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c c

 

m mm
 m     !"
# $%% & '#    ! ()*)# %%%+
A. Bilevel pressure
B. Expiratory time
C. Inspiratory time
D. Peak inspiratory pressure
E. PEEP

? ,!-  --$%./0% 1 -#    2% 


#   %%&3%  $  &$3 %  4
A. Increase FiO2 from 50 - 100% - љHPV ї љPVR ї јB-T shunt Q
B. Esmolol 70 mcg
C. Phenylephrine 35 mcg (vasopressors are relatively ineffective in children - systemic pressures are
determined by CO (HR x SV) and filling ALSO this is a massive dose)
D. Morphine 1 mg
E. 1/2 NS with 2.5% dex 70 mls

A.Ê FiO2 to 100% this is a real answer and will also improve HPV and increase B-T shunt Q
B.Ê Beta blocker may help slow heart rate and increase diastolic filling and preload, and MAY
help to increase diameter of RVOT.
C.Ê Phenylephrine will increase SVR and therefore left-sided pressures, thereby reducing right-to-
left shunt. BEST ANSWER
D.Ê Morphine will probably make little difference to a patient who is paralysed and ventilated,
E.Ê Crystalloid will increase preload if a big enough bolus is given, and this may dilate RVOT and
decrease right-to-left shunt.

Giving 100% oxygen may reduce hypoxic pulmonary vasoconstriction, pulmonary vascular resistance
and allow more blood to flow through the Blalock-Taussig aortopulmonary shunt where it can be
oxygenated. Other PVR lowering strategies include
@Ê sodium bicarbonate 1-2 mmol/kg
@Ê low inspiratory pressure ventilation with long expiratory times (although I suspect this may
produce hypercapnoea)
@Ê general anaesthesia
@Ê Phenylephrine 35 mcg is quite a high dose in a 7kg infant (I have read here 0.5 - 2 mcg/kg)
but is one of the methods cited to increase SVR along with knee-chest positioning
@Ê abdominal pressure on the aorta
@Ê Finally RV filling with reduction in RVOT obstruction can be facilitated by B-blockers which
slow HR, likewise opioids (although morphine 1 mg to 7 kg child is excessive), general
anaesthetics (particularly the inhaled ones) and fluid loading. Given that the question was
remembered with doses, I wonder if the key to the question lies there rather than the choice
of drug.

‰  5m67 08% % %%%  4


A. increased risk of malignant hyperthermia
B. meningiomas
C. peripheral neuropathy
D. pheochromocytomas
E. poor dentition
D - Von HippelʹLindau disease (VHL) is a rare, autosomal dominant genetic condition[1]:555 in which
hemangioblastomas are found in the cerebellum, spinal cord, kidney and retina. These are associated
with several pathologies including renal angioma, renal cell carcinoma and phaeochromocytoma.
VHL results from a mutation in the von HippelʹLindau tumor suppressor gene on chromosome 3p25.3
Wikipedia - Disco 28/6/10

5   %/9:(  %30  1 # %16/  %5 ;%%, 7!/* 0!!< 


  
A. Enoxaparin
B. Fondoparinux - looks promising but at this stage awaiting larger, multi-centre RCTs to
demonstrate efficacy
C. Heparin by infusion
D. Lepirudin - recombinant anticoagulant from leaches - direct IIa inhibitor; monitored with APTT
(best answer at this stage); dose 0.08mg/kg/hr no load + titrate to APTT
E. Warfarin - can cause procoagulant state and gangrene

Management of HIT:
First task is to discontinue unfractionated heparin from ALL sources (including heparin-coated lines,
etc). LMWH can also cause HIT, therefore not suitable as a replacement. Fondaparinux is an indirect
Factor-Xa inhibitor (synthetic pentasaccharide), and there are some reports of it being used in HIT
successfully. Warfarin (Vit K antagonist) is contraindicated in acute HIT (or if suspected HIT), as it can
cause skin necrosis or venous limb gangrene.
Current recommendations are to treat with DTI's (lepirudin, argatroban, bivalirudin) or danaparoid.
Although danaparoid is a LMW heparinoid, there is an extremely low cross-reactivity rate with HIT
antibodies, and this is rarely clinically significant.
As danaparoid is not an option, the best answer is therefore a direct thrombin inhibitor (DTI), and
lepirudin is the only one listed, so answer is D.
References:
Greinacher A. Heparin-induced thrombocytopenia, J Thromb Haemost 2009;7(Suppl. 1):9-12.
Shantsila, et.al. Heparin-Induced Thrombocytopenia: A Contemporary Clinical Approach to Diagnosis
and Management, Chest 2009; 135:1651-1664.
Therapeutic Guidelines - Cardiovascular (electronic version), 2008.

 7  


A. Chovostek's sign
B.
C.
D.
E. Short QT

= 1 % =%  %% m  ) #  -3 


A. Do case while taking both.
B. Do case while stopping both.
C. Stop Prasugrel for 7 days, keep taking aspirin.
D. Stop Prasugrel for some other different time
E. Post-pone for 6 months
I had never heard of prasugrel until I read this question, but it is the same class of drug as clopidogrel
(not surprising given the context). As per AHA/ACC Guidelines, recommended to continue dual anti-
platelet therapy for 365 days, and I would consider prasugrel the same as clopidogrel. Given that this
is an elective procedure, and the potential for blood loss (while usually minimal) is significant
(especially given dual anti-platelet therapy), the procedure should be delayed for another 6 months
(i.e. 12 months from time of stent placement. The risk of an in-stent thrombosis is high if both anti-
platelet drugs are not continued for the full 12 months.

 2 % % %7%% 3 '% +


A. ?
B. can have had an uneventful 'triggering' anaesthetic
C. Recommended to use an anaesthetic machine which has not had volatiles through it
D. ?
E. there have been case reports of MH occurring up to 48 h post op

B is TRUE - may have had an uneventful trigger-type anaesthetic previously. (Oxford Handbook of
Anaesthesia, 2nd Ed, p. 260)
C is not strictly true (depending how you interpret the question). If a machine that has never had
volatiles through it is available then that's great, but in practice you need to remove the vaporisers,
change the circuit and CO2 absorber, and flush with high fresh gas flows for 20-30 minutes. (Oxford
Handbook of Anaesthesia, 2nd Ed, p. 263)
E is TRUE also. Oxford Handbook states that rarely it can develop 2-3 days post-op and manifest as
massive myoglobinuria +/- renal failure secondary to rhabdomyolysis. (Oxford Handbook of
Anaesthesia, 2nd Ed, p. 260)

 > .?7 m?$2 ?m $2 ?=$7 ‰? ‰$.)0m %%  +
A. Chronic renal failure
B. Malignant hyperthermia
C. Diabetic ketoacidosis
D. End-stage respiratory failure
E. Ethylene glycol toxicity

A.Ê FALSE - CRF will give a metabolic acidosis with compensatory respiratory alkalosis
B.Ê TRUE - MH will give metabolic lactic acidosis and elevated PCO2 (mixed acidosis)
C.Ê FALSE
D.Ê FALSE
E.Ê FALSE - Ethylene Glycol acutely causes a high AG metabolic acidosis with hyperventilation
Kussmaul breathing

l  # % '%-% +;<


A. Euphoria
B. ?
C. ?
D. ?
E. Miosis (causes mydriasis or dilated pupils)

m % ;  %,-<- ;   m4m <-% 


 %   @ 
A. 3 mg/kg
B. 7 mg/kg
C. 15 mg/kg
D. 25 mg/kg
E. 35 mg/kg

Apparently up to 35-55 mg/kg of lignocaine has been "safely" used in this technique, although you
would have to have a low threshold for suspecting toxicity.
mm   $3# %
A. Twice as potent
B. Three times as potent
C. Four times as potent
D. Five times as potent
E. Same potency
If procaine =1, then lignocaine potency=2, and bupivacaine potency =8. Therefore bupivacaine is 4
times as potent as lignocaine (Foundations of Anesthesia: Basic Sciences for Clinical Practice by
Hemmings & Hopkins, 2nd edn, p.394)
Other recommended texts (Primary exam pharm texts) give differing values compared to procaine,
but all give a ratio of 4x potency for buipvacaine:lignocaine (Stoelting and Katzung)

m?   3 %%  2-A - A 1( 1 ;)< 2 $7(


 A$*   $( %%   '+
A.
B. Metaraminol
C. Check TOF
D. Nothing
E. Increase TCI
A.Ê
B.Ê MAP OK - there is no reason to be chasing ICPs or anything at this stage
C.Ê TRUE - response entropy of 70 suggests the patient may not be adequately paralysed, so
check TOF
D.Ê maybe
E.Ê whilst entropy is up slightly I would wait for the trend and with a MAP of 70 and a CPP of ?55
I would not increase the propofol

m‰ 2%   / %m;?&< B# % - mA,#%  


3  '  3 3,/ m;?&<+
A. 5 min
B. 10 min
C. 30 min
D. 60 min
E. 90 min
A study by Naguib et. al. showed that after an initial intubating dose of atracurium, and spontaneous
recovery of the first twitch (T1) to 10% of its control height, a maintenance dose of 0.1mg/kg of
mivacurium resulted in a time of 25 minutes to regain T1=10%. My guess would be the answer is C,
but it's still a guess
Reference: Naguib, et al. Interactions between Mivacurium and Atracurium. BJA 1994; 73:484-89

m5 2 6% 
A.? something with fresh gas flows
B. Relies on a constant flow of pressurised gas
C. Out of circle
D. Not temperature compensated
E. volatile injected into fresh gas slow?

A-?
B - TRUE. Upstream gas source required to push fresh gas through the vaporizer (opposite to Draw-
over vaporizer)
C - ? FALSE. Don't exactly understand the question/stem. You can use a plenum vaporizer with OR
without a circle (e.g. T-piece in paeds)
D - FALSE. Most ARE temperature compensated
E - FALSE. Not necessarily, although some can. Not true exclusively.

m ! %  3,$ %       +


A. Anterior
B. Posterior
C. Caudal
D. Cranial
E. Superficial

Answer is B (see Oxford handbook of Anaesthesia, 2nd Edn, p. 1077). Phrenic nerve stimulation
occurs if you are too anterior.

m= '% *6(  2m 7$62$2'2m$ 8A+


A. ?0.8
B. ?3
C. 520
D. 1280
E. 1520 dynes.sec/cm-5

SVR = (Systemic A-V Pressure difference) / Flow


Therefore SVR = (100-5)/5 = 95/5 = 19 mmHg/L/min
To convert to dynes.sec/cm-5 then multiply by 80; this gives us 1520 dynes.sec/cm-5. Therefore
ANSWER is E.

m      6 -%  .? %
   %% %
A. Get vascular surgeon to repair it and continue with surgery and heparin
B. Leave it in. Do CABG. Pull it out post op.
C. Pull it out, compress. Delay surgery for 24hrs
D. Pull it out compress. Continue with surgery + heparin.
E. Pull it out. Compress. Continue with surgery no heparin.

m *  ;(   %<


A. Anterior to scalenius anterior
B. ?
C. ?
D. ?
E. ?

The stellate ganglion lies ANTERIOR to the scalenius anterior muscle ("Anaesthesia UK" website -
Stellate Ganglion Block - http://www.frca.co.uk/article.aspx?articleid=100538)

ml /   # ;()2)/<
A. can be blocked at the elbow immediately medial to the brachial artery
B. can be blocked at the wrist between palmaris longus and flexor carpi ulnaris
C. can be blocked at the wrist medial to flexor carpi ulnaris
D. is formed from the lateral, medial, and posterior cords of the brachial plexus
E. provides sensation to the ulna half of the palm
A.Ê TRUE
B.Ê FALSE - between palmaris longus and flexor carpi radialis
C.Ê FALSE - lateral to flexor carpi ulnarus
D.Ê FALSE - The median nerve is formed by a lateral and medial head (from the lateral and
medial cords respectively) and has no contribution from the posterior cord. It runs down the
upper arm initally lateral to the brachial artery, but changes to be medial to the artery about
halfway down the arm, and is therefore MEDIAL to the brachial artery at the elbow
E.Ê FALSE - sensation to the lateral 3 and a half fingers and corresponding lateral area of palm -
radial side

? 2 -,     % %  %-  #   -
%  - ? % -m%% ?5%%$  % 
% % 3 - , '% % +
A. Compression neurapraxia (i think it said due to torniquet)
B. DVT
C. Muscle ischaemia (muscle is good for 4hrs of warm ischaemic time)
D. Damage to femoral nerve - femoral nerve does not flex knee
E. Spinal cord damage - unilateral and no neuraxial intervention makes this unlikely
Inability to flex the knee is not a femoral nerve problem - it is sciatic. This problem seems to have
?m     % %%;##  m m?< ? %%   3
  % %  %    
A. Continue with surgery
B. Beta block then continue
C. Get myocardial perfusion scan
D. Postpone surgery awaiting AVR
E. Postpone surgery awaiting balloon valvotomy

Median life expectancy


5 - syncope
3 - angina
2 - dyspnoea

According to ACC/AHA Guidelines on Perioperative Cardiovascular Evaluation and Care for


Noncardiac Surgery (2009 version with B-blocker update), my answer would be D=TRUE. We are told
the man has moderate AS, and his valve area of 1.1 cm2 confirms that. We are told he gets mild
dyspnoea on exertion but is otherwise asymptomatic. However, the fact that he does get SOB means
he has symptomatic aortic stenosis. Unable to say how many METS he can do from the short history.
The guidelines recommend that "if the aortic stenosis is symptomatic, elective noncardiac surgery
should generally be postponed or cancelled. Such patients require aortic valve replacement before
elective but necessary noncardiac surgery" (see p. e184, Section 3.5 Valvular Heart Disease). It is a
bit unclear if this section just refers to severe aortic stenosis, although one could make that
argument. However, logically a patient with moderate symptomatic AS at age 75 may well be a
candidate for a valve replacement anyway, purely from the cardiac point of view. The natural history
is that average progression of moderate AS is a decrease in valve area of 0.1 cm2 per year, and once
symptoms occur average survival is 2-3 years. Also, the table that defines "active cardiac conditions"
shows that severe aortic stenosis is defined as mean P gradient > 40mmHg OR valve area < 1.0 cm2
OR symptomatic. You could therefore argue that symptomatic AS is an "active cardiac condition"
and should be evaluated first.

?? %3# $ -- 3%%;3  # %C%C<$%- %%


3  % %$   %-3 - 3 
A. Medium risk surgery, medium risk patient
B. Medium risk surgery, high risk patient
C. High risk surgery low risk patient
D. High risk surgery, medium risk patient
E. High risk surgery, high risk patient.

Fem-pop bypass is HIGH risk surgery (although an angioplasty would not be if done under LA +/-
sedation).

stratifying patient risk ACC/AHA Guidelines:


1.Ê "active cardiac conditions" that when present indicate major clinical risk
@Ê Unstable coronary syndromes
áÊUnstable or severe angina (CCS class III or IV)
áÊRecent MI
@Ê Decompensated HF
áÊNYHA class IV
áÊWorsening or new-onset HF
@Ê Significant arrhythmias
áÊHigh-grade A-V block
áÊMobitz type II A-V block
áÊ3rd degree A-V block
áÊSymptomatic ventricular arrhythmias
áÊSVT (incl AF) with uncontrolled ventricular rate (HR>100bpm @ rest)
áÊSymptomatic bradycardia
áÊNewly recognised VT
@Ê Severe valvular disease
áÊSevere AS (mean P gradient > 40mmHg; valve area < 1.0cm2; symptomatic)
€Ê OR symptomatic AS regardless of the grade
áÊSymptomatic mitral stenosis (progressive SOBOE, exertional presyncope, or
HF)
2.Ê Intermediate risk denoted by the presence of "clinical risk factors"
@Ê ischaemic heart disease
@Ê compensated or prior heart failure
@Ê diabetes mellitus
@Ê renal insufficiency (creatinine >2mg/dL, which is >177umol/L)
@Ê cerebrovascular disease
3.Ê minor predictors
@Ê Age >70
@Ê Abnormal ECG (LVH; LBBB; ST-T abnormalities)
@Ê Rhythm other than sinus
@Ê Uncontrolled systemic hypertension

(7‰; )'<?‰ . %-*30/ D%3,+


A. inferonasal
b. inferotemporal
c. medial canthus
d. superior nasal
e. superior temporal

?5 .3 /  % %-3333%#%%3  


. %    +
A. Bag and mask ventilate
B. Intubate and ventilate
C. position head up, insert suction catheter in oesophagus (or to stomach?)
D. Place prone, head down to allow contents to drain
E. Insert gastrostomy

A - FALSE. Not unless the baby is in respiratory distress and/or hypoxic. May inflate stomach by
ventilating through fistula.
B - FALSE. Just because the baby has been diagnosed with TOF is not an immediate indication for
intubation in and of itself.
C - TRUE. Neonates with TOF should have a "nasogastric" tube inserted into the oesophageal stump
to drain secretions and prevent accumulation in the blind-end pouch. The NGT should be connected
to continuous suction. The infant should be nursed prone or in the lateral position with 30 degrees
head up tilt to decrease the risk of aspiration. See A Practice of Anesthesia for Infants and Children -
4th edition by Cote, Lerman, Todres; p.755. Saunders (2009)
D - FALSE. Can nurse prone, but lateral with head up tilt seems to be the recommended and most
commonly cited method.
E - FALSE. Initial management as above (see C - TRUE), and then repair. Gastrostomy may be
performed, but not best immediate management.

? =    %%%$- %% % $


  % %%$)/ ?   
A. Adrenaline
B. CPR
C. CPB
D. Place prone

I don't know if this was a bit of a trick question but setting aside the complexities and potential side-
effects/complications of mediastinal masses, the answer may be that in the event of cardiac arrest
you must perform CPR. If CPB has been organised pre-op and/or is available then that's great, but
the first response would be to attempt to resuscitate the patient with CPR and look for/treat
reversible causes. Answer=B.
However - significant compression of vascular structures (including the heart) can occur secondary
to large mediastinal masses, and changing patient position may improve things. Perhaps the answer
should be to turn prone and see if there is improvement? Any ideas?

Reference: Curr Opin Anesthesiology 2007 20:1-3

Options are reposition (lateral or prone) vs emergency sternotomy and decompression great vessels.

?= 2%  $ 2"-‰  % 1 # % %% %% %, 


% +
A. Hypercalcemia from taking parathyroids - causes hypocalcaemia
B. Bilateral laryngeal nerve palsies - chronicity wrong
C. bleeding and haematoma
D. Tracheomalacia - chronicity wrong, will have obstruction immediately after extubation
E.

? . %  #       % ;(  @ %<
A. Prewarming of patient
B.
C.
D. Warm IV fluids
? -3# %
A. complete heart block
B. congestive cardiac failure
c. VF
D.

According to Yao & Artusio (6th edn, p.236-7), biventricular pacing is defined as a lead in the RV to
pace the interventricular septum, and a lead in the coronary sinus which can pace the LV lateral free
wall. This is apparently most commonly used in patients with LBBB which can cause dyssynchronous
contraction of the LV leading to impaired systolic function. The biventricular pacing "resynchronises"
LV contraction and improves systolic function.
They quote indications as:
(i) severe cardiomyopathy (EF<35%),
(ii) LBBB with NYHA class III or IV symptoms despite maximal medical therapy.

?l 1 %- /)=#% $3  /%% /3 % 


A. vapouriser is tilted
B. Hotter than 39C
C. On battery power
D. Interlock not engaged, or not seated properly (or something like that)
E. other vapouriser is already on

‰ 1 %- #% $  3 % -


A. High SVP
B. High boiling poing
C. Low SVP
D. High MAC
E. Low MAC

‰m  -=0;(   %<


A. Wrist flexion and extension

‰? *=%% -  %


A. PE
B. AFE
C. Haemorrhage
D. Preeclampsia
E. cardiomyopathy

‰‰ %,  /?  % %-03% % ‰? ,%


A. Loss of beat to beat variability
B. No change
C. Late decels
D. Variable Deccels
E. uterine contractions
CTG can be used from about 18-20 weeks gestation. Fetal heart rate (FHR) variability is present by
25-27 weeks. The most likely thing in non-obstetric surgery during pregnancy is that the CTG will not
change (assuming all goes well with the surgery, and the mother's physiology is maintained close to
normal). However, the most common signs of fetal distress will be a change in the baseline FHR, and
loss of beat-to-beat variability. If this occurs you should assess and correct any maternal physiologic
parameters that are abnormal. (Answer=B). Ref: Chestnut's Obstetric Anesthesia: Principles and
Practice (4th Edn), Chestnut, Polley, Tsen, Wong. Mosby, 2009; p. 352.
Reference: Practical Approach to Obstetric Anesthesia 2009 p84:

Consider A-Loss of beat to beat variability:

Normal CTG under GA = Loss of beat to beat variability, no decelerations.

Normal CTG under neuraxial block without sedation = No change

‰5 '% /%%   # %+;(  @ %<


A. Cirrhosis
B. Psoriasis
C. Arthritis
D.
E.

IBD (and specifically UC) is associated with arthritis - more commonly in Crohn's (C=True, and NOT
the answer). Colectomy usually cures arthritis. IBD is also associated with Primary Sclerosing
Cholangitis (PSC) which "frequently" leads to cirrhosis and hepatic failure (A=True and NOT the
answer). Dermatologic associations of IBD include erythema nodosum, pyoderma gangrenosum,
pyoderma vegetans, pyostomatitis vegetans, Sweet's syndrome, Psoriasis, and skin tags. Therefore
B=True and also NOT the answer. Answer obviously one of the stems that was not remembered.
Ref: Harrison's 16th edn, pp.1783-84.

‰ 'D% %  - % %+;  


@ %<
A. TOFC
B. TOFratio
C. Post tetanic count

‰= 'D%  3+7-- - $- -  3 ;  @< 
A. 27%
B. 32%
C. 42%
D.
E.
‰ /% %$ D%% -+;(  @ %<
A. Amiodarone
B. Isoprenaline
C.
D.
E.

‰ /  -/; (  % / %  / #<


A. Magnesium
B. ?
C. ?
D. ?

‰l 7 $6 %$ D% -%  +


A. defibrillate
B. amiodarone
C. Intubate and ventilate
D. Pre-cordial thump
E. adrenaline

5 2   % %   7(ml $%3 .2m A=   %% 
# # %   +
A. adenosine 6mg - this comes after vagal manoeuvres in the algorithm
B. DCR
C. amiodarone
D. Atenolol
E. ?

5m /  %3 # 4


A. Arises from T2 trunk
B. Is usually blocked in brachial plexus block
C. Supplies antecubital fossa
D. can be damaged by torniquet
E. Arises from inferior trunk
A.Ê False. Arises from lat. cut. branch of 2nd intercostal nerve (from T2 originally, but not directly
from the trunk)
B.Ê False. It joins the medial cutaneous nerve of the arm which comes from the medial cord, but
does not form part of the brachial plexus, and is not blocked in brachial plexus blocks.
C.Ê False. Supplies medial side of upper arm, and joins medial cutaneous nerve of arm which
supplies medial side of upper arm down to the elbow.
D.Ê TRUE. Any nerve compressed by a tourniquet can be damaged. Would have tobe high up the
arm/close to axilla to compress it.
E.Ê False. Not part of brachial plexus, or a branch from it. Arises from lat. cut. branch of 2nd
intercostal nerve.
REF: Anatomy For Anaesthetists - Ellis, Feldman & Harrop-Griffiths (8th edn) - pp 182 and 317.

5? 2127; <-C  %%  C   % /%% 


A. headache Immediately after procedure
B. Frontal headache only - FALSE and the answer as usually frontal and occipital
C. Starts 24hrs post
D. Auditory symptoms
E. Neck stiffness
A=FALSE. Usually starts 24-48 hrs after dural puncture.
B=True. Typically fronto-occipital, but can be frontal, occipital or nuchal (Evidence-Based Obstetric
Anaesthesia, Halpern & Douglas, BMJ Books; Blackwell, 2005; p.192)
C=True. Most commonly starts 24-48 hrs later.
D=True. Hearing loss and/or tinnitus are features.
E=True. Neck stiffness and photophobia are common.

5‰ 83 % %  -    /% %% 


A. Increased sepsis
B. Increased investigations for sepsis
C. increased non shivering thermogenesis
D. Increased need for resuscitation
E. Cerebral Palsy
Labour epidural analgesia is associated with an increase in maternal core body temperature, but also
with an increased neonatal temperature and fetal heart rate. Several studies have shown that labour
epidural analgesia is associated with increased neonatal neonatal sepsis evaluations, but no increase
in neonatal sepsis. Answer=B.
Ref: Chestnut's Obstetric Anesthesia: Principles and Practice (4th Edn), Chestnut, Polley, Tsen, Wong.
Mosby, 2009; p. 457.

55   % , %%-)$8 -2 %%- 


%@% % 
A. Pathonomonic
B. Supportive
C. Only found at postmortem
D. Irrelevant
E. Incidental
A = False. No finding is pathognomonic of AFE. It is a diagnosis of exclusion.
B = True. This finding (whether at post-mortem, or whether aspirated from pulmonary artery
catheter in a surviving patient) is suggestive, but not pathognomonic. Fetal squames have been
found in pulm. art. catheter aspirates in women with no evidence of AFE, and conversely there are
reports where they have been unable to detect fetal squames in women diagnosed with AFE. The
finding is suggestive/supportive only.
C = False. Can be found in pulmonary artery aspirates in women still alive, and even with no
symptoms.
D = False. This finding is not irrelevant, but not diagnostic. It needs to be considered with all other
clinical information.
E = ? Given the less than ideal specificity of the test, one could argue that it is incidental, although the
BJA CEACCP article states that it is suggestive of AFE, which implies it is more than an incidental
finding.
ANSWER=B.
Refs: Chestnut's Obstetric Anesthesia: Principles and Practice (4th Edn), Chestnut, Polley, Tsen,
Wong. Mosby, 2009; p. 845. and BJA CEACCP 2007; 7(5):152-56.

5 : #D%  %% -%3% /    -  


 #  
A. Autonomy
B. Nonmaleficience
C. Justice
D. Paternalism
Autonomy is the right of the patient to think/decide/act freely. The patient has the right to decide
what treatment they do or don't want to have, and even if the doctor disagrees with their decision
(and/or reasoning) the patient has the right to decide for themselves. Answer is A.
It is Autonomy not to transfuse them if required, as per their wishes. it is Justice to afford them
access to the same standard of health care as everone else. i think C.

5= = % #      3 % * %   -- 
 %A3  -$3  #      %  B % /  
% %% 3   +
A. Dignity
B. Competence
C. Non-maleficience
D. Paternalism
E. Futility

5 !%  18/  .    '-  %% - -8 -#%(
3%
A. Trachealis muscle
B. "there are 3 lobes in right lung"
C. LMB longer than right
D. Angle of RMB vs left
E. Three segments of RUL

5 B  -3%$3 % - / % --3 


%, %4
A. Right upper lobe
B. RML
C. RLL
D. LUL
E. Lingula <br

5l )7-- -/-3
A. 2hrs
B. 8hrs
C. 12hrs
D. 24hrs
E. 15 minutes
"Stoelting" and "Anesthetic Pharmacology" both state that the half life of tirofiban is in the order of
2-4 hours.

 2 !*)% 
A. Increase CVA
B. Anaphylaxis
C. renal failure
D. Increased AMI

m '%  %  %


A. Poor taste
B. High inter-individual pharmacokinetic variability
C. Not licensed for <10yo
D. not as effective as adult when given in ?weight adjusted dose?
A.Ê FALSE - as far as I am aware it doesn't have a particularly nasty taste, and is used in cough
suppressants, so FALSE.
B.Ê TRUE - Variations in CYP2D6 function affect how much codeine is converted to morphine,
and therefore how effective it is, but also how "sensitive" patients are to codeine. (?10% of
caucasian population are poor metabolisers)
C.Ê FALSE
D.Ê FALSE

? 2 3 -  ? % 2 3 E 
  $% %%   .2%+? A0  % 
A. IV hydralazine
B. IV Magnesium
C. Propofol
D. Epidural lignocaine bolus
E. Esmolol

A - ?FALSE. Duration of action may be a problem, as once tumour is out you may need a vasopressor
and won't want the hydralazine hanging around. Plasma half-life is 2-3 hours (significantly more in
renal impairment, but may be less in "rapid acetylators"). Anyway, 4 half-lives is 8-12 hours (less if
you're a fast acetylator), and that's not ideal.
B - TRUE. Oxford Handbook says this is a good option.
C - False. Not the best option.
D - False. Epidural bolus will not negate the effects of circulating vasoactive catecholamines. also the
duration is likely to be in the order of hours
E - False. Esmolol for tachycardia, but not for BP control.

‰ ?+‰A5  % 3 %% -  .2m5 Al$ 


%  % . % %3 -   
A. Coagulation screen
B. Hb
C. Platelet count
D. skin bleeding time
E.
Thalassemia trait is a red-herring. No effect on clotting/epidural placement. Money is on pre-
eclampsia Main thing to look at is the platelet count. Answer is C.
See Oxford Handbook 2nd edn - p.744.
- If plt>100, proceed.
- If plt<100, do coags.
- If plt 80-100, and coags normal - regional is OK.

5   +‰lA5  .2mAmm$5F $% !1 $m 8%-,


  - %- % !  
A. 500mL Crystalloid bolus
B. IV hydralazine - this is the priority here - aim for <160 with hydralazine 5mg IV Q15min/PRN
C. IV Magnesium - this would be second job
D. insert epidural - not before assessment of coagulation profile

 . %   % %#  1 % %73 - % 0   


A. Omeprazole
B. Cimetidine
C. Ranitidine - IV ranitidine works within 40mins and lasts several hours and is part of the SIG obs
guideline (you would also give sodium citrate)
D. Sodium citrate

From the ANZCA Obstetric SIG - Ranitidine has been the most extensively studied (Escolano et al
1996, Level II; Lin et al 1996, Level II; Rout et al 1992, Level II). To date, no other agent has been
consistently demonstrated to be more effective than ranitidine and most are more expensive. A
number of studies have been done in the non-obstetric elective surgery setting. Maltby et al (1990,
Level II) showed that 150 mg of oral rantitidine when given two to three hours before surgery
resulted in a mean gastric pH of 5.86 (+/- 1.73) and with only one out of 49 patients having an ͚at
risk͛ combination of pH <2.5 plus gastric volume of >25 mL.

This doesn't however say specifically that the volume and pH are better than others... It also says
that Sodium citrate is the most effective agent for immediate neutralisation of acidic gastric content.
The reported effects on gastric volume are inconsistent with either no change (Dewan et al 1985,
Level II) or a slight increase (Jasson et al 1989, Level II; Yau et al 1992; Level II

= %  % % ;  <


A. VSD
B. PDA
C. ?
D. ?
ACYANOTIC defects: VSD=35%, ASD=9%, PDA=8%, Pulm. stenosis=8%, Aortic stenosis=6%,
Coarctation=6%, Atrioventricular septal defect=3%
CYANOTIC defects: Tetralogy=5%, Transposition=4%

 # 5  /%G% %$% % ;  <


A. Venous hum

    %    


A. Guillain-Barre syndrome
B. Organophosphate poisoning
C. Spinal cord injury
D. Stroke
E. Prolonged NMBD use

A - False. Effectively a denervation injury which causes UP-regulation.


B - TRUE. Organophosphate poisoning causes increases in miniature-end-plate potential (MEPP), and
thus can cause DOWN-regulation of ACh receptors. Apparently continuous exposure to
organophosphates can cause degeneration of pre-junctional and post-junctional structures.
C - False. Denervation causes UP-regulation.
D - False. As for spinal cord injury.
E - Prolonged NMBD use can cause UP-regulation of ACh receptors.
REFS: Miller (7th edn) - p.358

  % #%0-  %  -%# )H)2/


A. Prolonged disease
B. High dose Rx
C. Previous respiratory crisis
D. Increased sensitivity to NMB's - they will all be sensitive
E. bulbar dysfunction
Reference: CEPD Reviews 2002 p88- and OHA 246-

risk factors for IPPV postop (thymectomy) are:


1.Ê FVC<2.9L
2.Ê Concommitant COAD
3.Ê Acute fulminant crisis or respiratory involvement (grade 3)
4.Ê Myasthenic crisis (grade 4)
5.Ê OHA adds:
a.Ê Duration of disease >6yrs
b.Ê Pyridostigmine dose >750mg/d
c.Ê Major body cavity surgery
d.Ê Bulbar palsy that is predictive of intra and postop airway protection.

l 1%"-. 23 %;  <


A. SOB post pneumonectomy dyspnoea
B. Confusion post CABG

= ! #-8;  <


A. the internal branch of the superior branch of the...
B.
C.
D.
E. Cuff compression of recurrent laryngeal nerve against thryoid can cause palsy

=m '%3- 3 # ;  <


A. Auricultemporal
B. Great Auricular ʹ superficial cervical plexus
C. ?

=? ( %  # I;  <


A. Haemodynamically stable
B. Low grade injury on CT
C. ?

=‰ '   % %;  <


A. No improvement cooling Grade I to III
B. ?
C. ?

=5 %%%  !!!%


A. soft palate
B. hard palate
C. Epiglottis
D. arytenoid cartillage
E. opening to ?

= / ( 4/$7 !I?*$!2%$3 %  -  ;  <


A. Propofol/fentanyl
B. Propofol / nitrous
C. Other options with volatiles
== 1 /%     0@ % %4 % !2# +% 
  % E $ % ;  <
A. Morphine
B. Phenytoin
Most anticonvulsants are contraindicated (such as phenytoin, carbamazepine, thiopentone) because
they induce hepatic P450 enzymes. (This consumes heme and thus reduces the negative feedback on
ALA synthesase which is then free to generate heme/porphyrins products.) Drugs considered safe to
use in convulsing porphyriacs include: midazolam, propofol, gabapentin and magnesium.

= (  % % %4


A. pyridostigmine has slow onset of effect
B. physostigmine does not rely on renal metabolism/excretion
C. neostigmine cannot reverse centrally acting cholinergics
D. edrophonium is less reliable in reversal?

= @ %3 % %%;<4


A. exacerbated with heat

=l @ %3%%% %%;<4


A. mm fasciculation
B. dry skin

  # 3,-- % 


A. lateral femoral cutaneous nerve
B. femoral nerve

m   %7$ $ 3 % %-7;@<


A. muscle biopsy on pregnant lady
B. negative muscle biopsy of her father
C. genetic testing of pregnant lady

? /  # % -%,3      %4


A. subcostal nerve
B. ilioinguinal nerve
C. genitofemoral nerve
D. femoral nerve
E. lat cutaneous femoral nerve

The lateral cutaneous branch of the last thoracic nerve is large, and does not divide into an anterior
and a posterior branch. It perforates the Obliqui internus and externus, descends over the iliac crest
in front of the lateral cutaneous branch of the iliohypogastric (Fig. 819), and is distributed to the skin
of the front part of the gluteal region, some of its filaments extending as low as the greater
trochanter. http://education.yahoo.com/reference/gray/illustrations/figure?id=820 When you look
at the assoc. picture, it looks like this nerve will supply this bit skin (Lat cut br of the 12th Thoracic
nerve).

‰ 7 %    #    A;<4


A. 6% HES 130/0.4

5 2% %%;<
A. alkaline then acid urine
B. ?
C. ?
 ' #  # -  8A%m5?% -  

A. jet ventilation using pressure 400KPA
B. oxygen flush button on anaesthetic machine
C. oxygen tubing on oxygen port on anaesthetic machine at 12L/min
D.
E. none of the above

=   ;<


A. "there is hyperplasia of pulmonary arterioles"
B.

 $ %# +.2 A5 H(    % %*/( ?8B2 *!/!6) 


C3 % %% %%     %%C;<
A. intraop TOE
B. TTE

 !6 
A. late plasma levels around the same as oral
B. highly protein bound
C. ?30%? renally excreted
D. VD 10L/kg

A.Ê TRUE
B.Ê FALSE - PPB 0-5%
C.Ê FALSE - renal excretion unchanged < 2%
D.Ê FALSE - Vd = 1L/kg

l 7 /    $ % %%+


A.Global injury
B.Optic nerve injury
C.Horners syndrome
D.Tenstentorial herniation - with CNIII stretch
E.....

  %3 ?8%  1 %%  %%  3 % 


a. High Frequency
b. Penumbra effect
c. ? Dissipation of energy
d
e.

m 2  %%- !%% 34


a. Restrictive cardiomyopathy
b. Dilated cardiomyopathy
c.
d.
e.

? %  %% ;<


a. high SVR
b. tachycardia
‰ 0%3 % % '% 3 %  %3 % -+
A. Inter-quartile range
B. Standard deviation
C. Standard error of the mean
D. ?
E. ?

5 '  % 3 -      - %#% % 4
A. Sensitivity
B. Specificity
C. Positive predictive value
D. Negative predictive value

 !- %% # $  #  % % 4


A. Sensitivity
B. Specificity
C. Positive Predictive Value
D. Negative Predictive Value

= 4%-- ;<
A. F9
B. F13

 %,  %-;<4


A. intraop myocardial ischaemia
B. post op myocardial ischaemia

  ,   3  %%%


A. Euvolaemic
B.
C.
D.
E. urinary Na <20 (not enough ADH and large consequent free water diuresis with low urinary
sodium and hypernatraemia)

l !-  %% -*1


a. Primun < 3cm (primum may involve the atrioventricular valves and are an endocardial cushion
defect that is usually corrected surgically)
b. Primun > 3cm
c. Secundum < 3 cm
d. Secundum > 3cm
e. sinus venosus ASD

l /- %- # %


a. 1-2 days
b. 3-4 days
c. 5-6 days
annoyingly the OHA says 2-3days!

lm * % 


A. predict intraop anaesthetic risk
B. Predict intraop surgical and anaesthetic risk
C. Standardise the physical status classification of patients
D. Predict periop anaesthetic risk
E. Predict periop anaesthetic and surgical risk

l? 2%%%%4;  %% , 0% #  %0  , .2 -<


A. Reduced BP on inspiration unlike normal (ie normally increased on insp)
B. Reduced BP on inspiration exaggerated from normal
C. Reduced BP on expiration unlike normal
D. Reduced BP on expiration exaggerated from normal
E. ?

l? ( %-@ %%# 3


A. abdominal distension
B. an increase in chest wall spasticity - this splints their chest wall and prevents "flail" with
diaphragmatic descent
C. interscalene nerve block
D. the upright position
E. unilateral compliance reduction

l‰ !  (()/%     #%%% %


A. autonomic dysfunction is a predictor for worse long term survival after myocardial infarction
B. heart rate responses are primarily mediated through the sympathetic nervous system
C. inhalation anaesthetics all impair autonomic reflex responses
D. autonomic dysfunction is a predictor for haemodynamic instability following anaesthetic
induction
E. low heart rate variability is associated with worse cardiac outcomes following non-cardiac surgery

l5  %  %  0%- 0# % - - 
)H)2/
A. in obstructive disease the expiratory curve has a scooped out or concave appearance
B. in restrictive disease expiratory flows are usually decreased in relation to lung volume
C. in restrictive disease the expiratory curve has a convex appearance
D. the expiratory curve is largely effort independent
E. the inspiratory curve is effort dependent

l 3 % %%% -%---%3 % 


A. is cheap and readily available
B. is slow to be absorbed from the peritoneum and thus safer
C. is not as dangerous as some other gases if inadvertently given intravenously
D. provides the best surgical conditions for vision and diathermy
E. will not produce any problems with gas emboli as it dissolves rapidly in blood

l=  #  %    % %$ D%%9F % %
=  0m # - 3   0m 0 #  /%  @ %;%%
  D,3- %-0D % %  # %   ((
A$ % %, %   <
A. an intravenous infusion of CaCl2 (10 mls over 20 minutes) this is still just moderate hyperkalaemia
and in the absence of ECG changes this is not yet necessary
B. arterial blood gases to ascertain the acid/base status
C. potassium exchange resins rectally - temporising measure to help the cadaveric kidney out
D. sodium bicarbonate infusion (50- 100 mEq over 5- 10 minutes) - only if acidotic
E. urgent haemodialysis - if temporising measures fail and kidney does not kick in
l % 0-  4
A. Fine inspiratory crepitations
B. Systolic murmur at apex
C. Systolic murmur at left sternal edge - classical L heart valvular disease
D. Murmur at apex with opening snap
E. Pericardial rub

l 7%   % % % /% 4


A. Tachycardia
B. Myocardial depression
C. Coronary artery vasodilatation
D. Prolonged PR interval
E. Decreased impulse conduction

ll 2 0% -3 %%% 


A. otic ganglion - has post ganglionic sympathetic fibres from around middle meningeal artery
B. carotid body - glossopharyngeal (parasympathetic)
C. ciliary ganglion (sympathetic fibres pass through the ganglion but do not synapse there and
they're post ganglionic)
D. coeliac ganglion - part of the sympathetic prevertebral chain so pre-ganglionic fibres pass to it
E. all of the above

m . %- 3 #  /  


A. auriculotemporal nerve
B. long buccal nerve
C. lingual nerve
D. great auricular nerve
E. chorda tympani nerve - facial nerve
The chorda tympani is a nerve that branches from the facial nerve (cranial nerve VII) inside the facial
canal, just before the facial nerve exits the skull via the stylomastoid foramen.
Chorda tympani is a branch of the facial nerve (the seventh cranial nerve) that serves the taste buds
in the front of the tongue, runs through the middle ear, and carries taste messages to the brain.
(Wikipedia) Disco 30/6/10

m m !$ % $  %3    %


% %   -%-  %   /  %%% 

Complication present Complication absent

Exposed to new drug 50 25


NOT exposed 25 25

From this data


A. the relative risk of this complication with drug exposure CANNOT be determined (retrospective)
B. the odds ratio of this complication with drug exposure CANNOT be determined
C. the relative risk of this complication with drug exposure is 2
D. the odds ratio of this complication with drug exposure is 1.33
E. none of the above
A.Ê TRUE - this study is a retrospective case control and RR is not used rather OR
B.Ê FALSE - OR calculation is appropriate
C.Ê FALSE - RR not relevant
D.Ê FALSE - OR = 2
E.Ê FALSE

m ? .2 %  0#  % % 4


A. big (wide) cuff - underestimates
B. skinny arm - underestimates
C. severely peripherally vasoconstricted
D. atherosclerosis (it was arteriosclerosis - yes indeed) - rigid artery ї cuff pressure must be higher
to compress them
E. slow cuff deflation - false fast deflation will overestimate DBP and underestimate SBP

m ‰  #   %m --   #   %% %--- 
5 % %%4
A. Class 1 device
B. Equipotential earthing
C. LIM
D. Residual Current Device
E. Fuse

m 5 2%0%-% %%%%%  


A. jaundice in over 50% of patients
B. development of chronic disease in less than 10% of patients - 85-90% will develop chronic HCV
C. hepatitis B in the majority of patients - hep C in the majority although now it is 1 in 3.6million and
HBV is 1 in a million.
D. the presence of antigen or antibody to hepatitis C
E. elevation of serum alkaline phosphatase - usually not elevated ie not a transaminase

m  !  @2     J%3%, $% # 2-


A. A
B. B
C. AB - would argue that these people do not have Abs to ABO antigens ie less risk of a reaction
D. O
E. Blood group of FFP in this situation does not matter

m =   %- %  % - % ;/"(2<%  - - 
)H)2/
A. agitation
B. angina
C. bradycardia
D. nausea
E. tinnitus

m  / %- @   %  %


A. arrhythmia
B. cyanosis
C. sweating
D. tachycardia + јETCO2 (after MMS)
E. rigidity

m  '- - %3% 0-(!+


A. cochlear implant -
B. heart valve prosthesis - fixed to fibrous tissue
C. ICD - malfunction likely
D. pacemaker - malfunction likely
E. intracranial clips - if ferromagnetic

m l ( # % %- %  %% 4


A. LBBB
B. Pulmonary hypertension - will tend to cause narrowed normal splitting ie less P2 delay
C. Acute pulmonary embolus - congestion will cause larger end-diastolic volumes and ejection will
take longer (normal split despite increased PA pressures)
D. ASD - will cause a fixed split that does not vary with respiratory cycle
E. Severe MR - will tend to accentuate normal split owing to faster LV ejection

ë
   ë   occurs on inspiration owing to entrainment of blood into the RV relative to the
LV. RV ejection then takes longer resulting in a slightly delayed P2. On expiration this is minimise
owing to the opposite effect.
  ë  occurs withLBBB, PPM (where uncoordinated ventricular ejection causes P2 to go
first), AS or HOCM (prolonged LV ejection)

mm -34
A. Cardioversion results in longer life expectency than rate control
B. Need to stay on warfarin following cardioversion
C. Pt with HR <80 generally do not require anticoagulation
D.

mmm *%%%   % 


A. one third of the blood loss occurs postoperatively
B. major blood loss is frequently accompanied by a consumptive coagulopathy
C. surgery will halt progression of the restrictive lung deficit
D. the major neurological deficits that occur are usually due to damage to the posterior columns of
the spinal cord - would have thought that anterior spine is more vulnerable in the setting of
hypoperfusion of anterior spinal artery territory
E. the use of aprotinin reduces blood loss

mm5 1--   3    3   


A. Equipotential earthing

mm ' %  % % +


A. cortisol
B.
C. TSH
D. growth hormone

mm= %%  / 3 % -  3 %4


A. anterograde perfusion via coronary vessel
B. retrograde perfusion via jugular vein
C. thiopentone IV
D. hypothermia to 20 degrees celcius

mm * -%%  %


A. chance of a positive test in people with the disease
B. chance of a negative test in people without disease
C. chance of...
mm  #  # # %%  %
A. chance of a positive test in people with the disease
B. chance of a negative test in people without disease
C. chance of ...
(NB there were definitely two questions with identical options a. through e. (and each option was
wordy and a bit confusing). The stems were definitely specificity and NPV)

mml 2 -3% / 3 %   % %4;% 5<


A. angle of the bronchus
B. length of the bronchus
c. RUL
D. trachealis muscle (posterior)

m? *%-   4;% <


A.
B.
C. seizures - coma only
D. short ST segment - FALSE, shortening of QT interval + prolonged PR + QRS prolongation + T wave
flattening + heart block + digoxin accentuation

features of hypercalcaemia
1.Ê weakness/N+V/lethargy/metal changes/coma
2.Ê ECG changes above
treatment
1.Ê rehydrate
2.Ê frusemide diuresis
3.Ê palmidronate (long lasting)
4.Ê calcitonin ї љ Ca and PO4 secretion from bone (transient)
5.Ê hydrocortisone 200-400mg IV (if secondary to malignancy)
6.Ê HD if secondary to renal failure

m?m 2 6 % '% +


A. if resistant to defibrillation should give amiodarone 5mg/kg
B.
C. commonly associated with respiratory arrest
D. is the most common form of arrest in this patient group
E. should defibrillate with 5J/kg - false 2 and then 4J/kg

m?‰  86  - m & ? . % %4;<
A. CPAP 5cm top lung - this will allow oxygen insufflation and slight distension of the non-dependent
lung/you get 150mL TV with contralateral lung insufflation anyway. this is a good start (could
increase to 10cmH2O
B. CPAP 10cm top lung
C. PEEP 5cm bottom lung - will increase shunt to non-dependent lung (this is a desperate
manoeuvre)
D. CPAP 5cm top + PEEP 5cm bottom

one lung ventilation CEACCP 2002


surgical indications:
1.Ê lung
2.Ê oesophageal
3.Ê mediastinal
4.Ê spinal
pre-operative assessment
@Ê attempts to determine the patient's ability to tolerate OLV and possible lung resection
@Ê assess assuming pneumonectomy since
áÊ disease may be more extensive than expected
áÊ oedema + atelectasis ї post op lung function may be significantly impaired
@Ê Hx
áÊ functional capacity
€Ê SOB at rest (NYHA IV) or cor pulmonale ї bodes poorly
áÊ cardiac problems
@Ê investigations
áÊ spirometry
€Ê FEV1 < 2L ї probability of postop respiratory failure ї 40%

áÊ ABG - hypoxia at rest poor predictor/hypercapnia indicates respiratory failure


áÊ evaluation of individual lung function
€Ê technetium scanning to determine the post operative FEV1. FEV1 < 0.85L
associated with respiratory failure post op
áÊ pulmonary artery catheterisation and occlusion of the artery on the proposed side of
the pneumonectomy, will test the remaining lung.
€Ê PA pressure > 40mmHg or PaO2 < 45mmHg or PCO2 > 60mmHg ї survival
unlikely
€Ê dicey test
physiology of OLV
@Ê lateral decubitus ї V/Q mismatch
áÊ 60% flow to dependent lung BUT more ventilation to non-dependent lung
áÊ  compliance and FRC of dependent lung owing to weight of mediastinum +
elevated position of diaphragm (abdominal contents pushing up)
@Ê open chest
áÊ r compliance of non-dependent lung ї r dead space of non-dependent lung + r
shunt in dependent lung (A-a gradient r)
@Ê collapse of non-dependent lung ї shunt
@Ê if minute ventilation remains constant there will be a small increase in pCO2 owing to
reduced ventilation
@Ê in theory with OLV, a shunt fraction of 50% is possible, that cannot be treated with rFiO2.
in reality several factors reduce this to about 20% of the pulmonary blood flow:
áÊ increased perfusion of dependent lung
áÊ collapse of the non-dependent lung causes mechanical obstruction to circulation
áÊ HPV causes shunt to dependent lung
@Ê factors affecting pulmonary BF
áÊ volatiles
€Ê 1MAC isoflurane ї 20% HPV
€Ê N2O only 10% HPV
áÊ IV anaesthesia - no affect on HPV
áÊ vasodilators HPV
áÊ vasoconstrictors constrict vessels in the dependent lung and increase BF to non-
dependent lung and shunt fraction (dopamine may do this less and is the first choice
if vasopressor is required)
áÊ rFiO2 ї PVR in dependent lung (favourable)
áÊ CO -
€Ê rCO ї recruitment and distension in the non-dependent lung ї rshunt
€Ê CO ї Sv02 ї SaO2 if shunt fraction large
áÊ PEEP
€Ê rPVR ї r flow to non-dependent lung ї rshunt
conduct of anaesthesia
@Ê GA with controlled ventilation
@Ê goals
áÊ blunt airway reflexes - remifentanil
áÊ minimise HPV inhibition - propofol TIVA (no demonstration clinical benefit but
theoretically sound)
áÊ maintain haemodynamic stability
áÊ rapid offset drugs to avoid prolonged ventilation post op - remifentanil and TIVA
áÊ good post operative analgesia
€Ê thoracic epidural - large meta-analysis showed
@Ê atelectasis
@Ê LRTIs
@Ê pulmonary complications
€Ê paravertebral catheter (Sx or anaesthetic percutaneous)
€Ê intercostal blocks at the start to avoid opioids during surgery
áÊ restrictive fluid administration ї better lung outcomes; vasopressor might be a
better choice
@Ê practical aspects
áÊ DLT
€Ê MALE - 39-41Fr
€Ê FEMALE - 37-39Fr
€Ê children - 26Fr OK for 8-10yrs
€Ê L sided DLT more commonly used - L bronchus is longer and so less chance of
obstructing the L upper lobe bronchus than a R DLT on the R obstructing the
R upper lobe bronchus
@Ê contraindications incl. L bronchial lesions/L bronch stump
€Ê clinical manoeuvres include auscultation and clamping
€Ê fibreoptic bronchoscopic evaluation gold std - want to see the blue cuff just
beyond the carina
áÊ bronchial blockers
€Ê children (DLT too big)
€Ê normal ETT then bronchoscopic placement of blocker
áÊ single lumen ETT
€Ê eg for TOF or bleeding lung
€Ê eureka type intubation for R main
€Ê for L main - turn child's head to R and advanced the ETT with the concavity
facing posteriorly
áÊ equipment
€Ê invasive BP
€Ê CVL
€Ê temperature
€Ê spirometry - for pressure/volume loops
€Ê OLV - TV and rRR 20%
@Ê permissive hypercapnia to avoid barotrauma
áÊ resus - treatment of hypoxia on OLV
€Ê 100% oxygen
€Ê let surgeon know
€Ê check tube postition for slip +/- bronch eg cuff herniation
€Ê check circuit
€Ê check CO
€Ê insufflate non-dependent lung with oxygen (TV of 150mL/min due to
contralateral lung ventilation
@Ê small amounts of PEEP can be applied to the non-dependent lung
with a flow rate of 1L/min (Ayres T-piece can be used here)
€Ê CPAP to non-dependent lung (5-10cmH2O) ї distension of non-dependent
lung but no haemodynamic instability/surgical interference (can do this with
the ambibag
€Ê consider PEEP to ventilated lung ї rFRC and shifts the lung up to the
steeper part of the compliance curve allowing better volume for a given
pressure BUT rPEEP ї rPVR ї rflow to non-dependent lung + r shunt.
This needs to be balanced carefully
€Ê ultimately intermittent ventilation of the non-dependent lung may be
required
€Ê surgical clamping of the non-dependent PA will eliminate shunt.