Anaesthetics Flashcards
Pre-operative assessment (optimisation)
History and examination
Relevant investigations
Risk assessment tools: ASA, surgery grade, exercise tolerance (METs)
Optimise control of chronic conditions
Advantages of pre-operative assessment
Reduces
- Anxiety
- Delays
- Cancellations
- Complications
- Length of stay
- Mortality
Disadvantages of pre-operative assessment
Iatrogenic harm of over-investigation
Pre-operative medication changes
- Most medications continue as normal
- Possible exceptions: stop metformin (prevent metabolic acidosis) + anticoagulants (prevent bleeding)
Pain
Personal experience influenced by biological, psychological and social factors (life experiences)
Benefits of treating pain
Basic Human Right
For patient:
- Physical: improve sleep, appetite, fewer medical complications
- Psychological: reduced suffering, depression, anxiety
- Improve quality of life
For family:
- Improved functioning
For society:
- Lower health costs
- Contribute to community
Classification of pain
Duration
- Acute
- Chronic: >3 months (pain lasts after normal healing, often no cause)
- Acute on chronic
Cause
- Cancer: progressive
- Non-cancer
Mechanism
- Nociceptive
- Neuropathic
Nociceptive pain
Obvious tissue injury
- Well localised
- Sharp, dull
Neuropathic pain
Nervous system damage/abnormality causing abnormal processing of pain signal
- Not well localised
- Burning, shooting, numbness, pins and needles
Pain physiology
- Tissue injury and release of chemicals (prostaglandins, Substance P)
- Stimulation of nociceptors (pain receptors)
- Signal travels in A-Delta or C nerve to dorsal horn and synapses (first relay station)
- Second nerve ascends in spinothalamic tract (on opposite side)
- Synapses in thalamus (second relay station)
- Pain perception in cortex
- Descending pathway from brain to dorsal horn (decreases pain signal)
Gate theory
Distraction stimulus travel in large nerve fibres to inhibitor neuron.
- Inhibits transmission of afferent nociceptive fibres in dorsal root ganglia
Pathological pain mechanisms
- Increased receptor numbers
- Abnormal sensitisation of nerves
- Chemical changes in dorsal horn
- Loss of normal inhibitory modulation
Pain assessment
- Verbal rating score
- Numerical rating score
- Visual analogue scale
- Smiling faces
- Abbey Pain Scale (confused)
- Functional assessments
Non-pharmacological management of pain
- Rest, ice, elevation
- Nursing
- Surgery, acupuncture, massage, TENS, physiotherapy
- Psychological: explanation, reassurance, counselling
Acute (nociceptive) pain management
WHO pain ladder
- Mild: paracetamol, NSAIDs, aspirin
- Moderate: mild opioids (codeine, dihydrocodeine, tramadol) +/- non-opioids
- Severe: strong opioids (morphine, oxycodone, fentanyl) +/- non-opioids
RAT: recognise, assess (severity, type), treat, reassess
Neuropathic pain management
Antidepressants (amitriptyline, duloxetine)
Anticonvulsants (carbamazepine, sodium valproate, gabapentin)
Triad of anaesthesia
- Hypnosis
- Unconsciousness
- General anaesthetic - Analgesia
- Suppress autonomic response to pain
- Opiates, local anaesthetic - Relaxation (skeletal muscle)
- Immobility, access to body cavities, artificial ventilation
- Interacts with nicotinic ACh receptor at NMJ
Balanced anaesthesia: use different drugs to achieve desired anaesthetic state
General anaesthesia
Producing insensibility in the whole body using central acting drugs, usually causing loss of consciousness
- Provide hypnosis and little muscle relaxation and analgesia
- Potent
Mechanisms: globally suppress neuronal activity
- Open chloride channels - bind allosterically to GABA receptors (hyperpolarise neurons, suppress excitatory synaptic activity)
General anaesthesia
- Pharmacological kinetics
Most common sequence: IV induction followed by inhalational maintenance
IV (thiopentone, propofol)
- Rapid onset/recovery (redistribution, metabolism)
- Target Controlled Infusion pump system
Inhalation (halogenated hydrocarbons)
- Low MAC (minimum alveolar concentration) = high potency
- Slow induction
Regional anaesthesia
Producing insensibility in an area of the body using local anaesthetics applied to nerves supplying relevant area
- Applied between spinal cord and periphery (anaesthesia distal to injection)
- Only pain sensation needs to be removed
Local anaesthesia
Producing insensibility in only the relevant part of the body using local anaesthetics applied directly to tissues.
- Lihnocaine, Bupivacaine, Ropivacaine
Mechanism: blocks Na channels and prevents propagation of axonal action potential
- No hypnosis
- Risk of toxicity
Sedation
Some awareness of what is occurring
ASA system
1: normal, fit patient
2: mild systemic disease
3: severe systemic disease
4: severe systemic disease with threat to life
5: not expected to survive
6: brain dead, organ retrieval usually
Anaesthetic effect on CVS
General: depress cardiovascular centre
- Reduce sympathetic outflow
- Negative inotropic effect on heart
- Reduce vasoconstrictor tone (decreases peripheral resistance and venous return/CO)
Local/Regional - proportional to size of area
- Veno/vasodilation
Anaesthetic effect on respiratory system
General: depress respiratory centre
- Reduce hypoxic/hypercarbic drive
- Decrease tidal volume
- Increase RR
Paralyse cilia
Decrease FRC: V/Q mismatch, low lung volumes
Local/Regional: (neuraxial block)
Inspiratory function spared
Expiratory function impaired
Preparation for general anaesthesia
Pre-operative assessment
- Check in
- 5 pieces of monitoring present
- IV access
- Pre-oxygenation
Induction of general anaesthesia
ABC - serious CVS effect
Intubation - Guedel, LMA, ETT
Reduce minor complications
- Corneal injury: tape eyes
- Hypothermia
- Pressure/nerve injury
Guedel’s classification - 4 planes/stages of anaesthesia
- Analgesia and amnesia
- Delirium to unconsciousness
- Surgical anaesthesia
- Apnoea to death
Maintenance of general anaesthesia
Vapour or IV anaesthesia
Anti-emesis
Documentation
Communication - key moments in surgery
Important: vigilance, constant adjustment, anticipation
Emergence from general anaesthesia
- Reversal of neuromuscular blockade
- Stop anaesthetic agent
Spontaneous breathing and airway reflexes return
- Suctioning and removal of airway device
Recovery from general anaesthesia
Transfer to specific area
Continuous ABC
Management of nausea
Post-operative analgesia, fluid balance and organ support
Monitoring an unconscious patient
- ECG
- Non-invasive BP
- Oxygen sats
- End tidal CO2
- Airway pressure
ABC of unconscious patient
Airway (loss of airway reflexes and patency)
- Triple airway manoeuvre: head tilt, jaw thrust, open mouth
Intubation:
- Oropharyngeal/Guedel airway
- Laryngeal mask airway
- Endotracheal tube
Breathing
- Spontaneous, controlled or supported ventilation
Circulation
- BP every 5 minutes
- Vasoactive drugs
Anaesthesia risks
- Anaphylaxis
- Regurgitation (aspiration)
- Airway obstruction (hypoxia)
- Laryngospasm
- CVS instability
- Cardiac arrest
- Awareness
- Eye/corneal injury
- Hypothermia
- Pressure injury
- VTE (TED stockings)
- Nerve injury (positioning)
Levels of care
1: Ward-based
2: HDU - single organ support
3: Critical care - multiple organ support
Respiratory Failure
Type 1: oxygenation failure
- Level 1 care
- Nasal cannula, Hudson mask, Trauma mask (with bag)
Type 2: oxygenation and ventilation (CO2 clearance) failure
- Critical care
- High flow nasal cannula, non-invasive ventilation, intubation, tracheostomy
Cardiovascular failure
Shock: acute circulatory failure with inadequate tissue perfusion resulting in cellular hypoxia
- Distributive (septic)
- Hypovolaemic
- Anaphylactic
- Neurogenic
- Cardiogenic
Treatment: vasopressors, inotropes
Distributive/septic shock
Peripheral vasodilation with normal heart function
Hypovolaemic shock
Decrease in blood volume
- Primary: blood loss
- Secondary: dehydration
Anaphylactic shock
Peripheral vasodilation with abnormal heart function (reduced HR)
Neurogenic shock
Peripheral vasodilation due to disruption of sympathetic NS (spinal cord injury)
Cardiogenic shock
Abnormal heart function (unable to pump blood)
Arterial line
Site: radial, brachial, femoral
- Repeated blood sampling
- Instantaneous BP reading
Central venous line
Site: internal jugular, subclavian, femoral
- Repeated blood sampling
- CVP measurement
- Multiple potent drug administration
- Long duration of access
Vasopressors
Vasoconstrictors
- Improve preload - decrease venous volume
- Improve afterload - constrict arterioles
Metaraminol: alpha 1 agonist and little beta action (+ve contractility)
Noradrenaline: same as ^ but more potent
Inotropes
Support contractility
Adrenaline: alpha and beta agonism
Dobutamine: beta agonism
Neurological failure
Reduced conscious level
- Confusion
- Disorientation
- Delirium
- Lethargy
- Stupor
- Coma
Compromised ability to breath, ventilate and protect airway
Causes:
- Metabolic
- Head trauma
- Infection - meningitis, encephalitis
- Stroke
Colloids
Fluid with large osmotically active molecules (starches, gelatines, dextrans, albumin, blood products)
- Holds fluid in vascular tree
Crystalloids
Fluid with small molecules
- Fluid moves out of vascular tree (ECF expansion)
- 0.9% saline, Hartmann’s, plasmalyte-148, dextrose
0.9% saline components
Crystalloid
- Na 154 mmol/L
- Cl 154 mmol/L
High salt content (9g/L)
- Complications: hypercholaemic acidosis, decreased GFR
Hartmann’s components
- Na 131
- Cl 111
- K 5
- Ca2+ 2
- Lactate 29
5R’s of fluid prescription
Resuscitation:
- Replenish fluid (increase CO)
- Fluid challenge: 500ml crystalloid over 15 mins and reassess
Routine maintenance (nil by mouth):
- Prevent dehydration
- 30ml/kg/hr (never exceed 100ml/hr)
- 1 mmol/kg/day Na, K, Cl
- 50-100 g/day glucose
Replacement
Redistribution
- Fluid loss to sensible/insensible losses
Repletion of electrolytes
Reassessment
- May require vasopressors
