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Anaesthetics Flashcards

1
Q

Pre-operative assessment (optimisation)

A

History and examination
Relevant investigations
Risk assessment tools: ASA, surgery grade, exercise tolerance (METs)
Optimise control of chronic conditions

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2
Q

Advantages of pre-operative assessment

A

Reduces

  • Anxiety
  • Delays
  • Cancellations
  • Complications
  • Length of stay
  • Mortality
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3
Q

Disadvantages of pre-operative assessment

A

Iatrogenic harm of over-investigation

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4
Q

Pre-operative medication changes

A
  • Most medications continue as normal

- Possible exceptions: stop metformin (prevent metabolic acidosis) + anticoagulants (prevent bleeding)

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5
Q

Pain

A

Personal experience influenced by biological, psychological and social factors (life experiences)

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6
Q

Benefits of treating pain

A

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
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7
Q

Classification of pain

A

Duration

  • Acute
  • Chronic: >3 months (pain lasts after normal healing, often no cause)
  • Acute on chronic

Cause

  • Cancer: progressive
  • Non-cancer

Mechanism

  • Nociceptive
  • Neuropathic
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8
Q

Nociceptive pain

A

Obvious tissue injury

  • Well localised
  • Sharp, dull
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9
Q

Neuropathic pain

A

Nervous system damage/abnormality causing abnormal processing of pain signal

  • Not well localised
  • Burning, shooting, numbness, pins and needles
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10
Q

Pain physiology

A
  1. Tissue injury and release of chemicals (prostaglandins, Substance P)
  2. Stimulation of nociceptors (pain receptors)
  3. Signal travels in A-Delta or C nerve to dorsal horn and synapses (first relay station)
  4. Second nerve ascends in spinothalamic tract (on opposite side)
  5. Synapses in thalamus (second relay station)
  6. Pain perception in cortex
  7. Descending pathway from brain to dorsal horn (decreases pain signal)
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11
Q

Gate theory

A

Distraction stimulus travel in large nerve fibres to inhibitor neuron.
- Inhibits transmission of afferent nociceptive fibres in dorsal root ganglia

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12
Q

Pathological pain mechanisms

A
  • Increased receptor numbers
  • Abnormal sensitisation of nerves
  • Chemical changes in dorsal horn
  • Loss of normal inhibitory modulation
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13
Q

Pain assessment

A
  • Verbal rating score
  • Numerical rating score
  • Visual analogue scale
  • Smiling faces
  • Abbey Pain Scale (confused)
  • Functional assessments
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14
Q

Non-pharmacological management of pain

A
  • Rest, ice, elevation
  • Nursing
  • Surgery, acupuncture, massage, TENS, physiotherapy
  • Psychological: explanation, reassurance, counselling
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15
Q

Acute (nociceptive) pain management

A

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

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16
Q

Neuropathic pain management

A

Antidepressants (amitriptyline, duloxetine)

Anticonvulsants (carbamazepine, sodium valproate, gabapentin)

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17
Q

Triad of anaesthesia

A
  1. Hypnosis
    - Unconsciousness
    - General anaesthetic
  2. Analgesia
    - Suppress autonomic response to pain
    - Opiates, local anaesthetic
  3. 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

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18
Q

General anaesthesia

A

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)

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19
Q

General anaesthesia

- Pharmacological kinetics

A

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
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20
Q

Regional anaesthesia

A

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
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21
Q

Local anaesthesia

A

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
22
Q

Sedation

A

Some awareness of what is occurring

23
Q

ASA system

A

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

24
Q

Anaesthetic effect on CVS

A

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

25
Q

Anaesthetic effect on respiratory system

A

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

26
Q

Preparation for general anaesthesia

A

Pre-operative assessment

  • Check in
  • 5 pieces of monitoring present
  • IV access
  • Pre-oxygenation
27
Q

Induction of general anaesthesia

A

ABC - serious CVS effect

Intubation - Guedel, LMA, ETT

Reduce minor complications

  • Corneal injury: tape eyes
  • Hypothermia
  • Pressure/nerve injury
28
Q

Guedel’s classification - 4 planes/stages of anaesthesia

A
  1. Analgesia and amnesia
  2. Delirium to unconsciousness
  3. Surgical anaesthesia
  4. Apnoea to death
29
Q

Maintenance of general anaesthesia

A

Vapour or IV anaesthesia
Anti-emesis

Documentation
Communication - key moments in surgery

Important: vigilance, constant adjustment, anticipation

30
Q

Emergence from general anaesthesia

A
  • Reversal of neuromuscular blockade
  • Stop anaesthetic agent

Spontaneous breathing and airway reflexes return

  • Suctioning and removal of airway device
31
Q

Recovery from general anaesthesia

A

Transfer to specific area

Continuous ABC

Management of nausea

Post-operative analgesia, fluid balance and organ support

32
Q

Monitoring an unconscious patient

A
  • ECG
  • Non-invasive BP
  • Oxygen sats
  • End tidal CO2
  • Airway pressure
33
Q

ABC of unconscious patient

A

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
34
Q

Anaesthesia risks

A
  • Anaphylaxis
  • Regurgitation (aspiration)
  • Airway obstruction (hypoxia)
  • Laryngospasm
  • CVS instability
  • Cardiac arrest
  • Awareness
  • Eye/corneal injury
  • Hypothermia
  • Pressure injury
  • VTE (TED stockings)
  • Nerve injury (positioning)
35
Q

Levels of care

A

1: Ward-based
2: HDU - single organ support
3: Critical care - multiple organ support

36
Q

Respiratory Failure

A

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
37
Q

Cardiovascular failure

A

Shock: acute circulatory failure with inadequate tissue perfusion resulting in cellular hypoxia

  • Distributive (septic)
  • Hypovolaemic
  • Anaphylactic
  • Neurogenic
  • Cardiogenic

Treatment: vasopressors, inotropes

38
Q

Distributive/septic shock

A

Peripheral vasodilation with normal heart function

39
Q

Hypovolaemic shock

A

Decrease in blood volume

  • Primary: blood loss
  • Secondary: dehydration
40
Q

Anaphylactic shock

A

Peripheral vasodilation with abnormal heart function (reduced HR)

41
Q

Neurogenic shock

A

Peripheral vasodilation due to disruption of sympathetic NS (spinal cord injury)

42
Q

Cardiogenic shock

A

Abnormal heart function (unable to pump blood)

43
Q

Arterial line

A

Site: radial, brachial, femoral

  • Repeated blood sampling
  • Instantaneous BP reading
44
Q

Central venous line

A

Site: internal jugular, subclavian, femoral

  • Repeated blood sampling
  • CVP measurement
  • Multiple potent drug administration
  • Long duration of access
45
Q

Vasopressors

A

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

46
Q

Inotropes

A

Support contractility

Adrenaline: alpha and beta agonism
Dobutamine: beta agonism

47
Q

Neurological failure

A

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
48
Q

Colloids

A

Fluid with large osmotically active molecules (starches, gelatines, dextrans, albumin, blood products)
- Holds fluid in vascular tree

49
Q

Crystalloids

A

Fluid with small molecules

  • Fluid moves out of vascular tree (ECF expansion)
  • 0.9% saline, Hartmann’s, plasmalyte-148, dextrose
50
Q

0.9% saline components

A

Crystalloid

  • Na 154 mmol/L
  • Cl 154 mmol/L

High salt content (9g/L)
- Complications: hypercholaemic acidosis, decreased GFR

51
Q

Hartmann’s components

A
  • Na 131
  • Cl 111
  • K 5
  • Ca2+ 2
  • Lactate 29
52
Q

5R’s of fluid prescription

A

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

Systems (9 decks)

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