Restrictive Lung Diseases Flashcards
Restrictive Lung Diseases
Description & Key Characteristics
Diseases that restrict the lung from expanding fully
Ex. chest wall (boney), muscular (NM diseases), parenchyma
DEC compliance > DEC negative pressure > DEC air entry
- Inspiratory problem
- NEED (-) pressure in lungs compared to the atmosphere (high-low pressure)
- Volume of air in the lungs is decreased (DEC ventilation - V/Q mismatch)
Results in INC work of breathing:
- INC RR (may lead to hyperventilation: DEC PaCO2)
- INC accessory mm use
- INC pressure required to maintain lung expansion & ventilation (exert against a greater pressure)
- INC fatigue - poor ventilation = DEC O2 in system to supply tissue = fatigue easier
Restrictive Lung Diseases
(4)
- Interstitial Pulmonary Fibrosis
- Sarcoidosis
- Atelectasis
- ARDS
Interstitial Pulmonary Fibrosis
Definition
Thickening of the interstitium of the alverolar walls which progress to fibrosis or scarring
Interstitial Pulmonary Fibrosis: Pathophysiology
(4)
- DEC lung compliance (results in INC airway resistance on inhalation)
- INC elastic recoil
- INC fibroblasts result in INC collagen leading to fibrosis or scarring
- DEC diffusion capacity - gases cannot move across the membranes
Interstitial Pulmonary Fibrosis: Etiology
(4)
- Idiopathic (most common)
- Environmental exposure to inorganic dust, toxis gases, and certain drugs
- There may be a genetic factor
- Some connective tissue disorders are associated with IPF (ie RA)
- Hypothesized: Inflammation causes the fibrosis - abnormal wound repair
Interstitial Pulmonary Fibrosis:
Clinical Presentation
(6)
Inspection:
- Dyspnea
- INC RR + shallow breathing (tachypneic breathing)
- Dry, unproductive cough - irritation (do not need to expel anything)
- Clubbing
- Cynaosis
Later/ more progressed disease results in hypoxeamia - DEC O2 in blood & manifests in these S/S
- DEC chest expansion - bilaterally
Palpation:
- Tactile Fremitus: INC (more vibrations - thicker lung)
Percussion:
- Dull
Ascultation:
- Late fine dry inspiratory crackles - “velcro”
ABGs:
- DEC PaO2
- DEC PaCO2
INC RR, breathing out more frequently BUT do NOT get enough air in = poor diffusion of gas
CXR:
- Small contracted legs
- Raised diaphragm - bilaterally
- Diffuse reticular markings (mainly in lower lobes)
MESH appearance - fibrosis w/ air behind it
- High resolution CT is more commonly used to help assess the severity of IPE > Ground glass opacities is a key feature seen in IPF using HRCT
Sarcoidosis
Defintion & Patho & Etiology
A disease involving granuloma development (collection of inflammatory cells that form a lump) in the lungs, skin, lymph nodes, & other organs
Patho:
- Too complicated, do not need to know
Etiology
- Unknown
Atelectasis
Definition
Collapse of alveoli or lung tissue
May hve sub-segmental, segmental, or lobar distributions
Atelectasis:
Pathophysiology & Etiology
(6)
- Obstruction - ie mucus plug, trumor, foreign body
** Any alveoli DISTAL to a block will collapse - DEC nitrogen - helps keep open the alveoli
- DEC surfactant (INC surface tension)
- Compression - foregin substance, tumor - stuck close & collapse
- Hyperventilation
- Hypoventilation - breathing to shallow & not enough
Occur: post-op - not ventilating alveoli d/t incision sites
PNEUNOTHORAX always = atelectasis
Atelectasis: Clinical Presentation
(6)
Inspection:
- Dyspnea
- Cyanosis
- INC RR + shallow breathing (tachypneic breathing)
- IPSILATERAL trachael deviation - side of the atelectasis
Greater atelectasis = greater shift
Palpation:
- Tactile Fremitus: DEC (over a larger surface area & feeling vibrations over a more broad general area = feeling a lack of vibrations from that collapse area that has no lung tissue there (mostly empty space). Net affect is a DEC in tactile fremitus
- Chest wall excursion: DEC (on affected side)
Percussion:
- Dull (over atelectasis)
- Resonant - other areas will be normal
Auscultation:
- DEC BS or absent
- Dry inspiratory crackles (alveoli are opening - popping - open)
ABGs:
- DEC PaO2 - poor ventilation / good diffusion
CXR:
- Ipsilateral shift of metastinum
- INC density in area of atelectasis (whiteness)
- Elevated hemi-diaphragm (tenting)
Unilaterally less volume - diaphragm elevates
V/Q Complications
(2)
SHUNT
- Issue with ventilation - deoxygenated blood is passing by w/o being oxygenated
DEAD SPACE:
- Opposite of shunt - issues with perfusion (Q)
- O2 is available but gases are not getting exchanged
Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.
Acute Respiratory Distress Syndrome
Description
An acute lung injury which is characterized by respiratory distress, severe hypoxemia, & increased permeability of the alveolar-capillary membrane
Clinical phenotype - not a disease itself
ARDS: Pathophysiology
(4)
- INC permeability of capillaries d/t injury. This will lead to edema in interstitial space & then into alveoli
Edema > interstitium > alveoli > lung - DEC surfactant production leading to INC alvelor surface tension causing DEC lung compliance
- V/Q mismatch > right to left shunt > aterial hypoxemia
Passing through w/o picking up O2
Good perfusion BUT poor ventilation (edema) - Rapid fibrosis in later disease progression = DEC lung compliance even after the ARDS resolves
ARDS: Etiology
(5)
- Shock (any type)
- Severe pneumonia
- Severe trauma
- Sepsis
- Aspiration (inhaled toxins)
ARDS: Clinical Presentation
(6)
Inspection:
- Severe dyspnea (often require mechanical ventilation at high PEEP)
PEEP = Positive Expiratory End Pressure: pressure to hold alveoli open & helps recruit more alveoli for gas exchange
- Cyanosis - hypoxaemia
- INC RR + shallow breathing (tachypneic breathing)
Palpation:
- Tactile Fremitus: INC (pulmonary edema + fibrosis)
Percussion:
- Dull
Auscultation:
- Inspiratory crackles, diffuse wheezes (obstruction)
ABGs:
- Severe DEC PaO2 & PaCO2 - hyperventilation (breathing so rapidly)
- Respiratory alkolosis
CXR:
- Patchy infiltrate in periphery of lungs (edema/fibrosis)
