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Pulmonary Pathophysiology

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... diseases are asthma, chronic bronchitis, and emphysema. ... Emphysema ... Primary emphysema linked to an inherited deficiency of the enzyme alpha 1 ... – PowerPoint PPT presentation

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Title: Pulmonary Pathophysiology


1
Pulmonary Pathophysiology
2
Reduction of Pulmonary Function
  • Inadequate blood flow to the lungs
    hypoperfusion
  • Inadequate air flow to the alveoli -
    hypoventilation

3
Nosocomial infections
  • Factors that reduce airflow also compromise
    particle clearance and predispose to infection.
  • Restricted lung movement and ventilation may
    arise due to
  • Positioning
  • Constricting bandages
  • Central nervous system depression
  • Coma
  • High rate of pneumonia in hospital patients due
    in large part to impaired ventilation and
    clearance.

4
Signs and Symptoms of Pulmonary Disease
  • Dyspnea subjective sensation of uncomfortable
    breathing, feeling short of breath
  • Ranges from mild discomfort after exertion to
    extreme difficulty breathing at rest.
  • Usually caused by diffuse and extensive rather
    than focal pulmonary disease.

5
Dyspnea cont.
  • Due to
  • Airway obstruction
  • Greater force needed to provide adequate
    ventilation
  • Wheezing sound due to air being forced through
    airways narrowed due to constriction or fluid
    accumulation
  • Decreased compliance of lung tissue

6
Signs of dyspnea
  • Flaring nostrils
  • Use of accessory muscles in breathing
  • Retraction (pulling back) of intercostal spaces

7
Cough
  • Attempt to clear the lower respiratory passages
    by abrupt and forceful expulsion of air
  • Most common when fluid accumulates in lower
    airways

8
Cough may result from
  • Inflammation of lung tissue
  • Increased secretion in response to mucosal
    irritation
  • Inhalation of irritants
  • Intrinsic source of mucosal disruption such as
    tumor invasion of bronchial wall
  • Excessive blood hydrostatic pressure in pulmonary
    capillaries
  • Pulmonary edema excess fluid passes into airways

9
  • When cough can raise fluid into pharynx, the
    cough is described as a productive cough, and the
    fluid is sputum.
  • Production of bloody sputum is called hemoptysis
  • Usually involves only a small amount of blood
    loss
  • Not threatening, but can indicate a serious
    pulmonary disease
  • Tuberculosis, lung abscess, cancer, pulmonary
    infarction.

10
  • If sputum is purulent, and infection of lung or
    airway is indicated.
  • Cough that does not produce sputum is called a
    dry, nonproductive or hacking cough.
  • Acute cough is one that resolves in 2-3 weeks
    from onset of illness or treatment of underlying
    condition.
  • Us. caused by URT infections, allergic rhinitis,
    acute bronchitis, pneumonia, congestive heart
    failure, pulmonary embolus, or aspiration.

11
  • A chronic cough is one that persists for more
    than 3 weeks.
  • In nonsmokers, almost always due to postnasal
    drainage syndrome, asthma, or gastroesophageal
    reflux disease
  • In smokers, chronic bronchitis is the most common
    cause, although lung cancer should be considered.

12
Cyanosis
  • When blood contains a large amount of
    unoxygenated hemoglobin, it has a dark red-blue
    color which gives skin a characteristic bluish
    appearance.
  • Most cases arise as a result of peripheral
    vasoconstriction result is reduced blood flow,
    which allows hemoglobin to give up more of its
    oxygen to tissues- peripheral cyanosis.
  • Best seen in nail beds
  • Due to cold environment, anxiety, etc.

13
  • Central cyanosis can be due to
  • Abnormalities of the respiratory membrane
  • Mismatch between air flow and blood flow
  • Expressed as a ratio of change in ventilation (V)
    to perfusion (Q) V/Q ratio
  • Pulmonary thromboembolus - reduced blood flow
  • Airway obstruction reduced ventilation
  • In persons with dark skin can be seen in the
    whites of the eyes and mucous membranes.

14
  • Lack of cyanosis does not mean oxygenation is
    normal!!
  • In adults not evident until severe hypoxemia is
    present
  • Clinically observable when reduced hemoglobin
    levels reach 5 g/ dl.
  • Severe anemia and carbon monoxide poisoning give
    inadequate oxygenation of tissues without
    cyanosis
  • Individuals with polycythemia may have cyanosis
    when oxygenation is adequate.

15
Pain
  • Originates in pleurae, airways or chest wall
  • Inflammation of the parietal pleura causes sharp
    or stabbing pain when pleura stretches during
    inspiration
  • Usually localized to an area of the chest wall,
    where a pleural friction rub can be heard
  • Laughing or coughing makes pain worse
  • Common with pulmonary infarction due to embolism

16
  • Inflammation of trachea or bronchi produce a
    central chest pain that is pronounced after
    coughing
  • Must be differentiated from cardiac pain
  • High blood pressure in the pulmonary circulation
    can cause pain during exercise that often
    mistaken for cardiac pain (angina pectoris)

17
Clubbing
  • The selective bulbous enlargement of the end of a
    digit (finger or toe).
  • Usually painless
  • Commonly associated with diseases that cause
    decreased oxygenation
  • Lung cancer
  • Cystic fibrosis
  • Lung abscess
  • Congenital heart disease

18
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19
Respiratory Failure
  • The inability of the lungs to adequately
    oxygenate the blood and to clear it of carbon
    dioxide.
  • Can be acute
  • ARDS or pulmonary embolism
  • Direct injury to the lungs, airways or chest wall
  • Indirect due to injury of another body system,
    such as the brain or spinal cord.

20
  • Chronic respiratory failure
  • Due to progressive hypoventilation from airway
    obstruction or restrictive disease
  • Respiratory failure always presents a serious
    threat
  • Dysnpea always present, but may be difficult to
    detect a change in a chronic patient
  • Since nervous tissue it highly oxygen-dependent,
    see CNS signs and symptoms
  • Memory loss, visual impairment, drowsiness
  • Headache due to increased intracranial pressure
    due to cerebral vasodilation

21
Two principal patterns
  • Hypoxic Respiratory Failure
  • Seen when pO2 falls to or below 60 mm Hg
  • Typically seen in chronic bronchititis and
    emphysema, in lung consolidation due to bacterial
    infection, or in lung collapse, pulmonary
    hypertension, pulmonary embolism and ARDS.
  • Initially, produces headache and nervous
    agitation, soon followed by a decline in
  • mental activity, and confusion.

22
  • With a progressive lowering of pO2, more
    widespread tissue damage and loss of
    consciousness can be expected.
  • In the event of brain stem hypoxia, CNS output to
    the heart and systemic arterioles can produce
    circulatory shock
  • Renal hypoxia can cause loss of homeostatic
    balance and accumulation of wastes to complicate
    the problem

23
Hypoxic-Hypercapnic Respiratory Failure
  • When arterial pCO2 (normally 40 mm Hg) exceeds 45
    mm HG, condition is called hypercapnia
  • Most often, obstructive conditions produce this
    form of respiratory failure, as can
    hypoventilation from CNS problem, thoracic cage
    or neuromuscular abnormalities

24
  • Attempts to compensate include increased heart
    rate and vasodilation, which produces warm, moist
    skin.
  • CNS effects produce muscular tremors, drowsiness
    and coma.
  • Hypercapnia also produces acidosis.

25
Pulmonary Disorders
  • Acute Respiratory Failure
  • Acute Respiratory Distress Syndrome
  • (or Adult Respiratory Distress Syndrome)
  • Rapid and severe onset of respiratory failure
    characterized by acute lung inflammation and
    diffuse injury to the respiratory membrane with
    noncardiogenic edema.

26
ARDS
  • Identified in last 25 years
  • Affects 200 -250 thousand people each year in
    U.S.
  • Mortality in persons lt 60 is 40 (? 67)
  • Those over 65 and immunocompromised still have
    mortality over 60
  • Most survivors have almost normal lung function 1
    year after acute illness.

27
Pathophysiology of ARDS
  • All disorders causing ARDS acutely injure the
    respiratory membrane and produce severe pulmonary
    edema, shunting, and hypoxemia.
  • Shunting blow flow is normal, but gas exchanged
    is decreased. V/Q ratio changes the same effect
    as if blood were shunting or bypassing the lungs.

28
  • Damage can occur directly
  • Aspiration of acidic gastric contents
  • Inhalation of toxic gases
  • Or indirectly
  • Chemical mediators from systemic disorders

29
Result is massive inflammatory response by lungs
  • Initial injury damages the pulmonary capillary
    epithelium, causing platelet aggregation and
    intravascular thrombus formation.
  • Platelets release substances that attract and
    activate neutrophils.
  • Damage also activates the complement cascade
    which also activates neutrophils and the
    inflammatory response.

30
  • Role of neutrophils is central to the development
    of ARDS.
  • Neutrophils release inflammatory mediators
  • Proteolytic enzymes
  • Toxic oxygen products
  • Prostaglandins and leukotrienes
  • Platelet activating factors
  • These damage the respiratory membrane and
    increase capillary permeability, allowing fluids,
    proteins, and blood cells to leak into alveoli ?
    pulmonary edema and hemorrhage

31
  • Reduces pulmonary ventilation and compliance
  • Neutrophils and macrophages release mediators
    that cause pulmonary vasoconstriction ? pulmonary
    hypertension
  • Type II alveolar cells also damaged, see
    decreased surfactant production
  • Alveoli fill with fluid or collapse.
  • Lungs become less compliant, and ventilation
    decreases.

32
  • After 24 48 hours hyaline membranes form
  • After about 7 days, fibrosis progressively
    obliterates the alveoli, respiratory bronchioles
    and interstitium
  • Result is acute respiratory failure

33
  • In addition, chemical mediators often cause
    widespread inflammation, endothelial damage and
    increased capillary permeability throughout the
    body
  • This leads to systemic inflammatory response
    syndrome, which leads to multiple organ
    dysfunction syndrome (MODS)
  • Death may not be caused by ARDS alone, but by MODS

34
Clinical manifestations
  • Symptoms develop progressively
  • Hyperventilation? repiratory alkalosis? dyspnea
    and hypoxemia? metabolic acidosis? respiratory
    acidosis ? further hypoxemia ? hypotension,
    decreased cardiac output, death

35
Evaluation and Treatment
  • Diagnosis based on physical examination, blood
    gases and imaging
  • Treatment is based on early detection, supportive
    therapy and prevention of complications, esp.
    infection
  • Often requires mechanical ventilation

36
  • Many studies underway for treatment
  • Prophylactic immunotherapy
  • Antibodies against endotoxins
  • Inhibition of inflammatory mediators
  • Inhalation of nitric oxide to reduce pulmonary
    hypertension
  • Surfactant replacement

37
Postoperative Respiratory Failure
  • Same pathophysiology as ARDS, but usually not as
    severe.
  • Smokers are at risk, esp. if have pre-existing
    lung disease.
  • Also individuals with chronic renal failure,
    chronic hepatic disease, or infection
  • Thoracic and abdominal surgeries carry greatest
    risk
  • Individuals usually have a period of hypotension
    during surgery, and many have sepsis.

38
Prevention includes
  • Frequent turning
  • Deep breathing (spirometry)
  • Early ambulation to prevent atelectasis and
    accumulation of secretions
  • Humidification of air to loosen secretions
  • Supplemental oxygen and antibiotics as
    appropriate
  • Respiratory failure may require mechanical
    ventilation for a time.

39
Obstructive Pulmonary Disease
  • Characterized by airway obstruction that is worse
    with expiration. More force is required to expire
    a given volume of air, or emptying of lungs is
    slowed, or both.
  • The most common obstructive diseases are asthma,
    chronic bronchitis, and emphysema.
  • Many people have both chronic bronchitis and
    emphysema, and together these are often called
    chronic obstructive pulmonary disease - COPD

40
  • Major symptom of obstructive pulmonary disease is
    dyspnea, and the unifying sign is wheezing.
  • Individuals have increased work of breathing, V/Q
    mismatching, and a decreased forced expiratory
    volume.

41
Asthma
  • More intermittent and acute than COPD, even
    though it can be chronic
  • Factor that sets it apart from COPD is its
    reversibility
  • Occurs at all ages, approx. half of all cases
    develop during childhood, and another 1/3 develop
    before age 40
  • 5 of Adults and 7-10 of children in U.S. have
    asthma

42
  • Morbidity and mortality have risen in past 20
    years in spite of increased numbers and
    availability of antiasthma medications.
  • Runs in families, so evidence genetics plays a
    role.
  • Environmental factors interact with inherited
    factors to increase the risk of asthma and
    attacks of bronchospasm
  • Childhood exposure to high levels of allergens,
    cigarette smoke and/or respiratory viruses
    increases chances of developing asthma.

43
  • The major pathological feature of asthma is
    inflammation resulting in hyperresponsiveness of
    the airways.
  • Major events in an acute asthma attack are
    bronchiolar constriction, mucus hypersecretion,
    and inflammatory swelling.

44
  • Exposure to allergens or irritants causes mast
    cells to release granules and trigger the release
    of many inflammatory mediators such as histamine,
    interleukins, immunoglobulins, prostaglandins,
    leukotrines and nitric oxide.
  • See vasodilation and increased capillary
    permeability
  • Chemotactic factors attract neutrophils,
    eosinophils and lymphocytes to the area
    bronchial infiltration

45
  • Smooth muscle spasm in bronchioles due to IgE
    effect on autonomic neurons - ACh
  • Vascular congestion
  • Edema formation
  • Production of thick, tenacious mucus
  • Impaired mucociliary function
  • Thickening of airway walls
  • Increased bronchial responsiveness
  • Untreated, this can lead to airway damage that
    is irrevesible.

46
  • Obstruction increases resistance to air flow and
    decreases flow rates
  • Impaired expiration causes hyperinflation of
    alveoli distal to obstruction, and increases the
    work of breathing

47
Clinical manifestions
  • During remission individual is asymptomatic and
    pulmonary function tests are normal
  • Dyspnea
  • Often severe cough
  • Wheezing exhalation
  • Attacks usually of one to two hours duration, but
    may be severe and continue for days or even weeks.

48
  • If bronchospam is not reversed by usual measures,
    the individual is considered to have severe
    bronchospasm or status asthmaticus
  • If continues can be life threatening.

49
Management
  • Avoid triggers (allergens and irritants)
  • Patient education
  • Acute attacks treated with corticosteroids and
    inhaled beta-agonists
  • Chronic management based on severity of asthma
    and includes regular use of inhaled
    antiinflammatory medications corticosteroids,
    chromolyn sodium or leukotriene inhibitors.
  • Inhaled bronchodilators
  • Immunotherapy allergy shots, etc.

50
  • Bronchoconstriction may be a normal means of
    restricting airflow and intake of irritants and
    allergens. Their long term use may actually
    increase exposure to these factors and cause more
    pronounced and chronic symptoms.
  • Antiinflammatory agents have better long term
    effects.

51
COPD
  • Pathological changes that cause reduced
    expiratory air flow
  • Does not change markedly over time
  • Does not show major reversibility in response to
    pharmacological agents
  • Progressive
  • Associated with abnormal inflammatory response of
    the lungs to noxious particles or gases.

52
  • Fourth leading cause of death in U.S.
  • Increasing in incidence over the past 30 years
  • Primary cause is cigarette smoking
  • Both active and passive smoking have been
    implicated
  • Other risks are occupational exposures and air
    pollution
  • Genetic susceptibilities identified

53
Chronic Bronchitis
  • Hypersecretion of mucus and chronic productive
    cough for at least 3 months (usually winter) of
    the year for at least two consecutive years.
  • Incidence may be increased up to 20 times in
    persons who smoke and more in persons exposed to
    air pollution.

54
Pathophysiology
  • Inspired irritants result in inflammation of the
    airways with infiltration of neutrophils,
    macrophages, and lymphocytes into the bronchial
    wall.
  • Causes bronchial edema and increases size and
    number of mucus glands and goblet cells.
  • Mucus is thick and tenacious, and cant be
    cleared because of impaired ciliary function.
  • Increases susceptibility to infection and injury

55
  • Initially affects only larger bronchi, but
    eventually all airways involved.
  • Airways collapse in early expiration, blocked by
    mucus, and air is trapped in distal portion of
    the tract.
  • Leads to ventilation/perfusion mismatch
  • Hypoxemia occurs
  • Air trapping prevents respiratory muscles from
    functioning efficiently (barrel chest), and get
    hypoventilation and hypercapnia.

56
Treatment
  • Best treatment is PREVENTION because changes are
    not reversible.
  • Cessation of smoking halts progression of the
    disease
  • Bronchodilators, expectorants, and chest physical
    therapy are used as needed.
  • Acute attacks may require antibiotics, steroids
    and possibly mechanical ventilation.
  • Chronic oral steroids as a last resort.
  • Home oxygen therapy

57
Emphysema
  • Abnormal, permanent enlargement of the
    gas-exchange airways and destruction of the
    alveolar walls.
  • Obstruction results from changes in lung tissue
    rather than mucus production and inflammation.
  • Major mechanism is loss of elastic recoil

58
  • Major cause is cigarette smoking
  • Other causes are air pollution and childhood
    respiratory infections
  • Primary emphysema linked to an inherited
    deficiency of the enzyme alpha 1- antitrypsin
    which inhibits action of many proteolytic enzymes
    which can affect lung tissue.
  • With this deficiency, smokers are even more
    susceptible.

59
Pathophysiology
  • Begins with the destruction of the alveolar
    septa, which eliminates portions of the capillary
    bed, and increases the volume of air in the
    alveolus.
  • Inhaled oxidants inhibit the activity of
    endogenous antiproteases, and stimulate
    inflammation with increased activity of proteases.

60
  • See continued alveolar loss and loss of elastic
    recoil
  • Expiration becomes difficult
  • Hyperinflation of alveoli produce large air
    spaces (bullae) and air spaces adjacent to the
    pleura (Blebs)
  • These are not effective in gas exchange and
    result in hypoxemia
  • Air trapping causes hyperexpansion of the chest,
    which puts respiratory muscles at a mechanical
    disadvantage.

61
  • This makes breathing so difficult that late in
    the disease individuals develop hypoventilation
    and hypercapnia.

62
Clinical manifestations
  • Dyspnea
  • Barrel chest
  • Minimal wheezing
  • Prolonged expiration
  • Hypoventilation and polycythemia late in the
    progression of the disease

63
Treatment
  • Similar to chronic bronchitis
  • Stop smoking
  • Bronchodilating drugs
  • Breathing retraining
  • Relaxation exercises
  • Antibiotics for acute infections
  • Severe COPD may require inhaled or oral steroids,
    and home oxygen
  • Some can benefit from lung reduction surgery or
    lung transplant.
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