Review Flashcards
(148 cards)
1
Q
Normal temp
A
37
2
Q
Normal HR
A
60-100 bpm
Bradycardia = <60
Tachycardia = >100
3
Q
Normal BP
A
120/80
Hypo = 90/60
Hyper = 140/90
4
Q
Normal resp rate
A
12-16
Bradypnea <10
Tachypnoea >20
5
Q
5 key respiratory questions in a patient interview
A
Cough
Sputum
Breathlessness
Wheeze
Chest pain
6
Q
Questions around breathlessness
A
- Shortness of breath
- Work of breathing
- Aggs, eases
- Positions of ease
- Distance, stairs
7
Q
Questions around cough
A
- Frequency (daytime, nocturnal, after eating or drinking, acture/chronic)
- Effectiveness (pain and weakness → do these impact effectiveness)
- Productive/non productive Is phlegm produced
- Quality → Wet/dry, wheezy ect
8
Q
Questions around sputum
A
Secretions, mucus and phlegm all mean the same → once is has been coughed out it is called sputum
- Quantity
- Quality
- Consistency
- Colour
- Haemoptysis 0Blood → specs of blood are ok but fresh blood stop treatment
9
Q
Concerns for interview if patient is post srugery
A
- Dizziness
- Drowsiness
- Nausea
- Vomiting
10
Q
Concerns relating to epidural
A
- P/N
- Numbeness
- Weakness
- Headache
11
Q
Outline of physical exam
A
General observation
Respiratory observation
Palpation
Auscultation
Cough
Lower limbs
Specific assessment
12
Q
What is being noted during observation
A
General
- Position, posture, facial expression, level of consciousness, tone, attachments
- Distal clubbing and cyanosis (blue tips of fingers and lips)
- When observing attachments also use top to toe approach
Respiratory
Rate, chest shape
Breathing pattern, following pump and bucket handle
Accessory muscle use
13
Q
Hand placement for palpation
A
- Bilateral
- Around ribs 7-10 - anterior at opening of subcostal angle (this should increase during resp)
- May place hand on AP (sternum and thoracic spine) to feel for pump handle
14
Q
What is being noted during palpation
A
- Amount of movement and symmetry
- Temperature
- Fremitus - feels like a rumble due to retained secretions
- Subcutaneous emphysema which is just under the skin
15
Q
What causes a wheeze during asculation
A
- Due to touching of the opposite sides of the airway due to bronchoconstriction, mucus, tumor, foreign body
- Intrathoracic (within thorax)
- Inspiration = airway open so wheeze normally less intensity
- Expiration = Airway narrows due to pressure gradient so wheezy likely more intense
16
Q
Does it need to be noted if a wheeze disappears
A
If a wheeze disappears this can be a red flag as it can indicate airflow has dropped to the point that a wheeze cannot be produced
17
Q
What is stridor
A
- Extra thoracic
- Occurs during inspiration
- Occurs with croup, tracheal stenosis
- Is opposite to wheeze as the pressure gradients are reversed meaning decreased diameter in upper tract during inspiration
18
Q
What do crackle indicate
A
- Coarse crackles (thunder) normally indicate secretion or diffuse small airway disease and can occur on inspiration or expiration as the air passes these secretions. Similar to wheeze absence of crackles does not mean absence of secretion as the airflow may not be enough to produce the sound.
- Fine end inspiratory crackles normally indicate atelectasis which is a sudden opening of distal airways due to pressure equalisation
19
Q
Assessment of cough
A
Similar to respiratory questions in PI.
- Strength
- Dry/moist
- Effective
- Productive (quantity and quality of sputum)
20
Q
Lower limb check during assessment
A
- Oedema
- DVT
- Colout, temp, palpation, Homan’s sign (DF of ankle should cause pain at back of calf due to increased pressure)
- Skin integrity
- Circulation
- Dorsalis pedis pulse
- Post tib pulse
- Capillary refill
21
Q
Order of auscultation
A
2 - 4 - 6
- Right and left upper lobe = Ribs 2-4 anteriorly
- Right middle lobe ribs 4-6 on the right
- Left Upper lob = ribs 4 -6
- Right and left lower lobes, ribs 6 - 8 both anterior and lateral
- Right and left apical portion of Right and left lobe T3-T7 posterior
- Right and left posterior potrtion of lower lobe T8-T10
22
Q
Normal pH on ABG
A
7.35-7.45
23
Q
Normal PaCO2 on ABG
A
35-35 mmHg
24
Q
Normal HCO3 on ABG
A
22-28 meq/l
25
Normal PaO2 on ABG
80-100 mmHg
26
If PaCO2 has increased then acidity is
Acidic
27
Levels of normal respiration that can be impaired resulting in pathology
Respiratory controller (involuntary control)
Respiratory muscles
Rib cage and pleura
Abdomen pressure changes
Movement of air
Alveolar ventilation
28
What is FRC
This is the volume of gas left in the lung after normal expiration. Differs to residual capacity as this is the amount of air left in the lungs after forced expiation.
29
How is FRC changed
This is the volume of gas left in the lung after normal expiration. Differs to residual capacity as this is the amount of air left in the lungs after forced expiation
FRC also changes with age with the CC getting closer to FRC in older ages meaning that positioning may not have enough effect
FRC also decreases with obesity
30
What is closing capacity
Volume of air in the lung when the small airways in dependent lung start to collapse during expiration and thus trapping air inside.
Most young health people the CC = RV
However if CC > FRC during normal expiration there may be collapse of the airways in dependent lung areas causing reduced ventilation in these areas.
31
What is hypoxaemic pulmonary vasoconstriction
Hypoxaemic is decrease O2
This is a protective response causing constriction of pulmonary vessel in a state of V/Q mismatch (Decrease PaO2). This will divert blood to areas with greater ventilation (increase perfusion to areas with increase ventilation) which will increase PaO2
32
What is atelectasis
Collapse of alveoli if they’re not ventilated or unstable.
Can be contained to small groups, lung segment or the whole lung
33
Types of atelectasis (5)
- Micro atelectasis
- Patchy areas not resulting in shift of structures, all post surgery patients will have this.
- If not treated may become major
- Plate Atelectasis
- Small areas of collapse (thin white lines on CXR)
- Compression
- Physical structure causing the collapse. Tumor, pleural effusion, increase pleural pressure
- Absorption
- Brochus or bronchiole is blocked meaning the gas distal to this is trapped but the gas uptake by blood still occurs meaning the gas pocket will collapse.
- Can also occur in oxygen therapy when FiO2 is high leading to decrease nitrogen which can cause a V/Q mismatch
- Surfactant impairment
- Surfactant reduces surface tension of alveoli to prevent collapse meaning if it is decreased collapse can occur
- Effected by anaesthesia, supplemental O2, infection
34
Effects of atelectasis
- V/Q mismatch which can cause hypoxemia or sometimes hypercapnia
- Decreased FRC
- Decreased compliance → difficult to reinflate (balloon analogy), increase WOB, increased O2 consumption
35
Clinical and CXR signs of atelectasis
- Decrease chest wall movement on palpation (either uni or bilaterally), may also have increased temperature
- Decreased or absent breathsound on ausculation, fine end inspiratory crackles can also be present
- Decreased SpO2
- Shift of structures towards the collapse
- Increased density (white) in the collapsed lobe due to crowding of vessels
- Crowding of ribs
36
Risk factors for atelectasis (S')
- Surgery
- Shallow breathing
- Supine or slumped
- Increased Secretion
- Decreased Surfactant
- Senior
- Supplemental oxygen
- Smoking history
- Size (obesity)
37
What is critical opening pressure
This is the pressure needed to overcome the surface tension for initial inflation of collapsed regions
Think about the balloon analogy
38
What is Newtonian Law of Viscosity
Sticky surfaces peel apart more easily when done slowly
This is why slow lamina flow is the gold standard during inspiration
- Allow regions with long time constants to fill
- Fill lower lung regions (which are the dependent parts at risk of collapse)
- Encourage opening of the alveoli
39
What is collateral ventilation
Blockage or atelectasis can be overcome through inflation of alveoli via connecting channels.
40
What is alveolar interdependence
Refers to the stretching force impaired by neighbouring alveoli. This is increased with deeper breathing.
41
What are time constants are why are they important
= compliance x resistance of an alveolar unit
In health lungs the time constants of all alveoli are relatively uniform meaning the same rate and pressure will inflate all alveoli.
However in an impaired lung the time constants are differed meaning different rates and pressure will inflate different alveoli
- Units with increased resistance take longer
- Alveoli with increased compliance take longer
- Alveoli with decreased compliance take a greater inspiratory effort to fill
Net result is increased time to fill alveoli with fresh air and empty alveoli of stale air.
This is why inspiratory holds are used, to allow for different time constants.
42
2 P's for physio to improve ventilation
Pain relief
Aiming to optimist inspiratory volume which can be pain inhibited
- Support and positioning
- Timing physio with medication
Positioning
High sitting, standing are best to increase FRC
Ensures that there is increased perfusion in the based limiting the event of a V/q mismatch
High sitting → can be done off bed SOOB, obese patient may need to sit <60 degrees
Side lying → good lung on the bottom to improve gas exchange (makes it dependent)
43
Management for increased work of breathing
- Positioning
- Supported positioned (forward lean sitting and standing)
- Using axiohumeral muscles, the supported positioned also the muscle to be used in reverse origin-insertion to assists in respiration
- Breathing control
- Gentle tidal breathing
- Emphasis on lower chest not upper
- Inspire through nose
44
Other than the 2 P's what are 5 other techniques used to improve ventilation
Breathing exercises
Demand ventilation (mobilisation)
Facilitation techniques (quick stretch, neurophysiological)
Incentive spirometry
PEPs
45
Number of TEE that should be done
No more than 5 at a time
46
What is hypoxaemia and why can this occur
Low oxygen in blood
PaO2 < 80mmHg is classified as hypoxaemia and if is it < 60mmHg this is severe hypoxaemia
Can be from a few reasons:
- V/Q mismatch (most common)
- Hypoventilation (atelectasis or low long volume)
- Diffusion limitation
47
What is hypoxia and why can this occur
O2 delivery to the tissues is inadequate to meet metabolic needs
Results from:
- Hypoxaemia
- Decreased cardiac output
- Decreased haemoglobin (therefore decreased carrying capacity)
- Increased metabolic rate (burns)
48
What is hypercapnia
Increased partial pressure of CO2
>50 mmHg
Normal = 35-45
Results from:
- Hypoventilation
49
What are the early and late signs for respiratory distress
Clinical signs:
- Respiratory compensation
- Increased RR
- Increased accessory muscle use
- Nasal flaring
- Intercostal recession
- Increased sympathetic tone
- Increase HR, BP and sweating
If long term than can cause end organ hypoxia:
- Altered mental status (confusion, aggression)
- ECG changes
- Cyanosis
50
What are the two types of respiratory failure
When the resp system is unable to provide adequate gas exchange for metabolic requirements.
Type 1 = PaO2 < 60 mmHg (severe hypoxaemia)
Type 2 = above +PaCO2 > 50 mmHg (hypoxaemia with hypercapnia)
51
Features of type 1 resp failure
- Restlessness
- Confusion
- Aggression
- Sweating
- Plucking
- Increased RR, HP and BP
- Pallor
- ECG changes
52
Features of type 2 respiratory failure
Type 2 → leads to vasodilation
- Drowsiness
- Headache
- Flushed skin
- Bounding pulse
- Warm peripheries
53
Aims of oxygen therapy
- Correct hypoxaemia → limit tissue hypoxia
- Decreased WOB
- Decrease cerebral vasodilation (type 2 resp failure)
54
Dangers of oxygen therapy (4)
- Patients with COPD
- PaO2 becomes the main stimulus to breath (normal is PaCO2) so supplimental oxygen can increase PaO2
- Oxygen toxicity
- For long period oxygen therapy can have pulmonary changes such as pulmonary oedema and decreased pulmonary compliance. Need to keep supplemental oxygen levels as low as possible for all patients.
- Depression of ciliary function
- Thickening of secretions will further increased secretion retention (cycle)
- Absorption atelectasis
- Nitrogen has a structural role to hold alveoli open, with increased O2 in alveoli the nitrogen is moved out. End result is a V/Q mismatch.
55
How to minimise the dangers of oxygen therapy
How to minimise these
- Ensure correct flow and FiO2
- Monitor improvements and deterioration
- Minimise supplemented O2
- Humidification
56
2 main mechanisms that are involved in normal airway clearance
- Mucociliary clearance (MCC)
- Effective cough (as a backup for impaired MCC)
57
When does impaired airway clearance occur
This occurs when one of the two previously mentioned mechanisms has failed which leads to increased secretions, obstruction and +/- atelectasis.
58
Two mucosal layers
- The outer gel layer which has less amount of water but it more viscous meaning it is able to catch foreign material
- The inner sol layer which has increased amounts of water and is not as viscous, this is the layer in which the cilia beat. Due to the water content it means that dehydration ect can decreased the water in this layer making the cilia beat less effective.
59
How does MCC work
- This is the process of the cilia propelling the mucous
- This occurs in a uni direction wave like motion and it moves particles towards the trachea so they can be coughed out
60
2 factors that decrease mucociliary clearance
- Decreased cilial beating
- This can be temporary such as from medications (this is why it is important to consider airway clearance post surgery), high FiO2 concentrations, atelectasis, lack of sleep. Or it can be permanent such as from smoking or a disease
- Increased secretion volume or thickness
- Infection, dehydration, disease
61
Effects of a congested airway (one with increased secretions)
- Decreased cilial function
- Increased WOB → fatigue
- Decreased ventilation → decreased V/Q ration → decreased PaO2
- Long term damage
62
Aims of ACTs (3)
- Get air behind secretion
- Secretion mobilisation
- Secretion removal
63
Number of huffs and TEE that should be done in a row
TEE no more than 5, huff 2-3
64
2 main goals of TEE for airway clearance
- Increase lung volume
- Collateral ventilation → air behind secretions → mobilise these secretions
- Re expand lung
- Alveolar interdependence
- Increase surfactant production
- Allow for time constants
- Newtonians law of viscosity
65
Duration of ACBT
- Repeat until effective huff to low lung volume has become dry sounding and non productive OR when pt becomes fatigued
- Normally 10 to 30 mins
66
What is the role of the pericardial fluid?
The pericardial fluid lubricates and creates a frictionless environment for the heart. An
increase in pericardial fluid will compress the heart and impair its ability to pump. This is
termed cardiac tamponade
67
Systole and diastole
Systole = heart contracts
Diastole = heart relaxes
68
What 3 mechanisms affect BP
HR, SV and total peripheral resistance
69
What 3 mechanisms can increase SV
1. Increased venous return (Frank Starling’s law)
2. Reduced after-load
3. Increased contractility of the ventricle (inotropy)
70
Process of TEE in ACBT
- Slow laminar flow with IH for 3 sec
- Encourage lower chest expansion
- 3-4 TEE then back to BC
71
Two main goals of TEE
- Increase lung volume
- Collateral ventilation → air behind secretions → mobilise these secretions
- Re expand lung
- Alveolar interdependence
- Increase surfactant production
- Allow for time constants
- Newtonians law of viscosity
72
How does PEP work
Aim is to reinflate collapsed parts of the lung by collateral ventilation. With collapsed parts of the lung secretions can be stuck distal to this. EPP aims to splint the airways open during expiration which can then get air behind the secretions and mobilise upwards.
73
Ratio of inspiration to expiration in PEP and what to do if this isnt occuring
Ratio of inspiration to expiration 1:3 (seconds)
The size of the resistor will determine the amount of POP generated, smaller resistor number (smaller hole) will mean increased PEP generated (toilet roll and straw analogy)
74
Inhaler use
Shake for 20 seconds
Breath in as press
Hold for at least 10 seconds (or as long as you an)
Breath out throw nose
Wait 20 seconds before next dose
75
What is Pneumonia
Acute disease that is marked by inflammation of lung tissue as well as alveoli infiltration
76
What are different types of PPCs
- CXR report atelectasis/consolidation
- Temp >38
- Raised WCC (white cell count) or prescription of ABs specific for lung infection
- SpO2 <90
- NEW production of yellow/green sputum
- Positive signs of infection on sputum
- Diagnosis of pneumonia/chest infection
- Readmission to or prolonged stay in ICY with resp problems
Atelectasis, consolidation or infection
77
Atelectasis considerations post surgery
- All post op patients will have microatelectasis
- If high FiO2 from oxygen therapy this can lead to decreased nitrogen which is a structural unit in the airways causing them to become less stable → V/Q mismatch
- Surfactant affected by anaesthesia, supplemental O2 and mechanical ventilation
78
Risk factors for PPC's - patient related
- Advanced age
- Increased CC, decreased elastic recoil
- ASA comorbidity score 3-5
- Impaired functional status
- Resp and CV disease
- Recent infection
- Increased secretions, decrease MCC
- Smoking history (especially in last 8 weeks)
- Sleep apnoea
- Other → impaired cognition, cancer, immunocompromised
79
4 key post surgery questions
Nausea, dizziness, drowsy, vomiting
80
Risk factors for PPC's - procedure related
- Anaesthesia >180 mins
- Impaired airway clearance → drying of cilia, secretion retention, loss of cough reflex
- Impaired ventilation → decreased FRC, atelectasis, decreased alveolar ventilation
- Surgery type → upper abdo, thoracic (these two will effect deep breath in and cough), neuro
- Emergency or elective surgery (emergency gives less time for pre op)
81
What is medical Air?
Has 21% pp of O2
82
Flow rate for nebulisation
>6L
83
Flow rate and FiO2 for nasal prongs
Flow rate of 1-4 and FiO2 depends on the flow rate (0.24-0.36)
84
Flow rate and FiO2 for face mask
Needs a flow rate >5L to prevent rebreathing of exhaled gas. FiO2 0.4-0.6
85
Flow rate for rebreather and non rebreather
A non rebreather has a valve between the bag and mask so cant rebreath Co2. Partial = 6-10 L, FiO2 <9.6. Non rebreather 10-15 L FiO2 0.8-0.9
86
Components of the ISBAR
- Identify
- Situation
- Reason for admission
- Background
- Past medical history, previous surgical, investigations ordered, vital signs, medication, socials history, functional history.
- Analysis
- Current problems/risks,
- Recommendation
- Plans for management, any requests?
87
What does a moist cough on assessment indicate
Can indicate sputum present
88
What is the purpose of a nebuliser
Reduce viscosity of secretion and support mobilisations of secretions. Can be done on medical air.
89
Flow rate for nebuliser
>6L
90
When would you use medical air instead of O2 for nebulisation
When the patient has a hypoxic drive to breath
91
Dangers of oxygen therapy
* Pts with chronic respiratory failure (COPD)
* Oxygen toxicity
* Depression of ciliary function
* Absorption atelectasis
92
How can oxygen therapy lead to absorption atelectasis
Nitrogen = structural role to hold alveoli open
With ↑O2 in alveoli, nitrogen is moved out
structural collapse (atelectasis)
alveoli perfused but not ventilated
V/Q mismatch
93
3 principles that help t reveres atelectasis
Critical opening pressure
Slow laminar flow (Newtonian law)
Inspiratory holds (time constants, collateral ventilation, alveolar interdependence)
94
Components of a epidural assessment
Observe the insertion site
P/I -> p/n, numbness, weakness, headache, pain at site
Sensation using a reference point above (arm)
Muscle strength
95
Components of circulation check
Dorsil pedis - navicular, medial
Tib post - near medial malleoli
Capillary refill
96
When would you use incentive spirometry over TEE
Patient needs visual queues
Not responding to tactile
Pain -> gives incentive
97
Easy way to remember pH and PaCO2 on ABGs
pH is 7.34-7.45 which is the same as PaCO2 35-45
98
Increase and decrease of HCO will cause blood to become
Decrease is acidotic and increase is alkalosis
99
What does intrathoracic pressure do to venous return and why is this important for patients with low BP
Increase in intrathoracic pressure will decrease venous return. This is important when doing techniques to improve lung volumes. Avoid consecutive big breaths in as this will increase intrathoracic pressure and there fore decrease venous return and BP
100
Considerations for manual hyper inflation of a high resp rate patient
If doing manual hyperinflation then need to make sure that this is timed with patient’s normal breathing. If not then it make suppress there hypoxic drive to breath,
101
Resp failure type 1 and 2 on problems list
Impaired ventilation and impaired gas exchange
102
Management of type 1 and type 2 resp failure
1
-Increase ventilation (breahting ex, demand, positioning)
-ACT
- NIV
2
-O2 therapy via fixed device
-Ventilation
103
What is NBM
Nil by mouth
104
Diabetes consideration for physio
Need to check blood sugar levels prior to mobilising
105
Signs of acute ischemia
6 p's
➢ Pain
➢ Pallor
➢ Polar
➢ Pulseless
➢ Paralysis
➢ Paraesthesia
106
2 factors that can reduce MCC
2 main factors that do this:
- Decreased cilial beating
- This can be temporary such as from medications (this is why it is important to consider airway clearance post surgery), high FiO2 concentrations, atelectasis, lack of sleep. Or it can be permanent such as from smoking or a disease
- Increased secretion volume or thickness
- Infection, dehydration, disease
107
Adverse effects of narcotics (PCA)
* Respiratory depression (eg RR<8bpm)
* Postural hypotension, syncope (fainting)
* Drowsiness
* Nausea, vomiting
* Paralytic ileus
* Pruritis / itchiness
* Urinary retention
108
Fempop ROM limitations
Ensure hip does not exceed 60° flexion when knee is extended
109
Axillo femoral bypass restriction
- shoulder flexion >90o
- hip flexion > 60
- sidelying
110
Pre op AAA physio assessment
Whether or not you should include cough in your assessment of the patient depends on whether there has been a leak from the aneurysm, and the size of the aneurysm:
* < 6 cm - limit cough / FET; depends on chest condition and indication for coughing
* > 6 cm - risk of rupture, therefore no cough preoperativelyO
111
O2 devices implication for physio
Check the device is worn correctly (ie, not dislodged) and that the correct flow rate /
FiO2 is being delivered to the patient
* Monitor SpO2 with pulse oximeter
* Mobilise post-op patients with portable O2 (if appropriate), or if removed use portable
pulse oximeter, and ensure oxygen device replaced when returned to bed / chair.
* Be aware of negative effects of oxygen; monitor and manage these (see Module 1)
112
IDC implication for physio
* Do not dislodge; take special care when mobilising
* Ensure bag is not too full prior to mobilising
* Keep bag below level of catheter insertion
113
ICC implication for physio
* Do not dislodge; if accidentally disconnected, reconnect and assess system
* Check whether the fluid is swinging, draining or bubbling (see lecture)
* Keep bottle system below level of insertion into patient’s chest wall so no danger of
fluid entering pleural cavity
* If the bottle breaks: if previously no bubbling – double clamp, quickly change bottles; if
previously bubbling – do not clamp, quickly change the bottle
114
What is oxygen toxicity
High FiO2 (.5-.6) for long periods causes pulmonary changes -> pulmonary oedema -> reduced pulmonary compliance
115
Relationship between flow rate and FiO2
Flow rate and FiO2 are directly related, starting at 0.24 FiO2 for 1L/min and increasing 0.04 for each L/min after that.G
116
GOR implication for pshyio
Will need to limit PD positions
117
Long term CS use
No percs and vibs, care with handling
118
Implications of Hyperinflation
No IH, for TEE facilitate abdo
119
IHD implications
May experience Angina during mobilisation
120
SOB management
Positioning in upright and recovery position to increase FRC and also reverse origin in section for axio humeral muscles which can be used in respiration.
Breathing control focusing on diaphragm activation as Henry has increase AP movement
121
2 stages for PEP handheld devices
Can be used for mobilisation and clearance → similar to FETs with the first needed a slightly deeper breath and the second needing the deepest breath in. Meaning it has with two stages
122
Considerations for treatment if patient usually uses walking aid
Will need to use this for treatment
123
Implication of DVT history
circulation exercises, mobilisation asap; monitor signs;
replace TEDs if removed for Ax / mobilisation
124
Results of emphysema
Impaired gas exchange, loss of elastic recoil causing decreased FRC
125
Path of Bronchitis
Affects bronchi & bronchioles:
* Inflammation due to mucous gland hyperplasia +
mucus hypersecretion
* Smooth muscle hypertrophy and hyperplasia →
thickening of bronchial wall
* Mucociliary function → mucous retained in airways
* These factors lead to obstruction
126
Path of emphysema
*Affects more distal parts of the airway (compared with chronic
bronchitis):
* Destruction of alveolar septa → joining of adjacent alveoli
* Permanent enlargement of the terminal air spaces (distal to
terminal bronchiole)
* Destruction of lung parenchyma
Impaired gas exchange due to loss of available surface area for gas exchange with physiological dead space
2. Airflow limitation, gas trapping and hyperinflation due to premature closing from loss of elastic recoil / radial traction on small airways. The unsupported airways narrow and collapse, particularly during expiration. Also results in FRC (functional residual capacity)
as stale air is ‘trapped’ in the lungs due to incomplete expiration
127
Path of Bronchiectasis
* Abnormal and permanent dilatation of the
bronchi
Increased secretions (not directly), because they have decreased MCC function
* Destruction of muscular and elastic components of bronchial walls
* Usually associated with inflammation
* Surrounding undamaged lung exerts a contractile force which results in hypertrophy and hyperplasia of tissue in the area and a loss of elasticity
128
What is pneumonia
Acute inflammatory consolidation of alveoli, or infiltration of the interstitial cells with inflammatory cells, or combination of both. Usually caused by bacteria, but can refer to non-bacterial infections e.g. viral pneumonias, atypical pneumonias
129
MDP post segment of right and left upper
1/4 turn from prone with drainage side up
130
MDP Anterior segments of upper lobes
Supine
131
MDP right middle lobe and ligular segment of left upper
1/4 turn from supine with drainage side up
132
MDP Apical and post segment of lower lobe
Prone
133
MDP Anterior segment of lower lobe
Supine
134
MDP lateral segment of lower lobe
Side lying with drainage side up
135
Infective exacerbation consideration for physio
Infection control, use PPE, frequent sanitisation and bare below elbows.
136
PEP use and nebulisation
- Often positioned in forward lean in sitting
- Therapist has hand on abdomen or lateral chest wall to palpate muscle activity
- Patient takes breath slightly deeper than usual
- Pressure on manometer 10-20 H2O for 3-5 seconds of expiration
- When assembling the mask make sure the resister is on the expiration side
- Mouth piece PEP can be combined with nebulisation which is an advantage over the mask
137
Mini trach indications and info
* Inserted for retained secretions or UAO
* Paediatric size tracheotomy but used in adults as well for
above reasons
* Maintain own airway, eat, talk
* No need for humidification, may need
NaCl 0.9% during suction
* Use size 8 or 10 FG catheter to suction ie clean tube
138
Precautions to suctioning
- Pulmonary oedema
- Haemoptysis
- Respiratory burns
- Head injuries
- High levels of PEEP, FiO
- Severe infection
139
Different sized French Gauge (FG) catheters and their indications
FG 8 - Paeds and minitrache
FG 10 - Minitrach
FG 12 - Adults
FG 14 - Adults
140
Brochiectasis
Abnormal and permanent dilation of the bronchi. Destruction of the muscular and elastic components of the bronchial walls.
The surrounding undamaged tissues exerts a contractile force which causes hypertrophy and hyperplasia of tissue in the area and a loss of elasticity.
Impaired MCC and predisposes airways to chronic infection. Infections causes inflammation and obstruction due to poor airway clearance which becomes a cycle.
141
Questions for epidural
- P/N
- Numbness
- Weakness
- Headache
142
What does GA do to surfactant
Decreases it
143
Contraindications to PEEP
Low BP/CO
Peep increases intrathoracic pressure and therefore decreases venous return
144
Humidification vs nebulsation
Humidification
Add moisture to the air
Used when patient is receiving O2 therapy to prevent drying of the airways
Nebulisation
Converts liquid medication into a mist that can be inhaled
145
PEP prescription
8-10 breaths per cycle repeated 5-10 times
146
What must the patient do before exhaling in PEP
hold the breath for 3 seconds
147
PEP precautions
x Active haemoptysis
x Lung surgery (lobectomy, transplant)
x Pneumothorax (drained or undrained)
x Undrained empyema or lung abscess
x Emphysematous bullae
x Inc WOB
x Haemodynamic instability
x Facial fractures or surgery
x Middle ear infection
x Sinusitis
148
3 main path features of asthma
Airflow obstruction
Airway hyper responsiveness
Airway inflammation
