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Principles of anaesthesia > Common accidents and anaesthetic emergencies > Flashcards

Common accidents and anaesthetic emergencies Flashcards

1
Q

Airway problems during anaesthesia

A

Difficult intubation

Under-inflation of ETT

Over-inflation of ETT

ETT occlusion

Bronchocontriction

Sudden loss of capnograph trace

Hypoventilation

Apnoea/respiratory arrest

Hypercapnia

Rebreathing of CO2

Tachypnoea

Barotrauma/volutrauma

Regurgitation

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2
Q

Difficult intubation

A

E.g. brachys, oral mass, inability to open the mouth

Always pre-oxygenate

Always use a laryngoscope

Change position

Use a stylet or guide tube

Check for adequate plane of anaesthesia

Use topical anaesthetic

Flexible fibre-optic endoscope

IF STILL NOT WORKING - temporal tracheostomy or retrograde intubation

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3
Q

When is a CO2 trace at 0?

A

At the end of inspiration

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4
Q

Transitional part of the CO2 curve

A

The bit going up

Represents the mixing of dead space and alveolar gas

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5
Q

The alpha angle of a CO2 curve

A

Represents the change from airway gas to alveolar gas

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6
Q

Alveolar part of a CO2 curve (top bit)

A

Represents the plateau average alveolar CO2 concentration

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7
Q

End-tidal CO2 on the CO2 curve

A

The highest point of the curve, usually the second corner at the top

Represents the maximal alveolar CO2 concentration

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8
Q

Normal end-tidal CO2 (ETCO2 values)

A

35-45 mmHg

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9
Q

CO2 trace of oesophageal intubation

A

Some very small waves then nothing

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10
Q

CO2 trace of endobronchial intubation

A

Distinct step on the alveolar part of the curve

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11
Q

Under-inflation of ETT

A

Risk of aspiration pneumonia

Leak of anaesthetic agent
- environmental pollution
- safety of personnel

Check ETT before use

CO2 curve will look more rounded rather than having a nice plateau

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12
Q

Over-inflation of ETT

A

Risk of tracheal ischaemic necrosis

Recommened sat ETT cuff pressure range: 20-30 cmH2O

Methods of measuring cuff pressure
- palpation of pitot balloon
- minimum occlusive volume technique
- syringe devices

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13
Q

ETT occlusion

A

By mucous, blood etc.

Gives the CO2 trace a sharkfin appearance

Can use suction, or re-intubation

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14
Q

What can be the cause for sudden loss of the capnograph trace

A

Disconnection from ETT

Extubation

ETT kinking - armed ETT

Apnoea

Cardiopulmonary arrest

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15
Q

Causes of hypoventilation

A

Obesity

Positioning (e.g. dorsal recumbency, trendelenburg position (feet higher than head))

Abdominal distension (fluid, pregnancy, lap surgery)

Pulmonary disease/airway obstruction

Neuromuscular disease

Anaesthesia induced respiratory depression (inhalational agents, induction agents, opioids)

Hypothermia

Pain

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16
Q

Types of hypoventilation

A

Alveolar hypoventilation

Atelectasis (collapsed lung)

Ventilation/Perfusion (V/Q) mismatch

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17
Q

Treatment for hypoventilation

A

Administer O2

Manual or mechanical ventilation

Recruitment manoevres

Decrease anaesthetic depth

Address causes

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18
Q

Causes of apnoea/respiratory arrest

A

Drugs (induction agents, ketamine, opioids)

Excessive depth of anaesthesia

Cardiac arrest

Vagal stimulation (intubation, visceral traction)

Weaning from ventilator

Nerve damage (i.e. ventral slot)

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19
Q

Treatment of apnoea/respiratory arrest

A

O2 administration

Ventilation

Decrease depth of anaesthesia

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20
Q

Hypoxaemia

A

Low concentration of O2 in arterial blood (PaO2)

PaO2 < 60mmHg

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21
Q

Causes of hypoxaemia

A

Hypoventilation

Impaired diffursion: pulmonary oedema, pneumonia, pulmonary fibrosis

Ventilation/perfusion (V/Q) mismatch: pulmonary oedema, pneumonia, atelectasis, increase in dead space

Right to left shunt

Decreased inspired fraction of O2 (FiO2): inadequate O2 supply, hypoxic mixture, airway obstruction

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22
Q

Consequences of hypoxaemia

A

Initially: SNS activation (tachycardia + increase in myocardial contractility + vasoconstriction)

Decrease in myocardial O2 delivery, arrhythmias

Then: bradycardia, hypotension

Respiratory depression

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23
Q

Treatment of hypoxaemia

A

Pre-oxygenation

O2 administration

Mechanical ventilation, recruitment manouvres for atelectasis

Improve cardiac output + arterial blood pressure to improve perfusion (fluid therapy, vasopressors…)

Treat underlying disease

Avoid causes of increased O2 consumption (pain, shivering, hyperthermia)

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24
Q

Hypercapnia

A

Increased ETCO2

ETCO2 > 45mmHg

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25
Causes of hypercapnia
Hypoventilation Increased metabolism (increased cardiac output, fever, malignant hyperthermia, drugs, hyperthyroidism...) Rebreathing
26
Consequences of hypercapnia
Up to 60 mmHg: stimulation of sympathetic nervous system Above 60-90 mmHg: - decrease in cardiac contractility - vasodilation - central nervous system depression -> apnoea - respiratory acidosis - arrhythmias - shift of oxy-haemaglobin dissociation curve to the right
27
Rebreathing of CO2
Inspiration of CO2 Seen on the CO2 curve by it never returning to the baseline Normally inspired fraction of CO2 (FiCO2) should be 0
28
Causes of rebreathing
Increased dead space Inadequate fresh gas flow in non-rebreathing systems Exhausted CO2 absorber in rebreathing systems Inspiratory or expiratory valve dysfunction in rebreathing system
29
Causes of tachypneoa
Inadequate anaesthetic depth Pain Increased CO2 production (hyperthermia..) Hypoxaemia Hypercapnia Drug administration (opioids in conscious animals)
30
Barotrauma/volutrauma
Excessive pressure/volume causes rupture of alveolar walls Causes pneumomediastinum and/or pneumothorax Do NOT administer peak airway/excessive tidal volume when ventilating Do NOT use O2 flush when patient is connected Check the APL valve in breathing system is OPEN If manual ventilation is performed make sure you re-open the APL valve
31
What does a shark fin CO2 trace indicate?
Obstruction / bronchospasm
32
What does a curare cleft (dip on upper plateau) on a CO2 trace indicate?
Asynchronous breathing
33
What CO2 pressure are you aiming for when performing CPR?
10mmHg
34
Causes of regurgitation
Inadequate fasting times Drugs (e.g. alpha 2s, opioids) Hiatal hernia or other comorbidities
35
How to prevent / minimise the risk of aspiration pneumonia in GA
Adequate fastnig time Rapid sequence induction + ensure ETT is properly cuffed Suction device ready Adequate depth of anaesthesia Avoid changes of position Drugs: metoclopramide, maropitant, omeprazole, ranitidine
36
Treatment of peri-operative regurgitation
Head down Suction +/- lavage with saline/tap water Measure pH of regurgitated material: if acidic instil sodium bicarbonate 8.4% diluted 1:1 with water into oesophagus Careful with sedation level
37
Causes of bradycardias under anaesthesia
Drugs: opioids, alpha 2s, etc. Raised intracranial pressure - Cushings reflex Vagal response (change of position, surgical stimulation...) Hypothermia Electrolyte imbalance (hyperkalaemia...)
38
Treatment of bradycardia under anaesthetic
Address potential causes Reverse alpha 2s (before anti-cholinergics) Anti-cholinergic agents: atropine, glycopyrrolate
39
Treatment for AV blocks under anaesthetic
Drug reversal (e.g. alpha 2s) Anticholinergic drug administration Pacemaker if 3rd degree
40
First degree AV block
R is far from the p wave
41
Second degree mobitz type I AV block
There is a longer and longer gap between p wave and QRS and then the QRS is dropped and it starts again
42
Second degree mobitz type II AV block
Occasionally no QRS but all other p to QRS gaps the same
43
Third degree AV block
p waves do not have an aligning QRS and then there are VPCs and ventricle tries its best
44
Causes of tachycardia under anaesthetic
Sympathetic nervous system stimulation (pain, inadequate anaesthetic depth) Drugs (anticholinergic) Cardiac disease Anaemia, haemorrhage, hypovolaemia Hypoxaemia Hypotension Pheochromocytoma
45
Treatment of tachycardia under anaesthetic
Address the underlying cause B blocker administration
46
Treatment for VPCs, accelerated idioventricular rhythm (AIVR), and ventricular tachycardia under anaesthesia
Lidocaine bolus +/- CRI if effect on cardiac output and blood pressure
47
Treatment for pulseless ventricular tachycardia
Defibrillation
48
Anaphylactic shock
Usually a type 1 hypersensitivity reaction, IgE mediated Mast cell and basophil activation: release histamine, leukotriens, prostaglandins etc.
49
Causes of anaphylactic shock during anaesthesia
Drugs (antibiotics, pethidine, morphine...) Mast cell tumour degranulation
50
Clinical signs of anaphylactic shock whilst under anaesthesia
Tachycardia, arrhythmias Vasodilation, hypotension Urticaria, angioedema Laryngeal and pulmonary oedema, bronchoconstriction
51
Treatment of anaphylactic shock whilst under anaesthesia
Adrenaline Antihistamine (chlorphenamine) Corticosteroids (dexamethasone) Bronchodilators (terbutaline) O2, ventilation Fluid therapy Vasopressors (noradrenaline, dopamine, phenylephrine)
52
Parameters for hypotension when under anaesthesia
MAP < 60-70 mmHg SAP <90 mmHg
53
Causes of hypotension under anaesthesia
Hypovolaemia (haemorrhage, dehydration, vomiting, polyuria...) Vasodilation: drugs (inhalational agents, propofol...), sepsis, anaphylaxis Decreased myocarial contractility or cardiac output (cardiac structural disease, cardiac tamponade, arrhythmias...) Decreased venous return (mechanical ventilation, pneumothorax, abdominal distension, surgery...)
54
Treatment for hypotension caused by hypovolaemia
Fluid therapy - blood products - crystalloids - colloids
55
Treatment for hypotension caused by vasodilation
Decrease vasodilation by: - decreasing inhalational agents - MAC sparing techniques - antagonise drugs causing hypotension Vasocontrict: drugs
56
Treatment of hypotension caused by decreased cardiac contractility or decreased cardiac output
Increase cardiac contractility Drugs i.e. dobutamine Antagonise drugs with negative inotropic effect Treat arrhythmias
57
Treatment of hypotension caused by decreased venous return
Treat cause Decrease ventilatory settings
58
Dopamine
Dopaminergic receptors at <2.5 mcg/kg/min Beta receptors at 2.5-10 mcg/kg/min Alpha receptors at >10 mcg/kg/min Vasodilation (dopaminergic) Increased inotropy (beta) Vasocontriction (alpha) Constant rate infusion (CRI)
59
Dobutamine
Beta receptors at 1-5 mcg/kg/min Increased inotropy and HR CRI
60
Ephedrine
Alpha and beta receptors, and stimulates noradrenaline release and inhibits its reuptake Increased inotropy and vasoconstriction HR increased or decreased Bolus 0.1 mg/kg IV
61
Noradrenaline
Beta receptors at <0.5 mcg/kg/min Alpha receptors at higher dose, up to 1 mcg/kg/min Increased inotropy, HR, and vasoconstriction CRI
62
Phenylephrine
Alpha receptors 1-3 mcg/kg/min Vasoconstriction CRI
63
Haemorrhage
Decreased plasma volume, haemaglobin concentration, decreased O2 carrying capacity of the blood Body response: increase CO, minute volume, and O2 tissue extraction... up to a certain level. Then hypoxaemia, lactic acidosis, hypotension Replace with whole blood, packed red blood cells, haemoglobin based O2 products Consider if the loss is >20% of blood volume or if seeing clinical signs
64
Blood volume in cats
60 ml/kg
65
Blood volume in dogs
90 ml/kg
66
Clinical signs of haemorrhage under anaesthesia
Tachycardia Hypotension Change in EtCO2 values Increased lactate
67
Hypertension
Increase in blood pressure values above the normal limits Risks of myocardial ischaemia, arrhythmias, retinopathy, blindness, renal failure
68
Causes of hypertension under anaesthesia
Pain/nociception Light plane of anaesthesia Hypercapnia, metabolic acidosis, hypoxaemia Underlying renal issues i.e. CKD Pheochromocytoma
69
Treatment of hypertension under anaesthesia
Identify and treat the cause (i.e. administer analgesia) Use drugs that will cause vasodilation - increase concentration of anaesthetic agents - ACP administration
70
Clinical signs of inadequate depth of anaesthesia
Sudden increase in HR, or ABP Change of respiratory rate/pattern Change of eye position Presence of strong palpebral reflex Change in jaw tone Sudden movement
71
Dysphoria on recovery
State of stress, anxiety, characterised by vocalisation, panting, restlessness Patient may not be mentally appropriate Differentiate between pain and anaesthesia related dysphoria: difficult Recent opioid administration?
72
Treatment of dysphoria on recovery
Sedation - alpha 2 bolus or CRI - ACP (delayed onset) - propofol (may need to re-intubate) - consider opioid reversal (nalaxone) but removes analgesic effect

Principles of anaesthesia (9 decks)

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