Glossary of Pathophys joint 1
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- Why use pulmonary function tests?
- -Categorize physiology
-Follow progression of disease
-Assess response to treatment
-Measure effects of exposures
-Help identify surgical risks
- 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 isovolumic flow
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
Late volume changes
- Restriction on a spirogram
- Rapid upstroke
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?
- VC+RV or IC+ERV+RV
- 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
- 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?
- distortion of lung by fluid
- What causes the dyspnea?
- inefficiency of respiratory muscles
- 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
- 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
On the other...
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
Relax bronchial smooth muscle
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
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 otherwis
- 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 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
-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 becau
- 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?
- 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
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
- What are the effects of hypocapnia on the CNS?
- decrease flow, ICP
increase in O2 demand
- What are the effects of hypocapnia on the Lungs?
increased vascular perm
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
- hypoventilation in the lung dz
- What are the primary physiological events in hypoventilation?
- increased PaCo2
- What are the seoncdary consequences?
- increase bicarb, Cl
arousal from sleep
- What are the clincal manifestations of hypoventilation?
- 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
Post-sedation or anesthesia
- Psychogenic Central alveolar hypoventilation
- Dyspnea absent
Normal MVV, MIP, MEP, PFT
incresed PCO2, HCO3
Hypoxemia secondary to hypercapnea
- What is the Rx for Central alveolar hypoventilation
- Respiratory stimulants
- What are Dx clues for Neuromuscular hypoventilation
- psychogenic Neuromuscular hypoventilation
- Dyspnea, orthopnea
decreasedMVV, MIP / MEP, ± restrictive PFTs
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
- 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
- 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
-Commonly in heart failure
- 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
- 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
- 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
- What are the underlying factors contributing to apnea?
- Negative Oropharyngeal
-Small Pharyngeal Cavity
-High Pharyngeal Compliance
-Decreased Upper Airway
-High Upstream Resistance
- What are the underlying factors contributing to hypoxia, hypercarbia, and acidosis?
- Baseline Arterial PO2
Degree of Diffuse Airways
- What are the underlying factors contributing to arousal from sleep?
- Chemoreceptor Sensitivity
- OSA Clinical Features
- daytime sleepiness
snoring w alt. slience
- What causes the morning headaches in OSA?
- nocturnal CO2 retention
- What is another name for Pickwickian syndrome and what are the symptoms?
- Obesity hypoventilation
- 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
Idiopathic Pulmonary Fibrosis
- What is affected in ILD?
- What is the consequence of affected interstitium?
- POOR OXYGENATION
REDUCED LUNG COMPLIANCE
- what is the interstitium?
- refers to the area that separates the alveolar pace from the vessels
- What causes the poor oxygenation?
- Access to air
Alveolar capillary membrane
- 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
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
- You see a chest xray with: -bilateral infiltrates
-small lung volumes
What is your differential?
- What is a classic CT for idiopathic pulmonary fibrosis?
- -bilateral infiltrates
-peripheral distribution (pleural based)
-areas of fibrosis (honey combing)
- 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
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
- Chest xray shows:
-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
-Remove from environment
-Treat: Oxygen Exercise/Rehabilitation
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