ePathoPlusPage

Respiratory

Outline
A. Review of Terms

1.

a. Tidal Volume = amount of air you normally breathe in and out
b. Vital Capacity = maximal volume that can be exhaled after a maximal inspiration without the use of force or rapid effort

 

2. Forced Expiratory Volume (FEV)  - to measure ask the client to inhale deeply, then forcefully exhale. The amount of air exhaled in a unit time is the FEV.
            a. in all Obstructive Lung diseases the FEV is decreased below norms

3.Minute ventilation
                VE =  VT X  f       (  f = frequency)

4. Dead space (VD) = volume of air that does not exchange with pulmonary blood
            1. anatomic dead space (for example volume of air in trachea)
            2. alveolar dead space (alveoli that are ventilated but not being perfused)

5. Compliance = change in volume that occurs for a given change in pressure

a. as compliance decreases, it becomes harder to inflate the alveoli, in Restrictive type lung diseases this is a major feature

6. Elastance = reverse of compliance, the extent to which lungs are able to return to their barely stretched position

a. in emphysema elastance is greatly diminished so that, although, it is easy to inflate the lungs, it is difficult to get the air out (hence a decreased FEV)

7. Resistance- the smaller the radius of the airway, the great the resistance,

       a.  R =   1/r4

         (R = resistance, r = radius of airway, by halving the airway you get a 16 fold increase in resistance)

              b. in asthma the resistance increases quickly make it difficult to breathe in
                    and out, (Hence a decreased FEV)

    8. Inspiratory to Expiratory ratio (I:E) = 1:2
            i.e normally it takes about twice as long to breathe out as it does to breathe in

    9. Atelectasis = areas of lung where alveoli are collapsed (cannot fill with air)
        a. compression atelectasis - due to pressure pushing down on alveoli and
             collapsing them

b. absorption atelectasis - when alveoli collapses because all the gas inside of  the alveoli is absorbed into the pulmonary blood, for example, if the alveoli were to fill 100% with oxygen, all the oxygen would be absorbed leaving no gas behind in the alveoli to prevent it from collapsing

    10. consolidation - when the alveoli are filled with fluid or inflammatory exudates, this is what happens in cases of pneumonia's

B.Distinction between Obstructive type lung diseases and Restrictive type lung diseases

C. Chronic Obstructive Pulmonary Disease (COPD)
    1. includes three diseases
            Chronic Bronchitis
            Emphysema
            Asthma

    2. chronic bronchitis and emphysema can occur together. The spectrum ranges from bronchitis with no emphysema to emphysema with no bronchitis and all stages in between possible

    3. Chronic Bronchitis
        a. physiologically it is the hypertrophy and hypersecretion of bronchial mucous glands

b. symptomatically it is defined as the hypersecretion of mucus and recurrent or productive cough for a minimum of 3 months per year for at least 2 consecutive years in patients for whom other causes have been excluded

c. causes
     1. inhalation of physical or chemical irritants (almost always cigarette smoke)
     2. viral or bacterial infections

d. pathophysiology: inflammatory response  causes ulceration and destruction of bronchial wall- granulation and fibrotic tissue replace normal ciliated epithelium- scarring leads to stenosis and airway obstruction

e. Clinical picture
   1. earliest symptom = productive cough
   2. increased susceptibility to infections
   3. breathlessness
   4. cyanosis
   5. pulmonary function tests show : decreased FEV, reduced vital capacity,  increased residual volume (but TLC within normal limits), low PO2, elevated PCO2

f. blue bloater

g. cor pulmonale

4. Emphysema
a. defined by destructive changes in alveolar walls and enlargement of air spaces distal to the terminal non respiratory bronchiole

b. physiologically - increased compliance, decreased elastance

c. Causes
     1. inhalation of  physical or chemical irritants (almost always cigarette smoke)
     2. genetic (very rare)

d. pathophysiology: PMN wbc and or alveolar macrophages release protease (elastase) in response to stimulus, protease if it contacts lung connective tissue will destroy it (instead of bacteria or virus)

1. normally the liver produces alpha 1 antitrypsin which circulates to the lungs and neutralizes the protease before it damages alveolar tissue, however, if inflammation is chronic, the liver may not be able to produce sufficient quantities to continuously neutralize

  e. clinical picture
               1. decreased FEV, increased TLC (cause barrel chest), increased residual volume   

                2. vital capacity may be normal or only slightly reduced until later stages of disease

                3. use of accessory muscles to aid in exhalation of air ( pursed lip breathing)

                4. X-ray- may show blebs (air pockets from ruptured alveoli) and or bullae (air spaces within lung parenchyma)

    5. Asthma
        1. differs from chronic bronchitis and emphysema because it results in intermittent rather than continuous airway obstruction

2. Two basic types
    a. Immunologic (Allergic, Extrinsic)
         1. usually occurs in childhood,
         2 often follows other allergic diseases such as eczema
         3. levels of IgE elevated

    b. Nonimmunologic ( Nonallergic, Intrinsic)
        1. usually does not occur to adulthood
        2. associated with recurrent resp tract infection
        3. levels of IgE not greatly elevated

     c. a mixed pattern ( i.e. combination of above two) may occur

3. airway in state of easy provocation, episode may be triggered by
        change in temperature
         humidity
        irritating fumes
        strong odors
        physical exertion
         emotional stress ?

4. pathophysiology: mast cells degranulate (easy provocation) releasing histamine, slow reacting substance of anaphylaxis (SRSA) and eosinophilicchemotactic factor of anaphylaxis (ECF-A), leading to
             a. constriction of smooth muscles of both large and small airways
                 (bronchospasm)

             b. increased capillary permeability- leads to mucosal edema- further
                   narrows airway
                     c. increased mucous gland secretions and production

5.status asthmaticus

D. Pneumonia
    1. more than 1 million new cases per year
    2. occurs most during winter months, assoc. with upper respiratory infections
    3. most common causative agents
        a. gram + bacteria (more serious infection than caused by gram - , mortality  approaches 50%) , e.g. strep pneumonia (most common community acquired),   mycoplasma pneumonia, staph aureus

  b. gram - bacteria,  (most cases of nosocomial acquisition), e.g. E. coli,  P. aeruginosa, proteus

c. non bacterial
     1. pneumocystis carinii
     2. fungi
     3. viruses
     4. Legionella

4. mode of transmission
      a. inspiration - aerosolization from talking, coughing

     b. aspiration of oropharyngeal secretions

     c. circulation

5. in bacterial pneumonia the bacteria releases endotoxins which stimulate an inflammatory reaction that damages lung tissue, the alveoli and terminal bronchioles fill with infectious debris and exudates (consolidation)

6. viral pneumonia's are usually milder and self limiting

7. clinical manifestations
     a.fever, chills

     b. productive or dry cough
     c. malaise

     d. pleural pain

             e. dypnea, hemoptysis

     f. leukocytosis

     g. chest x-ray shows infiltrate (consolidation) of single lobe = lobar pneumonia, or more diffuse = bronchopneumonia     

     h. pathogen identified by sputum culture or blood culture (if viral scant sputum)
             1. strep pneumonia produces rusty colored sputum
              2. staph aureus produces salmon colored sputum
             3. pseudomonas aeruginosa produces a greenish sputum with
                      distinct odor

E. Tuberculosis
1. one of leading causes of death worldwide, increasing in U.S

2. caused by mycobacterium tuberculosis

3. transmitted by aerosolization
4. pathophysiology: forms tubercles (granulomas) in lung, may become hard (no necrosis occurs) or soft (necrosis occurs). Necrosis occurs as a result of caseation (i.e. centers of tubercles filled with bacilli, dead wbc and necrotic lung
         tissue, a cheeselike substance), which is released into adjacent airways when tubercle ruptures ( a process called liquefaction). When liquid (caseous) material has been released  it leaves behind an air filled cavity (cavitation)

5. may develop extrapulmonary TB

6. primary (first) TB infection
     a. only about 5% of Americans infected with TB develop active, clinical disease

     b. causes a cell mediated immune reaction which leads to formation of sensitized T cells and which is detectable by a positive reaction to a skin test, this occurs  2-6 weeks after primary  infection and is maintained as long as living bacilli are maintained in body

     c. N.B. a positive reaction to a tuberculin skin test indicates the person has  been infected at some time with TB bacilli but does not indicate whether infection is currently active or inactive. Also, absence of a positive test does not always mean TB is absent

     d. primary TB infections are often not recognized
 

Discussion  

    Dyspnea is a symptom, a sensation felt by the patient that can be defined as difficult, labored, uncomfortable breathing. Rarely, is dyspnea the only symptom. Dyspnea is subjective. It is perceived and interpreted solely by the patient. It cannot be measured accurately with pulmonary function tests or ABG's. It should not be confused with hyperventilation, tachypnea or hyperpnea- all of which can be measured. Dyspnea may depend in part on past conditioning experiences. A patient's awareness of dyspnea does not necessarily mean the presence of disease. Certainly, respiratory conditions such as obstructive disorders and restrictive diseases can cause dyspnea, but other non- respiratory conditions such as anemia, diabetes and hepatic insufficiency can also result in dyspnea.
    Cough is defined as an explosive expiratory maneuver that helps protect the tracheobronchial tree from entry of a foreign substance or the accumulation of bronchopulmonary secretions. A cough that is chronic, i.e. persists for a month or longer, and is persistent is usually due to chronic bronchitis or other chronic respiratory disorders. In most cases, cough is involuntary, although it can be voluntary. It begins with mechanical stimulation of receptors in the pharynx, larynx or tracheobronchial tree or along the vagus nerve (this is why sometimes when you do an otoscopic exam you may stimulate coughing in the patient because movement of the ear can stimulate the vagus nerve).  The impulse travels from the receptor via  the vagus nerve or glossopharyngeal nerve to a cough center located in the medulla. Stimulation of this cough center causes three phases to occur: 1. deep inhalation (distends the trachea and hyperinflates the lungs), 2. compression (glotis closes, active contraction of expiratory muscles causing an increase in intrathoracic and abdominal pressures) and 3. expiration   (glotis opens and explosive release of trapped intrathoracic air.  Note- the vital capacity must be sufficient to ensure a deep breath. If it is not, then the cough is inadequate and secretions will be retained.  Pain, weakness or CNS depression can limit Inspiratory and expiratory efforts. In COPD (because of reduced FEV) expiratory cough effort is reduced. Environmental irritants, smoking (most common), inhalation of allergens, aspiration from pharynx, infections, lesions or cooling or drying of tracheobronchial secretions can all stimulate the cough reflex.  Coughing often causes fatigue and loss of appetite.  In some people with increased ICP coughing may be dangerous.

Clinically  

    Measurement of PEFR (peak expiratory flow rates)  provides data   that allows for estimates of FEV. In clients with asthma,  such measurements are extremely useful. Once a baseline, "personal best" measurement of PEFR is obtained, repeated measurements can be compared to this value and appropriate interpretations and actions initiated. For example, if on a given day PEFR falls below 80% of personal best, then the patient can be taught to increase medication, if it falls below another arbitrary percentage, they can seek medical help etc. Often PEFR's drop prior to onset of significant symptoms, thus providing the opportunity to prevent an asthmatic attack if medication is increased at that time. PEFR can be used to judge the efficacy of medication.
    Respiratory disorders can be considered from several different vantage points, depending on which set of physiological criteria are being considered. One such vantage point is to determine if a respiratory condition is causing more of a deadspace effect or a shunt effect. Deadspace occurs when the alveoli are normally ventilated but the perfusion to that alveoli is absent or decreased. For example, a classical situation causing increased deadspace would be a pulmonary embolus which blocks blood flow to a segment of the lung. The body attempts to compensate for increased deadspace by increasing ventilation to the normal units. A shunt occurs when perfusion to the alveoli is normal but their is decreased or no ventilation to the alveoli. For example, consider the case of ARDS (Adult Respiratory Distress Syndrome). In this condition the alveoli have collapsed or nearly collapsed because the capillaries have become "leaky". The resultant shift of fluids from the capillaries into surrounding tissue (non cardiogenic edema) pushes down on alveoli (compliance is greatly decreased) causing them to collapse. The body attempts to compensate for increased shunting by increasing perfusion to the normal units, it does this by increasing cardiac output.