Respiratory Flashcards

1
Q

What is the 4 main functions of the respiratory system?

A

Gas exchange

Protection against harmful particles

pH homeostasis

Vocalisation/speech

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2
Q

What is the function of the upper respiratory system?

A

Not gas exchange

Warms air to preserve body temperature

Humidifies air so gas exchange tissue doesn’t dry air

Nasal hair coated with mucous trap large particles to filter air before gas exchange

Speech

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3
Q

What does the upper respiratory tract consist of?

A

Nasal cavity

Pharynx

Larynx

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4
Q

What does the lower respiratory tract consist of?

A

Trachea

Bronchus

Lung

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5
Q

Lungs smooth muscle layer contains:

A

Autonomic nervous system

Sympathetic nerves stimulate beta-2-adrenergic receptors to increase airway diameter

Parasympathetic nerves stimulate muscarinic receptors to reduce airway diameter

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6
Q

The branching airways:

A

Trachea - bronchi - 2nd bronchi - bronchioles - alveoli

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7
Q

Large airways (bronchus) are lined by…

A

Goblet cells = produce mucous that traps particles

Ciliated cells = move mucous towards pharynx (throat) to be swallowed

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8
Q

Alveoli walls are composed of…

A

single layer of simple squamous epithelium

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9
Q

There are 2 types of alveolus cells:

A

Larger type 1 cells

Smaller type 2 cells

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10
Q

Larger type 1 alveoli cells:

A

Primary gas exchange site - oxygen to carbon dioxide exchange between alveolar gas and pulmonary capillary blood

Have thin walls and large surface area to maximise gas exchange.

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11
Q

Smaller type 2 alveoli cells:

A

Secrete surfactant – reduces surface tension to ease expansion of lungs and prevent collapse of alveoli

These cells have limited regeneration capabilities (smoking destroys them)

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12
Q

How is the diffusion of gas maximised?

A

Haemoglobin is needed for gaseous exchange = there is a dense network of capillaries surrounding the alveoli

Membranes of capillaries and alveoli are almost fused

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13
Q

What does the connective tissue between alveoli contain?

A

Elastin (elastic fibres) – allows the lungs to expand during inspiration and recoil during expiration.

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14
Q

How does air get into lungs?

A

Boyles law

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15
Q

Boyles law:

A

Increase volume – pressure decreases

Decrease volume – pressure increases

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16
Q

Change in lung volume causes airflow:

A

When lungs expand - volume increases and pressure decreases

Pressure in the lungs falls below atmospheric

Air flows in - inspiration

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17
Q

Lungs contained within pleural sac….

A

Lung adheres to the thoracic wall by cohesive forces of pleural membranes

As the respiratory muscles cause thoracic cage to move, lung volume changes = inspiration and expiration.

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18
Q

Muscles involved in inspiration:

A

Diaphragm

External intercostals

Scalenes

Stemocleidomastoids

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19
Q

Muscles involved in expiration:

A

Internal intercostals

Abdominal muscles

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20
Q

Ventilation =

A

Breathing = Moving air in and out of lungs

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21
Q

Oxygen pathway:

A

air inhaled through nostrils  nasal cavity  pharynx  larynx  trachea  mainstream bronchus  conducting bronchioles  terminal bronchioles  respiratory bronchioles  alveolar duct  alveoli  capillary  body

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22
Q

Passive inhalation:

A

Diaphragm contracts downwards

Chest muscles pull ribs outward

Increased intrathoracic volume

Decreased intrathoracic pressure

Air moved into lungs (flows down pressure gradient)

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23
Q

Passive exhalation:

A

Diaphragm relaxes (returns to resting position)

External intercostal muscles relax

Thoracic cage recoils

Elastic lung recoil

Decreased intrathoracic volume

Increased intrathoracic pressure

Air pushed out of lungs

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24
Q

Volume changes lead to gas movement according to Boyle’s law:

A

Volume changes cause pressure changes.

Pressure changes cause the flow of gases equalize pressure

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25
Factors Influencing Pulmonary Ventilation:
- The resistance of the airways - The surface tension of the alveoli - The compliance of the lung tissue
26
Resistance =
force that opposes flow of air
27
The effect of resistance on the pulmonary system:
Resistance impedes airflow into lungs. Increased Resistance = increased energy needed to breathe in. Airways generate 80% of resistance. Diameter of airway is inversely proportional to the resistance it produces.
28
In healthy patients, resistance...
...is insignificant, as total diameter of airways is large. Large airway diameters in beginning of conducting zone Resistance disappears in terminal bronchiole → diffusion drives gas exchange
29
reduced total airway diameter =
increased resistance to overcome in order to breathe
30
Diseases that increase resistance:
Smooth muscle of airway constricts (e.g., asthma) Mucous plugging of airways (e.g., COPD, bronchitis, cystic fibrosis) Obstruction of bronchioles and alveoli by infectious material (e.g., pneumonia)
31
Alveolar surface tension =
Water molecules stick to other water molecules Resists any force that tends to increase surface area of liquid Occurs in alveoli due to the water molecules inside them If left unchecked, keeps alveoli from stretching during inspiration
32
Surfactant:
Type II alveolar cells (pneumocytes) synthesize pulmonary surfactant Decreases alveolar surface tension by separating water molecules from each other Allows easier expansion during inspiration and prevents alveoli from collapsing during expiration
33
Anything that destroys surfactant...
can cause pulmonary disease e.g. the lack of surfactant in premature infants leads to infant respiratory distress syndrome. e.g. chronic smokers produce less surfactant, leading to issues seen in COPD.
34
Compliance =
Measure of volume change with given change in transpulmonary pressure
35
Compliance is determined by...
tensile properties of lung tissue (how stiff the lungs are)
36
Effect of compliance on the pulmonary system:
High compliance = increased lung stiffness = increased energy to stretch during inspiration Ventilation is more efficient in areas of lung with increased compliance. Areas with reduced compliance expand less.
37
Compliance of lungs is influenced by gravity:
o Apex is less compliant. o Base is more compliant.
38
Healthy lungs have higher compliance because of:
 Distensibility of lung tissue  Reduced alveolar surface tension
39
Reduced lung compliance appears in:
 Fibrosis (e.g., acute respiratory surfactant distress syndrome, scarring after chemotherapy)  Reduced production of surfactant (e.g., premature lungs, COPD)  Reduced flexibility of thoracic cage (e.g., scoliosis, cerebral palsy)
40
Too much lung compliance appears in:
 Pulmonary emphysema
41
Indications For Performing Lung Function Tests:
Detect presence and severity of lung disease Determine the effects of intervention Assess preoperative risk
42
Contraindications for lung function tests:
Haemoptysis (coughing up blood) Pneumothorax Unstable cardiovascular status Aneurysms - danger or rupture due to increased thoracic pressure Recent eye surgery (wait 4 weeks due to increased pressure at back of eye) Nausea/vomiting Recent thoracic or abdominal surgery Can worsen Angina due to blood pressure changes
43
Things to avoid before respiratory tests:
Smoking 24hrs – has impact on gas transfer Alcohol for at least 4hrs – reduces gas exchange A large meal for 2hrs Bronchodilators – stop taking inhaler if possible Vigorous exercise for at least 30mins Wearing tight clothing or surgical appliances
44
Calibration of equipment is required to...
ensure accuracy
45
Lung volumes =
specific volumes of air contained by different portions of lungs at specific points in the respiratory cycle
46
Tidal volume (TV) =
volume of air inhaled or exhaled with each breath under resting conditions (during the respiratory cycle)
47
Residual volume (RV) =
volume of air left in lungs after forced exhalation
48
Expiratory reserve volume (ERV) =
volume of air that can be forcefully exhaled after normal tidal volume exhalation
49
Inspiratory reserve volume (IRV) =
maximum volume of air that can be forcefully inhaled after normal tidal volume inhalation
50
Lung capacities are...
a combination of 2 or more volumes
51
Total lung capacity (TLC) =
Maximum volume of air contained in lungs after maximum inspiration tidal volume + residual volume + expiratory reserve volume + inspiratory reserve volume
52
Vital capacity (VC) =
Maximum volume of air that a person can move in or out of lungs (air expelled by a full expiration after full inspiration) tidal volume + expiratory reserve volume + inspiratory reserve volume
53
Functional residual capacity (FRC) =
Volume of air remaining in lungs after tidal (normal) expiration expiratory reserve volume + residual volume
54
Inspiratory capacity (IC) =
Maximum volume of air that can be inspired after normal expiration (from the position of functional residual capacity) tidal volume + inspiratory reserve volume
55
Thoracic Gas Volume (TGV) =
Absolute volume of gas in the thorax at any point in time and at any alveolar pressure (FRC-pleth)
56
Dead space =
air that enters and exits lungs but does not make it to areas where gas exchange can occur Total dead space = alveolar dead space + anatomical dead space
57
Anatomical dead space =
air in airways that does not reach alveoli or respiratory bronchioles
58
Alveolar dead space =
air in alveoli that cannot be absorbed into bloodstream due to lung disease or blood flow limitations
59
Minute ventilation =
Volume of air moved in and out of lungs per minute breathing frequency expressed in breaths/minute × tidal volume
60
Alveolar ventilation =
Volume of air reaching alveoli per minute and is available for gas exchange breathing frequency expressed in breaths/minute - total dead space
61
work of breathing =
the amount of energy a person needs to breathe Elastic work: done to overcome elastic recoil of chest wall and pulmonary parenchyma and surface tension of alveoli Resistive work: done to overcome resistance of airways and tissues
62
Measurements of residual volume and total lung capacity requires...
the use of helium dilution or plethysmography.
63
Helium dilution =
a gas of known helium concentration is breathed through a closed circuit and the volume of gas in the lungs is calculated from a measure of the dilution of the helium (helium is an inert gas that is not absorbed or metabolised)
64
Body plethysmography =
a large airtight box that allows pressure-volume relationships in the thorax to be determined. When the plethysmograph is sealed, changes in lung volume are by a change in pressure within the box
65
Static lung volumes test =
A method of assessing the size of the lungs. Used to determine the elastic properties and the compliance of the lung and identify pathophysiology. Provides information on the functional status of the lungs, assessment of disease severity, course of disease and response to treatment. Identify hyperinflation and gas trapping.
66
How are static lung volumes measured?
Static lung volumes cannot be measured directly (there is always some air in the lungs). We calculate them from indirect measurements made using static lung volume techniques. There are 3 techniques: whole body plethysmography, nitrogen washout and helium dilution (the differences between these could be an exam question) Whole body plethysmography is the gold standard.
67
What is the procedure for body plethysmography?
1) Patient sits in box, box volume is corrected for patient weight, nose clip and mouthpiece attached. 2) door is sealed and the subject is asked to sit for 1 minute, allowing temperature to settle. Patient is asked to breathe normally. 3) Shutter is closed at end of normal tidal expiration and patient is asked to pant softly against the shutter at a frequency of 1 breath per second 4) Panting graph generated shows changes in box pressure and mouth pressure 5) Shutter is reopened, patient asked to breathe in fully to maximal inspiration and then breath out fully to empty (like a sigh) 6) The test finishes with a big breath back in to full 7) steps are repeated until 3 technically acceptable traces are obtained
68
Spirometry =
a method of assessing lung function by measuring the volume of air that the patient is able to expel from the lungs after a maximal inspiration (also measures speed/flow). The results of the test are represented graphically as a plot of volume against time = forced expiratory spirogram. It is a reliable method of differentiating between obstructive and restrictive diseases. It can also help to monitor disease severity.
69
Obstructive airways disorders examples...
chronic obstructive pulmonary disease asthma
70
Restrictive diseases examples...
fibrotic lung disease
71
Spirometry provides several important measures:
FEV1 = forced expiratory volume in 1 second FVC = forced vital capacity FEV1/FVC ratio
72
FEV1 =
forced expiratory volume in 1 second maximum volume of air forcefully expired in the first second after maximal inspiration
73
FVC =
forced vital capacity maximum volume of air forcefully expired after maximal inspiration = the total volume of air that the patient can forcibly exhale in one breath.
74
FEV1/FVC ratio =
the ratio of FEV1 to FVC expressed as a percentage
75
Values of FEV1 and FVC are expressed as ...
a percentage of the predicted normal for a person of the same sex, age and height
76
How is spirometry done?
Patient is asked to take big breath in and blow out normally. Then do another big breath in before blasting it out as hard as can until empty.
77
The graph produced by spirometry is...
The expiratory volume-time graph
78
The expiratory volume-time graph should ...
be smooth and free from abnormalities caused by: Coughing during expiration, extra breath during expiration, slow start to forced expiration, sub-maximal effort.
79
Common errors of spirometry:
Slow Start Mouth Leak – weakness in face muscles = cannot get lips tight around mouth piece Coughing in first second Variable effort Glottis Closure (opening between the vocal folds)
80
Spirometry criteria for acceptability:
Free from common errors Reproducible A minimum of 3 technically acceptable manoeuvres are required, of which the best two curves should be within 5% of each other The chosen values for FVC and FEV1 should not differ from the next best values for FVC and FEV1 by more than 150mL.
81
Restrictive spirometry:
FVC can be reduced in any condition that limits the lungs ability to achieve a ‘full’ inspiration... - Reduced lung compliance (lung fibrosis, loss of lung volume) - Chest deformity - Muscle weakness (myopathy, myasthenia gravis) When lung volume is restricted FEV1 also reduces in proportion = FEV1:FVC ratio is normal
82
Obstructive spirometry:
FEV1 is reduced in any condition that reduces vital capacity, but it is particularly reduced when there is diffuse airway obstruction = FEV1:FVC ratio is reduced - most commonly seen in asthma and COPD.
83
Peak expiratory flow:
maximum rate of airflow that can be achieved during a sudden forced expiration after full inspiration It gives an indication of diffuse airway obstruction.
84
How is peak expiratory flow measured?
The patient takes a full inspiration, applies their lips to the mouthpiece and makes a sudden maximal expiratory blast. A piston is pushed down the inside the cylinder, progressively exposing a slot in the top, until a position of rest is reached. The position of the piston is indicated by a marker and PEF is read from a scale. The best of 3 attempts is accepted as the peak flow rate. It is somewhat dependent on patient effort.
85
Forced expiratory manoeuvres can be displayed by...
measuring peak expiratory flow or plotting flow against volume on a flow volume loop (provide same information)
86
Flow volume loops:
Airflow is represented on the vertical axis and lung volume is on the horizontal axis Expiratory flow appears above the line, inspiratory flow below the line At TLC airways are stretched (dilated) and airway resistance is minimised, so maximum (peak) expiratory flow is reached quickly after the start of forced expiration. As expiration continues, lung volume progressively diminishes, airway resistance increases and maximum flow achievable (at each lung volume) declines. In a healthy patient this declining portion of the expiratory limb is quite straight. When no further air can be exhaled, flow is zero and the loop reaches the horizontal axis. The inspiratory manoeuvre can then begin.
87
Flow volume loops can be used to assess ...
narrowing of the airways
88
When recording a flow volume loop the patient is asked...
1) take a full inspiration 2) maximal forced expiration 3)maximal forced inspiration
89
What is measured by a flow volume loop?
* PEF = peak expiratory flow * RV = residual volume * PIF = peak inspiratory flow * FEF = forced expiratory flow
90
Pressure difference across resistance is directly proportional to...
...the flow of gas. The flow signal is integrated to derive volume.
91
Obstructive flow volume loop:
concave expiratory part of loop (sudden drop in flow early in expiration due to collapse of airways) normal inspiratory part of loop Reduced FEV1 (<80%) FVC reduced to a lesser extent Reduced FEV1/FVC Ratio (<0.7)
92
Restrictive flow volume loop:
Curve reaches top of expected but drops faster Proportional reduction in FEV1 and FVC (<80%) FEV1/FVC Ratio remains normal (>0.7) Flow volume loop cannot tell you what restrictive ventilatory defect they have
93
Gas trasfer =
describes the rate of transfer of a gas between alveoli and the erythrocytes in the alveolar capillaries pressure difference between two sites (how good lungs are at passing O2 from alveoli to bloodstream)
94
What gas is used to measure gas transfer?
Carbon monoxide is used as O2 is difficult to measure o similar properties to oxygen o technically easier to use o safe at low concentrations
95
What measurements are taken during gas transfer?
Transfer Coefficient (KCO) = Rate of disappearance of CO from alveolar gas during 10s breath hold. Alveolar Volume (VA) = Lung Volume ‘seen’ by inhaled CO during the measurement
96
Gas transfer calculation:
Carbon Monoxide Transfer Factor (TLCO) = Total ability of lungs to transfer gas across into bloodstream Calculated by multiplying the Transfer Coefficient (KCO) X VA
97
Why is it difficult to measure the transfer of oxygen?
transfer of oxygen into the blood quickly becomes limited by the saturation of haemoglobin = carbon monoxide used to measure gas transfer instead
98
To measure diffusion capacity/transfer factor (DLCO/ TLCO) we need to know:
The amount of carbon monoxide (CO) transferred per minute The pressure gradient across the alveolar membrane (alveolar partial pressure)
99
Single-breath method to measure gas transfer:
the patient inspires a gas mixture of helium and carbon monoxide, hold their breath for 10 sec and then breathes out. A sample of expired gas is collected and analysed for alveolar concentrations of helium and carbon monoxide. The change in concentration of helium (which is an inert gas and not absorbed or metabolised) between the inspired and alveolar samples is the results of gas dilution and gives a measurement of alveolar gas volume.
100
Why hold breath fro 10 seconds during gas transfer measurement?
because CO (carbon monoxide) and CH4 (methane) have to have time to get to alveoli where gas exchange takes place
101
Tracer Gas:
Inert gas, almost insoluble (doesn’t react or diffuse through membranes) Chemically stable, almost inactive and have negligible leakage into the blood Provides estimate of alveolar volume Dilution effect on CO Can use Helium, Argon, Neon, Methane
102
Why Carbon Monoxide for gas transgfer tests?
CO and O2 bind to same sites(behaves like O2 – attaches to haemoglobin) COHb levels are negligible in non-smokers Readily measure CO in low concentrations COHb and O2Hb dissociation curves same shape and affected in same manner Even when large amounts of CO combine with Hb, the PCO remains low
103
Reproducibility of gas transfer test:
A minimum of two technically acceptable gas transfer manoeuvres should be performed with a maximum of five. Five gas transfer manoeuvres will increase carboxyhaemoglobin (COHb) by approximately 3.5%, which will ultimately decrease measured transfer factor by 3.5%). TLco results should be within the repeatability criterion of 0.67 mmol/min/kPa. Kco within 0.10 mmol/min/kPa/L VA within 5%. The mean of two technically acceptable manoeuvres should be reported.
104
Causes of decreased DLCO and/or KCO:
COPD, Pulmonary fibrosis, Pulmonary vascular disease, Renal failure, Cardiac failure, Mitral valve disease, Cirrhosis, Collagen diseases.
105
Causes of increased DLCO and/or KCO =
Asthma – increase in gas exchange. Often get increase in blood supply around lungs Pneumonectomy – DLCO reduces because less lung but KCO increases Extrapulmonary restriction - type of restrictive lung disease, indicated by decreased alveolar ventilation with accompanying hypercapnia (buildup of carbon dioxide in your bloodstream)
106
Gas transfer in emphysema (obstructive):
alveoli destruction and distention TLCO ↓ KCO ↓ Diffusion distance ↑ SA for gas exchange ↓ = gas exchange reduces
107
Gas transfer in asthma (obstructive):
TLCO ↓ (but can be ↑) KCO tends to be ↑ Reason not known Hyperaemia of airways Greater perfusion of lung apices in asthma
108
Gas transfer in intra-pulmonary disease (restrictive):
e.g. Fibrosis fibrotic tissue makes it hard for gas exchange = TLCO ↓ KCO ↓
109
Gas transfer in extra-pulmonary disease (restrictive):
e.g. Muscle weakness, scoliosis, pleural disease underinflated lungs = less air into them = TLCO ↓ KCO ↑
110
Boyle’s Law:
At a constant temperature, the volume (V) of a given mass of an ideal gas is inversely proportional to its pressure (P), that is, PV=K. The constant (K) is proportional to the mass of the gas (the number of moles) and its absolute temperature. Assuming that temperature remains constant (isothermal conditions of measurement): P1 × V1=P2 × V2. I.e. if the volume of a closed container is doubled, the pressure will fall by half
111
Using Boyle’s Law in Body phethysmography:
1. Determination of transfer gas volume (FRC-pleth) is possible if the lungs are treated as a closed compartment and alveolar pressure can be measured at the same time as changes in volume. 2. At the end of tidal expiration (at FRC) the alveolar pressure approximates mouth pressure and thus can be measured at the mouthpiece 3. When the airway is occluded at the end of the mouthpiece, the lungs can then be treated as a closed compartment, this prevents airflow and holds the lung at a constant volume (FRC) 4. The patient is asked to pant gently against the shutter, causing pressure changes within the thoracic cavity, resulting in rarefaction (inspiratory efforts) and compression (expiratory efforts) of the air within the cavity (lungs) 5. Changes in the thoracic volume are recorded by changes in box pressure, these changes can be used to calculate TGV (FRC-pleth) 6. By relating changes in alveolar pressure (reflected by changes in mouth pressure), to changes in thoracic gas alveolar volume (reciprocal to changes in the box pressure during panting). TGV (FRC-pleth) can be calculated at the moment of occlusion (at the end of a normal breath- FRC)
112
During Body Plethysmography calibration...
a known volume is injected into the box resulting in an increase in box pressure, therefore, box pressure changes during the manoeuvre can be converted to volume changes own volume is injected into the box resulting in an increase in box pressure, therefore, box pressure changes during the manoeuvre can be converted to volume changes
113
Calculating lung volume subdivisions during body plethysmography:
FRC measured during the test. When FRC has been calculated, we calculate the other subdivisions of the lungs by asking the patient to fully inhale and exhale: ERV and VC measured at the end of the test
114
Errors in body Plethysmography:
the line should be straight errors can be caused by excessive force leading to hysteresis, excessive panting or box leakage
115
Reproducibility of body Plethysmography:
At least three FRCpleth values that are technically acceptable and agree within 5% (ie, the difference between the highest and lowest values divided by the mean is ≤5%) should be obtained and the mean value reported. If there is a larger deviation, additional values should be obtained until three values agree within 5% of their mean, and the mean value should be reported
116
Clinical use of body Plethysmography:
Calculating Lung Compliance = change in volume ÷ change in pressure
117
Lung compliance:
a measure of the lungs ability to stretch and expand. It is a measure of the dispensability of the elastic tissue. the measurement of lung compliance can be useful in determining the effects of a disease on the structure of the lung.
118
Reduced compliance =
stiff lungs (restrictive defect- pulmonary fibrosis)
119
Increased compliance =
floppy lungs (obstructive - emphysema)
120
Body Plethysmography: Obstructive lung disease
lungs are bigger = more air in lungs than there should be increased total lung capacity (TLC) but airways tighter = cannot expel air Increased functional residual capacity (FRC) - due to air trapping increased residual volume (RV) due to air trapping Reduced vital capacity (VC) - less air moved in and out of lungs lungs become floppy = increased compliance
121
Body Plethysmography: Restrictive lung disease
smaller lungs due to... intrinsic = stiff lungs that do not expand/contract properly extrinsic = crushing lungs due to overweight or scoliosis Reduced TLC, FRC, RV, VC Z score is lower than expected for all (-)
122
Whole body plethysmography vs other techniques
In patients with obstructive pulmonary disease, who may have gas trapping and hyperinflation, FRC measured by body plethysmography is usually higher than when measured using dilution or washout techniques. Gas trapping and hyperinflation in obstructive disease involves areas of the lung being unventilated, due to airway collapse. – gas isn’t going to disperse into areas that are collapsed = underestimated volumes Body plethysmography measures all gas in the thorax and will incorporate unventilated areas of the lung, whereas dilution and washout techniques can only measure areas of ventilated lung due to the measurement technique.
123
Respiratory muscle function tests:
Weakness of the respiratory muscles causes a restrictive ventilatory defect, with reduced TLC and VC. Comparison of VC when sitting upright and in a supine position allows assessment of the diaphragm strength – pressure of the abdominal contents on a weak diaphragm causes a fall of VC in the supine position by ~30%. Global respiratory muscle function can be assessed by measuring mouth pressures.
124
Restrictive lung disease definition:
pulmonary disorders defined by restrictive patterns on spirometry Characterised by a reduced distensibility of the lungs, compromising lung expansion and thus reduced lung volumes, particularly with reduced total lung capacity.
125
There are 2 types of restrictive lung disease:
Intrinsic = lung parenchymal involvement – e.g. interstitial lung disease Extrinsic = outside pressure reducing lung volume – obesity, neuromuscular disorders, chest wall deformities (scoliosis, kyphosis)
126
Those with a restrictive lung disease pattern can often have...
decreased lung volumes increased work of breathing inadequate ventilation Inadequate oxygenation. Spirometry shows a decrease in the forced vital capacity (FVC).
127
Interstitial lung disease definition
conditions affecting the lung interstitium (space between an alveolus and its surrounding capillaries). there is inflammation and fibrosis (scarring) in the lung interstitium.
128
Primary ILD:
unknown cause - Idiopathic pulmonary fibrosis - Interstitial pneumonia
129
Secondary ILD:
known cause - Connective tissue and autoimmune disease: Sarcoidosis, Rheumatoid arthritis - Infective: Mycoplasma pneumonia, Pneumocystis pneumonia - Environmental: Asbestosis, Silicosis - Drugs: Methotrexate, Amiodarone, Bleomycin
130
Risk factors for ILD include:
- Male sex - Cigarette smoking - Regular dust exposure (could be occupational)
131
the commonest type of ILD is...
idiopathic pulmonary fibrosis
132
Idiopathic pulmonary fibrosis:
Type of ILD characterised by fibrosis in the lung interstitium, which is irreversible.
133
How does Idiopathic pulmonary fibrosis occur:
Fibrosis is triggered by repeated injury to the lung tissue (e.g. from inhaled toxins). Usually, fibroblasts respond to this lung injury by secreting extracellular matrix, which repairs the injuries. In ILD, genetic mutations lead to excess secretion of extracellular matrix, which accumulates in the lung interstitium, leading to fibrosis. The lung interstitium becomes thicker, increasing the diffusion distance for oxygen to travel from the air in the alveoli to the blood in the surrounding capillaries. Hence, gas exchange in the lungs is compromised.
134
Typical symptoms of ILD include:
- Progressive exertional dyspnoea (usually presents slowly, over many weeks and months) - Dry cough - Connective tissue disease symptoms, such as arthralgia, difficulty swallowing and dry eyes - General malaise and fatigue (due to underlying connective tissue disease or vasculitis)
135
How to diagnose ILD:
Lung function tests: typically show a restrictive pattern (reduced FVC, reduced FEV1, normal ratio)
136
Medical management varies for each type of ILD:
- Idiopathic pulmonary fibrosis: antifibrotics - Connective tissue disease: corticosteroids
137
Some patients with ILD may benefit from LTOT...
Indications for long-term oxygen therapy: o Resting PaO2 ≤ 7.3kPa o Resting PaO2 ≤ 8.0kPa with peripheral oedema/polycythaemia/pulmonary hypertension
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ILD related complications
- Respiratory failure: due to failure of gas exchange in the lungs. - Pulmonary hypertension: due to chronic hypoxic pulmonary vasoconstriction (constriction of blood vessels supplying fibrotic areas of the lung, to direct blood to healthier areas of the lung).
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Chronic obstructive pulmonary disease (COPD) definition:
disease characterised by progressive, largely irreversible airflow obstruction = chronic bronchitis + emphysema
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Respiratory failure:
Occurs when the respiratory system fails to maintain gas exchange. Respiratory failure is classified according to blood gas abnormalities type 1 = low oxygen level type 2 = high carbon dioxide level
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Type 1 respiratory failure
hypoxemic = low oxygen level in blood paO2 <60mmHg with normal/below normal paCO2 Gas exchange is impaired at level of alveolo-capillary membrane Caused by lung damage that prevents adequate oxygenation of the blood (hypoxaemia), but remaining lung is still sufficient to excrete the carbon dioxide produced by tissue metabolism
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type 1 respiratory failure is characterised by (V/Q ratio) mismatch...
Ventilation (V) = air that reaches alveoli Prefusion (Q) = blood that reaches the alveoli mismatch causes hypoxemia
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Type 2 Respiratory failure
hypercapnic – too much CO2 in blood o PaCO2 >50mmHg o Low pO2 = Hypoxemia is common due to respiratory pump failure Alveolar ventilation is insufficient to excrete carbon dioxide produced = CO2 retention in lungs As lungs become less efficient, CO2 increases = chemoreceptors act to increase drive to breathe. Overtime, CO2 becomes too high.
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Causes of type 2 respiratory failure
The most common cause is COPD Airway obstruction (e.g. blockage of trachea by choking = underventilation) Respiratory muscle weakness (e.g. Guillain-Barre syndrome)) Central loss of drive (e.g. opiates – lead to loss of drive to breathe) Chronic lung disease (re-setting of central drive)
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causes of type 1 respiratory failure:
Occurs due to damage to lung tissue pulmonary oedema severe pneumonia COVID-19 acute respiratory distress syndrome (ARDS) emphysema
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type 2 respiratory failure can have complications:
damage to vital organs due to hypoxaemia central nervous system depression due to increased carbon dioxide levels respiratory acidosis (carbon dioxide retention) ultimately fatal unless treated
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Diagnosis of respiratory failure:
- Arterial blood gases- measures oxygen and carbon dioxide levels in the blood - Pulmonary function tests - identifies obstruction, restriction, and gas diffusion abnormalities.
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Management of respiratory failure:
Correction of Hypoxemia - The goal is to maintain adequate tissue oxygenation, generally achieved with an arterial oxygen tension (PaO2) of 60 mmHg or arterial oxygen saturation (SaO2) at about 90%. Un-controlled oxygen supplementation can result in oxygen toxicity and CO2 narcosis. Inspired oxygen concentration should be adjusted at the lowest level, which is sufficient for tissue oxygenation. Oxygen can be delivered by several routes depending on the clinical situations in which we may use a nasal cannula, simple face mask nonrebreathing mask, or high flow nasal cannula.
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In chronic COPD there is adaptation of central chemoreceptors to high CO2. What is the risk of giving oxygen?
Too high levels of oxygen, too quickly, results in death by hypercarbia – the drive to breathe has been taken away (peripheral chemoreceptors need time to adjust) = low levels (controlled oxygen) is required
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Bronchiectasis definition:
A type of obstructive lung disease. It is a chronic respiratory disease characterised by permanent bronchial dilation, due to irreversible damage to the bronchial wall.
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What causes bronchiectasis?
An initial insult to the bronchi (e.g. infection) results in immune cells being recruited. These immune cells secrete cytokines and proteases, leading to inflammation in the bronchi. Inflammation damages the muscle and elastin found in the bronchial walls, leading to bronchial dilation.
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In patients with bronchiectasis, several factors prevent the bronchial dilation from reversing ...
impaired muco-ciliary clearance and dysregulated immunity
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The bronchial dilation seen in bronchiectasis can cause...
Dilated bronchi are predisposed to persistent microbial colonisation, as mucus traps in the dilated bronchi. Blockage of the airways – if airway is occluded air cannot get down = alveoli are not going to be perfused = whole areas of lung cannot function.
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What does obstructive lung disease do to air resistance?
increases airway resistance in airways due to narrowing = increased work of breathing + patients are unable to fully expel air during exhalation
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Examples of obstructive lung disease:
asthma, chronic bronchitis, emphysema, obstructive sleep apnoea, bronchiectasis
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What does Restrictive lung disease do to compliance?
decrease in compliance of lungs = increasing amount of work needed to expand and contract lungs = Patients are unable to completely stretch the lungs to breathe in sufficient air = increased work of breathing
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Do restrictive or obstructive lung disease influence oxygen saturation?
Restrictive diseases effect all of lung parenchyma = cause reduced oxygen saturation unless obstruction is widespread, patients can continue to have normal or near-normal oxygen saturation
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Pulmonary causes of restrictive lung disease:
pulmonary fibrosis neonatal respiratory distress syndrome sarcoidosis Pneumoconiosis
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Examples of mixed lung disease:
Lung diseases often have elements of both restrictive and obstructive pathologies. The most common example of mixed lung disease is cystic fibrosis, where airways are narrowed and the lung parenchyma is stiffened.
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Typical spirometry findings in obstructive lung disease include:
Reduced FEV1 (<80% of the predicted normal) Reduced FVC (but to a lesser extent than FEV1) FEV1/FVC ratio reduced (<0.7)
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Non- pulmonary causes of restrictive lung disease:
Skeletal abnormalities (e.g. kyphoscoliosis), Neuromuscular diseases (e.g. motor neuron disease, myasthenia gravis, Guillan-Barre syndrome), Connective tissue diseases, Obesity or pregnancy.
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Typical spirometry findings in restrictive lung disease include:
Reduced FEV1 (<80% of the predicted normal) Reduced FVC (<80% of the predicted normal) FEV1/FVC ratio normal (>0.7)
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How to test if asthma is the cause of obstructive airway disease?
assess reversibility with a bronchodilator administer 400 micrograms of salbutamol and repeat spirometry after 15 minutes presence of reversibility is suggestive of a diagnosis of asthma absence of reversibility suggests COPD Partial reversibility may suggest a coexisting diagnosis of asthma and COPD
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Spirometry if FEV1/FVC is <70%
= obstructive FEV1 >80% = mild obstruction FEV1 50-80% = moderate obstruction FEV1 30-50% = severe obstruction FEV1 <30% = very severe obstruction
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Spirometry if FEV1/FVC is >70%
= normal or restrictive VC >85% = within normal limits VC 75-85% = borderline restriction VC <75% = probable restriction
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Lung compliance is a description of...
lung expandability (stretch)
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there are 2 factors of lung compliance...
elasticity from elastin surface tension which is decreased by surfactant
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decreased lung compliance =
more resistance = difficult to stretch + readily recoils stiff lung due to high elastic recoil thick balloon
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increased lung compliance =
less resistance = easily stretched + doesn't easily recoil plastic bag
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compliance =
change in volume / change in pressure
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Diseases characterised by reduced lung compliance:
Restrictive lung diseases (compromised lung expansion) * Intrinsic - Interstitial Lung Disease (ILD) - e.g. pulmonary fibrosis (scarring of lung tissue) * extrinsic - poor muscular effort (muscular dystrophy, Myasthenia Gravis, Guillain-Barre Syndrome) or structural limitation (scoliosis/obesity) Reduced surfactant = increased surface tension (e.g. neonatal/acute respiratory distress syndrome where fluid builds up in alveoli)
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emphysema and lung compliance:
degeneration of parenchyma = loss of alveoli elastic recoil harder for lungs to expand extra work required to exhale increased lung compliance
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pulmonary fibrosis and lung compliance:
scarring/hardening of lung tissue elastin replaced by collagen decreased stretch (stiff) decreased lung compliance increased work of breathing
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reduced surfactant =
reduced compliance
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FRC =
functional residual capacity volume of air in lungs at rest
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spirometry measures...
all lung volumes except residual volume FEV1 = forced expiratory volume in 1 sec FVC = forced vital capacity = volume of air forcibly exhaled after full inspiration VC = vital capacity = max air exhaled when blowing out as fast as possible PEF = peak expiratory flow = max flow exhaled when blowing out at steady rate
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FEV1/FVC ratio
allows identification of obstructive or restrictive ventilatory defects
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obstructive spirometry
FEV1/FVC <70% FEV1 is reduced more than FVC
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restrictive spirometry
FEV1/FVC >70% FVC reduced more than FVC
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hypercapnia =
Too much carbon dioxide (CO2) in the blood caused by hypoventilation of the body can eventually cause hypoxaemia due to reduced respiratory drive can conversely be caused by long term hypoxaemia = body tries to compensate = increased CO2 in the blood. This is known as type 2 respiratory failure.
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Type 2 respiratory failure
PaCO2 greater than 4.2kPa and PaO2 less than 8kPa caused by reduced respiratory drive common in advanced COPD patients due to: long term hypoxaemia or lack of gas exchange occurring in the alveoli thanks to poor tissue quality patient will present as drowsy and with low respiratory rate as a result of the increased CO2 in the brain
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Hypoxaemia
Abnormally low partial pressure of oxygen in the blood
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hypoxia
tissue oxygen delivery is inadequate to support normal the aerobic metabolism of the tissues
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COPD
emphysema + chronic bronchitis chronic inflammation from prolonged exposure to noxious particles or gases, most commonly cigarette smoke Chronic inflammation causes airway narrowing and decreased lung recoil
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how are lung volumes measured?
All except residual volume measured using spirometry Body plethysmography or helium dilution used to measure functional residual capacity (FRC) - this can be used to calculate residual volume (FRC-expiratory reserve volume)
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helium dilution
used to measure lung volumes 1) fixed amount of helium mix in reservoir 2) normal tidal breathing 3) at the end of a normal expiration (at FRC) shutter closed 4) patient begins to breath in helium mixture 5) helium moves into lungs until equilibrium is reached and helium level in resiovoir levels off Helium not absorbed across alveoil-capillary membrane = initial amount of helium is equal to final amount can calculate FRC measures volume of air in upper airway only (doesn't measure air in emphysema bullae)
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Nitrogen washout
1) patient breathes in 100% oxygen 2) exhales nitrogen containing gas initially left in lungs 3) measured over course of several minutes until nitrogen reduces to 0 initial nitrogen in lungs = total nitrogen exhaled can calculate FRC disadvantage = can cause oxygen retention in patients with severe COPD due to 100% oxygen overcoming pulmonary hypoxic vasoconstriction = worsening VQ mismatch
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respiratory failure =
respiratory system fails to maintain gas exchange classified by blood gas
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Type 1 respiratory failure:
hypoxemic (low oxygen in blood) paO2 <60mmHg normal paCO2 gas exchange is impaired at the level of the alveolar-capillary membrane Examples: pulmonary oedema, COVID, severe pneumonia
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Type 2 respiratory failure:
hypercapnic (high carbon dioxide in blood) paCO2 >50mmHg hypoxemia (tissue oxygen delivery is inadequate) caused by respiratory pump failure
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hypoxemia =
low partial pressure of oxygen in blood
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hypercapnia =
too much carbon dioxide in blood caused by co2 retention (failure to remove) can lead to hypoxemia due to reduced respiratory drive or can be caused by long-term hypoxemia (body compensates leading to increased co2 in blood
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Advanced COPD can lead to...
long term hypoxemia due to lack of gas exchange = retention of co2 = hypercapnia = type 2 respiratory failure
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V/Q ratio
ventilation/perfusion ratio per min air reaching alveoli/blood reaching alveoli via capillaries
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V/Q mismatch causes
hypoxemia
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type 1 respiratory failure occurs because of...
damage to lung tissue (pulmonary oedema, pneumonia, acute respiratory distress syndrome) damage prevents adequate oxygenation of blood = hypoxemia (<60mmHg) remaining lung is still sufficient to excrete carbon dioxide being produced by tissue metabolism = normal co2 level in blood
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type 2 respiratory failure occurs because of...
Pump failure = hypercapnia Decreased ventilatory effort or inability to overcome high resistance alveolar ventilation is insufficient to excrete co2 being produced = co2 retention lung is affected as a whole = co2 accumulates = respiratory acidosis
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complications of type 2 respiratory failure
damage to organs due to hypoxemia CNS depression due to hypercapnia fatal if not treated
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type 1 respiratory failure symptoms -
hypoxemia = dyspnea (SOB), confusion, cyanosis Body tries to accommodate = tachycardia, tachypnea
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Type 2 respiratory failure symtoms -
hypercapnia change in behaviour, headache, coma
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Evaluation of respiratory failure
arterial blood gases - measure o2 and co2 in blood renal (kidney) function liver function pulmonary function ECG chest radiography
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Management of respiratory failure
correction of hypoxemia - controlled o2 supplementation (uncontrolled = oxygen toxicity/co2 narcosis) ventilatory support - e.g. non-invasive positive pressure ventilation
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restrictive lung disease
compromised lung expansion decreased lung volumes (reduced TLC) increased work of breathing inadequate ventilation/oxygenation reduced FVC
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dyssomnias
hypersomnia or insomnia
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3 main types of dyssomnia
intrinsic = arising from within body (idiopathic insomnia, narcolepsy, OSA) extrinsic = secondary to environment (inadequate sleep hygiene, alcohol sleep disorder) circadian rhythm disruption (shift work, jet lag)
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insomina =
daily complaints of insufficient sleep or not feeling rested
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hypersomnia =
excessive sleepiness daytime sleep episodes
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narcolepsy =
sudden + uncontrolled sleep attacks
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4 symtoms of narcolepsy =
cataplexy = sudden bilateral loss of muscle tone usually after strong emotion sleep paralysis = aware of surroundings but unable to move hypnagogic hallucinations = sensations that feel real but are imagined automatic behaviour = doing things without thinking and not remembering
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thoracic gas volume =
measured at end of normal expiration = functional residual capacity (FRC) body plethysmography used to measure (panting against closed shutter)
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low KCO =
carbon monoxide transfer coefficient alveoli problem with reduced gas exchange COPD emphysema - destruction go alveoli Pulmonary fibrosis - scarring of alveoli
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HIgh KCO =
carbon monoxide transfer coefficient incomplete alveolar expansion with preserved gas exchange - extra-parenchymal restriction (scoliosis, chest wall deformity, neuromuscular) increased pulmonary blood floe from areas with low gas exchange to areas with better gas exchange (asthma)
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Two Process Model of Sleep:
1. Circadian rhythm (body clock) = 24 hour cycle, rhythmic, intrinsic process, Generated from the suprachiasmatic nucleus (SCN) of the hypothalamus- linked to retinol ganglion cells (responding to light entering the eye) 2. Homeostatic drive (sleep pressure) = Dependent on previous sleep quality/ duration, Pressure to sleep builds up the longer we are awake
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Sleep Homeostasis:
Circadian pacemaker is linked to light exposure The longer you are awake and alert with neuronal activation, there is a build-up of adenosine which causes an increased sleep need (homeostatic drive)
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Zeitberger =
= an environmental agent/event that provides the stimulus for a biological clock Most potent Zeitberger affecting sleep/wake is light. Without a Zeitberger (light) the clock runs at 25 hours naturally - can occur in blindness.
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Melatonin:
Hormone that causes sleepiness Produced by the Pineal gland Released/suppressed in response to light/dark = Important to seek light during the day and dim light in the evening Linked to photoreceptor in the eye that detect light intensity (Retinol ganglion cells) Blue light has the greatest power to switch off melatonin (high blue light levels in natural light and in LED light)
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Dark to light (sunrise)
Pineal gland switched off and Melatonin release is suppressed
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Light to dark (sunset)
Pineal gland switched on and Melatonin is released
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We sleep in cycles –
Each cycle lasts around 90 minutes: - Stage 1 sleep (5%) - Stage 2 sleep (50%) - Stage 3 (Delta) sleep = slow wave/deep sleep) (20%) - REM (rapid eye movement) sleep (25%)
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Non-REM sleep =
Stage 1-3 = voluntary muscle paralysis
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REM sleep =
hypotonia of skeletal muscles only diaphragm working ensures we don’t act out our dreams
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Polysomnography EEG
EEG during polysomnography investigations is used to stage sleep by monitoring electrical activity of the brain - Each stage of sleep exhibits different waveforms
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Epworth sleepiness scale
survey to score the chance of dozing when completing certain tasks
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Why should OSA be treated before other sleep disorders?
Obstructive sleep apnoea will exacerbate all other sleep problems and may be the primary cause
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Obstructive sleep apnoea =
Characterized by periodic narrowing and obstruction of the pharyngeal (upper) airway during sleep, despite ongoing effort to breathe Muscles relax during sleep- soft tissue at the back of the throat collapses and can block or partially obstruct the upper airway Leads to partial reductions (hypopnoea) and/or complete cessation (apnoea) of airflow that last at least 10 seconds Leads to reduction in blood oxygen levels and an increase in carbon dioxide levels The brain responds causing the patient to rouse = airway reopens There is an adrenaline response and a surge in heart rate as well as blood pressure surges
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Snoring =
partial obstruction of airway
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Screening for Obstructive Sleep Apnoea:
Familial history Epworth sleepiness score>10 Obesity (extra weight on throat) Snoring >40 years old Witnessed apnoea More common in males (due to deposition of fat) Restless sleep Crowded/narrow pharynx
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Pathophysiology of OSA:
The pharynx walls are susceptible to collapse Due to muscle relaxation during sleep, there is loss of the necessary contraction of the pharyngeal dilators leading to narrowing/collapse
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Pathway of OSA:
sleep = relaxation of muscles apart from diaphragm With OSA = pharynx collapses Impaired alveolar ventilation = hypoxaemia + hypercapnia arousal threshold reached = adrenergic response = increase in catecholamines = increase heart rate, contraction of smooth muscle, blood pressure surges pharynx reopens = blood gas levels return to open patient goes back to sleep
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OSA sleep investigation results:
Apnoea-hypopnoea index = >5 events per hour saw tooth dipping - following apnea spO2 slowly falls, then quickly returns to baseline as airflow restored Usually snore is observed Heart rate and blood pressure rises in response to each event Respiratory effort is maintained but there is a reduction in respiratory effort during events
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central sleep apnoea =
loss of respiratory effort
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Intermittent hypoxia results in...
activated inflammatory pathways, increasing risk of disease
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Episodic surgery in blood pressure during OS...
puts pressure on blood vessels = can lead to sustained hypertension
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OSA can lead to...
systemic hypertension increased inflammation and oxidative stress metabolic dysfunction insulin resistance/glucose dysregulation - poorly controlled diabetic weight gain hyper coagulability - atherosclerosis/ stroke endothelial dysfunction congestive heart failure/arrythmias
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Upper airway resistance syndrome sleep test results:
Apnoea hypopnoea index within normal range (<5 events per hours) Oxygen levels stay steady Snoring observed Significant heart rate variability throughout Flow limitation observed on trace (but flow not reduced enough to be marked as a hypopnoea- >30%) Can have similar clinical issues as OSA
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Treatment of OSA:
weight loss Continuous positive airway pressure (CPAP) therapy Mandibular Advancement Devices positional therapy tonsil reduction/tonsillectomy nasal surgery hypoglossal nerve stimulation
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Mandibular Advancement Devices
mouthguard that keeps airway open Mild-moderate OSA with a near to normal BMI Used for symptomatic snoring
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Hypoglossal Nerve Stimulation
Implanted in chest and connected to the nerve under the tongue - causes genioglossus muscle activation and decreases upper airway collapsibility Stimulation timed with breathing- during each inspiration the system delivers a signal to the hypoglossal nerve
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Neuromuscular Electrical Stimulation Therapy
Training of the upper airway dilator muscles using neuromuscular electrical stimulation Therapy consists of a series of pulse bursts
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Continuous positive airway pressure (CPAP) therapy
Gold standard in treating moderate/severe OSA – first line treatment Delivered pressurised air through a mask sealed over nose/mouth to splint the airway Works immediately, resolves apnoea's, desaturations and HR variability Side effects are minimal - dry mouth/nose, red marks on face, air leak = noise
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Obesity Hypoventilation Syndrome
combination of obesity (BMI> 30kg/m2) and daytime hypercapnia (PCO2 >45mmHg or >6kPa) Nocturnal alveolar hypoventilation Arises from a complex relationship between sleep disordered breathing, diminished respiratory drive and obesity-related respiratory impairment Increased risk of pulmonary hypertension and heart failure
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How do Obesity Hypoventilation Syndrome patients present?
Significantly obese Morning headaches Daytime sleepiness/morning grogginess May have peripheral oedema Polycythaemia (high red blood cells) Often have a degree of OSA sleep study = SpO2 staying low throughout the night- not returning to baseline An arterial blood gas will confirm type 2 respiratory failure
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Arterial Blood Gas:
Blood gas changes can be metabolic or respiratory in origin ABG’s are used to identify the presence of type 1 and 2 respiratory failure In health, we are driven to our next breath by the PaCO2, which is linked to pH Additional receptor (the hypoxic centre) in the brainstem monitors PaO2- spends most of the time ‘asleep’, unconcerned about minor fluctuations in oxygenation level
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Standard assessment to screen for daytime hypercapnia is...
hypercapnia = CO2 retention measurement of arterial blood gas (PaCO2)
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Obesity Hypoventilation Syndrome with OSA
NIV = Non-invasive ventilation Process of supporting ventilation with the aim to normalise blood gases Delivers two different pressures to assist or establish adequate ventilation
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Central Sleep Apnoea:
Drive to breath has been lost Apnoea’s occur with no respiratory effort O2 desaturation is slow No snoring (no narrowing at back of throat)
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Treatment for CSA:
Adaptive servo-ventilation (not safe in patients with HF) Treat the underlying cause of the condition: o Heroin/opioids o Heart failure o COPD o Brainstem dysfunction o Myotonic dystrophy o High altitude o Severe obesity
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Overlap Syndrome:
- OSA and COPD - Poorer outcomes - Pulmonary hypertension - CPAP needed
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Upper Airway Resistance Syndrome (UARS)
Respiratory Effort Related Arousals Increased upper airway resistance = Increased respiratory effort = Arousals occur results in excessive daytime sleepiness
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Obstructive Sleep Apnoea
Severe upper airway resistance Obstructive apnoea and hypopneas Sleep fragmentation Hypoxemic episodes – dips in O2 levels throughout night
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Central Sleep Apnoea
Repetitive absent respiratory efforts during sleep – drive to breathe is effected Open airway Sleep fragmentation Hypoxemic episodes
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NREM Parasomnias
o Cataphrenia o Night terrors o Sleep eating o Sleep walking
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REM Parasomnias
o REM behaviour disorder o Nightmares
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Insomnia
Problems getting to sleep Difficulty staying asleep through the night Common causes = Stress, Irregular sleep schedule, Poor sleeping habits, Mental health issues, Physical illnesses, Medications, Neurological problems
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Restless Legs Syndrome
Overwhelming urge to move the legs when they are at rest. These unpleasant sensations keep many people from falling asleep since they constantly want to move their legs.
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Periodic limb movement disorder
Repetitive movements in sleep, most typically in the lower limbs. Brief muscle twitches, jerking movements or an upward flexing of the feet.
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Narcolepsy
Cataplexy = Sudden loss of postural tone brought on by emotion e.g. Laughter Excessive sleepiness = not relieved by adequate sleep, persistent throughout day Sleep paralysis = Onset of sleep or on awakening Hypnagogic hallucinations = Dream imagery at onset or end of sleep
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Sleep studies
Respiratory Polygraphy = Pulse oximetry, Oronasal airflow, Chest and/or abdominal movements, Sound, Body position and movements Polysomnography = respiratory polygraphy + Sound, EEG, Tibial EMG
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Pulse Oximetry measures Oxygen Saturation and pulse rate:
Cessation of airflow (Apnoea) = arterial blood passing through the lungs picks up less oxygen = Reduction in levels of saturation (desaturation) Airflow returns to normal = Oxygen saturation returns to the original level.
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pulse oximetry measure pulse rate Increases in pulse rate are seen in subjects with –
with any arousals from sleep - Periodic Limb Movement Disorder - Sleep Related Breathing Disorders
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Normal sleep pulse oximetry
high and steady O2 levels low and steady heart rate
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OSA pulse oximetry
Dips in O2 levels throughout the night – airway collapses and then opens up again following arousal. blood pressure changes with pulse rate changes = increases risk of high blood pressure
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Upper airway resistance pulse oximetry
Resistance of upper airway that doesn’t restrict airway enough to reduce amount of O2 in lungs but causes arousal due to increased effort. Pulse rate rises and falls = patients sleep is disturbed.
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Neuromuscular disorder pulse oximetry
Good baseline of O2 saturation. Dips caused by muscle weakness – when patient goes into REM sleep (every 90min) muscles work at lower level making breathing harder.
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hypopnoea
reduced airflow
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apnoea
no airflow
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Sleep study OSA
upper airway collapses = portions of no airflow (slight dip in O2) but still effort throughout
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Sleep study CSA
central drive to breathe is interrupted = portions of no effort + no airflow
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Electroencephalogram (EEG)
Essential for sleep staging, identifying arousal Non polarisable silver electrodes stuck to head
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Electrooculogram (EOG)
Rapid eye movement sleep The potential between two electrodes placed 1cm above and 1 cm below outer canthus of R and L eye
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Submental EMG
The potential between two electrodes placed 2cm apart on the skin of chin . The chin (submental) muscle: - High activty when awake - Low activity when sleep (paralysis of skeletal muscles during REM sleep)
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awake EEG
alpha waves (regular pattern of 8-12Hz)
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stage 1 EEG
slow rolling eye movements positive occipital sharp transients of sleep central theta activity enhance beta activity attenuation of alpha rhythm
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stage 2 EEG
sleep spindles (short runs of rhythmical EEG waves of 12-16Hz) K complexes (duration 0.5s with well delineated sharp wave 12-14Hz)
277
stage 3 EEG
delta waves (slow EEG waves 1-2Hz)
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REM EEG
EEG looks like stage 1 rapid eye movement appears on EOG recording EMG = low amplitude (paralysis of skeletal muscles)
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What causes the change in thoracic volume during inspiration…
70% of volume change due to diaphragm 30% due to rib movements
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Compliance =
Change in volume ÷ change in pressure
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Lung compliance increases with
lung volume and lung recoil pressure
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Lung elastic recoil pressure or transpulmonary pressure =
the difference between the pressure inside the lungs (the alveolar pressure) and the pressure outside the lungs (the pleural pressure).
283
lung compliance in pulmonary fibrosis
An overproduction of collagen and scaring on the lungs = stiff small lungs = reduced compliance
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lung compliance in COPD/emphysema
The elastic recoil of the lungs is required to expire gases, thus even though floppy lungs will not be stiff and could indicate increased compliance, this lack of elasticity actually reduces compliance.
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Chemoreceptors:
chemical control of breathing Central Chemoreceptors = main ones located in the brain stem Peripheral (arterial) chemoreceptors = reserve/back up located in carotid & aortic bodies
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Central chemoreceptors
Respond to pH of cerebrospinal fluid CO2 diffuses across the blood-brain barrier and changes pF
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Peripheral chemoreceptors
Respond to low levels of oxygen Low levels of oxygen cause hypoxic drive to breath causing an increase in respiration. High levels of oxygen reduce hypoxic drive to breath so inspiration levels reduce.
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The normal range:
predicted value+/- 1.645 SD This includes 90% of the normal population. Values outside this range statistically likely to be abnormal
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Standard Residuals (z scores):
R = (observed – predicted)/SD A positive z score indicates a value higher than predicted, a negative z score indicates a value lower than predicted.
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Z-score positive =
higher than predicted
291
Z-score negative =
lower than predicted
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FEV1
reduced in obstructive reduced in restrictive
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FVC
Normal (may be slightly reduced) in obstructive reduced in restrictive
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FEV1/FVC ratio
reduced in obstructive Normal in restrictive
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Z score/SR: more negative than -1.645
obstructive
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Z score/SR: more positive than +1.645
restrictive
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Why use Z socre/SR
percent predicted can have the potential to over diagnose those older and underdiagnose those younger
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Crackly lungs =
Idiopathic pulmonary fibrosis (IPF)
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