upper respiratory tract
lower respiratory tract
primary functions of resp tract (3)
Exchange oxygen and carbon dioxide between blood and the atmosphere
Olfaction – smell and taste
secondary functions of resp tract (5)
Warming and humidifying incoming air
Moistening of cell lining
Keeping lining clean
Keeping airways open during pressure changes
Keeping alveoli open against surface tension
anatomy of the upper resp tract
blood supply ensures inspired air enters lungs at body temp and fully saturated with water vapour.
Hairs -> filter harmful material
air cavities in the cranial bones
clarity + tone of voice
lighten weight of skull hence body can support he weight
Speech – pitch and volume
Strength of expiration contributes to volume
Preventing material reaching LRT – during swallowing larynx closes and pulled upwards to assist process
Supplied with vagal receptors which form the sensory side of cough reflex – stimulation of larynx by ingested matter produces strong cough reflex
what is it filled with?
Each lung is surrounded by two membranes (pleurae)
The outer (parietal) pleura - attached to the chest wall and sensitive to pain
The inner (visceral) pleura - attached to the lung and viscera and is perfused by the pulmonary circulation
Pleural space is filled with fluid - reduces friction between layers during respiration
provides surface tension that keeps the lung surface in close apposition with the chest wall –
allows optimal inflation of the alveoli during respiration.
Also transmits pressures from the chest wall to the visceral pleural surface (and hence, the lung)
trachea and main bronchi anatomy
where birfucates? what do the rings support?
which bronchi is longer? effect?
what does the bronchi subdivide into? numbers?
Ends where it bifurcates into 2 main bronchi at the level of the sternal angle (the Angle of Louis)
Horseshoe shaped cartilaginous rings supporting the anterior and lateral walls (allow cough reflex to happen)
The posterior wall is flaccid and bulges forward during coughing.
Left main bronchus – longer than right and leaves the trachea at a more abrupt angle
The right main bronchus is more directly in line with the trachea so that inhaled material tends to enter the right lung more readily than the left
Bronchi subdivide into lobar bronchi – upper mid and lower on right, upper and lower on left, then segmental bronchi and until terminal bronchioles reached
functional area of alveoli
describe bronchi? bronchioles?
what is acinus?
large airways vs conducting airways?
Bronchi – airways with cartilage –smooth muscle spiral internal to cartilage (maintain airflow)
Bronchioles – small airways with no cartilage
Terminal bronchiole supplies the acinus (functional unit of lung)
Each acinus contains branching respiratory bronchioles communicating with alveoli
The large airways relatively rigid, and consist of muscle and cartilage. They are responsible for maintaining air-flow - but smooth muscle present can reduce diameter of airway.
The conducting bronchioles can contract greatly – allowing regulation of airflow
type 1 and type 2 pneumocytes?
when is small gap between capillaries and alveolar present?
0.1-0.2 microns diameter
Lined with single layer of flattened epithelial cells
Type I pneumocytes comprise 92-95% of the cells – direct contact with pulmonary capillaries for gaseous exchnage
Type II pneumocytes cover the remaining surface and secrete surfactant (reduce surface tension) also repair function
There is a small gap between the basement membrane of the capillaries and the alveolar cells which is only apparent in disease states, when it might contain fluid.
cytology in nasal cavity
where is olfactory mucosa? cytology?
rest of nasal cavity cytology?
what counteract effect of incoming dry air?
what do goblet cells do?
Nasal cavity lined by skin with hairs to provide first filter
The olfactory mucosa is found only in small area in roof of nasal cavity. It contains highly pseudostratified epithelium, is ciliated, and contains olfactory cells
Rest of nasal cavity lined by respiratory mucosa –
pseudostratified columnar epithelium with cilia and goblet cells
Serous and mucous glands under epithelium - counteract effect of dry incoming air
Beneath epithelium is venous plexus – thin walled veins and venules – warm incoming air
Goblet cells – mucus secretion onto surface of epithelium – traps small particles
cytology in lower resp
epithelium change along the tree?
what cell decreases as you go down?
Epithelium – transition from pseudostratified in nose and trachea to simple cuboidal in terminal bronchioles
Pseudostratified epithelium function in secretion and absorption
Respiratory epithelium down to terminal bronchioles is ciliated and contains goblet cells Goblet cells decrease but cilia are found as far distally as respiratory bronchioles
cytology in resp tract
what is mucocillary escalator?
what lines most of resp tract?
Mucous membrane (mucosa) lines most of respiratory tract.
Cilia are covered with a thin layer of mucus – function to trap foreign particles, and propel them towards pharynx – hence protection against infection
Move in co-ordinated waves sweeping mucus layer towards pharynx where swallowed – mucociliary escalator
physiology of lungs
2 main things?
Mechanical – ventilation
Gas exchange - perfusion
Gas transfer – distribution and diffusion
ventilation - inhalation
what happens during higher levels of ventilation?
Normal/quiet breathing: Diaphragm flattens External intercostal muscles contract Volume of thoracic cavity increases Lungs expand Air flows down pressure gradient into lungs
High levels of ventilation:
Inspiratory muscles – neck and chest
Expiratory – internal intercostal muscles, abdominal muscles
Elastic and non-elastic resistance
what is normally active and what is passive?
what bring chest to position after expiration?
what is used when there ius abnormal resistance?
when is elsatic work increased?
when is non-elastic work increased?
Elastic and non-elastic resistance
Normally inspiration is active and expiration is passive
Elastic forces in lungs and chest wall – bring chest to position at the end of normal expiration. Kinetic energy brings chest to resting position
Inspiration or expiration against abnormal resistance may require use of accessory muscles
Elastic work is increased when lungs are more rigid e.g. fibrosis
Non-elastic forces – work is increased by rapid breathing and obstructive lung disease such as asthma
muscles? effect of this?
Functionally - elastic bags resembling balloons.
Lack muscle which would allow them to expand or
do children breath faster or slower?
does all air reach alveoli?
what happens is aleveolar ventilation increase or decrease?
Children tend to breathe faster
Not all reaches alveoli but remains in larger airways – dead space (20-30%) - can increase in disease.
If alveolar ventilation reduced in proportion to CO2 excretion, PCO2 rises (hypercapnia) and if alveolar ventilation becomes excessive, arterial PCO2 falls (hypocapnia)
what is it?
what is distensibility of lungs?
what balances retractive forces of lung?
what effect does gravity have on lungs?
Compliance – a measure of ease of lung expansion
Distensibility of lungs – the elastic properties of lungs cause them to retract from chest wall
Expressed as change in lung volume
Retractive forces of lung balanced by semi-rigid structure of the thoracic cage. Gravity results in weight of lungs keeping upper parts under greater stretch. Upper parts are less compliant and less receptive to air entry during inspiration. So lower zones receive more ventilation than upper zones.
where does this occur in normal individual?
in disease, where does it occur?
Distribution of air in lungs uneven
Airway resistance to airflow in normal individual occurs in larger airways
In disease airway resistance occurs in peripheral airways
what is it? total lung capacity? tidal volume? functional residual capacity? residual volume? vital capacity?
Spirometry is a means of measuring ventilation.
The total lung capacity is the volume of gas in the lungs after a full inspiration
The tidal volume is the amount of air which enters and leaves the lungs during normal breathing
The functional residual capacity is the volume of gas within the lungs at the end of normal expiration
After a full expiration there is still some gas remaining in the lungs – the residual volume
The vital capacity is the volume of air expelled by a maximum expiration from a position of full inspiration
total lung capacity
volume of gas in the lungs after a full inspiration
amount of air which enters and leaves the lungs during normal breathing
functional residual capacity
volume of gas within the lungs at the end of normal expiration
After a full expiration there is still some gas remaining in the lungs
volume of air expelled by a maximum expiration from a position of full inspiration
where does it receive blood from?
what does efficiency of gas exchange depend on?
why is distribution of ventilation and perfusion not perfect in normal lung?
Lungs receive blood supply from pulmonary and systemic circulation
Efficiency of gas exchange depends on alveolar distribution and blood flow in all parts of lungs
Pulmonary capillary network in alveolar walls is dense – large surface area
Even in normal lung, distribution of ventilation and perfusion not perfect – e.g. effects of gravity - perfusion preferentially in base of lungs
Lung perfusion - Respiratory quotient (RQ)
what is rq?
why is PCO2 a measure of alveolar ventilation?
what happens when alveolar ventilation drops?
The possible values of the ventilation:perfusion ratio (VA/Q) is between ∞ (ventilation and no perfusion) and 0 (perfusion but no ventilation)
Respiratory Quotient (RQ)
At steady state: CO2 produced by body and O2 absorbed depends on metabolism
Typically 0.7 during pure fat metabolism to 1.0 during pure carbohydrate metabolism. RQ usually 0.8 (assume 1.0)
When CO2 produced at constant rate, PCO2 of alveolar air depends on amount of outside air that the CO2 is mixed with in alveoli. i.e. PCO2 is measure of alveolar ventilation
When alveolar ventilation drops, PCO2 rises
Distribution – Oxygen transport
heamoglobin? sub units? saturation? what happens at tissue? what affects dissociation of O2? what causes diffusion across alveolar membrane? left and right shift meaning?
Haemoglobin contains 4 haem units
Hb almost saturates with O2 as blood passes through alveolar capillaries
Once in tissue, O2 released and PO2 decreases
Dissociation of O2 affected by pH and temperature
Diffusion across alveolar membrane due to pressure gradient
Left shift: higher O2 affinity
Right shift: lower O2 affinity
Distribution – Carbon Dioxide transport
where is co2 carried to?
what is the cause of diffusion?
CO2 carried from tissues to lungs
Diffusion from cell to blood across the alveolar membrane due to pressure gradient
24x more soluble than O2 – no carrier
Sensory control of ventilation
where are they found?
what activates the receptors? effect?
when does this stop? important when?
Mechanoreceptors – found in walls of bronchi and bronchioles.
Main function is to prevent over inflation of lungs.
Inflation activates the receptors which inhibit the neurones in the respiratory centre via vagus nerve.
Once expiration starts, activation of the stretch receptors ceases allowing inspiratory neurones to become active again. This is important in infants but in adults it is only functional during exercise when the tidal volume is larger than normal.
Sensory control of ventilation
what do chemo receptors respond to?
how do they detect it?
what does this stimulate?
when is this response decreased?
where are the two types of chemo recepotrs found?
what do they both respond to?
Chemoreceptors respond to O2, CO2 and H+
Central chemoreceptors –Lie on ventrolateral surface on either side of medulla.
They respond mainly to hypercapnia but not directly due to gas pressure but to changes in levels of H+ in the CSF.
When PCO2 in blood increases, CO2 diffuses into the CSF and liberates H+
They stimulate an increased ventilatory rate and increased depth of ventilation
The response is reduced by factors including sleep, increasing age, narcotic analgesics, alcohol, athletic training and anaesthetics
Peripheral chemoreceptors are found in the carotid bodies at the origin of the internal carotid artery and in the ascending aortic wall.
They respond mainly to hypoxia.
They also stimulate and increased ventilatory rate and increased depth of breathing
control of breathing
what is the prime effector of ventilatory control?
when can another factor become a more potent effector?
what can reduce sensitivity of resp centre?
name a non-resp cause that can do this
drugs that can stimulate and depress resp centre?
Under normal circumstances, the prime effector of ventilatory control is alteration in arterial pCO2.
However, in circumstances of hypoxia (PO2 <8 Kpa), the PO2 is the most potent stimulus to ventilation.
Raised PCO2 is accompanied by increasing acidity of blood and CSF and stimulates both peripheral and central chemoreceptors
Chronic CO2 retention reduces sensitivity of the respiratory centre.
H+ also increased by non-respiratory causes such as diabetic ketoacidosis
Drugs – aspirin can stimulate respiratory control centres directly. Other drugs e.g. sedatives may depress it
Neural control of breathing
UMN effect on LMN
what are UMN
what does activity in UMNS do?
how do impulses reach spinal motor neurones?
LMNs - cell bodies where?
impulses that have a conscious change travel via?
The distribution and organisation of the respiratory centre highly complex
Upper motor neurones (UMNs) “drive” lower motor neurones
The UMNs originate in the medulla and forebrain
Activity in UMNs controls frequency and duration of LMN discharge to muscles of breathing
Impulses reach spinal motor neurones via reticulospinal tract. Lower motor neurones (LMNs) – cell bodies in anterior horn of spinal cord at C3-C5 (phrenic nerve to diaphragm) and T1-T12 (external and internal intercostal nerves/muscles)
Impulses mediating conscious change travel via corticospinal tract
ventilation and UMN/LMN
effect of UMN and LMN during quiet/normal breathing?
change during higher levels of ventilation?
Inspiratory UMNs fire strongly enough only to excite a few inspiratory LMNs
The expiratory UMNs are also active but not sufficiently to
High levels of ventilation: UMN activity increases LMNs start to fire Inspiratory intercostal muscles then abdominal muscles make the LMNs fire.
cholinergic innervation effect?
noradrenergic innervation effect?
Airways contain afferent (sensory) and efferent (motor) nerves
Stimulation of the vagus nerve causes the release of Ach – leads to contraction of airway smooth muscle which constricts bronchi and mucus secretion
Human airways have little or no noradrenergic innervation but there are b2 adrenoceptors in human lung, primarily in airway smooth muscle of intermediate and small diameter bronchi. Allow airway tone to be regulated by circulating adrenaline.