Random FFICM Questions Flashcards

1
Q

What causes a high mixed venous oxygen saturation (SvO2)?

A

↑ SvO2

• ↑ O2 delivery, e.g.
↑ FiO2, hyperbaric O2
• ↓ O2 extraction,
e.g. hypothermia, general anaesthetic, neuromuscular blockade
• ↑ Flow states, e.g. sepsis, thyrotoxicosis, severe liver disease

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2
Q

What causes a low mixed venous oxygen saturation (SvO2)?

A

↓ SvO2

• ↓ O2 delivery, e.g. shock states, hypoxemia, anaemia
• ↑ O2 extraction, e.g. hyperthermia, shivering, pain, seizures

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3
Q

What is a mixed venous oxygen saturation (SvO2)?

A

SvO2 is obtained from a pulmonary artery catheter. It measures the end result of O2 consumption and delivery, and contains blood from both the SVC and IVC. The normal range is approximately 65–70%.

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4
Q

What is ScvO2?

A

ScvO2 measures oxygen saturation in the SVC, taken from an internal jugular, subclavian or axillary vein catheter and is sometimes used as a surrogate for SvO2.

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5
Q

What is the relationship between SvO2 and ScvO2?

A

Typically, in healthy individuals, SvO2 > ScvO2 because the brain (SVC-drained) has a higher oxygen demand compared to organs like the kidneys (IVC-drained) with lower oxygen demands.
ScvO2 can surpass SvO2 in cases where the brain’s metabolic requirement decreases, such as during anaesthesia, in TBI, or in shock, when body oxygen extraction increases, which leads to reduced oxygen saturation in the IVC.

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6
Q

What is functional residual capacity (FRC)?

A

• FRC = expiratory reserve volume + residual volume.

• It is the volume of air in the lungs after normal expiration, measured by either gas dilution or body plethysmography.

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7
Q

What factors affect functional residual capacity (FRC)?

A

↑ FRC :
• Standing position
• Asthma/COPD
• PEEP/CPAP

↓ FRC
• Supine position
• Obesity
• Pregnancy
• Restrictive lung disorders
• General anaesthesia

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8
Q

What should be the normal cuff pressure of a tracheostomy and how often should it be checked and why?

A

20–30 cm H2O
It should be checked every 8–12 hours, (or more frequently depending on the clinical picture)
Higher cuff pressures may compress tracheal capillaries, limit blood flow, and predispose to tracheal necrosis (ischaemic damage).

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9
Q

What is the difference between cardiac output and cardiac index and what are their normal values?

A

• Cardiac Output = Heart Rate × Stroke Volume
Normal range ~ 4–8 L/min
• Cardiac Index = Cardiac Output/Body
Surface Area
Normal range ~ 2.5–4 L/min

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10
Q

What is the physiological role of C‐reactive protein?

A

• A pentraxin protein synthesised in the liver
• ↑ In response to inflammation
• Binds to phosphocholine on the surface of dead/dying cells, which activates the complement system

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11
Q

Which cardiac structural abnormality may the presence of a right bundle branch block in a young adult indicate?

A

Atrial septal defect

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12
Q

What are some of the causes of a raised MCV?

A

DRAMATIC

D - Drugs, e.g. anticonvulsants, antimicrobials, chemotherapy
R - Reticulocytosis
A - Alcohol abuse
M - Megaloblastic anaemia, e.g. pernicious anaemia, B12/folate deficiency
A- Artefact, e.g. aplasia, myelofibrosis, hyperglycaemia, cold agglutinins
T - Thyroid (hypothyroidism)
I - Immature bone marrow cells, e.g. myelodysplastic syndrome
C - Chronic liver disease

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13
Q

What is the dose of IV salbutamol in treating life‐threatening asthma, and what are some side effects?

A

• Dose: 3–20 mcg/min

• Side effects: tachycardia, arrhythmias,
tremors, hyperglycaemia, hypokalaemia, and type B lactic acidosis

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14
Q

What are the mechanisms of drug‐induced hyperkalaemia?

A

K+ supplements
• Sando-K
• IV fluids with K+

Drugs that impair K+ distribution
• Beta blockers
• Arginine
• Digoxin
• Suxamethonium

Drugs that ↓ renal K+ excretion
• Calcineurin inhibitors, e.g. tacrolimus and ciclosporin
• Potassium-sparing diuretics,
e.g. spironolactone,
eplerenone
• Some antibiotics, e.g.
trimethoprim

Drugs that impact on the RAAS
• NSAIDs
• ACE inhibitors, ARBs
• Heparin

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15
Q

When do you control hypertension in the first 24 hours after an acute ischaemic stroke according to NICE?

A

NICE advises against actively managing hypertension during this period, except in the following situations:

• To facilitate thrombolysis–target BP < 185/110.
• In cases of pre-eclampsia, aortic dissection, or hypertensive encephalopathy/nephropathy/cardiac failure.

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16
Q

What percentage TBSA burn would meet the criteria for referral to a burns centre on area alone?

A

> 40% Total Body Surface Area (TBSA)

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17
Q

Where is propofol predominantly metabolised?

A

Liver: Hepatic metabolism, primarily via glucuronidation and sulfation pathways.

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18
Q

What is the dose of IV magnesium in the management of acute asthma, and how does it work as a bronchodilator?

A

Dose:
1.2–2 g IV over 20 minutes

Mechanism as a bronchodilator:
1. Calcium blocker in bronchial smooth muscle
2. ↓ Ach release at the NMJ
3. ↑ Sensitivity of β-receptors to catecholamines

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19
Q

What is the Parkland formula for IV fluid replacement after a burn, and does it take into account pre-hospital fluid administration?

A

4 mL/kg/%TBSA over 24 hours

Half of total is given in the first 8 hours after the injury.

When calculating TBSA, erythematous regions are omitted unless there is additional blistering or underlying evidence of a partial- thickness burn.

This formula takes into account pre- hospital fluid administration. Therefore, any prehospital fluid is subtracted from total.

Aiming for 0.5ml/kg/hour urine output

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20
Q

What did the PROPPR trial (2015) demonstrate for blood product administration in a 1:1:1 ratio compared to a 1:1:2 plasma:platelet:red
cell ratio in patients with severe trauma and major bleeding?

A

• No difference in all-cause 24-hour or 90-day mortality
• Post-hoc analysis found a significant reduction in death by exsanguination within the first 24 hours and a higher rate of achieving haemostasis in the 1:1:1 group compared to the 1:1:2 group.

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21
Q

What are the 12 physiological variables of the APACHE II score, how do you calculate the score and what does it mean?

A

CNS:
GCS
CVS:
MAP
HR
Resp:
RR
PaO2
Renal:
Arterial pH
Na+
K+
Creatinine
Micro/Haem:
Temperature
WCC
Hct

The worst of these variables within the first 24 hours of critical care admission is used

Effects of age and chronic health are incorporated to give a single score with a maximum of 71. A score of >25 represents a predicted mortality of >50%.

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22
Q

What dose of adrenaline do you give in adult anaphylaxis?

A

IM: 0.5–1mL of 1:1,000 (0.5–1mg)
OR
IV: 0.5–1mL of 1:10,000 (50–100 mcg)

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23
Q

What is the difference between intra‐ abdominal hypertension (IAH) and abdominal compartment syndrome (ACS), and how do you measure intra-abdominal pressure (IAP)?

A

• IAH: sustained or repeated pathological elevation of IAP ≥ 12 mmHg
• ACS: sustained IAP > 20 mmHg + new organ dysfunction/failure +/− abdominal perfusion pressure (APP) < 60 mmHg

IAP is measured:
• Direct: puncture of the abdominal cavity
• Indirect: via a urinary catheter in the bladder or a balloon-tipped catheter inserted into the stomach. Correlates well with direct measurements but can be inaccurate when there are adhesions, pelvic fractures, and abdominal packs.

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24
Q

Where in adults does the trachea start and divide anatomically?

A

• Starts at C6
• Extends to T4 where it bifurcates
• It is approximately 10–12 cm long
• The right main bronchus separates at a
25° angle and the left main bronchus separates at a 45° angle.

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25
Q

What is the evidence for a decompressive hemicraniectomy (DH) in malignant middle cerebral artery syndrome according to the DECIMAL (2007), HAMLET (2009) and DESTINY II (2011) trials?

A

• Mortality: Decompressive hemicraniectomy significantly reduces mortality compared to conservative treatment in all three studies. This benefit appears to be particularly strong when surgery is performed early (within 48 hours) after stroke onset.
This was observed in younger patients (18–55 years in DECIMAL) and older patients (≥61 years in DESTINY II), as well as in the varied population of HAMLET.

• Neurological Disability: The findings on functional outcome are more complex and are potentially dependent on factors like age, stroke severity, and time to surgery:
Decompressive hemicraniectomy did not significantly improve the proportion of patients achieving a ‘good’ functional outcome (mRS ≤ 3) at 6 or 12 months in DECIMAL and HAMLET.
However, it significantly increased the proportion of patients achieving a ‘moderate’ functional outcome (mRS ≤ 4) at six months in DECIMAL and DESTINY II.
Notably, no surviving patients in DESTINY II achieved the best possible functional outcome (mRS 0–2).

Overall: Decompressive hemicraniectomy offers a clear and substantial mortality benefit. While it may not guarantee good recovery and return to pre-stroke levels of function, it can increase the chances of achieving moderate disability as opposed to severe disability or death. This decision requires individualised assessment and MDT involvement.

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26
Q

How do you distinguish between moderate, severe and life-threatening acute asthma?

A

Moderate PEFR > 50%
No features of severe asthma

Severe PEFR 33–50%
RR ≥ 25
HR ≥ 110
Inability to complete sentences in one breath

Life‐threatening
Features of severe asthma + at least one of:
• PEFR < 33%
• SpO2<92%
• Normal or ↓ PCO2: implies poor ventilation
• Cyanosis, confusion or coma
• Hypotension or ↓ HR
• Exhaustion or poor
respiratory effort
• Silent chest
• Tachy(arrhythmia)

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27
Q

When is it safe to use suxamethonium after a significant burn injury?

A

• Within the first 24 hours after the burn
• One year after the burn

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28
Q

How do you calculate the internal diameter of an endotracheal tube in the paediatric population?

A

Cuffed : [age / 4] + 3.5

Uncuffed : [age / 4] + 3.5 + 0.5

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29
Q

What is the recommended therapeutic management for a variceal haemorrhage that continues to bleed despite pharmacological intervention, endoscopic banding and balloon tamponade?

A

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

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30
Q

When is damage control surgery more preferable than definite surgery in trauma?

A

When there is severe haemorrhagic shock and/or ongoing bleeding.

This is particularly necessary if the lethal diamond is present (hypothermia, acidosis, coagulopathy and hypocalcaemia) and in patients who have inaccessible major venous injuries or those who require time-consuming procedures.

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31
Q

What risk is associated with the administration of suxamethonium after a spinal cord injury, and how soon after the injury does this risk occur?

A

• Life-threatening hyperkalaemia
• 72 hours after spinal cord injury

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32
Q

How is the rapid shallow breathing index (RSBI) useful as a weaning predictor?

A

RSBI = RR / Tv (TV in Litres not mls)

• RSBI < 105: 80% chance of successful extubation
• RSBI >105: strongly suggests weaning failure

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33
Q

What happens to pulmonary artery pressure after a cardiac arrest?

A


Multifactorial reasons why this may occur include:

Post-ROSC
o ↑ PVR secondary to hypoxia/acidosis o ↑ PAP secondary to cardiac dysfunction as part of post-cardiac
arrest syndrome

Precipitant of cardiac arrest
o ↑ PAP secondary to cardiac
dysfunction (e.g. STEMI) or pulmonary embolism

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34
Q

What is meant by intention to treat analysis in a randomised controlled trial?

A

• All participants are analysed based on their originally assigned treatment groups, regardless of whether they completed or received the intended treatment.
• This approach helps maintain the randomisation and avoids biases caused by crossover or dropout.

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35
Q

Which clinical features in someone with a burn may indicate the need for early intubation?

A

• GCS<8
• Respiratory distress or failure
• Noticeable swelling or blistering in the lips, tongue or oropharynx
• Voice changes, e.g. hoarseness or stridor
• Singed nasal hair
• Carbonaceous sputum
• Extensive burns of the face or neck,
including circumferential burns

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36
Q

How does digoxin work in treating atrial fibrillation with a fast ventricular rate?

A

Direct:
Inhibits cardiac Na+/ K+-ATPase causing an
↑ Intracellular Na+ which leads to
Exchange of Na+ for Ca2+ via the Na+/Ca2+ pump causing
↑ Intracellular Ca2+ and↓ Intracellular Na+

↑ Intracellular Ca2+ causes ↑ cardiac contraction
↓ Intracellular Na+ prolongs refractory time of the bundle of His

Indirect:
↑ Acetylcholine at cardiac muscarinic receptors
Resulting in prolongation of the refractory period at the AV node and bundle of His

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37
Q

Which alternative drug can be used in the management of AVNRT if adenosine is contraindicated?

A

Verapamil 2.5–5 mg IV

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38
Q

Why may someone with primary hyperaldosteronism (Conn’s syndrome) develop muscle weakness and tetany?

A

Due to hypokalaemic metabolic alkalosis
Conn’s syndrome causes a low renin hypertension.
It is diagnosed by a ↑ aldosterone:renin ratio.

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39
Q

What modifications have been implemented in advanced life support algorithms for resuscitating individuals with hypothermia?

A

• Refrain from administering adrenaline or any other drugs until the temperature is >30°C.

• When the temperature ranges from 30°C to 35°C, double the dose intervals for ALS drugs.

• In cases of VF, consider delivering up to three shocks if needed, but hold off on further shocks until the temperature is >30°C.

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40
Q

What is the most likely diagnosis if someone develops hypocalcaemia and seizures two days after starting chemotherapy?

A

Tumour lysis syndrome (TLS) – electrolyte abnormalities can precipitate neurological dysfunction.

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41
Q

What are the common biochemical abnormalities seen in tumour lysis syndrome?

A

Common abnormalities include:
• ↓ Calcium
• ↑ Phosphate, potassium, urate, LDH,
lactate

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42
Q

What causes and what cancers are associated with Tumour Lysis Syndrome?

A

TLS is due to the sudden and large-scale death of cells following the initiation of chemotherapy. It is often associated with acute leukaemias and high-grade lymphomas, e.g. Burkitt’s.

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43
Q

What are the most likely causes for developing drowsiness one week after undergoing endovascular coiling for a subarachnoid haemorrhage, when a CT scan indicates no rebleeding, infarction or hydrocephalus?

A

• Delayed cerebral ischaemia (DCI)
o Cerebral vasospasm
o Local hypoperfusion or disordered
autoregulation

• Non-convulsive seizures

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44
Q

What’s the rationale for including clindamycin or linezolid alongside broad- spectrum antibiotics in the treatment of necrotising fasciitis?

A

For the termination of toxin production

45
Q

Besides hypothermia, what are some alternative reasons for the presence of J-waves on an ECG?

A

Normal variant (early repolarisation)
HABIT:
Hypercalcaemia
Angina – vasospastic
Brain injury including a subarachnoid
haemorrhage
Idiopathic ventricular fibrillation
Type 1 Brugada syndrome

46
Q

When would you consider placing an inferior vena cava (IVC) filter after a pulmonary embolism (PE)?

A

• If anticoagulation is contraindicated, e.g. the bleeding risk is very high

• If thrombosis has recurred despite adequate anticoagulation

• If temporary cessation of anticoagulation within one month is anticipated, e.g. pregnant patients within one month of the expected date of delivery

IVC filters have no long-term mortality benefit. As foreign material, they are thrombogenic (↑ incidence of DVT).

47
Q

What is the utility of the LRINEC (Laboratory Risk Indicator for Necrotising Fasciitis) score?

A

• The LRINEC score distinguishes necrotising fasciitis from other soft tissue infections, e.g. cellulitis.
• The score incorporates CRP, WCC, Hb, sodium, creatinine and glucose.
• A LRINEC score of ≥6 could be used as a potential tool to rule in necrotising fasciitis, but a score <6 should not be used to rule out the diagnosis.
• A score ≥8 has a positive predictive value >90%.

48
Q

Is it necessary to check digoxin levels during and after administering digoxin‐specific antibody fragments for digoxin toxicity?

A

No – the assay measures both digoxin bound to antibody fragments and free digoxin. This overestimates free levels.

49
Q

What fibrinogen level may warrant administering cryoprecipitate in a trauma patient?

A

Fibrinogen < 1.5–2 g/L

50
Q

What is the normal axis for left ventricular depolarisation in an adult, and what are the Sokolow-Lyon criteria for left ventricular hypertrophy (LVH)?

A

• Normal axis: −30 to +90 degrees
• LVH: If the height of the R wave in
V5/6 + the depth of the S wave in V1/2 is
≥35 mm
• The most common cause of LVH is
hypertension

51
Q

What are the two pathways of coagulation?

A

Intrinsic Pathway (APTT): Factors 8, 9, 11, 12
Extrinsic Pathway (PT): Factors 3, 7
Joint: Factors 2, 5, 10, prothrombin, fibrinogen

52
Q

Which substances are primarily responsible for crystal nephropathy in tumour lysis syndrome?

A

Uric acid and calcium phosphate

↑ Cell turnover →
↑ purine metabolism →
↑ serum urate↑ Cell lysis →
↑ serum phosphate which binds
to calcium

Uric acid precipitates readily in the presence of calcium phosphate, and calcium phosphate precipitates readily in the presence of uric acid.

53
Q

According to the BTS guidelines, when do you insert a chest drain for a spontaneous pneumothorax (PTX)?

A
  1. Primary PTX when aspiration fails. Aspiration is indicated for a primary PTX when breathless and/or size is >2 cm.
  2. Secondary PTX when aspiration fails. Aspiration is indicated for a secondary PTX when the size is 1–2 cm.
  3. Secondary PTX when the patient is breathless and/or the size of the pneu- mothorax is >2 cm.
54
Q

What clinical feature would indicate a
haemodynamically unstable pulmonary embolism (previously called a massive or high-risk PE)?

A

Significant hypotension:
Blood pressure of <90 mmHg OR a drop of >40 mmHg from baseline, which is not explained by something else, e.g. arrhythmia, hypovolaemia or sepsis.

55
Q

What makes ketamine effective in enhancing lung function and alleviating bronchospasm in asthma?

A

It is a bronchodilator.
It is a phencyclidine derivative. It has
little effect on the laryngeal reflexes,
and a patent airway can often be maintained. However, it can induce ↑ secretion production, potentially leading to laryngospasm due to these retained reflexes.

56
Q

What CT features are associated with an increased severity of acute pancreatitis?

A

• Extensive fat stranding
• Peri-pancreatitis fluid collections
• Pancreatic necrosis

57
Q

On which side of the body do traumatic diaphragmatic injuries tend to occur?

A

Left

58
Q

What are the principles of ventilating someone with life‐threatening asthma and which strategies can achieve this?

A

Principles:
Lung protective ventilation:
• Limit peak and
mean airway
pressures
• Allow for a prolonged
expiratory time
• Maintain adequate
oxygenation

Strategies:
• ↓ Tidal volume
• ↓RR
• ↓ Or removal of
extrinsic PEEP
• ↓ Inspiratory time or
↑ expiratory time
• Permissive
hypercapnia
• Intermittent
disconnection from ventilator and manual chest decompression

59
Q

Why should care be taken when giving flumazenil?

A

It reverses the effects of benzodiazepines.
It has a relatively short half-life when compared to benzodiazepines and has a risk of provoking seizures when administered.

60
Q

What do the Berlin criteria for ARDS entail?

A

Berlin criteria:

Timing:
Within one week of a known clinical insult or new/worsening respiratory symptoms

Oxygenation (P/F ratios):
PaO2/FiO2 < 40 kPa (≤300 mmHg) with a minimum PEEP of
5 cm H2O
• Mild ≤ 39.9 kPa
• Moderate ≤ 26.6 kPa
• Severe ≤ 13.3 kPa

CXR or CT:
Bilateral opacities not explained by effusions/collapse/nodules

Origin of oedema:
Respiratory failure NOT fully explained by cardiac failure or fluid overload

61
Q

What are the four key recommendations of the New Global Definition of ARDS that expand upon the Berlin Criteria?

A

• Intubation is not required for making
a diagnosis. This includes patients on high-flow nasal oxygen (HFNO) ≥ 30 L/min or NIV/CPAP with end-expiratory pressure ≥ 5 cmH2O.

• Uses SpO2/FiO2 as an alternative to P/F to assess oxygenation. A SpO2/ FiO2 ≤ 315 + SpO2 ≤ 97% is indicative of compromised oxygenation.

• The requirement of bilateral lung opacities as an imaging criterion remains, but now includes using ultrasound, provided it is performed by a well-trained operator.

• In settings with limited resources, the following are not essential for diagnosis: PEEP, specific oxygen flow rates, or particular types of respiratory support devices.

62
Q

Which ion has the most significant impact on the resting potential of neural tissue?

A

Potassium – This has a large concentration gradient across the cell membrane and the greatest permeability at rest.

Every cell membrane has a transmembrane potential difference of –70 mV. This difference is dependent on two factors: The transmembrane concentration gradient and the permeability of the membrane to the ions.

63
Q

What are some general respiratory changes that occur by the third trimester of pregnancy?

A

Increases:
TV, RR, pH, PaO2, Maternal 2,3-DPG

Decreases:
Chest wall compliance, airway resistance, FRC, Bicarb, PaCO2

Lung compliance stays the same

64
Q

What is the pathogenesis of hepatic encephalopathy (HE) in chronic liver disease and what are some treatment options?

A

• Pathogenesis:
HE occurs when the
liver cannot remove ammonia from enteric sources. This ammonia enters the systemic circulation. It goes to the brain to cause neurotoxicity and cerebral oedema.

• Management:
Treat any precipitating factor, e.g.
SBP, UGIB, electrolyte disturbances. May also need organ support on ICU, e.g. for ↓ GCS in Grade 4 HE

Lactulose & Rifaximin: ↓ Ammonia levels in the gut by ↑ transit time and ↓ bacterial numbers

LOLA: Removes ammonia from the blood through extrahepatic metabolism of ammonia to glutamine. This treatment is not widely available and has little evidence of benefit.

65
Q

Which parameters on a blood gas are directly and indirectly measured?

A

• Direct: pH, PaO2, PaCO2
• Indirect: Standard bicarbonate, base
excess, SaO2

66
Q

How do you treat prilocaine toxicity?

A

Methylthioninium chloride (methylene blue) 1 mg/kg IV

• Prilocaine is metabolised in the liver to O-toluidine.
• O-toluidine oxidises haemoglobin into methaemoglobin.
• Methaemoglobin has ↓ oxygen-carrying capacity resulting in cyanosis.
• Methylene blue accelerates the reduction of methaemoglobin.

67
Q

How do you distinguish between
hyperacute, acute and subacute liver failure using the O’Grady classification?

A

Acute liver failure is triad of jaundice, coagulopathy and encephalopathy. It is classified according to the time from the onset of jaundice to the development of encephalopathy:
• Hyperacute disease: <7 days
• Acute disease: 1–4 weeks
• Subacute disease: 4–12 weeks

68
Q

What is meant by pulsus paradoxus and in which clinical contexts may it be present?

A

An amplification of the typical drop in systolic BP during inhalation by >10 mmHg. When severe, the radial pulse vanishes during inspiration.
The ‘paradox’ is that the pulse disappears despite cardiac contraction. It is often due to pericardial disease, particularly cardiac tamponade, but can occur in many contexts including (‘PRACTICE’):
• Pulmonary embolism
• RV infarction and Restrictive
cardiomyopathy
• Asthma and COPD (severe)
• Cardiac tamponade and Constrictive
pericarditis
• Tension pneumothorax
• Iatrogenic during surgery
• Compression (obesity, pectus
excavatum)
• Effusions (large bilateral pleural effusions)

69
Q

What ECG pattern has developed if a person who took a large quantity of cocaine now has ST elevation in V 1-3 and T wave inversion in V 1-2?

A

Drug induced Brugada

70
Q

What type of lung injury does a titrated PEEP strategy aim to decrease when treating ARDS?

A

Atelectotrauma

71
Q

What are the King’s criteria for non‐ paracetamol‐induced acute liver failure?

A

INR > 6.5
(PT > 100 seconds)

OR

Any three of the following:
• Aetiology: Non-A, non-B hepatitis or idiosyncratic drug reaction
• Bilirubin > 300 μmol/L
• Age < 11 or > 40 years
• INR > 3.5 (PT > 50 seconds)
• Time from onset
of jaundice to encephalopathy > 7 days

72
Q

Which three clinical signs make up Beck’s triad in acute pericardial tamponade?

A

• ↓BP
• ↓ Heart sounds (quiet/muffled)
• ↑ CVP – distended neck veins

73
Q

How does mannitol reduce intracranial pressure (ICP)?

A

Mannitol is a diuretic and ‘free radical scavenger’. It is freely filtered through the glomerulus and is not re-absorbed. It decreases ICP in two main ways:

Immediate (Plasma Expansion):
Plasma expansion results in:↓ Blood viscosity↑ Intravascular volume ↑ Cardiac output
Overall, these effects result in ↑ regional cerebral blood flow and compensatory cerebral vasoconstriction in brain regions where autoregulation is intact

Delayed (Osmotic):
↑ Plasma osmolality → shifts water from cerebral extracellular space into plasma → ↓ cerebral oedema (if the BBB is intact)

74
Q

Which arrhythmias can cause cannon‐A waves in the JVP waveform?

A

• Complete heart block
• Ventricular tachycardia
• Junctional rhythms including AVNRT

75
Q

Which complication of heparin therapy carries the highest mortality?

A

Type 2 HIT (heparin-induced thrombocytopaenia) due to arterial/venous thrombotic complications

Type 2 HIT: Onset time 5-14 days (compared to 1-4 in type 1), causes arterio/venous thrombosis, need to stop heparin and start alternative anticoagulant

76
Q

How may somatosensory evoked potentials (SSEPs) suggest poor neurological outcome post-cardiac arrest?

A

They test the somatosensory pathway integrity.
Stimulating a peripheral nerve, e.g. median nerve can be detected at the cortical level. The bilateral absence of the N20 spike on SSEP testing can be used as part of neuro-prognostication in predicting
poor neurological outcome in comatosed patients following cardiac arrest.

77
Q

What is the classical CSF finding in Guillain– Barré syndrome (GBS)?

A

Albuminocytological dissociation
(↑ CSF protein, normal glucose and no pleocytosis)

GBS is a post-infectious immune-mediated acute inflammatory demyelinating polyneuropathy (AIDP). The majority of cases occur within one month of a respiratory
or GI infection, e.g. Campylobacter
jejuni, Mycoplasma pneumoniae, CMV or EBV. The pathogenesis is a cross reaction
of antibodies with gangliosides in the peripheral nervous system. Anti-ganglioside antibodies (e.g. anti-GM1) are present in 25% of patients. The majority of cases exhibit Landry’s ascending paralysis, areflexia and autonomic dysfunction. Sensory symptoms tend to be mild/absent.

78
Q

Which reversal agent can you use to manage major bleeding in someone who takes dabigatran?

A

Idarucizumab–5 mg IV bolus

This is humanised monoclonal antibody fragment that binds to dabigatran and its metabolites.

HD or HF can also remove dabigatran.

79
Q

What are the RIFLE criteria for acute kidney injury?

A

Risk:↑ Cr × 1.5, >25% ↓in Egfr, UOut
<0.5 mL/kg/hr for 6 hrs

Injury:↑ Cr × 2, >50% ↓in Egfr, Uout
<0.5 mL/kg/hr for 12 hrs

Failure:↑ Cr × 3, Uout <0.3 mL/kg/hr for 24 hrs OR Anuria for 12 hrs

Loss: Loss of renal function > Four weeks

End stage: Loss of renal function > Three months

80
Q

Why is atropine ineffective for treating bradycardia in a heart transplant?

A

The heart is completely denervated. Therefore, the lack of a vagal input would prevent any anticholinergic effects of atropine. Sympathomimetic agents are used instead for chronotropy or inotropy.

81
Q

Which organism is most likely to cause right- sided infective endocarditis in an intravenous drug user?

A

Staphylococcus aureus

82
Q

How may hyperoxia cause harm in an acute myocardial infarction?

A

• Through free radical production
• Through coronary vasoconstriction

83
Q

What are the four mechanisms of AKI in rhabdomyolysis?

A
  1. Myoglobin combines with Tamm–Horsfall protein to form insoluble casts and tubular obstruction.
  2. Hyperuricaemia worsens this tubular obstruction.
  3. The haem moiety is directly nephrotoxic.
  4. There is inappropriate renal vasocon-striction because of hypovolaemia and third-spacing.
84
Q

Why may peripheral oedema develop in cor pulmonale if there is preserved ventricular function?

A

Chronic hypoxia causes sympathetic stimulation. This activates the renin– angiotensin–aldosterone system (RAAS) which results in fluid retention.

85
Q

What is meant by FVC, FEV1/FVC ratio, TLC and DLCO?

A

• FVC: Volume from maximal inspiration to maximal expiration
• FEV1/FVC ratio: The portion of FVC exhaled in the first second
• TLC: The total volume of gas in the lungs at maximal inspiration
• DLCO: Lung diffusion capacity for
carbon monoxide, approximating oxygen transfer from alveoli to red blood cells

86
Q

Which laxative class is least likely to cause diarrhoea?

A

Bulk-forming laxatives, e.g. psyllium, methylcellulose
These laxatives work by absorbing water in the intestine, which increases stool bulk and stimulates peristalsis.

87
Q

What is meant by pre‐excitation in electrophysiology?

A

There is an accessory pathway between the atria and ventricles. This prematurely activates the ventricles.

88
Q

How do you calculate static compliance?

A

Cstatic = Vt / (Pplat - PEEP)

89
Q

What are the two types of amiodarone‐ induced thyrotoxicosis (AIT)?

A

Pre‐existing thyroid disease?:
T1 - Often, T2 - No

Pathology:
T1 - Excessive hormone synthesis due to excess iodine found in amiodarone
T2 - Excessive release of preformed hormones due to thyroiditis

Goitre:
T1 - Mostly multinodular
T2 - Absent or small

Radioiodine isotope uptake:
T1 - Normal, T2 -↓/ absent

Thyroid ABS:
T1 - Present, T2 - Absent

IL‐6:
T1 - Normal/mildly raised, T2 - Very high

Treatment options:
T1:
• Stop amiodarone
• Antithyroid drugs
• K+ perchlorate
• Thyroidectomy
T2:
• Stop amiodarone
• Anti- inflammatory drugs, e.g. prednisolone

90
Q

When should you send blood for mast cell tryptase in anaphylaxis?

A

• Initial sample as soon as possible
• Second sample at 1–2 hours
• Third sample at 24 hours or in
convalescence

91
Q

Why may Torsades de Pointes (TdP) develop after giving amiodarone to treat atrial fibrillation?

A

Amiodarone prolongs the QT interval. QT prolongation increases the risk of TdP

92
Q

What are the five different types of myocardial infarction (MI)?

A

Type 1:
Acute coronary syndrome
Caused by coronary artery disease with atherothrombotic plaque rupture or erosion leading to either an occlusive or partially occlusive thrombus

Type 2:
Supply– demand imbalance
Myocardial cell death secondary to an oxygen supply–demand imbalance to the myocardium, e.g. septic shock, hypoxia or hypovolaemia

Type 3:
MI causing death
Symptoms indicative of MI with presumed new ECG changes or ventricular fibrillation, but biomarker samples not obtained before death
MI detected at autopsy
examination

Type 4:
PCI‐related
Type 4a: Procedure-related MI occurring 48 hours after PCI
Type 4b: MI due to stent or scaffold thrombosis following PCI
Type 4c: Restenosis associated with PCI

Type 5:
CABG‐ related
Procedural myocardial injury during or ≤ 48 hours after CABG/cardiac surgery

93
Q

What is normal pleural fluid pH and what pH would you expect in a parapneumonic effusion?

A

Normal: 7.6 - 7.66
Uncomplicated parapneumonic effusion: >7.2
Complicated parapneumonic effusion: <7.2
Empyema: Tis Pus

94
Q

How would you manage someone with longstanding atrial fibrillation with adverse signs if their INR was 1.3?

A

Sedation + synchronised DC cardioversion
The risk of embolisation (~6.8%) is outweighed by the need for urgent HR control.
There is no difference in the incidence of embolic phenomena between chemical or electrical; electrical cardioversion occurs faster.

95
Q

What are the grades of hepatic encephalopathy (HE)?

A

1:
Mild confusion,↓ Attention, Mild asterixis/ tremor

2:
Lethargy, Disorientation, inappropriate behaviour, Asterixis, slurred speech

3:
Somnolent but rousable, Bizarre behaviour, Rigidity, clonus, hyperreflexia

4:
Coma, Abnormal posturing

96
Q

What are some causes of an overdamped A-line trace?

A

• Tubing: Overly compliant, narrow or kinked
• Obstruction: Air bubbles, blood clots
• Pressure bag: Underinflated or low flush
bag pressure
• Connections: Loose connections in
the fluid-filled part of the electronic
monitoring system
• Artery: Arterial spasm

97
Q

What kind of inspiratory pattern does volume‐controlled ventilation produce?

A

Square inspiratory flow pattern

98
Q

What makes noradrenaline a suitable option to manage hypotension following elective surgery in someone with known severe aortic stenosis (AS) with a peak transvalvular gradient of 80 mmHg?

A

Noradrenaline → ↑ SVR → ↑ DBP → ↑ coronary perfusion
In severe AS, maintaining good coronary perfusion is essential as the LV is hypertrophied and prone to ischaemia if the DBP falls.
Drugs that ↓ afterload or ↑ heart rate (↓ diastolic time) should be avoided.

99
Q

How do you diagnose peritoneal dialysis (PD) peritonitis and which organisms are implicated?

A

Two of the following:
• The presence of signs/symptoms such as fever, abdominal pain, nausea, vomiting or cloudy effluent
• A white cell count >100 per mL of effluent with >50% neutrophils after a 2-hour dwell
• A positive culture from the effluent

The most common organisms are coagulase-negative Staphylococcus, non- Pseudomonas Gram-negative organisms and Staphylococcus aureus. Treatment should include intra-peritoneal antibiotics.

100
Q

What are the absolute contraindications to full face mask NIV in an acute exacerbation of COPD?

A

• Patient refusal
• Severe facial deformity
• Facial burns
• Fixed upper airway obstruction
• Pneumothorax (unless a chest drain is inserted)
• Recent upper GI surgery

101
Q

Which Mapleson circuits are best suited for neonates?

A

Mapleson E and F

102
Q

Which pathophysiological mechanism would increase peak airway pressure but not plateau pressure?

A

↑ Airway resistance

103
Q

Which drugs are recommended to treat cocaine‐associated hypertension, and why are beta-blockers not recommended first-line?

A

• Benzodiazepines (e.g. diazepam)
• Nitrates (e.g. glyceryl trinitrate)
• Alpha-blockers (e.g. phentolamine)

Cocaine is an indirectly acting sympathomimetic. It causes hypertension due to ↓ reuptake of noradrenaline at sympathetic nerve terminals.

Beta blockade results in unopposed alpha stimulation. This can worsen coronary artery vasoconstriction and systemic hypertension.

104
Q

Which triggers are used to support a patient‐ initiated breath on a ventilator?

A

• Flow: A pre-set flow rate generated by the patient triggers a supported breath.
• Pressure: A ↓ in pressure below a pre-set value within the ventilator circuit triggers a supported breath.

105
Q

Which anion and cation are the most prevalent intracellularly?

A

• Anion: Phosphate
• Cation: Potassium

106
Q

How do you define a sub‐massive pulmonary embolism (PE) (intermediate-risk PE)?

A

PE + RV dysfunction/myocardial necrosis without systemic hypotension/ haemodynamic instability
• RV dysfunction: dilated RV on CT/TTE, new RBBB, S1Q3T3, ↑ BNP
• Myocardial necrosis: ↑ Cardiac enzymes, e.g. Troponin

107
Q

Which chromosome contains the predisposing gene for malignant hyperthermia (MH) and what is MH?

A

Chromosome 19 – close to the gene for the ryanodine/dihydropyridine receptor complex
• During anaesthesia, abnormal skeletal muscle contraction and metabolism lead to ↑ temperature and ↑ muscle rigidity.
• Triggers are volatile agents and suxamethonium.
• A rapid ↑ in ETCO2 is one of the earliest signs. Other features may include CVS instability and cyanosis. The reaction can be delayed for several hours.
• Muscle biopsies may appear histologically normal, and the caffeine halothane contracture test is the gold standard for diagnosis.
• Treatment is with IV dantrolene.

108
Q

What is central cord syndrome and what are its main clinical features?

A

Bleeding, infarction or oedema involving the central grey matter of the spinal cord.

Features:
Motor loss in upper limbs > motor loss

Upper limbs:
Mixed UMN and LMN signs
Loss of pain and temperature

Lower limbs:
UMN signs
Variable sensory changes