Applied anatomy, physiology and pharmacology for IV sedation Flashcards Preview

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Flashcards in Applied anatomy, physiology and pharmacology for IV sedation Deck (77)
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1

Minimal sedation:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
(4)

1. Normal response to verbal commands
2. Airway unaffected
3. Ventilation unaffected
4. Cardiovascular unaffected

2

Moderate sedation:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
(4)

1. Purposeful response to verbal or tactile stimulation
2. Airway maintained without intervention
3. Ventilation adequate
4. Cardiovascular usually maintained

3

Deep sedation:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
(4)

1. Purposeful response following repeated or painful stimulation
2. Airway intervention may be required
Ventilation may be inadequate
4. Cardiovascular usually maintained

4

GA:
1. responsiveness
2. airway
3. ventilation
4. cardiovascular
(4)

1. Unrousable even with painful stimulation
2. Airway intervention often required
3. Ventilation frequently inadequate
4. Cardiovascular may be impaired

5

5 parts of respiration (5)

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

6

Learn upper airway anatomy

Learn upper airway anatomy

7

Learn lower airway anatomy

Learn lower airway anatomy

8

Inspiration vs expiration (4)

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

9

Normal rate of ventilation

10-18 per minute

10

Gas exchange
-where
-how
(5)

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

11

Action of haemoglobin (7)

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

12

Cellular respiration simple equation (5)

Glucose + 6O2 --> 6CO2 + 5H2O + ATP

13

Control of respiration (3)

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

14

Monitoring respiration: basic clinical signs (4)

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

15

Monitoring respiration: advanced (2)

Pulse oximetry (mandatory)
Carbon dioxide monitoring (optional)

16

Limitations of pulse oximetry (5)

Ambient light
Movement
Cold peripheries
Nail varnish
Measurement lag

17

What is capnography? (2)

Detected exhaled CO2 in breath
Usually via nasal prongs

18

How does capnography work? (3)

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

19

Name 2 respiratory complications (2)

Upper airway obstruction
Hypoventilation

20

Describe upper airway obstruction (3)

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

21

Signs of airway obsruction (5)

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

22

Management of airway obstruction (4)

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

23

Detection of hypoventilation (2)

Monitoring of respiratory rate
Drop in oxygen saturation

24

Describe hypoventilation and its effects (4)

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

25

Management of hypoventilation (2)

Reversal of sedation with Flumazenil or Naloxone
Assisted ventilation with self-inflating AMBU bag

26

Basic function of the CV system (2)

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

27

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

Organs and tissues quickly begin to fail:
-cardiac ischaemia --> angina --> MI
-cerebral ischaemia --> faint/ collapse --> stroke
-lung --> hypoxia

28

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

Blood pressure

29

How is blood pressure displayed? (3)

systolic, diastolic and mean (MAP)
e.g. 120/60 (80)

30

How is the MAP calculated? (1)

Diastolic + 1/3 (systolic - diastolic)
-modern machines calculate it for you

31

What is a normal MAP? (1)

Around 80mmHg

32

What is autoregulation? (2)

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

33

What is blood pressure determined by? (2)

1. Cardiac output (CO)
2. Systemic vascular resistance (SVR)

34

What is cardiac output? (1)

The amount of blood ejected by the heart per minute

35

What is the average cardiac output? (1)

5litres / min

36

How is cardiac output determined? (2)

By heart rate and stroke volume
-HR between 50-180 have little effect

37

When is stroke volume reduced? (3)

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

38

What is systemic vascular resistance? (2)

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

39

Effect of dilation and constriction on SVR (2)

Constriction increases SVR and hence BP
Dilation decreases SVR and hence BP

40

SVR is decreased by (3)

Sedative drugs
Anaphylaxis
Sepsis/ infection

41

Acute blood pressure control (3)

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

Chronic blood pressure system (3)

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

43

Monitoring BP: basic clinical signs (5)

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

44

Monitoring BP: advanced (2)

Non-invasive blood pressure (mandatory)
ECG monitoring

45

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

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

46

What is NIBP affected by? (2)

Movement
Wrong size cuff

47

What is sedation? (1)

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

48

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

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

Name 3 cardiovascular complications (3)

1. Hypotension
2. Cardiac arrhythmias
3. Cardiac arrest

50

Causes of CV hypotension (2)

Vasodilation caused by sedative drugs
Some drugs decrease strength of heart contraction

51

Risk factors in CV hypotension (2)

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

52

Treatment for CV hypotension (5)

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

Risk factors/ causes of cardiac arrhythmias (4)

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

Treatment for cardiac arrhythmias (2)

Call for expert help
ALS standard algorithms

55

Commonly used drug types in moderate sedation (3)

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

56

Mode of action of Midazolam

***

57

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

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

Dosing of midazolam (4)

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

Midazolam: cautions (2)

Decrease initial dose to 1.5mg in the elderly
If used with a pre-med then reduce dose by 1/3

60

Advantages of Midazolam (3)

Quick onset
Short action of duration
Minimal cardiovascular effects

61

Adverse effects of Midazolam (2)

Respiratory depression
Airway obstruction

62

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

Reverse benzodiazepine effects quickly
Onset within 1-2mins, peak effect within 6-10mins

63

Dose of Flumazenil (2)

Dose of 200mcg every 1-2mins as required

64

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

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

65

Dosing of Fentanyl (1)

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

66

Advantages of Fentanyl (3)

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

67

Adverse effects of Fentanyl (3)

Hypotension and bradycardia
Respiratory depression
Nausea and vomiting

68

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

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

69

Advantages of Remifentanil (2)

Excellent analgesic properties
Extremely short duration of action (8 minutes)

70

Adverse effects of Remifentanil (3)

Hypotension
Bradycardia
Respiratory depression and apnoea

71

What is Propofol including onset and duration (3)

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

72

Dosage of Propofol (2)

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

73

Advantages of Propofol (2)

Very potent sedative
Rapid onset

74

Adverse effects of Propofol (3)

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

75

General tips for IV sedation (4)

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

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

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

Disadvantages of polypharmacy (3)

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