e-LFH - Core Training - Clinical

Question 1

Which standard classes of drugs should be prepared before each patient(5)?

Answer 1

Standard drugs typically consist of:

IV induction agent, e.g. propofol
IV opioid, eg fentanyl. Note: these are in the controlled drug cupboard
Neuromuscular blocking agents (NMBA), e.g. atracurium and vecuromium
Antibiotics
IV fluids

Question 2

Which emergency drugs should be drawn up before each patient?

What may be worth preparing for unstable patients?

Answer 2

Emergency drugs are:

• Suxamethonium:
  Draw up in a syringe with blue needle on it, in case it is necessary to give it IM in an emergency
• Atropine or glycopyrrolate
• Ephedrine and/or metaraminol

It may be worth drawing up adrenaline in 10 μg/ml concentration (place 1 ml of 1 in 1000 in a 100 ml bag of NaCl 0.9 %) for unstable patients.

Question 3

Sequence of checks when administering drugs?

Answer 3

It is recommended that anaesthetists use the same sequence when administering any drug:

Check the drug
Check the ampoule
Check the dilution
Check the syringe
Check the route of administration

Question 4

Common types of controlled drug(3)?

Answer 4

Controlled drugs (CD) are:

• Opioids, e.g. fentanyl, morphine, diamorphine, alfentanil
• Benzodiazepines, e.g. midazolam
• Cocaine

Ketamine is not officially a CD but most theatres feel it is good practice to observe the same standards for this drug.

Question 5

Main pre-op checks when preparing to anaesthetise patient (4)?

Additional questions (7)

Answer 5

• Correct patient
• Correct operation
• Correct site and side
• Check consent form

Additional checks

• Whether patient has any allergies
• Dentures, caps or crowns
• Whether patient has any metalwork in their body
• When patient last ate and drank
• That medical records/x-rays are available
• That surgeon is available and ready
• Blood glucose control if diabetic

Question 6

Care of the unconscious patient
- Things to check (5)

Answer 6

• Tape eyes shut once the patient is anaesthetized to:
  -Prevent drying of the cornea and subsequent injury
• Prevent trauma to the cornea which could result in a corneal abrasion
• Take special care with elbows, legs and heels to prevent nerve injury and pressure sores
• Ensure that the patient is not lying on leads or cables, and that equipment is not pressing on the patient’s skin
• Keep all arm angles <90 ° to prevent nerve injury, especially when the patient is in the prone position
  -With an arm out on a board, ensure the head does not
  face away from the arm, putting tension on the
  brachial plexus
• Ensure the patient is positioned in a way that would be tolerated by them when conscious

Question 7

The NAP 5 audit on accidental anaesthetic awareness found the risk of medication critical incidents was associated with (3)?

Answer 7

The NAP 5 audit on accidental anaesthetic awareness found the risk of medication critical incidents was associated with:

Very junior anaesthetists
Non-elective anaesthesia
Outside of normal working hours

Question 8

Advantages of nasal intubation (2)?

Disadvantages (3)?

Answer 8

Advantages

Nasal intubation leaves the oral cavity clear for oral surgery.

For patients in the Intensive Care Unit (ICU), nasal intubation is more easily tolerated than oral intubation and less sedation is required.

Disadvantages

Nasal intubation is more difficult than oral intubation and may cause a nose bleed due to the rich blood supply to the nasal mucosa

A nasal tube may create a false passageway, e.g. beneath the nasal mucosa or, in patients with basal skull fractures, into the cranium

In long-term intubation, nasal intubation may be associated with infection of the paranasal air sinuses

Question 9

Which bones form the hard palate (2)?

Answer 9

The hard palate is formed of the palatine process of the maxilla and the horizontal part of the palatine bone

Question 10

What are the afferent and efferent sides of the gag reflex?

Answer 10

The afferent side of the reflex is glossopharyngeal, the efferent side is vagal.

Question 11

What is the pharynx and how is it divided?

Answer 11

The pharynx is the area common to the upper respiratory and alimentary tracts. It is divided into the nasopharynx, oropharynx and laryngopharynx

Question 12

Which area do fish bones commonly lodge?

Answer 12

Recesses either side of the larynx form the piriform fossae. This is the site where fish bones commonly lodge.

Question 13

Where are the palatine tonsils located?

Answer 13

The palatine tonsils, more commonly simply referred to as the tonsils, are collections of lymphoid tissue between the palatoglossal and palatopharyngeal arches, the ‘pillars of the fauces’.

Question 14

What is the sensory nerve supply to the tonsils?

How are they best anaesthetised?

Answer 14

The sensory nerve supply to the tonsil is from branches of three nerves, i.e. the glossopharyngeal, maxillary and mandibular nerves. Infiltration analgesia into the tonsillar bed is more effective than attempting nerve blockade.

Question 15

How is aspiration prevented during swallowing (5)?

Answer 15

Aspiration during swallowing is prevented by

• closure of the laryngeal sphincter
• upward movement of the larynx behind the base of the tongue
• reflex inhibition of breathing
• channelling of liquid or food laterally by the epiglottis into the piriform fossae.
• The epiglottis may also act as a ‘lid’ to the larynx to prevent substances entering the trachea.

Question 16

At what vertebral level is the larynx?

What structures is it close to (2)?

Answer 16

The larynx is in the midline, opposite the 4th to 6th cervical vertebrae and has a close relationship to the carotid artery and jugular vein.

Question 17

Which articulating cartilages make up the larynx?

Which three laryngeal cartilages are paired?

Answer 17

The framework of the larynx consists of articulating cartilages:

• Thyroid
• Cricoid
• Epiglottis

The following three cartilages are paired:

• Arytenoid
• Corniculate
• Cuneiform

Question 18

How are the true and false vocal cords also known?

How is the gap between the vocal cords?

Answer 18

The vestibular folds are known as the false vocal cords, whilst the vocal folds are known as the true vocal cords.

The gap between the vocal cords is known as the rima glottidis or, simply, the ‘glottis’. It is the narrowest part of the airway in the adult.

Question 19

What is the function of the extrinsic muscles of the larynx?

What is the funciton of the intrinsic muscles of the larynx?

Answer 19

The muscles of the larynx are composed of the extrinsic and intrinsic muscles.

The extrinsic muscles work with other muscles attached to the hyoid to move the larynx up and down during swallowing.

The intrinsic muscles open the vocal cords during inspiration, close the cords and laryngeal inlet during swallowing and alter the tension of the cords during phonation.

Question 20

What is the function of the posterior circoarytenoids?

Answer 20

Posterior cricoarytenoids

These muscles abduct the vocal cords on inspiration. They are the only true abductors. The muscles achieve this by pulling the posterior ends of the arytenoid cartilages together medially. The resulting pivoting movement abducts the anterior ends of the cartilages, to which the vocal cords are attached

Question 21

What is the function of the lateral and transverse arytenoids?

Answer 21

Lateral cricoarytenoids, transvere arytenoids

These are adductors of the cords and close the vocal cords

Question 22

What is the shared function of the aryepiglottic and thryoepiglottic muscles?

Answer 22

Aryepiglottics, thyroepiglottics

These are the laryngeal sphincters and close the laryngeal inlet during swallowing

Question 23

What is the function of the cricothyroid musles?

Answer 23

The cricothyroids are the tensors of the cords, acting by tilting the cricoid cartilage (and the attached arytenoids) on the thyroid cartilage (Fig 5).

Question 24

What is the function of the thyroarytenoid muscles?

And vocalis?

Answer 24

Thyroarytenoids, vocalis

The thyroarytenoids are relaxors of the cords. The vocalis are responsible for the fine adjustment of the cords

Question 25

What is the sensory supply to the larynx above the vocal cords? Which branches are there and what do they do?

How can laryngoscopy induce vagal reflexes?

Answer 25

The sensory supply to the larynx is from the:

Superior laryngeal nerve - above the vocal cords

• The external laryngeal branch provides the motor supply to the cricothyroid muscle.
• The internal laryngeal branch passes beneath the mucosa of the piriform fossa, and provides the sensory supply to the interior of the larynx as far as the vocal cords.

Laryngoscopy may induce vagal reflexes via stimulation of the internal laryngeal nerve, which provides the sensory supply to the vallecula.

Question 26

Which nerve provides the sensory supply to the larynx below the vocal cords?

What other function does this nerve have?

Answer 26

Recurrent laryngeal nerve - below the vocal cords

This provides the sensory supply to the larynx below the vocal cords and the motor supply to all the intrinsic muscles of the larynx, apart from the cricothyroid muscle.

Question 27

What are the paths of the right and left recurrent laryngeal nerves to ascend to the larynx?

Answer 27

The right recurrent laryngeal nerve passes under the subclavian artery to ascend to the larynx in the groove between the oesophagus and the trachea.

The left recurrent laryngeal nerve passes under the aortic arch to ascend in the groove between the oesophagus and the trachea.

Question 28

What does damage the superior laryngeal nerve result in (2)?

Answer 28

Superior laryngeal nerve damage

Damage to the superior laryngeal nerve results in:

• A hoarse voice due to loss of function of the tensor of the cord (cricothyroid). The hoarseness is temporary as the muscle on the other side compensates
• An increased risk of aspiration resulting from loss of sensation above the cords

Question 29

What does unilateral damage to the recurrent laryngeal nerve result in?

And bilateral damage?

Answer 29

Unilateral recurrent laryngeal nerve damage produces the following problems:

• Vocal cord palsy, with complete inability to abduct and a resulting cord position towards the midline. This produces a hoarse voice that is corrected to an extent as the other cord moves across to compensate. It also means the glottis is unable to close tightly so that the patient cannot generate a positive intrathoracic pressure to cough effectively, which can lead to respiratory problems postoperatively.
• The risk of aspiration is increased because of the infraglottic loss of sensation.

Bilateral vocal cord palsy resulting from damage to both recurrent laryngeal nerves produces severe respiratory distress, presenting as stridor as the flaccid vocal cords flap together.

Urgent intubation is required acutely, with a tracheostomy likely to follow.

Question 30

What does the cricothyroid membrane lie between?

Which structures may be damaged during cricothyroidectomy?

Answer 30

The cricothyroid membrane lies between the thyroid cartilage above and the cricoid cartilage below.

The vocal cords are in close proximity and may be damaged during cricothyroid puncture.

Question 31

Between which vertebral levels does the trachea extend?

How long is it? How much is above the suprasternal notch? Rough diameter?

Answer 31

The trachea extends from its attachment to the cricoid cartilage (C6) to the tracheal bifurcation at the carina (T5-6).

In adults it is 15 cm in length; 5 cm above the suprasternal notch, 8 cm if the neck is fully extended. The diameter of the trachea is approximately the same as the patient’s index finger.

Question 32

What are the anterior and posterior walls of the trachea formed of?

Answer 32

Patency is maintained by C-shaped cartilages anteriorly.

The trachea is completed posteriorly by the trachealis muscle.

Question 33

Which tracheal rings does the thyroid isthmus overlie?

Answer 33

The trachea lies in the midline, anterior to the oesophagus, with the thyroid isthmus overlying the 2nd to 4th tracheal rings.

Question 34

Where does the right upper lobe bronchus arise from the right main bronchus?

Answer 34

The right upper lobe bronchus arises 2.5 cm from the carina.

Question 35

How many lobes does each lung have?

Answer 35

The right lung is divided into three lobes and the left lung into two lobes, plus the lingula: the remnant of the left middle lobe.

Question 36

During which common procedures may the pleural cavity be inadvertently opened to cause a pneumothorax (4)?

Answer 36

The pleural cavity be inadvertently opened to cause a pneumothorax during:

• Insertion of a central line, i.e. subclavian or internal jugular
• Supraclavicular brachial plexus block
• Intercostal nerve block
• Surgery on the kidney or adrenal gland

Question 37

How many bronchopulmonary segments does each bronchus divide into?

Answer 37

Ten segments

Right lung

• Upper lobe - Apical, posterior, anterior
• Middle lobe - Lateral, medial
• Lower lobe - apical, medial basal, anterior basal, lateral basal, posterior basal

Left lung

• Upper lobe - Apical, posterior, anterior
• Middle lobe - Superior lingular, inferior lingular
• Lower lobe - apical, medial basal, anterior basal, lateral basal, posterior basal

Question 38

Which lung segment is most commonly affected by aspiration during anaesthesia?

Answer 38

The apical segment of the right lower lobe.

Aspiration is more likely to occur into the right side than the left. The apical bronchus of the right lower lobe is the first segmental bronchus to arise posteriorly and is most commonly affected in the supine patient.

Question 39

How does the bronchiolar wall differ from the bronchus? What is it lined with?

Answer 39

The bronchiolar wall contains smooth muscle but no cartilage. It is lined by ciliated cuboidal epithelium.

Question 40

What epithelium lines the alveoli?

Answer 40

The alveoli are lined by a single fine layer of non-ciliated cuboidal epithelium

Question 41

How many compartments are in the mediastinum?

Answer 41

The mediastinum is the space between the two pleural cavities.

It is divided into four compartments by relationship to the pericardium:

• Anterior
• Middle (containing the pericardium)
• Posterior
• Superior

Question 42

Why is a mass in the anterior mediastinum a major risk factor for anaesthesia?

Answer 42

A mass in the anterior mediastinum is a major risk factor for anaesthesia. Loss of muscle tone after induction may allow the mass to fall back to compress the heart, great vessels and major airways.

Question 43

Which nerves and roots supply the diaphragm?

Answer 43

The nerve supply to the diaphragm is from the phrenic nerves which originate from the spinal cord at cervical level C3, C4 and C5.

Question 44

What proportion of tidal volume does the diaphragm contribute?

Answer 44

The diaphragm contributes 60-75% of the tidal volume.

Question 45

What effect does a damaged phrenic nerve have on the diaphragm? How is it diagnosed?

Answer 45

Phrenic nerve palsy causes upward paradoxical movement of the diaphragm on that side during inspiration. Diagnosis is made by screening the diaphragm by fluoroscopy.

Question 46

What are the three types of intercostal muscle?

Which direction does each run in?

What is the function of each?

Answer 46

External

• The external intercostal muscles slope downward and forward.
• They contract on inspiration to pull the ribs upward and outward, increasing the anteroposterior and lateral diameter of the thorax.

Internal

• The internal intercostal muscles slope downward and backward.
• They are only used in active expiration and pull the ribs downward and inward to decrease the volume of the thoracic cavity. They stiffen the intercostal spaces to prevent them from bulging during straining.

Innermost

• The innermost intercostals consist of a thin layer of muscle linking the ribs together to stabilize the chest wall.

Question 47

Which groups form the accessory muscles of respiration (4)?

What are their functions?

Answer 47

Scalene

• These muscles elevate the first two ribs.

Sternomastoids

• The sternomastoid muscles elevate the sternum.

Alae nasi

• The indicative flaring of the nostrils is commonly seen in children with mild respiratory distress.

Small muscles of the head and neck

• ‘Head bobbing’ is a sign of severe respiratory distress in children.

Question 48

Approximate depths of the tracheal tube in adult males and females?

Answer 48

In an adult male, the depth of the tracheal tube is usually around 23 cm at the lips. In an adult female, the depth is 21 cm at the lips.

Question 49

Which ribs should be visible in an inspiratory film?

Answer 49

At least six ribs should be visible anteriorly and 10 ribs posteriorly.

Question 50

How many layers are in the pericardium?

What are the attachements?

Answer 50

The pericardium has three layers: fibrous, parietal and visceral.

The attachments of the fibrous pericardial sac are to the great vessels superiorly, to the posterior aspect of the sternum and the central tendon of the diaphragm.

Question 51

What is a normal cardiothoracic ratio?

What can lead to an abnormally high CTR?

Answer 51

In an adult, the cardiothoracic ratio should be less than 50% on a posterior-anterior (P-A) film.

A misleadingly high cardiothoracic ratio can result from:

• Taking an A-P film rather than a P-A
• The heart being pushed more horizontally by upward abdominal pressure, such as obesity or pregnancy

Question 52

Which vessel supplies the SA node 65% of people?

Answer 52

RCA

Question 53

Which vessel supplies the AV node in 80% of people?

Answer 53

The A-V node is supplied by the right coronary artery in 80% of people.

Question 54

From where does the sympathetic supply of the heart originate?

Answer 54

The sympathetic supply originates from the lateral horns of the spinal cord (T1-4).

Question 55

Lorazepam

Dose?

Onset?

Adverse effects?

Metabolism?

Answer 55

Dose - 1-2mg

Onset - 1-3 mins (IV), 2hr (PO)

Respiratory depression

Metabolised by the liver - half life 14 hours

Question 56

Temazepam

Dose?

Onset?

Adverse effects (1)?

Metabolism?

Excretion?

Answer 56

• Commonly used as a ‘night time’ hypnotic at a dose of 10-20 mg
• A similar dose may also be used to produce anxiolysis preoperatively. Higher doses are usually required during the day to produce sleep. The effects of larger doses may continue to be seen in the postoperative period
• Usually administered 1-2 h prior to surgery
• Has no significant effect on the cardiovascular system and only depresses the respiratory system at higher doses
• Is metabolized in the liver and mainly excreted in the urine

Question 57

The three stages of giving an anaesthetic?

Answer 57

Giving an anaesthetic involves three stages:

• Induction - putting the patient to sleep
• Maintenance - keeping the patient asleep
• Reversal - waking the patient up

Question 58

Alternatives to benzodiazepines for medication?

Answer 58

IM opioids - morphine, papaveretum, pethidine

These are occasionally used today, but have, in the main, been replaced by oral anxiolytics.

Question 59

How should patients with gastro-oesophageal reflux be induced?

What are the goals of premedication?

Answer 59

A Rapid Sequence Induction (RSI) is the technique of choice for these patients.

The goals of premedication in reflux disease are an increased gastric pH and a reduced gastric volume.

Question 60

Anti-reflux pre-med examples and doses (3)

Answer 60

PPI: Omeprazole, 20 mg orally

H2 antagonist: Ranitidine, 150 mg orally

Metoclopramide 10-20mg

Question 61

NSAIDs

Doses and routes for:

• Ibuprofen
• Diclofenac
• Ketorolac

Answer 61

Ibuprofen - Up to 1200mg daily in divided doses - PO

Diclofenac - Up to 150mg daily in divided doses - PO, PR, IV

Ketorolac - Up to 40mg daily - IV (usually 10-30mg)

Question 62

Side effects of NSAIDs (4)

Answer 62

Gastric irritation

Exacerbation of asthma

Renal injury

Platelet dysfunction

Question 63

How long after a dose of LMWH can neuraxial blockage be safely peformed? Why?

Answer 63

There is a potential conflict between the use of LMWH for thromboembolic prophylaxis and neuraxial blockade, i.e. spinal or epidural anaesthesia or analgesia, since such procedures are contraindicated within 10 h of a dose of LMWH. This is to prevent the rare complication of epidural haematoma.

Question 64

Examples of different classifications of thromboprophylaxis risk:

Minor (2)

Medium (3)

High (5)

Answer 64

Minor risk

• Minor surgery <30min, no risk factor other than age
• Major gen surg (>30 min), age <40, no other risk factors

Medium risk

• Major general, urological, gynaecological, cardiothoracic, vascular or neurological surgery; age >40 or with one or more risk factors
• Major medical illness: heart or lung disease, cancer, inflammatory bowel disease
• Minor surgery, trauma or illness in patients with previous DVT or PE, thrombophilia

High risk

• Fracture or major orthopaedic surgery of pelvis, hip or leg
• Major pelvic or abdominal surgery for cancer
• Major surgery, trauma or illness in patients with previous DVT or PE, thrombophilia
• Lower limb paralysis
• Critical leg ischaemia or major leg amputation

Question 65

Which medications should be omitted prior to surgery(4)?

How long should they be omitted for in each case?

Answer 65

• ACEi/ARBs - should be omitted on day of surgery
• Warfarin - stop 5-7 days before surgery
• Clopidogrel - ideally 7 days prior to neuraxial blockade
• Oral contraceptive - ideally 6 weeks prior

Question 66

2 approaches to pre-op management of insulin-dependent diabetes

Answer 66

VRIII

A variable rate intravenous infusion of insulin plus concomitant intravenous dextrose and potassium containing fluid

• A syringe containing 50 units of human actrapid in 50 ml of 0.9% saline.
• Intravenous dextrose-containing fluids must also have potassium added to run at 100 ml/h.

While a patient is managed with intravenous insulin, they should have their blood sugar monitored hourly.

Alberti regimen

The Alberti regimen is based upon the addition of actrapid insulin to intravenous dextrose-containing fluids. The amount of insulin added can be varied. The standard intravenous fluid used is 10% dextrose with ten units of actrapid and 1 g of potassium in 500 ml.

Question 67

Short-acting oral hypoglycaemic agents (2)

Long-acting oral hypoglycaemic agent (4)

Answer 67

Short-acting hypoglycaemic agents

• Gliclazide
• Repaglinide

Long-acting hypoglycaemic agents

• Glibenclamide
• Metformin
• Glipizide
• Rosiglitazone

Question 68

Management of T2DM pre-op

Morning of surgery (2)

Medication changes pre-admission?

Risk to patient?

Plan for minor surgery vs major surgery?

Answer 68

• On the day of surgery, the patient should be starved to the local protocol and their morning dose of hypoglycaemic agent withheld.
• Ideally, long-acting agents should be converted to short-acting agents a week or so before surgery.
• The risk to the patient is hypoglycaemia, particularly after an overnight fast.
• For minor surgery, no further action is required as long as the blood sugar is well controlled.
• Where it is poorly controlled, and for major surgery, an insulin sliding scale is required with regular blood sugar measurements.

Question 69

Which colour labels denote induction agents?

Answer 69

IV induction agents are identified by yellow labels.

Question 70

What physicochemical property must induction agents share?

Answer 70

They must all be very lipid-soluble to cross the blood-brain barrier.

Question 71

What are the following induction agents presented in?

• Propofol
• Thiopental
• Etomidate

Answer 71

• Propofol is an emulsion containing 1% propofol in a lipid medium.
• Thiopental is a weak acid and can be dissolved in water as long as it is mainly in the ionized form, i.e. when the pH is very high. Therefore, it is stored as its sodium salt, as a powder mixed with sodium carbonate, so that when 20 ml of water is added it produces a 2.5% solution of thiopental with a pH of 10.5.
• Etomidate is soluble, but is stabilized by 35% propylene glycol to give a 0.2% solution.

Question 72

How to convert % solution to mg/ml?

Answer 72

Multiply by 10

Question 73

Why is it important to introduce a volatile agent as soon as possible after IV induction?

Answer 73

The effect of the IV agent lasts only a few minutes. To maintain anaesthesia it is important to introduce a volatile agent as soon as possible. Although the anaesthetic effects of induction agents and volatile agents are synergistic, it takes longer for the alveolar concentration of the volatile agent to reach a maximum than it does for the effect of the induction agent to wear off.

Question 74

Doses of induction agents required for a fit adult?

• Propofol
• Thiopental
• Etomidate

Answer 74

• For propofol: 1-2.5 mg/kg
• For thiopental: 3-7 mg/kg
• For etomidate: 0.25-0.3 mg/kg

Question 75

Propofol

• Onset time
• Offset time
• Metabolism?
• CVS side effects (2)
• RS side effect
• Other effects (3)
• Relative contraindication to use?

Answer 75

• Onset time - 30 seconds
• Offset time - 3-7 minutes
• Metabolism? - Two pathways: conjugated in the liver to the glucuronide and hydroxylated to the quinol, which is subsequently glucuronidated.
• CVS side effects (2) - Direct myocardial depression and reduction in SVR causing hypotension
• RS side effect - Dose-dependent respiratory depression.
• Other effects (3)
  
  • Pain on injection, which can be reduced by the use of lidocaine.
  • Nausea and vomiting is much less likely after propofol than other agents.
  • Hypersensitivity reactions: Approximately 1 in 100 000.
• Relative contraindication to use - Not licensed for children under three.

Question 76

What chemical class does propofol belong to?

pKA?

How does it exist in plasma?

Answer 76

It is a phenol derivative and extremely lipid-soluble, more so than thiopental. It has a pKa of 11, so exists almost entirely in the unionized, i.e. more lipid-soluble, form. About 98% is bound to plasma proteins.

Question 77

Thiopental

• Onset time
• Offset time
• Metabolism?
• CVS side effects (2)
• RS side effect
• Problems with use (2)
• Absolute contraindication to use?

Answer 77

• Onset time: 30 seconds
• Offset time: 5-10 minutes
• Metabolism: In the liver to the active oxybarbiturate derivative pentobarbital and two other inactive metabolites.
• CVS: Direct myocardial depression with hypotension and reduction in cardiac output. Use with caution in the hypovolaemic patient.
• RS: Dose-dependent reduction in minute ventilation, commonly with a short period of apnoea.
• Problems with use
  
  • Extremely painful and limb-threatening if given intra-arterially. Urgent treatment includes: Saline dilution, papaverine 40 mg to dilate the artery and sympathetic blockade to improve blood flow.
  • Hypersensitivity reactions: Approximately 1 in 15 000.
• Absolute contraindication to use - Porphyria.

Question 78

What chemical class does thiopental belong to?

pKa?

How does it exist in plasma?

What is the dose of thiopental for induction of anaesthesia?

Answer 78

It is a thiobarbiturate, highly lipid-soluble and a weak acid with a pKa of 7.6. Approximately 60% of free thiopental is in the unionized form, which is more lipid-soluble. About 75-80% is bound to plasma proteins.

3-7 mg/kg.

Question 79

Etomidate

• Onset time
• Offset time
• Metabolism?
• CVS side effects
• RS side effect
• Other effects (4)
• Relative contraindications to use (2)

Answer 79

• Onset time - 30 seconds
• Offset time - 3-7 minutes
• Metabolism - Etomidate is an ester and undergoes ester hydrolysis in both plasma and the liver.
• CVS side effect - Very little effect on heart rate (HR), CO and systemic vascular resistance (SVR).
• RS side effect - Minimal and transient dose-dependent respiratory depression.
• Other effects
  
  • Pain on injection, which is reduced by the use of the preparation in lipid, i.e. Etomidate-Lipuro®.
  • Nausea and vomiting is common compared with propofol.
  • Adrenocortical suppression, especially if used by infusion.
  • Hypersensitivity reactions: Approximately 1 in 75 000.
• Relative contraindication to use
  
  • Sedation in intensive care. Avoid in porphyria.

Question 80

What chemical class does etomidate belong to?

How does it exist in plasma?

Dose for induction?

Answer 80

It is a carboxylated imidazole derivative, both lipid-soluble and water-soluble, i.e. much more water-soluble than propofol. About 70% is bound to plasma proteins.

0.25-0.3 mg/kg.

Question 81

The phrase that distinguishes pharmacokinetics from pharmacodynamics?

Answer 81

Pharmacokinetics is often described as ‘what the body does to the drug’ to distinguish it from pharmacodynamics, which describes the effects a drug has on the body, i.e. ‘what the drug does to the body’.

Question 82

Which two processes account for the rapid fall in plasma concentration of induction agent after a bolus? Which is the larger contributor?

What determines to which tissues the drug is initially distributed?

Answer 82

• The drug is moving out of the bloodstream and is being distributed to other tissues (main process)
• The drug is being metabolized and/or excreted from the body

The blood flow. Tissues that have a high blood flow, i.e. vessel-rich tissues, take up the drug more quickly.

Question 83

Which is metabolised faster: propofol or thiopental?

Answer 83

Propofol and thiopental are metabolized by the liver. Propofol is much more rapidly broken down than thiopental and has no active metabolites, whereas thiopental is metabolized more slowly, but has an active metabolite-pentobarbital.

Question 84

Three questions that influence choice of induction agent?

Answer 84

Are any agents absolutely contraindicated?

• Previous hypersensitivity reaction to the active agent
• Thiopental and etomidate in porphyria

Are there any patient-related factors that may influence choice?

• Resuscitation state of patient: propofol and thiopental produce more CVS depression than etomidate, so hypovolaemia is a relative contraindication
• Rapid sequence induction needed: thiopental has a slightly faster onset than propofol
• Epilepsy: thiopental is antiepileptic
• Age of patient: presence of ischaemic heart disease

Are there any drug-related factors that may influence choice?

• Previous reaction to a drug presented in propylene glycol: this should exclude use of etomidate
• Egg allergy: some consider this a relative contraindication to propofol, although there is no supporting evidence

Question 85

Difference between a gas and a vapour? Which are inhalational anaesthetics?

Answer 85

Any agent that can exist as a liquid at room temperature is correctly called a vapour. Any agent that cannot be liquefied at room temperature, whatever the pressure, is correctly called a gas. Volatile anaesthetic agents are all liquids at room temperature, so strictly speaking are vapours and not gases.

Question 86

Definition of a MAC?

Answer 86

The MAC is that concentration required to prevent 50% of patients moving when subjected to a standard midline incision

Question 87

MACs

• Isoflurane
• Sevoflurane
• NO2

Answer 87

Isoflurane -1.2

Sevoflurane - 2.0

Nitrous oxide - 103.0

Question 88

Factors increasing MAC (7)

Answer 88

1. Stimulants
2. Chronic alcohol dependence
3. Exogenous catecholamine use
4. Hyperthyroidism
5. Hyperthermia
6. Young age
7. Anxiety and stress

Question 89

Factors reducing MAC (10)

Answer 89

1. Nitrous oxide
2. Alpha2 adrenergic agents
3. Benzodiazepines
4. Intravenous anaesthetics used by infusion
5. Opioid analgesics
6. Acute alcohol intoxication
7. Reduced GCS
8. Hypothermia
9. Hypothyroidism
10. Increasing age

Question 90

Which two coefficients describe the solubility of volatile agents in body tissues? Which correlates with potency in terms of MAC?

Answer 90

There are two important partition coefficients that describe solubility of volatile agents in body tissues. One is the blood:gas (B:G) partition coefficient and the other the oil:gas (O:G) partition coefficient.

Volatiles must reach the CNS to have their effect and this requires them to cross the blood-brain barrier. Only lipid-soluble drugs can gain access to the brain.

Potency follows the order of O:G solubility

Question 91

O:G partition coefficients

• Isoflurane
• Sevoflurane
• N2O

Answer 91

Isoflurane - 98

Sevoflurane - 80

N2O - 1.4

Question 92

What determines speed of onset when using a volatile agent for induction?

Which coefficient determines this rate?

Answer 92

The speed of onset of anaesthesia when using a volatile agent for induction of anaesthesia depends on how rapidly the alveolar concentration reaches the inspired concentration of the agent.

The curves for each agent all reach the same end-point, but at different rates, dependent on their blood:gas solubility coefficient. The more insoluble the agent is in blood, the faster its FA/FI ratio approaches 1.

Question 93

What is overpressure and why is it used?

Which volatile agent can this not be used for?

Answer 93

Overpressure involves setting the initial concentration on the vaporizer above that actually needed for maintenance and then, over 5 min or so, reducing it towards a maintenance value of approximately 1 MAC.

This is easy to achieve in practice with sevoflurane, but harder with isoflurane as it is an airway irritant, and may precipitate coughing in unparalyzed patients. Initial steady increases over a minute or so will minimize this.

Question 94

A low blood-gas partition coefficient has what effect on onset of anaesthesia?

Answer 94

Volatile agents with a low blood-gas partition coefficient have a rapid speed of onset of anaesthesia.

Question 95

How would minute ventilation affect speed of onset of anaesthesia with a volatile agent?

If the patient’s cardiac output increases, what effect might this have on speed of onset of anaesthesia?

Answer 95

If minute ventilation is increased, more volatile agent reaches the alveoli, so speed of onset of anaesthesia is quicker.

If a cardiac output increases, then blood passes more quickly through the lungs and less anaesthetic is taken up in the same time. As a result speed of onset of anaesthesia is slower. The converse is true if the cardiac output falls.

Question 96

Blood:gas partition coefficients

• Isoflurane?
• Sevoflurane?
• N2O?

Answer 96

Isoflurane - 1.4

Sevoflurane - 0.6

Nitrous oxide - 0.47

Question 97

What is the concentration effect?

Answer 97

The concentration-effect refers to the principle that the concentration of inspired anesthetic gas influences both (1) the alveolar concentration that may be attained and (2) the rate at which that concentration may be attained. The rate of rise of alveolar end tidal concentration is thus dependent upon and accelerated by a high initial inspired concentration of anesthetic gas. The concentration effect is only clinically relevant with nitrous oxide, although it may occur with other gases.

Question 98

What is the second gas effect?

Answer 98

The second gas effect

When a high inspired concentration of N2O is used for induction along with a volatile, not only does the alveolar concentration of N2O rise more rapidly than predicted, but so does that of the volatile. As a result induction is more rapid than might be expected.

Question 99

What is diffusion hypoxia? How is it mitigated?

Answer 99

Diffusion hypoxia

At the end of an anaesthetic N2O will diffuse back into the alveoli more rapidly than N2 can diffuse into blood. If air is given without oxygen supplementation this will have the effect of diluting the amount of oxygen, and so reducing its concentration in the alveoli. This carries a risk of hypoxia, so all patients should be given supplementary oxygen at the end of an anaesthetic when N2O has been used.

Question 100

How do volatile agents affect tidal volume?

Answer 100

All volatile agents cause a dose-dependent reduction in tidal volume accompanied by an increase in respiratory rate. However, with high concentrations, alveolar ventilation will become inadequate.

Question 101

Which volatile is used for gas inductions? Why?

Answer 101

Sevoflurane. Isoflurane is an irritant vapour and may cause coughing.

Question 102

How do the effects of sevoflurane and isoflurane on minute ventilation differ? Why is this important for gas inductions?

Answer 102

Sevoflurane is more potent than isoflurane in reducing minute ventilation and may cause apnoea.

For a gaseous induction using sevoflurane overpressure with 8% is commonly used. Once the patient is almost asleep it is important to reduce the vaporizer setting to maintain adequate alveolar ventilation. If this reduction is not made and 8% sevoflurane is continued then alveolar ventilation is reduced and eventually apnoea will follow.

Question 103

How do volatile agents affect SVR and cardiac contractility?

• Isoflurane
• Sevoflurane
• N2O

Answer 103

All volatile agents, including isoflurane and sevoflurane, cause a dose-dependent reduction in systemic vascular resistance (SVR). Both agents slightly reduce cardiac contractility.

• Isoflurane causes a greater reduction in SVR than sevoflurane. This drop in SVR is accompanied by reflex tachycardia. Isoflurane has also been associated with coronary steal.
• Sevoflurane causes a less pronounced fall in SVR; blood pressure and heart rate are better preserved.
• Nitrous oxide reduces cardiac contractility very slightly, but this is usually offset by an increase in sympathetic activity so that there is little overall effect.

Question 104

What is coronary steal? Which volatile is it associated with?

Answer 104

Isoflurane causes vasodilatation of normal coronary arteries. Blood may be diverted away from stenotic vessels by vasodilatation of normal vessels. As a result, cardiac muscle supplied by the stenosed coronary vessel may become ischaemic.

Question 105

What sort of chemical compounds are isoflurane and sevoflurane?

How are they metabolised and by which enzyme?

Which is metabolised to the greater extent?

Which product of sevoflurane metabolism could theoretically cause renal issues?

Answer 105

Isoflurane (Fig 1) and sevoflurane (Fig 2) are both halogenated ethers and are metabolized in the liver by CYP2E1, one of the cytochrome P450 family of enzymes.

Sevoflurane is metabolized to a greater extent than isoflurane.

Metabolism produces significant amounts of fluoride ions, which are known to cause renal impairment. Despite this, sevoflurane does not appear to impair renal function, even after prolonged exposure.

Question 106

How do carbon dioxide absorbers interact with sevoflurane?

Answer 106

Increasingly, breathing systems with carbon dioxide absorbers are being used. These interact with sevoflurane to produce a range of potentially toxic compounds, which have, rather unimaginatively, been called compound A, compound B, etc, through to compound E.

Only compound A has the potential to induce significant clinical effects. However, even after prolonged exposure, and despite potentially toxic levels being reached, there have been no reports of actual renal toxicity.

Question 107

Which side effect can prolonged exposure to nitrous oxide cause?

Answer 107

Megaloblastic anaemia

Although nitrous oxide is not metabolized to any significant extent, it does interfere with DNA synthesis in the bone marrow. Prolonged exposure may start to produce megaloblastic changes.

Question 108

Difference between opioid and opiate?

Answer 108

The term ‘opiate’ is usually reserved for naturally-occurring opioid drugs such as morphine.

‘Opioid’ is a more generic term that includes the synthetic drugs such as fentanyl.

Question 109

Which colour label identifies opioid drugs?

Answer 109

Blue

Question 110

What dose of fentanyl is given at induction? Why? Time to onset? Duration of effect?

Answer 110

An initial bolus dose of 1-3 µg/kg is usually given at induction, often before the intravenous induction agent, as it takes about 5 min to have an effect.

One of fentanyl’s effects is to reduce the response to laryngoscopy.

Repeated doses of fentanyl may be given intraoperatively, usually 50-100 µg, depending on the duration of surgery and analgesic plans. The duration of analgesic effects of fentanyl depend on the dose given and the level of surgical stimulation, but for the doses described above analgesia lasts about 15-30 min

Question 111

Standard concentration of fentanyl?

Answer 111

It comes in 2 ml and 10 ml ampoules, each containing a clear solution of 50 μg/ml

Question 112

How does fentanyl compare to morphine in terms of lipid solubility? What does this mean for its effect?

How is it metabolised?

Answer 112

Fentanyl is 580 x more lipid soluble. When given as a single intravenous bolus dose, fentanyl is a short-acting drug. Its plasma concentration falls rapidly due to distribution to vessel-rich tissues. If multiple repeated doses or an infusion are used, then there is some accumulation in fat and the recovery time increases. Metabolism, to inactive products, occurs in the liver.

Question 113

What are the common side effects of fentanyl (6)?

Which rare complication can occur?

Answer 113

• Bradycardia
• Hypotension
• Respiratory depression
• Nausea and vomiting postoperatively
• Urinary retention
• Constipation and itching

Occasionally chest wall rigidity is seen when fentanyl is used in a large dose as part of induction of anaesthesia.

Question 114

How is morphine dosed intraop? How long do effects last?

How and when should morphine be given if severe pain is anticipated post-op?

Answer 114

The intraoperative dose of morphine, after initial use of fentanyl, is usually a 2-5 mg bolus, depending on how stimulating the surgery is and the duration of the procedure. Requires redosing every 30-40 mins.

An intravenous bolus dose of morphine of 0.1-0.15 mg/kg can be given about 45 min before the end of surgery. The longer onset time to peak effects means that the timing of intraoperative morphine requires care.

Question 115

What is the standard presentation of morphine? How is it normally diluted for use?

Answer 115

1 ml ampoules containing a clear solution of 10 mg/ml. For intravenous use, this is normally diluted with saline to give a solution of 1 mg/ml.

Question 116

How does morphine’s potency compare to fentanyl?

How is morphine metabolised? In which patients is this important?

Answer 116

Around 100x less potent.

Metabolism occurs in the liver; an active metabolite is morphine-6-glucuronide, which is more potent than morphine. The presence of an active metabolite is only important in patients with renal failure who receive repeated doses of morphine.

Question 117

Uses for neuromuscular blockade (3)

Answer 117

NMBs are used to facilitate:

• Tracheal intubation
• Surgery where muscle relaxation is essential
• Mechanical ventilation

Question 118

What type of muscle relaxant is succinylcholine?

Answer 118

Depolarizing

Question 119

How do depolarising and non-depolarising NMBs compare with respect to the following?

• Speed of onset
• Activation before block
• Speed of offset
• May require reversal?

Answer 119

Depolarising

• Speed of onset - Fast
• Activation before block - Yes, see twitching
• Speed of offset - Fast
• May require reversal - No

Non-depolarising

• Speed of onset - Slower
• Activation before block - No
• Speed of offset - Slower
• May require reversal - Yes

Question 120

When is RSI indicated?

What is omitted from an RSI in contrast to standard induction?

Why?

Answer 120

Indicated in situations where the patient is at risk of aspiration of gastric contents.

Preoxygenation is followed by an induction agent and then immediately by the depolarizing neuromuscular blocker succinylcholine, without checking for mask ventilation.

There are two reasons for this:

This technique aims to minimize the time between induction and intubation

Succinylcholine wears off after a few minutes, allowing spontaneous respiration to restart. The alveolar reservoir of oxygen achieved by preoxygenation should limit any hypoxia until spontaneous respiration restarts

Question 121

Why is important to check that the effects of succinylcholine have worn off before using a non-depolarizing agent?

Answer 121

To exclude succinylcholine apnoea.

Occasionally, patients have genetically abnormal plasma cholinesterase (the enzyme that metabolizes succinylcholine) so that its effects are significantly prolonged. In this situation paralysis could be still be present at the end of surgery.

If a non-depolarizing relaxant had been given without using the nerve stimulator to confirm recovery from succinylcholine, it would be unclear which muscle relaxant was responsible for the continued paralysis.

Question 122

What colour label denotes non-depolarising NMBs?

And depolarising NMBs?

Answer 122

The national colour-coding for labels on syringes containing non-depolarizing NMBs is red.

Succinylcholine (Fig 3) has a black and red label to show that it is a depolarizing rather than a non-depolarizing NMB.

Question 123

How are intubating and maintenance doses of NMBs dosed?

Answer 123

Intubating doses are based on body weight while maintenance doses are titrated according to response determined by the peripheral nerve stimulator.

Question 124

Vecuronium

Standard concentration?

Intubating dose?

Maintenance dose?

Answer 124

• Standard concentration - 2mg/ml
• Intubating dose - 0.1mg/kg
• Maintenance dose - 1-2mg

Question 125

Actracium

Standard concentration?

Intubating dose?

Maintenance dose?

Answer 125

Standard concentration - 10mg/ml

Intubating dose - 0.5mg/kg

Maintenance dose - 10-20mg

Question 126

Succinylcholine

Presentation?

Intubating dose?

Maintenance dose?

Answer 126

Presentation - 2 ml glass vial, 100 mg total.

Intubating Dose - 1-2 mg/kg

Succinylcholine should not be used to maintain neuromuscular blockade.

Question 128

Why is muscle fasciculation seen with succinylcholine?

How is it metabolised?

Contraindications to use (3)

Answer 128

Succinylcholine is structurally related to acetylcholine and produces muscle relaxation by x As a result, muscle fasciculation is seen in many patients soon after succinylcholine administration.

Succinylcholine has a short duration of action as it is metabolized in the plasma by pseudocholinesterase.

Patient-related contraindications, history of:

• Malignant hyperpyrexia
• Anaphylaxis to succinylcholine
• Succinylcholine apnoea

Question 129

Patient-related contraindications to succinylcholine use (3)

Clinical contraindications (2)

Answer 129

Patient-related contraindications, history of:

• Malignant hyperpyrexia
• Anaphylaxis to succinylcholine
• Succinylcholine apnoea

Clinical contraindications:

• The presence of widespread denervation injury, especially after burns and spinal cord injury
• The presence of an open, penetrating eye injury

Question 130

How can succinylcholine cause acute onset hyperkalemia?

Answer 130

When it is used in presence of denervation injuries, altered expression of acetylcholine receptors (throughout the muscle membrane rather than the junctional area only) leads to a greater efflux of intramuscular potassium upon depolarisation.

Question 131

Adverse effects of succinylcholine (4)

Answer 131

• Hyperkalemia
• Bradycardia (due to structural similarity to acetylcholine, most often seen after a second dose)
• Sux pains - uncoordinated muscle fasciculations leading to jaw and neck pain that persist for a day or two (most likely in women)
• Transient raised pressure in the eye, stomach and cranium

Question 132

The common mechanism of non-depolarising NMBs?

Classified into which two groups by structure?

Answer 132

The non-depolarizing NMBs are all competitive antagonists of acetylcholine at the neuromuscular junction.

They are classified according to their structure. There are two groups:

• Aminosteroids, e.g. Vecuronium
• Benzylisoquinoliniums, e.g. Atracurium

Question 133

How is vecuronium metabolised? And excreted?

What regular meds can mean a higher dose is required?

Answer 133

It is metabolized in the liver and excreted in the bile and urine. Its effects may be prolonged with hepatic and renal dysfunction.

Patients with induced liver enzymes, e.g. due to carbamazepine therapy, have a higher dose requirement.

Question 134

How is atracurium broken down? (2)

Which groups of patients does this make it suitable for(2)?

Answer 134

Hofmann degradation is unique to atracurium and involves spontaneous breakdown to laudanosine and acrylate.

Ester hydrolysis is caused by non-specific esterases, which are distinct from plasma cholinesterase

In the body this breakdown is independent of enzyme systems, so atracurium can be eliminated by an organ-independent mechanism, which is an advantage in patients with renal or hepatic failure

Question 135

In which patients is atracurium avoided? Why?

Answer 135

Atracurium commonly causes local histamine release, with redness or a wheal-and-flare reaction. Occasionally there is systemic histamine release, which may precipitate small airway obstruction and wheeze, especially in asthmatics and when a large dose is given quickly. It may also cause vasodilation and hypotension

Question 136

Things that may potentiate effects of non-depolarising NMBs?

Answer 136

The effects of both agents may be potentiated by:

• acidosis
• high-dose gentamicin
• magnesium therapy

Question 137

What % of nicotinic receptors do non-depolarizing agents need to occupy to produce blockade?

Answer 137

Although acetylcholine only needs to occupy a small proportion of receptors to trigger muscle contraction, non-depolarizing muscle blockers need to occupy the majority (about 90%) of the receptors to produce blockade.

Question 138

How does neostigmine affect the heart?

How can it be overcome?

Answer 138

Question: Neostigmine acts at all sites where AChE is present and this includes the heart. What effect might this have?

Answer: Bradycardia.

Question: How might this be overcome?

Answer: Give an anticholinergic, such as glycopyrrolate or atropine, with neostigmine.

Question 139

Recommended dose of neostigmine?

Answer 139

The recommended dose of neostigmine is 0.05 mg/kg. It is presented in a 1 ml ampoule of 2.5 mg alone or premixed with glycopyrrolate 0.5 mg.

Question 140

How is a Train of Four delivered? What current is used?

Answer 140

The Train of Four (TOF) describes four supramaximal stimuli, each with a duration of 0.1 msec, delivered at 2 Hz

Typically a current >60 mA is sufficient.

Question 141

Which two pieces of information do you get from a train of four?

Answer 141

The TOF count - this relates to the number of twitches seen

The TOF ratio - this is the ratio of the fourth twitch height to the first twitch height, T4:T1.

Question 142

What approximate occupancy does each number of twitches of TOF represent?

Why is TOF count unhelpful in assessing the reversal of NMB?

Answer 142

4 - 0-85%

3 - 90%

2 - 92%

1 - 95%

A TOF count of four covers a huge range of receptor occupancy, which in a clinical context makes it unhelpful when assessing reversal of neuromuscular blockade.

Question 143

How does TOF ratio change as a non-depolarizing block wears off?

Answer 143

During partial non-depolarizing block the TOF ratio is <0.7, i.e. T4 is much smaller than T1. As the non-depolarizing block wears off or is reversed, the TOF ratio approaches one.

Question 144

What are the commonly used types of peripheral nerve stimulation patterns? (3)

Answer 144

• The Train of Four (TOF)
• The Double Burst
• Tetany

Question 145

How is tetany delivered via peripheral nerve stimulation?

What is fade?

Answer 145

Tetany describes a constant stimulus to the nerve at 50 Hz. At 60 mA it is very painful for an awake patient.

Tetanic fade refers to the diminishing muscle twitch response from an evoked potential stimulation of muscle under the effect of a non-depolarizing neuromuscular blocking agent.

Question 146

What is post-tetanic facilitation?

Answer 146

Following a tetanic stimulus the response to a single twitch is greater than normal, a phenomenon known as ‘post-tetanic facilitation’. The TOF is stronger and the TOF count may increase when a tetanic stimulus is applied during partial blockade.

Question 147

How does lipid solubility affect potency of local anaesthetics?

Answer 147

The more lipid soluble the agent, the more potent it is

Question 148

Which is more potent, lidocaine or bupivacaine?

Answer 148

Bupivacaine: it is approximately four times more potent than lidocaine.

Question 149

How does ionisation of local anaesthetics affect passage across a membrane and subsequent activity?

Answer 149

The unionized form of the local anaesthetic must cross the axonal lipid membrane to reach the inside. Once inside, it is the ionized form of the drug that is effective in blocking the channel.

Question 150

What determines the proportion of any drug in the ionized form compared with the unionized form? (3)

Answer 150

There are three factors:

• Whether the drug is a weak acid or a weak base
• The pKa of the drug, i.e. the pH at which the ionized and unionized forms are present in equal amounts
• The pH of the environment

Question 151

Are local anaesthetic weak acids or bases?

How does pKa affect local anaesthetics at pH 7.4?

How does this affect speed of onset when comparing lidocaine and bupivicaine?

Answer 151

Local anaesthetics are weak bases; weak bases are ionized below their pKa. Both lidocaine and bupivacaine have a pKa above plasma pH. At pH 7.4 both these drugs are mainly ionized, but for lidocaine approximately 25% is unionized, whereas for bupivacaine just 15% is unionized.

Lidocaine has a faster onset of block than bupivacaine.

Question 152

Which two main factors determine duration of LA block?

Answer 152

Once placed around the nerve, the duration of a block is determined by two main factors:

• Protein binding
• Rate of removal from the site and subsequent metabolism

Question 153

How does the addition of adrenaline affect the use of lidocaine? (2)

Answer 153

The addition of 1 in 200 000 adrenaline can be used to prolong the duration of a block. It can be useful when added to lidocaine. However, because the duration of action of bupivacaine is determined mainly by tissue binding, the addition of adrenaline is not clinically useful.

By restricting lidocaine absorption into the blood stream, the addition of adrenaline allows a higher dose of lidocaine to be used: 7 mg/kg rather than 3 mg/kg.

Question 154

Max dose of lidocaine? And with adrenaline?

Answer 154

Lidocaine alone - 3 mg/kg

With adrenaline - 7 mg/kg

Question 155

Two classes of local anaesthetics?

How does this structural difference influence the pharmacokinetics of these agents?

Answer 155

The local anaesthetic agents fall into two chemical groups, depending on the chemical linkage present:

• Amide local anaesthetics
• Ester local anaesthetics

Ester linkages are more readily broken down, because esterases are present in a variety of tissues as well as in the bloodstream. Amide bonds are broken by amidases, which are found in the liver. Therefore, ester local anaesthetics have a shorter duration of action than amide local anaesthetics and are less commonly used for local blocks. In addition, amides are more highly protein-bound, which also increases their relative duration of action.

Question 156

Which functional groups are common to all local anesthetics? (2)

Answer 156

All local anaesthetics have a lipid-soluble ring linked to an amine-containing group. The two groups of local anaesthetic differ in the type of linkage.

Question 157

Difference between Marcain and Marcain Heavy?

Answer 157

Marcain®. Colourless solution 0.25% and 0.5%.

Marcain®. Heavy: 0.5% bupivacaine with glucose 80 mg/ml, 4 ml ampoule, for subarachnoid block.

Question 158

Max dose bupivicaine with or without adrenaline

Unwanted effects (2)

Answer 158

2 mg/kg

Myocardial depression

CNS convulsions then coma

Levobupivacaine less toxic.

Question 159

Examples of ester local anaesthetics (2)

Answer 159

Tetracaine (amethocaine)

Cocaine

Question 160

Contents of ametop vs contents of EMLA?

Differences in effect (3)

Answer 160

Ametop: Tetracaine (amethocaine) 4% as a gel

EMLA: Lidocaine 2.5% and prilocaine 2.5% in a cream

Ametop takes 30 minutes to work effectively

It is faster-acting than EMLA

Does not last as long.

It does not cause vasoconstriction like EMLA

Can cause hypersensitivy

Question 161

Ephedrine

Presentation?

Dose?

Mode of action?

What effect is seen with repeated doses?

Answer 161

Presentation - 30mg in 10ml normal saline (3mg/ml)

Dose - 3-6mg titrated to effect. Less effective beyond total dose 30mg.

Mode of action - indirect action, causing release of noradrenaline at the sympathetic nerve terminals. Acts on alpha and beta adrenoreceptors causing increase CO + SVR.

What effect is seen with repeated doses - Tachyphylaxis due to depletion of noradrenaline stores

Question 162

Phenylephrine

Presentation

Dose

Mode of action

Adverse effect

Answer 162

Presentation - 10mg in 100ml normal saline (100µg/ml)

Dose - 50-100µg, titrated to effect

Mode of action - Acts only on alpha adrenoceptors. Causes vasoconstriction and in increased SVR.

Adverse effect - Reflex bradycardia which can cause a fall in cardiac output if a large dose is given

Question 164

Metaraminol

Presentation

Dose

Mode of action

Adverse effect

Answer 164

Presentation - 10mg in 20ml normal saline (0.5mg/ml)

Dose - 0.5mg dose titrated to effect

Mode of action - It acts mainly via alpha-adrenoceptors causing an increase in BP via an increase in systemic vascular resistance. It has only minimal effects on beta-adrenoceptors and hence cardiac contractility

Adverse effect - Reflex bradycardia

Question 165

Most common causes of intraoperative bradycardia (2)

Answer 165

Intraoperative bradycardia, i.e. rate <50 bpm, is usually due to either vagal stimulation or the combination of a well beta-blocked patient and a general anaesthetic.

Question 166

Causes of intraoperative vagal stimulation (4)

Answer 166

Vagal stimulation may be due to stretching or pulling of any part of the airway or gut that is innervated by the vagus nerve. Stimulation of the inferior surface of the epiglottis, pneumoperitoneum (especially higher pressures) and manipulation of the bowel may all cause bradycardia. Traction on structures innervated by the sacral parasympathetic outflow, particularly those of the genito-urinary system, may also cause bradycardia.

Question 167

Why is glycopyrrolate is free of the unwanted central effects of atropine, such as sedation?

Answer 167

Atropine can cross the blood-brain barrier but glycopyrrolate cannot because, unlike atropine, it carries a permanent charge on its nitrogen atom, which makes it much less lipid soluble.

Question 168

Atropine

Presentations (2)

Dose

Mechanism

Answer 168

Presentation - Usually 600µg/ml but for cardiac arrests prepacked 3mg in 10ml (300µg/ml)

Dose - 500g up to max 1.2mg

Mechanism - Blocks acetylcholine (cholinergic muscarinic antagonist)

Question 169

Glycopyrrolate

Presentation

Dose

Mechanism

Answer 169

Presentation - Usually presented at a concentration of 200 μg/ml.

Dose - Titrated to effect with doses of 100-200 μg, up to 600 μg.

Mechanism - Blocks acetylcholine (cholinergic muscarinic antagonist)

Question 170

Acute bronchospasm

Three non-pharmacological interventions (3)

Immediate pharmacological interventions (5)

Answer 170

Three non-pharmalogical interventions are:

• Adequate expiratory time when ventilated, to avoid air trapping
• Consider pressure-controlled ventilation
• Optimizing patient position, i.e. minimize pneumoperitoneum

Immediate pharmacological interventions

• Oxygen
• Inhaled anaesthetics
• Salbutamol
• Aminophylline
• Adrenaline

Question 171

IV salbutamol

Presentation

Dose

Why not inhaled or nebulised?

Answer 171

Presentation - 1 ml ampoules containing 500 μg/ml; there is also a 5 ml ampoule containing 5 mg salbutamol. The recommended dilution is 50 μg/ml.

The recommended dose is 250 μg by slow IV injection. In theatre this should be given over at least 20 minutes, taking care to avoid tachycardia. The intensive care unit (ICU) recommended rate of infusion is 5 μg/min.

For inhalers, the patient is required to produce a high inspiratory flow rate in order to get the drug into the lungs. It is not possible to achieve this in an anaesthetized patient. Nebulizers can be successfully attached to ICU ventilators, but for the most part this is not possible in theatres.

Question 172

Aminophylline

Presentation

Dose

Mechanism

Caution

Answer 172

Presentation - It is presented as 250mg in a 10 ml ampoule, so further dilution is not required

Dose - 250 mg titrated to effect over 20 minutes.

Mechanism - It acts as a non-specific phosphodiesterase inhibitor to increase cAMP within cells, leading to smooth muscle relaxation.

Caution - Should not be used in patients who are normally controlled on a preparation containing theophylline, because the plasma concentrations may easily enter the toxic range and result in seizure activity and arrhythmias.

Question 173

How should adrenaline be given to treat refractory bronchospasm?

Answer 173

Low dose adrenaline, starting with 50 μg-0.5 ml of 1 in 10 000 adrenaline (100 μg/ml), titrated to effect.

At low dose, adrenaline is mainly active at beta-adrenoceptors

Question 174

Rate of anaphylaxis due to anaesthetic drugs? Which are most commonly involved?

Answer 174

Anaphylaxis due to anaesthetic drugs has an incidence of about 1 in 10-20 000.

This translates into about 55 suspected anaphylactic reactions per year in the UK. Data from France suggests that neuromuscular blocking drugs are the most commonly-involved group.

Question 175

Malignant hyperthermia

Inheritance?

Triggers?

Features (4)

Treatment (4)

Answer 175

Autosomal dominant condition.

It may be triggered by volatile anaesthetic agents and succinylcholine, but not necessarily at the first exposure.

The common clinical features are increasing end tidal CO2, tachycardia and increased oxygen consumption. Hyperthermia is not an early sign.

Treatment involves:

• Removing the suspected triggering agent
• Ventilating with a high minute volume in a high FIO2
• Administering dantrolene at 2 mg/kg up to 10 mg/kg
• Active cooling

Question 176

Dantrolene

Presentation

Dose

Mechanism

Answer 176

Presentation - Dantrolene is presented in a glass vial containing only 20 mg

Dose - 2mg/kg - For an average man of 80 kg, 2 mg/kg requires 160 mg (= 8 vials)

Mechanism - uncouples the action potential from the contractile process within skeletal muscle by binding to the ryanodine receptor (i.e. stops the release of calcium from the sarcoplasmic reticulum).

Question 177

Definition of a gas

Answer 177

A gas is a compressible fluid phase in which no liquid can be formed at that temperature.

Question 178

Definition of critical temperature

Answer 178

The threshold above which a substance exists as a gas is its critical temperature

Question 179

Definition of a vapour

Answer 179

A vapour is a gaseous phase which is in a state of equilibrium with the same substance in liquid form. A vapour can only exist below its critical temperature

Question 180

What is Boyle’s Law?

How are the pressure and volume of a gas related in two different settings?

Answer 180

P is inversely proportional to V

P ∝ 1/V

The relationship of P and V for a gas in two different settings is therefore:

P1V1 = P2V2

Question 181

How much oxygen does a 5L cylinder containing O2 at 100 atm provide at 1atm?

Answer 181

A 5 L cylinder containing oxygen at a pressure of 100 atmospheres provides a supply of 500 L at 1 atmosphere.

Question 182

Charles’s Law?

Answer 182

Volume is proportional to absolute temperature

(in a closed system with a fixed mass of gas)

Question 183

Gay-Lussac’s Law

Answer 183

If a fixed mass of gas is kept at a constant volume in a closed system, its pressure is directly proportional to the absolute temperature

P∝T

Question 184

The Combined Gas Law

Answer 184

The laws of Boyle, Charles and Gay-Lussac are assimilated to produce the Combined Gas Law, which relates pressure, volume and temperature.

PV/T=k

Question 185

The Ideal Gas Law

Answer 185

PV = nRT

Question 186

Why does the ideal gas law not apply to N2O at room temperature?

Answer 186

Because nitrous oxide has a critical temperature of 36.5°C, the cylinder contains liquid and vapour, so the gas laws do not apply. A cylinder of nitrous oxide has to be weighed to measure its contents.

Question 187

How are partial pressure and total pressure related?

Whose Law is this?

Answer 187

The total pressure is the sum of the pressures of the individual gases, as if they were alone in the same volume (Dalton’s Law).

The pressure exerted by each gas is termed its partial pressure, and it is assumed that the temperature is constant and that they do not react with each other.

Question 188

Definition of saturated vapour pressure?

Answer 188

As a liquid continues to evaporate into a space above it, the pressure of its vapour increases. A point of equilibrium is reached at which the rate of evaporation equals that of condensation, when the space becomes saturated.

Question 189

Why do liquids cool during vapourization?

Answer 189

Liquid molecules require energy to become vapour. This is the latent heat of vaporization. If this energy cannot be obtained from external sources then it is drawn from the liquid causing it to cool. This occurs in a vaporizer or when a nitrous oxide cylinder is used.

Question 190

How is the temperature when saturated vapour pressure equals atmospheric pressure also known?

Answer 190

The temperature at which the saturated vapour pressure equals the atmospheric presure is the boiling point.

Question 192

Henry’s Law

Answer 192

The amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid.

Question 193

How does temperature affect the solubility of gas in a liquid?

Answer 193

As the temperature increases, the molecules in the solution have more energy to get out of the liquid and so solubility falls.

Conversely, a fall in temperature increases the solubility of a gas in a liquid.

Question 194

The danger of an electric shock is influenced by? (3)

Answer 194

• Overall strength of current
• Type and frequency of current
• Local current density

Question 195

In the UK, mains electricity supply is:

• AC or DC?
• Hz?

Answer 195

In the UK, the mains supply is alternating current (AC), with a frequency of 50 Hz.

Question 196

What is Ohm’s Law?

Answer 196

Voltage = Current × Resistance (V = IR).

Question 197

Which term replaces resistance when dealing with alternating current?

Answer 197

For alternating current, the term impedance (Z) is used instead of resistance, and can be similarly used in Ohm’s Law to calculate current. Impedance varies with frequency.

Question 198

How is electrical current measured?

What determines current in a circuit?

Answer 198

Electrical current is measured in amperes (A). Current (I) in a circuit depends on the electrical barrier presented to the voltage (V) applied.

Question 199

What is the effect of the following currents when applies to the skin?

• Up to 5mA
• 10-20 mA
• 50 mA
• 100-300 mA

Answer 199

• Up to 5mA - Tingling but generally harmless
• 10-20 mA - Pain, sustained muscular contraction.
• 50 mA - Risk of arrhythmias, e.g. ventricular ectopics
• 100-300 mA - Risk of ventricular fibrillation.

Question 200

What is the typical impedance of dry skin?

Using Ohm’s Law, what current would be produced by touching mains voltage of 240V?

What increases the risk of shock by reducing skin impedance? (2)

Answer 200

A typical impedance value for dry skin is 10 kΩ.

I=V/Z

= 240/10000

=24 x 10^-3 A

= 24mA

Skin impedance falls, and therefore the risk becomes greater, with:

• A high surface area of contact
• Wet skin

Question 201

How does current density change with cross sectional area?

How is this used in unipolar diathermy?

Answer 201

A current passing through the body does so via all the tissues between the entry and exit points. As the cross-sectional area becomes larger, e.g. going from the arm to the thorax, the current density is much reduced. However, if there is a marked narrowing in the circuit at any point, the current density increases markedly in this area.

Unipolar diathermy is used to cut tissues or cauterize vessels during surgery. A high-frequency current is passed through a fine blade or forceps, returning via a large, low impedance pad. The current density is very high at the tip producing an intense heating effect.

Question 202

What is microshock?

Answer 202

If an aberrant current were to occur in a faulty device connected to an intra-cardiac catheter, e.g. CVP line, external pacemaker, there is a risk that the entire current could enter the myocardium through a small area, thus generating a high current density

Under these circumstances, a current as low as 0.1 mA may be sufficient to trigger VF. This effect, called microshock, may be evident even at low voltages.

Question 203

Three classes of insulation according to British Standards?

Answer 203

Class I

• Used in most low risk equipment
• Any exposed metal parts, e.g. the case, must be connected to earth
• Functions in combination with a cut-out device

Class II

• This equipment is often called double-insulated, all exposed parts having two layers of insulation
• An earth connection is not required

Class III

• These devices are powered internally, usually by a battery, and run at a voltage of less than 40 V DC
• If an AC supply is used then an isolating transformer is incorporated
• Though there is still a risk of electric shock, the major hazard arising from mains voltage has been removed

Question 204

How does a fuse work (in terms of impedance and current)?

Answer 204

For most standard major electrical items a fuse is incorporated into the live supply and the earth wire is connected to the equipment casing.

In the event of a fault that makes the casing live, the earth provides a low impedance return pathway to the sub-station. The sudden surge in current melts the fuse, thereby disconnecting the live supply.

The fuse must be appropriately rated so that it does not blow with normal use.

Question 205

How does a circuit breaker work?

Answer 205

The Current-Operated Earth Leakage Circuit Breaker (COELCB) is a widely used device which monitors the current flowing in the live and neutral conductors.

A difference in the flowing current indicates that current may be flowing to earth by another means. If such a difference is detected, the circuit breaker rapidly operates a relay on the live conductor, switching off power.

A current difference as low as 30 mA may trip the device and it can switch off in 30 ms. If it switches off, then the supply should not be re-established until the cause is rectified.

Question 206

1 atm is equates to (approximately) how many:

• bar
• psi
• kPa
• cmH2O

Answer 206

1 atmosphere equates to (approximately):

• 1 bar
• 15 pounds per square inch (psi)
• 100 kPa
• 1033.23 cmH2O

Question 207

What is the SI unit of pressure and what is it equivalent to?

Answer 207

The SI unit of pressure is the pascal (Pa) and is equivalent to a force of 1 newton applied over an area of 1 m2.

Question 208

How is the hospital’s oxygen supply stored in most hospitals?

At what pressure is the pipeline for delivery into the main hospital?

Answer 208

In most hospitals oxygen is stored as a liquid in a large vacuum flask, i.e. a Vacuum Insulated Evaporator or VIE.

The oxygen is liquefied by cooling it to -150 degrees C and is kept at a pressure of 1000 kPa (10 atmospheres).

The oxygen is allowed to warm up to room temperature so that it turns back into a gas and the pressure is regulated to a pressure of 440 kPa.

Question 209

What is Entonox?

Cylinder colour and pressure?

Why must it be kept above -6 degrees C?

Answer 209

Entonox is a 50:50 mixture of nitrous oxide and oxygen

Entonox ® is stored in white or blue cylinders with blue and white shoulders. It is supplied in cylinders at a pressure of 137 bar and must be stored above its pseudocritical temperature of -6 degrees C.

Below this temperature the nitrous oxide liquefies in a process called lamination.

Question 210

To what do the following pipeline colours correspond?

• White
• Blue
• Black
• Yellow
• Clear

Answer 210

White - Oxygen

Blue - Nitrous oxide

Black - Air

Yellow - Suction

Clear - Anaesthetic gas scavenging

Question 212

Which volatile is the odd one out and requires a heated vapouriser?

Answer 212

Desflurane is the odd one out in terms of vaporization: because of its low boiling point it is delivered from a heated vaporizer which has to be plugged into a mains electricity supply to operate. It is also filled from a sealed bottle system and has a built in low level alarm.

Question 213

What are the three sizes of connector used in adult breathing systems?

Answer 213

The connectors used in adult breathing systems, up to the final connections to the endotracheal tube or laryngeal mask airway, are made up of a 22 mm conical male and female connector.

Another set of connectors used in the breathing system itself are the smaller 15 mm male and female connectors. They are used on both endotracheal tubes and laryngeal mask airways

The third commonly used connector in adult breathing systems is a 30 mm-sized conical connector. It is used with Anaesthetic Gas Scavenging Systems (AGSS).

Question 214

What does APL stand for?

What are the three functions of an APL?

Answer 214

An adjustable pressure limiting (APL) valve

The APL is a specialized valve that has three important functions:

• As a one-way exhaust valve
• As a mechanism to enable adjustable positive pressure ventilation using a reservoir bag
• As a safety blow-off valve in the breathing system

Question 215

In which situations may blood pressure be more important than flow? (2)

Answer 215

An organ requiring a certain perfusion pressure (e.g. the kidney)

A disease state in which an obstruction in the circulation requires a high pressure to overcome it (e.g. carotid stenosis)

Question 216

What equation links pressure, flow and resistance?

What are the equivalent values for the circulation?

Answer 216

Pressure = Flow x Resistance

BP = CO x SVR

Question 217

What is the most efficient type of flow?

Which equation calculates laminar flow?

Answer 217

The most efficient type of flow is laminar, in which fluid layers move smoothly over each other. Under laminar conditions flow can be calculated from Poiseuille’s formula.

Q = ΔPπr⁴ / 8ηL

Question 218

What is the dicrotic notch in arterial pressure waveform?

Answer 218

The change in shape during the descending part of the wave is the dicrotic notch. It is generally thought to represent the elastic recoil of the aortic wall immediately after aortic valve closure.

Question 219

Where is the biggest fall in pressure in the circulation? Why?

How are these vessels also known?

Answer 219

The biggest fall in pressure in the circulation occurs in the arterioles, particularly those supplying the major organs. They are often called resistance vessels. Their small radius produces a high resistance. Resistance is inversely proportional to the fourth power of the radius.

Question 220

What are capacitance vessels? When is their volume reduced?

Answer 220

The pressure in the veins is low, but they hold a large proportion of the circulating blood volume: the capacitance vessels.

In hypovolaemia, when the body’s responses lead to vasoconstriction, particularly in the skin/gut with most of the blood kept in the central circulation to perfuse the vital organs.

Question 221

Why can an increase in HR lead to myocardial ischaemia?

Answer 221

Less time spent in diastole and therefore less time for perfusion.

Question 222

What are the two main body systems that regulate the cardiovascular system?

Which provides rapid response to hypotension?

How do carotid sinus baroreceptors react to changes in BP?

Answer 222

• Autonomic nervous system (seconds to minutes)
• Humoral system (minutes to hours)

They are activated by stretch produced by a rise in blood pressure.

Because they respond to stretch, activation of the baroreceptors results in an inhibitory effect on the cardiovascular system, causing a fall in heart rate and vasodilatation.

Vasoconstriction and tachycardia result from a decrease in activity in the baroreceptors when the blood pressure falls.

Question 223

How does the juxtaglomerular apparatus exert control on blood pressure?

Answer 223

Hypotension, leading to a reduction in flow through the renal tubule, is sensed by the juxtaglomerular apparatus.

This releases renin that activates the cascade which ultimately produces angiotensin II, a powerful vasoconstrictor.

Renin also stimulates aldosterone release from the adrenal cortex, leading to Na+ and H2O retention.

Question 224

How are the classes of shock defined by:

• Blood loss (ml)
• Blood loss (%)
• HR
• CRT
• BP

Answer 224

• Blood loss (ml)
  
  • Class 1 <750ml, Class 2 750-1500, Class 3 1500-2000m Class 4 >2000
• Blood loss (%)
  
  • Class 1 <15%, Class 2 15-30, Class 3 30-40, Class 4 >40
• HR
  
  • Class 1 <100, Class 2 100-120, Class 3 120-140, Class 4 >140
• CRT
  
  • Normal, >2m >5, Not detectable
• BP
  
  • Normal, normal, reduced, v low

Question 225

How is the simultaneous contraction of fibres in cardiomyocytes achieved?

Answer 225

Simultaneous contraction of all fibres is achieved by the specialized conduction system, the syncitial nature of cardiac muscle and by prolonging the action potential via slow Ca2+ inflow through L-type channels, thus ensuring total ventricular depolarization.

Question 226

What is the natural firing rate of the SA node?

Answer 226

100-120/min. The heart rate is normally slower because of dominant vagal parasympathetic activity.

Question 227

How big is the area for alveolar gas exchange in an adult?

Answer 227

80-90 m2, approximately half the size of a singles tennis court.

Question 228

Normal TV?

Volume of anatomical dead space?

Answer 228

500ml

150ml

Question 229

Approximate values for a fit young male:

• TLC?
• FRC?
• VC?
• RV?

Answer 229

VT Tidal volume (500 mL)

IRV Inspiratory reserve volume (3000 mL)

ERV Expiratory reserve volume (1500 mL)

RV Residual volume (1000 mL)

TLC Total lung capacity (6000 mL)

VC Vital capacity (5000 mL)

FRC Functional residual capacity (2500 mL)

Question 230

Which inward and outward forces determine FRC?

Answer 230

Its position is determined by the inward forces (lung elasticity) balanced against the outward forces (respiratory muscle tone).

Question 231

Two main reasons that FRC is important to anaesthetists?

Answer 231

During apnoea it provides the reservoir in the lungs from which oxygen can be taken to maintain arterial oxygenation – the greater the oxygen reservoir, the longer the time before hypoxaemia develops

FRC has a major influence on the distribution of ventilation within the lung by determining where the starting position of each area of the lung is on the compliance curve

Question 232

Approximate number of airway branches between trachea and alveoli?

To what level of branching is gas flow a result of respiratory effort? What occurs after that?

In what structures does gas exchange first take place?

Answer 232

From the trachea to the alveoli, branching of the airway occurs approximately 23 times.

Flow of gas resulting from respiratory effort only occurs down to division 16. Below this, gases move passively by diffusion along partial pressure gradients, between the alveoli and higher airways.

Respiratory bronchioles.

Question 233

How much pressure is generated during spontaneously breathing?

How much is required to achieve the same tidal volumes via IPPV?

Answer 233

When breathing spontaneously, inspiratory flow occurs by creating a small negative pressure in the alveoli (~ 2-3 cm H2O below atmospheric).

A higher pressure is normally needed (~ 10-15 cm H2O) to deliver the same tidal volume during IPPV.

Question 234

Which factors influence rate and depth of respiration feeding into the brain’s respiratory centres? (4)

Which is most important?

Answer 234

Rising CO2 (central chemoreceptors) - most important (Arterial PCO2 is closely maintained between
5.1–5.5 kPa)

Falling O2 (peripheral chemoreceptors)

Voluntary control (cortex)

Muscle activity (stretch receptors)

Question 235

How is PaCO2 related to minute ventilation? Why does the curve flatten at low PaCO2 values?

How do opioids or anaesthetic agents affect this curve?

Answer 235

As the arterial PaCO2 rises, the Vmin increases in an attempt to bring it back to the normal range. The lower end of the curve flattens out because automatic firing from the respiratory centre maintains a minimum Vmin.

Drugs that depress the CNS make the chemoreceptors less sensitive to PaCO2, moving the curve to the right and making it less steep

Question 236

How do obstructive and restrictive lung diseases affect lung resistance and compliance respectively?

Answer 236

An increase in resistance is seen in obstructive airways disease.

A decrease (worsening) in compliance occurs with restrictive lung disease.

Question 237

How does ventilation change between apices and bases in normal breathing?

And perfusion?

Answer 237

Ventilation

In a normal patient breathing spontaneously, the resting position of the lung is such that the apices are already reasonably expanded, whilst the bases are more squashed (though not collapsed). The resulting positions on the compliance diagram mean that the bases and mid-zones are on the steep part of the curve and receive more ventilation.

Perfusion

The effect of gravity reduces the perfusion pressure by 1 cm H2O for every cm in height above the level of the heart, with a similar increase below. This means that perfusion at the apices reduces to virtually zero, and increases progressively down to the bases.

Question 238

What is shunt in terms of V & Q?

Answer 238

No ventilation (V/Q = 0)

Question 239

What is alveolar dead space in terms of V & Q?

Answer 239

No perfusion (V/Q = ∞)

Perfusion may cease because of occlusion by embolus (thrombus or air) or because of a fall in cardiac output leading to an inadequate pressure to perfuse the upper part of the lung.

Question 240

How does an increase in dead space affect etCO2?

Answer 240

The end-tidal CO2 will fall because the gas not involved in respiratory exchange will dilute the CO2 concentration coming from areas of lung that have been.

Question 241

How does general anaesthesia generally affect V/Q mismatching?

Answer 241

General anaesthesia almost inevitably produces some degree of V/Q mismatching because of the associated fall in FRC, which moves the lung down the compliance curve.

The bases are now on the lower (unfavourable) part of the curve and receive less ventilation, whilst the apices become more compliant and receive more.

The distribution of perfusion - influenced largely by gravity - is unchanged, with the mid-zones and bases receiving most of the blood flow, resulting in V/Q mismatch.

Question 242

How much O2/min does the body use at rest?

Equation for calculating oxygen consumption?

Answer 242

The body uses approximately 250 mL O2/min at rest.

Oxygen consumption at rest can be calculated by measuring the difference between inspired (Fi = 21%) and expired (FE = 16%) oxygen concentration and then multiplying that by the alveolar minute volume (VA = 5 L/min):

O2 consumption = VA x (Fi – FE)

= 5000 x (0.21 – 0.16)

= 250 mL/min

Question 243

Solubility of oxygen in plasma?

Answer 243

0.23 mL/L/kPa

Question 244

What is the main regulator of Hb production?

Answer 244

The main regulator of Hb production is erythropoietin (EPO), which is secreted by kidney in response to tissue O2 level.

Question 245

How many oxygen molecules can each Hb bind?

How does oxygen binding to haemoglobin change as more molecules attach?

Answer 245

Four - one to each haem group

Initial binding of O2 is difficult, but as the first O2 molecule binds it changes the shape of the Hb molecule slightly, making other binding sites more accessible.

Subsequent binding of the second and third O2 molecules is therefore easier (cooperativity), but once these sites are occupied, full saturation with the fourth molecule becomes more difficult as only one free binding site remains.

Question 246

At rest, approximately how much oxygen is extracted by tissues?

What is P50 (with respect to the Hb-O2 saturation curve?

Answer 246

At rest, approximately 25% of the available O2 is extracted by the tissues, resulting in a venous saturation of 75% and a PO2 of around 5.3 kPa.

The P50 is the PO2 at which the Hb-O2 saturation is 50%, normally around 3.5 kPa. It is a reference point that describes the position of the curve and changes as the curve moves under different conditions.

Question 247

3 ways to express blood oxygen level?

Answer 247

Partial pressure (PaO2)

Saturation (SpO2)

Content (CaO2)

Question 248

Atmospheric oxygen content in kPa?

Answer 248

21kPa

Question 249

What is the oxygen cascade and what are its parts (3)?

Answer 249

Oxygen cascade

The normal PaO2 (13 kPa) is reached after a three stage fall from the atmospheric level (21 kPa), known as the oxygen cascade:

• In the upper airway, humidification adds water vapour
• In the alveoli, O2 is taken up in exchange for CO2
• In the circulation, from the small physiological shunt caused by the bronchial circulation and thebesian veins

Question 250

Equation for oxygen content of blood?

What is normal CaO2 of arterial blood?

Answer 250

CaO2= Hb-bound + dissolved

= ([Hb] x 1.34 x satn) + (0.23 x PO2)

= (150 x 1.34 x 0.98) + (0.23 x 13)

= 197 + 3

= 200 mL/L

Question 251

What is VO2?

Things that increase VO2? (5)

And VO2 max?

Answer 251

The rate of O2 consumption (VO2) is higher during muscular activity (including shivering), in pregnancy, in childhood and in states that increase metabolic rate (e.g. pyrexia, thyrotoxicosis).

The maximum extent to which an individual can increase his/her O2 consumption during exercise (VO2 max) is increasingly being used as a measure of cardiopulmonary fitness.

Question 252

At what level of deoxy-Hb is cyanosis seen?

Why does it not always correspond to measured SpO2?

Answer 252

It is detected clinically when ≥ 5 g/dL deoxy-Hb can be seen in the skin or mucous membranes.

Cyanosis is seen in capillary blood, whilst a pulse oximeter reading is based on the arterial value, which will be substantially higher because:

• PO2 is slightly higher in the artery than the capillary
• The saturation curve in the capillary has a small right shift (Bohr effect)

Question 253

How does anaemia affect CaO2 and SpO2?

Answer 253

Because almost all O2 is carried bound to Hb, anaemia reduces O2 content approximately in proportion to the fall in Hb.

The saturation will be unaffected as all the Hb present is saturated and the PO2 is unchanged as it measures the level in plasma.

Question 255

How are cholinergic receptors subdivided? (2)

How do their mechanisms of action differ? Which type of ion channel are they?

Where can each subtype be found?

Answer 255

Cholinergic receptors are subdivided into nicotinic and muscarinic receptors.

They can be artificially stimulated respectively by the alkaloids:

• Nicotine, found in the tobacco plant
• Muscarine, from the poisonous amanita mushroom

Nicotinic receptors are transmembrane channels that open to allow Na+ ions to flow through in response to activation by ACh. This is an example of a ligand-gated ion channel.

Nicotinic receptors exist throughout the body in:

• All autonomic ganglia
• The adrenal medulla
• The neuromuscular junction

Muscarinic receptors are predominantly found at parasympathetic postganglionic junctions and work instead by G-protein linkage.

Question 256

What is the resting membrane potential of a neuron?

Answer 256

Neurones have a constant resting membrane potential (RMP), set at about -70 mV. The inside is negative relative to the exterior.

Question 258

Timing with respect to anaesthesia for the following pharmacological measures in patients with high aspiration risk:

• PPI
• H2 antagonist
• Antacids
• Prokinetics

Answer 258

• PPI - 90 mins prior
• H2 antagonist - 90 mins prior
• Antacids - Immediately before
• Prokinetics- 90 mins prior

Question 259

Virchow’s triad?

Answer 259

Hypercoagulability

Vessel wall injury

Venous stasis

Question 261

Which two sets of neurons make up the efferent pathways for both the SNS and PNS? Where do they synapse?

Where are their cell bodies?

What type of fibres are they?

Answer 261

The efferent pathways for both the SNS and PNS consist of two sets of neurones, ‘preganglionic’ and ‘postganglionic’, that synapse in an intermediary ganglion.

The cell bodies of the preganglionic neurones are in the brain or spinal cord. Each preganglionic cell anastomoses with 8-9 postganglionic cells to produce the diffuse responses characteristic of the ANS

Preganglionic axons are myelinated slow conducting B fibres.

The axons of the postganglionic neurones are mainly unmyelinated C fibres.

Question 262

Where do sympathetic nervous system efferents originate?

Where are their preganglionic cell bodies found?

What are the three ways they can terminate?

Answer 262

The sympathetic efferents have a thoracolumbar outflow from spinal roots T1-L2.

Preganglionic cell bodies are found in the lateral horns of the spinal cord, and their axons can terminate in one of three ways:

1. Most synapse in the paravertebral sympathetic chain
2. Some pass through the sympathetic chain via the splanchnic nerves to synapse in a peripheral autonomic ganglion in the abdomen or pelvis (e.g. coeliac, mesenteric)
3. Direct synapse with chromaffin cells in medulla of adrenal gland

Question 263

Where do parasympathetic efferents originate?

Where are their cell bodies originate? (2)

How do the majority synapse? What are the four discrete intermediary ganglia?

Answer 263

The parasympathetic efferents have a cranio-sacral outflow from cranial nerves III, VII, IX and X and spinal roots S2-4.

The preganglionic cell bodies are in the cranial nerve nuclei or the lateral horns of the sacral spinal cord.

Parasympathetic ganglia from the vagus and sacral efferents are usually diffusely located in the walls of the viscera they supply (heart, lungs, gut).

Cranial nerves III, VII and IX that supply the head and neck synapse in four discrete intermediary ganglia: the ciliary, sphenopalatine, submaxillary or otic ganglion.

Question 264

How does sympathetic outflow reach the head and pelvic regions?

Which sympathetic ganglia supply the head?

Where is the stellate ganglion found?

Answer 264

There is no direct sympathetic outflow to the head and neck or pelvic region, rather neurones travel up or down from the thoracolumbar sympathetic chain to cervical or sacral ganglia

The sympathetic outflow to the head and neck is via the superior, middle and inferior cervical ganglia.

The inferior cervical ganglion is often fused with the first thoracic ganglion to form the stellate ganglion at the level of C6, just in front of the neck of the first rib.

Question 265

How do visceral autonomic afferents travel back to the CNS?

Which organs have parasympathetic visceral pain fibres? (3)

Which organs have sympathetic visceral pain fibres? (2)

Answer 265

Visceral autonomic afferents and pain fibres travel with autonomic efferent nerves (but synapse in the brain and spinal cord).

Pain fibres from the lungs, bronchi and pelvis travel with parasympathetic nerves

Pain fibres from the abdominal viscera and heart travel with sympathetic nerves.

Question 266

How are the following blocks used?

• Thoracic sympathectomy
• Lumbar sympathectomy
• Coeliac plexus block

Answer 266

Thoracic sympathectomy is used for the treatment of severe Reynaud’s phenomenon or hyperhidrosis (sweaty palms).

Lumbar sympathectomy is used for circulatory insufficiency of the lower limb or phantom limb pain.

Coeliac plexus block is used for the pain associated with upper GI malignancy or acute or chronic pancreatitis.

Question 267

What are the two main neurotransmitters in the ANS?

Which neurotransmitter is used by:

• all pre-ganglionic neurones?
• all post-ganglionic parasympathetic neurones?
• post-ganglionic sympathetic neurones that innervate sweat glands and skeletal muscle blood vessels?
• All other post-ganglionic sympathetic neurones?

Answer 267

Acetylcholine + Noradrenaline

Which neurotransmitter is used by:

• all pre-ganglionic neurones - ACh
• all post-ganglionic parasympathetic neurones - ACh
• post-ganglionic sympathetic neurones that innervate sweat glands - ACh
• All other post-ganglionic sympathetic neurones - NA

Question 268

What are the two types of acetylcholine receptors?

Where are each type found?

What is the receptor mechanism for each?

Which is affected by atropine?

Answer 268

Muscarinic receptors, M1-M5, are:

• Found in smooth muscle, glands, the heart and the brain
• G protein-linked; their actions are mimicked by muscarine
• Blocked by atropine

Nicotinic receptors are:

• Found in the sympathetic ganglia and the motor end-plates of skeletal muscle
• Ligand-gated ion channel receptors; their actions are mimicked by nicotine, but unaffected by atropine

Question 269

How does neostigmine reverse neuro-muscular blockade?

How are unwanted muscarinic effects avoided?

Answer 269

An anticholinesterase (neostigmine) is given to increase ACh levels. at the motor end-plate of the neuromuscular junction blocker (nicotinic) this reverses the effect of the muscle relaxant.

Unwanted muscarinic effects of the ACh are prevented by the use of an agent such as atropine or glycopyrrolate.

Question 270

What are the two main types of adrenergic receptor?

By what mechanism do they all work?

Answer 270

There are two main types of adrenergic receptors, alpha (α) and beta (β), both linked to G-proteins and each with subtypes

Question 271

Are the following pre- or post-synaptic?

• Alpha 1
• Alpha 2
• Beta 1
• Beta 2

Does noradrenaline have a greater affinity for alpha or beta receptors? And adrenaline?

Answer 271

α1, β1 and β2 receptors are all post-synaptic.

α2 receptors may be presynaptic and post-synaptic.

Noradrenaline has a greater affinity for α receptors, adrenaline for β receptors.

Question 272

Effects of stimulating the following receptors:

• Alpha 1 (2)
• Alpha 2 (2)
• Beta (3)

Second messenger for each?

Answer 272

• Alpha 1 - Phospholipase C - Smooth muscle contraction, glycogenolysis
• Alpha 2 - Adenyl cyclase - Inhibition of norad release, smooth muscle contraction
• Beta - Adenyl cyclase - Contraction of cardiac muscle, smooth muscle relaxation, glycogenlysis

Question 273

How does parasympathetic stimulation affect the pupil?

And sympathetic stimulation?

Which muscles are involved?

Answer 273

The sphincter of the iris: parasympathetic stimulation produces pupil constriction (miosis)

The radial muscle of the iris: sympathetic stimulation produces pupil dilation (mydriasis) (α1)

Question 274

What is the effect of spinal block for Caesarean section on blood pressure?

How may this be managed?

What additional effect does high spinal block have on the cardiovascular system?

Answer 274

Blood pressure falls due to associated sympathetic block that produces widespread vasodilation (T4-L2).

Fluid loading and use of a directly acting vasoconstrictor such as phenylephrine.

More profound hypotension due to greater sympathetic block and bradycardia from loss of sympathetic supply to the heart (T1-4).

Question 275

How long should surgery be delayed for post-MI?

And post-PCI?

Answer 275

The risk of dying in the month after an MI is about 50 times the risk of dying in the month before an MI. By 12 months the relative risk has fallen to between 3 and 1.5 times average. Between the first and twelfth month the relative mortality risk probably falls exponentially.

Normally surgery should be delayed for 3-6 months following MI.

Six months after placement of stents the risk of dying is no longer elevated. But if clopidogrel is stopped (for surgery) in patients with drug-eluting stents their risk of dying will increase, perhaps five times. he management of patients with stents who are receiving anti-platelet medication should be jointly planned with the cardiologist.

Question 276

Why is rate control for AF required for surgery?

Answer 276

In patients with atrial fibrillation (AF) a marked sudden increase in ventricular rate may compromise adequate ventricular filling.

Patients in AF should ideally should have their rate controlled to <100 bpm pre-operatively.

Question 277

Aspirin is continued in most surgeries except for those involving the following? (3)

When should it be stopped if it is?

Answer 277

The risk of bleeding if aspirin is continued is exceeded by the risk of thromboses, except for surgeries in:

• The brain
• Spinal canal
• Prostate

Orthopaedic surgeons and general surgeons vary in their practices.

If stopping aspirin, this should be done at least five days pre-operatively.

Question 278

Frequency of failed intubation in elective GAs?

And emergency GAs?

Frequency of failed mask ventilation?

Answer 278

Failed intubation occurs about 1 in 2000 elective general anaesthetics and 1 in 300 emergency anaesthetics.

Failed mask ventilation occurs in about 1 in 1500 anaesthetics.

Question 279

Patient groups with a potentially unstable cervical spine (3)?

Answer 279

Trauma, rheumatoid arthritis, Down’s syndrome

Question 280

Adverse anatomical features suggesting a difficult airway (7)

Answer 280

1. Small mouth
2. Receding chin
3. High arched palate
4. Large tongue
5. Bull neck
6. Morbid obesity
7. Large breasts

Question 281

Acquired problems leading to airway difficulty? (5)

Answer 281

Obvious acquired problems include:

1. Burns
2. Tumours
3. Abscesses
4. Radiotherapy
5. Other scars

Question 282

Mechanical deformities leading to airway difficulties (3)

Answer 282

Fixed cervical spine, reduced temporo-mandibular movement and mouth opening.

Question 283

Why do airway tests tend often fail to predict difficult airways?

Answer 283

The tests have low specificity and low positive predictive value. This means there are a large number of false positives, and a positive test is only infrequently followed by true difficulty.

Question 284

What can be seen in a Grade 2a vs 2b view?

Answer 284

2a - Partial view of the glottis

2b - Posterior vocal cords or arytenoids just visible

Question 285

Cook’s modified classification of laryngoscopy

What are the classes?

Answer 285

Easy - Views require no adjuncts

Restricted - Views require a gum elastic bougie

Difficult - Views require advanced techniques

Question 286

What does an inter-incisor gap of <3cm predict? And less than 2.5cm?

Answer 286

If the gap is less than 3 cm, intubation difficulty is more likely. If the gap is less than 2.5 cm LMA insertion will also be difficult.

Question 287

History factors associated with difficult mask ventilation? (2)

Examination factors? (6)

Answer 287

History

• A history of snoring
• A history of sleep apnoea

Examination

• Facial abnormalities preventing mask seal
• Markedly receding jaw
• Markedly prognathic jaw
• Gross obesity
• Facial hair
• Poor dentition

Question 288

Which patients need a pre-op ECG? (3, surgical severity, +systemic disease)

Which patients need a pre-op FBC? (3)

Which patients need pre-op U+Es? (4)

Answer 288

ECG - >60yrs and surgical severity at least 3 or Any cardiovascular disease or severe renal disease?

FBC - Older than 60 years AND surgical severity at least grade 2.
All adults if surgical severity at least grade 3. Severe renal disease.

U+E - Older than 60 years AND surgical severity at least grade 3.
All adults if surgical severity at least grade 4.Any renal disease.
Severe cardiovascular disease.

Question 289

Which analgesic drugs work in the brain/thalamus? (4)

How does each work?

Answer 289

Opioids - Act at opioid receptors in the CNS: both in the brain and the dorsal horn of the spinal cord

Paracetamol - Central COX3 inhibition to reduce prostaglandin synthesis

Clonidine - Alpha-agonst, mainly central via pre-synaptic alpha 2 but also some spinal action

Ketamine - Acts central in brain and spinal cord.

Question 290

For each drug, what is the following when used for conscious sedation?

• Initial adult dose
• Initial onset time (min)
• Peak effect time (min)

1. Propofol
2. Midazolam
3. Ketamine
4. Fentanyl

Answer 290

• Propofol
  
  • 10 - 20 mg
  • ½ - 1 min
  • 1 - 2 mins
• Midazolam
  
  • 1-2mg
  • 1-2 mins
  • 3-4 mins
• Ketamine
  
  • 10-30 mg
  • 1/2 - 1 min
  • 1-2 mins
• Fentanyl
  
  • ​25-75mcg
  • 1-2 mins
  • 3-5 mins

Question 291

What are the three types of neuraxial block?

Answer 291

Spinal/subarachnoid block

Epidural/caudal block

Combined spinal epidural

Question 292

Minimum standards of monitoring for sedation in AAGBI guideline (5)

Answer 292

The following are listed as minimum standards of monitoring for sedation in AAGBI guidelines:

• Anaesthetist present
• Pulse oximeter
• ECG
• NIBP

Although not essential, monitoring ETCO2 is very useful.

Question 293

What are the monitoring requirements of regional anaesthesia vs general anaesthesia?

Answer 293

Monitoring of SpO2, ECG and BP is required. The AAGBI states that ‘The same standards of monitoring apply when the anaesthetist is responsible for a local/regional anaesthetic or a sedative technique for an operative procedure’.

Question 294

Why are patients undergoing regional anaesthetic generally fasted?

Answer 294

Patient fasting is mandatory for most regional techniques, because failure of the block or complications of the block might necessitate rapid conversion to a general anaesthetic (GA).

Question 295

In regional anaesthesia, which three techniques are commonly used to confirm the correct placement of the needle in relation to the nerves?

Answer 295

Three techniques are commonly used to confirm the correct placement of the needle in relation to the nerves:

• Seeking of paraesthesia
• Nerve stimulators
• Ultrasound guidance

Question 296

Which regional anaesthesia techniques are associated with the highest plasma concentrations of LA? (2)

Answer 296

Intercostal and interpleural

Question 297

Common complications of neuraxial blocks (6)

Frequency of rare complications?

Rare complications (5 main ones, 7 very rare others)

Answer 297

Common complications of neuraxial blocks include

• post-dural puncture headache
• hypotension
• nausea
• inadequate block
• shivering
• urinary retention.

Rare (all 1 in >5000) complications are:

• Cardiac arrest
• Respiratory failure
• Systemic LA toxicity
• Meningitis
• Spinal/epidural haematoma

Additional rare (all 1 in >5000) complications are:

• Anaphylaxis
• Spinal/epidural abscess
• Paraplegia
• Radiculopathy
• Conus medullaris injury
• Cauda equina syndrome
• Anterior spinal artery syndrome

Question 298

Three absolute contraindications to neuraxial anaesthesia?

Relative contraindications (5)

Answer 298

There are three absolute contraindications to neuraxial anaesthesia:

• Patient refusal
• Local, overlying, sepsis
• Significant uncorrected hypovolaemia

Relative contraindications include:

• Coagulopathy/anticoagulant therapy
• Aortic/mitral stenosis. There is a risk of profound hypotension from sympathetic blockade
• Previous back surgery. There may be a technical difficulty
• Systemic sepsis. There is a risk of ‘seeding’ an abscess
• Pre-existing neurological disease. There may be medicolegal disputes about ‘new’ symptoms

Question 299

Thrombocytopenia cut-off for epidural from ASRA guideline?

And for spinal?

Answer 299

Epidural <100

Spinal <50

Question 300

Why do the gases need heating prior to inspiration?

Answer 300

Heating allows the gases to become more saturated with water vapour. Thus humidifiers have an essential role in maintaining a healthy respiratory tract.

Question 301

Which microbe has been implicated in transmission by breathing equipment?

Answer 301

Hepatitis C.

Question 302

What are the two main types of breathing system filter?

Which is most efficient?

What problems are associated with filters (3)?

Answer 302

There are two main types of filter:

• Electrostatic
• Hydrophobic

Hydrophobic filters are the most efficient and long-lasting type of filter.

Associated problems are:

• An increase in dead-space, especially in children
• An increased resistance to flow, especially if wet
• In severe cases the filter may block with secretions, blocking the anaesthetic circuit