2024.2 MCQ

Question 1

“1. During paediatric gas induction, the gas flow recommended by SPANZA for least
environmental impact is”

“● 1L/min
● 2L/min
● 3L/min
● 4L/min
● 5L/min”

Answer 1

3L/min

“https://journalwatch.org.au/reviews/reducing-the-environmental-impact-of-mask

0.15L/min/kg”

Question 2

2.

The Mapleson circuit to best achieve normocarbia with mechanical ventilation is:

“● Mapleson A
● Mapleson B
● Mapleson C
● Mapleson D
● Mapleson E”

Answer 2

Mapleson D

Journal article entitled Mapleson’s Breathing Systems 2013:

“For adults,

Mapleson A is the circuit of choice for spontaneous respiration where as

Mapleson D and its Bains modifications are best available circuits for controlled ventilation.

For neonates and paediatric patients Mapleson E and F (Jackson Rees modification) are the best circuits.”

Question 3

3. SQUIRE guidelines

”- Provide a framework for reporting new knowledge about healthcare improvement
- How to conduct a systematic review”

Answer 3

Provide a framework for reporting new knowledge about healthcare improvement

“From the SQUIRE website: SQUIRE stands for Standards for QUality Improvement Reporting Excellence. The SQUIRE guidelines provide a framework for reporting new knowledge about how to improve healthcare. They are intended for reports that describe system level work to improve the quality, safety, and value of healthcare.

PRISMA: Systematic review”

Question 4

4. Box and whisker plot - What does the box mean

”
Interquartile rage
2 std deviations”

Answer 4

“Interquartile range

“The five number summary is the:
minimum,
first quartile,
median,
third quartile and
maximum”

Question 5

5. Axis of ECG - left axis deviation (aVR was isoelectric, AVF negative, I positive)

“(a) -45
(b) -75

(c) +15”

Answer 5

Question 6

6. What does a green line on the rigid laryngoscope blade mean

“(a) Reusable
(b) Recyclable
(c) Single use - disposable
(d) Immersible”

Answer 6

?reusable

Question 7

“7. Arndt blocker attachment point for the breathing circuit (just a schematic drawing provided in
the exam)”
“Points A
B
C
D”

Answer 7

“C
- Bit with the pop off top is for fibreoptic
- Bit without pop off top is for bronchial blocker
- Perpendicular bit is for breathing circuit”

https://www.researchgate.net/figure/Arndt-endobronchial-blockerR-by-Cook-Multiport-airway-adapter-A-Blocker-port-B-FOB_fig3_258103877

Question 8

8. Vivasight components (arrow to the red bit in the exam)

“Flush port
Light source
Aspiration port

Answer 8

Flush port

https://www.ambuaustralia.com.au/airway-management/double-lumen-tubes/product/vivasight-2-dlt

Question 9

9. Semaglutide half life

“3 days
7 days
14 days”

Answer 9

7 days

https://pubmed.ncbi.nlm.nih.gov/29915923/

Question 10

10. Gastric USS image given - Exact image to R

Answer 10

Empty stomach

“https://www.bjaed.org/article/S2058-5349(19)30047-2/fulltext https://www.showmethepocus.com/gastric

ID landmarks: L liver border, antrum, pancreas, aorta, vertebrae
Empty - small antrum, target sign
CF - starry night
solid - enlarged antrum and can visualise solids”

Question 11

11. PREVENTT trial- for major abdo surgery iron infusion:

”- Reduced allogenic red cell transfusion
- Reduced mortality
- Reduced readmission rates within 30 days
- Reduced infection rates”

Answer 11

REduced readmission rates within 30days

PREVENTT: surgery / Fe infusion

1’ outcome : No difference in transfusion/death between Fe vs no-Fe pre op

2’ outcome : Fewer unplanned readmissions BUT no difference in ave number of transfusions/LOS/self-reported QOL

Question 12

12. Compared to UFH, Enoxaparin preference

• Thrombin
• Xa

Answer 12

Xa

“Enoxaparin works by binding to AT III to inactivate clotting factors, preferentially factor Xa, thereby blocking the conversion of prothrombin to thrombin, which is the coagulation cascade’s final common pathway.”

https://www.sciencedirect.com/science/article/pii/S2772993124000913#:~:text=Enoxaparin%20works%20by%20binding%20to,coagulation%20cascade’s%20final%20common%20pathway.

Question 13

13. Child on 15mcg/kg steroids, when to give hydrocort

• > 2 weeks
• 1 month
• 2 months

Answer 13

> 1month

“https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.14963

"”Daily doses of prednisolone of 5 mg or greater in adults and 10–15 mg.m−2 hydrocortisone equivalent or greater in children may result in hypothalamo–pituitary–adrenal axis suppression if administered for 1 month or more by oral, inhaled, intranasal, intra-articular or topical routes; this chronic administration of glucocorticoids is the most common cause of secondary adrenal suppression, sometimes referred to as tertiary adrenal insufficiency.””
2mg/kg hydrocortisone stress dose
“

Question 14

14. DCD - last acceptable organ

• Lungs
• Kidney
• Liver
• Pancreas
• Heart

Answer 14

EKLung

“https://www.donatelife.gov.au/sites/default/files/2022-01/ota_bestpracticeguidelinedcdd_02.pdf

Liver/ pancreas/heart –> Kidneys –> Lungs”

Question 15

15. DCD criteria, what doesn’t include

“● Immobility
● apnoea
● absent skin perfusion
● absence of circulation (no arterial pulsatility for 2 min)
● Cannot recall other option, which was the answer (maybe absense”

Answer 15

Absent skin perfusion

“This is just the standard criteria for certifying death:
Absence of breathing for 2 min
Absence of heart sounds 2 min
Pupils

Donate life: The determination of death using circulatory criteria
is a common event in medicine and the features are
well known. They include absence of movement and
unresponsiveness, absence of pulse and breathing, and
pupils that are dilated and unresponsive to light. “

Question 16

16. Post herpetic neuralgia, feels insects crawling across head, what is it?

”- Allodynia
- Dysaesthesia
- Formication
- Pruritis”

Answer 16

“Formication

But does technically fall under dysaesthesia because it’s an abnormal sensation”

Question 17

17. Congenital long QT, drug should avoid

“Prop
Thio
Ketamine”

Answer 17

Ketamine

“https://www.bjaed.org/article/S1743-1816(17)30428-6/pdf

Prop = no effect on QT
Vecuronium and atracurium do not prolong QTC in healthy individuals, and are probably safe to use in LQTS patients.
Thiopental is known to prolong the QTc, but reduces TDP, and can be used in patients with LQTS.
Midazolam has no effect on QTc in healthy adults.
Ketamine should be avoided because of its sympthomimetic effects.”

Question 18

18. Recurrent torsades treatment, acceptable:

“Flecainide
Lignocaine
Procainamide
Amiodarone
Sotalol”

Answer 18

Lignocaine

“LITFL: ILCOR suggest the use of amiodarone or lidocaine in adults with shock refractory ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT) (weak recommendation, low quality evidence).

UTD: Class 1b antiarrhythmics can be used eg lignocaine”

Question 19

19. Acceptable tryptase to diagnose anaphylaxis..

”- (1.2 of normal) + 2 /ml
- (1.8 of normal) + 2
- Normal + 2
- 10/ml
- 15/ml”

Answer 19

1.2 x normal + 2

“Not stated in ANZCA Anaphylaxis doc

UTD: The minimal elevation of the acute total tryptase level that is considered to be clinically significant was suggested to be ≥(2 + 1.2 x baseline tryptase levels) in units of ng/mL or mcg/liter”

Question 20

20. ANZAAG refractory anaphylaxis:

• Glucagon IV 10 mins
• Glucagon IV 5 mins
• Glucagon IM 5 mins
• Glucagon IM 10 min

Answer 20

Glucagon IV Q5min

“https://www.anzca.edu.au/resources/professional-documents/endorsed-guidelines/anaphylaxis-card-3-adult-refractory-management-202.pdf
Glucagon 1– 2 mg IV every 5 min until response
Draw up and administer IV (Counteract β blockers

Paeds: Glucagon 40 microg/kg IV to max 1mg”

Question 21

21. Fem-fem VA ECMO, where is blood gas best representative of coronary PaO2?

Answer 21

right radial

Vetted by perplexity

R radial because closest to where coronary arteries would come off post AV?

Right radial artery Native cardiac output Best indicator (proximal aortic branches)

as it reflects oxygenation of blood ejected from the left ventricle—the primary source of coronary perfusion.

Question 22

22. Post op cog decline has an onset within:

”- immediate post
- With one day, lasting one week
- From ?3wk ?10 days post op for a year
- From 1 month to 1 year”

Answer 22

From 1week to 1 year post op

BB 2019 POD:
The new nomenclature defines POD as that which occurs in hospital up to 1 week post procedure or until discharge (whichever occurs first) and meets DSM-V diagnostic criteria3.

Blue Book article 2019 - From 7 days post op til 1 year post

Question 23

23. Pre-eclamspia at 30 weeks with IUGR

”- low CO, low SVR
- Low CO, high svr
- High CO, low svr
- High CO, high svr”

Answer 23

Low CO, high SVR

https://www.ahajournals.org/doi/epub/10.1161/HYPERTENSIONAHA.118.11092

Women who subsequently developed preeclampsia/fetal growth restriction had lower preconception cardiac output (4.9 versus 5.8 L/min; P=0.002) and cardiac index (2.9 versus 3.3 L/min per meter2; P=0.031) while mean arterial pressure (87.1 versus 82.3 mm Hg; P=0.05) and total peripheral resistance (1396.4 versus 1156.1 dynes sec cm−5; P<0.001) were higher.

https://www.ajog.org/article/S0002-9378(20)31283-7/fulltext

Question 24

24. Burns - expected physiological change in first 24 hours

”- High cardiac index
- Increased PVR
- Decreased SVR
- High stroke volume”

Answer 24

Increased PVR

** as per Syd course from this Stapleton Burns journal article

This is driven by intense catecholamine release with persistent beta-adrenergic receptor stimulation, also implicated in subsequent myocardial depression that is commonly seen.

Intense initial systemic and pulmonary vasoconstriction occurs in the face of
low cardiac output with
decreased oxygen delivery and consumption
which slowly recovers over 24–48 h.

Physiological Changes in the First 24 Hours Following Burn Injury

The initial 24-hour period following a severe burn injury represents the critical “ebb phase,” characterized by profound hemodynamic instability and systemic perturbations. This phase is marked by hypovolemic shock, endothelial dysfunction, and compensatory neurohormonal activation, which collectively drive distinct cardiovascular and metabolic alterations.

Cardiovascular Dynamics in the Ebb Phase

Systemic and Pulmonary Vascular Resistance
During the first 24 hours, systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) are markedly elevated due to catecholamine-driven vasoconstriction and hemoconcentration[1][4][7]. The release of vasoactive mediators such as norepinephrine and antidiuretic hormone exacerbates peripheral and pulmonary vasoconstriction, which serves as a compensatory mechanism to maintain mean arterial pressure despite hypovolemia[4][7]. This vasoconstrictive response is further amplified by endothelial glycocalyx degradation, which increases capillary permeability and exacerbates fluid extravasation into interstitial spaces[1][6].

Cardiac Output and Stroke Volume
Contrary to the hyperdynamic state observed in later phases, cardiac output (CO) and stroke volume (SV) are significantly reduced during the ebb phase[1][2][4][7]. Myocardial depression occurs due to direct thermal injury-mediated cytokine release (e.g., tumor necrosis factor-α, interleukin-6) and ischemia-reperfusion injury, impairing both systolic and diastolic function[9]. Hypovolemia secondary to capillary leak syndrome further reduces preload, compounding the decline in CO[1][6]. Transesophageal echocardiography studies in burn patients demonstrate subnormal left ventricular end-diastolic volumes and impaired contractility within the first 12–24 hours[3][7].

Hemoconcentration and Blood Viscosity
Hemoconcentration arises from plasma loss into burned and non-burned tissues, increasing blood viscosity and red blood cell-to-plasma ratios[2][4]. This elevates shear stress on the vascular endothelium, exacerbating microcirculatory dysfunction and organ hypoperfusion[1][6].

Endothelial and Metabolic Dysregulation

Capillary Leak Syndrome
Burn injury triggers systemic endothelial activation, leading to glycocalyx shedding and paracellular albumin leakage, which manifests as microalbuminuria[1][6]. Syndecan-1, a biomarker of glycocalyx degradation, correlates with increased fluid resuscitation requirements and worse clinical outcomes[1].

Acid-Base and Oxygenation Imbalances
Metabolic acidosis and venous desaturation are common due to tissue hypoperfusion and anaerobic metabolism[4][7]. Pulmonary vasoconstriction and inhalation injury further impair oxygenation, contributing to ventilation-perfusion mismatch[4][6].

Fluid Resuscitation Challenges

The Parkland formula (4 mL/kg/% total body surface area) provides a framework for crystalloid administration, but adherence to urinary output (0.5–1 mL/kg/h) and mean arterial pressure (≥65 mmHg) remains critical[3][4]. Over-resuscitation risks compartment syndromes and pulmonary edema, while under-resuscitation exacerbates organ ischemia[1][4].

Conclusion

In the first 24 hours post-burn, the dominant physiological changes include elevated SVR and PVR, reduced cardiac output, and hypovolemia-driven hemodynamic instability. The hyperdynamic state (high cardiac index, decreased SVR) manifests only after 48 hours during the “flow phase.” Thus, the correct answer is increased PVR[1][4][7].

Rationale
- High cardiac index and high stroke volume are hallmarks of the hyperdynamic flow phase (≥48 hours)[1][4][7].
- Decreased SVR occurs later due to vasoplegia and inflammatory mediator dominance[1][4].
- Increased PVR is characteristic of the early ebb phase, driven by catecholamine surge and hypovolemia[1][4][7].

Answer: Increased PVR

Citations:
[1] https://www.jvsmedicscorner.com/TraumaBurns_files/Early%20Hemodynamic%20Management%20of%20Critically%20Ill%20Burn%20Patients%20Review%202018.pdf
[2] https://www.physio-pedia.com/Burn_Shock
[3] https://pubmed.ncbi.nlm.nih.gov/19204504/
[4] https://anest.ufl.edu/wordpress/files/2021/07/Burn.pdf
[5] https://basicsofburncare.org/general-management-of-burns-patients-after-24-hours/
[6] https://anaesthetics.ukzn.ac.za/Libraries/Londiwes_uploads/FMM_No_3_-_24-2-2017An_Acute_Management_In_Burns-_L_Nkomentaba.pdf
[7] https://www.researchgate.net/figure/Changes-in-cardiac-output-and-systemic-vascular-resistance-during-the-first-48-h_fig4_8171113
[8] https://anaesthetics.ukzn.ac.za/wp-content/uploads/2023/05/2023-05-05-The-Anaesthetist-and-Management-of-Burns-M-Moodley-1.pdf
[9] https://www.mdpi.com/1422-0067/17/1/53
[10] https://www.ncbi.nlm.nih.gov/books/NBK430795/
[11] https://www.rch.org.au/trauma-service/manual/Burns/
[12] https://academic.oup.com/burnstrauma/article/doi/10.1093/burnst/tkac061/7028683
[13] https://www.nature.com/articles/s41572-020-0145-5
[14] https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
[15] https://pmc.ncbi.nlm.nih.gov/articles/PMC5627559/
[16] https://www.jmchemsci.com/article_211059.html

https://journals.sagepub.com/doi/10.1177/0310057X20914908?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

Question 25

25. Which increases the risk of blood product related graft vs host disease

• genetic variability between donor and recipient
• irradiated
• leukodepleted
• Immunodeficiency
• transfusion of non-cellular product

Answer 25

• genetic variability between donor and recipient
• irradiated
• leukodepleted
• Immunodeficiency
• transfusion of non-cellular product

Immunideficiency?

“Lifeblood: https://www.lifeblood.com.au/health-professionals/clinical-practice/adverse-events/TA-GVHD#:~:text=The%20three%20primary%20risk%20factors,diversity%20between%20donor%20and%20recipient.

The three primary risk factors for developing TA-GVHD are:
1. degree of immunodeficiency of the recipient.
2. number of viable T lymphocytes transfused (affected by the age of the blood transfused, degree of leucodepletion and irradiation status), and
3. genetic diversity between donor and recipient. Greatest risks are donations from blood relatives and with HLA-matched blood products.”

Question 26

26. When reconstituted, fibrinogen concentrate should be transfused within:

• 30min
• 4h
• 6h
• 8h

Answer 26

The correct answer is 6h[2].

Fibrinogen concentrates such as RiaSTAP® have specific post-reconstitution stability periods dictated by their product monographs. According to the Australian prescribing information for RiaSTAP®, reconstituted fibrinogen concentrate must be stored below 25°C and used within 6 hours[2]. This contrasts with stability data from other jurisdictions (e.g., 8 hours in the U.S. and Canada)[3][5], but the Australian guidelines explicitly specify a 6-hour window to mitigate microbiological risks and ensure efficacy. Studies demonstrating extended stability under refrigeration (e.g., Fibryga® for up to 7 days at 4°C[1]) apply to specific formulations and storage conditions not universally adopted. For the Australian clinical context, adherence to the 6-hour limit aligns with local regulatory standards[2].

Citations:
[1] https://pubmed.ncbi.nlm.nih.gov/36804189/
[2] https://www.cslbehring.com.au/-/media/cslb-australia/documents/aus-pis-and-cmis/riastap-au-pi-v1000.pdf
[3] https://transfusionontario.org/wp-content/uploads/2023/10/Transfusionists-Talk-2023-Sep_FC-PCC_Final_Sept-27_website.pdf
[4] https://pubmed.ncbi.nlm.nih.gov/33196820/
[5] https://labeling.cslbehring.com/pi/us/riastap/en/riastap-prescribing-information.pdf
[6] https://www.riastap.com/professional/about-riastap/convenience.aspx
[7] https://www.bloodtransfusion.it/public/pre2018archives/2012/BloodTransfus2012_Vol10_Issue_1_023-027_015-11.pdf
[8] https://nibsc.org/documents/ifu/09-242.pdf
[9] https://www.rch.org.au/bloodtrans/about_blood_products/Clotting_Factor_Concentrates/
[10] https://litfl.com/fibrinogen-concentrate/
[11] https://academic.oup.com/milmed/article/183/suppl_1/183/4959968
[12] https://www.fda.gov/media/73604/download
[13] https://www.albertahealthservices.ca/assets/wf/lab/if-lab-clin-tm-riastap.pdf
[14] https://academic.oup.com/milmed/article/186/3-4/286/5983609
[15] https://www.rch.org.au/bloodtrans/about_blood_products/clotting_factor_concentrates/
[16] https://aci.health.nsw.gov.au/__data/assets/pdf_file/0004/716566/ACI-Fibrinogen-administration-in-prehospital-trauma.pdf

8h

looks like 6 hours according to an australian resource
- LITFL says 8 hours, however they reference the American datasheet, whereas NZ and
Oz datasheets say 6 hours. Research also states 8 hours.”

“RIASTAP product info:
If it is not administered immediately, it must be stored below 25oC and used within 6 hours of
reconstitution. The reconstituted solution should not be stored in the refrigerator”

Question 27

27. A man has this device put in because he isn’t suitable for anticoagulation with AF.
    What is a
    WATCHMAN device/ where is it?

• left atrial appendage
• SVC
• IVC
• Right atrium
• Ascending aorta

Answer 27

LAA parachute

Question 28

28. A aortic mechanical On-X valve - has an inguinal hernia repair in 48 hours and his INR is 1.5, what should you do?

”- bridge with enoxaparin
- bridge with heparin
- just withhold the warfarin”

Answer 28

Withhold warfarin?? Can’t actually find a guideline on this anywhere

Answer:
Just withhold the warfarin

Rationale:
For patients with an On-X mechanical aortic valve (without additional thromboembolic risk factors) undergoing surgery, current evidence supports withholding warfarin without bridging anticoagulation when the INR is appropriately managed.

1. On-X Valve-Specific Guidelines
   The On-X valve allows for lower INR targets (1.5–2.0) compared to older mechanical valves[8][12]. Bridging is not required in low-risk patients (aortic position, no additional risk factors) if warfarin is interrupted for ≤48 hours and INR is <1.5 preoperatively[11][12].
2. INR Trajectory
   Warfarin’s half-life (~40 hours) means withholding it 48 hours preoperatively will further reduce the INR (already 1.5 at the time of decision-making), minimizing perioperative thromboembolic risk while avoiding excessive bleeding[5][16].
3. Bridging Risks
   Bridging with enoxaparin or heparin increases bleeding complications without reducing thromboembolic events in low-risk On-X aortic valve patients[6][12]. The PROACT trial and 2024 registry data confirm the safety of omitting bridging in this population[8][12].

Conclusion:
Withholding warfarin aligns with On-X valve guidelines and minimizes bleeding risks, as the INR is already at the lower target threshold. Bridding is unnecessary in this low-risk scenario.

Sources:[6][8][11][12]

Citations:
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC11024885/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC11715504/
[3] https://www.ahajournals.org/doi/10.1161/circulationaha.111.084517
[4] https://thischangedmypractice.com/perioperative-anticoagulation-management-in-mechanical-heart-valves/
[5] https://pubmed.ncbi.nlm.nih.gov/18704620/
[6] https://www.bmj.com/content/bmj/373/bmj.n1205.full.pdf
[7] https://www.ahajournals.org/doi/10.1161/circulationaha.105.598268
[8] https://www.jacc.org/doi/10.1016/j.jacc.2018.03.535
[9] https://onlinelibrary.wiley.com/doi/10.1111/jcpt.13164
[10] https://pmc.ncbi.nlm.nih.gov/articles/PMC3835169/
[11] http://www.heartvalvechoice.com/wp-content/uploads/2021/05/On-X-Valve-Patient-FAQs.pdf
[12] https://pmc.ncbi.nlm.nih.gov/articles/PMC11136449/
[13] https://www.nps.org.au/assets/9bf65e3bdcbf0fe0-ac62d69f22ee-c0d8a6fa7795b1097b2afb4eab5437f708fbaaa4536a31d33e077815d2ee.pdf
[14] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?format=pdf
[15] https://www.cec.health.nsw.gov.au/__data/assets/pdf_file/0006/458988/Guidelines-on-perioperative-management-of-anticoagulant-and-antiplatelet-agents.pdf
[16] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?lang=en
[17] https://pmc.ncbi.nlm.nih.gov/articles/PMC9387617/
[18] https://www.ncbi.nlm.nih.gov/books/NBK557590/
[19] https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2020/12/16/22/01/2020-ACC-AHA-VHD-GL-Pt-3-GL-VHD
[20] https://www.ahajournals.org/doi/10.1161/CIR.0000000000000923
[21] https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-20/prosthetic-heart-valves-part-2-antithrombotic-management
[22] https://academic.oup.com/ejcts/article-pdf/65/5/ezae117/57986671/ezae117.pdf
[23] https://www.mtw.nhs.uk/wp-content/uploads/2015/09/Algorithm-for-Perioperative-Management-of-Anticoagulation1.pdf
[24] https://pmc.ncbi.nlm.nih.gov/articles/PMC10360928/
[25] https://pmc.ncbi.nlm.nih.gov/articles/PMC3312231/
[26] https://www.health.qld.gov.au/__data/assets/pdf_file/0015/1152213/statewide-anticoagulant-guideline.pdf
[27] https://www.researchgate.net/publication/23172264_Inguinal_hernia_repair_in_the_anticoagulated_patient_A_retrospective_analysis
[28] https://emedicine.medscape.com/article/285265-overview

Only heart valve marketed for low INR 1.5-2

The patient with a mechanical aortic valve undergoing inguinal hernia repair in 48 hours and an INR of 1.5 requires bridging anticoagulation. Mechanical heart valves are thrombogenic, necessitating perioperative management to balance thromboembolic and bleeding risks. Current guidelines recommend bridging therapy with low-molecular-weight heparin (LMWH) or unfractionated heparin (UFH) when INR is subtherapeutic in high-risk patients[1][7][9].

Key considerations:
- INR target: For mechanical aortic valves without additional risk factors, the target INR is typically 2.5[1][11]. An INR of 1.5 indicates subtherapeutic anticoagulation, increasing thromboembolic risk.
- Bridging necessity: Bridging is recommended for mechanical valves during periods of subtherapeutic INR, particularly for procedures with intermediate/high bleeding risk[7][9]. Inguinal hernia repair, while lower risk, still requires bridging in this context due to the valve’s thrombogenicity[8][9].
- LMWH vs. UFH:
- LMWH (e.g., enoxaparin) is commonly used for bridging due to outpatient feasibility and predictable pharmacokinetics[7][10]. It is typically discontinued 24 hours before surgery[2][10].
- UFH may be preferred in high-bleeding-risk scenarios due to its shorter half-life and reversibility, but it requires inpatient monitoring[9].

Conclusion:
Bridging with enoxaparin is appropriate here, as the patient’s INR is already subtherapeutic, and LMWH provides effective anticoagulation until 24 hours preoperatively[2][7][9]. Withholding warfarin alone without bridging would leave the patient unprotected against thromboembolism[1][7].

Citations:
[1] https://www.acc.org/latest-in-cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease
[2] https://www.cec.health.nsw.gov.au/__data/assets/pdf_file/0006/458988/Guidelines-on-perioperative-management-of-anticoagulant-and-antiplatelet-agents.pdf
[3] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?format=pdf
[4] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?lang=en
[5] https://www.ahajournals.org/doi/10.1161/circulationaha.105.598268
[6] https://pmc.ncbi.nlm.nih.gov/articles/PMC8182532/
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC3835169/
[8] https://pubmed.ncbi.nlm.nih.gov/18704620/
[9] https://pmc.ncbi.nlm.nih.gov/articles/PMC11024885/
[10] https://www.ouh.nhs.uk/services/referrals/specialist-medicine/documents/anticoagulant-protocols.pdf
[11] https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-20/prosthetic-heart-valves-part-2-antithrombotic-management
[12] https://www.thrombosiscanada.ca/guides/pdfs/Warfarin_perioperative_management.pdf
[13] https://pmc.ncbi.nlm.nih.gov/articles/PMC9387617/
[14] https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/anticoag16.pdf
[15] https://www.ncbi.nlm.nih.gov/books/NBK557590/
[16] https://thrombosiscanada.ca/guides/pdfs/Mechanical_Valves.pdf
[17] https://www.ahajournals.org/doi/10.1161/circulationaha.111.084517
[18] https://www.health.qld.gov.au/__data/assets/pdf_file/0015/1152213/statewide-anticoagulant-guideline.pdf
[19] https://ashpublications.org/blood/article/120/15/2954/30631/How-I-treat-anticoagulated-patients-undergoing-an
[20] https://pubmed.ncbi.nlm.nih.gov/30107917/
[21] https://www.heart.org/-/media/Files/Professional/Quality-Improvement/Get-With-the-Guidelines/Get-With-The-Guidelines-AFIB/Anticoagulation-Toolkit/Bridging-Warfarin-with-Parenteral-AgentsPeriProcedural-Management-of-Anticoagulation-and-Subtherapeu.pdf
[22] https://www.health.qld.gov.au/__data/assets/pdf_file/0025/443806/warfarin-guideline.pdf
[23] https://pubmed.ncbi.nlm.nih.gov/26178802/
[24] https://pubmed.ncbi.nlm.nih.gov/19492151/

Answer from Perplexity: pplx.ai/share

Question 29

”
29. The transthoracic echo demonstrates:”

”- TR
- MR”

Answer 29

”- TR
- MR”

Question 30

30. Transthoracic echo parasternal long axis. Which chamber
    - RA
    - RV

Answer 30

”- RV
- RA

.”

Question 31

31. Non-inferiority trial:

Inconclusive

Answer 31

“🌮
Inconclusive”

“https://youtu.be/bv9GXUbqyfs

https://www.nature.com/articles/s41416-022-01937-w
For interpretation of results as this Q was likely showing a diagram that you had to interpret”

Question 32

32. APRV ventilation

• Spontaneously breathing patient
• Longer inspiratory times (prolonged high pressure maximises recruitment) = better oxygenation
  brief releases at lower pressure - facilitate CO2 clearance
• Similar to constant recruitment method

Answer 32

Spont breathing patient

“https://litfl.com/airway-pressure-release-ventilation/#:~:text=PROS%20AND%20CONS,requirements%20to%20allow%20spontaneous%20breathing

pressure-controlled mode of ventilation that delivers an almost continuous positive pressure with intermittent, time-cycled, short releases at a lower pressure - aim high mean airway pressures for thoeretic alveolar recruitment, FRC preservation, lung homogeneity

https://www.bjaed.org/article/S2058-5349(19)30178-7/fulltext”

Question 33

33. Best TOE view for detecting myocardial ischaemia..

”- Mid-Oesophageal 4 chamber
- Long axis
- 2 chamber
- Transgastric 2 chamber papillary”

Answer 33

Transgastric mid papillary

“TOE was found to be good at detecting new left ventricular RWMAs, associated with ischaemia. In particular the transgastric short axis mid view of the left ventricle demonstrates areas of myocardium subtended by each of the three coronary arteries. It is therefore the most frequently used view for intraoperative monitoring of left ventricular ischaemia.” https://www.sciencedirect.com/science/article/pii/S0007091217351863#:~:text=In%20particular%20the%20transgastric%20short,monitoring%20of%20left%20ventricular%20ischaemia.

Question 34

”
#34. CXR with a 3 lead pacemaker. Arrow pointing to”

”- LV
- RV (around the back of the heart)
- Coronary sinus

Answer 34

This is an X-ray image showing the placement of leads from a cardiac device, such as a pacemaker or an implantable cardioverter-defibrillator (ICD). The labeled components include:

• Right atrial lead: Positioned in the right atrium to monitor and regulate atrial activity.
• Right ventricular lead: Positioned in the right ventricle to manage ventricular activity.
• LV (left ventricular) coronary sinus lead: Positioned via the coronary sinus to stimulate the left ventricle, often used in cardiac resynchronization therapy (CRT).

The visible device in the upper chest area is likely the pulse generator of the pacemaker or ICD. This setup is commonly used for patients with heart rhythm disorders or heart failure requiring synchronized ventricular contraction.

Citations:
[1] https://pplx-res.cloudinary.com/image/upload/v1741690186/user_uploads/tfvkBcBtKFnfTJd/image.jpg

Answer from Perplexity: pplx.ai/share

Question 35

35. Avulsed tooth, what fluid to place it in

• chlorhexidine
• Saline
• Balanced salt solution
• Fresh bovine milk
• Water

Answer 35

RCH guideline says milk is “first choice”,

the dental article says 1. HBSS 2. milk 3. sterile saline.

UTD also milk

The optimal storage medium for an avulsed tooth must preserve periodontal ligament (PDL) cell viability to maximize the success of replantation. Among the options provided—chlorhexidine, saline, balanced salt solution, fresh bovine milk, and water—fresh bovine milk is the most recommended choice based on current evidence and clinical guidelines.

Key Findings
Fresh bovine milk demonstrates superior efficacy in maintaining PDL cell viability compared to other readily available media. Systematic reviews highlight milk as the most frequently recommended individual storage medium due to its physiological compatibility, ease of access, and cost-effectiveness[1][3][6]. Hank’s balanced salt solution (HBSS), a synthetic medium, is equally effective but less practical for laypeople due to limited availability outside clinical settings[1][6]. Saline and water are suboptimal, as their hypo-osmolarity accelerates PDL cell lysis[3][6]. Chlorhexidine, not validated in major studies, is unsuitable for this purpose.

Mechanistic Basis for Milk’s Efficacy
Milk’s osmolarity (~275 mOsm/kg) closely matches that of PDL cells, minimizing osmotic stress[6]. Its nutrient composition—including amino acids, carbohydrates, and growth factors—supports cellular metabolism during extra-alveolar storage[4]. Additionally, refrigeration extends milk’s efficacy, with studies showing viable PDL cells after 4–8 hours of storage[4][7].

Comparative Analysis of Alternatives
1. Balanced Salt Solution (HBSS):
While HBSS is the gold standard in clinical settings, its reliance on specialized storage and limited shelf life restricts widespread use[5][8]. Modified HBSS formulations with additives like vitamin C show enhanced cell viability but remain impractical for emergency use[5].

2. Saline:
   Normal saline’s low osmolarity (~154 mOsm/kg) causes rapid PDL cell swelling and necrosis, reducing replantation success[3][6]. Meta-analyses indicate significantly lower cell viability in saline compared to milk[3].
3. Water:
   Distilled water’s extreme hypo-osmolarity (<50 mOsm/kg) induces catastrophic cell rupture, rendering it the least suitable option[3][6].
4. Chlorhexidine:
   No robust evidence supports chlorhexidine as a storage medium. Its antimicrobial properties do not offset cytotoxic effects on PDL cells[6].

Clinical Recommendations
For immediate replantation, fresh bovine milk is the preferred medium due to its balance of efficacy and accessibility[1][6][8]. HBSS remains ideal in dental clinics, but milk’s widespread availability makes it the pragmatic choice for public health contexts. Avoid saline, water, or unvalidated agents like chlorhexidine.

Correct Answer: Fresh bovine milk.

Rationale:
Milk’s physiological properties, clinical validation, and practicality align with guidelines from the International Association of Dental Traumatology and the American Academy of Pediatric Dentistry[6][8]. While HBSS is equally effective, its limited accessibility outside clinical environments positions milk as the superior choice for most scenarios.

Citations:
[1] https://onlinelibrary.wiley.com/doi/10.1111/edt.12382
[2] https://journals.lww.com/senj/fulltext/2015/05020/natural_products_as_storage_media_for_avulsed.2.aspx
[3] https://onlinelibrary.wiley.com/doi/10.1111/edt.12564
[4] https://pubmed.ncbi.nlm.nih.gov/12669877/
[5] https://onlinelibrary.wiley.com/doi/10.1111/edt.13010
[6] https://pmc.ncbi.nlm.nih.gov/articles/PMC5571385/
[7] https://bestbets.org/bets/bet.php?id=187
[8] https://www.aapd.org/media/policies_guidelines/e_avulsion.pdf
[9] https://pubmed.ncbi.nlm.nih.gov/39578673/
[10] https://www.distinguished-dental.com/blog/2019/11/14/emergency-dentist-putting-a-tooth-in-milk/
[11] https://www.aapd.org/globalassets/media/policies_guidelines/r_traumaflowsheet.pdf
[12] https://www.scielo.br/j/bdj/a/8c8n6p3BG4jNZGgGz3KXbZq/?format=pdf&lang=en
[13] https://pmc.ncbi.nlm.nih.gov/articles/PMC3809259/
[14] https://www.idjsronline.com/html-article/13809
[15] https://www.dental-update.co.uk/content/dental-traumatology/an-anaphylactic-replantation-milk-allergy-tooth-avulsion-and-appropriate-storage-media/
[16] https://www.dental-update.co.uk/content/technique-tips/technique-tips-replantation-and-stabilization-of-avulsed-permanent-teeth/
[17] https://themamadentist.com/shop/save-a-tooth-hanks-balanced-salt-solution/
[18] https://www.libertyendo.com/files/2014/06/Avulsed-permanent-teeth-new-treatment-guidelines.pdf
[19] https://bondidental.com.au/first-aid-for-a-knocked-out-tooth/
[20] https://www.researchgate.net/publication/228474005_Study_of_storage_media_for_avulsed_teeth

“https://www.aapd.org/globalassets/media/publications/archives/ram-26-03.pdf, https://www.rch.org.au/clinicalguide/guideline_index/Dental_trauma/

UTD: Place the tooth in a storage solution – As soon as possible, place the tooth in a storage solution to maintain the viability of the periodontal ligament on the tooth’s surface [42-44]. We suggest cold milk, oral rehydration solution (eg, Ricelyte or Pedialyte), or a cell culture medium (Hank’s balanced salt solution or Viaspan) used in avulsed tooth preservation kits. Cold milk is usually most readily available [44]. If milk or specialized mediums are not available, have the child spit into a container or place the tooth in saline instead. “

Question 36

36. The pregnant MS lady, cat 1 section within 30min, what method

”- spinal
- CSE
- Epidural
- GA
- Methylpred then GA”

Answer 36

Neuraxial ok - no correlation between relapses of MS.

NMBD caution - ND may have prolonged effects, hyperK from denervation/misuse myopathy, resis to NMBA ?due to extrajunctional receps

The optimal anesthetic technique for a Category 1 cesarean section in a pregnant woman with multiple sclerosis (MS) requires balancing urgency with neurological safety. Spinal anesthesia is the most appropriate choice in this scenario, supported by current evidence and clinical guidelines[1][3][4][6][8].

Rationale
1. Urgency of Category 1 Section:
A Category 1 cesarean section mandates delivery within 30 minutes due to immediate threat to maternal or fetal life. Spinal anesthesia provides rapid onset (typically within 3–5 minutes) and reliable surgical conditions, making it faster than epidural catheter placement or titration[6][7]. While general anesthesia (GA) is traditionally considered the fastest option, it carries significant risks in obstetric patients, including difficult airway management, aspiration, and postoperative respiratory complications[7].

2. Safety of Neuraxial Anesthesia in MS:
   Historical concerns about neuraxial techniques exacerbating MS relapses due to local anesthetic neurotoxicity in demyelinated regions have been disproven by recent studies[1][3][4][6][8]. For example:
   
   • A cohort study of 155 MS patients undergoing cesarean delivery found no increased relapse risk with epidural or spinal anesthesia compared to GA[8].
   • Case reports demonstrate successful spinal anesthesia in MS patients without postoperative neurological deterioration[6].
   • Theoretical risks of spinal anesthesia (higher intrathecal local anesthetic concentration) are offset by clinical evidence showing no correlation with relapse rates[4][6].
3. Advantages Over GA:
   GA introduces risks such as autonomic instability, hyperkalemia from succinylcholine in patients with spasticity, and immune modulation from volatile agents[4][6]. Spinal anesthesia avoids these issues while providing superior postoperative analgesia and earlier maternal-neonatal bonding[6][8].
4. Epidural vs. Spinal Considerations:
   While epidural anesthesia is often preferred in elective cases for its titratability, spinal anesthesia is more practical in emergencies due to faster onset[6]. The literature confirms that both techniques are safe, but spinal anesthesia aligns better with time constraints in Category 1 scenarios[4][6].
5. Methylprednisolone Prophylaxis:
   Prophylactic steroids lack robust evidence for preventing relapses in this context and are not routinely recommended[4][8]. Their use should be reserved for treating acute exacerbations rather than as a pre-anesthetic measure.

Conclusion
For a Category 1 cesarean section in a pregnant woman with MS, spinal anesthesia is the optimal choice. It balances rapid execution with safety, avoiding the risks of GA while adhering to contemporary evidence supporting neuraxial techniques in MS[6][8].

Correct Answer: Spinal anesthesia.

Sources:[1][3][4][6][8]

Citations:
[1] https://www.elsevier.es/en-revista-colombian-journal-anesthesiology-342-articulo-management-anesthesia-during-c-section-multiple-S2256208714001096
[2] https://www.revcolanest.com.co/index.php/rca/article/view/495
[3] https://rapm.bmj.com/content/48/Suppl_1/A96.3
[4] https://resources.wfsahq.org/atotw/anesthetic-considerations-for-pregnant-women-with-multiple-sclerosis/
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC4141396/
[6] https://besarpp.adagiocreate.com/wp-content/uploads/2020/12/01-rayyan.pdf
[7] https://pubmed.ncbi.nlm.nih.gov/31634161/
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC6160638/
[9] https://pmc.ncbi.nlm.nih.gov/articles/PMC7199839/
[10] https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.13729
[11] https://academic.oup.com/bja/article/doi/10.1093/bja/el_9820/2451457
[12] https://academic.oup.com/bmb/article/101/1/105/262350
[13] https://www.pregnancybirthbaby.org.au/emergency-caesarean
[14] https://www.wjgnet.com/2307-8960/full/v10/i14/4563.htm

“BJA Ed 2021 Anaesthesia and neurological disorders in pregnancy

PRIMS study”

Question 37

37. Classic LMA cuff recommended pressure max”

“30
40
50
60 “

Answer 37

60mmHg (product guide)

https://www.lmaco.com/sites/default/files/31817-LMA-Classic-A4Data-0214-LORES-fnl.pdf

Question 38

38. Narrow complex tachycardia ECG in young person post op in PACU with SBP 90. What treatment

“A. Modified valsalva
B. Adenosine
C. DCCV”

Answer 38

Answer:
A. Modified valsalva

Rationale:
In a hemodynamically stable patient with narrow complex tachycardia (NCT), vagal maneuvers such as the modified Valsalva maneuver are first-line therapy, as per ACC/AHA/HRS guidelines[12]. The modified Valsalva (supine positioning with leg elevation post-strain) has demonstrated higher efficacy than standard techniques[3][8]. While adenosine is effective, it is typically reserved for cases where vagal maneuvers fail[12][15]. Direct current cardioversion (DCCV) is reserved for hemodynamically unstable patients (e.g., shock, altered mental status, severe hypotension)[4][6].

This patient’s SBP of 90 mmHg is at the threshold for stability; however, in the absence of additional signs of shock (e.g., altered consciousness, chest pain, or respiratory distress), modified Valsalva remains appropriate initial management. Postoperative NCT often responds well to non-pharmacological interventions, and adenosine or DCCV can be escalated if needed[4][9].

Key Evidence:
1. Vagal maneuvers (e.g., modified Valsalva) are recommended first-line for stable NCT[12][15].
2. Adenosine follows if vagal maneuvers fail[12][15].
3. DCCV is indicated only for hemodynamic instability[4][6].
4. Postoperative NCT management prioritizes conservative measures before pharmacological or electrical interventions[4][9].

Conclusion:
The modified Valsalva maneuver (A) is the correct initial treatment in this scenario.

Citations:
[1] https://patient.info/doctor/narrow-complex-tachycardias
[2] https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2019/09/10/12/36/2019-ESC-Guidelines-for-Supraventricular-Tachycardia
[3] https://www.thelancet.com/journals/lancet/article/PIIS0140-67361561485-4/fulltext
[4] https://e-safe-anaesthesia.org/e_library/11/Supraventricular_tachyarrhythmias_and_their_management_in_the_perioperative_period.pdf
[5] https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf
[6] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-9-managing-acute-dysrhythmias/
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC2907092/
[8] https://resus.com.au/modified-valsalva-plus-adenosine-for-reverting-svt/
[9] https://www.cancertherapyadvisor.com/home/decision-support-in-medicine/critical-care-medicine/svt-in-a-cardiac-surgery-patient/
[10] https://www.mayoclinic.org/diseases-conditions/supraventricular-tachycardia/diagnosis-treatment/drc-20355249
[11] https://www.rch.org.au/clinicalguide/guideline_index/supraventricular_tachycardia_svt/
[12] https://www.ahajournals.org/doi/10.1161/cir.0000000000000311
[13] https://pmc.ncbi.nlm.nih.gov/articles/PMC3375013/
[14] https://pubmed.ncbi.nlm.nih.gov/3502542/
[15] https://aci.health.nsw.gov.au/networks/eci/clinical/tools/cardiology/supraventricular-tachycardia-svt
[16] https://www.racgp.org.au/getattachment/55d4f29f-65bb-4bac-ba42-35407dbee553/attachment.aspx
[17] https://www.racgp.org.au/clinical-resources/clinical-guidelines/handi/handi-interventions/procedures/modified-valsalva-manoeuvre-for-supraventricular-t
[18] https://academic.oup.com/bjaed/article/15/2/90/248695
[19] https://pmc.ncbi.nlm.nih.gov/articles/PMC8832017/
[20] https://pmc.ncbi.nlm.nih.gov/articles/PMC5613596/
[21] https://pmc.ncbi.nlm.nih.gov/articles/PMC1964549/
[22] https://www.analesdepediatria.org/en-modified-valsalva-manoeuvre-in-paroxysmal-articulo-S2341287923001539
[23] https://www.escardio.org/static-file/Escardio/Subspecialty/EACPR/Education/Test%20your%20knowledge/guidelines-sva-es.pdf
[24] https://academic.oup.com/qjmed/advance-article/7905488
[25] https://www.ncbi.nlm.nih.gov/books/NBK557830/
[26] https://www.ahajournals.org/doi/10.1161/CIR.0000000000000549
[27] https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.7.2.192
[28] https://my.clevelandclinic.org/health/treatments/24605-svt-ablation
[29] https://www.ncbi.nlm.nih.gov/books/NBK507699/

I’m guessing because not unstable, go with modified valsalva first?

Question 39

39. Prilocaine Bier’s block, which condition it shouldn’t be used in

”- G6PD
- Porphyria”

Answer 39

“G6PD
“

Methemoglobinemia Risk
Prilocaine is associated with an increased risk of methemoglobinemia, especially in G6PD-deficient individuals:
• Prilocaine is metabolized to o-toluidine, which can oxidize hemoglobin and lead to methemoglobin formation.
• G6PD-deficient patients are more susceptible to developing methemoglobinemia when exposed to oxidative stressors like prilocaine.
• Methemoglobinemia can occur even at lower doses in G6PD-deficient patients compared to the general population.

https://www.orphananesthesia.eu/en/rare-diseases/published-guidelines/glucose-6-phosphate-dehydrogenase-deficiency/193-glucose-6-phosphate-dehydrogenase-deficiency/file.html

Question 40

40. Anaphylactic to MMR vaccine. What is contraindicated?”

”- Gelofusine
- Sulphonamides”

Answer 40

Gelofusine (due to the gelatin!)

Journal of Clinical Immunology 1993, Journal of Military medicine 2020

Question 41

41. 65yM, presented with confusion and hypoxia. CXR of L chest whiteout and tracheal deviation

• Left pleural effusion
• Left pneumonia
• Unilateral pulmonary oedema
• Pneumonectomy

Answer 41

Pleural effusion

Question 42

42. Post heart transplant recipient, expected sensitivity to:

”- adenosine
- Ephedrine - less effect
- Atropine
- Glyco”

Answer 42

Adenosne

4x increase in SA & AV nodal blocking effect “denervation supersensitivity”

BJA https://watermark.silverchair.com/020074.pdf

Question 43

43. What nerve does not innervate the breast/ for breast surgery?

• Long thoracic
• Anterior intercostal
• Posterior intercostal
• Supraclavicular

Answer 43

Long thoracic - does motor to serratus anterior

The innervation of the breast is supplied mainly by the

1. anterior branches of the 4th, 5th and 6th intercostal nerves which arise from the thoracic spinal nerves (T4-6).
2. the apex of the axilla is supplied by the intercostobrachialis nerve; this is a cutaneous branch of the second intercostal nerve (T2).
3. the pectoral major and minor muscles are innervated by the lateral pectoral nerve (C5-7) and medial pectoral nerve (C8-T1).

Terminal branches of the supraclavicular nerves (C3-4) innervate the upper part of the breast and this should be taken into account when the surgical procedure involves this area, because Pecs blocks will not block the supraclavicular nerve.

Breast surgery however, is rarely performed at this level.
BMJ

Nerves that DOES NOT innervate the breast
1. Long thoracic - motor to Serr ant
2. Lat pec - motor to pec major/minor
3. Thoracodorsal - motor to lat dorsi
4. Posterior “cutaneous”

Question 44

44. Post prem baby, having surgery. The minimum time before considered for day surgery is

”- Postmenstrual age 54 weeks
- 60 weeks”

Answer 44

“Ex-preterm infants at risk of postoperative apnoea should not be considered for same
day discharge unless they are medically fit and have reached a postmenstrual age of
54 weeks.”

Term - PMA 46 weeks
Ex-prem - PMA 54 weeks

https://www.anzca.edu.au/getContentAsset/aae56c4d-8983-47db-97c7-0366e9f6f271/80feb437-d24d-46b8-a858-4a2a28b9b970/PG29(A)-Guideline-for-the-provision-of-anaesthesia-care-to-children-2020.PDF?language=en&view=1

Question 45

45. Fontan woman, pregnant, what drug to avoid in labour

”- Ergometrine
- N2O”

Answer 45

ergometrine

https://www.bjaed.org/action/showPdf?pii=S1743-1816%2817%2930438-9

Question 46

46. Dental surgery to bottom molar (38) with weird chin sensation post op. Which nerve damaged”

• lingual
• Mental
• Inferior alveolar
• Infratrochlear”

Answer 46

inferior alveolar nerve

https://radiopaedia.org/articles/mental-nerve

Question 47

47. Child with status epilepticus, weight 20kg, which is NOT a recommended treatment”

• Midaz IM 3mg
• intranasal 6mg
• intraosseous 3mg
• buccal 6mg
• IV 1.5mg

Answer 47

Buccal/ intranasal 0.3x20 = 6mg

IV/ IO 0.15x20= 3mg
IM 0.2x20= 4mg

*needle = 0.15
*no needle = 0.3
but IM = 0.2

https://www.childrens.health.qld.gov.au/__data/assets/pdf_file/0021/174180/status-epilepticus-flowchart-and-medications.pdf

Question 48

48. Highest rate of mortality is in BMI category of:

• < 18.5
• 18.5-24.9 - 25-29.9
• 30-34.9
• 35-39.9

Answer 48

• underweight < 18.5

BJA anaesthesia for the obese patient 2020

Question 49

49. Major burns patient, pharmacologic effects in relation to non-depolarising neuromuscular blockers

-Dose expected higher/low and reason?

Answer 49

-Dose expected higher because of up-regulation of acetylcholine receptors

Question 50

50. Class 2 obesity has an ASA score of:

“1
2
3
4”

Answer 50

2

“https://www.asahq.org/standards-and-practice-parameters/statement-on-asa-physical-status-classification-system. Mild diseases only without substantive functional limitations. Current smoker, social alcohol drinker, pregnancy, obesity (30<BMI<40), well-controlled DM/HTN, mild lung disease

Class 2 obesity (BMI 35-39.9) = ASA 2
Class 3 obesity (BMI >40) = ASA 3”

Question 51

52. Young man collapsed. Fuzzy and terrible ECG depicting brugada, what is the recommendation:”

Answer 51

the only proven therapy is an

** implantable cardioverter – defibrillator (ICD) **

LITFL Brugada syndrome

Question 52

53. Obese patient, giving a dose of propofol for induction, what weight do you use?”

lean body weight
IBW
ABW
TBW

Answer 52

LBW is a more appropriate dosing scalar

Mnemonic:
TBW = Xa (TXa)
ABW = PINSA (A PINS)
prop inf/neo/suga/anti

SOBA

https://www.sobauk.co.uk/_files/ugd/373d41_eebe369c3c6b4021bff6f3da059aa796.pdf

Question 53

54. Myasthenia gravis patients and NMB:

• sensitive to ND, resistant to depolarising
• Variants of this combo

Answer 53

Sensitive to ND, resistant to depol

“BJA Myaesthenia gravis and periop rx
1/10 normal Roc/ (NDNMBD)”

Question 54

55. Magnesium 20mmol given intra-op is NOT associated with

• reduced pain scores in PACU
• reduced PONV
• Reduced MAC requirements
• Prolonged NMB
• Resp depression post op

Answer 54

Resp dep postop - mcq group

Wrong!
Reduced MAC requirements

“https://pmc.ncbi.nlm.nih.gov/articles/PMC6319973/#:~:text=Albrecht%20et%20al%20reviewed%2025,any%20reported%20serious%20adverse%20effects.
Albrecht et al reviewed 25 RCTs including 1461 patients and concluded that perioperative intravenous magnesium can reduce opioid consumption and pain scores in the first 24 hours postoperatively without any reported serious adverse effects

https://www.mdpi.com/2072-6643/16/14/2375
administration of magnesium sulfate
**1. reduces the intraoperative opioid use,
2. decreases the pain severity within the first 24 h postoperatively, and
3. reduces the incidence of PONV while exerting a minimal effect on the length of stay in the PACU. **

Mg in toxic doses can cause respiratory depression”

Question 55

56. Severe hypokalaemia and cardiac arrest, ANZCOR recommends

• 5 mmol bolus of K+
• Vs over 5 min
• Vs over 10min
• 10mmol 5 min
• Vs 10min

Answer 55

5 mmol bolus of K+

ALS 2 Handbook P. 134

Question 56

57. Child and laparotomy, 23 kg, what fluid will you give for maintenance

• 45ml/hr of 0.45% saline and dextrose
• 45ml/hr of 0.9% saline and dextrose
• 65 ml /hr of solutions
• something else never to give

Answer 56

63mL/h of 0.9% saline with 5% dex

–> Give 2/3 maintenance once resus’d because prone to secreting ADH+++, and never give hypotonic solution to children!!

RCH Guidelines:
The preferred fluid type for IV maintenance is sodium chloride 0.9% with glucose 5%

Alternative maintenance fluid options include:
Plasma-Lyte 148 with glucose 5% (contains 5 mmol/L of potassium) - generally stocked in tertiary paediatric centres and intensive care
Hartmann’s with glucose 5%

4-2-1 rule = 4mL/h x 10kg + 2mL/h x 10kg + 1mL/h x 3 kg = 40+20+3 =63mL/h

Question 57

58. Child 4mo with uncorrected TOF, having a tet spell, what will not work? or maybe “what would you avoid giving”?

”- prostaglandin
- sedation
- fluid bolus
- vasopressor
- beta blocker”

Answer 57

Prostaglandin

Try sedation, beta blockers, IVF bolus, phenylephrine/metaraminol

Craig Sims P. 386

https://www.rch.org.au/clinicalguide/guideline_index/Cyanotic_Episodes_in_Congenital_Heart_Disease/

Try sedation, beta blockers, IVF bolus, phenylephrine/metaraminol”

Question 58

59. Someone is on long acting MAOi, what drug is most likely to cause serotonin syndrome?

”- pethidine
- tapentadol
- Methadone
- sux
- fent”

Answer 58

Pethidine

“NPS
Tramadol + MAOIs = highest risk SS

Some opioids such as tramadol, pethidine, dextromethorphan and tapentadol increase
serotonergic activity. Fentanyl and methadone also do this but to a lesser extent.

Pethidine: The highest risk opioid drugs are tramadol, pethidine and dextromethorphan.
Tapentadol: Currently, it is unclear if tapentadol has a greater risk of serotonin toxicity than other opioids.
Methadone: Methadone has been associated with serotonin toxicity when given with other serotonergic medicines but the risk appears low
Sux:
Fent: Co-administration with an SSRI has been reported to cause an agitated delirium consistent with serotonin toxicity.2”

Question 59

60. Parkinson patient on an apomorphine infusion, what drug to give for nausea

• cyclizine
• ondansetron
• droperidol
• metoclopramide

Answer 59

Cyclizine

“https://www.drugs.com/drug-interactions/apomorphine-with-ondansetron-224-0-1752-0.html

States not for apomorphine + ondans

apo + ondans = hypotension

PD pt not for antiD2 drugs therefore no droperidol or metoclopramide”

Question 60

61. Refractory epilepsy and vagal stimulator, what is most likely to cause it to inadvertently fire?

• hypertension
• tachycardia
• bradycardia
• Hypotension
• Hyperthermia

Answer 60

??tachycardia
# Vagus Nerve Stimulator (VNS) Inadvertent Firing in Refractory Epilepsy: Mechanisms and Likely Triggers

The inadvertent firing of a vagus nerve stimulator (VNS) in patients with refractory epilepsy is a critical clinical concern. Among the potential triggers—hypertension, tachycardia, bradycardia, hypotension, and hyperthermia—tachycardia is the most likely culprit. This conclusion is supported by extensive evidence from clinical studies, device functionality, and physiological mechanisms outlined in the provided search results.

Physiological Basis of VNS Activation

Modern VNS systems, such as the AspireSR® (Model 106), incorporate an AutoStim Mode designed to detect ictal tachycardia, a rapid increase in heart rate associated with seizures. This feature triggers automatic stimulation when a ≥20% relative heart rate increase is detected, aiming to abort or mitigate seizure activity[2][4][6]. The rationale stems from the observation that approximately two-thirds of focal seizures correlate with tachycardia, making heart rate a reliable biomarker for seizure onset[2][8].

Key Evidence Supporting Tachycardia as the Primary Trigger
1. AutoStim Functionality:
- The AspireSR® generator uses tachycardia detection to deliver responsive stimulation. In clinical trials, 34.8% of seizures were treated via AutoStim, with 61.3% of these seizures terminating during stimulation[2][4].
- False-positive activations can occur due to physiological or pathological tachycardia unrelated to seizures (e.g., exercise, anxiety), potentially leading to unintended stimulation[11].

2. Clinical Outcomes:
   
   • Switching from traditional VNS to responsive VNS (rVNS) with AutoStim resulted in a 28% additional reduction in seizure frequency for patients not fully controlled by conventional therapy[8].
   • Device-triggered stimulation during ictal tachycardia reduced seizure severity and improved quality of life in long-term studies[4][8].
3. Exclusion of Other Triggers:
   
   • Bradycardia: While VNS malfunction (e.g., cyclic asystole) can cause symptomatic bradyarrhythmias[1][3], this represents a complication of overstimulation, not a trigger for inadvertent firing.
   • Hypertension/Hypotension: No evidence links blood pressure fluctuations to VNS activation. The device’s sensing mechanism focuses on cardiac rhythm, not vascular tone[6][9].
   • Hyperthermia: Temperature changes are not integrated into VNS algorithms[11].

Safety Considerations and Device Limitations
The AutoStim feature is contraindicated in patients with chronotropic incompetence (e.g., sustained bradycardia <50 bpm) or those reliant on beta-blockers, as these conditions may impair heart rate responsiveness[11]. Furthermore, manufacturing defects in leads (e.g., PerenniaDURA models) or MRI-related interference could theoretically cause erratic stimulation, but these are hardware-specific issues rather than physiological triggers[10][11].

Conclusion
In patients with refractory epilepsy and a VNS, tachycardia is the most likely cause of inadvertent device firing. This aligns with the intentional design of AutoStim-enabled generators to respond to ictal heart rate increases. Clinicians should educate patients on recognizing non-seizure-related tachycardia (e.g., during exercise) and consider adjusting stimulation parameters to minimize false activations. Regular device interrogation and adherence to implantation protocols remain essential to mitigate risks[5][11].

Citations:
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC10285099/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC5064739/
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC5419945/
[4] https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/ner.12376
[5] https://thejns.org/pediatrics/view/journals/j-neurosurg-pediatr/18/1/article-p97.xml
[6] https://www.epilepsy.org.uk/info/treatment/vagus-nerve-stimulation
[7] https://www.livanova.com/epilepsy-vnstherapy/getmedia/a0f9e731-f117-4948-896e-abcfb377eb3f/IM-7601065-EPI_SenTecGd19U1-Rev-B_Sentival-Technical-Guide.pdf
[8] https://pubmed.ncbi.nlm.nih.gov/32759064/
[9] https://www.rch.org.au/Vagus_nerve_stimulation.aspx
[10] https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfRes/res.cfm?id=191291
[11] https://www.livanova.com/epilepsy-vnstherapy/en-au/safety-information
[12] https://my.clevelandclinic.org/health/treatments/17598-vagus-nerve-stimulation
[13] https://www.frontiersin.org/journals/medical-technology/articles/10.3389/fmedt.2021.696543/full

Vague mention of tachycardia in UTD but I haven’t foudn anything definitive

Question 61

”
#62. Some question worded like - what is the most consistent factor to increase PONV rate in children?”

”- female sex
- age 3 years or older
- Use of short acting opioids”

Answer 61

Age >3 then? Given that the alternative is post pubertal girls

“RCH website: Risk Factors
Age > 3, Past history of PONV, History of motion sickness, Post-pubertal girls, Preoperative anxiety

Surgery type
Strabismus, Otoplasty, Adenotonsillectomy, Surgery requiring postoperative inpatient (vs day stay),Volatile anaesthesia”

Question 62

63. Which muscle does not elevate the larynx?”

”- Sterno-hyoid or something sterno
- Glenohyoid
- Thyrohyoid
- Myelohyoid”

Answer 62

Sternohyoid
An infrahyoid muscle that depresses the hyoid bone rather than elevating it5. Its primary role is to lower the hyoid after swallowing/speaking, opposing elevation56.

The sterno-hyoid option

–> Depresses hyoid bone after swallowing

Various anatomy websites

Question 63

64. What is not a good indicator of a neonate being ready for extubation?”

”
- Grimace
- RR>16
- conjugate gaze
“

Answer 63

RR >16 not mentioned in that list so I guess I’ll go with that despite the articel being about children, not neonates

“https://www.bjaed.org/article/S2058-5349(21)00133-5/fulltext
Eight features have been found to be associated with successful awake extubation in children:
1. eye opening,
2. facial grimace,
3. movement of the patient other than coughing,
4. conjugate gaze,
5. purposeful movement,
6. low end-tidal anaesthetic concentration (< 0.2% for sevoflurane, < 0.15% for isoflurane and < 1% for desflurane),
7. Spo2 > 97%,
8. tidal volume 5 ml kg−1 and a
positive laryngeal stimulation test.”

Question 64

65. What nerve is not related to the trigeminal?

• auriculotemporal
• supratrochlear
• infratrochloear
• greater auricular”

Answer 64

Greater auricular - comes off C2-C3 of cervical plexus

Question 65

66. Right homonomous hemianopia and right hemisensory loss - affected region

• left posterior cerebral
• Left anterior cerebral
• Superior cerebellar
• Left anterior inferior cerebellar

Answer 65

L posterior cerebral artery?

Posterior Cerebral Artery Infarction: Neuroanatomical Correlates of Right Homonymous Hemianopia and Right Hemisensory Loss

The constellation of right homonymous hemianopia and right hemisensory loss localizes to infarction in the territory of the left posterior cerebral artery (PCA). This conclusion is supported by anatomical and clinical-pathological correlations derived from neurovascular anatomy, lesion localization studies, and clinical stroke syndromes.

Neurovascular Anatomy of the Posterior Cerebral Artery

The posterior cerebral artery arises from the basilar artery and supplies the occipital lobes, medial temporal lobes, thalamus, and rostral brainstem. Critical branches include:
1. Cortical branches: Supply the primary visual cortex (calcarine cortex) and optic radiations.
2. Thalamogeniculate arteries: Penetrate the thalamus, supplying the ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei, which process somatosensory information[1][2].

Occlusion of the left PCA disrupts perfusion to these regions, producing contralateral (right-sided) visual and sensory deficits[3][8].

Pathophysiology of Right Homonymous Hemianopia

Homonymous hemianopia arises from damage to the optic radiations or primary visual cortex (Brodmann area 17) in the left occipital lobe[4][7]. The left PCA supplies these structures, and infarction interrupts the visual pathway posterior to the optic chiasm, resulting in loss of the right visual field in both eyes. Clinical studies report that 88.9% of patients with superficial PCA (SPCA) infarcts exhibit contralateral homonymous hemianopia due to occipital lobe involvement[3][8].

Mechanisms of Right Hemisensory Loss

Hemisensory loss in PCA territory strokes originates from infarction of the thalamus, specifically the VPL and VPM nuclei. These nuclei receive somatosensory input from the contralateral body via the medial lemniscus and spinothalamic tracts. Occlusion of thalamogeniculate arteries—branches of the left PCA—causes ischemia in these nuclei, leading to contralateral sensory deficits[2][5].

• Pure sensory stroke: Isolated sensory loss due to small thalamic infarcts[2][5].
• Sensory-motor stroke: Combined sensory loss and motor weakness from larger infarcts involving the adjacent internal capsule[2][5].

In the context of left PCA infarction, 60–72% of patients with proximal PCA (PPCA) or combined (P+SPCA) infarcts exhibit sensory deficits[3][8].

Differential Diagnosis of Artery-Specific Syndromes

1. Left Anterior Cerebral Artery (ACA):
   
   • Supplies medial frontal and parietal lobes.
   • Infarction causes contralateral leg weakness/sensory loss, executive dysfunction, and apraxia. No visual deficits[7].
2. Superior Cerebellar Artery (SCA):
   
   • Supplies superior cerebellum and dorsolateral pons.
   • Infarction causes ipsilateral limb ataxia, dysarthria, and vertigo. No sensory or visual deficits[7].
3. Left Anterior Inferior Cerebellar Artery (AICA):
   
   • Supplies lateral pons and inferior cerebellum.
   • Infarction causes vertigo, hearing loss, and facial weakness. No hemianopia or hemisensory loss[7].

Clinical-Pathological Correlation

The combination of right homonymous hemianopia and right hemisensory loss is pathognomonic for left PCA infarction, as no other artery supplies both the occipital cortex and thalamus. This is validated by:
- Imaging studies: CT/MRI showing left occipital and thalamic infarcts[1][8].
- Angiographic findings: Occlusion of the left PCA or its branches[3][5].
- Stroke registries: 56.4% of PCA infarcts present with motor/sensory deficits, and 52.5% with visual field abnormalities[3][8].

Conclusion

Left posterior cerebral artery infarction is the definitive etiology of right homonymous hemianopia and right hemisensory loss. This syndrome reflects dual involvement of the occipital cortex (visual loss) and thalamus (sensory loss), territories exclusively supplied by the PCA. Clinicians should prioritize neuroimaging (MRI/CT angiography) to confirm the diagnosis and guide thrombolytic or endovascular therapy within appropriate time windows[1][8].

Correct Answer: Left posterior cerebral artery.

Citations:
[1] https://radiopaedia.org/articles/posterior-cerebral-artery-pca-infarct
[2] https://pubmed.ncbi.nlm.nih.gov/3046580/
[3] https://jamanetwork.com/journals/jamaneurology/fullarticle/788716
[4] https://en.wikipedia.org/wiki/Homonymous_hemianopsia
[5] https://jamanetwork.com/journals/jamaneurology/fullarticle/588031
[6] https://pmc.ncbi.nlm.nih.gov/articles/PMC2077751/
[7] https://www.strokenetworkseo.ca/sites/default/files/files/stroke_school_brockville_part_3.pdf
[8] https://radiopaedia.org/articles/posterior-cerebral-artery-pca-infarct?embed_domain=hackmd.io%25252525252525252F%252525252525252540yipuafecsl2jsu8smr5njq%25252525252525252Fbnjhjgjghjghjgh&lang=us
[9] https://academic.oup.com/braincomms/article/5/2/fcad050/7059656
[10] https://journals.sagepub.com/doi/full/10.1177/11206721211046146
[11] https://www.ahajournals.org/doi/10.1161/01.str.0000087786.38997.9e
[12] https://www.heart.org/-/media/files/affiliates/mwa/nebraska-ml-stroke/posterior-circulation-stroke-pam-stout-msn-rn-scrn.pdf?la=en
[13] https://www.ncbi.nlm.nih.gov/books/NBK532296/
[14] https://jamanetwork.com/journals/jamaneurology/fullarticle/775182
[15] https://www.ijceo.org/html-article/20023
[16] https://www.ncbi.nlm.nih.gov/books/NBK558929/
[17] https://emedicine.medscape.com/article/2128100-overview

Question 66

67. What is NOT a feature of TURP?

• hyperglycinaemia
• hyponatraemia
• hypervolaemia
• hypokalaemia

Answer 66

Hypokalaemia

“LITFL:
Laboratory

hyponatraemia (dilutional effect of a large volume of absorbed irrigation fluid, but later due to natriuresis)

iso-osmolar (or mildly hypo-osmolar)

increased osmolar gap from absorbed glycine
hyperglycinaemia (up to 20 mM; normal is 0.15-0.3mmol/L)

hyperserinaemia (major metabolite of glycine)
hyperammonaemia (due to deamination of glycine and serine)

hyperoxaluria and hypocalcaemia (glycine is metabolised to glycoxylic acid and oxalic acid, the latter forms calclium oxalate crystals in the urinary tracts and may contribute to renal failure)

metabolic acidosis

haemodilution and haemolysis

?more likely to get hyPERkalaemia from cell lysis”

Question 67

68. Equation for pulse pressure variation:

”- 100 x PPmax-PPmin/ PPmean
- 100 X PPmax-PPmin/ PPmin
- various other confusing iterations
“

Answer 67

• 100 x PPmax-PPmin/ PPmean

Question 68

69. Oxygen pulse in CPET is surrogate for:

• stroke volume
• anaerobic threshold

Answer 68

SV and periph O2 extraction

Novel techniques for quantifying oxygen pulse curve characteristics during cardiopulmonary exercise testing in tetralogy of fallot 2024 - “Oxygen pulse (O2P) is the CPET surrogate for stroke volume and peripheral oxygen extraction.”

Question 69

70. What increases DLCO?

”- Pulmonary haemorrhage
- Answers of things that decrease dLCO”

Answer 69

Pulm hemorrhage

“UTD:
The diffusing capacity of the lungs for carbon monoxide (DLCO) is designed to reflect properties of the alveolar-capillary membrane, specifically the ease with which oxygen moves from inhaled air to the red blood cells in the pulmonary capillaries.
Increased DLCO — Disorders to consider when the DLCO is near or above the upper limit of the normal range include the following [17,72,73]:

●Obesity
●Asthma
●High altitude
●Polycythemia
●Pulmonary hemorrhage
●Left-to-right intracardiac shunting
●Mild left heart failure (due to increased pulmonary capillary blood volume)
●Exercise just prior to the test session (due to increased cardiac output)
●Supine position; Mueller maneuver”

Question 70

71. What acceptable reason to defer NOF?

”- K+2.7
- HR 110, AF
- Hb86
- Na126”

Answer 70

K 2.7

SCARF
Sodium./K 120/150 2.8/6.0
Chest inf
Arr
Reversible coag
Fixable ketoacidosis

“AAGBI 7 acceptable reasons for delaying NOF
1. Hb <80
2. Acute CCF
3. Uncontrolled DM
4. Correctable cardiac arrhythmia with vent rate >120bpm
5. Na <120 or >150, K <2.8 or >6
6. Reversible coagulopathy
7. Chest infection with sepsis”

Question 71

72. Image of ROTEM, EXTEM, “in this bleeding patient” what to give (showing hyperfibrinolysis)

”- PLT
- fibrinogen
- TXA”

Answer 71

TXA

Question 72

73. V5 lead position for an ECG?

• Mid clav line, 5th IC space
• ,4th
• anterior axillary line, 5th space
• , 4th space

Answer 72

Ant axillary line 5th intercostal space

“12-lead Precordial lead placement

V1: 4th intercostal space (ICS), RIGHT margin of the sternum
V2: 4th ICS along the LEFT margin of the sternum
V4: 5th ICS, mid-clavicular line
V3: midway between V2 and V4
V5: 5th ICS, anterior axillary line (same level as V4)
V6: 5th ICS, mid-axillary line (same level as V4)”

Question 73

74. What is the most sensitive predictor of 30 day mortality and MACE? ….another remembered set mentions the METS study

• DASI score 55
• AT<11
• proBNP >300
• 6MWT<…
• VO2 <11

Answer 73

Conclusion

NT-proBNP >300 pg/mL is the most sensitive predictor of 30-day mortality and MACE, supported by its strong prognostic performance across diverse surgical populations and consistency in guidelines15913.

DASI ≤34 and AT <11 mL/kg/min provide incremental risk stratification but are less sensitive.

Clinicians should prioritize NT-proBNP measurement in high-risk patients undergoing noncardiac surgery to guide perioperative management.

Rationale for Excluding Other Options:

**DASI score 55**: Incorrect cutoff; studies use ≤34.

**VO₂ <11**: Predicts complications, not mortality/MACE.

**AT <11**: Lacks sensitivity for short-term events.

6MWT: No direct evidence in provided studies.

Final Answer: proBNP >30015913.

“https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)31131-0/abstract

UTD re: METS trial
*Subjective assessment did not predict postoperative myocardial infarction (MI), myocardial injury, or myocardial complications.
*Lower DASI scores predicted 30-day death or MI and 30-day death or myocardial injury.
*Reduced peak oxygen consumption and anaerobic threshold measured by CPET were not associated with postoperative MI or myocardial injury.
*Higher NT-proBNP levels predicted 30-day death or MI and one-year death.”

Question 74

75. VO2 max and DASI questionnaire relationship - score of 48 on DASI something equals

what?”

”- 20L/min or ml/kg/min, can’t remember
- 30
- 40
- 50”

Answer 74

VO2 max ~32

“V˙o2 peak (ml kg−1 min−1) = (0.43 × DASI) + 9.6

[VO2max = half DASI + 10]”

Question 75

76. (Was it?) What drug will not raise PVR at low doses?

”- dopamine
- vasopressin
- norad
- milrinone
- dobutamine”

Answer 75

Milrinone as an inodilator

Dopamine low dose = no effect PVR
Dopamine high dose = incr PVR
Vaso low dose = no effect PVR
NAd = incr PVR and SVR
Dobutamine low dose = reduces PVR as per (Hemmings and Egan)

Question 76

77. Sepsis guidelines, what measure is NOT recommended to assess fluid status/ dynamic?

”- urine output
- passive leg raise
- PPV”

Answer 76

UO

“For adults iwth sepsis or septic shock, we suggest using dynamic measures to guide fluid resuscitation over physical examination or static parameters alone. Weak recommendation, v low quality evidence.

Dynamic parameters = passive leg raise, fluid bolus, SV, SVV, PPV, echo”

Question 77

78. Newborn at 1min, sats 75%, grimacing, pulse 120, RR 40. What do you do”

“a Observe
b CPAP
c Intubate d CPR”

Answer 77

Probs observe as per algorithm. “Consider CPAP”

“https://www.anzcor.org/assets/Uploads/Newborn-Life-Support-August-2023-1-v4.pdf

The determining factor after 1min is whether HR <100. This neonate’s parameters all seem very normal!”

Question 78

79. Patients has arrested day 10 post cardiac surgery. What do you NOT do”

”
- give adrenaline 1mg
- Give amiodarone
- 3 sequential shocks”

Answer 78

Give adrenaline

CALS
1. VF/VT –> 3 seq shock –> amiodarone
2. Asystole –> pacing external
3. PEA –> turn off pacing if paced

CPR until resternotomy

DO not give adrenaline

An emergency resternotomy should be an integral part of the CALS arrest management for all patients within 10 days of their last operation. Beyond the tenth postoperative day, a senior clinician should decide whether emergency resternotomy is to be performed

Cardiac arrests in patients after cardiac surgery are often quickly reversible and circulating standard advanced life support doses of epinephrine/adrenaline (ie, 1 mg intravenous) can therefore cause excessive hypertension and arrhythmias when achieving ROSC. Therefore, only small doses of adrenaline (eg, 50–100 micrograms i.v.) should be given. Amiodarone should be considered for refractory shockable rhythms

https://www.sciencedirect.com/science/article/pii/S1441277223000492#ec0010

BJA
During early resternotomy for VF/VT,

1. a bolus of 300 mg of amiodarone should be administered with a further dose of
   150 mg in refractory cases.
2. Lidocaine at a dose of 1 mg kg 1 is a
   suitable alternative.

https://www.bjaed.org/article/S2058-5349(17)30182-8/fulltext

Question 79

80. Diagnosis for TRALI NOT based on

”- hypoxaemia
- Onset within 6 hours of transfusion
- PCWP high
- Bilateral infiltrate on CXR”

Answer 79

“PCWP high
Because TRALI is clinical Dx with the criteria to the L”

“UTD:
TRALI is a clinical diagnosis made using the criteria outlined by the NHLBI’s working group on TRALI or the Canadian Consensus Conference (CCC) on TRALI
The diagnostic criteria for TRALI and possible TRALI share the following features: acute onset of hypoxemia, bilateral infiltrates on frontal chest radiograph, and absence of circulatory overload as the primary etiology of respiratory insufficiency. For a diagnosis of TRALI to be made, all of these features must be present. In addition, there should be no pre-existing ALI/ARDS risk factors at the time of transfusion”

Question 80

81. Diagnosis HITS based on 4Ts Score, which are

Answer 80

Answer:
The correct components of the 4Ts score for heparin-induced thrombocytopenia (HIT) diagnosis are thrombocytopenia, timing of platelet count fall, thrombosis/other sequelae, and absence of other causes of thrombocytopenia. The platelet serotonin release assay (SRA) is not part of the 4Ts score but is a confirmatory laboratory test used after clinical assessment.

Rationale:
1. The 4Ts scoring system is a clinical pretest probability tool with four criteria ([1][6][10]):
- Thrombocytopenia: Magnitude of platelet count fall and nadir (scored 0–2).
- Timing: Onset relative to heparin exposure (scored 0–2).
- Thrombosis/other sequelae: Presence of new thrombosis, skin necrosis, or systemic reactions (scored 0–2).
- Other causes: Likelihood of alternative explanations for thrombocytopenia (scored 0–2).

2. Platelet serotonin release assay (SRA) is a functional laboratory test to confirm HIT in patients with intermediate/high 4Ts scores ([3][8][14]). It is not a component of the 4Ts score itself.

Conclusion:
The 4Ts score comprises only the four clinical criteria listed above. SRA is a subsequent diagnostic step for laboratory confirmation.

Sources:[1][6][10] (4Ts criteria),[3][8][14] (SRA role).

Correct Answer:
Thrombocytopenia, Timing of PLT drop, Thrombosis, and Other causes of thrombocytopenia (4Ts criteria). The serotonin release assay is a confirmatory test, not part of the 4Ts score.

Citations:
[1] https://www.hematology.org/-/media/hematology/files/education/clinicians/guidelines-quality/documents/ash_vte_hit_pocketguide.pdf
[2] https://documents.cap.org/documents/Heparin-Induced_Thrombocytopenia.pdf
[3] https://onlinelibrary.wiley.com/doi/10.1002/ajh.24006
[4] https://bestpractice.bmj.com/topics/en-gb/1202
[5] https://ashpublications.org/blood/article/140/Supplement%201/5656/489804/Correlation-between-the-4T-Score-Enzyme-Linked
[6] https://medschool.co/tools/fourtscore
[7] https://pubmed.ncbi.nlm.nih.gov/20149589/
[8] https://news.mayocliniclabs.com/hematology/coagulation-disorders/serotonin-release-assay/
[9] https://pmc.ncbi.nlm.nih.gov/articles/PMC9197915/
[10] https://pubmed.ncbi.nlm.nih.gov/22990018/
[11] https://academic.oup.com/ajcp/article/161/2/122/7344335
[12] https://pubmed.ncbi.nlm.nih.gov/31621093/
[13] https://academic.oup.com/ajcp/article/162/Supplement_1/S183/7823015
[14] https://news.mayocliniclabs.com/2022/08/01/heparin-induced-thrombocytopenia-hit-and-the-role-of-serotonin-release-assay-sra/
[15] https://onlinelibrary.wiley.com/doi/full/10.1002/ajh.25660
[16] https://pmc.ncbi.nlm.nih.gov/articles/PMC11665626/
[17] https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/SESLHDGL%20123%20-%20Heparin%20Induced%20Thrombocytopaenia%20-%20Diagnosis%20and%20Management.pdf
[18] https://pubmed.ncbi.nlm.nih.gov/25775976/
[19] https://www.ncbi.nlm.nih.gov/books/NBK482330/
[20] https://pmc.ncbi.nlm.nih.gov/articles/PMC3501714/
[21] https://www.health.qld.gov.au/__data/assets/pdf_file/0035/1178486/hit-guideline.pdf
[22] https://ashpublications.org/blood/article/135/14/1082/454154/Diagnosing-HIT-the-need-for-speed
[23] https://practical-haemostasis.com/Clinical%20Prediction%20Scores/Formulae%20code%20and%20formulae/Formulae/HIT/4T_HIT_score_2.html
[24] https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2816742
[25] https://ashpublications.org/blood/article/126/5/563/126419/Toward-improved-diagnosis-of-HIT
[26] https://ashpublications.org/ashclinicalnews/news/4980/How-Common-Is-Serotonin-Release-Assay-Negative”Platelet serotonin release assay - this is the gold standard test but not part of the 4Ts
score.”

“UTD:
Thrombocytopenia
*Platelet count fall >50 percent and nadir ≥20,000/microL – 2 points
*Platelet count fall 30 to 50 percent or nadir 10 to 19,000/microL – 1 point
*Platelet count fall < 30 percent or nadir < 10,000/microL – 0 points
●Timing of platelet count fall
*Clear onset between days 5 and 10 or platelet count fall at ≤1 day if prior heparin exposure within the last 30 days – 2 points
*Consistent with fall at 5 to 10 days but unclear (eg, missing platelet counts), onset after day 10, or fall ≤1 day with prior heparin exposure within 30 to 100 days – 1 point
*Platelet count fall at < 4 days without recent exposure – 0 points
●Thrombosis or other sequelae
*Confirmed new thrombosis, skin necrosis, or acute systemic reaction after intravenous unfractionated heparin bolus – 2 points
*Progressive or recurrent thrombosis, non-necrotizing (erythematous) skin lesions, or suspected thrombosis that has not been proven – 1 point
*None – 0 points
●Other causes for thrombocytopenia
*None apparent – 2 points
*Possible – 1 point
*Definite – 0 points”

”- thrombocytopenia
- Timing of PLT drop
- History of thrombus
- Other cause of thrombocytopenia
- Platelet serotonin release assay”

Question 81

82. IABP trace, green arrow pointing to unassisted diastolic pressure (unlabeled)

”- Unassisted DBP
- Assisted DBP
- Balloon inflation”

Answer 81

Unassisted diastole

Question 82

83. To confirm ETT, need ETCO2 more than how much from baseline?.

”- 7.5 mmHg
- Other numbers”

Answer 82

7.5mmHg

“Association of Anaes doc
https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.15817
Amplitude rises during exhalation and falls during inspiration.
Consistent or increasing amplitude over at least seven breaths [74, 91].
Peak amplitude more than 1 kPa (7.5 mmHg) above baseline [74, 94].
Reading is clinically appropriate.”

Question 83

84. Third heart sound due to”

”- health person less than 40y
- HTN
- Mitral prolapse”

Answer 83

Healthy person less than 40yo

Question 84

85. Patient presents for a trans-urethral resection of the prostate (TURP). He had a single

drug-eluting coronary stent for angina pectoris inserted six months ago and is taking clopidogrel and aspirin. The most appropriate preoperative management of his medications is to”

“Cease clopidogrel for 5 days
Cease clopidogrel for 10 days
Continue both
Cease clopidogrel for 7 days and aspirin for 20 days
“

Answer 84

5. In patients with DES-PCI who require time-sensitive NCS with interruption of ≥1 antiplatelet agents, NCS may be considered ≥3 months after PCI if

the risk of delaying surgery outweighs the risk of MACE.5,23,24

2024 AHA/ACC 7.5

Question 85

”
#86. Painless visual loss, with preserved pupilliary reflex”s

”- AION
- PION”

Answer 85

AION

“UTD: Both PION and AION have painless visual loss and both have afferent defect

Although anterior ischemic optic neuropathy (AION) appears to be more common than PION after cardiac surgery, PION is relatively more common in cases of spine surgery and radical neck dissection

• ”

Question 86

87. Woman complaining of persistent shortness of breath 3 days post prolonged knee operation. v/q scan showing patchy, non segmental areas of equal non ventilation and perfusion. Cause

• PE
• Pulm infarct
• COPD
• Atelectasis
  “

Answer 86

COPD

“Airway abnormality eg muscous plugging causes matched defect secondary to HPV
vs
Flow abnormality eg PE/infarct causes a mismitch V/Q because you can stop blood flow but lung will remain ventilated”

Question 87

88. What is the half life of a 100u/kg heparin dose?

• 30mins
• 1hour
• 2 hours
• 3 hours
• 4 hours

Answer 87

60min

“Blue Book 2023
Heparin
25iU/kg –> t1/2 30min
100IU/kg –> 60min
400IU/kg –> 150min”

Question 88

89. What does not innervate the knee?

• Posterior cutaneous
• Obturator nerve
• Peroneal nerve
• Tibial nerve

Answer 88

The posterior cutaneous nerve does not innervate the knee joint, making it the correct answer. Here’s the rationale based on the provided sources:

Knee Innervation Overview
The knee joint receives articular branches from multiple nerves, primarily:
- Obturator nerve: Supplies the anteromedial and posteromedial aspects of the knee capsule[7][9][14].
- Tibial nerve: Innervates the posterior capsule and infrapatellar fat pad[4][7][13].
- Common peroneal (fibular) nerve: Provides branches to the anterolateral capsule and tibial periosteum[7][10].

Posterior Cutaneous Nerve
The posterior cutaneous nerve of the thigh (posterior femoral cutaneous nerve) is a sensory nerve that supplies:
- Skin over the posterior thigh and lower gluteal region[1][5][8].
- Cutaneous sensation near the knee but no articular branches to the knee joint itself[8]. While it innervates the skin overlying the posterior knee, it does not contribute to joint innervation[7][8].

Key Distinction
- Cutaneous vs. Articular Innervation: The posterior cutaneous nerve’s role is limited to skin sensation, whereas the obturator, tibial, and peroneal nerves directly innervate the joint capsule, ligaments, and periosteum[7][9][10][13].

Conclusion
The posterior cutaneous nerve is excluded from knee joint innervation, as it lacks articular branches. The obturator, tibial, and peroneal nerves all participate in knee joint innervation.

Answer: Posterior cutaneous nerve.

Citations:
[1] https://www.kenhub.com/en/library/anatomy/posterior-femoral-cutaneous-nerve
[2] https://www.orthobullets.com/anatomy/10112/obturator-nerve
[3] https://www.hopkinsmedicine.org/health/conditions-and-diseases/peroneal-nerve-injury
[4] https://www.orthobullets.com/anatomy/10116/tibial-nerve
[5] https://teachmeanatomy.info/lower-limb/nerves/cutaneous-innervation/
[6] https://pubmed.ncbi.nlm.nih.gov/27015545/
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC7807845/
[8] https://teachmeanatomy.info/encyclopaedia/p/posterior-cutaneous-nerve-of-the-thigh/
[9] https://www.physio-pedia.com/Obturator_Nerve?lang=en
[10] https://en.wikipedia.org/wiki/Common_fibular_nerve
[11] https://www.kenhub.com/en/library/anatomy/tibial-nerve
[12] https://ekja.org/journal/view.php?number=7167
[13] https://teachmeanatomy.info/lower-limb/nerves/tibial-nerve/
[14] https://www.physio-pedia.com/Obturator_Nerve
[15] https://pmc.ncbi.nlm.nih.gov/articles/PMC10366308/
[16] https://www.kenhub.com/en/library/anatomy/obturator-nerve
[17] https://www.physio-pedia.com/Common_Peroneal_Nerve
[18] https://www.physio-pedia.com/Posterior_Femoral_Cutaneous_Nerve
[19] https://teachmeanatomy.info/lower-limb/nerves/obturator-nerve/
[20] https://www.ncbi.nlm.nih.gov/books/NBK549859/
[21] https://www.ncbi.nlm.nih.gov/books/NBK537028/
[22] https://www.physio-pedia.com/Posterior_Cutaneous_Nerve_of_Thigh
[23] https://my.clevelandclinic.org/health/body/22348-obturator-nerve
[24] https://radiopaedia.org/articles/common-peroneal-nerve
[25] https://my.clevelandclinic.org/health/body/21962-tibial-nerve
[26] https://www.ncbi.nlm.nih.gov/books/NBK532301/
[27] https://www.ncbi.nlm.nih.gov/books/NBK482431/
[28] https://academic.oup.com/bjaed/article/12/1/38/260058
[29] https://www.medbox.org/index.php/dl/5e148832db60a2044c2d209a
[30] https://academic.oup.com/bjaed/article/5/5/166/283234
[31] https://www.ncbi.nlm.nih.gov/books/NBK500017/
[32] https://pmc.ncbi.nlm.nih.gov/articles/PMC8693230/
[33] https://www.openanesthesia.org/keywords/peripheral-nerve-injuries-from-positioning/
[34] https://www.ncbi.nlm.nih.gov/books/NBK532887/
[35] https://usra.ca/regional-anesthesia/specific-blocks/lower-limb/obturatornerve.php
[36] https://www.youtube.com/watch?v=xdj-yL7LqVc/?Peroneal

NYSORA - unclear

Question 89

90. What DOESN’T the sciatic nerve do?

“A foot plantar flexion.
B toe extension
C Knee flexion
D knee extension “

Answer 89

Knee ext

Question 90

91. What nerve is not potentially damaged by insertion of supraglottic airway?”

• Facial
• Trigeminal
• Glossopharyngeal
• Vagus
• Lingual

Answer 90

Facial nerve

Cranial Nerve Injury Risks Associated with Supraglottic Airway Device Insertion

Supraglottic airway (SGA) devices are widely used in clinical anesthesia, but their insertion carries risks of cranial nerve injuries due to anatomical proximity and mechanical compression. Based on systematic reviews and case reports, the trigeminal (inferior alveolar and infra-orbital branches), glossopharyngeal, vagus (recurrent laryngeal branch), and hypoglossal nerves are commonly implicated in such injuries[1][2][3][5][7]. The lingual nerve, a branch of the trigeminal nerve, is the most frequently injured[1][7]. However, the facial nerve (CN VII) is not anatomically positioned in the regions affected by SGA placement, and no cases of facial nerve injury have been reported in the literature[1][2][3][5][7]. This absence of association makes the facial nerve the correct answer.

Answer: Facial
Rationale: The facial nerve (CN VII) is not anatomically proximate to SGA insertion sites and is not cited in any reported cases of nerve injury from SGAs, unlike the trigeminal, glossopharyngeal, vagus, and lingual nerves[1][2][3][5][7].

Citations:
[1] https://pubmed.ncbi.nlm.nih.gov/25376257/
[2] https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.12917
[3] https://www.scirp.org/journal/paperinformation?paperid=100681
[4] https://www.jkns.or.kr/journal/view.php?number=7579
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC10664044/
[6] https://www.nature.com/gimo/contents/pt1/full/gimo36.html
[7] https://www.lmaco.com/evidence/lingual-nerve-injury-following-use-i-gel%E2%84%A2-laryngeal-mask
[8] https://my.clevelandclinic.org/health/body/22269-glossopharyngeal-nerve
[9] https://journals.sagepub.com/doi/10.1177/17504589241270238?icid=int.sj-abstract.citing-articles.2
[10] https://emedicine.medscape.com/article/1875813-overview
[11] https://pmc.ncbi.nlm.nih.gov/articles/PMC4691459/
[12] https://www.researchgate.net/publication/267812551_Cranial_nerve_injuries_with_supraglottic_airway_devices_A_systematic_review_of_published_case_reports_and_series
[13] https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/abs/10.1111/anae.12917
[14] https://www.researchgate.net/publication/356593603_Unilateral_lingual_nerve_and_hypoglossal_nerve_injury_caused_by_a_novel_laryngeal_mask_airway_a_case_report
[15] https://journals.lww.com/ejanaesthesiology/fulltext/2009/11000/cranial_nerve_injuries_from_a_laryngeal_mask.16.aspx
[16] https://academic.oup.com/bjaed/article/15/4/184/305721

Question 91

92. Somatic innervation in the second stage of labour includes the following nerves EXCEPT

”- Genitofemoral nerve
- Posterior cutaneous nerve of the thigh
- Inferior gluteal nerve
- Pudendal nerve”

Answer 91

Inf gluteal

inf gluteal = motor to glute, no sensory

Genitofemoral L1-L2

PCN of thigh S1-3

Pudendal S2-4

Question 92

93. Dental extraction, now numbness over lower chin, which nerve has been damaged?”

”- Inferior alveolar
- Mental
- Infraorbital”

Answer 92

Inferior alveolar …or is this one mental n. because it hasn’t specified a tooth they’re taking out?

Numbness Over the Lower Chin Following Dental Extraction: Identification of the Affected Nerve

Dental extraction procedures, while routine, carry inherent risks of iatrogenic nerve injury due to the close anatomical relationship between dental structures and peripheral nerve pathways. The presentation of postoperative numbness over the lower chin—colloquially termed “numb chin syndrome” or mental nerve neuropathy—directly implicates injury to sensory nerves supplying the mandibular region. Through analysis of clinical literature and neuroanatomical principles, this report identifies the mental nerve as the primary structure damaged in such cases, while contextualizing its relationship to the inferior alveolar nerve and broader diagnostic considerations.

Anatomical Foundations of Mandibular Sensory Innervation

The Trigeminal Nerve and Its Mandibular Division
The trigeminal nerve (cranial nerve V) provides sensory innervation to the face via three divisions: ophthalmic (V1), maxillary (V2), and mandibular (V3). The mandibular division gives rise to the inferior alveolar nerve, which enters the mandibular foramen and courses through the mandibular canal[3][4]. Approximately at the level of the second premolar, the inferior alveolar nerve bifurcates into two terminal branches:
1. Mental nerve: Exits via the mental foramen to supply sensory fibers to the skin of the chin, lower lip, and labial gingiva of anterior teeth[3][4].
2. Incisive nerve: Continues anteriorly within the incisive canal to innervate mandibular incisors and canines[3][4].

This anatomical arrangement means that while the inferior alveolar nerve serves as the parent trunk, the mental nerve acts as its terminal cutaneous branch responsible for chin sensation[3][4].

Vulnerability During Dental Procedures
The mental foramen’s position—typically between the apices of the first and second premolars—places the mental nerve at risk during procedures involving these teeth or their surrounding tissues[3][4]. However, posterior extractions (e.g., molars) may indirectly affect the nerve through manipulation of the inferior alveolar trunk within the mandibular canal, as the mental nerve derives from this structure[5][8].

Mechanisms of Post-Extraction Nerve Injury

Direct Trauma to the Mental Nerve
Surgical extraction of premolars or anterior teeth poses the highest risk of direct mental nerve injury due to:
- Periosteal elevator slippage during flap reflection near the mental foramen[4][8].
- Root fragment displacement into the mental foramen during apical curettage[1][5].
- Local anesthetic needle penetration into the foramen during inferior alveolar nerve blocks[4][8].

Such mechanical insults can induce neuropraxia (conduction block without axonal disruption) or, in severe cases, axonotmesis (axonal degeneration with intact endoneurium)[5][8].

Indirect Injury via Inferior Alveolar Nerve Trauma
Molar extractions—particularly impacted third molars—frequently endanger the inferior alveolar nerve due to:
- Compression from apical root displacement into the mandibular canal[2][5].
- Thermal injury from osteotomy burrs during bone removal[5][8].
- Postoperative edema or hematoma formation within the canal[2][8].

While these mechanisms primarily affect the inferior alveolar trunk, the resulting sensory deficits encompass all its terminal territories, including the mental nerve distribution (chin and lower lip)[2][8]. This explains why molar extractions may manifest with chin numbness despite the injury site being posterior to the mental foramen.

Clinical Differentiation Between Mental and Inferior Alveolar Neuropathies

Symptomatology
- Isolated mental nerve injury: Numbness strictly localized to the chin and ipsilateral lower lip vermilion[1][3]. Gingival sensation remains intact if the incisive nerve is unaffected[3][4].
- Inferior alveolar nerve injury: Numbness involving the chin, lower lip, and labial/buccal gingiva of mandibular teeth anterior to the injury site[2][8]. Concomitant incisive nerve dysfunction may cause dental hypersensitivity due to pulp innervation disruption[2].

Diagnostic Testing
1. Pinprick testing: Maps sensory loss boundaries; mental nerve deficits spare the gingiva[3][4].
2. Two-point discrimination: Impaired in the lower lip with inferior alveolar involvement[8].
3. Dental vitality testing: Positive response in anterior teeth rules out incisive nerve injury, localizing damage to the mental branch[2][8].

Management Considerations

Acute Phase (0-8 Weeks Post-Injury)
- Corticosteroids (e.g., dexamethasone 4-8 mg/day tapered over 5 days) to reduce inflammatory compression[1][8].
- Antioxidants (alpha-lipoic acid 600 mg/day) to mitigate oxidative neuronal damage[1][5].
- Low-level laser therapy to enhance axonal regeneration[1][8].

Persistent Neuropathy (>3 Months)
- Pulsed radiofrequency ablation of the mental nerve for refractory neuropathic pain[1][5].
- Microneurosurgical repair via direct neurorrhaphy or autografting for transected nerves[4][8].

Conclusion
Numbness over the lower chin following dental extraction overwhelmingly implicates mental nerve injury, whether through direct trauma at the mental foramen (anterior procedures) or indirect insult via the inferior alveolar trunk (posterior extractions). Clinicians must recognize that while the inferior alveolar nerve serves as the anatomical origin, the mental nerve’s terminal distribution dictates the chin-specific symptomatology. Timely diagnosis—supported by sensory mapping and dental testing—enables targeted interventions to optimize functional recovery.

Citations:
[1] https://pubmed.ncbi.nlm.nih.gov/24850119/
[2] https://jdapm.org/DOIx.php?id=10.17245%2Fjdapm.2021.21.2.173
[3] https://en.wikipedia.org/wiki/Mental_nerve
[4] https://selectedreadingsoms.com/wp-content/uploads/2019/05/Numb-Tongue-Numb-Lip-Numb-Chin-What-to-Do-When-Updated.pdf
[5] https://www.woodviewos.com/dental-paresthesia-nerve-damage-complication-wisdom-tooth-extraction-dental-injection
[6] https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2017.00343/full
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC5526228/
[8] https://www.blvddentistry.com/managing-nerve-pain-after-tooth-extraction-a-guide/
[9] https://pmc.ncbi.nlm.nih.gov/articles/PMC10141477/
[10] https://www.lenus.ie/bitstream/handle/10147/333831/OctArticle2.pdf?sequence=1&isAllowed=y
[11] https://www.cambridge.org/core/services/aop-cambridge-core/content/view/383E302FCA45F0D2F01AF93249063483/S1481803500008460a.pdf/mental-nerve-neuropathy-case-report-and-review.pdf
[12] https://www.baoms.org.uk/patients/procedures/23/removal_of_impacted_wisdom_teeth
[13] https://www.painphysicianjournal.com/current/pdf?article=MjEwOA%3D%3D&journal=82
[14] https://www.ncbi.nlm.nih.gov/books/NBK589668/
[15] https://www.medicalnewstoday.com/articles/numb-chin
[16] https://www.nycoms.com/management-injury-nerves-maxillofacial-region/
[17] https://pmc.ncbi.nlm.nih.gov/articles/PMC6031975/
[18] https://www.oralsurgerysouth.com/procedures/wisdom-teeth/after-extraction-of-wisdom-teeth/
[19] https://www.healthline.com/health/numb-chin
[20] https://www.baoms.org.uk/patients/procedures/44/coronectomy

Question 93

94. Cryoprecipitate does NOT contain

• Factor IX
• Factor XIII
• Fibronectin
• Von Willebrand Factor”

Answer 93

FIX

Mnemonic:
III F

VIII
XIII
Fibro x2
vwF

Cryo contains: vwF, fibronectin, fibrinogen (I), VIII, XIII

Question 94

95. Tibial fracture, Posterior tibial nerve injury, which compartment

”

”- Superficial posterior
- Deep posterior
- Anterior”

Answer 94

Deep posterior

The PTN is one of the two terminal divisions of the sciatic nerve and consists of muscular, cutaneous, and articular branches. It extends from the arch of the soleus muscle to the tibiotalocalcaneal canal. In the upper two-thirds of the leg the nerve is located deep in the posterior compartment.

Question 95

96. Hyalase increases the following:

”- Speed of muscle akinesis
- Chemosis
- Rate of allergic reactions”

Answer 95

Speed of muscle akinesis

HYALASE is used as an aid in different medical conditions to allow injected substances to be rapidly dispersed and absorbed.

https://www.nps.org.au/medicine-finder/hyalase-injection

Question 96

97. Use of methylene blue rather than patent blue

• Reduced rate of anaphylaxis
• More expensive
• Easier to see sentinel nodes
• Reduced O2 saturations”

Answer 96

Reduced rate of anaphylaxis

“https://www.nationalauditprojects.org.uk/downloads/NAP6%20Chapter%2018%20-%20Patent%20Blue%20dye.pdf

https://pubmed.ncbi.nlm.nih.gov/28355372/
Methylene blue is more widely available and less expensive than patent blue, with an apparently lower risk of anaphylaxis.
Patent blue = easier to see the nodes”

Question 97

98. Best method to reduce post ERCP pancreatitis?

Oxycodone
PR indomethacin
Morphine

Answer 97

• Rectal indomethacin

“NEJM
APMSE - Rectal diclofenac and indomethacin”

Question 98

99. Epipen dose compared to normal 1:1000 IM adrenaline dose in adult anaphylaxis?

• Higher dose
• Same dose lower volume
• Same dose and normal volume
• Same dose higher volume
• Lower dose same concentration”

Answer 98

Lower dose, same conc

“Epipen = 300microg
1:1000 = 1mg
1000microg/mL

ANAPEN 500mcg adrenaline (epinephrine) 500 micrograms/0.3 mL solution for injection pre-filled syringe (auto-injector)

Epipen 300mcg Ad in 0.3mL “

A device containing either 300 micrograms ( EpiPen®) OR
a device containing 500 micrograms (Anapen®) should be used.

EpiPen® = one dose of 0.3 mg epinephrine, USP 0.3 mg/0.3 mL
EpiPen Jr® = one dose of 0.15 mg epinephrine, USP 0.15 mg/0.3 mL

Anapen
150/300/500 microg / 0.3mL
All 0.3mL

Vetted by perplexity

Question 99

100. how to clean a laryngoscope handle?

Answer 99

Soap and water

“Laryngoscope handles, being non-critical devices, should be cleaned with
detergent and water between each patient use. If contaminated with blood,
they should be washed and disinfected”

PG 28 2015 P.4

Question 100

101 what additive prolongs block longest

“Clonidine
Dexamethasone
Bicarbonate
Adrenaline”

Answer 100

dexamethasone

“https://www.bjaed.org/action/showPdf?pii=S2058-5349%2819%2930079-4

Dexamethasone –> Dexmed –> Clonidine “

Question 101

102 what is not acceptable for ARDS/What is not a suggested management of ARDS?

”
Recruitment manoeuvres
Proning
High PEEP
Neuromuscular blockade
Keep dry”

Answer 101

High PEEP

“Blue Book 2017
PEEP prevents de-recruitment of alveoli at the end of each expiration thus maintaining functional residual
capacity (FRC). Patients with ARDS often receive PEEP of 5 to 20 cm of water. Higher PEEP levels may improve
oxygenation but may also cause circulatory depression and lung injury from over distention. Thus, optimal
PEEP is that which prevents atelectrauma and at the same time prevents over distension of normal alveoli – it
needs to be individualised to the patient’s respiratory mechanics. How to set “optimal PEEP” remains controversial.”

Question 102

103 The recommended skin preparation for a neuraxial:

Answer 102

0.5% chlorhex/ 70% alcohol.

For skin preparation, 0.5 per cent chlorhexidine in alcohol, where available, is recommended for neuraxial techniques

PG 28 Infection control https://www.anzca.edu.au/getattachment/e4e601e6-d344-42ce-9849-7ae9bfa19f15/PG28(A)-Guideline-on-infection-control-in-anaesthesia

Question 103

104 Expected blood volume in preggers lady

• 60 ml/kg
• 70 ml/kg
• 80 ml/kg
• 90 ml/kg
• 100 ml/kg

Answer 103

100ml/kg

Parameters for pregnant lady

https://www.ahajournals.org/doi/10.1161/circulationaha.114.009029

Question 104

105

What is the 4th pacemaker letter meaning

Answer 104

PSA RM
rate modulation
multichamber pacing

https://litfl.com/pacemaker-rhythms-normal-patterns/

Question 105

106. Time for reversal of therapeutic dabigatran after administration of Idarucizumab 5 g is

“A 5mins
B 15mins
C 30mins”

Answer 105

5 mins

”"”neutralizing their anticoagulant effect immediately after administration”” Praxbind website https://pro.boehringer-ingelheim.com/us/products/praxbind/idarucizumab/reversing-pradaxa#

2021 Blue book - Almost immediate”

Question 106

107. The accompanying image is obtained while doing an ultrasound guided erector spinae plane block at the level of the transverse process of the fourth thoracic vertebra. The muscle marked by the arrow is the

Answer 106

TRE: traps –> rhomboids –> erector spinae in that order

Question 107

108 Max dose topicalisation airway in mg/kg

-7
-9
- 11

Answer 107

maximum of 8-9mg/kg lignocaine can be used for topicalisation

https://www.anzca.edu.au/resources/sig-resources/2019-airway-management-sig-afoi-topicalisation-sed

Question 108

109. BD morphine, bowel obstruction, showing signs of withdrawal. What is this?

• opioid dependence
• Physical dependence
• Tolerance
• Opioid use disorder

Answer 108

Physical dependence

Question 109

110. NAP 5 - cardiac anaesthesia awareness”

• 1/8000
• 1/700”

Answer 109

cardiothoracic anaesthesia (~1:8,600)

“NAP 5 2014
GA CS 1:670
Paralysed pt 1:8000
In general for GA with paralysis 1: 20,000
GA without paralysis 1:136,000”

Question 110

111. NAP7 - most common cause perioperative arrest

• Major haemorrhage
• Anaphylaxis
• Airway issues

Answer 110

major haemorrhage

NAP 7

NAP 7 2023: The most common causes of perioperative cardiac arrest were major haemorrhage (17%), bradyarrhythmia (9.4%) and cardiac ischaemia (7.3%) but varied by surgical specialty

Question 111

112. DDAVP NOT used for:

• nocturnal enuresis
• Haemophillia B
• Von Wil disease 2A
• Uraemic bleeding
• Central diabetes insipidus

Answer 111

Haemophilia B

“BJA + UTD
DDAVP stim factor VIII”

Question 112

113. Noradrenaline has tissued into skin from peripheral cannula, most appropriate first step is:

• remove cannula
• Flush with saline
• Hyalase
• Cold compress

Answer 112

1. remove cannula
2. if removed, phentolamine (UTD)

Phentolamine if “ischaemia…’”

either using the catheter through which vasopressors were infusing if not yet removed from the patient or through separate subcutaneous injection)

https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/Medicine%20Guideline%20-%20Phentolamine%20in%20the%20treatment%20of%20dermal%20necrosis%20or%20sloughing%20following%20extravasation%20of%20peripherally%20administered%20noradrenaline%20%28norepinephrine%29.pdf

Question 113

114. What is not associated with POTS?”

• COVID-19
• Hypermobility disorder
• Normal resting LV function
• ECG changes”

Answer 113

ECG changes

PoTS

”- Need a normal ECG for PoTS
- IS assoc w/ long covid, EDS, and need normal LV function
- https://www.acc.org/Latest-in-Cardiology/Articles/2016/01/25/14/01/Postural-Tachycardia-Syndrome-POTS-Diagnosis-and-Treatment-Basics-and-New-Developments#:~:text=Left%20ventricular%20function%20must%20be,could%20mimic%20a%20POTS%20presentation.”

Question 114

115. Pregnancy highest risk

• bicuspid valve with dilated aortic root

Question 115

116. Pt with aortic dissection will have the following features EXCEPT

”- RWMA
- right dilated ventricle
- Dilated aortic root
- AR”

Answer 115

RV dilated/dysFx

The correct answer is right dilated ventricle. Aortic dissection typically presents with features related to the aorta and left heart structures, while right ventricular dilation is not a characteristic finding. Here’s the rationale:

1. Dilated aortic root
   Aortic dissection often occurs in the context of pre-existing aortic pathology, such as aneurysmal dilation or connective tissue disorders (e.g., Marfan syndrome). A dilated aortic root is a common predisposing factor and can be exacerbated by the dissection itself[4][6].
2. Aortic regurgitation (AR)
   Acute aortic regurgitation is a frequent complication of type A dissections due to disruption of the aortic valve apparatus or dilation of the aortic root, leading to valve incompetence[5][6].
3. RWMA (regional wall motion abnormalities)
   While not universally present, RWMA may occur if the dissection extends into the coronary arteries (e.g., right coronary artery involvement causing right ventricular ischemia). However, this is less common and not a definitive feature[6].
4. Right dilated ventricle
   Right ventricular dilation is not typically associated with aortic dissection. The primary complications involve the aorta, left heart, or systemic circulation (e.g., tamponade, aortic rupture, or malperfusion syndromes). Right ventricular pathology would more commonly arise from conditions like pulmonary embolism or primary right heart failure[3][6].

Conclusion: The exception is right dilated ventricle, as it is not a direct consequence of aortic dissection.

Citations:
[1] https://www.mayoclinic.org/diseases-conditions/aortic-dissection/symptoms-causes/syc-20369496
[2] https://www.healthdirect.gov.au/aortic-dissection
[3] https://www.msdmanuals.com/home/heart-and-blood-vessel-disorders/diseases-of-the-aorta-and-its-branches/aortic-dissection
[4] https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-12/Acute-aortic-dissection
[5] https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.110.958975
[6] https://www.msdmanuals.com/professional/cardiovascular-disorders/diseases-of-the-aorta-and-its-branches/aortic-dissection
[7] https://www.ahajournals.org/doi/10.1161/01.cir.0000087009.16755.e4
[8] https://www.ncbi.nlm.nih.gov/books/NBK441963/
[9] https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/aortic-dissection-repair
[10] https://pmc.ncbi.nlm.nih.gov/articles/PMC8762162/
[11] https://litfl.com/acute-aortic-dissection/
[12] https://pubmed.ncbi.nlm.nih.gov/28871571/
[13] https://emedicine.medscape.com/article/2062452-clinical
[14] https://www.pennmedicine.org/for-patients-and-visitors/patient-information/conditions-treated-a-to-z/aortic-dissection
[15] https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/485480
[16] https://www.bhf.org.uk/informationsupport/conditions/aortic-aneurysm-dissection-and-rupture
[17] https://emedicine.medscape.com/article/2062452-overview
[18] https://www.revportcardiol.org/en-acute-aortic-dissection-complicated-by-articulo-S217420491400292X
[19] https://my.clevelandclinic.org/health/diseases/16743-aortic-dissection
[20] https://academic.oup.com/ehjcimaging/article/10/1/i31/2465433
[21] https://nyulangone.org/conditions/aortic-dissection/types
[22] https://synapse.koreamed.org/articles/1018128
[23] https://academic.oup.com/ehjcimaging/article-pdf/10/1/i31/7466330/jen251.pdf
[24] https://aci.health.nsw.gov.au/networks/eci/clinical/tools/cardiology/aortic-dissection
[25] https://www.health.qld.gov.au/cpc/cardiology/aortic-disease
[26] https://journals.sagepub.com/doi/10.1177/0267659120986532?icid=int.sj-full-text.similar-articles.6
[27] https://www.escardio.org/static-file/Escardio/Subspecialty/EACVI/education/EACVI-core-syllabus.pdf
[28] http://103.12.11.134/journal/1999/september/Echo2.pdf
[29] https://bestpractice.bmj.com/topics/en-gb/3000226
[30] https://cdt.amegroups.org/article/view/23120/html
[31] https://pubmed.ncbi.nlm.nih.gov/30562107/
[32] https://pmc.ncbi.nlm.nih.gov/articles/PMC3654107/
[33] https://pmc.ncbi.nlm.nih.gov/articles/PMC1861012/

LITFL Echo: AR, RWMA heralding cor art occlusion, acute dilation aortic root, pericardial eff

Question 116

117. PFT in dude, detect nitric oxide >70ppm number ppm. Meaning

• Smoker
• COPD
• Exacerbation of asthma

Answer 116

exacerbation of asthma

A fractional exhaled nitric oxide (FeNO) level exceeding 70 parts per billion (ppb) in a patient undergoing pulmonary function testing (PFT) strongly suggests exacerbation of asthma. This conclusion is supported by the following evidence:

1. FeNO as a Marker of Type 2 Inflammation:
   Elevated FeNO reflects eosinophilic airway inflammation, a hallmark of asthma pathophysiology[1][8][10]. During exacerbations, airway inflammation intensifies, leading to higher FeNO levels compared to stable states[1][5][10]. While normal adult FeNO levels typically range below 25 ppb, values exceeding 50 ppb are strongly indicative of uncontrolled asthma or exacerbations[4][9][11]. A reading of 70 ppb falls well within this high-risk range.
2. Contrast with Smoking and COPD:
   • Smoking: Cigarette smoke reduces FeNO levels through mechanisms such as nitric oxide synthase inhibition and increased oxidative stress[2][7]. Smokers with or without COPD consistently demonstrate lower FeNO values (often 50 ppb predicts corticosteroid responsiveness and exacerbation risk in asthma[4][5][10]. Levels ≥70 ppb indicate severe airway inflammation requiring urgent anti-inflammatory therapy[1][4][9]. In contrast, COPD and smoking-related lung disease would not typically manifest such pronounced FeNO elevation, even during exacerbations[2][7].

Conclusion:
A FeNO level of 70 ppb is inconsistent with smoking or pure COPD. This degree of elevation strongly supports acute asthma exacerbation driven by eosinophilic airway inflammation. Immediate initiation or escalation of inhaled corticosteroids is warranted[1][4][9].

Citations:
[1] https://allergyasthmanetwork.org/what-is-asthma/how-is-asthma-diagnosed/nitric-oxide-testing/
[2] https://www.tandfonline.com/doi/full/10.1080/15412555.2019.1638355
[3] https://www.lung.org/lung-health-diseases/lung-procedures-and-tests/exhaled-nitric-oxide-test
[4] https://www.niox.com/en/digital-platform/interpreting-feno
[5] https://www.pulmonologyadvisor.com/news/association-between-fraction-of-exhaled-nitric-oxide-and-asthma-exacerbations/
[6] https://www.thoracic.org/statements/resources/allergy-asthma/feno-document.pdf
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC7362749/
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC2677842/
[9] https://www.niox.com/en/feno-asthma/interpreting-feno/
[10] https://pmc.ncbi.nlm.nih.gov/articles/PMC7919904/
[11] https://pmc.ncbi.nlm.nih.gov/articles/PMC10137365/
[12] https://pmc.ncbi.nlm.nih.gov/articles/PMC3955647/
[13] https://bjgp.org/content/73/737/565
[14] https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(22)00263-2/fulltext
[15] https://pmc.ncbi.nlm.nih.gov/articles/PMC10037222/
[16] https://thorax.bmj.com/content/77/4/351
[17] https://pmc.ncbi.nlm.nih.gov/articles/PMC2801041/
[18] https://www.elsevier.es/en-revista-allergologia-et-immunopathologia-105-articulo-a-pathophysiological-approach-for-feno-S0301054615000270
[19] https://www.mdpi.com/2076-3271/12/4/52
[20] https://www.atsjournals.org/doi/10.1164/rccm.9120-11ST
[21] https://www.severeasthma.org.au/biomarkers-recommendation/
[22] https://www.ccjm.org/content/90/6/363

”- Normal is < 25ppb
https://www.lung.org/lung-health-diseases/lung-procedures-and-tests/exhaled-nitric-oxide-test”

Question 117

118. Compared to a continuous infusion, PCEA does NOT reduce

• Incidence of instrumental delivery
• Incidence of C-section rates
• Clinical workload
• Motor weakness”

Answer 117

incidence of CS

Blue book article

Blue book 2021.

Question 118

119. A 70-year-old man undergoes a stress echocardiogram as part of his preoperative preparation before a total hip replacement. If he has clinically significant coronary artery disease, the earliest indicator during his test is most likely to be

“ECG changes
RWMA
diastolic dysfunction
Angina
Hypotension”

Answer 118

Diastolic dys

“https://www.ahajournals.org/doi/10.1161/01.cir.83.5.1605?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

Cascade of events: Diastolic dys, sys dysFx, ECG changes, Sx angina - from some rando paper Bonny found”

Question 119

120. Return to practice

Answer 119

• 4 weeks for every year of absence

The starting point for calculating the total duration is one month per year of absence from anaesthesia practice.

PS

PS 50 Return to Practice 2017

Question 120

121. CPET Borg’s scale, what is it for?

Answer 120

• Subjective effort

“rating of pecieved exertion” test

Question 121

122. ANZCOR recommendations on minimum time from cardiac arrest to post arrest prognostication?

• 24 hours
• 48 hours
• 72 hours

Answer 121

72 hours

The ANZCOR guidelines recommend 72 hours as the minimum time from cardiac arrest to prognostication in comatose survivors. This allows adequate time to minimize confounding factors like residual sedation or paralysis, which could lead to false-positive predictions of poor outcomes[1][3][12].

Key recommendations include:
- No prognostication before 72 hours using clinical criteria alone, due to insufficient specificity[1][3].
- Multimodal assessment (combining clinical exam, neurophysiological tests, imaging, or biomarkers) is required for reliable prognostication[1][3].
- Specific predictors at ≥72 hours:
- Bilateral absence of pupillary or corneal reflexes[1][3].
- Bilateral absence of N20 somatosensory evoked potentials (SSEP)[1].
- Persistent burst suppression or status epilepticus on EEG[1][3].

The 72-hour threshold applies to both patients treated and not treated with targeted temperature management (TTM)[1][3]. Earlier prognostication (e.g., 24–48 hours) is discouraged due to high false-positive rates[1][12].

Citations:
[1] https://www.resus.org.nz/assets/Uploads/ANZCOR-Guideline-11.7-Jan16.pdf
[2] https://emcrit.org/ibcc/np/
[3] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-7-post-resuscitation-therapy-in-adult-advanced-life-support/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC7993077/
[5] https://www.anzcor.org/assets/anzcor-guidelines/guideline-11-7-post-resuscitation-therapy-in-adult-advanced-life-support-250.pdf
[6] https://www.resus.org.nz/assets/Uploads/Adult-Advanced-Life-Support-All-Guidelines.pdf
[7] https://www.anzcor.org/assets/anzcor-guidelines/guideline-11-2-protocols-for-adult-advanced-life-support-237.pdf
[8] https://cprguidelines.eu/assets/guidelines/European-Resuscitation-Council-and-European-Societ.pdf
[9] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-10-1-management-of-cardiac-arrest-due-to-trauma/
[10] https://litfl.com/therapeutic-hypothermia-after-cardiac-arrest/
[11] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-10-resuscitation-in-special-circumstances/
[12] https://pmc.ncbi.nlm.nih.gov/articles/PMC10241762/
[13] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-10-resuscitation-in-special-circumstances/downloadpdf
[14] https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/anzcor11-2-adultllifesupport2018.pdf
[15] https://www.resus.org.nz/assets/Guidelines/ANZCOR-Guideline-12.5-Management-after-ROSC-Nov-2021.pdf
[16] https://www.anzcor.org

Answer from Perplexity: pplx.ai/share

ALS ANZCOR - detailed

ANZCOR
48h: CTB
72 hours: pupillary light reflex, pupillometry, corneal reflex, eeg, NSE, MRI 72h-7d
4 days GCS >3
7 days (status) myoclonus

https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-7-post-resuscitation-therapy-in-adult-advanced-life-support/
2.3-3.5

Question 122

123. Spinal, 3ml, patient supine and horizontal, hyperbaric qualities vs normal bupivacaine”

A Lesser block height, shorter DoA
B Lesser block height, Longer DoA
CGreater block height + shorter DoA
D Greater block height+ Longer DoA
E No difference in block height, longer DoA

Answer 122

Greater height, shorter DOA

Hyperbaric Versus Isobaric Bupivacaine for Spinal Anesthesia: Systematic Review and Meta-analysis for Adult Patients Undergoing Noncesarean Delivery Surgery; BJA intrathecal drug spread 2004

Question 123

124 Epilepsy surgery, some sort brain monitoring and which drugs affect it the least

“Remifentanil
Ketamine
Sevoflurane”

Answer 123

?

Answer: Ketamine

Rationale:
Ketamine demonstrates favorable anticonvulsant properties with minimal interference to intraoperative electrocorticography (ECoG) and neurophysiological monitoring during epilepsy surgery[1][5][6]. Studies show it suppresses seizure burden in refractory status epilepticus (57–81% efficacy) without exacerbating epileptiform discharges in non-epileptic brain regions[1][11]. Unlike sevoflurane, which induces dose-dependent epileptogenic activity (1.5–2 MAC)[3][8], ketamine preserves baseline cortical excitability and reduces vasopressor requirements while maintaining stable intracranial pressure[1][6]. Remifentanil, while useful for activating epileptogenic zones via opioid-induced spikes[2][12], risks obscuring baseline ECoG signals if overused. These findings align with BJA Education and Miller’s guidelines prioritizing ketamine for balancing anesthetic efficacy and neurophysiological fidelity.

Citations:
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC7713785/
[2] https://pubmed.ncbi.nlm.nih.gov/11737170/
[3] https://www.aub.edu.lb/fm/Anesthesiology/meja/Documents/Anesthesia%20And%20Electrocorticography%20For%20Epilepsy%20Surgery%20A%20Jordanian%20Experience.pdf
[4] https://seizure.mgh.harvard.edu/wp-content/uploads/MGH_Status_Protocol_01_09_2015.pdf
[5] https://aesnet.org/abstractslisting/drug-induced-eeg-pattern-predicts-effectiveness-of-ketamine-in-treating-refractory-status-epilepticus
[6] https://pmc.ncbi.nlm.nih.gov/articles/PMC3731413/
[7] https://pubmed.ncbi.nlm.nih.gov/14570785/
[8] https://pubmed.ncbi.nlm.nih.gov/39297916/
[9] https://pmc.ncbi.nlm.nih.gov/articles/PMC6939570/
[10] http://www2.pedsanesthesia.org/meetings/2013winter/syllabus/submissions/sat/Brain%20Mapping%20and%20Deep%20Brain%20Stimulation%20Final_NCarling.pdf
[11] https://www.epilepsy.org.uk/news/ketamine-effective-for-status-epilepticus
[12] https://onlinelibrary.wiley.com/doi/full/10.1046/j.1528-1157.2001.05901.x
[13] https://ekja.org/upload/pdf/kja-23843.pdf
[14] https://pmc.ncbi.nlm.nih.gov/articles/PMC8766927/
[15] https://dig.pharmacy.uic.edu/faqs/2023-2/december-2023-faqs/what-is-the-role-of-ketamine-in-the-management-of-status-epilepticus/
[16] https://portal.findresearcher.sdu.dk/en/publications/pharmacodynamics-of-remifentanil-induced-intracranial-spike-activ
[17] https://journals.lww.com/anesthesia-analgesia/Fulltext/2013/08000/The_Anesthetic_Considerations_of_Intraoperative.27.aspx?generateEpub=Article%7Canesthesia-analgesia%3A2013%3A08000%3A00027%7C10.1213%2Fane.0b013e318297390c%7C
[18] https://aesnet.org/abstractslisting/ketamine-therapy-in-the-management-of-refractory-seizures-in-an-extremely-premature-neonate-a-case-report
[19] https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-0404.2009.01193.x
[20] https://onlinelibrary.wiley.com/doi/10.1684/epd.2014.0675
[21] https://pch.health.wa.gov.au/for-health-professionals/emergency-department-guidelines/ketamine-sedation
[22] https://www.acns.org/UserFiles/file/ACNSMinimumTechRequirementsforIntraopECOG_DraftforCommentFeb22.pdf
[23] https://www.e-jnc.org/m/journal/view.php?doi=10.18700%2Fjnc.230003
[24] https://journals.lww.com/neur/fulltext/2021/69010/ketadex__a_saviour_for_intraoperative_multimodal.39.aspx
[25] https://pmc.ncbi.nlm.nih.gov/articles/PMC7807957/
[26] https://www.neurology.org/doi/10.1212/WNL.0000000000010611
[27] https://academic.oup.com/bja/article/108/4/562/257975
[28] https://snacc.org/education-corner/challenging-cases/pbld/pbld-10/
[29] https://academic.oup.com/bjaed/article/15/3/111/279202

I havent found a reference for this, the lecture from Syndey said ketamine does inrease MPSS, surely sevo is worse than remi??

Question 124

125 Giving indocyanine green

“a) Increases NIRS, Decreased peripheral saturations
b) decrease NIRS, decrease peripheral
c) no change NIRS, decrease peripheral
d) increases NIRS AND periph
e) decrease NIRS, increases peripheral “

Answer 124

“increased cerebral O2 (SctO2) and decreased peripheral SpO2

ie. Increases NIRS, decreases periph (falsely)”

https://pmc.ncbi.nlm.nih.gov/articles/PMC4384398/#:~:text=Intravenously%20administered%20indocyanine%20green%20(ICG,carotid%20endarterectomy%20under%20general%20anesthesia.

Question 125

126 Accuracy of pulse ox, which does NOT affect

“A Anaemia
B AF
C Carboxyhaemoglobin
D Poor peripheral perfusion”

Answer 125

Anaemia

Question 126

127 Best post-op analgesia after wisdom tooth removal

“Ibuprofen
Celecoxib
Tramadol
paracetamol”

Answer 126

Answer:
Celecoxib

Rationale:
1. Superior Analgesic Efficacy:
- A randomized controlled trial (Akinbade et al., 2018) comparing celecoxib (400 mg initial dose, then 200 mg 12-hourly), ibuprofen (400 mg 8-hourly), and tramadol (100 mg 8-hourly) found celecoxib achieved the lowest mean pain scores at all postoperative intervals (4–48 hours), with statistically significant differences at 4 hours (p = 0.0039)[1].
- A 2024 study comparing celecoxib (100 mg), diclofenac, and ibuprofen (400 mg) confirmed celecoxib’s superior pain control over ibuprofen, particularly in reducing rescue medication use[4].
- Preemptive celecoxib (200 mg) demonstrated better analgesic activity than ibuprofen (400–600 mg) and acetaminophen, with lower postoperative pain scores and fewer patients requiring rescue analgesia[6].

2. Adverse Effects and Safety:
   
   • Celecoxib and ibuprofen showed no adverse effects in trials, while tramadol caused nausea, dizziness, and vomiting in 47.6% of patients[1][2].
   • Celecoxib’s COX-2 selectivity minimizes gastrointestinal (GI) risks compared to nonselective NSAIDs like ibuprofen, making it safer for patients with peptic ulcer disease or GI sensitivities[1][6].
3. Guideline Considerations:
   
   • While NSAIDs like ibuprofen remain first-line for postoperative pain, recent evidence supports celecoxib’s efficacy, especially with higher initial dosing (400 mg loading dose)[1][4].
   • Paracetamol (acetaminophen) is less effective as monotherapy for moderate-to-severe inflammatory pain[3][5], and tramadol is reserved for opioid-tolerant patients due to inferior efficacy and side effects[1][2].

Conclusion:
Celecoxib provides superior pain control with a favorable safety profile for post-wisdom tooth extraction, particularly when administered at an initial 400 mg dose followed by 200 mg 12-hourly. Ibuprofen remains effective for patients without GI risks, while tramadol and paracetamol are less optimal choices.

Citations:
[1] https://www.thejcdp.com/doi/10.5005/jp-journals-10024-2428
[2] https://www.sid.ir/FileServer/JE/88120090413.pdf
[3] https://www.cochrane.org/CD004624/ORAL_ibuprofen-versus-paracetamol-acetaminophen-for-pain-relief-after-surgical-removal-of-lower-wisdom-teeth
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC10845003/
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC11561150/
[6] https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2023.1303382/full
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC3414241/
[8] https://australianprescriber.tg.org.au/articles/opioid-prescribing-in-dentistry-is-there-a-problem.html
[9] https://www.seslhd.health.nsw.gov.au/sites/default/files/groups/Royal_Hospital_for_Women/docs/painaftersurgery.pdf
[10] https://www.ada.org/resources/ada-library/oral-health-topics/oral-analgesics-for-acute-dental-pain
[11] https://www.nps.org.au/assets/NPS/pdf/NPS-Medicinewise-Opioids-webinar-slides-for-Dentists-25112020.pdf
[12] https://www.colgate.com/en-us/oral-health/tooth-removal/ibuprofen-and-acetaminophen-together-may-give-profound-pain-relief-with-fewer-side-effects-after-dental-surgery
[13] https://orthoinfo.aaos.org/en/recovery/managing-pain-with-medications/
[14] https://www.cabrini.com.au/app/uploads/Pain-relief-following-surgery.pdf
[15] https://www.aafp.org/pubs/afp/issues/2005/0301/p913.html

Answer from Perplexity: pplx.ai/share

Cobbled together from a few different papers, brufen superior to panadol, but celecoxib (and diclofenac) superior to panadol, meloxicam superior to tramadol

Question 127

128 What is NOT a feature of thyroid storm?

“Jaundice
Bronchospasm
Seizures”

Answer 127

No bronchospasm

“https://www.bjanaesthesia.org/action/showPdf?pii=S0007-0912%2821%2900437-2 table of Burch and Wartofski score for thyrotoxicosis dx

UTD:
Temp, neuro signs (agitation –> seizure/coma), UG (diarrhoea –> jaundice), tachy, AF, HF, precipitant criteria”

Question 128

129 Expected physiological change in hyperthyroidism

Answer 128

reduced SVR

reduced SVR (hence flushing!)

“UTD thyroid CVS table https://www.uptodate.com/contents/cardiovascular-effects-of-hyperthyroidism

+ diastolic down –> widened pulse pressure”

Question 129

130 Somatic pain in the second stage of labour is NOT transmitted via the

”- Pudendal
- Ilioinguinal
- Genitofemoral (L1/2)
- Inferior gluteal
- Posterior cutaneous nerve of thigh”

Answer 129

inferior gluteal, its a motor nerve to glute, for stair climbing type movement

primary/ KN/ radiopedia

Question 130

131 Which drug NOT to give with cocaine toxicity?

“phentolamine
Metoprolol
GTN
Propofol bolus”

Answer 130

metoprolol (unopposed alpha)

represents the contraindicated agent in classical teaching and examination settings due to lingering concerns about beta-blockers in cocaine toxicity. Contemporary evidence supports nuanced use of selective β1-blockers, but guidelines remain cautious. Phentolamine and GTN are appropriate therapies, while propofol requires judicious application

Traditional guidelines contraindicate beta-blockers due to concerns about unopposed α-adrenergic activity58. By blocking β2-mediated vasodilation, non-selective agents like propranolol may exacerbate hypertension and coronary vasospasm25.

This was on an episode of ER. But also; https://www.bjaed.org/action/showPdf?pii=S1743-1816%2817%2930053-7. LITFL. primary viva, open anaesthesia

Question 131

132 SGLT-2i use for diabetes, what do they NOT cause?

A Glycosuria
B Reduced eGFR
C Euglycaemic ketosis
D Hypoglycaemia

Answer 131

least likely hypoglycaemia?? , they can cause all of these things..

“2019 blue book article

Initial increase in Cr which normalises over time”

“2019 blue book article Initial increase in Cr which normalises over time

https://www.tga.gov.au/sites/default/files/auspar-empagliflozin-171026-pi.pdf SGLT2-i monotherapy does not cause hypoglycaemia”

Question 132

133 Buprenorphine patch stopped, when will plasma levels drop by 50%

“12
24
48
72
“

Answer 132

12h

The plasma concentration of buprenorphine decreases by approximately 50% within 12 hours after removal of the transdermal patch, with a reported range of 10–24 hours[1][2]. This initial decline reflects the gradual depletion of the subcutaneous depot of buprenorphine that persists after patch removal. The pharmacokinetic profile is characterized by a biphasic elimination pattern, where the rapid initial decline (median 12 hours) transitions to a slower terminal elimination phase with a half-life of ~26 hours[1][5][7].

Rationale:
- Direct evidence from multiple manufacturer studies (NORSPAN® and BuTrans®) demonstrates a 50% plasma reduction within 12 hours post-removal[1][2].
- The 26-hour terminal half-life cited in other sources[3][5] refers to the subsequent elimination phase after the initial 50% drop, not contradicting the rapid initial decline.
- Clinical guidelines emphasize withholding subsequent opioids for ≥24 hours after patch removal due to this pharmacokinetic profile[2][5].

Correct Answer:
12 hours

Citations:
[1] https://www.researchreview.com.au/MUND0082PI.pdf
[2] https://www.purdue.ca/wp-content/uploads/2021/09/BUTRANS-PM-E-Jul2021.pdf
[3] https://www.drugs.com/medical-answers/long-buprenorphine-stay-system-3566034/
[4] https://www.rxfiles.ca/rxfiles/uploads/documents/butrans-qanda.pdf
[5] https://www.safercare.vic.gov.au/sites/default/files/2021-02/GUIDANCE_Opioid%20Conversion%20FINAL_0.pdf
[6] https://academic.oup.com/painmedicine/article/19/10/1988/4283321
[7] https://www.tga.gov.au/sites/default/files/auspar-buprenorphine-161213.pdf
[8] https://reference.medscape.com/drug/butrans-buprenorphine-transdermal-999581
[9] https://pmc.ncbi.nlm.nih.gov/articles/PMC3004620/
[10] https://www.nps.org.au/medicine-finder/norspan-5-transdermal-patch
[11] https://www.nps.org.au/medicine-finder/buprenorphine-sandoz
[12] https://pmc.ncbi.nlm.nih.gov/articles/PMC1661652/
[13] https://academic.oup.com/painmedicine/article-pdf/19/10/1988/25842049/pnx235.pdf
[14] https://pmc.ncbi.nlm.nih.gov/articles/PMC6822392/
[15] https://healthpsychologyresearch.openmedicalpublishing.org/article/27241-buprenorphine-for-chronic-pain-a-safer-alternative-to-traditional-opioids
[16] https://www.medicines.org.uk/emc/product/10079/smpc

APMSE
Steady state reached after 3d
Terminal t1/2 12h
vs
Fent patch onset 12-24h
t1/2 17h”

Question 133

134 Autonomic dysreflexia is more likely seen in spinal lesions at the level of:

“T5 incomplete injury
T5 complete injury
T10 incomplete
T10 complete”

Answer 133

50-70% above T6, and more likely if complete

https://www.bjaed.org/article/S2058-5349(17)30152-X/pdf

Question 134

135 5 kPa is approximately equivalent to:

“37 mmHg
45 mmHg”

Answer 134

5 x 7.5= 37.5mmHg

its in the blue book article about hyperbaric medicine: 1kpa = 7.5mmHg

Question 135

136 Baby swallows battery, what to give

Answer 135

Honey

“50-150ml 0.25% sterile acetic acid to neutralise residual alkali (LITFL), sulcrafate recommended by USA Poisons centre.

RCH: Honey at home, suculfate in ED”

Question 136

137 Risk of AFE is highest in:

“Caesarean
Induction of labour
Labour augmented by oxytocin infusion”

Answer 136

Induction

https://www.bjaed.org/article/S2058-5349(18)30060-X/fulltext. “strong evidence that induction of labour by any method increases the risk of AFE”

Question 137

138. You have induced a patient (I forget this part) and ten minutes later - reduced air entry left side, sats 85%, hypotensive. Lung USS on the left side shows no sliding and a lung point sign.

”- Left needle decompression 2nd IC space
- Left chest drain insertion
- Left finger thoracostomy
- Pull the ETT back 2cm
- Get a chest XR”

Answer 137

BMJ says needle decompression first, then definitive rx with ICC to follow

“https://qualitysafety.bmj.com/content/qhc/14/3/e18.full.pdf. Crisis management during anaesthesia: pneumothorax
“

Question 138

139. Compared with open mechanical aortic valve repair, TAVI has:

• Reduced mean gradient
• Reduced vascular injury
• Reduced arrhythmia
• Reduced paravalvular leaks

Answer 138

TAVI: reduced
1. all cause mortality,
2. stroke,
3. AKI
4. new onset AF (arrhythmias),
5. major bleed
6. anticoag requirement
7. LOS reocvery time

TAVI higher
1. major vascular complication (haematoma, dissection, retroperitoneal bleeding)
2. PPM (LBBB and PPM dependency)
3. Paravalvular leak (PVL)

No difference = mean gradient

TAVI: >80yo or life expectancy < 10 years

2019 European heart journal https://www.escardio.org/Sub-specialty-communities/European-Association-of-Percutaneous-Cardiovascular-Interventions-(EAPCI)/Research-and-Publications/Commented-articles/transcatheter-aortic-valve-implantation-vs-surgical-aortic-valve-replacement-fo

Question 139

140. The number of segments in the left lower lobe of the lung is:

-3
-4 four
-2

Answer 139

“four bronchopulmonary segments:

superior segment
anteromedial segment
lateral segment
posterior segment”

radiopedia

Question 140

141. Current ANZCA recommendations for a child 7 months old fasting prior to surgery are:

• Clear fluids one hour, breast milk 3 hours
• Clear fluids two hours, breast milk 3 hours

Answer 140

CF 1h, Br milk 3 hours

< 12 mo: 1:3:4
> 12 mo: 1:3:6
CF:BF:Formula
CF 3mL/kg/hr

PG07 https://www.anzca.edu.au/resources/professional-documents/guidelines/ps07-guidelines-on-pre-anaesthesia-consultation-an

Question 141

142. In relation to ECHO, TAPSE refers to:

• right ventricular contraction
• Tricuspid valve something

Answer 141

RV contraction from these options

“LITFL https://litfl.com/right-ventricular-function-and-haemodynamic-assessment-echocardiography/. measure of RV Systolic function:
TAPSE (Tricuspid Annular Plane Systolic Excursion) normal is >1.7cm (less useful post some cardiac surgery) [measured in AP4C w/ M Mode]”

Question 142

143. EPO given peri-operatively

a) Less transfusion, same thrombosis
b) Less transfusion, more thrombosis
c) No change in transfusion or thrombosis
d) No change in transfusion, more thrombosis

Answer 142

Answer:
a) Less transfusion, same thrombosis

I think this was remembered incorrectly, BJA says decreased transfusion in cardac and ortho patients, and INCREASED mortality and thrombotic complications therefore dont give to surgical patients , as per NICE guidelines

Impact of Preoperative Erythropoietin on Transfusion Requirements and Thrombotic Risk in Major Surgery

The administration of erythropoietin-stimulating agents (ESAs) prior to major surgery has emerged as a critical component of patient blood management strategies. A synthesis of evidence from randomized controlled trials and meta-analyses demonstrates that preoperative erythropoietin significantly reduces the need for allogeneic blood transfusions without increasing the risk of thromboembolic complications. This conclusion holds across diverse surgical contexts, including cardiac, orthopedic, and general elective procedures.

Mechanisms of Erythropoietin in Preoperative Optimization

Erythropoiesis Stimulation and Hemoglobin Augmentation
Erythropoietin functions by binding to receptors on erythroid progenitor cells in the bone marrow, stimulating red blood cell production and increasing hemoglobin concentrations[1][6]. In surgical patients with preoperative anemia, this mechanism directly addresses the oxygen-carrying capacity deficit, reducing reliance on transfusions. Meta-analyses report that ESA administration elevates preoperative hemoglobin by 1.2–1.8 g/dL compared to placebo, with sustained effects into the postoperative period[3][7].

Synergy with Iron Supplementation
The efficacy of erythropoietin is enhanced when combined with intravenous iron, which addresses underlying iron deficiency present in 40–60% of anemic surgical patients[6]. This combination therapy corrects both erythropoietic drive and substrate availability, achieving hemoglobin optimization in 75–90% of cases[7].

Transfusion Reduction Across Surgical Specialties

Cardiac Surgery
In coronary artery bypass grafting and valve replacement procedures, preoperative erythropoietin reduces transfusion rates by 45% (risk ratio [RR] 0.55, 95% CI 0.37–0.81)[1]. This effect persists despite the high baseline transfusion risk in cardiac operations, where 50–60% of patients typically require blood products[4].

Orthopedic Surgery
Total hip and knee arthroplasty data demonstrate even greater benefit, with a 64% reduction in transfusion requirements (RR 0.36, 95% CI 0.28–0.46)[1]. Erythropoietin-treated patients maintain higher hemoglobin levels at all perioperative time points—preoperative (12.1 vs 11.3 g/dL), postoperative day 1 (10.4 vs 9.1 g/dL), and discharge (11.2 vs 10.1 g/dL)[3].

General Surgery
For non-cardiac procedures, ESA therapy decreases transfusion risk by 17% (RR 0.83, p=0.049) while reducing mean units transfused per patient from 1.8 to 1.2[7]. These outcomes are particularly significant in cancer resections, where anemia prevalence exceeds 30%[8].

Thrombotic Safety Profile

Venous Thromboembolism Risk Analysis
Pooled data from 28 randomized trials (n=4,750 patients) show no increased risk of deep vein thrombosis or pulmonary embolism with erythropoietin use (RR 1.02, 95% CI 0.78–1.33)[1][4]. This finding contradicts earlier concerns derived from oncology studies, where ESAs increase thrombosis risk by 93% (OR 1.93, p500 mL
- Contraindications to autologous donation
- Iron deficiency (ferritin <100 ng/mL or transferrin saturation <20%)[7]

Economic and Logistical Considerations

Cost-Benefit Analysis
While ESA therapy adds $800–$1,200 per patient, this is offset by:
- 56% reduction in transfusion costs ($320 saved per unit avoided)
- $2,100 average savings from shorter hospitalization
- $4,800–$7,500 per quality-adjusted life year gained through complication avoidance[6]

Blood Supply Implications
Widespread ESA adoption could decrease perioperative transfusion demand by 18–22%, enhancing blood bank sustainability during shortages[1][4].

Conclusion

Preoperative erythropoietin administration safely reduces allogeneic blood transfusion requirements across surgical specialties without increasing thrombotic risk. This dual benefit—achieved through physiological erythropoiesis stimulation and adherence to standardized thromboprophylaxis—positions ESAs as a cornerstone of modern blood management programs. Future research should focus on protocol standardization and long-term outcomes in high-risk subgroups.

Answer:
a) Less transfusion, same thrombosis

Citations:
[1] https://pubmed.ncbi.nlm.nih.gov/30649068/
[2] https://pubmed.ncbi.nlm.nih.gov/39168487/
[3] https://www.dovepress.com/a-meta-analysis-and-systematic-review-evaluating-the-use-of-erythropoi-peer-reviewed-fulltext-article-TCRM
[4] https://journals.lww.com/anesthesia-analgesia/fulltext/2019/05000/preoperative_erythropoietin_vs_placebo__what_does.1.aspx
[5] https://ashpublications.org/ashclinicalnews/news/2547/Erythropoiesis-Stimulating-Agents-and-the-Risk-of
[6] https://www.cochrane.org/CD012451/ANAESTH_use-erythropoietin-plus-iron-correct-anaemia-surgery-reduce-risk-blood-transfusion
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC8885371/
[8] https://cco.amegroups.org/article/view/1347/html

https://watermark.silverchair.com/mkw061.pdf

Question 143

Dabigatran - which test is test for monitoring from a standard coags test (unsure if “standard” was used in the previous repeat of this Q)

Answer 143

?
TT - most sensitive
Ecarin Clotting Time

aPTT - qualitative

Perplexity