Every cell in the body needs a constant supply of oxygen to produce energy to grow, repair or replace itself and to maintain
normal vital functions. The respiratory system is the body's link to its supply of oxygen. It includes the diaphragm and chest
muscles, the nose and mouth, the pharynx and trachea, the bronchial tree and the lungs. The bloodstream, heart and brain are
also involved. The bloodstream takes oxygen from the lungs to the rest of the body and returns carbon dioxide to them to be
removed. The heart creates the force to move the blood at the right speed and pressure throughout the body. The smooth functioning
of the entire system is directed by the brain and the autonomic nervous system.
Air containing oxygen enters the body through the nose and mouth. From there it passes through the pharynx on its way to the
trachea. The trachea divides into two main bronchi upon reaching the lungs. One bronchus serves the right lung and the other
serves the left lung. The bronchi subdivide several times into smaller bronchi, which then divide into smaller and smaller
branches called bronchioles. After many subdivisions, the bronchioles end at the alveolar ducts. At the end of each alveolar
duct are clusters of alveoli. The oxygen transferred through the system is finally transferred to the bloodstream at the alveoli.
Blood vessels from the pulmonary arterial system accompany the bronchi and bronchioles. These blood vessels also branch into
smaller and smaller units ending with capillaries, which are in direct contact with each alveolus. Gas exchange occurs through
this alveolar-capillary membrane as oxygen moves into and carbon dioxide moves out of the bloodstream (perfusion). In the
blood, oxygen is transported in two forms: dissolved in plasma (which is measured by PO2) and bound to hemoglobin (measured by SpO2). The amount of oxygen bound to hemoglobin is much larger than the amount dissolved in plasma. The "matching" of ventilation
and perfusion is important to proper lung function. It does no good to ventilate an alveolus that is not being perfused (alveolar
dead space) or to perfuse an alveolus that is not being ventilated because of atelectasis. In the normal lung, ventilation
and perfusion are not evenly matched (known as V/Q mismatch) and this worsens with lung disease and dorsal or lateral recumbencies.
Both ventilation and perfusion increase toward the dependant regions of the lung, but since blood is heavier than lung parenchyma,
perfusion increases at a faster rate than ventilation. Vasodilation or vasoconstriction, caused by disease or anesthetic drugs,
enhances V/Q mismatching and hypoxemia. From an anesthetic point of view, alveolar ventilation is very important because this
will control the amount of volatile or gaseous anesthetic agent that can diffuse into the bloodstream. Any increase in alveolar
ventilation will increase anesthetic uptake into the pulmonary blood.
The movement of air into and out of the lungs is called ventilation. The contraction of the inspiratory muscles, mainly the
diaphragm, causes the chest cavity to expand, creating negative pressure. This is inspiration. During maximal inspiration,
the diaphragm forces the abdominal ventrally and caudally. The external intercostal muscles are also involved. These muscles
contract and raise the ribs during inspiration, increasing the diameter of the chest cavity.
Normal expiration is a passive process resulting from the natural recoil or elasticity of the expanded lung and chest wall.
However, when breathing is rapid, the internal intercostal muscles and the abdominal muscles contract to help force air out
of the lungs more fully and quickly. At the end of inspiration, the elasticity of the lung causes it to return to its smaller
interbreath size. The ability to do this is called elastic recoil. The volume of air remaining in the lung at the end of a
normal breath (the end expiratory lung volume) is the functional residual capacity (FRC). FRC is composed of the expiratory
reserve volume and the residual volume. On expiration, there is still air left in the lungs, if there weren't, all of the
alveoli would collapse. FRC decreases slightly in supine and lateral recumbency compared to prone. FRC is diminished with
small airway diseases. At FRC the alveoli in the non-dependant lung sections is larger than those in the dependant regions
because of gravity and the weight of the lung. Alveoli in the dependant regions are squashed and compressed by the weight
of the overlying lung tissue. In lateral or dorsal positions the dependant alveoli are also compressed by the weight of the
mediastinal structures and by the weight of the abdominal contents pressing against the diaphragm. In patients with large
abdominal masses or excessive bloating (GDV) the problem becomes especially significant.
In spite of many protective mechanisms in place in the lungs, including FRC, small airway and alveolar collapse (atelectasis)
still occurs in the normal animal. Atelectasis is especially prominent in the dependant lung regions when an animal is recumbent.
Intermittent deep positive pressure breaths in the anesthetized patient can help minimize small airway and alveolar collapse.
The use of positive end expiratory pressure (PEEP) has been proven to help as well. PEEP increases airway pressure and FRC
to help keep small airways and alveoli open. PEEP valves are commercially available (in 5, 10, and 15 cm H2O) and can be added
to the anesthesia machine for this purpose. Unfortunately, once atelectasis has occurred, it is very difficult to open the
closed alveoli. Applying excessive pressure in an attempt to open alveoli (as in the case of attempting to re-inflate a packed
off lung during a thoracotomy) tends only to damage the already working tissue (barotrauma) before re-inflation takes place.
Re-inflation is a slow, delicate process and will happen on its own in healthy tissue over time or once recumbency or insult
The degree of stiffness or compliance of the lung tissue affects the amount of pressure needed to increase or decrease the
volume of the lung. With increasing stiffness, the lung becomes less able to return to its normal size during expiration.
Virtually all diseases cause the compliance of the lungs to decrease.
The amount of airflow resistance can also affect lung volumes. Resistance is the degree of ease in which air can pass through
the airways. It is determined by the number, length and diameter of the airways. An animal with a high degree of resistance
may not be able to exhale fully, thus some air becomes trapped in the lungs.
Ventilation is the process by which gas in closed spaces is renewed or exchanged. As it applies to the lungs, it is a process
of exchanging the gas in the airways and alveoli with gas from the environment. Breathing provides for ventilation and oxygenation.
Tidal volume is the volume of gas passing into and out of the lungs in one normal respiratory cycle. Normal tidal volume for
mammals is 10-20 ml/kg. Minute volume is used to describe the amount of gas moved per minute and is approximately 150-250
ml/kg/minute. Minute volume = tidal volume x respiratory rate. It is alveolar ventilation that is important for gas exchange
however. Tidal volume is used to ventilate not only the alveoli, but also the airways leading to the alveoli. Because there
is little or no diffusion of oxygen and carbon dioxide through the membranes of the airways, they comprise what is known as
dead space ventilation. The other part of dead space is made up of alveoli with diminished capillary perfusion. Ventilating
these alveoli is ineffective and will do nothing to improve blood gases. The non-perfused alveoli and the airways are known
as physiologic dead spaces. Therefore tidal volume has a dead space component and an alveolar component. Dead space ventilation
is about 30-40% of tidal volume and minute volume in a normal patient breathing a normal tidal volume. Dead space ventilation
has a purpose. It assists in humidifying and tempering inhaled air and it cools the body as in panting. Panting is predominantly
dead space ventilation. During panting, the respiratory frequency increases and the tidal volume decreases, so that alveolar
ventilation remains approximately constant. This is the reason that when animals under anesthesia pant, they very often wake
up. They are not effectively ventilating their alveoli and exchanging gas well. Often times these patients will be hypercarbic
because they are not able to effectively reduce their carbon dioxide levels. Slower, deeper breaths are usually more efficient.
Certain pieces of anesthesia equipment can add to the anatomical dead space of a patient by "extending" their airways. Endotracheal
tubes that are too long and extend far beyond the patient's nose would be an example. Adding this dead space presents a further
challenge to patients trying to effectively ventilate.
Monitoring ventilation on patients under anesthesia can be done a number of ways. Ventilation is assessed in terms of rate,
rhythm, and tidal volume. First of all, a good look at the patient's chest excursions should be done to evaluate for quality
and effort. Auscultation of the lungs should be performed prior to sedating or anesthetizing any patient. Normal lung sounds
should be heard on both sides of the chest. Any abnormal sounds should be investigated prior to moving forward with anesthesia
as anesthetic drugs can depress respiration and ventilation and may worsen existing problems.
Mucous membrane color should be assessed regularly. The tongue and gums should be pink. Any change in color, especially blue
or purple tingeing can indicate hypoxemia.
Respirometers can be used to measure tidal volume and minute volume. Expired gas passes through oblique slits, which creates
circular gas flow in a chamber, causing rotation of a double-vaned rotor. The rotor is coupled via a set of linkage gears
to a display indicator dial and needle. Accumulated minute volume is recorded and each breath's tidal volume can be viewed.
The respirometer measures volume in one direction only. Flow can be calculated by averaging recorded volumes over time. Owing
to inertia in the system it tends to overestimate higher volumes and underestimate lower volumes.
Apnea or respiratory monitors detect the movement of gas through the proximal end of the endotracheal tube. They provide no
information on tidal volume or the physiologic state of the patient. They can be falsely activated by pressure on the chest
or abdomen of the patient or by cardiac oscillations that cause gas movement in the trachea.