Useful Methods for Studying Respiratory Abnormalities

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 Note total volume is about the same, but the rate of expiration is very different

o 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