Restrictive Resp. disorders

Decreased compliance (expansion/elasticity) of the lungs or chest wall or both

• CNS: head injury, tumor, stroke, narcotic or barbiurate OD
• Neuromuscular disorders: Guillian-Barre Syndrome, Amyotropic Lateral Sclerosis, Myasthenia Gravis, Musculr Dystrophy
• Chest wall orgin: chest trauma (flail chest, fractured ribs), Pickwickian syndrome (pt. morbidly obese and can't expand lungs), Kyphoscoliosis
• Pleural disorders: pleural effusion, pleurisy, pneumothorax
• lung parenchymal disorders: atelectasis, pneumonia, intestitial lung disease, ARDS (acute resp. distress syndrome)

• -Decr. inspiratory values
• -reduced vital capacity
• -reduced TLC total lung capacity

They affect the alveoli, blood vessels, and surrounding support tissue of the lungs rather than the airways, they are restrictive

alveoli becomes inflammed and leads to pulmonary fibrosis, or scarring that becomes stiff, and noncompliant w/ poor recoil and expanision and poor gas exchange

exertional dyspnea. you may also hear fine crackles and see rapid shallow resps, and clubbing

• -ABG's show hypoxia
• -CXR shows characteristic infiltrative patterns

cor pulmonale is a result of pulm HTN, as the heart can no longer pump efficiently against the stiff lung, it leads to L sided heart failure and death

• caused by occupational exposure
• 1) pneumoconioses- inhalation of inorganic dust and particulate matter (asbestos, silicosis, coal workers "black lung" disease) has a poor prognosis
• 2)hypersensitivity pneumonitis (exposure to cotton dust, sugar cane fiber)

reduce inflammatory response, prevent disease progression, manage dyspnea and provide supportive care late in the disease

• -corticosteroids and other immunosuppressants (most common med)
• -preventative teaching to environmental hazards
• -smoking cessation
• -vaccines
• -adequate fluids
• -home O2
• -hospice care...reduction of dyspnea by providing morphine: oral, parenteral or nebulized

• -A restrictive resp disorder of unknown cause that mostly affects the lungs.
• -involves a autoimmune response- T-lymphocytes incr. and cause damage to alveolar cells . Normally T-lymphocytes are protective but w/ Sarcoidosis they form granulomas on the alveoli that cause fibrosis that reduces lung compliance and gas exchange...cor pulmonale often results

• -enlarged lymph nodes in the hilar area of the lungs
• -lung infiltrate on CXR (the first indication of the disease may be an abnormal CXR in an otherwise healthy pt.)
• -cough, dyspnea, hemoptysis and chest discomfort

• -The goal of therapy is to lessen the s/sx and prevent fibrosis.
• -Corticosteroids for severe manifestations, hepatic insufficiency, cardiac dysrhythmias, CNS involvement or disfiguring skin lesions
• -Immune modifiers (e.g. chloroquine, indomethacin, azathiaprine, methotrexate)
• -If asymptomatic and normal PFT's- no treatment.

• -Teach about corticosteroids: do not stop abruptly, take w/ food or milk to minimize GI upset, limit Na and incr. K
• -symptom relief of inflammatory symptoms (arthralgias, eye inflammation)

Pneumonia= an inflammatory process that results in edema of ung tissue and movement of fluid into the alveoli, causing hypoxemia

The normal protective mechanisms are overcome (warming, filtraionand humididfication of inspired air, closure of epitlottis over trachea, cough reflex, mucociliary movement, secretion of Immunoglobin A, alveolar macrophages)

• 1) community aquired (CAP), most common streptococcus pneumonia (gram +) treated w/ PCN or cephlosporins
• 2) Hospital-aquired (nosocomial), most common staphylococcus areus (gram +) treated w/vanco, zosyn, levaquin

Nonsosomial has a high mortality rate: mechanical ventilation incr. risk, contaminated respiratory equipment, immunosuppression and general debilitaion.

• 1) Lobar- w/ consolidation ina segment or entire lobe
• 2) bronchopneumonia- w/ diffusely scattered patches around the bronchi

• -fibrin and edema of inflammation stiffen the lung= decr. lung compliance and vital capicity
• -decr. producting of surfactant leads to atelectasis
• -venous blood passes thru underventilated areas, leading to hypoxemia
• -tissue necrosis can result when multiplying organisms from abscesses that perforate bronchial wall
• -can lead to sepsis

• -presents w/ rapid onset of shaking, fever, cough of rust-colored purulent sputum
• -pleuritic pain common
• -fine crackles over affected lobe
• -signs of pulm. consolidation (dullness to percussionincr. fremitus, bronchial BS)

• -have gradual and atypical presentations d/t interstitial rather than alveolar inflammation
• -HA, myalgias, fatigue sore throat, n&v, diarrhea, crackles, dry hacking, nonproductive cough
• -elderly pts may present w/ confusion or stupor as the primary finding
• -typical in younger population aka "walking pneumonia"...treated w/ azithromycin or erythromycin (typical PCN or cephlosporins won't work)

• 1) bacterial- rust color
• 2) pseudomonis- green
• 3) staph- yellow

• 1)Pneumococcus or
• 2) Klebsiella

• 1)viral
• 2)legionella
• 3)fungal

Necrotizing infection w/ S. aureus, gram neg bacteria or mycobacterium TB

pleural effusion

before AB therapy is started

low O2 levels

• >15,000 w/ presence of bands (immature neutrophils)
• unless they are elderly/immunocompromised and can't muster up a rxn and show elevated counts

• -emperic AB
• -O2 PRN
• -analgesics, antipyretics
• -rest
• -postural drainage, chest physiotherapy to mobolize secretions
• -FLUIDS! (IV or oral) at least 3000 mL/day unless contraindicated
• -nutritional support of at least 1,500 cal/day, small frequent meals
• -Amantadine and Rimantidine for Influenza A Virus. During influenza epidemics, recommended as chemoprophylaxis for nursing home pts, immunocompromised or unvaccinated pts
• -vaccines!

• -A restrictive resp. disorder that is highly communicable caused by Mycobacterium tuberculosis, a gram-pos acid fast bacillus
• -TB usually involves the lungs but may also occur in the larynx, kidneys, bones, adrenal glands, lymph nodes, meninges...can be disseminated throughout entire body
• -significant public health concern d/t incr. numbers of impoverished/homeless perosns and multi-drug resistant strains

• airborne transmission-infected person coughs, sneezes etc, droplet nuclei inhaled by others, TB multiplies freely when it reaches a susceptible site
• -non-specific pneumonitis occurs and resolves in healthy individuals but 5-15% aquire the disease
• -cell mediated immunity develops in 2-10 wks, resulting in a positive TB test

• -Granulomatous inflammation created by the tubercle bacillus in the lung becomes surrounded by collagen, fibroblasts and lymphocytes
• -Necrosis ("caseation" cheese like) occurs in the center of the lesion. "Ghon tubercle" shows on CXR and is the primary lesion...necrotic areas may calcify and liquify
• -calcified "Ghon complex" may form and enter a latent period, then can be reactivated if hosts immune mechanisms are impaired
• -if liquefacation occurs, the liquid empties into a bronchus and the evacuated area becomes a cavity.
• -bacilli continue to grow in the necrotic cavity wall and spreade via tracheobronchial lymph nodes to new areas of the lung

• -may be asymptomatic in early stage
• -fatigue, malaise, anorexia, wt. loss, low-grade fevers (fever spike tends to happen in the afternoon), night sweats
• -wt.losslater in disease
• -frequent cough of purulent sputum
• -dull or tight chest pain

• -positive smear for acid-fast bacilli
• -confirmation by sputum culture (best collected in AM)- can identify in 1-3 wks (slow growing)
• -repeat cultures after tx, should be neg. after 3 months
• -cavitation and calcified lesions may be seen on CXR but aren't specific enough to be sole basis for diagnosis
• -TB skin test

• -duration of tx is 6-12 mo.
• -Directly Observed Therapy (DOT) is recommended for patients at risk for noncompliance
• -resp. isolation until 3 neg smears
• -negative pressure, UV light directed at upper part of room, HEPA (high efficency particulate air) filter
• -evaulation of susceptible family members
• -major s/e of INH, RIF and PZI is hepatitis, monitor LFTs

• -interferes w/ DNA metabolism of tubercle bacillus
• -s/e= hepatotoxicity (monitor LFTs) peripheral neuritis, hypersensitivity (skin rash, arthralgia, fever), optic neuritis, vit B6 neuritis, may inhibit metabolism of phenytoin, carbamazepine and warfarin
• -nursing considerations: pyridixine (Vit. B6) supplements needed during high-dose therapy (Vit B6 can cause terrible nightmares)
• -INH is used as single prophylactic agent for individuals when PPD converts positive
• -taken on empty stomach

• -has broad spectrum effects, inhibits RNA polymerase of tuvercle bacillus
• -s/e: hepatotoxicity (monitor LFTs), febrile rxn, GI upset, peripheral neuropathy, may enhance elimination of theophylline, steroids, oral hypoglycemics, warfarin
• -nursing considerations: most commonly used w/ INH, low incidence of s/e
• -suppresses birth control pills
• -causes orange discoloration of body secretions/urine. teach pt. to continue taking med

cipro and levaquin

• Severe Acute Respiratory Distress Syndrome, an atypical pneumonia first identified in China in 2002
• -caused by SARS-CoV which is widespread among cattle, pigs, rodents, cats, dogs- virus mutates and transfers to humans but not human to human
• -s/sx range from simple febile resp. illness to severe pneumonia and death
• -incubation period= 2-7 days but can be as long as 10 days
• -viral shedding peaks in resp. specimens and stools at around day 10 after the onset of the clinical illness (unlike other viral illnesses where the contagious period is early in the disease process)

• -fever over 100.4, HA, arthralgias, fatigue, sore throat, N/V, diarrhea
• -in 2-4 days nonproductive cough and difficulty breathing, SOB, low O2 sats, and cyanosis =more severe illness!
• -lab tests show lyphopenia, mild thrombocytopenia, elevated liver enzymes, cultures to r/o other causes
• -CXR may be normal in first wks of illness an dlater have an ARDS type picture...these pts probably need to be on a vent
• -viral culture may or may not isolate SARS-CoV form nasopharyngeal swab during first week, but after week 1 of illness get a stool specimen
• -presence of antibody more than 21 days after sx onset

• -supportive, no effective tx known
• -steroids and antivirals-AB may be considered for concurrent CAP
• -Infection control:
• -pt's w/ over a 100.4 fever or resp. sx should be given a surgical mask and asked about travel hx
• -if suspected SARS put pt in private room and notify infection control
• -airborne and contact precautions in neg. pressure room, N-95, gown and gloves
• -follow up CXR after 1 week after discharge
• -if at home pts should stay home for 10 days after resolution of fever, in seperate bedroom, bathroom, own eating utensils and linen (bc SARS shed in stool)