Drugs used in an emergency Flashcards

1
Q

What is the definition of hypotension for healthy patients otherwise undergoing an uncomplicated anaesthetic?

A

85mmHg

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2
Q

Hypotension, Rash and bronchospasm??

A

Suspect anaphylaxis

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3
Q

How is the definition of hypotension different for patients with significant CVS disease?

A

Significant hypotension may be present at a higher systolic BP

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4
Q

What is the most common side effects of IV and general anaesthetic agents?

A

Hypotension

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5
Q

Give an example of a directly acting and an indirectly acting sympathomimmetic

A

Direct: phenylephrine
Indirect: Ephedrine

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6
Q

Which anticholinergic drug can be used for simple hypotension?

A

Atropine and glycopyrrolate

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7
Q

When would an anticholinergic considered for the treatment of hypotension?

A

When it is associated with pronounced bradycardia

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8
Q

Discuss the presentation and preparation of ephidrine

A

1 ml glass ampoule with 30mg Ephidrine

Preparation: 9ml saline plus 1 ml ephidrine in 10 ml syrinage = 3mg/ml

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9
Q

What is the dose of ephidrine and at what dose do the effects become less pronounced

A

3-6 mg (1ml) bolus doses are titrated to effect

Effects become less pronounced beyond the total dose of 30mg

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10
Q

What is the mode of action of ephidrine

A

Ephidrine causes release of NA from SNS nerve terminals, which then stimulates adrenoreceptors non-specifically

TACHYPHYLAXIS is seen as a result of depletion of noradrenalin stores

Ephidrine also has a weak direct effect on adrenoreceptors

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11
Q

What are the effects of ephidrine

A

Non-specific activation of alpha and beta receptors cause increase CO and increase SVR –> increase in BP

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12
Q

How long do the CVS effects last

A

a few minutes (Google says 1 hour)

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13
Q

When is ephidrine used?

A

Modest hypotension with normal or slow heart rate

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14
Q

What is the presentation and preparation of phenylephrine?

A

10mg/ml –> add to 100 ml of 0.9% NaCl –> 100ug/ml

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15
Q

What is the dose of phenylephrine

A

50 - 100 ug titrated to effect

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16
Q

What is the mode of action of phenylephrine

A

Acts directly on alpha receptors –> no effect on beta receptors

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17
Q

What are the effects of phenylephrine?

A

alpha 1 stimulation –> vasconstriction and increased SVR

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18
Q

What are the side effects of phenylephrine?

A

Reflex bradycardia due to increased SVR and no beta receptor stimulation

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19
Q

What is phenylephrine used for

A

Severe hypotension with normal or FAST heart rate

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20
Q

What is the presentation and preparation of mataraminol

A

10mg/ml. Dilute to 20 ml syringe with NaCl 0.9%. 0.5 mg/ml

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21
Q

What is the dose of metaraminol

A

0.5 mg bolus doses titrated to effect

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22
Q

What is the mode of action and effects ofmetaraminol

A

Same as phenylephrine with minimal effects on beta-adrenoreceptors

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23
Q

What is the use of metaraminol

A

Same as phenylephrine: hypotension and normal or fast heart rate

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24
Q

What are the most common causes of intra-operative bradycardia (rate<50)?

A

Vagal stimulation

Combination of well beta blocked patient and a general anaesthetic

Severe hypoxia

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25
Q

How does vagal stimulation occur

A

Stretching or pulling of any part of the airway or gut that is innervated by the vagus nerve.
Stimulation of
1. Inferior surface of the epigottis
2. Pneumoperitoneum (esp. higher pressures)
3. Manipulation of bowel

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26
Q

Apart from vagus stimulation, stimulation of what other nerves may cause bradycardia

A

Traction on structures innervated by the sacral parasympathetic outflow (GUS)

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27
Q

What is the treatment of intraoperative bradycardia

A
  1. Remove the stimulus
  2. Treat pharmacologically –> allowing the stimulus to be repeated if required.

If bradycardia is recurrent an delaying surgery, pharmacological treatment may be needed.

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28
Q

What is the fundamental similarity and difference between atropine and glycopyrrolate?

A

Both drugs contain Nitrogen atoms

Glycopyrrolate N atom carries permanent + charge –> unable to cross the BBB

Atropine N atom does not carry a + charge –> crosses BBB

Therefore, glycopyrrolate is free of unwanted central effects of atropine, such as sedation

29
Q

Compare the presentation of Atropine and Glycopyrrolate

A

Atropine: 0.5 mg/ml or 0.6 mg/ml
Glycopyrrolate: 0.2 mg/ml

30
Q

Compare the dose of Atropine and Glycopyrrolate for the treatment of bradycardia

A

Atropine: 0.5 mg doses every 3 to 5 minutes titrated to effect (max 3mg)

Glycopyrrolate: 0.2 mg doses every 3 to 5 minutes titrated to effect(max 0.6 mg)

31
Q

Compare the Mechanism of action of Atropine and Glycopyrrolate

A

Same

Block M receptors in the heart –> increasing heart rate

32
Q

When does acute bronchospasm most commonly occur

A

Shortly after induction of anaesthesia

33
Q

Under which circumstances is bronchospasm more likely

A
  1. Asthmatics
  2. Atopy
  3. Smokers
  4. Drugs that release histamine (Morphine/Atracurium)
34
Q

How is bronchospasm differentiated from anaphylaxis?

A

Anaphylaxis is usually associated with severe hypotension and cutaneous signs

35
Q

List 3 non-pharmacological interventions for bronchospasm

A
  1. Optimise I:E ration (1:4) - avoid air trapping
  2. Consider pressure controlled ventilation
  3. Optimize patient position: minimize pneumoperitoneum
36
Q

List 5 immediate pharmacological interventions

A
Oxygen
Inhaled anaesthetics
Salbutamol
Aminophylline
Adrenaline
37
Q

Since isoflurane is an irritant, can it be administered to a patient with bronchospasm?

A

Isoflurane is an upper airway irritant
Isoflurane relaxes bronchial smooth muscle

It will be beneficial to administer isoflurane to a patient with bronchospasm

38
Q

Why should FiO2 be increased in bronchospasm

A

Acute bronchospasm may lead to reduced alveolar ventilation –> Increase FiO2 to ensure sufficient

39
Q

What is the most effective way to administer salbutamol to a patient in theatre

A

Intravenously

40
Q

Describe the presentation, preparation and dose of salbutamol and aminophylline

A

Salbutamol

  • 500ug/ml –> dilute to 500ug/10ml (50ug/ml)
  • Theatre dose 250 ug over 20 minutes
  • ICU dose: 250 ug over 50 minutes

Aminophylline

  • 250mg/10mls (further dilution not required)
  • 250 mg over 20 minutes
41
Q

Compare the mechanism of action of Salbutamol to aminophylline

A

Salbutamol
Beta 2 agonist (at high doses it acts on beta 1)

Aminophylline
Non-specific phosphodiesterase inhibitor –> increasing cAMP within cells –> smooth muscle relaxation

42
Q

Compare the side effects of salbutamol with aminophylline

A

Salbutamol

  • Tachycardia
  • dysrhythmia
  • exacerbate hypokalaemia

Aminophylline
- contra-indicated in patient’s already on theophylline –> if plasma concentrations become toxic: seizures/dysrhythmias

43
Q

What is the treatment of acute SEVERE bronchospasm –> almost no air movement possible after intubation

A

0.5ml of 1:10 000 Adrenalin titrated to affect

50ug

44
Q

Describe how the dose of adrenalin affects the action at the different adrenoreceptors

A

At low dose (e.g. 50 ug increments in bronchospasm) - adrenalin is mainly active at beta receptors. Potent Beta 2 stimulation is achieved with low dose adrenalin

At high dose (1mg in cardiac arrest) - alpha adrenoreceptor affects predominate to increase coronary perfusion by increasing SVR

45
Q

What common equipment related issue might mimmic acute SEVERE bronchospasm

A

Blockages at any point in the breathing circuit

46
Q

What is the incidence of anaphylaxis due to anaesthetic drugs

A

1 in 10 000 - 20 000

55 suspected anaphylactic reactions per year in the UK

47
Q

Which group of drugs are the most commonly involved in causing anaphylaxis?

A

Neuromuscular blocking Agents –> especially the Benzylisoquinolinium drugs (Atracurium, Cisatracurium, Mivacurium)

48
Q

What is the triad for the most common features of anyphylaxis

A

CVS collapse
Bronchospasm
Widespread erythema

49
Q

Describe the initial management of a patient with anaphylaxis

A
  1. Stop suspected agent
  2. Call for HELP
  3. Airway, O2 100%, patient flat and elevate legs
  4. Adrenalin IV: 50ug -100ug increments
    Adrenalin IM: 0.5mg - 1 mg repeated as required every 10 minutes
50
Q

Can undiluted adrenalin be given IV for anaphylaxis

A

No - it is not possible to give the chosen dose accurately

51
Q

Describe the secondary management of anaphylaxis

A

Isotonic balanced salt solution IV administration
Chlorphenamine - 10mg IV
Hydrocortisone - 100mg IV

52
Q

What does adrenalin 1: 1000 mean

A

1g in 1000 mls
1000mg in 1000ml
1mg/ml

53
Q

What does adrenalin 1: 10 000 mean

A

1g in 10 000 ml
0.1mg/ml
100ug/ml

54
Q

Describe the mendelian inheritance of malignant hyperthermia

A

Autosomal dominant

55
Q

Which agents can trigger malignant hyperthermia

A

Volatile anaesthetic agents and succinylcholine

56
Q

In patient’s with genetic predisposition for malignant hyperthermia, does this condition manifest on first exposure to a precipitating agent

A

Not necessarily manifested on first exposure

57
Q

What are and what are not common clinical features of malignant hyperthermia?

A

Common clinical features

  1. Increasing ETCO2
  2. Tachycardia
  3. Increased O2 consumption

Hyperthermia is NOT an early sign

58
Q

What is the significance of masseter muscle spasm and generalied muscle rigidity after succinylcholine?

A

These clinical findings indicate a high risk of malignant hyperthermia but RARELY progress to full blown MH and are usually transient

59
Q

Describe the treatment for malignant hyperthermia

A
  1. Call for help
  2. Remove trigger
  3. FiO2 100%
  4. Dantrolene 2mg/kg up to 10mg/kg
  5. Active cooling
  6. ICU postop as recurrence occurs
60
Q

What is the modern mortality for malignant hyperthermia and why has it decreased from 70 - 80 % which it was in the past

A

5 - 10 %

  1. Early detection via capnography
  2. Early use of dantrolene sodium
61
Q

Describe the morbidity rate of malignant hyperthermia

A

Overall: 34.8%

Renal dysfunction 97%
Coma - 9 %
Cardiac dysfunction - 9%
Pulmonary oedema - 9%
DIC - 9%
Hepatic dysfunction - 4.5%
62
Q

What dose and why is adrenalin given during cardiac arrest

A

1mg every 3 - 5 minutes

High dose adrenalin –> predominant alpha-adrenergic effect –> increasing cardiac and cerebral perfusion by increasing peripheral SVR

63
Q

When should amiodarone be given during cardiac arrest?

A

For refractory: VF/pulseless VT. Expert consensus suggests that if VT/VF persists after 3 shocks: Amiodarone 300mg bolus

One additional bolus of 150mg can be given after 3 - 5 minutes if VF/VT still present

64
Q

When can lignocaine be given during cardiac arrest and what is the dose?

A

For refractory VF/VT persistent after 3 shocks when amiodarone is not available and NOT when amiodarone has already been given

Dose: 1,5 mg/kg followed by 0.5mg/kg (max 3mg/kg)

65
Q

When should MgSO4 be given during cardiac arrest?

What is the dose?

A
  1. For refractory VF where hypomagnesaemia is suspected
    - potassium-losing diuretics
    - alcoholic/malnourished
  2. Torsades de Pointes
  3. Digitalis toxicity

Dose: 2g in 10ml slow bolus

66
Q

When should Sodium Bicarbonate be administered in cardiac arrest and what is the dose?

A
  1. Severe hyperkalaemia
  2. Overdose
    - TCA
    - Aspirin
    - Cocaine
  3. Severe Metabolic acidosis present (must be intubated)

Dose: 1ml/kg of 8.5% solution

67
Q

When is Calcium chloride indicated in cardiac arrest and what is the dose?

A
  1. Severe hyperkalaemia
  2. BB or CCB overdose
  3. Hypocalcaemia
  4. Magnesium overdose (Rx pre-eclampsia)

Dose: 10ml of 10% slow IV bolus

68
Q

Which drugs in cardiac arrest cannot be administered through the same IV line

A

Calcium containing solutions and sodium bicarbonate –> PRECIPITATION

69
Q

What is a quaternary Nitrogen and give an example of a drug whose pharmacodynamics are altered by the presence of this

A

A quaternary nitrogen atom is permanently charged –> Glycopyrrolate has a quaternary N atom which means that it cannot cross the BBB. Therefore the unwanted central effects of the agent are avoid unlike atropine (which does not contain a quaternary nitrogen atom and crosses the BBB)