General Duties Flashcards
Ideal body weight calculation
Height in cm - 100 for men or 105 for women
List some parametric tests
Two sample t-test
Paired t-test
ANOVA
Pearson’s correlation coefficient
List some non-parametric tests
Mann-Whitney U test
Wilcoxon rank-sum
Kruskal-Wallis test
Spearman’s rank correlation coefficient
What is the concentration of intralipid for LA toxicity?
20%
What is the initial bolus dose required for intralipid in LA toxicity?
1.5ml/kg
What is the infusion rate of intralipid for LA toxicity?
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
What is the maximum cumulative dose of intralipid?
12ml/kg (?)
Name the structures in the paravertebral space
Parietal pleura (anteriorlateral)
Superior costotransverse ligament (posterior) - need to go through this to get to paravertebral space
Intercostal nerve
?sympathetic chain
List common complications associated with paravertebral block at T4
Pneumothorax Vascular puncture Dural puncture Horner’s syndrome Harlequin syndrome
What are the features of Harlequin syndrome?
Contra-lateral hyperperfusion
So the face on the opposite side is all red
After a PVB a patient has ipsilateral miosis. What condition is this likely to be and how would you confirm your diagnosis?
Horner’s syndrome
Ptosis, miosis, anhydrosis & enopthalmos
Describe the features of Parkinson’s disease
Tremor Bradykinesia Rigidity Autonomic features - BP control GI - constipation CNS - low mood/dementia Quiet voice, slow speech
Describe the classes of drugs used in PD
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
What other treatments exist for Parkinson’s Disease?
Deep brain stimulation - electrodes into subthalamic nuclei connected to pulse generator
What drugs should be avoided for anaesthesia of a PD patient?
Atropine Halothane High dose Fentanyl/Alfentanil DIRECT ACTING sympathomimetics DA antagonists Serotonin syndrome - Tramadol
What considerations are needed for a PD patient having an operation?
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
What PD drugs can be given via a different route to PO?
Rotigotine
Apomorphine
These discussions should be made with a PD specialist (and a patient)
Critical care admission may be required
How do you describe doing a nerve block?
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
Definition of major haemorrhage?
150ml/min blood loss
Loss of 50% blood volume in <3 hours
Loss of entire circulating blood volume in 24 hours
How would you manage a major trauma ?
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
What parameters do you transfuse to in major haemorrhage? (Or other parameters you want to stick to)
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
What is damage control resuscitation?
Maintain circulating blood volume, control haemorrhage and correct lethal triad of trauma (hypothermia/acidaemia/coagulopathy)
What are the principles of damage control resuscitation?
Damage control surgery
Permissive hypotension (except in head injury)
Rapid rewarming
Limit crystalloid
Early blood component therapy
Correct hypofibrinogenaemia & coagulopathies
What is damage control surgery?
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)
What is the mechanism behind acute traumatic coagulopathy?
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
Define neuropraxia
Temporary physiological interruption of conduction without loss of atonal continuity
Define axonotmesis
Loss of relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve
Define neurotmesis
Total severance or disruption of the entire nerve fibre with no distal nerve conduction
What is prehabilitation?
The process of enhancing an individual’s functional capacity to enable them to withstand a forthcoming stressor such as major surgery
What are the 2 main models to describe frailty?
Frailty phenotype
Frailty index
Give an example of a tool to describe frailty
Edmonton Frail Scale
Canada Study of Health and Ageing (CSHA) frailty index
List some risk factors for frailty
Age Female sex Lower socioeconomic class Depression Disability Comorbidities such as cardiovascular disease Diabetes Stroke Cancer Arthritis COPD Anaemia
What are the 4 main components of prehabilitation?
Medical optimisation
Physical activity
Nutritional support
Psychosocial support
What are the potential benefits of prehabilitation?
Shorter length of stay
Reduced post operative pain
Fewer post-op complications
What 3 physiological benefits may be gained from physical training as part of a prehabilitation program?
Improve functional reserve Improve mitochondrial oxygen uptake Improved lean body weight/weight loss Improved anaerobic threshold Improved VO2 max.
Give 4 benefits of carbohydrate preloading and nutritional optimisation
Shorter fasting time Improved wound healing Reduced length of stay Reduced infection Decreased insulin resistance Promotes anabolic state
Define delirium
Acute disturbance in cognitive state with fluctuations in orientation
What drugs are safe to use in porphyria?
Propofol
Fentanyl
Atracurium
What drugs need to be avoided in acute haemolytic porphyria?
Thiopentone Etomidate Ketamine Anything that stimulates P450 Antibiotics (although penicillins are ok) Antifungals Dexmedetomidine Anti-arrhythmics Ergometrine Anti-epileptics
What is acute hepatic porphyria?
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
What are some features of a Neurovisceral attack in Acute Hepatic Porphyria?
Abdo pain Hypertension Seizures Confusion N&V Peripheral neuropathy
What investigation would you do to confirm an attack of AHP?
PBG (urine)
Has to be taken at the time of the attack
Can also do plasma and faecal sample for porphyrin
What are the anaesthetic principles for a patient with AHPorphyria?
Minimise starvation time
Avoid precipitant drugs
Minimise stress by using good analgesia and avoiding PONV
Consider early epidural in obstetrics
How would you manage an acute attack of AHP?
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)
What perioperative consequences may be associated with pre-operative anaemia?
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
What adaptions occur to offset effects of anaemia?
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
Describe perioperative events that will worsen the effects of anaemia?
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
What further blood tests may help the classification of this anaemia?
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
What scoring systems can be used to help predict perioperative risk before major surgery?
ASA POSSUM SORT Revised CRI Nottingham hip fracture score V-POSSUM Carlisle risk calculator for elective AAA
What are the main measures of fitness obtained by CPET?
Anaerobic threshold - the level of O2 delivery at which anaerobic metabolism occurs
VO2 peak
Workload
What abnormalities seen at time of testing in CPET may suggest cardio-respiratory disease?
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
How can frailty be assessed?
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)
What drugs would you use in a hypertensive response to phaeochromocytoma tumour handling?
Mg Phentolamine GTN Sodium nitroprusside Nicardipine Esmolol
Define difficult airway
Difficulty with face mask ventilation/supraglottic device ventilation/endotracheal intubation or all 3
>2 attempts at laryngoscopy using direct laryngoscopy
What are the contraindications to AFOI?
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
What are the muscles of the larynx and what do they do?
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
What is the nerve supply to the larynx?
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
You used AFOI to intubate the patient. How would you be sure the patient is safe at extubation?
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
State three factors that affect blood viscosity
Temperature
Flow rate
Haematocrit
List intraoperative strategies to maintain perfusion to a free flap
Normothermia Normovolaemia Vasodilatation from anaesthetic agents Sympathetic blockade - paravertebrals/epidurals Minimised handling of flap
List 2 surgical and 2 non-surgical causes of free flap failure
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
How do you assess a free flap?
Colour CRT Skin turgor Skin temperature Bleeding on pinprick Doppler
What happens at the initiation of exercise?
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
What is the maximum HR?
Maximum HR = (220 - age) +/- 11
What is the anaerobic threshold?
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
What is VO2?
Oxygen consumption
What is CPET?
A dynamic, non-invasive assessment of cardiopulmonary system at rest and during exercise
Determines functional capacity
What are the CPET-derived variables?
What other measurements can CPET record?
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
Which CPET-derived variables are associated with poor postoperative outcomes?
Anaerobic threshold <11
Peak O2 consumption (VO2peak) <15
Ventilatory efficiency for CO2 (VE/VCO2) 36
Mortality/morbidity/ICU admission/LoS
What is the normal CVS response to exercise?
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
How is CPET done?
What equipment is needed?
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
What is VO2peak?
What is VO2max?
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
What are the CPET numbers that puts patients at higher risk of perioperative complications?
VO2peak <15ml/kg/min
AT <10.2mlO2/kg/min
ECG changes (ischaemic) SpO2 should be >95% throughout
In CPET, how is maximal effort defined/represented?
Achieving >80% of predicted work rate/load
Achieving >80% of predicted maximum HR
Achieving a RER (VCO2/VO2) of >1.15
What is VO2max influenced by?
CVS ability to deliver O2 to tissues
Ability for muscles to use O2 for ATP production aerobically
-this is due to capillary density
What abnormalities seen on CPET may suggest cardiorespiratory disease?
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
When might CPET be impractical?
Lower limb amputation Severe PVD Severe OA Balance/coordination problems Inability to tolerate face mask - claustraphobia
Other than CPET, how else can a patient’s functional capacity be assessed?
Duke Activity Status Index
6 minute walk test
Incremental shuttle walk test
Hand crank CPET
What are the contraindications to CPET?
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%)
List the patient related risk factors for PONV
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 (?)
List the anaesthetic related risk factors for PONV
Use of volatile
Use of nitrous
Intra- and post-operative opioid use
Increased duration of anaesthesia
What are the unwanted effects of PONV in adults?
Patient dissatisfaction Prolonged hospital admission Delayed oral intake Suture dehiscence Dehydration Electrolyte imbalance Aspiration Oesophageal rupture
Which non-pharmacological interventions have been shown to be effective in reducing PONV?
Acupuncture Wrist bands/acupressure Avoidance of GA (use of regional) Aromatherapy Avoidance of dehydration
Describe how 5HT3 antagonists work
Enterochromaffin cells release 5HT
5HT stimulates vagus - terminate in chemoreceptor trigger zone/vomiting centre
5HT3 receptors in CRTZ are blocked by e.g. ondansetron
Give some examples of chemotherapy
Alkylating agents
Tyrosine kinase inhibitors
Hormonal agents
List some systemic complications of chemotherapy
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
What is the function of the spleen?
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
What vaccines do you need if you’ve had a splenectomy?
Pneumococcal vaccine
Hib
Meningococcal C
2 weeks after traumatic splenectomy
What are the WHO classifications of obesity?
BMI 30-35 = Obese class I BMI 35-40 = Obese class II BMI >40 = Obese class III
Define:
- Total Body Weight
- Ideal Body Weight
- Lean Body Weight
- Adjusted Body Weight
- The actual weight of the patient
- What the patient should weigh with a normal ratio of lean mass to fat mass. (Calculation = height in cm - 100 or 105)
- Patient’s weight excluding fat
- 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
List the physiological changes that occur in the respiratory system due to obesity?
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
What are the new guidelines for anaesthesia for hip fracture?
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
What assessment tools should be used for hip fracture patients?
4AT/delirium assessment
Frailty assessment/score
Nottingham Hip Fracture Score
Involve orthogeriatricians
What are the 7 acceptable reasons for delaying hip fracture surgery?
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
What are the transfusion thresholds for hip fracture patients?
Hb should be >90g/L
Or >100g/L in IHD
What is the STOPBANG scoring tool?
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
What are the endocrine consequences of OSA?
Impaired glucose tolerance
Dyslipidaemia
Altered cortisol/ACTH
Testicular/ovarian dysfunction
What are the CVS consequences of OSA?
Systemic HTN Pulmonary HTN RV failure Dysrhythmias Increased risk of MI/stroke Pickwickian syndrome
List absolute contraindications to CPET
Acute MI Uncontrolled arrhythmia Syncope Active endocarditis Unstable angina Symptomatic severe AS Uncontrolled heart failure Uncontrolled asthma Suspected dissecting or leaking AAA
State the number of METS associated with:
- Resting, fasted for >12 hours
- Walking at 2.5mph on the flat
- Climbing 2 flights of stairs without stopping
- Jogging
- 1 MET
- 3
- 4
- 8
What are the contributors to ‘oxygen debt’?
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
What is the dose of dantrolene in malignant hyperthermia?
2-3mg/kg
Repeat 1mg/kg every 5mins until ETCO2<6kPa and temp <38.5
What is the management of a suspected Malignant Hyperthermia case?
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
What are the factors that affect IOP?
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
What factors affect choroidal blood volume?
Blood flow to eye is auto-regulated
Arterial PaCO2
Hypoxaemia
Vasodilation
Transient rise with acute systolic BP increase
Venous pressure - coughing/prone position
What are some predisposing factors for delirium post-operatively?
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
What are some modifiable risk factors to prevent delirium?
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
What are the associations/systemic effects of myotonic dystrophy?
CVS: conduction defects; arrhythmias; cardiomyopathy
CNS: cognitive impairment
Endocrine: insulin resistance; hypothyroidism
GI: poor GI transit
MSK: contractures; myotonia
What are the precipitants of myotonic contractures?
How would you treat it?
Hypothermia
Shivering
Electrical stimulation
Restore physiological homeostasis
What is the calculation for SVR?
MAP x 80
———
CO
x80 is to convert from Wood unit (mmHg/L/min) to dynes/sec/cm5
What is the calculation for PVR?
80 x (MPAP - PCWP)
———————————
CO
List patient factors that may require a vitreoretinal surgery to take place under GA?
Inability to lie still Chronic cough/movement disorder Dementia/cognitive impairment Inability to lie flat - CCF/COPD Longer duration required for this surgery
List the principles of GA for intraocular eye surgery
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
What are the features of a fat embolus?
RS: dyspnoea, tachypnoea and hypoxaemia
CNS: consfusion, drowsiness, seizures
Skin: petechial rash in mucous membranes, skin folds
Fat embolism index scoring
What are the features of a fat embolus?
Tachycardia Pyrexia MI Drop in platelets ESR Lipouria Fat in sputum
What are the 2 theories for fat embolus?
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
What are the prevention strategies for fat embolism?
Early immobilisation
Early fixation
Use of venting holes intra-operatively
Avoiding IM nail
What are the cartilages of the larynx?
3 paired:
- Cuneiforms
- Arytenoids
- Corniculates
3 unpaired:
- Epiglottis
- Thyroid
- Cricoid
Describe the oculocardiac reflex
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
What are the contraindications to day case surgery in children?
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
Describe the pathogenesis of AIP
Autosomal dominant
Variable expression
Disorder of haem biosynthesis pathway
Deficiency of enzyme PBG-deaminase
Which commonly used anaesthetic drugs should be avoided in AIP?
Ketamine Thiopentone Sevoflurane Ephedrine Diclofenac Metaraminol
What is the management of a porphyric crisis?
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
What is meant by:
- MRI safe
- MRI conditional
- Equipment poses no additional risk in the MRI
2. No additional risk in specified environment with specific conditions
What precautions should be taken with a patient in MRI?
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
What are the absolute contraindications to MRI?
Aneurysm clips Ocular implants Cochlear implants ICDs PPMs Neurostimulation devices
What is the course of the Vagus nerve (CN X)?
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
What are the sensory functions of the Vagus nerve?
Auricular nerve - innervation external auditory canal/external ear
Internal laryngeal nerve - superior aspect of larynx/laryngopharynx
Cardiac fibres
GI tract - up to splenic flexure
What are the common side effects of chemotherapy agents?
Pulmonary Cardiac Renal Hepatic Neurological Haematological
Classify cytotoxic drugs
Alkylating agents (platins) Anti-metabolites (MTX) Plant alkaloids (vinca alkaloids) Topoisomerase inhibitors Antitumour antibiotics Hormones (steroids/testosterone/tamoxifen) Monoclonal antibodies (rituximab)
What is Stroke Volume Variation?
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
What are the nuclei of the Vagus Nerve?
Motor: Nucleus ambiguous
Sensory: Nucleus tractus solitarius
Parasympathetic: Dorsal nucleus
Describe the course of the Vagus nerve
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
Describe the course of the LEFT Vagus Nerve (CN X) below the neck
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
Describe the course of the RIGHT Vagus Nerve (CN X) below the neck
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
What are the main branches of the Vagus Nerve arising in the head and neck?
Head - auricular branch
Neck - Pharyngeal nerve
Superior laryngeal nerve
Right recurrent laryngeal nerve
Superior cardiac plexus
What are the main branches of the Vagus Nerve arising in the Thorax and Abdomen?
Thorax:
- Left RLN
- Inferior cardiac plexus
- Pulmonary plexus
- Oesophageal plexus
- Anterior Vagal Trunk (LVN)
- Posterior Vagal Trunk (RVN)
Abdomen:
- Gastric
- Hepatic
- Intestinal
- Coeliac plexus
What are the clinical features of vagus nerve transection?
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)
Describe how you would perform an AFOI
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
How would you perform an AFOI?
STOP (in a weird order)
- Oxygenate - HFNO
- Topicalise:
- Co-phenylcaine to nose
- 10 sprays of 10% lidocaine to oropharynx
- x5 1ml syringes of 2% lidocaine -SAYG - Sedate - Remi TCI
- Perform:
- including two point check at the end
What is in cophenylcaine?
5% lidocaine with 0.5% phenylephrine
What is the resting membrane potential in:
- skeletal muscle cell?
- nervous tissue cell?
- cardiac muscle cell?
- —90mV
- —70mV
- —90mV
What are the major components of the neuromuscular junction?
- Alpha-motor neurone
- Synaptic cleft
- Motor end plate of the muscle fibre
How is acetylcholine synthesised and stored within the nerve terminal?
ACh made from choline and acetyl co-A
80% stored in vesicles
1% in ‘active zone’ for immediate release
20% in cytoplasm (dissolved)
How does neuromuscular transmission occur?
- 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
Describe the nicotinic ACh receptor
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
Describe the synthesis of thyroid hormones
- 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)
What are the effects of thyroid hormones?
- 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
What are some examples of hypoxic pulmonary vasoconstriction in clinical practice?
Foetal circulation
Pneumonia
High altitude
Upper lobe diversion in cardiogenic pulmonary oedema
Describe the anatomy of the retroperitoneal space.
Anterior pararenal space: duodenum, pancreas, ascending/descending colon
Perirenal space: kidneys, adrenals, proximal ureters
Posterior pararenal space: contains fat
Great vessel compartment: aorta, IVC
What are some of the difficulties with retroperitoneal surgery?
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
What are the anaesthetic considerations for patients having a renal transplant?
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)
What are the anaesthetic considerations when anaesthetising a patient with myasthenia gravis?
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
What is the inheritance for Malignant Hyperthermia?
Autosomal Dominant
Tested on muscle biopsy or genetic testing
Database in Leeds
What is the pathophysiology of malignant hyperthermia?
—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
How would you anaesthetise a patient that may have MH?
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?
How would you treat MH if diagnosed intraoperatively?
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
What happens at aortic cross clamp?
Above clamp:
—sudden increase in SVR
—increase myocardial work
—increase BP
Below clamp:
—blood supply from collaterals
Describe the mediastinum
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
What is ultrasound?
> 20kHz sound waves
Medical US usually 2.5-15MHz
What are the stages of hypothermia?
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
Outline the coagulation process
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)
What are the contraindications to ECT?
—Raised ICP —Recent stroke —Cerebral aneurysm —Recent MI —Heart failure —Severe HTN —Osteoporosis
How would you anaesthetise for ECT?
—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
What do you need to form a clot?
—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
What do platelets release when activated?
- Vasoconstrictors: serotonin, thromboxane
- ADP
- Platelet activating factor
- vWF
- Fibrinogen
- Thrombin
- Ca2+
- Platelet derived growth factor
What are the steps involved in haemostasis?
Initiation Vasoconstriction Propagation Formation of platelet plug Formation of fibrin clot
What is the nerve supply to the abdominal muscles?
Intercostal nerves T7-11
Subcostal nerve T12
Iliohypogastric L1
Ilioinguinal L1
What are the indications for carotid endarterectomy?
European carotid surgery trial: symptomatic TIA + >70% stenosis of affected side
What is the function of the parathyroid gland?
Regulate calcium
And phosphate
What does parathyroid hormone do?
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
How is body pH regulated?
- Buffering system
—Intracellular: Phosphate, proteins
—Extracellular: HCO3, Hb - Respiratory regulation
—metabolic acidosis sensed by carotid bodies->stimulate respiratory centre
—hypercapnoea sensed by peripheral (carotid/aortic bodies) & central (medulla) chemoreceptors - Renal regulation
—Re-absorption of HCO3
—excretion of acids/H+
What mechanisms does the body have to prevent infection?
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
What are immunoglobulins? What are their function?
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
What are the stages of haemostasis?
Initiation
Propagation - large amount of thrombin generated converts fibrinogen to fibrin
Stabilisation - fibrin stabilises platelet plug
Vasoconstriction
What haemodynamic parameters can be deduced from Oesophageal Doppler?
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
How is COPD classified?
Using the GOLD criteria:
- Mild = FEV1 >80% predicted
- Moderate = FEV1 >50 <80% predicted
- Severe = >30 <50% predicted
- Very severe = <30% predicted
Confirmed on spirometry with post-bronchodilator FEV1/FVC of <0.7
What is intra-abdominal hypertension?
> 12mmHg is hypertension
Abdo compartment syndrome = >20mmHg with organ dysfunction
Grades I-IV
Measured by direct or indirect
Describe the cardio-respiratory physiology during the respiratory cycle
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
What happens to thyroid function in critical illness?
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
