Anaesthesia Flashcards

1
Q

What is analgesia?

A

Decrease or absence of pain.

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2
Q

What is pain?

A

Conscious perception of a noxious stimuli

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3
Q

What is local anaesthesia?

A

A loss of sensation restricted to a small body area (e.g. finger)
Achieved by blocking specific terminal nerves using LA.

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4
Q

What is regional anaesthesia?

A

Loss of sensation in a more extended body are (e.g. limb)

Achieved by blocking major nerves or multiple terminal nerves using LA or analgesic drugs.

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5
Q

What is general anaesthesia?

A

Pharmacologically induced state of absence of consciousness.
The patient will not respond to any stimuli (including pain).
Achieved by administering intravenous or inhalant anaesthetics.
Should always be combined with analgesia & muscle relaxation.

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6
Q

What is sedation?

A

Pharmacologically induced state of reduced level of consciousness.
May be associated with a lack of memory.
When combined with analgesia, can further reduce level of pain perception.

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7
Q

What are the 4 stages of anaesthesia?

A
  1. disordered consciousness, voluntary movement.
  2. excitement.
  3. surgical anaesthesia.
  4. overdose
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8
Q

What happens in stage 1 anaesthesia?

A

Patient is conscious but not acting normal.
Agent acts on cerebral cortex, rendering its function more acute but unbalanced (except for pain perception).
Profoundly modified by pre-medication.

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9
Q

What happens in stage 2 anaesthesia?

A

Unconsciousness.
Patient may exhibit signs of excitement.
Patient can move through stage 2 quicker if drugs are administered faster.
May be unnoticeable with heavy pre-medication.

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10
Q

What happens in stage 3 anaesthesia?

A
Tranquil phase of narcosis (resembling natural sleep).
Goal of anaesthesia: to maintain this level of narcosis for as long as required.
4 planes (light, medium & deep)
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11
Q

What happens in stage 4 anaesthesia?

A
Signs of severe shock.
Weak pulse.
Not breathing.
Dilated pupils.
Reflexes absent.
Loss of sphincter tones.
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12
Q

To which stage of GA does the following clinical signs in a dog correspond:
Eyes ventro-medial, decreased RR, palpebral reflex absent, corneal reflex present, relaxed jaw tone?

A

Stage 3, plane 2 (ideal GA for surgery).

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13
Q

What does pre-anaesthetic patient evaluation include?

A
  1. History.
  2. Physical exam.
  3. Pain assessment.
  4. Clinical diagnostics (at least CBC/biochem: PCV, TS, BUN, BG)
  5. Other considerations (e.g. breed, recent trauma, concurrent drugs).
  6. Classification of physical status (ASA status).
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14
Q

What 3 systems are most heavily affected by GA?

A

CNS, cardiovascular & respiratory (must assess in physical exam).

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15
Q

How does pain affect GA?

A

Pain increases dosage of anaesthetic needed, thus causing more side effects.
Pain also causes patient stress and reduces healing.
Consider NSAIDs and/or opioids for prophylactic pain treatment.

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16
Q

Why consider prophylactic treatment of pain?

A

Reduces GA dose needed.
Minimise wind-up and hyperalgesia.
Synergistic with pre-medication (improves sedation).

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17
Q

What are the 6 different ASA physical statuses?

A
  1. normal healthy patient.
  2. patient with mild systemic disease (e.g. obesity)
  3. patient with severe systemic disease.
  4. patient with severe systemic disease that is a constant threat to life (e.g. GDV)
  5. moribund patient who is not expected to survive without operation (e.g. late GDV)
  6. declared brain-dead patient whose organs are being removed for donor purposes.
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18
Q

Why is fasting recommended in most patients?

A

GA relaxes lower oesophageal sphincter and decreases GI motility:
Risk of regurgitation & aspiration.
Risk of bloat (presses on diaphragm and restricts respiration).
Risk of ileus (painful and poor recovery).

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19
Q

What are is difference in pre-anaesthetic patient preparation between monogastrics, ruminants and small mammals/birds/neonates?

A

Monogastrics (dogs, cats, horses): withhold food 12 hrs, no withholding of water.
Ruminants: withhold food 12-36 hrs, water for 12 hrs.
Small mammals, bids and neonates: short to no fast (risk of hypoglycaemia), no withholding of water.

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20
Q

What is the protocol for pre-anaesthetic preparation in diabetic patients?

A

Schedule procedure for 1st of the morning.
Evening meal and insulin the night before.
Small meal in the middle of the night with 1/2 dose insulin.
No morning meal.
Check glucose pre-op:
If normal (<500g/dL) no AM insulin).
If >500g/dL): 1/2 dose insulin.
If low - provide supplemental glucose.

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21
Q

What are the aims of premedication?

A

To calm the patient.
To provide peri-operative analgesia.
To reduce the total amount of anaesthetic (and its side effects).
To reduce nausea & vomiting.
To smoothen recovery.
To reduce autonomic side effects (HR, BP less reactive during surgery - CNS less reactive to noxious stimuli).

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22
Q

What factors dictate the type of agents used for pre-medication?

A

Animal temperament:
e.g. alpha-2 agonists like medetomidine for more aggressive patients Vs. benzodiazepines or phenothiazines (acepromazine) for more docile patients.
Duration of procedure:
e.g. ACP lasts 6-8 hrs and is long acting (good for longer procedure).
Ability to antagonise the agent:
e.g. important for very sick/old patient that cannot metabolise agents well on their own.
Health status of patient:
e.g. choosing agents with less effects on the cardiovascular system (NOT alpha 2s, possibly small dose ACP) for patients with cardiovascular disease.
Availability of the drug.
Personal preference.

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23
Q

Why combine traquilizer/sedative agents with opioids for premedication?

A

Synergistic effects (decrease the dose of both sedation & analgesia required, meaning less side effects).
Produces reliable & safe sedation.
Reduced the dose of induction and maintenance anaesthetic agent.
Provides pre-emptive analgesia.

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24
Q

What agents can we use for sedation?

A

Phenothiazines (e.g. ACP)
Alpha 2 agonists (e.g. xylazine LA, medetomidine SA, dex-medetomidine SA, romifidine LA , detomidine LA).
Benzodiazepines (e.g. diazepam, midazolam).

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25
Q

What are the effects of acepromazine?

A

Tranquillisation/sedation.
Anti-arrhythmic (reduces myocardium sensitivity to catecholamines).
Anti-emetic.
Spasmolytic (relieve spasm of smooth muscles - e.g. GIT)
Anti-histamine (don’t use on patient going for skin allergy test)
Alpha 1 receptor antagonists (vasodilation, decreased BP and increased HR).
NO analgesia.

Side effects:
Hypotension (care with hypovolaemic patients).
Collapse in Boxers.
Decreased seizure threshold (should not use in patients with brain trauma, space occupying lesion in brain).
Hypothermia.

26
Q

Where are alpha 2 adrenoceptors distributed throughout the body?

A

Sympathetic NS.
Vascular endothelium.
CNS.
Also platelets, uterus & gut.

27
Q

What are the general effects of alpha 2 agonists?

A
Sedation/hypnosis (dose dependent).
Analgesia (very good).
Muscle relaxation (very good).
Respiratory depression (mild).

Phase 1: drug effects blood vessels.
Initial period of hypertension (vasoconstriction) followed by a reflex bradycardia.
Phase 2: drugs reach brain.
Drop in BP (back to normal or below) and low HR due to parasympathetic activation.

Cardiac arrhythmias (AV blocks 1 & 2)

Also hyperglycaemia, diuresis,, decreased intestinal motility, vomiting.

28
Q

Should anticholinergic drugs (e.g. atropine) be administered with alpha 2 adrenoceptors agonists to offset bradycardia?

A

No.
Anticholinergic will increase HR and also BP so patient will become hypertensive.
The reflex bradycardia is protective.

29
Q

What are the effects of xylazine?

A

Sensitises myocardium to catecholamine (increased risk of arrhythmias).
Emesis.

30
Q

What is the difference between medetomidine and dex-medetomidine?

A

Levo-medetomidine removed from medetomidine to produce dex-medetomidine.

Levo-medetomidine is inactive, has alpha 2 antagonistic properties, high alpha 1 affinity (anti-sedative, myometrial activity, arrhythmias).

31
Q

Is there an alpha 2 antagonist?

A

Only one licensed is antisedan.
Will reverse xylazine, medetomidine and dexmedetomidine).
Will not full reverse CV depression.

32
Q

Main effects of benzodiazepines (diazepam, midazolam)?

A
Muscle relaxation.
Anxiolytic.
Appetite stimulation.
Minimal cardiovascular and respiratory effects.
Anti-convulsant.
Anti-arrhythmic.
Potential for complete reversal (flumazenil).
Thrombophlebitis with diazepam.
33
Q

What are the clinical uses of benzodiazepines?

A

Increases muscle relaxation during anaesthesia.
Offset muscle hypertonicity caused by ketamine.
Stimulate appetite in anorexic patients.
Treatment of seizures.
To decrease dose of induction agent.

Excellent sedation agents in very young/sick/senile patients, either alone or in combination with opioid drugs.

Unreliable in healthy adult patients.

34
Q

What can we use for analgesia?

A

Opioids.

Full (pure μ) agonists (best analgesia).
e.g. morphine, methadone, hydromorphone, fentanyl, meperidine, alfentanil, remifentanil.

Partial μ agonists (not as good but still good)
e.g. buprenorphine

κ agonists and μ antagonists (unreliable analgesia)
e.g. butophanol (good sedative), nalbuphine

35
Q

Why use full μ agonist opioid analgesics over partial or kappa agonists?

A

Full agonists are reliable analgesics and can be titrated to effect.
Best choice for sever pain.
Can be topped up.

Partial μ or kappa agonists can be potent analgesics but tend to be unreliable.

36
Q

What are the physiological effects of opioid analgesics?

A

CNS depression in dogs BUT excitement in cats and horses.

Minimal CVS effects, possible sinus bradycardia.

Respiratory sytem depression..

Also histamine release, GIT depression, release of ADH (urine retention), hypothermia, (can be hyperthermia in cats, horses and pigs), emesis, pupillary diameter (miosis in dogs and midriasis in cats).

37
Q

What are differences between the different opioid analgesics?

A

Morphine (gold standard, may cause vomiting in pain-free/ambulatory patients, histamine release possible with IV administration, duration of 4 hrs in dogs and 6-8 hrs in cats).

Methadone (similar to morphine but no vomiting).

Hydromorphone (eight times stronger than morphine, better sedation, emesis less likely, no histamine release).

Alfentanil & fentanyl (50-100x potency of morphine, short acting agents mainly used for intra-op as bolus/infusion, useful for severe pain BUT bradycardia and respiration depression).

38
Q

Are there any contraindications to the use opioids?

A

Pre-existing respiratory depression.
Head trauma (respiration depression will lead to increased CO and increased ICP - must control respiration of patient).
Pancreatitis (increases pain and issues)

39
Q

What are the factors that determine the rate & speed of onset of anaesthesia?

A

The anaesthetic used:

  • lipid solubility (access brain faster e.g. alfaxalone, propofol)
  • molecular size (big molecules cannot cross BBB)
  • protein binding (more protein binding = less available to brain)
  • ionisation (will not cross BBB if ionised)

Dose.
Rate of administration.
Route of administration (e.g. IV vs subcut vs IM).

Animals level of consciousness (more sedated = less anaesthesia required, more excited = more agent req).

Acid-base levels (low pH, more sensitive to drug), electrolytes and serum protein status.

Cardiac output (lower CO= longer induction IV, VUT faster induction for inhalants).

40
Q

What are the possible IV agents used for induction of GA?

A
Barbiturates (e.g. thiopental)
Dissociative agents (e.g. ketamine)
Imidazole derivative (e.g. etomidate)
Steroids (e.g. alfaxalone)
Phenol derivatives (e.g. propofol)
41
Q

What are the effects of thiopental?

A

CNS:
Depression (via GABA receptors)
No analgesia (anti-analgesic at sub-hypnotic doses)

CVS: (depression) 
Decrease in arterial BP (vasodilation).
- Decreased peripheral resistance.
- Decreased SV.
- Decreased myocardial contractility.
Increase in HR (to compensate).
Increased sensitivity of myocardium to catecholamine (arrhythmias common). 

Resp:
Post induction apnoea common (esp following opioid pre-med).
Decreased ventilatory rate and tidal volume.

42
Q

What dictates induction and arousal in anaesthesia with thiopental?

A

Depends largely on redistribution NOT metabolism (hepatic metab = 5% total dose per hour).

Do not use in patient with no fat (young, sighthounds) - stays in blood and slows recovery.

Not good as an infusion due this redistribution.

43
Q

What are the precautions for thiopental?

A

IV ONLY (other methods = skin slough/burn).
Thin dogs.
Hypovolaemia (decrease in MAP is marked)
Liver dysfunction (metab even slower)
Age (metab even slower)
Obesity (requires higher dose)
Hypo-proteinaemia/acidosis (requires smaller dose)

44
Q

What are the effects of ketamine?

A
Cataleptic state:
CNS excitation
Analgesia
Immobility
Dissociation from one's env.
Amnesia.
CNS effects:
Acting on GABA and NMDA receptors.
Increases ICP (not for patients with history of seizures or brain lesions).
Can cause seizures in dogs &amp; cats.
Analgesia (somatic > visceral)
NMDA antagonist (acts against chronic pain).
Hallucinations/delirium in recovery.
Oculo-palpebral reflex maintained.
CVS (stimulation)
Increased sympathetic tone.
Increased HR and contractility.
Increased CO &amp; arterial BP.
Increased myocardial oxygen demands.
Little change in peripheral resistance.
BUT do not use in very sick patient (CVS will crash - ketamine requires intact adrenergic system)

Resp:
Transient apnoea possible with IV administration)
Ventilation usually well maintained (unlike other agents).
Laryngeal and pharyngeal reflexes maintained.
Broncho-dilation.
Apneustic breathing (breathe in, pause, breathe out).

45
Q

Explain ketamine’s pharmacokinetics in dogs/horses vs cats.

A

Extensive hepatic metabolism in dogs and horses.
Mainly excreted unchanged via kidney in cats.
Do NOT use in cats with renal dysfunction.

Rapid recovery in most species due to redistribution from CNS to body tissues.

46
Q

What are ketamine’s adverse effects?

A

CNS stimulation.
Pain on injection due to low pH (not with IV).
Emergence delirium (swinging head from side to side).
Hypertension and tachycardia.
Prolonged recovery.
Salivation.
Increased muscle tone (requires muscle relaxants)

47
Q

Why use etomidate?

A

No CVS effects.
Mild resp depression.
Good induction agent for high risk/sick patients.
BUT not in AUS.

48
Q

Why use alfaxalone?

A

High therapeutic index.
Lack of cumulation in body (ideal of CRI and infusion).
Rapid, complete recovery of consciousness.
Lack of irritant effects and activity when given IM/SC.

*NOTE:
No preservative (keep in fridge).
Twitching/paddling in recovery is possible in cats (removed with good sedation, dim room, removal of stimulation).
Respiratory depression at induction AND decrease in arterial BP (give to effect and slowly).

49
Q

Why use propofol?

A

Quick “to effect” induction & recovery.
Can be used as infusion (does not prolong recovery).
Can be used as total IV anaesthesia (like alfaxalone).

Lack of excitement at induction.
Lack of hangover at recovery.
Non-cumulative nature.
Ability to use as CRI.
Can be given to patients with kidney/liver damage.
50
Q

What are the adverse effects of propofol?

A

Cardiovascular depression.
Respiratory depression.
Pain on injection (esp cats)

Dose dependent like alfaxalone.

51
Q

Can you use opioids as an induction agent?

A

In combination with benzodiazepines (e.g. fentanyl + diazepam).
May be adequate for intubation if patient is debilitated (very sick patient)
Minimal systemic effects.
Bradycardia, respiratory depression and GI effects.
Great analgesia/reversibility.

52
Q

What is TIVA, PIVA & balanced anaesthesia?

A

TIVA = total intra-venous anaesthesia (only IV agents used to provide balanced anaesthesia).
PIVA = partial intravenous anaesthesia (inhalant and IV agents used concurrently to provide balanced anaesthesia).
Balanced anaesthesia = judicious use of hypnotic and analgesic agents to minimise side-effects of each while providing anaesthesia and analgesia.

53
Q

What are the hazards of volatile agents?

A

CVS:
CV depression (enflurane>halothane>isoflurane)
CV stimulation (desflurane)
Coronary steal in horses (isoflurane) - alteration of circulation patterns leads to a reduction in the blood directed to the coronary circulation.

Resp:
Irritancy (des>iso>halo) - leading to broncho-constriction.
Blocks hypoxic pulmonary vasoconstriction reflex - when lung are collapsed (i.e. when lying down), areas not oxygenated properly will normally shunt blood to other areas.

CNS:
Cerebral vasodilation (increase ICP).
Epileptic activity (enflurane).

Toxicity:
Nephrotoxicity (methoxyflurane, sevoflurane).
Hepatotoxicity (all)
Malignant hyperthermia (reaction to gas leading to massive muscular spasm - can be fatal).
Operating room pollution (i.e abortions)

54
Q

What are the hazards of nitrous oxide?

A

No benefits in vet med.
Prevents admin of high partial pressure of oxygen.
Diffusion into gas-filled areas (e.g. GIT, pneumothorax).
Air embolism.
Bone marrow toxicity.
Nervous system, cardiovascular, hepatic and reproductive effects in humans.

Very stable in atmosphere.
Destroys ozone.
Significant greenhouse gas.

55
Q

What are advantages of TIVA?

A

Guaranteed rapid, smooth induction & recovery (PIVA may require lots of sedation)
Seamless transition from induction to maintenance (PIVA requires induction with IV bolus, then must intubate and begin admin of inhalant agents before conc. of IV agent drops up/requires top up).
Easy to deepen anaesthesia (quicker to increase infusion rate compared to gases - which depends on patients breathing, etc.)
Rapid predictable recovery of better quality.
Safe for patients with MH, asthma & other allergic conditions.
Less “stress response” to surgery.
Absence of nausea and vomiting (appetite stimulation instead - propofol).

Absence of theatre contamination (allow patient to breathe pure oxygen - no need to scavenge gases)
Small contribution to reduction in global warming.

56
Q

What are the limitations of TIVA?

A

Expensive (alfaxalone>propofol)

Varying response to standard dose (age, sex, obesity, haemodynamic states).

57
Q

Which agents are suitable for TIVA?

A
Alfaxan CD 
- rapid clearance
- minimal cumulation
Propofol
- rapid clearance 
- predictable metabolism
- minimal cumulation
58
Q

How do we deliver TIVA to the patient?

A

Intermittent bolus:
Give bolus IV, begin procedures, when patient gets lighter give another bolus & repeat.
OK for very short cases (up to 30 minutes)
Simple & no special equipment req.
BUT poor quality (peaks and troughs) - costs more to re-anaesthetise patient.
Large total drug dose.
Slow recovery.

Constant rate infusion (CRI):
Smoother anaesthesia.
Accumulates with time (deeper patient).
Risk of awareness or side effects (depending on rate).

Variable rate infusion: 
Modify rate of infusion depending on state of patient (reduced accumulation effect).
Smoother.
Lower total drug dose.
Faster recovery.
Frequent adjustment needed.

Target controlled infusion:
A computer with a set of pharmacokinetic parameters specific for a given agent and pop’n.
Computer controls the rate of infusion depending on blood concentration of the target.

Co-infusion:
Propofol & alfaxalone.
Poor reflex suppressant.
No analgesia (requires opioids).

59
Q

Which opioids do we use with TIVA?

A

Traditional opioids not optimal for infusion (morphine, pethidine).

  • difficult to titrate to effect.
  • active metabolites (can lead to histamine release).
  • limited potency

Aim for potent analgesic with a similar profile to alfaxalone/propofol (easily titratable to effect, rapid recovery).
E.g. Fentanyl, alfentanil, remifentanil.
*NOTE: remifentanil will have same speed of recovery no matter how long you give the agent (half life every 3 mins)
BUT fentanyl recovery will increase the longer you give the agent.

60
Q

What is the role of an endotracheal tube?

A

Secure the airway during anaesthesia (deglutition reflexes are lost).
Delivery of inhalant anaesthetics and mechanical ventilation.