S1 L2 Clinical Application in Ventilation and Lung Mechanics Flashcards
- *Quick overview: Quickly describe each of the flowing -**
- Atelectasis
- Interstitial lung disease
- Hypoventilation
- Pneumothorax
- Obstructive lung disease (COPD and Asthma)
- Respiratory Distress syndrome
ATELECTASIS – complete or partial lung collapse – several causes INTERSTITIAL LUNG DISEASE - Lung expansion difficult secondary to stiff lungs from increased collagen in alveolar walls – decreased compliance/increased elastic recoil
HYPOVENTILATION - Inability to expand chest and ventilate - many causes
PNEUMOTHORAX - Air in the intrapleural space with loss of pleural seal OBSTRUCTIVE LUNG DISEASE (COPD&ASTHMA)- ↑airways resistance and, in emphysema decreased elastance/elastic recoil secondary to loss elastic fibres – compliance increased but elastic recoil decreased
RESPIRATORY DISTRESS SYNDROME – NEW BORN - ↓ surfactant leads to increased surface tension and decreased compliance
Structure of a bronchus compared to the structure of a bronchiole?
How do bronchioles keep open?
Structure of a bronchus compared to the structure of a bronchiole?
Bronchiole - No cartilage in bronchiole
Bronchus - Cartilage keep bronchus open
Bronchioles stay open due to: Radial traction
• Due to Radial traction (outward tugging action) of the surrounding alveolar walls on bronchioles
• Prevents collapse of bronchioles during expiration
• Why would bronchioles collapse during expiration?
- *Clinical correlates: Chronic Obstructive Lung Disease (COPD)**
- What is this?
- Main cause
- Overdiagnosed? Underdiagnosed?
What is it?
Clinical syndrome characterised by chronic respiratory symptoms with associated pulmonary abnormalities – all conditions share impaired airflow that is not fully reversible – classic definition encompasses two medical conditions:
– Chronic bronchitis
– Emphysema
– Above two conditions co-exist
Cause:
Primarily caused by smoking and/or inhaled pollutants interacting with genetic vulnerability
COPD greatly underdiagnosed – considered disease of the older adult but may start in people in their 30’s though typical age presentation 60’s -
Should be recognised earlier! Earlier interventions slow lung function decline
- *Clinical correlates: Chronic bronchitis**
- type of disease
- What happens in this disease to cause symptoms?
- Effects of these, lead to…
Type of disease:
Chronic bronchitis is a disease of the small airways
- *What happens in this disease to cause symptoms:** (inflammation, reduced cilia, mucous production increase, less surfactant)
- Inflammation in the smaller bronchi and bronchioles - airways chronically inflammed
- Mucous hypersecretion (from goblet cell hyperplasia & sub mucousal glands)
- Reduced cilia and impaired function – mucous is not cleared effectively - narrows airways
- Epithelial remodelling - also narrows airwayS
- Loss of small airways (remember watering can? Fewer holes! Less flow) - Increased airway surface tension - fewer clara cells (less surfactant-like material in airways)
Effects of above lead to:
– Increased air flow resistance– worse on expiration
– Alteration of airway surface tension(increased) predisposing to small airway collapse - worse on expiration
- *Clinical correlates: Emphysema**
- Type of disease
- Causes
- Process (flow diagram) of what happens
- Talk about elastic recoil and compliance
- Effect on radial traction
- Signs and Symptoms
- Microscopic images of alveoli
Type of disease:
Air sacs disease/lung parenchyma
Causes:
smoking, alpha-1 anti trypsin (this is an anti-proteinase, leads to the desruction of elastin)
- *What happens:**
- Abnormal, permanent enlargement of the air spaces distal to the terminal bronchiole
- With destruction of alveolar walls (No fibrosis) –>
- Inflammatory cells accumulate –>
- which release elastases and oxidants that destroy alveolar walls and elastin
Reduced elastic recoil is a key problem:
Lack of elastic tissue means the lungs are easier to expand ->
Increase compliance ->
Reduced elastic recoil ->
Leaves lungs hyperinflated
Also surface area is reduced, so gas exchange is less efficient
Radial traction:
Reduced radial traction in the small airway
- *Signs and Symptoms:**
- Reduced exercise tolerance
- SOB
- Barrel chest
- *Clinical correlates: Emphysema**
- What is Barrel chest?
- Which does it happen?
Air trapping and descreased elastic recoil
Increased air flattends diaphragm (due to hyperinflation) as compliance has increased and elastic recoil has reduced ->
can’t contract as effectively ->
Impaired inspiration ->
Less room for new air with more oxygen and less CO2
- *Airway obstruction in COPD**
- Cause of airway obstruction in chronic bronchitis
- Cause of airway obstruction in emphysema
Cause of airway obstruction in chronic bronchitis:
Small airways narrowed through thickening of the bronchiolar periphery wall by inflammation and fixed narrowing as a result of fibrosis
Cause of airway obstruction in emphysema:
disruption of alveolar attachments as a result of emphysema (affects radial traction)
- *Clinical correlates: Atelectasis**
- Three reasons for atelectasis
- Why can surgery lead to atelectasis
- Impaired pulmonary surfactant production: alveoli collapse secondary to increased surface tension
- Compression atelectasis: pressure on alveoli – Air in pleural cavity (pneumothorax) – Fluid in the pleural cavity (pleural effusion) – Abdominal obesity or – GI surgery post-op distention pushing up& compressing alveoli (post-operative)
• Resorption collapse: due to obstruction – Airway obstructed e.g. by tumour, mucus plug, foreign object ->
Prevents alveoli from ventilating ->
Air distal to obstruction is reabsorbed into the blood stream ->
Alveoil collapse ->
This lobe of the lung collapses (due to reduced pressure)
- *Surgery:**
e. g. anaethesia, pain relief, intubation, sedatives etc, can lead to the patient breathing more shallower, meaning alveoli may not infiltrate adequately causing them to collapse
Clinical correlates: Atelectasis
2 main problems
- Alveoli not ventilated – So can’t participate in gas exchange – impaired oxygenation and CO2 elimination
- Collapsed alveoli more suggestible to lung infection including pneumonia
- *Clinical correlates: Interstital Lung Disease
- **Another name for Interstitial lung disease
- 2 main problems for ventilation (clue: think about equations) and respiration
Diffuse lung fibrosis
1.
Thickening of the pulmonary interstitium (interstitial space between the capillary basement membrane and alveolar cells)
Sometimes reversible, sometimes not
(interstitium - space contains, collagen fibres, elastin fibres, fibroblasts)
This leads to reduced compliance - lungs are stiff, harder to expand
Increase elastic recoil - the resting lung volume is smaller than normal (nut rate of airflow is not impaired)
2.
Gas exchange is also affected - i.e. not just air movement in an airway – also a diffusion problem
• alveolar capillary membrane is thickened
• Increases diffusion distance for O2 and CO2 (Diffusion defect)
• Impairs gas exchange (more session 3)
- *Clinical correlates: Interstial lung disease**
- Causes
idiopathic - means no cause identified
In GW:
Pneumoconiosis (DLF caused by coal dust)
- *Clincal correlates: Interstitial lung disease**
- Symptoms
- Signs
- In DPF (Diffuse Pulmonary Fibrosis, another name for interstitial lung disease), is the functional residual capacity increased or reduced?
Signs:
- decreased lung excursion on palpation
- reduced chest movement
- bi-basal end inspiratory lung crackles (sounds like velcrow)
- Finger clubbing (increase in tissue at bottow of nails)
- Small pleural effusions
Symptoms:
- Dry cough
- Dyspnoea on exertion progressing to at rest
- Fatigue
- Typically gradual, insidious progression Sx
- Reduced exercise tolerance
- Tachypnoae
- Tachycardia
FRC:
Decreases, as lung can’t expand as much (reduced compliance, stiffer walls)
- *Clinical correlates: Neonatal Respiratory Distress Syndrome (NRDS)**
- Premature babies - time when born - where nearly all have NRDS?
- Which molecule is affected?
- Leads to?
- What does this mean for ventilation and respiration?
- Signs and symptoms
- Explain the reason for intercostal recession
- Premature babies - time when born - where nearly all have NRDS?
produced by type II pneumocytes, starts at 24-28 weeks gestation, so all babies born before and around this time have NRDS
- Which molecule is affected and leads to…
Lack of surfactant = Increased surface tension in fluid lining the alveoli
- What does this mean for ventilation and respiration?
Both have stiff lungs, Both decreased compliance and increased elastic recoil, Different underling mechanisms
- Signs and symptoms (from birth):
Ø Grunting, Ø Nasal flaring, Ø Intercostal and subcostal retractions Ø Rapid respiratory rate (tachypnoea) Ø Cyanosis
- Explain the reason for intercostal recession:
As air can’t flow freely as alveoil can’t expand as much, pressure in the lungs decreases, this leads to the intercostal muscle pulling sharply inwards. More obviously seen in babies with soft skin.
- *Clinical correlates: Pneumothorax**
- What happens in a pneumothorax
Chest wall or the lung is breached - tear in parietal or visceral pleura ->
A communication is created between pleural space and atmosphere ->
Air flows from atmosphere (higher pressure) ->
into the pleural cavity (lower pressure) ->
Until the pleural pressure = atmospheric pressure ->
The pleural seal is lost ->
Lung elastic recoil not counter-balanced by negative pleural pressure/chest wall ->
Lung collapses to unstretched size
Emphysematous dominant COPD vs Pulmonary fibrosis
Emphysema vs Pulmonary fibrosis - Compliance
- *Clinical correlates: Hypoventilation**
- What is this
- Causes for this
Hypoventilation - failure to breath rapidly enough (low respiratory rate) or deeply enough (low tidal volume)
leads to hypercapnia
