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FRCA & FICM > General Duties > Flashcards

General Duties Flashcards

1
Q

Ideal body weight calculation

A

Height in cm - 100 for men or 105 for women

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2
Q

List some parametric tests

A

Two sample t-test
Paired t-test
ANOVA
Pearson’s correlation coefficient

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3
Q

List some non-parametric tests

A

Mann-Whitney U test
Wilcoxon rank-sum
Kruskal-Wallis test
Spearman’s rank correlation coefficient

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4
Q

What is the concentration of intralipid for LA toxicity?

A

20%

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5
Q

What is the initial bolus dose required for intralipid in LA toxicity?

A

1.5ml/kg

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6
Q

What is the infusion rate of intralipid for LA toxicity?

A

15ml/kg/hr
2 further bolus doses can be given 5 mins apart
Double rate of infusion to 30ml/kg/hr if clinical situation unchanged

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7
Q

What is the maximum cumulative dose of intralipid?

A

12ml/kg (?)

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8
Q

Name the structures in the paravertebral space

A

Parietal pleura (anteriorlateral)
Superior costotransverse ligament (posterior) - need to go through this to get to paravertebral space
Intercostal nerve
?sympathetic chain

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9
Q

List common complications associated with paravertebral block at T4

A 
Pneumothorax
Vascular puncture
Dural puncture
Horner’s syndrome
Harlequin syndrome
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10
Q

What are the features of Harlequin syndrome?

A

Contra-lateral hyperperfusion

So the face on the opposite side is all red

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11
Q

After a PVB a patient has ipsilateral miosis. What condition is this likely to be and how would you confirm your diagnosis?

A

Horner’s syndrome

Ptosis, miosis, anhydrosis & enopthalmos

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12
Q

Describe the features of Parkinson’s disease

A 
Tremor
Bradykinesia
Rigidity
Autonomic features - BP control
GI - constipation
CNS - low mood/dementia
Quiet voice, slow speech
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13
Q

Describe the classes of drugs used in PD

A

Dopamine - Levodopa (plus something to try and prevent peripheral L-dopa breakdown)
Domaine agonists - apomorphine/rotigotine
MAO-B inhibitors - selegiline
COMT inhibitors - entacapone
Anti-cholinergics

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14
Q

What other treatments exist for Parkinson’s Disease?

A

Deep brain stimulation - electrodes into subthalamic nuclei connected to pulse generator

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15
Q

What drugs should be avoided for anaesthesia of a PD patient?

A 
Atropine
Halothane
High dose Fentanyl/Alfentanil
DIRECT ACTING sympathomimetics
DA antagonists
Serotonin syndrome - Tramadol
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16
Q

What considerations are needed for a PD patient having an operation?

A

Surgery timing (first)
Ensure drug regime continued and minimise disruption
Avoid prolonged starvation
RA vs GA
Poor swallow - airway concerns
Interference/artefact with electrical equipment - from tremor
Think if they have a DBS - diathermy, checking the machine still works afterwards etc
May not be able to work PCA
May need critical care admission if severe PD - complex multisystem disease

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17
Q

What PD drugs can be given via a different route to PO?

A

Rotigotine
Apomorphine
These discussions should be made with a PD specialist (and a patient)
Critical care admission may be required

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18
Q

How do you describe doing a nerve block?

A 
Consent
Block name
Equipment needed: trained assistant, AAGBI monitoring, venous access, access to resus equipment/intralipid
Patient position
Asepsis & LA to skin
US +/- NS settings
Probe orientation and location
Structures identified; needle end point
Injection method - slow incremental injection with rate always <20ml/min
Post block instructions
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19
Q

Definition of major haemorrhage?

A

150ml/min blood loss
Loss of 50% blood volume in <3 hours
Loss of entire circulating blood volume in 24 hours

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20
Q

How would you manage a major trauma ?

A 
Trauma call
ABC
-secure airway
-apply O2
IV access
Crossmatch
Activate major haemorrhage protocol
Give TXA

Early diagnosis of bleeding points and management - CT/surgery/binders/haemostatic dressings

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21
Q

What parameters do you transfuse to in major haemorrhage? (Or other parameters you want to stick to)

A 
Systolic BP ~100mmHg
Aim for Hb 90-100 during bleed; above 80 afterwards
Hct >0.3
Plts >100
Fibrinogen >1.5g (2 in obstetrics)
Ionised calcium Ca2+ >1mmol/L
pH >7.2
BE 36
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22
Q

What is damage control resuscitation?

A

Maintain circulating blood volume, control haemorrhage and correct lethal triad of trauma (hypothermia/acidaemia/coagulopathy)

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23
Q

What are the principles of damage control resuscitation?

A

Damage control surgery
Permissive hypotension (except in head injury)
Rapid rewarming
Limit crystalloid
Early blood component therapy
Correct hypofibrinogenaemia & coagulopathies

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24
Q

What is damage control surgery?

A

Limited surgery interventions to control haemorrhage and minimise contamination

Come back later when patient more stable
These patients have reduced acidaemia/hypothermia/coagulopathy on arrival to ICU if the surgery is SHORT (<1hour)

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25
Q

What is the mechanism behind acute traumatic coagulopathy?

A

Activated protein C causes anticoagulation
Endothelial glycocalyx releases heparin when disrupted
Loss of fibrinogen
Platelet dysfunction from initial hyper activation as a result of widespread ADP release from endothelial cells

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26
Q

Define neuropraxia

A

Temporary physiological interruption of conduction without loss of atonal continuity

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27
Q

Define axonotmesis

A

Loss of relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve

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28
Q

Define neurotmesis

A

Total severance or disruption of the entire nerve fibre with no distal nerve conduction

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29
Q

What is prehabilitation?

A

The process of enhancing an individual’s functional capacity to enable them to withstand a forthcoming stressor such as major surgery

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30
Q

What are the 2 main models to describe frailty?

A

Frailty phenotype

Frailty index

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31
Q

Give an example of a tool to describe frailty

A

Edmonton Frail Scale

Canada Study of Health and Ageing (CSHA) frailty index

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32
Q

List some risk factors for frailty

A 
Age
Female sex
Lower socioeconomic class
Depression
Disability
Comorbidities such as cardiovascular disease
Diabetes
Stroke
Cancer
Arthritis
COPD
Anaemia
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33
Q

What are the 4 main components of prehabilitation?

A

Medical optimisation
Physical activity
Nutritional support
Psychosocial support

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34
Q

What are the potential benefits of prehabilitation?

A

Shorter length of stay
Reduced post operative pain
Fewer post-op complications

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35
Q

What 3 physiological benefits may be gained from physical training as part of a prehabilitation program?

A 
Improve functional reserve
Improve mitochondrial oxygen uptake
Improved lean body weight/weight loss
Improved anaerobic threshold
Improved VO2 max.
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36
Q

Give 4 benefits of carbohydrate preloading and nutritional optimisation

A 
Shorter fasting time
Improved wound healing
Reduced length of stay
Reduced infection
Decreased insulin resistance
Promotes anabolic state
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37
Q

Define delirium

A

Acute disturbance in cognitive state with fluctuations in orientation

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38
Q

What drugs are safe to use in porphyria?

A

Propofol
Fentanyl
Atracurium

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39
Q

What drugs need to be avoided in acute haemolytic porphyria?

A 
Thiopentone
Etomidate
Ketamine
Anything that stimulates P450
Antibiotics (although penicillins are ok)
Antifungals
Dexmedetomidine
Anti-arrhythmics
Ergometrine
Anti-epileptics
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40
Q

What is acute hepatic porphyria?

A

Group of AUTOSOMAL DOMINANT conditions
Partial deficiency in the activity of enzymes involved in haem synthesis

Most common = AIP
Then hereditary coproporphyria and variegateporphyria

Build up of products - ALA & PBG - build up and cause attacks
Haem suppresses the whole pathway and stops attaches

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41
Q

What are some features of a Neurovisceral attack in Acute Hepatic Porphyria?

A 
Abdo pain
Hypertension
Seizures
Confusion
N&V
Peripheral neuropathy
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42
Q

What investigation would you do to confirm an attack of AHP?

A

PBG (urine)
Has to be taken at the time of the attack

Can also do plasma and faecal sample for porphyrin

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43
Q

What are the anaesthetic principles for a patient with AHPorphyria?

A

Minimise starvation time
Avoid precipitant drugs
Minimise stress by using good analgesia and avoiding PONV
Consider early epidural in obstetrics

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44
Q

How would you manage an acute attack of AHP?

A 
Remove or treat participating factor
Maintain carb intake
Effective pain management 
Control PONV
Exclude other causes of abdominal pain
Monitor for neuropathy
Send urinary PBG
Involve UK NAPS to arrange giving HAEM ARGINATE (reduces duration of attack but causes severe thrombophlebitis)
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45
Q

What perioperative consequences may be associated with pre-operative anaemia?

A

Risk of cancellation of case - delayed treatment
Poor wound healing
Longer hospital stay
Higher risk of complications - MI, wound infections/LRTI/UTI
Increased all cause morbidity and mortality
High risk of needing blood transfusion and its assoc risks

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46
Q

What adaptions occur to offset effects of anaemia?

A

Increased O2 extraction
Increased CO - decreased SVR from reduced blood viscosity/sympathetic response
R shift of OHDC due to increased 2,3DPG
Redistribution of cardiac output to high demand areas

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47
Q

Describe perioperative events that will worsen the effects of anaemia?

A 
Shivering
Pain
Stress response
Fever
Hypoxaemia if inadequate oxygen therapy etc
Reduced CO from anaesthetic agents
Blood loss from surgery
Reduced erythropoiesis due to inflammatory response
Hypothermia causing L shift of OHDC
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48
Q

What further blood tests may help the classification of this anaemia?

A

B12
Folate
Iron
Ferritin
Reticulocyte count - low count = bone marrow problem; high count = haemolysis
Total iron binding capacity - raised in IDA
Transferrin saturations - low in IDA

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49
Q

What scoring systems can be used to help predict perioperative risk before major surgery?

A 
ASA
POSSUM
SORT
Revised CRI
Nottingham hip fracture score
V-POSSUM
Carlisle risk calculator for elective AAA
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50
Q

What are the main measures of fitness obtained by CPET?

A

Anaerobic threshold - the level of O2 delivery at which anaerobic metabolism occurs
VO2 peak
Workload

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51
Q

What abnormalities seen at time of testing in CPET may suggest cardio-respiratory disease?

A 
Rapid rise in HR
Reduced peak O2 pulse (reduced SV)
ECG abnormality
Reduced BP with exercise
Raised ventilatory equivalent for CO2/O2
Spirometry abnormalities such as significant reductions in FVC, FEV1
Reduced SpO2 at peak exercise
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52
Q

How can frailty be assessed?

A

End of the bed/first clinical impression of an experienced doctor/clinician
ASA score
Clinical frailty scale (score 1-9)
Edmonton Frail Scale
Canadian Study of Health and Aging clinical frailty scale
Electronic Frailty Index (using SystemOne)

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53
Q

What drugs would you use in a hypertensive response to phaeochromocytoma tumour handling?

A 
Mg
Phentolamine
GTN
Sodium nitroprusside
Nicardipine
Esmolol
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54
Q

Define difficult airway

A

Difficulty with face mask ventilation/supraglottic device ventilation/endotracheal intubation or all 3
>2 attempts at laryngoscopy using direct laryngoscopy

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55
Q

What are the contraindications to AFOI?

A 
Inexperienced operator
Basal skull fracture
Allergy to LA
Infection/contamination of upper airway - bleeding/friable tumour/abscess
Distorted anatomy
Impending airway obstruction (cork in a bottle)
Uncooperative patient
Penetrating eye injury
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56
Q

What are the muscles of the larynx and what do they do?

A

Cricothyroid - tenses vocal cords
Thyroarytenoid and vocalis - slacken vocal cords
Lateral cricoarytenoid and transverse arytenoids - adduction of vocal cords
Posterior cricoarytenoid - abduction of vocal cords

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57
Q

What is the nerve supply to the larynx?

A

Recurrent laryngeal to all intrinsic muscles of larynx except cricothyroid (external laryngeal)
Recurrent laryngeal - sensation below glottis
Superior laryngeal nerve - internal branch - sensation above glottis

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58
Q

You used AFOI to intubate the patient. How would you be sure the patient is safe at extubation?

A

Extubate in theatre with assistant
Appropriate drugs ready for reintubation
Appropriate equipment for reintubation
Verbalise plan
Surgical team in theatre
Observation in theatre prior to transfer to recovery
Ensure: CVS stability, RS stability, Metabolic/Temp stability, Neuromuscular function returned

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59
Q

State three factors that affect blood viscosity

A

Temperature
Flow rate
Haematocrit

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60
Q

List intraoperative strategies to maintain perfusion to a free flap

A 
Normothermia
Normovolaemia
Vasodilatation from anaesthetic agents
Sympathetic blockade - paravertebrals/epidurals
Minimised handling of flap
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61
Q

List 2 surgical and 2 non-surgical causes of free flap failure

A

Surgical:

  • Arterial - vessel spasm/trauma/thrombus/technical problems with anastomoses
  • Venous - kicking of anastomosis, thrombus, haematoma compressing drainage

Non-surgical:

  • Oedema from excess fluid
  • Hypercoagulable state
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62
Q

How do you assess a free flap?

A 
Colour
CRT
Skin turgor
Skin temperature
Bleeding on pinprick
Doppler
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63
Q

What happens at the initiation of exercise?

A

Resp and CVS increase O2 demand
Increased CO and Vasodilatation through:
-Vasodilatory metabolites - H+, K+, PO4, AMP and adenosine
-Improved O2 dissociation through increased temp/reduced pH
-Increased muscle blood flow

CO increases:

  • SV increase from increased venous return and increased inotropy from catecholamines
  • HR increase from SNS stimulation and vagal inhibition
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64
Q

What is the maximum HR?

A

Maximum HR = (220 - age) +/- 11

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65
Q

What is the anaerobic threshold?

A

The point at which O2 demand of muscles exceeds the ability of the cardiopulmonary system to supply O2
Where blood lactate rises as metabolism switches from aerobic to anaerobic

Marker of exercise intensity
Occurs from:
-Low muscle O2
-Accelerated glycolysis
-Recruitment of fast twitch fibres
-Reduced rate of lactate removal
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66
Q

What is VO2?

A

Oxygen consumption

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67
Q

What is CPET?

A

A dynamic, non-invasive assessment of cardiopulmonary system at rest and during exercise

Determines functional capacity

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68
Q

What are the CPET-derived variables?

What other measurements can CPET record?

A

Anaerobic threshold - AT
Peak O2 consumption - VO2peak
Ventilatory efficiency for CO2 - VE/VCO2
Maximum workload/rate

Respiratory exchange ratio (RER) - VCO2/VO2
Work rate (in Watts)
Ventilatory measurements:
-SpO2
-VE
-Vt
-RR
-VE/VO2 & VE/VCO2

CVS:

  • HR
  • ECG ST segment changes
  • NIBP
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69
Q

Which CPET-derived variables are associated with poor postoperative outcomes?

A

Anaerobic threshold <11
Peak O2 consumption (VO2peak) <15
Ventilatory efficiency for CO2 (VE/VCO2) 36

Mortality/morbidity/ICU admission/LoS

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70
Q

What is the normal CVS response to exercise?

A 
Increase in systolic BP
Reduced SVR (increasing muscle perfusion)
Increased venous return

CO increases in proportion to intensity of exercise from increase HR and SV

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71
Q

How is CPET done?

What equipment is needed?

A 
Electromagnetically braked cycle ergometer
Rapid gas analyser
Pressure differential pneumotachograph
ECG
SpO2
NIBP

Measurements taken:

  • at rest
  • during unloaded cycling
  • during increasing resistance
  • in recovery phase after cessation of exercise

Inputting patient gender/height/weight/age calculates a normal value which is then compared to those obtained

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72
Q

What is VO2peak?

What is VO2max?

A

VO2max is the maximum VO2 achievable by an individual performing a specific type of exercise
-often not achieved by elderly/co-morbid
The plateau of O2 uptake at a certain work rate
The O2 intake during exercise at which actual O2 intake reaches a maximum beyond which no increase in effort can raise it

VO2peak is the highest VO2 measured

  • often the point at which the test is terminated
  • regardless of the subject’s effort
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73
Q

What are the CPET numbers that puts patients at higher risk of perioperative complications?

A

VO2peak <15ml/kg/min
AT <10.2mlO2/kg/min

ECG changes (ischaemic)
SpO2 should be >95% throughout
74
Q

In CPET, how is maximal effort defined/represented?

A

Achieving >80% of predicted work rate/load
Achieving >80% of predicted maximum HR
Achieving a RER (VCO2/VO2) of >1.15

75
Q

What is VO2max influenced by?

A

CVS ability to deliver O2 to tissues

Ability for muscles to use O2 for ATP production aerobically
-this is due to capillary density

76
Q

What abnormalities seen on CPET may suggest cardiorespiratory disease?

A 
Rapid rise in HR at low level of work
Reduced HR reserve
Reduced peak O2 pulse (reflection of SV)
Reduced BP with exercise
ECG changes - ischaemia or arrhythmia

Raised VEO2 or VECO2
Spirometry abnormalities in FEV1, FVC etc
Reduced O2 SpO2 at peak exercise

77
Q

When might CPET be impractical?

A 
Lower limb amputation
Severe PVD
Severe OA
Balance/coordination problems
Inability to tolerate face mask - claustraphobia
78
Q

Other than CPET, how else can a patient’s functional capacity be assessed?

A

Duke Activity Status Index
6 minute walk test
Incremental shuttle walk test
Hand crank CPET

79
Q

What are the contraindications to CPET?

A 
Acute MI within 5 days
Unstable angina
Uncontrolled arrhythmia causing compromise
Syncope
Uncontrolled asthma
Active endocarditis
Severe AS
Acute PE or VTE
Suspected dissecting aneurysm
Pulmonary oedema
Low SpO2 prior to start (<85%)
80
Q

List the patient related risk factors for PONV

A 
Female gender
History of PONV
History of travel sickness/motion sickness
Non smoker
Anxiety
ASA 1/2
History of migraine
Age - >3years old risk increases but then declines throughout adulthood
FH of PONV (?)
81
Q

List the anaesthetic related risk factors for PONV

A

Use of volatile
Use of nitrous
Intra- and post-operative opioid use
Increased duration of anaesthesia

82
Q

What are the unwanted effects of PONV in adults?

A 
Patient dissatisfaction
Prolonged hospital admission
Delayed oral intake
Suture dehiscence
Dehydration
Electrolyte imbalance
Aspiration
Oesophageal rupture
83
Q

Which non-pharmacological interventions have been shown to be effective in reducing PONV?

A 
Acupuncture
Wrist bands/acupressure
Avoidance of GA (use of regional)
Aromatherapy
Avoidance of dehydration
84
Q

Describe how 5HT3 antagonists work

A

Enterochromaffin cells release 5HT
5HT stimulates vagus - terminate in chemoreceptor trigger zone/vomiting centre
5HT3 receptors in CRTZ are blocked by e.g. ondansetron

85
Q

Give some examples of chemotherapy

A

Alkylating agents
Tyrosine kinase inhibitors
Hormonal agents

86
Q

List some systemic complications of chemotherapy

A

Hypertension/arrhythmias/MI/CCF/cardiomyopathy
Pneumonitis/PE/Pneumonia
Diarrhoea/vomiting/mucositis/electrolyte disturbance
Hepatocellular necrosis/fibrosis/cirrhosis
Anaemia/neutropenia/thrombocytopenia
Peripheral neuropathy/seizures/encephalopathy/autonomic neuropathy

87
Q

What is the function of the spleen?

A

Immune:

  • stores lymphocytes
  • innate immune response - removes macrophages/pathogens
  • adaptive immune response - stores B cells and T cells

Non-immune:

  • Removes old blood cells
  • Store of platelets
  • Removes old platelets
  • Spleen acts as a blood reservoir
88
Q

What vaccines do you need if you’ve had a splenectomy?

A

Pneumococcal vaccine
Hib
Meningococcal C

2 weeks after traumatic splenectomy

89
Q

What are the WHO classifications of obesity?

A 
BMI 30-35 = Obese class I
BMI 35-40 = Obese class II
BMI >40 = Obese class III
90
Q

Define:

  • Total Body Weight
  • Ideal Body Weight
  • Lean Body Weight
  • Adjusted Body Weight
A
  1. The actual weight of the patient
  2. What the patient should weigh with a normal ratio of lean mass to fat mass. (Calculation = height in cm - 100 or 105)
  3. Patient’s weight excluding fat
  4. Calculated by adding 40% of excess weight to IBW, as obese individuals have increased lean body mass and an increased volume of distribution for drugs
91
Q

List the physiological changes that occur in the respiratory system due to obesity?

A 
Reduced FRC
Increased O2 consumption
Reduced closing capacity
Restrictive lung disease due to decreased diaphragmatic movement/weight on thorax
Decreased lung compliance
Increased PVR
Increased OSA
Increased V/Q mismatch
Obese hypoventilation syndrome
Higher incidence of difficult airway
Higher incidence of regurgitation/aspiration
92
Q

What are the new guidelines for anaesthesia for hip fracture?

A

GA vs Spinal - no difference
Avoid intra-operative hypotension
Single-shot nerve blocks supplement both anaesthesia techniques
Single shot block in ED and at surgery (as long as >6 hours apart)
Surgery within 36 hours

93
Q

What assessment tools should be used for hip fracture patients?

A

4AT/delirium assessment
Frailty assessment/score
Nottingham Hip Fracture Score

Involve orthogeriatricians

94
Q

What are the 7 acceptable reasons for delaying hip fracture surgery?

A 
Hb <80g/L
Na <120 or >150; K <2.8 or >6
Uncontrolled diabetes
Uncontrolled LV failure
Correctable cardiac arrhythmia with ventricular rate >120bpm
Chest infection with sepsis
Reversible coagulopathy
95
Q

What are the transfusion thresholds for hip fracture patients?

A

Hb should be >90g/L

Or >100g/L in IHD

96
Q

What is the STOPBANG scoring tool?

A 
Scoring tool for OSA
Snore
Tired in the day
Observed apnoea
P - high BP
BMI >35
Age >50
Neck circumference >40cm
Gender - male gender

High risk if >3 criteria

97
Q

What are the endocrine consequences of OSA?

A

Impaired glucose tolerance
Dyslipidaemia
Altered cortisol/ACTH
Testicular/ovarian dysfunction

98
Q

What are the CVS consequences of OSA?

A 
Systemic HTN
Pulmonary HTN
RV failure
Dysrhythmias
Increased risk of MI/stroke
Pickwickian syndrome
99
Q

List absolute contraindications to CPET

A 
Acute MI
Uncontrolled arrhythmia
Syncope
Active endocarditis
Unstable angina
Symptomatic severe AS
Uncontrolled heart failure
Uncontrolled asthma
Suspected dissecting or leaking AAA
100
Q

State the number of METS associated with:

  1. Resting, fasted for >12 hours
  2. Walking at 2.5mph on the flat
  3. Climbing 2 flights of stairs without stopping
  4. Jogging
A
  1. 1 MET
  2. 3
  3. 4
  4. 8
101
Q

What are the contributors to ‘oxygen debt’?

A

Oxygen debt - the O2 used to restore the body to its resting state

Restoration of ATP
Restoration of myoglobin O2 stores
Restoration of muscle and liver glycogen
Dissipation of heat
Restoration of intracellular electrolytes to normal concentrations
Repair/hypertrophy of muscle fibres
102
Q

What is the dose of dantrolene in malignant hyperthermia?

A

2-3mg/kg

Repeat 1mg/kg every 5mins until ETCO2<6kPa and temp <38.5

103
Q

What is the management of a suspected Malignant Hyperthermia case?

A

Call for help
Increase FiO2
Find QRH and use

—Eliminate trigger drug:
Turn off vaporisers
Hyperventilate on clean circuit:
-Charcoal filters on both limbs of circuit
-Change soda lime and breathing circuit when feasible

—Dantrolene:
2-3mg/kg immediate IV bolus (about 200mg in normal sized adult)
Repeat 1mg/kg every 5 mins until ETCO2<6kPa and temp <38.5

—Active cooling
Turn off warming
Cold IV fluids
Cold packs to axillae/groins

—Manage complications:
Arrhythmia
Hyperkalaemia
DIC
IV access/lines
ICU
Genetic testing
104
Q

What are the factors that affect IOP?

A

Intraocular contents:

  • Choroidal blood volume
  • Aqueous humour - Na/K ATPase dependent active secretory process; independent of ocular pressure (still produces 0.15ml/hr)
  • Vitreous humour

External pressure:

  • Direct pressure
  • Retro-bulbar haematoma
  • Extrinsic muscle tone
  • Venous congestion

Scleral rigidity:

  • Severe myopia
  • Older age
105
Q

What factors affect choroidal blood volume?

A

Blood flow to eye is auto-regulated

Arterial PaCO2
Hypoxaemia
Vasodilation
Transient rise with acute systolic BP increase
Venous pressure - coughing/prone position

106
Q

What are some predisposing factors for delirium post-operatively?

A 
Age
Comorbidities
Frailty
Severe illness
Dementia
Emergency surgery
Type of surgery - hip fracture/AAA repai
Years of education
Previous delirium
Sensory impairment - visual/hearing
Vascular risk factors
Smoking
Alcohol
Depression
Lab measures - dehydration, CRP, abnormal Na/K, low albumin, low haematocrit

From AAGBI guidelines in 2019

107
Q

What are some modifiable risk factors to prevent delirium?

A

Intra-operative:

  • BIS monitoring to avoid excessive anaesthesia
  • BP variance - maintain physiological homeostasis as much as possible
  • Temperature
  • Anaemia
  • Glucose/electrolyte control
  • Acid/base disturbances

Post operative:

  • Dehydration
  • Sensory impairment
  • Sleep deprivation
  • Constipation/urinary retention
  • Sepsis
  • Pain
  • Drugs - opioids, benzos
108
Q

What are the associations/systemic effects of myotonic dystrophy?

A

CVS: conduction defects; arrhythmias; cardiomyopathy
CNS: cognitive impairment
Endocrine: insulin resistance; hypothyroidism
GI: poor GI transit
MSK: contractures; myotonia

109
Q

What are the precipitants of myotonic contractures?

How would you treat it?

A

Hypothermia
Shivering
Electrical stimulation

Restore physiological homeostasis

110
Q

What is the calculation for SVR?

A

MAP x 80
———
CO

x80 is to convert from Wood unit (mmHg/L/min) to dynes/sec/cm5

111
Q

What is the calculation for PVR?

A

80 x (MPAP - PCWP)
———————————
CO

112
Q

List patient factors that may require a vitreoretinal surgery to take place under GA?

A 
Inability to lie still
Chronic cough/movement disorder
Dementia/cognitive impairment
Inability to lie flat - CCF/COPD
Longer duration required for this surgery
113
Q

List the principles of GA for intraocular eye surgery

A

Minimise increases in IOP
Use of prophylactic antimuscarinic against oculocardiac reflex
Control PaCO2
Avoid nitrous
Avoid coughing/straining - use of muscle relaxants
Smooth emergence using Remi/flexiLMA
Avoid PONV

114
Q

What are the features of a fat embolus?

A

RS: dyspnoea, tachypnoea and hypoxaemia
CNS: consfusion, drowsiness, seizures
Skin: petechial rash in mucous membranes, skin folds

Fat embolism index scoring

115
Q

What are the features of a fat embolus?

A 
Tachycardia
Pyrexia
MI
Drop in platelets
ESR
Lipouria
Fat in sputum
116
Q

What are the 2 theories for fat embolus?

A

Mechanical - fat from marrow enters venous circulation and embolisms in pulmonary circulation

Toxic intermediaries - embolised fat agglutinate in plasma and degrades, releasing free fatty acids

117
Q

What are the prevention strategies for fat embolism?

A

Early immobilisation
Early fixation
Use of venting holes intra-operatively
Avoiding IM nail

118
Q

What are the cartilages of the larynx?

A

3 paired:

  • Cuneiforms
  • Arytenoids
  • Corniculates

3 unpaired:

  • Epiglottis
  • Thyroid
  • Cricoid
119
Q

Describe the oculocardiac reflex

A

Usually traction on medial rectus muscle
Afferent: long and short ciliary nerves of Trigeminal (V1) nerve to motor nucleus of vagus nerve
Efferent: Vagus to sino-atrial node (bradycardia) and medulla (cessation of breathing) and vomiting centre (N&V)

Low CO2 sensitises the reflex

120
Q

What are the contraindications to day case surgery in children?

A 
Term baby <1month in age
Preterm or ex-preterm <60weeks PCA
Poorly controlled systemic disease
Inborn errors of metabolism
—-including diabetes
Complex cardiac disease
Sickle cell disease
Active infection
Poor housing
No telephone
Parent unable to care for child
Live >1 hour from hospital
No transportation
121
Q

Describe the pathogenesis of AIP

A

Autosomal dominant
Variable expression

Disorder of haem biosynthesis pathway
Deficiency of enzyme PBG-deaminase

122
Q

Which commonly used anaesthetic drugs should be avoided in AIP?

A 
Ketamine
Thiopentone
Sevoflurane
Ephedrine
Diclofenac
Metaraminol
123
Q

What is the management of a porphyric crisis?

A 
Remove precipitating cause if possible
Give IV haem arginate and continue for 4 days
Treat pain with paracetamol/morphine
PCA
Antiemetic
Beta blockers for tachycardia

Give carbs to prevent catabolic state
Monitor U&Es
Admit to HDU
Send urinary PBG

124
Q

What is meant by:

  1. MRI safe
  2. MRI conditional
A
  1. Equipment poses no additional risk in the MRI

2. No additional risk in specified environment with specific conditions

125
Q

What precautions should be taken with a patient in MRI?

A 
Equipment:
—Fibreoptic pulse ox
—MRI safe ECG electrodes
—Avoid loops
—NIBP with non ferrous connection
—MRI compatible anaesthetic machine
—or long breathing circuit
—MRI safe pumps
-or long infusion lines
—MRI safe monitors
Anaesthetic:
—MRI safety check of patient
—MRI safety check of staff
—Transfer onto MRI trolley (non ferrous)
—Stabilise patient outside the 5 Gauss MRI scanner area
—Secure the airway (difficult to access in MRI)
—Tape pilot balloon
—Plan for rapid retrieval in emergency
126
Q

What are the absolute contraindications to MRI?

A 
Aneurysm clips
Ocular implants
Cochlear implants
ICDs
PPMs
Neurostimulation devices
127
Q

What is the course of the Vagus nerve (CN X)?

A

Originates in brainstem
Exits via jugular foramen with CN IX & XI
Into carotid sheath

R Vagus nerve:

  • Anterior to subclavian
  • Forms posterior vagal trunk

L Vagus nerve:

  • Between carotid and subclavian
  • Forms anterior vagal trunk
  • Left recurrent laryngeal from under arch of aorta
128
Q

What are the sensory functions of the Vagus nerve?

A

Auricular nerve - innervation external auditory canal/external ear
Internal laryngeal nerve - superior aspect of larynx/laryngopharynx
Cardiac fibres
GI tract - up to splenic flexure

129
Q

What are the common side effects of chemotherapy agents?

A 
Pulmonary
Cardiac
Renal
Hepatic
Neurological
Haematological
130
Q

Classify cytotoxic drugs

A 
Alkylating agents (platins)
Anti-metabolites (MTX)
Plant alkaloids (vinca alkaloids)
Topoisomerase inhibitors
Antitumour antibiotics
Hormones (steroids/testosterone/tamoxifen)
Monoclonal antibodies (rituximab)
131
Q

What is Stroke Volume Variation?

A

A method of measuring a patient’s dynamic cardiac output; represented as a percentage

Reflects the change in SV beat to beat; if >10% then fluid-responsive

SVmax - SVmin/SVmean

132
Q

What are the nuclei of the Vagus Nerve?

A

Motor: Nucleus ambiguous
Sensory: Nucleus tractus solitarius
Parasympathetic: Dorsal nucleus

133
Q

Describe the course of the Vagus nerve

A

Arises from medulla
Through jugular foramen within the dural sheath along with the Accessory Nerve (CN XI)
Into carotid sheath; posterior to internal carotid
Paths of R and L then differ

134
Q

Describe the course of the LEFT Vagus Nerve (CN X) below the neck

A

Enters thorax and travels posterior to L brachiocephalic vein
Descends anterior to aortic arch (giving off Recurrent Laryngeal Nerve)
Descends posterior to lung root (giving off L pulmonary plexus)
Unites with Right Vagus to form oesophageal plexus
Anterior Vagus nerve formed from oesophageal plexus - passes through diaphragm at T10 anterior to oesophagus
Gives off gastric, pyloric and hepatic branches

135
Q

Describe the course of the RIGHT Vagus Nerve (CN X) below the neck

A

Gives off Right Recurrent Laryngeal Nerve in the neck at level of subclavian
Descends behind brachiocephalic vein
Forms R pulmonary plexus
Unites with L vagus nerve to form oesophageal plexus
Forms the Posterior Vagus Nerve
Enters abdomen posterior to oesophagus at T10
Forms coeliac branch/ganglion - supplies intestines, kidneys & adrenals

136
Q

What are the main branches of the Vagus Nerve arising in the head and neck?

A

Head - auricular branch

Neck - Pharyngeal nerve
Superior laryngeal nerve
Right recurrent laryngeal nerve
Superior cardiac plexus

137
Q

What are the main branches of the Vagus Nerve arising in the Thorax and Abdomen?

A

Thorax:

  • Left RLN
  • Inferior cardiac plexus
  • Pulmonary plexus
  • Oesophageal plexus
  • Anterior Vagal Trunk (LVN)
  • Posterior Vagal Trunk (RVN)

Abdomen:

  • Gastric
  • Hepatic
  • Intestinal
  • Coeliac plexus
138
Q

What are the clinical features of vagus nerve transection?

A

Lower lesions more common
Due to infection/trauma/neoplasm

  • Dysphonia
  • Bovine cough
  • Nasal speech
  • Abnormal swallowing
  • Reduced bowel motility
  • Loss of vagal reflexes (gag, cough, oculocardiac, carotid sinus)
139
Q

Describe how you would perform an AFOI

A

Speak and consent patient
Calculate maximum anaesthetic dose
Oxygenate - HFNO
Topicalise - 10 sprays 10% lidocaine to oropharynx; cophenylcaine to nose
Test topicalisation using soft suction catheter.
X5 1ml syringes of 2% lidocaine to spray as you go

Sedate - Remi Minto Cet 1-3 +/- midazolam if 2nd anaesthetist
Perform - appropriate tube; sitting up; facing patient; clear secretions

Confirm placement: misting ETCO2, ventilation
Check position using FOB

140
Q

How would you perform an AFOI?

A

STOP (in a weird order)

  1. Oxygenate - HFNO
  2. Topicalise:
    - Co-phenylcaine to nose
    - 10 sprays of 10% lidocaine to oropharynx
    - x5 1ml syringes of 2% lidocaine -SAYG
  3. Sedate - Remi TCI
  4. Perform:
    - including two point check at the end
141
Q

What is in cophenylcaine?

A

5% lidocaine with 0.5% phenylephrine

142
Q

What is the resting membrane potential in:

  1. skeletal muscle cell?
  2. nervous tissue cell?
  3. cardiac muscle cell?
A
  1. —90mV
  2. —70mV
  3. —90mV
143
Q

What are the major components of the neuromuscular junction?

A
  • Alpha-motor neurone
  • Synaptic cleft
  • Motor end plate of the muscle fibre
144
Q

How is acetylcholine synthesised and stored within the nerve terminal?

A

ACh made from choline and acetyl co-A

80% stored in vesicles
1% in ‘active zone’ for immediate release
20% in cytoplasm (dissolved)

145
Q

How does neuromuscular transmission occur?

A
  • Motor nerve depolarises
  • Voltage gated Ca++ channels open on pre-synaptic membrane
  • Ca++ causes vesicles to move and fuse and release their contents
  • Creates motor end place potential and localised depolarisation of muscle fibre membrane, causing excitation-contraction coupling
146
Q

Describe the nicotinic ACh receptor

A

Pentameric, ligand gated ion channel

Consists of 2 alpha, 1 beta, 1 gamma, 1 delta subunits

Undergoes conformational change when bound to allow Na+/K+ into cell

147
Q

Describe the synthesis of thyroid hormones

A
  • Iodine taken up by gut and into thyroid via active transport
  • iodine oxidised by peroxidase
  • binds to tyrosine found on thyroglobulin to form T1 or T2
  • these couple up to form T3 or T4
  • T3/T4 stored on thyroglobulin
  • transported bound to plasma proteins (albumin/T4-binding globulin)
148
Q

What are the effects of thyroid hormones?

A
  • Metabolic
    Basal metabolic rate
    Catecholamine sensitivity in vasculature
    Control breakdown of proteins/calcium from bone
  • Growth
    Direct tissue growth; allow GH to function
  • Nervous system
    Required for normal myelination and nervous system development
  • Other
    Sex functions
149
Q

What are some examples of hypoxic pulmonary vasoconstriction in clinical practice?

A

Foetal circulation
Pneumonia
High altitude
Upper lobe diversion in cardiogenic pulmonary oedema

150
Q

Describe the anatomy of the retroperitoneal space.

A

Anterior pararenal space: duodenum, pancreas, ascending/descending colon

Perirenal space: kidneys, adrenals, proximal ureters

Posterior pararenal space: contains fat

Great vessel compartment: aorta, IVC

151
Q

What are some of the difficulties with retroperitoneal surgery?

A

Positioning
Bleeding - may be hard to detect
Pleural breach - if operating near diaphragm; behaves as a pneumothorax but as is made of CO2 is often resolved once abdomen deflated, as CO2 rapidly reabsorbed. May need chest drain (unlikely) or re-attempt with lower inflation pressures

152
Q

What are the anaesthetic considerations for patients having a renal transplant?

A

Pre-op:
—General: ECG/ECHO/bloods and normal history/examination & comorbidities that may affect anaesthetic
—Specific: dialysis?/fistulae?/anuric?/fluid state/potassium

Intra-op:
—Immunosuppression
—Positioning/arterial line vs BP cuff on fistula
—Muscle relaxation choice and re-dosing

Post-op:
—Fluid
—PCA
—Post op destination (specialist ward vs HDU)

153
Q

What are the anaesthetic considerations when anaesthetising a patient with myasthenia gravis?

A

Pre-op: history, drugs

Intra-op:
—RSI if bulbar
—sensitivity to non-depolarising NMBDs
—cholinesterase inhibitors may precipitate cholinergic crisis

Post-op:
—ventilation may be required

154
Q

What is the inheritance for Malignant Hyperthermia?

A

Autosomal Dominant

Tested on muscle biopsy or genetic testing
Database in Leeds

155
Q

What is the pathophysiology of malignant hyperthermia?

A

—Exposure of the trigger (Sux/Volatile) causes dysregulation of excitation/contraction coupling in skeletal muscle.
—Changes in Ryanodine receptor
—Sustained release of Calcium into cytosol
—Increased metabolic demand for ATP causes increase CO2 production/increased O2 consumption
—Rise in CO2 stimulates sympathetic nervous system
—Muscle contraction causes acceleration of heat production and muscle rigidity

156
Q

How would you anaesthetise a patient that may have MH?

A

Pre-op:
—If possible to contact Leeds - have a database of all those with MH
—

Intra-op:
—Monitor for MH
—TIVA; avoidance of sux
—MH anaesthetic machine
—Charcoal filters
—Have DANTROLENE nearby

Post-op:
—Monitor for MH
—Potential for HDU admission?

157
Q

How would you treat MH if diagnosed intraoperatively?

A 
Call for help
Stop the trigger, give 100% O2, hyperventilate
Use charcoal filters
Switch to TIVA
DANTROLENE - 2.5mg/kg
Active cooling - fluids etc
Lines & catheter
Treat acidosis, hyperkalaemia, AKI, coagulopathy
ICU post op
158
Q

What happens at aortic cross clamp?

A

Above clamp:
—sudden increase in SVR
—increase myocardial work
—increase BP

Below clamp:
—blood supply from collaterals

159
Q

Describe the mediastinum

A

Contains all thoracic viscera except the lungs
Sternum to vertebral column and pleura either side

Split into:
—Superior - trachea/bronchi/aortic arch/SVC/phrenic, Vagi and RLN
—Anterior - remnants of thymus/lymph nodes
—Middle - heart/pericardium/phrenic nerves
—Posterior - oesophagus/descending aorta/anyhow veins/vagus nerve/greater,lesser,least splanchnic nerves

160
Q

What is ultrasound?

A

> 20kHz sound waves

Medical US usually 2.5-15MHz

161
Q

What are the stages of hypothermia?

A

Mild: 33-35; increased HR/RR, cold skin, shivering, poor judgement, confusion, apathy

Moderate: 27-33; increasing confusion, decreased HR/RR, shivering stops

Severe: <27; low BP/HR; coma, arrhythmias, death

162
Q

Outline the coagulation process

A

EXTRINSIC/TISSUE FACTOR PATHWAY (most important):
—Tissue factor released on injury, causing Factor VII to activate.
—Factor VIIa (and calcium) activates Factor X
—Factor Xa converts Prothrombin (II) to Thrombin (IIa) (N.B. this is inhibited by the action of Antithrombin III - think heparin)
—Other clotting factors and platelets are activated
—Thrombin converts Fibrinogen (I) to Fibrin

CONTACT ACTIVATOR PATHWAY
—Factor XII -> Factor XI ->Factor IX (plus Calcium)
—IXa, VIIIa, phospholipid and calcium activated Factor X

—Fibrin mesh + platelets = CLOT
Clot broken down by Plasmin (enhanced by tPA)

163
Q

What are the contraindications to ECT?

A 
—Raised ICP
—Recent stroke
—Cerebral aneurysm
—Recent MI
—Heart failure
—Severe HTN
—Osteoporosis
164
Q

How would you anaesthetise for ECT?

A 
—Normal history etc
—IV access
—Low dose induction; sux at 0.5mg/kg (check their last anaesthetic and go the same or less)
—Bite block
—O2 via facemask and hyperventilate (low CO2 decreases seizure threshold)
—Consider glyco
—Seizure up to 2mins is tolerated
—Monitor post ECT
165
Q

What do you need to form a clot?

A 
—Tissue Factor
Initiates the external clotting cascade (Factor X -> Factor II/Thrombin ->Factor I/Fibrin)
—Collagen exposed
Releases Tissue Factor
—vWF
Important to bind platelets to collagen
—Platelets
Bound via vWF to collagen, change shape and bind to each other via ADP
166
Q

What do platelets release when activated?

A
  • Vasoconstrictors: serotonin, thromboxane
  • ADP
  • Platelet activating factor
  • vWF
  • Fibrinogen
  • Thrombin
  • Ca2+
  • Platelet derived growth factor
167
Q

What are the steps involved in haemostasis?

A 
Initiation
Vasoconstriction
Propagation
Formation of platelet plug
Formation of fibrin clot
168
Q

What is the nerve supply to the abdominal muscles?

A

Intercostal nerves T7-11
Subcostal nerve T12
Iliohypogastric L1
Ilioinguinal L1

169
Q

What are the indications for carotid endarterectomy?

A

European carotid surgery trial: symptomatic TIA + >70% stenosis of affected side

170
Q

What is the function of the parathyroid gland?

A

Regulate calcium

And phosphate

171
Q

What does parathyroid hormone do?

A 
Released in response to low calcium
Increases serum calcium by:
—stimulating osteoclasts to resorb bone
—increasing gut uptake of calcium (via Vit D)
—decreasing renal loss of calcium
172
Q

How is body pH regulated?

A
  1. Buffering system
    —Intracellular: Phosphate, proteins
    —Extracellular: HCO3, Hb
  2. Respiratory regulation
    —metabolic acidosis sensed by carotid bodies->stimulate respiratory centre
    —hypercapnoea sensed by peripheral (carotid/aortic bodies) & central (medulla) chemoreceptors
  3. Renal regulation
    —Re-absorption of HCO3
    —excretion of acids/H+
173
Q

What mechanisms does the body have to prevent infection?

A

Innate immune system (rapid, non-specific):
—Barriers
—Complement
—White cells - neutrophils/macrophages/eosinophils/NK lymphocytes
—Inflammation/acute phase reactants

Acquired immune system (slower, specific):
—Cytotoxic T cells against intracellular pathogens
—B cells/T helper cells for antibody-mediated immunity
—Plasma cells (from B cells) - antibody factories

174
Q

What are immunoglobulins? What are their function?

A

From adaptive immune system (v similar to antibody, but bound to cell instead)
Proteins with 2 heavy/2 light chains and antigen binding sites

Types:
—IgG - crosses the placenta; most abundant
—IgM - bind large antigens
—IgE - mast cell degranulation
—IgA - mucosa
175
Q

What are the stages of haemostasis?

A

Initiation
Propagation - large amount of thrombin generated converts fibrinogen to fibrin
Stabilisation - fibrin stabilises platelet plug

Vasoconstriction

176
Q

What haemodynamic parameters can be deduced from Oesophageal Doppler?

A

Cardiac output (SV x HR)

Stroke volume - area under the systolic part of the curve

Flow time (corrected); FTc = preload

Peak velocity = contractility

Heart rate

Afterload - FTc and PV interpreted together

177
Q

How is COPD classified?

A

Using the GOLD criteria:

  1. Mild = FEV1 >80% predicted
  2. Moderate = FEV1 >50 <80% predicted
  3. Severe = >30 <50% predicted
  4. Very severe = <30% predicted

Confirmed on spirometry with post-bronchodilator FEV1/FVC of <0.7

178
Q

What is intra-abdominal hypertension?

A

> 12mmHg is hypertension
Abdo compartment syndrome = >20mmHg with organ dysfunction
Grades I-IV

Measured by direct or indirect

179
Q

Describe the cardio-respiratory physiology during the respiratory cycle

A

Spont inspiration:
-intrathoracic pressure decreases
-increased RV venous return; increased RV output
-IV septum pushed across, impairing LV filling
-pooling of blood in pulmonary venous vessels so decreased LV venous return
-decreased LV output
Spont expiration = converse

Positive pressure ventilation:
-reduction in RV preload and RV output during inspiration
-increase in LV preload as pulmonary vessels are squeezed, increasing venous return to the LV
-decrease in LV afterload during inspiratory PPV

At the end of expiratory PPV- decrease LV SV and MAP

180
Q

What happens to thyroid function in critical illness?

A

Initially increase in TSH & T4
Then increase in rT3 and reduced T3
General suppression of TSH/T4 as critical illness progresses

Normally, there is nocturnal secretion of TSH which is suppressed in critical illness
Peripheral conversion of T4 to T3 becomes less reliable and converts to rT3

Usually, thyroid function synergises with sympathetic nervous system, which may be decreased in critical illness

FRCA & FICM (9 decks)

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