Two often-confused words are analgesia and anaesthesia. Analgesia is ‘the removal of pain sensation’ whereas anaesthesia is ‘the loss of sensation in general’ (including pain). This difference in meaning is often lost, with many people (and publications) using the terminology ‘local anaesthesia’ when ‘local analgesia’ is what is meant. Local analgesia is the effect that dental practitioners aim to achieve in normal clinical activity; however, ‘local anaesthesia’ is the term commonly used in medicine and dentistry, and is used in this publication.
Pharmacology of Local anaesthetics
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Local anaesthetics
Mechanism of action
Properties
Local anaesthetic solutions: concentrations used for various types of anaesthesia (Table 1.8)
Precautions
Adverse effects
Individual drugs
Use in dentistry

Individual local anaesthetic drugs
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Individual local anaesthetic drugs

Lignocaine
Lignocaine is an aminoamide local anaesthetic and is also an antiarrhythmic drug. In specialised pain management units, intravenous or continuous subcutaneous infusions of lignocaine are used for neuropathic pain. Alkalinisation with sodium bicarbonate increases the rate of onset of block (see Wounds and lacerations for information). Allergy rarely occurs. See Table 1.7 for duration of action and maximum doses.
Topical lignocaine has a role in managing localised neuropathic pain such as postherpetic neuralgia. A eutectic mixture of lignocaine 2.5% and prilocaine 2.5% is used topically to produce dermal anaesthesia before cannula insertion and minor surgical procedures, and is commonly used in children. This mixture is usually applied topically under an occlusive dressing for 30 to 60 minutes.
For adverse effects of local anaesthetics, see Adverse effects.
Prilocaine
Prilocaine is equipotent to lignocaine, but is less toxic and has a slightly longer duration of action. Prilocaine is the preferred agent for regional intravenous local anaesthesia (Bier block). See Table 1.7 for duration of action and maximum doses.
Prilocaine is also used topically in combination with lignocaine.
The main disadvantage is methaemoglobinaemia at high doses in susceptible patients. Doses greater than 600 mg, or 8 mg/kg, can lead to reduced blood oxygen-carrying capacity and cyanosis, often with delayed onset. Prilocaine should be used cautiously in infants under three months of age due to their lower levels of methaemoglobin reductase compared to adults. For further adverse effects, see Adverse effects.
Bupivacaine
Bupivacaine is a long-acting local anaesthetic. It is used for infiltration, peripheral nerve and plexus blocks, and epidural and spinal anaesthesia or analgesia. Onset time is about five minutes after infiltration, up to 20 minutes after epidural and major plexus blocks, and rapid after intrathecal use, although peak effect is further delayed (eg 15 minutes after intrathecal and 30 to 45 minutes after epidural use). See Table 1.7 for duration of action and maximum doses. For adverse effects, see Adverse effects.
Levobupivacaine
Levobupivacaine is the S-isomer of bupivacaine and may confer some safety advantages over bupivacaine. For continuous epidural analgesia, levobupivacaine can be co-administered with fentanyl, morphine or clonidine. The 0.75% solution (75 mg/10 mL) can be used to achieve a dense local anaesthetic block, but is not approved for obstetric or paediatric use. See Table 1.7 for duration of action and maximum doses. For adverse effects, see Adverse effects.
Ropivacaine
Ropivacaine is a long-acting analogue of bupivacaine produced as the pure S-enantiomer. It has lower arrhythmogenic and cardiac depressant effect than racemic bupivacaine. An advantage of ropivacaine is the greater differential in the response of sensory and motor nerves to local anaesthetic block. Profound sensory and motor block can be obtained when administered at high concentration via the epidural route, whereas lower concentrations allow analgesic block without significant motor impairment. The addition of adrenaline confers no advantage in the clinical use of ropivacaine. See Table 1.7 for duration of action and maximum doses. For adverse effects, see Adverse effects.
Procaine
Procaine is a benzoic acid ester local anaesthetic with low toxicity and some vasodilator activity. See Table 1.7 for duration of action and maximum doses. For adverse effects, see Adverse effects.
Amethocaine
Amethocaine (tetracaine) is a benzoic acid ester local anaesthetic, primarily used in topical anaesthesia (eg ophthalmic procedures). As a 4% gel or cream formulation, amethocaine has been shown to be effective topically to produce dermal anaesthesia before cannula insertion and minor surgical procedures. It may have a faster onset than lignocaine+prilocaine. Localised erythema has been noted. It is only available for hospital use [Note 1]. Amethocaine use in other local anaesthetic techniques is limited due to its systemic toxicity. For adverse effects, see Adverse effects.
Cocaine
Cocaine is a benzoic acid ester local anaesthetic that also causes local vasoconstriction. Toxicity and potential for abuse have limited its clinical use. Cocaine is used primarily for topical anaesthesia of the upper respiratory tract. Topical solutions, with a concentration of 1% to 10%, can be applied using cotton applicators or packs, or be instilled, or used as a spray on the mucous membranes of the oral, laryngeal, and nasal cavities. For adverse effects, see Adverse effects.
Note 1: Contact your regional drug information service or the NPS Therapeutic Advice and Information Service (tel. 1300 138 677) regarding availability.
Local anaesthetics: adverse effects
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Local anaesthetics: adverse effects
Local anaesthesia is an effective and relatively safe method of pain control, and has a very low incidence of significant adverse effects. Different anaesthetic drugs can have different complications. The adverse effects of local anaesthetics include:

central nervous system effects—light-headedness, nervousness, apprehension, euphoria, confusion, dizziness, drowsiness, blurred or double vision, twitching, tremors, convulsions and unconsciousness, difficulty swallowing, slurred speech, sensations of heat or cold
respiratory effects—respiratory depression, respiratory arrest
cardiovascular effects—bradycardia, hypotension, cardiovascular collapse, cardiac arrest
allergic responses (usually to the ester group of local anaesthetics)—cutaneous lesions, urticaria, oedema, anaphylactoid reactions
local complications
methaemoglobinaemia (prilocaine, dose-dependent).
Clinicians using local anaesthetics should be familiar with the diagnosis and management of drug-related toxicity. Other acute emergencies can arise with nerve blocks. Resuscitation drugs and equipment, including oxygen, should always be available for the immediate management of adverse reactions. An intravenous cannula should be inserted before complicated procedures.

Systemic toxicity can arise after inadvertent intravascular injection of local anaesthetic, rapid systemic absorption, excessive dose administration or impaired drug clearance.

Local anaesthetics can cause circumoral and tongue numbness, light-headedness, visual and auditory disturbances, generalised muscular twitching, loss of consciousness, seizures, coma, respiratory arrest and cardiovascular collapse.

With the majority of local anaesthetics, minor central nervous system effects are seen before seizures or the onset of cardiovascular toxicity, and can act as a warning of serious events. However, longer-acting local anaesthetic agents, notably bupivacaine, can cause cardiovascular effects before any central nervous system effect. Changes in cardiac conduction, excitability, refractory period, contractility and peripheral vascular resistance can occur at therapeutic blood concentrations. Higher concentrations lead to life-threatening atrioventricular block, ventricular arrhythmias and depressed cardiac contractility. Bupivacaine has relatively greater cardiotoxicity than levobupivacaine and ropivacaine. Due to the potential for systemic toxicity, bupivacaine, levobupivacaine and ropivacaine are contraindicated for use in intravenous regional anaesthesia (Bier block). Limited case reports suggest that infusion of fat emulsions may be of clinical benefit in managing cardiac toxicity related to long-acting amide local anaesthetics (eg bupivacaine, ropivacaine) in patients not responding to standard resuscitative measures. A number of Australian hospitals are now stocking 20% fat emulsion in ward areas that routinely administer local anaesthetics.

Allergic reactions to aminoester local anaesthetics can be due to the drug itself, or to the preservatives (eg methylparaben) or antioxidants (eg sodium metabisulfite) that are in some preparations. Cross-sensitivity can also occur, as many foods, drugs and skin preparations contain similar preservatives.
Allergy to the aminoamide local anaesthetics is very rare, but has been reported.
Positive skin testing to one local anaesthetic does not provide any information about other drugs.
Local anaesthetics: precautions
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Local anaesthetics: precautions
Figures for maximum safe dose are imprecise, due to the influence of multiple factors. Use the lowest dose and concentration required to produce effective anaesthesia. Following careful aspiration to avoid inadvertent intravascular bolus or unwanted intrathecal injection, local anaesthetic solutions should be administered incrementally. Local anaesthetics rapidly cross the placenta and can expose the fetus to dangerous levels of the drug in some procedures, depending on the dose and technique of administration. Solutions containing preservative should not be used for intrathecal use.

Aminoamide local anaesthetics are metabolised in the liver and should be used with caution in patients with significant hepatic impairment. Lignocaine, bupivacaine and ropivacaine have metabolites that can contribute to activity and toxicity. Many metabolites are formed by the cytochrome P450 isoenzymes 3A4, 2C9 and 1A2. Prilocaine is metabolised to ortho-toluidine (o-toluidine), which can oxidise haemoglobin to methaemoglobin.

Atypical plasma cholinesterase (pseudocholinesterase deficiency) is a hereditary condition (affecting 1:3000 people) that results in molecular differences in the pseudocholinesterases, resulting in the poor metabolism of the ester molecules and an increased risk of adverse outcomes with ester-based local anaesthetics.
It is important to read the manufacturer’s guidelines as the concentrations of the local anaesthetics and associated vasoconstrictors change as new products come on to the market.
Local anaesthetic solutions: concentrations used for various types of anaesthesia (Table 1.8)
By Piscean | | Posted in , , | With 0 comments

Local anaesthetic solutions: concentrations used for various types of anaesthesia (Table 1.8)
Use Lignocaine (%) Prilocaine (%) Bupivacaine/levobupivacaine (%) Ropivacaine (%) Procaine (%)
topical
4 to 10
(2.5 in combination with prilocaine 2.5%)
2.5 (in combination with lignocaine 2.5%)
–
–
–
infiltration
0.5 to 1
0.5 to 2
0.25 to 0.5
0.2 to 0.75
0.25 to 0.5
regional nerve block
1 to 1.5
1.5 to 2
0.25 to 0.5
0.75
0.5 to 2
IV regional (Bier block)
0.25 to 0.5
0.25 to 0.5
contraindicated
contraindicated
–
epidural block (surgical)
1 to 2
2
0.25 to 0.5 (bupivacaine)
0.5 to 0.75 (levobupivacaine)
0.75 to 1
–
epidural infusion or block for analgesia
1
1
0.1 to 0.25
0.2
–
intrathecal
2
–
0.5
0.5
–
Local anaesthetics: properties
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Local anaesthetics: properties
A local anaesthetic molecule comprises a lipophilic head, a hydrophilic tail, and a linking intermediate chain. The intermediate chain can be an ester (aminoester group) or an amide (aminoamide group). Aminoester local anaesthetics are more water soluble, and are primarily metabolised in plasma by pseudocholinesterases. Aminoamide local anaesthetics are less water soluble, and are primarily metabolised in the liver by de-ethylation. See Table 1.7 for characteristics of local anaesthetic drugs.

Efficacy of a particular drug is determined by its concentration at the site of action. This depends on the dose and concentration injected, diffusion to the relevant site if this is distant from the injection point, and on removal by the circulation, which in turn depends on the vascularity of the tissue. Increased lipid solubility of the local anaesthetic enhances absorption. Increased ionisation, which depends on the pKa of the drug and the pH at the site, decreases absorption (see Table 1.7).

Systemic absorption can be reduced by co-administration with a vasoconstrictor such as adrenaline, which prolongs and intensifies the local anaesthetic action, reduces surgical bleeding, and lowers peak blood concentrations of the local anaesthetic and the risk of systemic toxicity. A local anaesthetic solution with 1:200 000 adrenaline (5 micrograms/mL) is often used. Adrenaline is contraindicated in the presence of ischaemic heart disease, ventricular arrhythmias or uncontrolled hypertension, and for digital or penile nerve blocks, and intravenous block.

The uses of the different local anaesthetic solutions are summarised in Table 1.8.
Characteristics of local anaesthetics (Table 1.7)
Drug pKa Onset Duration (hours) [NB1] Maximum single adult dose [NB2] pH of solution [NB3] Protein binding (%)
Aminoamides
lignocaine
7.9
fast
0.5 to 2
3 mg/kg;
7 mg/kg (with adrenaline)
6.5
65
prilocaine
7.9
fast
1 to 3
6 mg/kg;
8 mg/kg (with adrenaline)
5.0 to 7.0
55
bupivacaine
8.1
intermediate to slow
4 to 12
1.5 to 2 mg/kg
2 to 3 mg/kg (with adrenaline)
4.0 to 6.5
95
levobupivacaine
8.1
intermediate to slow
4 to 12
1.5 to 2 mg/kg
4.0 to 6.5
95
ropivacaine
8.1
intermediate to slow
3 to 6
300 mg (major nerve block)
4 to 6
94
Aminoesters
procaine
8.9
slow
0.5 to 1.5
8 mg/kg
5 to 6.5
6
amethocaine (tetracaine)
[NB4]
–
fast
at least 15 minutes
single dose
4.5 to 6.5
-

NB1: variable, dependent upon dose and route of administration
NB2: variable, dependent upon route of administration
NB3: pH lower by 1.0 to 1.5 units for adrenaline-containing solutions
NB4: characteristics apply to topical use in ophthalmic procedures. See Use of local anaesthetics in children regarding its use as a topical local anaesthetic in children
Local anaesthetics: mechanism of action
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Local anaesthetics: mechanism of action
Local anaesthetics inhibit the generation of electrical impulses and their conduction along the neuronal axon membrane, by reversible block of sodium ion channels. The progression of local anaesthetic block relates to nerve fibre diameter, myelination, and conduction velocity. In general, loss of nerve function occurs in the order of loss of autonomic activity, followed by loss of pain sensation, other sensory functions and finally motor activity.
Use of local anaesthetics in children
By Piscean | Thursday, September 29, 2011 | Posted in , , , | With 0 comments

Use of local anaesthetics in children

Introduction
Local anaesthetics provide excellent pain relief, are an important part of multimodal analgesia, and can significantly decrease opioid requirements. It is important that the total dose of local anaesthetic does not exceed the maximum doses. Appropriate resuscitation equipment and personnel should be available for the management of local anaesthetic toxicity.

For topical and transdermal administration, 
Local infiltration should be used routinely in children for surgery and for procedures such as intravenous cannulation or lumbar puncture. Buffered lignocaine causes minimal pain when used with local infiltration, and works rapidly.

Do not use adrenaline-containing solutions in end-artery regions (eg digits, penis).

Regional blocks
Femoral nerve block and axillary brachial plexus block are examples of regional blocks.
Use of these blocks requires a detailed knowledge of the relevant anatomy, and an intravenous cannula should be inserted before the block, in case there is an adverse reaction.
A volume of 0.5 mL/kg of local anaesthetic agent is usually required. The concentration of local anaesthetic may need to be decreased to avoid toxicity.

Many peripheral nerve blocks are performed under general anaesthesia for postoperative pain control. Care should be taken with dressings, pressure areas, and positioning, because that part of the body will have no sensation.

Central neural blocks  
(eg epidural administration of local anaesthetic and opioid drugs) should only be performed by experienced practitioners (eg paediatric anaesthetists) and only in institutions where there is expertise to care for these children. They are usually inserted under general anaesthesia and can provide excellent analgesia after major surgery.

The anatomy of the paediatric epidural space differs from that of the adult in that it is:
relatively superficial in a child compared with an adult
less densely packed with fat, so that relatively larger volumes of local anaesthetic are required.

Maximum paediatric local anaesthetic single dose by any route (Table 1.20)

Drug Maximum dose (mg/kg)
lignocaine without adrenaline
5
lignocaine with adrenaline
7
bupivacaine with or without adrenaline
2.5
ropivacaine with or without adrenaline
2 to 3
levobupivacaine with or without adrenaline
2.5
Duration of action and maximum doses of local anaesthetics used in dentistry
By Piscean | Tuesday, September 27, 2011 | Posted in , , , | With 0 comments

Duration of action and maximum doses of local anaesthetics used in dentistry
Drug Duration (minutes) [NB1] Maximum dose [NB2] Approximate maximum number of 2.2 mL cartridges that can be used in a 70 kg person (and dose contained in it)
pulp soft tissue
lignocaine 2% (20 mg/mL)
5 to 10
60 to 120
4.4 mg/kg to an absolute maximum of 300 mg in an adult
not available in cartridges in Australia
lignocaine 2% (20 mg/mL) with adrenaline 1:80 000 (12.5 micrograms/mL)
60 to 90
180 to 300
4.4 mg/kg to an absolute maximum of 300 mg in an adult
7 (308 mg)
lignocaine 2% (20 mg/mL) with adrenaline 1:100 000 (10 micrograms/mL)
60 to 90
180 to 300
4.4 mg/kg to an absolute maximum of 300 mg in an adult
7 (308 mg)
prilocaine 4% (40 mg/mL)
30 to 45
60 to 180
6 mg/kg to an absolute maximum of 400 mg in an adult
4.5 (396 mg)
prilocaine 3% (30 mg/mL) with adrenaline 1:300 000 (3.3 micrograms/mL)
30 to 90
120
6 mg/kg to an absolute maximum of 400 mg in an adult
6 (396 mg)
prilocaine 3% (30 mg/mL) with felypressin 0.03 international units/mL
40 to 90
150 to 210
6 mg/kg to an absolute maximum of 400 mg in an adult
6 (396 mg)
articaine 4% (40 mg/mL) with adrenaline 1:100 000 (10 micrograms/mL)
60 to 75
180 to 360
7 mg/kg to an absolute maximum of 500 mg in an adult
5.5 (484 mg)
mepivacaine 3% (30 mg/mL)
20 to 40
120 to 180
4.4 mg/kg to an absolute maximum of 300 mg in an adult
4.5 (297 mg)
mepivacaine 2% (20 mg/mL) with adrenaline 1:100 000 (10 micrograms/mL)
60 to 90
90 to 180
4.4 mg/kg to an absolute maximum of 300 mg in an adult
7 (308 mg)
bupivacaine 0.5% (5 mg/mL) with adrenaline 1:200 000 (5 micrograms/mL)
90 to 180
240 to 540
1.3 mg/kg to an absolute maximum of 90 mg in an adult
8 (88 mg)
NB1: variable, dependent upon dose and route of administration
NB2: variable, dependent upon route of administration, medical history and many other factors. Maximum doses are unlikely to be reached in most adult dental patients for most dental procedures. This might not be so in children and the elderly. Maximum doses are expressed in terms of the local anaesthetic, not the vasoconstrictor. Many guidelines have different maximum doses for local anaesthetics with and without vasoconstrictors. In this publication, the maximum doses have not been adjusted for the inclusion of a vasoconstrictor (this is in line with the recommendations given in Malamed S. Handbook of local anasthesia. 5th ed. St Louis: Mosby; 2004). As with all medications, it is recommended that the clinician confirms details of dosages with the relevant data provided through the manufacturer
Local anaesthetics: properties
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Local anaesthetics: properties
A local anaesthetic molecule comprises a lipophilic head, a hydrophilic tail, and a linking intermediate chain. The intermediate chain can be an ester (aminoester group) or an amide (aminoamide group). Aminoester local anaesthetics are more water soluble, and are primarily metabolised in plasma by pseudocholinesterases. Aminoamide local anaesthetics are less water soluble, and are primarily metabolised in the liver by de-ethylation. See Table 1.7 for characteristics of local anaesthetic drugs.

Efficacy of a particular drug is determined by its concentration at the site of action. This depends on the dose and concentration injected, diffusion to the relevant site if this is distant from the injection point, and on removal by the circulation, which in turn depends on the vascularity of the tissue. Increased lipid solubility of the local anaesthetic enhances absorption. Increased ionisation, which depends on the pKa of the drug and the pH at the site, decreases absorption 

Systemic absorption can be reduced by co-administration with a vasoconstrictor such as adrenaline, which prolongs and intensifies the local anaesthetic action, reduces surgical bleeding, and lowers peak blood concentrations of the local anaesthetic and the risk of systemic toxicity. A local anaesthetic solution with 1:200 000 adrenaline (5 micrograms/mL) is often used. Adrenaline is contraindicated in the presence of ischaemic heart disease, ventricular arrhythmias or uncontrolled hypertension, and for digital or penile nerve blocks, and intravenous block.
The uses of the different local anaesthetic solutions are summarised in Table 1.8.
Characteristics of local anaesthetics (Table 1.7)
Drug pKa Onset Duration (hours) [NB1] Maximum single adult dose [NB2] pH of solution [NB3] Protein binding (%)
Aminoamides
lignocaine
7.9
fast
0.5 to 2
3 mg/kg;
7 mg/kg (with adrenaline)
6.5
65
prilocaine
7.9
fast
1 to 3
6 mg/kg;
8 mg/kg (with adrenaline)
5.0 to 7.0
55
bupivacaine
8.1
intermediate to slow
4 to 12
1.5 to 2 mg/kg
2 to 3 mg/kg (with adrenaline)
4.0 to 6.5
95
levobupivacaine
8.1
intermediate to slow
4 to 12
1.5 to 2 mg/kg
4.0 to 6.5
95
ropivacaine
8.1
intermediate to slow
3 to 6
300 mg (major nerve block)
4 to 6
94
Aminoesters
procaine
8.9
slow
0.5 to 1.5
8 mg/kg
5 to 6.5
6
amethocaine (tetracaine)
[NB4]
–
fast
at least 15 minutes
single dose
4.5 to 6.5
-
NB1: variable, dependent upon dose and route of administration
NB2: variable, dependent upon route of administration
NB3: pH lower by 1.0 to 1.5 units for adrenaline-containing solutions
NB4: characteristics apply to topical use in ophthalmic procedures.regarding its use as a topical local anaesthetic in children
Thiopentone
By Piscean | Friday, September 9, 2011 | Posted in , , , | With 0 comments

Thiopentone is a barbiturate, and therefore potentiates the inhibitory effects of gamma amino butyric acid (GABA) in the central nervous system. After a single dose, unconsciousness occurs approximately 10 to 20 seconds after injection and recovery occurs after 5 to 10 minutes. Rapid recovery is largely due to redistribution rather than hepatic metabolism. Due to interindividual variation, doses are titrated incrementally to effect. Intravenous cannulae must be thoroughly flushed after administration of thiopentone due to the risk of precipitation, especially in combination with the neuromuscular blocking agents. Bronchospasm may occur; therefore thiopentone is best avoided in asthma. Respiratory depression may be prolonged in myasthenia gravis and muscular dystrophy. Hypotension and myocardial depression are common. Patients may notice a 'garlic' taste during induction. Thiopentone is cerebroprotective, which can be useful in head injury and status epilepticus. Thiopentone should not be used for short procedures where a patient may be discharged rapidly, as full recovery may take up to 24 hours. Extravasation can result in local tissue necrosis.
Propofol
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The mechanism of action of propofol is poorly defined, but its main central nervous system depressant action is thought to be via gamma-amino-butyric acid (GABA) receptors at a site of action other than that of benzodiazepines and barbiturates.
Propofol is an oil at room temperature, and therefore is formulated for intravenous administration in a lipid emulsion containing soya oil and egg lecithin. After intravenous administration, the onset of action is within 30 seconds and recovery generally occurs within three to five minutes. This rapid recovery and absence of 'hangover' effects has resulted in its increasing role in procedural sedation and short-term sedation of mechanically ventilated patients, particularly in emergency medicine.
There is a wide variation in the dose required to achieve sedation or unconsciousness, therefore doses should be titrated incrementally. Patients over the age of 55 years tend to require lower doses than younger patients.
Propofol does not possess any analgesic activity. It is associated with hypotension, bradycardia, pain at the injection site and muscle excitation resulting in tremors and involuntary movements. Brief apnoea and respiratory depression requiring ventilatory support is generally more common with propofol than with midazolam/opioid combinations used in procedural sedation.

Ketamine
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Ketamine is an N-methyl-D-aspartate antagonist (NMDA) that induces dissociative anaesthesia due to dissociation between the cortical and limbic systems. In addition to other pharmacological effects, it interacts with opioid receptors. It produces good analgesic effects at subanaesthetic doses.
For information on ketamine abuse, 

Use for acute or chronic pain

When used in subanaesthetic doses, ketamine can assist in controlling acute or chronic pain, particularly severe pain that is not well controlled by other agents, and particularly if there is evidence of central sensitisation. Ketamine should only be used in consultation with a specialist in pain medicine, anaesthesia or palliative care. When used for pain, it can be given by the subcutaneous route, either as intermittent doses or as a continuous infusion, often combined with an opioid analgesic. In persistent pain, it can be effective when given in short bursts of 3 to 5 days, then ceased and recommenced if pain returns or increases. Ketamine has also been used as a nasal spray.

Use for procedural sedation
Ketamine may be administered intramuscularly, intravenously or by continuous intravenous infusion. When administered intramuscularly, its onset of action is almost as rapid as when administered intravenously. The duration of its effect is partly dependent on the total dose administered. Amnesia may persist for one to two hours.

Precautions
Ketamine should be avoided in the following situations:
conditions where elevations in blood pressure and heart rate would be deleterious, such as uncontrolled hypertension, acute stroke, acute coronary syndromes, intracranial haemorrhage, stenotic valve disease, tachyarrhythmias and hyperthyroidism
raised intraocular pressure, including penetrating eye injuries
history of hallucinations
procedures involving the posterior pharynx, due to the risk of laryngospasm. 
Adverse effects
Common adverse effects include hypersalivation and increased muscle tone resulting in random or purposeful movements that may resemble seizures. Emergence reactions, involving vivid dreams, confusion, hallucinations and irrational behaviour may occur during recovery and for up to 24 hours. In rare cases, these effects have recurred days or weeks after ketamine administration. Emergence phenomena occur less frequently in children (aged 15 years or less), in the elderly and with intramuscular administration. They can be minimised by monitoring the patient in a quiet, low-stimulus environment during recovery. Benzodiazepines, such as midazolam, have been used to prevent and treat such reactions. Ketamine may be useful in asthmatic patients due to its direct relaxant effects on bronchial smooth muscle and absence of respiratory depression. It is the induction agent of choice in status asthmaticus.