Alveolar ventilation Flashcards
Extra information about factors impacting alveolar ventilation and partial pressures
What drives airflow?
How do you work out the resistance of airways to airflow?
Pressure difference between mouth and alveolar drives flow i.e.atmospheric pressure to +/-1cmH2O atmospheric
Airway resistance (Raw) is based on the pressure gradient (difference between alveolar pressure and the airway opening pressure) divided by the airflow. (analogous to ohms)
Raw=(PA-Pao)/V.
Resistance is normally very low consider 1L/seconds dirven by pressure drop of 1 cmH2O
What determines airway resistance?
Viscosity of air (very low and therefore flows easily e.g. compare blood to air)
Dimensions of airways, normally the greatest resistance to airflow is in the larger bronchi and trachea as although they are larger the small number = total cross section is less than in the much smaller, but more numerous (65000) terminal bronchioles in parallel. In disease, however, terminal bronchioles are more vulnerable.
The way airflows in the lungs - laminar flow or at increased speed transitional or turbulent flow.
How does airway resistance change in normal airways?
Turbulence common in the trachea especially in exercise or when coughing. It is transitional in the larger bronchi and always laminar in the smaller terminal bronchioles.
Resistance to laminar flow =1/r4 demonstrating the importance of radius (e.g. if half radius increases resistance by a factor of 16)
About half of the airway resistance is in the nasopharynx- hence breathing is easier through an open mouth. Remaining resistance in the lungs depends on radius of airway and the number of airways in parallel to give an indication of the amount of resistance at that specific level of branching. Medium size bronchi represent the level of branching with the highest airway resistance, hence narrowing of these airways in disease can have a significant impact. Peak flow monitoring picks up more of the narrowing at the medium bronchi than in other parts of the lung.
How can smaller bronchioles impact on airflow resistance in disease?
There small size means they are easily occluded by muscle contraction in their walls, oedema in their walls and mucus collecting in the lumen of bronchioles.
Sympathetic stimulation of beta adrenergic receptors in the bronchioles by epinephrine and norepinephrine released into the blood stream result in bronchiole dilation.
Parasympathetic stimulation of the bronchioles by small branches of the vagus nerve releasing acetylcholine results in bronchiole constriction. Drug atropine is an acetylcholine blocker that can reverse this effect in disease processes. Reflexes in the lung as a result of irritation of the epithelial membrane can also trigger this parasympathetic response as too can microemboli in small pulmonary arteries.
What secretory factors can impact on bronchiolar constriction?
Histamine and slow reactive substance of anaphylaxis released by mast cells in allergic reactions can result in airway constriction.
What factors help to maintian the lumen of the respiratory passageways?
A layer of mucus coats the respiratory passageway all the way to the terminal bronchioles. This is released by goblet cells and submucosal glands in the epithelial lining of airways. This mucus keeps the airway moist and traps dirt. The epithelium is ciliated to the level of the terminal bronchiols forming a ciliary escalator with power stroke beating towards the pharynx (down from nose and up through trachea etc).
Cough/sneeze reflex irritation of the mucosa creates nerve impulse from vagus nerve to medulla (trigeminal nerve to medulla in sneeze). then 2.5L air rapidly inspired, epiglottis closes, vocal cords shut trapping the air, abdominal muscles and other expiratory musles contract forcefully creating pressure rise and explosive force of air. The non-cartilaginous parts of airway invaginate creating slits the air has to pass through. In sneeze the uvula is also depressed so air passes through the nose.
What is the normal function of the nose?
Warm the air
Humidify the air
Filter the air by passing through the hair, but also the conchae resulting in rapid direction changes of the air and the particles with greater weight than the air are unable to change direction at the same speed and are suspended and continue forward into the obstruction and become trapped in the mucosa.
Why does a tracheostomy improve alveolar ventilation in those in respiratory distress or poor blood gas composition?
Alveolar ventilation (V<strong>.</strong>A) = f(VT-VD)
Respiratory rate *(Tidal volume - Dead space)
Alveolar ventilation can therefore be increased by increasing the respiratory rate, increasing the tidal volume or decreasing the dead space. A tracheostomy impacts on the later.
What is the Bohr equation?
What is Fowler’s method?
The Bohr equation gives another way to measure deadspace. It is based on the assumption that CO2 volume is all expired (as inspired values are negligible under normal conditions
VD = VT * (PACO2 - PECO2)/PACO2
A- Alveolar
E-Expired i.e. how much is it diluted by the dead space air. This is a measure of physiological dead space.
Fowler’s method measures the anatomical dead space by measuring CO2 concentration at the lips. Zero to low CO2 represents the anatomical dead space, and sharp rise and plateau represents the alveolar air giving the volume of each.
What is the relationship between the ventilation of the alveolar and the fraction of CO2 in alveolar gas and therefore its partial pressure in alveolar gas?
CO2 enters the alveolar from the blood at a rate of V<strong>.</strong>CO2
And is washed out by ventilation at a rate of V<strong>.</strong>A (i.e. alveolar ventilation) * FACO2 (i.e. Fraction of alveolar gas which is CO2)
V<strong>.</strong>CO2=FACO2*V<strong>.</strong>A
FACO2=V<strong>.</strong>CO2/V<strong>.</strong>A
So the fraction of Alveolar gas that is CO2 is equal to the amount that flows into the alveolar divided by the rate of ventilation. Consequently as ventilation increases the fraction of alveolar gas that is CO2 goes down.
Multiply by a constant gives PACO2
PACO2 = K*(V<strong>.</strong>CO2/V<strong>.</strong>A)
So when ventilation increases so too does PACO2
Hyperventilation therefore increases arterial and alveolar PCO2 and Hypoventilation does the reverse as is seen in COPD exacerbations. (link to acidosis and alkalosis)
What is the relationshp between alveolar ventilation and the partial pressure of oxygen in the alveolar?
PAO2= PIO2 - K*(V<strong>.</strong>O2/V<strong>.</strong>A)
Meaning the partial pressure of oxygen in the alveolar is equal to the inspired partial pressure less (the flow of oxygen into the alveolar from the pulmonary arteries divided by the ventilation of the alveolar) multiplied by a constant. This explains that as ventilation is increased the deduction is reduced and therfore the partial pressure is closer to the inspired value and vice versa a fall in ventilation results in a fall in alveolar PO2.
What is the alveolar gas equation?
As both the partial pressure of oxygen and carbon dioxide are related to the alveolar ventilation these equations can be combined to give the alveolar gas equation:
PAO2=PIO2- (PACO2/R)
R is the respiratory quotient or respiratory exchange ratio. In normal lungs 5ml oxygen/100ml blood is transported to the tissue, whilst 4ml carbon dioxide/100ml blood is transported from the tissue to the lung. This gives a ratio of 0.8. This figure is dependent on the energy source for metabolism - exclusively carbohydrate diets give a ratio of 1, when oxygen reacts with fats some of it will react with hydrogen to form water and therefore the ratio is closer to 0.7.
Due to the solubility of CO2 the partial pressure can be taken from either the alveolar or the arterial value = 40mmHg
Partial pressure of inspired air must include the deduction for humidification (47mmHg)
PIO2=[0.21*(760-47)] = about 150mmHg
PAO2=150-50 = 100mmHg
How can the alveolar gas equation be used in clinical practice?
The arterial PO2 is usually no more than 10mmHg lower than alveolar PO2. When arterial blood gases are taken these can be used to estimate the alveolar PO2 based on the arterial PCO2, which will be the same as the alveolar level, and will also give the arterial level. An increased difference is indicative of reduced gas exchange usually caused by increased ventilation perfusion mismatch.
How can you work out the partial pressure of inspired O2?
PiO2 = FiO2 * (PB -PSVP)
This tells us that the inspired partial pressure of O2 is the fraction of inspired oxygen (room air is 21% up to 100% if receiving oxygen therapy) multiplied by the (Barometric pressure, which at sea level is 760mmHg or 101KPa, less the saturation vapour pressure, which is 47mmHg or 6.3KPa)
How does ventilation vary across the lung?
The lower lung is most ventilated, then the middle zone and the upper zone is least ventilated. This holds for standing or sitting.
This is due to the uneven distribution of intrapleural pressure at functional residual capacity and the curved relationship between intrapleural pressure and compliance. Gravity means that at FRC the base of the lung is more compressed and therefore has a less negative pleural pressure than the apex of the lung. This means that as the lungs expand and pleural pressure falls whilst they may fall by the same amounts the apex of the lung is less compliant and therefore the volume of increase per cmH2O decrease is less. The elastin and collagen at the apex is already stretched even at FRC and it’s therefore less compliant.
