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Acute Care > Anaesthetics > Flashcards

Anaesthetics Flashcards

1
Q

What is a critical illness?

A

Any patient at risk of serious deterioration/ has actual or impending organ failure

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2
Q

Give a differential of airway obstruction?

A
  • reduced GCS
  • foreign body
  • aspiration
  • oedema - anaphylaxis, burns etc
  • bronchospasm
  • pulmonary oedema etc
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3
Q

Wheeze is inspiratory

A

Stridor is expiratory

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4
Q

See-saw breathing e.g. paradoxical chest and abdominal movements are a sign of complete airway obstruction

A

S

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5
Q

What is the tidal volume?

A

The volume of air that moves in and out per breath

usually about 500ml

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6
Q

What is the inspiratory reserve volume?

A

IRV is the amount of air above the tidal volume that a person can maximally inhale

(often around 3L)

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7
Q

What is the expiratory reserve volume?

A

The maximum amount, above the tidal volume that a patient can exhale

(normally about 1.2L)

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8
Q

What is the residual volume?

A

The amount of air left in the lungs after maximal exhalation

normal 1.2L

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9
Q

What is the functional residual capacity?

A

The FRC is the volume of air left in the lungs after normal expiration

(Normally 2.4 L)

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10
Q

What is the vital capacity?

A

The maximal amount of air that can be exhaled after a maximum inhale.

(Normally 4.7L)

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11
Q

What is an atomic dead space in the lungs?

A

All parts of the conducting airways e.g. trachea apart from alveoli which are not involved in gas exchange
About 1/3 of the tidal volume is lost to dead space

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12
Q

Physiological dead space - anatomical dead space + functional dead space (some alveoli do not have a good enough blood supply). How is it calculated?

A

Using the Bohr equation

e.g. physiological dead space may be increased in emphysema

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13
Q

How do you calculate the minute volume?

A

Tidal volume x respiratory rate

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14
Q

What is alveolar ventilation?

A

The portion of minute volume involved in gas exchange e.g. Minute volume - dead space

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15
Q

What is a shunt?

A

When perfusion exceeds ventilation e.g. there is a problem with the airways

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16
Q

What is dead space with regard Q/V?

A

When ventilation exceeds perfusion e.g. no oxygen can be gained as blood supply is inadequate

Examples include pulmonary oedema, pneumonia, ptx etc

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17
Q

CO2 is removed via alveolar ventilation (down a pressure gradient)

A

CO2 retention suggests low alveolar ventilation)

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18
Q

Some patients develop hypercapnia secondary to reduced hypoxia drive. What is the commonest cause?

A

Opiod analgesics which decrease respiratory drive

COPD is the other important cause

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19
Q

Partial pressure is the pressure that would be exerted by 1 gas in a mixture if it occupied an area on its own.

A

The partial pressure of 02 decreases from 21kPa in air to just 1 - 5 kPa in mitochondria

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20
Q

What are the 4 different types of hypoxia?

A

1) hypoxic hypoxia. —>pO2< 12 due to low ventilation, shunt or ventilation problems Vv
2) anaemic hypoxia —> anaemia or CO poisoning
3) Ischaemic hypoxia —> O2 OK but reduced blood flow e.g. clot or cardiac failure
4) Cytotoxic hypoxia —> tissues are unable to use O2 e.g. cyanosis

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21
Q

GIVE 3 clinical signs that suggest patients are ‘at risk’ of respiratory failure?

A

1) RR > 25
2) Sp02 < 94%
3) PaO2 <10 (normal is > 10.6)

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22
Q

Which 2 investigations should be performed in all patients with respiratory failure?

A

ABG

CXR

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23
Q

What is the difference between a fixed and variable performance oxygen device?

A
  • fixed e.g. Venturi deliver fixed oxygen concentration regardless of respiratory effort. Should be used if you want to know the FiO2
  • variable performance e.g. nasal cannulae - the O2 delivery depends on patient respiratory effort and size
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24
Q

Normal Fi02 = 0.21 as 21% of normal air is oxygen

This in increased to 0.28-0.36 by nasal cannula

A

Hudsons masks (the common ones) provide FiO2 of 0.4

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25
Q

Trauma masks e.g. non-rebreather masks provide an FiO2 of 60-80% but need a high flow rate (10-15L/min) to achieve this

A

Hudson masks use a flow of >4L/ min

Nasal cannula = 2-4L per minute

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26
Q

What are the target PaO2?

A

For a patient on air the PaO2 should be 10-13kPa

For a patient on oxyge, the PaO2 should be 10kPa less than the FiO2 concentration e.g. target Pao2 of 30 if FiO2 is 0.4

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27
Q

Venturi masks are the main fixed performance device

A

Remember the masks tell you what flow rate is required to get desired FiO2

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28
Q

Last reminder:

Shunt = inadequate ventilation e.g. wasted perfusion

Dead space = wasted ventilation as perfusion is inadequate

A

Hypoxia is usually due to s shunt

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29
Q

Shock is the failure to perfume vital organs

A

Shock is failure to perfume vital organs

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30
Q

What is the equation of oxygen delivery?

A

Cardiac output x arterial oxygen concentration

(remember that arterial oxygen concentration is a product of oxygen saturation x 1.34

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31
Q

What effect will systemic vascular resistance have on CO?

A

It will increase the afterload which decreases CO

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32
Q

What is the difference between BP and CO?

A

BP = pressure of blood in the systemic circulation

CO = flow of blood through the circulation

—> BP = CO x systemic vascular resistance

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33
Q

Cardiogenic shock = pump failure, typically due to reduction in SV. List some causes

A
  • MI
  • Acute valve incompetence
  • VT
  • Complete Heart Block

It is the contractility that is primarily affected

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34
Q

Obstructive shock is a reduced CO due to reduced SV as a result of compression. Give some examples?

A

PE
Cardiac tamponade
Tension ptx

It is the preload/ afterload that is primarily affected e.g. heart cannot fill or cannot empty

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35
Q

Distributive shock e.g. in anaphylaxis/ sepsis is caused by peripheral vasodilatation which reduces SVR —> fall in BP

A

Important that although CO increases, the tissue distribution is inappropriate so shock occurs (as well as reduced BP)

36
Q

Where are arterial baroreceptors located?

A

1) Aortic arch (vagus)

2) Carotid sinus (glossopharyneal)

37
Q

Remember that angiotensin 2 is potent vasoconstrictor.

A

It is produced in the lungs after conversion from angiotensin 2. Angiotensin 2 is produced by the action of renin on angiotensin 1

Angiotensin 11 also helps Na and water reabsorption

38
Q

What are the 3 main consequences of shock?

A

1) Cellular hypoxia/ organ hypoperfusion
2) Effects of lactic acidosis
3) Inflammatory response

39
Q

Normally glucose is metabolised to pyruvate the normal way, producing 36 molecules of ATP

A

In anaerobic metabolism, glucose is converted to lactate acid, producing only 2 molecules o ATP

(And eventually a metabolic acidosis)

40
Q

What is the difference between severe sepsis and septic shock?

A

Severe sepsis = sepsis + evidence of end organ damage/ hypoperfusion

Septic shock = sepsis + refractory hypotension

41
Q

List some signs of hypovolaemia

A
  • tahcycardia
  • hypotensive
  • postural dizziness
  • cool, slow cap refill
  • oliguria
42
Q

Signs of fluid overload

A
  • SOB, crackles
  • ankle oedema
  • hypertension
  • Increased JVP
  • tachycardia (don’t forget)
43
Q

Signs of sepsis:

A
  • flushed, sweaty
  • hypotensive
  • tachycardia
  • tachypnoea
  • reduced LOC
  • oliguria
  • signs of underlying cause
  • fever
44
Q

Sepsis should ALWAYS be considered as a cause of hypovolaemia, especially if there is a poor response to fluid challenge

A

Sepsis should ALWAYS be considered as a cause of hypovolaemia, especially if there is a poor response to fluid challenge

45
Q

What is the difference between crystalloid and colloid fluid?

A

Crystaloid = in solution can diffuse through a semi-permeable membrane e.g. saline

Colloid = are a suspension rather than a solution and will therefore not diffuse through a semi-permeable membrane

46
Q

What is the defining abnormality of hypervolaemia?

A

A raised preload

47
Q

In a bradycardic patient, what features on ECG suggest risk of asystole and therefore need for atropine?

A

1) Mobitz 11
2) Recent asystole
3) Complete heart block
4) Ventricular pause >3s

48
Q

Patient with HR of 180 and signs of shock. After getting ECG etc what do you do?

A

Patient is unstable so up to 3 DC shock

If unsuccessful then give amiodarone 300mg over 10-20 minutes

49
Q

Regular broad complex tachycardia = VT (amiodarone)

A

Regular narrow complex tachycardia = SVT (vagal and adenosine)

50
Q

Course of action in an unconscious patient with a bedside glucose reading of <3.5mmol/L

A

Give 100ml of 10% glucose IV

(If any evidence of malnutrition or alcoholism, given 1mg/kg thiamine at the same time to prevent Werncike’s encephalopathy - confusion, opthalmoplegia and ataxia)

51
Q

What is the triad of opiate toxicity?

A

Unconscious
Pin-point pupils
Respiratory depression

(consider naloxone - 0.4mg IV)

52
Q

Always remember to use BEST response when considering GCS

A

The patient could have a focal weakness or similar

53
Q

List 6 important causes of unconsciousness which require urgent investigation and management?

A

1) Sepsis/ shock
2) Drugs/ opiates
3) Raised ICP
4) Hypoxia
5) Meningitis/ encephalitis
6) Hypoglycaemia

54
Q

What are the 3 areas of consideration when prescribing fluids?

A

1) Basal requirement
2) Existing deficit
3) Predicted losses

55
Q

What is in saline?

A

154 of Na and Cl

NaCl goes into the extracellular fluid e.g. interstitial and plasma BUT beware in hypernatraemia

56
Q

What is in Hartmann’s?

A

Na 131
Cl 110
K 5

Just like NaCl it goes into the ECF

57
Q

Why is 5% dextrose rubbish for resuscitation?

A

It is essentially just water so equilibrates between ICF and ECF equally

58
Q

What is in gelofusine?

A

0.9% NaCl —> 154 Na, 154 Cl

+ Big molecules which exert an oncotic pressure

59
Q

What is pain?

A

‘An unpleasant sensory of emotional experience associated with actual or potential tissue damage

60
Q

Remember pain activates the sympathetic nervous system, prevents deep breathing/ cough reflex and reduces mobility —> DVT, pressure sores etc

A

Remember pain activates the sympathetic nervous system, prevents deep breathing/ cough reflex and reduces mobility —> DVT, pressure sores etc

61
Q

Describe the Tayside 0-3 pain scale

A

0 - no pain at rest or movement
1 - no pain at rest, mild on movement
2 - intermittent at rest, moderate on movement
3 - continuous at rest, severe on movement

62
Q

Remember we normally step up from paracetemol —> paracetemol + opioid —> opioid + non-opioid

A

In post-op pain we start at the top and step down

63
Q

What is the standard way to treat acute pain?

A

1) Dilute morphine to a 1mg in 1ml solution

2) Titrate in 1-2mg increments until patient is comfortable

64
Q

In opioid induced poisoning naloxone is given as a bolus of 400 micrograms

A

In opioid induced sedation e.g. excess post-op analgesia it is given in 40 microgram increments with continual reassessment

65
Q

What are the side effects of an epidural?

A

1) post-dural puncture headache
2) hypotension
3) infection
4) epidural haematoma
5) inadequate relief

66
Q

What is the standard PCA prescription?

A

1mg morphine with 5 minute lockout

67
Q

How do you convert from IV to oral morphine?

A

Double it e.g. 60mg IV = 120mg oral

68
Q

What is isoflurane?

A

A general anaesthetic

69
Q

Ranitidine is a gastric acid inhibitor

A

ACTRAPID is an anti-hyperglycaemic

70
Q

Salbutamol is a beta 2 agonist which can cause hypokalaemia

A

Salbutamol is a beta 2 agonist which can cause hypokalaemia

71
Q

Remember antibiotics generally increase activity of warfarin (bleeding more likely)

A

OCP, carbamazepine and barbituates generally reduce activity

72
Q

Atenolol is a cardioselective beta 1 receptor antagonist

A

Reduce heart rate and contractility

Can mask signs of hypoglycaemia

73
Q

How does morphine work?

A

It binds to the mu opiod receptor and stimulates dopamine release

Morphine has extensive 1st pass metabolism —> t1/2 = 3 hours

74
Q

Benzos work by binding to and enhancing the activity of GABA receptors

A

Remember GABA is the main inhibitory neurotransmitter

Glutamate is main excitatory transmitter

75
Q

What does a central line measure?

A

It is placed in the subclavian vein and then threaded to the SVC
It measures central venous pressure in the RA —> preload

76
Q

What is an intra-arterial line used for?

A

1) continuous BP measurement
2) continuos ABG
3) can be used for drawing blood samples

77
Q

How does paracetamol cause problems?

A

1) Normally it is absorbed, conjugated and peed out
2) In overdose, the conjugation is overwhelmed and paracetamol is metabolised via an alternative pathway —> NAPQI
(N-acetyl - p - benzoquinine imine)
3) This is initially OK as it is inactivated by glutathione
4) BUT glutathione is used up quickly —> free NAPQI which causes necrosis of the liver/ kidneys
5) Toxicity is increased with other activators of the P450 system e.g. alcohol

78
Q

Doses for the treatment of anaphylaxis?

A

1) Adrenaline = 500 micrograms
2) Fluid challenge 500ml
3) Hydrocortisone 200mg
4) Cholrphenamide 10mg

79
Q

PR interval

A

AV conduction time

Normally 0.12-0.2 (3-5 small squares)

80
Q

what should be given to a post patient with a RR of 6 who is drowsy and difficult to rouse due to opioids?

A

Naloxone - give 40 microgram increments, titrated to effect

81
Q

when is warfarin stopped prior to elective surgery?

A

5 days

82
Q

which drug do you give in asystole?

A

1mg adrenaline IV

83
Q

what is the typical blood gas in a patient who has had a sudden cardiac arrest?

A

respiratory and metabolic acidosis due to apnoea and ischaemia

84
Q

Where is the epidural space?

A

outside the dura mater (epidural is the same as extra-dural)

85
Q

What is in the epidural space?

A

Adipose tissue
Spinal nerve roots
venous plexus

86
Q

Why does an epidural cause reduction in CO and BP?

A

it blocks the sympathetic system –> vasodilatation

Acute Care (4 decks)

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