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ACUTE > INTRA-OP CARE > Flashcards

INTRA-OP CARE Flashcards

1
Q

What is anaesthesia and what are its 3 roles?

A

A drug-induced reversible loss of consciousness which allows for surgery and invasive procedures
The 3 roles are analgesia, hypnosis and muscle relaxation

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2
Q

What are the types of anaesthesia?

A

General
Local
Regional - indlcudes Spinal and epidural
Sedation

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3
Q

What are the 4 levels of anaesthesia?

A

Stage 1 = analgesia only
Stage 2 = excitation
Stage 3 = surgical anaesthesia
Stage 4 = medullary depression

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4
Q

What are the signs of the excitation stage of anaesthesia in.e. Stage 2?

A

Delirium with struggling
Rapid and irregular respirations
Frequent eye movements
Increased pupil diameter
Amnesia

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5
Q

What are the 4 planes of surgical anaesthesia i..e stage 3?

A

Plane 1 = decrease in eye movements and some pupillary constriction
Plane 2 = loss of corneal reflex
Plane 3 and 4 = loss of pharyngeal reflex and progressive decrease in thoracic breathing and general muscle tone

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6
Q

What is stage 4 anaesthesia i.e. medullary depression?

A

Loss of spontaneous respiration
Progressive depression of cardiovascular reflexes
No eye movements
Requires respiratory and circulatory support

We dont want to reach this! This occurs when too much Anaesthesia is given

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7
Q

What can be given as pre-medication before a GA?

A

A H2 receptor antagonists can be used if GORD or emergency surgery - to prevent regurgitation and aspiration of gastric contents
Benzos can be given to reduce anxiety
Analgesia and antiemetics can be given

Antimuscarinics can be given to combat the bronchial and salivary secretions and muscarinic side effects of neostigmine - this is less common now

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8
Q

What are the 4 stages of anaesthesia?

A

Induction
Maintenance
Emergnce
Recovery

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9
Q

What is induction?

A

The transition from awake to the anaesthetised state

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10
Q

What is the standard induction regimen?

A

Quick acting opioid e.g. fentanyl + propofol

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11
Q

When are muscle relaxants required for anaesthetics

A

If intubation is required

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12
Q

What muscle relaxant agents are used?

A

Depolarising - suxamethonium
Non-depolarising - rocuronium

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13
Q

What is the additional benefit of giving analgesia in induction of anaesthesia?

A

It reduces the sympathetic response so stops tachycardia and hypertension to stimuli e.g. laryngoscopy

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14
Q

What are IV drug options for anaesthesia?

A

Propofol
Ketamine
Thiopental
Etomidate

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15
Q

When should we always choose tracheal intubation over a supraglottic device e.g. LMA?

A

If there is any risk of airway soiling e..g regurg or anticipated difficulty with ventilation e.g. lung pathology/obesity

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16
Q

When should rapid sequence induction be used?

A

When pt is considered high risk of airway aspiration

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17
Q

What is rapid sequence induction?

A

A technique that involves rapid, successive administration of induction and neuromuscular blocking drugs to achieve a state of unconsciousness and paralysis in the shortest time possible to secure the airway

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18
Q

What is the MOA of propofol?

A

It potentiates GABA A and therefore enhances its inhibitory effects

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19
Q

What are the benefits of propofol?

A

Rapid induction due to high lipid solubility
Rapid recovery (as half life is 2-4 minutes)
Less hangover effects
Has some anti-emetic effects
Does not accumulate so an continuous infusion can be used
Can also be used for sedation in ICU or for diagnostic procedures

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20
Q

What are the adverse effects of propofol?

A

Dose-dependant hypotension
May also cause a dose-dependant respiratory depression
Causes pain on IV injection due to activation of the pain receptor TRPA1 (this can be reduced by including IV lidocaine)

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21
Q

Why does propofol cause hypotension?

A

It inhibits the sympathetic nervous system (causing vasodilation, negative inotropic effect, direct cardiac depression) and impairs the baroreflex regulatory mechanisms

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22
Q

Contraindications for propofol?

A

Hypotension
Hypersensitivity to the drug, eggs or soy

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23
Q

To prevent hypoxia what should inhalation anaesthetics always contain?

A

25% oxygen (higher >30% if NO is being used)

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24
Q

What is the Minimum Alveolar Concentration?

A

A measure of the potency - its the concentration of the anaesthetic when 50% of the population will fail to respond to a single noxious stimuli e.g. first surgical incision

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25
Q

What does it mean that NO has a MAC >100%?

A

This means that it would take a concentration of NO >100% to achieve its desired effect i.e. it alone cannot put the pt to No has a low oil:gas partition coefficient i..e it is relatively insoluble in blood and tissues and thus is lipid insoluble = low potency

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26
Q

What are examples of volatile liquid anaesthetics?

A

Sevoflurane, isoflurane and desflurane

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27
Q

What are examples of inhalational anaesthetics?

A

volatile liquid anaesthetics and NO

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28
Q

What are the possible adverse effects of isoflurane?

A

HR is generally stable but can rise in younger pt. Systemic arterial pressure and CO can fall causing decreased systemic vascular resistance. It can potentiate the effects of muscle relaxant drugs

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29
Q

When is isoflurane the preferred anaesthetic?

A

In obstetrics

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30
Q

Why is desflurane not recommended for the induction of anaesthesia?

A

As it irritates the URT

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31
Q

What are the benefits of desflurane over isoflurane?

A

Rapid acting. Emergence and recovery are particuarly rapid due to low solubility.

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32
Q

What are the benefits of sevoflurane over the other volatile liquid anaesthetics?

A

Rapid acting. More potent than desflurane. Emergency and recovery are more rapid than isoflurane (although slower than desflurane). Non-irritant so can be used for induction. Little effect on heart rhythm.

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33
Q

MOA of thiopental sodium?

A

A barbiturate
Potentiates GABA A

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34
Q

Adverse effects of thiopental sodium?

A

Dose-related cardiovascular and respiratory depression can occur
Metabolism is slow so sedative effects can persist for up to 24 hours
Can cause laryngospasm

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35
Q

Moa of etomidate?

A

Potentiates GABA A

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36
Q

Adverse effects of etomidate?

A

High incidence of myoclonus
Can cause primary adrenal suppression as it reversible inhibits 11 beta hydroxylase
Postoperative nausea and vomiting are more common with etomidate than propofol or barbiturate induction

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37
Q

Benefits of etomidate over propofol and thiopental sodium?

A

Rapid recovery without a hangover effect
Causes less hypotension

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38
Q

Whats the MOA of ketamine?

A

Works by blocking NMDA receptors

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39
Q

When is ketamine used as an induction agent?

A

Paediatrics
Good for trauma as causes less hypotension

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40
Q

Adverse effects of ketamine as an induction agent?

A

Recovery is slow
High incidence of myoclonus and disorientation
High incidence of transient psychotic effects - hallucinations
Not sure this is a bad thing… Produces dissociative anaesthesia - marked sensory loss, analgesia and amnesia but without complete LOC

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41
Q

What does entonox consist of?

A

50% NO 50% O2

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42
Q

What is NO used for in anaesthetics?

A

Maintenance and analgesia
Note: its a weak sedative and muscle relaxant

It cannot be used as a sole anaesthetic as it lacks potency but it is useful as part of a combination of drugs as it allows for a significant reduction in dosage

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43
Q

When should NO not be used?

A

If there are air-containing spaces e.g. pneumothorax or intracranial air as it can worsen these by increasing the volume of

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44
Q

Why are IV agents better than inhaled anaesthetic agent for induction?

A

IV agents are infused straight into the blood so can reach an effective concentration very quickly
Inhalational meds need to diffuse across the lung tissue and then into the blood

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45
Q

What is TIVA?

A

Total IV Anaesthesia - using an IV med for induction and maintenance as a slow continuous infusion
Most commonly done with propofol

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46
Q

Mao of non-depolarising neuromuscular blockade agents?

A

Competitive antagonists of nicotonic acetylcholine receptors at the NMJ and this decreases skeletal muscle tone

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47
Q

What are the 2 types of neuromuscular blockades?

A

Depolarising and non-depolarising

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48
Q

Examples of non-depolarising neuromuscular blockers?

A

Atracurium
Rocuronium
Pancuronium
Cisatracurium
Mivacurium

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49
Q

Examples of depolarising neuromuscular blockers?

A

Suxamethonium

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50
Q

Why are neuromuscular blockers give in anaesthesia?

A

They block the transmission of signals between motor nerve endings and skeletal muscles, preventing the affected muscles from contracting and also reducing their resting tone.
Thus they paralyse the jaw and the vocal cords facilitating laryngoscopy and tracheal intubation, and various other muscles whose paralysis may facilitate artificial ventilation and surgery.

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51
Q

How do you reverse the action on non-depolarising neuromuscular blockers?

A

With neostigmine - an anticholinesterase inhibitor

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52
Q

When trying to reverse the action of rocuronium, why might you give an antimuscarinic e.g. atropine alongside neostigmine?

A

You may give it to prevent the bradycardia or excessive salivation you may get by stimulation of muscarinic receptors

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53
Q

Mao of depolarising neuromuscular blockade agents?

A

Binds to nicotinic acetylcholine receptors resulting in persistent depolarisation of the motor end plate

54
Q

Adverse effects of non-depolarising neuromuscular blocking drugs?

A

Hypotension

55
Q

Adverse effects of depolarising neuromuscular blocking drugs?

A

Malignant hyperthermia
Transient hyperkalaemia
Can cause muscle fasciculations

Very prolonged paralysis occurs in 1 in 2000 people who have a genetic defect of pseudocholinesterase as this is what usually hydrolyses it

56
Q

When is suxamethonium CI?

A

For pt with penetrating eye injuries or acute narrow angle glaucoma
As it increases intra-ocular pressure

57
Q

Which neuromuscular blocker is the drug of choice for RSI?

A

Suxamethonium

58
Q

What analgesia is commonly used in anaesthetics?

A

Opiates - fentanyl, morphine, remifentanyl
NSAIDs and IV paracetamol
Spinal and epidural anaesthesia

59
Q

What are important points about maintenance in anaesthesia?

A

Usually done by volatile drugs but can be done as IV infusion
Think about correct positoning
Keep pt warm as susceptible to hypothermia
Think about fluid balance
May need antibiotics

60
Q

Why is desflurance not used for induction?

A

As it has irritant effects on the lungs

61
Q

Outline the ways in which thermoregulation is impaired in the post-op period?

A
  • using IV fluids
  • irrigation of the body cavities
  • exposure to cold theatre environment
  • use of cold skin prep fluids
  • muscle relaxants stop the shivering
  • spinal and epidurals prevent peripheral vasoconstriction by decreasing the sympathetic tone
62
Q

Why is it important to maintain pt temperature?

A

As when cold the proteins and enzymes do not work optimally. This means anaesthetic drugs are metabolised more slowly. This also affects the platelets, Coag system and immune system

63
Q

What is “thermoregulation in the perioperative period?

A

Thermoregulation from 1 hour prior to surgery until 24 hours after the surgery has been completed q

64
Q

Risk factors for perioperative hypothermia?

A

ASA grade of 2 or above
Major surgery
Low body weight
Large volumes of unwarmed IV infusions
Unwarmed blood transfusions

65
Q

NICE guidance on perioperative thermoregulation?

A

Pt temp measures in pre-op phase and if lower than 36.0, active warming should commence immediately. Pt should not be moved to theatre if temp is <36.0 unless they have a time critical condition
Forced air warming devices should be used from the onset for any anaesthetic duration >30 mins or any high risk pt
Fluid volumes >500ml should be warmed prior to administration
Following surgery pt temp should be measured and repeated every 15 mins until transfer to the ward
Pt should not be transferred to the ward if their temp is <36.0

66
Q

Complications of perioperative hypothermia?

A

Coagulopathy: it reduces blood’s ability to clot, increasing intra-operative blood loss.
Prolonged recovery from anaesthesia: small decreases in body temperature can cause drastic prolongation of anaesthetic drugs, both neuromuscular blocking agents, propofol and inhalational agents.
Reduced wound healing: hypothermia leads to local vasoconstriction which reduces perfusion to the skin, this reduces the necessary immune moderators available at the site to promote healing.
Infection: a combination of poorer incisional site healing and also reduced number of immune cells able to access the skin leads to a significantly increased risk of infection.
Shivering: whilst shivering appears benign in the healthy population, it can cause a significant increase in metabolic rate which can in certain patient groups even result in myocardial ischaemia.

67
Q

What is emergence in anaesthetics?

A

When the unconsciousness and paralysis are reversed

68
Q

Outline how emergence is done?

A

Anticholinesterases can be given to reverse the effects of neuromuscular blockers
Once paralysis is reversed the inhaled anaesthetic can be stopped.
When pt wakes up and is breathing for themselves they can be extubated

69
Q

Which antiemetics are most commonly used in anaesthetics?

A

Ondansetron
Dexamethasone
Cyclizine

70
Q

When should you avoid using dexamethasone as an antiemetic in anaesthetics?

A

When the pt has diabetes (increases CBG) or is in an immunocompromised state

71
Q

What are the possible risks of a general anaesthetic?

A

Sore throat
Confusion and memory loss
Post op N&V
Aspiration
Difficult passing urine
Bruising and pain
Dental injury if laryngooscpe is used
Anaphylaxis
Cardiovascular events
Accidental awareness
Malignant hyperthermia
Death

72
Q

MOA of local anaesthetic agents?

A

Prevent nerve transmission by inhibiting depolarisation of the cell by blocking the voltage-gated Na+ channels

73
Q

What factors influence the action of LA?

A

Local concentration
Size of nerve fibre
Nerve myelination
Length of nerve exposed to LA

74
Q

When giving LA, why is temperature discrimination lost before pain sensation?

A

As LA tend to affect the smaller nerve fibres first such as the C fibres which react to thermal /mechanical/chemical stimuli to produce a delayed dull, aching, burning pain. Whereas the larger A delta fibres are affected late which are responsible for thr fast sharp pain caused by mechanical pressure

75
Q

Why are LAs affected by pH?

A

As they are weak bases

76
Q

What is pKa of a LA?

A

The pKa is the pH at which the ionised and un-ionised forms are present in equal amounts.
For bases, such as local anaesthetics, the higher the pKa, the greater the ionised fraction in solution. The rate of diffusion across a nerve sheath and membrane is related to the proportion of non-ionised drug so LA with low pKa have a faster onset of action e.g. lidocaine pKa 7.8 has a faster onset than bupivacaine pKa 8.1 as at pH7.4 a greater proportion of lidocaine exists in the non-ionised form

77
Q

What does it mean to say LAs are use-dependant?

A

when nerves are stimulated more frequently, LAs tend to work more effectively.
This is because LAs primarily block sodium channels, which are responsible for transmitting nerve impulses. When nerves are firing rapidly, more sodium channels are open, providing more targets for the local anesthetic to block, hence enhancing its efficacy.

78
Q

How can LA be used?

A

As topical anaesthesia
As infiltration anaesthesia
As a peripheral nerve block
Epidural
Spinal anaesthesia
IV regional anaesthesia

79
Q

What is an epidural?

A

A slow infusion via a catheter of an aqueous solution in the epidural space to produce anaesthesia above and below the site of injection
Levobupivacaine is often used with or without fentanyl

80
Q

What are the adverse effects of epidurals in labour?

A

Risk of prolonged second stage and increased probability of instrumental delivery

low bp
temporary loss of bladder control
itchy skin
feeling sick
headaches
nerve damage

81
Q

What is a peripheral nerve block?

A

A type of regional anaesthesia where LA is injected around specific nerves causing the area distal to be anaesthetised but the pt can remain awake
This is done under USS and sometimes requires a nerve stimulator

82
Q

What is spinal anaesthesia?

A

A type of regional anaesthesia where LA is injected into the CSF in the subarachnoid space at L3/L4 or L4/L5 to cause numbness and paralysis of the areas innervated by the spinal nerves below the level of injection

83
Q

What is the spread of the LA in a spinal anaesthetic CEPD at on?

A

The posture of the pt in the first 10-15 minutes and the density of the solutions i..e an LA in 10% glucose is more dense than the CSF

84
Q

What is IV regional anaesthesia?

A

an anesthetic technique on the body’s extremities where a local anesthetic is injected intravenously and isolated from circulation in a target area. A double tourniquet is applied to do this

Often used for reduction of fractures

85
Q

What are examples of amide-based LAs?

A

Lidocaine
Bupivacaine
Ropivacaine
Prilocaine
Mepivacaine

86
Q

What are ester-based local anaesthetics?

A

Cocaine
Procaine
Tetracaine
Benzocaine
Chloroprocaine

87
Q

How are amide and ester LAs metabolised differently?

A

Amides are biotransformed in the liver but esters are hydrolyzed in the bloodstream by plasma esterases.

88
Q

What drugs does lidocaine interact with?

A

Beta blockers
Ciprofloxacin
Phenytoin

89
Q

What can Lidocaine be given with to limit systemic absorption and prolong duration. Of action?

A

Adrenaline - causes vasoconstriction

90
Q

When is lidocaine with adrenaline contraindicated?

A

In patients taking MAOI’s or tricyclic antidepressants

91
Q

What is the max dose of lidocaine you can give with and without adrenaline?

A

Lidocaine - 3mg/kg
Lidocaine + adrenaline - 7mg/kg

92
Q

What are the following brand names for: Denela, EMLA, LMX4, Nulbia?

A

Topical lidocaine “numbing cream”

93
Q

Why is cocaine no longer regularly used as an LA?

A

As it has the potential for abuse
It had systemic adverse effects e.g. tachycardia and arrhythmias

94
Q

Which LA must never be used for regional blockade?

A

Bupivacaine as cardiotoxic - risky if tornoqiet fails

95
Q

Which LA is the agent of choice for IV regional anaesthesia?

A

Prilocaine - less cardiotoxic than others

96
Q

Differences between amide and ester-based LAs?

A

Amides - metabolised in liver (important to know in case pt has liver deficiency), generally have a longer duration of action, pKa value is lower at 7.6-8.1 so less ionised meaning faster onset of action
Esters - more common to have allergic reactions, metabolised in plasma by pseudocholinesterase (important to know in case pt has a defiency), pKa value is higher at 8.5-9.0 so more ionized than amides

97
Q

Unwanted local effects of local anaesthetic?

A

some discomfort when the injection is given
a tingling sensation as the medicine wears off
possibly some minor bruising, bleeding or soreness where the injection was given
Ischaemic from the use of vasoconstrictor agents e.g. adrenaline

98
Q

Signs of LA toxicity?

A

Early: Perioral tingling, tinnitus and slurred speech
Sudden alteration in mental status, severe agitation, or loss of consciousness. Sometimes seizures
Cardiovascular collapse: sinus bradycardia, conduction blocks, asystole, VTs

99
Q

Management of LA?

A

Call for help
Maintain airway
Give 100% oxygen
Establish IV accesss
Control seizures
Give IV intralipid

Once stabilised exclude pancreatitis with daily amylase or lipase

100
Q

Max dose of bupivacaine?

A

2mg/kg

101
Q

Max dose of Prilocaine?

A

6mg/kg or 9 with adrenaline

102
Q

What is an arterial line?

A

A special type of cannula inserted into an artery which can accurately monitor the real time BP
Can also be used to take samples e.g. ABG

103
Q

What is a central line?

A

A central venous catheter
A long thin tube inserted into a large vein with the tip located in the vena cava. It can be inserted into the internal jugular vein, subclavian vein or femoral vein
They have separate lumens that can be used for giving meds and taking blood samples

They are more reliable and last longer than peripheral cannulas

104
Q

What are the types of central lines?

A

PICC line
Hickman line
Vascath line
Portacath line
Pulmonary artery catheter

105
Q

What is a vascath?

A

A temporary line in the internal jugular or femoral vein
Often used for short term haemodialysis

106
Q

What is a PICC line?

A

A peripherally inserted central catheter
A Catheter which is inserted into a peripheral vein and fed through the venous system until the tip is in a central vein.

107
Q

What is a Hickman line?

A

A type of tunnelled central venous catheter
Enters the skin on the chest, enters the subclavian or jugular veins nd then the tip sites in the SVC. There is a cuff surrounding the catheter near skin insertion which promotes adhesion of tissue to the cuff making the catheter more permenant and preventing infection
Can be used longer time and for regular IV treatment

108
Q

What is a Portacath?

A

There is a small port under the skin at the top of the chest to access the device. The chamber is cleated to a catheter that enters the subclavian vein with a tip that sits in the SVC or RA. It will be a bump on the chest wall when nothing is attached.
Last the longest of all central lines.
Fully internalised so low risk of infection

109
Q

What are the 2 zones in the lungs?

A

The conducting zone and the respiratory zone

110
Q

How much dead space is in the lungs

A

2-3L

111
Q

What is residual volume of the lungs?

A

The volume of gas remaining in the lungs after a forced expiration

112
Q

What is expiratory reserve volume of the lungs?

A

The volume of gas forcefully expired after normal tidal expiration

113
Q

What is the tidal volume of the lungs?

A

The volume of gas inspired and expired during normal breathing

114
Q

What is the inspiratory resevere volume of the lungs?

A

The volume of gas inspired over the normal tidal inspiration

115
Q

What is the total lung capacity?

A

The volume of gas in the lungs at the end of maximal inspiration

116
Q

What is the vital capacity of the lungs?

A

the maximum amount of air you can forcibly exhale from your lungs after fully inhaling.
Tidal volume + inspiratory reserve volume + expiratory reserve volume

117
Q

What is the functional residual capacity?

A

the volume remaining in the lungs after a normal, passive exhalation
Expiratory reserve volume + residual volume

118
Q

Outline how pre-oxygenation before induction of anaesthesia can increase time to desaturation?

A

Typical functional residual capacity volume is 2.2L and normally contains 21% oxygen. Since tota; body oxygen consumption is about 250mls/min, the normal store of oxygen will only last just over 1 minute with apnoea. Pre-oxygenation is defined as breathing 100% from a close fitting mask for 3-5 minutes to denitrogenate the lungs and increase the oxygen stores to in excess of 1800mls thus increasing time to desaturation to about 7-8 minutes assuming an oxygen consumption of 250mls/min

119
Q

What is the average circulating volume in an adult?

A

5L

120
Q

How to calculate cardiac output?

A

Blood pressure / systemic vascular resistance

121
Q

How can we increase the bp after induction of anaesthesia?

A

Increase preload - elevated legs to augment venous return, give bolus of fluid
Increase after load - vasopressors drugs to increase SVR e.g. andrenaline.
Increase contractility with inotropes = increases HR

122
Q

Whats the science behind safety checklists, briefings and debriefings?

A

Reduces wrong-site surgery
Encourages teamwork
Encourages communication
Ensures no preventable errors or adverse events
Ensures pt safety

123
Q

Outline the diffiuclt intubation guidelines?

A

Laryngoscopy and tracheal intubation (after 3+1 attempts no further attempts should be made)
If this fails use a supraglottic airway. If this fails try face mask ventilation. If this works wake pt up
If this doesnt work -> cricothyroidotomy

124
Q

What are the signs you have intubated the trachea rather than the oesophagus?

A

Visually you can see the tube passing through the glottis aperture
6 consecutive normal capnograph traces (end tidal CO2)
Inflation of chest
Mist on mask from CO2

125
Q

What is rapid sequence induction?

A

A way to gain control over the airway as quickly and safely as possible after induction where a pt needs to be intubated in an emergency scenario and detailed pre-planning is not possible.
This is considerably more risky as pt has not been fasted and anaesthetist has not had the chance to plan for individual factors and potential problems.
The biggest concern is aspiration so cricoid pressure may be used to compress the oesophagus and prevent this reflux

126
Q

Why is optimal positoning important in surgery?

A

To provide best surgical access
To minimise risks from the surgery e.g. abrasions
To avoid peripheral nerve injuries
To avoid ocular injuries
To avoid pressure sores

127
Q

VTE prophylaxis before surgery?

A

• VTE risk assessment should be performed as part of the pre-op assessment
• Women should be advised to stop oestrogen containing drugs 4 weeks before surgery
• Encourage mobilisation and hydration asap after surgery
• Pharmacological thromboprophylaxia can be given for some pt
• Mechanical thromboprophyalxis is for all surgical pt - anti-embolism stockings and pneumatic compression devices - new evidence out about this not being as useful??

128
Q

Diameter of ETT for women and men?

A

7-7.5 women
8-8.5 for men

129
Q

What can be used to assist with a tricky ETT?

A

A laryngoscope
A bougie
A stylet

130
Q

What is awake fibre-optic intubation?

A

When an ETT is inserted with the pt awake under guidance of an endoscope
This is used when there is trismus or difficult anatomy so that there is no delay in intubation and therefore no risk of hypoxia

131
Q

Whats the diffference between a LMA and an I-gel?

A

SADs with inflatable cuffs are called laryngeal mask airways (LMA). I-gel is a type of non-inflatable SAD that uses a gel-like cuff that moulds to the larynx.

132
Q

Indications for a tracheastomy?

A

Respiratory failure where long-term ventilation may be required (e.g., after an acquired brain injury)
Prolonged weaning from mechanical ventilation (e.g., ICU patients that are weak after critical illness)
Upper airway obstruction (e.g., by a tumour or head and neck surgery)
Management of respiratory secretions (e.g., in patients with paralysis)
Reducing the risk of aspiration (e.g., in patients with an unsafe swallow or absent cough reflex)

ACUTE (17 decks)

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