Gas diffusion and exchange across the alveolar Flashcards
Describe the functions of the conducting and respiratory zones and relate their anatomical and histological features
Conducting zones:
‘Tubes’. E.g. the bronchioles.
Functions: To warm, filter and moisten air (aids gas solubility and exchange)
Respiratory zones:
The site of gas exchange between the air and the blood, such as alveoli.
Thin and large SA for exchange. Loading of oxygen into blood and CO2 into lungs for expiration.
Define the terms ‘anatomical’ and ‘physiological’ dead space and explain influential factors on the volumes of each.
Anatomical dead space:
Air becomes trapped within the conducting airways of the respiratory system - refers to stagnant air.
* The wider the tubes the greater the anatomical dead space
*Obstruction –> increased dead space
* Posture can increase dead space. E.g. head back –> Increase
Physiological dead space:
Refers to the dead space within the whole system. Includes anatomical dead space and also the areas at which exchange is not occurring e.g. alveoli not perfused or damaged.
In health anatomical and physiological dead space are normally equivalent. Physiological dead space is increased in pathology.
Explain the principles underlying gas flow and exchange across the alveolar-capillary walls
Ficks Law:
Proportional to SA
Inversely proportional to thickness of the surface
Related to the gas diffusion constant (D) - determined by the properties of the individual gas.
Explain how factors in health and disease can affect this process and how pulmonary diffusion can be measured
Pathologies may influence some of the determinants of diffusion.
Emphysema: Compliance (recoil) is reduced
Pneumonia: Consolidation and fibrosis causes increased thickness and decreased SA
Cystic fibrosis: Decreases the SA
Measuring pulmonary diffusion - D^L (gas):
- Rate of transfer of air across the air blood barrier.
- Single breath method
- Patients inhale a test gas, with small CO concentration (0.01%), hold breath for 10 seconds
- Rate of disappearance of the gas is measured (expired and inspired air are compared)
- 25 ml/min/mmHg = normal
- Transfer factor is obtained
Describe the partial pressure gradients for oxygen and carbon dioxide exchange and state normal values for their partial pressures in arteriole and venous blood in alveoli gas (mmHg/kPa)
Oxygen: High inspired value, gradually decreases as it travels through the alveoli (A), arterioles (a) and into the veins (V)
PIO2 160 mmHg –> PAO2 100 mmHg –> Mixes with O2 poor blood from anatomoses and shunts –> PaO2 95 mmHg –> Tissues use O2. Metabolic demand dependent –> PvO2 40 mmHg
Carbon dioxide:
Produced in the tissues and seen in high amounts in the veins (PVCO2), decreases slightly as it passes to the alveoli (PACO2) and decreases further as it is expired (PECO2)
Carbon dioxide produced by the tissues and transported to the lungs –> PVCO2 46 mmHg –> Venous blood arrives at the lungs and mixes with the alveolar air –> PACO2 40 mmHg –> Carbon dioxide diffuses from the blood, into the alveoli and into the air –> PECO2 32 mmHg
* Despite CO2 partial pressure being lower the rate of exchange is equal - this is due to CO2 being x20 more soluble
Explain the clinical relevance of ventilation-perfusion matching
For efficient gas exchange matching of ventilation (V) and perfusion (Q) is required. Allows for maximum exchange.
V = 5 L air/min
Q = 6 L blood/min
This is a range in exchange throughout the lung, much better at the base (x1.6 V and x3 Q at the base)
Explain how respiratory dysfunctions can disrupt VQ matching
Ventilation and perfusion (VQ) mismatch is the most common cause of PaO2 decrease in respiratory disease.
VQ mismatch sees an increase in physiological dead space.
Partial pressure of oxygen decreases (PaO2), the oxygen gradient between the alveoli and arterioles increases, breathing rate increases.
A range of pathologies can cause this e.g. lack of circulation, alveolar structural problems.
Poiseulle’s Law - flow, pressure and resistance govern air and blood flow
- If the diameter of the conducting zone/vessel is changed then the flow will change
- Bronchioles provide most resistance to airflow (V)
- Arterioles can increase or decrease blood flow accordingly (Q)
Hypercapnia –> Bronchioles dilate –> Increases airflow
Hypoxia –> arterioles constrict –> Reduce flow and redirect blood to better perfused areas. - Opposite to systemic response - this is in THE LUNGS
- Continuous local changes are seen, throughout the lungs.
Type I respiratory failure
- Reduced PaO2 –> Hypoxia
- Could be caused by acute conditions such as hypoventilation, increased metabolic demand (fever)
Chronic conditions: Cardiac failure, a section of the lungs being unventilated (Fallor’s tetralogy)
Respiratory dysfunctions: Adult respiratory distress syndrome, pneumonia, asthma, pulmonary oedema, COPD
Type II respiratory failure
Sees hypoxia, follow by hypercapnia
Arterial hypoxemia
Arteriole PaO2 is below normal levels
Hypoxia
Oxygen supply is insufficient to meet metabolic demands
Hyper and hypo capnia
High or low levels or CO2
Normal plasma pH
7.35 - 7.45
Factors involved in blood pH homeostasis
Respiratory rate
Metabolic: Production of HCO3-, excessive secretion of stomach acid (e.g. vomiting), excessive loss of water (e.g. diarrhoea)
Chemical buffers: protein (Hb and plasma proteins), phosphate (bone) and carbonic acid-bicarbonate buffer (MAJOR BUFFER SYSTEM) systems
Adjusting renal acid/alkali secretion.