Critical Care Flashcards
(82 cards)
1
Q
Level 0 care
A
Normal ward
2
Q
Level 1 care
A
- Enhanced care
- 3:1 ratio of patients to nurses
- Monitored
3
Q
Level 2 care
A
- High dependency (HDU)
- 2:1 ratio of patients to nurses
- Single organ failure (not ventilated)
4
Q
Level 3 care
A
- Intensive care (ICU)
- Recovery units
- 1:1 ratio of patients to nurses
- Multiorgan failure
- Ventilation
5
Q
Criteria for discharge to ward from recovery
A
- Spontaneous airway maintenance
- Awake and non-drowsy
- Comfortable and pain free
- Haemodynamically stable
- No evidence of haemorrhage
6
Q
Pulse oximetry infrared wavelength
A
660-940nm
7
Q
How does pulse oximetry calculate oxygen saturation
A
- A constant ‘background’ amount of infrared light is absorbed by skin, venous blood, fat
- A changing amount is absorbed by the pulsatile arterial blood
- The difference between the constant and variable amount is calculated
- Oxygenated Hb and Deoxygenated Hb absorb different amounts at the two wavelengths the saturated Hb can be calculated from the ratio between the two
8
Q
What can be the delay between a fall in PaO2 and SaO2
A
15-20 seconds
9
Q
What can limit the effectiveness of pulse oximetry
A
- Delay
- Abnormal pulses e.g. AF
- Abnormal Hb or pigments e.g. carbon monoxide poisoning
- Interference e.g. shivering, diathermy
- Poor tissue perfusion
- Nail varnish
10
Q
Indications for intra-arterial monitoring
A
- Critically ill/shocked patients
- Major surgery
- Surgery for phaeochromocytoma
- Induced hypotension
- Those requiring frequent ABG e.g. lung disease
- Monitoring use of inotropes
11
Q
Complications of intra-arterial monitoring
A
- Embolisation
- Haemorrhage
- Arterial damage and thombosis
- AV fistula formation
- Distal limb ischaemia
- Sepsis
- Tissue necrosis
- Radial nerve damage
12
Q
Normal CVP range
A
8-12cmH2O
13
Q
What can CVP monitoring be useful for
A
- Assessing circulating volume status
- Assessing myocardial contractility
(- Also for administering TPN or toxic drugs)
14
Q
Where should the tip of the CVP lie
A
SVC
15
Q
When during respiration should the CVP reading be taken
A
During respiratory end expiration
16
Q
Common complications of CVP lines
A
- Sepsis
- Pneumothorax
- Incorrect placement (should be confirmed with CXR)
17
Q
How is cardiac output calculated using TOE
A
- US records the change in frequency of the signal that is reflected of the RBCs in the ascending aorta = velocity
- Velocity is multiplied by the cross-sectional area of the aorta = stroke volume
- Stroke volume x heart rate = CO
18
Q
Where should the tip of a Swan-Ganz (pulmonary artery pressure) catheter lie
A
- Right atrium to be inflated (proximal lumen remains here)
2. Floated through right ventricle into pulmonary artery (distal lumen/tip)
19
Q
What is CVP monitoring best for
A
Assessing adequacy of intravascular volume status by testing with fluid challenge (should cause a prolonged rise in CVP)
20
Q
What can be measured using a Swan-Ganz catheter
A
- Stroke volume
- SVR
- Pulmonary artery resistance
- Oxygen delivery (and consumption)
21
Q
How is cardiac output calculated using Swan-Ganz catheter
A
Fick principle
22
Q
What is the tidal volume
A
- Volume of air moved on quiet respiration
- 0.5L in males
- 0.34L in females
23
Q
What is the inspiratory reserve volume
A
- Maximul volume inspirable following normal inhalation
- 3L
24
Q
What is the expiratory reserve volume
A
- Maximum volume expirable after tidal volume expiration
- 1L
25
What is residual volume
- The volume remaining in the lungs after maximum expiration
- FRC-ERV = 1.5L
26
What is vital capacity
- The volume that can be expired after a maximum inspiratory effort
- 5.6L
- 70ml/KG
27
What is functional residual capacity
- Volume of air remaining in the lungs at the end of normal expiration
- RV + ERV = 2.5L
28
What is forced vital capacity
The volume of air that can be maximally forcefully exhaled
29
How is respiratory minute volume calculated
Tidal volume x respiratory rate
30
What constitutes anatomical dead space
- Mouth
- Nose
- Pharynx
- Larynx
- Trachea
- Bronchi
31
What constitutes alveolar dead space
Volumes of disease parts of the lung unable to perform gaseous exchange
32
What is the physiological dead space
Anatomical dead space plus alveolar dead space
33
Typical volume of dead space
150ml
34
What is the effect of ventilators on dead space
Increased due to the length of tubing
35
How can type 1 respiratory failure be managed
CPAP
36
How can type 2 respiratory failure be managed
BiPAP
37
Diagnostic features of acute lung injury
- Pulmonary infiltrates on CXR
- Pulmonary artery wedge pressure <18
- Hypoxaemia
- Known cause
38
ARDS mortality rate
50-60%
39
Preferred intubation method in paediatrics
Nasal intubation
40
Contraindications to nasotracheal intubation
- Apnoea
- Basal skull fractures
- Facial fractures
41
Male and female ET tube diameters
- Male = 8-9mm
| - Female = 7-8mm
42
Male and female ET tube lengths (to teeth)
- Male = 23cm
| - Female = 21cm
43
Role of the cuffed end of the ET tube
- Creates a seal
- Helps prevent aspiration
- Can cause stenosis and tracheomalacia if high pressure
44
Hazards of ET tube insertion
- Oesophageal intubation (hence end-tidal CO2 is measured)
- Tube advanced too far to right main bronchus
- Airway damage or rupture
45
Effect of tracheostomy on dead space
Reduced
46
Early complications of percutaneous tracheostomy
- Asphyxia
- Aspiration
- Creation of false track
- Laceration of oesophagus or trachea
47
Late complications of percutaneous tracheostomy
- Vocal fold paralysis/hoarseness
- Cellulitis
- Laryngeal stenosis
- Tracheomalacia
48
Site of percutaneous tracheostomy
Between 2nd and 4th tracheal rings
49
Role of PEEP
- Prevents alveolar collapse at the end of expiration
| - Recruits collapsed alveoli
50
Disadvantages of PEEP
- Reduces physiological shunting
- Reduces venous return
- Barotrauma
51
Advantages of PEEP
Increases lung volume and improves oxygenation
52
Advantages of CPAP
- Increases lung volumes and oxygenation
- Reduces respiratory effort
- Reduces cardiac work by reducing transmural tension
53
Benefits of BiPAP over CPAP
Allows lower overall airway pressures to be used, reducing the risk of barotrauma
54
List the four processes involved in nociception (pain)
1. Transduction (anti-inflammatories act here)
2. Transmission (local anaesthetics act here)
3. Modulation (TENS exploits this)
4. Perception (opiates act here)
55
Describe transduction of pain stimuli
Translation of noxious stimuli into electrical activity at the sensory endings of nerves
56
What is primary hyperalgesia
Decreased nocicpetive threshold in damaged tissue resulting in exaggerated response
57
What is secondary hyperalgesia
Lower pain threshold in areas beyond the site of injury
58
What innervates peripheral nociceptors
- A fibres (fast)
| - C fibres (slow - unmyelinated)
59
What type of pain do A fibres transmit
Acute sharp pain
60
What type of pain do C fibres transmit
Slow chronic pain
61
Where do A fibres terminate in the dorsal horn
Lamina 1 and 5
62
Where do C fibres terminate in the dorsal horn
Lamina 2 and 3 (Substantia gelatinosa)
63
Neurotransmitter between A/C fibres and second-order neurones in the dorsal horn
Substance P
64
How do pain stimuli ascend the spinal cord to the brain
- Second order neurones cross over in the white commissure one segment rostrally
- Ascend in the lateral spinothalamic tract
- Becomes the spinal lemniscus in the brainstem
- Synapse in the thalamus (ventral posterolateral nucleus)
65
How do pain stimuli travel from the ventral posterolateral nucleus of the thalamus to the somaesthetic area of the brain
1. Third-order neurones pass through the internal capsule
| 2. Reach the somaesthetic area in the postcentral gyrus of the cerebral cortex
66
Where do C fibres terminate
Reticular formation
67
Describe the central mechanism for the modulation of pain
- Descending anti-nociceptive tract in the dorsal horn of the spinal cord
- Enkephalins cause presynaptic inhibition of incoming pain fibres
68
Describe the mechanical inhibition of pain
- Stimulation of mechanoreceptors in the area of the body where pain originates can inhibit pain
- Occurs by stimulating large A fibres
- How TENS works
69
How is visceral pain from the thoracic and abdominal viscera transmitted
C fibres within the sympathetic nerves
70
Where is pain perceived
Thalamus and sensory cortex
71
What causes referred pain
Branches of visceral pain fibres synapse in the spinal cord with some of the same second-order neurones that receive pain fibres from the skin
72
What do tracheostomy sizes correlate to
Their inner diameter
73
What is the minimum time from insertion should a tracheostomy be changed
At least 3 days to permit track formation
74
NSAID mechanism of action
- Cyclo-oxygenase inhibitor
| - Results in the inhibition of prostaglandin synthesis which sensitises pain receptors to noxious stimuli
75
Why do NSAIDs cause peptic ulceration
Prostaglandins are necessary for gastric mucous and bicarbonate production
76
Preferred pain management option for extensive abdominal laparoscopy
TAP block
77
First line analgesic for neuropathic pain
- Amitriptyline OR
| - Pregabalin
78
Second line analgesic regime for neuropathic pain
Amitriptyline AND pregabalin
79
Flow through a cannula is proportional to
Radius to the power of 4
80
Where is the basilic vein identified for venous cut-down
2cm medial to the brachial artery
81
By what method are central venous catheters inserted
Seldinger technique
82
From where can the IJV be accessed
1. Posterior border of SCM (most common)
2. Anterior border of SCM
3. Lower end between the two heads of SCM
