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Pain and Anxiety for FINALS > Applied anatomy, physiology and pharmacology for IV sedation > Flashcards

Applied anatomy, physiology and pharmacology for IV sedation Flashcards

1
Q 
Minimal sedation:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
 (4)
A
  1. Normal response to verbal commands
  2. Airway unaffected
  3. Ventilation unaffected
  4. Cardiovascular unaffected
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2
Q 
Moderate sedation:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
 (4)
A
  1. Purposeful response to verbal or tactile stimulation
  2. Airway maintained without intervention
  3. Ventilation adequate
  4. Cardiovascular usually maintained
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3
Q 
Deep sedation:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
 (4)
A
  1. Purposeful response following repeated or painful stimulation
  2. Airway intervention may be required
    Ventilation may be inadequate
  3. Cardiovascular usually maintained
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4
Q 
GA:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
 (4)
A
  1. Unrousable even with painful stimulation
  2. Airway intervention often required
  3. Ventilation frequently inadequate
  4. Cardiovascular may be impaired
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5
Q

5 parts of respiration (5)

A
  1. Ventilation of gas into and out of lungs
  2. Diffusion of gases from lungs into blood
  3. Transport of oxygen by blood to cells and transport away of carbon dioxide
  4. Diffusion of gases from blood to cells
  5. Oxidation: use of oxygen to produce energy within cell and production of carbon dioxide
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6
Q

Learn upper airway anatomy

A

Learn upper airway anatomy

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7
Q

Learn lower airway anatomy

A

Learn lower airway anatomy

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8
Q

Inspiration vs expiration (4)

A

Active vs passive
Initiated by diaphragm vs elastic recoil of lungs
Inspiration supported by intercostals, accessory muscles for more vigorous inhalation
Forced expiration involves abdominals and intercostals

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9
Q

Normal rate of ventilation

A

10-18 per minute

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10
Q

Gas exchange
-where
-how
(5)

A 
Occurs within the alveoli
Wall single layer thick
0.2 micrometers
Adjacent to pulmonary capillary wall
Gases diffuse down concentration gradients
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11
Q

Action of haemoglobin (7)

A

O2 binds to haemoglobin
Each molecule can carry 4 O2 molecules
Carried within red blood cells
CaO2= 1.34 x Hb x SpO2
Rely on adequate circulation to transport to tissues
Delivery = CaO2 x Cardiac Output
Properties of haemoglobin mean it releases O2 when it gets to the tissues

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12
Q

Cellular respiration simple equation (5)

A

Glucose + 6O2 –> 6CO2 + 5H2O + ATP

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13
Q

Control of respiration (3)

A

Autonomic nervous system: brainstem, medulla and pons
Respiratory centre
Respond to blood CO2 levels

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14
Q

Monitoring respiration: basic clinical signs (4)

A

Respiratory rate 10-18 per minute
Depth of breathing
Pattern of breathing
Cyanosis

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15
Q

Monitoring respiration: advanced (2)

A 
Pulse oximetry (mandatory)
Carbon dioxide monitoring (optional)
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16
Q

Limitations of pulse oximetry (5)

A 
Ambient light
Movement 
Cold peripheries
Nail varnish
Measurement lag
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17
Q

What is capnography? (2)

A

Detected exhaled CO2 in breath

Usually via nasal prongs

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18
Q

How does capnography work? (3)

A

Waveform displayed on a monitor
Allows confirmation of adequate ventilation and an open airway
Patient has to be breathing through their nose

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19
Q

Name 2 respiratory complications (2)

A

Upper airway obstruction

Hypoventilation

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20
Q

Describe upper airway obstruction (3)

A

Sedation leads to a decrease in tone of the muscles of the pharynx
Leads to pharyngeal collapse, tongue falls against back wall of pharynx
Mild cases lead to partial airway obstruction, more severe leads to complete obstruction

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21
Q

Signs of airway obsruction (5)

A 
Snoring
Stridor
Drop in O2 saturations
Loss of CO2 trace
Seesaw respiration
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22
Q

Management of airway obstruction (4)

A

Supplementary oxygen
Careful titration of sedation
Basic airway opening manoeuvres
Airway adjuncts

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23
Q

Detection of hypoventilation (2)

A

Monitoring of respiratory rate

Drop in oxygen saturation

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24
Q

Describe hypoventilation and its effects (4)

A

Sedative drugs also sedate the Respiratory center in the brain
Also reduce receptor sensitivity to CO2
Leads to reduced respiratory rate or complete cessation of breathing
CO2 levels can build up leading to narcosis

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25
Q

Management of hypoventilation (2)

A

Reversal of sedation with Flumazenil or Naloxone

Assisted ventilation with self-inflating AMBU bag

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26
Q

Basic function of the CV system (2)

A

Deliver oxygenated blood to body organs and tissues for metabolism
“Tissue perfusion”

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27
Q 
What happens with inadequate perfusion in
-cardiac ischaemia
-cerebral ischaemia
-lung
(4)
A

Organs and tissues quickly begin to fail:

  • cardiac ischaemia –> angina –> MI
  • cerebral ischaemia –> faint/ collapse –> stroke
  • lung –> hypoxia
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28
Q

What is the main determinant of organ perfusion? (1)

A

Blood pressure

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29
Q

How is blood pressure displayed? (3)

A

systolic, diastolic and mean (MAP)

e.g. 120/60 (80)

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30
Q

How is the MAP calculated? (1)

A

Diastolic + 1/3 (systolic - diastolic)

-modern machines calculate it for you

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31
Q

What is a normal MAP? (1)

A

Around 80mmHg

32
Q

What is autoregulation? (2)

A

Ensures adequate perfusion over a range of MAPs
Limits will shift in people with chronic hypertension
(graph)

33
Q

What is blood pressure determined by? (2)

A
  1. Cardiac output (CO)

2. Systemic vascular resistance (SVR)

34
Q

What is cardiac output? (1)

A

The amount of blood ejected by the heart per minute

35
Q

What is the average cardiac output? (1)

A

5litres / min

36
Q

How is cardiac output determined? (2)

A

By heart rate and stroke volume

-HR between 50-180 have little effect

37
Q

When is stroke volume reduced? (3)

A

Dehydration / blood loss
Ischaemic heart disease / heart failure
Anaesthetic drugs

38
Q

What is systemic vascular resistance? (2)

A

The resistance produced by the vascular system to the flow of blood, predominantly small arterioles throughout body

39
Q

Effect of dilation and constriction on SVR (2)

A

Constriction increases SVR and hence BP

Dilation decreases SVR and hence BP

40
Q

SVR is decreased by (3)

A

Sedative drugs
Anaphylaxis
Sepsis/ infection

41
Q

Acute blood pressure control (3)

A

Baroreceptors in aortic arch and internal carotids
Send signals to brain stem
Autonomic nervous system alters rate and strength of heart contraction and constriction of blood vessels

42
Q

Chronic blood pressure system (3)

A

Renin-angiotensin system
Aldosterone
Chronic regulation of blood sodium concentration and body fluid retention

43
Q

Monitoring BP: basic clinical signs (5)

A 
Heart rate (from pulse oximeter)
Heart rhythm
Conscious level
Skin colour
Capillary refill
44
Q

Monitoring BP: advanced (2)

A

Non-invasive blood pressure (mandatory)

ECG monitoring

45
Q

How does non-invasive blood pressure (NIBP) work? (3)

A

Automated machines
Cuff around arm or calf
Automatic cycling - every 5 minutes

46
Q

What is NIBP affected by? (2)

A

Movement

Wrong size cuff

47
Q

What is sedation? (1)

A

Is a continuum which extends from normal alert consciousness to complete unresponsiveness

48
Q

ECG monitonitoring: what can it detect and when is it used? (2)

A

Used in pts with history of significant CV disease
Can detect arrythmias and also signs of cardiac ischaemia and infarction
Usually a 3-lead configuration

49
Q

Name 3 cardiovascular complications (3)

A
  1. Hypotension
  2. Cardiac arrhythmias
  3. Cardiac arrest
50
Q

Causes of CV hypotension (2)

A

Vasodilation caused by sedative drugs

Some drugs decrease strength of heart contraction

51
Q

Risk factors in CV hypotension (2)

A

Dose related

More likely to occur in elderly, and those with existing CV disease

52
Q

Treatment for CV hypotension (5)

A

Prevention better than the cure!
Pre-assessment of comorbidity (recent IHD)
Stop administering agent
Place patient head down and with feet elevated
IV fluids may be required

53
Q

Risk factors/ causes of cardiac arrhythmias (4)

A

Multi-factorial aetiology
May be precipitated by adrenaline in LA
More likely in elder and those with CVS disease
Raised blood CO2 levels also increase risk

54
Q

Treatment for cardiac arrhythmias (2)

A

Call for expert help

ALS standard algorithms

55
Q

Commonly used drug types in moderate sedation (3)

A

Benzodiazepines: Midazolam
Opiates: Fentanyl, Remifentanil
Others: Propofol, Ketamine, Dexomethomedine

56
Q

Mode of action of Midazolam

A
57
Q

How is Midazolam given including onset, peak and duration? (5)

A 
IV for moderate sedation
-onset: 1-3mins
-peak: 5-7mins
-duration: 20-30mins
Titrate dose to desired end-point e.g. slurring of speech
58
Q

Dosing of midazolam (4)

A

Initial dose ≈ 2.5mg given over 2 minutes
Wait at least 2 minutes for effect
Subsequent doses of 1mg
Usually no more than 5mg total

59
Q

Midazolam: cautions (2)

A

Decrease initial dose to 1.5mg in the elderly

If used with a pre-med then reduce dose by 1/3

60
Q

Advantages of Midazolam (3)

A

Quick onset
Short action of duration
Minimal cardiovascular effects

61
Q

Adverse effects of Midazolam (2)

A

Respiratory depression

Airway obstruction

62
Q

What does flumazenil do including onset and peak effect (3)

A

Reverse benzodiazepine effects quickly

Onset within 1-2mins, peak effect within 6-10mins

63
Q

Dose of Flumazenil (2)

A

Dose of 200mcg every 1-2mins as required

64
Q

What is fentanyl and what does it do including onset, peak and duration (5)

A 
Man-made synthetic opiate drug
Provides analgesia and sedation
Onset:	1 - 2 mins
Peak:	10 - 15 mins
Duration:	30 - 60 mins
65
Q

Dosing of Fentanyl (1)

A

25mcg (0.5ml) bolus up to 200mcg max

66
Q

Advantages of Fentanyl (3)

A

Provides analgesia as well as sedation
Fast onset
Short duration of action

67
Q

Adverse effects of Fentanyl (3)

A

Hypotension and bradycardia
Respiratory depression
Nausea and vomiting

68
Q

Remifentanil: what is it and how it is administered? (3)

A

Ultra short acting opiate
Very potent analgesic effect
Has to be administered by continuous infusion via syringe driver

69
Q

Advantages of Remifentanil (2)

A

Excellent analgesic properties

Extremely short duration of action (8 minutes)

70
Q

Adverse effects of Remifentanil (3)

A

Hypotension
Bradycardia
Respiratory depression and apnoea

71
Q

What is Propofol including onset and duration (3)

A

IV induction agent
Onset: 30s
Duration: 10-15mins

72
Q

Dosage of Propofol (2)

A

10-20mg (1-2mls) every 5mins
OR
By continuous infusion

73
Q

Advantages of Propofol (2)

A

Very potent sedative

Rapid onset

74
Q

Adverse effects of Propofol (3)

A

Only for use by trained sedationist or anaesthetic staff
Can rapidly progress to general anaesthesia
Significant cardiovascular and respiratory depression

75
Q

General tips for IV sedation (4)

A

Use single drug if possible - avoid ‘polypharmacy’
Give small incremental boluses to titrate effect in individual patient
Easier to give a bit more than to deal with effects of giving too much
Knowledge of time to onset and peak effect of the drug you are using

76
Q

What is polypharmacy and what are the good aspects? (4)

A

Use of more than one drug
Can have advantages
Different drugs give different effects e.g. Opiate + Benzodiazepine gives both sedation and analgesia
Giving a second drug means you can use less of the first drug and so potentially reducing side effects

77
Q

Disadvantages of polypharmacy (3)

A

Opens the door for greater risk of overdosing and over-sedating patients
Drugs with the same side effects will have synergistic action and make those side effects even more likely
Must be aware of time to peak effect of the drugs you are using as not waiting for full effect of first drug may lead to dosing of 2nd drug peaking with 1st drug –> significant over-sedation and side effects

Pain and Anxiety for FINALS (7 decks)

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