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![Page 1: Charles University in Prague, 1 st Medical Faculty, Lab. of biocybernetics & Computer-Aided Learning Assessment of respiratory system function Stanislav.](https://reader036.fdocuments.in/reader036/viewer/2022062803/56649f0e5503460f94c22e99/html5/thumbnails/1.jpg)
Charles University in Prague, 1st Medical Faculty, Lab. of biocybernetics & Computer-Aided Learning
Assessment of respiratory system function
Stanislav Matoušek
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What is the function of lungs?
Alveolus• Ventilation – mechanical function of
the lung – get air in and out • Perfusion with blood – get blood in
and out • Diffusion – get gas molecules from air
to blood and back• Matching of ventilation and perfusion
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Possible respiratory system disturbances
• // ventilation • // perfusion • // distribution of ventilation and per-
fusion = ventilation perfusion mismatch• // diffusion • Important: Ventilation, perfusion
and their distribution are feedback regulated processes.
• Disturbance: – 1. In the effector part (lungs, resp.
muscles for ventilation, heart for perfusion)
– 2. In the regulator part (sensors, CNS eg. in uremia, liver in hepatopulmonary syndrome)
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The overall measure of respiratory system function
• pO2 & pCO2 in arterial blood - („Astrup“)
• O2 solubility in water is low => need of Hemoglobin
• pO2 = 13,3 kPa = 100 Torr• pCO2 = 5,3 kPa = 40 Torr (1 kPa = 10 cm H2O = 7,6 mmHg or
Torr)
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Solubility of gases in liquids
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Oxygen-hemoglobin dissociation curve
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Ventilation
• Is carried out by respiratory muscles, that change volume of thorax.
• Volume changes cause changes of pressures
• Changes of pressure in alveoli cause air flow (
• ↑ transthoracic pressure – expiration;
• ↓ transthoracic ressure – inspiration)
• Flow behaves according to Ohm’s law
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Spirometry - Measure of ventilation volumes (and air flow)
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Spirometry
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Spirometry – Volume-flow loop
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Pressures in the lungs
Transthoracic pressure
Transpulmo-nary pressure
-12 mmHg
+1 mmHg
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Normal lung
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Lung compliance
• Is a measure of the pressures developed by the effect of the lung elasticity while the lung is at rest.
• C = Vbreath/ (pendin.- pendexp.) = ΔV /Δ p • The pressures are not pressures needed to make
the air flow (it is measured at rest/0 flow points• They are pressures needed to keep the lung inflated
!!• The more you want to have the lung inflated, the
more pressure you need• Decreased compliance = stiff lung = restrictive
disease• Increased compliance - loose lung – emphysema –
(increased compliance does not cause problems by itself. However, it causes increased resistance during expiration)
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Restrictive disease
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Lung resistence
• Depends on pressures needed to make the air flow (transthoracic in normal breathing)
• R = (penviron.- palv.)/ F = Δ p / F
• Increased resistance – obstruction in the lungs – obstructive desease
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Obstructive disease
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Measuring of the Compliance of the lungs
• C = Vbreath / (pendin.- pendexp.)• Direct – difficult, because
you need to measure the transpulmonary pressure difference
• Easy in artificial ventilation
• Indirect - decreased lung compliance = stiff lung - will cause ↓ decreased static lung volumes, especially ↓ in VC a FVC.
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Measuring of the resistance of the airways
R = (penviron.- palv.)/ FDirect: Temporary
occlusion method (spirometry, whole body pletysmography)
Indirect: Increased airway resistance = blonchoconstriction will cause decrease of flow and „dynamic lung volumes“ FEV1, FEF25-75% and MEFs.
-12 mmHg
+1 mmHg
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What type of lung disease?
a)
b)
c)
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Normal spirogram
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Obstruction- medium degree
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Obstruction parameters
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Restrictive disease
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Real world situation
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Whole body plethysmography
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Other methods of measuring Residual volume and TLC
• Nitrogen washout method -person breathes in pure oxygen - concentration of N2 in the
expired air is measured• Helium dilution method
– Given amount of Helium
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Ventilation disorders
• Lung impairment (mechanical properties change) – Obstructive disease - ↑ increased resistance R of
airways (R = “dynamic lung resistance”)– Restrictive disease – ↓decreased lung compliance C (‘↑
static resistance” `; C = 1/ static lung resistance)• Chest wall impairment
– ↓ decreased C of chest wall – severe scoliosis, extensive fibrosis, serial fractures
• Insufficient activity of respiratory muscles (// innervation or // muscle strength , // of CNS ) – E.g.. Respiratory centre suppression in barbiturate poisoning, myasthenia gravis
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Perfusion
• All the blood volume flows through lungs
• Also behaves according to Ohm’s law
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Disorders of perfusion
• Causes– Embolization to the pulmonary artery
(increased resistante to the blood flow)– Pulmonary hypotension (right heart failure)– Pulmonary hypertension
• Manifestation– Pulmonary hypertension causing ever right
heart failure in massive embolism – Decrease in pO2 (increase in pCO2),
• Increase of shunting • Blood flows fast through a small part of the lungs
only – the rest functions as dead space
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Measuring perfusion
• a) Ventilation - perfusion scan - diagnosis of pulmonary embolism and parenchymal lung disease should be performed in all clinically stable patients with the suspicion of pulmonary embolismshould be performed in all clinically stable patients with the suspicion of pulmonary embolism- Ventilation scan - 133Xe gas- Perfusion scan – microspheres of albumin (50-100 mm labeled with gamma emitting isotope 99mTc- “Mismatch” in ventilation and perfusion is characteristic for PTE
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Lung scintigraphy -perfusion
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Lung scintigraphy - ventilation
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West’s weir
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Physiological ventilation distribution
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Distribution of ventilation and perfusion
• In healthy lung, the most perfused part is at the base… this part is at the same time the most ventilated one (No mismatch )
• Various pathologies can cause ventilation perfusion mismatch
• Every lung region (size is on us to decide) has its ventilation perfusion ratio VA/Q - number from O to ∞ … norm 0,8 - 1
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Pulmonary shunt• Extreme case of ventilation perfusion
mismatch• Zero local ventilation VA/Q = OCauses:
– Atelectasis– Lung edema (alveolar)– Lung inflammation (inflammatory exsudate)– Collapsed lung (pneumothorax)
• Blood leaving the defect area has low ↓ pO2 and high ↑ pCO2 (no gas exchange)
• After mixing with blood from healthy regions, ↓ pO2 stays low, but pCO2 normalizes. Why?
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Dead space
• Opposite extreme case of ventilation-perfusion mismatch. No perfusion.
• VA/Q = ∞• Increases of dead space:
– Embolism– Emphysema– Bronchiectasia
• Ventilation of dead space has by itself no influence on blood gases, but it is wasted respiratory work! =>
• Excessive ventilation of dead space can lead to insufficient ventilation of healthy alveoli.
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Physiological dead space
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Ventilation perfusion mismatch
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Ventilation perfusion mismatch
• Is a very common cause of hypoxemia - ↓ pO2 (low ↑ pCO2 might probably not occur)
• Etiological factor of dyspnea onset in:– ARDS– COPD, especially chronic bronchitis
(smoker)– Asthma
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Diffusion
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Diffusion in lungs
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Rate of diffusion
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Diffusion impairments
Decrease ↓ of diffusion surface S:• Emphysema• Pneumothorax
Increase ↑ in diffusion distance d:• Lung fibrosis • Lung edema• Interstitial pneumonia
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Measuring „diffusion“
• Transfer factor / Lung diffusion capacity
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Respiratory insufficiency!!
• Respiratory insufficiency type I (partial, hypoxemic)– pO2 is ↓ low, but pCO2 is normal or
even also ↓ lower
• Respiratory insufficiency type II (global, hypoventilation)– pO2 is ↓ low and pCO2 is ↑ high
(respiratory a….)
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Partial respiratory insufficiency(Type I)
• Impaired // distribution – Ventilation perfusion mismatch -
uneven VA/Q in different lung regions
– True shunting (right-left)
• Impaired // diffusion • Through water O2 diffuses about 20x slower
than CO2
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Global respiratory insufficiency(type II)
• Impaired // ventilation - overall alveolar hypoventilation
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ARDS
• Adult/acute respiratory distress syndrom • Cause: Sudden damage to alveolo-capillary
membrane – interstice and alveoli get infiltrated by plasma and proteins
• Ventilation-perfusion mismatch appears, in some parts of lungs to the degree of shunting
• Consequence: Partial respiratory insufficiency in serious cases evolving into global respiratory insufficiency
• With edema, lung compliance decreases ↓C , where only interstitial edema => // diffusion
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ARDS
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Signs of ARDS
• Dyspnea – decrease ↓ pO2• Low ↓ lung compliance – breathing
faster and more shallow, increased breathing effort
• Dry irritating cough (sometimes pink sputum)
• CO2 often decreased ↓ !! = hypocapnia – respiratory acidosis
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<
Osmotic pressure
C1 C2 > = P2P1 > =
Membrane permeable to water, but NOT to solutes
H2O
H2O
H2O
H2O
[H2O]1 [H2O] 2 =
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Cell
Isotonic environment
290 ± 10 mmol/l
Vessel
Interstice
H 20
Gradient of
hydraulic pressuresGradient
of oncotic pressures
H 20
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arteriolevenule capillary
Oncotic pressure gradient
Hydraulic pressure gradient
filtrate movementLymphatic drainage
Lymphatic drainage
proteins
proteins
Interstitialliquid
Movement of H2O across the lung capillary
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arteriolevenule capillary
Oncotic pressure gradient
Hydraulic pressure gradientFiltrate movement
Lymphatic drainage
Lymphatic drainage
proteins
proteins
Interstitialfluid
ARDS
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Causes of ARDS
• Shock and inflammation– Circulatory shock and
severe hypotension – Pulmonary embolism– DIC – Extensive burns– Extensive pneumonia – Sepsis and septic shock– Post-transfusion TRALI
• Damage from alveolar side– Inhalation of toxic
gases and fumes – Long-time O2 toxicity– Aspiration of gastric
content– Water aspiration in
drowning• Other
– Lung contusion and chest trauma
– Head trauma– Pancreatitis– Heroin overdose
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Summary