phys chapter 37
Mechanics of Pulmonary Ventilation
 Lungs can be expanded and contracted in two ways
o Downward and upward movement of diaphragm to lengthen or shorten chest cavity
o Elevation and depression of ribs to increase and decrease anteroposterior diameter of chest cavity
 During normal breathing, inspiration is almost entirely contraction of the diaphragm and expiration is elastic
recoil of lungs, chest wall, and abdominal structures
 During heavy breathing, elastic relaxation is not enough, so abdominal muscles contract, pushing abdominal
contents upward against bottom of diaphragm, forcefully compressing lungs to expel air
 When rib cage is elevated, ribs project almost directly forward (instead of normal downward), so sternum moves
forward, making anteroposterior thickness of chest about 20% greater during maximum inspiration than during
expiration
o Most important muscles that do this are external intercostals, but they are helped by
sternocleidomastoid, serratus anterior, and scalenes
o Muscles that pull rib cage down are rectus abdominis and internal intercostals
 Lung is only held in place by the hilum, so it is free to move in thoracic cavity, but continual suction of excess
fluid into lymphatic channels maintains slight suction between visceral surface of lung pleura and parietal
pleural surface of thoracic cavity, so lungs are held to thoracic wall as if glued there
 Pleural pressure – pressure of fluid in space between lung pleura and chest wall pleura
o Normal pleural pressure at the beginning of inspiration is about -5 cm H2O, which is the amount of
suction required to hold lungs open to resting level
o During normal inspiration, expansion of chest cage pulls outward on lungs, creating average force of
about -7.5 cm H2O
 Alveolar pressure – pressure of air inside lung alveoli
o When glottis is open and no air is flowing into or out of lungs, all of respiratory tree pressure is equal to
air pressure (0 cm H2O)
o During normal inspiration, alveolar pressure decreases to about -1 cm H2O, enough to pull 0.5 liter of air
into lungs in the 2 sec required for normal quiet inspiration
o During expiration, the above process reverses, and alveolar pressure is about +1 cm H2O
 Transpulmonary pressure – difference between alveolar pressure and pressure on outer surfaces of lungs –
measure of elastic forces in lungs that tend to collapse lungs at each instant of respiration (recoil pressure)
 Lung compliance – extent to which lungs expand for each unit increase in transpulmonary pressure (if allowed to
reach equilibrium) – expressed in mL/cm H2O
o
o
Above curves are expiratory compliance curve and inspiratory compliance curve
Determined by elastic forces of lungs (elastic forces of lung tissue and elastic forces caused by surface
tension of fluid lining inside walls of alveoli and other lung air spaces
 Elastic forces of lung tissue caused by elastin and collagen fibers in lung parenchyma
 Elastic forces due to surface tension – when lungs are filled with air, there is an interface
between alveolar fluid and air in alveoli – if lungs were filled with saline, for example, there
would not be this interface, and lung would have much less compliance (fluid-air interface
represents about 2/3 of compliance of lung tissue)
Surfactant, Surface Tension, and Collapse of Alveoli

When water forms a surface with air, water molecules on surface of water have an especially strong attraction
for one another, causing water surface to always attempt to contract – in the lung, this results in an attempt to
force air out of alveoli through bronchi and, in doing so, causes alveoli to try to collapse – net effect is to cause
an elastic contractile force of the entire lungs (surface tension elastic force)
o Surfactant is surface active agent in water (greatly reduces surface tension)
 Type II alveolar cells (10% of surface area) – granular, containing lipid inclusions that are secreted in surfactant
o Most important surfactant ingredients are dipalmitoylphosphatidylcholine (phospholipid), surfactant
apoproteins, and Ca2+ ions
o Phospholipids responsible for reducing surface tension because they do not dissolve uniformly in fluid
lining of alveolar surface (part of molecule dissolves while remainder spreads over surface of water)
 Pressure = 2(surface tension)/(radius of alveolus)
o This is especially significant in small premature babies, many of whom have alveoli with radii less than
one quarter that of an adult
o Surfactant does not normally begin to be secreted into alveoli until 6-7 months of gestation, and in some
cases, even later than that
o Both of above points lead to lung collapse in premature infants (respiratory distress syndrome)
 If air passages leading from alveoli are blocked, surface tension in alveoli tends to collapse it, creating positive
pressure in alveoli, attempting to push air out
 Compliance of combined lung-thorax system is almost exactly one half that of lungs alone
o When lungs are expanded to high volumes or compressed to low volumes, limitations of chest become
extreme; when near these limits, compliance of combined lung-thorax system can be less than 1/5 that
of lungs alone
 Work of inspiration can be divided into three fractions
o that required to expand lungs against the lung and chest elastic forces (compliance or elastic work)
o that required to overcome viscosity of lung and chest wall structures (tissue resistance work)
o that required to overcome airway resistance to movement of air into lungs (airway resistance work)
 One of major limitations on intensity of exercise that can be performed is person's ability to provide enough
muscle energy for respiratory process alone (during strenuous exercise, work can be 50x normal value)
Pulmonary Values and Capacities
 Spirometry – recording volume movement of air into and out of lungs
 Tidal volume (VT) is volume of air inspired or expired with each normal breath
 Inspiratory reserve volume (IRV) is extra volume of air that can be inspired over and above normal tidal volume
 Expiratory reserve volume(ERV) is maximum extra volume of air that can be expired by forceful expiration after
end of normal tidal expiration
 Residual volume (RV) is volume of air remaining in lungs after most forceful expiration
 Inspiratory capacity (IC) = VT + IRV
 Vital capacity (VC) = IC + ERV
 Total lung capacity (TLC) = VC + RV
 Functional residual capacity (FRC) = ERV + RV

FRC is an important value because changes in its volume could be indicative of some types of pulmonary disease
o Can be measured with spirometer with helium in it – person breathes out then inhales from spirometer
and FRC is calculated by:
FRC = (CiHe/CfHe – 1)ViSpir
where CiHe is the initial concentration of He in spirometer, CfHe is final concentration of He in spirometer,
and ViSpir is initial volume of spirometer
 Minute respiratory volume – total amount of new air moved into respiratory passages each minute (VT x number
of breaths per minute) – this is indicated by putting a dot over the V (can’t do this in Word)
Alveolar Ventilation
 Alveolar ventilation – rate at which new air reaches alveoli
 Dead space air – air in areas where gas exchange does not occur (such as nose, trachea, etc.)
 Dead space volume can be calculated by having the patient take a deep breath of pure oxygen, then having
them exhale into a rapidly recording nitrogen meter, which makes a figure like below
first portion of expired air comes from dead space regions of respiratory passageways, where air has been
completely replaced by oxygen (alveoli will contain residual volume of previously inspired air) and dead space
volume (VD) is calculated by (VE is total expired air volume)
VD = (Gray area x VE)/(pink area + gray area)
 Dead space air volume increases slightly with age
 Anatomic dead space – measured as VD above; volume of all space of respiratory system other than areas
where gas exchange normally occurs
 Physiologic dead space – total volume of respiratory tract that is not actively participating in gas exchange (this
includes nonfunctional alveoli) – usually relatively equal to anatomic dead space in a normal, healthy person
 Rate of alveolar ventilation is calculated by
VA = Freq x (VT – VD )
Where VA is the volume of alveolar respiration per minute, and Freq is the frequency of respiration per minute
Functions of Respiratory Passageways
 Alveolar enlargement through respiration is what keeps the bronchioles open (those spaces without cartilage
rings or plates)
 Walls of trachea, bronchi, and bronchioles (not respiratory bronchioles) made of smooth muscle – excessive
contraction is result of many obstructive diseases
o Other causes of obstructive diseases are edema in bronchiole walls or mucus collecting in lumens of
bronchioles
 SNS stimulation caused by norepinephrine and epinephrine, and PNS stimulation caused by acetylcholine
o Atropine blocks acetylcholine and can be used to help with asthma
o Irritation of epithelial membrane of respiratory passageways by noxious gases, dust, cigarette smoke, or
bronchial infection can also activate PNS nerves
 Histamine and slow reactive substance of anaphylaxis – substances released by mast cells during allergic
reactions (especially those caused by pollen)
o Smoke, dust, sulfur dioxide, etc., can act directly on lung tissues to initiate local, non-nervous reactions
that cause obstructive constriction of airway

Mucus secreted by goblet cells and small submucosal glands keeps surfaces moist and traps small particles of
inspired air to keep it from reaching alveoli (remember mucous escalator system from histo) – cilia in respiratory
tract beat upwards and those in nose beat downwards to bring mucous to pharynx for expulsion or swallowing
 Cough reflex – particles touching bronchi or trachea (carina and larynx especially sensitive) cause cough
o Afferent nerves – vagus nerve; this goes to medulla of brain, which signals efferent response
o Large breath is inspired, epiglottis closes, and vocal cords shut tightly to entrap air within lungs;
abdominal muscles contract forcefully, pushing against diaphragm, and other accessory expiratory
muscles contract forcefully; pressure in lungs rises, and vocal cords and epiglottis suddenly open widely
so that air under high pressure in lungs explodes outward – rapidly moving air brings particles with it
o Strong compression of lungs collapses bronchi and trachea by causing noncartilaginous parts to
invaginate inward, so exploding air passes through bronchial and tracheal slits
 Sneeze reflex – CN V carries afferent impulses to medulla, where reflex is triggered
o Cough reflex is initiated except that uvula is depressed, so large amounts of air pass rapidly through
nose instead of out mouth, clearing nasal passages of foreign matter
Normal Respiratory Functions of Nose
 Nose conchae warm and humidify air for inspiration, and nasal passages partially filter air
o Inspired air rises to within 1o F of body temperature and within 2-3% of full saturation with water vapor
before it reaches the trachea
 If person breathes through tracheostomy tube or other such artificial way without conditioned air, serious lung
crusting and infection can ensue
 Nasal hairs at entrance to nostrils are important for filtering out large particles, and most of other particles
removed by turbulent precipitation
o Air passes over conchae and becomes turbulent as it passes over these and hits nasal septum and
pharyngeal wall; each time air hits one of the obstructions, it must change direction, and particles
suspended in the air (having much more mass and momentum than air) cannot change direction of
travel and will be trapped by the mucous coating and transported by the cilia to be expelled
o Nasal filtration system is so efficient that almost no particles larger than 6 µm (smaller than RBCs) can
pass into lungs through nose
 Particles not removed by nasal filtration – many 1-5 µm in size settle in smaller bronchioles by gravitational
precipitation (this is why black lung is common in coal miners)
 Particles that are less than 1 µm diffuse against walls of alveoli and adhere to alveolar fluid – these are removed
by alveolar macrophages and carried away by lymphatic system
 Particles less than 0.5 µm in diameter remain suspended in alveolar air and are expelled by expiration
 Excess of particle inhalation can cause growth of fibrous tissue in alveolar septa, leading to permanent debility
Vocalization
 Speech is composed of 2 mechanical functions: phonation (achieved by larynx) and articulation (modification of
sounds through structures of mouth and pharynx)
 Closer vocal cords are to each other, the louder the noise they will make
 Pitch is determined by degree of stretch of vocal cords and somewhat by how tightly cords are approximated to
one another and mass of their edges
 Vocal cords attached by vocal ligaments to thyroid cartilage (anteriorly) and by vocal process to arytenoid
cartilages (posteriorly)
 Vocal cords can be stretched by either forward rotation of thyroid cartilage or posterior rotation of arytenoid
cartilages
 Slips of muscles within the vocal cords can change shapes and masses of vocal cord edges, sharpening them to
emit high-pitched sounds and blunting them for more bass sounds
 Muscles between arytenoid cartilages and cricoid cartilage can rotate arytenoid cartilages inward or outward or
pull bases together or apart to give various configurations of vocal cord sounds