Long case


65 year old lady with a hemiparesis from a cerebral
haemorrhage 6 months ago. Cerebral angiography
reveals 2 cerebral aneurysms, not amenable to coiling.
She presents for an elective craniotomy.
She has a permanent pacemaker fitted 3 years ago for
complete heart block, has treated hypertension and was a
heavy smoker but now smokes only 10 cigarettes a day.
She is short of breath after 50 to 100 yards.
Medication:Felodipine, ramipril, fluoxetine, clopidogrel,
salbutamol, tiotropium, becotide inhalers, lansoprazole
On examination, BP 140/90 P 75 weight 60kg, height
1.61m, chest sounds clear
CXR: hyperexpanded lung fields but clear, heart size
normal, dual chamber permanent pacemaker
ECG: Paced rhythm 75/min. Only ventricular pacing
spikes seen
FEV1 0.83l
FVC 2.53l
FEV1/FVC ratio 33%
PEFR reduced
ABG air: pH 7.45


Summarise the case. Tell me what each of the drugs are.
What do you think about the CXR, ECG, lung function
tests and blood gases? Are there any post-op
implications? What may be the problem intra-operatively
with having a pacemaker? –fixed CO, causing fall in MAP
and CPP, diathermy.
What would be your main anaesthetic concern about this
operation –haemorrhage. What would you like to do to
prepare this lady for theatre. How would you anaesthetise
this lady?- wanted to know about monitoring pre-induction
and intra-operatively. What sort of central line would you
use and where would you put it? Wanted quadruple lumen
at least. What are the options for which anaesthetic you
would use?- volatile/ TIVA/ remifentanil. What are the
advantages of TIVA and of remifentanil. Is this operation
painful. Apart form her poor respiratory function, what
other reason may she require ventilation post-operatively-
haemorrage, raised ICP, cardiovascular instability. What is
the mortality form this procedure?


You are in the middle of a laparoscopy for a 30 year old
lady. Suddenly, you see the ETCO2 read zero. What are
the causes? – disconnection/ monitor problem/ obstruction
to airway or breathing system/ ETT, Cardiac arrest, which
may be due to anaphylaxis, arrythmia, PE, venous air
What would you do to diagnose the cause? If this was a
venous air embolism, how would you manage it? What
other changes on the monitor may you notice? Why do
you put patients head down and left lateral? What can
cause a systemic air embolism?

What does this ECG show? How do you work out the
axis? Draw the conducting system of the heart. What
implications does this have for anaesthesia? If this patient
was having a carotid end-arterectomy, is there anything
specifically about this operation that would make you
worry with this ECG. Would you still be worried if he was
coming for a big toe operations!?
3. AAA:

You are called to the ward to see a 79 year old man BP
60/40 who has a bleeding abdominal aortic aneurysm.
What will your initial management be?. Wanted me to
include that you would not resuscitate to a systolic BP of
greater than 100 as this would cause more bleeding.
Would you take every patient to theatre? Wanted me to
mention about quality of life and co-morbities, discussion
with relatives if time . Who makes the the decision to go to
theatre? Do bleeding abdominal aortic aneurysms
otherwise always go to theatre? How would you induce
the patient. Wanted pre-induction A-line of stable. What
drugs would you use for induction. Mentioned fentanyl,
thiopentone, suxamethonium and wanted to know what
dose of thiopentone I would use.


Tell me the course of the phrenic nerve. What does it supply?- motor to diaphragm. Does it have any sensory branches? –pleura and peritoneum covering upper and lower parts of central diaphragm, some sensory fibres to mediastinal parietal pleura and to the pericardium What are its relations in the the neck? C3,C4,C5 roots unite at the level of the lateral border of the scalenus anterior muscle, at the level of the cricoid. It runs vertically downards across the anterior border of scalenus anterior, from lateral to medial, behind the prevertebral fascia. What about in the thorax? It enters the thorax by passing in front of the subclavian artery and behind the brachiocephalic vein. The right phrenic nerve descends in the thorax along the right side of the right brachiocephalic vein and passes in front of the root of the right lung and runs along the right side of the pericardium. It descends on the right side of the IVC to the diaphragm. It terminal braches pass through the caval opening to supply the undersurface of the diaphragm. The left phrenic nerve descends in the thorax to the left of the left subclavian artery. It crosses the left side of the aortic arch and the crosses in front of the root of the left lung and descends over the left surface of the pericardium. The terminal branches pierce the muscle of the diaphragm to supply the underaspect. Where does it pass relative to the pericardium? –anterior. What sort of procedures may damage the phrenic nerve? Central venous cannulation, interscalene block, cardiac and thoracic surgery. How would you diagnose a phrenic nerve palsy? How would you manage a phrenic nerve palsy. How would you manage a long term phrenic nerve palsy- phrenic nerve stimulation. 2. BLOOD TRANSFUSION:

What happens if a patient gets an incompatible blood
transfusion? What are the symptoms of this? Tell me
about the ABO blood groups. Explain how an immune
haemolytic transfusion reaction occurs? What is the most
common cause of ABO incompatibility? –clerical error. At
what stages can this occur? How can you minimise the
risk of this? Are there any other ways by which the patient
can be identified other than using the nameband?-no.
Have you heard of the SHOT report? What does it stand
for and what did it show? Roughly what percentage of
transfusion reactions are due to clerical error?


You have an asthmatic for an elective operation. How
would you assess the severity of their asthma? What
affects bronchomotor tone? Wanted things like autonomic
nervous system, histamine, irritants, prostaglandins,
leukotrienes, magnesium. How would this affect which
drugs you would not use on an asthmatic patient. Eg
thiopentone, NSAIDS. What induction agent may be
particularly beneficial in asthma?

4. NMJ:

Explain how the NMJ works. How does tetanus occur?
How does fade occur? How can you monitor the NMJ?
What patterns of stimulation can you get with the
peripheral nerve stimulus and when would they be useful?
How does the peripheral nerve stimulator used to perform
peripheral blockade differ from the one used to monitor
neuromuscular junction function?

Source: http://www.nosats.org.uk/Kay's%20Final%20SOEs.pdf

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