Professional Documents
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15 Lectures by Major
15 Lectures by Major
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.
1
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Salim, M.
Basics of pain medicine
1. Pain
2. Medicine
Includes index
616.849-dc22
ISBN: 969-8963-00-6
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2
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.
FORMERLY:
Professor of Anaesthesiology
Army Medical College, Rawalpindi.
Advisor in Anaesthesia
Armed Forces of Pakistan.
3
4
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
Index………………………………………………………..………………………………………………………133
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LECTURE 1
PREOPERATIVE ASSESSMENT
AND PREMEDICATION
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.
14
Q: WHAT PHYSICAL EXAMINATION SHOULD BE DONE BY AN
ANAESTHETIST?
1. Respiratory System:
Cyanosis.
Finger clubbing.
Pattern of breathing.
Mediastinal shift.
Localizing signs.
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.
15
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.
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.
16
Q: WHAT ARE THE EFFECTS OF PRE- EXISTING DURG
THERAPY?
17
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.
18
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.
EQUIPMENT
19
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.
20
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.
21
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. O 2 cylinder
pressure is 137 bars N2O cylinder pressure is 44 bar at 15C.
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:-
22
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:-
ENDOTRACHEAL TUBES
There are many designs of endotracheal tubes. The general
considerations determining their construction as follow.
MATERIAL
Red rubber
- Not normally disposable
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- 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 37C
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.
LARYNGOSCOPES
These are the instruments to see larynx.
There are many designs for use, depending on requirement:
24
25
Fig: INTRODUCING A LARYNGOSCOPE.
26
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”.
27
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.
28
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.
29
LECTURE 2
30
Fig: HOLDING THE MASK WITH ONE HAND.
31
Q: WHAT IS THE CLASSIFICATION OF INHALATIONAL
ANAESTHETIC AGENTS?
NITROUS OXIDE
32
Q: HOW IS NITROUS OXIDE STORED?
Sweet smelling.
Non irritating.
Colorless.
Non inflammable but supports combustion.
Formula N2 O
Molecular wt: 44
Boiling point: -89oC
Critical temperature: 36.5oC
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.
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.
Nausea and vomiting are likely to occur.
33
Crosses placental barrier but does not cause respiratory
depression in fetus.
HALOTHANE
34
Blood gas solubility: 2.5 at 37oC
MAC: 0.75 V %
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
Uterine relaxation and bleeding only in parturient uterus.
35
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 4o 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?
ENFLURANE
F F F
H ----- C ---- O ----- C ----- C ------ H
F E CI
36
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
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.
MUSCLE RELAXATION
37
Enhances the effect of non-depolarizing muscle relaxants.
38
ISOFLURANE
F H F
H ----- C ------ C ----- O ----- C ------ H
F CI F
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.
CNS
39
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.
SEVOFLURANE
MAC 2.0
Blood: gas solubility at 37C 0.65
Boiling point 58.5C
Saturated vapour pressure at 20C 170
mmHg
DESFLURANE
40
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 37C 0.45
Boiling point 22.8C
Saturated vapour pressure at 20C 66
mmHg
41
LECTURE 3
Thiopentone sodium:
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.
INDICATIONS:
42
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.
KETAMINE:
Dosage:
2-mg/kg i.v. for induction.
1 – 1.5 mg/kg for maintenance.
8 – 10-mg/kg i.m.
PROPOFOL
43
2, 6, di-isopropylphenol: 1% solution in egg white lecithin emulsion.
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
Transient apnoea
44
Decreased rate and tidal volume
Depression of laryngeal reflexes more than barbiturate
HEPATIC
None
RENAL
Decreased cardiac output may decrease renal blood flow
MISCELLANEOUS
45
LECTURE 4
MUSCLE RELAXANTS
Tubocurarine
Doxacurium
Pancuronium (commonly used)
Gallamine (not used due to its ganglion blocking effects)
Intermediate Acting
Short Acting
Mivacurium
46
Q: WHAT ARE THE SALIENT FEATURES OF DEPOLARIZING
MUSCLE BLOCKING DRUGS?
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.
ATRACURIUM
Physical structure:
It is an isoquinolon compound belonging to quaternary group.
Pharmacokinetics:
Absorption: from I/M and I/V routes.
47
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.
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.
48
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.
49
Congenital
1. PROLONGED APNOEA:
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
50
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.
Family history of malignant hyperpyrexia.
51
LECTURE 5
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
Etidocaine
52
Q: WHAT IS THE SITE OF ACTION OF LOCAL ANAESTHETIC
AGENTS?
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).
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.
Age, physical status and weight of patient.
53
Q: WHAT ARE THE SIGNS OF TOXICITY IN VARIOUS ORGAN
SYSTEMS?
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.
Cross sensitivity.
54
Q: HOW CAN YOU IMPORVE DURATION AND QUALITY OF
LOCAL ANAESTHETIC?
Remember: 1 ml of 1% lignocaine = 10 mg
55
Lecture 6
REGIONAL ANAESTHESIA
SPINAL ANAESTHESIA
Indications are:-
56
i) Skin and subcutaneous tissues
ii) Supraspinous ligament
iii) Interspinous ligament
iv) Ligamentum Flavum
v) Durmamater
vi) Arachnoid mater
57
Complications are:-
i) Hypotension.
ii) Post dural puncture headache (PDPH).
iii) Nausea and vomiting.
iv) Meningitis.
v) Urinary retention.
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
Boundaries:
58
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.
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.
It gives rapid, dense and predictable anaesthetic effect.
In epidural anaesthesia:-
59
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.
60
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 4th 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.
61
Tuohy’s needle is passed in the intervertebral space, while passing
through the skin, supraspinous ligament, interspinous ligament and
ligamentum flavum.
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
62
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.
63
Q: WHAT ARE ITS INDICATIONS?
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.
Pain on injection.
Backache.
Headache.
Urinary retention.
Vascular injury, Nerve injury.
Rarely in obstetric practice, injury to fetal head when placing the
needle.
Infections.
64
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.
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.
65
After a few seconds stretch his mucous membrane at the site of
the injection and quickly pierce it with the bevel of the needle parallel
to the bone. Inject quickly – there is nothing more painful than a local
dental anaesthetic given slowly.
Once you are through his mucosa, you can pause a little while
you find the landmarks. When your needle is in the right position,
inject. You cannot aspirate with a dental cartridge.
Test for analgesia. If you are going to fill a patient’s tooth, drill its
exposed dentine.. Before pulling it out, test the sensitivity of the gum
around it.
66
Fig: BLOCKING THE LINGUAL AND INFERIOR ALVEOLAR NERVES. A, is an injection which is too lateral
and B is one which is too medial. X, is the initial position for the syringe, and Y, its final position. C, is the position of
your fingers feeling the ascending ramus of the patient’s mandible. D, is the position to aim for , midway between your
two fingers.
LOCAL INFILTRATION
Labially in a patient’s lower jaw. Hold his lip out of the way
so that you can see the sulcus clearly. Insert the needle next the
chosen tooth, so that its point lies against the outside of his mandible,
level with the tip of the root. Inject half a cartridge.
67
Lingually in the lower jaw. Insert the needle a short distance
at the point where the mucosa is reflected off the lingual side of his
alveolus, as in A, Fig. You may have to hold his tongue out of the way
to see the floor of his mouth. Inject about a quarter of a cartridge.
There will be a small swelling, which will quickly disappear.
Try not to enter his mental foramen, because you may injure the
vessels that come out of it, and so cause a large haematoma.
Lingually inject his premolars in the same way as for his lower incisors
and canines.
68
Fig: INFILTRATING THE LOWER GUMS. A, infiltrating the lingual and B, the labial gum.
69
Feel the anterior and posterior borders of the ascending ramus of his
mandible between the thumb and index finger of your left hand, as in
C. Make sure that your index finger is as far up his mandible as it will
go. The tips of your fingers should lie at either end of line QR. Aim at
the mid point between them – usually 2 cm behind point R. Rest the
syringe on the occlusal surfaces of the teeth.
Fig: INFILTRATION ANAESTHESIA FOR THE TEETH. A, when you infiltrate a patient’s gum, put
the needle into his buccal sulcus, make the bevel face his periosteum and inject just outside it.
B, to anaesthetize his palatal gums inject at the point marked “X”. C, infiltrating the palatal
gum of his first molar. D, infiltrating the buccal aspect of his third molar (tuberosity block). E,
infiltrating the gum of his lateral incisor. F, blocking his mental nerve. His mental foramen lies
on a vertical line between his 4th and 5th teeth, and in a young person is half way up his
mandible.
70
The block Now you know the landmarks, put your left index finger into
the patient’s mouth, above his lower third molar, as in the upper
diagram in Fig. you will feel a depression in the bone immediately
above and behind it (retromolar fossa). Behind this you will find a ridge
(the oblique line), on the inner surface of his mandible.
CAUTION! (1) Don’t’ push the needle completely into the patient’s
tissues, if it breaks you will have great difficulty removing it. (2) Before
starting to extract a tooth, press the beak of the forceps hard on both
sides of the tooth. If he feels pain, give him another injection.
71
Fig: INSERTING THE NEEDLE TO BLOCK THE INFERIOR ALVELAR NERVE. Notice the position of the point
of the needle.
72
Lecture 7
FLUID MANAGEMENT
1. HISTORY:-
History of abnormal fluid loss.
History of NPO hours.
2. PHYSICAL EXAMINATION:-
Physical examination is important to assess whether the patient is
suffering from hypovolemia or hypervolemia.
Signs of hypovolemia:-
Skin turgor is lost.
Dry mucous membranes.
Dull sensorium.
Weak peripheral pulses.
Increased pulse rate.
Decreased blood pressure.
Orthostatic changes in pulse and blood pressure.
Urine output less than 0.5 ml/kg/hr.
Late signs of hypervolemia are:-
Tachycardia.
Pulmonary rales.
Cyanosis.
Wheezing.
Pink frothy sputum.
Presacral or pretibial pitting edema.
Increased urinary flow.
3. HAEMODYNAMIC MEASUREMENT:-
73
Body fluid status can be measured by measurement of
CVP (Central Venous Pressure).
PCWP (Pulmonary Capillary Wedge Pressure).
4. LABORATORY EVALUATION:-
Blood:-
Serum haematocrit ---- increases with dehydration.
Arterial pH ---- metabolic acidosis in dehydration.
Serum sodium ---- increases in dehydration.
Serum urea ---- increases in dehydration.
Urea to creatinine ratio ---- 10:1.
Urine:-
Urine specific gravity ---- 1.010.
Urine osmolarity > 650 m. osmol/kg.
Urinary sodium concentration < 20meq/l.
Urinary chloride concentration is decreased.
Crystalloids.
Colloids.
74
Losses that involve both water and electrolyte deficit should
be replaced with isotonic electrolyte solutions.
Antiplatelets effect.
May interfere with blood typing.
May prolong bleeding time.
May cause renal failure.
Mild to severe anaphylactic reactions can occur.
75
GIT secretions.
Sweating.
Insensible loss from skin and respiratory tract.
This is a hypotonic loss and is replaced with solutions such as.
5% Dextrose water with saline.
5% Dextrose water without saline.
Pre-existing deficits
Fluid deficit due to period of fasting before surgery:-
Normal maintenance rate X duration of fast
Abnormal fluid loses
Pre operative bleeding
Vomiting
Diuresis
Diarrhoea
Occult loses
Third spacing
Ascites
Increased insensible losses due to hyperventilation, fever and
sweating
To replace pre-existing deficits fluid should be similar in
composition to the fluid lost.
Surgical fluid losses:-
Blood loss is estimated;
Suction container.
Visual estimation of blood loss.
Sponges 4’’ x 4’’ --- 10 ml.
Laparotomy pads ---- 100 – 150 ml.
Blood loss can be measured by weighing sponges before and after
use and by serial haematocrit and hemoglobin concentrations.
76
Across serosal surface (Ascites).
Into bowel lumen.
Significant loss of lymphatic fluid may occur during extensive
retroperitoneal dissection.
Total 110ml/hr
Paediatric Cases
First 10kg 4ml/kg/hr
Next 10kg 2ml/kg/hr
Then Next 1ml/kg/hr
BLOOD TRANSFUSION
77
Hb % less than 7 gm/dl and / or
Haematocrit less than 21% (in a patient undergoing elective
surgery)
10-20% blood volume loss
1. Infection
a. Viruses
Hepatitis C
Hepatitis B
HIV
Cytomegalovirus
b. Bacteria
Syphilis
c. Protozoa:
Malaria, toxoplasmosis
2. ABO incompatibility
3. Anaphylaxis
4. Adverse transfusion reaction
5. Massive transfusion problems
a. Hyperkalemia: high K+ levels in blood, may be if
transfusion more than 1.5 ml/kg/min.
b. Hypocalcaemia: citrate chelates ionized calcium
c. Hypomagnesaemia
d. Acid-base derangements: initial acidosis becomes alkalosis
as citrate metabolized to bicarbonate
e. Hypothermia
6. Oxygen dissociation curve shifts to the left, so less oxygen is
delivered to the tissue
7. Micro embolism
8. Hyperglycaemia
9. Dilutional thrombocytopenia
10. Dilutional coagulopathy
11. Transfusion-related acute lung injury
78
Red cells last well in refrigerated (4-6 C) stored blood. More than 70%
survive 24 hrs after transfusion. Clotting factors deteriorate
progressively after 24 hrs storage. Citrate-phosphate-dextrose (CPD)
blood contains no functional platelets after 48h. citrate-phosphate –
dextrose blood plus adenine preserves its adenosine triphosphate (ATP)
and 2,3-DPG levels for up to 2 weeks with slow fall thereafter and is
stored for up to 35 days.
In the conscious
1. Headache
2. Precordial or lumbar pain
3. Urticaria or pruritus
4. Burning in limbs
5. Bronchospasm
6. Dyspnoea
7. Tachycardia
8. Restlessness
9. Suffused face
10. Nausea and vomiting
11. Pyrexia and rigors
12. Circulatory collapse
13. Later, haemoglobinaemia, haemoglobinuria and oliguria.
Under anaesthesia
Sometimes not easy to distinguish from the effects of hemorrhage
itself, especially during rapid transfusion > 100 ml/min.
79
Immediate
1. Rapid severe and progressive hypotension
2. Tachycardia
3. General oozing from wound
4. Urticarial rash
5. Bronchospasm, raising airway pressures on intermittent
positive pressure ventilation.
Late
Jaundice and oliguria in 5-10% of these patients. It strongly
resembles anaphylactic reaction and treatment is similar.
The blood unit should be rechecked against blood slip and patient’s
identity bracelet (Patient’s Chart). Blood should be drawn to identify
haemoglobin and coagulation tests.
80
Lecture 8
pH:
It is the negative logarithmic value of H+ concentration
pH= 1/[H+]
Acids:
Substances that produce H+ when dissolved in water.
Acid-Base disorders:
Normal pH of body fluids is 7.36-7.44
Acidosis:
Process that cause acids to accumulate
Acidemia:
Present when pH < 7.36
Alkalosis:
Process that cause base to accumulate
Alkalemia:
Present when pH > 7.44
METABOLIC ACIDOSIS
81
Clinical features:-
Decreased cardiac output
Pulmonary hypertension
Arrhythmias
Kussmaul breathing
Hyperkalaemia
Causes
Overproduction of acids:-
Diabetic ketoacidosis
Lactic acidosis
Exogenous acid:-
Salicylates
Reduced excretion:-
Renal failure
Treatment
Identification of cause and its treatment. If pH < 7.2, measures taken
to restore pH. Sodium bicarbonate can be used for restoration of pH
towards normal.
Bicarbonate requirement: body wt. (in kg) x base deficit x 0.3
METABOLIC ALKALOSIS
Characterized by primary increase in HCO3 and a variable degree of
alkalemia. Compensatory respiratory hypoventilation is very limited
and not effective. For diagnostic point of view, metabolic alkalosis is
divided into:
Chloride responsive
Chloride resistant
Chloride responsive:
Loss of acid
Vomiting
N/G suction
Gastrocolic fistula
Chloride depletion
Diarrhoea
Diuretic abuse
Excessive alkalies
NaHCO3 administration
Chloride resistance
Primary or secondary hyperaldosteronism
Cushing syndrome
Severe hypokalemia
82
Treatment
In chloride responsive alkalosis, administration of saline causes volume
expansion and results in excretion of excess bicarbonate; if K + is
required, it should be given as KCl. In patients to whom volume is
administered, the use of acetazolamide results in renal loss of HCO 3
and an improvement in pH.
In life threatening metabolic alkalosis, rapid correction is necessary
and may be achieved by administration of H+ in the form of dilute HCl.
Acid is given as 0.1 normal HCl in glucose 5 % at a rate no more than
0.2 mmol/kg/hr.
RESPIRATORY ACIDOSIS
Characterized by an increase in CO2, which results in acidemia
proportional to degree of hypercapnia. Compensation is through
kidneys, which excrete acid.
Clinical features
Usually hypoxemia and manifestations of underlying disease dominate
the clinical picture but hypercapnia per se may result in coma, raised
ICP and hyper dynamic CVS resulting, from release of catecholamine.
Causes:-
CNS
Drug over dosage
Trauma
Tumor
PNS
Polyneuropathy
Myasthenia gravis
Poliomyelitis
Tetanus
Primary pulmonary disease
Airway obstruction:-
Asthma
Parenchymal disease:-
ARDS
Loss of mechanical integrity:-
Flail chest
Treatment
Treatment of underlying cause and mechanical ventilation if required.
RESPIRATORY ALKALOSIS
Primary decrease PaCO2, which increase pH above 7.44
Clinical features:-
83
Lightheadedness
Confusion
Seizures
Circumoral paraesthesia
Hyperreflexia
Tetany
Causes
Hyperventilation voluntarily or hysteria
Pain, anxiety
Specific conditions
CVS disease
Meningitis
Tumor
Trauma
Respiratory disease
Pneumonia
Pulmonary embolism
Shock
Cardiogenic
Hypovolaemic
Treatment
Treatment of underlying cause
ELECTROLYTE BALANCE
SODIUM BALANCE
Q: DEFINE HYPERNATREMIA?
84
Q: WHAT ARE THE VARIOUS CAUSES OF HYPERNATREMIA?
Q: DEFINE HYPONATREMIA?
85
Q: WHAT ARE THE CAUSES OF HYPONATRAEMIA?
HYPONATREMIA
EVALUATION OF EXTRACELLULAR FLUID VOLUME
HYPOVOLAEMIA HYPERVOLAEMIA
NORMOVOLEMIA
(EDEMA)
plasma
osmolarity
- Acidosis
Urine sodium Urine sodium Urine sodium
> 20mmol/l < 15mmol/l <20mmol/l
Urine Sodium
variable
DEPLETIONAL SYNDROMES DILUTIONAL SYNDROMES
SALINE REQUIRED FLUID RESTRICTION REQUIRED
* Syndrome to inappropriate ADH Secretion
86
** Syndrome of inappropriate intravenous therapy
Intracellular overhydration
Cerebral odema
Raised intracranial pressure
Nausea, Vomiting, Delerium, Convulsions, Coma
POTASSIUM BALANCE
Q: DEFINE HYPOKALEMIA?
Causes Comments
Reduced intake Usually only contributory
Tissue Insulin therapy, alkalaemia, B2- adrenergic agonists,
redistribution familial periodic paralysis, vitamin B12 therapy.
Increased loss
Gastrointestinal Diarrhoea, vomiting, fistulae, nasogastric suction,
colonic villous adenoma.
(Urine K+ <
20mmol/l)
Renal Loss Diuretic therapy, primary or secondary
hyperaldosteronism, Malignant hypertension, renal
artery stenosis (high renin), Renal tubular acidosis,
hypomagnesemia, renal failure.
87
Q: WHAT ARE THE SYMPTOMS OF HYPOKALEMIA?
Q: DEFINE HYPERKALEMIA
88
EFFECTS
Skeletal muscle weakness.
Peaked T wave.
Shortened QT interval.
Ventricle fibrillation.
Asystole.
TREATMENT
Calcium gluconate 10% i/v. (0.5 ml/kg to maximum of 20 ml) given
over 5 min. no change in plasma [K+]. Effect immediate but
transient.
Glucose 50 gm (0.5-1.0g/kg) plus insulin 20 units (0.3 unit/kg) as
single i.v. bolus dose.
Sodium bicarbonate 1.5 – 2.0 mmol/kg i.v. over 5-10 min.
Calcium resonium 15 g p.o. or 30 p.r. 8-hourly.
Peritoneal or haemodialysis.
89
Lecture 9
BLOOD GASES
Arterial Venous
7.35-7.45 pH 7.31-7.41
80-100 mm Hg pO2 30-40 mm Hg
35-45 mm Hg pCO2 41-51 mm Hg
21-25 mEq/L HCO3 22-29 mEq/L
95% - 99% O2 sat 60% - 85%
- 2 to + 2 BE 0 to +4
In a patient > 60 years old, PaCO2 is equal to 80 mm Hg minus 1 mm
Hg for every year over 60.
1. Check pH
= Alkalosis
= Acidosis
2. Check pCO2
= CO2 retention (hypoventilation); respiratory acidosis or
compensating for
metabolic alkalosis.
= CO2 blown off (hyperventilation); respiratory alkalosis or
compensating
for metabolic acidosis.
3. Check HCO3
= Nonvolatile acid is lost; HCO3 gained (metabolic alkalosis or
compensating
for respiratory acidosis)
= Nonvolatile acid is added; HCO3 is lost (metabolic acidosis or
compensating for respiratory alkalosis)
4. Determine imbalance
5. Determine if compensation exists
90
Q: WHAT CHANGES IN PARAMETERS WILL HELP YOU TO
DETERMINE IMBALANCE IN ABG’s?
If
pH and pCO2
or Then respiratory disorder
pH and pCO2
If
pH and HCO3
or Then metabolic disorder
pH and HCO3
If
pCO2 and HCO3
or Then compensation is occurring
pCO 2 and HCO3
If
pCO2 and HCO3
or Then mixed imbalance
pCO 2 and HCO3
PH = 7.30 – 7.50
PaCO2 = 30-50 mm Hg
Now
- If PaCO2 is normal and pH is outside the range – the disorder is
uncompensated
- If PaCO2 is increased or decreased and pH is outside the range –
the disorder is partially compensated
- If PaCO2 is increased or decreased and pH is within range – the
disorder is fully compensated.
91
See for example.
If ph = 7.26, PaCO2= 56, HCO3 = 24 then respiratory acidosis is
uncompensated
If ph = 7.38 PaCO2= 76, HCO3 = 24 then respiratory acidosis is
compensated
If ph=7.2, PaCO2=40, HCO3 =9 then metabolic acidosis is either acute
or uncompensated
If ph = 7.36 PaCO2= 25, HCO3 = 15 then metabolic acidosis is
compensated
PULSE OXIMETRY
1. A probe positioned on the finger, toe, ear lobe or nose. The light
emitting diodes (LEDs) producing beams at red and infrared
frequencies on one side and a sensitive photodetector on the
other side. The LEDs operate in sequence.
92
3. The microprocessor is programmed to mathematically analyze
both the DC and AC components. The result is the arterial
saturation.
Q: WHAT IS A CAPNOGRAPH?
Gases with molecules that contain at least two dissimilar atoms absorb
radiation in infrared region of spectrum. Using this property, carbon
dioxide concentration can be measured directly and continuously
throughout the respiratory cycle. End-tidal carbon dioxide reflects
accurately the arterial carbon dioxide tension in the individuals with
normal lungs.
93
1. CO2 absorbs the infrared radiation particularly at a wavelength of
4.3 um.
2. The amount of radiation absorbed is proportional to the number
of CO2 molecules (partial pressure of CO 2) present in the
chamber.
3. The electrical output from the detector is proportional to the
partial pressure of CO2 in the chamber.
4. In the same way a beam of light passes through the reference
chamber, which contains air. The absorption detected from the
sample chamber is compared to that in the reference chamber.
This allows the calculation of values.
94
3. Dilution of end-tidal CO2 can occur, whenever there are loose
connections or system leaks.
4. Nitrous oxide absorbs infrared light with an absorption spectrum
overlapping that of CO2, thus causing inaccuracy.
5. The absorption of CO2 is increased due to the presence of nitrous
oxide or nitrogen.
95
Lecture 10
Q: CLASSIFY HYPERTENSION.
96
Give slow I/V injection of anaesthetic agents.
Stabilize the heart with I/V narcotic analgesic like ultra short
acting Fentanyl.
Inhalation of volatile anaesthetics over 5 mins with N2O: Oxygen.
Give lignocaine 1mg/kg IV bolus dose to attenuate reflexes at
intubation.
2. Excessive hypertension during intubation:-
Intubation leads to excessive sympathetic discharge,
tachycardia, and dysrythmias.
Give lignocaine 1mg/kg body wt.
Short acting beta blockers such as esmolol I/V.
Local spray of cords.
3. Acute hypertension during maintenance:-
Titrate volatile anaesthetic.
Avoid hypocapnia and hypercapnia.
4. Rebound hypertension during recovery:-
If diastolic BP <120mmHg, no active measure.
Give proper analgesia and avoid hypoxia.
If diastolic BP >120mm Hg, give anti-hypertensive agents such
as nitroprusside, nitroglycerine.
ASTHMA
97
Q: WHAT ARE THE IMPORTANT HISTORICAL FEATURES OF AN
ASTHMATIC PATIENT?
Anaesthetic management:-
98
Incomplete relaxation
Regurgitation
Avoid beta blockers
(Cardio selective, Metoprolol 2-10 mg may be used)
Q: WHAT IS THE TREATMENT OF ACUTE BRONCHOSPASM?
1. PREOPERATIVE EVALUTAION
a) Pulmonary function tests
b) ABG’s
c) Chest X-ray
99
2. PREOPERATIVE PREPARATION
a) Minimizing bronchospasm
b) Smoking cessation at least 2 weeks prior to surgery.
3. ANAESTHETIC MANAGEMENT
a) Intubation
1) Direct oral: appropriate if intubation difficulty not
suspected.
2) Fibroptic: appropriate for difficult airway
3) Nasal
4) Awake: indications include difficult airway, high risk of
gastric aspiration, anatomic risk for inadequate cord
visualization, jaw malformation, head and neck scar,
congenital abnormalities of upper airway, morbid obesity
5) Endobronchial: appropriate when one lung ventilation
desired
b) Hypercarbia
1) May prolong time for resumption of spontaneous
ventilation at the end of case
2) Increases cerebral blood flow
c) Hypocarbia
1) May prolong time for resumption of spontaneous
ventilation at the end of case
2) Decreases cerebral blood flow
d) Hypoxemia: greatest risk
1) Low F1O2 due to anaesthetic circuit leakage or
disconnection
2) Endobronchial intubation
3) Bronchospasm
4) Pulmonary odema
5) Pneumothorax
6) Unplanned extubation
7) Endotracheal tube obstruction
8) Airway obstruction in nonintubated patient
9) Alveolar hypoventilation
10) Atelactasis
11) Worsening of underlying pulmonary disease
1. Atelactasis
2. Pneumonia
100
101
Lecture 11
CARDIOPULMONORY RESUSCITATION
Q: DEFINE CPR.
Hypovolemia.
Hypoxia.
Hydrogen Ion (Acidosis).
Hyper / Hypokalemia.
Hypothermia.
2. 5Ts are:-
Tablets (Drugs).
Temponade.
Tension pneumothorax.
Thrombosis, coronary.
Thrombosis, pulmonary.
102
Q: WHAT ARE THE TWO COMMONLY USED TYPES OF CPR.
B – Breathing,
Assess breathlessness
Give two normal breaths that make chest rise (1 sec)
1. Head tilt and Chin lift Maneuver. This is done in patients where it
is confirmed that there is no risk of neck injury e.g. cardiac arrest
in home,
arrest in hospital wards.
103
Assess breathing by using three senses i.e. look, listen and feel. Look
for the movements of abdomen, listen the breath sounds, and feel the
air coming out of patient’s nose or mouth by placing your ear near
patient’s nose and mouth.
If the person is breathing place him in recovery position, call for help
and monitor his breathing efforts.
If the person is not breathing then give two normal breaths that make
chest rise, by blowing from your mouth after pinching his nose and
getting a proper mouth to mouth seal. After two initial breaths give two
breaths after every thirty chest compressions.
A – Airway
104
B – Breathing
C – Circulation
IV access
Rhythm appropriate drugs
D – Differential Diagnosis
1. Oxygen 10 – 15 l/min.
2. Adrenaline 1mg every 3 – 5 minutes.
3. Amiodarone 300mg IV push in adults and 5mg/kg in children
4. Atropine 0.5 – 1mg (maximum dose is 0.03 to 0.04 mg/kg body
weight).
5. Lignocaine 1 – 1.5 mg/kg body weight.
6. Magnesium sulphate 1 – 2 g IV in adults.
7. Procainamide up to 17 mg/kg body weight.
8. Sodium Bicarbonate 1 mmol/kg only in protracted CPR, known
cases of bicarbonate responsive acidosis, hyperkalaemia.
105
ALGORHITHM FOR BASIC LIFE SUPPORT
Check responsiveness
Shake and shout
Unresponsive Shout
for help
No breathing two
effective breaths
No circulation
Compress chest
100/min.30:2ratio
Cardiac arrest
106
BLS algorithm if
appropriate
Precordial thump if
appropriate
Attach defib/monitor
Assess
rhythm
During CPR
If not already:
VF/Pulseless VT Asystole or
Check electrode/paddle
positions and contact
PEA
Attempt/verify: ETT
i.v.access
Defibrillate Shock Give adrenaline every 3min
360J Monophasic Correct reversible causes
120-200J Biphesic Consider: buffers
antiarrhythmics
atropine/pacing
107
Fig: MOUTH – TO – MOUTH AND MOUTH –TO – NOSE VENTILATION. Start mouth – to – mouth, and if this
fails try mouth – to – nose. A, and B, extend the patient’s head, pinch his nose and watch his chest expand. B, and C,
when you ventilate mouth to nose, put one hand on his forehead and hold his chin up with the other one.
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30:2
Fig: CARDIOPULMONARY RESUSCITATION. Note that the operator is using the heel of his hand.
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Q: HOW WOULD YOU KEEP THE AIRWAY CLEAR?
Try these methods in the following order. If one method fails, quickly
move on to the next.
FLEX THE PATIENT’S NECK AND TILT HIS HEAD While he is lying flat,
grasp his head with one hand and tilt it so that his nostrils point
upwards. At the same time, flex his neck forward. Extending his head
without flexing his neck is less effective. This combination of
movements raises his mandible away from his cervical spine, and lifts
his tongue off the posterior wall of his pharynx. A pillow under his head
and neck helps to maintain this position.
LIFT HIS CHIN Pull it upwards. This will usually clear the airway of a
young adult with a good set of teeth.
Fig: TWO WAYS OF KEEPING A PATIENT’S AIRWAY CLEAR. Tilting a patient’s head backwards will usually
clear his airway. If this does not, insert Guedel’s airway.
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LIFT THE ANGLES OF HIS JAW Sit at the head of the table, rest your
elbows on it, and lift both the angles of his jaw with your middle
fingers. Your thumb and first fingers will then be free, if necessary, to
hold the mask, as in Fig.
Lifting his chin, if it succeeds, is better than lifting the angles of his jaw,
because lifting them can make his jaw stiff, and at worst dislocate it.
Lifting the angles of the jaw is for more difficult patients only.
Fig: GUEDELS’S AIRWAY IN PLACE. If lifting a patient’s chin fails to clear his airway, you may need to lift the
angles of his jaw.
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NASAL AIRWAY Put a soft wide rubber tube down one of his nostrils,
and hold it with a large safety pin. This is useful in severe maxillofacial
injuries, when opening the patient’s mouth may be impossible or
painful.
FERGUSSON’S GAG is useful if the patient clenches his teeth shut, and
prevents you inserting an airway. Push the gag between his back teeth,
and use it to open his jaw. Keep pieces of rubber tube on the ends of
the gag to prevent them injuring his teeth. If his teeth are complete, so
that you cannot insert a gag, force a wedge between his teeth. Rock it
to and fro between them, until they are far enough apart for you to
insert the ends of the gag. The danger of this is that you will break his
teeth, but you may have to take this risk.
If you don’t have a gag or a wedge, press your fingers between his
gums behind his molar teeth. This will open his jaws enough for you to
pass a laryngoscope. This is less traumatic than using a gag. Many
anaesthetists prefer this method and seldom, if ever, use a gag.
Main Changes
1. Children are classified into only 2 age groups: infants < 1year and
children (1year to puberty).
2. There are 5 initial rescue breaths (no mention that 2 must be
effective).
3. When doing pulse check it is now a “circulation check: as follows:
Start chest compressions if any of the following are present:
Absent central pulse for up to 10 seconds (carotid, brachial or
femoral).
Inadequate pulse (< 60 bpm for all ages of Child) with signs of
poor perfusion (include pallor, lack of responsiveness and poor
muscle tone).
No signs of a circulation (include movement, coughing or normal
breathing but not agonal gasps).
4. Chest compressions must compress the lower third of the sternum
by one third of the anteroposterior diameter (use 2 fingers, 1 hand
or 2 hands as needed to achieve this depending on age and size).
5. Position for all ages is 2 finger breadth above the xiphisternum.
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6. In infants hand encircling technique is best.
7. For all infants and children the ratio is 15 compressions 2
ventilations.
8. For all adults the ratio is 30 compressions to 2 ventilations.
Lecture 12
PAIN
Q: DEFINE PAIN.
Pain is divided into two types, acute pain and chronic pain.
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3. Numerical Rating Scales (NRS’s)
4. Visual Analogue Scales (VAS’s)
1. NSAIDs
Paracetamol
Aspirin
Diclofenac
Piroxicam
Mefenamic acid
Ketorolac
2. OPIODS
Morphine
Pethidine
Tramadol
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Nalbuphine
Buprenorphine
Pentazocine
Plexuses blocks
Brachial plexus block
Paravertebral block
Nerve blocks
Sciatic nerve block
Suprascapular nerve block
Ulnar nerve block
Radial nerve block
Peroneal nerve block
Bier’s block: IV Local anaesthetic is given after applying tourniquet to
an extremity.
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Anaesthetists in conjunction with other specialties, including
rheumatology, neurology, neurosurgery, psychiatry and other
disciplines including nursing, usually head the pain clinics. The roles of
pain clinic in patient care are:
Decrease subjective pain experience.
Increase general level of activity.
Decrease drug consumption.
Return to employment or full quality of life.
Decrease further use of health care resources.
Essential pain clinic equipment will include suitable imaging,
suitable monitoring for sedation, radio-frequency lesion generator,
cryoprobe machine and peripheral nerve stimulator. Pain clinics
have been shown to be effective both for nerve block treatments
and for psychologically based therapeutics.
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Intrathecal neurolysis using phenol or alcohol for trunk pain.
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Lecture 13
ICU
Q: DEFINE ICU.
118
Sedation.
MONITORING
ARTIFICIAL VENTILATION
TYPES:-
1. Negative pressure ventilation (not used nowadays).
2. Positive pressure ventilation.
Q: CLASSIFY VENTILATORS.
Indications:
PaO2 < 60mm Hg.
PaCO2>50mm Hg.
PH<7.2
SPO2<80%
Respiratory rate > 35 or < 07
Unconscious patient not breathing.
Elective ventilation e.g. post thoracotomy, V/Q mismatch etc.
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Q: WHAT IS THE CRITERIA FOR WEANING OFF THE
VENTILATOR?
Patient should be weaned off early in the morning when all the
consultants are present.
PaO2 is more than 60 mmHg
PaCO2 is less than 50 mmHg
pH is greater than 7.2
SpO2 is greater than 80%
Respiratory rate < 35/min
Normal vital signs.
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Lecture 14
COMPLICATIONS OF ANAESTHESIA
Q: WHAT ARE THE COMPLICATIONS OF ANAESTHESIA?
Respiratory complications.
Cardiovascular complications.
Complications resulting from posture.
Vomiting and regurgitation.
Neurological complications.
Awareness during Anaesthesia.
Malignant hyperpyrexia.
Accidental hypothermia.
Anaphylactic reactions.
Electrical hazards.
Miscellaneous complications.
Ophthalmologic complications.
Spontaneous rupture of tympanic membrane.
Minor sequelae.
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Obstruction at the glottis, due to laryngeal spasm, impaction of
epiglottis into the larynx, incomplete reversal of relaxants or foreign
bodies
Fault of apparatus
Bronchospasm
Due to
Asthma.
Surgical or airway stimulation.
Drug reaction.
Respiratory infection.
Pulmonary oedema.
Severe reduction in lung volume as in a tension Pneumothorax.
Coughing
Due to
Inadequate depth of Anaesthesia.
Chemical or infective inflammation of upper airways.
Irritation of larynx.
Hiccup
Due to
Stimulation of sensory nerve endings.
Sputum retention and atelectasis
Due to
Inadequate coughing due to pain.
Residual neuromuscular block.
Sedatives.
Impairment of mucociliary transport in lungs due to inhalation
of cold, dry gases.
Aspiration pneumonitis
Sleep apnoea
Due to
Airway obstruction.
Central respiratory depression (Ondine’s curse).
Pulmonary barotraumas
DVT and pulmonary embolism
Cardiac dysrhythmias
Associated with
Cardiac pathology.
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Hypercapnia or hypoxia.
Toxins, malignant hyperpyrexia, drugs, anaphylaxis.
Electrolyte imbalance.
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Any Avoid compression of lateral
Ulnar humerus
Any Padding at elbow, forearm
Supination
Retinal ischemia Prone, Sitting Avoid pressure on globe
Skin necrosis Any Padding over bony
prominences
Clinical manifestations:-
Cardiovascular system
Hypotension
Tachycardia
Dysrythmias
Pulmonary
Bronchospasm
Cough
Dyspnoea
Pulmonary oedema
Laryngeal oedema
Hypoxia
Dermatologic
Urticaria
Facial oedema
Pruritus
Treatment:-
Discontinue drug administration.
Administer 100% oxygen.
Epinephrine (0.01 – 0.5 mg IV or IM).
Intravenous fluids (1-2 L lactated Ringer’s injection).
Aminophylline (5-6 mg/kg IV).
Diphenhydramine (50-75 mg IV).
Gas supply
Failure of N2O supply.
Gas leaks in the breathing circuit.
Failure to flush a circle system.
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Vaporizer
Empty.
Not turned on.
Wrong agent in it.
Ventilators
Mixing of driving gas with respired gases.
Monitors
No agent monitor.
No N2O monitor.
No adequate monitor of awareness.
Technique
Insufficient sedation, premedication.
Total intravenous Anaesthesia.
Miscalculation of doses of intravenous drugs.
Difficult Intubation.
Patients
Resistance to Anaesthesia.
Alcoholism.
Very sick cases.
Emergencies.
Surgery
Obstetrics.
Cardiopulmonary bypass.
Bronchoscopy.
Dental injury.
Trauma to pharynx.
Sore throat.
Transient hoarseness.
Arytenoids dislocation.
Vocal cord paralyses.
Disruption of laryngeal ability to protect the airway.
Persistent postoperative hoarseness.
Laryngeal injury.
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Airway obstruction related to head and neck pathology.
Bleeding at the surgical site.
Tracheal compression from a goiter.
Unexpected laryngeal oedema.
Laryngeal edema from prolonged upper airway surgery.
Post-tonsillectomy pulmonary oedema.
Excessive sedation or anaesthetic agent.
Inappropriate fluid management.
Persistent muscle relaxant effect.
Miscellaneous (sepsis, transfusion reaction, bronchospasm,
inappropriate intubation).
Definition
Malignant hyperpyrexia is an inherited autosomal disorder in
which heat production exceeds heat loss in the body to cause a rise of
temperature of at least 2C/h.
Management
Withdraw volatile anaesthetic agents and hyperventilate with
oxygen.
Cool patient with ice, wet sheets, fan, cold-water gastric and
peritoneal lavage.
Get help.
Measure the temperature, blood gases, and electrolytes.
Insert an arterial line, acidosis is corrected with bicarbonate.
Give Dantrolene 1-2 mg/kg, and repeat up to 10 mg/kg.
Hyperkalaemia can be corrected with glucose 50% (1liter) and
insulin 100 units. Promote a diuresis.
Give dexamethasone 20 mg, methylprednisolone 10 mg/kg or other
steroid.
Abandon the operation if possible.
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127
Lecture 15
Intraoperative factors
Surgical procedure.
Surgeon.
Type of anaesthesia.
Relaxant/reversal status.
Unexpected surgical or anaesthetic events.
Intraoperative vital sign ranges.
Estimated blood loss.
Urine output.
Drugs given.
Time/amount of opioids administration.
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Expected airway and ventilatory status.
Acceptable urine output and blood loss.
Surgical instructions.
3 2 1 0
Airway can cough or maintains holding of holding of
jaw
and
Cry airway without jaw needed other
measures
holding jaw taken to
maintain
airway
Behaviour can lift the head can open eyes some non- no
movement at all
and show tongue purposeful
Movements
Consciousness fully awake, awake but needs responds tono
response
Can talk, well support stimuli only
Oriented
A score of 8 is the minimal for discharge from the recovery.
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Q: HOW WOULD YOU DIFFERENTITATE PAIN, HYPERCAPNIA,
AND HYPOVOLEMIA IN RECOVERY ROOM?
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Decreased protein binding.
Redistribution.
Drug interaction.
Metabolic
Hypoxia or Hypercapnia.
Hepatic, renal, or endocrine end organ dysfunction.
Hypoglycemia, hyperosmolar – hyperglycemia, diabetic
ketoacidosis.
Electrolyte imbalance (Na+, Ca++, Mg+).
Neurologic injury
Intracranial hemorrhage.
Cerebral ischemia.
Cerebral embolus.
Cerebral contusion.
Subclinical seizures.
Enlarging pneumoencephalus.
Drug
Withdrawal (beta blockers, clonidine)
Theophylline
Atropine
Beta-2 antagonists
Epinephrine
Vasodilators
Ketamine
Others
Hypovolemia, hypervolemia
Anemia
Fever
Hypercarbia
Hypoxemia (early sign)
Cardiac tamponade
Tension pneumothorax
Thromboembolism
Hyperthyroid, pheochromocytoma
Pain
Anxiety, Shivering
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Bladder distention
Allergy
Hypoglycemia
Acute porphyria
Preexisting hypertension.
Withdrawal of antihypertensive medications.
Hypercarbia.
Volume overload.
Bladder distention.
Increased intracranial pressure.
Pain.
Drugs.
Pressors, epinephrine, Ketamine.
Reversal with naloxone.
Indirect acting vasopressor with chronic MAO use.
Autonomic hyperreflexia.
Pheochromocytoma.
Carotid surgery.
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hyperventilation Pain
(PaCO2 low) Abdominal distention
Obesity
Tight dressings
Pneumo-/haemothor
ax
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Fig: A, THE RECOVERY POSITION is the only safe one for a patient on the trolley on his way to the ward, and in
his bed when he gets there. Show your nurses how to place an unconscious patient on his side, with his uppermost arm
and leg supporting his body. This position helps to keep his airway clear, it allows his tongue to fall forwards, and it lets
blood and secretions drain from his mouth. B, sucking out his nose. Pinch one of this nostrils shut while you suck
through the other.
134
Fig: ALL SET FOR A SAFE RECOVERY on a trolley which has sides and can tip. There is an oxygen cylinder and a
mask, a bell to summon help, a sphygmomanometer, and a sucker.
135
Q: WHAT IS THE CLINICAL ASSESSMENT OF THE ADEQUACY
OF REVERSAL OF NEUROMUSCULAR BLOCK?
Subjective:-
Grip strength
Adequate cough
Objective:-
Ability to sustain head lift for at least 5 sec.
Ability to produce vital capacity of at least 10 ml/kg
Infections
Immunologically mediated processes
Drug reactions
Blood reactions
Tissue destruction (rejection)
Connective tissue disorders
Granulomatous disorders
Tissue damage
Trauma
Infarction
Thrombosis
Neoplastic disorders
Metabolic disorders
Thyroid storm (thyroid crisis)
Adrenal crisis
Pheochromocytoma
Malignant hyperthermia
Acute gout
Acute porphyria
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APPENDIX
Eyes open
Spontaneously 4
To command 3
To pain 2
No response 1
Motor response
Obeys command 6
Localizes pain 5
Withdraws 4
Flexion (abnormal) 3
Extension (abnormal) 2
No response 1
Verbal response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensive sounds 2
No response 1
Structure Normal
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Findings Possible Diagnosis
INTUBATION/EXTUBATION GUIDELINES
Intubation:-
Tube size:-
Orotracheal Nasotracheal
Males: 8-8.5 mm i.d. <7.5 mm i.d.
Females: 7-8 mm i.d.
Cuff pressure:-
>20 mm Hg increases risk for tracheal damage
<15 mm Hg increase risk of aspiration around cuff
Ventilation:-
Auscultate the lateral aspect of the chest midaxillary line for
presence of breath sounds.
Inspect chest for equal expansion.
Auscultate over the epigastric area. Gurgling sounds indicate
esophageal intubation
Minimal occlusive technique:-
Place stethoscope at larynx.
Slowly remove air (in 0.2 ml amounts) from cuff until air leak is
heard.
Slowly reinsert air (in 0.2 ml amounts) until the inspiratory leak
stops.
Stabilize tube:-
Remember :- Regarding tube – when in doubt take it out.
Extubation:
Elevate HOB. (Head of Bed).
Preoxygenate (100%).
Suction endotracheal tube, above tube cuff, from patient’s mouth.
138
Instruct patient to take in a deep breath; deflate cuff and remove
tube on peak inspiration.
Administer prescribed oxygen.
Assess signs and symptoms indicative of respiratory distress and
increased effort.
139
6. Give O2 + N2O + Volatile agents through mask or endotracheal tube
through out the surgical procedure, the muscle relaxant are given if
necessary.
7. At the end of operation muscle relaxants are reversed with
neostigmine and atropine/pyrrolate.
8. Patient is sent to recovery room for further care.
These are based on body weight: For the first 10kg – 100ml/kg/day (or
approximately 4 ml/kg/hr). For the next 10kg – 2ml/kg/hr). Remember,
infants need 4 ml/kg/hr of fluid in and at least 2 ml/kg/hr of urine
output. Bigger children need 2 ml/kg/hr in and 1 ml/kg/hr out.
140
Lactic acidosis
Ethylene glycol, Ethanol intoxication
Salicylate intoxication
141
Fig: THE TEN GOLDEN RULES, If these rules were always followed, there would be far fewer anaesthetic deaths:
(1) Assess and prepare a patient adequately. (2) Starve him. (3) Put him on a tipping table. (4) Check the machine and
cylinders before you start. (5) Have a sucker ready. (6) Have airways ready. (7) Be ready to control his ventilation. (8)
Have a vein open. (9) Monitor his pulse and blood pressure. (10) Have someone around who can apply cricoid
pressure, and who can be relied on in an emergency.
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LOG BOOK
PROCEDURES
143
DEPARTMENT OF ANAESTHESIOLOGY
____________________________________________________________
____________________________________________________________
Name: ____________________________________________
Year: _________________________________________________
_______________________________________________________
VIVA __________
ATTENDANCE __________
____________________________
SIGN HEAD OF
DEPARTMENT
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Key Viva Attendance
A Excellent 80% >75%
B Good 70- 60-75%
80%
C Satisfactory 65- 50-60%
70%
D Poor 60% 50%
PERFORMED
PROCEDURE DATES WITH INITIALS
1 Pre-Operative assessment
2 Venepunctures
5 LMA Insertion
6 Spinal Block
8 Fluid Resuscitation
9 CPR (Basics)
____________________________
SIGN HEAD OF
DEPARTMENT
ATTENDANCE RECORD OF 15 DAYS
145
_______________ ________________________
Total Attendance Sign Head of Department
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SUGGESTED READING
Students those who are interested to become anaesthetist and planning for post-
graduation in anaesthesiology are suggested to read the following books:-
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