Phys Ch 42
Useful Methods for Studying Respiratory Abnormalities
 Blood pH measured using miniature glass pH electrode – voltage generated by glass electrode is direct measure
of pH
 When weak solution of sodium bicarbonate is exposed to CO2 gas, CO2 dissolves in solution until equilibrium
state is established – using Henderson-Hasselbalch equation
pH = 6.1 + log (HCO3-/CO2)
 Concentration of oxygen can be measured by polarography – electric current is made to flow between small
negative electrode and solution; if voltage is more than -0.6 volt different from voltage of solution, oxygen will
deposit on electrode
o Rate of current flow through electrode is directly proportional to concentration of O2
o Negative platinum electrode is used, separated from blood by thin plastic membrane that allows
diffusion of oxygen but not proteins or other substances that will “poison” electrode
 Very often pH, PO2, and PCO2 are all determined by the same machine at once in modern practice
 In many respiratory diseases, particularly asthma, resistance to airflow becomes especially great during
expiration
o Maximum expiratory flow – when person expires with great force, expiratory airflow reaches maximum
flow beyond which flow cannot be increased anymore, even with greatly increased additional force
o Maximum expiratory flow is much greater when lungs are filled with large volume of air than when they
are almost empty
o Increased pressure from within tends to collapse bronchioles at the same time as expelling air from
alveoli, causing still greater increase in alveolar pressure and increasing degree of bronchiolar collapse
and airway resistance, preventing further increase in flow
o As lung volume becomes smaller, maximum expiratory flow rate becomes less because enlarged lung
partially holds bronchi and bronchioles open by elastic pull on their outsides by lung structural elements,
but as lung becomes smaller, these structures are relaxed so bronchi and bronchioles are collapsed
more easily by external chest pressure
 Constricted lungs have both reduced total lung capacity (TLC) and reduced residual volume (RV); because lung
cannot expand to normal maximum volume, maximal expiratory flow cannot rise to equal that of normal curve
o Constricted lung diseases include tuberculosis, silicosis, kyphosis, scoliosis, and fibrotic pleurisy
 Airway obstruction has more difficulty expiring than inspiring because of tendency of airways to close is greatly
increased by extra positive pressure required in chest to cause expiration – extra negative pleural pressure that
occurs during inspiration pulls airways open at same time that it expands alveoli, so air tends to enter lung and
becomes trapped, increasing both TLC and RV – because they collapse more easily than normal airways,
maximum expiratory flow rate is greatly reduced
o Airway obstruction diseases include asthma and some stages of emphysema
 Forced expiratory vital capacity (FVC) – person first inspires maximally to total lung capacity and then exhales
into spirometer with maximum expiratory effort as rapidly and completely as possible; total distance of
downslope represents FBC
o
o
Note total volume is about the same, but the rate of expiration is very different
FEV1 is forced expiratory volume during first second – used to calculate percentage of air expelled in the
first second (should be around 80% for a healthy person)
Chronic Emphysema
 Pulmonary emphysema stages and development
o Chronic infection caused by inhaling smoke or other substances that irritate bronchi and bronchioles
that messes up normal protective mechanisms of airways, including partial paralysis of cilia of
respiratory epithelium (can be caused by nicotine)
 Also stimulates excess mucus secretion, exacerbated by fact that cilia are paralyzed and cannot
expel it properly
 Inhibition of alveolar macrophages occurs so they become less effective in combating infection
o Infection, excess mucus, and inflammatory edema of bronchiolar epithelium cause chronic obstruction
of many smaller airways
o Obstruction of airways makes it especially difficult to expire, causing entrapment of air in alveoli and
overstretching them
 Causes marked destruction of 50-80% of alveolar walls
 Physiologic effects of chronic emphysema depends on severity of disease and relative degrees of bronchiolar
obstruction versus lung parenchymal destruction
o Bronchiolar obstruction increases airway resistance and results in greatly increased work of breathing
o Marked loss of alveolar walls greatly decreases diffusing capacity of the lung, reducing ability of lungs to
oxygenate blood and remove carbon dioxide from blood
o Obstructive process is worse in some parts of lung, while others are well ventilated, causing extremely
abnormal ventilation-perfusion ratios (physiologic shunts in areas of low Va/Q and physiologic dead
space in areas of very high Va/Q
o Loss of large portions of alveolar walls decrease number of pulmonary capillaries through which blood
can pass, causing marked increase in pulmonary vascular resistance and resultant hypertension,
overloading right side of heart and causing right-sided heart failure
 Chronic emphysema usually progresses slowly over many years – patient develops both hypoxia and
hypercapnia because of hypoventilation of many alveoli plus loss of alveolar walls
Pneumonia
 Pneumonia – any inflammatory condition of the lung in which some or all of alveoli are filled with fluid and
blood cells
 Pneumococci – bacterial pneumonia; begins with infection in alveoli, pulmonary membrane becomes inflamed
and highly porous so fluid and RBCs and WBCs leak out of blood into alveoli – spreads as bacteria spreads from
alveolus to alveolus
 Consolidated area of lung – area of lung filled with fluid and cellular debris

Early stages of pneumonia include a localized area with alveolar ventilation reduced while blood flow through
the lung continues normally – causes reduction in total available surface area of respiratory membrane and
decreased ventilation-perfusion ratio – causes hyoxemia (low blood oxygen) and hypercapnia (high blood CO2)
Atelectasis
 Atelectasis – collapse of alveoli that can occur because of total obstruction of the airway or lack of surfactant in
fluids lining alveoli – can occur in localized areas of lung or whole lung
 Airway obstruction atelectasis results from blockage of many small bronchi with mucus or obstruction of major
bronchus by either large mucus plug or some solid object such as a tumor
o Air entrapped beyond block is absorbed within minutes to hours
o If lung tissue is pliable enough, this will lead to collapse of alveoli
o If lung is rigid because of fibrotic tissue and cannot collapse, absorption of air from alveoli creates very
negative pressures in alveoli, which pull fluid out of pulmonary capillaries into alveoli, causing alveoli to
fill completely with edema fluid
o Massive collapse – when entire lung becomes atelectatic (usually due to rigid lung and buildup of edema
fluid)
o Collapse of lung occludes alveoli and increases resistance to blood flow through pulmonary vessels
because of lung collapse compressing the vessels and because hypoxia in collapsed alveoli causes
additional vasoconstriction
o Most of blood becomes routed through ventilated lung and becomes well aerated (5/6 of blood sent to
ventilated lung)
 In a number of diseases, such as hyaline membrane disease (respiratory distress syndrome), quantity of
surfactant secreted is so greatly depressed that surface tension of alveolar fluid becomes several times normal –
lung can then collapse or become filled with fluid by the same mechanisms as obstruction lung collapse
Asthma
 Asthma – characterized by spastic contraction of smooth muscle in bronchioles, which partially obstructs
bronchioles
 Usual cause is contractile hypersensitivity of bronchioles in response to foreign substances in air
o In 70% of patients under 30, it is caused by allergic hypersensitivity to pollen
o Older people almost always caused by hypersensitivity to nonallergenic types of irritants such as smog
 Patient’s body creates large amounts of IgE antibodies that are mainly attached to mast cells present in lung
interstitium in close association with bronchioles and small bronchi
o When person breathes in allergen, it reacts with mast cell-attached antibodies and causes mast cells to
release histamine, slow-reacting substance of anaphylaxis (mixture of leukotrienes), eosinophilic
chemotactic factor, and bradykinin
o Combined effects of all of the above are to produce localized edema in walls of small bronchioles, as
well as secretion of thick mucus into bronchiolar lumens, and produce spasm of bronchiolar smooth
muscle
 Asthmatic person often can inspire quite adequately, but has great difficulty expiring because bronchospasm is
exacerbated because of normal compression during exhalation
 Results in greatly reduced maximum expiratory rate and reduced timed expiratory volume, producing air hunger
(dyspnea)
 Functional residual capacity and residual volume of lung become especially increased during acute asthma
attack because of difficulty in expiring air from lungs
 Over a period of years, chest cage becomes permanently enlarged (barrel chest), and both functional residual
capacity and lung residual volume become permanently increased
Tuberculosis
 Tubercle bacilli cause invasion of infected tissue by macrophages and walling off of lesion by fibrous tissue to
form “tubercle”
o Walling off process helps limit further transmission of tubercle bacilli in lungs and is part of protective
process against extension of infection
o In 3% of people who contract tuberculosis, walling off process fails and tubercle bacilli spread
throughout lungs, often causing extreme destruction of lung tissue with formation of large abscess
cavities

Late stages of tuberculosis characterized by many areas of fibrosis throughout lungs
o Causes increased work for respiratory muscles to cause pulmonary ventilation and reduced vital capacity
and breathing capacity
o Causes reduced total respiratory membrane, causing progressively diminished pulmonary diffusing
capacity
o Causes abnormal ventilation-perfusion ratio in lungs, further reducing overall pulmonary diffusion of
oxygen and CO2
Classifications of Hypoxia
 Inadequate oxygenation of blood in lungs because of extrinsic reasons
o Deficiency of oxygen in atmosphere
o Hypoventilation (neuromuscular disorders)
 Pulmonary disease
o Hypoventilation caused by increased airway resistance or decreased pulmonary compliance
o Abnormal alveolar ventilation-perfusion ratio (either increased physiologic dead space or increased
physiologic shunt)
o Diminished respiratory membrane diffusion
 Venous-to-arterial shunts (i.e., right-to-left cardiac shunts)
 Inadequate oxygen transport to tissues by blood
o Anemia or abnormal hemoglobin
o General circulatory deficiency
o Localized circulatory deficiency (peripheral, cerebral, coronary vessels)
o Tissue edema
 Inadequate tissue capability of using oxygen
o Poisoning of cellular oxidation enzymes (i.e. cyanide poisoning, which blocks cytochrome oxidase)
o Lack of tissue cellular oxidative enzymes (i.e., beriberi, where several important steps in tissue utilization
of oxygen are compromised because of vitamin B deficiency)
o Diminished cellular metabolic capacity for using oxygen because of toxicity, vitamin deficiency, or other
factors
Effects of Hypoxia on the Body
 Hypoxia, if severe enough, can cause death of cells throughout body
 Causes depressed mental activity, sometimes culminating in coma
 Causes reduced work capacity of muscles
Oxygen Therapy in Different Types of Hypoxia
 Can be administered by placing the patient’s head in a “tent” that contains air fortified with oxygen, via oxygen
mask, or via intranasal tube
 If patient is suffering from atmospheric hypoxia, oxygen therapy can completely correct depressed oxygen level
 In hypoventilation hypoxia, putting the patient on 100% oxygen will help them move five times as much oxygen
into alveoli with each breath as when breathing normal air, so it can be extremely beneficial (but does not help
excess blood CO2 caused by hypoventilation)
 In hypoxia caused by impaired alveolar membrane diffusion, oxygen therapy can increase PO2 in lung alveoli to
about 6x normal value, raising oxygen pressure gradient for diffusion of oxygen from alveoli to blood, allowing
pulmonary blood to pick up oxygen 3-4 times as rapidly as would occur with no therapy
 In hypoxia caused by anemia, oxygen therapy is of much less value because the problem is that one or more of
mechanisms for transporting oxygen from lungs to tissues is deficient, not a lack of oxygen in general
o Small amount of extra oxygen can be transported in dissolved state in blood, and sometimes this small
amount of extra oxygen may be difference between life and death for patient
 Hypoxia caused by inadequate tissue use of oxygen would not benefit from oxygen therapy at all because there
is no availability of oxygen problem or transportation problem
Cyanosis
 Cyanosis – blueness of skin caused by excessive amounts of deoxygenated hemoglobin in skin blood vessels,
especially capillaries (deoxygenated hemoglobin has an intense dark blue-purple color)

Definite cyanosis appears whenever arterial blood contains more than 5 g of deoxygenated hemoglobin in each
100 mL of blood
o People with anemia is almost never cyanotic because there isn’t enough hemoglobin to have 5 g
deoxygenated
o People with excess RBCs (as occurs in polycythemia vera), great excess of available hemoglobin that can
become deoxygenated frequently leads to cyanosis, even if actual oxygen content is normal
Hypercapnia in Body Fluids
 Hypercapnia usually occurs in association with hypoxia only when hypoxia is caused by hypoventilation or
circulatory deficiency
o Hypoxia caused by too little oxygen in air, too little hemoglobin, or poisoning of oxidative enzymes only
has to do with availability of oxygen or use of oxygen by tissues, so does not cause hypercapnia
o Hypoxia resulting from poor diffusion through pulmonary membrane or through tissues usually does not
have severe hypercapnia because CO2 diffuses 20x as rapidly as O2 – if hypercapnia does begin to occur,
this immediately stimulates pulmonary ventilation, which corrects hypercapnia, but not necessarily
hypoxia
o Hypoxia caused by hypoventilation – CO2 transfer between alveoli and atmosphere is affected as much
as O2 transfer, so hypercapnia can result
o Hypoxia caused by circulatory deficiency – diminished flow of blood decreases carbon dioxide removal
from tissues, resulting in tissue hypercapnia on top of tissue hypoxia
 Transport capacity for CO2 is more than 3x that of O2, so resulting hypercapnia is much less than
tissue hypoxia
 If alveolar PCO2 rises to 60-75 mm Hg, a normal person begins to breathe as rapidly and deeply as they can (air
hunger) and severe dyspnea ensues
 If alveolar PCO2 rises to 80-100 mm Hg, person becomes lethargic and sometimes semicomatose
 Anesthesia and death can result when PCO2 rises to 120-150 mm Hg because excess CO2 begins to depress
respiration rather than stimulate it, causing a vicious cycle (more CO2 causes further decrease in respiration,
which causes more CO2 retention)
Dyspnea
 Dyspnea – mental anguish associated with inability to ventilate enough to satisfy demand for air (air hunger)
 Factors that enter into development of sensation of dyspnea
o Abnormality of respiratory gases in body fluids, especially hypercapnia and to a lesser extent hypoxia
o Amount of work that must be performed by respiratory muscles to provide adequate ventilation
 Respiratory gases may be at normal levels at this point, but forceful activity of respiratory
muscles required to maintain normal blood gas levels can give the person dyspnea
o State of mind – called neurogenic dyspnea or emotional dyspnea
 Often the type of dyspnea that occurs with people with claustrophobia or fears of crowded
rooms, etc. – mental belief that there is not enough air will cause feeling of mild dyspnea
Artificial Respiration
 Resuscitator – consists of tank supply of oxygen or air and a mechanism for applying intermittent positive
pressure and (with some machines) negative pressure
o Mask that fits over face or connector to endotracheal tube used
o Intermittent positive-pressure cycle forces air into lungs, and period between allows for passive
exhalation (with some machines, mild negative pressure can simulate exhalation with accessory
exhalation muscles)
o Positive pressure can be adjusted so as not to overfill or underfill lung
 Tank respirator (iron lung) – patient’s body inside the tank with head sticking out flexible, air-tight collar
o At end of tank opposite patient’s head, motor-driven leather diaphragm moves back and forth with
sufficient excursion to raise and lower pressure inside tank (works like normal diaphragm) – valves are
for checking pressure levels so as not to cause too forceful inspiration or expiration

Effect of resuscitator or tank respirator on venous return – in both cases, pressure inside lungs becomes greater
than pressure everywhere else in patient’s body
o Flow of blood into chest and heart from peripheral veins is impeded – over time, this can reduce cardiac
output, sometimes to lethal levels