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Diploma in Anaesthesia > Emergence from anaesthesia > Flashcards

Emergence from anaesthesia Flashcards

1
Q

Define slow/failed recovery

A

A patient with slow or failed recovery is someone in whom a progressive return of pre-operative function does not occur within the predicted time frame. It may include failure to:

Regain consciousness appropriately
Restore adequate ventilation or oxygenation
Sustain adequate cardiovascular function

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2
Q

Describe two high priority reversible causes of slow/failed recovery

A

Hyponatraemia in TURP
Hypoglycaemia in DM
Hypothermia after prolonged surgery

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3
Q

What device can help differentiate between central and peripheral causes

A

Peripheral nerve stimulator

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4
Q

What preoperative factors may suggest a cause for delayed recovery

A 
Check anaesthetic chart:
Patients usual medications 
- opioids
- amitriptyline
- anticonvulsant

Premedication

  • Benzodiazepine
  • Gabapentin
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5
Q

What intra-operative factors may cause slow/failed recovery

A

Length of anaesthesia

Intra-operative drugs
OPIOIDS - pinpoint pupils
- Rx incremental doses of naloxone: 0.1 - 0.2 mg
BENZOS
- Rx incremental doses of flumazenil: 0.1 mg (max 1 mg)
- may cause seizures, hypertension and dysrhythmias

Neuraxial/Nerve block

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6
Q

Which patients are at risk for hypoglycaemia

A

Children

Diabetics
Recent alcohol consumption
Malnourished
Sepsis
Liver failure
Hypoadrenalism

Rx: 50 ml 50% dextrose

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7
Q

Why can hypothermia lead to delayed/failed recovery

A

All drug metabolism is temperature dependent –> hypothermia increases likelihood of residual drug effect

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8
Q

What are three effects of severe hypothermia relevant to anaesthesia

A

Can cause unconsciousness itself
Cogaulopathy
Shivering –> increases O2 consumption

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9
Q

Describe the presentation of incomplete NMBD reversal and the approach to resolving this?

A

HPT and tachycardia with poor power and co-ordination

Use peripheral nerve stimulator to confirm degree of block, bearing in mind that it is painful

Sedate/maintain anaesthesia until NMB is fully reversed

SUX apnoea –> ventilation may be required for many hours

Further dose of neostigmine + glycopyrrolate may be given as indicated by peripheral nerve stimulator

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10
Q

If incomplete reversal of NMBD is excluded, what is the next step

A 
Full examination
? RSP cause: CXR/ABG
? CVS cause: cerebral hypoperfusion
? CNS cause: Intracranial event - CTB
? Metabolic: Acidosis/hypercapnoea - prolonged effects of NMB: ABG/UE/TFT
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11
Q

When can a diagnosis of “emergence phenomena” be made

A

In retrospect - diagnosis of exclusion

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12
Q

What is central anticholinergic syndrome

A

Associated with signs of peripheral anticholinergic activity

Blind as a bat,
dry as a bone,
full as a flask (can’t urinate),
hot as a hell
red as a beet,
mad as a hatter (concrete, easily describable, often Lilliputian hallucinations),
tacky (tachycardic) as a leisure suit (pink flamingo); phantom behaviors (“woolgathering”)

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13
Q

Describe how the patient/surgery/polypharmacy interact to potentially cause delayed recover by affecting the pharmacokinetics of the drugs

A

Absorption
Distribution
Metabolism
Excretion

Metabolism and excretion
- SUX apnoea (homozygous atypical plasma cholinesterase)

  • Renal/hepatic impairment
  • Hypothermia
  • Hypovolaemia
  • Acidosis
    All impair metabolism and excreiton of many drugs but mainly opioids and NMBDs

Distribution and excretion
- Prolonged surgery: inhalational agents will accumulate in tissues delaying their excretion

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14
Q

Describe how the patient/surgery/polypharmacy interact to potentially cause delayed recover by affecting the pharmacodynamics of the drugs

A

Wide range of sensitivity to different drugs especially opioids and especially elderly

Combined drugs can be synergistic –> prolonged action

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15
Q

How can local anaesthetics prolong recovery?

A

Directly:
1. High spinal/epidural –> hypotension/respiratory difficulty delaying recovery

  1. Interscalene nerve block may cause respiratory problems by anaesthesia of the phrenic nerve

Indirectly
Local anaesthetic systemic toxicity –? cardiac arrythmias/hypotension/CNS toxicity

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16
Q

Describe an approach to the causes of hypoventilation

A 
Anatomical approach
Brain
1. Loss of central drive
- COPD/OSA
- Intracranial pathology (CVA)
- drug overdose (including local anaesthetic toxicity)
- RICP

Airway
- Obstruction

Lungs
- COPD/Atalectasis/sputum plugging/BS/consolidation/ARDS

Muscles
- NMJ dysfunction: Incomplete NMBD reversal/myaesthenia gravis/muscle disorders

Chest wall

  • Obesity: reduced compliance
  • Pain
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17
Q

Describe the ‘other’ patient factors that can lead to delayed/failed recovery

A

There are 4 major areas to consider:

Endocrine
Hypoglycaemia
Hyperglycaemia
Hypothyroidism

Renal
Hypokalaemia
Uraemia
Hyponatraemia
Hypernataraemia
Hypermagnesaemia

Hepatic
Failed drug metabolism
Hepatic encephalopathy

Metabolic
Hypothermia – this is very common and may also increase bleeding postoperatively
Acidosis

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18
Q

Which procedures are high risk for surgical causes of delayed/failed recovery?

A

Carotid endarterectomy
Neurosurgical
Thoracic

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19
Q

Name 5 drugs that caused prolonged effects of NMBDs

A 
Volatile anaesthetics
Diuretics
CCB
Aminoglycosides
Lithium
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20
Q

Name 5 non-pharmacoological factors that prolong the effects of NMBDs

A

Hypokalemia and Hypermagnaesaemia (Hyperpolarization)

Hypothermia (reduced rate of metabolism)

Acidosis (donating proton to the tertiary amines –> increasing ionization and receptor affinity)

Myaesthenia gravis

Hepatic/renal insufficiency

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21
Q

Under which circumstances is the duration of depolarizing NMB prolonged

A

Atypical cholinesterase
Pregnancy
Liver disease

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22
Q

How is the duration of action of SUX affected in children

A

Duration of action is shorter in children

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23
Q

Describe the steps required for extubation

A

FIRST: A. Confirm neuromuscular function is adequate. This should be your first move. It is distressing for patients to emerge from anaesthesia while still partially paralyzed. Their respiratory function and ability to clear secretions will also be impaired.

SECOND: C. Stop anaesthetics drugs and give 100% oxygen. High flow oxygen (>6 L/min) will speed this process, but it still takes several minutes for washout of the inhaled anaesthetic agents to occur.

THIRD: E. Apply suction to the airway. Patients can’t swallow under anaesthesia. Saliva and other debris will accumulate in the mouth and pharynx and this could be inhaled during emergence. It’s best to do this before the patient is fully awake, to avoid biting on the suction device.

FOURTH: B. Ensure breathing is adequate. The ventilator should be turned off and the reservoir bag observed for the return of spontaneous respiration. Gentle assistance may be required by squeezing the bag manually.

FIFTH: D. Place patient in a suitable recovery position. As we shall see, there are several suitable positions, depending on the circumstances.

SIXTH: F. Assess wakefulness and ability to maintain airway. This is the final consideration. But remember, ‘every extubation is a trial of extubation’ and very occasionally reintubation will be necessary.

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24
Q

what are the two patterns of peripheral nerve stimulation than can detect ‘fade’

A 
Train of four (TOF)
Double burst (DB)
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25
Q

When can the NMB reversal agent be given?

A

TOF stimulus: at least 2 twitches

DB: one twitch

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26
Q

Why must there be some evidence of spontaneous return of neuromuscular transmission before giving reversal agents?

A

Attempts to reverse with more profound paralysis may be unsuccessful.

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27
Q

What level of neuromuscular reversal must be present prior to extubation

A

Full recovery of neuromuscular function (ie, train-of-four [TOF] ratio of ≥0.9) must be achieved prior to extubation of the trachea.

28
Q

Name the unwanted effects associated with neostigmine. What agents are given to prevent these side effects?

A

A: Excessive salivation
B: Bronchospasm
C: Tachycardia

Muscarinic antagonists:

  1. Atropine (enters CNS)
  2. Glycopyrrolate (Does not enter CNS)
29
Q

What other method for reversal of non-depolarising muscle relaxants exist? What is their mechanism and onset of action?

A

Sugammadex - SELECTIVE RELAXANT BINDING AGENT

Binds to AMIOSTEROID muscle relaxants (Rocuronium/vecuronium)

Onset of action: RAPID

30
Q

How long should preoxygenation prior to extubation be?

A

3 - 5 minutes or ET O2 >80%

31
Q

How can spontaneous ventilation be stimulated near the end of surgery?

A

Turn down respiratory rate –> allow CO2 to accumulate. Respiratory centre is less sensitive to PaCO2 in the presence of opioids

32
Q

After preoxygenation and circuit washout, what is the ext step in extubation?

A

Suction and clear the airway (no swallowing possible during anaesthetic)

33
Q

How is breathing assessed once airway is cleared

A

Insert Geudel airway –> prevent tube biting
Observe capnograph, ET volatile, reservoir bag and chest rise.
If insufficient, assist with assisted manual ventilation.

34
Q

Why should a Geudel airway be sited during the assessment of breathing phase

A
  1. Prevent ETT biting/obstruction
  2. Maintain airway after ETT removal
  3. Useful access for suction catheter
35
Q

Once the patient is breathing spontaneously –> the patient will be waking up. What occurs during this phase

A

Presence of ETT –> coughing, straining and breath holding. This must be minimized as it increases arterial, intracranial and intraocular pressure

36
Q

Why is the left lateral position preferred to the right lateral position as a recovery position?

A

Laryngoscopy and re-intubation are easier on this side when using a standard Mcintosh blade

37
Q

When is the supine position an appropriate recovery position?

A

Patient awake with good airway patency and there is minimal risk of regurgitation

38
Q

Name another recovery position and when it is contraindicated

A

Sitting up

- Contraindicated in hypotension and C-spine injury

39
Q

What are the problems with extubating a patient who is lightly anaesthetized versus awake with fully recovered airway reflexes?

A

High complication rate when extubated ‘light’.

  • Laryngospasm
  • Breath holding
40
Q

When is deep extubation done

A

Often during tonsillectomy –> patient placed in left lateral and monitored closely in recovery area

41
Q

How does diffusion hypoxia occur an what is done to avoid this

A

N2O diffuses into the alveoli faster than nitrogen enters into pulmonary capillary blood - adminsitration of O2 after extubation. Contents of alveoli are therefore diluted, including O2.

42
Q

reasons for inadequate reversal of NMB

A
  1. Hypothermia
  2. Premature reversal NMB
  3. Drugs
    Volatile anaesthetics
    Diuretics
    CCB
    Aminoglycosides
    Lithium
  4. Electrolyte abN
    Hypokalemia, hyponatraemia, hypocalcaemia Hypermagnaesaemia
  5. Acidosis/Hypovolaemia
  6. Renal/hepatic impairment
  7. Myaesthenia gravis
43
Q

With regard to transfer to recovery: how does this differ for a patient in whom RSI was done to those who were anaesthetized with an LMA?

A

RSI - Need to be completely awake when extubated.

LMA - Likely to be transferred to recovery partially anaesthetized with LMA in situ

44
Q

What are the potential problems as a patient awakens with an LMA in situ?

A 
Aspiration
Dental damage
Hypoxia
Laryngospasm
Negative pressure pulmonary oedema
45
Q

Which patients are most at risk for airway complications in recovery?

A

Children

  • Increased BMR and VO2 with decreased O2 reserves
  • oropharyngeal obstruction: secretion/muscle tone/OSA/FB (pack)
  • laryngeal obstruction: larygospasm/secretions
46
Q

How is postoperative hypertension defined

A

Increase BP 20% above baseline (tends to be short lived)

Common causes:

  • Patient factors: agitation/pre-operative hypertension/pain
  • Inadequate ventilation: hypoxaemia/hypercapnoea
  • Bladder distension
  • Drug related
47
Q

What are common causes of hypotension in recovery

A
  1. Hypovolaemia: blood loss/third space losses
  2. Vasodilation: subarachnoid/extradural block/residual effects anaesthetics and analgaesics/rewarming/sepsis
  3. Myocardial depression anaesthetic agents
48
Q

Classify the causes of delayed return of consciousness

A

Pharmacological: benzo/opioid/IV anaesthetics/volatiles

Metabolic: hypo/hyperglycaemia, hypo/hypernatraemia, uraemia, hypothermia

Respiratory failure

49
Q

What are the main aims of effective symptoms control in recovery

A
  1. Pain
  2. PONV
  3. Shivering
50
Q

What actions should be taken if analgaesia is insufficient in recovery

A
  1. ? Site of cannula/epidural/PCA functioning
  2. ? Cause - ? distended bladder/hematoma or standard surgical pain
    - -> administer morphine as prescribed titrated so that the patient can cough comfortably and moves comfortably
51
Q

What causes shivering and what is the treatment?

A
  1. Hypothermia
  2. Side effect ofGA/neuraxial blockade

Rx: exclude hypothermia
If excluded consider pethidine 15 - 25 mg IV in ADULTS

52
Q

How much does shivering increase O2 consumption?

A

4 - 5 fold –> predisposing to hypoxia

53
Q

What is the definition of hypoxaemia

A

PaO2 < 8 kPa

54
Q

What is the difference between hypoxaemia and hypoxia

A

Hypoxaemia is a a PaO2 < 8 kPa

Hypoxia describes a condition where there is either inadequate O2 for cellular respiration and/or when cells are unable to utilize the O2 supplied –> lactate production via anaerobic metabolism

55
Q

How does PaO2 change with age?

A

Elderly: PaO2 ± 10 kPa is normal for elderly patients breathing room air

56
Q

Temporary inspiratory noise followed by apnoea and desaturation subsequent to LMA removal in recovery. what is the most likely diagnosis? Describe the Rx of this condition

A

Laryngospasm.

  1. Call for help
  2. Optimize airway position
  3. CPAP with FIO2 100% via a water’s circuit (Mapelson C)
  4. If total airway obstruction persists: IV induction agent ± SUX –> restore oxygenation and ventilation: BVM + OPA
  5. Suction and clear airway (look for throat packs)
57
Q

Differentiate the clinical findings in complete and partial airway obstruction

A

PARTIAL
Look: Accessory muscle use, tracheal tug, reduced expansion
Listen: Noisy, stridor (larynx), gurgling (pharynx) wheeze (bronchioles)
Feel: diminished airflow

COMPLETE
Look: Initial: See-saw paradoxical chest movements. Later –>no respiratory effort
Listen: Silent
Feel: No flow

58
Q

When should LMAs be removed?

A

Laryngeal mask airways should be removed with the patient either deeply anaesthetized or wide awake. This avoids provoking laryngospasm whilst in a light plane of anaesthesia.

59
Q

What is the risk of instrumenting the patient’s airway during light anaesthesia?

A

Instrumenting the airway of a lightly anaesthetized patient may provoke laryngospasm.

60
Q

Describe the use of the water’s circuit (Mapelson C) in recovery

A

High concentrations of oxygen can be administered with a Waters’ circuit via a tight fitting face mask or laryngeal mask airway.

By adjusting the adjustable pressure limiting valve (APL valve), either continuous positive airways pressure (CPAP) can be administered to improve airway patency and/or assisted ventilations can be delivered.

A fresh gas flow equal to twice the minute ventilation is required to prevent re-breathing with this circuit.

61
Q

Compare the maximum flow rates for the various sources of oxygen

A

Piped O2 supply - 15 L/min (but greater flows are possible)

Cylinder O2 supply - 15L/minute - 25 L/minute

Emergency O2 flush on anaesthetic machine > 30 L/minute –> high risk of barotrauma

62
Q

With regard to oxygen delivery, what are variable performance devices? What FiO2 can be delivered by these devices

A
  1. Variable performance face masks
    - at O2 flow of 4L/minute FiO2 ± 40%
  2. Nasal Cannulae
    - at O2 flow of 3 L/minute FiO2 ± 30
  3. Face mask with reservoir bag
    - at O2 flow of 10 - 15 L/minute FiO2 ± 80%
63
Q

With regard to variable performance oxygen delivery devices, what factors make the performance (FiO2? variable?

A
  1. O2 flow rate
  2. Quantity of entrained air
  3. Respiratory rate and pattern of ventilation
  4. Mask fit
64
Q

What are fixed performance oxygen delivery devices?

A

Venturi devices

65
Q

Define the Bernoulli principle

Define the Venturi effect

Describe a practical application of the Venturi effect

A

The Bernoulli Principle:
An increase in the flow velocity of an ideal fluid will be accompanied by a simultaneous reduction in its pressure.

The Venturi effect:
The effect by which the introduction of a constriction to fluid flow within a tube causes the velocity of fluid to increase, therefore, reducing the pressure of the fluid.

Practical application of the Venturi effect:
In a Venturi device, the reduction in pressure (subsequent to a constriction) causes ambient air to be entrained at a CONSTANT RATIO at the site of constriction to flow, the size of the constriction determining the final concentration of inspired oxygen.

66
Q

Are fixed performance oxygen delivery devices dependent on respiratory dynamics

A

No. The total gas flow is greater than the patient’s peak inspiratory flow rate, additional entrainment of air via side holes in the face mask is avoided and the inspired oxygen concentration is independent of respiratory dynamics.

Diploma in Anaesthesia (73 decks)

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