15 LECTURE's Final for Print

15

LECTURES IN ANAESTHESIOLOGY

FOR

MEDICAL STUDENTS

BY

PROF. BRIG. M. SALIM SI(M)

MBBS: MCPS (Pak); D.A. (London); FFARCSI (Dublin) FRCA (London); FCPS (Pak); Ph.D ,FRCP; FICS, FACS.

Diploma in Acupuncture (China); D.Sc. (Hony) Fellow Medicina Alternativa.

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Salim, M.

Basics of pain medicine

1. Pain 2. Medicine

Includes index 616.849-dc22

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First Edition 2007 (Published by HEC) Second Edition 2014

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15

LECTURES IN ANAESTHESIOLOGY

FOR

MEDICAL STUDENTS

BY

PROF. BRIG. M. SALIM SI(M)

MBBS: MCPS (Pak); D.A. (London); FFARCSI (Dublin) FRCA (London); FCPS (Pak); Ph.D ,FRCP; FICS, FACS.

Diploma in Acupuncture (China); D.Sc. (Hony) Fellow Medicina Alternativa.

 Professor of Anaesthesiology & Pain Medicine Islamic International Medical College, Rawalpindi.

 Honorary Consultant & Instructor

Armed Forces Post Graduate Medical Institute, Rawalpindi.  President: Society for Treatment and Study of Pain (STSP)

 Chief Editor, JIIMC

 Chief Editor, Anaesthesia, Pain & Intensive Care  Patron,, Rawal Medical Journal

FORMERLY:

 Prof. of Anaesthesia, Rawalpindi Medical College

Holy Family Hospital, Rawalpindi.  Professor of Anaesthesiology

Army Medical College, Rawalpindi.  Advisor in Anaesthesia

Armed Forces of Pakistan.

 Dean faculty of Anaesthesiology

CONTENTS

List of figure ………vii

Dedication……….………...ix

Forewords……….………...xi

Preface……….xiii

Introduction………..xv

Lecuter-1 Preoperative Assessment and Premedication……….……….……..1

Lecuter-2 Inhalational Anaesthetic Agents………...15

Lecuter-3 Intravenous Anaesthetic Agents ………..………27

Lecuter-4 Muscle Relaxants ………..………..………..31

Lecuter-5 Local Anaesthetic Agents ………..………..37

Lecuter-6 Regional Anaesthesia...41

Lecuter-7 Fluid Management ………..…………...57

Lecuter-8 Acid-Base & Electrolyte Balance ……….………...65

Lecuter-9 Blood Gases, Pulse Oximetry and Capnography………..………...73

Lecuter-10 Anaesthesia and Related Diseases ………..……….79

Lecuter-11 Cardiopulmonary Resuscitation………...……….…..85 Lecuter-12 Pain………..……….…...95 Lecuter-13 ICU………..….99 Lecuter-14 Complications of Anaesthesia ……….………..103 Lecuter-15 Post Operative Recovery and Care ……….………111

Appendix………..………...119

Suggested Reading………..………131

LECTURE 1

PREOPERATIVE ASSESSMENT

AND PREMEDICATION

Q:

WHAT IS THE AIM OF PREOPERATIVE ASSESSMENT?

The preoperative management affects outcome for better or worse, and central to achieving the best possible outcome is a thorough preoperative evaluation intended to:

 Identify the health problems that place the patient at increased risk.  Resolve and control diseases as well as possible.

 Define a management plan that minimizes preoperative, intraoperative, and especially postoperative risks.

 The Aim of preoperative evaluation is to reduce morbidity and mortality.

Q:

WHAT POINTS WOULD YOU KEEP IN MIND WHILE TAKING

THE HISTORY?

1. General medical and surgical history. Ask especially about:

 Cardiovascular system --- hypertension, angina, orthopnoea, ankle swelling, previous MI, rheumatic fever, valvular heart disease.

 Respiratory system --- shortness of breath, cough, sputum, wheezing, asthma, tobacco abuse.

 Hepatic --- viral hepatitis, jaundice, cirrhosis.  Renal --- renal failure.

 Gastrointestinal --- peptic ulcer disease.

 CNS --- seizures, peripheral neurological deficit, stroke, muscle dystrophies.

 Musculoskeletal --- osteoarthritis, rheumatoid arthritis.  Endocrine --- diabetes mellitus, thyroid disease.

 Haematology --- easy bruising or prolonged bleeding.

 Dental --- temporomandibular joint disorder, loose or missing teeth. 2. Previous anaesthetics and ill effects.

3. Drug therapy including oral contraceptives and aspirin. 4. Excessive alcohol intake.

5. Allergies. 6. Pregnancy.

7. Time of last intake of food and drink. 8. A consent form.

Q:

WHAT PHYSICAL EXAMINATION SHOULD BE DONE BY AN

ANAESTHETIST?

 Presence of added sounds on auscultation.

2. Cardiovascular system:

 Pulse (rate, rhythm and character).

 Venous pressure and character.

 Peripheral dependant oedema.

 Blood pressure.

 Apex beat.

 Thrills.

 Extra heart sounds and murmurs.

3. State of nutrition, malnutrition and obesity.

4. Skin colour, especially pallor, cyanosis, jaundice or pigmentation.

5. Psychological state of the patient, especially anxiety. 6. The airway(The Airway are assessed by Mallampati scoring

system).

7. Ease of venous cannulation.

Q:

WHAT INVESTIGATIONS SHOULD BE AVAILABLE AT

PREOPERATIVE ASSESSMENT?

Depending upon the age and condition of the patient following investigations may be required:

1. Urine tests, especially for sugar, ketones and protein. 2. Haemoglobin and blood count.

3. Blood urea and Creatinine. 4. Serum electrolytes.

6. E.C.G.

7. Chest X-ray. 8. Echocardiogram.

9. Bedside pulse oximetry.

10. Other special investigations may be ordered when indicated.

The above investigations help to assess the status of the patient condition. The anaesthetist should correct any abnormality in the investigation before giving anaesthesia. He may refer the patient to appropriate consultant.

Q: WHAT IS ASA (AMERICAN SOCIETY OF

ANAESTHESIOLOGISTS) SCORING SYSTEM?

The ASA scoring system describes the preoperative condition of a patient. It makes no allowances for the patient’s age, smoking history, any obesity or pregnancy. Addition of postscript E indicates emergency surgery.

THE ASA SCORING SYSTEM

I Healthy patient.

II Mild systemic disease, no functional limitations.

III Moderate systemic disease, definite functional limitation. IV Severe systemic disease that is a continuous threat to life.

V Moribund patient, unlikely to survive 24 hours with or without operation.

Q: WHAT IS MALLAMPATI SCORING SYSTEM?

Clinical assessment of airway is very essential. In Mallampati scoring system, the patient sits opposite the anesthetist with mouth open and tongue protruded. The structures visible at the back of the mouth are noted as described below.

 Class 1 – faucial pillars, soft palate and uvula visible.

 Class 2 – faucial pillars and soft palate visible, uvula masked by base of tongue.

 Class 3 – only soft palate visible.

 Class 4 – soft palate not visible.

Mallampati scoring system helps the anaesthetist for easy intubation. Patients in class1 and 2 are intubated easily for other classes anaesthetist adopted other measures to intubate the patients such as stylet or fiber optic laryngoscope.

Q: WHAT ARE THE EFFECTS OF PRE- EXISTING DURG

THERAPY?

1. Antihypertensive drugs are normally continued up to the time of surgery, otherwise hypertensive crisis may occur. Adequate therapy restores a normal blood volume and minimizes the risk of a dangerous fall of arterial pressure at induction of anaesthesia. The avoidance of hypovolaemia during surgery is important. Bradycardia is common in those taking beta-blocking drugs.

2. Antianginal drugs such as calcium channel blockers or nitrates should not be stopped before surgery without a very specific reason, or angina may recur.

3. Lithium should be stopped 2 days before major surgery as it potentiates the non-depolarizing group of relaxants. In emergency cases Suxamethonium and regional blocks should be considered.

4. Monoamine oxidase inhibitors such as phenelzine should be discontinued 2 weeks before surgery, otherwise hypo or hypertensive crisis may occur and its prolongs analgesics effect particularly pethidine and opioids.

5. Levodopa should be continued upto the time of surgery to prevent the recurrence of severe Parkinsonism, dysphagia and aspiration pneumonia.

6. Steroid therapy suppresses ACTH production by the anterior pituitary. In time the adrenal cortex atrophies and is thus unable to increase its secretions in response to stress. This results in profound hypotension during and after anaesthesia with decreased sensitivity to catecholamine. Thus it is generally safer to assume some diminution of adrenal reserve and to give extra hydrocortisone over the period of surgery, e.g. hydrocortisone 100 mg i.m. just before surgery, and continued 6 to 8 hourly for 24 hours after minor surgery, or for 3 days in case of major surgery.

7. insulin should be continued. The patient should be NPO after midnight, no IV fluids, and half of the usual morning subcutaneous dose given. Hypoglycemia and hyperglycemia should be avoided.

8. Oral contraceptives should be discontinued 4 weeks prior to surgery as they increase the risk of DVT.

Q: WHAT ARE THE REASONS FOR THE ADMINISTRATION OF

PREMEDICANTS?

 To reduce saliva secretion.

 To prevent vagal reflexes, due to surgical stimulation or associated with medication.

 For specific therapeutic affects, e.g. steroids, H2 blockers, etc.

Q: WHAT ARE THE DIFFERENT DRUGS USED FOR

PREMEDICATION?

SEDATIVES

BENZODIAZEPINES

These are all good premedicants and can be given orally producing sedation, amnesia and freedom from anxiety.

Midazolam: has been used for night sedation before surgery (7.5 – 15

mg) or as premedication. Dose is 70-100 mcg/kg i.v. 30-60 min before surgery.

Diazepam: 10-20 mg, orally or i.v. duration 4-8 hrs. ANALGESICS

Long acting NSAIDs gives useful background analgesia. Ketoprofen (100-200 mg oral or rectal, 30 mg i.m, i.v.), Piroxicam (20-40 mg oral), Diclofenac (50-100 mg oral or rectal) will all give useful analgesia in patients suffering from pain preoperatively. Pethidine or Morphine can also be used.

ANTICHOLINERGIC AGENTS

ATROPINE

Effects on nervous system:

 Competitive blocking action on muscarinic receptors supplied by postganglionic cholinergic nerves.

 Complete vagal blockade requires a dose of 3mg.

 Inhibits sweating.

 Stimulates the medulla and higher centres. Effects on eye:

 Dilated pupils.

 Loss of accommodation. Effects on respiratory system:

 Sweat, bronchial and salivary glands are inhibited.

 Bronchodilatation.

 Slight increase in anatomical dead space. Effects on circulatory system.

 Tachycardia.

 Increased myocardial oxygen consumption.

 Cardiac output and blood pressure is increased. Effects on alimentary system.

 Tone and peristalsis of gut are decreased.

 Increases chances of regurgitation.

Dose: usual adult dose, 0.6 mg i.m. (in children 0.015 mg/kg) 1 hr before operation. With neostigmine the dose is 1-2 mg.

HYOSCINE HYDROBROMIDE:

Used as a gastrointestinal antispasmodic. It is a tertiary amine, so crosses the blood-brain barrier and causes sedation. Occasionally it produces central anticholinergic syndrome. It is a mild respiratory stimulant, while its actions on iris, salivary, sweat and bronchial glands are stronger than atropine. It is a moderately powerful antiemetic. Dose 10-30 mg.

GLYCOPYRONIUM BROMIDE:

It reduces the tone of lower oesophageal sphincter. It suppresses gastric secretions better than atropine or hyoscine. It causes tachycardia; so effective in preventing bradycardia due to suxamethonium. It efficiently dries up salivary secretion.

Dose: premedication 0.2-0.4 mg (adult); 4-8 mcg/kg (child). Intravenous use to protect against bradycardia (adult) 0.2 mg, 4 mcg/kg (child).

ANTACIDS

These are commonly prescribed for patients thought to be at risk of regurgitation and aspiration. Ranitidine, 150 mg orally or 50 mg i.m.

DRUGS FOR SPECIFIC EFFECTS

These include all drugs used to ensure optimal treatment of specific conditions up to the time of surgery, e.g. salbutamol inhalation for asthmatics.

NOTE: It is usually quoted that sympathetic words and reassurance to

patients act as sedative effect.

Remember:- reassurance + sympathetic words = 10 mg diazepam.

EQUIPMENT

Q1: WRITE SHORT

NOTES:-1. Anaesthesia Machine 2. Cylinders

3. Vaporizers

1. ANAESTHESIA MACHINE

Def: Machine which delivers measured amount of gases & volatile anaesthetic agents from source of supply to patient through tubing. Basic functions of

machine:- To deliver compressed gases to patient at a safe pressure.

 To allow the flow & composition of the gases to be easily adjusted.

 To permit the addition of a precise concentration of volatile anaesthetic such as isoflurane.

 To deliver this mixture to a common gas outlet & hence, to a breathing circuit on ventilation.

Types of Anaesthesia Machine: - There are two types of

Anaesthesia Machine.

I) Continuous Flow: - Machine delivers a mixture of gases

& vapours at a continuous flow set by anaesthetist into a reservoir bag from which the patient inhales.

II) Demand Flow: - Machine delivers the preset mixture of

gas at flow rates demanded by breathing pattern of the patient without interposition of reservoir bag.

Fig: The system is an anaesthetic machine of the Boyle’s type. Nitrous oxide and oxygen from cylinders on the left are measured by rotameters (flow meters). Control levers determine what proportion of the total flow goes through the bottle. A rod raises or lowers the hood.

This is a simple anaesthetic apparatus design by Edmond Boyle. He was commonly known as “Cookie”. In place of ether vaporizer (as shown in the figure) these days other vaporizers such as halothane, isoflurane, sevoflurane etc are installed.

Components of Anaesthesia Machine:

- Gas inlets receive medical gases from attached cylinders or hospital’s gas delivery system.

 Pressure regulators reduce gas pressure.

 Oxygen-Pressure failure devices signals low oxygen pressure.

 A fresh gas out-let delivers the final gas composition to the breathing circuit.

2. CYLINDERS.

Cylinders are constructed from molybdenum steel.

Cylinders are tested hydraulically every 5 years to ensure that they can withstand hydraulic pressures considerably in excess of those to which they are subjected in normal use & the tests recorded by a mark stamped on the neck of the shoulder. Gas cylinders are tested by

I) Tensile test.

II) Flattening, impact & band tests. III) Hydraulic or pressure test.

Filling ratio of a cylinder is the ratio of weight of gas in the cylinders to weight of water the cylinder could hold. Great care is taken that the gases are free from water vapours, otherwise when the cylinder is opened, temperature fall & water vapours would freeze & block the exit valve.

Cylinder are identified

by:-i. Size of cylinder e.g. oxygen cylinder are 6 different sizes C,D,E,F,G,J, & N2O cylinders are 5 different sizes C,D,E,F,G

ii. Colour Codes

a. N2O cylinder has Blue body & Shoulder.

b. O2 cylinder carries black body & white shoulder.

c. CO2 cylinder has grey body & shoulder.

iii.Pin Index System is a device to prevent interchangeability of

cylinders of different gases. The pegs on the inlet connection slot into corresponding holes (pits) on the cylinder valve.

e.g. position of pit on cylinders:

O2 --- 2, 5

N2O --- 3, 5

CO2 --- 1, 6

Different gas cylinders carry different pressures e.g. O2 cylinder

pressure is 137 bars N2O cylinder pressure is 44 bar at 15C.

Cylinder valves should be opened slowly to prevent sudden surges of pressure & should be closed with no more force that is necessary otherwise valve seating may be damaged.

3. VAPORIZERS

Definition: - A vaporizer is a device for adding clinically useful

concentration of anaesthetic vapours to a stream of carrier gas.

Types:-i. Drawover vaporizers: In this type of

vaporizers, gas is pulled through the vaporizer when the patient inspires, creating a

subatmospheric pressure.

Resistance to gas flow through a draw over vaporizer must be extremely small.

ii. Plenum Vaporizers : - In this type of vaporizers

gas is forced through the vaporizer by the pressure of fresh gas supply.

Resistance of plenum vaporizers may be high enough to prevent its use as draw over vaporizers.

Principles of both devices are similar. All the anaesthetic gas entering the vaporizer passes through the anaesthetic liquid and becomes saturated with vapour. 1 ml of liquid anaesthetic is equivalent of approximately 200ml of anaesthetic vapors.

Concentration of anaesthetic in the gas mixture emerging from the outlet port is dependent

upon:- Saturated Vapour Pressure of the anaesthetic liquid in the vaporizer.

 Temperature of liquid anaesthetic agent, as this determines its saturated vapour pressure.

 Splitting ratio i.e. the flow rate of gas through the vaporizer chamber in comparison with that through by-pass.

 Surface area of anaesthetic agent in the vaporizer.

 Duration of use as the liquid in the vaporizing chamber evaporate, its temperature falls & thus its saturated vapour pressure decreases. This leads to reduction in concentration of anaesthetic in mixture leaving the exit port.

 Nature of liquid

 Fresh gas flow

Q2: WRITE SHORT NOTE ON ENDOTRACHEAL TUBES?

There are many designs of endotracheal tubes. The general considerations determining their construction as follow.

MATERIAL Red rubber

- Relatively irritant, and not ideal for prolonged Intubation

- Firm/curvature predetermined - May transmit infection

Plastic (PVC)

- Disposable

- Non-irritant (implantation-tested) - Moulds to body contours at 37C CUFFS

Red rubber cuffs are firm and rounded so that a seal between the endotracheal tube and the trachea exists over small areas. The mucosa is likely to be damaged, not only because of the chemical irritants but also because of compression, and hence hypoxia, of the mucosa.

PVC tubes have cuffs of varying shapes. The shape of the cuff can be more cylindrical, thus, by increasing the area of seal, there is a reduction in the pressure necessary in the cuff.

The seal between tracheal mucosa and endotracheal tube is required to prevent the escape of gas (during IIPV) and also to prevent the aspiration of saliva or gastric contents into the tracheobronchial tree.

Age/4 + 4.5 is the accepted formula for determining the size (mm) of the endotracheal tube, for a child.

The length of the tube for a child is determined by: Age/2 + 12 cm (oral)

Age/2 + 15 cm (nasal)

Q3: WRITE A SHORT NOTE ON LARYNGOSCOPES

LARYNGOSCOPES

These are the instruments to see larynx.

There are many designs for use, depending on requirement: 1. NEONATAL – STRAIGHT BLADE

The epiglottis is relatively large and floppy; a straight blade is necessary to flatten and hold the epiglottis forward to allow the cords to be visualised.

2. INFANT–STRAIGHT OR CURVED BLADE

The tongue of the infant is large in relation to the buccal cavity and blade design is aimed at keeping it out of the way. Blades which are almost tubular are used in infants with tissue flaps associated with palatal defects. The most commonly used paediatric laryngoscopes are the Anderson, Magill and the Robertshaw.

Fig: HOW TO USE A LARYNGOSCOPE. (A) Insert the laryngoscope with your wrist straight, then extend your wrist. (B) Finally, lift the patient’s jaw forwards. (C)The secret of success is to have the patient’s head extended on his neck before you begin. (D) and to have his neck flexed forwards. (E). Arrange the pillow under his neck and shoulders so that you can achieve this. This has been likened to the position of “sniffing the morning air”.

3. ADULT – STRAIGHT OR CURVED BLADE

The primary aim is deflection of the tongue from the line of vision of the vocal cords; however, a variety of other problems have been overcome.

a. A laryngoscope with an obtuse angle between the handle and the blade – to facilitate insertion into the mouth of patients with difficult access, e.g. in an iron lung, in severe fixed flexion or in a halo splint for stabilization of the cervical spine.

b. A ‘left – handed blade’ – for use is patients where the right side of the mouth is invaded by tumour, or access is otherwise compromised.

c. The addition of a prism to the blade allows the vocal cords to be visualized when they are not in direct line of sight. d. McCoy Laryngoscope. Resembles a conventional

laryngoscope, but the distal part of the blade is hinged and can be tilted up or down by a lever on the handle. Allows

the larynx to be ‘lifted’ to improve vision in case of difficulty.

4. LARYNGEAL MASK AIRWAY (LMA)

A revolution in airway control. The LMA is inserted into the mouth and advanced until it comes to lie against the posterior pharyngeal wall opposite the larynx. The large cuff is then inflated and this creates a seal around the laryngeal opening. The seal of airway to trachea is not so reliable as when using an endotracheal tube and a number of studies have shown some leakage past the LMA which could potentially enter the trachea. Some doubts have been expressed as to the suitability of the LMA for use during controlled ventilation and for surgery within the mouth and pharynx, e.g., tonsillectomy. Nevertheless, it has been used widely for these situations. Great care must be taken to ensure that airway inflation pressures remain low if using an LMA for controlled ventilation.

5. FIBREOPTIC LARYNGOSCOPE

A thin flexible fibreoptic device that will pass through a tracheal tube. The fiberscope is passed through the nose or mouth (the nose is usually easier) and advanced under direct vision until it lies within the trachea. The tracheal tube, which has been previously slid onto the fiberscope is then advanced using the fiberscope as a guide. The fiberscope is then withdrawn. The use of the fibreoptic laryngoscope requires previous training. It is the safest technique for securing the airway is case of anticipated difficult Intubation and may be performed with the patient awake following local anaesthesia to the airway.

Fig: THE POSITIONS OF PTIENTS OF DIFFERENT AGES DURING INTUBATION. Put the pillow under an adult’s head and neck, but under a child’s back.

LECTURE 2

INHALATIONAL ANAESTHETIC AGENTS

Q: WHAT ARE THE CHARACTERISTICS OF AN IDEAL VOLATILE

ANAESTHETIC AGENT?

The characteristics of an ideal volatile anaesthetic agent are: 1. Non-inflammable, non explosive.

2. Stable physical characteristics.

3. Appropriate volatility, having low boiling point and high SVP. 4. Potent.

5. Cardiovascular and respiratory stability.

6. Low blood-gas solubility giving rapid induction/recovery. 7. Analgesic.

8. Low incidence of nausea and vomiting.

9. Should not sensitize the myocardium to adrenaline. 10. Non-irritant and pleasant smelling.

11. Non-metabolized.

12. Non-hepatotoxic and nephrotoxic. 13. Non-teratogenic.

14. Cheap.

15. No effect on CBF and intracranial pressure or effect easily antagonized by hyperventilation.

Fig: HOLDING THE MASK WITH ONE HAND.

Q:

WHAT IS THE CLASSIFICATION OF INHALATIONAL

ANAESTHETIC AGENTS?

A: VOLATILE ANAESTHETIC AGENTS

1. ETHERS.

 Methoxyflurane (not in use due to its nephrotoxic effects).

 Enflurane.  Isoflurane. 2. HALOGENATED HYDROCARBONS.  Halothane.  Sevoflurane.  Desflurane.

 Chloroform(not used these days due to its toxic effects).

B: GASEOUS ANAESTHETIC AGENTS

2. CYCLOPROPANE (not used these days due to its toxic effects and explosion hazards).

NITROUS OXIDE

Q: HOW IS NITROUS OXIDE PREPARED?

Nitrous oxide is also known as laughing gas. It is prepared commercially by heating Ammonium Nitrate crystals to a temperature of 245-270o_C.

Heat

NH4NO3 ---N2O + H2O

Q: WHAT ARE THE IMPURITIES FORMED ALONG WITH N

O?

The chief impurities

are:- Nitrogen which dilutes the anaesthetic.

 Nitric oxide which combines with hemoglobin to produce anemic type of hypoxia.

 Nitric acid causes pulmonary oedema.

 Nitrogen dioxide which may damage the valves.

 Ammonia.

 Nitrous acid.

Q: HOW IS NITROUS OXIDE STORED?

Nitrous oxide is stored in compressed form as a liquid in blue cylinders at a pressure of 50 bar (5000kPa; 750 lb.in2_{). Because the cylinder}

contains liquid and vapour, the total quantity of nitrous oxide contained in cylinder can be ascertained only by weighing. Nitrous oxide cylinders should be kept in a vertical position during use so that the liquid phase remains at the bottom of the cylinder.

Q: WHAT ARE THE PHYSICAL PROPERTIES OF NITROUS

OXIDE?

 Sweet smelling.

 Non irritating.

 Colorless.

 Non inflammable but supports combustion.

 Formula N2O

 Molecular wt: 44

 Boiling point: -89o_C

 Critical temperature: 36.5o_C

 Critical pressure: 71.7 Atm.

 Blood/gas solubility coefficient: 0.468

 Eliminated unchanged from the body mostly via lungs.

 Stable.

 Not affected by soda lime.

Q: WHAT ARE THE EFFECTS OF NITROUS OXIDE ON VARIOUS

SYSTEMS OF THE BODY?

1. CNS

 Causes CNS depression.

 Paralysis of respiratory and vasoactive centre does not occur.

2. RESPIRATORY SYSTEM

 Respiration is stimulated (both depth and rate).

 Reduces the MAC of volatile anaesthetics by about 50%.

3. MUSCULAR SYSTEM

 Depression of skeletal system is minimal.

4. MISCELLANEOUS

 No effect on kidney or liver function.

 Crosses placental barrier but does not cause respiratory depression in fetus.

Q: WHAT ARE THE SIDE EFFECTS OF NITROUS OXIDE?

 May cause exhilaration and euphoria during induction.

 Unpleasant hallucinations and dysphoria can occur.

 Continual use for days or weeks may cause neutropenia or macrocytic anaemia.

 Interferes with nucleic acid synthesis.

 Diffuses into cavities and cause otological disturbances in middle ear.

 Prolonged use can lead to bone marrow depression and teratogenic effect.

 Respiratory depression and diffusion hypoxia.

 Pollution problem.

 Expensive.

 Difficulties of cylinder transport.

HALOTHANE

Q: WRITE A SHORT NOTE ABOUT THE CHEMISTRY AND

PHYSICAL

PROPERTIES OF HALOTHANE?

Halothane is 2-bromo-2-chloro-1, 1, 1-triflouroethane. Its formula is CI F

 

H--- C --- C ---F  

Br F The physical properties are:-

 Halogenated hydrocarbon.

 Non inflammable and non explosive.

 Colourless and sweet smelling.

 Unstable in light.

 Stored in amber coloured bottles with thymol as preservative.

 Mol. wt: 197

 Boiling point: 50.2o_C

 L.H.V: 35.2 Calories/gm

 Blood gas solubility: 2.5 at 37o_C

 MAC: 0.75 V %

Q: WRITE DOWN BRIEFLY THE EFFECTS OF HALOTHANE ON

VARIOUS ORGAN SYSTEMS?

CVS:

 Blocks sympathetic ganglion

 Increases vagal tone causing bradycardia

 Direct myocardial depressant effect.

 Direct depressant of vasomotor center.

 Increases impulse discharge from baroreceptors.

 Depresses S-A node.

 Direct depressant of vasculature of smooth muscles.

 Dose dependent hypotension due to decreased cardiac output and lowered peripheral resistance.

 Sensitizes heart to arrhythmic effects of adrenaline.

 Coronary artery vasodilator.

CNS

 Increases the CSF pressure and cerebral blood flow.

 Blunts autoregulation of cerebral blood pressure.

 Not a very good analgesic.

RESPIRATORY SYSTEM

 Depresses respiration with shallow rapid breathing.

 Rate increases with depth of anaesthesia.

 Bronchodilator.

 Increases apneic threshold.

 Hypoxic drive depressed.

 Attenuates airway reflex.

 Depresses clearance of mucous secretions from respiratory tract.

MUSCULAR SYSTEM

 Potentiates the effect of non depolarizing muscle relaxant.

 Moderate relaxation.

 Triggering agent for malignant hyperpyrexia.

UTERUS

LIVER

 Halothane hepatitis.

 Decreases hepatic blood flow.

 Slows down the metabolism of drugs like fentanyl, phenytoin, verapamil.

HORMONAL EFFECTS

 Increase in growth hormone, serum thyroxine.

 Sensitivity to insulin is increased.

BODY TEMPERATURE

 Causes 1o _{C drop of esophageal temperature and 4}o _{C rise of skin}

temperature.

MISCELLANEOUS

HALOTHANE SHAKES: recovery from halothane is sometimes associated with restlessness or shivering. Cover with blankets and ensure adequate oxygenation.

Q: WHAT ARE THE CONTRAINDICATIONS TO THE USE OF

HALOTHANE?

 Patient with hepatic dysfunction.

 Patient with increased intracranial pressure.

 Patient having history of malignant hyperpyrexia.

 Patients with hypovolaemia and severe cardiac disease such as aortic stenosis.

ENFLURANE

Q: WRITE A SHORT NOTE ABOUT THE CHEMISTRY AND

PHYSICAL

PROPERTIES OF ENFLURANE.

Enflurane is defluoro methyl ether of 1, 1, 2 trifluro-2-Chloroethane.

F F F

  

H --- C ---- O --- C --- C --- H

  

F E CI

are:- Stable, colourless without added chemical stabilizers.

 Non inflammable, non explosive.

 Pleasant ethereal smell.

 Does not decompose when circulated with oxygen and water vapours through warm soda lime.

 Blood/gas solubility coefficient: 1.8

 MAC: 1.7%

 Boiling point: 56oC

 SVP: 175 mmHg at 20oC

Q: WHAT ARE THE EFFECTS OF ENFLURANE ON VARIOUS

ORGAN SYSTEMS?

CVS

 Dose dependant depression of myocardial contractility.

 Reduction in cardiac output.

 Less likely to sensitise the heart to adrenaline.

 Dose dependant reduction in arterial pressure.

 No central vagal effect.

 Hypotension leads to reflex tachycardia.

 Preferable to halothane during surgery involving pheochromocytomas and other tumours associated with excessive secretion of catecholamines.

RESPIRATORY SYSTEM

 Non irritant.

 Does not increase salivary or bronchial secretions.

 Dose dependant depression of alveolar ventilation with reduction in tidal volume and an increase in ventilatory rate.

 Pharyngeal and laryngeal reflexes are diminished quickly.

UTERUS

Dose related relaxation of uterine muscle.

CNS

 Dose dependant depression of EEG activity.

 Produces epileptiform spike activity.

 Twitching of face and arm muscles.

 Avoided in epileptic patients.

Enhances the effect of non-depolarizing muscle relaxants.

Q: WHAT ARE THE INDICATIONS FOR THE USE OF

ENFLURANE?

 For induction and maintenance of general anaesthesia.

 For dental anaesthesia in view of rapidity of action and recovery with stability of cardiovascular system.

ISOFLURANE

Q: WHAT IS THE FORMULA AND THE MAJOR PHYSICAL

CHARACTERISTICS OF ISOFLURANE?

Isoflurane, which is 1-chloro-2, 2, 2-triflouroethyl diflouromethyl ether, is an isomer of enflurane. Its formula is

F H F

  

H --- C --- C --- O --- C --- H

  

F CI F

Its physical properties include

 Colorless, volatile anaesthetic

 Slightly pungent odour

 Does not require preservatives

 Non inflammable

 Vapor pressure 240 mmHg at 20o_C

 MAC 1.2

 Blood/gas partition coefficient 1.4

Q: WHAT ARE THE EFFECTS OF ISOFLURANE ON VARIOUS

ORGAN SYSTEMS?

RESPIRATORY SYSTEM

 Dose dependant depression of ventilation.

 Decrease in tidal volume with increase in ventilatory rate.

 Blunts response to hypoxia and hypercapnia.

 Bronchodilator.

CVS

 Myocardial depressant but less depression of cardiac output than halothane potent peripheral vascular dilator.

 Systemic hypotension due to reduction in systemic vascular resistance coronary vasodilatation leading to Coronary Steal Syndrome.

 Does not sensitize the myocardium to catecholamines.

 High inspired concentrations, Minimum Alveolar Concentration (MAC) > 1 lead to vasodilatation, an increased cerebral blood flow and intracranial pressure.

 No seizure activity on EEG.

 Does not blunt autoregulation.

 Decreases CMRO2 (Cerebral Metabolic Rate of Oxygen

consumption).

MUSCULAR SYSTEM

 Dose dependant depression of neuromuscular transmission with potentiation of non depolarizing neuromuscular blocking drugs.

RENAL

 Decreases renal blood flow, GFR and urine output.

HEPATIC

 Total hepatic blood flow is decreased but to lesser extent than halothane

 LFT’s minimally affected.

Q: WRITE SHORT NOTE ON SEVOFLURANE.

SEVOFLURANE

This is non-flammable ether. It is devoid of significant cardio/respiratory side-effects. The major advantage is that its very low blood: gas solubility coefficient (0.6) allows its use for rapid face mask induction of anaesthesia, especially in children. It is in wide clinical use in Japan.

It is 3% metabolised.

 MAC 2.0

 Blood: gas solubility at 37C 0.65

 Boiling point 58.5C

 Saturated vapour pressure at 20C 170

mmHg

Q: WRITE SHORT NOTE ON DESFLURANE

DESFLURANE

Desflurane is also halogenated ether and is licensed for use in Europe and North America. It is not unpleasant to inhale and is non-irritant to the respiratory tract at low concentrations. It has a very low blood; gas

solubility (0.42) and is thus associated with short induction and wake-up times. It is 0.02% metabolised.

 MAC 6.0

 Blood: gas solubility at 37C 0.45

 Boiling point 22.8C

 Saturated vapour pressure at 20C 66 mmHg

Both these agents are expensive to produce. They offer advantages over other anaesthetic vapours but sevoflurane produces a toxic product on contact with soda-lime whilst desflurane increases heart rate and is a respiratory irritant at concentrations > 1MAC.

LECTURE 3

INTRAVENOUS ANAESTHETIC AGENTS

Q: DEFINE INTRAVENOUS ANAESTHETIC AGENTS?

I/V anaesthetic agents may be defined as “drugs that will induce loss of consciousness in one arm brain circulation time when given in appropriate dosage”.

Q: NAME THE COMMON INTRAVENOUS AGENTS.

Common I/V anaesthetic agents include: 1. Thiopentone sodium

2. Ketamine.

3. Propofol. 4. Etomidate. 5. Methohexitone.

Q: WRITE A SHORT NOTE ON THIOPENTONE?

It is the most commonly used I/V anaesthetic agent. It is usually used for induction of anaesthesia. It is a sodium salt of barbituric acid and is the sulphur analogue of pentobarbitone. The 2.5% solution, which is commonly prepared, has a pH of 10.5.

 It produces anaesthesia usually in less than 30 sec. after i/v injection.

 Duration of action is 5 – 10 min.

 Myocardial contractility is depressed and peripheral vasodilatation occurs, which leads to Hypotension.

 Ventilatory drive is decreased and a short period of apnoea is common, preceded by a few deep breaths.

 Skeletal muscle tone is reduced due to suppression of spinal cord reflexes.

 Intraocular Pressure (IOP) is reduced by 40%

 Antanalgesic

 If injected accidentally in the artery it will cause sever pain in the fingers. One should keep the needle in-situ and inject papaverine (Vasodilator) and local anaesthetic procaine to relief pain.

Induction of anaesthesia, Maintenance of anaesthesia, Basal narcosis by rectal administration, Status epilepticus, Reduction of intracranial pressure.

ABSOLUTE CONTRAINDICATIONS:

 Airway obstruction.

 Porphyria

 Previous hypersensitivity reaction.

DOSE:

 3 – 5 mg/kg body weight as 2.5% solution.

Q: WRITE A SHORT NOTE ON KETAMINE?

This is a phencyclidine derivative. It produces dissociative anaesthesia.

 After i.v. injection it induces anaesthesia in 30 – 60 sec. duration of action is 10 – 15 min. After i.m. injection the effect starts within 3-4 min. and duration of action is 15 – 25 min.

 There may be emergence delirium, restlessness, disorientation, nightmares and hallucinations.

 Arterial pressure increases by up to 25%.

 Heart rate increases by upto 20%. Myocardial oxygen demand also increases.

 Transient apnoea may occur after i.v. injection, but ventilation is well maintained thereafter.

 Pharyngeal and laryngeal reflexes and a patent airway are well maintained.

 Muscle tone is increased & spontaneous movements may occur.

 IOP increases.

Dosage:

 2-mg/kg i.v. for induction.

 1 – 1.5 mg/kg for maintenance.

 8 – 10-mg/kg i.m.

PROPOFOL

2, 6, di-isopropylphenol: 1% solution in egg white lecithin emulsion.

Q: WHAT ARE THE PHYSICAL PROPERTIES AND

PRESENTATION?

Propofol is extremely lipid soluble, but almost insoluble in water. It is formulated in a white, aqueous emulsion containing soybean oil and purified egg phosphatide.

Q: WHAT ARE THE PHARMACOKINETICS OF PROPOFOL?

 Distributed rapidly

 Termination of action occurs by redistribution

 Metabolized at both hepatic and extra hepatic sites

 Very high clearance

 Excretion through kidneys

Q: WHAT IS THE DOSE OF PROPOFOL?

 2-3 mg/kg IV induction

 100-200 μg/kg/min maintenance

 Sedation: 25-100 μg/kg/min

Q: WHAT ARE THE PHARMACOLOGIC ACTIONS OF

PROPOFOL?

CNS

EEG frequency decreases and amplitude increases

Cerebral blood flow, intracranial pressure and cerebral metabolic oxygen demand decreases

May have anticonvulsant effect Occasional excitatory activity

CVS

Venous dilatation, decreased peripheral resistance and cardiac depression lead to hypotension

Heart rate may increase

RESPIRATORY

Decreased rate and tidal volume

Depression of laryngeal reflexes more than barbiturate

HEPATIC

None

RENAL

Decreased cardiac output may decrease renal blood flow

MISCELLANEOUS

Less postoperative nausea than barbiturates Possible antipruritic effect at low dose

Q: WHAT ARE THE ADVERSE EFFECTS?

1. Very low incidence of anaphylaxis 2. Caution if lipid disorder present 3. Cardiovascular depression 4. Respiratory depression 5. Excitatory phenomena 6. Pain on injection

LECTURE 4

MUSCLE RELAXANTS

Q:

CLASSIFY MUSCLE RELAXANTS.

Muscle relaxants are classified as:

1. Depolarizing Muscle Relaxants

 Succinyl choline (commonly used)

 Decamethonium

2. Non-Depolarizing Muscle Relaxants.

 Long Acting

 Tubocurarine  Doxacurium

 Pancuronium (commonly used)

 Gallamine (not used due to its ganglion blocking effects)  Intermediate Acting

 Atracurium (commonly used)  Vecuronium

 Rocuronium  Short Acting

 Mivacurium

Q:

WHAT ARE THE SALIENT FEATURES OF

NON-DEPOLARIZING

MUSCLE BLOCK?

1. Do not cause muscle fasciculation. 2. Very hydrophilic.

3. Relatively slow onset.

4. Reversed by neostigmine and other anticholinesterases. 5. Effects reduced by acetylcholine and adrenaline.

6. Potentiated by volatile agents, Mg2, and hypokalemia.

7. Mild cooling antagonizes their effects.

Q:

WHAT ARE THE SALIENT FEATURES OF DEPOLARIZING

MUSCLE BLOCKING DRUGS?

1. Cause muscle fasciculation’s but not in myasthenia gravis.

2. Repolarization is interfered with; the resting membrane potential is held up until phase II block develops, when it returns to -70 mV.

3. Not reversed with neostigmine and other anticholinesterases. 4. potentiated with isoflurane, enflurane, Ach, respiratory alkalosis,

hypothermia and Mg2+_.

5. Antagonized by ether, halothane, acidosis and non-depolarizing relaxants.

6. Fast dissociation constants at receptor.

Q:

WHAT CLINICAL SIGNS INDICATE THE NEED OF MORE

RELAXANT

DURING SURGERY?

1. Hiccup, due to contraction of periphery of the diaphragm. 2. Rigidity of abdominal wall.

3. Increased resistance to inflation of lung. 4. Bucking or coughing on tracheal tube. 5. As indicated by neuromuscular monitoring.

Q:

WHAT ARE THE CLINICAL SIGNS OF INCOMPLETE

REVERSAL?

1. Shallow respiration. 2. Jerky respiration.

3. “Tracheal tug” and “see-saw” respiration where, as the abdomen moves out, the chest moves in.

4. Cyanosis.

5. A restless, frightened, struggling patient, who says that he or she cannot breathe.

6. Diplopia.

7. Inability to raise head or extrude tongue.

Q:

WRITE A SHORT NOTE ON ATRACURIUM?

ATRACURIUM

Physical structure:

It is an isoquinolon compound belonging to quaternary group.

Pharmacokinetics:

Distribution: Throughout ECF.

Metabolism: Hoffmann degradation.

Alkaline ester hydrolysis in plasma.

Pharmacodynamics:

Dose: 0.5-mg/kg i.v. as bolus dose.

Top ups 0.3- 0.1mg/kg i.v.

Neonates are slightly more resistant so dose is 0.3 mg/kg.

Speed of onset: 1-2 min. Duration: 20-40 min .

Reversed with: neostigmine.

Side effects and clinical considerations

1. Release of histamine.

2. Hypotension and tachycardia, if given in excess of 0.5mg/kg bronchospasm so avoid in patients with bronchial asthma.

3. Laudanosine, a breakdown product of Hoffmann degradation, is epileptogenic.

4. Duration of action can be markedly prolonged in hypothermia and acidotic patients.

5. Atracurium precipitates as a free acid if given into an i.v. line containing an alkaline solution such as thiopentone.

Q:

WRITE A SHORT NOTE ON PANCURONIUM?

Physical structure:

It is a long acting quaternary amino-steroid, devoid of hormonal activity. It resembles two acetylcholine molecules bound together.

Pharmacokinetics:

 Strongly bound to gamma globulin and moderately bound to albumin.

 Metabolized by deacytylation in liver to limited degree.

 Excretion primarily through kidney (40%) but 10% is cleared through bile.

 Patients with renal failure show prolonged block.

 Patients with cirrhosis require increased loading dose due to large volume of distribution but decreased maintenance dose due to decreased plasma clearance.

Dose:

0.05mg/kg i.v. bolus. Duration: 40-60 min.

1. Can cause stimulation of the myocardium with rise in pulse rate and blood pressure.

2. Vagal blockade and catecholamines release. 3. Increased incidence of ventricular dysrythmias. 4. Releases histamine from tissues.

5. Should be avoided in renal failure and total biliary obstruction.

Q: WHAT IS SUXAMETHONIUM AND WHAT IS ITS

PHARMACOKINETICS?

Suxamethonium is a dicholine ester of succinic acid. It belongs to quaternary ammonium group.

Pharmacokinetics:

Absorption: I/V, I/M or S/C.

Distribution: throughout the ECF and slightly through the

placenta.

Metabolism: hydrolysis by plasma cholinesterases. Dose: 1-1.5 mg/kg Duration: 10-15 min.

Q: WHAT ABNORMALITIES CAN OCCUR IN SUXAMETHONIUM

METABOLISM, WHICH CAN PROLONG ITS DURATION OF

ACTION?

1. Abnormal plasma cholinesterase (inherited)

 Atypical cholinesterase.

 Fluoride resistant cholinesterase.

 Silent gene.

2. Plasma cholinesterases deficiency:

 Acquired

 After X-ray therapy

 After organophosphorous poisoning  In hyperpyrexia  In cardiac failure  Uraemia  Hypoproteinemia  Myasthenia gravis  Pregnancy  Myxoedema  Asthma  Obesity

 Following treatment with: cyclophosphamide, ecothiopate, ketamine, pancuronium, MAO inhibitors, and oral contraceptives.

 Congenital

3. Plasma cholinesterase Antagonism: by anticholinesterases

such as neostigmine.

Q: WHAT ARE THE SIDE EFFECTS OF SUXAMETHONIUM.

The commonest causes are:

 Atypical serum cholinesterases.

 Dehydration and electrolyte imbalance.

 An overdose of muscle relaxant.

 A low serum cholinesterase level in blood.

 An excessive formation of succinyl monocholine.

 Dual block.

The management includes

 Artificial ventilation and sedation are maintained until monitoring shows that the block has worn off.

 A blood sample is taken for cholinesterase analysis.

 Fresh frozen plasma given.

2. HYPERKALEMIA

A rise in serum potassium of 0.2-0.4 mmol/l occurs due to release from muscle, especially in burn patients.

3. RAISED INTRA-OCCULAR PRESSURE

Suxamethonium, 1 mg/kg, raises the pressure an average of 7 mm Hg.

4. MUSCLE PAIN

More frequent in women and middle-aged patients.

5. RAISED INTRAGASTRIC PRESSURE 6. MALIGNANT HYPERPYREXIA

Incidence is 1 in 100000 adults.

7. EXACERBATES DYSTROPHIA MYOTONIA

8. DIRECT MYOCARDIAL DEPRESSANT LEADING TO BRADYCARDIA AND CARDIAC ARREST

9. MUSCARINIC EFFECTS 10. ANAPHYLAXIS

Q: WHAT ARE THE INDICATIONS FOR USE OF

SUXAMETHONIUM?

 Endotracheal intubation.

 ECT.

 Short orthopaedic procedures.

 Short surgical procedures.

Q: WHAT ARE THE CONTRA-INDICATIONS TO THE USE OF

SUXAMETHONIUM?

 Hyperkalemia.

 Known case of atypical pseudocholinesterase.

 Hypersensitivity.

 In patients with increased intraocular pressure.

LECTURE 5

LOCAL ANAESTHETIC AGENTS

Q: WHAT ARE LOCAL ANAESTHETIC AGENTS?

Local anaesthetics cause reversible blockade of peripheral nerve conduction or inhibition of excitation at nerve endings with resultant loss of sensation in the particular area of the body.

Q: HOW DO YOU CLASSIFY LOCAL ANAESTHETIC AGENTS.

A) ACCORDING TO STRUCTURE 1. HAVING ESTER LINKAGE

 Chloroprocaine

 Cocaine

 Procaine

 Tetracaine

2. HAVING AMIDE LINKAGE

 Lignocaine

 Bupivacaine

 Etidocaine

 Cinchocaine

B) ACCORDING TO POTENCY

1. LOW POTENCY AND SHORT DURATION

 Procaine

 Chloroprocaine

2. INTERMEDIATE POTENCY AND DURATION

 Mepivacaine

 Prilocaine

 Lignocaine

3. HIGH POTENCY AND LONG DURATION

 Tetracaine

 Bupivacaine

Q: WHAT IS THE SITE OF ACTION OF LOCAL ANAESTHETIC

AGENTS?

The site of action of local anesthetics drugs is at the surface membrane of cells of excitable tissues. In a myelinated nerve the site of action is the node of Ranvier.

Q: WHAT IS DIFFERENTIAL BLOCK?

The minimum concentration of local anaesthetic drug necessary to cause block of a nerve fiber of given diameter is known as the Cm. The thicker the diameter of a nerve fibre the greatest the Cm required. In practice the sequence of blockade is autonomic, sensory, and finally motor block according to fibre diameter.

Q: WHAT DOES THE UPTAKE OF LOCAL ANAESTHETICS

DEPEND UPON?

Local anaesthetic drugs are lipid-soluble bases, which act by

penetrating lipo-protein cell membranes in the non-ionized state. The blocking quality of a local anaesthetic drug depends on its:

- Potency.

 Latency (time between its injection and maximum effect) – this in turn depends on nerve diameter, local pH, diffusion rate and concentration of local drug.

 Duration of action.

 Regression time (time between commencement and completion of pain appreciation).

Q: WHAT FACTORS INFLUENCE LOCAL ANAESTHETIC

TOXICITY?

 Quantity of solution.

 Concentration of drug.

 Presence or absence of adrenaline.

 Vascularity of site of injection.

 Rate of absorption of drug.

 Rate of metabolism of drug.

 Hypersensitivity of patient.

Q: WHAT ARE THE SIGNS OF TOXICITY IN VARIOUS ORGAN

SYSTEMS?

CENTRAL NERVOUS SYSTEM

 Central stimulation followed by depression.

 Restlessness.  Hysterical behaviour.  Vertigo.  Tremors.  Convulsions.  Respiratory failure.

Treatment:- Artificial ventilation with O2 or air.

 Intravenous injection of Suxamethonium or just sufficient Thiopentone to control convulsions (10-150 mg).

 Diazepam.

CARDIOVASCULAR SYSTEM

 Hypotension.

 Acute collapse – primary cardiac failure, feeble pulse and cardiovascular collapse, bradycardia, pallor, sweating and hypotension.

Treatment:- Elevate legs.

 Give oxygen by IPPV.

 Rapid intravenous infusion.

 Raise blood pressure.

 Cardiac massage.

RESPIRATORY SYSTEM

 Apnoea.

 Medullary depression.

 Respiratory muscle paralysis.

ALLERGIC PHENOMENA

 Bronchospasm.

 Urticaria.

 Angioneurotic oedema.

Q: HOW CAN YOU IMPORVE DURATION AND QUALITY OF

LOCAL

ANAESTHETIC?

 Addition of adrenaline, 1:200 000 to 1:500 000 solution.

 Injection closer to nerve.

 The amount of free base.

 Adjusting the pH to about 7.

Q: WHAT ARE THE DIFFERENT METHODS OF LOCAL

ANESTHESIA?

 Simple topical application at operative site.

 Infiltration analgesia to abolish pain.

 Field block.

 Nerve block (conduction anaesthesia).

 Refrigeration analgesia (Cryoanalgesia).

 Intravenous local analgesia.

 Central neural blockade.

Q: WHAT IS THE MAXIMUM DOSE OF LOCAL ANAESTHETICS?

Lignocaine 3 to 7 (with adrenaline)

Bupivacaine 2.5

Lecture 6

REGIONAL ANAESTHESIA

Q:

What is the anatomy of spinal cord?

Spinal cord is a part of CNS, extending from foramen magnum to lower border of L1 or upper border of L2 in adults and L3 L4 in children. It is

covered by fibro fatty tissue known as meninges. It consists of grey mater and white mater which represent ascending and descending tracts. There are 8 cervical. 12 thoracic, 5 lumbar and 5 sacral spinal nerves.

SPINAL ANAESTHESIA

Q: DEFINE SPINAL ANAESTHESIA?

Spinal anaesthesia is a type of regional block in which local anaesthetic is injected into the subarachnoid space. It causes major conduction block, which refers to blockade of spinal nerve roots. The resultant nerve block provides surgical anaesthesia as far cephalad as upper abdomen.

Q:

WHAT ARE THE INDICATIONS OF SPINAL ANAESTHESIA?

Indications

are:-i) Lower abdominal surgery e.g. Cesarean Section, Herniotomy, Transvesical prostatectomy, TURP, Cystoscopies etc.

ii) Perineal surgery e.g. haemorrhoidectomy, fistulectomy, TURP, cystoscopies etc.

iii) Lower limb surgery e.g. Arthroscopy, amputation, open reduction internal fixation (ORIF) of fractures etc.

Q:

AT WHICH LEVELS THE BLOCK IS PERFORMED?

A typical subarachnoid block is performed in the lumbar region below the level of spinal cord i.e. L 3-4 in children and L2-3 in adults.

Q:

WHICH STRUCTURES ARE PIERCED WHILE PERFORMING

THE BLOCK?

forward:-i) Skin and subcutaneous tissues ii) Supraspinous ligament

iii) Interspinous ligament iv) Ligamentum Flavum v) Durmamater

vi) Arachnoid mater

Fig: EQUIPMENT FOR EPIDURAL AND SUBARACHNOID ANAESTHESIA.

Q:

WHAT ARE THE COMPLICATIONS OF SPINAL

Complications are:-i) Hypotension.

ii) Post dural puncture headache (PDPH). iii) Nausea and vomiting.

iv) Meningitis.

v) Urinary retention.

Q:

WHICH AGENTS ARE COMMONLY USED?

Agents commonly used are:-i) Inj. Lignocaine 2%. ii) Inj. Bupivacaine 0.5%. iii) Inj. Bupivacaine 0.75%.

Q:

WHAT ARE THE CONTRAINDICATIONS OF SPINAL

ANAESTHESIA?

Contraindications

are:-i) Patient’s disapproval.

ii) Infection at the injection site. iii) Increased intracranial pressure. iv) Coagulopathy.

v) Meningitis.

vi) Hypovolaemia and Hypotension. vii) Valvular heart disease.

EPIDURAL ANAESTHESIA

Q:

WHAT IS EPIDURAL ANAESTHESIA?

In Epidural Anaesthesia local anaesthetics are injected in the epidural space. The epidural space lies just outside the dural sac, where there is a negative pressure. The structures pierced by epidural

needle:- Skin.

 Subcutaneous fat.

 Supraspinous ligament.

 Interspinous ligament.

 Ligamentum Flavum, and then is the epidural space.

Q:

DESCRIBE THE ANATOMY OF EPIDURAL SPACE?

Superiorly: closed at foramen magnum.

Inferiorly: closed at sacro-cocccygeal membrane.

Anteriorly: posterior longitudinal ligaments, vertebral bodies.

Posteriorly: vertebral lamina and Ligamentum Flavum. Laterally: open, pedicles and intervertebral foramina

Shape: Triangular, with apex posteriorly.

Contents: Veins, arteries, fat, lymphatic, nerve roots and dural cuffs.

Fig: LUMBAR EPIDURAL ANAESTHESIA. Notice how the anaesthetist’s right hand rests against the patient’s back to support the needle.

Q:

DIFFERENTIATE BETWEEN SPINAL AND EPIDURAL

ANAESTHESIA?

In spinal

anaesthetic:- A small amount of local anaesthetic drug is placed directly in the CSF producing a total neural blockade caudal to the injection site.

 Ten-fold increase in dose of local anaesthetic (in comparison to spinal) is required to fill the potential epidural space.

 The onset is slower.

 The anaesthesia is segmental i.e. a band of anaesthesia is produced extending above and below the injection site.

Advantages of epidural anaesthesia:

 Epidural anaesthesia causes less hypotension as compared to spinal anaesthesia. Catheter can be introduced inside the epidural space and drugs can be given repeatedly for post-operative pain relief.

 Epidural analgesia is a popular technique for painless delivery.

 Epidural anaesthesia can be applied at any level of vertebral column by expert hands.

Fig: THE ANATOMY OF EPIDURAL AND SUBARACHNOID ANAESTHESIA. A, the anatomy for lumbar puncture with a patient in the sitting position. B, with the patient in the lying position. The line between his iliac crests passes between his 3rd _{and 4}th _{lumbar spines. C and epidural}

needle goes first through his interspinous ligament and then through his ligamentum flavum before it reaches his extradural space. In this figure his interspinous ligament has been dissected away in the segment through which the needle is passing. For subarachnoid anaesthesia the needle goes further on through his dura and arachnoid mater into his subarachnoid space, which is filled with CSF.

Tuohy’s needle is passed in the intervertebral space, while passing through the skin, supraspinous ligament, interspinous ligament and ligamentum flavum.

Two methods are applied for identification of epidural space.

 Loss Of Resistance (LOR) method, using syringe.

 Hanging drop method.

Q:

WHAT ARE THE CONTRAINDICATIONS OF EPIDURAL

ANAESTHESIA?

Following are the contraindications of epidural

anaesthesia:- Patient’s refusal.

 Sepsis with haemodynamic instability.

 Uncorrected hypovolaemia.

 Coagulopathy.

Q:

WHAT ARE THE COMPLICATIONS OF EPIDURAL

ANAESTHESIA?

These

are:- Hypotension, which can be prevented by fluid preload.

 Intravascular injection of local anaesthetic.

 Dural puncture and total spinal anaesthesia.

 Epidural haematoma.

CAUDAL ANAESTHESIA

Q:

DEFINE CAUDAL ANAESTHESIA?

The sacral epidural is called caudal anaesthesia. In this block local anaesthetic is injected through sacral hiatus into the epidural space. The caudal space is the sacral component of the epidural space, and access is through the sacral hiatus, a midline defect of caudal most aspect of the sacrum. The space is covered by sacrococccygeal ligament.

Fig: CAUDAL EPIDURAL ANAESTHESIA. A, the position of the needle in relation to the sacrum. B, the patient ready for the anaesthetic with a pillow under his pubis. C, making a triangle with the anatomical landmarks. D, injecting.

Q:

WHAT ARE ITS INDICATIONS?

 Surgical and obstetric procedures involving perineum and sacral distributions, such as anorectal region.

 Postoperative pain relief for operations on the lower extremities, perineum, male genitals and lower abdomen.

Q:

WHAT ARE ITS CONTRAINDICATIONS?

Absolute

 Sepsis.

 Bacteremia.

 Skin infection at injection site.

 Severe hypovolaemia.

 Coagulopathy.

 Therapeutic anticoagulation.

 Increased intracranial pressure.

 Lack of consent.

 Sacral decubitus ulcers.

Relative

 Peripheral neuropathy.

 Mini-dose heparin.

 Aspirin or other antiplatelet drugs.

 Certain cardiac lesions.

 Psychologic or emotional instability.

 Morbid obesity.

 Prolonged surgery.

 Surgery of uncertain duration.

Q:

WHAT ARE THE COMPLICATIONS?

 Pain on injection.

 Backache.

 Headache.

 Urinary retention.

 Vascular injury, Nerve injury.

 Rarely in obstetric practice, injury to fetal head when placing the needle.

Q: HOW WOULD YOU GIVE LOCAL BLOCKS FOR THE MOUTH

AND TEETH?

(Following pages are for dental students. The students may practice these local blocks under the supervision of their teachers.)

A tooth and its surrounding gum are innervated from three directions: (1) Its pulp is supplied by a nerve which passes up its root. The gum on (2) its labial and (3) its lingual sides is innervated separately. The tooth socket is partly supplied by the nerve that supplies the root and partly by those that supply the gum. If you are going to remove a patient’s tooth painlessly, you will have to anaesthetize all three sets of nerves.

You can easily anaesthetize a patient’s labial and lingual gums by local infiltration, but instead of blocking his palatal gums close to this teeth, it is easier to block them in his palate. Infiltrating his gums or his palate will at the same time block the nerves that supply most of the roots of his teeth. The exceptions are his lower molars and second premolars. To anaesthetize them you will have to block his inferior alveolar nerve as it enters his mandibular canal.

A patient’s inferior alveolar nerve supplies all the teeth of his lower jaw, so blocking this nerve should make all his lower teeth completely anaesthetic. Unfortunately, anaesthesia is sometimes incomplete, because small accessory branches enter the bone through other foramina and so escape the block. Also, his incisors may not be completely anaesthetized by a single block, because they are innervated from both sides.

ANAESTHETIZING THE TEETH

DRUGS AND EQUIPMENT For all methods, use 0.5% bupivacaine, or

2% lignocaine with or without adrenaline, preferably in 2 ml cartridges. If possible, a 10% lignocaine spray, or 5% lignocaine paste. A dental cartridge type syringe. If necessary, you can use an ordinary one, preferably one with a “Luer-lok”. Use thin needles – 0.323 and 42 mm. A spirit lamp to flame the end of the cartridge which has to be pierced. A pair of straight – nosed pliers, or artery forceps, to remove the broken end of a needle. A decontaminant, such as 0.5% chlorhexidine. Forceps and some pledgets of cotton wool.

GENERAL METHOD

Sedate the patient with diazepam 10 to 20mg. Explain to him what your are going to do. Clean his mucosa with the antiseptic. If possible, spray his mucosa with 10% lignocaine, or apply it as a 5% paste.