Anaesthesia 4

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ANAESTHESIA
PROMETRIC
EXAM
PRACTICE
MODULE
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What factors show that intubation of the larynx will be difficult enough to indicate
fibroptic intubation?
Notes for an answer:
1. Examination of patient
a) history of rheumatoid arthritis; known history of difficult intubation - Cormack & Lehane
scores from previous laryngoscopies;
b) poor mouth opening (< 3fb);
c) low Malampatti score;
d) thyromental distance (< 6cm);
e) small mandible size, inability to protrude jaw;
f) neck stiffness or injury (need to mention neck X-rays), atlanto-occipital distance, atlanto-
odontoid distance (> 3mm);
g) Frontal crowns, awkward front teeth.
2. Trismus.
3. Congenital abnormalities of the face or neck.
4. Known or suspected laryngeal obstruction (need to mention soft tissue X-ray of neck).
5. Previous suxamethonium masseter spasm (if rapid sequence induction is needed).
This answer needs a note on whether any of these factors are absolute indications, and how
many of the predictive factors need to be present to indicate fibreoptic intubation.
Serious omissions likely to cause a fail:

Failure to note at least four predictive factors; failure to mention laryngeal obstruction.
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Page 4
How do you manage the physiological consequences of surgical manoeuvres during

abdominal laparoscopy?
Physiological upsets (with management in brackets):
1. Vascular reflexes; bradycardia (atropine 0.2-0.5 mg will correct this).
2. Gas in peritoneum causes diaphragmatic splinting (IPPV is required).
3. Gas in blood vessels causes air embolism (requiring "air embolism drill").
4. Excess absorption of CO2 (moderate hyperventilation).
5. Haemorrhage (you need to state that this can be massive, requiring urgent group-specific
transfusion).
6. Gas in pleural cavity causes tension pneumothorax (this requires a comment on how to
make the correct diagnosis and the insertion of a needle in correct side of chest).
7. Surgical emphysema - can cause severe pain.

Failure to mention diaphragmatic splinting and gas embolism.
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What are the factors that prolong the action of nondepolarising relaxants?
1. Structure of relaxant - basic scientific knowledge (bonus marks if you state what difference the
structure makes).
2. Physiology of patient - hypokalaemia, hypocalcaemia, hypothermia, acidosis, poisons (e.g.,
botulinus toxin).
3. Volatile anaesthetics.
4. Myasthenia and other rare diseases (bonus marks if you can name any).
5. Other drugs, especially local anaesthetics and aminoglycoside and lincomycin antibiotics in
high dosage.
6. Age of patient, very young and very old.
Comment: This is common everyday anaesthetic practice and would be marked severely.

Failure to mention electrolyte abnormalities, volatile anaesthetics, and age factors.
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Page 5
What are the ''anaesthetic" problems caused by morbid obesity?

1. Definition of morbid obesity in terms of body mass index is required (greater than 30 kg/M2).
Problems:
Respiratory system — increased work of breathing, diaphragmatic splinting, difficult intubation,
underventilation, reduced lung volumes, pulmonary "shunting", hypercapnia, hypoxia (operative
and postoperative), slow equilibration with inhaled anaesthetics.
Cardiovascular system — blood volume increased, increased cardiac work, hypertension and
coronary disease, risk of DVT, less water per unit of body weight;
Miscellaneous — hiatus hernia, regurgitation.
Technical — difficult to move, lift and nurse — spontaneous respiration restricted, difficult to
intubate, especially when front dental crowns are present, difficult venepuncture, estimation of
drug dosage is difficult, inaccuracy of noninvasive arterial pressure monitoring, regional and
local blocks are technically difficult, surgery is often more prolonged.
Comment: This is a large answer to complete in 10-15 minutes, unless you have thought it out
beforehand.

Failure to mention respiratory problems, and regurgitation risks.
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How do you prevent unplanned awareness during general anaesthesia?

1. History from patient (previous unplanned awareness; physiological resistance to anaesthesia;
alcoholism, etc.).
2. Preoperative checks of machine, vaporisers (or syringe drivers if using total intravenous
anaesthesia). Vaporisers are refilled before they become empty.
3. Monitoring of breathing system — including agent, especially when using the closed circle
system. 1 MAC of volatile anaesthetic is normally sufficient.
4. Adequate premedication, especially benzodiazepines.
5. Use of ear muffs or plugs on patient during surgery.
6. Monitoring of patient (this needs a very brief discussion of the value of "clinical" signs,
and a few details about the available awareness monitors).
7. Not placing reliance on opioids to prevent awareness.

Failure to mention anaesthetic agent monitoring.
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How would you detect unplanned awareness during general anaesthesia?

1. Monitoring of breathing system — (including anaesthetic agent), and/or syringe driver system.
2. Monitoring of patient
a) Clinical;
b) Cerebral function monitoring;
c) Spectral Edge Frequency analysis;
d) Bisectral Index;
e) Frontalis EMG etc.;
f) Evoked potentials and responses;
g) Respiratory Sinus Arrythmia analysis;
h) Oesophageal contraction rate.
A brief comment on the usefulness and inadequacies of these monitors is required.

Failure to mention the monitoring of anaesthetic agents. In practice, this is routine.
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What are the advantages and limitations of the laryngeal mask airway?
Advantages: general ease of use, does not require neck movement for insertion; good in difficult
airway situations, bearded patients; allows remoteness from mouth for head and neck
operations. (Some comment on sizes is helpful.)
Limitations: can cause laryngospasm; can turn, kink and obstruct in other ways; no airway
protection from gastric reflux, logistic difficulties of sterilisation, pharyngeal damage on
insertion, especially if the cuff is too tightly evacuated, dental damage, occlusion by biting, if
anaesthesia is too light or the patient wakes up with the laryngeal mask in situ.
Comment: The laryngeal mask does not guarantee anything, but it is wonderfully useful.

Failure to mention obstruction of airway.
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Page 7
How do you manage total intravenous anaesthesia?

The following are required:
1. Reliable IV cannula.
2. Reliable syringe pump — with battery backup, alarms for blockage, disconnection, and empty
syringe.
3. Reliable full monitoring of airway, breathing (anaesthetic bag movements, SpO2, EtCO2),
Circulation (ECG, arterial pressure, SpO2) and depth of anaesthesia (details not needed).
4. Use of reliable drugs (e.g., propofol) and typical infusion rates (e.g., 10-6 mg/kg/hr for
propofol).

Failure to mention the need for full monitoring, especially respiration.
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Write short notes on ondansetron

This answer needs most of the following headings:
Pharmacy:
Type of chemical, storage (plastic ampoules) preparation, concentration
Pharmacodynamics:
Mode of action, 5HT3 serotonin antagonism
Clinical effects: antiemetic
Dose, 4-8 mg
Onset,
minutes
Duration, 8
hrs.
Pharmacokin
etics:
Routes of administration, IV< IM< oral
Metabolism, liver
Side effects, constipation, headache, flushing, transient
visual disturbances Plus other features: especially
useful in chemotherapy.
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Page 8
How do you manage sedoanalgesia?

(This is sedation plus local anaesthesia)
1. Sedative drugs used, benzodiazepines, ketamine, opioids, phenothiazines, the doses required
and undesirable side-effects.
2. Methods of local analgesia; e.g., regional/local/topical.
3. Monitoring — you need to state that this is complete as for full general anaesthetic,
because the patients selected for this type of anaesthesia are sometimes very ill.
4. A brief discussion of a strategy for coping with failed local analgesia, e.g., appropriate
analgesics.

Failure to mention full monitoring.
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Under what circumstances should general anaesthesia for elective cases be postponed and
why?
Uncontrolled hypertension, recent myocardial infarction, colds, URTI, chest infection, head
injury, acute pancreatitis, acute LVF, uncontrolled arrythmia, inadequate preparation or
investigations; serious electrolyte abnormality, e.g., hypokalaemia; serious acute anaemia;
uncontrolled shock.
Comment: This is a safety question, and needs only a brief reason for each area noted here.

Failure to mention shock, myocardial infarction and respiratory tract infections.
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Page 9
How would you determine the causes of arterial hypotension (80/60 mmHg.) during a
prostatectomy, and how would you manage it?
1. Bloodloss — inspection and analysis of bladder washouts — requires a discussi on of
difficulty of assessment.
2. TURP syndrome — clinical signs, use of ethanol marker and breathalyser monitoring.
3. Anaesthetic — too deep, severe hypocapnia, severe bradycardia, spinal block too extensive,
or made more severe by presence of significant cardiac disease.
4. Other medical conditions — myocardial infarction, co-existing aortic stenosis, cardiac
failure — need comment about usefulness of monitoring.

Failure to mention TURP syndrome, bloodloss and myocardial infarction.
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What are the causes and management of hypoventilation immediately following

anaesthesia?
Causes:
1. Obstructed airway.
2. Anaesthetic drugs — especially volatiles and opioids.
3. Incomplete reversal of relaxants.
4. Pain.
5. Shock.
6. CO2 narcosis (caused by, and a cause of, hypoventilation).
7. Obesity and medical problems of the patient, e.g., myasthenia, pulmonary disease, raised
intracranial pressure.
Management:
Oxygen, ventilation of lungs, reversal of cause.
Comment: This is a question about everyday anaesthetic practice.

Failure to mention obstructed airway.
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Page 10
What causes bradycardia during general anaesthesia and what is the management of this
condition?
First of all, this needs a comment about what pulse rates constitute bradycardia.
Causes: deep anaesthesia, hypoventilation (e.g., disconnected ventilator), hypoxia, hypotension
(which may also be caused by bradycardia), oculocardiac and other vagal reflexes, drugs
(opioids, neostigmine, B-blockers), cardiac ischaemia/failure/ bradyarrythmias, cerebral
compression, high spinal blockade.
Management: assess reasons for it and state what limits
should provoke action. Mention use of anticholinergic drugs,
e.g., atropine.
Treat cause if possible.
Comment: A common problem.

Failure to mention opioids and vagal reflexes.
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Page 11
List the causes and briefly note the management of tachycardia (> 100 bpm) during
general anaesthesia in an adult
Causes: light anaesthesia, hypercarbia, hypovolaemia, hypotension, tachy-arrythmia, drugs
(atropine, adrenaline), endocrine problems (thyroid crisis, phaeochromocytoma), malignant
hyperpyrexia, toxaemia.
General Management:
a) assess significance: (e.g., associated with hyper- or hypotension — pulse rates well
above 100 bpm may adversely affect circulation), state need for experienced help;
b) treat cause if possible. The target pulse rate is 70-100 bpm.
Tachyarrythmias: mention of DC defibrillation shock if hypotensive.
Specific Managements:
Sinus tachycardia — carotid sinus massage; Beta-blockers (and contraindications to these drugs).
Supra Ventricular Tachycardia —carotid sinus massage, adenosine,
amiodarone, verapamil is controversial. Atrial fibrillation or Flutter — digoxin,
amiodarone; DC shock may be needed.
Ventricular tachycardia — amiodarone (lignocaine, flecaine and verapamil are used much less).

Inadequate details of general management; failure to mention malignant hyperpyrexia.
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Page 12
Why do some patients suffer circulatory collapse at the induction of general anaesthesia
and how would you manage it?
Causes:
1. Nature of patient's disease e.g., untreated hypertension, sudden arrythmia, cardiac failure
(for example in emergency CABG), severe aortic stenosis, pacemaker failure,
phaeochromocytoma, and other rare syndromes
2. Anaphylaxis (hypotension, bronchospasm, flushing, oedema).
a) Stop injecting the anaesthetic agent.
b) O2/ventilation.
c) Adrenaline 50-100µg.
d) Head down position and 2L colloid volume load.
e) Antihistamines.
f) Steroids.
g) Blood samples.
h) Prevent
awareness. (an
d then later. . .
i) Inform patient).
3. Fainting — vasovagal shock. Atropine, and elevation of legs etc.
4. Shock. Prevented by pre-emptive correction of hypovolaemia.
5. Overdose of anaesthetic agent. Prevention is better than cure!
6. Myocardial infarction. ECG will show this.
General Management:
Firstly, diagnosis of the cause, based on knowledge of the patients preoperative medical
condition, and full monitoring.
In general, anticipation of the problem, with full monitoring; elevation of the legs and careful
use of catecholamines. ACLS plus control of the cause if the collapse progresses to cardiac
arrest.
Comment: There is no simple way of categorising the answer to this one!

Failure to mention anaphylaxis.
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Page 13
What signs would lead you to suspect that a patient under general anaesthesia was
developing malignant hyperpyrexia? Describe Your immediate management
Signs:
• high tachycardia; hypercapnia; cyanosis/hypoxia; hypothermia; muscle rigidity;
metabolic and respiratory acidosis; initial hypertension; followed by cardiovascular
failure; mottled rash.
Management:
• hyperventilate with oxygen; stop trigger agents; repeatedly measure blood gases; electrolytes
and temperature;
• inject dantrolene, 1mg/kg, i.v., repeated (to inhibit sarcoplasmic Ca++ release);
• i.v. sodium bicarbonate, 0.3 mmol/kg;
• active cooling;
• insulin/dextrose to control hyperkalaemia;
• diuresis to prevent renal failure;
• ITU admission.

Failure to mention dantrolene, and stopping the anaesthetic.
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Page 14
What is the pathophysiology of malignant hyperpyrexia? How would you investigate it?
1. Abnormal Ca++ flux with uncontrolled release of Ca++ from sarcoplasmic reticulum on
exposure to triggers gives rise in Ca++ pump activity; binding of troponin C causes
massive muscle contraction and uncoupling of oxidation from phosphorylation.
2. The role of the ryanodine receptor is central to this process.
3. The condition is inherited as an autosomal dominant.
4. Masseter spasm in children may be associated with it.
5. Triggers: suxamethonium, halothane, physiological stress and many other agents.
Investigation:
• During the crisis: CPK levels > 20,000.
• After the crisis: muscle biopsy (MHSusceptible, MHEquivocal, MHNonsusceptible).
MHEcould be exposed to ryanodine.
• Investigate the family.

Failure to mention calcium and at least some of the triggers.
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Page 15
You are asked to construct a question sheet for day-case patients to answer on admission
to hospital. What questions would you ask?
• What do you weigh?
• How tall are you?
• Can you do normal activities?
• Is your general health good?
• Have you ever had an operation? If so, please list them.
• Have you ever had an anaesthetic? If so, did you have any problem with it?
• Have your relatives had any problems with anaesthetics?
• Do you have any loose or crowned teeth? If so, which ones?
• Have you had any medical illnesses? If so, which ones?
• Are you taking any sort of medicine, pill or tablet? If so, which ones?
• Are you allergic or sensitive to any medicine?. . . or anything else?
• Do you smoke? If so, how many?
• How many stairs can you climb quickly before you get short of breath?
• Are you short of breath on lying flat?
• Do you have a cough or wheeze? If so, how often?
• Do you get pain in the chest or palpitations? If so, how often?
• Have you had a heart attack or a ''stroke"? If so, when?
• Do you know if you are anaemic?
• Could you possibly be pregnant?
• Are you a "drug user" or homosexual?
• Have you ever been jaundiced? If so, when?
• Have you got someone to take you home and stay with you for the night after the operation?
Comment: This is a question of communication as well as preoperative skills.

Failure to mention previous anaesthetics, and the need for a responsible adult to take the patient
home.
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Page 16
What protocol would you construct to guide surgeons on selecting adultpatients for day-
case anaesthesia?
Operations to Avoid:
• those which are lengthy (more than 30 min), painful, haemorrhagic, enter thorax or abdomen.
Patients to Avoid:
• those with previously bad reactions to anaesthetics;
• those with COAD;
• breathless on ascent of 10 stairs; orthopnoea; breathless at rest, cyanosis;
• myocardial infarction in last year, or multiple or severe previous infarctions with restriction of
activity; Angina;
• any degree of left ventricular failure;
• untreated hypertension; severe anaemia;
• electrolyte abnormalities;
• CVA in last year;
• obesity (BMI greater than 30);
• Insulin-dependent diabetes mellitus;
• ASA grades III or more;
• patients with severe congenital abnormalities;
• those with no-one to take them home and look after them;
• patients over the age of 70 years.
Comment: This question includes communication skills with colleagues.

Failure to mention those with previously bad reactions to anaesthetics.
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Page 17
Describe the anaesthetic arrangements involved in a gynaecological day-case list of 15

patients for dilatation and curettage of the uterus
Prior to the Day of the List:
1. There is a need for a selection protocol for surgeons choosing the patients (e.g., patients may
be obese).
2. Preadmission questionnaire for patients.
3. Preadmission investigations complete before day of operation.
On the Day of the List:
4. Organisation of the day of operation: preoperative visits, confirmation of the correct order of
the list/no waiting for patients/coffee break for staff! Routine checks of patient identity and
expected operation.
5. Anaesthetic techniques for rapid awakening (e.g., sevoflurane, desflurane, or TIVA) and no
nausea (routine use of antiemetics).
6. Organisation to avoid "log-jams" in recovery.
7. Discharge protocol — accompanied by responsible adult/no driving/alcohol.
8. Written discharge instructions.
After the List:
9. Postoperative visit.
10. Follow-up audit.
Comment: This is a test of important anaesthetic management skills.

Failure to mention pre- and postoperative factors.
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Page 18
Write short notes on rocuronium

Pharmacy:
Type of chemical, storage (solution in glass ampoules,) preparation, concentration
Pharmacodynamics:
Mode of action, nondepolarising neuromuscular blockade
Clinical effects, relaxation
Dose, 0.5 mg/kg.
Onset, 60 secs.
Duration, 45-60 mins.
Pharmacokinetics:
Routes of administration, i.v.
Metabolism, liver
Interactions, volatile and local anaesthetics, aminoglycoside antibiotics
Plus other features: rapid onset due to low receptor occupancy, with high biophase
concentrations.
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Page 19
Give an account of the pharmacology of propofol

Pharmacy:
Type of chemical (phenol), storage (glass ampoules), preparation (emulsion), concentration (10
mg/ml.).
Pharmacodynamics:
Brain (reduction CMRO2 and anaesthesia), heart, bloodvessels (vasodilator), respiratory
depression.
clinical effects: anaesthesia.
Pharmacokinetics:
Doses (1-2 mg/kg.), blood levels (3.5-4.5 µg/ml.), onset (one circulation time), lipid solubility
(high), distribution (initially to extracellular fluid, brain, then other sites, especially fat), short
half life; 99% metabolised.
Side effects: extrapyramidal movements, mild relaxation of muscles; depression of pharyngeal
reflexes.
Contraindications:
a) Absolute: hypersensitivity, upper airway obstruction.
b) Relative: severe cardiovascular disease, hypovolaemia, aortic stenosis, extremes of age.
Total Intravenous Anaesthesia — infusion rates (10-8-6 mg/kg/hr.).
Interactions with other drugs e.g., alfentanil — (increases duration).
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Compare and contrast halothane and desflurane.

This should include the following:
An ethane (halothane) compared with a more highly fluorinated ether (desflurane); physical
properties, MAC values, rates of onset and offset, pharmacodynamics, metabolism, side
effects, vaporiser design.

Failure to mention MAC values.
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Page 20
What are the pharmacological problems presented by a patient taking monoamine-oxidase

inhibitors (MAOI) who requires emergency anaesthesia for a bleeding duodenal ulcer?
discuss the pharmacological problems presented.
Problem of cardiovascular support and need for inotropes (with their interactions), place of
dopamine in renal support; need mention of careful volume replacement before and during
anaesthesia. This answer needs a mention of strategies for analgesia and the problem of
interaction with pethidine causing hypotension and coma.
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List the causes of "suxamethonium apnoea". How would you diagnose and manage it once
it had occurred?
Causes:
1. Congenital — genotypes e, f, s, a; with homo- and heterozygotes. Inheritance as dominant.
2. Acquired — pregnancy, malnutrition, plasmapheresis, myxoedema, the newborn, lupus, and
drug-induced.
3. Antagonism — anticholinesterases, e.g., neostigmine, ecothiopate.
Diagnosis:
a) history from patient;
b) Failure of suxamethonium to wear off within 5-10 minutes;
c) Neuromuscular monitoring;
d) Later — investigation of patient and relatives. Dibucaine no.; fluoride no.; serum
cholinesterase levels.
Management:
Oxygenation; IPPV and sedation for about 1-2 hr. until muscle power returns.

Failure to mention both congenital and acquired forms.
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Describe the Bain system and its functions

Bain system — modified Mapleson D, coaxial, outlet valve by machine, small deadspace,
always some rebreathing except at very high flows, breaks of central tube gives high
deadspace — safety check before use, not antistatic, sterilising procedures. the outlet valve
usually has an airway pressure limiting device, set at 50-60 mm Hg., which prevents
barotrauma, but not pressure effects on pulmonary circulation.
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Page 21
What are the safety devices involved in delivery of oxygen from a cylinder on an
anaesthetic machine to an anaesthetised patient through a Bain system?
Pin-index on cylinders, tap on cylinders, pressure reducing valve, filter, flow restrictor, needle
valve, rotameter (on the left in UK), vaporiser with adequate gas seals, machine pressure relief
valve, standardised 22mm outlet, bag, coaxial pipes, mask, Heidbrink exit valve with airway
pressure limiting device (50-60 mm Hg).

Failure to mention pin index and the airway pressure limiting device.
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Compare two types of anaesthetic breathing system used for a healthy spontaneously
breathing child weighing 20kg
Issues for discussion (any descriptions of the systems should be very brief).
• Simplicity of use.
• Safety for patient (valves (or lack of them); ease of disconnections; antistatic protection; risks
of hypoxia, prevention of pulmonary barotrauma).
• Economy.
• Fresh Gas Flows — requires figures for the systems you describe.
• Humidification and warming.
• Likelihood of rebreathing at various gas flows.
• Ease of sterilisation and crossinfection.
Comment: The size of the patient in question here has been chosen to allow you the maximum
choice of breathing systems.

Failure to mention the safety factors.
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Page 22
Write short notes on desflurane

Pharmacy:
type of chemical (fourinated ether), storage (glass bottles)
Pharmacodynamics:
Mode of action, inhalation volatile anaesthetic
Clinical effects, anaesthesia
Dose, MAC = 6%
Onset, very rapid, due to low solubility
Duration, N/A
Pharmacokinetics:
Routes of administration, inhalation
Metabolism, very small
Excretion, rapidly, via lungs
Side effects, coughing, laryngospasm, excitement on inhalation induction
Plus other features (low solubility, blood/gas partition coefficient 0.4, oil/gas 18.7; high SVP (88
@ 20° C; MAC50 6%; Boiling point 22.8° C; vaporiser designed to run above boiling point).
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Page 23
Describe the circle system for anaesthesia. What are its advantages and limitations?
Corrugated tubes, soda lime, low-resistance, NON-stick valves, gas entry port on inspiratory
limb.
Advantages
Economy, low pollution, warming of gases, humidification.
Soda lime — 90% Ca(OH)2, 5% NaOH, 1% KOH, silicates and water. Used to absorb CO2 (up
to 20% of its own weight). Granule size, air spaces important, Colour indicator change on
exhaustion.
Limitations
1. Risk of
• hypoxia
• hypercapnia
• awareness due to slow equilibration with large volumes
• overdose of anaesthetic, disconnections
• deadspace problems (a sticking valve causes a large dead-space)
• carbon monoxide generation during rest, if very dry
• degradion of sevoflurane by heat
2. Needs monitoring of:
• O2
• CO2
• anaesthetic agents

Failure to mention the soda-lime; monitoring of gases.
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Page 24
What are the features of an anaesthetic machine which are designed to minimise the risk of
delivering hypoxic gas mixtures?
The features which should be mentioned are: colour coding of cylinders, pin-index, pressure
gauge, Schrader valves and colour- coded pipe for pipelines, flow control by rotameters,
O2/N2O interlock, O2 failure warning device, O2 monitor, safety checklist card.
Issues for discussion — effectiveness, proof against operator failure, areas of failure of
reliability, need for audible alerts for operator, operator involvement in safety checks, effect of
electrical failure.

Failure to mention the pin-index and Schrader valves.
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Write short notes on dantrolene

Pharmacy:
Type of chemical, storage (powder, with mannitol), i.v. preparation is very highly alkaline
Pharmacodynamics:
Mode of action, muscle fibre relaxant, acting at excitation-contraction coupling zone, preventing
Ca++ release from sarcoplasmic reticulum
Clinical effects, treatment of malignant hyperpyrexia (and other spasm)
Dose, 1 mg/kg., repeated
Onset, rapid
Duration, 10-
30 mins.
Pharmacokinet
ics:
Routes of administration, i.v., oral
Metabolism, liver
Interactions, with veapamil in
anaesthetised animals Plus other
features: difficult to dissolve
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Page 25
Write short notes on ketamine

Pharmacy:
Type of chemical (a cyclohexanone), storage (aqueous solution in glass ampoules)
preparation, concentration (10, 50, and 100 mg/ml.)
Pharmacodynamics:
Mode of action, NMDM receptor agonist
Clinical effects, analgesia; anaesthesia
Dose, 5mg/kg i.m.; 2mg/kg. i.v.; 0.5mg/kg. i.v. for sedoanalgesia
Onset, one circulation time, i.v.; 5 mins i.m.
Duration, 10-30 mins.
Pharmacokinetics:
Routes of administration, i.v.; i.m.; oral; epidural
Metabolism, liver
Side effects, dreams and hallucinations, vasoconstrictor — hypertension, mild rises of ICP and
IOP, salivation, PONY, increased muscle tone and movements.
Interactions, dreams and hallucinations prevented by low dose benzodiazepines.
Prolonged hypnosis with barbiturates. Plus other features: low-dose use in
sedoanalgesia. Has been used in patients with full stomachs without regurgitation.
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Page 26
List the physical properties of desflurane, and describe the characteristics of a suitable
vaporiser
1. Molecular wt: 168 Daltons.
2. Boiling point 22.8° C.
3. SVP @ 20° C: 88.5 kPa.
4. Oil/gas Sol.: 18.7.
5. MAC: 6%.
6. Blood/gas partition coefficient 0.4.
Vaporiser characteristics:
Splitting of gas inflow, temperature controlled @ 39° C, calibration independent of flow,
electronic vapour injection with differential pressure transducer system, electronic monitoring
of liquid content with alarm, keyed filling ports and bottles, spill-proof device, easily mounted
and demounted from machine, interlocks to allow only one in use, at any one time.
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How do you estimate bloodloss during various types of surgery?

1. Clinical condition of patient e.g., capillary refill, warm periphery, quality and volume of pulses
in various parts of body.
2. Monitoring CVP; arterial pressure — invasive and noninvasive (with comment on pressures
needed for production of urine) (MAP 70 mm Hg.).
3. Visual assessment of swabs, drapes and sucker bottle, allowing for volume of saline washouts.
4. Other weigh swabs.
5. Hb estimation of TURP irrigation fluid and calculation of bloodloss.
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Page 27
Write short notes on minimum alveolar concentration

Definition: a measure of the potency of volatile anaesthetics. MAC50 is the minimum alveolar
concentration required to prevent physical reaction to skin incision in 50% of subjects.
Isoflurane 1.15%; enflurane 1.7%; desflurane 6%;
sevoflurane 2%; halothane 0.75%. It varies with age, greatest
at one month; lowest in premature babies and old age.
Increased by: adrelaline, severe
surgical stimulus. Decreased by:
sedation, analgesia, pregnancy.
MAC95 is the minimum alveolar concentration required to prevent reaction to
skin incision in 95% of subjects. Other features: in mixtures of anaesthetic
gases, the various MAC's are additive.
<><><><><><><><><><><><>
Write short notes on propofol

Pharmacy:
Type of chemical (phenol) storage (emulsion in soybean oil, in glass ampoules) concentration
(10mg/ml.)
Pharmacodynamics:
Mode of action, hypnosis via GABA receptors
Clinical effects, anaesthesia
Dose, 1-2 mg/kg; infusion 10-6 mg/kg/hr. effective blood level is 3.5-4.5 µg/ml.
Onset, one circulation time
Duration, 1-5 mins.
Pharmacokinetics:
Metabolism, liver
Side effects, vasodilation, hypotension, respiratory depression, relaxation
Interactions, prolongs action of alfentanil
Plus other features: long infusion leads to
green urine colour In low dosage it is used
as a sedative
Note the similarity to the question and answer on p22
<><><><><><><><><><><><>
Page 28
Write short notes on mivacurium

Pharmacy:
Type of chemical (benzylisoquinoline), storage, (aqueous, in glass ampoules) preparation,
concentration 10mg/ml
Pharmacodynamics:
Mode of action, nondepolarising neuromuscular drug
Clinical effects, relaxant
Dose, 0.1-0.2 mg/kg.
Onset, 3 mins.
Duration, 10 mins.
Pharmacokinetics:
Routes of administration,
i.v. Metabolism, serum
cholinesterase Side effects,
histamine release
Interactions, volatile and local anaesthetics, aminoglycoside antibiotics, other relaxants
<><><><><><><><><><><><>
Write short notes on hyoscine

Pharmacy:
Type of chemical, storage, preparation (aqueous, tablet or syrup), concentration (400 µg/ml.)
Pharmacodynamics:
Mode of action, anticholinergic
Clinical effects, parasympathetic blockade; sedative; antiemetic; locally acting mydriatic
Dose, 7 µg/kg.
Onset, one
circulation time
Duration, 3hrs
Pharmacokinetics:
Routes of administration, oral, i.m.; i.v.
Metabolism, liver
Side effects, central anticholinergic syndrome, tachycardia, dry mouth
<><><><><><><><><><><><>
Page 29
Write short notes on glycopyrronium (glycopyrollate)

Pharmacy:
Type of chemical, storage (aqueous solution in glass ampoules,) preparation, concentration 200
µg/ml.
Pharmacodynamics:
Mode of action, anticholinergic
Clinical effects, parasympathetic blockade
Dose, 7 µg/kg.
Onset, one circulation time
Duration, 4-6 hrs.
Pharmacokinetics:
Routes of administration, i.v; i.m.
Metabolism, liver
Side effects, Tachycardia, dry mouth
Plus other features: does not cross blood brain barrier
<><><><><><><><><><><><>
Page 30
Chapter 3
Paediatric Anaesthesia
Page 31
How does the physiology of children aged 1 year differ from that of adults?
Infants have:
1. More increased heart and respiratory rates in response to demands than adults. The ribs are
more horizontal, and the respiration is more diaphragmatic.
2. Higher metabolic rate — more rapid onset of cyanosis.
3. Reduced renal concentrating function — need more water.
4. Greater risk of hypothermia due to relatively larger surface area.
5. Greater sensitivity to opioids, partly due to nervous system immaturity, partly to hepatic
clearance.
6. Larger volume of distribution for water-soluble drugs.
Comment: the question sounds complex, but the answer is quite simple!

Failure to mention sensitivity to opioids.
<><><><><><><><><><><><>
Write short notes on EMLA cream

Pharmacy:
Type of chemical (eutectic mixture of local anaesthetics), storage (cream in a tube),
preparation, concentration (2.5% lignocaine; 2.5% prilocaine)
Pharmacodynamics:
Mode of action, local analgesia
Clinical effects, to make venpuncture painless
Dose, 5 ml.
Onset, 1 hr.
Duration, as long as applied
Pharmacokinetics:
Routes of administration, topical
Metabolism, liver
Side effects, Risk of being eaten (with its dressing) by a child
<><><><><><><><><><><><>
Page 32
What psychological factors influence your anaesthesia for children aged 2-3 years?
1. Very easily frightened — need to be seen with parents and spoken to kindly; need discussion
of place of premedication, including day cases.
2. Highly dependent on parents — development of rapport with them is a high priority.
3. Tolerate pain badly
a) need EMLA or similar cream for venepuncture and discussion of management of gaseous
induction
b) need careful analgesia (but sensitive to opioids and not able to control own PCA) — need
discussion of pro's and con's of the main techniques for pain relief.
Comment: The question sounds complex, but the answer is quite simple!

Failure to mention fear and pain.
<><><><><><><><><><><><>
What facilities are required for transfer of a 2-month old baby to a paediatric unit?
A trolley which is easily mobile and physically secure, warm, with O2 supply, humidification,
IPPV available (secure tracheal tube if appropriate), good IVI. Monitoring which is portable,
shakeproof, battery powered (need SpO2, EtCO2, ECG, pulse meter, thermometer;
laryngoscopes, spare tracheal tubes and i.v. cannulas.)
Drugs and other facilities for CPR. Easy access to the patient.
Trained assistants/facilities for, and rapport with, accompanying parent.
<><><><><><><><><><><><>
Page 33
A 6-week old child has projectile vomiting and is presented for laparotomy. Describe the
general anaesthetic problems of this case.
1. Alkalosis (needs treatment to lower the serum bicarbonate below 30 mmol/L).
2. Dehydration (needs IVI and full rehydration).
3. Hyponatraemia (need IVI with half strength saline).
4. Hypokalaemia.
5. Full stomach (regurgitation risk — need for preoperative nasogastric tube with clear
washouts and rapid sequence induction of anaesthesia).
6. Small size of patient, with special paediatric problems — risk of hypothermia, risk of
overventilation, risk of fluid overload, sensitivity to opioids, narrow cricoid ring, short
trachea, more difficult intubation. If the patient is a premature baby, extra risk of
intracranial haemorrhage.
Comment: This is a safety question.

Failure to mention alkalosis and regurgitation risk.
<><><><><><><><><><><><>
Describe the management of acute epiglottitis in a child of three years.

Rapport with parents. Minimum interference with child prior to careful transfer to theatre with
humidified O2, ENT surgeon standing by, careful O2/halothane or sevoflurane induction,
difficult intubation (with possible use of steroid cream), throat swab; then — need for IV
infusion, blood tests for bacteria and RSV, antibiotics (usually cephalosporin for Haemophilus
A), IPPV, sedation, humidification, transfer to ITU, fluid management, protocol for eventual
extubation.
Comment: This condition is rapidly becoming rare.

Failure to mention careful gas induction and difficult intubation.
<><><><><><><><><><><><>
Page 34
Describe the management of acute laryngotracheitis in a child of three years of age,

presenting with cyanosis
Rapport is established with parents.
Humidified O2 therapy; cyanosis makes this case severe enough to require intubation; induction
of anaesthesia (gas or iv), potentially difficult intubation, throat swab; need for rehydration by
i.v. infusion, blood cultures for bacteriology and virology, antibiotics (broad spectrum in the first
instance), ITU, IPPV, sedation, humidification, paediatric fluid management, protocol for
eventual extubation.
<><><><><><><><><><><><>
What are the aims of premedication in children? Describe the pharmacology of two such
premedicant drugs
1. Needs a comment on sedation, analgesia, drying secretions, routes of administration; and
about which patients need greater and which need lower dosage.
2. Needs comment on selection criteria for premedication in children and influence on
dosages of premedicants in children with relevant concomitant diseases, e.g., effect of
Downs syndrome on dosages of sedatives.
3. Details about two drugs, e.g., benzodiazepines, atropine, hyoscine, trimeprazine; using the
format described for answers on ''write short notes on" questions.
Comment: An easy answer for those who premedicate children. In answer to the first part of the
question, it would also be acceptable to argue the case against premedicating children!
<><><><><><><><><><><><>
Page 39
Chapter 4
Neuroanaesth
esia
Page 40
How does concomitant head injury influence your anaesthetic management of operation
for a fracture of the hand?
Monitoring of head injury required as it may be getting worse — monitoring of GCS. The
intracranial critical volume/pressure compliance point may be reached suddenly.
If the head injury is unstable, cerebral oedema would be worsened by coughing, straining,
vomiting, and jugular venous obstruction. Hypoxia, and hypercapnia may critically compress
brain, and hypotension would carry risk of cerebral hypoxia. Operation may need to be
postponed.
If head injury is stable and improving, brachial plexus and wrist blocks and local infiltration
are OK, Biers block OK, but care is needed with dosages of local anaesthetics because of side
effects.

Failure to mention intracranial pressure, and regional blockade.
<><><><><><><><><><><><>
What monitoring do you consider necessary for a posterior fossa craniotomy? What are
the possible sources of error associated with two of the monitors you mention?
List of monitors (with sources of
error in brackets). Noninvasive BP
(inaccurate on large arms).
Invasive arterial pressure (damping, clotting in cannula, zero errors, height of transducer).
Pulse oximetry (mechanical and electrical interference; digit too large or too small for
transducer; abnormal haemoglobins; venous pulsation; delay in alerting hypoxia).
Capnography (sampling site too far from lungs, blocked sample tube, interference by N2O, leak
in sample tube, monitor wrongly calibrated).
Agent monitoring (interference by N2O).
FiO2 (blocked sample tube, leak in sample tube, monitor wrongly calibrated, fuel cell dead).
Pulse (if counting from ECG, a high T wave can apparently double the rate, if counting from a
digit, electrical and mechanical interference).
Air embolus doppler (errors due to wrong direction).
CVP (catheter tip peripheral — reading is too high, catheter tip in right ventricle — reading is
too high; damping, clotting in cannula, zero errors, height of transducer).
Page 41
Describe the physiological effects of high arterial carbon dioxide tension (10 kpa, 70
mmHg.)
Effects of high CO2:
On general circulation — increased arterial pressure; raised arteriolar tone, dilation of skin
blood vessels.
On cerebral circulation — vasodilation, increase in flow and volume of vessels. Raising of ICP.
On respiration — stimulation of
rate and depth. On oxygen
dissociation curve — move to the
right. On coronary flow — increase.
On heart — arrythmias; increased force of myocardial contraction,
On muscle — increased tone.
On pH — reduction
On adrenal — secretion of
adrenalin. Rise of
intraocular pressure.
CO2 narcosis may supervene.

Failure to mention cerebral circulation.
<><><><><><><><><><><><>
What factors affect cerebral blood flow? State briefly their importance in relation to
anaesthesia within 12 hours of head injury
Control Factors
• a rise of CO2, increases it;
• a rise of venous pressure reduces it;
• arterial pressure (autoregulation controls it between MAP of 40-140);
• extracellular pH (acidaemia increases it);
• PO2 (hypoxia increases it);
• temperature (cold reduces it);
• neurogenic factors — various effects.
Pathological Factors
• raised intracranial pressure, due to vomiting coughing and straining reduces it;
Drugs
• examples are thiopentone, propofol, mannitol.
Serious omissions likely to cause a fail

Failure to mention effects of drugs.
Page 42
How may cerebral bloodflow be affected by general anaesthesia?

General anaesthesia — disruption of controlling factors by the anaesthetic; e.g., cardiovascular
instability, raised jugular venous pressure (coughing, vomiting, fluid loading, hypoxia,
intubation, IPPV, cardiac failure) hypercapnia, hypocapnia, hypothermia; hyperventilation with
low CO2 tension causes cerebral vasoconstriction;
• drugs — induction agents e.g., propofol, thiopentone (reduce it);
• anaesthetic volatile agents (increase it);
• Other drugs, for example fentanyl, ketamine.
Comment: This answer also needs a little discussion of the significance to the anaesthetist of
raised intracranial pressure.
<><><><><><><><><><><><>
Page 43
Chapter 5
Obstetric Anaesthesia
Page 44
How do obstetric factors affect the management of anaesthesia for the removal of a
retained placenta?
1. A retained placenta can cause severe blood loss, therefore good IV access essential,
and that potential hypovolaemia is as dangerous in regional block as in general
anaesthesia.
2. Acid gastric juice — with risks of severe pneumonitis from regurgitation and aspiration.
3. Pre-partum narcotic drugs may have been given, which will accentuate responses to
anaesthesia.
4. The possible presence of an existing epidural for obstetric analgesia, which can be used for the
anaesthetic.
5. The sensitivity of the postpartum uterus to the relaxing effect of halothane.
6. Oxytocic-induced vomiting and the need for antiemetics.

Failure to mention haemorrhage and shock; and risk of aspiration of gastric acid.
<><><><><><><><><><><><>
Write short notes on ranitidine

Pharmacy:
Type of chemical, storage (glass ampoules, tablets)
Pharmacodynamics:
Mode of action, H2 antagonist
Clinical effects, reduction of volume and acidity of gastric juice
Dose, 150 mg.
Onset, 1 hr.
Duration, 4 hrs.
Pharmacokinetics:
Routes of administration, oral, i.m., i.v.
Metabolism, liver
Excretion
Side effects, cardiovascular disturbances, bradycardia, AV block, asystole; CNS disturbances
— mental confusion, headache dizziness; anaphylaxis, nosocomial pneumonia
Interactions, in porphyria and
phenylketonuria Plus other
features: no effect on cytochrome
P450
Page 45
Describe the anaesthetic management of massive intrapartum haemorrhage requiring

emergency operation
1. Give oxygen.
2. Stop haemorrhage — need for oxytocics; immediate delivery and even emergency
hysterectomy. Need for large, fast infusion to replace bloodloss.
3. Anaesthetic for severely shocked patient (hypovolaemia, acute anaemia, oxygen carriage
problems), who may have a full stomach with acid gastric juice.
4. Organisation for massive transfusion.
5. Risk of DIC — organisation for fresh frozen plasma.
6. Preservation of renal and splanchnic function with dopamine, dopexamine, diuretics.
7. Later — ARDS or MSOF or ileus may require intensive care.

Failure to mention massive transfusion; renal and other organ function.
<><><><><><><><><><><><>
Describe the pathophysiological processes of pre-eclamptic toxaemia of pregnancy

Pre-eclamptic toxaemia arises from changes in the placenta which lead to:
• hypertension;
• albminuria;
• DIC, with coagulopathy;
• low platelets (function may be reduced by aspirin);
• intrauterine haemorrhage;
• convulsions (exact process not clear) with hypoxia;
• placental failure (baby at risk);
• sodium retention;
• patients are waterlogged, yet hypovolaemic;
• HELLP syndrome may occur.

Failure to mention abnormalities of haemostasis, convulsions and placental failure with risk to
baby.
Page 46
You are asked to help with a case of severe pre-eclamptic toxaemia of pregnancy. What is
your management?
1. Assessment: hypertension, proteinuria, weight gain. How serious and how acute is it?
2. Monitoring the baby. Is there temporary or continuous bradycardia?
3. Clinical monitoring of the mother. Is there hyper-reflexia or incipient convulsions?
4. Monitoring: arterial pressure, blood gases, platelet levels, coagulation screen, CVP, urinalysis.
5. Treatment: there should be a continuous attempt to make all abnormal parameters
normal. Arterial pressure control is a high priority (IV colloid, epidural, hydrallazine,
alphamethyldopa), magnesium sulphate to prevent convulsions.
FFP for coagulopathy, attempt at early delivery. If general anaesthetic is required, upper
airway oedema may make intubation difficult.
The risks to mother may continue after operation.

Failure to mention magnesium sulphate or to consider the baby.
Page 47
Chapter 6
Cardiothoracic Anaesthesia
Page 48
Describe the anatomy of the trachea, including its relations

Origin (cricoid, C6); termination (carina, T4); tubular midline structure of horseshoe-shaped
cartilages (keep airway open), fascia and muscle; lined by ciliated epithelium, which moves
mucus. Innervated by recurrent laryngeal nerves and vagi; blood supply from thyroid arteries,
draining to inferior thyroid plexus.
Relations:
Neck – pretracheal fascia, strap muscles, thyroid, platysma; laterally – carotid sheath, recurrent
nerves and vagi, posteriorly – oesophagus.
Chest – anteriorly innominate artery, vein, aorta; laterally subclavian arteries, recurrent nerves
and pleura on right side; posteriorly oesophagus. Carina is related to pulmonary artery
bifurcation.
Comment: In an anatomy question, extra marks can often be gained by noting the function of
the structure in question. In this case it is simply the airway!
<><><><><><><><><><><><>
Describe the anatomy of the diaphragm, including its relations

A sheet of muscle, arising from the lower 6 costal cartilages, the xiphisternum, arcuate
ligaments and crura; inserted into central tendon. There are three main openings – for
oesophagus, aorta, and inferior vena cava. (Also perforated by thoracic duct and hemiazygos
vein).
Function:
Rhythmic respiration and abdominal straining. Innervated by phrenic nerve (C345); blood
supply from surrounding vessels, e.g., internal mammary artery.
Relations:
Above – pleura, pericardium, lungs, heart, ribs, spine, oesophagus (passing through hiatus)
aorta, inferior vena cava; below – stomach, spleen, liver, kidneys, arcuate ligament.
Page 49
Describe the arterial blood supply of the myocardium

1. R coronary (dominant in 50%) from right coronary sinus, between aorta and right auricle,
goes down right atrioventricular groove (marginal branch down right ventricle), to posterior
atrioventricular groove, to anastomose with left coronary, with posterior interventricular and
posterolateral branches. Supplies SA node, AV node, Bundle of His, pulmonary conus.
2. L coronary (dominant in 20%) from left (posterior) sinus between left auricle and
pulmonary trunk, gives left anterior descending (anterior interventricular) branch which
supplies anterior left ventricle, septum and bundle branches. It continues as circumflex in
atrioventricular groove, with obtuse, marginal and left lateral branches.
<><><><><><><><><><><><>
Describe the venous drainage of the myocardium

1. Thebesian veins (venae cordis minimae) drain into the cavities of the heart. Anterior cardiac
veins open into right atrium.
2. The coronary sinus drains 90% of left ventricular blood supply from five tributaries
(great, middle and small cardiac veins; posterior vein of left ventricle, and oblique vein
of left atrium).
3. It lies in the atrioventricular groove, and drains into the right atrium to the left of the opening
of the inferior vena cava.
Page 50
Describe the conducting system of the heart

This system is specialised myocardial tissue and has pacemaker activity and conduction
functions.
SA node on right side of SVC root, near the top of the crista terminalis and the right auricle.
There are 3 internodal pathways (anterior, middle, posterior).
Function:
It contains P cells which generate impulses.
Other (pathophysiological) pathways: Bundle of Kent bypasses AV node, James fibres go to
Bundle of His.
AV node on right side of central fibrous body (has labyrinthine structure which delays
conduction and limits number of impulses coming through), has atrionodal, nodal and nodal-His
regions. Bundle of His is inferoposterior to membranous portion of septum. left bundle (below
posterior cusp of aortic valve) has 2 branches which ramify in the muscle of left ventricle and
interventricular septum. right bundle goes under base of anterior papillary muscle of tricuspid
valve (as the moderator band) and ramifies in the muscle of the right ventricle.

Sinuatrial and atrioventricular nodes.
<><><><><><><><><><><><>
How may abnormalities of cardiac conduction be revealed by the electrocardiogram?

• Atrial fibrillation;
• Heart block;
• Bundle branch block;
• Re-entry arrythmias, and their significance (usually ischaemic). Mention of oesophageal and
intracardiac leads;
• Sick Sinus Syndrome.
Comment: Each one needs a small description of what the abnormality looks like.
Page 51
Describe the anatomy of the bronchial tree

1. The bronchial tree extends from the carina to the bronchioles.
2. It is a branching tubular structure, stiffened by small rings and plates of cartilage. Lined
by pseudostratified columnar ciliated epithelial cells with goblet and serous cells.
Bronchial artery supply from aorta (and third right posterior intercostal artery), to
pulmonary and azygos veins.
3. Nerve supply from the pulmonary plexus — vagus is constrictor, adrenergic is dilator;
nonadrenergic, noncholinergic (NANC) system is bronchodilator and mucus secreting.
4. R main 15mm x 2cm from carina to intermediate bronchus. Branches — upper — APA,
middle — LM, lower — AMALP. (Each letter represents the name of a branch)
5. L main 13mm x 5cm, Branches: left upper APA (lingular SI), lower-APAL.
6. Lower bronchi down to 16th division end as terminal bronchioles.
<><><><><><><><><><><><>
Describe the nerve supply of the larynx

Branches of vagus nerve:
Superior laryngeal nerves — external — motor to cricothyroid; internal — sensory from mucosa
above cords.
Recurrent laryngeal nerves — sensory below cords and motor to the other small muscles. They
arise in the chest, curve round the aorta and subclavian artery, and return to the neck alongside
trachea and oesophagus. They enter the larynx behind the cricothyroid joints, beneath the
lower part of the pyriform recess.
Comment: This is an easy question!
Page 52
Describe the anatomy of the first rib, including its relations

First rib has upper and lower surfaces (lower surface featureless), curves downwards and
forwards, sickle shaped, head articulates with body of T1, and tubercle with transverse process,
muscle insertions: scalenus anterior inserted into scalene tubercle (vein in front, artery behind),
lev. costae and serratus anterior inserted into lateral border. Function: formation of rib cage
and respiration.
Relations:
• lower surface — pleura;
• medially — pleura, thoracic duct;
• neck of rib — root of T1, vagus, phrenic nerves and sympathetic chain;
• laterally — posterior triangle of neck;
• inferiorly — first intercostal space, with intercostal muscles vessels and nerves;
• superiorly — clavicle, subclavius, the brachial plexus crosses from superomedial to
inferolateral, the subclavian artery and vein cross the medial end of the first rib and join the
brachial plexus.
Page 53
Chapter 7
Trauma and Emergency Anaesthesia
Page 54
What are the effects of an overdose of a tricyclic antidepressant drug?

1. Autonomic; sympathetic stimulation and anticholinergic effects.
2. Brain; sedation, convulsions, coma.
3. Cardiac; tachyarrythmias; cardiac failure (most inotropes make tachyarrythmias worse).
4. Drug overdose effects in general; often overdosed with other drugs and alcohol, loss of
airway control, regurgitation risk, skin necrosis, hypothermia, retention of urine.
Comment: It helps to categorise these effects.

Failure to mention convulsions and tachyarrythmias
<><><><><><><><><><><><>
A child of 12 years has been admitted following a road accident. At emergency

laparotomy the surgeon announces that the liver is ruptured. Describe your management
of the case up to the end of the operation
This is severe road trauma and needs a comment about search for, and possible presence of,
other injuries, especially head injury.
• organise massive blood crossmatch, and supplies of fresh frozen plasma;
• circulatory support (drugs and colloids and crystalloids in severe haemorrhage), citrate
problems;
• diagnosis of blood clotting abnormalities, with intraoperative coagulation screening;
• keeping the patient warm;
• blood glucose support;
• organisation of ITU;
• keeping parents informed of progress;
• perhaps consider secondary transfer to liver unit.

Failure to mention managing massive transfusion.
<><><><><><><><><><><><>
Page 55
Write short notes on Hartmann's solution

Pharmacy:
type of chemical (intravenous electrolyte solution) storage (glass or plastic) preparation,
concentration (isotonic) Na+ 131; K+ 5; Cl- 111; Ca++ 2; Lactate 29; mmol/l.
Pharmacodynamics:
mode of action, water and electrolyte replacement
clinical effects, rehydration
dose, appropriate to clinical situation — e.g., 500ml/4-6 hrs
onset,
immediate
duration,
N/A
Pharmacokin
etics:
routes of administration, i.v.
excretion, kidney
interactions, lactate load is unsuitable for
diabetic patients Plus other features: same
electrolyte concentrations as plasma
<><><><><><><><><><><><>
Describe the adverse affects of blood transfusion. How may they be reduced?
1. Acute and delayed haemolytic reaction, circulatory overload, hypothermia, embolism,
hyperkalaemia, citrate intoxication, crossinfection, ARDS, immunosuppression,
hypomagnesaemia, hypocalcaemia, coagulopathy.
2. Reduction of adverse effects:
a) Set up a good transfusion service! (the administrative side, including correct labelling is as
important as the technical side);
b) Warm the blood during transfusion;
c) Ca++ and fresh frozen plasma are given to correct coagulopathy. Platelet transfusion may be
needed;
d) Autotransfusion, cell savers and predonation solve many of these problems;
e) Monitor the patient for overload and transfusion reactions.

Most of the complications.
<><><><><><><><><><><><>
Page 56
Describe the alternatives to donor blood transfusion

1. Colloid infusion (which will be limited by progressive anaemia).
2. Autologous transfusion — predonation/perioperative haemodilution cell savers/salvage with
reinfusion.
3. Fluorocarbons—fluosol emulsion 5ml/dl. O2 carriage @ FiO2 1.0.
4. Haemoglobin infusion with 2,3 DPG analogue (nephrotoxicity of red cell stroma).
Comment: The above items should be described in detail.
<><><><><><><><><><><><>
What are the contents of a unit of transfusion blood? Describe briefly the alternatives
which can be used in an emergency haemorrhage situation until transfusion blood
becomes available
Contents:
350 ml. blood, 150 ml. CPD adenine or SAGM. (Most is plasma-reduced and therefore low in
albumin and globulins). It becomes progressively more hyperkalaemic and acidotic during
storage, with lower clotting factors and low platelets.
Alternatives:
Colloids: dextran 70, gelofusine, hespan, haemaccel, hetastarch, albumin.
Crystalloids: normal saline, Hartmann's solution, 5% dextrose.
<><><><><><><><><><><><>
Page 57
Write short notes on Gelatin-based plasma substitutes

Pharmacy:
Type of chemical (high molecular weight colloids 30-70 K.Daltons) storage (glass or plastic),
preparation, concentration (frequently slightly hypertonic)
Pharmacodynamics:
Mode of action, expansion of the plasma
compartment Clinical effects, resuscitation
from shock and haemorrhage Dose,
appropriate to clinical situation
Onset, immediate
Duration, hours
Pharmacokinetics:
Routes of
administration, i.v.
Metabolism, very little
Excretion, via kidneys
Side effects, allergy, risk of overinfusion
Comment: This answer will also need details of the various types of product.
<><><><><><><><><><><><>
Describe the features of the Boyle's anaesthetic machine and Bain system which protect
the patient from pulmonary barotrauma
The following items need to be addressed:
1. Reducing valve and flow restrictor for cylinders, needle valves on flowmeters to restrict
flow, thin-walled bag, which limits pressure rises, heidbrink valve (the pressure relief
valve protects the machine, not the patient).
2. Airway pressure limiter (and its limitations).
<><><><><><><><><><><><>
Page 58
What physiological changes follow acute hypovolaemia?

Definition: imbalance between circulating volume and capacity of circulation.
1. Blood volume falls causing reduced venous return; reduced RA pressure, CO.
2. Reduced cardiac output causes systolic and pulse pressure fall.
3. Baroreceptors firing reduced, leads to tachycardia, vasoconstriction, adrenaline secretion,
Cortisone secretion, redistribution of CO from skin, muscle and viscera to heart and brain. BP
maintained till loss of 20% volume.
4. Atrial receptors cause ADH secretion (resulting in oliguria and water retention).
Aldosterone secretion (causes Na+ retention), thirst, endorphin secretion, water transfer
from ECF to circulation, resulting in dilutional anaemia.
5. Carotid chemoreceptors stimulation causes hyperventilation.
6. Cold periphery, pallor, cyanosis, reduced capillary refill.

Baroreceptors, ADH, shift of water into circulation.
<><><><><><><><><><><><>
What is the physiological response to the rapid loss of 1 litre of blood in the adult?
1. General description of the clinical picture in the hypovolaemic patient with fall of
cardiac output, vasoconstriction and hypotension. Some indication of signs—reduced
capillary refill, tachycardia, oliguria, distress, loss of muscle tone.
2. Compensation:
a) baroreceptors—arteriolar resistance, venoconstriction, cardiac effects (tachycardia,
raised diastolic) respiratory effects (hyperventilation);
b) pituitary renal/adrenal axis, renin, angiotensin, ACTH, ADH;
c) fluid shifts from ECF to blood, with timescale.
Comment: This is similar to the previous question, and demonstrates that any subject may be
asked in several different ways.
<><><><><><><><><><><><>
Page 59
Outline the factors responsible for the maintenance of cardiac output

1. Venous return, myocardial contractility (Starling's Law of the heart).
2. Sympathetic and parasympathetic activity.
3. Diastolic coronary blood flow and PaO2, supplying the substrates for muscle action.
4. Inotropic hormones, PaCO2 levels, and heart rate (especially in children)—Bowditch effect.

Failure to mention Starling's law, inotropic hormones and nerve control of heart.
<><><><><><><><><><><><>
What are the causes and effects of hypothermia?

Causes:
Conduction, convection, radiation, and cooling of the blood.
radiation to cold surroundings (note the importance of ambient temp),e.g., drowning;
convection: evaporation of skin prep or water vapour from exposed serous cavities during
operation, especially when there is vasodilation, loss of hypothalamic control, absent shivering
response (due to anaesthesia or alcohol intoxication); dry, cold inspired gases;
conduction of heat to cold surroundings, as when a limb is packed in snow, or a donor organ
transported in melting ice;
cooling of the blood: cold IV infusions, deliberate hypothermia during cardiopulmonary bypass.
Effects:
Dysrythmias at < 31° C. Prolonged action of general anaesthetics and relaxants, slow
metabolism of drugs and citrate, increased Hb oxygen affinity, fall in CBF, reduced O2
consumption, peripheral vasoconstriction, acidosis, coagulation problems, shivering and
hypoxia on recovery.
<><><><><><><><><><><><>
Page 60
Describe the immediate rescusitation (in the first hour) of an unconscious patient admitted
to the A & E department after falling off a ladder
Primary survey—the main elements of ATLS. Airway, Breathing, Circulation—pulse, BP,
capillary refill (hypotension is likely to be due to extracranial bleeding or spinal injury);
Disability of cerebrum (level of consciousness, pupils, GCS monitoring is commenced);
Exposure (other injuries).
Cervical support collar is placed until cervical spine is
known to be stable. Resuscitation.
IV access is
established.
O2 is given.
Items A and B; O2, intubation (with care of cervical spine); cricoid pressure (because of the
vomiting risk); note of the appropriate anaesthetic drugs; and IPPV.
C: volume replacement as necessary with monitoring of arterial pressure,
capillary refill, urine output and CVP. Monitoring: ECG, arterial pressure,
CVP, pulse oximetry, capnography.
Investigations: FBC, Cross-match, ABG's. Blood sample for drug
levels if history indicates this. X ray: chest, skull, neck, pelvis.
Secondary survey: more detailed examination and repeated further assessments.

Cervical collar, oxygen, the vomiting risk, and the main elements of ATLS.
<><><><><><><><><><><><>
Page 61
Chapter 8
Acute and Nonacute Pain Management
Page 62
What are the medical effects of opioid drugs?

1. Analgesia
2. Addiction
3. Respiratory depression
4. Nausea and vomiting
5. Bradycardia
6. Miosis
7. Sedation
8. Hallucinations
9. Bronchospasm
10. Biliary spasm
11. Renal colic
12. Slowing of premature labour
13. Itching
14. Histamine release
15. Muscle rigidity

Failure to mention respiratory depression and addiction.
<><><><><><><><><><><><>
Write short notes on pethidine

Pharmacy:
Type of chemical, (phenylpiperidine) storage (aqueous in glass ampoules), preparation
(synthetic) concentration
Pharmacodynamics:
Mode of action opioid agonist
Clinical effects, analgesia, respiratory depression, nausea and vomiting, sedation, addiction,
relaxation of smooth muscle
Dose, 1
mg/kg.
Onset,
minutes
Duration, 2-4
hrs.
Pharmacokin
etics:
Routes of administration, oral, im., i.v., epidural
Metabolism, liver
Side effects, respiratory depression, nausea and vomiting, addiction, histamine release,
Interactions, MAOI's—collapse and coma
Plus other features: related to atropine, synthesised in 1939.
Page 63
Discuss the methods available for the relief of pain following abdominal hysterectomy
Advantages:
• NSAID's (reasonably powerful, no respiratory depression or vomiting).
• Other oral analgesics: very safe but most are not so powerful.
• IM opiates (powerful and safe).
• PCA (powerful, swift reaction to pain, patients can customise dosage to their own needs).
• Epidural catheters (superb, powerful analgesia).
This answer needs a note about customising treatment for the individual patient and discussing
patient preferences!
Complications:
• NSAID's (haemorrhage, ulcers, renal failure and bleeding).
• IM opiates (nausea, vomiting and delay in action).
• PCA (needs common sense, reasonably strong fingers and may cause vomiting and
hallucinations. Serious overdose has occurred.).
• Epidural catheters (weak, numb legs and risk of unrecognised apnoea from opiates; and
hypotension).

Failure to mention PCA, and the dangers of epidural opiates.
<><><><><><><><><><><><>
Page 64
Write short notes on tenoxicam

Pharmacy:
Type of chemical (nonsteroidal anti-inflammatory drug), storage (powder or tablet), preparation,
concentration
Pharmacodynamics:
Mode of action, local prostaglandin inhibition
Clinical effects, analgesia
Dose, 20-40
mg. Onset,
minutes
Duration, 10-
12 hrs.
Pharmacokinet
ics:
Routes of administration, oral, i.m., i.v.
Metabolism, liver
Side effects, platelet inhibition, gastric irritation, tendency to renal failure
Interactions, other NSAIDs
<><><><><><><><><><><><>
Describe the principles involved in prevention and treatment of postherpertic neuralgia in

the upper limb
Place of preventive analgesia of herpes zoster, acyclovir cream. This is neuropathic pain and is
self-limiting; may be helped by tricyclic drugs and other coanalgesics, local analgesics,
capsaicin cream, IV guanethidine block.
<><><><><><><><><><><><>
Compare and contrast pethidine and codeine

Both Controlled Drugs, analgesics and constipators; but codeine doesn't sedate and has less
respiratory depression by IM route. The examiner also needs to see the usual pharmacological
details e.g., using the answer format for questions which start ''Write short notes on. . .".

Respiratory depression.
<><><><><><><><><><><><>
Page 65
Describe the adverse reactions which may follow the use of non-steroidal anti-
inflammatory drugs
PGE1 synthase inhibition causing (reversible) gastric irritation, renal failure, exacerbation of
asthma, angioedema, rashes, water retention, aseptic meningitis in patients with SLE, hepatic
damage. Thromboxane A inhibition causes irreversible loss of the adhesiveness of existing
platelets.
Renal failure.
<><><><><><><><><><><><>
Describe the pharmacological eeffects of pparacetamol

Pharmacy:
Type of chemical (simple analgesic drug), storage (powder or tablet)
Pharmacodynamics:
Mode of action, central prostaglandin inhibition
Dose, 10-15
mg/kg. Onset,
minutes
Duration, 4-6
hrs.
Pharmacokinet
ics:
Routes of administration, oral
Metabolism, liver
Side effects, overdose causes serious hepatic damage
Interactions, potentiates other analgesics
<><><><><><><><><><><><>
Page 66
Describe the P0armacological effects of dextropropoxyphene

Pharmacy:
preparation (tablet), it is an opiod
Pharmacodynamics:
Mode of action, simple analgesia
Dose, 30-65
mg. Onset,
minutes
Duration, 6-8
hrs.
Pharmacokin
etics:
Metabolism, liver
Side effects, respiratory depression and acute heart failure; overdose convulsions
Interactions, potentiates other analgesics
<><><><><><><><><><><><>
Page 67
Chapter 9
Intensive
Therapy
Page 68
A patient is admitted to the intensive care unit with a relapse of myasthenia gravis. How
do you cope with the medical problems of this situation?
1. Identification of what caused relapse and treatment of infections if appropriate.
2. Problems of inability to swallow and excessive secretion of saliva due to anticholinesterases;
nasogastric tube and enteral nutrition will be required.
3. Respiratory failure (and how it is diagnosed) would indicate intubation and IPPV, with risk
of chest infections. Antibiotics may be needed for this.
4. Protection of the eyes because of inability to blink.
5. Prevention of bedsores and use of physiotherapy.
6. Plasmapheresis may be needed.
7. Steroid cover may be required.
Comment: The mention of ITU indicates that this relapse is severe, and the answer should
address this.

Failure to mention anticholineserases and respiratory failure.
<><><><><><><><><><><><>
A patient is admitted to the intensive care unit with Guillain Barre Syndrome. How do you
cope with the medical problems of this situation?
1. Identification of the degree of disability.
2. Problems of inability to move and the unhappiness this causes.
3. Intubation and IPPV for respiratory failure, with risk of infections. Antibiotics may be needed.
4. Prevention of bedsores and use of physiotherapy.
5. Steroid cover may be required.
6. Will this be a short- or long-term case? How will nutrition be provided?
<><><><><><><><><><><><>
Page 69
Why do some patients develop ARDS following colectomy? What are the
pathophysiological processses?
The sequence of events may be:
gut wall ischaemia — endotoxinaemia — eicosanoid secretion — endothelial damage —
capillary closure — tissue hypoxia and oedema — destruction of type I cell — proliferation of
type II cells — hyaline membrane formation — shunting, hypoxia — deadspace, hypercapnia—
barotrauma (due to IPPV)—lung destruction.

Failure to mention endotoxin and generalised endothelial damage.
<><><><><><><><><><><><>
Describe the complications of endotracheal intubation.

Short Term:
• cardiovascular—reflexes due to intubation;
• bronchospasm;
• endobronchial intubation resulting in one-lung ventilation;
• oesophageal intubation by mistake;
• kinking of tube with respiratory obstruction;
• obstruction of tip against tracheal wall;
• herniation of cuff;
• laryngospasm on extubation;
• sore throat;
• subglottic oedema and stenosis in children;
• throat packs left in, causing obstruction.
Longer Term:
• candida/haemorrhage/crusting/dilation of trachea/stenosis of trachea.

Failure to mention obstruction and nosocomial infection in the longer term.
<><><><><><><><><><><><>
Page 70
What is the venturi principle? Describe the clinical uses of high frequency jet ventilation
Principle:
High speed gas jet causes suction on surrounding areas with
entrainment of surrounding gas. Rates: 1-1.5 Hz. 1.5-5 Hz. 5-10 Hz.
(high frequency oscillation).
Uses:
• rigid bronchoscopy and intratracheal surgery;
• for the development of intrinsic PEEP in the intensive care case;
• reduction of pulmonary barotrauma in ARDS;
• to allow reduced requirement for sedation during IPPV;
• reduction of pulmonary leak during IPPV in cases of bronchopleural fistula.
<><><><><><><><><><><><>
Describe the anatomy of the subclavian vein

The subclavian is the continuation of the axillary vein, from lower border of first rib. Arches
up across rib, then medial, downwards and forwards, across scalenus anterior insertion to enter
thorax, and join internal jugular vein behind sternoclavicular joint. Anterior is clavicle, postero-
laterally lies subclavian artery and pleura, posteriorly is vagus and phrenic nerves.
<><><><><><><><><><><><>
Describe the anatomy of the internal jugular vein

Jugular—large thin-walled vein, traverses the neck from jugular bulb to subclavian vein; in
carotid sheath with artery and vagus. From above lies posterior, then lateral, then anterior to
artery. The lower part is behind sternomastoid. It lies in front of prevertebral fascia, vertebral
muscles, transverse processes, and lower down, subclavian artery, phrenic, vagus, and cupola
of pleura.
<><><><><><><><><><><><>
Page 71
What are the possible complications of internal jugular vein cannulation, and how do you
avoid them?
Complications:
Air embolism, pneumothorax, carotid or vertebral artery puncture with cerebral damage,
haematoma, sepsis, sympathetic trunk damage, surgical emphysema.
Avoidance:
a) position of patient, head down;
b) careful preparation of skin;
c) landmarks; (midpoint between mastoid and manubrium, lateral to carotid artery);
d) use of seldinger wire system and careful direction of insertion;
e) avoidance of unwanted damage to other structures in neck by good knowledge of anatomy
and inserting needle in upper half of neck to avoid pleura;
f) aspiration test for position of cannula tip;
g) chest X-ray for position of cannula tip.

Failure to mention pneumothorax and carotid artery puncture.
<><><><><><><><><><><><>
What are the possible complications of subclavian vein cannulation, and how do you avoid
them?
Complications:
Air embolism, pneumothorax, artery puncture, haematoma, sepsis, thoracic duct injury on left,
surgical emphysema.
Avoidance of Complications:
a) position of patient — head down;
b) careful preparation of skin;
c) landmarks; 1 cm below midpoint of clavicle;
d) use of seldinger system and careful direction of insertion towards suprasternal notch;
e) avoidance of unwanted damage to other structures e.g., pleura by not allowing needle to go
between ribs;
f) aspiration test for position of cannula tip;
g) chest X-ray for position of cannula tip.

Failure to mention pneumothorax.
<><><><><><><><><><><><>
Page 72
Describe the pharmacology of a drug used to relieve severe pulmonary vasoconstriction

An example would be: prostacyclin (inhibits platelet aggregation, half life 3 min., infusion 2-5
µg/kg/min, side effects — pulmonary and systemic vasodilation, bradycardia, flushing,
headaches hypotension, pallor, sweating, severe anticoagulation with heparin);
thrombocytopenia.
a description of nitric oxide is also appropriate
<><><><><><><><><><><><>
List the properties of an ideal inotrope. Compare the properties of dopamine with this
ideal
Effective in normal and abnormal hearts, doesn't raise myocardial VO2; raises renal and
splanchnic perfusion, preventing endotoxinaemia; no side effects, no alpha effects, no
arrythmias. Dopamine comes out quite well!
<><><><><><><><><><><><>
List the factors which determine the supply of oxygen to the tissues of the body. How may
these factors be altered by septic shock?
Factors:
• O2 supply to lungs;
• respiratory drive and adequacy of ventilation;
• pulmonary O2 transfer (shunting and V/Q mismatch);
• Hb level and O2 affinity of haemoglobin, including shifts of the O2 dissociation curve;
• cardiac output and blood distribution;
• capillary function;
• body temperature.
Alteration by Septic Shock:
• reduction of lung function, cardiac output, arterial pressure;
• unbalanced blood distribution;
• endothelial swelling, capillary closure;
• tissue oedema;
• bypass of capillaries via arteriovenous anastomoses.
<><><><><><><><><><><><>
Page 73
Write short notes on gastric tonometry

Need a description of how pHi is derived and measured (catheter with a balloon, completely
filled with saline. CO2 from gastric mucosa diffuses into this, and a sample is withdrawn and
measured. At the same time, serum bicarbonate is measured, and pHi derived from the
Henderson-Hasselbalch equation) and in which situations it is deranged (pHi is reduced in
shock, sepsis and hypotension).
<><><><><><><><><><><><>
Write short notes on pulmonary capillary wedge pressure

Need comment on:
• method of inserting the flotation catheter, e.g., via internal jugular line;
• pressures during insertion, in the superior vena cava, right atrium, right ventricle, and
pulmonary artery;
• interpretation of readings;
• complications of technique (e.g., infection, arrythmias, damage to pulmonary vessels).
<><><><><><><><><><><><>
Write short notes on Sucralfate

Pharmacy:
Type of chemical, storage (liquid), preparation, concentration
Pharmacodynamics:
Mode of action, physical protection of gastric mucosa
Clinical effects, at pH < 4 polymerises and adheres to ulcer craters, preventing peptic ulceration
Dose, 2 g. twice
daily Onset,
immediate
Duration, hours
Pharmacokinetics:
Excretion, via GI tract
Side effects, no effect on gastric pH
Plus other features: the name means sucrose (aluminium) sulphate — it increases gastric
production of mucus, and does not cause nosocomial pneumonia.
<><><><><><><><><><><><>
Page 74
Write short notes on dopamine

Pharmacy:
Type of chemical (catecholamine), storage (aqueous solution in coloured glass ampoules),
preparation, concentration
Pharmacodynamics:
Mode of action, stimulation of adrenergic and dopamine receptors
Clinical effects, inotrope, renal vasodilator
Dose, 1-10 µg/kg/min.
Onset, immediate
Duration, very transient unless infused
Pharmacokinetics:
Metabolism, liver
Side effects, vasoconstriction in high dosage
<><><><><><><><><><><><>
Discuss the occurrence of metabolic acidosis in patients in the intensive care unit
1. Causes — tissue hypoxia, renal failure, insulin antagonism (with the various acids involved).
2. Prevention — The methods of preventing the above, and their considerable limitations.
3. Treatment — need discussion of the problems of bicarbonate.
<><><><><><><><><><><><>
Give a brief account of the pulmonary problems that occur during intermittent positive
pressure ventilation of the lungs in ARDS
Notes for an answer should include the following aspects:
misplacement of tracheal tube, crusting, deadspace problem due to capillary blockage, shunting
problem due to hyaline membrane, diffusion problem due to oedema, barotrauma due to
hyperventilating normal lung in juxtaposition to areas of stiff diseased lung. Secondary
nosocomial infection.
<><><><><><><><><><><><>
Page 75
Write short notes on prostacyclin

Pharmacy:
Type of chemical (natural hormone), storage (aqueous solution in glass ampoules)
Pharmacodynamics:
Mode of action, inhibits platelet aggregation
Clinical effects, pulmonary and systemic vasodilation, used in haemofiltration
Dose, infusion 2-5 µg/kg/min.
Onset, immediate
Duration, half-life
3 min.
Pharmacokinetics:
Metabolism, liver
Side effects, pulmonary and systemic vasodilation, bradycardia, flushing, headaches
hypotension, pallor, sweating
Interactions, severe anticoagulation
with heparin Plus other features:
used in haemofiltration
<><><><><><><><><><><><>
Page 77
Chapter 10
Clinical Measurement
Page 78
Describe the physical principles of the pulse oximeter

Hb and HbO have different absorption spectra. Light absorbed depends on their concentrations
and the thickness of the medium.
(Beer-Lambert Law; there is some doubt about the relevance of this.) Comparison of
absorption at different wavelengths (not necessarily the isobestic point) gives relative
concentrations of HbO and Hb, the SpO2. Infrared light from diode emitter passes through or is
reflected from skin to a photodetector. The steady (DC) component is rejected. The pulsing
(AC) component is amplified and displayed digitally or graphically. Calibration of each model
(at the top end of the SpO2 scale) is done using volunteers.
<><><><><><><><><><><><>
Describe the physical principles of a capnograph. How may it be calibrated?

Principle of the infrared device: two different atoms in a molecule cause infrared absorption;
infrared beam splits and passes through a reference and sample gas chambers. CO2 absorbs the
infrared and emergent beams are compared by photoelectric cells. Analyser sites may be direct
(instream) or indirect via withdrawn sample.
Calibration: electronic/physical; zero = air; span — using accurately known CO2 sample from
machine, cylinder or reference cell

Failure to mention zeroing the calibration.
<><><><><><><><><><><><>
Page 79
What information can a capnograph give about an anaesthetic?

End-tidal carbon dioxide monitoring may indicate:
• adequacy of ventilation;
• oesophageal intubation (no CO2 in gas);
• rebreathing (graph does not return to zero on inspiration);
• sodalime exhaustion (rising CO2);
• fall of cardiac output (falling CO2);
• PE; air embolism (sudden fall of CO2 excretion);
• MH (fast rising CO2);
• shock (low CO2 production);
• disconnection of anaesthetic system (sudden fall of CO2 to zero), emphysema, airtrapping
(sloping plateau);
• wearing off of relaxants (notching of capnograph plateau);
• death (cessation of CO2 production).

Failure to mention oesophageal intubation.
<><><><><><><><><><><><>
What are the sources of error of the pulse oximeter?

1. Sources of error: interference; mechanical (fingers too large for probe, movement artefacts),
electrical, light, nail polish and dirt.
2. COHb counted as HbO, so SpO2 falsely high.
3. Methylene blue, methaemoglobin and bilirubin counted as Hb, so SpO2 falsely low.
Inaccurate in presence of venous congestion (venous pulsation) or low SpO2 (not calibrated
in this range).
4. Warning of central hypoxia may be delayed.
5. Fails during poor tissue perfusion (a useful sign of poor perfusion).
6. Inaccurate during cardiopulmonary bypass.
Comment: In spite of these sources of error, pulse oximetry
is an excellent monitor!
<><><><><><><><><><><><>
Page 80
What arrangements are required for an adult head-injured patient, during transfer to a
neurosurgical unit?
1. Identification tag for patient.
2. Clear notes of injuries, with investigations (e.g., X-rays), and ongoing Glasgow Coma Score
chart.
3. Hard collar if cervical spine injury is suspected.
4. Intravenous infusion (or central line).
5. Intubation and ventilation of patients who are comatose, depressed conscious level, or who
have fitted; with added oxygen.
6. Monitoring, pulse oximetry, capnography, arterial pressure.
7. Administration of analgesic and relaxant.
8. Administration of mannitol or frusemide, if not already given.
9. Smooth slow journey, head-up position, trained escort.
<><><><><><><><><><><><>
What information can be gained from measuring central venous pressure?

a) Normal range: (with variations erect/supine/head down; spont./IPPV; and effect of tachycardia
and bradycardia);
b) Diagnosis and subsequent management of shock;
c) Managing fluid and blood transfusion;
d) Monitoring cardiac performance, esp. right side of heart, and acute left ventricular failure;
note also assessment of venous waves a, c, v.

Failure to mention treatment of shock.
<><><><><><><><><><><><>
Page 81
Chapter 11
Regional and Local Analgesia
Page 82
What are the dangers and complications of intradural spinal analgesia?

Immediate: inappropriate dosage causing total spinal; hypotension, respiratory depression,
apnoea; bradycardia; intravascular injection of local anaesthetic; headache, itching,
incontinence, retention of urine, paralysis of legs preventing ambulation.
Later complications: arachnoiditiis, meningitis, backache, epidural haematoma and abscess;
neurological damage from inadvertent injection of toxins; spinal artery syndrome; foreign body
left in dural space.
Comment: There is still a widespread misconception that spinals are always safe!

Failure to mention apnoea and hypotension.
<><><><><><><><><><><><>
Write short notes on ephedrine

Pharmacy:
Type of chemical (catecholamine), storage (aqueous solution in glass ampoules), concentration
(30mg/ml.).
Pharmacodynamics:
Mode of action, alpha and beta agonist
Clinical effects, rise of arterial pressure, bronchodilation, relief of nasal congestion
Dose, 3-30 mg.
Onset, seconds
Duration, 3-30
mins.
Pharmacokine
tics:
Routes of administration, i.m., iv., topical
Metabolism, liver
Side effects, increases awareness during light anaesthesia
Interactions, other catecholamines
potentiated Plus other features: a
very safe and effective drug
<><><><><><><><><><><><>
Page 83
What are the dangers and complications of extradural analgesia?

The hazards of epidural anaesthesia:
• Inadvertent spinal or total spinal. Subdural injection, with effects similar to total spinal.
• Systemic toxicity from local anaesthetic absorption,
a) cardiovascular; low arterial pressure; low cardiac output; low systemic vascular resistance;
bradycardia
b) convulsions followed by depression.
• Cardiovascular — hypotension, bradycardia.
• Respiratory — respiratory depression, apnoea; impaired cough and tidal volume.
• Other systems — Urinary retention or incontinence.
• Increased gut tone and relaxation of sphincters.
• Nausea, vomiting, headache, restlessness.
• Backache.
• Abducens palsy.
• Neurological damage, spinal artery syndrome, arachnoiditis, radiculitis, sepsis (meningitis or
abscess).
• Broken needle or catheter.
• Epidural or spinal haematoma, spinal abscess.
• Inadequate block (failed, unilateral, missed segment, patchy).
Comment: It is difficult to know where to stop with this list! These are only the main
complications.

Failure to mention total spinal, systemic toxicity, hypotension.
<><><><><><><><><><><><>
Page 84
What are the advantages and disadvantages of the local anaesthetic and epidural
anaesthetic techniques for the repair of an inguinal hernia?
Ilioinguinal
Advantages:
• simple;
• no hypotension;
• no resp. depression in patients with respiratory failure;
• control of own airway;
• conscious;
• no IPPV;
• avoids use of opioids.
Disadvantages:
• does not always work, especially on the hernia sac;
• ilioinguinal nerve may be damaged;
• moderate failure rate.
Epidural
Advantages:
• control own airway;
• conscious, avoids IPPV in patients with respiratory failure;
• catheter for longer analgesia;
• avoids systemic opioids.
Disadvantages:
• more complex technique;
• hypotension;
• hypovolaemia;
• backache;
• infection;
• drug toxicity;
• total spinal;
• haematoma;
• foreign body may be left in spinal canal.

Failure to mention value in patients with respiratory failure; failure to list the
disadvantages of epidural analgesia.
Page 85
Write short notes on prilocaine

Pharmacy:
Type of chemical (amide), storage (aqueous solution in glass ampoules).
Pharmacodynamics:
Mode of action, blockade of nerves
Clinical effects, local analgesia
Dose, up to 8 mg/kg. of 0.5-2% solution
Onset, minutes
Duration, 1-2
hours
Pharmacokinet
ics:
Routes of administration, infiltration, epidural,
intravenous regional block Metabolism, liver, to
orthotoluidine (causes methaemoglobinaemia)
Excretion, kidney
Side effects, methaemoglobinaemia
Plus other features: one of the safest local analgesics.
<><><><><><><><><><><><>
Page 86
What factors would influence your decision to choose a regional technique in preference to
a general anaesthetic for transurethral resection of the prostate?
Indications for Regional Analgesia (RA):
Patient preference in favour of RA, COAD, good postoperative analgesia; reduction of
haemorrhage due to parasympathetic blockade.
Contraindications of RA:
Patient preference against RA, uncooperative patient, untreated hypertension, ischaemic heart
disease, fixed cardiac output, physical abnormalities (spinal deformity), local sepsis, disorders
of haemostasis, e.g., anticoagulants.
The following are also relevant to this answer:
Advantages (Reasons for Choosing) of Regional Analgesia:
• Avoidance of respiratory depression in the obese and in respiratory failure; easier
recognition of TURP syndrome, less bleeding, easier recovery as patient is fully awake.
Disadvantages (Reasons for not Choosing) of Regional Analgesia:
• Immediate: inappropriate dosage causing total spinal; hypotension, respiratory
depression, apnoea, bradycardia, intravascular injection of local anaesthetic, headache
itching, incontinence, retention of urine, paralysis of legs preventing ambulation.
• Later complications: arachnoiditis, meningitis, backache, epidural haematoma and abscess;
neurological damage from inadvertent injection of toxins; spinal artery syndrome; foreign
body left in dural space.
Comment: It is very helpful in an answer like this to categorise your points.

Failure to mention advantage of regional analgesia in respiratory failure and morbid obesity.
<><><><><><><><><><><><>
Page 87
Write short notes on midazolam

Pharmacy:
Pharmacodynamics:
Mode of action, benzodiazepine receptor agonist
Clinical effects, sedation, amnesia
Dose, 1-10 mg.
Onset, minutes
Duration, 1-2
hours
Pharmacokine
tics:
Routes of administration, i.m., i.v., oral
Metabolism, liver
Excretion, kidney
Side effects, overdose causes unconsciousness, with loss of airway control, and hypoxia
Interactions, reversed by flumazenil
<><><><><><><><><><><><>
What factors influence the choice of anaesthetic for insertion of arteriovenous shunt for
haemodialysis?
The effect of general anaesthetics on renal function (risks of hypoxia and hypotension; the effect
of NSAIDS on renal function).
Effect of renal failure on general anaesthetics — the following are relevant:
• anaemia;
• hyperkalaemia (suxamethonium, cardiac arrythmias — not a problem if patient has been
dialysed very recently);
• many nondepolarising relaxants greatly prolonged.
Thus regional blocks are ideal, for example plexus block may dilate blood vessels and make the
operation easier; and they avoid the problems of general anaesthetics, but some patients may
prefer general anaesthesia in addition. Furthermore, brachial plexus block would be
contraindicated if the patient were anticoagulated.
Comment: There is no right or wrong technique here, there are merely advantages and
disadvantages.

Failure to mention anaemia and hyperkalaemia
<><><><><><><><><><><><>
Page 88
Write short notes on naloxone

Pharmacy:
Type of chemical, (oxymorphone derivative), storage (aqueous solution in glass ampoules),
preparation, concentration
Pharmacodynamics:
Mode of action, opiate antagonist with receptor affinity but no
receptor stimulation Clinical effects, reversal of respiratory
depression caused by natural and synthetic opioids Dose, 7
µg/kg.
Onset, rapid
Duration, 30 mins-6hrs (i.m.)
Pharmacokinetics:
Routes of administration, i.m, i.v.
Metabolism, liver
Side effects, reverses nitrous oxide anaesthesia
<><><><><><><><><><><><>
Describe the effects and treatment of bupivacaine overdosage

Effects:
1. Vascular — hypotension, cyanosis.
2. Cardiac — arrythmias, negative inotropy, arrest.
3. Cerebral — convulsions, hypoxia.
Treatment:
Oxygen, IPPV, ACLS for cardiac arrest; diazepam, anticonvulsants. Careful volume loading,
needs mention of dangers of inotropes in worsening of arrythmias, and dangers of some
anticonvulsants, e.g., thiopentone in worsening of cardiac failure.
Comment: This is a question of safety and omissions would be marked severely.

Failure to mention cardiac arrest and convulsions. Failure to mention the need for oxygen in
treatment.
<><><><><><><><><><><><>
Page 89
What are the advantages and disadvantages of the supraclavicular and axillary approaches
to the brachial plexus block
Supraclavicular:
Advantages:
wider area of block.
Disadvantages:
pneumothorax risk, vessel damage (inc. thoracic duct); risk of intravascular injection; location of
plexus may be difficult.
Axillary:
Advantages:
much less risk of pneumothorax; location of plexus is usually easier.
Disadvantages:
inadequate block above elbow unless large volumes of analgesic are used; vessel damage;
axillary skin may be infected; risk of intravascular injection.
Comment: An easy question for those who have performed these blocks!

Failure to mention pneumothorax.
<><><><><><><><><><><><>
Write short notes on adrenaline

Pharmacy:
Type of chemical (amine), storage (aqueous solution in glass
ampoules or syringes).
Pharmacodynamics:
Mode of action, stimulates sympathetic receptors, alpha 1 and 2; beta 1 and 2
Clinical effects, rise of pulse rate and atrerial pressure, redistribution of circulation, dilate
bronchus and pupil raise central excitatory state, quieten gut
Dose, 0.1 mg for anaphylaxis; 1mg for CPR; 1/200,000 vasoconstrictor for local anaesthetics
Onset, rapid
Duration, 10
mins
Pharmacokin
etics:
Routes of administration, i.v. and infiltration
Metabolism, catechol-o-methyl transferase and monoamine oxidase
Side effects, feelings of panic!
Interactions, monoamine oxidase inhibitors, cocaine
<><><><><><><><><><><><>
Page 90
What is the place of local analgesic nerve blocks in the anaesthetic technique for
cholecystectomy (excluding ''spinal" and extradural techniques)? State briefly how they
are performed. What are their shortcomings? What are their risks?
Place: very helpful for supplementary and postoperative analgesia, using long-acting agents.
Shortcomings: Note that these blocks by themselves are inadequate for surgery, because the gall
bladder is often innervated by vagus and/or phrenic nerves.
Performance: Clean skin first, have i.v. access and available resuscitation equipment.
Subcostal block: infiltrate subcostal area of abdominal wall in both subcutaneous and muscle
layers, with local analgesic.
Risk: peritoneal, pleural or pericardial puncture.
Intrapleural block: insert i.v. or special cannula into pleural space at angle of rib, taking care to
avoid pneumothorax and intercostal artery puncture.
Risk: pneumothorax, and volumes of local analgesic required are close to toxic doses.
Intercostal block: short bevel needle inserted just below rib, posterior to angle, into subcostal
groove.
Risk: haematoma and pneumothorax. The problem of overlap of innervation from adjacent
intercostal nerves is solved by blocking multiple spaces.
Comment: There is a great risk of over-running your allotted time. Keep this answer in note
form.

Failure to mention at least two of these blocks.
<><><><><><><><><><><><>
Page 91
Give a brief description of the sensory nerve supply of the thoracic cage and abdominal
wall
Supraclavicular nerves in pectoral region.
The thoracic intercostal nerves T1-T12; each one has sensory input to dorsal horn; these
nerves cross intra- and extradural spaces, and traverse intervertebral foramina, T1 goes via
brachial plexus, other anterior divisions travel in subcostal grooves. Cutaneous branch given
off in midaxillary line; intramuscular branch continues, both cross the costal cartilages, and
enter abdominal wall (in subcutaneous and intramuscular layers respectively), and proceed to
midline, where intramuscular branch surfaces. T4 to sternum, T10 to umbilicus. Lumbar nerve
of L1 supplies inguinal region, scrotum and labia.
Comment: A diagram would be helpful here.

Failure to mention the cutaneous branch.
<><><><><><><><><><><><>
Write short notes on ropivacaine

Pharmacy:
Type of chemical (amide), storage (aqueous solution in glass ampoules), concentration (0.5-1%).
Pharmacodynamics:
Mode of action, inhibition of nerve conduction
Clinical effects, local analgesia
Dose, 0.5-1%
Onset, 20 mins.
Duration, 8-9 hrs.
Pharmacokinetics:
Routes of administration, infiltration, epidural
Metabolism, liver
Side effects, less toxic than bupivacaine
Plus other features: better motor block than bupivacaine
<><><><><><><><><><><><>
Page 92
Briefly describe the anatomical relations of the brachial plexus

Relations:
Transverse processes of C5-T1; scalenus anterior and medius, whose fascia helps to form its
sheath.
In the posterior triangle of the neck, it lies on the upper surface of the first rib. Under the
clavicle and subclavius it joins the subclavian vessels, and lies on the second rib and first
intercostal space, which separate it from the pleura. The shoulder joint and humerus lie
laterally as it traverses the axilla.
Comment: It is a great help to have thought this answer out before meeting it in an examination!

Failure to mention the neck, the first rib and the axilla.
<><><><><><><><><><><><>
What are the complications of the supraclavicular and axillary brachial plexus blocks and
how do you recognise them?
Complications (with signs for recognition in brackets):
1. Nerve damage (pain on injection, involuntary movement of arm, failure to recover function
after block wears off).
2. Vessel damage (intravascular injection, with immediate toxic effects; later, haematoma and
ensuing thrombosis).
3. Pleural damage with pneumothorax (cough, collapse, cyanosis, hypoxia, seen on chest X-ray).
4. Thoracic duct damage (development of chyloma).
5. Infection (heat, redness, swelling, pain, loss of function).
6. Toxic effects of local analgesic (hypotension, arrythmias, convulsions, hypoxia).
Comment: Extra marks for identifying major and minor complications and their frequency.

Failure to mention pleural damage or pneumothorax.
<><><><><><><><><><><><>
Page 93
Describe the anatomy of the sacral canal and its contents

Extends from the lower border of L5 to sacral hiatus, S4-5; bounded posteriorly by fused
laminae, anteriorly by fused vertebral bodies, laterally by pedicles and sacral intervertebral
foraminae. It is lined with periosteum. Contents—fat, cauda equina with pia mater, filum
terminale, veins, lymphatics and minor arteries, dura (to lower border of S1 or upper border of
S2 (S3 in small children).
Comment: This is essential anatomical knowledge for anaesthetists.

Failure to mention cauda equina and dura.
<><><><><><><><><><><><>
Describe the anatomy of the epidural space at the level of the fourth lumbar vertebra
A canal formed anteriorly by body of vertebra and discs; posteriorly by neural arch (laminae),
laterally by pedicles with neural foraminae. Lined by periosteum with posterior longitudinal
ligament anteriorly, ligamentum flavum posteriorly.
Contents: epidural space—fat veins lymphatics, nerves with dural cuff.
Traversed by dural sac—dura and arachnoid maters, subarachnoid space and CSF. This is
traversed by cauda equina with pia mater (cord ends at L2), and filum terminale.
Comment: This is essential anatomical knowledge for anaesthetists.

Failure to mention cauda equina and dura.
<><><><><><><><><><><><>
Page 95
Chapter 12
Medicine and Surgery Related to Anaesthesia
Page 96
What precautions should you take when anaesthetising a patient known to have suffered
from viral hepatitis?
1. Protect staff and other patients—assessment of infectivity of patient (HBAge, Hepatitis A,
Hepatitis C and other infective diseases), information to all staff, use of disposable equipment
and safe disposal. Use of gloves etc., practice of correct "sharps drill". Check Hepatitis B
immunisation status of all staff.
2. Protect patient—liver function tests to assess hepatic reserve, and appropriate care with
dosages of drugs.
Comment: It would be difficult to know how much detail to give in this answer. This would have
to be dictated by the time available.

Failure to mention protection of staff.
<><><><><><><><><><><><>
Write short notes on verapamil hydrochloride

Pharmacy:
Type of chemical, storage (tablets, aqueous solution), preparation, concentration
Pharmacodynamics:
Mode of action, Ca++ channel blocker, mainly slow channel cardiac effects
Clinical effects, class 4 antiarrythmic; increases refractory period, reduces excitability and
dilates arterioles
Dose, oral—100-500 mg/day, adult; 2.5 mg i.v.
Onset,
minutes
Duration,
hours
Pharmacokin
etics:
Side effects, constipation
Interactions, digoxin, volatile anaesthetics, beta blocking drugs
<><><><><><><><><><><><>
Page 97
How would you manage atrial fibrillation which occurs during anaesthesia? What could be
done to prevent it?
ECG monitoring is essential for recognition.
1. Management:
a) Use of adenosine, 3mg i.v.—for diagnosis;
b) Use of DC shock (bonus marks for management of this during regional analgesia);
c) digoxin 0.5mg i.v. to control ventricular rate if > 100bpm;
d) amiodarone 1g infusion to prevent recurrence;
e) use of beta blockade in thyrotoxicosis;
f) need for notes about the care of resulting cardiac failure and embolism problems.
2. Prevention:
a) recognition of the at-risk patients (thyrotoxicosis/myocardial ischaemia/ mitral
stenosis/previous atrial fibrillation/Sick sinus syndrome/elderly with hypokalaemia).
Preoperative ECG is essential for this;
b) Avoidance of hypotension at induction in the elderly;
c) Preoperative correction of hypokalaemia.

Failure to mention the ECG and the resulting cardiac failure
<><><><><><><><><><><><>
Write short notes on the diagnosis and treatment of pneumothorax

1. Diagnosis:
The answer needs comments about when this is likely to confront the anaesthetist, and the
difficulty of locating the side.
a) symptoms: pain, dyspnoea, cyanosis, cardiovascular collapse, especially in tension
pneumothorax or bilateral pneumothorax;
b) signs: abnormal breath sounds, abnormal chest movement, coin test;
c) tests: CXR—mediastinal shift, loss of lung markings in periphery.
2. Treatment:
This may be a major life-threatening emergency. IPPV may make the condition worse! Need for
(i.v.) cannula in third ribspace anteriorly, and chest drain techniques, after which IPPV will be
safer.
<><><><><><><><><><><><>
Page 98
Write short notes on doxapram

Pharmacy:
Type of chemical, storage (aqueous solution in glass ampoules and plastic bags), preparation,
concentration (2 mg or 20 mg/ml.)
Pharmacodynamics:
Mode of action, peripheral
chemoreceptor stimulant Clinical
effects, nonspecific respiratory
stimulant Dose, 1 mg/kg., better
given as infusion
Onset,
minutes
Duration, 1
hour
Pharmacokin
etics:
Metabolism, liver
Side effects, tachycardia, dizziness, sweating, muscle fasiculations.
Interactions, MAOI's; aminophylline (agitation)
<><><><><><><><><><><><>
Write short notes on aminophylline

Pharmacy:
Storage (aqueous solution in glass ampoules)
Pharmacodynamics:
Mode of action, cyclic AMP inhibition
Clinical effects, bronchodilator and stabiliser of cardiac rhythm
Dose, 100-
250 mg.
Onset, rapid
Duration, 4-6
hrs.
Pharmacokin
etics:
Routes of administration, oral, i.v.
Side effects, gastric irritation, CNS stimulation, hypokalaemia
Interactions, Ephedrine (in children); phenytoin, carbamazepine,
barbiturates, doxapram Plus other features: regular monitoring
of theophylline levels required
<><><><><><><><><><><><>
Page 99
What problems does hiatus hernia pose for the anaesthetised patient and how do you cope
with them?
1. Regurgitation and aspiration of highly acidic juice causes pulmonary airways burn; if
this occurs, it is managed by tracheal washout, IPPV, possibly steroids and antibiotics.
2. Haemorrhage from peptic ulcer, if present; oesophagitis; resultant anaemia.
3. The giant hiatus hernia may interfere with lung function.
4. Managed by premedication with H2 antagonist and metoclopramide. Cricoid pressure is
needed during induction, with tracheal intubation to protect lungs.
Needs discussion of difficulty of insertion of nasogastric tube and pHi estimation.
Failure to mention cricoid pressure, and H2 antagonists.
<><><><><><><><><><><><>
What is the relevance to anaesthetic management of ankylosing spondylitis? What

strategies would you employ to overcome them?
Problems:
Stiff neck and jaw—intubation difficulty; reduced pulmonary function needs assessment, esp. if
kyphotic.
Strategies:
1. Use of regional blocks; spinal blocks are desirable but difficult!—spinal X -ray is needed.
2. Elective fibreoptic intubation or tracheostomy may be needed if general anaesthesia is
unavoidable, especially if there is:
a) known history of difficult intubation—Cormack & Lehane scores from previous
laryngoscopies;
b) poor mouth opening (< 3fb);
c) low Malampatti score;
d) short thyromental distance (< 6cm);
e) small mandible size and inability to protrude jaw;
f) neck stiffness (you would need to mention neck X-rays here). This is perhaps the most critical
of these features.

Failure to mention difficult intubation and reduced lung function.
<><><><><><><><><><><><>
Page 100
Write short notes on nifedipine

Pharmacy:
Storage (liquid in capsules)
Pharmacodynamics:
Mode of action, calcium channel antagonist
Clinical effects, percentage lowering of arterial pressure in hypertension; coronary vasodilation.
Dose, 10 mg.
Onset,
minutes
Duration, 4-8
hrs.
Pharmacokin
etics:
Routes of administration, oral,
sublingual Side effects,
headaches dizziness and
flushing Interactions,
potentiated by cimetidine
Plus other features: fast onset; no rise of intraocular pressure
<><><><><><><><><><><><>
How does the presence of aortic stenosis affect the management of an anaesthetic?
Fixed cardiac output, with risk of severe hypotension on induction; vasodilation is to be
avoided. Coronary flow reduced, risk of endocarditis (need for antibiotic cover) and
subendocardial ischaemia if inotropes are given in large dosage. (Bonus marks for stating that
HOCM is worsened by inotropes).
Comment: It is particularly important to mention that coronary flow is dependent on diastolic
pressure, and that tachycardia is to be avoided as it shortens diastolic interval.

Failure to mention fixed cardiac output, with risk of severe hypotension on induction.
<><><><><><><><><><><><>
Page 101
What would happen if a full dose of thiopentone was given to a patient with acute
intermittent porphyria and why?
The patient would become anaesthetised, but:
Thiopentone stimulates hepatic delta ALA synthase, giving excess porphyrins, causing:
a) neuropathy, epilepsy, psychiatric symptoms;
b) abdominal pain and vomiting;
c) tachycardia, hypertension, acute LVF;
d) red urine.
This is a dose-related effect.
Neuropathy may last for weeks, needing IPPV, and intensive care.

Failure to mention delta ALA synthase, and neuropathy.
<><><><><><><><><><><><>
What is the management of an acute sickle cell crisis?

1. Remove precipitating factor, e.g., cannabis, hypoxia, cold, acidosis.
2. Give oxygen and rehydrate the patient.
3. Prevent cold, hypoxia and acidosis occurring during treatment.
4. Control very severe pain with large doses of opiates.
5. Prevent joint and organ damage which can be fatal.
6. Exchange transfusion has been used with success.

Failure to mention pain and need for oxygen.
<><><><><><><><><><><><>
Page 102
In what ways does Down's Syndrome affect the management of an anaesthetic?

1. Resistance to sedatives.
2. Large size and difficult veins.
3. Excess salivation and large tongue.
4. Associated ASD and VSD, with risk of intracardiac shunting and endocarditis (need for
antibiotics).
5. Immune deficiency with risk of infection and cross infection.
6. Communication problems resulting in fear and failure to comply with instructions (rapport
with parents essential).
Comment: Anaesthetists should be professionally competent in these situations.

Failure to mention the cardiac complications.
<><><><><><><><><><><><>
What precautions should be taken when anaesthetising a patient with dystrophia

myotonica?
1. Prevention of aspiration of stomach contents.
2. Prevention of prolonged apnoea by avoiding thiopentone.
3. Prevention of cardiovascular depression and dysrhythmias by being sparing with volatile
agents.
4. Prevention of severe myotonia by avoiding suxamethonium.
5. Awareness that nondepolarising relaxants do not stop myotonia.
6. Awareness that anticholinesterases may worsen myotonia.
7. Dantrolene may reduce myotonia and should be available.
8. Central neural blockade is useful (if appropriate).
9. Postoperative IPPV may be required.
10. Preparedness for these patients to be very heavy for their age.
Comment: This is rare but important.

Failure to mention the risks of thiopentone and suxamethonium.
<><><><><><><><><><><><>
Page 103
How do the intraoperative surgical complications of excision of thyroid goitre affect the
management of the anaesthetic?
1. Stimulation of carotid baroreceptors by surgical manipulations may destabilise arterial
pressure. Surgery may cause haemorrhage, pneumothorax; splitting of sternum would require
IPPV; recurrent laryngeal palsy and external laryngeal palsy may cause postoperative airway
obstruction; concomitant parathyroidectomy may cause early postoperative tetany.
2. Damage to the trachea (including tracheomalacia) may occur with postoperative airway
obstruction.
3. Finally—the surgical elbow in the patient's eye!

Failure to mention need for IPPV; postoperative airway obstruction.
<><><><><><><><><><><><>
What are the anaesthetic problems posed by surgical removal of a phaeochromocytoma?

1. Preoperative unstable arterial pressure requiring alpha and (later) beta blockade with
restoration of circulating blood volume.
2. Avoid histamine releasers in premed and anaesthetic—they may cause a crisis.
3. Vasodilators may be needed for operative hypertension.
4. Vasoconstrictors (adrenaline, noradrenaline, angiotensin) needed for post-removal
hypotension.
5. Requires full-scale monitoring (details needed).
6. Secondary phaeochromocytomas may be missed at operation, with postoperative ongoing
symptoms.

Failure to mention unstable arterial pressure; histamine releasers and need for full-scale
monitoring.
<><><><><><><><><><><><>
Page 104
What are the anaesthetic problems posed by surgical removal of a parathyroid adenoma
and how do you cope with them?
1. Excessively high Ca++ would pose a risk of serious arrythmias (may need emergency
lowering of Ca++, antiarrythmic drugs and K+ infusion).
2. Pneumothorax (prevention by IPPV, treatment by chest drain).
3. Air embolus (prevention by avoiding too steep head-up tilt, treatment by turning patient on
side and evacuation by central line).
4. Haemorrhage (treated by infusion and transfusion).
5. Recurrent nerve damage (with postoperative obstruction, requiring reintubation).
6. Postoperative tetany requiring Calcium injection (needs details of preparations and doses).
Comment: This is an easy question.

Failure to mention postoperative tetany requiring Calcium.
<><><><><><><><><><><><>
What are the complications of mitral valve disease during anaesthesia and how do you
prevent them?
1. Fixed cardiac output, with risk of serious vascular instability (avoidance of cardiac depression,
vasodilation and tachycardia).
2. Acute left ventricular failure, with pulmonary oedema, requiring diuresis with frusemide.
3. Bacterial endocarditis, (requiring antibiotic cover).
4. Atrial fibrillation (requiring control of rate and treatment of left ventricular failure). This may
cause:
a) arterial thromboembolism, prevented by anticoagulation;
b) cardiac failure, requiring careful use of inotropes.

Failure to mention atrial fibrillation and bacterial endocarditis.
<><><><><><><><><><><><>
Page 105
A patient's arterial pressure on admission for moderately urgent appendicectomy is

170/115 mmHg. Describe your anaesthetic management
The anaesthetist checks it for himself! (It can be due to pain, a full bladder, and the answer
requires a brief discussion of hypertension due to fear.)
Investigation of Causative Conditions:
a) generalised vascular disease, possible renal and other rare causes of hypertension (e.g.,
phaeochromocytoma);
b) is the patient's abdominal pain due to another, medical, cause? Could it be angina due to
hypertensive crisis?
Management:
Prevention of risks;
• hypotension under anaesthesia;
• myocardial infarction;
• cerebral haemorrhage;
• ECG required;
• this diastolic pressure is too high for safety. The operation is postponed for emergency
medical treatment, involving relevant specialists.
Relevant Drugs:
• nifedipine;
• beta blockers;
• ACE inhibitors;
• Ca channel blockers;
• clonidine, with rapid and carefully monitored intravascular volume replacement.
Antibiotics are required to cope with a short period of postponement of operation. Spinal
anaesthesia not advisable because of cardiovascular instability.
Comment: The answer to this is longer than many in this book.

Failure to mention emergency medical investigation and treatment of
hypertension; and risk of severe hypotension under anaesthesia.
<><><><><><><><><><><><>
Page 106
A patient with congestive cardiac failure presents for hip replacement. Describe your
management for the anaesthetic
Postpone the operation and control the
cardiac failure. Problems:
1. The implication is that the patient has serious cardiac and possibly other organ disease,
and requires full investigation, e.g., by ECG, echocardiography and relevant blood tests.
2. Cardiac depression by anaesthetics, and
3. uncontrolled vasodilation from cement are the notable risk points, with the emphasis on
prevention.
4. Haemorrhage may be considerable with need for accurate volume replacement with
monitoring.
Comment: This is not an uncommon scenario.

Failure to mention postponement of operation.
<><><><><><><><><><><><>
A patient presenting for prostatectomy has a pulse rate of 39 beats per minute. Describe
the common causes and management of this
This answer needs a comment on what pulse rates are acceptable and what the
target pulse rate would be. Causes:
1. Heart block (will need anticholinergics and possibly pacing).
2. Treatment with beta blockers (reduce the dose and/or use other drugs; premedicate with
anticholinergics).
3. Sick sinus syndrome (common in this patient population with risk of atrial fibrillation,
supraventricular tachycardia, ventricular tachycardia and ventricular fibrillation).
4. Failure of implanted pacemaker (needing referral to cardiologist).
This all implies serious cardiovascular disease.
ECG and full drug history is essential (esp. beta blockade). Specialist medical advice is helpful.
Operation will need to be postponed until the pulse rate is normal.
Risk of further bradycardia during and after anaesthetic.

Failure to mention that this sign usually indicates serious cardiovascular disease.
<><><><><><><><><><><><>
Page 107
How does the common cold influence fitness for anaesthesia?

1. A genuine cold presents a risk of postoperative chest infection, which depends on severity of
cold and need for intubation.
2. Risk of laryngeal spasm/bronchospasm/cyanosis during operation.
3. Risk of cardiac arrest in children—up to 4-6 weeks after infection.
This answer requires a brief discussion about difficulty in diagnosis because of fast onset of
colds in children, and differentiation from teething, and blocked nose due to adenoid
hypertrophy—the presence of pyrexia is a useful sign.
Tonsillectomy during a cold may cause marked haemorrhage and local infection.

Failure to mention the risk of laryngospasm and cardiac arrest in children.
<><><><><><><><><><><><>
Write short notes on atrial fibrillation

Causes: ischaemia, rheumatic heart disease, thyrotoxicosis; triggers: hypotension and
hypokalaemia.
Diagnosis: irregularly irregular pulse (including deficit), and cannon waves. The ECG makes
the diagnosis. The answer needs a comment on the significance of uncontrolled rate.
Complications: poor cardiac output, left ventricular failure, emboli (requiring anticoagulation).
Treatment: need to mention adenosine, DC shock, amiodarone, digoxin, and the indications for
anticoagulation.

Failure to mention cardiac failure.
<><><><><><><><><><><><>
Page 108
How do you judge the significance and plan the management of preoperative anaemia?
Significance: What has caused it? How severe is it? (When the Hb is below 10g/dl. it will
cause reduced oxygen carriage). Is it acute or chronic (with compensation by raised 2.3 DPG)?
Does the patient have chronic renal failure (high blood urea and creatinine)/ carcinomatosis
(skeletal X-ray survey)/leukaemia (blood film)/malnutrition (red cell volume)/coagulopathy
(coagulation profile, drug history)/chronic bloodloss from gut, bladder or uterus
(microcytosis)/aspirin or NSAID usage? There will be reduced O2 flux and possibly high output
cardiac failure if severe.
Investigations: The medical history will have indicated which lines should be further
investigated.
Management: The relevant issues are:
a) how severe;
b) how acute the anaemia is and whether it is ''renal" (accept Hb of 7-8g/dl); and how
urgent surgery is (emergency indicates transfusion, and possibly urgent need to stop
cause of bleeding if possible).
The non-urgent situation calls for discussion of Fe++ therapy, erythropoeitin, and correction of
haemostasis factor levels.
Comment: This is a common problem but not an easy question to answer.

Failure to mention oxygen carriage.
<><><><><><><><><><><><>
Page 109
A patient with non-insulin-dependent diabetes is to undergo amputation of an infected

gangrenous leg. What is the correct peri-operative management of the diabetes?
You need to state that this diabetes will be
out of control. Issues to mention include:
a) History of patients previous diabetic status.
b) Involvement of diabetologist.
c) Assessment of current biochemical status plus awareness of possible loss of control due to
gangrene—danger of hyper- and hypoglycaemia—requiring assessment of blood glucose,
electrolytes, hydration status (Hartmann's solution is avoided because of lactate load).
d) Preoperative management—antibiotics, rehydration urine output, hourly blood glucose
and electrolyte monitoring, insulin prescription (sliding scale/Alberti regime: K+, insulin,
glucose infusion).
e) Operative management—maintain diabetic regime, monitor blood sugar (intervals of 1 hour on
average).
f) Postoperative management—Awareness of rapid improvement in diabetes, use of sliding
scale, timing of return to preoperative regime.
Comment: This is quite a common clinical situation.

Failure to mention diabetes will be out of control, with need for insulin.
<><><><><><><><><><><><>
Page 110
How would you judge the significance of preoperative jaundice?

Causes:
Is there infective hepatitis?—need to test for HBAge, Hepatitis A, Hepatitis C, and enquire
about malaria, glandular fever. Would there be a crossinfection risk for staff?
Is it due to; drugs (paracetamol, halothane), with risk of fulminating hepatic failure (what is the
drug history?); gallstones; Gilbert's syndrome; haemolysis; cirrhosis; Ca pancreas; pancreatitis
(Serum amylase and blood glucose levels are required)?
Effects:
Has it affected blood coagulation, and therefore jeopardise haemostasis? Is there hepatic failure
(function tests needed)? Is there concomitant renal failure (electrolyte tests)?
Are there cerebral effects, e.g., in the neonate?

Failure to mention the appropriate tests.
<><><><><><><><><><><><>
How do antihypertensive drugs affect the management of anaesthesia?

1. They reduce raised arterial pressure (this needs a little discussion of the limits, and target
pressures at different ages).
2. They commonly vasodilate the patient, which requires care in the use of vasodilating
anaesthetics.
3. They commonly increase circulating volume, which is a safety factor, and the indication
for continuing medication through the perioperative period.
4. Beta blockers may limit changes of cardiac rate and output and cause severe bradycardia.
5. Some cause renal failure in certain situations, with problems of anaemia, hyperkalaemia,
acidosis and prolongation of relaxants.
6. Clonidine will potentiate anaesthetics and analgesics.
7. Thiazides lower the serum K+, prolonging and potentiating nondepolarising relaxants.
8. Withdrawal of some antihypertensives cause excessive rebound of arterial pressure.
Comment: This is common clinical scenario.

Failure to mention lowered arterial pressure.
<><><><><><><><><><><><>
Page 111
What are the functions of the thyroid gland and how are they controlled? What are the
effects of thyroid dysfunction on anaesthesia?
Functions: production of thyroxine and T3 to control metabolic rate, growth, cerebral activity.
They interact with other hormones.
Control: TSH from anterior pituitary; negative feedback control.
Effect of Dysfunction:
a) myxoedema—sensitivity to anaesthetics and cold, instability of circulation;
b) thyrotoxicosis—atrial fibrillation, thyroid crisis.

Failure to mention myxoedema and atrial fibrillation.
<><><><><><><><><><><><>
In what circumstances may fluid overload occur during operation? How is it diagnosed
and managed?
1. Overestimation of the operative losses (e.g., in laparoscopic operations), with overinfusion.
2. TURP syndrome, with absorption of irrigant.
3. In severe toxaemia with capillary hyperpermeability, causing pulmonary oedema.
4. Where the patient has inappropriate ADH secretion, renal failure, acute left ventricular failure.
5. During and after cardiopulmonary bypass.
Diagnosis: onset of hypoxia, rise of ventilation pressures, auscultation of crepitations in the
lungs, froth in tracheal tube. Management: diuretics, treatment of acute heart failure,
oxygenation, fluid restriction, triple strength albumin if appropriate. Comment: CEPOD have
emphasised the importance of this.
Failure to mention TURP syndrome and overinfusion.
<><><><><><><><><><><><>
Page 112
Name and define the different types of hypoxia. Where are they seen clinically?
1. Hypoxic—PaO2 is low (inadequate respiration, low FiO2).
2. Anaemic—Hb and O2 carriage is low (anaemia; Hb < 10g/dl).
3. Stagnant—bloodflow is slow (poor cardiac output, obstruction of peripheral vasculature).
4. Histotoxic—tissues are unable to utilise delivered O2 (CO poisoning, cyanide poisoning).
Comment: This is basic physiology upon which anaesthetic practice is based.
Failure to mention all four types.
<><><><><><><><><><><><>
What is the mode of action of the following in lowering arterial pressure?

• Isoflurane — vasodilation
• Halothane — negative inotropy and vasodilation
• Propofol — vasodilation
• Lignocaine — negative inotropy
• Enflurane — negative inotropy and vasodilation
• Desflurane — vasodilation
• Thiopentone — negative inotropy and vasodilation
• GTN — vasodilation
• Pulmonary embolism — physical obstruction of circulation
• Ruptured aortic aneurysm — reduction of bloodvolume and afterload
• Septic shock syndrome — negative inotropy, pulmonary vasoconstriction, opening of A-V
anastomoses
• Ventricular fibrillation — no cardiac output
• Spinal anaesthesia — vasodilation
• Anaphylactic shock — vasodilation
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Page 113
Describe all the clinical actions of one anaesthetic agent and two other drugs you might use
to lower arterial pressure during anaesthesia
Many drugs can do this, e.g., halothane, enflurane, isoflurane, desflurane, alpha and beta
blockers, ganglion blockers, direct vasodilators (SNP and nitrates), hydrallazine clonidine.
Comment: Space forbids a full treatment of all the possibilities for this answer. The
pharmacodynamics and side-effects should all be mentioned as in the answers to the "Write
short notes on. . ." questions).
<><><><><><><><><><><><>
Write short notes on amiodarone

Pharmacy
Pharmacodynamics:
Mode of action, a K+ channel blocker which uncouples beta receptors from the regulatory unit of
the adenylate cyclase complex
Clinical effects, class 3 antiarrythmic, control of ventricular and supraventricular arrythmias
Dose, 100-
250 mg.
Onset, rapid
Duration,
months
Pharmacokin
etics:
Routes of administration, oral, i.v.
Metabolism, liver (halflife 26-107 days)
Side effects, mild negative inotrope; microdeposits of drug in cornea; pulmonary interstitial
infilatration.
Interactions, prolongs life of digoxin; potentiates other antiarrythmics;
Plus other features: affects thyroid function; avoid in porphyria, contains iodine.
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Page 114
Write short notes on adenosine

Pharmacy:
Type of chemical (endogenous nucleoside)
Pharmacodynamics:
Mode of action, stimulation of A1 receptors
Clinical effects, negative chronotropy on sinus node, negative dromotropy on atrioventricular
node; termination of supraventricular tachycardias
Dose, 3 mg.
Onset, one
circulation time
Duration, 1 minute
Pharmacokinetics:
Interactions, alteration of potency of anaesthetics
Plus other features: avoid in sick sinus syndrome, heart block, and asthma
<><><><><><><><><><><><>
Page 115
Chapter 13
Faciomaxillary, Ophthalmic and ENT
Page 116
What complications of operations on the bony structures of the lower half of the face may
affect the anaesthetic management, and how do you deal with them?
1. "Oculocardiac" reflex — bradycardia — atropine needed.
2. Interference with tracheal tube, the nasal route may be preferable, and armoured tube may be
required.
3. Massive haemorrhage, requiring massive crossmatch and massive transfusion, with CVP
monitoring.
4. Postoperative airway problems, due to swelling and pre-existing abnormalities.
5. Postoperative vomiting problems when the jaws have been wired together, requiring
antiemetics, awake extubation and strategy for emergency unwiring.
Comment: This is another example of demonstrating your skills in an important clinical
scenario.

Failure to mention bradycardia, massive haemorrhage and airway problems.
<><><><><><><><><><><><>
A patient requires an anaesthetic for removal of an infected molar tooth which is causing
severe trismus. Describe the problems and outline the anaesthetic methods
1. Problems — woody swelling in pharynx, unable to open mouth, severe local infection and
toxaemia, pus in pharynx. Local anaesthesia is unhelpful. Relaxants will not usually relax
trismus, because the spasm arises in the muscles of mastication themselves.
2. The airway should be secured, and needs a brief discussion of four methods: General
anaesthesia; awake fibreoptic intubation; blind nasal (not easy because of swollen tissues);
tracheostomy (difficult if the neck is also swollen); induction of general anaesthesia: the
safest is inhalation induction, using high O2, spontaneous breathing, e.g., with halothane or
sevoflurane; not IV induction.
3. Trismus relaxes under general anaesthesia and cords may be visualised in the usual way.
There is still the problem that pus may be in the pharynx.
4. Awake extubation is safest for the airway.
Comment: This question is about a safety issue.

Failure to mention trismus not releasing with relaxants; and three of the above
approaches to intubation, with problems.
<><><><><><><><><><><><>
Page 117
Describe the anaesthetic management for a patient with a perforating eye injury who had a
large meal in the last hour
1. Postpone the operation if possible; if not possible:
Premedication with metoclopramide and H2 antagonist.
2. The use of suxamethonium is controversial as it raises intraocular pressure.
3. The use of intubation is controversial as it also raises intraocular pressure. Opiates are
important here.
4. If intubation is essential, cricoid pressure is required, and a very careful laryngeal spray with
lignocaine.
5. Laryngeal mask has been used successfully, after a period of saturation.
6. Postoperatively, prevention of coughing and vomiting is important.
<><><><><><><><><><><><>
Describe the anaesthetic management for a 5-year-old patient who requires reoperation
for haemorrhage an hour after tonsillectomy
1. Assessment and resuscitation: intravenous infusion of colloids and blood until the patient is
clinically not shocked (details needed). Oxygen is required.
2. Premedication: not usually required for tonsillar haemorrhage in the first six hours after
operation.
3. Induction of anaesthesia: rapid sequence induction with cricoid pressure and intubation.
4. Maintenance of anaesthesia: light anaesthetic, a nasogastric tube is passed and the stomach
emptied.
5. Postoperative care: further assessment of shock, anaemia, and analgesia. Oxygen is required.
<><><><><><><><><><><><>
Page 118
How would you perform a block of the maxillary nerve?

1. Preoperative: assess patient (details required, including anticoagulation); gain consent.
2. Operative: availability of resuscitation equipment, i.v. access, clean skin. Full monitoring is
applied.
3. Short-bevel needle is inserted below mid point of zygoma, above mandible, and advanced
towards contralateral eyeball until it meets pterygoid plate. It is then angled upwards and
forwards and advanced 1 cm. to enter the pterygomaxillary fissure, close to the maxillary
nerve. Aspiration is performed:
a) nothing aspirated — inject 2 mls of local analgesic;
b) blood is aspirated — move needle slightly to exit bloodvessel;
c) air is aspirated — withdraw needle 0.5-1cm — the tip is in the nasal cavity!
<><><><><><><><><><><><>
Page 119

Anaesthesia 4

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Page 2

Serious omissions likely to cause a fail:

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Serious omissions likely to cause a fail:

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Serious omissions likely to cause a fail:

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Serious omissions likely to cause a fail:

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Serious omissions likely to cause a fail:

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Serious omissions likely to cause a fail:

Serious omissions likely to cause a fail:

Serious omissions likely to cause a fail

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Serious omissions likely to cause a fail:

Write short notes on ranitidine