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INFOGRAPHICS in ANAESTHESI by Dr. Tushar Chokshi.pptx

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INFOGRAPHICS in ANAESTHESI by Dr. Tushar Chokshi.pptx

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Respected Sir/Madam/Colleague Greeting from Dr. Tushar Chokshi, Vadodara I have completed 20 months journey of my Infographics in Anesthesiology. I am extremely thankful and honored for allowing, accepting, tolerating and inspiring continuous endeavoring of my infographics. In September 2020 I started my first Infographics in Anesthesia on MgSO4. And till date I have completed almost 130 + infographics in our subjects. (लोग साथ आते गए और कारवााँ बनता गया) I was inspired to make infographics in anesthesia by one little 5 year old child. He was having online education during corona period from his school every day through infographics on different subjects. He was accepting theme of story or any subject very nicely and not only that he was remembering very well (As our vision is most valuable sense then hearing and remembers 70 to 90 %). And from this I had taken ideas of making infographics in anesthesia. Now every time for each medication, procedure or other things, it becomes easy for me and others to refer in single page as one slider infographics. For each making of infographics, I usually take 5 to 10 hours to make it readable with graphics, shapes, colors, & informations by visually appealing. Before each infographics I read, write, correct, and understand detailed information for particular infographics from journals, textbooks and online articles. Not only that, in doubt I always consult my colleagues who are experts and masters in their subjects by phone calls, messages or emails. Still some informations may be written wrongly with spellings or dose or without my deep knowledge. But my intentions are very clear to respect all my colleagues. I will be humbled if you can guide and advice me personally. I will still advice you to refer textbooks or other articles for particular infographics. In my life whatever I learned, taught and experienced from my teachers, seniors and colleagues, I want to give it back to society. I am lifetime student of my subject and I will exchange my knowledge throughout the life with you. Lastly, I fall in love with my infographics, & not just the end product of my work. I believe to Die Empty and Unleash my best work everyday. Show must go on. Your Infographics Colleague, Dr. Tushar Chokshi InfographicS Aspire to Inspire before we Expire of
Dedicated to My Family
Dr. Tushar M. Chokshi Area of Expertise Other Highlights Affiliations Current Position Consultant Private Practicing Anesthesiologist in Vadodara (Gujarat, INDIA)  Sterling Hospital  Urocare Hospital  Dhwani ENT Hospital  Arpan Surgical Hospital 30 Years of Experience TIVA, OFA and NORA  Uro Anaesthesia  Lapro Anaesthesia ENT Anesthesia Paediatric Anesthesia  Founder of TIVA and OFA Face book Groups in INDIA  National and State Level Speaker Started Smartphone and Tele- Anesthesia practice in INDIA Started Infographics in Anaesthesia  9825062245 chokshitushar@hotmail.com MD (Anaesthesiology) https://sites.google.com/site/tusharchokshisite National Origami Teacher Visual Storyteller & Vlogger Happy Go To Lucky Fellow Always believe in exchange of Knowledge
List of Drugs Adrenaline Atracurium Bupivacaine Calcium Cis-Atracurium Clonidine Dentrolene Dexamethasone Desflurane Dexmedetomidine Ephedrine Diclofenac Sodium Esmolol Etomidate Fentanyl Flumazenil Furosemide Glycopyrrolate Hydrocortisone Isoflurane Ketamine Levo Bupivacaine Lidocaine MgSO4 Midazolam Morphine Naloxone Nitrous Oxide Neostigmine Ondansetron Paracetamol Propofol Remifentanil Remimazolam Rocuronium Bromide Ropivacaine Sevoflurane Sodium Thiopental Suxamethonium Sugammadex Tranexamic Acid Xenon Paediatric Drug Dose PAC PDPH Risk of Anaesthesia PONV MH LAST List of Volatile Agents SGD Antidotes in Anaesthesia Adjuvants in L/A TIVA Kingdom Ane Drugs Label Colour Infertility Tests Infertility Tests Thyroid Function Tests Blood Sugar Tests Urine Tests Cardiac Blood Tests Lipid Profile Tests Liver Function Tests Complete Blood Count Kidney Function Tests Furosemide Transdermal patch Anaphylaxis NG tubes IV fluids 37 38 39 40 41 42 43 44 45 46 47 49 48 50 51 52 53 54 19 20 21 22 23 24 25 26 27 28 29 31 30 32 33 34 35 36 55 56 57 58 59 60 61 62 63 64 65 67 66 68 69 70 71 73 1 2 3 4 5 6 7 8 9 10 11 13 12 14 15 16 17 18 Infographics Infographics Infographics Infographics Mephentermine
Letter Pulmonary Embolism Different Positioning OFA Mnemonics Dobutamine Bain circuit Vecuronium Norepinephrine Chloroprocaine Mepivacaine Tetracaine Prilocaine Methoxyflurane Procaine Halothane Enflurane Cardiac Blood Flow Lung Physiology Haemodynamics Effects of Anaesthesia Pulmonary Circulation Antidotes in Anaesthesia TOF & PTC Segmental Spinal Anesthesia Geriatric Anaesthesia 1 Geriatric Anaesthesia 3 Geriatric Anaesthesia 2 ERCP Anae. Mx TEE Awareness EEG Intravascular volume monitoring Circulatory system Pulse Oximetry Central venous monitoring Ventilation Cricothyrotomy Neuropathic Pain Cancer Pain PA form for CVS Common Pain Syndromes Non opioid Rx chronic pain Musculoskeletal pain i-gel Opioid Mx of chronic pain Interventional pain therapy Pain management by RA Physiology in trauma Initial Mx in trauma Types of Trauma Airway Mx in trauma Trauma Bay Haemodynamics in trauma Intraoperative Mx of trauma CPNBs Ciprofol Medication Errors 109 110 111 112 113 114 115 116 117 118 119 121 120 122 123 124 125 126 92 93 94 95 96 97 98 98 99 100 101 103 102 104 105 106 107 108 127 128 129 130 131 132 133 134 135 74 75 76 77 78 79 80 81 82 83 84 86 85 87 88 89 90 91 Infographics Infographics Infographics Infographics Anticholinesterases Drugs Nondepolarizing NMBDs Depolarizing NMBDs Temperature Monitoring Site Magnesium Actions
1962-2009 1957-1961 Dexamethasone 1886-1990 Magnesium Sulphate 1956 Paracetamol 1973-1988 Diclofenac Sodium 1961-1966 Clonidine 1980-1987 Esmolol 1920-1928 Ephedrine 1971-1985 Mephentermine 1860 Cocaine 1905 Procaine 193--1941 Tetracaine 1943-1949 Lidocaine 1950 Chloroprocaine 1960 Mepivacine 1957 Bupivacine 1980 Ropivacaine 1980 Levobupivacaine 1900 Tubocurarine Chloride 1906-1951 Suxamethonium 1947 Gallamine Triethiodide 1964 Pancuronium 1974-1983 Atracurium 1984 Vecuronium 1984 Mivacurium 1989-1995 Cisatracurium 1994 Rocuronium 1830 Chloroform 1846 Ether 1920 Trichloroethylene 1956 Halothane 1963-1966 Enflurane 1979 Isoflurane 1970-1987 Desflurane 1971-1990 Savoflurane 1804 Morphine 1937-1943 Pethidine 1959-1968 Fentanil 1974 Sufentanil 1996 Remifentanil 1974 Carfentanyl 2020 Oliceridine 1930-1934 Sodium Thiopental 1962-1964-1970 Ketamine 1964-1972 Etomidate 1977-1989 Propofol 1999 Dexmedetomidine 1901 Atropine 1975 Glycopyrrolate 1964-1979 1981 Metoclopramide Ranitidine 1980-1991 Ondansetron 1959-1963 Diazepam 1963-1977 Lorazepam 1975-1990 Midazolam 1772 Nitrous Oxide 1774 Oxygen 1881 Cyclopropaine 1898 Xenon 1996 Atipamazole 1961-1971 1982 Naloxone Doxapram 1987 Flumezenil 1931 Neostigmine 2007-2015 Sugammdex 1967 Dentrolene 2014-2020 Remimazolam Anesthesia Adjuvant IV Anesthetic Local Anesthetic Gas Opioid/Narcotics Premedication Inhaltion Anesthetic Benzodiazepine Muscle Relaxant Anti MH Agent Benzodiazepine Reversal Agent IV Reversal Agent Opioid Reversal Agent Relaxant Reversal Agent Opioid with Benzodiazepine I N F O G R A P H I C S A N E S T H E S I A D R U G S O F Total 69 Drugs In Use 50 Drugs Tranexamic acid 1895-1904 Adrenaline 1959-1964 Lasix 1964 Metoclopramide
ADRENALINE Physiological Response of Adrenaline Heart : Increases heart rate, Contractility and Conduction across AV node Lungs : Increases Respiratory Rate & Bronchodilation Liver : Stimulates Glycogenolysis Muscle : Stimulates Glycogenolysis and Glycolysis Brain : Vasoconstriction and Vasodilation Systemic : Triggers Lipolysis Muscle Contraction Mechanism of Action Acts on both alpha and beta-adrenergic receptors. The rise in BP is 3-fold: a direct myocardial stimulation that increases the strength of ventricular contraction (positive inotropic action), an increased HR (positive chronotropic action), and peripheral vasoconstriction Side effects of Adrenaline Pharmacokinetics and Pharmacodynamics Formula : C9H13NO3 Molar mass : 183.207 g·mol−1 Receptors : Adrenergic receptors Metabolism : Adrenergic synapse (MAO and COMT) Protein binding : 15–20% Metabolites : Metanephrine Onset of action : Within 30 seconds Elimination half life : 2 minutes Duration of action : 5 minutes Excretion : Urine Store : Between :20° to 25°C Solution : Clear, Colorless & Sterile Solution For Extravasation And Tissue Necrosis With IV Infusion : Antidote is infiltrate the area with 10mL-15mL of saline solution containing from 5mg-10mg of phentolamine, an adrenergic blocking agent Dosage and Strength Available as 1 mg/mL (1:1000) 1mL amp. and 30 ml vial. And 1 mL amp. contains 1 mg adrenaline, 9.0 mg NaCl, 1.0 mg sodium metabisulfite, hydrochloric acid to adjust pH, and water for injection In Anaphylaxis : 0.3-0.5 mg(0.3-0.5 mL) of undiluted adrenalin administered IM or S/C in the anterolateral aspect of the thigh, maximum of 0.5 mg(0.5 mL) per injection, repeated every 5 to 10 minutes as necessary In Hypotension Associated With Septic Shock Dilute 1 mL (1 mg) of adrenaline from its vial to 1,000 mL of a 5 % dextrose or 5 % DNS solution to produce a 1 mcg per mL dilution and give infusions of adrenaline into a large vein and avoid the veins of the leg Routes IV IM Endotracheal Intracardiac Nasal Eye drop S/C Medical use Anaphylaxis Cardiac arrest To prevent superficial bleeding Asthma & Inhaled adrenaline for Croup Anxiety, Apprehensiveness Restlessness Tremor Weakness Dizziness Sweating Palpitations Pallor Nausea Vomiting Headache Respiratory difficulties Cardiovascular Angina, Arrhythmias, Hypertension, Pallor, Palpitations, Tachycardia Tachyarrhythmia, Vasoconstriction Ventricular Ectopy and Stress Cardiomyopathy Neurological Disorientation, Impaired memory, Panic, Psychomotor Agitation, Sleepiness, Tingling Contraindications for Adrenaline None Invented in 1895 & In use 1904 Also known as Epinephrine (Hormone) Produced both by the adrenal glands and by a small number of neurons in the medulla oblongata Gives Fight-or-Flight response Overdose Produce extremely elevated blood pressure and Cerebrovascular hemorrhage Treatment is supportive with alpha-adrenergic blocking and beta-adrenergic blocking drugs Adrenaline level in blood is normally less than 10 ng/L During Exercise increase by 10-fold & in Stress 50-fold In Pheochromocytoma levels of 1000–10,000 ng/L IV Adrenaline produce 10,000 to 100,000 ng/L BP Effect The onset of BP increase after IV dose in < 5 minutes & the time to offset BP occurs within 15 minutes Precautions Renal Impairment Cardiac Arrhythmia & Ischemia Patients on MAOI and Anti- depressant Never inject into digits, hands, or feet with LA because vasoconstr -iction causes loss of blood flow to the tissue & necrosis
ATRACURIUM History Invented by George H. Dewar Atracurium was licensed by Strathclyde University to the Wellcome Foundation UK First named this compound "33A74” Non-steroidal skeletal muscle relaxant Bisquaternary ammonium benzylis- oquinoline compound Mechanism of Action  Antagonize the neurotransmitter action of acetylcholine by binding competitively with cholinergic receptor sites on the motor end-plate  Binding of the postsynaptic nicotinic receptor by atracurium prevents depolarization of the motor end plate & subsequent skeletal muscle contraction Extra Shots Overdosage increase the risk of histamine release and cardiovascular effects It is advisable to reverse atracurium with an anticholinesterase reversing agent such as neostigmine, edrophonium, or pyridostigmine in conjunction with atropine or glycopyrrolate Avoid in rapid sequence intubation Side Effects Histamine release Cutaneous flushing (Face & Arm) Hypotension & reflex tachycardia  Bronchospasm & Secretions Seizures Erythema and Itching  Rare Allergic reactions (anaphylactic or anaphylactoid) Inadequate block, prolonged block Indications An adjunct to general anesthesia to facilitate endotracheal intubation To provide skeletal muscle relaxation during surgery or mechanical ventilation To facilitate the placement of a Supraglotic Airway Off label use : in ARDS and Shivering due to hypothermia following arrest Precautions to Use  Allergy and asthmatic patients  Myasthenia Gravis/Burns Injury  Eaton-Lambert syndrome  Electrolyte disorders  Malignant hyperthermia  Long term use in ICU ( > 10 days ) Pregnancy is not contraindication but careful it is teratogenic Pharmacokinetics Bioavailability 100 % (IV)  Protein binding 82%  Elimination half-life 17–21 minutes Metabolism Hofmann elimination and ester hydrolysis by nonspecific esteras (45 %)  Pregnancy Category C  Formula C65H82N2O18S2 Molar mass 1243.49g·mol−1 Dose of Atracurium  Only IV administration & never give IM injection because it causes tissue irritation  IV Bolus dose is 0.4 to 0.5 mg/kg & intubation can be expected in 2 to 2.5 minutes in most patients  First dose lasts 20 to 35 minutes  Maintenance dose is 0.08 to 0.10 mg/kg (last upto 20 min) Less than 2 yrs child dose is 0.3 to 0.4 mg/kg For continuous infusion 5 to 9 mcg/kg/minute (for GA & ICU) Infusion can be diluted in 5% Dextrose, 0.9% Sodium Chloride and 5% Dextrose with 0.9% Sodium Chloride (DNS)  Contains 10 mg/ml atracurium besylate  Available as 2.5 ml amp, 5 and 10 ml multidose bulbs Storage under 2° to 8° C Upon removal from refrigeration to room temperature use in 14 days Invented 1974 & In Use 1983 Most commonly used muscle relaxant Non Depolarizing Muscle Relaxant with short duration of action Atracurium should not be administered until patient has recovered from succinylcholine induced neuromuscular block It has an acid pH, should not be mixed with alkaline solutions in the same syringe 10 mL multidose vials only contain benzyl alcohol, so as far as avoid this vial in neonates and infants Laudanosine is major biologically active metabolite of atracurium without neuromuscular blocking activity In Renal and Hepatic failure or Critically ill patients No dose adjustment Reduce dose in long volatile anaesthesia Onset of action takes Approximately 2 minutes Renal Excretion is less than 5 % Slower injection speed, from 30 to 60 seconds, reduce histamine release, and the associated adverse effects Atracurium Hoffman elimination is a temperature and pH-dependent process and is slowed by acidosis and hypothermia No cumulative effect with repeat doses or continuous infusion It does not provide pain control, sedation, or amnesic effects
 BUPIVACAINE  Pharmacokinetic Bioavailability - n/a  Protein binding - 95%  Metabolism - Liver  Onset of action - Within 15 min  Elimination half-life - 3.1 hours (adults) 8.1 hours (neonates)  Duration of action - 2 to 8 hr  Excretion - Kidney 4–10%  Routes of administration Parenteral, Topical and Implant  Formula - C18H28N2O  Molar mass - 288.435 g·mol−1 Melting point - 107 to 108 °C  Pregnancy category - AU: A US: C  Peak effect - 35 to 40 minutes 1957 An implantable formulation of bupivacaine was approved for medical use in USA in August 2020 for open hernia surgery  Sometimes used in combination with epinephrine to prevent systemic absorption and extend the duration of action  The 0.75% (most concentrated) formulation is used in retro- bulbar block Indications  Local Infiltration  Peripheral nerve block  Sympathetic nerve block  Epidural & Spinal Anesthesia Caudal blocks Safely given in pregnancy and lactation Contraindications  Known hypersensitivity  Obstetrical paracervical blocks  Intravenous regional anaesthesia (Bier block)  0.75% formulation in epidural anesthesia during labor  Intra articular infusions Side effects Sleepiness Muscle twitching Ringing in the ears Changes in vision Low blood pressure Irregular heart rate Low Sexual Desire Compared to other local anesthetics, bupivacaine is markedly Cardiotoxic Bupivacaine can cause chondrolysis after continuous infusion into a joint space Treatment of overdose is intravenous lipid emulsion CNS Toxicity Circumoral numbness Facial tingling Vertigo/ Tinnitus Restlessness Anxiety/Dizziness Seizures/Coma CVS Toxicity Hypotension Arrhythmia Bradycardia Heart block Cardiac arrest GI Toxicity Nausea/ Vomiting High Spinal Anesthesia with Bupivacaine causes Paresthesia, Paralysis, Apnea, Hypoventilation, Fecal Incontinence, and Urinary Incontinence Mechanism of Action (Amino-Amide anesthetic)  Bupivacaine binds to the intracellular portion of voltage- gated sodium channels and blocks sodium influx into nerve cells, which prevents depolarization. Without depolarization, no initiation or conduction of a pain signal can occur The amino-amide anesthetics are more stable and less likely to cause allergic reactions Levobupivacaine is the (S)-(–)-enantiomer of bupivacaine, with longer duration of action, producing less vasodilatation Bupivacaine is available as a generic medication and is not very expensive Bupivacaine Dosage  Epidural Block  0.75% concentration : 75 to 150 mg (10 to 20 mL) for complete motor block  0.5% concentration 50 to 100 mg (10 to 20 mL) moderate to complete motor block  0.25% concentration: 25 to 50 mg (10 to 20 mL) partial to moderate motor block  Epidural Anesthesia:  0.5% and 0.75% solutions Epidural Anesthesia in Obstetrics:  only 0.5% and 0.25% Available as spinal heavy amp., preservative free and 0.25 % & 0.5 % solution bulb Bupivacaine Dosage  Caudal Block: 0.25% to 0.5% concentration (15 to 30 mL)  Peripheral Nerve Block : 0.25% to 0.5% concentration  Retrobulbar Block 0.75% concentration (2 to 4 mL)  Sympathetic Block: 0.25% concentration (20 to 50 mL)  Local Infiltration: 0.25% concentration max dose of 175 mg  Spinal anesthesia : 0.5 % heavy solution with dextrose (2 to 4 ml) preservative free 0.75% bupivacaine in 8.25% dextrose ( 1 to 1.6 ml) Usual dose of Bupivacaine is 2 mg/kg with or without adrenaline Rapid injection of a large volume of bupivacaine solution should be avoided and fractional or incremental doses should be used Local Anesthetic
Pharmacokinetics Atomic No. : 20 Formula : C12H22CaO14 Molar Mass : 430.373 g·mol−1 Routes : Oral / IV/ Topical Bioavailability : 100 % Metabolism : Direct Elimination : Renal Ca Ca Ca Ca IV CALCIUM M/A : Calcium plays a central role in a large number of physiological actions that are essential for life which include cardiac automaticity; excitation–contraction coupling in myocardial, smooth and skeletal muscle; blood coagulation; neuronal conduction; synaptic transmission; hormone secretion and mitotic division A normal 70-kg adult contains about 1.2 kg calcium, of which more than 99% is located in the bone In the plasma, the normal total calcium concentration is about 2.25–2.55 Mol/L−1 (9.0–10.2mg/dL−1) 50% of this is free ionized calcium, 10% is calcium combined with various anions, 40% is bound to proteins, mainly albumin Calcium inj. is given IV only, S/C or IM injections are not allowed because causes severe necrosis or sloughing Avoid rapid injection, it may cause Cardiac Arrest Dosing Regimen A bolus dose of 100 mg elemental calcium diluted in 100 mL isotonic saline and given over 5-10 min. It raise the total serum calcium by 0.5 mg/dL, but level of calcium begins to fall after 30 min. Therefore, the bolus dose of calcium should be followed by a continuous infusion at a dose rate of 1 to 2 mg/kg/h (elemental calcium) for at least 6 hours IV calcium available as 100 mg/ml Ca Chloride 10 ml 10 % (272 mg) Ca Gluconate 10 ml 10% (93 mg) Gluconate is less irritant to veins Precautions for giving Calcium Injection Calcium infusions can promote vasoconstriction and ischemia in any of the vital organs & and seen high in patients with low cardiac output Aggressive calcium replacement can promote intracellular calcium overload, which can produce lethal cell injury, particularly in patients with circulatory shock, so avoid it Always give calcium solution in large or central veins with small intracath, due to hyperosmolarity of calcium solutions Hypocalcemia(< 6) & Hypercalcemia(> 14) Sudden decreases in serum calcium may be seen in the early postoperative period after thyroidectomy or parathyroidectomy and may cause laryngospasm (Give Calcium accordingly) Hypercalcemia results from increased calcium reabsorption from the gastrointestinal tract, in renal insufficiency and increased bone resorption of calcium ( Treat with Isotonic saline Infusion, Furosemide, Calcitonin, Glucocorticoid, Biphosphonate & Dialysis ) Symptomatic Hypocalcemia must be treated before giving any type of anesthesia  Antidote of Calcium is Magnesium First isolated by Humphry Davy in 1808 It is classified as a calcium salt Most widely used is Calcium Gluconate Calcium Gluconate introduced in 1920 No dose adjustment is required in geriatric hepatic or renal impairment patients Always monitor ECG & serum calcium level every 4 hours in IV calcium therapy patients Calcium is prime drug in Cardiac arrest and cardiotoxicity due to hyper kalemia or hyper magnesemia  Common Side Effects - Warmth/Nausea/Vomiting/Paresthesias - Tingling /Heavy feeling/Bradycardia - Chalky taste in your mouth - Upset stomach/Gas/Constipation Serious Side Effects - Little or No Urination - Irregular Heart Beats - Light headedness - Feeling tired/Muscle weakness - Swelling/Weight gain Indications - Hypocalcemia/Tetany - Hydrofluoric acid burns -Hyperkalemia/Hyper Magnesemia - β-blocker toxicity - Calcium-channel blocker (CCB) toxicity - Allergic conditions/ Spider Bites - Pruritus due to drugs Contraindications Digitalized patients, VF & Hypercalcemia Usual Dosage Adults: 500 mg - 2 grams (5-20 mL) Children: 200-500 mg (2-5 mL) Infants: no more than 200 mg (not more than 2 mL) Careful of extravasation in IV Calcium and Antidote is Hyaluronidase
CARBON DIOXIDE Chemical Formula : CO2 Molar mass 44.009 g·mol−1 Colorless gas  Low concentrations: No odour  High concentrations Sharp & Acidic odour Density : 53 % higher than dry air Frozen solid form of CO2 known as dry ice Dissolves in water to form carbonic acid CO2 is necessary for the survival of life on earth like oxygen In Body Produced in the tissues and removed from the lungs by ventilation carried in the blood as dissolved gas, e.g. bicarbonate, and small amount bound to hemoglobin as carbamino hemoglobin Dissociation curve for carbon dioxide is essentially linear Increased Carbon Dioxide Production Fever Malignant hyperthermia Systemic absorption during laparoscopy procedures Thyroid storm Tourniquet release Administration of sodium bicarbonate Increased Dead space Decreased Minute Ventilation CO2 Narcosis (Paco2 > 80 mm of Hg) is a condition that develops when excessive CO2 is present in the bloodstream, leading to a depressed level of consciousness & largely results from lung disease, hypoventilation, or environmental exposure Respiratory Acidosis is a condition that occurs when the lungs can't remove enough of the CO2 produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic, due to failure of ventilation CO2 is the most important end-product of tissue metabolism Exists in three forms: (1) as free carbon dioxide, winch is dissolved in the water of the blood, (2) as bicarbonate of the plasma, and (3) as carbamino compounds in combination with haemoglobin CO2 tension of the body cell is greater than that in the capillary blood, thus CO2 moves into the blood The partial pressure of CO2 in mixed venous blood, PvCO2 (44-46 mm Hg) is greater than that in the alveoli of the lungs, Paco2 (38-40 mm Hg) CO2 used in anaesthesia since the late 1920s, principally to stimulate breathing after a period of hyperventilation Hypercarbia or Hypercapnia (High Paco2) Hypercapnia defined as the Paco2 being greater than 45 mm Hg. If the Paco2 is greater than 45 mm Hg, and the PaO2 is less than 60 mm Hg, a patient is said to be in hypercapnic respiratory failure Also known as Hypercarbia or CO2 Retention & confirmed by ABG analysis Exhausted carbon dioxide absorbents and malfunctioning expiratory valves on the anesthesia delivery circuit are possible causes hypercapnia Hypercapnia causes delayed awakening in the post anesthesia care unit Hypocarbia, or hypocapnia, occurs when levels of CO2 in the blood become abnormally low (Paco2 < 35 mm Hg). Hypocarbia is confirmed by arterial blood gas analysis. Hypocarbia, especially if only transient, is usually well tolerated by patients. Deliberate hyperventilation, leading to hypocarbia, is often used to decrease intracranial pressure in neurosurgical patients Seen in hypovolemia, hypotension, hypothermia & hypothyroidism Also seen in deep anaesthesia, iatrogenic hyperventilation, pulmonary embolism , CNS pathology and decreased metabolism Hypocarbia causes decreased myocardial oxygen supply, increased myocardial oxygen demand, decreased cerebral blood flow & respiratory alkalosis Treated by assessing oxygenation status, decreasing minute ventilation and restoring circulation to improve cardiac output Initial treatment of hypercapnia is oxygen therapy with the goal of increasing the inspired oxygen volume In anaesthesia common causes are over sedation, hypoventilation, inadequate gas flow and increased dead space In operation theatre it is detected by capnography and now a days capnography monitoring is must for CO2 like oxygen monitoring Both hypercapnia & hypocapnia are dangerous to the life Capnography It is a monitoring of the concentration or partial pressure of carbon dioxide in the respiratory gases as end-tidal carbon dioxide (EtCO2) Normal values for patients regardless of age, sex, race, or size range between 35-45 mm Hg In high EtCO2 value think respiratory failure In low EtCO2 value think poor systemic perfusion with shock
CHLOROPROCAINE An ester local anesthetic Chloroprocaine has one of the lowest partition coefficients (low lipophilicity) and has low potency relative to other local anesthetics Formula : C13H19ClN2O2 Molar mass : 270.76 g·mol−1 Metabolized by pseudo cholinesterase the liver Excretion through Kidney Chloroprocaine is used commonly for epidural anaesthesia Uses of Chloroprocaine in Anaesthesia Used in Regional Anaesthesia including Spinal, Caudal and Epidural anaesthesia Used in Local Anaesthesia including Brachial plexus block, Cervical nerve block and Occipital Maxillary/Mandibular block for Dental anaesthesia and Infraorbital block for Ophthalmic anaesthesia Also in Ulnar, Paravertebral, Intercostal, Sciatic, Lumbar Sympathetic, Stellate ganglion & Paracervical blocks Mechanism of Action Causes reversible nerve conduction blockade by decreasing nerve membrane permeability to sodium Binds to a specific region of the alpha subunit on the cytoplasmic region to inhibit voltage-gated sodium channels This binding activity increases the threshold for excitation in the nerve and slows nerve impulse propagation Chloroprocaine is vasodilator Dose and Strength Supplied as a 1%, 2%, and 3% solution For Spinal is 1% and preservative-free 50 mg Maximum recommended dose for infiltration, or peripheral nerve block is 11 mg/kg when administered alone, not to exceed 800 mg When given with adrenaline, dose is 14 mg/kg not exceeding 100 mg 2% / 3% is used in Lumbar epidural for LACS The effect last for 60-70 minutes Available as Chloroprocaine HCL injection Adverse Effects Most common adverse effect is pain related to the procedural injection due to high allergic reactions Sometimes in regional use Hypotension, Bradycardia, Nausea, and Headache Accidental intrathecal injection during epidural placement, with large dose may produce ‘ Total Spinal ‘ leading to fixed and dilated pupil Rarely Cauda Equina Syndrome in S/A Cautions & Contraindications In patients with a known allergy to para- aminobenzoic acid Caution to use Chloroprocaine to provide epidural, spinal, caudal, peripheral nerve and infiltrative anesthesia in lactating women Use with caution in patients with end-stage liver disease Avoid in pediatric patients younger than four years old (Dosing is not established) Doses more than 11 mg/kg may cause LAST Available as 1% and 2%, in multidose vials with methylparaben as preservative 2% and 3%, in single dose vials without preservative and EDTA ( Note for S/A) Always Keep from freezing, with Protect from light and Store at 20° to 25°C Monitoring during Chloroprocaine Anae. According to the ASA, oxygenation, ventilation, and circulation should be continuously monitored The Pulse Oximeter is the most commonly used with Oxygen supply During regional block with minimal or no sedation practiced The temperature should be assessed whenever possible BP & HR every 5 minutes interval taken Never use in Intravenous Regional anesthesia due to the risk of thrombophlebitis Chloroprocaine does not itself appear to be neurotoxic at clinical concentrations but formulations that contain EDTA can cause burning back pain when used in epidurals A preservative-free formulation of Chloroprocaine may be a drug of choice in short-acting spinal anesthesia and might even replace Lidocaine Chloroprocaine shelf life is 24 months Never autoclave Chloroprocaine injections Different Doses in Different Blocks Brachial Plexus 30 to 40 mL (600 to 800 mg) as a 2% solution Caudal epidural 15 to 25 mL of 2% or 3% methylparaben-free (MPF) solution, repeated every 40-60 min Infraorbital 0.5 to 1 mL (10 to 20 mg) as a 2% solution Paracervical 3 mL per each of 4 sites as a 1% solution, total dose up to 120 mg  Pudendal 10 mL on each side as a 2% solution, total dose 400 mg Digital 3 to 4 ml 1 %
Also called as CYCLOPOFOL  Invented in CHINA in Feb. 2021 & patented in Dec. 2021 Sedative, Hypnotic & Anaesthetic Trade Name is Sishuning (HSK3486) In china price is Rs. 3800/- per 20 ml amp. Ciprofol is Class 1 IV Anaesthetic & Propofol analogue with improved pharmacokinetic properties  Phase I, IIa, IIb Trails are completed  recently Phase III Trial started on 2nd August 2022  just now only available in CHINA  Ciprofol developed by Haisco Pharma. Group Dose Schedule Initial dose is 0.4 mg/kg for 30 seconds In geriatric 0.3 mg/kg Supplemental dose is 0.1mg/kg/ time as IV bolus for 10 seconds & minimum 2 minute with each dose Range from 0.3 to 0.6 mg/kg Maintenance infusion dose is 0.1 to 0.3 mg/kg/h Almost one forth dose is required than Propofol Available as 50 mg in 20 ml borosilicate glass ampoule solution & 200 mg in 20 ml under development phase Ciprofol is a Propofol analogue with improved pharmacokinetic properties & pharmacodynamic characteristics New intravenous anesthetic agent characteristics of a rapid rate of onset and recovery in pre- clinical experiments It is γ-aminobutyric acid (GABA) receptor agonist & novel 2,6- disubstituted phenol derivative Circulating metabolites are nonhypnotic and nontoxic Non inferior to Propofol in all trials with characteristics Indications Induction & Maintenance of anesthesia in all elective surgeries As sedation in NORA procedures As a sedation in mechanical ventilation in ICU Adjuvant in TIVA Not studied in < 18 years old pt. In all phase trials indicated in gastroscopy, hysteroscopy colonoscopy, ERCP, bronchoscopy, cystoscopy & Gynec procedures Works as status epilepticus and as an anti-emetic like Propofol Better than Propofol in all transplant Induction Superior to Propofol Five times More potent than Propofol Almost no pain on IV injection Less hemodynamic instability ( less hypotension & depression) Only dose dependent respiratory depression, apnea and hypoxia Myoclonus and infusion syndrome are extremely rare Better in prolonged infusion Less serious AEs (adverse events) than Propofol in all trials Ciprofol induction is associated with more stable BIS changes than Propofol Ciprofol binds to the γ-aminobutyric acid type A (GABAA) receptor more tightly than Propofol and exhibits reduced lipophilicity and more suitability Pharmacokinetics  Ciprofol Injection content are soya bean oil for injection, medium chain triglyceride, refined egg yolk lecithine, sodium oleate, glycerin, sodium hydroxide & water for injection Ciprofol is white or off-white homogenous milky liquid  Validity period 24 is months Not studied in pregnant and lactating women Storage at 25 degree c in airtight & do not freeze Metabolism: oxidation to form mono oxyglucuronic acid In Short Compared to Propofol, it has the advantages of "two fast and five few" rapid onset, rapid recovery; less dosage, wider safety window; less respiratory depression, risk reduction by more than 60%; less cardiovascular adverse events , stable circulation; less pain on injection, the incidence is only 1/10 of Propofol; less lipid infusion Highly effective, easy to control, safe and comfortable It takes effect quickly and wakes up quickly Ketamine+Ciprofol combo is viable Extra Shots Effect last for 3 to 5 minutes Awakening time is about 3 min Overdose causes cardiovascular & respiratory depression Approved by the China & Australian State Food and Drug Administration for studies Excretion through renal 80 % and fecal 20 % Not known that it is excreted in human milk Till now 12 major trials are done on Ciprofol in China & Australia  May be game changer or another experimental IV anesthetic drug CIPROFOL (IV Anaesthetic)
Non-Depolarising Neuromuscular Blocking Drug One of the ten isomers of the parent molecule, Atracurium M/A Acts by competitive antagonism Binds with nicotinic acetyl chonline receptors (nAChRs) on the motor end-plate of neuromuscular junction to produce neuromuscular blockade Drug of choice in Cardiac compromise patients ARDS patients Hepatic failure patients Renal failure patients Ideal in Neuro Surgical patients Chemo and Obese patient Systemic Actions No change in Heart Rate, Contractility, SVR and Blood Pressure Lung protective through its anti inflammatory properties Metabolism is through Hofmann reaction Reduces ICP, cerebral perfusion and it is neuroprotective Does not produce any autonomic effect Ideal Neuromuscular Blocking Agent - Best intubating condition - - Non-depolarizing mechanism of action - - Rapid onset enabling quick intubation - - Rapid complete and predictable recovery - - Short elimination half life - - No cumulative effect - - No histamine release - - High potency - - Has pharmacologically inactive metabolites - - Reversible by cholinesterase inhibitors - - Elimination pathways less dependent on organ function - - Lack clinically important Cardiovascular side effects - Dose is 0.15 to 0.20 mg/kg (50-60 minutes) Maintenance dose is 0.02 to 0.03 mg/kg (20-25 minutes) OT and ICU Infusion 1-3 mcg/kg/minute Paediatric dose is 0.10-0.15 mg/kg Below 1 mth not recommended Indications It is intermediate onset and duration action of drug Mainly indicated for inpatients and outpatients adjunct to general anaesthesia To facilitate tracheal intubation To provide skeletal muscle relaxation during surgery For mechanical ventilation in ICU Pregnancy, Labour, Delivery and Nursing mother (drug of choice) Contraindications Known hypersensitivity Patients with myasthenia gravis or myasthenia syndrome History of prior anaphylactic reactions to neuromuscular blocking agents Adverse Effects Uncommon with the use of Cisatracurium Less than 1% - Brady, Hypo, Spasm, Myopathy, Prolonged Effect - Kept refrigerated at 2 to 8 degrees Celsius - Protected from light - Rate of loss of potency is as high as 5% per month at 25 degrees Celsius - Once removed from refrigeration to room temperature storage, it should be used within 21 days - Undergoes 80 % Hofmann elimination - Renal Excretion of is only 16 % - Elimination half-life is 20–29 minutes - Hypothermia and Hyperthermia, increase and decrease the duration of action - Sedative, Volatile agents, Local anaesthetics and Anti-epileptic agents will prolong the effect Avoid in Rapid Sequence intubation As ICU relaxant more than one week Burns injury Cerebral palsy Hemiplegia (on the affected side) Muscular denervation (peripheral nerve injury) Severe chronic infection Tetanus Botulism Cis gives uniform recovery from anesthesia  
CLONIDINE Invented in 1961, Medical use in 1966, Epidural use in 1984 First approved to treat HT and in 2010 approved for ADHD in children  It is given by Oral/IV/IM/Epidural/Spinal/Skin Patch  Imidazole compound & partial α2 receptors agonist  It causes bradycardia, by increasing signaling through the vagus nerve   Mechanism of Action   Clonidine treats high blood pressure by stimulating α2 receptors in the brain stem, which decreases peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2 receptors in the vasomotor center in the brainstem  This binding has a sympatholytic effect, suppresses release of norepinephrine ATP, renin, and neuropeptide Y which if released would increase vascular resistance When given IV, it temporarily increase BP by stimulating α1 receptors in smooth muscles in blood vessels like Dex Clonidine crosses the blood-brain barrier   Indications  To treat high BP Menopausal Flushing Drug withdrawal (Alcohol/Opioids/Smoking) Spasticity and certain pain conditions ADHD and Diarrhoea   Use in Anaesthesia practice   Administration of clonidine in combination with a local anaesthetic to prolongs analgesia and motor blockade in Epidural and Spinal When used IV or IM it gives sedation, hypnosis, analgesia, opioid need reduction and anti-sympathetic response, to surgical trauma response But its use is limited by its principal effects of hypotension and bradycardia Oral Premedication : 2 to 4 mcg/kg IV : 1-2 mcg/kg as bolus, slowly  IV infusion : 0.2 mcg/kg/minute Spinal : 0.5-1 mcg/kg with L/A Epidural : 1-2 mcg/kg with L/A Continuous Epidural Infusion : 30 mcg/hr Patch : 0.1 mg or 0.2 mg per day   Pharmacokinetic   Formula : C9H9Cl2N3 Molar mass : 230.09 g·mol−1 Bioavailability : 70–80% (oral),60–70% (transdermal) Protein binding : 20–40% Metabolism : Liver to inactive metabolites (50 %) Elimination : Renal another 50 % Elimination half-life : 6-23 hrs, in Renal Failure 41 hrs Elimination half-life in S/A : 1.5 hrs Store : 20° to 25°C Shelf Life : 60 months  Highly Lipid Soluble   Contraindications   Allergic reactions to clonidine Severe Bradyarrhythmia Above the C4 dermatome Bleeding diathesis Sick Sinus Syndrome AV block of second or third degree No specific antidote for clonidine overdosage (Naloxone and Atropine are used sometimes) Epidural clonidine is not recommended for obstetrical, post-partum, or peri-operative pain management Spinal clonidine as an adjuvant to Cesarean Section anesthesia is well established ( No neonatal side effect) Available Ampule : 150 mcg/ml Bulb : 100 mcg/ml 10 ml vial & 500 mcg/ml 10 ml vial Tablets : 0.1/0.2/0.3 mg Patch : 0.1 mg or 0.2 mg > 10% Dizziness Fatigue Orthostatic hypotension Somnolence (dose-dependent) Dry mouth Headache (dose-dependent) Bradycardia Skin reactions (if given transdermally) Hypotension In 1-10% Pain below the ear (salivary gland) Sedation (dose-dependent) Erectile dysfunction Weight gain/loss Nausea/vomiting Abnormal LFTs Constipation Skin Rash Malaise Anxiety Overdose Cause Hypotension Bradycardia Respiratory- depression Hypothermia Drowsiness Clonidine in the treatment of chronic neoplastic pain, used epidurally in the dose of 10-50 μg/h Clonidine has also got benefit in the treatment of Postoperative Shivering Clonidine is now slowly replaced by Dexmedetomidine ( Dex is full α2 receptors agonist) If clonidine is used then Volatile Anaesthetics requirement are reduced by 50 % Clonidine is a versatile drug that is used in the critical care setting for sedation and to treat opioid induce Hyperalgesia
D A N T R O L E N E Oral Dantrolene was first described in the scientific literature in 1967, IV in 1979 Dantrolene is Hydantoin derivatives, a new class of muscle relaxant Dantrolene was widely used in the management of spasticity as Oral Rx Efficacy in treating Malignant Hyperthermia was discovered by South African anesthesiologist Gaisford Harrison and reported in a landmark 1975 article published in the British Journal of Anaesthesia Side Effects Drowsiness Dizziness Weakness General malaise Fatigue Diarrhea Indications Primary drug used for the treatment and prevention of malignant hyperthermia, during General Anaesthesia Neuroleptic Malignant Syndrome, Muscle Spasticity /Spasms Poisoning by 2,4-dinitrophenol Contraindications Oral Dantrolene Pre-existing liver disease Compromised lung function Severe cardiovascular impairment Hypersensitivity to Dantrolene Pediatric patients under five years of age People who need good muscular balance Nausea IV Dantrolene People with a known hypersensitivity to Dantrolene Mechanism of Action Dantrolene is a postsynaptic muscle relaxant that lessens excitation-contraction coupling in muscle cells Work directly on the Ryanodine receptor to prevent the release of calcium Dantrolene does not act at the neuromuscular junction and has no effect on the passive or active electrical properties of the surface and tubular membranes of skeletal muscle fibers IV Dantrolene have normal EMG results Pharmacokinetics Formula C14H10N4O5 Molar mass 314.257 g·mol−1 Bioavailability 70% Metabolism Liver Excretion Biliary, Kidney Routes Oral and IV  Protein binding Mostly to albumin Half Life 4 to 8 hrs  Trade names Dantrium, Ryanodex Dose of Dantrolene The recommended dose of Dantrolene is 1-2.5 mg/kg, repeated as necessary, every 4-6 hrs for 24 – 48 hrs (Max 10 mg) It is recommended that each hospital keep a minimum stock of 36 Dantrolene vials (720 mg), sufficient for maximum four doses in a 70-kg person (20 mg/Vial) Risk of Death in MH : 5% if treated, 95% if not treated with Dentrolene Extra Shots The poor water solubility of Dantrolene leads to certain difficulties in its use. A more water-soluble analog of Dantrolene, Azumolene, is under development for similar indications. Azumolene has a bromine residue instead of the nitro group found in Dantrolene, and is 30 times more water-soluble Dantrolene Malignant Hyperthermia Association of the United States guidelines state Dantrolene must be available within 10 min of the decision to treat MH wherever volatile anesthetics or succinylcholine are administered Dantrolene for IV administration is supplied in 70 mL vials, containing 20 mg Dantrolene sodium and 3 g Mannitol. It must be diluted with 60 mL of sterile, preservative-free, distilled water Phlebitis is a most common side effect of Dantrolene IV administration, noted in approximately 10% of patients, so intermittent bolus is preferred than continuous IV administration Invasive hemodynamic monitoring is necessary while giving IV Dantrolene Serum potassium must be closely monitored during Dantrolene therapy Oral Dantrolene is effective in reducing muscle pain after IV suxamethonium in GA Repeated dosing of Dantrolene should be guided by clinical and laboratory signs Dantrolene 20 mg vial cost is Rs. 6000/- (36 vials cost are Rs. 216000/-) Antidote of MH $ 82/Vial
DEXAMETHASONE  Universal Friend  Anti Nauseatic & Anti Emetic Early Discharge from Anaesthesia Anti Inflammatory Weak anti pyretic effect Anti Edema drug Anti Shivering Systemic Analgesic Effect Increase Quality of Recovery  Synthetic Glucocorticoids with minimal mineralocorticoid activity  Most potent anti inflammatory than Hydrocortisone and prednisolone  Biological half-life is 3 hours  Metabolism in liver with inactive metabolites  Renal excretion upto 65% in urine within 24 hours Readily available  Price is very cheap   Most ideal perioperative agent   Superior to ondensetron to reduce PONV   Reduce opioid Consumption   Decrease Analgesic effect upto 24 hours   Always to be given prior to surgery   Best TIVA and OFA adjuvant   Great psychological effect  Prevents any allergic reaction  Invented in 1957 & In use 1961  Dose Schedule  PONV – 0.1 mg/kg (IV)   Anti Inflammatory – 0.2 mg/kg(IV)   Analgesic – 0.1 mg/kg(IV)   Epidural -- 8 to 10 mg   Blocks – 0.1 mg/kg   S/A - 8 mg  Mechanism of Actions  Depletion of γ-aminobutyric acid (GABA) stores and reduction of blood brain barrier to emetogenic toxins,  Inhibition of central prostaglandins and serotonin  Membrane stabilizing effect on nerves and on spinal cord Dexona IN DM  4 mg is ideal dose 8 -10 mg dose Increase around 25 mg/dl glucose postop upto 24 hrs Dexona in Sepsis Does not increase any risk of wound infection with or without DM in any surgical procedure Acute Side Effect Flushing Perineal Itching Dexona Is the only adjuvant in anesthesia given irrespective of age, sex, disease or ASA status Safe in Onco Anesthesia Avoid in Psychiatric patients Be careful in Immuno compromised patients Improves Cognitive function In Elderly 8 8 8 8 8 8 8 8
DESFLURANE Pharmacokinetics  Formula C3H2F6O, Store at 15°-30°C  Metabolism : Not metabolized  Elimination half-life : Elimination dependent on minute ventilation  Routes of administration : Inhalation  Molar mass : 168.038 g·mol−1  Boiling point : 23.5 °C or 74.3 °F (at 1 atm)  Brain: Gas coefficient : 0.54  Density :1.465 g/cm³(at 20 °C)  Molecular Weight : 168  Vapor pressure : 88.5 kPa672 mmHg(at 20 °C) & 107 kPa804 mmHg(at 24 °C)  Blood:Gas partition coefficient : 0.42  Oil:Gas partition coefficient : 19  MAC : 6 vol %  Non-flammable Specific Gravity : 1.465  Shelf Life : 3 years  Desflurane Vaporizer color is Blue Most rapid onset and offset of the volatile anesthetic used for general anesthesia due to its low solubility in blood Though it vaporizes very readily, it is colorless liquid at room temperature  Drawbacks of desflurane are its low potency, its pungency and its high cost Cause tachycardia and airway irritability when administered at concentrations greater than 10 vol % Due to airway irritability, desflurane is infrequently used to induce anesthesia via inhalation techniques Mechanism of Action  Desflurane is known to act as a positive allosteric modulator of the GABAA and glycine receptors, and as a negative allosteric modulator of the nicotinic acetylcholine receptor, as well as affecting other ligand-gated ion channels Does not corrode stainless steel, brass, aluminum, anodized aluminum, nickel plated brass, copper, or beryllium Provides good relaxation for intubation Ideal volatile agent for day care surgery In adults, a starting concentration of 3% is recommended & increased in 0.5-1.0% increments every 2 to 3 breaths. Inspired concentrations of 4-11% of desflurane usually produce surgical anaesthesia in 2-4 minutes Can be safely use in Obstetric anesthesia, compromised renal and hepatic patients ( it is less hepatotoxic) Because of its low blood-gas partition coefficient, desflurane allow more rapid emergence and recovery than Halothane, Isoflurane, or even Sevoflurane  CVS effect : Dose dependent tachycardia and hypertension Depression in myocardial contractility, Decrease in SVR, Coronary vasodilator  CNS effect : Dose dependent Cerebral vasodilatation Increase CBF, Cerebral blood volume, Intracranial pressure, Cerebral oxygen consumption decreased  Respiratory effect : Potent respiratory depressant, Decrease tidal volume, Increase RR, Extremely irritant to respiratory airways  Invented in 1970 & Medical use in 1987 Indicated as an inhalation agent for induction of anesthesia for inpatient and outpatient surgery in adults Contraindicated as an inhalation agent for the induction and maintenance of anesthesia in non intubated pediatric patients because of a high incidence of moderate to severe upper airway adverse events including coughing, laryngospasm, and secretions Near to ideal inhalational anesthetic agent Vaporizer specifically designed and designated for use with desflurane should be utilized for its administration  Should not be used as the sole agent for anesthetic induction in patients with coronary artery disease or patients where increases in heart rate or blood pressure are undesirable  In case of contact with skin or eye, immediately flush skin and eye with plenty of water at least 15 minutes  The predicted effects of acute over exposure by inhalation of Desflurane include headache, dizziness or (in extreme cases) unconsciousness  If individuals smell vapors, or experience dizziness or headaches, they should be moved to an area with fresh air Age N O2 100% N N2O 60%/40% O2 2 weeks 6 9.2 ± 0.0 - - 10 weeks 5 9.4 ± 0.4 - - 9 months 4 10.0 ± 0.7 5 7.5 ± 0.8 2 years 3 9.1 ± 0.6 - - 3 years - - 5 6.4 ± 0.4 4 years 4 8.6 ± 0.6 - - 7 years 5 8.1 ± 0.6 - - 25 years 4 7.3 ± 0.0 4 4.0 ± 0.3 45 years 4 6.0 ± 0.3 6 2.8 ± 0.6 70 years 6 5.2 ± 0.6 6 1.7 ± 0.4 Effect of Age on Minimum Alveolar Concentration Triggers Malignant Hyperthermia
Sedation Anxiolysis DEXMEDETOMIDINE Analgesic Anaesthetic FDA December 1999 Market August 2000  Agonist of α2-adrenergic receptors   Most ideal anesthetic agent available  M/A Induces sedation by decreasing activity of noradrenergic neurons in the locus ceruleus in the brain stem, thereby increasing the activity of inhibitory gamma- aminobutyric acid (GABA) neurons in the ventrolateral preoptic nucleus  Popular in pediatric TIVA with ketamine   Patients sedated, but arousable, alert and respond without uncomfortable like conscious sedation  No effect on Respiratory System  Transient Hypertension followed by Hypotension  No Direct effect on Myocardium IOP Insulin Release  Overdose may cause 1st or 2nd degree AV Block  - Nasal - ~ 84 % bioavailability Indications Pre Anaesthetic sedation (IM/IV) As Induction Agent In maintenance of Anaesthesia As adjuvant in TIVA Intra thecal with Regional Ane. In Post Operative Analgesia As ICU sedation(only for 24 hrs) Relative Contraindication  Infusion over 24 hours  In pre existing severe bradycardia  Brady dysrhythemia  Patient with < 30% EF  Partial or Complete AV block  In patients more than 65 y of age, a higher incidence of bradycardia and hypotension Compatibility - 0.9% sodium chloride in water - 5% dextrose in water - 20% mannitol - Lactated Ringer's solution - 100 mg/ml MgSo4 solution - 0.3% potassium chloride solution - With other Anesthetic agents e.g. Propofol, Ketamine, Etomidate Available as Ampoules or Bulb 50 mcg / 0.5ml 100 mcg / 1 ml 200 mcg / 2ml Sileo Gel for Dogs (Dexmedetomidine Oromucosal Gel) 0.09 mg/ml, 3 ml syringe (BIPHASIC BLOOD PRESSURE RESPONSE) (BRADYCARDIA IS BECAUSE OF DOUBLE EFFECT) (DECREASE OPIOID REQUIREMENT BY 50 %) (BETTER THAN CLONIDINE IN ALL ASPECTS)
 DICLOFENAC SODIUM   Introduced By Ciba-Geigy in 1965  Nonsteroidal anti-inflammatory drug  Available worldwide  Generic Medication  Available as both a sodium and a potassium salt  Given by Mouth, Rectally, IM, IV injection and Topical Skin Gel/Spray Pharmacokinetic  Formula C14H11Cl2NO2  Protein binding More than 99%  Metabolism Liver, oxidative, primarily by CYP2C9  Onset of action Within 4 hours Topical,30 min Oral, 15 minutes IM, 5 minutes IV and 30 minutes Rectal  Elimination half-life 1.2–2 hr  Excretion 40% bile duct and 60% urine  Molar mass 296.15 g·mol−1 Mechanism of action  The primary mechanism responsible for its anti- inflammatory, antipyretic, and analgesic action is thought to be inhibition of prostaglandin synthesis by inhibition of the transiently expressed prostaglandin- endoperoxide synthase-2 (PGES-2) also known as cycloxygenase-2 (COX-2).  Blockage of voltage-dependent sodium channels  Blockage of acid-sensing ion channels It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis Avoid use of multidose bulb/vial  Positive allosteric modulation of KCNQ- and BK-potassium channels  It inhibits the lipoxygenase pathways, thus reducing formation of the leukotrienes  It also may inhibit phospholipase A2 as part of its mechanism of action  These additional actions may explain its high potency – it is the most potent NSAID on a broad basis Contraindications  Hypersensitivity against diclofenac  History of allergic reactions (COPD, bronchospasm, shock, rhinitis, urticaria) Active stomach and/or duodenal ulceration or GI bleeding Severe congestive heart failure Severe liver insufficiency Severe chronic kidney disease Pre-existing hepatic porphyria Avoid during dengue fever Patients with fluid retention In worsening of pre-existing hypertension Inflammatory bowel disease such as Crohn's disease or ulcerative colitis Serious skin adverse events e.g. exfoliative dermatitis, Stevens–Johnson syndrome, toxic epidermal necrolysis Powerful NSAID in TIVA/OFA with analgesia and anti-inflammatory action  Use aqueous solution only Best is given in single dose of 1.5 mg/kg IV slowly and maximum is 150 mg  It is opioid sparing drug  Always give before surgical incision to inhibit prostaglandin receptors, which control the haemodynamic response to surgical stimulation  Diclo should not be mixed with any drug except paracetamol in same syringe  Given with any IV Infusion Always dilute diclo with DW and give slowly to avoid injection pain Dose  Oral 50 mg 2 or 3 times a day  Extended-release tablets 100 mg once a day  Potassium immediate-release tablets 50 mg orally 2 or 3 times a day  Sodium enteric-coated tablets 75 mg orally 2 times a day  IV/IM 1 to 1.5 mg/kg, repeat after 8 hours  Rectally 1 to 1.5 mg/kg ( Paediatric patients) Diclo is better than paracetamol to control post operative fever & pain In anaesthesia practice Diclo Is used as an adjuvant for perioperative acute pain management  Diclofenac is an effective analgesic for acute pain in children as part of the analgesic regime in the peri operative period with dose range from 0.5 to 2.5 mg/kg  Infusion line pain or irritation to vein is very common during IV Diclo, so better prefer large venous line Major side effects of diclo are 1) Abdominal or Stomach pain, Cramping, or Burning 2) Bloody or black, tarry stools 3) Bloody urine and decreased frequency or amount of urine 4) Heartburn or Indigestion 5) Diarrhea 6) Increased thirst and Loss of appetite 7) Vomiting of blood or material that looks like coffee grounds 7) Very rare anaphylactic or anaphylactoid reaction  Some time single dose or overdose of Diclo may cause Acute Renal Failure  As far as avoid Diclo in geriatric age group of patients ( paracetamol is preferred )
DOBUTAMINE Approved in 1970 - 1978 Works by direct stimulation of β1 receptors Formula C18H23NO3 Given by IV & Intraosseous Onset of action within 2 min Elimination half life 2 min Dobutamine is predominantly a β1-adrenergic agonist, with weak β2 activity, and α1 selective activity Stimulation of the β1-adrenoceptors of the heart, increase contractility and cardiac output dobutamine is less prone to induce hypertension than is dopamine Dobutamine has mild β2 agonist activity, which makes it useful as a vasodilator Adverse effects Hypertension(> 50 mm of Hg) Angina Arrhythmia (Most Dangerous) Use with caution in AF Tachycardia(>30 beats/min) Palpitation Sometime bronchospasm and shortness of breath Urinary urgency(at high dose) Nausea and Headache Phlebitis and very rare Cutaneous necrosis Overdose Terminate the infusion and arrhythmia treated with lidocaine & beta blocker & sublingual nitrate Indications Patients who require a positive inotropic support in the treatment of cardiac decompensation due to depressed contractility Cardiogenic shock characterized by heart failure with severe hypotension Septic Shock Used for detection of myocardial ischemia (dobutamine stress echocardiography) In Paediatric population (neonates- 18 years) in cardiomyopathies & Cardiogenic shock Dose & Formation Available as 50 mg/ml in 5 ml 10 ml & 50 ml amp/bulb Dose ranges from 2.5-10 µg dobutamine/kg/min Neonate-18 years an initial dose of 5 mcg/kg/minute, range from 2 – 20 mcg/kg/min Low dose 2.5 µg/kg/min (15 drops/min) Medium dose 5 g/kg/min(30 drops/min) High dose 10 µg/kg/min(60 drops/min) Always dilute dobutamine with final concentration 0.5 mg/ml in DNS/D5/NS/DW & not in RL Contraindications Known hypersensitivity Pericardial Tamponade Constrictive Pericarditis Hypertrophic Obstructive Cardiomyopathy Severe Aortic Stenosis Hypovolaemic conditions Recent MI Severe heart failure Chronic Arrhythmia Hypovolemia Acute pericarditis, Myocarditis or Endocarditis Aortic Aneurysm  Inadequately treated arterial hypertension Shelf Life : 3 years Dilution of Dobutamine used within 24 hrs and kept in freeze for 2°C to 8° Sometimes immediately after opening the ampoule, there may be a sulfuric odour lasting for short period Solutions containing Dobutamine may have a pink coloration, which may become darker over time, This is due to a slight oxidation of the active substance Unused solution discarded Pharmacokinetics Dobutamine & Dopamine Dobutamine produced a distinct increase in cardiac index, while lowering left ventricular end- diastolic pressure and leaving mean aortic pressure unchanged Dopamine also significantly improved cardiac index, but at the expense of a greater increase in heart rate than occurred with dobutamine Dobutamine is preferred when there is a need to improve low cardiac output.  Dopamine increase global blood flow Wide Ball Hypotension occurs in almost 40% of all anesthetized patients Dopamine is recommended for patients with kidney disease due to its ability to increase renal blood flow Dobutamine is preferred when there is a need to improve low cardiac output Dobutamine should be avoided in patients affected by outflow obstructions, pulmonic stenosis, or hypertrophic obstructive Cardiomyopathy Dobutamine Infusion Rate of administration and duration of dobutamine infusion is based on blood pressure, heart rate, frequency of ectopic activity, and urine flow; cardiac output, central venous pressure, and pulmonary capillary wedge pressure Initial dose: 0.5 to 1 mcg/kg/min IV infusion Maintenance dose: 2 to 20 mcg/kg/min IV infusion Maximum dose: 40 mcg/kg/min IV infusion Always label the infusion It is Synthetic catecholamine Haemodynemic changes occur during anaesthesia and surgery in elderly patients, Dobutamine corrects the perioperative decrease in cardiac output and blood pressure, and might prevent postoperative neurological disorders Dobutamine is only given with guidelines of institution and when indicated For routine administration it is too dangerous Monitoring with ECG is must during therapy
ENFLURANE MECHANISM OF ACTION Enflurane acts as a positive allosteric modulator of the GABAA, glycine, and 5- HT3 receptors, and as a negative allosteric modulator of the AMPA, kainate, and NMDA receptors as well as of nicotinic acetylcholine receptors. So it act on different ion channels within the nervous system by blocking excitatory channels and augmenting inhibitory channels Enflurane is (2-chloro-1,1,2,-trifluoroethyl- difluoromethyl ether) is a halogenated ether Developed by Ross Terrell in 1963, first used clinically in 1966 Approved by the FDA in 1972 Withdrawn from the US market due to more Seizure activity, increased Cardio Depressant effects and Slow onset of action Increasingly used for inhalational anesthesia during the 1970s and 1980s, now no longer in common use PHARMACOKINETICS Clear, colorless, mild sweet odor , Stable nonflammable and non explosive liquid whose purity exceeds 99.9% Formula : C3H2ClF5O, Molar mass : 184.49 g·mol−1 Protein binding : 97%, Boiling point at 1 atm 56.5 °C Blood:Gas partition coefficient 1.9, Oil:Gas partition coefficient 98 Vapor pressure at 20 °C22.9 kPa (172 mm Hg), MAC : 1.68 Specific gravity (25º/25ºC) is 1.517 The MAC in man is 1.68% in pure oxygen, 0.57 in 70% nitrous oxide, 30% oxygen, and 1.17 in 30% nitrous oxide, 70% oxygen Rapidly absorbed into the circulation through the lungs Metabolized : by the CYP2E1 enzyme in the liver upto only 9 % Storage at 15º-30ºC (59º-86ºF) Enflurane sensitizes the heart to catecholamines such as epinephrine  Usually not recommended in Paediatric Anaesthesia as induction DOSAGE AND ADMINISTRATION Orange colored Vaporizers calibrated specifically for Enflurane Preanesthetic medication should be selected according to patient Induction may be achieved using Enflurane alone with oxygen or in combination with oxygen-nitrous oxide mixtures Inspired concentrations of 2.0 to 4.5% Enflurane produce surgical anesthesia in 7 to 10 minute Surgical levels of anesthesia maintained with 0.5 to 3.0% Enflurane Enflurane 0.25 to 1.0% provides analgesia for vaginal delivery AVAILABLE In 125 and 250 mL amber-colored bottles Contains no additives Expire date is five years Take Precautions to give Enflurane in Patients of Acute Kidney & Liver injury, Epileptic patients, Neurotoxic patient SIDE EFFECTS Malignant hyperthermia Movements of various muscle groups and/or Seizures Cardiac depression and arrhythmias Hypotension, Respiratory depression Hypoxia, Hypocapnia, Arrhythmias Shivering, Nausea and Vomiting Moderate to severe liver injury Perioperative hyperkalemia Cardio – Hepato – Neuro - Renal toxicity CONTRAINDICATIONS Seizure disorders Known sensitivity or other halogenated anesthetics Suspected genetic susceptibility to Malignant Hyperthermia Preeclampsia and Eclampsia Accidental occupational exposure to Enflurane causes eye irritation, central nervous system depression, analgesia, anesthesia, convulsions, and respiratory depression INDICATIONS : Induction and maintenance of general anesthesia (mainly as maintenance) Used to provide analgesia for vaginal delivery, Low concentrations used to supplement other GA agents during delivery by Cesarean section, High dose relaxes the uterus in pregnant women giving more blood loss The Blood-Pas partition coefficient is slightly lower than that of Halothane, So induction of anaesthesia and awakening is relatively slower than Halothane 250 ml capacity with 7.35 kg. weight History
ESMOLOL  Emergency friend of Anaesthesiologist  Cardioselective beta1 receptor blocker  Shortest acting beta blocker Class II Antiarrhythmic Safely given in broncho- spastic and vascular dis.  Gives central analgesia Opioid sparing adjuvant in OFA and TIVA No significant intrinsic sympathomimetic or membrane stabilizing activity at therapeutic dosages Dosages forms and Strengths Infusion bags 2 g/100 ml, 2.5 g/250 ml, 5 g/500 ml Injectable solution 10 mg/ml and 20 mg/ml Compatible with all common solvents Incompatible with NaHCO3 Never infuse in small veins or by butterfly  Never stop abruptly due to withdrawal effect Pharmacokinetic Bioavailability 90 % Protein binding 55-60% Metabolism Erythrocytic (in blood by hydrolysis of its methyl ester) Elimination half-life 9 minutes Distribution half life 2 minutes Duration of action 10-30 minutes Excretion Kidney (73-78%) Vd 3.4 liter/kg Storage at room temperature Safely given in pediatric Patients ( > 2 Years) Careful in Pregnancy Uses To terminate supra- ventricular tachycardia In episodic atrial fibrillation or flutter Arrhythmia during perioperative period To reduce HR and BP during and after cardiac surgery In early treatment of myocardial infarction In blunting the haemodynemic response to laryngoscopy and intubation To reduce intra and post operative hypotension Brady is less Intraoperative Tachycardia and Hypertension Immediate control 1 mg/kg over 30 sec then 0.15-0.3 mg/kg/min infusion Postoperative control 0.5 mg/kg iv for 1 min then 0.1 mg/kg/min infusion If not control then repeat bolus doses For supraventricular tachycardia 0.5 mg/kg over 1 min then 0.05 mg/kg/min infusion Hypo Is more PONV is less Best adjuvant in Ane Contraindication Sinus bradycardia, Sick sinus syndrome AV heart block, Heart failure Pulmonary hypertension Hypersensitivity Side Effects 10 % or more Hypotension asymptomatic ( 25%) Hypotension symptomatic (12%) Bradycardia (15 %)  1 – 10 % Injection site pain (8%) Agitation (7%) Dizziness(3%)  1 % or less Chest pain Anxiety/Depression Dry Mouth/Dyspepsia Redness of the face and neck Headache Mechanism of Action Esmolol decreases the force and rate of heart contractions by blocking beta-adrenergic receptors of the sympathetic nervous system, which are found in the heart and other organs of the body  Esmolol prevents the action of two naturally occurring substances: epinephrine and norepinephrine
Etomidate decrease in level of circulating cortisol IV 100 to 200 mg hydrocortisone is given before etomidate Pharmacokinetics Onset of Action : within 30 to 60 seconds Peak Effect : In 1 minute Duration : 3 to 5 minute and terminated by redistribution Protein Binding : 76 % Metabolism : Hepatic & Plasma Esterase Half-Life Distribution : 3 Minutes ( Anesthesia ) Half-Life Redistribution : 30 Minutes ( Sedation ) Half-Life Elimination : 3 hours ( Drowsiness ) Etomidate + Ketamine Mixture Most suitable mixture for short procedure Best combination for RSI in trauma and sepsis patients Good alternative in pediatric patients compare to ketofol and ketodex Both counter act each other adverse effects like myoclonus, nystagmus, injection site pain Dose is 0.1mg/kg etomidate + 1 mg/kg ketamine Mechanism of Action • Carboxylated Imidazole agent • Imidazole agent in IV anesthetic drugs • R-1-(1-ethylphenyl)imidazole-5-ethyl ester • Acts directly on the (GABA) receptor complex blocking neuroexcitation producing sedation/hypnosis/ anesthesia without analgesia • Acidic pH - 6.9, pKa – 4.2, • poorly water soluble • soluble in 35 % propylene glycol History - Janssen Pharma in 1964 at Belgium First introduced as Anti-Fungal agent - Introduced as IV Anesthetic agent (due to potent sedative properties ) - In Europe 1972 - In USA 1983 - In India 2013 Doses in different situations • For Sedation : 0.1 mg/kg up to three doses • For G/A 0.3 to 0.4 mg/kg IV over 30-60 seconds • In ICU : As continuous infusion 0.04 to 0.05 mg/kg/hr with continuous monitoring • In Cushing Syndrome or law cortisol level patients 0.2 mg/kg • In Geriatric patients : 0.2 mg/kg • In Pregnancy : 0.2 mg/kg • In Pediatric Patients : 0.1-0.3 mg/kg Available as Milky White and Clear Solution in 2 mg/ml 10 ml Bulb or MCT/LCT preparation Etomidate is most preferred drug in Hemodynamically unstable patients then any other anesthetic agents for induction of anesthesia Indications • As Sedation • As Conscious Sedation • As Hypnotic Agent • Etomidate Interview in Lie Detector Test • As Anesthetic Agent ( preferred in cardiac patients) • In Rapid Sequence Intubation (RSI) • In Cardio version as Premedication • In ICU as infusion in ventilated or nonventilated patient • As eSAM ( Etomidate Speech And Memory Test) Contra-Indications • Proven sepsis with unstable hemodynamic patients • Abnormally Low Blood Pressure even with Rx • Decreased Function of the Adrenal Gland • Hypersensitivity of Etomidate • Pediatric Patients less than 10 years age (but people have started using etomidate up to 2 years age with risk-benefit profile) • In Pregnancy try to avoid as induction agent if other anesthetic agents are available • In Geriatric Patients with caution Adverse effects • Transient Injection site pain up to 80 % patients • Skeletal Muscle movements mainly myoclonic ( peripheral limb movements ) up to 30 % patients • Opsoclonus ( uncontrolled eye movements ) • Adrenal Suppression up to 10 % patients • Hiccups • Apnea up to 90 seconds • Less frequently nausea vomiting laryngospasm, snoring, arrhythmia & increase in PaCO2 CNS – Decrease ICP, Cerebral Blood flow and Cerebral Metabolism But cerebral perfusion pressure maintained CVS -- No or Minimal changes in Heart Rate, Blood Pressure and Cardiac Output No hemodynamic changes in response to pain No effect on Sympathetic tone RS – Minimal changes in Respiratory Rate and Tidal Volume Slight elevation in arterial carbon dioxide tension (PaCO2) Transient apnea up to 90 seconds - No histamine release - Very rare allergic reactions - Hepatic and Renal blood flow decreased Administration of Drug • Never dilute Etomidate with DW in same Syringe • Preferably Large Vein for IV administration • Pre administration of lidocaine if possible (2 ml) • First dose to be completed within one arm-brain circulation (60-90 seconds ) • All muscle relaxants, benzodiazepines, narcotics and ketamine are compatible with etomidate in same syringe except vecuronium and Vit-C Different Effects ETOMIDATE In Pregnancy with Heart Dz. etomidate is drug of choice
- FENTANYL - Bioavailability 92% (transdermal) 89% (intranasal) 65% (buccal) 54% (sublingual) 100% (intramuscular) 100% (intravenous) 55% (inhaled) Protein binding : 80–85% Metabolism : Liver(CYP3A4) Onset of action : IV within 5 minutes Elimination half-life Formula C22H28N2O Intravenous Molar mass : 336.479 g·mol−1 6 mins (T1/2 α) Melting point : 87.5 °C 1 hours (T1/2 β) Crosses BBB & Placenta 16 hours (T1/2 ɣ) Intranasal : 6.5 hrs. Transdermal : 20–27 hrs. Sublingual/buccal (single dose) : 2.6–13.5 hrs. Duration of action IV : 30–60 minutes Excretion : 75% Urine, 10% feces, 10% unchanged Routes of Administration Buccal Epidural/Spinal IM IV Nasal Nebulizer Sublingual Skin patch Oral Used as Recreational drug & also in Veterinary Anesthesia Side Effects Vomiting, Constipation, Sedation, Urinary retention, Confusion, Hallucinations Injuries related to poor coordination Symptoms of Overdose Respiratory depression, Somnolence, Stupor, Coma, Skeletal muscle flaccidity, Cold and clammy skin, Pupillary constriction, Pulmonary edema, Bradycardia, Hypotension, Airway obstruction, Atypical snoring, and Death A potent OPIOID agonist 100 times more stronger than Morphine Fentanyl invented by Paul Janssen in 1960 and approved for medical use in 1968 Most widely used synthetic opioid Hyperalgesia is common with Fentanyl Fentanyl patches for cancer pain is WHO List of Essential Medicines Mechanism of Action Fentanyl binds to opioid receptors, especially the mu opioid receptor, which are coupled to G-proteins. Activation of opioid receptors causes GTP to be exchanged for GDP on the G- proteins which in turn down regulates adenylate cyclase, reducing concentrations of cAMP. Reduced cAMP decreases cAMP dependant influx of calcium ions into the cell. The exchange of GTP for GDP results in hyperpolarization of the cell and inhibition of nerve activity Fentanyl Antagonist -Naloxone- -Nalmefene- -Naltrexone- Doses -Loading dose: IV 25-100 mcg or 1-2 mcg/kg -Maintenance dose: IV 25-50 mcg or 0.35-0.5 mcg/kg every 30 to 60 minutes -Continuous infusion: 50-200 mcg/hour (Ane.) -TIVA : 0.5 to 2 mcg/kg -NORA : 0.5 to 1 mcg/kg -Rapid sequence intubation : 1 to 3 mcg/kg -Continuous infusion : 50-100 mcg/hour (ICU) -Epidural : 0.5-1 mcg/kg/hr -Never exceed single doses of 3 mcg/kg   (IM : 1-2 mcg/kg) Uses of Fentanyl 1) As analgesic with other anaesthetic drugs 2) For maintenance in all anesthesia technique (TIVA, NORA, Volatile, Regional) 3) In post operative pain relief 4) Management of chronic pain e.g. cancer 5) In Palliative Care 6) In ICU for mechanically ventilated patient 7) In Breakthrough pain 8) In Combat medicine in Military 9) Suppression of the cough reflex Available Strengths of Fentanyl (schedule II drug) IV injection : 0.05 mg(50 mcg)/ml 2ml, 10ml and 50 ml vials Transdermal Patch 12.5,25,37.5,50,62.5,75,100 mcg/hr Fentanyl Buccal Tablet : 100 mcg Intranasal Spray : 100mcg, 300mcg, 400mcg/100mcL spray Given from Neonates to Geriatric patients Extra Shots -Dose reduction is 50 % in acute renal and hepatic impairment -Do not abruptly discontinue fentanyl in patient -It can be mixed with propofol, ketamine, lidocaine, etomidate and midazolam -It also can be mixed in 5% dextrose, RL and 0.9 % normal saline for continuous infusion -No histamine release, thus preferred narcotic for asthmatic patients Extra Shots -Fentanyl is contraindicated in patients who are on MAO-Inhibitors -Rapid administration cause muscle rigidity, so always give IV injection slowly -Fentaketacaine (Fentanyl + Ketamine + Lidocaine) drip is used for postoperative analgesia -Fentanyl is also used in Neuroleptanalgesia -Recently fentanyl use extend in treatment of epilepsy -Narcotic delirium is common with fentanyl Opioid epidemic with fentanyl is very common Fentanyl is high potential for addiction
FLUMAZENIL History & Important Information  Also known as Flumazepil First characterized in 1981, First marketed in 1987, FDA approval in 1991, Patent rights lost in 2008, So it is now generic formulation  Flumazenil short half-life requires multiple doses Administration of the drug requires careful monitoring by an anesthesiologist due to potential side effects  If the patient fails to awaken after receiving the maximal dose of IV flumazenil (5 mg over 1 hour), other causes of the persistent sedation or respiratory depression should be considered  In undifferentiated coma it’s use is absolutely contraindicated Mechanism of Action Flumazenil is an imidazobenzodiazepine derivative and a potent benzodiazepine receptor antagonist that competitively inhibits the activity at the benzodiazepine recognition site on the GABA/benzodiazepine receptor complex, thereby reversing the effects of benzodiazepine on the central nervous system, so acts both as antagonist and antidote Does not antagonize the central nervous system effects of drugs affecting GABA ergic neurons by means other than the benzodiazepine receptor  Benzodiazepine overdose rarely cause mortality Indications in Anaesthesia For the complete or partial reversal of the sedative effects of benzodiazepines in sedation or general anaesthesia For the management of benzodiazepine overdose Other Indications To treat overdoses of non- benzodiazepine hypnotics, such as Zolpide, Zaleplon and Zopiclone (also known as "Z-drugs") To treat Idiopathic Hypersomnia  In Hepatic Encephalopathy Pharmacokinetics Formula : C15H14FN3O3 Molar Mass : 303.293 g/mol Routes of Administration : IV Metabolism : Hepatic, Complete Excretion : Urine 90–95%, Feces 5–10% Onset of Action : Within 1 or 2 minutes Peak Effects : 7 to 10 minutes Elimination Half Life : Initial (7-15 min), Brain (20-30 min), Terminal (40-80 min) (Average : 53 minutes) Protein Bound : 40 to 50 % Available : 5 or 10 ml multidose vial ( 100 μg/ml) Compatible : With 5% Dextrose in water, Lactated Ringer‘s and Normal Saline solutions Storage : At 25°C & solution is stable for 24 hrs. Dose Reduction : In Geriatric, Renal & Hepatic Pt. Dosage Forms & Strengths Reversal of Sedation and General Anesthesia - 0.2 mg IV over 15 sec - IF after 45 sec no response, administer 0.2 mg again over 1 min; may repeat at 1 min intervals; not to exceed 4 doses (1 mg) -IF resedation occurs, may repeat doses at 20-min intervals; not to exceed 1 mg/dose or 3 mg/hr Benzodiazepine Overdose - 0.2 mg IV over 15-30 sec - IF no response after 30 sec, administer 0.3 mg over 30 sec 1 min later; IF no response, repeat dose of 0.5 mg IV over 30 sec at 1-min intervals to max cumulative dose of 3 mg/hr -Rarely patient may require titration up to total dose 5 mg Adverse Effects  > 10% Nausea and vomiting (11%)  1-10% Dizziness (10%), Abnormal/blurred vision (3-9%), Agitation (3-9%) Dyspnea (3-9%). Hyperventilation (3-9%), Pain at injection site (3-9%) Xerostomia (3-9%), Diaphoresis (1-3%), Emotional disturbance (1-3%) Fatigue (1-3%), Headache (1-3%), Paresthesia (1-3%), Tremor (1-3%) Weakness (1-3%) 1% Delirium, Abnormal hearing, Thick tongue, Generalized seizure Precautions for IV Administration  Slowly over 15 to 30 seconds  To minimize pain, administer through a freely running IV infusion line into a large vein Avoid extravasation Relative Contraindication to Use Head Injury/Seizures patients/ Patient under 1 year of age Should not be used until the effects of neuromuscular blockade have been fully reversed.  In Psychiatric Patients /Status Epileptics/Myoclonus/Hypertonia  Use In Drug- and Alcohol-Dependent Patients
 FUROSEMIDE/FRUSEMIDE (LASIX)  Loop Diuretic Use - 1964 Bioavailability : 43 - 69 % ; Protein Binding : 91 - 99 % Metabolism : Liver & Kidney, Glucuronidation Crosses placenta, enters breast milk Elimination Half Life : upto 100 min Excretion : Kidney 66 % & Bile Duct 33 % Formula : C12H11ClN2O5S; Molar Mass : 330.7 g·mol−1 Serious Side Effects Electrolyte Imbalance Low Blood Pressure Hearing Loss Excessive Urination  Feeling Thirsty Common Side Effects Light headed on stand Ringing in Ears Sensitivity to Light Hypokalemia Dizziness & Dry Mouth Mechanism of Action  Rapid acting, highly efficacious diuretic Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule. Increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium. Effectiveness persists in impaired renal function Special Action (Diuresis) The action on the distal tubules is independent of any inhibitory effect on carbonic anhydrase or aldosterone; it also blocks negative, as well as positive, free water clearance. Bioavailability with end-stage renal disease 43 – 46% Elimination half-life is prolonged in CCF & ARF General Indications Edema due to heart or lung failure, hepatic impairment, or renal disease & in ARF or CRF Hypertension Therapeutic Effects Diuresis & subsequent mobilization of excess fluid e.g. edema, pleural effusions) Decreased BP Diuretic Effect Relative Contraindication Diabetes Hyperuricemia Low Magnesium Low calcium Low Chloride Low Sodium Low Potassium Known C/O BPH Hearing Loss patients Anuria Continuing loop diuretics Perioperatively is relatively safe Study confirms that Furosemide before surgery does not lead to intraoperative Hypo Furosemide infusion (during intra- and early postoperative period) has a renal protective effect during major surgeries Dosage ( Oral ) Edema 20–80 mg/day as a single dose initially, may repeat in 6–8 hr Hypertension 40 mg twice daily initially Hypercalcemia 120 mg/day in 1–3 doses Dosage ( IV/IM ) 20–40 mg, may repeat in 1–2 hr and ↑ by 20 mg every 1–2 hr until response is obtained, maintenance dose may be given every 6–12 hr; Continuous infusion– Bolus 0.1 mg/kg followed by 0.1 mg/kg/hr, double every 2 hr to a maximum of 0.4 mg/kg/hr. Dosage in Paediatrics Oral 2 mg/kg as a single dose; may be ↑ by 1–2 mg/kg every 6–8 hr (maximum dose = 6 mg/kg). IV/IM 1–2 mg/kg/dose every 6– 12 hr; Continuous infusion– 0.05 mg/kg/hr Neonates : 1-2 mg/kg Available as IV/IM 10 mg/ml 2 ml or 4 ml Oral 20 mg or 40 mg Oral solution for paediatric 10 mg/ml More than 10 % patient are getting Hyperuricemia and Hypokalemia after giving Furosemide IV/IM Avoid use of Furosemide in Pregnancy and Lactation, Only Use in Life- Threatening emergencies when no safer drug available Pharmacokinetics
GLYCOPYRROLATE Full name is Glycopyrronium bromide  Muscarinic anticholinergic group  Glycopyrronium was first used in 1961 to treat peptic ulcers  Since 1975, intravenous glycopyrronium has been used before surgery to reduce salivary, tracheobronchial, and pharyngeal secretions  In June 2018, glycopyrronium was approved by the FDA to treat excessive underarm sweating, becoming the first drug developed specifically to reduce excessive sweating  In inhalable form it is used to treat chronic obstructive pulmonary disease (COPD)  Also used to treat Sialorrhea & Ménière's disease Side effects  Dry mouth (Xerostomia)  Urinary retention  Headaches/ drowsiness  Vomiting/diarrhea,  Constipation Blurry vision/ Mydriasis  Urticaria / Pruritus Since glycopyrronium reduces the body's sweating ability, it can even cause hyperthermia & heat stroke in hot environments  Mechanism of action : Glycopyrronium competitively blocks muscarinic receptors thus inhibiting cholinergic transmission  Oral Administration : 1 hour before meals or 2 hours after meals, because high fat food reduces orally bioavailability  Glycopyrrolate is associated with a more stable cardiovascular system, fewer arrhythmias and superior control of oropharyngeal secretions at the time of reversal Pharmacokinetics  Glycopyrronium bromide affects the gastrointestinal tracts, liver and kidney but has a very limited effect on the brain and the central nervous system  Formula : C19H28NO3 +  Molar mass : 318.437 g·mol−1  Elimination half-life : 0.6–1.2 hours  Excretion : 85% renal  Routes of Administration : Mouth, Intravenous, Inhalation, Topical Glycopyrronium has a relatively slow diffusion rate, and in a standard comparison to atropine, is more resistant to penetration through the blood-brain barrier and placenta  Used topically and orally to treat hyperhidrosis, in particular, gustatory hyperhidrosis Dosages of Glycopyrrolate Tablets : 1mg/1.5mg/2mg Oral solution : 1mg/5mL Injectable solution : 0.2mg/mL Preoperative : 4mcg/kg (IV/IM) 30-60 min before surgery Intraoperative: 0.1 mg IV/IM; may repeat every 2-3 minutes Control of Secretions : 0.004-0.01 mg/kg IM/IV every 6 hours Dosages of Glycopyrrolate Pediatric Children 1 month to 2 years (4 mcg/kg (IM); may increase to 8 mcg/kg Children > 2 years : 4 mcg/kg (IM) Neuromuscular Blockade Reversal 0.2 mg (IV) per 1 mg of neostigmine or 5 mg of pyridostigmine in same syringe  Most preferred drug in reversal by anaesthesiologist than atropine Relative Contraindications Angle-closure glaucoma  Obstructive Uropathy GI obstruction / Paralytic ileus  Intestinal atony of elderly or debilitated patient  Unstable cardiovascular status  In Acute Hemorrhage  Severe Ulcerative Colitis  Toxic Megacolon, Myasthenia Gravis, Reflux Esophagitis  Hiatus Hernia / Mitral Stenosis Use caution in patients with hepatic impairment and renal impairment  Glycopyrrolate is a synthetic quaternary amine that crosses the blood-brain barrier poorly and is less likely to cause altered mental status or tachycardia than atropine  It has approximately twice the potency of atropine and more potent than atropine in its antisialogogue effect For overdose antidotes are Neostigmine and Pyridostigmine
HALOTHANE Discovered by C. W. Suckling in 1951 and commercial use started in 1956 Continued till 1990s as volatile induction No longer commercially available in the United States and replaced by Sevoflurane A potent trigger for Malignant Hyperthermia Since 2000 Isoflurane & then Sevoflurane replaced halothane as volatile induction in Anesthesia practice Mechanism of Action The exact mechanism of the action of general anesthetics has not been delineated. Halothane activates GABAA and glycine receptors It also acts as an NMDA receptor antagonist, inhibits nACh and voltage- gated sodium channels, and activates 5- HT3 and twin-pore K+ channels It does not affect the AMPA or kainate receptors  Potent anesthetic with a MAC of 0.75%  Oil:Gas partition coefficient : 224  Blood:Gas partition coefficient : 2.3  Boiling point : 50.2 °C(at 101.325 kPa)  Molar mass 197.38 g·mol−1  Formula : C2HBrClF3,  Packaged in dark-colored bottles Unstable in light  Stored at room temperature  Nonflammable and Nonirritant  Colorless and Pleasant Smelling  Metabolism : Hepatic(CYP2E1)  Excretion : Kidney & Respiratory  Routes of Administration : Inhalation General inhalation anesthetic used for induction and maintenance of general anesthesia King of inhalation agent from 1956 to 1990 The only inhalational anesthetic containing bromine, which makes it radiopaque Contains 0.01% Thymol as a stabilizing agent Available as 30/100/250 ml bottle Actions of Halothane on body Progressively Depresses Respiration, Tachypnea with Reduced tidal volume & alveolar ventilation , causes Bronchodilatation No increase in salivary or bronchial secretions Pharyngeal and laryngeal reflexes are rapidly obtunded., Causes Hypotension, Bradycardia and sometime Cardiac Arrhythmias Causes dilation of the vessels of the skin and skeletal muscles. Potent Uterine relaxant and Produces moderate muscular relaxation Gives Moderate induction and very slow Recovery  Not good Analgesic Common Side Effects Nausea, Vomiting, Chills, and Headache Serious side effects  Hives  Difficulty in breathing,  Swelling of face, lips, tongue, or throat  Abnormal heart rhythm  Decreased lung function  Decreased oxygen in the tissues or blood  Hepatitis  Kidney damage  Malignant hyperthermia  Problems with circulation  Yellowing of the skin or eyes (jaundice) Contraindication : In obstetric anaesthesia except Uterine Relaxation is required Halothane Hepatitis Repeated exposure to halothane in adults causes severe liver injury (1 in 10000) called as halothane hepatitis, immuno allergic in origin and this hepatitis syndrome had a mortality rate of 30% to 70%, but it is lower in pediatric patients Halothane and Heart It sensitizes the heart to catecholamines, causing cardiac arrhythmia, particular ventricular which is occasionally fatal It is potent trigger for MH But safe in Por- phyria Dose and MAC Induction dose varies from patient to patient but is usually within the range of 0.5% to 3%. & maintenance dose varies from 0.5% to 1.5% Halothane vaporizer is red colour Age : MAC % Infants : 1.08, 3 yrs : 0.91, 10 yrs. : 0.87, 15 yrs. : 0.92, 24 yrs. : 0.84, 42 yrs. : 0.76, 81 yrs. : 0.64 Reduce with N2O & Oxygen Ane. Precautions to Use Used only in halothane vaporizers In patients with markedly raised intracranial pressure Liver Diseases (any type) Malignant Hyperthermia suspected patient In renal failure With use of epinephrine or norepinephrine Overdose No antidote available, drug administration stopped & assisted/controlled ventilation with pure oxygen initiated Fever is very common after 2-3 days of Haloth. Ane
HYDROCORTISONE Uses of Hydrocortisone Mainly used as an Immunosuppressive Drug in Anaphylaxis and Angioedema Perioperatively in patients on long-term steroid treatment to prevent an adrenal crisis Adrenocortical Insufficiency Adrenogenital Syndrome High blood Calcium / Ulcerative Colitis Anemia, Thrombocytopenia & Lymphoma Rheumatoid Arthritis / Thyroiditis Dermatitis ( Eczema, Psoriasis & Itching )  Asthma & COPD Injected into inflamed joints e.g. Gout Congenital Adrenal Hyperplasia Topical Creams and Ointments Ranging from 0.1 % to 2.5 % ( 1 mg to 25 mg in 1 gm ) Oral ( Always after Food) 20 mg to 240 mg orally per day (In 3 to 4 Dose) IM Dose 100 to 500 mg Intravenous Dose 100 mg IV (Over 1-2 minutes ), followed by IV infusion of 200 mg over 24 hours OR 50 mg IV every 6 hours ( Maximum 500 mg in a day) 2 to 3 mg/kg ( Usual dose ) Pediatric Dose : 0.56 to 8 mg/kg/day oral or IV Patented in 1936 Medical use in 1941 Hydrocortisone is the name for the hormone Cortisol when supplied as a medication Hydrocortisone is a Corticosteroid, acting specifically as both a Glucocorticoid and as a Mineralocorticoid It is an agonist of the glucocorticoid and mineralocorticoid receptors Compared to hydrocortisone, Prednisolone is about 4 time potent and Dexamethasone about 40 times as potent in terms of Anti- inflammatory effect Mood changes / Headache Increased risk of infection Edema / Weight Gain Swollen Ankle Long-term use common side effects Osteoporosis, Upset of Stomach, Physical Weakness, Easy Bruising, Candidiasis, Sodium Retention, Potassium Loss & Convulsions Pharmacokinetics Formula : C21H30O5 Molar mass : 362.466 g·mol−1 Bioavailability : 100 % in IV, IM & Oral Elimination half-life : 1.5 hrs. (IV or IM) Routes of Administration : Oral, IV, IM, Topical & Rectal Store : Room Temperature Metabolism : Liver & Excretion : Renal In September 2020, WHO approved Hydrocortisone is effective in reducing mortality rate of critically ill COVID-19 patient Compatible with DW, Normal Saline and Dextrose Solutions Available as Injectable ampoule or bulb 100/200/250/500/1000 mg Hydrocortisone Sodium Succinate as powder & Phosphate as solution Dose No Dose adjustment in Renal, Hepatic or Geriatric patients Hydrocortisone in Anaesthesia  Preoperative : 100 mg IV and dose adjustment according to surgery, infection, trauma with 200 mg IV infusion over 24 hours  In Etomidate GA Induction (Specially Infusion) Always give higher dose in obese patients and drugs that induce CYP3A4 For patients undergoing any minor to major anesthesia Hydrocortisone 100 mg is as good as Dexamethasone 6–8 mg, & should be administered at time of induction of anesthesia  In Laryngospasm, Bronchospasm, Laryngeal Edema & Pulmonary Edema, 100 to 200 mg dose is indicated followed by infusion Mechanism of Action Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes Works by calming down our body's immune response to reduce pain, itching and swelling (Inflammation)
ISOFLURANE Physical properties Molecular weight : 84.5 g/mol  Boiling point (at 1 atm): 48.5 °C  Density (at 25 °C) : 1.496 g/mL  MAC : 1.15 vol %  Water solubility 13.5 mM (at 25 °C)  Blood:gas partition coefficient: 1.4  Oil:gas partition coefficient: 98  Routes of administration : Inhalation  Formula : C3H2ClF5O Invented in 1979, Non-flammable It vaporizes readily but is a liquid at room temperature Isoflurane is halogenated ether Mechanism of action 1) Isoflurane binds GABA glutamate and glycine receptors, but has different effects on each receptor. 2) It acts as a positive allosteric modulator of the GABAA receptor in electrophysiology studies of neurons and recombinant receptors. 3) It potentiates glycine receptor activity, which decreases motor function. 4) It also inhibits receptor activity in the NMDA glutamate receptor subtypes. 5) It inhibits conduction in activated potassium channels. 6) It also affects intracellular molecules. 7) It activates calcium ATPase by increasing membrane fluidity The average lifetime of Isoflurane in the atmosphere is 3.2 years Dosage Forms & Strengths Inhalation solution  Available as 30 ml, 100 mL & 250 mL Anesthesia Induction & Maintenance  Use calibrated vaporizer  Induction: 1.5-3% can produce surgical anesthesia in 7-10 minutes  Maintenance: 1-2.5% with nitrous oxide  Additional 0.5-1% may be needed if given with oxygen alone Adverse Effects 1-10%  Nausea, Vomiting, Shivering, Hypotension <1%  Arrhythmias  Malignant hyperthermia (rare)  Elevations in white blood count  May decrease creatinine and increase BUN  Ileus, if severe (fatal)  Hepatic dysfunction (postoperative period) (rare)  Respiratory depression (rare)  Elevated carboxyhemoglobin levels  Hyperkalemia Contraindications  Hypersensivity  Malignant Hyperthermia Careful in use  Coronary heart disease Chronic Renal and Liver Diseases  Hyperkalemia  Ventricular Dysfunction  Prolong use in GA  Latent neuromuscular disease  Obstetrical Anesthesia Pharmacokinetics  Onset: Rapid (7-10 min)  Duration: Short  Metabolism: Liver (0.2%)  Clear, Colorless, Stable liquid  Containing no additives or chemical stabilizers  Pungent, musty, ethereal odor Isoflurane stored in indirect sunlight in clear, colorless glass for five years Used for induction and maintenance of general anesthesia Premedication with anticholinergic drug is must before Isoflurane Drinking Isoflurane cause drowsiness dizziness Headache, nausea & vomiting Isoflurane has more incidence of airway hyper reactivity compared to Sevoflurane Isoflurane gives analgesia and relaxes muscles during anesthesia Not advisable as mask induction in pediatric patient Isoflurane cause decrease in intellectual function for 2 or 3 days after GA Extra Shots  Isoflurane causes cerebral vasodilation leading to increase in CBF and ICP and markedly reduces the CMRO2  95 % of inhaled Isoflurane eliminated by exhalation  It is unsafe to consume alcohol after Isoflurane anesthesia Isoflurane bottles and vaporizers are in purple color  Coughing and laryngospasm are more common with Isoflurane Iso. Rs. 10/ml Sevo. Rs.30/ml Now use of Isoflurane is declining in anesthesia practice But widely used in Veterinary anesthesia
Main Features  Rapid-acting general anesthetic  Produce profound analgesia  Normal pharyngeal-laryngeal reflexes  Slightly enhanced skeletal muscle tone  Cardiovascular and respiratory stimulation  Transient and minimal respiratory depression. Contraindications > Angina, Stroke and very high blood pressure Psychiatric disorders, Uncontrolled Epilepsy In raised intraocular pressure & Eye injury Acute Porphyria  Age less than 3 months  Tracheal and Laryngeal Surgery - Bioavailability – 93 -100 % - Protein binding - 53.5% -Distribution half-life 1.95 min - Half Life - 186 minutes - Elimination - urine 91 % , 3 % in feces and 6 % unchanged - Clearance rate - 95 L/h/70kg Mechanism of action  Interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels  Does not interact with GABA receptors  Selectively depress the thalamoneocortical system before significantly obtunding the more ancient cerebral centers and pathways (reticular-activating and limbic systems) - Water and Lipid Soluble - Oral ketamine broken down by bile acids - Undergoes hepatic Metabolism - It can be mixed with any TIVA drugs - Compatible with all IV fluids Other uses > Emergency Dept. > Asthma > Seizures >Pain management > Depression > Vet Anesthesia Invented in 1962 ---- NMDA receptor antagonist with Dissociative Anesthesia ---- Approved in 1970 Most Popular Anesthetic Drug of Anesthesiologists Ketamine • I V Effect Starts -2 min Last – 25 min • IM Effect Starts – 5 min Last – 4-6 hrs • Oral – 30 min C13H16ClNO More Analgesia & Less Anesthesia  M/A Main Actions  Increase BP  Increase Salivation  Bronchodilation  Hallucination  Agitation  Catatonia  Prevent opioid induced Hyperalgesia  Best agent in Post anesthetic shivering Post Ketamine Double vision & Nystagmus are very common Dose Schedules 0.1-0.3 mg/kg – Analgesia 0.2-05 mg/kg – Recreational 0.4-0.8 mg/kg -- Partially dissociated 1-2 mg/kg – Fully Dissociated 1-2 mg/kg /IV – Procedural Sedation 4-8 mg/kg/IM – Procedural Sedation 0.1-0.2 mg/kg/hr – Postop Pain Relief (Infusion maximum 3 days only) IV Bioavailability -100 % IM Bioavailability – 93 % Dose Schedules 10 mg/kg /Oral – As Sedative Premedication(Bioavailability – 20 %) 0.7-0.9 mg/kg – Intrathecal (S/A) 0.2 mg/ml – Epidural for Postop pain Intra nasal 0.5-1 mg/kg (Bio-50%) Intrarectal 0.5-1 mg/kg (Bio-30%) Sublingually 0.5 -1 mg/kg (Bio-30%) Inhalation 0.5-1 mg/kg Topical Gel – 1% ketamine with other drugs Ketamine is the only drug which Is given by all routes In body U N I Q U E D R U G S C H E D U L E D R U G •Increase HR, high BP(20 %) •Increased intracranial pressure • Transient reddening of the skin • Reduced appetite, nausea • Increased salivation, vomiting •Pain, eruptions or rashes at the injection site • Tonic-Clonic movements • Double vision , involuntary eye movements, • Increased bronchial secretions • Anaphylaxis and Dependence • Cognitive Deficits • Emergence reaction Side Effect Pharmacokinetics •Rapid onset and short duration of action • Initially distributed to highly perfused brain tissues • Crosses Blood Brain barrier • Undergoes extensive redistribution • Major metabolite are norketamine and dehydronorketamine Combination • Ket+Propofol(Ketofol) • Ketamine+Dex(Dexket) • Ketamine+Fentanyl • Ketamine+Midazolam • Ketamine+Diazepam • Ket+Prof+Dex (KPD) WHO List of Essential Medicine
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INFOGRAPHICS in ANAESTHESI by Dr. Tushar Chokshi.pptx

  • 1. Respected Sir/Madam/Colleague Greeting from Dr. Tushar Chokshi, Vadodara I have completed 20 months journey of my Infographics in Anesthesiology. I am extremely thankful and honored for allowing, accepting, tolerating and inspiring continuous endeavoring of my infographics. In September 2020 I started my first Infographics in Anesthesia on MgSO4. And till date I have completed almost 130 + infographics in our subjects. (लोग साथ आते गए और कारवााँ बनता गया) I was inspired to make infographics in anesthesia by one little 5 year old child. He was having online education during corona period from his school every day through infographics on different subjects. He was accepting theme of story or any subject very nicely and not only that he was remembering very well (As our vision is most valuable sense then hearing and remembers 70 to 90 %). And from this I had taken ideas of making infographics in anesthesia. Now every time for each medication, procedure or other things, it becomes easy for me and others to refer in single page as one slider infographics. For each making of infographics, I usually take 5 to 10 hours to make it readable with graphics, shapes, colors, & informations by visually appealing. Before each infographics I read, write, correct, and understand detailed information for particular infographics from journals, textbooks and online articles. Not only that, in doubt I always consult my colleagues who are experts and masters in their subjects by phone calls, messages or emails. Still some informations may be written wrongly with spellings or dose or without my deep knowledge. But my intentions are very clear to respect all my colleagues. I will be humbled if you can guide and advice me personally. I will still advice you to refer textbooks or other articles for particular infographics. In my life whatever I learned, taught and experienced from my teachers, seniors and colleagues, I want to give it back to society. I am lifetime student of my subject and I will exchange my knowledge throughout the life with you. Lastly, I fall in love with my infographics, & not just the end product of my work. I believe to Die Empty and Unleash my best work everyday. Show must go on. Your Infographics Colleague, Dr. Tushar Chokshi InfographicS Aspire to Inspire before we Expire of
  • 3. Dr. Tushar M. Chokshi Area of Expertise Other Highlights Affiliations Current Position Consultant Private Practicing Anesthesiologist in Vadodara (Gujarat, INDIA)  Sterling Hospital  Urocare Hospital  Dhwani ENT Hospital  Arpan Surgical Hospital 30 Years of Experience TIVA, OFA and NORA  Uro Anaesthesia  Lapro Anaesthesia ENT Anesthesia Paediatric Anesthesia  Founder of TIVA and OFA Face book Groups in INDIA  National and State Level Speaker Started Smartphone and Tele- Anesthesia practice in INDIA Started Infographics in Anaesthesia  9825062245 chokshitushar@hotmail.com MD (Anaesthesiology) https://sites.google.com/site/tusharchokshisite National Origami Teacher Visual Storyteller & Vlogger Happy Go To Lucky Fellow Always believe in exchange of Knowledge
  • 4. List of Drugs Adrenaline Atracurium Bupivacaine Calcium Cis-Atracurium Clonidine Dentrolene Dexamethasone Desflurane Dexmedetomidine Ephedrine Diclofenac Sodium Esmolol Etomidate Fentanyl Flumazenil Furosemide Glycopyrrolate Hydrocortisone Isoflurane Ketamine Levo Bupivacaine Lidocaine MgSO4 Midazolam Morphine Naloxone Nitrous Oxide Neostigmine Ondansetron Paracetamol Propofol Remifentanil Remimazolam Rocuronium Bromide Ropivacaine Sevoflurane Sodium Thiopental Suxamethonium Sugammadex Tranexamic Acid Xenon Paediatric Drug Dose PAC PDPH Risk of Anaesthesia PONV MH LAST List of Volatile Agents SGD Antidotes in Anaesthesia Adjuvants in L/A TIVA Kingdom Ane Drugs Label Colour Infertility Tests Infertility Tests Thyroid Function Tests Blood Sugar Tests Urine Tests Cardiac Blood Tests Lipid Profile Tests Liver Function Tests Complete Blood Count Kidney Function Tests Furosemide Transdermal patch Anaphylaxis NG tubes IV fluids 37 38 39 40 41 42 43 44 45 46 47 49 48 50 51 52 53 54 19 20 21 22 23 24 25 26 27 28 29 31 30 32 33 34 35 36 55 56 57 58 59 60 61 62 63 64 65 67 66 68 69 70 71 73 1 2 3 4 5 6 7 8 9 10 11 13 12 14 15 16 17 18 Infographics Infographics Infographics Infographics Mephentermine
  • 5. Letter Pulmonary Embolism Different Positioning OFA Mnemonics Dobutamine Bain circuit Vecuronium Norepinephrine Chloroprocaine Mepivacaine Tetracaine Prilocaine Methoxyflurane Procaine Halothane Enflurane Cardiac Blood Flow Lung Physiology Haemodynamics Effects of Anaesthesia Pulmonary Circulation Antidotes in Anaesthesia TOF & PTC Segmental Spinal Anesthesia Geriatric Anaesthesia 1 Geriatric Anaesthesia 3 Geriatric Anaesthesia 2 ERCP Anae. Mx TEE Awareness EEG Intravascular volume monitoring Circulatory system Pulse Oximetry Central venous monitoring Ventilation Cricothyrotomy Neuropathic Pain Cancer Pain PA form for CVS Common Pain Syndromes Non opioid Rx chronic pain Musculoskeletal pain i-gel Opioid Mx of chronic pain Interventional pain therapy Pain management by RA Physiology in trauma Initial Mx in trauma Types of Trauma Airway Mx in trauma Trauma Bay Haemodynamics in trauma Intraoperative Mx of trauma CPNBs Ciprofol Medication Errors 109 110 111 112 113 114 115 116 117 118 119 121 120 122 123 124 125 126 92 93 94 95 96 97 98 98 99 100 101 103 102 104 105 106 107 108 127 128 129 130 131 132 133 134 135 74 75 76 77 78 79 80 81 82 83 84 86 85 87 88 89 90 91 Infographics Infographics Infographics Infographics Anticholinesterases Drugs Nondepolarizing NMBDs Depolarizing NMBDs Temperature Monitoring Site Magnesium Actions
  • 6. 1962-2009 1957-1961 Dexamethasone 1886-1990 Magnesium Sulphate 1956 Paracetamol 1973-1988 Diclofenac Sodium 1961-1966 Clonidine 1980-1987 Esmolol 1920-1928 Ephedrine 1971-1985 Mephentermine 1860 Cocaine 1905 Procaine 193--1941 Tetracaine 1943-1949 Lidocaine 1950 Chloroprocaine 1960 Mepivacine 1957 Bupivacine 1980 Ropivacaine 1980 Levobupivacaine 1900 Tubocurarine Chloride 1906-1951 Suxamethonium 1947 Gallamine Triethiodide 1964 Pancuronium 1974-1983 Atracurium 1984 Vecuronium 1984 Mivacurium 1989-1995 Cisatracurium 1994 Rocuronium 1830 Chloroform 1846 Ether 1920 Trichloroethylene 1956 Halothane 1963-1966 Enflurane 1979 Isoflurane 1970-1987 Desflurane 1971-1990 Savoflurane 1804 Morphine 1937-1943 Pethidine 1959-1968 Fentanil 1974 Sufentanil 1996 Remifentanil 1974 Carfentanyl 2020 Oliceridine 1930-1934 Sodium Thiopental 1962-1964-1970 Ketamine 1964-1972 Etomidate 1977-1989 Propofol 1999 Dexmedetomidine 1901 Atropine 1975 Glycopyrrolate 1964-1979 1981 Metoclopramide Ranitidine 1980-1991 Ondansetron 1959-1963 Diazepam 1963-1977 Lorazepam 1975-1990 Midazolam 1772 Nitrous Oxide 1774 Oxygen 1881 Cyclopropaine 1898 Xenon 1996 Atipamazole 1961-1971 1982 Naloxone Doxapram 1987 Flumezenil 1931 Neostigmine 2007-2015 Sugammdex 1967 Dentrolene 2014-2020 Remimazolam Anesthesia Adjuvant IV Anesthetic Local Anesthetic Gas Opioid/Narcotics Premedication Inhaltion Anesthetic Benzodiazepine Muscle Relaxant Anti MH Agent Benzodiazepine Reversal Agent IV Reversal Agent Opioid Reversal Agent Relaxant Reversal Agent Opioid with Benzodiazepine I N F O G R A P H I C S A N E S T H E S I A D R U G S O F Total 69 Drugs In Use 50 Drugs Tranexamic acid 1895-1904 Adrenaline 1959-1964 Lasix 1964 Metoclopramide
  • 7. ADRENALINE Physiological Response of Adrenaline Heart : Increases heart rate, Contractility and Conduction across AV node Lungs : Increases Respiratory Rate & Bronchodilation Liver : Stimulates Glycogenolysis Muscle : Stimulates Glycogenolysis and Glycolysis Brain : Vasoconstriction and Vasodilation Systemic : Triggers Lipolysis Muscle Contraction Mechanism of Action Acts on both alpha and beta-adrenergic receptors. The rise in BP is 3-fold: a direct myocardial stimulation that increases the strength of ventricular contraction (positive inotropic action), an increased HR (positive chronotropic action), and peripheral vasoconstriction Side effects of Adrenaline Pharmacokinetics and Pharmacodynamics Formula : C9H13NO3 Molar mass : 183.207 g·mol−1 Receptors : Adrenergic receptors Metabolism : Adrenergic synapse (MAO and COMT) Protein binding : 15–20% Metabolites : Metanephrine Onset of action : Within 30 seconds Elimination half life : 2 minutes Duration of action : 5 minutes Excretion : Urine Store : Between :20° to 25°C Solution : Clear, Colorless & Sterile Solution For Extravasation And Tissue Necrosis With IV Infusion : Antidote is infiltrate the area with 10mL-15mL of saline solution containing from 5mg-10mg of phentolamine, an adrenergic blocking agent Dosage and Strength Available as 1 mg/mL (1:1000) 1mL amp. and 30 ml vial. And 1 mL amp. contains 1 mg adrenaline, 9.0 mg NaCl, 1.0 mg sodium metabisulfite, hydrochloric acid to adjust pH, and water for injection In Anaphylaxis : 0.3-0.5 mg(0.3-0.5 mL) of undiluted adrenalin administered IM or S/C in the anterolateral aspect of the thigh, maximum of 0.5 mg(0.5 mL) per injection, repeated every 5 to 10 minutes as necessary In Hypotension Associated With Septic Shock Dilute 1 mL (1 mg) of adrenaline from its vial to 1,000 mL of a 5 % dextrose or 5 % DNS solution to produce a 1 mcg per mL dilution and give infusions of adrenaline into a large vein and avoid the veins of the leg Routes IV IM Endotracheal Intracardiac Nasal Eye drop S/C Medical use Anaphylaxis Cardiac arrest To prevent superficial bleeding Asthma & Inhaled adrenaline for Croup Anxiety, Apprehensiveness Restlessness Tremor Weakness Dizziness Sweating Palpitations Pallor Nausea Vomiting Headache Respiratory difficulties Cardiovascular Angina, Arrhythmias, Hypertension, Pallor, Palpitations, Tachycardia Tachyarrhythmia, Vasoconstriction Ventricular Ectopy and Stress Cardiomyopathy Neurological Disorientation, Impaired memory, Panic, Psychomotor Agitation, Sleepiness, Tingling Contraindications for Adrenaline None Invented in 1895 & In use 1904 Also known as Epinephrine (Hormone) Produced both by the adrenal glands and by a small number of neurons in the medulla oblongata Gives Fight-or-Flight response Overdose Produce extremely elevated blood pressure and Cerebrovascular hemorrhage Treatment is supportive with alpha-adrenergic blocking and beta-adrenergic blocking drugs Adrenaline level in blood is normally less than 10 ng/L During Exercise increase by 10-fold & in Stress 50-fold In Pheochromocytoma levels of 1000–10,000 ng/L IV Adrenaline produce 10,000 to 100,000 ng/L BP Effect The onset of BP increase after IV dose in < 5 minutes & the time to offset BP occurs within 15 minutes Precautions Renal Impairment Cardiac Arrhythmia & Ischemia Patients on MAOI and Anti- depressant Never inject into digits, hands, or feet with LA because vasoconstr -iction causes loss of blood flow to the tissue & necrosis
  • 8. ATRACURIUM History Invented by George H. Dewar Atracurium was licensed by Strathclyde University to the Wellcome Foundation UK First named this compound "33A74” Non-steroidal skeletal muscle relaxant Bisquaternary ammonium benzylis- oquinoline compound Mechanism of Action  Antagonize the neurotransmitter action of acetylcholine by binding competitively with cholinergic receptor sites on the motor end-plate  Binding of the postsynaptic nicotinic receptor by atracurium prevents depolarization of the motor end plate & subsequent skeletal muscle contraction Extra Shots Overdosage increase the risk of histamine release and cardiovascular effects It is advisable to reverse atracurium with an anticholinesterase reversing agent such as neostigmine, edrophonium, or pyridostigmine in conjunction with atropine or glycopyrrolate Avoid in rapid sequence intubation Side Effects Histamine release Cutaneous flushing (Face & Arm) Hypotension & reflex tachycardia  Bronchospasm & Secretions Seizures Erythema and Itching  Rare Allergic reactions (anaphylactic or anaphylactoid) Inadequate block, prolonged block Indications An adjunct to general anesthesia to facilitate endotracheal intubation To provide skeletal muscle relaxation during surgery or mechanical ventilation To facilitate the placement of a Supraglotic Airway Off label use : in ARDS and Shivering due to hypothermia following arrest Precautions to Use  Allergy and asthmatic patients  Myasthenia Gravis/Burns Injury  Eaton-Lambert syndrome  Electrolyte disorders  Malignant hyperthermia  Long term use in ICU ( > 10 days ) Pregnancy is not contraindication but careful it is teratogenic Pharmacokinetics Bioavailability 100 % (IV)  Protein binding 82%  Elimination half-life 17–21 minutes Metabolism Hofmann elimination and ester hydrolysis by nonspecific esteras (45 %)  Pregnancy Category C  Formula C65H82N2O18S2 Molar mass 1243.49g·mol−1 Dose of Atracurium  Only IV administration & never give IM injection because it causes tissue irritation  IV Bolus dose is 0.4 to 0.5 mg/kg & intubation can be expected in 2 to 2.5 minutes in most patients  First dose lasts 20 to 35 minutes  Maintenance dose is 0.08 to 0.10 mg/kg (last upto 20 min) Less than 2 yrs child dose is 0.3 to 0.4 mg/kg For continuous infusion 5 to 9 mcg/kg/minute (for GA & ICU) Infusion can be diluted in 5% Dextrose, 0.9% Sodium Chloride and 5% Dextrose with 0.9% Sodium Chloride (DNS)  Contains 10 mg/ml atracurium besylate  Available as 2.5 ml amp, 5 and 10 ml multidose bulbs Storage under 2° to 8° C Upon removal from refrigeration to room temperature use in 14 days Invented 1974 & In Use 1983 Most commonly used muscle relaxant Non Depolarizing Muscle Relaxant with short duration of action Atracurium should not be administered until patient has recovered from succinylcholine induced neuromuscular block It has an acid pH, should not be mixed with alkaline solutions in the same syringe 10 mL multidose vials only contain benzyl alcohol, so as far as avoid this vial in neonates and infants Laudanosine is major biologically active metabolite of atracurium without neuromuscular blocking activity In Renal and Hepatic failure or Critically ill patients No dose adjustment Reduce dose in long volatile anaesthesia Onset of action takes Approximately 2 minutes Renal Excretion is less than 5 % Slower injection speed, from 30 to 60 seconds, reduce histamine release, and the associated adverse effects Atracurium Hoffman elimination is a temperature and pH-dependent process and is slowed by acidosis and hypothermia No cumulative effect with repeat doses or continuous infusion It does not provide pain control, sedation, or amnesic effects
  • 9.  BUPIVACAINE  Pharmacokinetic Bioavailability - n/a  Protein binding - 95%  Metabolism - Liver  Onset of action - Within 15 min  Elimination half-life - 3.1 hours (adults) 8.1 hours (neonates)  Duration of action - 2 to 8 hr  Excretion - Kidney 4–10%  Routes of administration Parenteral, Topical and Implant  Formula - C18H28N2O  Molar mass - 288.435 g·mol−1 Melting point - 107 to 108 °C  Pregnancy category - AU: A US: C  Peak effect - 35 to 40 minutes 1957 An implantable formulation of bupivacaine was approved for medical use in USA in August 2020 for open hernia surgery  Sometimes used in combination with epinephrine to prevent systemic absorption and extend the duration of action  The 0.75% (most concentrated) formulation is used in retro- bulbar block Indications  Local Infiltration  Peripheral nerve block  Sympathetic nerve block  Epidural & Spinal Anesthesia Caudal blocks Safely given in pregnancy and lactation Contraindications  Known hypersensitivity  Obstetrical paracervical blocks  Intravenous regional anaesthesia (Bier block)  0.75% formulation in epidural anesthesia during labor  Intra articular infusions Side effects Sleepiness Muscle twitching Ringing in the ears Changes in vision Low blood pressure Irregular heart rate Low Sexual Desire Compared to other local anesthetics, bupivacaine is markedly Cardiotoxic Bupivacaine can cause chondrolysis after continuous infusion into a joint space Treatment of overdose is intravenous lipid emulsion CNS Toxicity Circumoral numbness Facial tingling Vertigo/ Tinnitus Restlessness Anxiety/Dizziness Seizures/Coma CVS Toxicity Hypotension Arrhythmia Bradycardia Heart block Cardiac arrest GI Toxicity Nausea/ Vomiting High Spinal Anesthesia with Bupivacaine causes Paresthesia, Paralysis, Apnea, Hypoventilation, Fecal Incontinence, and Urinary Incontinence Mechanism of Action (Amino-Amide anesthetic)  Bupivacaine binds to the intracellular portion of voltage- gated sodium channels and blocks sodium influx into nerve cells, which prevents depolarization. Without depolarization, no initiation or conduction of a pain signal can occur The amino-amide anesthetics are more stable and less likely to cause allergic reactions Levobupivacaine is the (S)-(–)-enantiomer of bupivacaine, with longer duration of action, producing less vasodilatation Bupivacaine is available as a generic medication and is not very expensive Bupivacaine Dosage  Epidural Block  0.75% concentration : 75 to 150 mg (10 to 20 mL) for complete motor block  0.5% concentration 50 to 100 mg (10 to 20 mL) moderate to complete motor block  0.25% concentration: 25 to 50 mg (10 to 20 mL) partial to moderate motor block  Epidural Anesthesia:  0.5% and 0.75% solutions Epidural Anesthesia in Obstetrics:  only 0.5% and 0.25% Available as spinal heavy amp., preservative free and 0.25 % & 0.5 % solution bulb Bupivacaine Dosage  Caudal Block: 0.25% to 0.5% concentration (15 to 30 mL)  Peripheral Nerve Block : 0.25% to 0.5% concentration  Retrobulbar Block 0.75% concentration (2 to 4 mL)  Sympathetic Block: 0.25% concentration (20 to 50 mL)  Local Infiltration: 0.25% concentration max dose of 175 mg  Spinal anesthesia : 0.5 % heavy solution with dextrose (2 to 4 ml) preservative free 0.75% bupivacaine in 8.25% dextrose ( 1 to 1.6 ml) Usual dose of Bupivacaine is 2 mg/kg with or without adrenaline Rapid injection of a large volume of bupivacaine solution should be avoided and fractional or incremental doses should be used Local Anesthetic
  • 10. Pharmacokinetics Atomic No. : 20 Formula : C12H22CaO14 Molar Mass : 430.373 g·mol−1 Routes : Oral / IV/ Topical Bioavailability : 100 % Metabolism : Direct Elimination : Renal Ca Ca Ca Ca IV CALCIUM M/A : Calcium plays a central role in a large number of physiological actions that are essential for life which include cardiac automaticity; excitation–contraction coupling in myocardial, smooth and skeletal muscle; blood coagulation; neuronal conduction; synaptic transmission; hormone secretion and mitotic division A normal 70-kg adult contains about 1.2 kg calcium, of which more than 99% is located in the bone In the plasma, the normal total calcium concentration is about 2.25–2.55 Mol/L−1 (9.0–10.2mg/dL−1) 50% of this is free ionized calcium, 10% is calcium combined with various anions, 40% is bound to proteins, mainly albumin Calcium inj. is given IV only, S/C or IM injections are not allowed because causes severe necrosis or sloughing Avoid rapid injection, it may cause Cardiac Arrest Dosing Regimen A bolus dose of 100 mg elemental calcium diluted in 100 mL isotonic saline and given over 5-10 min. It raise the total serum calcium by 0.5 mg/dL, but level of calcium begins to fall after 30 min. Therefore, the bolus dose of calcium should be followed by a continuous infusion at a dose rate of 1 to 2 mg/kg/h (elemental calcium) for at least 6 hours IV calcium available as 100 mg/ml Ca Chloride 10 ml 10 % (272 mg) Ca Gluconate 10 ml 10% (93 mg) Gluconate is less irritant to veins Precautions for giving Calcium Injection Calcium infusions can promote vasoconstriction and ischemia in any of the vital organs & and seen high in patients with low cardiac output Aggressive calcium replacement can promote intracellular calcium overload, which can produce lethal cell injury, particularly in patients with circulatory shock, so avoid it Always give calcium solution in large or central veins with small intracath, due to hyperosmolarity of calcium solutions Hypocalcemia(< 6) & Hypercalcemia(> 14) Sudden decreases in serum calcium may be seen in the early postoperative period after thyroidectomy or parathyroidectomy and may cause laryngospasm (Give Calcium accordingly) Hypercalcemia results from increased calcium reabsorption from the gastrointestinal tract, in renal insufficiency and increased bone resorption of calcium ( Treat with Isotonic saline Infusion, Furosemide, Calcitonin, Glucocorticoid, Biphosphonate & Dialysis ) Symptomatic Hypocalcemia must be treated before giving any type of anesthesia  Antidote of Calcium is Magnesium First isolated by Humphry Davy in 1808 It is classified as a calcium salt Most widely used is Calcium Gluconate Calcium Gluconate introduced in 1920 No dose adjustment is required in geriatric hepatic or renal impairment patients Always monitor ECG & serum calcium level every 4 hours in IV calcium therapy patients Calcium is prime drug in Cardiac arrest and cardiotoxicity due to hyper kalemia or hyper magnesemia  Common Side Effects - Warmth/Nausea/Vomiting/Paresthesias - Tingling /Heavy feeling/Bradycardia - Chalky taste in your mouth - Upset stomach/Gas/Constipation Serious Side Effects - Little or No Urination - Irregular Heart Beats - Light headedness - Feeling tired/Muscle weakness - Swelling/Weight gain Indications - Hypocalcemia/Tetany - Hydrofluoric acid burns -Hyperkalemia/Hyper Magnesemia - β-blocker toxicity - Calcium-channel blocker (CCB) toxicity - Allergic conditions/ Spider Bites - Pruritus due to drugs Contraindications Digitalized patients, VF & Hypercalcemia Usual Dosage Adults: 500 mg - 2 grams (5-20 mL) Children: 200-500 mg (2-5 mL) Infants: no more than 200 mg (not more than 2 mL) Careful of extravasation in IV Calcium and Antidote is Hyaluronidase
  • 11. CARBON DIOXIDE Chemical Formula : CO2 Molar mass 44.009 g·mol−1 Colorless gas  Low concentrations: No odour  High concentrations Sharp & Acidic odour Density : 53 % higher than dry air Frozen solid form of CO2 known as dry ice Dissolves in water to form carbonic acid CO2 is necessary for the survival of life on earth like oxygen In Body Produced in the tissues and removed from the lungs by ventilation carried in the blood as dissolved gas, e.g. bicarbonate, and small amount bound to hemoglobin as carbamino hemoglobin Dissociation curve for carbon dioxide is essentially linear Increased Carbon Dioxide Production Fever Malignant hyperthermia Systemic absorption during laparoscopy procedures Thyroid storm Tourniquet release Administration of sodium bicarbonate Increased Dead space Decreased Minute Ventilation CO2 Narcosis (Paco2 > 80 mm of Hg) is a condition that develops when excessive CO2 is present in the bloodstream, leading to a depressed level of consciousness & largely results from lung disease, hypoventilation, or environmental exposure Respiratory Acidosis is a condition that occurs when the lungs can't remove enough of the CO2 produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic, due to failure of ventilation CO2 is the most important end-product of tissue metabolism Exists in three forms: (1) as free carbon dioxide, winch is dissolved in the water of the blood, (2) as bicarbonate of the plasma, and (3) as carbamino compounds in combination with haemoglobin CO2 tension of the body cell is greater than that in the capillary blood, thus CO2 moves into the blood The partial pressure of CO2 in mixed venous blood, PvCO2 (44-46 mm Hg) is greater than that in the alveoli of the lungs, Paco2 (38-40 mm Hg) CO2 used in anaesthesia since the late 1920s, principally to stimulate breathing after a period of hyperventilation Hypercarbia or Hypercapnia (High Paco2) Hypercapnia defined as the Paco2 being greater than 45 mm Hg. If the Paco2 is greater than 45 mm Hg, and the PaO2 is less than 60 mm Hg, a patient is said to be in hypercapnic respiratory failure Also known as Hypercarbia or CO2 Retention & confirmed by ABG analysis Exhausted carbon dioxide absorbents and malfunctioning expiratory valves on the anesthesia delivery circuit are possible causes hypercapnia Hypercapnia causes delayed awakening in the post anesthesia care unit Hypocarbia, or hypocapnia, occurs when levels of CO2 in the blood become abnormally low (Paco2 < 35 mm Hg). Hypocarbia is confirmed by arterial blood gas analysis. Hypocarbia, especially if only transient, is usually well tolerated by patients. Deliberate hyperventilation, leading to hypocarbia, is often used to decrease intracranial pressure in neurosurgical patients Seen in hypovolemia, hypotension, hypothermia & hypothyroidism Also seen in deep anaesthesia, iatrogenic hyperventilation, pulmonary embolism , CNS pathology and decreased metabolism Hypocarbia causes decreased myocardial oxygen supply, increased myocardial oxygen demand, decreased cerebral blood flow & respiratory alkalosis Treated by assessing oxygenation status, decreasing minute ventilation and restoring circulation to improve cardiac output Initial treatment of hypercapnia is oxygen therapy with the goal of increasing the inspired oxygen volume In anaesthesia common causes are over sedation, hypoventilation, inadequate gas flow and increased dead space In operation theatre it is detected by capnography and now a days capnography monitoring is must for CO2 like oxygen monitoring Both hypercapnia & hypocapnia are dangerous to the life Capnography It is a monitoring of the concentration or partial pressure of carbon dioxide in the respiratory gases as end-tidal carbon dioxide (EtCO2) Normal values for patients regardless of age, sex, race, or size range between 35-45 mm Hg In high EtCO2 value think respiratory failure In low EtCO2 value think poor systemic perfusion with shock
  • 12. CHLOROPROCAINE An ester local anesthetic Chloroprocaine has one of the lowest partition coefficients (low lipophilicity) and has low potency relative to other local anesthetics Formula : C13H19ClN2O2 Molar mass : 270.76 g·mol−1 Metabolized by pseudo cholinesterase the liver Excretion through Kidney Chloroprocaine is used commonly for epidural anaesthesia Uses of Chloroprocaine in Anaesthesia Used in Regional Anaesthesia including Spinal, Caudal and Epidural anaesthesia Used in Local Anaesthesia including Brachial plexus block, Cervical nerve block and Occipital Maxillary/Mandibular block for Dental anaesthesia and Infraorbital block for Ophthalmic anaesthesia Also in Ulnar, Paravertebral, Intercostal, Sciatic, Lumbar Sympathetic, Stellate ganglion & Paracervical blocks Mechanism of Action Causes reversible nerve conduction blockade by decreasing nerve membrane permeability to sodium Binds to a specific region of the alpha subunit on the cytoplasmic region to inhibit voltage-gated sodium channels This binding activity increases the threshold for excitation in the nerve and slows nerve impulse propagation Chloroprocaine is vasodilator Dose and Strength Supplied as a 1%, 2%, and 3% solution For Spinal is 1% and preservative-free 50 mg Maximum recommended dose for infiltration, or peripheral nerve block is 11 mg/kg when administered alone, not to exceed 800 mg When given with adrenaline, dose is 14 mg/kg not exceeding 100 mg 2% / 3% is used in Lumbar epidural for LACS The effect last for 60-70 minutes Available as Chloroprocaine HCL injection Adverse Effects Most common adverse effect is pain related to the procedural injection due to high allergic reactions Sometimes in regional use Hypotension, Bradycardia, Nausea, and Headache Accidental intrathecal injection during epidural placement, with large dose may produce ‘ Total Spinal ‘ leading to fixed and dilated pupil Rarely Cauda Equina Syndrome in S/A Cautions & Contraindications In patients with a known allergy to para- aminobenzoic acid Caution to use Chloroprocaine to provide epidural, spinal, caudal, peripheral nerve and infiltrative anesthesia in lactating women Use with caution in patients with end-stage liver disease Avoid in pediatric patients younger than four years old (Dosing is not established) Doses more than 11 mg/kg may cause LAST Available as 1% and 2%, in multidose vials with methylparaben as preservative 2% and 3%, in single dose vials without preservative and EDTA ( Note for S/A) Always Keep from freezing, with Protect from light and Store at 20° to 25°C Monitoring during Chloroprocaine Anae. According to the ASA, oxygenation, ventilation, and circulation should be continuously monitored The Pulse Oximeter is the most commonly used with Oxygen supply During regional block with minimal or no sedation practiced The temperature should be assessed whenever possible BP & HR every 5 minutes interval taken Never use in Intravenous Regional anesthesia due to the risk of thrombophlebitis Chloroprocaine does not itself appear to be neurotoxic at clinical concentrations but formulations that contain EDTA can cause burning back pain when used in epidurals A preservative-free formulation of Chloroprocaine may be a drug of choice in short-acting spinal anesthesia and might even replace Lidocaine Chloroprocaine shelf life is 24 months Never autoclave Chloroprocaine injections Different Doses in Different Blocks Brachial Plexus 30 to 40 mL (600 to 800 mg) as a 2% solution Caudal epidural 15 to 25 mL of 2% or 3% methylparaben-free (MPF) solution, repeated every 40-60 min Infraorbital 0.5 to 1 mL (10 to 20 mg) as a 2% solution Paracervical 3 mL per each of 4 sites as a 1% solution, total dose up to 120 mg  Pudendal 10 mL on each side as a 2% solution, total dose 400 mg Digital 3 to 4 ml 1 %
  • 13. Also called as CYCLOPOFOL  Invented in CHINA in Feb. 2021 & patented in Dec. 2021 Sedative, Hypnotic & Anaesthetic Trade Name is Sishuning (HSK3486) In china price is Rs. 3800/- per 20 ml amp. Ciprofol is Class 1 IV Anaesthetic & Propofol analogue with improved pharmacokinetic properties  Phase I, IIa, IIb Trails are completed  recently Phase III Trial started on 2nd August 2022  just now only available in CHINA  Ciprofol developed by Haisco Pharma. Group Dose Schedule Initial dose is 0.4 mg/kg for 30 seconds In geriatric 0.3 mg/kg Supplemental dose is 0.1mg/kg/ time as IV bolus for 10 seconds & minimum 2 minute with each dose Range from 0.3 to 0.6 mg/kg Maintenance infusion dose is 0.1 to 0.3 mg/kg/h Almost one forth dose is required than Propofol Available as 50 mg in 20 ml borosilicate glass ampoule solution & 200 mg in 20 ml under development phase Ciprofol is a Propofol analogue with improved pharmacokinetic properties & pharmacodynamic characteristics New intravenous anesthetic agent characteristics of a rapid rate of onset and recovery in pre- clinical experiments It is γ-aminobutyric acid (GABA) receptor agonist & novel 2,6- disubstituted phenol derivative Circulating metabolites are nonhypnotic and nontoxic Non inferior to Propofol in all trials with characteristics Indications Induction & Maintenance of anesthesia in all elective surgeries As sedation in NORA procedures As a sedation in mechanical ventilation in ICU Adjuvant in TIVA Not studied in < 18 years old pt. In all phase trials indicated in gastroscopy, hysteroscopy colonoscopy, ERCP, bronchoscopy, cystoscopy & Gynec procedures Works as status epilepticus and as an anti-emetic like Propofol Better than Propofol in all transplant Induction Superior to Propofol Five times More potent than Propofol Almost no pain on IV injection Less hemodynamic instability ( less hypotension & depression) Only dose dependent respiratory depression, apnea and hypoxia Myoclonus and infusion syndrome are extremely rare Better in prolonged infusion Less serious AEs (adverse events) than Propofol in all trials Ciprofol induction is associated with more stable BIS changes than Propofol Ciprofol binds to the γ-aminobutyric acid type A (GABAA) receptor more tightly than Propofol and exhibits reduced lipophilicity and more suitability Pharmacokinetics  Ciprofol Injection content are soya bean oil for injection, medium chain triglyceride, refined egg yolk lecithine, sodium oleate, glycerin, sodium hydroxide & water for injection Ciprofol is white or off-white homogenous milky liquid  Validity period 24 is months Not studied in pregnant and lactating women Storage at 25 degree c in airtight & do not freeze Metabolism: oxidation to form mono oxyglucuronic acid In Short Compared to Propofol, it has the advantages of "two fast and five few" rapid onset, rapid recovery; less dosage, wider safety window; less respiratory depression, risk reduction by more than 60%; less cardiovascular adverse events , stable circulation; less pain on injection, the incidence is only 1/10 of Propofol; less lipid infusion Highly effective, easy to control, safe and comfortable It takes effect quickly and wakes up quickly Ketamine+Ciprofol combo is viable Extra Shots Effect last for 3 to 5 minutes Awakening time is about 3 min Overdose causes cardiovascular & respiratory depression Approved by the China & Australian State Food and Drug Administration for studies Excretion through renal 80 % and fecal 20 % Not known that it is excreted in human milk Till now 12 major trials are done on Ciprofol in China & Australia  May be game changer or another experimental IV anesthetic drug CIPROFOL (IV Anaesthetic)
  • 14. Non-Depolarising Neuromuscular Blocking Drug One of the ten isomers of the parent molecule, Atracurium M/A Acts by competitive antagonism Binds with nicotinic acetyl chonline receptors (nAChRs) on the motor end-plate of neuromuscular junction to produce neuromuscular blockade Drug of choice in Cardiac compromise patients ARDS patients Hepatic failure patients Renal failure patients Ideal in Neuro Surgical patients Chemo and Obese patient Systemic Actions No change in Heart Rate, Contractility, SVR and Blood Pressure Lung protective through its anti inflammatory properties Metabolism is through Hofmann reaction Reduces ICP, cerebral perfusion and it is neuroprotective Does not produce any autonomic effect Ideal Neuromuscular Blocking Agent - Best intubating condition - - Non-depolarizing mechanism of action - - Rapid onset enabling quick intubation - - Rapid complete and predictable recovery - - Short elimination half life - - No cumulative effect - - No histamine release - - High potency - - Has pharmacologically inactive metabolites - - Reversible by cholinesterase inhibitors - - Elimination pathways less dependent on organ function - - Lack clinically important Cardiovascular side effects - Dose is 0.15 to 0.20 mg/kg (50-60 minutes) Maintenance dose is 0.02 to 0.03 mg/kg (20-25 minutes) OT and ICU Infusion 1-3 mcg/kg/minute Paediatric dose is 0.10-0.15 mg/kg Below 1 mth not recommended Indications It is intermediate onset and duration action of drug Mainly indicated for inpatients and outpatients adjunct to general anaesthesia To facilitate tracheal intubation To provide skeletal muscle relaxation during surgery For mechanical ventilation in ICU Pregnancy, Labour, Delivery and Nursing mother (drug of choice) Contraindications Known hypersensitivity Patients with myasthenia gravis or myasthenia syndrome History of prior anaphylactic reactions to neuromuscular blocking agents Adverse Effects Uncommon with the use of Cisatracurium Less than 1% - Brady, Hypo, Spasm, Myopathy, Prolonged Effect - Kept refrigerated at 2 to 8 degrees Celsius - Protected from light - Rate of loss of potency is as high as 5% per month at 25 degrees Celsius - Once removed from refrigeration to room temperature storage, it should be used within 21 days - Undergoes 80 % Hofmann elimination - Renal Excretion of is only 16 % - Elimination half-life is 20–29 minutes - Hypothermia and Hyperthermia, increase and decrease the duration of action - Sedative, Volatile agents, Local anaesthetics and Anti-epileptic agents will prolong the effect Avoid in Rapid Sequence intubation As ICU relaxant more than one week Burns injury Cerebral palsy Hemiplegia (on the affected side) Muscular denervation (peripheral nerve injury) Severe chronic infection Tetanus Botulism Cis gives uniform recovery from anesthesia  
  • 15. CLONIDINE Invented in 1961, Medical use in 1966, Epidural use in 1984 First approved to treat HT and in 2010 approved for ADHD in children  It is given by Oral/IV/IM/Epidural/Spinal/Skin Patch  Imidazole compound & partial α2 receptors agonist  It causes bradycardia, by increasing signaling through the vagus nerve   Mechanism of Action   Clonidine treats high blood pressure by stimulating α2 receptors in the brain stem, which decreases peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2 receptors in the vasomotor center in the brainstem  This binding has a sympatholytic effect, suppresses release of norepinephrine ATP, renin, and neuropeptide Y which if released would increase vascular resistance When given IV, it temporarily increase BP by stimulating α1 receptors in smooth muscles in blood vessels like Dex Clonidine crosses the blood-brain barrier   Indications  To treat high BP Menopausal Flushing Drug withdrawal (Alcohol/Opioids/Smoking) Spasticity and certain pain conditions ADHD and Diarrhoea   Use in Anaesthesia practice   Administration of clonidine in combination with a local anaesthetic to prolongs analgesia and motor blockade in Epidural and Spinal When used IV or IM it gives sedation, hypnosis, analgesia, opioid need reduction and anti-sympathetic response, to surgical trauma response But its use is limited by its principal effects of hypotension and bradycardia Oral Premedication : 2 to 4 mcg/kg IV : 1-2 mcg/kg as bolus, slowly  IV infusion : 0.2 mcg/kg/minute Spinal : 0.5-1 mcg/kg with L/A Epidural : 1-2 mcg/kg with L/A Continuous Epidural Infusion : 30 mcg/hr Patch : 0.1 mg or 0.2 mg per day   Pharmacokinetic   Formula : C9H9Cl2N3 Molar mass : 230.09 g·mol−1 Bioavailability : 70–80% (oral),60–70% (transdermal) Protein binding : 20–40% Metabolism : Liver to inactive metabolites (50 %) Elimination : Renal another 50 % Elimination half-life : 6-23 hrs, in Renal Failure 41 hrs Elimination half-life in S/A : 1.5 hrs Store : 20° to 25°C Shelf Life : 60 months  Highly Lipid Soluble   Contraindications   Allergic reactions to clonidine Severe Bradyarrhythmia Above the C4 dermatome Bleeding diathesis Sick Sinus Syndrome AV block of second or third degree No specific antidote for clonidine overdosage (Naloxone and Atropine are used sometimes) Epidural clonidine is not recommended for obstetrical, post-partum, or peri-operative pain management Spinal clonidine as an adjuvant to Cesarean Section anesthesia is well established ( No neonatal side effect) Available Ampule : 150 mcg/ml Bulb : 100 mcg/ml 10 ml vial & 500 mcg/ml 10 ml vial Tablets : 0.1/0.2/0.3 mg Patch : 0.1 mg or 0.2 mg > 10% Dizziness Fatigue Orthostatic hypotension Somnolence (dose-dependent) Dry mouth Headache (dose-dependent) Bradycardia Skin reactions (if given transdermally) Hypotension In 1-10% Pain below the ear (salivary gland) Sedation (dose-dependent) Erectile dysfunction Weight gain/loss Nausea/vomiting Abnormal LFTs Constipation Skin Rash Malaise Anxiety Overdose Cause Hypotension Bradycardia Respiratory- depression Hypothermia Drowsiness Clonidine in the treatment of chronic neoplastic pain, used epidurally in the dose of 10-50 μg/h Clonidine has also got benefit in the treatment of Postoperative Shivering Clonidine is now slowly replaced by Dexmedetomidine ( Dex is full α2 receptors agonist) If clonidine is used then Volatile Anaesthetics requirement are reduced by 50 % Clonidine is a versatile drug that is used in the critical care setting for sedation and to treat opioid induce Hyperalgesia
  • 16. D A N T R O L E N E Oral Dantrolene was first described in the scientific literature in 1967, IV in 1979 Dantrolene is Hydantoin derivatives, a new class of muscle relaxant Dantrolene was widely used in the management of spasticity as Oral Rx Efficacy in treating Malignant Hyperthermia was discovered by South African anesthesiologist Gaisford Harrison and reported in a landmark 1975 article published in the British Journal of Anaesthesia Side Effects Drowsiness Dizziness Weakness General malaise Fatigue Diarrhea Indications Primary drug used for the treatment and prevention of malignant hyperthermia, during General Anaesthesia Neuroleptic Malignant Syndrome, Muscle Spasticity /Spasms Poisoning by 2,4-dinitrophenol Contraindications Oral Dantrolene Pre-existing liver disease Compromised lung function Severe cardiovascular impairment Hypersensitivity to Dantrolene Pediatric patients under five years of age People who need good muscular balance Nausea IV Dantrolene People with a known hypersensitivity to Dantrolene Mechanism of Action Dantrolene is a postsynaptic muscle relaxant that lessens excitation-contraction coupling in muscle cells Work directly on the Ryanodine receptor to prevent the release of calcium Dantrolene does not act at the neuromuscular junction and has no effect on the passive or active electrical properties of the surface and tubular membranes of skeletal muscle fibers IV Dantrolene have normal EMG results Pharmacokinetics Formula C14H10N4O5 Molar mass 314.257 g·mol−1 Bioavailability 70% Metabolism Liver Excretion Biliary, Kidney Routes Oral and IV  Protein binding Mostly to albumin Half Life 4 to 8 hrs  Trade names Dantrium, Ryanodex Dose of Dantrolene The recommended dose of Dantrolene is 1-2.5 mg/kg, repeated as necessary, every 4-6 hrs for 24 – 48 hrs (Max 10 mg) It is recommended that each hospital keep a minimum stock of 36 Dantrolene vials (720 mg), sufficient for maximum four doses in a 70-kg person (20 mg/Vial) Risk of Death in MH : 5% if treated, 95% if not treated with Dentrolene Extra Shots The poor water solubility of Dantrolene leads to certain difficulties in its use. A more water-soluble analog of Dantrolene, Azumolene, is under development for similar indications. Azumolene has a bromine residue instead of the nitro group found in Dantrolene, and is 30 times more water-soluble Dantrolene Malignant Hyperthermia Association of the United States guidelines state Dantrolene must be available within 10 min of the decision to treat MH wherever volatile anesthetics or succinylcholine are administered Dantrolene for IV administration is supplied in 70 mL vials, containing 20 mg Dantrolene sodium and 3 g Mannitol. It must be diluted with 60 mL of sterile, preservative-free, distilled water Phlebitis is a most common side effect of Dantrolene IV administration, noted in approximately 10% of patients, so intermittent bolus is preferred than continuous IV administration Invasive hemodynamic monitoring is necessary while giving IV Dantrolene Serum potassium must be closely monitored during Dantrolene therapy Oral Dantrolene is effective in reducing muscle pain after IV suxamethonium in GA Repeated dosing of Dantrolene should be guided by clinical and laboratory signs Dantrolene 20 mg vial cost is Rs. 6000/- (36 vials cost are Rs. 216000/-) Antidote of MH $ 82/Vial
  • 17. DEXAMETHASONE  Universal Friend  Anti Nauseatic & Anti Emetic Early Discharge from Anaesthesia Anti Inflammatory Weak anti pyretic effect Anti Edema drug Anti Shivering Systemic Analgesic Effect Increase Quality of Recovery  Synthetic Glucocorticoids with minimal mineralocorticoid activity  Most potent anti inflammatory than Hydrocortisone and prednisolone  Biological half-life is 3 hours  Metabolism in liver with inactive metabolites  Renal excretion upto 65% in urine within 24 hours Readily available  Price is very cheap   Most ideal perioperative agent   Superior to ondensetron to reduce PONV   Reduce opioid Consumption   Decrease Analgesic effect upto 24 hours   Always to be given prior to surgery   Best TIVA and OFA adjuvant   Great psychological effect  Prevents any allergic reaction  Invented in 1957 & In use 1961  Dose Schedule  PONV – 0.1 mg/kg (IV)   Anti Inflammatory – 0.2 mg/kg(IV)   Analgesic – 0.1 mg/kg(IV)   Epidural -- 8 to 10 mg   Blocks – 0.1 mg/kg   S/A - 8 mg  Mechanism of Actions  Depletion of γ-aminobutyric acid (GABA) stores and reduction of blood brain barrier to emetogenic toxins,  Inhibition of central prostaglandins and serotonin  Membrane stabilizing effect on nerves and on spinal cord Dexona IN DM  4 mg is ideal dose 8 -10 mg dose Increase around 25 mg/dl glucose postop upto 24 hrs Dexona in Sepsis Does not increase any risk of wound infection with or without DM in any surgical procedure Acute Side Effect Flushing Perineal Itching Dexona Is the only adjuvant in anesthesia given irrespective of age, sex, disease or ASA status Safe in Onco Anesthesia Avoid in Psychiatric patients Be careful in Immuno compromised patients Improves Cognitive function In Elderly 8 8 8 8 8 8 8 8
  • 18. DESFLURANE Pharmacokinetics  Formula C3H2F6O, Store at 15°-30°C  Metabolism : Not metabolized  Elimination half-life : Elimination dependent on minute ventilation  Routes of administration : Inhalation  Molar mass : 168.038 g·mol−1  Boiling point : 23.5 °C or 74.3 °F (at 1 atm)  Brain: Gas coefficient : 0.54  Density :1.465 g/cm³(at 20 °C)  Molecular Weight : 168  Vapor pressure : 88.5 kPa672 mmHg(at 20 °C) & 107 kPa804 mmHg(at 24 °C)  Blood:Gas partition coefficient : 0.42  Oil:Gas partition coefficient : 19  MAC : 6 vol %  Non-flammable Specific Gravity : 1.465  Shelf Life : 3 years  Desflurane Vaporizer color is Blue Most rapid onset and offset of the volatile anesthetic used for general anesthesia due to its low solubility in blood Though it vaporizes very readily, it is colorless liquid at room temperature  Drawbacks of desflurane are its low potency, its pungency and its high cost Cause tachycardia and airway irritability when administered at concentrations greater than 10 vol % Due to airway irritability, desflurane is infrequently used to induce anesthesia via inhalation techniques Mechanism of Action  Desflurane is known to act as a positive allosteric modulator of the GABAA and glycine receptors, and as a negative allosteric modulator of the nicotinic acetylcholine receptor, as well as affecting other ligand-gated ion channels Does not corrode stainless steel, brass, aluminum, anodized aluminum, nickel plated brass, copper, or beryllium Provides good relaxation for intubation Ideal volatile agent for day care surgery In adults, a starting concentration of 3% is recommended & increased in 0.5-1.0% increments every 2 to 3 breaths. Inspired concentrations of 4-11% of desflurane usually produce surgical anaesthesia in 2-4 minutes Can be safely use in Obstetric anesthesia, compromised renal and hepatic patients ( it is less hepatotoxic) Because of its low blood-gas partition coefficient, desflurane allow more rapid emergence and recovery than Halothane, Isoflurane, or even Sevoflurane  CVS effect : Dose dependent tachycardia and hypertension Depression in myocardial contractility, Decrease in SVR, Coronary vasodilator  CNS effect : Dose dependent Cerebral vasodilatation Increase CBF, Cerebral blood volume, Intracranial pressure, Cerebral oxygen consumption decreased  Respiratory effect : Potent respiratory depressant, Decrease tidal volume, Increase RR, Extremely irritant to respiratory airways  Invented in 1970 & Medical use in 1987 Indicated as an inhalation agent for induction of anesthesia for inpatient and outpatient surgery in adults Contraindicated as an inhalation agent for the induction and maintenance of anesthesia in non intubated pediatric patients because of a high incidence of moderate to severe upper airway adverse events including coughing, laryngospasm, and secretions Near to ideal inhalational anesthetic agent Vaporizer specifically designed and designated for use with desflurane should be utilized for its administration  Should not be used as the sole agent for anesthetic induction in patients with coronary artery disease or patients where increases in heart rate or blood pressure are undesirable  In case of contact with skin or eye, immediately flush skin and eye with plenty of water at least 15 minutes  The predicted effects of acute over exposure by inhalation of Desflurane include headache, dizziness or (in extreme cases) unconsciousness  If individuals smell vapors, or experience dizziness or headaches, they should be moved to an area with fresh air Age N O2 100% N N2O 60%/40% O2 2 weeks 6 9.2 ± 0.0 - - 10 weeks 5 9.4 ± 0.4 - - 9 months 4 10.0 ± 0.7 5 7.5 ± 0.8 2 years 3 9.1 ± 0.6 - - 3 years - - 5 6.4 ± 0.4 4 years 4 8.6 ± 0.6 - - 7 years 5 8.1 ± 0.6 - - 25 years 4 7.3 ± 0.0 4 4.0 ± 0.3 45 years 4 6.0 ± 0.3 6 2.8 ± 0.6 70 years 6 5.2 ± 0.6 6 1.7 ± 0.4 Effect of Age on Minimum Alveolar Concentration Triggers Malignant Hyperthermia
  • 19. Sedation Anxiolysis DEXMEDETOMIDINE Analgesic Anaesthetic FDA December 1999 Market August 2000  Agonist of α2-adrenergic receptors   Most ideal anesthetic agent available  M/A Induces sedation by decreasing activity of noradrenergic neurons in the locus ceruleus in the brain stem, thereby increasing the activity of inhibitory gamma- aminobutyric acid (GABA) neurons in the ventrolateral preoptic nucleus  Popular in pediatric TIVA with ketamine   Patients sedated, but arousable, alert and respond without uncomfortable like conscious sedation  No effect on Respiratory System  Transient Hypertension followed by Hypotension  No Direct effect on Myocardium IOP Insulin Release  Overdose may cause 1st or 2nd degree AV Block  - Nasal - ~ 84 % bioavailability Indications Pre Anaesthetic sedation (IM/IV) As Induction Agent In maintenance of Anaesthesia As adjuvant in TIVA Intra thecal with Regional Ane. In Post Operative Analgesia As ICU sedation(only for 24 hrs) Relative Contraindication  Infusion over 24 hours  In pre existing severe bradycardia  Brady dysrhythemia  Patient with < 30% EF  Partial or Complete AV block  In patients more than 65 y of age, a higher incidence of bradycardia and hypotension Compatibility - 0.9% sodium chloride in water - 5% dextrose in water - 20% mannitol - Lactated Ringer's solution - 100 mg/ml MgSo4 solution - 0.3% potassium chloride solution - With other Anesthetic agents e.g. Propofol, Ketamine, Etomidate Available as Ampoules or Bulb 50 mcg / 0.5ml 100 mcg / 1 ml 200 mcg / 2ml Sileo Gel for Dogs (Dexmedetomidine Oromucosal Gel) 0.09 mg/ml, 3 ml syringe (BIPHASIC BLOOD PRESSURE RESPONSE) (BRADYCARDIA IS BECAUSE OF DOUBLE EFFECT) (DECREASE OPIOID REQUIREMENT BY 50 %) (BETTER THAN CLONIDINE IN ALL ASPECTS)
  • 20.  DICLOFENAC SODIUM   Introduced By Ciba-Geigy in 1965  Nonsteroidal anti-inflammatory drug  Available worldwide  Generic Medication  Available as both a sodium and a potassium salt  Given by Mouth, Rectally, IM, IV injection and Topical Skin Gel/Spray Pharmacokinetic  Formula C14H11Cl2NO2  Protein binding More than 99%  Metabolism Liver, oxidative, primarily by CYP2C9  Onset of action Within 4 hours Topical,30 min Oral, 15 minutes IM, 5 minutes IV and 30 minutes Rectal  Elimination half-life 1.2–2 hr  Excretion 40% bile duct and 60% urine  Molar mass 296.15 g·mol−1 Mechanism of action  The primary mechanism responsible for its anti- inflammatory, antipyretic, and analgesic action is thought to be inhibition of prostaglandin synthesis by inhibition of the transiently expressed prostaglandin- endoperoxide synthase-2 (PGES-2) also known as cycloxygenase-2 (COX-2).  Blockage of voltage-dependent sodium channels  Blockage of acid-sensing ion channels It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis Avoid use of multidose bulb/vial  Positive allosteric modulation of KCNQ- and BK-potassium channels  It inhibits the lipoxygenase pathways, thus reducing formation of the leukotrienes  It also may inhibit phospholipase A2 as part of its mechanism of action  These additional actions may explain its high potency – it is the most potent NSAID on a broad basis Contraindications  Hypersensitivity against diclofenac  History of allergic reactions (COPD, bronchospasm, shock, rhinitis, urticaria) Active stomach and/or duodenal ulceration or GI bleeding Severe congestive heart failure Severe liver insufficiency Severe chronic kidney disease Pre-existing hepatic porphyria Avoid during dengue fever Patients with fluid retention In worsening of pre-existing hypertension Inflammatory bowel disease such as Crohn's disease or ulcerative colitis Serious skin adverse events e.g. exfoliative dermatitis, Stevens–Johnson syndrome, toxic epidermal necrolysis Powerful NSAID in TIVA/OFA with analgesia and anti-inflammatory action  Use aqueous solution only Best is given in single dose of 1.5 mg/kg IV slowly and maximum is 150 mg  It is opioid sparing drug  Always give before surgical incision to inhibit prostaglandin receptors, which control the haemodynamic response to surgical stimulation  Diclo should not be mixed with any drug except paracetamol in same syringe  Given with any IV Infusion Always dilute diclo with DW and give slowly to avoid injection pain Dose  Oral 50 mg 2 or 3 times a day  Extended-release tablets 100 mg once a day  Potassium immediate-release tablets 50 mg orally 2 or 3 times a day  Sodium enteric-coated tablets 75 mg orally 2 times a day  IV/IM 1 to 1.5 mg/kg, repeat after 8 hours  Rectally 1 to 1.5 mg/kg ( Paediatric patients) Diclo is better than paracetamol to control post operative fever & pain In anaesthesia practice Diclo Is used as an adjuvant for perioperative acute pain management  Diclofenac is an effective analgesic for acute pain in children as part of the analgesic regime in the peri operative period with dose range from 0.5 to 2.5 mg/kg  Infusion line pain or irritation to vein is very common during IV Diclo, so better prefer large venous line Major side effects of diclo are 1) Abdominal or Stomach pain, Cramping, or Burning 2) Bloody or black, tarry stools 3) Bloody urine and decreased frequency or amount of urine 4) Heartburn or Indigestion 5) Diarrhea 6) Increased thirst and Loss of appetite 7) Vomiting of blood or material that looks like coffee grounds 7) Very rare anaphylactic or anaphylactoid reaction  Some time single dose or overdose of Diclo may cause Acute Renal Failure  As far as avoid Diclo in geriatric age group of patients ( paracetamol is preferred )
  • 21. DOBUTAMINE Approved in 1970 - 1978 Works by direct stimulation of β1 receptors Formula C18H23NO3 Given by IV & Intraosseous Onset of action within 2 min Elimination half life 2 min Dobutamine is predominantly a β1-adrenergic agonist, with weak β2 activity, and α1 selective activity Stimulation of the β1-adrenoceptors of the heart, increase contractility and cardiac output dobutamine is less prone to induce hypertension than is dopamine Dobutamine has mild β2 agonist activity, which makes it useful as a vasodilator Adverse effects Hypertension(> 50 mm of Hg) Angina Arrhythmia (Most Dangerous) Use with caution in AF Tachycardia(>30 beats/min) Palpitation Sometime bronchospasm and shortness of breath Urinary urgency(at high dose) Nausea and Headache Phlebitis and very rare Cutaneous necrosis Overdose Terminate the infusion and arrhythmia treated with lidocaine & beta blocker & sublingual nitrate Indications Patients who require a positive inotropic support in the treatment of cardiac decompensation due to depressed contractility Cardiogenic shock characterized by heart failure with severe hypotension Septic Shock Used for detection of myocardial ischemia (dobutamine stress echocardiography) In Paediatric population (neonates- 18 years) in cardiomyopathies & Cardiogenic shock Dose & Formation Available as 50 mg/ml in 5 ml 10 ml & 50 ml amp/bulb Dose ranges from 2.5-10 µg dobutamine/kg/min Neonate-18 years an initial dose of 5 mcg/kg/minute, range from 2 – 20 mcg/kg/min Low dose 2.5 µg/kg/min (15 drops/min) Medium dose 5 g/kg/min(30 drops/min) High dose 10 µg/kg/min(60 drops/min) Always dilute dobutamine with final concentration 0.5 mg/ml in DNS/D5/NS/DW & not in RL Contraindications Known hypersensitivity Pericardial Tamponade Constrictive Pericarditis Hypertrophic Obstructive Cardiomyopathy Severe Aortic Stenosis Hypovolaemic conditions Recent MI Severe heart failure Chronic Arrhythmia Hypovolemia Acute pericarditis, Myocarditis or Endocarditis Aortic Aneurysm  Inadequately treated arterial hypertension Shelf Life : 3 years Dilution of Dobutamine used within 24 hrs and kept in freeze for 2°C to 8° Sometimes immediately after opening the ampoule, there may be a sulfuric odour lasting for short period Solutions containing Dobutamine may have a pink coloration, which may become darker over time, This is due to a slight oxidation of the active substance Unused solution discarded Pharmacokinetics Dobutamine & Dopamine Dobutamine produced a distinct increase in cardiac index, while lowering left ventricular end- diastolic pressure and leaving mean aortic pressure unchanged Dopamine also significantly improved cardiac index, but at the expense of a greater increase in heart rate than occurred with dobutamine Dobutamine is preferred when there is a need to improve low cardiac output.  Dopamine increase global blood flow Wide Ball Hypotension occurs in almost 40% of all anesthetized patients Dopamine is recommended for patients with kidney disease due to its ability to increase renal blood flow Dobutamine is preferred when there is a need to improve low cardiac output Dobutamine should be avoided in patients affected by outflow obstructions, pulmonic stenosis, or hypertrophic obstructive Cardiomyopathy Dobutamine Infusion Rate of administration and duration of dobutamine infusion is based on blood pressure, heart rate, frequency of ectopic activity, and urine flow; cardiac output, central venous pressure, and pulmonary capillary wedge pressure Initial dose: 0.5 to 1 mcg/kg/min IV infusion Maintenance dose: 2 to 20 mcg/kg/min IV infusion Maximum dose: 40 mcg/kg/min IV infusion Always label the infusion It is Synthetic catecholamine Haemodynemic changes occur during anaesthesia and surgery in elderly patients, Dobutamine corrects the perioperative decrease in cardiac output and blood pressure, and might prevent postoperative neurological disorders Dobutamine is only given with guidelines of institution and when indicated For routine administration it is too dangerous Monitoring with ECG is must during therapy
  • 22. ENFLURANE MECHANISM OF ACTION Enflurane acts as a positive allosteric modulator of the GABAA, glycine, and 5- HT3 receptors, and as a negative allosteric modulator of the AMPA, kainate, and NMDA receptors as well as of nicotinic acetylcholine receptors. So it act on different ion channels within the nervous system by blocking excitatory channels and augmenting inhibitory channels Enflurane is (2-chloro-1,1,2,-trifluoroethyl- difluoromethyl ether) is a halogenated ether Developed by Ross Terrell in 1963, first used clinically in 1966 Approved by the FDA in 1972 Withdrawn from the US market due to more Seizure activity, increased Cardio Depressant effects and Slow onset of action Increasingly used for inhalational anesthesia during the 1970s and 1980s, now no longer in common use PHARMACOKINETICS Clear, colorless, mild sweet odor , Stable nonflammable and non explosive liquid whose purity exceeds 99.9% Formula : C3H2ClF5O, Molar mass : 184.49 g·mol−1 Protein binding : 97%, Boiling point at 1 atm 56.5 °C Blood:Gas partition coefficient 1.9, Oil:Gas partition coefficient 98 Vapor pressure at 20 °C22.9 kPa (172 mm Hg), MAC : 1.68 Specific gravity (25º/25ºC) is 1.517 The MAC in man is 1.68% in pure oxygen, 0.57 in 70% nitrous oxide, 30% oxygen, and 1.17 in 30% nitrous oxide, 70% oxygen Rapidly absorbed into the circulation through the lungs Metabolized : by the CYP2E1 enzyme in the liver upto only 9 % Storage at 15º-30ºC (59º-86ºF) Enflurane sensitizes the heart to catecholamines such as epinephrine  Usually not recommended in Paediatric Anaesthesia as induction DOSAGE AND ADMINISTRATION Orange colored Vaporizers calibrated specifically for Enflurane Preanesthetic medication should be selected according to patient Induction may be achieved using Enflurane alone with oxygen or in combination with oxygen-nitrous oxide mixtures Inspired concentrations of 2.0 to 4.5% Enflurane produce surgical anesthesia in 7 to 10 minute Surgical levels of anesthesia maintained with 0.5 to 3.0% Enflurane Enflurane 0.25 to 1.0% provides analgesia for vaginal delivery AVAILABLE In 125 and 250 mL amber-colored bottles Contains no additives Expire date is five years Take Precautions to give Enflurane in Patients of Acute Kidney & Liver injury, Epileptic patients, Neurotoxic patient SIDE EFFECTS Malignant hyperthermia Movements of various muscle groups and/or Seizures Cardiac depression and arrhythmias Hypotension, Respiratory depression Hypoxia, Hypocapnia, Arrhythmias Shivering, Nausea and Vomiting Moderate to severe liver injury Perioperative hyperkalemia Cardio – Hepato – Neuro - Renal toxicity CONTRAINDICATIONS Seizure disorders Known sensitivity or other halogenated anesthetics Suspected genetic susceptibility to Malignant Hyperthermia Preeclampsia and Eclampsia Accidental occupational exposure to Enflurane causes eye irritation, central nervous system depression, analgesia, anesthesia, convulsions, and respiratory depression INDICATIONS : Induction and maintenance of general anesthesia (mainly as maintenance) Used to provide analgesia for vaginal delivery, Low concentrations used to supplement other GA agents during delivery by Cesarean section, High dose relaxes the uterus in pregnant women giving more blood loss The Blood-Pas partition coefficient is slightly lower than that of Halothane, So induction of anaesthesia and awakening is relatively slower than Halothane 250 ml capacity with 7.35 kg. weight History
  • 23.
  • 24. ESMOLOL  Emergency friend of Anaesthesiologist  Cardioselective beta1 receptor blocker  Shortest acting beta blocker Class II Antiarrhythmic Safely given in broncho- spastic and vascular dis.  Gives central analgesia Opioid sparing adjuvant in OFA and TIVA No significant intrinsic sympathomimetic or membrane stabilizing activity at therapeutic dosages Dosages forms and Strengths Infusion bags 2 g/100 ml, 2.5 g/250 ml, 5 g/500 ml Injectable solution 10 mg/ml and 20 mg/ml Compatible with all common solvents Incompatible with NaHCO3 Never infuse in small veins or by butterfly  Never stop abruptly due to withdrawal effect Pharmacokinetic Bioavailability 90 % Protein binding 55-60% Metabolism Erythrocytic (in blood by hydrolysis of its methyl ester) Elimination half-life 9 minutes Distribution half life 2 minutes Duration of action 10-30 minutes Excretion Kidney (73-78%) Vd 3.4 liter/kg Storage at room temperature Safely given in pediatric Patients ( > 2 Years) Careful in Pregnancy Uses To terminate supra- ventricular tachycardia In episodic atrial fibrillation or flutter Arrhythmia during perioperative period To reduce HR and BP during and after cardiac surgery In early treatment of myocardial infarction In blunting the haemodynemic response to laryngoscopy and intubation To reduce intra and post operative hypotension Brady is less Intraoperative Tachycardia and Hypertension Immediate control 1 mg/kg over 30 sec then 0.15-0.3 mg/kg/min infusion Postoperative control 0.5 mg/kg iv for 1 min then 0.1 mg/kg/min infusion If not control then repeat bolus doses For supraventricular tachycardia 0.5 mg/kg over 1 min then 0.05 mg/kg/min infusion Hypo Is more PONV is less Best adjuvant in Ane Contraindication Sinus bradycardia, Sick sinus syndrome AV heart block, Heart failure Pulmonary hypertension Hypersensitivity Side Effects 10 % or more Hypotension asymptomatic ( 25%) Hypotension symptomatic (12%) Bradycardia (15 %)  1 – 10 % Injection site pain (8%) Agitation (7%) Dizziness(3%)  1 % or less Chest pain Anxiety/Depression Dry Mouth/Dyspepsia Redness of the face and neck Headache Mechanism of Action Esmolol decreases the force and rate of heart contractions by blocking beta-adrenergic receptors of the sympathetic nervous system, which are found in the heart and other organs of the body  Esmolol prevents the action of two naturally occurring substances: epinephrine and norepinephrine
  • 25. Etomidate decrease in level of circulating cortisol IV 100 to 200 mg hydrocortisone is given before etomidate Pharmacokinetics Onset of Action : within 30 to 60 seconds Peak Effect : In 1 minute Duration : 3 to 5 minute and terminated by redistribution Protein Binding : 76 % Metabolism : Hepatic & Plasma Esterase Half-Life Distribution : 3 Minutes ( Anesthesia ) Half-Life Redistribution : 30 Minutes ( Sedation ) Half-Life Elimination : 3 hours ( Drowsiness ) Etomidate + Ketamine Mixture Most suitable mixture for short procedure Best combination for RSI in trauma and sepsis patients Good alternative in pediatric patients compare to ketofol and ketodex Both counter act each other adverse effects like myoclonus, nystagmus, injection site pain Dose is 0.1mg/kg etomidate + 1 mg/kg ketamine Mechanism of Action • Carboxylated Imidazole agent • Imidazole agent in IV anesthetic drugs • R-1-(1-ethylphenyl)imidazole-5-ethyl ester • Acts directly on the (GABA) receptor complex blocking neuroexcitation producing sedation/hypnosis/ anesthesia without analgesia • Acidic pH - 6.9, pKa – 4.2, • poorly water soluble • soluble in 35 % propylene glycol History - Janssen Pharma in 1964 at Belgium First introduced as Anti-Fungal agent - Introduced as IV Anesthetic agent (due to potent sedative properties ) - In Europe 1972 - In USA 1983 - In India 2013 Doses in different situations • For Sedation : 0.1 mg/kg up to three doses • For G/A 0.3 to 0.4 mg/kg IV over 30-60 seconds • In ICU : As continuous infusion 0.04 to 0.05 mg/kg/hr with continuous monitoring • In Cushing Syndrome or law cortisol level patients 0.2 mg/kg • In Geriatric patients : 0.2 mg/kg • In Pregnancy : 0.2 mg/kg • In Pediatric Patients : 0.1-0.3 mg/kg Available as Milky White and Clear Solution in 2 mg/ml 10 ml Bulb or MCT/LCT preparation Etomidate is most preferred drug in Hemodynamically unstable patients then any other anesthetic agents for induction of anesthesia Indications • As Sedation • As Conscious Sedation • As Hypnotic Agent • Etomidate Interview in Lie Detector Test • As Anesthetic Agent ( preferred in cardiac patients) • In Rapid Sequence Intubation (RSI) • In Cardio version as Premedication • In ICU as infusion in ventilated or nonventilated patient • As eSAM ( Etomidate Speech And Memory Test) Contra-Indications • Proven sepsis with unstable hemodynamic patients • Abnormally Low Blood Pressure even with Rx • Decreased Function of the Adrenal Gland • Hypersensitivity of Etomidate • Pediatric Patients less than 10 years age (but people have started using etomidate up to 2 years age with risk-benefit profile) • In Pregnancy try to avoid as induction agent if other anesthetic agents are available • In Geriatric Patients with caution Adverse effects • Transient Injection site pain up to 80 % patients • Skeletal Muscle movements mainly myoclonic ( peripheral limb movements ) up to 30 % patients • Opsoclonus ( uncontrolled eye movements ) • Adrenal Suppression up to 10 % patients • Hiccups • Apnea up to 90 seconds • Less frequently nausea vomiting laryngospasm, snoring, arrhythmia & increase in PaCO2 CNS – Decrease ICP, Cerebral Blood flow and Cerebral Metabolism But cerebral perfusion pressure maintained CVS -- No or Minimal changes in Heart Rate, Blood Pressure and Cardiac Output No hemodynamic changes in response to pain No effect on Sympathetic tone RS – Minimal changes in Respiratory Rate and Tidal Volume Slight elevation in arterial carbon dioxide tension (PaCO2) Transient apnea up to 90 seconds - No histamine release - Very rare allergic reactions - Hepatic and Renal blood flow decreased Administration of Drug • Never dilute Etomidate with DW in same Syringe • Preferably Large Vein for IV administration • Pre administration of lidocaine if possible (2 ml) • First dose to be completed within one arm-brain circulation (60-90 seconds ) • All muscle relaxants, benzodiazepines, narcotics and ketamine are compatible with etomidate in same syringe except vecuronium and Vit-C Different Effects ETOMIDATE In Pregnancy with Heart Dz. etomidate is drug of choice
  • 26. - FENTANYL - Bioavailability 92% (transdermal) 89% (intranasal) 65% (buccal) 54% (sublingual) 100% (intramuscular) 100% (intravenous) 55% (inhaled) Protein binding : 80–85% Metabolism : Liver(CYP3A4) Onset of action : IV within 5 minutes Elimination half-life Formula C22H28N2O Intravenous Molar mass : 336.479 g·mol−1 6 mins (T1/2 α) Melting point : 87.5 °C 1 hours (T1/2 β) Crosses BBB & Placenta 16 hours (T1/2 ɣ) Intranasal : 6.5 hrs. Transdermal : 20–27 hrs. Sublingual/buccal (single dose) : 2.6–13.5 hrs. Duration of action IV : 30–60 minutes Excretion : 75% Urine, 10% feces, 10% unchanged Routes of Administration Buccal Epidural/Spinal IM IV Nasal Nebulizer Sublingual Skin patch Oral Used as Recreational drug & also in Veterinary Anesthesia Side Effects Vomiting, Constipation, Sedation, Urinary retention, Confusion, Hallucinations Injuries related to poor coordination Symptoms of Overdose Respiratory depression, Somnolence, Stupor, Coma, Skeletal muscle flaccidity, Cold and clammy skin, Pupillary constriction, Pulmonary edema, Bradycardia, Hypotension, Airway obstruction, Atypical snoring, and Death A potent OPIOID agonist 100 times more stronger than Morphine Fentanyl invented by Paul Janssen in 1960 and approved for medical use in 1968 Most widely used synthetic opioid Hyperalgesia is common with Fentanyl Fentanyl patches for cancer pain is WHO List of Essential Medicines Mechanism of Action Fentanyl binds to opioid receptors, especially the mu opioid receptor, which are coupled to G-proteins. Activation of opioid receptors causes GTP to be exchanged for GDP on the G- proteins which in turn down regulates adenylate cyclase, reducing concentrations of cAMP. Reduced cAMP decreases cAMP dependant influx of calcium ions into the cell. The exchange of GTP for GDP results in hyperpolarization of the cell and inhibition of nerve activity Fentanyl Antagonist -Naloxone- -Nalmefene- -Naltrexone- Doses -Loading dose: IV 25-100 mcg or 1-2 mcg/kg -Maintenance dose: IV 25-50 mcg or 0.35-0.5 mcg/kg every 30 to 60 minutes -Continuous infusion: 50-200 mcg/hour (Ane.) -TIVA : 0.5 to 2 mcg/kg -NORA : 0.5 to 1 mcg/kg -Rapid sequence intubation : 1 to 3 mcg/kg -Continuous infusion : 50-100 mcg/hour (ICU) -Epidural : 0.5-1 mcg/kg/hr -Never exceed single doses of 3 mcg/kg   (IM : 1-2 mcg/kg) Uses of Fentanyl 1) As analgesic with other anaesthetic drugs 2) For maintenance in all anesthesia technique (TIVA, NORA, Volatile, Regional) 3) In post operative pain relief 4) Management of chronic pain e.g. cancer 5) In Palliative Care 6) In ICU for mechanically ventilated patient 7) In Breakthrough pain 8) In Combat medicine in Military 9) Suppression of the cough reflex Available Strengths of Fentanyl (schedule II drug) IV injection : 0.05 mg(50 mcg)/ml 2ml, 10ml and 50 ml vials Transdermal Patch 12.5,25,37.5,50,62.5,75,100 mcg/hr Fentanyl Buccal Tablet : 100 mcg Intranasal Spray : 100mcg, 300mcg, 400mcg/100mcL spray Given from Neonates to Geriatric patients Extra Shots -Dose reduction is 50 % in acute renal and hepatic impairment -Do not abruptly discontinue fentanyl in patient -It can be mixed with propofol, ketamine, lidocaine, etomidate and midazolam -It also can be mixed in 5% dextrose, RL and 0.9 % normal saline for continuous infusion -No histamine release, thus preferred narcotic for asthmatic patients Extra Shots -Fentanyl is contraindicated in patients who are on MAO-Inhibitors -Rapid administration cause muscle rigidity, so always give IV injection slowly -Fentaketacaine (Fentanyl + Ketamine + Lidocaine) drip is used for postoperative analgesia -Fentanyl is also used in Neuroleptanalgesia -Recently fentanyl use extend in treatment of epilepsy -Narcotic delirium is common with fentanyl Opioid epidemic with fentanyl is very common Fentanyl is high potential for addiction
  • 27. FLUMAZENIL History & Important Information  Also known as Flumazepil First characterized in 1981, First marketed in 1987, FDA approval in 1991, Patent rights lost in 2008, So it is now generic formulation  Flumazenil short half-life requires multiple doses Administration of the drug requires careful monitoring by an anesthesiologist due to potential side effects  If the patient fails to awaken after receiving the maximal dose of IV flumazenil (5 mg over 1 hour), other causes of the persistent sedation or respiratory depression should be considered  In undifferentiated coma it’s use is absolutely contraindicated Mechanism of Action Flumazenil is an imidazobenzodiazepine derivative and a potent benzodiazepine receptor antagonist that competitively inhibits the activity at the benzodiazepine recognition site on the GABA/benzodiazepine receptor complex, thereby reversing the effects of benzodiazepine on the central nervous system, so acts both as antagonist and antidote Does not antagonize the central nervous system effects of drugs affecting GABA ergic neurons by means other than the benzodiazepine receptor  Benzodiazepine overdose rarely cause mortality Indications in Anaesthesia For the complete or partial reversal of the sedative effects of benzodiazepines in sedation or general anaesthesia For the management of benzodiazepine overdose Other Indications To treat overdoses of non- benzodiazepine hypnotics, such as Zolpide, Zaleplon and Zopiclone (also known as "Z-drugs") To treat Idiopathic Hypersomnia  In Hepatic Encephalopathy Pharmacokinetics Formula : C15H14FN3O3 Molar Mass : 303.293 g/mol Routes of Administration : IV Metabolism : Hepatic, Complete Excretion : Urine 90–95%, Feces 5–10% Onset of Action : Within 1 or 2 minutes Peak Effects : 7 to 10 minutes Elimination Half Life : Initial (7-15 min), Brain (20-30 min), Terminal (40-80 min) (Average : 53 minutes) Protein Bound : 40 to 50 % Available : 5 or 10 ml multidose vial ( 100 μg/ml) Compatible : With 5% Dextrose in water, Lactated Ringer‘s and Normal Saline solutions Storage : At 25°C & solution is stable for 24 hrs. Dose Reduction : In Geriatric, Renal & Hepatic Pt. Dosage Forms & Strengths Reversal of Sedation and General Anesthesia - 0.2 mg IV over 15 sec - IF after 45 sec no response, administer 0.2 mg again over 1 min; may repeat at 1 min intervals; not to exceed 4 doses (1 mg) -IF resedation occurs, may repeat doses at 20-min intervals; not to exceed 1 mg/dose or 3 mg/hr Benzodiazepine Overdose - 0.2 mg IV over 15-30 sec - IF no response after 30 sec, administer 0.3 mg over 30 sec 1 min later; IF no response, repeat dose of 0.5 mg IV over 30 sec at 1-min intervals to max cumulative dose of 3 mg/hr -Rarely patient may require titration up to total dose 5 mg Adverse Effects  > 10% Nausea and vomiting (11%)  1-10% Dizziness (10%), Abnormal/blurred vision (3-9%), Agitation (3-9%) Dyspnea (3-9%). Hyperventilation (3-9%), Pain at injection site (3-9%) Xerostomia (3-9%), Diaphoresis (1-3%), Emotional disturbance (1-3%) Fatigue (1-3%), Headache (1-3%), Paresthesia (1-3%), Tremor (1-3%) Weakness (1-3%) 1% Delirium, Abnormal hearing, Thick tongue, Generalized seizure Precautions for IV Administration  Slowly over 15 to 30 seconds  To minimize pain, administer through a freely running IV infusion line into a large vein Avoid extravasation Relative Contraindication to Use Head Injury/Seizures patients/ Patient under 1 year of age Should not be used until the effects of neuromuscular blockade have been fully reversed.  In Psychiatric Patients /Status Epileptics/Myoclonus/Hypertonia  Use In Drug- and Alcohol-Dependent Patients
  • 28.  FUROSEMIDE/FRUSEMIDE (LASIX)  Loop Diuretic Use - 1964 Bioavailability : 43 - 69 % ; Protein Binding : 91 - 99 % Metabolism : Liver & Kidney, Glucuronidation Crosses placenta, enters breast milk Elimination Half Life : upto 100 min Excretion : Kidney 66 % & Bile Duct 33 % Formula : C12H11ClN2O5S; Molar Mass : 330.7 g·mol−1 Serious Side Effects Electrolyte Imbalance Low Blood Pressure Hearing Loss Excessive Urination  Feeling Thirsty Common Side Effects Light headed on stand Ringing in Ears Sensitivity to Light Hypokalemia Dizziness & Dry Mouth Mechanism of Action  Rapid acting, highly efficacious diuretic Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule. Increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium. Effectiveness persists in impaired renal function Special Action (Diuresis) The action on the distal tubules is independent of any inhibitory effect on carbonic anhydrase or aldosterone; it also blocks negative, as well as positive, free water clearance. Bioavailability with end-stage renal disease 43 – 46% Elimination half-life is prolonged in CCF & ARF General Indications Edema due to heart or lung failure, hepatic impairment, or renal disease & in ARF or CRF Hypertension Therapeutic Effects Diuresis & subsequent mobilization of excess fluid e.g. edema, pleural effusions) Decreased BP Diuretic Effect Relative Contraindication Diabetes Hyperuricemia Low Magnesium Low calcium Low Chloride Low Sodium Low Potassium Known C/O BPH Hearing Loss patients Anuria Continuing loop diuretics Perioperatively is relatively safe Study confirms that Furosemide before surgery does not lead to intraoperative Hypo Furosemide infusion (during intra- and early postoperative period) has a renal protective effect during major surgeries Dosage ( Oral ) Edema 20–80 mg/day as a single dose initially, may repeat in 6–8 hr Hypertension 40 mg twice daily initially Hypercalcemia 120 mg/day in 1–3 doses Dosage ( IV/IM ) 20–40 mg, may repeat in 1–2 hr and ↑ by 20 mg every 1–2 hr until response is obtained, maintenance dose may be given every 6–12 hr; Continuous infusion– Bolus 0.1 mg/kg followed by 0.1 mg/kg/hr, double every 2 hr to a maximum of 0.4 mg/kg/hr. Dosage in Paediatrics Oral 2 mg/kg as a single dose; may be ↑ by 1–2 mg/kg every 6–8 hr (maximum dose = 6 mg/kg). IV/IM 1–2 mg/kg/dose every 6– 12 hr; Continuous infusion– 0.05 mg/kg/hr Neonates : 1-2 mg/kg Available as IV/IM 10 mg/ml 2 ml or 4 ml Oral 20 mg or 40 mg Oral solution for paediatric 10 mg/ml More than 10 % patient are getting Hyperuricemia and Hypokalemia after giving Furosemide IV/IM Avoid use of Furosemide in Pregnancy and Lactation, Only Use in Life- Threatening emergencies when no safer drug available Pharmacokinetics
  • 29. GLYCOPYRROLATE Full name is Glycopyrronium bromide  Muscarinic anticholinergic group  Glycopyrronium was first used in 1961 to treat peptic ulcers  Since 1975, intravenous glycopyrronium has been used before surgery to reduce salivary, tracheobronchial, and pharyngeal secretions  In June 2018, glycopyrronium was approved by the FDA to treat excessive underarm sweating, becoming the first drug developed specifically to reduce excessive sweating  In inhalable form it is used to treat chronic obstructive pulmonary disease (COPD)  Also used to treat Sialorrhea & Ménière's disease Side effects  Dry mouth (Xerostomia)  Urinary retention  Headaches/ drowsiness  Vomiting/diarrhea,  Constipation Blurry vision/ Mydriasis  Urticaria / Pruritus Since glycopyrronium reduces the body's sweating ability, it can even cause hyperthermia & heat stroke in hot environments  Mechanism of action : Glycopyrronium competitively blocks muscarinic receptors thus inhibiting cholinergic transmission  Oral Administration : 1 hour before meals or 2 hours after meals, because high fat food reduces orally bioavailability  Glycopyrrolate is associated with a more stable cardiovascular system, fewer arrhythmias and superior control of oropharyngeal secretions at the time of reversal Pharmacokinetics  Glycopyrronium bromide affects the gastrointestinal tracts, liver and kidney but has a very limited effect on the brain and the central nervous system  Formula : C19H28NO3 +  Molar mass : 318.437 g·mol−1  Elimination half-life : 0.6–1.2 hours  Excretion : 85% renal  Routes of Administration : Mouth, Intravenous, Inhalation, Topical Glycopyrronium has a relatively slow diffusion rate, and in a standard comparison to atropine, is more resistant to penetration through the blood-brain barrier and placenta  Used topically and orally to treat hyperhidrosis, in particular, gustatory hyperhidrosis Dosages of Glycopyrrolate Tablets : 1mg/1.5mg/2mg Oral solution : 1mg/5mL Injectable solution : 0.2mg/mL Preoperative : 4mcg/kg (IV/IM) 30-60 min before surgery Intraoperative: 0.1 mg IV/IM; may repeat every 2-3 minutes Control of Secretions : 0.004-0.01 mg/kg IM/IV every 6 hours Dosages of Glycopyrrolate Pediatric Children 1 month to 2 years (4 mcg/kg (IM); may increase to 8 mcg/kg Children > 2 years : 4 mcg/kg (IM) Neuromuscular Blockade Reversal 0.2 mg (IV) per 1 mg of neostigmine or 5 mg of pyridostigmine in same syringe  Most preferred drug in reversal by anaesthesiologist than atropine Relative Contraindications Angle-closure glaucoma  Obstructive Uropathy GI obstruction / Paralytic ileus  Intestinal atony of elderly or debilitated patient  Unstable cardiovascular status  In Acute Hemorrhage  Severe Ulcerative Colitis  Toxic Megacolon, Myasthenia Gravis, Reflux Esophagitis  Hiatus Hernia / Mitral Stenosis Use caution in patients with hepatic impairment and renal impairment  Glycopyrrolate is a synthetic quaternary amine that crosses the blood-brain barrier poorly and is less likely to cause altered mental status or tachycardia than atropine  It has approximately twice the potency of atropine and more potent than atropine in its antisialogogue effect For overdose antidotes are Neostigmine and Pyridostigmine
  • 30. HALOTHANE Discovered by C. W. Suckling in 1951 and commercial use started in 1956 Continued till 1990s as volatile induction No longer commercially available in the United States and replaced by Sevoflurane A potent trigger for Malignant Hyperthermia Since 2000 Isoflurane & then Sevoflurane replaced halothane as volatile induction in Anesthesia practice Mechanism of Action The exact mechanism of the action of general anesthetics has not been delineated. Halothane activates GABAA and glycine receptors It also acts as an NMDA receptor antagonist, inhibits nACh and voltage- gated sodium channels, and activates 5- HT3 and twin-pore K+ channels It does not affect the AMPA or kainate receptors  Potent anesthetic with a MAC of 0.75%  Oil:Gas partition coefficient : 224  Blood:Gas partition coefficient : 2.3  Boiling point : 50.2 °C(at 101.325 kPa)  Molar mass 197.38 g·mol−1  Formula : C2HBrClF3,  Packaged in dark-colored bottles Unstable in light  Stored at room temperature  Nonflammable and Nonirritant  Colorless and Pleasant Smelling  Metabolism : Hepatic(CYP2E1)  Excretion : Kidney & Respiratory  Routes of Administration : Inhalation General inhalation anesthetic used for induction and maintenance of general anesthesia King of inhalation agent from 1956 to 1990 The only inhalational anesthetic containing bromine, which makes it radiopaque Contains 0.01% Thymol as a stabilizing agent Available as 30/100/250 ml bottle Actions of Halothane on body Progressively Depresses Respiration, Tachypnea with Reduced tidal volume & alveolar ventilation , causes Bronchodilatation No increase in salivary or bronchial secretions Pharyngeal and laryngeal reflexes are rapidly obtunded., Causes Hypotension, Bradycardia and sometime Cardiac Arrhythmias Causes dilation of the vessels of the skin and skeletal muscles. Potent Uterine relaxant and Produces moderate muscular relaxation Gives Moderate induction and very slow Recovery  Not good Analgesic Common Side Effects Nausea, Vomiting, Chills, and Headache Serious side effects  Hives  Difficulty in breathing,  Swelling of face, lips, tongue, or throat  Abnormal heart rhythm  Decreased lung function  Decreased oxygen in the tissues or blood  Hepatitis  Kidney damage  Malignant hyperthermia  Problems with circulation  Yellowing of the skin or eyes (jaundice) Contraindication : In obstetric anaesthesia except Uterine Relaxation is required Halothane Hepatitis Repeated exposure to halothane in adults causes severe liver injury (1 in 10000) called as halothane hepatitis, immuno allergic in origin and this hepatitis syndrome had a mortality rate of 30% to 70%, but it is lower in pediatric patients Halothane and Heart It sensitizes the heart to catecholamines, causing cardiac arrhythmia, particular ventricular which is occasionally fatal It is potent trigger for MH But safe in Por- phyria Dose and MAC Induction dose varies from patient to patient but is usually within the range of 0.5% to 3%. & maintenance dose varies from 0.5% to 1.5% Halothane vaporizer is red colour Age : MAC % Infants : 1.08, 3 yrs : 0.91, 10 yrs. : 0.87, 15 yrs. : 0.92, 24 yrs. : 0.84, 42 yrs. : 0.76, 81 yrs. : 0.64 Reduce with N2O & Oxygen Ane. Precautions to Use Used only in halothane vaporizers In patients with markedly raised intracranial pressure Liver Diseases (any type) Malignant Hyperthermia suspected patient In renal failure With use of epinephrine or norepinephrine Overdose No antidote available, drug administration stopped & assisted/controlled ventilation with pure oxygen initiated Fever is very common after 2-3 days of Haloth. Ane
  • 31. HYDROCORTISONE Uses of Hydrocortisone Mainly used as an Immunosuppressive Drug in Anaphylaxis and Angioedema Perioperatively in patients on long-term steroid treatment to prevent an adrenal crisis Adrenocortical Insufficiency Adrenogenital Syndrome High blood Calcium / Ulcerative Colitis Anemia, Thrombocytopenia & Lymphoma Rheumatoid Arthritis / Thyroiditis Dermatitis ( Eczema, Psoriasis & Itching )  Asthma & COPD Injected into inflamed joints e.g. Gout Congenital Adrenal Hyperplasia Topical Creams and Ointments Ranging from 0.1 % to 2.5 % ( 1 mg to 25 mg in 1 gm ) Oral ( Always after Food) 20 mg to 240 mg orally per day (In 3 to 4 Dose) IM Dose 100 to 500 mg Intravenous Dose 100 mg IV (Over 1-2 minutes ), followed by IV infusion of 200 mg over 24 hours OR 50 mg IV every 6 hours ( Maximum 500 mg in a day) 2 to 3 mg/kg ( Usual dose ) Pediatric Dose : 0.56 to 8 mg/kg/day oral or IV Patented in 1936 Medical use in 1941 Hydrocortisone is the name for the hormone Cortisol when supplied as a medication Hydrocortisone is a Corticosteroid, acting specifically as both a Glucocorticoid and as a Mineralocorticoid It is an agonist of the glucocorticoid and mineralocorticoid receptors Compared to hydrocortisone, Prednisolone is about 4 time potent and Dexamethasone about 40 times as potent in terms of Anti- inflammatory effect Mood changes / Headache Increased risk of infection Edema / Weight Gain Swollen Ankle Long-term use common side effects Osteoporosis, Upset of Stomach, Physical Weakness, Easy Bruising, Candidiasis, Sodium Retention, Potassium Loss & Convulsions Pharmacokinetics Formula : C21H30O5 Molar mass : 362.466 g·mol−1 Bioavailability : 100 % in IV, IM & Oral Elimination half-life : 1.5 hrs. (IV or IM) Routes of Administration : Oral, IV, IM, Topical & Rectal Store : Room Temperature Metabolism : Liver & Excretion : Renal In September 2020, WHO approved Hydrocortisone is effective in reducing mortality rate of critically ill COVID-19 patient Compatible with DW, Normal Saline and Dextrose Solutions Available as Injectable ampoule or bulb 100/200/250/500/1000 mg Hydrocortisone Sodium Succinate as powder & Phosphate as solution Dose No Dose adjustment in Renal, Hepatic or Geriatric patients Hydrocortisone in Anaesthesia  Preoperative : 100 mg IV and dose adjustment according to surgery, infection, trauma with 200 mg IV infusion over 24 hours  In Etomidate GA Induction (Specially Infusion) Always give higher dose in obese patients and drugs that induce CYP3A4 For patients undergoing any minor to major anesthesia Hydrocortisone 100 mg is as good as Dexamethasone 6–8 mg, & should be administered at time of induction of anesthesia  In Laryngospasm, Bronchospasm, Laryngeal Edema & Pulmonary Edema, 100 to 200 mg dose is indicated followed by infusion Mechanism of Action Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes Works by calming down our body's immune response to reduce pain, itching and swelling (Inflammation)
  • 32. ISOFLURANE Physical properties Molecular weight : 84.5 g/mol  Boiling point (at 1 atm): 48.5 °C  Density (at 25 °C) : 1.496 g/mL  MAC : 1.15 vol %  Water solubility 13.5 mM (at 25 °C)  Blood:gas partition coefficient: 1.4  Oil:gas partition coefficient: 98  Routes of administration : Inhalation  Formula : C3H2ClF5O Invented in 1979, Non-flammable It vaporizes readily but is a liquid at room temperature Isoflurane is halogenated ether Mechanism of action 1) Isoflurane binds GABA glutamate and glycine receptors, but has different effects on each receptor. 2) It acts as a positive allosteric modulator of the GABAA receptor in electrophysiology studies of neurons and recombinant receptors. 3) It potentiates glycine receptor activity, which decreases motor function. 4) It also inhibits receptor activity in the NMDA glutamate receptor subtypes. 5) It inhibits conduction in activated potassium channels. 6) It also affects intracellular molecules. 7) It activates calcium ATPase by increasing membrane fluidity The average lifetime of Isoflurane in the atmosphere is 3.2 years Dosage Forms & Strengths Inhalation solution  Available as 30 ml, 100 mL & 250 mL Anesthesia Induction & Maintenance  Use calibrated vaporizer  Induction: 1.5-3% can produce surgical anesthesia in 7-10 minutes  Maintenance: 1-2.5% with nitrous oxide  Additional 0.5-1% may be needed if given with oxygen alone Adverse Effects 1-10%  Nausea, Vomiting, Shivering, Hypotension <1%  Arrhythmias  Malignant hyperthermia (rare)  Elevations in white blood count  May decrease creatinine and increase BUN  Ileus, if severe (fatal)  Hepatic dysfunction (postoperative period) (rare)  Respiratory depression (rare)  Elevated carboxyhemoglobin levels  Hyperkalemia Contraindications  Hypersensivity  Malignant Hyperthermia Careful in use  Coronary heart disease Chronic Renal and Liver Diseases  Hyperkalemia  Ventricular Dysfunction  Prolong use in GA  Latent neuromuscular disease  Obstetrical Anesthesia Pharmacokinetics  Onset: Rapid (7-10 min)  Duration: Short  Metabolism: Liver (0.2%)  Clear, Colorless, Stable liquid  Containing no additives or chemical stabilizers  Pungent, musty, ethereal odor Isoflurane stored in indirect sunlight in clear, colorless glass for five years Used for induction and maintenance of general anesthesia Premedication with anticholinergic drug is must before Isoflurane Drinking Isoflurane cause drowsiness dizziness Headache, nausea & vomiting Isoflurane has more incidence of airway hyper reactivity compared to Sevoflurane Isoflurane gives analgesia and relaxes muscles during anesthesia Not advisable as mask induction in pediatric patient Isoflurane cause decrease in intellectual function for 2 or 3 days after GA Extra Shots  Isoflurane causes cerebral vasodilation leading to increase in CBF and ICP and markedly reduces the CMRO2  95 % of inhaled Isoflurane eliminated by exhalation  It is unsafe to consume alcohol after Isoflurane anesthesia Isoflurane bottles and vaporizers are in purple color  Coughing and laryngospasm are more common with Isoflurane Iso. Rs. 10/ml Sevo. Rs.30/ml Now use of Isoflurane is declining in anesthesia practice But widely used in Veterinary anesthesia
  • 33. Main Features  Rapid-acting general anesthetic  Produce profound analgesia  Normal pharyngeal-laryngeal reflexes  Slightly enhanced skeletal muscle tone  Cardiovascular and respiratory stimulation  Transient and minimal respiratory depression. Contraindications > Angina, Stroke and very high blood pressure Psychiatric disorders, Uncontrolled Epilepsy In raised intraocular pressure & Eye injury Acute Porphyria  Age less than 3 months  Tracheal and Laryngeal Surgery - Bioavailability – 93 -100 % - Protein binding - 53.5% -Distribution half-life 1.95 min - Half Life - 186 minutes - Elimination - urine 91 % , 3 % in feces and 6 % unchanged - Clearance rate - 95 L/h/70kg Mechanism of action  Interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels  Does not interact with GABA receptors  Selectively depress the thalamoneocortical system before significantly obtunding the more ancient cerebral centers and pathways (reticular-activating and limbic systems) - Water and Lipid Soluble - Oral ketamine broken down by bile acids - Undergoes hepatic Metabolism - It can be mixed with any TIVA drugs - Compatible with all IV fluids Other uses > Emergency Dept. > Asthma > Seizures >Pain management > Depression > Vet Anesthesia Invented in 1962 ---- NMDA receptor antagonist with Dissociative Anesthesia ---- Approved in 1970 Most Popular Anesthetic Drug of Anesthesiologists Ketamine • I V Effect Starts -2 min Last – 25 min • IM Effect Starts – 5 min Last – 4-6 hrs • Oral – 30 min C13H16ClNO More Analgesia & Less Anesthesia  M/A Main Actions  Increase BP  Increase Salivation  Bronchodilation  Hallucination  Agitation  Catatonia  Prevent opioid induced Hyperalgesia  Best agent in Post anesthetic shivering Post Ketamine Double vision & Nystagmus are very common Dose Schedules 0.1-0.3 mg/kg – Analgesia 0.2-05 mg/kg – Recreational 0.4-0.8 mg/kg -- Partially dissociated 1-2 mg/kg – Fully Dissociated 1-2 mg/kg /IV – Procedural Sedation 4-8 mg/kg/IM – Procedural Sedation 0.1-0.2 mg/kg/hr – Postop Pain Relief (Infusion maximum 3 days only) IV Bioavailability -100 % IM Bioavailability – 93 % Dose Schedules 10 mg/kg /Oral – As Sedative Premedication(Bioavailability – 20 %) 0.7-0.9 mg/kg – Intrathecal (S/A) 0.2 mg/ml – Epidural for Postop pain Intra nasal 0.5-1 mg/kg (Bio-50%) Intrarectal 0.5-1 mg/kg (Bio-30%) Sublingually 0.5 -1 mg/kg (Bio-30%) Inhalation 0.5-1 mg/kg Topical Gel – 1% ketamine with other drugs Ketamine is the only drug which Is given by all routes In body U N I Q U E D R U G S C H E D U L E D R U G •Increase HR, high BP(20 %) •Increased intracranial pressure • Transient reddening of the skin • Reduced appetite, nausea • Increased salivation, vomiting •Pain, eruptions or rashes at the injection site • Tonic-Clonic movements • Double vision , involuntary eye movements, • Increased bronchial secretions • Anaphylaxis and Dependence • Cognitive Deficits • Emergence reaction Side Effect Pharmacokinetics •Rapid onset and short duration of action • Initially distributed to highly perfused brain tissues • Crosses Blood Brain barrier • Undergoes extensive redistribution • Major metabolite are norketamine and dehydronorketamine Combination • Ket+Propofol(Ketofol) • Ketamine+Dex(Dexket) • Ketamine+Fentanyl • Ketamine+Midazolam • Ketamine+Diazepam • Ket+Prof+Dex (KPD) WHO List of Essential Medicine