Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STP 1st year exams > Respiratory > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the upper respiratory tract consist of?

A

Nasal cavity

Pharynx

Larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the lower respiratory tract consist of?

A

Trachea

Bronchus

Lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The branching airways:

A

Trachea - bronchi - 2nd bronchi - bronchioles - alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Alveoli walls are composed of…

A

single layer of simple squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

There are 2 types of alveolus cells:

A

Larger type 1 cells

Smaller type 2 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does air get into lungs?

A

Boyles law

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Boyles law:

A

Increase volume – pressure decreases

Decrease volume – pressure increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Muscles involved in inspiration:

A

Diaphragm

External intercostals

Scalenes

Stemocleidomastoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Muscles involved in expiration:

A

Internal intercostals

Abdominal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ventilation =

A

Breathing = Moving air in and out of lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Factors Influencing Pulmonary Ventilation:

A
  • The resistance of the airways
  • The surface tension of the alveoli
  • The compliance of the lung tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Resistance =

A

force that opposes flow of air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The effect of resistance on the pulmonary system:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

In healthy patients, resistance…

A

…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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

reduced total airway diameter =

A

increased resistance to overcome in order to breathe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diseases that increase resistance:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Alveolar surface tension =

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Surfactant:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Anything that destroys surfactant…

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Compliance =

A

Measure of volume change with given change in transpulmonary pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Compliance is determined by…

A

tensile properties of lung tissue (how stiff the lungs are)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Effect of compliance on the pulmonary system:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Compliance of lungs is influenced by gravity:

A

o Apex is less compliant.
o Base is more compliant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Healthy lungs have higher compliance because of:

A

 Distensibility of lung tissue
 Reduced alveolar surface tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Reduced lung compliance appears in:

A

 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Too much lung compliance appears in:

A

 Pulmonary emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Indications For Performing Lung Function Tests:

A

Detect presence and severity of lung disease

Determine the effects of intervention

Assess preoperative risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Contraindications for lung function tests:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Things to avoid before respiratory tests:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Calibration of equipment is required to…

A

ensure accuracy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Lung volumes =

A

specific volumes of air contained by different portions of lungs at specific points in the respiratory cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Tidal volume (TV) =

A

volume of air inhaled or exhaled with each breath under resting conditions (during the respiratory cycle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Residual volume (RV) =

A

volume of air left in lungs after forced exhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Expiratory reserve volume (ERV) =

A

volume of air that can be forcefully exhaled after normal tidal volume exhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Inspiratory reserve volume (IRV) =

A

maximum volume of air that can be forcefully inhaled after normal tidal volume inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Lung capacities are…

A

a combination of 2 or more volumes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Total lung capacity (TLC) =

A

Maximum volume of air contained in lungs after maximum inspiration

tidal volume + residual volume + expiratory reserve volume + inspiratory reserve volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Vital capacity (VC) =

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Functional residual capacity (FRC) =

A

Volume of air remaining in lungs after tidal (normal) expiration

expiratory reserve volume + residual volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Inspiratory capacity (IC) =

A

Maximum volume of air that can be inspired after normal expiration (from the position of functional residual capacity)

tidal volume + inspiratory reserve volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Thoracic Gas Volume (TGV) =

A

Absolute volume of gas in the thorax at any point in time and at any alveolar pressure

(FRC-pleth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Dead space =

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Anatomical dead space =

A

air in airways that does not reach alveoli or respiratory bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Alveolar dead space =

A

air in alveoli that cannot be absorbed into bloodstream due to lung disease or blood flow limitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Minute ventilation =

A

Volume of air moved in and out of lungs per minute

breathing frequency expressed in breaths/minute × tidal volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Alveolar ventilation =

A

Volume of air reaching alveoli per minute and is available for gas exchange

breathing frequency expressed in breaths/minute - total dead space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

work of breathing =

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Measurements of residual volume and total lung capacity requires…

A

the use of helium dilution or plethysmography.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Helium dilution =

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Body plethysmography =

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Static lung volumes test =

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How are static lung volumes measured?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the procedure for body plethysmography?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Spirometry =

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Obstructive airways disorders examples…

A

chronic obstructive pulmonary disease

asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Restrictive diseases examples…

A

fibrotic lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Spirometry provides several important measures:

A

FEV1 = forced expiratory volume in 1 second

FVC = forced vital capacity

FEV1/FVC ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

FEV1 =

A

forced expiratory volume in 1 second

maximum volume of air forcefully expired in the first second after maximal inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

FVC =

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

FEV1/FVC ratio =

A

the ratio of FEV1 to FVC expressed as a percentage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Values of FEV1 and FVC are expressed as …

A

a percentage of the predicted normal for a person of the same sex, age and height

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How is spirometry done?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

The graph produced by spirometry is…

A

The expiratory volume-time graph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

The expiratory volume-time graph should …

A

be smooth and free from abnormalities caused by: Coughing during expiration, extra breath during expiration, slow start to forced expiration, sub-maximal effort.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Common errors of spirometry:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Spirometry criteria for acceptability:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Restrictive spirometry:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Obstructive spirometry:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Peak expiratory flow:

A

maximum rate of airflow that can be achieved during a sudden forced expiration after full inspiration

It gives an indication of diffuse airway obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How is peak expiratory flow measured?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Forced expiratory manoeuvres can be displayed by…

A

measuring peak expiratory flow or plotting flow against volume on a flow volume loop (provide same information)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Flow volume loops:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Flow volume loops can be used to assess …

A

narrowing of the airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

When recording a flow volume loop the patient is asked…

A

1) take a full inspiration
2) maximal forced expiration
3)maximal forced inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is measured by a flow volume loop?

A
  • PEF = peak expiratory flow
  • RV = residual volume
  • PIF = peak inspiratory flow
  • FEF = forced expiratory flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Pressure difference across resistance is directly proportional to…

A

…the flow of gas. The flow signal is integrated to derive volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Obstructive flow volume loop:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Restrictive flow volume loop:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Gas trasfer =

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What gas is used to measure gas transfer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What measurements are taken during gas transfer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Gas transfer calculation:

A

Carbon Monoxide Transfer Factor (TLCO) = Total ability of lungs to transfer gas across into bloodstream

Calculated by multiplying the Transfer Coefficient (KCO) X VA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Why is it difficult to measure the transfer of oxygen?

A

transfer of oxygen into the blood quickly becomes limited by the saturation of haemoglobin = carbon monoxide used to measure gas transfer instead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

To measure diffusion capacity/transfer factor (DLCO/ TLCO) we need to know:

A

The amount of carbon monoxide (CO) transferred per minute

The pressure gradient across the alveolar membrane (alveolar partial pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Single-breath method to measure gas transfer:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Why hold breath fro 10 seconds during gas transfer measurement?

A

because CO (carbon monoxide) and CH4 (methane) have to have time to get to alveoli where gas exchange takes place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Tracer Gas:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Why Carbon Monoxide for gas transgfer tests?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Reproducibility of gas transfer test:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Causes of decreased DLCO and/or KCO:

A

COPD, Pulmonary fibrosis, Pulmonary vascular disease, Renal failure, Cardiac failure, Mitral valve disease, Cirrhosis, Collagen diseases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Causes of increased DLCO and/or KCO =

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Gas transfer in emphysema (obstructive):

A

alveoli destruction and distention

TLCO ↓
KCO ↓
Diffusion distance ↑
SA for gas exchange ↓ = gas exchange reduces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Gas transfer in asthma (obstructive):

A

TLCO ↓ (but can be ↑)
KCO tends to be ↑
Reason not known
Hyperaemia of airways
Greater perfusion of lung apices in asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Gas transfer in intra-pulmonary disease (restrictive):

A

e.g. Fibrosis

fibrotic tissue makes it hard for gas exchange = TLCO ↓ KCO ↓

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Gas transfer in extra-pulmonary disease (restrictive):

A

e.g. Muscle weakness, scoliosis, pleural disease

underinflated lungs = less air into them = TLCO ↓ KCO ↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Boyle’s Law:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Using Boyle’s Law in Body phethysmography:

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

During Body Plethysmography calibration…

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Calculating lung volume subdivisions during body plethysmography:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Errors in body Plethysmography:

A

the line should be straight

errors can be caused by excessive force leading to hysteresis, excessive panting or box leakage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Reproducibility of body Plethysmography:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Clinical use of body Plethysmography:

A

Calculating Lung Compliance = change in volume ÷ change in pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Lung compliance:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Reduced compliance =

A

stiff lungs (restrictive defect- pulmonary fibrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Increased compliance =

A

floppy lungs (obstructive - emphysema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Body Plethysmography: Obstructive lung disease

A

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
Q

Body Plethysmography: Restrictive lung disease

A

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
Q

Whole body plethysmography vs other techniques

A

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
Q

Respiratory muscle function tests:

A

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
Q

Restrictive lung disease definition:

A

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
Q

There are 2 types of restrictive lung disease:

A

Intrinsic = lung parenchymal involvement – e.g. interstitial lung disease

Extrinsic = outside pressure reducing lung volume – obesity, neuromuscular disorders, chest wall deformities (scoliosis, kyphosis)

126
Q

Those with a restrictive lung disease pattern can often have…

A

decreased lung volumes

increased work of breathing

inadequate ventilation

Inadequate oxygenation.

Spirometry shows a decrease in the forced vital capacity (FVC).

127
Q

Interstitial lung disease definition

A

conditions affecting the lung interstitium (space between an alveolus and its surrounding capillaries).

there is inflammation and fibrosis (scarring) in the lung interstitium.

128
Q

Primary ILD:

A

unknown cause

  • Idiopathic pulmonary fibrosis
  • Interstitial pneumonia
129
Q

Secondary ILD:

A

known cause

  • Connective tissue and autoimmune disease: Sarcoidosis, Rheumatoid arthritis
  • Infective: Mycoplasma pneumonia, Pneumocystis pneumonia
  • Environmental: Asbestosis, Silicosis
  • Drugs: Methotrexate, Amiodarone, Bleomycin
130
Q

Risk factors for ILD include:

A
  • Male sex
  • Cigarette smoking
  • Regular dust exposure (could be occupational)
131
Q

the commonest type of ILD is…

A

idiopathic pulmonary fibrosis

132
Q

Idiopathic pulmonary fibrosis:

A

Type of ILD

characterised by fibrosis in the lung interstitium, which is irreversible.

133
Q

How does Idiopathic pulmonary fibrosis occur:

A

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
Q

Typical symptoms of ILD include:

A
  • 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
Q

How to diagnose ILD:

A

Lung function tests: typically show a restrictive pattern (reduced FVC, reduced FEV1, normal ratio)

136
Q

Medical management varies for each type of ILD:

A
  • Idiopathic pulmonary fibrosis: antifibrotics
  • Connective tissue disease: corticosteroids
137
Q

Some patients with ILD may benefit from LTOT…

A

Indications for long-term oxygen therapy:
o Resting PaO2 ≤ 7.3kPa
o Resting PaO2 ≤ 8.0kPa with peripheral oedema/polycythaemia/pulmonary hypertension

138
Q

ILD related complications

A
  • 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).
139
Q

Chronic obstructive pulmonary disease (COPD) definition:

A

disease characterised by progressive, largely irreversible airflow obstruction = chronic bronchitis + emphysema

140
Q

Respiratory failure:

A

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

141
Q

Type 1 respiratory failure

A

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

142
Q

type 1 respiratory failure is characterised by (V/Q ratio) mismatch…

A

Ventilation (V) = air that reaches alveoli
Prefusion (Q) = blood that reaches the alveoli

mismatch causes hypoxemia

143
Q

Type 2 Respiratory failure

A

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.

144
Q

Causes of type 2 respiratory failure

A

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)

145
Q

causes of type 1 respiratory failure:

A

Occurs due to damage to lung tissue

pulmonary oedema

severe pneumonia

COVID-19

acute respiratory distress syndrome (ARDS)

emphysema

146
Q

type 2 respiratory failure can have complications:

A

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

147
Q

Diagnosis of respiratory failure:

A
  • Arterial blood gases- measures oxygen and carbon dioxide levels in the blood
  • Pulmonary function tests - identifies obstruction, restriction, and gas diffusion abnormalities.
148
Q

Management of respiratory failure:

A

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.

149
Q

In chronic COPD there is adaptation of central chemoreceptors to high CO2.
What is the risk of giving oxygen?

A

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

150
Q

Bronchiectasis definition:

A

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.

151
Q

What causes bronchiectasis?

A

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.

152
Q

In patients with bronchiectasis, several factors prevent the bronchial dilation from reversing …

A

impaired muco-ciliary clearance and dysregulated immunity

153
Q

The bronchial dilation seen in bronchiectasis can cause…

A

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.

154
Q

What does obstructive lung disease do to air resistance?

A

increases airway resistance in airways due to narrowing = increased work of breathing + patients are unable to fully expel air during exhalation

155
Q

Examples of obstructive lung disease:

A

asthma, chronic bronchitis, emphysema, obstructive sleep apnoea, bronchiectasis

156
Q

What does Restrictive lung disease do to compliance?

A

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

157
Q

Do restrictive or obstructive lung disease influence oxygen saturation?

A

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

158
Q

Pulmonary causes of restrictive lung disease:

A

pulmonary fibrosis

neonatal respiratory distress syndrome

sarcoidosis

Pneumoconiosis

159
Q

Examples of mixed lung disease:

A

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.

160
Q

Typical spirometry findings in obstructive lung disease include:

A

Reduced FEV1 (<80% of the predicted normal)

Reduced FVC (but to a lesser extent than FEV1)

FEV1/FVC ratio reduced (<0.7)

161
Q

Non- pulmonary causes of restrictive lung disease:

A

Skeletal abnormalities (e.g. kyphoscoliosis), Neuromuscular diseases (e.g. motor neuron disease, myasthenia gravis, Guillan-Barre syndrome), Connective tissue diseases, Obesity or pregnancy.

162
Q

Typical spirometry findings in restrictive lung disease include:

A

Reduced FEV1 (<80% of the predicted normal)

Reduced FVC (<80% of the predicted normal)

FEV1/FVC ratio normal (>0.7)

163
Q

How to test if asthma is the cause of obstructive airway disease?

A

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

164
Q

Spirometry if FEV1/FVC is <70%

A

= obstructive

FEV1 >80% = mild obstruction
FEV1 50-80% = moderate obstruction
FEV1 30-50% = severe obstruction
FEV1 <30% = very severe obstruction

165
Q

Spirometry if FEV1/FVC is >70%

A

= normal or restrictive

VC >85% = within normal limits
VC 75-85% = borderline restriction
VC <75% = probable restriction

166
Q

Lung compliance is a description of…

A

lung expandability (stretch)

167
Q

there are 2 factors of lung compliance…

A

elasticity from elastin

surface tension which is decreased by surfactant

168
Q

decreased lung compliance =

A

more resistance = difficult to stretch + readily recoils

stiff lung due to high elastic recoil

thick balloon

169
Q

increased lung compliance =

A

less resistance = easily stretched + doesn’t easily recoil

plastic bag

170
Q

compliance =

A

change in volume / change in pressure

171
Q

Diseases characterised by reduced lung compliance:

A

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)

172
Q

emphysema and lung compliance:

A

degeneration of parenchyma = loss of alveoli elastic recoil

harder for lungs to expand

extra work required to exhale

increased lung compliance

173
Q

pulmonary fibrosis and lung compliance:

A

scarring/hardening of lung tissue

elastin replaced by collagen

decreased stretch (stiff)

decreased lung compliance

increased work of breathing

174
Q

reduced surfactant =

A

reduced compliance

175
Q

FRC =

A

functional residual capacity

volume of air in lungs at rest

176
Q

spirometry measures…

A

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

177
Q

FEV1/FVC ratio

A

allows identification of obstructive or restrictive ventilatory defects

178
Q

obstructive spirometry

A

FEV1/FVC <70%

FEV1 is reduced more than FVC

179
Q

restrictive spirometry

A

FEV1/FVC >70%

FVC reduced more than FVC

180
Q

hypercapnia =

A

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.

181
Q

Type 2 respiratory failure

A

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

182
Q

Hypoxaemia

A

Abnormally low partial pressure of oxygen in the blood

183
Q

hypoxia

A

tissue oxygen delivery is inadequate to support normal the aerobic metabolism of the tissues

184
Q

COPD

A

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

185
Q

how are lung volumes measured?

A

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)

186
Q

helium dilution

A

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)

187
Q

Nitrogen washout

A

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

188
Q

respiratory failure =

A

respiratory system fails to maintain gas exchange

classified by blood gas

189
Q

Type 1 respiratory failure:

A

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

190
Q

Type 2 respiratory failure:

A

hypercapnic (high carbon dioxide in blood)

paCO2 >50mmHg

hypoxemia (tissue oxygen delivery is inadequate)

caused by respiratory pump failure

191
Q

hypoxemia =

A

low partial pressure of oxygen in blood

192
Q

hypercapnia =

A

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

193
Q

Advanced COPD can lead to…

A

long term hypoxemia due to lack of gas exchange = retention of co2 = hypercapnia = type 2 respiratory failure

194
Q

V/Q ratio

A

ventilation/perfusion ratio per min

air reaching alveoli/blood reaching alveoli via capillaries

195
Q

V/Q mismatch causes

A

hypoxemia

196
Q

type 1 respiratory failure occurs because of…

A

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

197
Q

type 2 respiratory failure occurs because of…

A

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

198
Q

complications of type 2 respiratory failure

A

damage to organs due to hypoxemia

CNS depression due to hypercapnia

fatal if not treated

199
Q

type 1 respiratory failure symptoms -

A

hypoxemia = dyspnea (SOB), confusion, cyanosis

Body tries to accommodate = tachycardia, tachypnea

200
Q

Type 2 respiratory failure symtoms -

A

hypercapnia

change in behaviour, headache, coma

201
Q

Evaluation of respiratory failure

A

arterial blood gases - measure o2 and co2 in blood
renal (kidney) function
liver function
pulmonary function
ECG
chest radiography

202
Q

Management of respiratory failure

A

correction of hypoxemia - controlled o2 supplementation (uncontrolled = oxygen toxicity/co2 narcosis)

ventilatory support - e.g. non-invasive positive pressure ventilation

203
Q

restrictive lung disease

A

compromised lung expansion
decreased lung volumes (reduced TLC)
increased work of breathing
inadequate ventilation/oxygenation
reduced FVC

204
Q

dyssomnias

A

hypersomnia or insomnia

205
Q

3 main types of dyssomnia

A

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)

206
Q

insomina =

A

daily complaints of insufficient sleep or not feeling rested

207
Q

hypersomnia =

A

excessive sleepiness
daytime sleep episodes

208
Q

narcolepsy =

A

sudden + uncontrolled sleep attacks

209
Q

4 symtoms of narcolepsy =

A

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

210
Q

thoracic gas volume =

A

measured at end of normal expiration = functional residual capacity (FRC)

body plethysmography used to measure (panting against closed shutter)

211
Q

low KCO =

A

carbon monoxide transfer coefficient

alveoli problem with reduced gas exchange

COPD emphysema - destruction go alveoli
Pulmonary fibrosis - scarring of alveoli

212
Q

HIgh KCO =

A

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)

213
Q

Two Process Model of Sleep:

A
  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
214
Q

Sleep Homeostasis:

A

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)

215
Q

Zeitberger =

A

= 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.

216
Q

Melatonin:

A

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)

217
Q

Dark to light (sunrise)

A

Pineal gland switched off and Melatonin release is suppressed

218
Q

Light to dark (sunset)

A

Pineal gland switched on and Melatonin is released

219
Q

We sleep in cycles –

A

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%)
220
Q

Non-REM sleep =

A

Stage 1-3 = voluntary muscle paralysis

221
Q

REM sleep =

A

hypotonia of skeletal muscles

only diaphragm working

ensures we don’t act out our dreams

222
Q

Polysomnography EEG

A

EEG during polysomnography investigations is used to stage sleep by monitoring electrical activity of the brain - Each stage of sleep exhibits different waveforms

223
Q

Epworth sleepiness scale

A

survey to score the chance of dozing when completing certain tasks

224
Q

Why should OSA be treated before other sleep disorders?

A

Obstructive sleep apnoea will exacerbate all other sleep problems and may be the primary cause

225
Q

Obstructive sleep apnoea =

A

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

226
Q

Snoring =

A

partial obstruction of airway

227
Q

Screening for Obstructive Sleep Apnoea:

A

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

228
Q

Pathophysiology of OSA:

A

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

229
Q

Pathway of OSA:

A

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

230
Q

OSA sleep investigation results:

A

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

231
Q

central sleep apnoea =

A

loss of respiratory effort

232
Q

Intermittent hypoxia results in…

A

activated inflammatory pathways, increasing risk of disease

233
Q

Episodic surgery in blood pressure during OS…

A

puts pressure on blood vessels = can lead to sustained hypertension

234
Q

OSA can lead to…

A

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

235
Q

Upper airway resistance syndrome sleep test results:

A

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

236
Q

Treatment of OSA:

A

weight loss

Continuous positive airway pressure (CPAP) therapy

Mandibular Advancement Devices

positional therapy

tonsil reduction/tonsillectomy

nasal surgery

hypoglossal nerve stimulation

237
Q

Mandibular Advancement Devices

A

mouthguard that keeps airway open

Mild-moderate OSA with a near to normal BMI

Used for symptomatic snoring

238
Q

Hypoglossal Nerve Stimulation

A

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

239
Q

Neuromuscular Electrical Stimulation Therapy

A

Training of the upper airway dilator muscles using neuromuscular electrical stimulation

Therapy consists of a series of pulse bursts

240
Q

Continuous positive airway pressure (CPAP) therapy

A

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

241
Q

Obesity Hypoventilation Syndrome

A

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

242
Q

How do Obesity Hypoventilation Syndrome patients present?

A

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

243
Q

Arterial Blood Gas:

A

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

244
Q

Standard assessment to screen for daytime hypercapnia is…

A

hypercapnia = CO2 retention

measurement of arterial blood gas (PaCO2)

245
Q

Obesity Hypoventilation Syndrome with OSA

A

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

246
Q

Central Sleep Apnoea:

A

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)

247
Q

Treatment for CSA:

A

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

248
Q

Overlap Syndrome:

A
  • OSA and COPD
  • Poorer outcomes
  • Pulmonary hypertension
  • CPAP needed
249
Q

Upper Airway Resistance Syndrome (UARS)

A

Respiratory Effort Related Arousals

Increased upper airway resistance = Increased respiratory effort = Arousals occur

results in excessive daytime sleepiness

250
Q

Obstructive Sleep Apnoea

A

Severe upper airway resistance

Obstructive apnoea and hypopneas

Sleep fragmentation

Hypoxemic episodes – dips in O2 levels throughout night

251
Q

Central Sleep Apnoea

A

Repetitive absent respiratory efforts during sleep – drive to breathe is effected

Open airway

Sleep fragmentation

Hypoxemic episodes

252
Q

NREM Parasomnias

A

o Cataphrenia
o Night terrors
o Sleep eating
o Sleep walking

253
Q

REM Parasomnias

A

o REM behaviour disorder
o Nightmares

254
Q

Insomnia

A

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

255
Q

Restless Legs Syndrome

A

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.

256
Q

Periodic limb movement disorder

A

Repetitive movements in sleep, most typically in the lower limbs.

Brief muscle twitches, jerking movements or an upward flexing of the feet.

257
Q

Narcolepsy

A

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

258
Q

Sleep studies

A

Respiratory Polygraphy = Pulse oximetry, Oronasal airflow, Chest and/or abdominal movements, Sound, Body position and movements

Polysomnography = respiratory polygraphy + Sound, EEG, Tibial EMG

259
Q

Pulse Oximetry measures Oxygen Saturation and pulse rate:

A

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.

260
Q

pulse oximetry measure pulse rate

Increases in pulse rate are seen in subjects with –

A

with any arousals from sleep

  • Periodic Limb Movement Disorder
  • Sleep Related Breathing Disorders
261
Q

Normal sleep pulse oximetry

A

high and steady O2 levels

low and steady heart rate

262
Q

OSA pulse oximetry

A

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

263
Q
A
264
Q
A
265
Q

Upper airway resistance pulse oximetry

A

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.

266
Q

Neuromuscular disorder pulse oximetry

A

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.

267
Q

hypopnoea

A

reduced airflow

268
Q

apnoea

A

no airflow

269
Q

Sleep study OSA

A

upper airway collapses = portions of no airflow (slight dip in O2)

but still effort throughout

270
Q

Sleep study CSA

A

central drive to breathe is interrupted = portions of no effort + no airflow

271
Q

Electroencephalogram (EEG)

A

Essential for sleep staging, identifying arousal

Non polarisable silver electrodes stuck to head

272
Q

Electrooculogram (EOG)

A

Rapid eye movement sleep

The potential between two electrodes placed 1cm above and 1 cm below outer canthus of R and L eye

273
Q

Submental EMG

A

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)

274
Q

awake EEG

A

alpha waves (regular pattern of 8-12Hz)

275
Q

stage 1 EEG

A

slow rolling eye movements

positive occipital sharp transients of sleep

central theta activity

enhance beta activity

attenuation of alpha rhythm

276
Q

stage 2 EEG

A

sleep spindles (short runs of rhythmical EEG waves of 12-16Hz)

K complexes (duration 0.5s with well delineated sharp wave 12-14Hz)

277
Q

stage 3 EEG

A

delta waves (slow EEG waves 1-2Hz)

278
Q

REM EEG

A

EEG looks like stage 1

rapid eye movement appears on EOG recording

EMG = low amplitude (paralysis of skeletal muscles)

279
Q

What causes the change in thoracic volume during inspiration…

A

70% of volume change due to diaphragm

30% due to rib movements

280
Q

Compliance =

A

Change in volume ÷ change in pressure

281
Q

Lung compliance increases with

A

lung volume and lung recoil pressure

282
Q

Lung elastic recoil pressure or transpulmonary pressure =

A

the difference between the pressure inside the lungs (the alveolar pressure) and the pressure outside the lungs (the pleural pressure).

283
Q

lung compliance in pulmonary fibrosis

A

An overproduction of collagen and scaring on the lungs = stiff small lungs = reduced compliance

284
Q

lung compliance in COPD/emphysema

A

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.

285
Q

Chemoreceptors:

A

chemical control of breathing

Central Chemoreceptors = main ones located in the brain stem

Peripheral (arterial) chemoreceptors = reserve/back up located in carotid & aortic bodies

286
Q

Central chemoreceptors

A

Respond to pH of cerebrospinal fluid

CO2 diffuses across the blood-brain barrier and changes pF

287
Q

Peripheral chemoreceptors

A

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.

288
Q

The normal range:

A

predicted value+/- 1.645 SD

This includes 90% of the normal population. Values outside this range statistically likely to be abnormal

289
Q

Standard Residuals (z scores):

A

R = (observed – predicted)/SD

A positive z score indicates a value higher than predicted, a negative z score indicates a value lower than predicted.

290
Q

Z-score positive =

A

higher than predicted

291
Q

Z-score negative =

A

lower than predicted

292
Q

FEV1

A

reduced in obstructive

reduced in restrictive

293
Q

FVC

A

Normal (may be slightly reduced) in obstructive

reduced in restrictive

294
Q

FEV1/FVC ratio

A

reduced in obstructive

Normal in restrictive

295
Q

Z score/SR: more negative than -1.645

A

obstructive

296
Q

Z score/SR: more positive than +1.645

A

restrictive

297
Q

Why use Z socre/SR

A

percent predicted can have the potential to over diagnose those older and underdiagnose those younger

298
Q

Crackly lungs =

A

Idiopathic pulmonary fibrosis (IPF)

299
Q
A

STP 1st year exams (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions