module 11 restrictive lung disease Flashcards
restrictive PFT
decreased inspiration amount FEV1: gets out less then normal - 2.5L FVC: less out in total - 3.0L FEV1/FVC: 83% - normal
restrictive lung diseases caused by
alterations in
- lung parenchyma
- pleura
- chest wall
- neuromuscular funtion
restrictive lung disease presenting s/s
more effort to expand lungs during inspiration
inc. respiratory rate; rapid, shallow
dec. tidal volume
dyspnea
characteristics of restrictive disorders
dec. vital capacity
dec. total lung capacity
dec. function residual capacity
dec. residual volume
- greater dec. in lung vol. the greater the severity of disease
restrictive disorders ABG
dec. PaO2
normal or dec. PaCO2
inc. pH
overview of restrictive lung disorders
parenchyma - diffuse interstitial lung disease - sarcoidosis - pneumonitis - occupational lung disease atelectatic disorders - ARDS - IRDS infection/inflammatoin plueral space - PTX - effusion neuromuscular disorders chest wall deformities
diffuse interstitial lung disease
restrictive lung disorder also called pulmonary fibrosis 3 pathological patterns - inflammation - fibrosis - destruction Causes thickening of alveolar interstitum
diffuse interstitial lung disease pathogenesis (pulmonary fibrosis)
inj. to alveolar or capillary endothelial cells
- > infiltration of lymphocytes, macrophages, plasma cells
- > obliteration of capillaries, reorganization of lung parenchyma, irreversible fibrosis
- >thickened alveolar wall and interstitium
- > formation of large air filled sacs/cysts and dilated terminal and respiratory bronchioles
diffuse interstitial lung disease s/s
progressive dyspnea irritating non productive cough rapid, shallow breathing clubbing of nail beds bibasilar end-expiratory crackles cyanosis: late anorexia and wt. loss
inflammatory pattern of diffuse interstitial lung disease
triggering event
- occupational, smoking, drugs, CT disease
- > inflammatory response
- > inj. to alveolar capillary basement membrane
- > inc. permeability -> fluids and debris into alveoli
- > fibroblastic proliferation -> deposition of collagen
fibrotic pattern of diffuse interstitial lung disease
inc. mesenchymal and fibroblasts in interstitium
thickened alveolar walls w/ inc. fibrous tissue
-> restriction, dec. compliance, inc. elastic recoil
destruction pattern of diffuse interstitial lung disease
loss of alveolar walls
xray: honeycomb lung
sarcoidosis
acute or chronic systemic disease of unknown cause
immunologic basis
- presence of CD4 T cells
activation of alveolar macrophage to unknown trigger
women in 20-30’s
- 1st degree relative w/ hx inc risk 5x
noncaseating granulomas: fibrotic surrounded by large histiocytes
sarcoidosis pathogenesis
development of multiple, uniform, noncaseating epithelioid granulomas: affect multiple organ systems
Abnormal T cell function
sarcoidosis s/s
malaise fatigue wt loss fever chest discomfort dyspnea dry nonproductive cough erythema nodosum (nodes on lower extremities) macules papules hyperpigmentation subQ nodules hepatosplenomegaly lymphadenopathy iritis uveitis
hypersensitivity pneumonitis
extrinsic allergic alveolitis
restrictive and occupational disease
>300 inhaled organic agents responsible for inflammatory proccess
- genetic predisposition
antigen combines with serum antibody in alveolar walls -> type 3 hypersensitivity reaction -> antigen- antibody complexes -> inflammation and lung tissue injury
leads to diffuse pulmonary fibrosis in upper lobes (hallmark)
hypersensitivity pneumonitis granulomatous inflammation
-> lung tissue injury
- thickening of alveolar walls
- formation of exudate in bronchiolar lumen
- infiltration of lymphocytes, plasma cells, and eosinophils
fibrotic lung changes occur in advanced cases
acute hypersensitivity pneumonitis s/s
4-6 hours after exposure, resolves in 18-24 hours chills sweating myalgia nausea lethargy HA malaise possible fever dyspnea at rest dry cough inc. RR chest discomfort cyanosis (late) crackles in bases
chronic hypersensitivity pneumonitis s/s
progressive diffuse pulmonary fibrosis in upper lobes cough dyspnea fatigue cor pulmonale
pneumoconiosis: occupational lung diseases
parenchymal lung disease caused by inhalation of inorganic dust particles; greater the exposure, the worse the consequence
- anthracosis: coal miners lung/ black lung
- silicosis: silica inhalation
- asbestosis: asbestos inhalation
pneumoconiosis pathogenesis
alveolar macrophages try to engulf and remove particles
macrophages secrete lysozymes to control foreign particle activity
-> damage to alveolar walls causing deposition of fibrous materials
pneumoconiosis s/s
none in early stages physical s/s w/ impaired pulmonary circulation d/t inc. pulm vascular resistance or development of infection - productive cough - dyspnea - progressive fatigue - clubbing of fingers Late - chronic hyposemia - cor pulmonale - respiratory failure
atelectatic disorders
atelectasis: collapse of lung tissue
compression
absorption
surfactant
compression atelectasis
tumors
fluid
air in pleural space
absorption atelectasis
obstructed alveoli
-> no intake of air into alveoli
- tumor, mucus plugs, foreign body
concentrated O2, replaces nitrogen content, or anesthetic agents
-> too much O2 absorbed from alveoli -> collapse
surfactant impairment atelectatic
dec. production or inactivation of surfactant prematurity ARDS anesthesia mechancial ventialtion
ARDS: acute (adult) respiratory distress syndrome
characterized by damage to the alveolar capillary membrane -> wide spread protein alveolar infiltrates and dyspnea
changes in alveolar diameter
injury to pulmonary circulation
disruptions in O2 transport and utilization
associated with dec. in PaO2 refractory (does not respond) to O2 therapy
common findings with ARDS
severe hypoxemia r/t intrapulmonary shunting of blood dec. lung compliance dec. FRC diffuse, fluffy alveolar infiltrates noncardiogenic pulmonary edema
early ARDS s/s
hx of precipitating event -> low blood volume state 1-2 days before resp. failure sudden respiratory distress slight inc. HR dyspnea dec O2 shallow, rapid breathing
progressive ARDS s/s
inc. HR
inc. RR
hypoTN
restlessness
AMS
frothy secretion
crackles, ronchi
retractions
late ARDS s/s
cyanosis
ARDS breakdown tissue trauma
alveolar capillary membrane injury
- > tissue trauma
- > inc. platelet aggregation -> release of proteases and kalikrein
- > microemboli in pulm. vessels
- > activated neutrophils: serotonin, bradykinin, histamin, thromboxan A2 -> free radicals
- > pulmonary platelet trapping and coagulation activation
- > inc. permeability of endothelium and epithelium
- > inc. interstital and alveolar edema
- > dec. alveolar and airway filling
- > consquencses
- dec. FRC
- inc. intrapulmonary shunting
- dec. lung compliance
- inc. dead space
- loss of hypoxic vasoconstriction
- hyaline membrane formation
ARDS breakdown type 1 alveolar epithelial defects
alveolar capillary membrane injury
- > type 1 alveolar defects
- > dec. surface area, leaky capillary
- > disrupted basement membrane
- > disorganized collagen in the interstitium
- > fluid accumulation in alveoli
- > damage to type 2 pneumocytes and type 1 alveolar cells
- > decreased surfactant
- > alveolar collapse
- > dec. alveolar and airway filling
- > consequences
high FiO2 and ARDS
leads to damage to type 2 pneumocytes and type 1 alveolar cells
inc. permeability of endothelium and epithelium
- paralysis of ciliary action
- atelectasis
- pulmonary edema
- alveolar cell hypertrophy
- damage to mitochondria of type 2 cells
pneumonia
inflammatory reaction in alveoli and interstitium caused by infectious agent
- aspiration of oropharyngeal secretions
- inhalation of contaminants
- contamination from systemic circulation
CAP pneumonia
community acquired
- mild/moderate
- severe
nosocomial pneumonia
medically acquired
- ventilator: VAP
- health care facility: HCAP (resting home)
- hospital: HAP
pneumothorax
air in pleural space spontaneous primary: rupture of small blebs -> air in pleural space -- spontaneous -- tall, thin men, 20-40 w.out underlying disease factors -- smoking inc. risk Secondary: rupture of bleb or cyst -- r/t complication of preexisting pulmonary disease - asthma - emphysema - cystic fibrosis - infectious - interstitial lung disease
tension pneumothorax
build up of air under pressure in pleural space
- traumatic orgin
- penetrating or nonpenetrating injury
- medical emergency
- > lung collapse on same side
- > forces mediastinum toward contralateral side
- > dec. venous return and CO
pneumothorax s/s
inc. HR
dec. or absent breath sounds
hyperresonance
sudden chest pain
dyspnea
Tension and large
- severe inc. HR
- hypoTN
- tracheal shift
- neck vein distention
- hyperresonance
- SubQ emphysema
pleural effusion
fluid in pleural space - transudate - exudate - empyema - hemothorax - chylothorax change in pleural capillary hydrostatic pressure, colloid oncotic pressure, or intrapleural pressure
transudative effusion
low protein and LDH - HF - cirrhosis - nephrotic syndrome - myxedema r/t inc. hydrostatic or dec. oncotic pressure
hemothorax effusion
blood and pleural fluid
- chest trauma
exudative effusion
high protein and LDH - malignancy - infection - sarcoidosis r/t inc. production of fluid d/t inc. permeability of pleural membrane or impaired lymphatic drainage
chylothorax effusion
traumatic leakage of lymph fluid
- rheumatoid effusion
- TB pleuritis
empyema effusion
r/t infection in pleural space
pleural effusion s/s
dyspnea pleuritic pain: sharp, worse with inspiration dry cough dec. chest wall movement no breath sounds dullness to percussion dec. tactile fremitus
neuromuscular disorders
diseases affecting the muscles of respiration or their nerve supply can lead to dyspnea and respiratory failure
- poliomyelitis
- ALS
- mascular dystrophies
- guillian-barre syndrome
- myasthenia gravis
chest wall deformities
physically restrict expansion
- kyphoscoliosis
- ankylosing spondylosis
- flail chest
- obesity
kyphoscoliosis
bone deformity of chest wall resulting from posterior curvature (hump back) and scoliosis- lateral curvature
-> compression of lung volume, atelectasis, hypoxemia
kyphoscoliosis s/s
dyspnea on exertion
rapid, shallow breathing
hypoxemia later on and eventually CO2 retention
Flail chest
multiple rib fx at 2 different sites
-> unstable, free floating chest wall segment
moves paradoxically; inward on inspiration, outward on expiration
-> pulmonary contusion, dec. compliance, resp. failure
flail chest s/s
SOB pain on inspiration hypoTN cyanosis hypoxemia
obesity
dec. ventilatory drive
inc. work of breathing
inc. abd. size -> compression of chest cavity
obesity s/s
dec. alveolar ventialtion somnolence severe hyposemia polycythemia cor pulmonale SOB
