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218 Cards in this Set

  • Front
  • Back
Why use pulmonary function tests?
-Categorize physiology
-Follow progression of disease
-Assess response to treatment
-Measure effects of exposures
-Help identify surgical risks
-Adjudicate disability
What is forced expiratory maneuver?
Spirometry-patient takes a couple of tidal breaths, exhales to residual volume, take a full breath in up to total lung capacity, forcibly exhale as hard as he/she can until the lungs are “completely” empty, and then take an inspiratory breath.
What is the theory of equal pressure point?
A driving pressure falls(recoil and pleural), there is a point when the surrounding atomsperepheric pressure and driving pressure are equal.
What makes up the upstream portion?
aveoli to EPP
What makes up the downstream portion?
EPP to airway outlet
What two factors determine the airflow velocity of all foreced exhalation?
recoil pressure and resistance in the downstream segment
Elastic recoil pressure/upstream resistance
when do you see intrathoracic flow limitation?
When do you see extrathoracic flow limitation?
What is a flow volume loop?
volume on the x axis starting at TLC and going to RV. y axis is flow.
What are the characteristics of the FVL with HIGH lung volume?
High Pel, low Rus, High Vmax, EPP is near mouth in large stiff airways, effort-dependent.
What are the characteristics of the FVL with LOW lung volume?
Low Pel, high Rus, low Vmax, EPP is near aveoli in small floppy airways, effort-independent.
What is the relationship between V50 of expiration and inspiration?
inspiration should be 1.5 times greater than expiration. If less than one think extrathracic obstruction.
Intrathoracic obstruction
-Decreased isovolumic flow
-Concavity expiratory limb
-Reflects increased Rus, decreased Pel or both
-Upward shift due to air trapping(left)
-Decreased VC
-Volumes shift down(right)
Increased Pel
Increased isovolumic flow
Normal Pel
No change in isovolumic flow
Extrathoracic obstruction
V50 of expiration is greater than inspiration
Fixed obstruction
both inspiration and expiration are limited, most common in tachea
Central, non-parenchymal intrathoracic obstruction
volume independent shoulder on expiratory limb
what are the major landmarks of spirogram?
VC-total volume breathed out
FEF25-75-forced expiratory flow
how do you determine presence of obstruction with reduced VC on spirogram?
look for air trapping
Obstruction on a spirogram
Slow initial upstroke
Reduced FEV1
Reduced FVC
Reduced FEV1/FVC
Late volume changes
Restriction on a spirogram
Rapid upstroke
Reduced FEV1
Reduced FVC
Normal FEV1/FVC
No late volume changes
Why do bronchodilator testing?
-Done for obstructive disorders
-Tests presence/absence of airways reactivity
-May suggest inadequate treatment
-Best result obtainable on that day
Use in preference to baseline for prognostication
-Does not predict response to treatment
bronchodilator response
take 2 puffs of meter-dosed inhaler and repeat spirogram 15 minutes later.
What defines a significant response?
FVC increases by > 12% and 200 ml
FEV1 increases by > 12% and 200 ml
bronchial inhalation challenge
used to diagnose asthma. looking for highest dose to cause 20% decrease in FEV1
Direct challenge
use methylcholine or histamine to directly stimulate muscle. normal is 8 mg/ml for mch
Indirect challenge
use chemical(AMP) or thermal
What are the determinants of lung volumes?
RV, FRC, and TLC
What are the two ways to determine TLC?
total lung capacity-balance between inspiratory muscles opposed by elastic recoil
functional residual capacity-determined by recoil of chest wall out and recoil of lungs in, no muscles involved
reserve volume-determined by expiratory muscles squeezing in, opposed by recoil of chest wall out and airway closure
What would the lung volume test reveal in obstruction?
RV increased
TLC may be increased
VC squeezed
What would the lung volume test reveal in restriction?
All volumes reduced
RV may be preserved if mixed picture
How do you measure compressible lung volume?
plethysmograph but it overestimates bc it cant distinguish belly gas
How do you measure communicating lung volume?
gas dilution methods such as helium dilution, nitrogen washout. Underestimates.
What is the DLCO method?
The patient breathes in a mixture of air (He, O2, small amount of CO), takes a deep breath in, holds it in for 10 seconds and then you measure what is breathed out
How do you interpret the DLCO method?
kCO and VA are the primary measurements in determining DLCO. DLCO is the product of kCO (CO uptake) and VA (alveolar volume) – DLCO = kCO * VA.
What can cause a low DLCO?
Low DLCO can be caused by low kCO due to poor CO uptake, low VA which results in reduced surface area for uptake, or both. So one needs to look at alveolar volume (VA) and DLCO/VA (kCO)
What are the three cardinal signs of COPD?
dyspnea, cough, wheeze
What causes the cough?
inflammation and mucus gland hyperplasia
What causes the dyspnea?
What causes the wheeze?
increased airway resistance and decrease elastic recoil
Define asthma
chronic inflammatory disorder of the airways characterized by increased responsiveness to various stimuli and is manifested by widespread narrowing of the airways that changes in severity either spontaneously or as a result of therapy.
What causes the inflammation in asthma?
dendritic cells release Il-4, 13 that trigger Th2 development leading to the release of IgE and??
What three things are involved in the pathogenesis of COPD?
Exaggerated inflammatory response
Oxidative stress
Protease/antiprotease balance
What player are involved in inflammatory response of COPD?
Neutrophils, macrophages, CD8 lymphocytes
-Eosinophils in exacerbations
IL4, IL8, TNFa
Changes persist even after smoking stops
How is oxidative stress involved in COPD?
-Cell dysfunction and death
-Damage to extracellular matrix
-Activation of NFkB, priming inflammatory cells
-DNA damage by histone acetylation
-Inactivation of antiproteases
What is involved in the protease balance of COPD?
On one side...
PMN: elastase, cathepsin G, proteinase 3
Macrophages: cathepsin B,L,S; MMP
Oxidative stress
On the other...
a1 antiproteinase
Secretory antiproteinase inhibitor
What is the end result of remodelling in asthma?
thickening of all layers of asthmatic airway
What are the typical histological changes in asthma?
Epithelial damage
Thickened lamina reticularis
Smooth muscle hypertrophy
Goblet cell hyperplasia
Loss of aveolar attachment
Loss of airway elastin
What are the small airway histological lesions in COPD?
Remodeling with collagen deposition
Peribronchial lymphoid aggregrates
Lumenal debris with infolding of epithelium
What in the net effect of pathology in asthma?
Net effect of disease is to decrease Vmax and decrease isovolumic flow; longer time contant which cuases hyperinflation
What is the consequence of hyperinflation?
increased work of brething and diaphragmatic disadvantage due to decrease curvature
Prolonged hypoxemia can cause what?
pulmonary hypertension and right heart failure (cor pulmonale)
What causes hypoxemia?
increased vent-perf mismatch(uneven ventilation due to incomplete filling and diffusion)
Shunt due to increased airway closure
Hypoventilation leading to respiratory failure
What are the therapeutic principles of obstruction?
Minimize/eliminate exposures
Optimize Vmax
-Increase Pel
-Decrease Rus
Relax bronchial smooth muscle
Reduce inflammation/edema
Minimize secretions
Improve dyspnea
Reduce hyperinflation
Reverse gas exchange disturbance
Normal functions of pleural space
-Facilitates movement of lung relative to chest wall
-Visceral pleura provides mechanical support to the lung
-Helps protect against the formation of alveolar edema
What makes up pleura?
Single layer of mesothelial cells
Connective tissue basement membrane
lymphatics/stoma(pareital only)
sensory nerves (pareital only)
What are the 5 anatomic layers of the pleura?
2.submesothelial connective tissue
3.superficial elastic layer
4. subpleural CT layer
5. deep fibroelastic layer
Pressures influencing pleural fluid formation
hydrostatic -5 sum
oncotic +5 sum
sum 6 from pareital into pleural space
Pleural fluid formation
-Arises from systemic pleural vessels on visceral and parietal pleural surfaces.
-Some fluid may be reabsorbed.
-Remainder flows across mesothelial layer into pleural space.
-Fluid leaves pleural space via parietal lymphatic stomata by bulk flow.
-Capacity to reabsorb fluid far greater than normal rate of fluid formation
Why doesnt pleural fluid collect in the pleural space?
Pleural fluid forms slowly and the reabsorption capacity of the PAREITAL pleura exceeds basal fluid formation rate by 30 fold.
Pleural effusion
abnormal collection of fluid in pleural space
What situations do plerual effusions arise?
-incresed capillary pressure
-decreased pleural hydro press
-increased capillary perm.
-increased interstitial onc. pres.
-decreased capillary onc. pres.
-decreased fluid resorption
-translocation of fluid from peritoneum
A 60 yo man with a 20 pack-year history of smoking, presents to the emergency room complaining of 3 day history of increased shortness of breath, cough productive of yellow sputum, pleuritic chest pain, and fever. He takes no medications and has otherwise felt well.

General - mildly dyspneic man with rapid respiratory rate.
Vital signs: Temp 38.2C, RR 20, HR 94, BP 135/78
Lungs - crackles are heard in the right lung; decreased breath sounds and dullness to percussion at the base of the right lung.
Vital signs: Temp 38.2C, RR 20, HR 94, BP 135/78
Lungs - crackles are heard in the right lung; decreased breath sounds and dullness to percussion at the base of the right lung.
What is your diagnosis?
Pneumonia complicated by right pleural effusion
Explain the patient’s symptoms
Fever and productive cough explained by pneumonia. Parapneumonic effusion contributes to dyspnea and chest pain.
What proportion of pleural fluid volume contributes to lung compression? increases chest wall?
1/3 compresses lung
2/3 expands hemithorax
How does pleural effusion affect lung function?
Lung volumes reduced by only a fraction of pleural fluid volume
Minimal effect on gas exchange (due to balanced reductions in ventilation and perfusion)
Reduced compliance which may icrease the work of breathing
What determines the symptoms of the pleural effusion?
underlying cause of effusion
size of effusion
underlying lung function
What are the common symtoms of pleural effusion?
Dyspnea or shortness of breath
Pleuritic chest pain
What causes the dyspnea?
inefficiency of respiratory muscles
What causes the cough?
distortion of lung by fluid
What causes the pleuritic chest pain (pain that worsens with respiratory effort)?
arises from irritation and involvement of parietal pleural nerve fibers
What accounts for the physical findings of crackles and depressed breath sounds and dullness?
Pneumonia produces the crackles in the right lung while the right effusion causes decreased breath sounds and dullness at the base of the right lung.
Where would you hear crackles or "rales"?
in the segment of the lung with pneumonia
How do you confirm the dx of pleural effusion?
chest x-ray- you see a settling of fluid to the lowest part of chest, blunting of costophrenic angle, and meniscus
How much fluid would you need in order to see a blunted costophrenic angle?
200 cc
What causes the meniscus sign?
As more pleural fluid accumulates, the level of fluid rises in the upright chest and “obliterates” adjacent structures. Fluid rises higher along the edge of a pleural effusion producing an upside down “U” or meniscus sign
Pleural fluid analysis
used for differential
obtained by thoracocentesis
basic assays use protein and LDH
Others commonly employed: glucose, cell count and differential, gram stain and culture, cytology, pH, etc.
Why is it important to measure LDH?
LDH typically found in capillaries--shows capillary perm.
Transudative pleural effusions
Occur when SYSTEMIC factors that regulate pleural fluid formation are altered
What systemic factors are involved in transudative pleural effusions?
increased hydrostatic pressure
decreased serum oncotic pressure
What would you find from the basic assay in TPE?
normal LDH
low protein content
Exudative pleural effusions
Occur when LOCAL disease in lung or a surrounding structure stimulates pleural fluid formation
What local factors are involved in exudative pleural effusions?
increased capillary perm.(eg pneumonia)
obstruction of lymphatic drainage (malignancy)
What is the protein content in exudative pleural effusions?
How would you diagnostically seperate exudative from transudative?
Exudative meets one of the following:
1.pleural fluid : serum protein ratio > 0.5
2.pleural fluid : serum LDH ratio > 0.6
3.pleural fluid LDH value > 2/3 upper limit normal for serum
What are the common causes of transudative pleural effusions?
-CHF- inc. hydro press
-cirrhosis w/ acities-translocation
-nephrosis-dec onc pres
-PE-inc. CVP
-atelectasis-dec intrapleural pressure
What are the common causes of exudative pleural effusions?
Pneumonia-inc. capillary leak
Malignant pleural Dz-lymphatic obstruction
PE-inc capillary leak
Tuberculosis-inc. capillary leak
What is the Tx for pleural effusions?
treat underlying disease and chest tube if needed
when is a chest tube required?
What is empyema?
defined as pus in pleural space
How is empyema detected?
-gross pus removed during thoracentesis, or
-gram stain of fluid demonstrates organisms
-pleural fluid cultures positive
What is parapneumonic effusion?
exudative pleural effusion associated with infection in lung
most resolve with appropriate antibiotic therapy
chest tube might be required if it is complicated.
What are the stages of parapneumonic effusion evolution?
Exudative stage
rapid outpouring of sterile fluid into pleural space due to pleural inflammation
appropriate antibiotics at this stage often result in resolution
Fibropurulent stage
bacteria invade pleural space
fibrin deposition on pleural surface
pockets / loculations begin to form
Organization stage
fibroblasts invade pleural space
pleural peel formation – inelastic membrane surrounding lung surface
can render underlying lung ineffective for gas exchange due to poor compliance
Malignant effusions
Malignant involvement of pleural space can cause large effusions and debilitating symptoms
What are the most common causes of malignant effusions?
malignant mesothelioma
metastases from other sites like lung, breast or lymphoma
what do you do if malignant effusions return after thoracocentesis?
What are the two ways to accomplish pleurodesis?
Chemical - place chest tube, drain fluid, and instill sclerosing agent (talc); obliterates pleural space by fusing visceral and parietal pleura
Surgical – pleural surfaces surgically abraded leading to obliteration of pleural space
A 28 yo male, previously healthy, medical student presents with complaints of shortness of breath and R-sided chest pain. His sx began suddenly 7-days ago while weight lifting at the gym. He continued to attend classes, but sought medical attention because of the persistence of the symptoms. He admitted smoking one-half pack cigarettes per day for the past 10 years.
Heart rate – 120 / min, Resp rate – 22 / min
General – tall, thin, healthy appearing man in no acute distress
Chest – increased resonance to percussion, decreased breath sounds throughout right lung.
what is the diagnosis?
pneumothorax-air in the pleural space
What are the different types of pneumothorax?
Spontaneous – occurs without antecedent trauma or other obvious cause
Traumatic – results from trauma to chest
Tension pneumothorax – air in pleural space under pressure
What is a primary spontaneous pneumothorax?
Primary spontaneous – occurs in absence of lung disease
Results from rupture of subpleural emphysematous blebs most commonly in apices of lung
More common in tall, thin male smokers
What is a secondary spontaneous pneumothorax?
Secondary spontaneous – occurs as a complication of underlying lung disease (e.g. COPD)
What is an example of traumatic pneumothorax?
Iatrogenic – intended or inadvertent consequence of a diagnostic of therapeutic maneuver
What is a pleural bleb?
Blebs are defined as cystic spaces occurring within the substance of the pleura
What is the effect of pneumothorax on lung function?
-pneumothorax causes greater decrease in lung volume than increase in volume of hemithorax which leads to dec. vital capacity
-hypoxemia related to increased A-a gradient and lowered ventilation: perfusion ratios
What are the symtoms of pneumothorax?
Chest pain
What is dyspnea depend on in a pt with pneumothorax?
patient’s underlying lung function
size of pneumothorax
What would exam findings show in pneumothorax?
increased RR, HR, expansion of hemithorax, resonance to percussion

decresed or absent breath sounds
What would you see on a chest x-ray in pneumothorax?
thin white line and absence of lung markings beyond the line
Tension Pneumothorax
Air enter hemithorax either from tear in lung or hole in chest wall on inspiration; does not exit on expiration
What would you see on CXR for tension pneumothorax?
Lung is compressed against mediastinum
Shift of heart and trachea to opposite side
What are the symptoms of tension pneumo?
Dyspnea – more severe than in simple pneumothorax
What are the exam findings in a patient with tension pneumo?
increased-RR, HR, expansion of hemithorax, resonance

decreased BP(lack of venous return), breath sounds

shifted trachea and mediastinal contents
What are the therapeutic implications of tension pneumothorax?
medical emergency – requires immediate chest tube placement
What are the therapeutic implications of small pneumothorax in general?
Small pneumothorax in pt. without underlying lung disease can be managed with observation alone plus/minus supplemental oxygen therapy
What are the therapeutic implications of large pneumothorax in general?
chest tube drainage
How do you prevent recurrence?
Chemical or surgical pleurodesis
Governance of the respiratory system
Medullary control send nerual output to respiratory muscles which send mechanical output to affect gas flow and gas exchange which sends sensory input to sensors that feed back to the medulla.
What does the carotid body respond to?
paO2-triggers changes once it drops below 60
Mechanisms of respiratory drive
Innate medullary pacemaker
Hypoxia (sensed primarily in the carotid body)
Hypercarbia (sensed primarily in the medulla)
Mechanoreceptors (sensed in the lungs)
How much of a change in co2 is needed for a respose from the medulla?
Medulla responds linearly, starting with even slight increases in PCO2
Pulmonary mechanoreceptors
Irritant receptors in the lung-respond to lung volume, irritants to activate vagus which can react to stimulate increase RR or cough.
What information does the central respiratory center output integrate?
Central respiratory pacer cells
Central chemoreceptors
Peripheral chemoreceptors
Upper airway / lung receptors
Conscious / “volitional” pathways
Increased minute ventilation which will lead to lower pCO2

PaCO2 < 35
Rate of production/minute ventilation
What are some physiologic causes of hyperventilation?
What are some non physiologic causes of hyperventilation?
What are some pharmacologic causes of hyperventilation?
aspirin, progesterone (pregnancy), beta-adrenergic agonists
What are the symptoms of hyperventilation?
Sense of dyspnea
Neurologic signs-Visual changes, Syncope, Seizures
CV-chest pain, arrhythmia
Muscular weakness
Carpopedal spasm
What are the effects of hypocapnia on the CNS?
decrease flow, ICP
increase in O2 demand
neuronal excite./seizures
What are the effects of hypocapnia on the Lungs?
increased vascular perm
decrease Cstat
trend towards hypoventilation
What are the effects of hypocapnia on the Heart?
Hyperventilation syndromes-What are Dx clues?
clinical cause may be evident: sepsis, PE, stroke, liver failure, pregnancy
check ABGs for pH, A-a gradient2, HCO3-
Kussmaul breathing may suggest acidosis
Psychogenic hyperventilation
voluntary hyperventilation, normal AaDO2, normal PCO2 in sleep
dizziness, sweating, palpitations, paresthesias
What is the Tx for hyperventilation?
treat underlying diseases
brown paper bag
What is the clinical parameter for hypoventilation?
PaCO2 > 45
hypoventilation in the central controller
-Congenital central hypoventilation
hypoventilation in the neuromuscular
Myasthenia Gravis
Muscular Dystrophy
hypoventilation in the lung dz
What are the primary physiological events in hypoventilation?
increased PaCo2
decreased pH
What are the seoncdary consequences?
increase bicarb, Cl
cerebral vasodilation
arousal from sleep
Hb desat
pulmonary vasoconstriction
What are the clincal manifestations of hypoventilation?
sleep disturbance
pulmonary HBP
cor pulmonale
Diagnostic signs of central controller hypoventilation.
normal PFT and muscle function
low hypoxic drive and CO2 drive
Diagnostic signs of neuromuscular hypoventilation.
decreased IC, ERV
reduced muscle function
rapid shallow hypoxic and CO2 drive
Diagnostic signs of lung (eg COPD) hypoventilation.
PFT-obstruction +/- resist.
muscle function norm or impaired
Hypoxic drive may be impaired
CO2 drive is impaired in hypercarbia
Diagnostic clues in Central alveolar hypoventilation
Congenital defect – a/w Hirschsprung’s
“Ondine’s curse”
Post-sedation or anesthesia
Psychogenic Central alveolar hypoventilation
Dyspnea absent
incresed PCO2, HCO3
Hypoxemia secondary to hypercapnea
What is the Rx for Central alveolar hypoventilation
Respiratory stimulants
Diaphragmatic pacing
Nocturnal ventilation
What are Dx clues for Neuromuscular hypoventilation
psychogenic Neuromuscular hypoventilation
Dyspnea, orthopnea
decreasedMVV, MIP / MEP, ± restrictive PFTs
Normal drive
Hypoxia due to FRC, poor cough
Cor pulmonale as terminal event
What is the Rx for Neuromuscular hypoventilation?
Nocturnal ventilation
Treat underlying condition
Stimulants NOT helpful
Acute Pulmonary hypoventilation
respiratory acidosis (both obstructive and restrictive physiologies)
What are some examples of acute pulmonary hypoventilation?
Hydrothorax / hemothorax / pneumothorax
Chronic Pulmonary hypoventilation
associated with variable levels of carbon dioxide
What are Dx clues for Pulmonary hypoventilation
obstructive-COPD, bronchiectasis

restrictive-pulmonary fibrosis
psychogenic Pulmonary hypoventilation
PFTs will reveal physiology c/w the disease state
Respiratory drive is likely impaired (hypercarbic > hypoxic)
Hypoxia d/t underlying dz and hypercarbia → cor pulmonale
What is the Rx for Pulmonary hypoventilation
Treat underlying disease
Careful oxygen supplementation
Nocturnal ventilation
Two types of apnea
Patient can’t breathe–Obstructive apnea

Patient won’t breathe – Central apnea
Central sleep apnea
A cessation of airflow during sleep due to a cessation of respiratory effort
The result of decreased ventilatory motor output
Patients have transient instability of ventilatory control (the undamped spring hypothesis)
why do people have trouble sleeping at high altitudes?
low o2 content in the air leads to hyperventilation which in turn gives an even lower set point of pCO2 at 30. So when you sleep it takes longer for your pCO2 to reach 45, the setpoint to go to sleep.
when is central sleep apnea common?
at sleep onset, drive to breathe goes down bc your setpoint for p CO2 is raised to 45.
how does apnea beget apnea?
1.Sleep onset moves subject to sleep control curve with lesser slope and higher apnea threshold
2.pCO2 rises, pO2 falls to point of arousal. Move back to awake curve, overshoot hyperventilation.
3.pCO2 settles back down
4.Subject goes back to sleep and cycle repeats
what are the two types of central sleep apnea?
Transient instability of drive
Sleep state oscillation between wakefulness and early sleep – may be normal
Cheyne-Stokes respirations
-Commonly in heart failure
-daytime hyperventilation
Decreased ventilatory output
Usually chronic respiratory failure, neurologic disease or neuromuscular degeneration
Frequently have already developed cor pulmonale
dec. PO2 , inc. PCO2
Causes of ventilatory instability in central sleep apnea--hypercapneic
Bad brain
Bad muscles
Bad lungs
Causes of ventilatory instability in central sleep apnea--normocapneic
Increased feedback delay
Increased chemoreflex loop gain
Why does congestive heart failure cause central sleep apnea?
circulatory delay which means the pCO2 level measurement is delayed due to poor circulation. This results in cheyne stokes.
Chemoreflex Loop gain
ventilation response/ventilatory stimulus--exaggerated response leading to overshoot hypocarbia followed by overshoot hypercarbia
Treatment of Central Sleep Apnea
Maintenance of respiratory drive through medications and O2
Treat underlying disorder (CHF) by afterload reduction or CPAP
Inspired CO2
44% of adult males
28% of adult females
clinically most important in disruption of partner and as a marker of more sever pathology
Pathophysiology of Obstructive Events
-Abnormal pharyngeal collapsibility
-In normal individuals, sleep is associated with pharyngeal narrowing and an increase in respiratory system resistance.
What is the progression from snoring to apnea?
Pharyngeal collapse
based on interaction between xsectional area and muscle tone. The smally the pharynx, the more tone needed.
What are the sites of pharyngeal collapse?
What happens when you sleep that contributes to pharyngeal collapse?
Increased apneic threshold(higher drive to breath)
Decreased upper airway tone, protective reflexes, and load compensation(cant breathe harder)
inspiratory flow limitation
as you inspire harder, greater pressure promote collapse resulting in a plateauing in inspiratory airflow
Obstructive Apnea
A complete blockage of the airway despite efforts to breath
Explain paradoxing in OSA
once the airway obstructs thoracic and abdominal efforts become inverse bc there is no air coming in. this goes on until the airway opens.
What happens to the blood oxygen levels in OSA?
Anatomical contributions to OSA
overbite, short mandible
thick tongue
hypertrophied lymphatics
nasal packing
What are the underlying factors contributing to apnea?
Negative Oropharyngeal
-Small Pharyngeal Cavity
-High Pharyngeal Compliance
-Decreased Upper Airway
-Muscle Activity
-High Upstream Resistance
What are the underlying factors contributing to hypoxia, hypercarbia, and acidosis?
Baseline Arterial PO2
Degree of Diffuse Airways
Lung Volume
What are the underlying factors contributing to arousal from sleep?
Chemoreceptor Sensitivity
CNS Arousability
OSA Clinical Features
daytime sleepiness
restless sleep
snoring w alt. slience
dec intelligence
sex dysfunction
What causes the morning headaches in OSA?
nocturnal CO2 retention
What is another name for Pickwickian syndrome and what are the symptoms?
Obesity hypoventilation
morbid obesity
alveolar hypoventilation
hypoxemia, cyanosis
cor pulmonale
What two things put you at high risk for pickwickians?
sleep apnea
Nasal CPAP
Acts as stent in hypopharynx
Stiffens hypopharynx by stimulating nerves
Increases FRC, prevents airway closure
Decreases work of breathing (titrates away the effects of autoPEEP)
Decreases pleural pressure swings, reduces GERD
Decreases venous return, reduces preload
What are some options for treating OSA?
jaw positioning devices
interstitial lung diseases
comprise a diverse group of lung infiltrations that cause disruption of alveolar structures and have in common clinical, radiographic, and physiologic consequences
Name the ILDs.
Granulomatous diseases
Collagen-vascular diseases
Inhalation causes
Specific syndromes
Idiopathic Pulmonary Fibrosis
Inherited causes
What is affected in ILD?
What is the consequence of affected interstitium?
what is the interstitium?
refers to the area that separates the alveolar pace from the vessels
What causes the poor oxygenation?
Access to air
Surface area
Alveolar capillary membrane
Gas diffusion
What is the manifestation of reduced lung compliance?
increased work of breathing
What causes ILD?
injury leads to inflammation which causes tissue remodelling.
If you can't control this, you get fibrosis.
Syndrome of ILD
Progressive dyspnea at rest or exertion
Bilateral interstitial changes on chest radiograph
Physiological abnormalities
Histology with inflammatory/fibrotic changes
What is the one thing you get when you suspect ILD?
high resolution CT
Idiopathic Pulmonary Fibrosis-prognosis and treatment?
PROGNOSIS-50% survival 3-5 years
TX: Lung Transplant Evaluation
Oxygen supplementation
Pulmonary Rehabilitation
You see a chest xray with: -bilateral infiltrates
-basilar distribution
-small lung volumes
-engorged vascular
-enlarged heart
What is your differential?
What is a classic CT for idiopathic pulmonary fibrosis?
-bilateral infiltrates
-peripheral distribution (pleural based)
-areas of fibrosis (honey combing)
-retraction bronchiectasis
What would the PFT show for idiopathic pulmonary fibrosis?
shrink flow volume loop and shift it right
What would the ABG show for idiopathic pulmonary fibrosis?
pH 7.46
pCO2 41
PO2 65
O2 Sat 90%

Ex O2 sat 83%
what is the histological pattern of IPF?
usual interstitial pneumonitis
Epidemiology of IPF
Males > Females
Higher incidence if > 75 years of age
100,000 patients
Chest xray shows:
-bilateral infiltrates
-upper lobe predominance
-preserved lung volumes
whats the differential?
Epidemiology of Sarcoidosis
Males = Females

Higher incidence if African-Americans
About 45,000 Americans with sarcoid
Approach and Treatment
of Sarcoidosis
-Remove from environment
-Treat: Oxygen Exercise/Rehabilitation
Lung Transplantation