e-LFH - Core Training - Clinical Flashcards

1
Q

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

A

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

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2
Q

Which emergency drugs should be drawn up before each patient?

What may be worth preparing for unstable patients?

A

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.

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3
Q

Sequence of checks when administering drugs?

A

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

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4
Q

Common types of controlled drug(3)?

A

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.

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5
Q

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

Additional questions (7)

A
  • 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
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6
Q

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

A
  • 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
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7
Q

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

A

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

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8
Q

Advantages of nasal intubation (2)?

Disadvantages (3)?

A

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

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9
Q

Which bones form the hard palate (2)?

A

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

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10
Q

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

A

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

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11
Q

What is the pharynx and how is it divided?

A

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

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12
Q

Which area do fish bones commonly lodge?

A

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

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13
Q

Where are the palatine tonsils located?

A

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’.

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14
Q

What is the sensory nerve supply to the tonsils?

How are they best anaesthetised?

A

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.

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15
Q

How is aspiration prevented during swallowing (5)?

A

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.
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16
Q

At what vertebral level is the larynx?

What structures is it close to (2)?

A

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.

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17
Q

Which articulating cartilages make up the larynx?

Which three laryngeal cartilages are paired?

A

The framework of the larynx consists of articulating cartilages:

  • Thyroid
  • Cricoid
  • Epiglottis

The following three cartilages are paired:

  • Arytenoid
  • Corniculate
  • Cuneiform
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18
Q

How are the true and false vocal cords also known?

How is the gap between the vocal cords?

A

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.

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19
Q

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

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

A

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.

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20
Q

What is the function of the posterior circoarytenoids?

A

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

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21
Q

What is the function of the lateral and transverse arytenoids?

A

Lateral cricoarytenoids, transvere arytenoids

These are adductors of the cords and close the vocal cords

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22
Q

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

A

Aryepiglottics, thyroepiglottics

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

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23
Q

What is the function of the cricothyroid musles?

A

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

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24
Q

What is the function of the thyroarytenoid muscles?

And vocalis?

A

Thyroarytenoids, vocalis

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

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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?
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.
26
Which nerve provides the sensory supply to the larynx below the vocal cords? What other function does this nerve have?
**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.
27
What are the paths of the right and left recurrent laryngeal nerves to ascend to the larynx?
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.
28
What does damage the superior laryngeal nerve result in (2)?
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
29
What does unilateral damage to the recurrent laryngeal nerve result in? And bilateral damage?
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.
30
What does the cricothyroid membrane lie between? Which structures may be damaged during cricothyroidectomy?
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.
31
Between which vertebral levels does the trachea extend? How long is it? How much is above the suprasternal notch? Rough diameter?
The trachea extends from its attachment to the cricoid cartilage (**C6**) to the tracheal bifurcation at the carina (**T5-6**). ## Footnote 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.
32
What are the anterior and posterior walls of the trachea formed of?
Patency is maintained by C-shaped cartilages anteriorly. The trachea is completed posteriorly by the trachealis muscle.
33
Which tracheal rings does the thyroid isthmus overlie?
The trachea lies in the midline, anterior to the oesophagus, with the thyroid isthmus overlying the **2nd to 4th tracheal rings.**
34
Where does the right upper lobe bronchus arise from the right main bronchus?
The right upper lobe bronchus arises 2.5 cm from the carina.
35
How many lobes does each lung have?
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.
36
During which common procedures may the pleural cavity be inadvertently opened to cause a pneumothorax (4)?
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
37
How many bronchopulmonary segments does each bronchus divide into?
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
38
Which lung segment is most commonly affected by aspiration during anaesthesia?
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.
39
How does the bronchiolar wall differ from the bronchus? What is it lined with?
The bronchiolar wall contains smooth muscle but no cartilage. It is lined by ciliated cuboidal epithelium.
40
What epithelium lines the alveoli?
The alveoli are lined by a single fine layer of non-ciliated cuboidal epithelium
41
How many compartments are in the mediastinum?
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
42
Why is a mass in the anterior mediastinum a major risk factor for anaesthesia?
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.
43
Which nerves and roots supply the diaphragm?
The nerve supply to the diaphragm is from the phrenic nerves which originate from the spinal cord at cervical level C3, C4 and C5.
44
What proportion of tidal volume does the diaphragm contribute?
The diaphragm contributes 60-75% of the tidal volume.
45
What effect does a damaged phrenic nerve have on the diaphragm? How is it diagnosed?
Phrenic nerve palsy causes upward paradoxical movement of the diaphragm on that side during inspiration. Diagnosis is made by screening the diaphragm by fluoroscopy.
46
What are the three types of intercostal muscle? Which direction does each run in? What is the function of each?
**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.
47
Which groups form the accessory muscles of respiration (4)? What are their functions?
**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.
48
Approximate depths of the tracheal tube in adult males and females?
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.
49
Which ribs should be visible in an inspiratory film?
At least six ribs should be visible anteriorly and 10 ribs posteriorly.
50
How many layers are in the pericardium? What are the attachements?
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.
51
What is a normal cardiothoracic ratio? What can lead to an abnormally high CTR?
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
52
Which vessel supplies the SA node 65% of people?
RCA
53
Which vessel supplies the AV node in 80% of people?
The A-V node is supplied by the right coronary artery in 80% of people.
54
From where does the sympathetic supply of the heart originate?
The sympathetic supply originates from the lateral horns of the spinal cord (T1-4).
55
_Lorazepam_ Dose? Onset? Adverse effects? Metabolism?
Dose - 1-2mg Onset - 1-3 mins (IV), 2hr (PO) Respiratory depression Metabolised by the liver - half life 14 hours
56
_Temazepam_ Dose? Onset? Adverse effects (1)? Metabolism? Excretion?
* 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
57
The three stages of giving an anaesthetic?
Giving an anaesthetic involves three stages: * Induction - putting the patient to sleep * Maintenance - keeping the patient asleep * Reversal - waking the patient up
58
Alternatives to benzodiazepines for medication?
IM opioids - morphine, papaveretum, pethidine These are occasionally used today, but have, in the main, been replaced by oral anxiolytics.
59
How should patients with gastro-oesophageal reflux be induced? What are the goals of premedication?
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.
60
Anti-reflux pre-med examples and doses (3)
PPI: Omeprazole, 20 mg orally H2 antagonist: Ranitidine, 150 mg orally Metoclopramide 10-20mg
61
_NSAIDs_ Doses and routes for: * Ibuprofen * Diclofenac * Ketorolac
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)
62
Side effects of NSAIDs (4)
Gastric irritation Exacerbation of asthma Renal injury Platelet dysfunction
63
How long after a dose of LMWH can neuraxial blockage be safely peformed? Why?
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.
64
Examples of different classifications of thromboprophylaxis risk: Minor (2) Medium (3) High (5)
_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
65
Which medications should be omitted prior to surgery(4)? How long should they be omitted for in each case?
* 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
66
2 approaches to pre-op management of insulin-dependent diabetes
**_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.
67
Short-acting oral hypoglycaemic agents (2) Long-acting oral hypoglycaemic agent (4)
Short-acting hypoglycaemic agents * Gliclazide * Repaglinide Long-acting hypoglycaemic agents * Glibenclamide * Metformin * Glipizide * Rosiglitazone
68
Management of T2DM pre-op Morning of surgery (2) Medication changes pre-admission? Risk to patient? Plan for minor surgery vs major surgery?
* 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.
69
Which colour labels denote induction agents?
IV induction agents are identified by yellow labels.
70
What physicochemical property must induction agents share?
They must all be very lipid-soluble to cross the blood-brain barrier.
71
What are the following induction agents presented in? * Propofol * Thiopental * Etomidate
* 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.
72
How to convert % solution to mg/ml?
Multiply by 10
73
Why is it important to introduce a volatile agent as soon as possible after IV induction?
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, i**t 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.**
74
Doses of induction agents required for a fit adult? * Propofol * Thiopental * Etomidate
* For propofol: 1-2.5 mg/kg * For thiopental: 3-7 mg/kg * For etomidate: 0.25-0.3 mg/kg
75
**_Propofol_** * Onset time * Offset time * Metabolism? * CVS side effects (2) * RS side effect * Other effects (3) * Relative contraindication to use?
* 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.
76
What chemical class does propofol belong to? pKA? How does it exist in plasma?
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.
77
**_Thiopental_** * Onset time * Offset time * Metabolism? * CVS side effects (2) * RS side effect * Problems with use (2) * Absolute contraindication to use?
* 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.
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?
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.
79
**_Etomidate_** * Onset time * Offset time * Metabolism? * CVS side effects * RS side effect * Other effects (4) * Relative contraindications to use (2)
* 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.
80
What chemical class does etomidate belong to? How does it exist in plasma? Dose for induction?
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.
81
The phrase that distinguishes pharmacokinetics from pharmacodynamics?
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'.
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?
* 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.
83
Which is metabolised faster: propofol or thiopental?
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.
84
Three questions that influence choice of induction agent?
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
85
Difference between a gas and a vapour? Which are inhalational anaesthetics?
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.
86
Definition of a MAC?
The MAC is that concentration required to prevent 50% of patients moving when subjected to a standard midline incision
87
MACs * Isoflurane * Sevoflurane * NO2
Isoflurane -1.2 Sevoflurane - 2.0 Nitrous oxide - 103.0
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Factors increasing MAC (7)
1. Stimulants 2. Chronic alcohol dependence 3. Exogenous catecholamine use 4. Hyperthyroidism 5. Hyperthermia 6. Young age 7. Anxiety and stress
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Factors reducing MAC (10)
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
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Which two coefficients describe the solubility of volatile agents in body tissues? Which correlates with potency in terms of MAC?
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
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O:G partition coefficients * Isoflurane * Sevoflurane * N2O
Isoflurane - 98 Sevoflurane - 80 N2O - 1.4
92
What determines speed of onset when using a volatile agent for induction? Which coefficient determines this rate?
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.
93
What is overpressure and why is it used? Which volatile agent can this not be used for?
Overpressure involves s**etting 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.
94
A low blood-gas partition coefficient has what effect on onset of anaesthesia?
Volatile agents with a low blood-gas partition coefficient have a **rapid speed** of onset of anaesthesia.
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?
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.
96
Blood:gas partition coefficients * Isoflurane? * Sevoflurane? * N2O?
Isoflurane - 1.4 Sevoflurane - 0.6 Nitrous oxide - 0.47
97
What is the concentration effect?
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.
98
What is the second gas effect?
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.
99
What is diffusion hypoxia? How is it mitigated?
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.
100
How do volatile agents affect tidal volume?
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.
101
Which volatile is used for gas inductions? Why?
Sevoflurane. Isoflurane is an irritant vapour and may cause coughing.
102
How do the effects of sevoflurane and isoflurane on minute ventilation differ? Why is this important for gas inductions?
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.
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How do volatile agents affect SVR and cardiac contractility? * Isoflurane * Sevoflurane * N2O
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.
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What is coronary steal? Which volatile is it associated with?
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.
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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?
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.
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How do carbon dioxide absorbers interact with sevoflurane?
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.
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Which side effect can prolonged exposure to nitrous oxide cause?
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.
108
Difference between opioid and opiate?
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.
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Which colour label identifies opioid drugs?
Blue
110
What dose of fentanyl is given at induction? Why? Time to onset? Duration of effect?
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
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Standard concentration of fentanyl?
It comes in 2 ml and 10 ml ampoules, each containing a clear solution of **50 μg/ml**
112
How does fentanyl compare to morphine in terms of lipid solubility? What does this mean for its effect? ## Footnote How is it metabolised?
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.
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What are the common side effects of fentanyl (6)? Which rare complication can occur?
* 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.
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How is morphine dosed intraop? How long do effects last? How and when should morphine be given if severe pain is anticipated post-op?
The intraoperative dose of morphine, after initial use of fentanyl, is usually a **2-5 mg bolu**s, 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.
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What is the standard presentation of morphine? How is it normally diluted for use?
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.
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How does morphine's potency compare to fentanyl? How is morphine metabolised? In which patients is this important?
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.
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Uses for neuromuscular blockade (3)
NMBs are used to facilitate: * Tracheal intubation * Surgery where muscle relaxation is essential * Mechanical ventilation
118
What type of muscle relaxant is succinylcholine?
Depolarizing
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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?
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
120
When is RSI indicated? What is omitted from an RSI in contrast to standard induction? Why?
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
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Why is important to check that the effects of succinylcholine have worn off before using a non-depolarizing agent?
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.
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What colour label denotes non-depolarising NMBs? And depolarising NMBs?
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.
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How are intubating and maintenance doses of NMBs dosed?
Intubating doses are based on body weight while maintenance doses are titrated according to response determined by the peripheral nerve stimulator.
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**_Vecuronium_** Standard concentration? Intubating dose? Maintenance dose?
* Standard concentration - 2mg/ml * Intubating dose - 0.1mg/kg * Maintenance dose - 1-2mg
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**_Actracium_** ## Footnote Standard concentration? Intubating dose? Maintenance dose?
Standard concentration - 10mg/ml Intubating dose - 0.5mg/kg Maintenance dose - 10-20mg
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**_Succinylcholine_** ## Footnote Presentation? Intubating dose? Maintenance dose?
Presentation - 2 ml glass vial, 100 mg total. Intubating Dose - 1-2 mg/kg Succinylcholine should not be used to maintain neuromuscular blockade.
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Why is muscle fasciculation seen with succinylcholine? How is it metabolised? Contraindications to use (3)
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
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Patient-related contraindications to succinylcholine use (3) Clinical contraindications (2)
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
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How can succinylcholine cause acute onset hyperkalemia?
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.
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Adverse effects of succinylcholine (4)
* 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
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The common mechanism of non-depolarising NMBs? Classified into which two groups by structure?
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
133
How is vecuronium metabolised? And excreted? What regular meds can mean a higher dose is required?
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.
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How is atracurium broken down? (2) Which groups of patients does this make it suitable for(2)?
**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**
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In which patients is atracurium avoided? Why?
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
136
Things that may potentiate effects of non-depolarising NMBs?
The effects of both agents may be potentiated by: * acidosis * high-dose gentamicin * magnesium therapy
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What % of nicotinic receptors do non-depolarizing agents need to occupy to produce blockade?
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.
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How does neostigmine affect the heart? How can it be overcome?
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 anticholinergi**c, such as glycopyrrolate or atropine, with neostigmine.
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Recommended dose of neostigmine?
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.
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How is a Train of Four delivered? What current is used?
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.
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Which two pieces of information do you get from a train of four?
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.
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What approximate occupancy does each number of twitches of TOF represent? Why is TOF count unhelpful in assessing the reversal of NMB?
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.
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How does TOF ratio change as a non-depolarizing block wears off?
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.
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What are the commonly used types of peripheral nerve stimulation patterns? (3)
* The Train of Four (TOF) * The Double Burst * Tetany
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How is tetany delivered via peripheral nerve stimulation? What is fade?
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.
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What is post-tetanic facilitation?
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.
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How does lipid solubility affect potency of local anaesthetics?
The more lipid soluble the agent, the more potent it is
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Which is more potent, lidocaine or bupivacaine?
Bupivacaine: it is approximately four times more potent than lidocaine.
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How does ionisation of local anaesthetics affect passage across a membrane and subsequent activity?
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.
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What determines the proportion of any drug in the ionized form compared with the unionized form? (3)
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
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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?
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.
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Which two main factors determine duration of LA block?
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
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How does the addition of adrenaline affect the use of lidocaine? (2)
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.
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Max dose of lidocaine? And with adrenaline?
Lidocaine alone - 3 mg/kg With adrenaline - 7 mg/kg
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Two classes of local anaesthetics? How does this structural difference influence the pharmacokinetics of these agents?
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.
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Which functional groups are common to all local anesthetics? (2)
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.
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Difference between Marcain and Marcain Heavy?
Marcain®. Colourless solution 0.25% and 0.5%. Marcain®. Heavy: 0.5% bupivacaine with glucose 80 mg/ml, 4 ml ampoule, for subarachnoid block.
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Max dose bupivicaine with or without adrenaline Unwanted effects (2)
2 mg/kg Myocardial depression CNS convulsions then coma Levobupivacaine less toxic.
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Examples of ester local anaesthetics (2)
Tetracaine (amethocaine) Cocaine
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Contents of ametop vs contents of EMLA? Differences in effect (3)
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
161
**_Ephedrine_** Presentation? Dose? Mode of action? What effect is seen with repeated doses?
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
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**_Phenylephrine_** Presentation Dose Mode of action Adverse effect
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
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**_Metaraminol_** ## Footnote Presentation Dose Mode of action Adverse effect
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
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Most common causes of intraoperative bradycardia (2)
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**.
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Causes of intraoperative vagal stimulation (4)
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.
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Why is glycopyrrolate is free of the unwanted central effects of atropine, such as sedation?
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.
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**_Atropine_** Presentations (2) Dose Mechanism
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)
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**_Glycopyrrolate_** ## Footnote Presentation Dose Mechanism
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)
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Acute bronchospasm Three non-pharmacological interventions (3) Immediate pharmacological interventions (5)
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
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**_IV salbutamol_** Presentation Dose Why not inhaled or nebulised?
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.
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**_Aminophylline_** Presentation Dose Mechanism Caution
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.
173
How should adrenaline be given to treat refractory bronchospasm?
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
174
Rate of anaphylaxis due to anaesthetic drugs? Which are most commonly involved?
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.
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**_Malignant hyperthermia_** Inheritance? Triggers? Features (4) Treatment (4)
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
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**_Dantrolene_** Presentation Dose Mechanism
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).
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Definition of a gas
A gas is a compressible fluid phase in which no liquid can be formed at that temperature.
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Definition of critical temperature
The threshold above which a substance exists as a gas is its critical temperature
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Definition of a vapour
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
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What is Boyle's Law? How are the pressure and volume of a gas related in two different settings?
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
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How much oxygen does a 5L cylinder containing O2 at 100 atm provide at 1atm?
A 5 L cylinder containing oxygen at a pressure of 100 atmospheres provides a supply of 500 L at 1 atmosphere.
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Charles's Law?
Volume is proportional to absolute temperature (in a closed system with a fixed mass of gas)
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Gay-Lussac's Law
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
184
The Combined Gas Law
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
185
The Ideal Gas Law
PV = nRT
186
Why does the ideal gas law not apply to N2O at room temperature?
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.
187
How are partial pressure and total pressure related? Whose Law is this?
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.
188
Definition of saturated vapour pressure?
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.
189
Why do liquids cool during vapourization?
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.
190
How is the temperature when saturated vapour pressure equals atmospheric pressure also known?
The temperature at which the saturated vapour pressure equals the atmospheric presure is the boiling point.
191
192
Henry's Law
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.
193
How does temperature affect the solubility of gas in a liquid?
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.
194
The danger of an electric shock is influenced by? (3)
* Overall strength of current * Type and frequency of current * Local current density
195
In the UK, mains electricity supply is: * AC or DC? * Hz?
In the UK, the mains supply is alternating current (AC), with a frequency of 50 Hz.
196
What is Ohm's Law?
Voltage = Current × Resistance (V = IR).
197
Which term replaces resistance when dealing with alternating current?
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.
198
How is electrical current measured? What determines current in a circuit?
Electrical current is measured in amperes (A). Current (I) in a circuit depends on the electrical barrier presented to the voltage (V) applied.
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
* 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.
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)
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
201
How does current density change with cross sectional area? How is this used in unipolar diathermy?
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.
202
What is microshock?
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.
203
Three classes of insulation according to British Standards?
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
204
How does a fuse work (in terms of impedance and current)?
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.
205
How does a circuit breaker work?
The Current-Operated Earth Leakage Circuit Breaker (COELCB) is a widely used device which **monitors the current flowing in the live and neutral conductor**s. ## Footnote A **difference in the flowing current indicates that current may be flowing to earth by another mean**s. 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.
206
1 atm is equates to (approximately) how many: * bar * psi * kPa * cmH2O
1 atmosphere equates to (approximately): * 1 bar * 15 pounds per square inch (psi) * 100 kPa * 1033.23 cmH2O
207
What is the SI unit of pressure and what is it equivalent to?
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.
208
How is the hospital's oxygen supply stored in most hospitals? At what pressure is the pipeline for delivery into the main hospital?
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.**
209
What is Entonox? Cylinder colour and pressure? Why must it be kept above -6 degrees C?
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.
210
To what do the following pipeline colours correspond? * White * Blue * Black * Yellow * Clear
White - Oxygen Blue - Nitrous oxide Black - Air Yellow - Suction Clear - Anaesthetic gas scavenging
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212
Which volatile is the odd one out and requires a heated vapouriser?
**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.
213
What are the three sizes of connector used in adult breathing systems?
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).
214
What does APL stand for? What are the three functions of an APL?
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
215
In which situations may blood pressure be more important than flow? (2)
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)
216
What equation links pressure, flow and resistance? What are the equivalent values for the circulation?
Pressure = Flow x Resistance BP = CO x SVR
217
What is the most efficient type of flow? Which equation calculates laminar flow?
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
218
What is the dicrotic notch in arterial pressure waveform?
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.
219
Where is the biggest fall in pressure in the circulation? Why? How are these vessels also known?
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.
220
What are capacitance vessels? When is their volume reduced?
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.
221
Why can an increase in HR lead to myocardial ischaemia?
Less time spent in diastole and therefore less time for perfusion.
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?
* 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.
223
How does the juxtaglomerular apparatus exert control on blood pressure?
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.
224
How are the classes of shock defined by: * Blood loss (ml) * Blood loss (%) * HR * CRT * BP
* 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
225
How is the simultaneous contraction of fibres in cardiomyocytes achieved?
Simultaneous contraction of all fibres is achieved by the **specialized conduction system**, the **syncitial nature of cardiac muscle** and by **prolonging the action potentia**l via slow Ca2+ inflow through L-type channels, thus ensuring total ventricular depolarization.
226
What is the natural firing rate of the SA node?
100-120/min. The heart rate is normally slower because of dominant vagal parasympathetic activity.
227
How big is the area for alveolar gas exchange in an adult?
80-90 m2, approximately half the size of a singles tennis court.
228
Normal TV? Volume of anatomical dead space?
500ml 150ml
229
Approximate values for a fit young male: * TLC? * FRC? * VC? * RV?
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)
230
Which inward and outward forces determine FRC?
Its position is determined by the inward forces (**lung elasticity**) balanced against the outward forces (**respiratory muscle tone)**.
231
Two main reasons that FRC is important to anaesthetists?
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**
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?
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.
233
How much pressure is generated during spontaneously breathing? How much is required to achieve the same tidal volumes via IPPV?
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.
234
Which factors influence rate and depth of respiration feeding into the brain's respiratory centres? (4) Which is most important?
``` 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)
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?
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
236
How do obstructive and restrictive lung diseases affect lung resistance and compliance respectively?
An increase in resistance is seen in obstructive airways disease. A decrease (worsening) in compliance occurs with restrictive lung disease.
237
How does ventilation change between apices and bases in normal breathing? And perfusion?
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.
238
What is shunt in terms of V & Q?
No ventilation (V/Q = 0)
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What is alveolar dead space in terms of V & Q?
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.
240
How does an increase in dead space affect etCO2?
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.
241
How does general anaesthesia generally affect V/Q mismatching?
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 r**eceive less ventilation**, whilst the apices become more compliant and receive more. The **distribution of perfusion** - influenced largely by gravity - is u**nchanged**, with the mid-zones and bases receiving most of the blood flow, resulting in V/Q mismatch.
242
How much O2/min does the body use at rest? Equation for calculating oxygen consumption?
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
243
Solubility of oxygen in plasma?
0.23 mL/L/kPa
244
What is the main regulator of Hb production?
The main regulator of Hb production is erythropoietin (EPO), which is secreted by kidney in response to tissue O2 level.
245
How many oxygen molecules can each Hb bind? How does oxygen binding to haemoglobin change as more molecules attach?
Four - one to each haem group ## Footnote 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.
246
At rest, approximately how much oxygen is extracted by tissues? What is P50 (with respect to the Hb-O2 saturation curve?
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.
247
3 ways to express blood oxygen level?
Partial pressure (PaO2) Saturation (SpO2) Content (CaO2)
248
Atmospheric oxygen content in kPa?
21kPa
249
What is the oxygen cascade and what are its parts (3)?
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
250
Equation for oxygen content of blood? What is normal CaO2 of arterial blood?
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
251
What is VO2? Things that increase VO2? (5) And VO2 max?
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.
252
At what level of deoxy-Hb is cyanosis seen? Why does it not always correspond to measured SpO2?
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)
253
How does anaemia affect CaO2 and SpO2?
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.
254
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?
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**.
256
What is the resting membrane potential of a neuron?
Neurones have a constant resting membrane potential (RMP), set at about -70 mV. The inside is negative relative to the exterior.
257
258
Timing with respect to anaesthesia for the following pharmacological measures in patients with high aspiration risk: * PPI * H2 antagonist * Antacids * Prokinetics
* PPI - 90 mins prior * H2 antagonist - 90 mins prior * Antacids - Immediately before * Prokinetics- 90 mins prior
259
Virchow's triad?
Hypercoagulability Vessel wall injury Venous stasis
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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?
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.
262
Where do sympathetic nervous system efferents originate? Where are their preganglionic cell bodies found? What are the three ways they can terminate?
The sympathetic efferents have a t**horacolumbar outflow from spinal roots T1-L2**. Preganglionic cell bodies are found in the **l****ateral 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
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Where do parasympathetic efferents originate? Where are their cell bodies originate? (2) How do the majority synapse? What are the four discrete intermediary ganglia?
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 cor**d. 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.**
264
How does sympathetic outflow reach the head and pelvic regions? Which sympathetic ganglia supply the head? Where is the stellate ganglion found?
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 ## Footnote 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.
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)
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 a**bdominal viscera and heart** travel with sympathetic nerves.
266
How are the following blocks used? * Thoracic sympathectomy * Lumbar sympathectomy * Coeliac plexus block
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.
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?
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
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?
**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 receptor**s; their actions are mimicked by nicotine, but u**naffected by atropine**
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How does neostigmine reverse neuro-muscular blockade? How are unwanted muscarinic effects avoided?
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.
270
What are the two main types of adrenergic receptor? By what mechanism do they all work?
There are two main types of adrenergic receptors, **alpha (α) and beta (β)**, both **linked to G-proteins** and each with subtypes
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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?
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.
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Effects of stimulating the following receptors: * Alpha 1 (2) * Alpha 2 (2) * Beta (3) Second messenger for each?
* 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
273
How does parasympathetic stimulation affect the pupil? And sympathetic stimulation? Which muscles are involved?
The sphincter of the iris: parasympathetic stimulation produces pupil constriction (miosis) The radial muscle of the iris: sympathetic stimulation produces pupil dilation (mydriasis) (α1)
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?
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).
275
How long should surgery be delayed for post-MI? And post-PCI?
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.
276
Why is rate control for AF required for surgery?
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.
277
Aspirin is continued in most surgeries except for those involving the following? (3) When should it be stopped if it is?
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.
278
Frequency of failed intubation in elective GAs? And emergency GAs? Frequency of failed mask ventilation?
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.
279
Patient groups with a potentially unstable cervical spine (3)?
Trauma, rheumatoid arthritis, Down’s syndrome
280
Adverse anatomical features suggesting a difficult airway (7)
1. Small mouth 2. Receding chin 3. High arched palate 4. Large tongue 5. Bull neck 6. Morbid obesity 7. Large breasts
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Acquired problems leading to airway difficulty? (5)
Obvious acquired problems include: 1. Burns 2. Tumours 3. Abscesses 4. Radiotherapy 5. Other scars
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Mechanical deformities leading to airway difficulties (3)
Fixed cervical spine, reduced temporo-mandibular movement and mouth opening.
283
Why do airway tests tend often fail to predict difficult airways?
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.
284
What can be seen in a Grade 2a vs 2b view?
2a - Partial view of the glottis 2b - Posterior vocal cords or arytenoids just visible
285
Cook's modified classification of laryngoscopy What are the classes?
Easy - Views require no adjuncts Restricted - Views require a gum elastic bougie Difficult - Views require advanced techniques
286
What does an inter-incisor gap of \<3cm predict? And less than 2.5cm?
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.
287
History factors associated with difficult mask ventilation? (2) Examination factors? (6)
**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
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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)
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.
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Which analgesic drugs work in the brain/thalamus? (4) How does each work?
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.
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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**
* **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
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What are the three types of neuraxial block?
Spinal/subarachnoid block Epidural/caudal block Combined spinal epidural
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Minimum standards of monitoring for sedation in AAGBI guideline (5)
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.
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What are the monitoring requirements of regional anaesthesia vs general anaesthesia?
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'.
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Why are patients undergoing regional anaesthetic generally fasted?
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).
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In regional anaesthesia, which three techniques are commonly used to confirm the correct placement of the needle in relation to the nerves?
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
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Which regional anaesthesia techniques are associated with the highest plasma concentrations of LA? (2)
Intercostal and interpleural
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Common complications of neuraxial blocks (6) Frequency of rare complications? Rare complications (5 main ones, 7 very rare others)
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
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Three absolute contraindications to neuraxial anaesthesia? Relative contraindications (5)
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
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Thrombocytopenia cut-off for epidural from ASRA guideline? And for spinal?
Epidural \<100 Spinal \<50
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Why do the gases need heating prior to inspiration?
Heating allows the gases to become more saturated with water vapour. Thus humidifiers have an essential role in maintaining a healthy respiratory tract.
301
Which microbe has been implicated in transmission by breathing equipment?
Hepatitis C.
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What are the two main types of breathing system filter? Which is most efficient? What problems are associated with filters (3)?
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
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