Respiratory System
Respiratory System
CHAPTER II
BODY
dioxide (CO2) is transmitted from the blood capillaries into the alveoli and then expelled
through the bronchi and the upper respiratory tract.
The inner surface of the lungs where the exchange of gases takes place is very large, due to
the structure of the air sacs of the alveoli.
7. The lungs a pair of organs found in all vertebrates.
The structure of the lungs includes the bronchial tree air tubes branching off from the
bronchi into smaller and smaller air tubes, each one ending in a pulmonary alveolus.
Inhalation the intake of air into the lungs through expansion of chest volume.
Exhalation the expulsion of air from the lungs through contraction of chest volume.
The chest cavity contracts thus increasing air pressure and causing the air in the lungs to be
expelled through the upper respiratory tract. Exhalation, too, is passive. Air passes from the
high pressure in the lungs to the low pressure in the upper respiratory tract.
Inhalation and exhalation are involuntary and therefore their control requires an effort.
Changes in chest volume during inhalation and exhalation note that it only shows the
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Source: Wikipedia
Measuring the functioning of the lungs is a medical tool for diagnosing problems in the
respiratory system.
Maximum lung volume is known as TLC (total lung capacity). It can be obtained by
maximum strenuous inhalation.
The maximum lung volume of a healthy adult is up to 5-6 liters. In children the maximum
lung volume is up to 2-3 liters, depending on age. In infants it is up to 600-1000 milliliters.
Note! Differences in lung volume can only be caused by gender, age, and height.
Essential air volume is the maximum volume utilized by the lungs for inhalation,
also known as VC (vital capacity).
Residual volume (RV) is the volume of air remaining in the lungs after strenuous
exhalation when the lungs feel completely empty. Residual volume prevents the
broncheoli and the alveoli from sticking together. Residual volume is approximately
1.5 liters (adults).
The differential between total lung capacity and residual volume is the maximal
volume utilized by the lungs in order to breath. It is known as vital capacity
(VC). In an adult, the VC is between 3.5 and 4.5 liters.
Tidal Volume or VT is the volume of air displaced between normal inspiration and
expiration. In a healthy adult the tidal volume is approximately 500 milliliters.
2. Rate of airflow through the respiratory airways (into and out of the lungs).This measures
the effectiveness of airflow.
3. Efficiency of diffusion of oxygen from the pulmonary alveoli into the blood (not dealt
with in this unit).
TLC (total lung capacity) of children
3. The patient is asked to continue to expel air for a few seconds, despite the strong urge
to breathe in.
4. The test is repeated twice or three times.
Respiratory rate
Children in the upper classes of elementary school breathe about 20 times per minute.
Every breath causes an inhalation of approximately 7 milliliters of air volume per kilogram of
body weight.
A child who weighs 30 kilos inhales approximately 210 milliliters of air volume (210X30). In
other words, in the duration of a minute some 4200 milliliters of air volume enters and be
expelled from the lungs.
Athletes breathe slightly deeper and slower. With every breath they inhale approximately 10
milliliters of air per kilogram. Thus an athletic child who weighs 30 kilos will only breathe 15
times in the duration space of a minute. Each inhalation will require some 300 milliliters of
air volume. In the space of a minute 4500 milliliters of air volume will enter and be expelled
from the his lungs. We can deduce from this that athletes ventilate their airways in a much
more efficient way.
When we are under strain we breathe faster and more deeply. Since the lungs contain a
reserve of air, we do not become tired because lack of air (oxygen) is causing respiratory
restriction, but because of strain and tiredness in our respiratory and heart muscles.
When we are under emotional stress (before an exam, in distress, or feeling very frightened)
we breathe faster, but our breathing is shallower. For example, under stress we inhale 30
times per minute but at a rate of only 4 milliliters per kilo. In other words, overall only 3600
milliliters per minute are passing through our airways, so we feel short of breath.
Health History
Any assessment begins with a health history that includes exploration of the patients chief
complains. Build the health history by asking open-ended quetions. Ask these quetions
systematically to avoid overlooking imortant information. If necessary, conduct the interview
in several short sessions, depending on the severity of the patients condition, his
expectations, and staffing constraints.
Most information obtained about a child will come from the family. Sometimes the chief
complaint the parent expresses may not be the actual reason shes seeking medical attention.
Always ask the patient if she has other concerns about the child. Asking such quetions as
was there anything else you wanted to ask me today? or Do you have any other
concerns? may invite the parent to share her concerns.
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The adolescent child usually responds to those who pay attention to him. Showing interest in
the adolescent (and not his problem) early in the interview will help build trust and begin a
rapport with him. Start the interview by first informally asking about his friends, school, or
hobbies. When rapport has been established, you can return to more open-ended questioning.
During the interview, establish a rapport with the patient by explaining who you are and what
youll do. The quantity and qualiti of the information gathered depends on the relationship
you build with the patient. Try to gain his trust by being sensitive to his concerns and
feelings. Be alert to nonverbal responses that support or contradict his verbal responses. He
may, for example, deny chest pain verbally but reveal it through hid facial expressions. If the
patients verbal and nonverbal responses contradict each other, explore this with him to
clarify you assessment.
Chief Complaint
Ask the patients to tell you about his chief complaint. Use such quetions as When did you
first notice you werent feeling well? and What has happened since then that brings you
here today? Because many respiratiry disorders are chronic, be sure to ask him how the
latest episode compared with the previous episode, and what relief measures were helpful or
unhelpful.
Next, ask the patient to characterize his symtoms. Have him describe :
Aggravating factors-the cause of increasd intensity; for example, if he has dyspnea,
ask him how many feet he can walk before he feels short of breath
Alleviating factors-the relieving measures; determine if hes using any home
remedies, such as over-the counter (OTC) medications, alternative therapies, or a
charge in sleeping position.
Associated factors-the other symtoms thst occur at the same time as the primary
symtom
Location-the area where he experience the symtoms; ask him to pinpoint it and
determine if it radiates to other areas
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Quality-the feeling that accompanies the symptom and if he has experienced similar
symptoms in the past; ask him to characterize the symptom in his own words he
chooses to describe pain, for example, sharp, stabbing, or throbbing.
Durration-the lenght of tim symptoms last
Setting-the place where the patient was when the symptom occurred; ask him what he
was doing and who was with him.
Be sure to document your findings
A patient with a respiratory disorder may complain of dyspnea, fatigue, cough,
sputum production, wheezing, and chest pain. Here are some helpful assessment
techniques to gain informatio about each of these signs and symptoms.
Dyspnea
Dyspnea, or shortness of breath, occurs when breathin is inappropriately difficult for
the activity that the patient in performing. When ventilation is distrubed and ventilatory
demands exceed the actual or perceived capacity of the lungs to respond, the patient becomes
short breath. In additio, dyspnea is caused bby decreased lung compliance, disturbances in the
chest bellows system, airway obstruction, or exogenous factors such as obesity.
Obtain the patients history of dyspnea by using several scales, ask the patient to rate
his usual level of dyspnea on a scale of 0 to 10, in wich 0 means no dyspnea and 10 means
the worst he has experienced. Then ask him to rate the level that day. Another method to
assess dyspnea is to count the number of words the patient speaks between breath. A normal
individual can speak 10 to 12 words. A saverely dydpneic patient may speak only 1 to 2
words per breath.
Ask the patient what he does to relieve the dyspnea and how well those measures
work. (See Grading dyspnea.)
To find out if the dyspnea stems from pulmonary disease, ask the patient about its
onset and severity:
A sudden onset may indicated an acute problem, such as pneumothorax or
pulmonary embolus, or may result from anxiety caused by hyperventilation.
A gradual onset suggests a slow, progressive disorder such as chronic ostructive
pulmonary disease (COPD), whwewA cute intermitten attacks may indicate asthma.
Normally , an ifants respirations are abdominal, gradually changing to costal by age 7.
Suspect dyspnea in an infant who breathes costally, in an older child who breathes
abdominally, or in a child who uses accessory musscles to aid in breathing.
Orthopnea
Orthopnea is increased dyspnea when the patient is in a supine position. Its
traditionally measured in pillows-as in the number (usually one to three) of pillows needed
to prop the patient before dyspnea resolves. A better method is to record the degree of head
elevation at wich dyspnea is relieved using a goniometer. This device is used by physical
therapists to determine range of motion and may be used to measure a patients orthopnea, for
example, relieved at 35 degrees.
Orthopnea is commonly associated with:
Asthma
COPD
Diaphragmatic paralysis
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Cough
If the patient is experience a cough, ask him these quetions: Is the cough productive?
If the cough is chronic problem, has it charged recently? If so, how? What makes the cough
better? What makes it worse?
Also investigate the characteristics of the couhg:
Changing sputum, from white to yellow or green-suggesting a bacterial infection
Chronic productive with mucoid sputum-signaling asthma or chronic bronchitis
Congested-suggesting a cold, pneumonia, or bronchitis
Dry-signaling a cardiac condition
Hacking-signaling pneumonia
Increased amounts of mucoid sputum-suggestion acute tracheobronchitis or acute
asthma
Occuring in late afternoon-indicating exposure to irritants
Occuring in the early morning-indicating chronic airway inflammation, possibly from
cigarette smoke
Occuring in the evening-suggesting chronic postnasal drip or sinusitis
Severe-it disrupts daily activities and causes chest pain or acute respiratory distress.
Sputum Production
When a patient produces sputum, ask him to estimate the amount produced in
teaspoons or some other common measurement. Find out what time of day he usually coughs
and the color and consistency of his sputum. Ask if his sputum is a chronic problem and if it
has recently changed. If it has, ask him how. Also as if he coughs up blood (hemoptysis); if
so, find out how much and how often.
Hemoptysis
Hemoptysis (coughing up blood) may result from violent coughing or from serious
disorder, such as pneumonia, lung cancer, lung abscess, tuberculosis (TB), pulmonary
embolism, bronchiectasis, and left-sided heart failure. If the hemoptysis is mild (sputum
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streaked with blood), reassure the patient and be sure to ask when he first noticed it and how
often it occurs.
If hemoptysis is severe, causing frank bleeding place the patient in a semirecumbent
position, note pulse rate, blood pressure, and general condition. When the patients condition
stabilized, ask whether he has ever experienced similar bleeding (see hemoptysis or
hematemesis?)
If an ederly patient experiences hemoptysis, check his medication history for use of
anticoagulants. Changes in diet or medications, including OTC drugs and herbal supplements,
may be necessary because the may after the anticoagulant effect of Coumadin.
In children, hemoptysis may stem from Goodpasstures syndrome, cystic fibrosis or,
rarely, idiopathic primary pulmonary hemosiderosis. In rare cases, pulmonary hemorrhage of
unknown cause occurs in the first 2 weeks of life; the prognosis in these patients is poor.
Sleep Distrubance
Sleep distrubances may be related to obstructive sleep apnea or other sleep disorder
requiring additional evaluation.
If the patient complains of being drowsy or irritable in the daytime, ask him how
many hours of continuous sleep he gets at night. Ask him if he awakens during the night and
if his family complains about his snoring or restlessness.
Wheezing
If a patient wheezes, initially determine the severity of the condition.
If the patient is in distress, immediately assess his ABCs-airway, breathing, and
circulation. Does he have an open airway? Is the breathing? Does he have a pulse? If any of
these is absent, call for help and start cardiopulmonary resuscitation.
Next, quickly check for signs of impending crisis:
Is the patient having difficulty breathing?
Is the using accessory muscles to breathe? If chest excursion is less than the normal 1
1/8 to 2 (3 to 5 cm), hell use accessory muscle retraction, and use of scalene and
sternocleidomastoid muscles.
Has his level of consciousness (LOC) diminished?
Is he confused, anxious, or agitated?
Does he change his body position to ease breathing?
Does he skin look pale, diaphoretic, or cyanotic?
If the patient isnt in acute distress, ask him these questions:
When does wheezing occur? What makes you wheeze? Do you wheeze loudly enought for
others to hear? What helps stop your wheezing?
Children are especially susceptible to wheezing due to their small airways, wich are
prone to rapid obstruction.
Chest Pain
If the patient has chest pain, ask him where the pain is located have the patient rate the
pain in a scale from 0 to 10. Ask him what the pain frrls like, if its sharp, stabbing, burning,
or aching, find out if it radiates to another area in his body and if so, where. Ask the patient
how long the pain lasts, what causes it to occur, and what makes it better.
When the patient is describing his chest pain, attempt to determine the type of pain
hes experiencing:
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Chest wall pain thats localized and tender (indicates an infection or inflammation of
the chest wall, intercostal nerves, or intercostal muscles or, possibly, blunt chest
trauma)
Esophageal pain thats burning sensation that intensifies with swallowing (indicates
local inflammation)
Pleural pain thats stabbing, knifelike, and increases with deep brething or coughing
(associated with pulmonary infarction, pneumothorax, or pleurisy)
Substernal pain thats sharp, stabbling pain in the middle of his chest (indicates
pneumonia or spontaneous pneumothorax)
Tracheal pain thats burning sensation that intensifies with deep breathing or caughing
(suggests oxygen toxicity or aspiration)
Regardless of the type of pain the patient describes, remember to assess assossiated
factors, such as breathing, body position, and ease or difficulty of movement.
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affecting the respiratory system. Its important to note medications that the patient is allergic
to. This information needs to be verified and documented properly.
Family History
Obtaining family history helps determine whether a patient is at risk for hereditary or
infectious respiratory disease. First, ask if any of his immediate blood relatives, such as
parents, siblings, and children, have had cencer, sickle cell anemia, heart disease, or a chronic
illness, such as asthma and emphysema. Remember that diabetes can lead to cardiac and
possibly, respiratory problems. If an immediate relative has one or more of these disorders,
ask for more information about the patients maternal and paternal grandparent, aunts, and
uncles.
Be sure to determine whether the patient lives with anyone who has an infectious
disease, such as influenza or TB.
Psychosocial History
Ask the patient about his psychosocial history to assess his lifestyle. Be sure to cover his
home, community, and other environmental factors that might influence how he deals with
his respiratory problems. For example, people who work in mining, construction, or chemical
manufacturing are commonly exposed to environmental irritants. Also ask about
interpersonal relationship, mental health status, stress management, and coping style. Keep in
mind that a patients sexual habits or drug use may be connected with pulmonary disorder
related to acquired immunodeficiency syndrome
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progessively severe, incapacitating respiratory failure. All these disorders can cause
obstruction of bronchial airflow.
What causes COPD?
Predisposing factors to COPD include cigarette smoking, air pollution, occupational exposure
to irritating dusts or gases, familial and hereditary factors, infection, allergies, aging, and
potentially harmful drugs and chemicals.
Habitual cigarette smoking is by far the most important of these factors; COPD rarely
occurs in nonsmokers.cigarette smoking impairs ciliary action and macrophagic activity. It
also causes inflammation of the airways, increased mucus production, destruction of alveoalr
sepate, and peribronchiolar fibrosis. Air pollution, combined with the effects of cigarette
smoking, exacerbates COPD by inducing bronchospasm and mucosal edema, which increase
airway resistance.
Although less common than cigarette smoking and air pollution, occupational
exposure to irritating dusts or gases also aggravates COPD. Exposure to silica and other
nonorganic dusts may cause lung fibrosis and focal emphysema, saverely altering pulmonary
function. Exposure to certain organic dusts, such as cotton fiber, may increase airway
resistance, sometimes causing permanent respiratory difficulty. Pulmonary edema and
bronchiolitis-and, occasionally, permanent parenchymal damage-may result from exposure to
irritating gases, such as chlorine. Occupational asthma may develop, too, from exposure to
irritating dusts or gases.
COPD can also result-at least partially-from familial and hereditary factor, for
example, familial emphysema result from an inherited deficiency of alpha,-antitrypsin, a
nonspecific proteolytic enzyme inhibitor, proteolytic enzymes derived from blood leukocytes,
alveolar macrophages, and bacteria cause lysis of lung tissue. Cystic fibrosis, a congenital
disorder transmitted as an autosomal recessive trait, is another hereditary factor that can
contribute to development of COPD.
Aging, yet another presdiposing factor for COPD, may be associated with mild
panlobular emphysema, a common condition in the elderly. Many elderly patients show no
outward signs of emphysema, but histopathologic examination confirms this condition.
Kyphosis, a structural abnormality of the dorsal spine, may lead to emphysema.
Infection is the primary cause of bronchiectasis. It usually results from cystic fibrosis,
whooping cough, influenza, tuberculosis, or cancer. Infection also contributes to the
exacerbation of all forms of COPD. Viruses and mycoplasma pneumoniae cause most acute
episodes. Streptococcus pneumoniae commonly causes bacterial pneumonia; Hemophilus
influenzae causes acute exacerbations of COPD.
The primary presdiposing factor in extrinsic asthma is exposure to allergic individuals
in response to exposure to an allergen, they may have high serum levels of IgE antibodies.
These antibodies attach to mast cell in the submucosa of bronchial epithelium. When an
allergic individual is exposed to the specific sensitizing allergen, an antigen-antibody reaction
occurs, releasing IgE from the mast cell and causing asthma.
Harmful drugs for some asthma patients include aspirin and various nonsteroidal
antiinflammatory drugs, such as indomethacin; potentially harmful chemicals include a
yellow food dye. Exercise exacerbates asthma and, in some individuals, may actually cause
the condition (exercise-induced asthma), probably from heat and moisture loss in the uppr
airways.
Pathophysiology
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In all forms of COPD, narrowing of the airways obstruct airflow to and from the lungs. Such
obstruction markedly increases the work of breathing and resistance to airflow. This
narrowing impairs ventilation by trapping air in the bronchioles and alveoli. The trapped air,
in turn, hinders normal gas exchanges and distends the alveoli. Other phatology of COPD
varies with each from of the disease.
Chronic Bronchitis
In this from of COPD, tissue irritation usually result from exposure to cigarette smoke or air
pollution. Tissue irritation causes hypertrophy of mucus-producing cells in the bronchi, thus
increasing mucus production. This, in turn, activates the cough refflex, leading to progressive
destruction of smaller bronchioles, increased susceptibility to respiratory infection, airway
obstruction, and inadequate gas exchanfe.
Because of these pathologic changes, the patient becomes increasingly dyspneic and
short of breath on exertion, which forces him to restrict his physical activities. The sputum
produced by his cough becomes increasingly tenacious, mucoid, and copious, particularly in
the morning after secretions have accumulated during the night.
As bronchitis progresses, more alveoli become inadequately ventilated, futher
disrupting gas diffusion and causing first a decreased PaO2 level and later an elevated PaCO2.
The patient now develops hypoxia and hypercapnia. Compensatory hyperventilation,
however-common in some other forms of respiratory dysfunction-doesnt usually occur
because of the insensitivity of the respiratory center in the brain stem to the sustained
hypercapnia and the reactions of peripheral chemoreceptors in the aortic arch and carotid
body to the evolving hypoxia.
Eventually, inadequately oxygenated hemoglobin may cause cyanosis. Also,
pulmonary vasoconstriction may occure secondary to a decreased PaO2. If this occurs,
increased pulmonary vascular pressure causes resistance to the blood ejected by the right
ventricle. In time, this may cause right ventricular hypertrophy and failure, with edema.
Because of his cyanosis and edema, the patient with chronic bronchitis is often called a blue
bloater.
Emphysema
Emphysema may develop after a long history of chronic bronchitis, during which air becomes
trapped in the alveoli because mucus is blocking the small terminal bronchioles and airway
walls have collapsed. The increase in mucus production, though slight, causes the chronic
nonproductive cough characteristic of emphysema. The patient usually only raises small
amounts of sputum from his spasmodic and fatiguing cough. Typically, even such minimal
exertion as talking initiates coughing. Particularly in the morning. Severse paroxysms of
coughing may cause nausea and vomiting.
Subsequently, reccurent inflammation, associated with the release of proteolytic
enzymes from cells in the lung, breaks down the alveolar walls and ducts and the respiratory
bronchioles. Clusters of alveoli then merge, forming larger airspaces and reducing the total
number of alveoli. The creation of these airspaces causes even more air to become trapped
from collapsed airway walls. The effort required to exhale trapped air causes dyspnea on
exertion. Eventually dyspnea occurs even at rest.
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Meanwhile, destruction of the alveolar walls disrupts parts of the pulmonary capillary
bed, located in the walls. The reduces the total alveolar capillary membrane area oof the lungs
available for ga exchange. The combined effects of trapped air and alveolar distention change
the size and shape of the patients chest. Eventually he develop a characteristic barrel chestthat is, a round, bulging chest with increase anteroposterior diameter. Unlike the blue bloater
with chronic broncitis, the patient with emphysema isnt usually hipoxic or cyanotic, but his
expiratory effort does become markedly increased. For this reason, hes called a pink
puffer.
Asthma
Unlike bronchitis and enphysema, asthma is characterized by bronchospasms, caused by
infection, hyperensitivity to irritans or psychological stress, exercise, or drug use. The
bronchospasms are accompanied by edema, inflammatory cell infitrates (with many
eoshinophils), and hypersecretion of mucus. In chronic asthma, the amount of smooth muscle
increases, inflammatory cells infiltrate the bronchial wall, the basement membrane thickens,
and mucus obstructs many small airways.
As in emohysema, airway obstruction in asthma is worst during expiration. This is
manifested by a prolongrd expiration time (more than 4 second) and wheezing.(however, if
the bronchospasm is severe enough to drastically reduce airflow, wheezing may be almost
absent.) A productive cough, caused by hypersecretion of mucus, usually accompanies the
wheezing. When the eosinophil content rises, sputum may appear purulent. It may also
contain Curschmanns spirals (coiled mucinous fibrils) and Carcot-Leyden crystals
(breakdown products from eosinophils). If airway obstruction is severe and the patients fluid
intke is low, mucous plugs may harden, rendering the patients cough ineffective and causing
mucoid impaction.
Overinflation of the distal airways increases as an asthmatic attack worsens.
Overinflation is caused by premature airway closure, mucosal edema, mucous plugging, and
increased exhalation time (from increased airflow resistance). It decreases forced expiratoty
volume in 1 second (FEV1 ) while increasing residual volume and functional residual
capacity. This in indicated by decrease diaphragmatic excursion and lateral chest expansion,
widened intercostal spaces, hyperresonance, and increased work of breathing. Increased total
lung capcity (TLC) is responsible for these findings. Other signs of an asthma attack include
flared nostrils, the use of accessory muscles to breathe, sternocleidomastoid retraction,
tachypnea, and, in a thin-chested patient, intercostal retraction during inspiration. As airway
obstruction becomes more severe, anxiety increases the bodys metabolic demands, inducing
fatigue and respiratory failure, with mental confusion, systolic hypertension, and if extreme
CO2 elevations are present, asterixis (flapping tremor).
Most the pathologic effects are reversible. However, chronic and sustained
bronchospasms can cause smooth muscle hypertrophy and permanent narrowing of the
respiratory tract, causing signs and symptoms like those that occur in emphysema and chronic
bronchitis.
Cystic Fibrosis
In cystic fibrosis, abnormally thick moucus secretions obstruct ducts in the pancreas, liver,
and lungs, leading to trapped air, mucous stasis, and lung infection. When the patient with
cystic fibrosis inhales, his airways dilate normally and air flows into the lungs and alveoli for
gas exchange. During expiration, however, his airways usually collapse, trapping air and
eventually causing barrel chest.
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Mucus trapped in the collapsed airways increases obstruction, causing mucous statis
and predisposing the patient to infection. In turn, infection can lead to more mucus
production and bronchial wall damage. Exacerbating airway obstruction. Continual repetition
of this cycle eventually destroys lung tissue. These pulmonary changes may produce
tachypnea, chronic cough with mucus production, barrel chest, clubbing of the fingernails
and toenails, shortness or breath on exertion, weight loss or failure to gain weight, cyanosis,
and eventually fatal pulmonary disease.
Brochiectasis
In bronchiectasis, chronically enlarged or dilated bronchi follow inflammatory weakening of
the broncial walls may produce large quantities of foul-smelling mucopurulent secretions,
predisposing the patient to frequent respiratory infections and ultimatey obstructing depends
mainly on the amount of pulmonary tissue involved. Advanced bronchiectasis may cause
pneumonia, cor pulmonale, or right ventricular failure.
CHAPTER III
CONCLUSION
The respiratory system is the system in the human body that enables us to
breathe.
The act of breathing includes: inhaling and exhaling air in the body; the
absorption of oxygen from the air in order to produce energy; the discharge of
carbon dioxide, which is the byproduct of the process.
The respiratory system is divided into two parts: Upper respiratory tract, Lower
respiratory tract, The trachea, The bronchi, The broncheoli, Pulmonary alveoli,
The lungs
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REFERENCE
1979.
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