Anesthetic Agents: General and Local Anesthetics T IMOTHY J
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Instructions for Anesthesiology Programs Requesting the Addition of a Clinical Base Year (CBY) to an Existing 3-Year Accredited Residency
Instructions for Anesthesiology Programs Requesting the Addition of a Clinical Base Year (CBY) to an Existing 3-year Accredited Residency MATERIALS TO BE SUBMITTED: Attachment A: Clinical Base Year Information Form Attachment B: Provide specific goals and objectives (competency-based terminology) for each block rotation and indicate assessment tools that will be utilized. Attachment C: Include a description of both clinical and didactic experiences that will be provided (lectures, conferences, grand rounds, journal clubs). Attachment D: Provide an explanation of how residents will evaluate these experiences as well as supervising faculty members. Attachment E: Provide a one-page CV for the key supervising faculty. Attachment F: Clarify the role of the resident during each of the program components listed. Information about Anesthesiology Clinical Base Year ACGME RRC Program Requirements 7/08 1) Definition of Clinical Base Year (CBY) a) 12 months of ‘broad education in medical disciplines relevant to the practice of anesthesiology’ b) capability to provide the Clinical Base Year within the same institution is desirable but not required for accreditation. 2) Timing of CBY a) usually precedes training in clinical anesthesia b) strongly recommended that the CBY be completed before the resident begins the CA-2 year c) must be completed before the resident begins the CA-3 year 3) Routes of entry into Anesthesiology program a) Categorical program - Resident matches into categorical program (includes CB year, approved by RRC as part of the accredited -
Chapter 11 Local Anesthetics
Chapter LOCAL ANESTHETICS 11 Kenneth Drasner HISTORY MECHANISMS OF ACTION AND FACTORS ocal anesthesia can be defined as loss of sensation in AFFECTING BLOCK L a discrete region of the body caused by disruption of Nerve Conduction impulse generation or propagation. Local anesthesia can Anesthetic Effect and the Active Form of the be produced by various chemical and physical means. Local Anesthetic However, in routine clinical practice, local anesthesia is Sodium Ion Channel State, Anesthetic produced by a narrow class of compounds, and recovery Binding, and Use-Dependent Block is normally spontaneous, predictable, and complete. Critical Role of pH Lipid Solubility Differential Local Anesthetic Blockade Spread of Local Anesthesia after Injection HISTORY PHARMACOKINETICS Cocaine’s systemic toxicity, its irritant properties when Local Anesthetic Vasoactivity placed topically or around nerves, and its substantial Metabolism potential for physical and psychological dependence gene- Vasoconstrictors rated interest in identification of an alternative local 1 ADVERSE EFFECTS anesthetic. Because cocaine was known to be a benzoic Systemic Toxicity acid ester (Fig. 11-1), developmental strategies focused Allergic Reactions on this class of chemical compounds. Although benzo- caine was identified before the turn of the century, its SPECIFIC LOCAL ANESTHETICS poor water solubility restricted its use to topical anesthe- Amino-Esters sia, for which it still finds some limited application in Amino-Amide Local Anesthetics modern clinical practice. The -
Cyclopropane Anaesthesia by JOHN BOYD, M.D., D.A
Cyclopropane Anaesthesia By JOHN BOYD, M.D., D.A. TLHIS paper is based on my experience of one thousand cases of cyclopropane anaesthesia personally conducted by me since October, 1938, both in hospital and in private. But before discussing these it might be convenient for me to mention here something about the drug itself. HISTORY. Cyclopropane was first isolated in Germany in 1882 by Freund, who also demonstrated its chemical structure, C3H6. He did not, however, describe its anaesthetic properties. Following its discovery it seems to have been forgotten until 1928, when Henderson and Lucas of Toronto, in investigating contaminants of propylene, another anesthetic with undesirable side-effects, and itself'an isomer of cyclopropane, found that the supposed cause of the cardiac disturbances was in reality a better and less toxic anaesthetic. They demonstrated its anaesthetic properties first on animals, and then, before releasing it to the medical profession for clinical trial, they anaesthetised each other, and determined the quantities necessary for administration to man. In 1933 the first clinical trials of cyclopropane were made by Waters and his associates of the University of Wisconsin. In October of that year Waters presented a preliminary report on its anaesthetic properties in man,1 confirming the findings of Henderson and Lucas. Rowbotham introduced it to England first in 1935, and since then its use has spread rapidly throughout the country. PREPARATION. Cyclopropane is prepared commercially by the reduction of trimethylene bromide in the presence of metallic zinc in ethyl alcohol. It is also made commercially from propane in natural gas by progressive thermal chlorination. -
Analgesia and Sedation in Hospitalized Children
Analgesia and Sedation in Hospitalized Children By Elizabeth J. Beckman, Pharm.D., BCPS, BCCCP, BCPPS Reviewed by Julie Pingel, Pharm.D., BCPPS; and Brent A. Hall, Pharm.D., BCPPS LEARNING OBJECTIVES 1. Evaluate analgesics and sedative agents on the basis of drug mechanism of action, pharmacokinetic principles, adverse drug reactions, and administration considerations. 2. Design an evidence-based analgesic and/or sedative treatment and monitoring plan for the hospitalized child who is postoperative, acutely ill, or in need of prolonged sedation. 3. Design an analgesic and sedation treatment and monitoring plan to minimize hyperalgesia and delirium and optimize neurodevelopmental outcomes in children. INTRODUCTION ABBREVIATIONS IN THIS CHAPTER Pain, anxiety, fear, distress, and agitation are often experienced by GABA γ-Aminobutyric acid children undergoing medical treatment. Contributory factors may ICP Intracranial pressure include separation from parents, unfamiliar surroundings, sleep dis- PAD Pain, agitation, and delirium turbance, and invasive procedures. Children receive analgesia and PCA Patient-controlled analgesia sedatives to promote comfort, create a safe environment for patient PICU Pediatric ICU and caregiver, and increase patient tolerance to medical interven- PRIS Propofol-related infusion tions such as intravenous access placement or synchrony with syndrome mechanical ventilation. However, using these agents is not without Table of other common abbreviations. risk. Many of the agents used for analgesia and sedation are con- sidered high alert by the Institute for Safe Medication Practices because of their potential to cause significant patient harm, given their adverse effects and the development of tolerance, dependence, and withdrawal symptoms. Added layers of complexity include the ontogeny of the pediatric patient, ongoing disease processes, and presence of organ failure, which may alter the pharmacokinetics and pharmacodynamics of these medications. -
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Mutations M287L and Q266I in the Glycine Receptor ␣1 Subunit Change Sensitivity to Volatile Anesthetics in Oocytes and Neurons, but Not the Minimal Alveolar Concentration in Knockin Mice Cecilia M. Borghese, Ph.D.,* Wei Xiong, Ph.D.,† S. Irene Oh, B.S.,‡ Angel Ho, B.S.,§ S. John Mihic, Ph.D.,ʈ Li Zhang, M.D.,# David M. Lovinger, Ph.D.,** Gregg E. Homanics, Ph.D.,†† Edmond I. Eger 2nd, M.D.,‡‡ R. Adron Harris, Ph.D.§§ ABSTRACT What We Already Know about This Topic • Inhibitory spinal glycine receptor function is enhanced by vol- Background: Volatile anesthetics (VAs) alter the function of atile anesthetics, making this a leading candidate for their key central nervous system proteins but it is not clear which, immobilizing effect if any, of these targets mediates the immobility produced by • Point mutations in the ␣1 subunit of glycine receptors have been identified that increase or decrease receptor potentiation VAs in the face of noxious stimulation. A leading candidate is by volatile anesthetics the glycine receptor, a ligand-gated ion channel important for spinal physiology. VAs variously enhance such function, and blockade of spinal glycine receptors with strychnine af- fects the minimal alveolar concentration (an anesthetic What This Article Tells Us That Is New EC50) in proportion to the degree of enhancement. • Mice harboring specific mutations in their glycine receptors Methods: We produced single amino acid mutations into that increased or decreased potentiation by volatile anesthetic in vitro did not have significantly altered changes in anesthetic the glycine receptor ␣1 subunit that increased (M287L, third potency in vivo transmembrane region) or decreased (Q266I, second trans- • These findings indicate that this glycine receptor does not me- membrane region) sensitivity to isoflurane in recombinant diate anesthetic immobility, and that other targets must be receptors, and introduced such receptors into mice. -
Hallucinogens - LSD, Peyote, Psilocybin, and PCP
Information for Behavioral Health Providers in Primary Care Hallucinogens - LSD, Peyote, Psilocybin, and PCP What are Hallucinogens? Hallucinogenic compounds found in some plants and mushrooms (or their extracts) have been used— mostly during religious rituals—for centuries. Almost all hallucinogens contain nitrogen and are classified as alkaloids. Many hallucinogens have chemical structures similar to those of natural neurotransmitters (e.g., acetylcholine-, serotonin-, or catecholamine-like). While the exact mechanisms by which hallucinogens exert their effects remain unclear, research suggests that these drugs work, at least partially, by temporarily interfering with neurotransmitter action or by binding to their receptor sites. This InfoFacts will discuss four common types of hallucinogens: LSD (d-lysergic acid diethylamide) is one of the most potent mood-changing chemicals. It was discovered in 1938 and is manufactured from lysergic acid, which is found in ergot, a fungus that grows on rye and other grains. Peyote is a small, spineless cactus in which the principal active ingredient is mescaline. This plant has been used by natives in northern Mexico and the southwestern United States as a part of religious ceremonies. Mescaline can also be produced through chemical synthesis. Psilocybin (4-phosphoryloxy-N, N-dimethyltryptamine) is obtained from certain types of mushrooms that are indigenous to tropical and subtropical regions of South America, Mexico, and the United States. These mushrooms typically contain less than 0.5 percent psilocybin plus trace amounts of psilocin, another hallucinogenic substance. PCP (phencyclidine) was developed in the 1950s as an intravenous anesthetic. Its use has since been discontinued due to serious adverse effects. How Are Hallucinogens Abused? The very same characteristics that led to the incorporation of hallucinogens into ritualistic or spiritual traditions have also led to their propagation as drugs of abuse. -
Local Anesthetic Half Life (In Hours) Lidocaine 1.6 Mepivacaine 1.9 Bupivacaine 353.5 Prilocaine 1.6 Articaine 0.5
Local Anesthetics • The first local anesthetics History were cocaine and procaine (Novacain) developed in ltlate 1800’s • They were called “esters” because of their chemical composition • Esters had a slow onset and short half life so they did not last long History • Derivatives of esters called “amides” were developed in the 1930’s • Amides had a faster onset and a longer half life so they lasted longer • AidAmides quiklickly repldlaced esters • In dentistry today, esters are only found in topical anesthetics Generic Local Anesthetics • There are five amide anesthetics used in dentistry today. Their generic names are; – lidocaine – mepivocaine – bupivacaine – prilocaine – artica ine • Each is known by at least one brand name Brand Names • lidocaine : Xylocaine, Lignospan, Alphacaine, Octocaine • mepivocaine: Carbocaine, Arestocaine, Isocaine, Polocaine, Scandonest • prilocaine : Citanest, Citanest Forte • bibupivaca ine: MiMarcaine • articaine: Septocaine, Zorcaine About Local Anesthetic (LA) • Local anesthetic (LA) works by binding with sodium channels in neurons preventing depolarization • LA is inactivated at the injection site when it is absorbed into the blood stream and redistributed throughout the body • If enough LA is absorbed, sodium channels in other parts of the body will be blocked, causing systemic side effects About LA • A clinical effect of LAs is dilation blood vessels, speeding up absorption and distribution • To counteract this dilation so anesthesia is prolonged, , a vasoconstrictor is often added to LAs • However, vasoconstrictors have side effects also Metabolism and Excretion • Most amide LAs are metabolized (inactivated) by the liver and excreted by the kidneys. • Prilocaine is partially metabolized by the lungs • Articaine is partially metabolized by enzymes in the bloo d as well as the liver. -
General Anaesthesia in Oral Surgery and Outpatient Surgery History
Department of Oral- and Maxillofacial Surgery, Semmelweis University Budapest Head of Department: Dr. Németh Zsolt General anaesthesia in oral surgery and outpatient surgery History 1844 Horace Wells nitrous oxide extraction of one of his own wisdom teeth by a colleague 1846 William Morton (pupil of Wells) ether extraction 1946 introduction of lidocaine General anaesthesia should be strictly limited to those patients and clinical situations in which local anaesthesia (with or without sedation) is not an option. Bourne JG. General anaesthesia in the dental surgery. B Dental J 1962; 113: 54-7. Coleman F. The history of nitrous oxide anaesthesia. Dental Record 1942; 62: 143-9 Naveen Malhotra General Anaesthesia for Dentistry ndian Journal of Anaesthesia 2008;52:Suppl (5):725-737 Types of general anaesthesia Outpatient anaesthesia • Dental chair anaesthesia Relative analgesia for simple extraction • Day care anaesthesia Conscious sedation (Sedoanalgesia) for minor oral surgery In patient anaesthesia Intubation with or without neuromuscular blocking for complicated extractions, oral- and maxillofacial surgical procedures Indications of general anaesthesia • Acute infection (pain) • Children • Mentally challenged patients • Dental phobia • Allergy to local anaesthetics • Extensive dentistry & facio-maxillary surgery Equipments • anaesthesia machine, vaporizers • oxygen, nitrous oxide • breathing circuits (adult and pediatric) • nasal and facial masks • oral and nasal air-ways • different laryngoscopes with all sizes of blades • nasal and -
Methohexital(BAN, Rinn)
1788 General Anaesthetics metabolic pathways include hydroxylation of the 3. Lökken P, et al. Conscious sedation by rectal administration of Methohexital Sodium (BANM, rINNM) midazolam or midazolam plus ketamine as alternatives to gener- cyclohexone ring and conjugation with glucuronic ac- al anesthesia for dental treatment of uncooperative children. Compound 25398; Enallynymalnatrium; Méthohexital Sodique; id. The beta phase half-life is about 2.5 hours. Keta- Scand J Dent Res 1994; 102: 274–80. Methohexitone Sodium; Metohexital sódico; Natrii Methohexi- 4. Louon A, et al. Sedation with nasal ketamine and midazolam for talum. mine is excreted mainly in the urine as metabolites. It cryotherapy in retinopathy of prematurity. Br J Ophthalmol crosses the placenta. 1993; 77: 529–30. Натрий Метогекситал 5. Zsigmond EK, et al. A new route, jet-injection for anesthetic in- C14H17N2NaO3 = 284.3. ◊ References. duction in children–ketamine dose-range finding studies. Int J CAS — 309-36-4; 22151-68-4; 60634-69-7. 1. Clements JA, Nimmo WS. Pharmacokinetics and analgesic ef- Clin Pharmacol Ther 1996; 34: 84–8. ATC — N01AF01; N05CA15. fect of ketamine in man. Br J Anaesth 1981; 53: 27–30. 6. Kronenberg RH. Ketamine as an analgesic: parenteral, oral, rec- tal, subcutaneous, transdermal and intranasal administration. J ATC Vet — QN01AF01; QN05CA15. 2. Grant IS, et al. Pharmacokinetics and analgesic effects of IM and Pain Palliat Care Pharmacother 2002; 16: 27–35. oral ketamine. Br J Anaesth 1981; 53: 805–9. Pharmacopoeias. US includes Methohexital Sodium for In- jection. 3. Grant IS, et al. Ketamine disposition in children and adults. Br J Nonketotic hyperglycinaemia. -
Excluded Drug List
Excluded Drug List The following drugs are excluded from coverage as they are not approved by the FDA ACTIVE-PREP KIT I (FLURBIPROFEN-CYCLOBENZAPRINE CREAM COMPOUND KIT) ACTIVE-PREP KIT II (KETOPROFEN-BACLOFEN-GABAPENTIN CREAM COMPOUND KIT) ACTIVE-PREP KIT III (KETOPROFEN-LIDOCAINE-GABAPENTIN CREAM COMPOUND KIT) ACTIVE-PREP KIT IV (TRAMADOL-GABAPENTIN-MENTHOL-CAMPHOR CREAM COMPOUND KIT) ACTIVE-PREP KIT V (ITRACONAZOLE-PHENYTOIN SODIUM CREAM CMPD KIT) ADAZIN CREAM (BENZO-CAPSAICIN-LIDO-METHYL SALICYLATE CRE) AFLEXERYL-LC PAD (LIDOCAINE-MENTHOL PATCH) AFLEXERYL-MC PAD (CAPSAICIN-MENTHOL TOPICAL PATCH) AIF #2 DRUG PREPERATION KIT (FLURBIPROFEN-GABAPENT-CYCLOBEN-LIDO-DEXAMETH CREAM COMPOUND KIT) AGONEAZE (LIDOCAINE-PRILOCAINE KIT) ALCORTIN A (IODOQUINOL-HYDROCORTISONE-ALOE POLYSACCHARIDE GEL) ALEGENIX MIS (CAPSAICIN-MENTHOL DISK) ALIVIO PAD (CAPSAICIN-MENTHOL PATCH) ALODOX CONVENIENCE KIT (DOXYCYCLINE HYCLATE TAB 20 MG W/ EYELID CLEANSERS KIT) ANACAINE OINT (BENZOCAINE OINT) ANODYNZ MIS (CAPSAICIN-MENTHOL DISK) APPFORMIN/D (METFORMIN & DIETARY MANAGEMENT CAP PACK) AQUORAL (ARTIFICIAL SALIVA - AERO SOLN) ATENDIA PAD (LIDOCAINE-MENTHOL PATCH) ATOPICLAIR CRE (DERMATOLOGICAL PRODUCTS MISC – CREAM) Page 1 of 9 Updated JANUARY 2017 Excluded Drug List AURSTAT GEL/CRE (DERMATOLOGICAL PRODUCTS MISC) AVALIN-RX PAD (LIDOCAINE-MENTHOL PATCH) AVENOVA SPRAY (EYELID CLEANSER-LIQUID) BENSAL HP (SALICYLIC ACID & BENZOIC ACID OINT) CAMPHOMEX SPRAY (CAMPHOR-HISTAMINE-MENTHOL LIQD SPRAY) CAPSIDERM PAD (CAPSAICIN-MENTHOL -
Pharmacology for Regional Anaesthesia
Sign up to receive ATOTW weekly - email [email protected] PHARMACOLOGY FOR REGIONAL ANAESTHESIA ANAESTHESIA TUTORIAL OF THE WEEK 49 26TH MARCH 2007 Dr J. Hyndman Questions 1) List the factors that determine the duration of a local anaesthetic nerve block. 2) How much more potent is bupivocaine when compared to lidocaine? 3) How does the addition of epinephrine increase the duration of a nerve block? 4) What is the maximum recommended dose of: a) Plain lidocaine? b) Lidocaine with epinephrine 1:200 000? 5) What is the recommended dose of a) Clonidine to be added to local anaesthetic solution? b) Sodium bicarbonate? In this section, I will discuss the pharmacology of local anaesthetic agents and then describe the various additives used with these agents. I will also briefly cover the pharmacology of the other drugs commonly used in regional anaesthesia practice. A great number of drugs are used in regional anaesthesia. I am sure no two anaesthetists use exactly the same combinations of drugs. I will emphasise the drugs I use in my own practice but the reader may select a different range of drugs according to his experience and drug availability. The important point is to use the drugs you are familiar with. For the purposes of this discussion, I am going to concentrate on the following drugs: Local anaesthetic agents Lidocaine Prilocaine Bupivacaine Levobupivacaine Ropivacaine Local anaesthetic additives Epinephrine Clonidine Felypressin Sodium bicarbonate Commonly used drugs Midazolam/Temazepam Fentanyl Ephedrine Phenylephrine Atropine Propofol ATOTW 49 Pharmacology for regional anaesthesia 29/03/2007 Page 1 of 6 Sign up to receive ATOTW weekly - email [email protected] Ketamine EMLA cream Ametop gel Naloxone Flumazenil PHARMACOLOGY OF LOCAL ANAESTHETIC DRUGS History In 1860, cocaine was extracted from the leaves of the Erythroxylon coca bush. -
Jebmh.Com Original Research Article
Jebmh.com Original Research Article A COMPARATIVE STUDY OF SMALL DOSE OF KETAMINE, MIDAZOLAM AND PROPOFOL AS COINDUCTION AGENT TO PROPOFOL Abhimanyu Kalita1, Abu Lais Mustaq Ahmed2 1Senior Resident, Department of Anaesthesiology, Assam Medical College, Dibrugarh. 2Associate Professor, Department of Anaesthesiology, Assam Medical College, Dibrugarh. ABSTRACT BACKGROUND The technique of “coinduction”, i.e. use of a small dose of sedative agent or another anaesthetic agent reduces the dose requirement as well as adverse effects of the main inducing agent. Ketamine, midazolam and propofol have been used as coinduction agents with propofol. MATERIALS AND METHODS This prospective, randomised clinical study compared to three methods of coinduction. One group received ketamine, one group received midazolam and one group received propofol as coinducing agent with propofol. RESULTS The study showed that the group receiving ketamine as coinduction agent required least amount of propofol for induction and was also associated with lesser side effects. CONCLUSION Use of ketamine as coinduction agent leads to maximum reduction of induction dose of propofol and also lesser side effects as compared to propofol and midazolam. KEYWORDS Coinduction, Propofol, Midazolam, Ketamine. HOW TO CITE THIS ARTICLE: Kalita A, Ahmed ALM. A comparative study of small dose of ketamine, midazolam and propofol as coinduction agent to propofol. J. Evid. Based Med. Healthc. 2017; 4(64), 3820-3825. DOI: 10.18410/jebmh/2017/763 BACKGROUND But, the major disadvantage of propofol induction are Propofol is the most frequently used IV anaesthetic agent impaired cardiovascular and respiratory function, which may used today with a desirable anaesthetic profile. It provides put the patients at a higher risk of bradycardia, hypotension faster onset of action, antiemesis, rapid recovery with and apnoea.