What does a spirometer measure and how?
Changes in lung volume. Movements recorded as pt. breathes in and out through mouthpiece. Generally pt. asked to take deepest breath they can and exhale into sensor as hard as possible.
Explain the following and give rough amounts:
1. Tidal vol - vol breathed out (same as vol breathed in) - normal breathing. Rough amount of each breath = 0.5L
2. Inspiratory reserve vol - max vol of air inspired above TV, usually 2-3L
3. Expiratory reserve vol - max vol expired after TV, usually 1-1.5L
4. Vital capacity - total amount of air moved in 1 breath from full inspiration to full expiration (TV + IRV + ERV), usually 4-6L
What is RV? Give a value.
What is FRC? Give a value.
Which measurements can't be taken directly by a spirometer?
Residual volume - 1.2L. Volume remaining in lung after full exhalation.
Functional residual capacity: volume of air present in lungs after passive exhlation, 3L
RV, FRC, TLC (IRV + TV + ERV + RV)
What is normal breathing rate and amount?
What is minute ventilation? Give normal amount.
12 breaths/min, about 0.5L each breath
VI : volume of air passing into lungs per min, 6L/min
What is a vitalograph? How is it different from a spirometer?
How is the vitalograph used?
What is FEV1 an indirect measure of?
Used in lung function clinics and GPs to measure air flow (L/s), whereas spirometer measures lung volume
Ask pt. to breathe out as hard and fast as poss for as long as poss. Can get PEF (peak expiratory flow, L/min), FEV1 and FVC from graph.
FEV1: reflection of speed of lung emptying and thus an indirect measure of airflow
What is FER? What values are considered normal?
Give an example of restrictive lung disease - what would happen to the FER?
Give an example of obstructive lung disease - what would happen to the FER?
Forced expiratory ratio, FEVI/FVC, values above 70-80% = normal.
Loss of alveolar volume. FEVI is reduced in proportion to loss of lung volume so FVC also lower, so that the FEVI/FVC remain the same
Asthma. FEVI reduced to a greater extend than the FVC, so the FEVI/FVC ratio is reduced. (Indicative of obstructive lung disease)
What creates pressure differences during breathing?
What is the relationship between air flow and pressure?
What happens to pressure during inspiration and expiration?
Changes in lung volume from muscular breathing movements (due to respiratory muscles) and recoil of elastic tissues
Air only flows from region of high pressure to low pressure.
Inspiration: pressure around elastic alveoli lowered by expanding chest Expiration: pressure increased by decreasing size of chest and compressing gas in lungs
What 2 things expand and contract the lungs?
Which muscles increase volume of thoracic cavity during quiet inspiration?
1. diaphragm movement 2. rib elevation and depression
Diaphragm, external intercostals
What innervates the diaphragm?
What 2 types of movement do the external intercostal muscles cause during inspiration?
What are the accessory muscles of breathing?
What is dyspnoea?
Diaphragm innervated by phrenic nerves. NB: its contraction comprises 75% of energy expenditure during quiet breathing
1. pump-handle 2. bucket-handle
Scalene muscles, SCM, assist in elevating ribcage
Respiratory distress - a sign is use of accessory muscles while at rest
What muscles decrease volume of thoracic cavity during forced expiration?
Why might expiratory muscles contract actively?
Abdominal muscles - most imp. expiratory muscles
High levels of breathing, or if airways obstructed by disease
Explain how the 2 muscles of expiration work.
1. abdominal muscles - squeeze contens of abdomen up against diaphragm and force it up into chest, thereby expelling air.
2. Internal intercostal muscles - pull ribs down and in thus assisting in decreasing thoracic volume.
What is alveolar ventilation?
What is hypo or hyperventilation?
What is anatomical dead space? What is its normal value and thus what is the usable portion of a typical TV?
Portion of total ventilation that reaches alveoli and participates in GE.
Insufficient or excess alveolar ventilation, occurs in many lung diseases.
System of tubes connecting alveoli to atmosphere - volume of air in mouth, pharynx trachea, and bronchi up to terminal bronchioles. Around 150ml of any breath. so usable portion = 500-150 = 350ml
What is alveolar dead space? What causes it?
What is physiological dead space?
What can change the normal value of physiological dead space?
Dead space within alveoli which have insufficient blood supply to act as effective respiratory membranes. Caused by age, disease.
Anatomic dead space + alveolar dead space (NB: alveolar dead space usually v small (less than 5ml) so anatomical and physiological dead space are roughly the same = around 150ml)
Lung volume (age, sex, training), breathing pattern, and can increase dramatically in some lung diseases
What is the normal value for alveolar ventilation?
What happens to airflow if PA < Patm? If PA > Patm?
What law defines the relationship between expansion and gas flow? How does this relate to alveoli?
What creates pressure differences in the lungs?
4.2L/min (12x350 = 4200mL/min)
Airflows into lungs. Air flows out of lungs.
Boyles law (if vol of gas is increaed, the pressure exerted by the gas decreaes). Thus as alveoli forced to expland, pressure inside them decreases and gas flows in from conducting airways.
Changes in lung volume.
What 2 balanced things determine lung volume?
What is recoil pressure?
How are lungs inflated?
Elastic properties of lung and chest wall.
Characteristic of elasticity - if inflate e.g. balloon, the elastic recoil produces recoil pressure.
By pressure reduction (like a plunger in a syringe)
What "locks" the lungs and chest wall together?
What is intrapleural pressure?
Is it positive or negative?
Intrapleural fluid in intrapleural space. Intrapleural cohesive forces mean that as the chest wall expands during inspiration, the lung follows (expand as 1 unit).
At end of expiration, there is tension between lungs, whose elasticity is causing them to collapse and chest wall whose elasticity is causing it to spring outwards. This generates intrapleural pressure Ppl in the intrapleural space.
Lowering plunger (diaphragm) reduces pressure around balloon (intrapleural pressure) and generates inspiration.
Usually -ve wrt atm (and air pressure in aveoli which is connected to atm)
Describe the changes in intrapleural pressure during respiration.
What happens if the pleural cavity is damaged/ruptured and air enters pleural space (b/c Ppl
Normal at beginning of inspiration is slightly -ve.
Inspiration - chest cage expansion pulls outwards on lungs and Ppl becomes more -ve. Expiration - Ppl becomes less -ve.
Ppl becomes equal to or exceeds the atm pressure and the pressure surrounding the lungs increases and the lungs may collapse -> pneumothorax
What is compliance?
What is the formula for compliance?
How does compliance change with pressure?
List conditions which:
1. reduce compliance
2. increase compliance
Elasticity of lungs - ease at which lungs expand under pressure. Changed by most lung disease.
Compliance = Change in vol / Change in pressure
At high expanding pressure the lung is stiffer and compliance is smaller.
1. pulmonary fibrosis, collapse/closure of lung, increase in pulm venous pressure
2. age, emphysema
Explain the hysteresis seen in the volume vs pressure around lung graph.
What 2 things generate the elastic properties of the lungs?
Lung vol at any given pressure during inhalation is less than the lung vol at any given pressure during exhalation (red line).
Even without expanding pressure the lung always has some air in it, due to airway closure which traps gas in alveoli.
1. Elastic fibres and collagen
2. Surface tension forces caused by the alveolar-liquid interface
What forms the bulk of the CT in alveoli walls?
What is the difference between ease of inflation of an air-filler and fluid-filed lung?
Air filled - hysteresis = need greater pressure to reach particular lung vol when inflating it rather than when deflating. Elastic forces and surface tension work together. Not present in fluid-filled - no -air-fluid interface to easier to exapand lungs - only elastic forces working.
Explain surface tension elastic force.
How does Laplaces law apply to alveoli?
How do the lungs compensate with the problem of pressure differences from having alveoli of different sizes?
Inner surface of alveoli: water surface trying to contract b/c of surface tension = alveoli try to collapse (force air out) = generates elastic contractile force throughout lungs = STEF.
The smaller the alveoli, the greater internal pressure required to keep it inflated.
Surfactant greatly reduces surface tension of water = reduce STEF.
Describe the composition of surfactant.
Describe the creation of surfactant.
What is infant respiratory distress syndrome?
Complex mix of lipids and proteins. About 50% is DPPtdCho. Amphipathic character (hyydrophillic).
Assembley occurs in lamellar bodies of the Type II Pneumocytes -> secreted into alveolar fluid -> structural changes to become tubular myelin -> form surfactant layer at air-water interface.
Baby produces surfactant 24-28 weeks. If premature, may not have enough and lungs collapse.
Describe chest and lung wall pulling directions under equilibrium.
How does emphysema affect the lungs?
Chest wall pulls out and lungs pull in = balance.
Destruction of lung architecture including elastic fibres and collagen. Also impaired elastic recoil and lungs don't deflate as easily. Lung more easily distended and compliance increased.
Describe the effect of emphysema compared to fibrosis on lung compliance.
Can structural changes affect chest compliance?
Emphysema: same amount of pressure, easier to inflate
Fibrosis: same amount of pressure, harder to inflate
Yes - structural change of thorax e.g. kyphoscoliosis will affect compliance. However, usually LUNG compliance affected rather than CHEST compliance.
What is Raw?
What is asthma?
What are the 2 types of airway flow?
What is poiseuille's law as applied to the lungs?
Airway resistance - reisistance to gas flow within lung airways. Affected by asthma.
Reduction in airway diameter from swelling due to inflammation.
1. laminar (streamlined, orderly) 2. turbulant (chaotic). Normally LAMINAR
Small changes in the diameter of airways lead to relatively big changes in air flow.
Where are almost half of the sites of airway resistance?
Why does major resistance to air flow not occur in airways with smaller radius (like Poiseuille's law says)?
Where is the main site of airway resistance?
Upper respiratory tract (nose, pharynx, larynx). Reduced resistance when breathe through mouth.
B/c total cross-sectional area increases as you go down the tracheobronchial tree, so although diameter of each airway is small, there are a larger number of them.
Small bronchi and bronchioles (increase in number of airways not yet exerted its effects and cross-sectional area is relatively small)
NB: resistnce of small bronchi and bronchioles is variable and under influence of neuronal and hormonal factors e.g. asthma is a spasm of bronchial SM
Describe the parasympathetic and sympathetic autonomic control systems of bronchial smooth muscle tone.
What other factors contribute to brochomotor tone?
Parasympathetic (vagus) nerves: postganglionic fibres release ACh -> stimulates muscarinic receptors on SM = contraciton.
Sympathetic: due to circulating catecholamines (no sympathetic nervous input). Adrenaline activates beta-2 receptors.
- Non-adrenergic non cholinergic systems (NANC): inc. bronchodilators
- Mediator release e.g. histamine: neutrophils, eosinophils
- Rapidly adapting pulmonary receptors (irritant/cough receptors)
- Slowly adapting / stretch pulmonary receptors: reduces bronchomotor tone
-CO2: causes bronchodilation in underventilated areas where gas builds up
What 2 things do respiratory muscles work to overcome?
What is the formula for the work of breathing?
How efficient is repiration for metabolism?
1. resistance to airflow 2. elastic recoil of lungs
W = P . change in V
(P = gas at constant pressure)
Very - small fraction of metabolism needed but this changes in disease.