Respiratory physiology

Dr Zarli Nyein
AP Anaesthesiologist
UM 2
FUNCTIONAL RESPIRATORY ANATOMY

• Rib Cage & Muscles of Respiration

• Rib cage contains the two lungs, each surrounded by its own pleura
• Contraction of the diaphragm—principal pulmonary muscle
• Diaphragmatic movement normally accounts for 75% of the change in
chest volume.
• Upward and outward rib movement expands the chest.
• External intercostal muscles are also responsible for inspiration
• Sternocleidomastoid, scalene, and pectoralis muscles can be recruited to
assist during inspiration
• Expiration is normally passive in the supine position but becomes active in
the upright position and with increased effort
• Some pharyngeal muscles are important in maintaining the patency of the
airway
• Genioglossus, levator palati, tensor palati, palatopharyngeus, and
palatoglossus muscles….
Tracheobronchial Tree
• trachea serves as a conduit for ventilation and
clearance of tracheal and bronchial secretions.
• Trachea begins at the lower border of the
cricoid cartilage, extends to the carina
• average length of 10 to 13 cm
• composed of C shaped cartilaginous rings,
which form the anterior and lateral walls of the
trachea and are connected posteriorly by the
membranous wall of the trachea
• Bifurcates into the right and left mainstem
bronchi at the level of the sternal angle.
• right mainstem bronchus
• more linear arrangement with the trachea,
• left mainstem bronchus
• more angular orientation with the trachea.
• Humidification and filtering of inspired air are functions of the upper airway
• Tracheobronchial tree serves to conduct gas flow to and from the alveoli.
• Dichotomous division (each branch dividing into two smaller branches),
starting with the trachea and ending in alveolar sacs, is estimated to involve 23
divisions, or generations
• estimated 300 to 500 million alveoli provide an enormous membrane surface
area (50–100 m2) for gas exchange in the average adult
Alveoli
• Each alveolus is in close contact with a network of
pulmonary capillaries.
• Pulmonary epithelium contains at least two cell
types
• Type I pneumocytes are flat and form tight (1-nm)
junctions with one another
• Type II pneumocytes, which are more numerous
than type I pneumocytes
• contain surfactant, an important substance
necessary for normal pulmonary mechanics.
• Unlike type I cells, type II pneumocytes are capable
of cell division and can produce type I
pneumocytes if the latter are destroyed
Pulmonary Circulation & Lymphatics
• lungs are supplied by two circulations, pulmonary and
bronchial.
• bronchial circulation arises from the thoracic aorta and
from intercostal arteries and provides a small amount
of blood flow (<4%of cardiac output), which sustains
the metabolic needs of the tracheobronchial tree.
• bronchial vessels anastomose with the pulmonary
arterial circulation and continue as far as the alveolar
duct.
• pulmonary circulation normally receives the total
output of the right heart via the pulmonary artery,
which divides into right and left branches to supply
each lung.
Innervation
• Motor innervation of the diaphragm,
along with sensory innervation of the
central diaphragm, is supplied by the
phrenic nerves, which arise from the
C3–C5 nerve roots.
• Sensory innervation of the peripheral
diaphragm is supplied by the adjacent
sixth through eleventh intercostal
nerves.
• Intercostal muscles are innervated by
their respective thoracic nerve roots.
• Vagus nerves provide sensory innervation to the tracheobronchial tree.
• Both sympathetic and parasympathetic autonomic innervation of bronchial
smooth muscle and secretory glands is present.
• Vagal activity mediates bronchoconstriction and increases bronchial
secretions via muscarinic receptors.
• Sympathetic activity (T1–T4) mediates bronchodilation and also decreases
secretions via β2-receptors.
REGULATION AND CONTROL OF BREATHING

• Basic elements of the respiratory control system are

• (1) strategically placed sensors
• (2) central controller
• (3) respiratory muscles
CENTRAL CONTROLLER:

• Breathing is mainly controlled at the level of brainstem.

• Respiratory centres located in the pons and medulla.
1. Medullary respiratory centre
• Dorsal medullary respiratory neurones are associated with inspiration:
• When the neurones are active their action potentials travel through
reticulospinal tract in the spinal cord and phrenic and intercostal nerves
and finally stimulate the respiratory muscles.
• Ventral medullary respiratory neurones are
associated with expiration.
• During heavy breathing increased activity of the
inspiratory centre neurones activates the
expiratory system.
• In turn, the increased activity of the expiratory
system inhibits the inspiratory centre and
stimulates muscles of expiration.
• Dorsal and ventral groups are bilaterally paired
and there is 8 cross communication between
them.
• As a consequence they behave in synchrony and
the respiratory movements are symmetric
2.Apneustic Centre:

• It is located in the lower pons.

• Exact role of this centre in the normal breathing is not known.
• Lesions covering this area in the pons cause a pathologic respiratory
rhythm with increased apnoea frequency.
• What is known is nerve impulses from the apneustic centre stimulate the
inspiratory centre and without constant influence of this centre respiration
becomes shallow and irregular.
3.Pneumotaxic centre:

• It is located in the upper pons.

• A group of neurones that have an inhibitory effect on the both inspiratory and apneustic
centres.
• It is probably responsible for the termination of inspiration by inhibiting the activity of the
dorsal medullar neurones.
• Primarily regulates the volume and secondarily the rate of the respiration.
• is responsible for the fine-tuning of the respiratory rhythm.
• Hypoactivation of this centre causes prolonged deep inspirations and brief, limited
expirations by allowing the inspiration centre remain active longer than normal.
• Hyperactivation of this centre on the other hand results in shallow inspirations.
• Breathing in some extent is also controlled consciously from higher brain
centres (e.g. cerebral cortex).
• This control is required when we talk, cough and vomit.
• It is also possible voluntarily change the rate of the breathing
• Other parts of the brain (limbic system, hypothalamus) can also alter the
breathing pattern e.g. affective states, strong emotions such as rage and
fear.
• In addition, stimulation of touch, thermal and pain receptors can also
stimulate the respiratory system.
SENSORS:
• 1.MECHANORECEPTORS:
• Placed in the walls of bronchi and bronchioles of the lung and the main
function of these receptors is to prevent the overinflation of the lungs.
• Inflation of the lungs activates these receptors and activation of the stretch
receptors in turn inhibits the neurones in inspiratory centre via vagus nerve.
• When the expiration starts activation of the stretch receptors gradually
ceases allowing neurones in the inspiratory neurones become active again.
• This phenomenon is called Hering-Breuer Reflex.
• It is particularly important for infants.
• In adults it is functional only during exercise when the tidal volume is larger
than normal
• 2.CHEMORECEPTORS:
• Chemoreceptors are specialised neurones
activated by changes in O2 or CO2 levels in the
blood and the brain tissue, respectively.
• Involved in the regulation of respiration
according to the changes in PO2 and pH.
• O2-sensitive chemoreceptors (Peripheral
chemoreceptors) are located at the bifurcation of
the carotid artery in the neck and the aortic arch.
• Connected to the respiratory centre in the
medulla by glossopharyngeal nerve (carotid
body chemoreceptors) and the vagus nerve
(aortic body).
• Central chemoreceptors are
located bilaterally in the
chemosensitive area of the
medulla oblongata and exposed to
the cerebrospinal fluid (CSF),
local blood flow and local
metabolism.
• Respond to changes in H+
concentration in these
compartments.
• When the blood partial PCO2 is
increased CO2 diffuses into the
CSF from cerebral vessels and
liberates H+.
• CO2 level is a major regulator of respiration.
• much more important than oxygen to maintain normal respiration.
• Even very small changes in carbon dioxide levels (5 mm Hg increase in
PCO2, hypercapnia) in the blood cause large increases in the rate and
depth of respiration (100 % increase in ventilation).
• only after 50 % decrease in PO2 can produce significant changes in
respiration.
• Due to the nature of O2-Hb saturation that at any PO2 level above 80 mm
Hg Hb is saturated with O2.
• In stroke patients or physiologically at high altitude blood PO2 level may
drop considerably and activate peripheral chemoreceptors and activate
stimulation (ability of the lung to eliminate CO2 is not affected, in
response to increased respiration, blood PCO2 is decreased)
MECHANISM OF BREATHING

• small cyclic pressure gradients established within the airways.

• During spontaneous ventilation, these gradients are secondary to
variations in intrathoracic pressure; during mechanical ventilation, they
are produced by intermittent positive pressure in the upper airway.
• During apneic oxygenation, gas exchange depends on the mass movement
of gases along concentration gradients
Spontaneous Ventilation

• The pressure within

alveoli is always greater
than the surrounding
(intrathoracic) pressure
unless the alveoli are
collapsed
• at end inspiration, volume is maximal, flow is zero, and alveolar pressure is
atmospheric.
• Diaphragmatic and intercostal muscle activation during inspiration expands
the chest and decreases intrapleural pressure from –5 cm H2O to –8 or –9
cm H2O
Mechanical Ventilation

• intermittently apply positive

airway pressure at the upper
airway
LUNG MECHANICS

• movement of the lungs

• elastic resistance of tissues and the gas–liquid interface and the nonelastic
resistance to gas flow….main determinant
• Elastic resistance governs lung volume and the associated pressures under static
conditions
Elastic Resistance
• Both the lungs and the chest wall have elastic properties.
• Chest tends to expand outward, whereas the lungs tend to collapse.

Surface Tension Forces

• Surface tension forces tend to reduce the area of the interface and favor alveolar
collapse.
• Laplace’s law can be used to quantify these forces
• pulmonary surfactant decreases alveolar surface tension in proportion to
its concentration within the alveolus.
• As alveoli become smaller, the surfactant within becomes more
concentrated, and surface tension is more effectively reduced.
• Conversely, when alveoli are overdistended, surfactant becomes less
concentrated, and surface tension increases.
• The net effect is to stabilize alveolar size: small alveoli are prevented from
getting smaller, whereas large alveoli are prevented from getting larger.
Compliance
• defined as the change in volume divided by the change in distending pressure.

• Measurements are usually obtained under static conditions (ie, at equilibrium).

• Dynamic lung compliance [Cdyn, L], which is measured during rhythmic breathing,
is also dependent on airway resistance.
• CL is normally 150 to 200 mL/cm H2O.
• A variety of factors, including lung volume, pulmonary blood volume, extravascular
lung water, and pathological processes (eg, inflammation and fibrosis), affect CL
Compliance is reduced when
• (1) The pulmonary venous pressure is increased and the lung becomes
engorged with blood
• (2) There is alveolar oedema due to insufficiency of alveolar inflation
• (3) The lung remains unventilated for a while e.g. atelectasis and
• (4) Because of diseases causing fibrosis of the lung e.g. chronic restrictive
lung disease
CHEST WALL COMPLIANCE: Changes in chest wall
compliance are less common than changes in the lung
compliance: (1) pathologic situations preventing the
normal movement of the rib cage, such as, distortion of
the spinal column, (2) pathologic (cancer) or physiologic
(pregnancy) reasons increasing the intra abdominal
pressure, (3) stiff chest, such as broken ribs

where transthoracic pressure equals atmospheric pressure

minus intrapleural pressure.
Normal chest wall compliance is 200 mL/cm H2O
Total compliance (lung and chest wall together) is 100 mL/cm
H2O and is expressed by the following equation
Lung Volumes

• Lung volumes are important parameters for both respiratory physiology

and clinical practice
• Lung capacities are clinically useful measurements that represent a
combination of two or more volumes.
Lung volumes and capacities

Spirogram showing static lung volumes. (Reproduced with

permission from Lumb A. Nunn’s Applied Respiratory
Physiology, 8th ed. St. Louis, MO: Elsevier; 2017.)
Functional Residual Capacity

• The lung volume at the end of a normal exhalation is called functional residual
capacity (FRC).
• FRC can be measured by nitrogen washout, helium wash-in technique, or body
plethysmography
Factors known to alter the FRC
• Body habitus: height, obesity
• Sex: FRC is reduced by about 10% in females compared with males.
• Increased intraabdominal pressure: laparoscopic procedures, pregnancy, significant
ascites
• Posture: FRC decreases as a patient is moved from an upright to a supine or prone
position.
• Lung disease: Decreased compliance of the lung, chest, or both is characteristic of
restrictive pulmonary disorders, all of which are associated with a low FRC
• Diaphragmatic tone: its contribution is evident with unilateral or bilateral phrenic
nerve paralysis
Closing Capacity
• Volume at which these airways begin to close in dependent areas of the lung is
called the closing capacity
• small airways lacking cartilaginous support depend on radial traction caused by
the elastic recoil of surrounding tissue to keep them open; patency of these
airways, particularly in dependent areas of the lung, is highly dependent on
lung volume.
• At lower lung volumes, alveoli in dependent areas continue to be perfused but
are no longer ventilated; the resulting intrapulmonary shunting of
deoxygenated blood (venous admixture) promotes hypoxemia.
• Closing capacity is normally well below FRC but rises steadily with age
• This increase is probably responsible for the normal age related decline in
arterial O2 tension.
• Unlike FRC, closing capacity is unaffected by posture.
• Closing capacity also approaches or exceeds FRC in morbid obesity
Vital Capacity

• Vital capacity (VC) is the maximum volume of gas that can be exhaled
following maximal inspiration.
• In addition to body habitus, VC is also dependent on respiratory muscle
strength and chest–lung compliance.
• Normal VC is about 60 to 70 mL/kg.