1 - Weebly

							1. Describe the mechanics of normal respiration
3 different pressures affect ventilation:
1. Atmospheric Pressure - Pressure exerted by weight of air in atmosphere on
objects on Earth’s surface - approximately 760mmHg at sea level (decreases w/
altitude)
2. Intraalveolar Pressure (Intrapulmonary p.) – the pressure of air in alveoli;
alveoli communicate with the atmosphere (via conducting airways)
- Air flows down pressure gradient any time intra-alveolar pressure differs from
atmospheric pressure - Airflow continues until 2 pressures equilibrate
3. Intrapleural Pressure (Intrathoracic p.) – the pressure within the pleural cavity.
This is usually less than atmospheric p. ~756mmHg. Atmospheric P is given the
reference value of 0mmHg, meaning IP = -4 mmHg. This negative pressure in the
alveolar space is important for keeping the airways open that do not have the benefit
of a cartilaginous ring – this is due to a pressure gradient in which the pleural pressure
is kept less than the pressure inside the conducting tubes (thus preventing collapse of
the tubes).

Two forces hold the thoracic wall and lungs in close proximity;
  - Intrapleural Fluid Cohesiveness – Pleural Cavity contains two surfaces, the
       Visceral and Parietal Pleural surfaces, and contains a fluid to prevent any
       friction occurring between the surfaces during the respiration process.
       However, the fluid inside the cavity contains polar water molecules which
       resist being pulled apart. This therefore acts to hold the pleural surfaces
       together. As a result, a change in thoracic volume equals a change in lung
       dimension, and the lung follows the movement of the chest wall.
  - Transmural pressure gradient - Net pressure of 4mmHg pushing outwards
       (760mmHg Intraalveolar/atmospheric pressure pushing outwards on pleural
       membranes, and only 756mmHg (pressure in pleural cavity) pushing inwards).
       = Intraalveolar P. – Intrapleural P.
NB// also a transmural pressure gradient across thoracic wall (atm. P - Ip. P)

Hence, increasing or decreasing volume of lungs will lead to a differential in pressure
causing air to flow in or out of the lungs until equilibrium is reached.
Inspiration
Expansion of chest cage causes more negative pressure in lungs. P becomes less than
760mmHg, which results in air flowing in. This occurs via;

– active diaphragm contraction, external intercostal contraction which increases the
vertical diameter of the chest
– costal elevation & expansion resulting in:
    - pump handle action of the upper 8 ribs (sternum) (increases the AP diameter
        of the chest)
    - bucket handle action of the lower 4 ribs (increases the transverse diameter of
        the chest

Accessory muscles of inspiration:
- Sternocleidomastoid muscles - lifts sternum
- Scalene muscles (anterior, middle and posterior) - attach to both cervical vertebral
column and to ribs 1&2
- Pectoralis Minor
- Serratus Anterior




Expiration
Is a passive process – elastic recoil of lungs upon relaxation of diaphragm & external
intercostals. Decreased volume leads to an increased pressure > than atmospheric and
air flows out.
– Gravity acting on the elevated rib cage reduces the vertical axis when intercostals
not contracted

Active or forced expiration is achieved by the action of internal intercostal muscles,
abdominal muscles and muscles of transversus thoracis
2. Explain the mechanisms leading to the consequences of airway
   obstruction (normal airway airflow, work of breathing,
   hyperinflation and gas trapping, alteration of V/Q relationships).
Flow depends not only on pressure gradient but also on the resistance to flow of the
vessel ie;

                                       F= ∆P/R
Where F=flow
        ∆P= Diff between alveolar and atmospheric pressure
        R= Resistance of airways - primarily determined by radii (Poiseuille’s Law)
Normally, airways offer such low resistance that only a small pressure gradient of
1-2 mmHg need to be created to achieve adequate rates of airflow in and out of the
lungs. These modest changes to airway size can be made via autonomic control;
    - Parasympathetic Nervous System – causes bronchiolar smooth muscle
        contraction ie bronchoconstriction which increases airway resistance
    - Sympathetic tone esp. via adrenalin causes bronchodilatation. This ensures
        that during high O2 demand, P caused by respiratory muscles achieves
        maximal flow rate with minimal resistance (thus adrenalin and similar drugs
        sometimes good to treat bronchial spasms)

Chronic Obstructive Pulmonary Diseases (COPD) are a group of lung diseases
characterised by increased airway resistance from narrowing of the lumen of lower
airways. it is the fact that the pleural pressure is less than the airway pressure that
keeps the airways open. Since the airways are severely constricted in asthma, this
pressure needs to be further decreased in an attempt to keep the airways open. This is
achieved by inflating the lungs further than what they would normally be ie
Hyperinflation. The increase in resistance also means that a larger pressure gradient
must be established to maintain normal airflow rate – the body must work harder to
breath and accessory muscles will be employed to aid breathing.

Examples of COPD include;

1. Chronic Bronchitis - stimulated by frequent Allergen/irritant exposure and chronic
inflammation, prolonged oedematous thickening of airway linings with
overproduction of thick mucous, and an inability to satisfactorily remove mucous due
to paralysed ciliary mucous elevator with resultant frequent bacterial infections.
2. Asthma (chronic) due to -
        a. Thickening of airway walls due to inflammation and histamine induced
        oedema.
        b. Plugging of airways by excessive secretion of thick mucous
        c. Airway hyper-responsiveness characterised by trigger induced excessive
        and spasmodic constriction of smooth muscle in smaller airways
3. Emphysema - collapse of smaller airways (increased IP P.) and breakdown of
alveolar walls which is irreversible due to;
- Excessive release of destructive enzymes from alveolar macrophages overwhelms
protective enzymes as response to chronic exposure to cigarette smoke
- A genetic deficiency of protective enzymes.
Airway collapse - Frictional losses cause airway P to fall below the surrounding
elevated intrapleural pressure. Small non-rigid airways become compressed closed
which blocks further expiration. Air is therefore trapped within alveoli ie Gas
Trapping. The Residual Volume (RV) is the amount of air left in alveoli after
maximal expiration and increases in COPD.


3. Understand blood-gas exchange, including oxygen saturation and
   partial pressure relationships, ventilation-perfusion relationships,
   physiological deadspace and shunting.

    Gases flow from regions of higher pressure to regions of lower pressure – this is
     called flow “down the pressure gradient”, and is a passive process.
    Dry atmospheric air is composed mainly of nitrogen (~79%) and oxygen (~21%),
     with small amounts of CO2, other gases and pollutants.
    Partial pressure is the amount of pressure an individual gas contributes to the
     total pressure exerted by a mixture of gases. The partial pressure is proportional
     to the molar amount of any gas. Atmospheric pressure is ~760 mmHg at sea
     level, and oxygen thus contributes 160mmHg (21% x 760 mmHg = 160 mmHg).
    In the mixture of gases that reaches the alveoli, the partial pressure of oxygen is
     considerably lower than 160 mmHg for two reasons. First, the air is humid in the
     airways, thus water vapour contributes to the pressure of the mixture. Secondly,
     not all air that enters the alveoli is freshly inspired (~150ml is air remaining in
     airways (Dead Space) after expiration).
    The partial pressure of oxygen in the lungs is usually ~100mmHg (denoted PAO2).
    This rule of gas movement also holds true at gas-liquid interfaces; the gas will
     dissolve in liquid along its pressure gradient. Some gases are more soluble than
     others. For example, CO2 is ~20x more soluble in blood than is O2. Thus, for a
     given pressure gradient, CO2 will dissolve much more quickly and more
     extensively than will O2.
    In the capillary bed of the lungs, O2 moves into blood, and CO2 moves out, into
     the alveolar air. The following table (adapted from Sherwood) summarizes the
     partial pressures of O2 and CO2 in the respiratory/vascular system:

Region                                               PO2 (mmHg)    PCO2 (mmHg)
Atmospheric air                                          160            0.03
Alveoli
Pulmonary veins (returning to heart)                     100             40
Systemic arteries
Tissue cell                                              <40            >46
Systemic veins
Pulmonary arteries (heart → lungs)                       40              46
NB Net diffusion gradients between the lungs & tissues

    The gases will diffuse between the alveoli air and the blood of the pulmonary
     capillary bed until equilibrium is reached. As previously stated, oxygen is not
     very soluble in blood; approximately 3mL O2 dissolves in 1L of blood.
    Most oxygen in the blood is associated with haemoglobin (approximately 98%),
     allowing oxygen content in the blood to reach ~200mL O2/L blood.
    Haemoglobin will bind O2 based on a characteristic “dissociation curve” (see
     kates LO’s from last week). This curve shows that under physiological
    conditions, the haemoglobin can reach it’s oxygen carrying capacity; that is, it
    will become saturated at PAO2 far less than 100 mmHg:




                           Fig. (Lectures by Jon Curlewis, Wk. 14/15, 2005)


   This curve also helps to explain that exchange of CO2 and O2 in the human lungs
    are “perfusion limited”, and not “diffusion limited” (NB// can be diffusion limited
    in conditions such as Emphysema and Pulmonary Oedema as they decrease the
    surface area and thickness of the respiratory membrane which ultimately affects
    diffusion rate). The equilibration of partial pressures occurs more rapidly than
    does the flow of blood i.e. all the diffusion that is going to occur does so within
    0.25 seconds; blood flows past the respiratory membrane in 0.75s. if O2
    consumption and CO2 production increase, an increase in blood flow (perfusion)
    will compensate (due to effects on respiratory centres in the brain).
   To maximize the efficiency of gas exchange, the body matches ventilation
    (delivery of inspired air) with perfusion (delivery of blood). This is done via the
    autonomic nervous system. Regions of poor ventilation will bronchodilate due to
    the build up in CO2. Regions of elevated perfusion will vasoconstrict due to
    decreased O2.
   If ventilation/perfusion mismatch cannot be compensated for by the above stated
    mechanism, Type I respiratory failure occurs. A typical example is asthma.
    Some capillary beds have high ventilation / perfusion ratios (V/Q), while others
    have low V/Q ratios. The result is decreased PaO2 and decreased PaCO2.
   Another type of respiratory disorder causing Type I failure is “shunting”. The
    blood gas levels are affected in a similar way to those seen in altered V/Q
    relationships. Shunting is basically an extreme form of V/Q mismatch; some
    regions of the lung are not being perfused at all.
   Clinically, V/Q mismatch can be distinguished from shunting by administering
    nearly pure oxygen to the patient. If shunting is occurring, PaO2 will be almost
    completely unchanged. If the patient is suffering a V/Q mismatch, PaO2 will
    increase. This is because the poorly ventilated regions of the lung will be getting
    more O2 delivered to them, effectively raising the V/Q to more normal levels.
4. Outline assessment of lung function, the methods used and
   interpretation of data.




Tidal Volume: Volume of air entering or leaving lungs during single breath ~500 mL
under resting conditions
Inspiratory Reserve Volume: Extra volume of air that can be maximally inspired
over TV
Inspiratory Capacity: Maximum volume of air that can be inspired at end of a
normal quiet expiration
Expiratory Reserve Volume: Extra volume of air that can be actively expired by
maximal contraction of expiratory muscles
Residual Volume: Minimum volume of air remaining in lungs even after a maximal
expiration (~1200 mL)
Functional Residual Capacity: Volume of air in lungs at end of normal passive
expiration
(2200 mL)
Vital Capacity: Maximum volume of air that can be moved out during a single breath
following a maximal inspiration (Inspires maximally + Expires maximally) ~ 4500
mL
Total Lung Capacity: Maximum volume of air that the lungs can hold (~5700 mL)

A variety of tests are used to measure lung function, including vitalograph spirometer
and pneumotachograph.

The vitalograph spirometer measures volume of expired air with respect to time. The
pneumotachograph is computer based, and measures airflow (inspired and expired)
with respect to volume of air (inspired or expired).
The vitalograph spirometer gives the following measurements:
Forced Vital Capacity (FVC) ; the total amount of air you can expire after maximal
inspiration
Forced Expiratory Volume at 1 second (FEV1); the amount of air expired after one
second, expressed as a percentage of FVC ~ 80% in healthy person

The pneumotachograph provides FVC, as well as:
Peak Expiratory Flow (PEF), and Peak Inspiratory Flow (PIF), which like FEV1
are a measure of resistance; in a healthy person without significant airway resistance,
PEF should be reached by the time 15% of FVC has been expired. PIF is usually
reached after ~50% of the FVC has been inspired. PEF>PIF due to elastic recoil of
lungs and abdominal muscles