PATHOLOGY OF OBSTRUCTUVE LUNG DISEASES (BOSCH)

Emphysema
Definition
o Enlarged air spaces distal to bronchioles
o Destruction of walls but no obvious fibrosis
Patho
o proteolysis and antiproteolysis destroy elastic tissue
radial traction and collapse small airways
Cause
o Cigarrete oxid stress PMN + Macs release of eleastase
and radicals elastolytic activity and oxid of alpha 1 antitrypsin
o Genetic alpha 1 abnormal chronic liver disease and alpha 1
elastase activity
Morpho subtypes
o *centrilobular(centriacinar)
Cigarette
Involves resp bronchioles anthracnosis in middle of lobe
Upper lung
May become panlobular
o Panlobular (panacinar)
Alpha 1 antitrypsin deficiency
Uniform destruction of lobule
Lower lobes
o Paraseptal (distal acinar)
Next to fibrosis
Destoy alveolar ducts and distal alveoli peripheral of lobule
Subpleural of Upper lobes
May become spontaneous pneumothorax (tall thin ppl)
o Interstitial
Dissection of air in CT w/in lungs, mediastinum, subcut tissue
Due to pulm tears due to trauma or intra alveolar pressure
Gross patho
o Hyperinflated lung w/ enlarged airspace
o Thin network of CT
Micro patho
o Irregular airspace w/ # of attenuated frag alveolar septa
Clinically
o Worsening dyspnea
o Nonproductive cough
o Tachypnea w/ prolonged expire phase + use of access muscles
o Near normal Hg sat Pink puffers
o Weight loss
o Flat diaphragm / AP diameter (Barrel chest)
Chronic Bronchitis
Definition
o Productive cough for 3 months for 2 years
Causes
o Pollutatns, smoke
o Resp tract infection
Patho
o Irritants mucus production / epithelial squamous metaplasia
Bronchiol and Bronchiolar patho
o Hyperplasia of goblet cells and glands Reid index
Index = ratio of thickness of mucous glands to wall
o SM due to bronchospasm
o Focal epithelial squamous metaplasia and dysplasia
Clinically
o Cough w/ sputum

o Dyspnea and cyanosis (hypoxemia and hypercapnia)

V/Q mismatch pulm vessels constrict to compensate
Pulm HTN Edema
Cyanosis + Edema = Blue bloater
Asthma
Defintiion
o Partially reversible obstruction w/ bronchospasm after agent
o Status asthmaticus = most severe type, meds dont work
Patho
o vasc perm (edema), neural/cytokine bronchoconstrict, mucus
hypersecrete
o Allergens Type 1 HS = Th2 response w/ IL4, IL5, IL13
IL4 = tell B cells to release IgE
IL5 = chemotactic to eosinophils
o Re-exposure Ag specific IgE bound to mast cell IgE cross
linking and mast cell degranulate and release mediators
Acute phase
Histamine perm
Leukotriene C4, D4, E = perm + bronchoconstrict
Late phase
Influx of eosinophils
Other causes
o Aspergillus HS
o Occupational (dusts, toluene, formaldehyde) HS
o Pollutants/drugs
o Virtal Resp tract infection Inflamm response
o Exercise and cold vasc perfusion
o Emotional Vagal stim
Gross Patho
o Overaerated lungs
o Mucus plugs
Microscopic Patho = airway remodeling
o Goblet cell metaplasia + gland hyperplasia (like CB)
o Mucous plugs = Curschmann spirals (epithelial cells), Charcot
Leyden Crystals (granules of eosinophils)
o Sub basement membrane fibrosis
o Eosinophils (not in CB)
o SM hyperplasia and hypertrophy
Note = eosinophils and BM in asthma only, everything else
common w/ CB
Clinical = wheezing, tachypnea, dyspnea
Bronchiectasis
Permanent dilatation due to recurrent bacterial infections w/ necrosis
Patho
o Airway block due to mucous plugs in CB or CF
o ciliary fxn and loss of structure
o Permanent dilation and clearance of secretion
Gross patho
o Dilated peripheral airways out to pleura
o Lower lobes
Clinically
o Cough w/ mucoid or purulent sputum, dyspnea, fever
Atelectasis = incomplete expansion
Def = collapse of previously inflated lung tissue (reversible)
Atelectasis Neonatorum = incomplete expansion at birth
Acquired Atelectasis types

o Obstructive complete block/mediastinal shift toward atelectic

lung/alveolar collapse/bronchial secretions
o Compression pulm compression/shift away / accum in
pleural cavity
o Contraction = due to pulm fibrosis
o Patchy = due to loss of surfactant

NEONATAL AND PEDIATRIC PULMONARY DISEASE(KRELL)

Canalicular stage
o At 16 weeks
o Bronchial and vasc dev completed
o Alvealor ducts form and air sacrs lined w/ cuboidal cells
precursors to type 1 and 2 alveolars cells
Form relationship to capillaries
Alveolar or viable stage
o Cuboidal cells thin out
o Type 2 cells make surfactant and are now seen
o Surfactant
Lines alveoli and ST
After first breath of air prevents collapse of alveoli on
exhalation
o Lung maturity determined by ratio of phospholipids lecithin and
sphingomyelin
o Lecithin w/ maturation and sphingomyelin
L/S w/ age
Things that accelerate this maturation
Cortisone, stress, thyroxin, prolactin, thyophylline,
sympathomimetics
That decrease
Insulin, metapyrone, barbiturates
Tracheo-esophageal fistula
o 4th week prenatal
o Fail to separate esophageal and lung buds from foregut
o Clinically
Neonatal feeding problems
Coughing w/ feeding
Aspirations into airways
Absence of lung or lobe
o 4 to 8 weeks
o Failrure of airway budding into mesenchyme
o Not symptomatic but reserves
Accessory or extra lobes
o Variant of airway branching
o Azygous = Right upper lung
o Cardic lobe = right lower
Cysts
o 4 to 12 weeks of preg
o Abnormal detachmet of lung tissue form primitive air buds
o Connected to bronchial tree by defective airway
o Cliically
Poor clearance of mucus / infections
CXR = persisitent infiltrates
o Blood supply from pulmonary circulation
Sequeastrations
o 1st Tri
o Ectopic lung tissue
o No connection to bronchial tree
o Connected to systemic supply so risk of bleeding
Infant Respiratory Distress syndrome

Hyaline membrane disease

Impaired or delayed surfactant
Low compliance, atelectasis (collapse) work
Epithelial necrosis
Frequent in diabetic moms
Clinically
Cyanosis
Tachypnea, grunting
Acidosis
Need O2 vent and surfactant replacement
o Complications
Lung injury to high FiO2 radicals
Retrolental fibroplasias (blindness, prevent w/ vit E)
Barotrauma
o Prevent w/ corticosteroids before delivery
SIDS
o Brain stem dev abnormal
o Pulm edema, petechiae
o Decreased chemoreceptor response
Cystic fibrosis
o Inherited disoreder of exocrine glands
o Gene mutation of CFTR
o cAMP regulated chloride channel
o Clin
Meconium iluus
Recurrent infections
Pancreatic insuff
Sweat chloride
Immotile cilia syndrome
o Lack of ciliary motion so fail to clear secretions
o Recurrent infections
o
o
o
o
o
o

 Biopsy not required when Hx, PFT, CXR all show occupational lung
disease
Dust macules
o Small scattered densities
o No progressive lung disease
Fibrotic Lung Diseases

PLEURAL DISEASES
Causes of pleural fluid accum =
o hydrostatic pressure = CHF = most common
o oncotic pressure = nephrotic
o perm = pneumonia
o Rupture of thoracic duct
Clinical signs
o Dyspnea and pleuritic chest pain
o Dullness to percussion, absence of fremitus, diminished breath
sounds, friction rub
Diagnosis
o CXR = Fluid layers due to gravity
o Thoracocentesis
No need if suspected CHF, low protein or cirrhosis
But if fever w/ CHF, then yes
Yes if pneumonia, cancer
Transudative
o Systemic factors influence formation and absorption are altered
CHF, cirrhosis increased filtration
Nephrotic syndrome, peritoneal dialysis
o <3g
Exudative
o When local factors that influence are altered
Pneumonia, malignancy
o Fluid Protein to serum protein >0.5
o Fluid LDH to serum LDH >0.6
o Total pleural fluid LDH > 2/3 upper limit of normal for serum
LDH
o Parapnuonic effusion
Typical effusion gram stain/culture negative
Complicated = gram stain culture positive fibrinopurulent
organization can become an Empyema
o Malignant effusion
lymphocyes
Low glucose, high LDH
o TB effusion
o Cyclothorax = milky fluid in space , triglyc
o Hemothorax = blood in space
Pneumothorax
o Gas in pleural space
o Iatrogenic type
o Traumatic type
o Primary spontaneous
No underlying disease, Tall thin body
o Tension pneumothorax = low BP b/c venous return

OCCUPATIONAL LUNG DISEASES (KRELL)

Silicosis
o Hard rock mining/sandblasting/stone cutting
o Acute silicosis/silicoproteinosis
Ground Glass appearance in Upper lobe
Fatal reaction to massive exposure
Impairment of ALv macs, cant clear surfactant
Diffuse, patchy, eosinophilic, lipoproteinaceous
o Chronic (simple) silicosis
Long standing Mac activation
Nodules/upper lung/eggshell calcification
Almost no change in PFT
Concentrically layered dense collagen
Birefringent silica
o Complicated silicosis
Nodules combine, large densities on CXR
Mainly Restrictive PFT
ANCA and RF +
Caplans syndrome
Pneumoconiosis + Rheumatoid arthritis
Big nodules but more benign
Palisading (in a row) fibroblasts
o Progressive massive fibrosis
Massive coalescence of Upper Lobe nodules
Traction on lower lung by fibrosing upper lobes Bullae at
base
Traction emphysema
Pleural adhesions
Compression of vena cava on esophagus
o Silicotuberculosis
Silica poisons Macs
High relapse rate, Weight loss, Fever
Coal workers pneumoconiosis
Black lung compensation
Anthracosis = least severe
o Lots of Carbon laden Macs in interstitium and nodes
Accum of coal dust in lungs + tissue rxn
Simple CWP
o Macules to Fine nodules, black sputum
o No scarring
o Centrilobular, upper lung
o PFT normal
Complicated CWP
o Can lead to progressive massive fibrosis (dense scar tissue)
o Upper lung
o Ischemic necrosis in center of nodules = cavitation
o Pulm dysfxn and pulm HTN
Asbestosis and related
Mining, Pipe fitters, boiler workers
Asbestos pleural disease

o Pleural plaques
Thickened parietal pleura and dome of diapragm
Calcified as hard white areas on CXR
o Exudative bloody pleural effusions
Asbestosis = pulm interstitial fibrosis
o Long fibers are worse than serpentine chrysotile, too large to be
ingested by Macs
o Fibers coated w/ beaded golden complex honeycomb lung
o Asbestos is tumor initiator and promotor and gen free radicals
o Lung Base
o Shaggy heart Border
o Dry cough, crackles
o PFT = restrictive w/ low lung volume
o Clubbing, cor pulmonale
Asbestos and malignancies
o Bronchogenic lung cancer
Worst if smoking and asbestos
o Malignant mesothelioma
Tumor of pleural mesothelial cells
Diff from benign by behavior rather than cell types
Worse than lung cancer = radiation or chemo dont work
Immunologic lung disease
Type 3 HS due to organic dusts = acute HS pneumonitis
o Immune complex formation and deposition in tissue
complement activation
Type 4 HS = chronic HS pneumonitis
o Delayed type HS (like berylliosis)
o Cytoxic T cell mediated HS
CD8
Farmers lung
o Bilateral reticulonodular infilatrates
o Will resolve w/in 1 day
o Lead to restrictive lung disease
Occupational asthma
o Temporal relationship
Berylliosis
o Metal alloy factory, nuclear power, electronics, aerospace
o Exposure both inhalation and skin
o Genetic predisp
o Type 4 HS
Activation of CD4 Th1 cells and Macs non necrotizing
granulomas and fibrosis
Toxic lung injury
o Soluble agents = HCl, ammonia, sulfur
Harsh upper airway irriatns
Less commonly leads to lung injury b/c ppl will leave
Diffuse alveolar damage Acute resp distress syndrome
Release of pro inflamm by Macs anc activation of endothelial
cells in lung intra capillary adhesion, activation of PMNs
release of free radicals, lysosomal proteases, leukotrienes
alveolar endothelial, epithelial damage
Early acute or exudative stage of ARDS = 1 2 weeks
o Hyperemia, edema
o Intralveolar hyaline membrane no pneumocytes seen
o Patchy atelectasis = loss of type 2 pneumocytes
Later proliferative or organizing stage
o Prolif of type 2 pneumocytes

o Interstitial and intra alveolar fibroblastic prolif

Mineral/Inorganic Dust pathogenesis
o Phag by Macs long standing activation of Macs
o Activate inflammasome IL-1B and IL-18
o Release radicals
o Make eicosanoids
o Secrete IL8 (chem PMN), TNF, IL1
o Make fibroblast growth factors

COPD/ILD, OSA/high altitude

Group 4 = Chronic thromboembolic disease
o Thrombus obstruction at prox or distal pulm arteries
o Pulm Emb also from parasites, tumor, foreign
o Tx = anticoagulate, Pulm endarterectomy (clots pulled out)
Group 5 - Misc
o Hematologic, systemic, metabolic
Clinically
o Pulm HTN prelaod to RV RV hypertrophy/dilate/fail
o Syncope w/ exertion
o Loud P2 heart sound, late pulmonv valve closure
o Edema of legs, ascites, hepatomegaly, pulsating liver, JVD
o Echocardiogram = most important
o Right heart catheterization = gold standard for PAH Dx
Classification of dyspnea
o 1 = ordinary activity no symptoms
o 2 = ordinary has symptoms CCB, PDE-5i
o 3 = less than ordinary ERA
o 4 = dyspnea at rest Start IV or SQ prostacyclin analog
6 minute walk test
o Oxygen sat and heart rate monitored

PULMONARY HYPERTENSION
Definition
o Mean pulm artery > 25 mm Hg
o When MPAP is >25, and pulm cap wedge is < 15 art HTN
o When MPAP is >25 and pulm wedge is >15 venous HTN
Group I = Pulm artery HTN
o Idiopathic
o Familial
o Patho
Vasoconstriction, cell prolif, fibrosis, thrombosis
Imbalance of humor mediators (unopposed vasoconstrict and
prolif)
TXA2, ET1, 5HT
PGI2, NO, VIP
o vasoconstrict and cell prolif area pulm pressure RV
fail
Hyperplasia of intima
Hypertrophy of media
In situ thrombi
o Treatment options
Calcium channel blockers
Endothelin receptor antagonists
PDE-5i
GC stim riociguat for group 4
Prostacyclin derivatives = pulm vasodilators
Group 2
o Pulm venous HTN
Pressure in Left heart pressure in pulm
o Due to
LA or LV disease
Left valvular disease
Group 3
o Pulm HTN due to Resp Distress/hypoxemia
Hypoxemia causes vasoconstriction

PULMONARY EMBOLISM/THROMBOEMBOLIC DISEASE

Virchows triad = risk factors for DVT
o Stasis
o Endothelial injury
o Hypercoagulable state
Highest risk of VTE in preg is near term and immediate post partum
Diagnosis
o Scoring systems = Wells score
o help in DX but not Diagnostic
CXR, ECG, blood gas
o Dippler ultra sound is most preferred for DVT dx
Clinical symptoms of PE + DVT by Doppler = no futher testing
needed
o Contrast venography is gold standard
o D-Dimer
Product of fibrinolysis
Neg = most likely embolism not present
Pos = further testing neede
o Multi detector CT is preferred for Dx of PE
High spec and sens for large PE/segmental PE
Poor for small subsegmental emboli
Pt needs to hold breath = hard
Radiation exposure
o Ventilation perfusion scan
Neg probabilty scan = not PE
High prob scan = lack of perfusion but normal ventilation = PE

PATHOLOGY OF INTERSTITIAL LUNG DISEASE

ILD definition
o Destroys alveoli and adds cells and fibrous tissue to interstitium
exchange surface

Thickening and stiffeing of septa

Restricting stretch
o Hypoxia in ILD ***
o Result in small non compliant lungs
o Known causes
Pneumoconiosis inorganic silicosis, asbestosis
o Unknown cause
Fibrotic lung disease assoc w/ collagen vascular disease ***
Rheumatoid arthritis/scleroderma, SLE, Sjogrens
Lymphangioleiomyomatosis (LAM) **** - women, abnormal
muscle prolif, cysts. Tuberous sclerosis = one cause of LAM

that is inherited
Usual interstitial pneumonia (UIP) = Idiopathic pulmonary fibrosis
(IPF)
o Patchy distribution
o Subpleural accentuation / peripheral densities
o Fibroblastic foci = myofibroblasts

o May lead to end stage / honeycomb lung irreg reticular

o Traction bronchiectasis
o Patho
Insult epithelial and BM damage inflamm
pneumocytes and myofibroblasts
If BM is preserved, recovery is seen w/ type 1 pneumo
restoration

If BM lost, fibroblasts and collagen production present

Pneumocytes become fibroblasts via EMT epithelial
mesenchymal transition
TGF-B fibroblasts and collagen
Fibroblasts come from bone marrow/resident fibroblasts and
EMT
Inhibitors of vascular and stromal growth factors (VEGF, GFG,
TFG-B) will inhbit progression of IPF
Tyrosine kinase inhibitor = Med
o Clinically
Bibasilar inspiratory crackles/Tachypnea/Clubbing
Restrictive Pulm physio w/ volumes and DLCO and wide Aa
gradient *****
Hyperplastic type 2 pneumo and loss of type 1
Desquamative interstitial pneumonitis (DIP)
o Smoking Link
o Responds to steroids (UIP doesnt respond)
o Good prognosis
o Patho
# of Macs, mild fibrosis
Same patho as UIP but linked to smoking
Alveoli filled w/ Macs
Uniform damage
Non specific interstitial pneumonia (NSIP)
o Prognosis differs based on if cellular or fibrotic subtype
Cellular = lymphocyte infiltration
Fibrotic(worse) collage infil
o Uniform fibrosis = diffuse alveolar fibrosis (unlike UIP)
o Ground glass CXR
o Responds to corticsteroids
o No subpleural accentuation
o Clinically*******
Restrictive Vent defects
FEV1 and FVC
Normal FEV1/FVC
TLC , DLCO
Compliance, Aa grad w/ 6 min walk
Hypersensitivy Pneumonitis
o ILD w/ known etiology = organic dust inhale
o Patho
Interstitial granulomas
Peribronchiolar inflamm
Small airway obstruct = Bronchiolitis obliterans orgranizing
pneumona = BOOP
Granulation tissue in alveoli/bronchi
Dont become Honeycomb
o Type 3 HS activate complement
o Type 4 cell med immunity granuloma formation
How to Dx
o Interdisciplinary
o Rule out exposure to other agents, drugs, bugs
o Rule out comoribid conditions
o CT/Radio picture
o Wedge resection sample
Sarcoidosis
o Common systemic disease , Upper lobe disease
o Non necrotizing granulomata
o Lymphangitic pattern, mediastinal lymph node affected
o Bihilar lymphadenopathy = butterfly lymph
o Extensive interstitial fibrosis
o Rule out infection otherwise if steroid is given it is bad

o Do transbroncioal biopsy for Dx

o Patho
Activation of T4/T8 (10:1)
Recruit and activate Macs
o Clinically
Upper lobe Honeycomb
Peribronchial distribution
Histiocytoses X
o Prolif of Langerhans cells
Dendriitc APCs
Strong assoc w/ smoking, symptoms get better when stopped
Stellate, peribronchiolar nodules
Upper lobe
Delicate folds of nuclear membrane
Birbeck granules
Racket shaped cytoplasmic inclusions
Positive Cd1a stain
o Unifocal = Lung or Bone
Eosinophilic granuloma of Lung (or bone)
Best prognosi
o Multifocal
Hand schuller christain disease
Age 1-3
Lung and bone, and systemic
Letterer Siwe disease
Age 0-1 yr
Worse prognosis

TUBERCULOSIS

o Pulm TB always should be treated

Transmission of TB
o Person to person
o Airborne droplet nuclei
o Nodular lesions have 10k but cavitary lesions have up to 1 bill
bacteria so highly infectious
o NTM has no airborn transmission
Patho
o Macs ingest tubercular bacilli
o They escape intracell killing and disrupt Macs
o 2-3 weeks later T cell immunity, Macs, kill bacteria
o HIV infection, diabetes, cancer, immunosupp agents bacteria
can reactivate
Immunology
o Pt needs cellular immune response to control
o Need CD4, IL12, IFy, TNF
o Epitheloid cells are stimulated Macs creating the granuloma
o Langerhans giant cell consist of fused Macs arount w/ multiple
nuclei in peripheral successful host response
o CD4 cells activate Macs to kill epithelioid granuloma
o CD8 suppress lyse Macs infected w/ mycobacteria to form
caseating granuloma
o Resistice to infection = Innate
o Resitiance to progression = adaptive
o Blockade of TNF-a reactivation high bacillary burden
o Extrapulm TB common in HIV patients
Clinically
o 10 to 100 bacilli needed for positive culture = gold standard
o Mantoux tb skin test (TST) = t cell med delayed type HS
2 to 8 weeks after infection to react to TST
o Interferon gamma release assays (IGRA) = presence of infection
by measuring immune response to TB proteins in whole blood
o TST and IGRA cannot differentiate between LTBI and active TB
o False positive TST in pts w/ NTM, BCG vaccine
o CXR
Primary TB = middle or lower zones w/ ipsi hilar adenopathy
Reactivation TB = upper lobe w/ caviation
o HIV infection is greatest risk factor
o Isolation discontinued when
Pt on adequate therapy for 2 weeks
Symptoms improve
3 consecutive neg AFB sputu smears

Mycobacterium TB
o Cell wall rich in lipids
o Acid fast bascilli
o Obligate aerobe
PNEUMONIA
o Niacin when cultured
o Virulence factors
Definition
Cord factor
o Infection of parenchyma due to pathogens at alveolar level and
Lipoarabinomannam = inhibit Mac activation
host response
Induces Mac to secrete TNF alpha = fever, weight loss, tissue Classification (in worsening order)
o CAP, HCAP, HAP/VAP
damage
Nontuberculous Mycobacteria
Patho
o No human to human transmission
o Inhalation o small droplets
o Classification of NTM depends on
o Aspiration of oral bacteria most common
Rate of growth
Sympstoms
Pigment production
o Fever, cough, chest pain, dyspnea
o M. fortuitum = rapid
o At least 2 of 4 + CXR for Dx
o Can be a colonizer
o CURB 65
Pulmonary NTM
Confusion, urea nitrogen > 20, Resp rate > 30, Low BP, older
o Dx of NTM = dont have to treat
than 65

 Adepuate sputum gram stain has >25 PMNs and <10 Squamous
epithelial cells per low power field
Infectious agents
o Strept pneumo = most common bacterial in CAP
o Rhinovirus = most common in CAP
Funal
o Coccidiomycosis
Acute = valley fever, self limited
Erythema nodosum = bumps on shin
Tx = itraconazole, fluconazole
o Blastomycosis
Acute = non spec, non prod cough, no self limited
Chronic = like TB
Skin lesions due to fungus
Tx = amphotericin B for severe, CNS
Itraconazole for mild to mod, Not CNS
o Histoplasmosis
Acute benign = no sputum
Acute severe
Chronic = productive cough
Dx via urine antigen , hilar enlargement
Tx = itra, fluco, ampho B
Outpatient Tx
o Typical bacterial
moxi-club + azithro
levo or moxi
o influenza = oseltamivir
o mycoplasma or chlamydophila = azithro or doxy
inpatient
o empirical
beta lactam(ceftr) + azithro
levo or moxi
o influenza = oseltamivir
o Staph aureus = vanco or linezolid
o PSA = anti PSA beta lactam
Use FQ antibiotic to cover typical and atypical
Penicillin resisitant S pneumo
o Chromosomally mediated, not beta lactamase mediated
o Use ceftriaxone or vanco
Do not repeat CXR until 4 weeks in uncomp
Prevention
o Flu vaccine > 6 mo, no if egg allergy
Pneumococcal vaccine for adults
o PVC 13 and 23 for >65
o PVC 13 for <65

RESPIRATORY FAILURE AND MECHANICAL

VENTILATION
Hypoxemia can be due to
o Low environmental
o Hypoventilation
o VQ mismatch
o Right left shunt
o Diffusion defect
Hypercapnic Resp failure
o alveolar ventilation = removal of CO2

o PaCO2 will rise when production of CO2 by body such as

catabolic states, high caloric intake, low min vent, high dead space
o Causes
CNS disease
Respiratory center in brainstem is suppressed
Chest wall abnormality
Structural = kyphosis or scoliosis
Functional = Neuro musc disease, lung hyperinflation due to
COPD where diaphragm is flat
Airway disease
Upper or lower airway obstruction
Hypoxemic respiratory fail
o In a pure hypoxemic fail, theres no problem w/ ventilation so
PaCO2 is normal
o Causes
Parenchymal lung disease
Infections, inflame or fibrotic disease, neoplasms
Due to VQ mismatch
CV disease
LV fail, RV fail, pulm embolism
Pulm edema
Cardiogenic = hydrostatic pressure due to LV fail
Noncardiogenic = fluid leaked to endothelium injury. ARDS
is best example
ARDS
o Patho
Inflamm infiltrate endothel damage fluid leaks out
edema
Disruption of walls and loss of surfactant
Dev of hyaline membrane and later on fibrosis
o Dx
Echocardiogram
Wedge pressure = LVEDP
Increased in cardiogenic pulm edema
Normal in noncardiogenic pulm edema
Mechanical Ventilation
o Mode
Pressure targeted = predetermined pressure
Volume targeted = predetermined Tidal volume = common
Controlled mandatory vent (CMV) = all VT equal
Assist controlled (AC) = pt triggers vent w/ neg pressure
Synchronized intermittent mandatory vent (SIMV) = VT
variable
o Rate, Tidal volume, FiO2, Flow pattern
o Monitor airway pressure
Peak insp pressure at tube end
Pleateu pressure at alveoli w/o mvmt of air during inspire
o PEEP = possitve pressure in alveoli at end of exhalation
Improves lung compliance, aids LV
o Flow rate
o Sensors volume, flow, pressure
Complications
o Barotrauma
o CV = LV aide might cause hypotension
o Auto PEEP = more air trapped w/ each breath dynamic
hyperinflation seen in COPD
Weaning from MV
o Rapid shallow breathing index = RSBI = best predictiability