Lect. 9 and 10 Chronic Obstructive Pulmonary diseases Dr. Kilgore
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COPD
o Airway disease
o Emphysema
commonality is a decrease in airflow
o Airflow limitation
o Asthma
Emphysema
o Enlarged air sacs with weakened and collapsed air sacs with excess mucus
COPD
o Characterized in general by abnormal airway inflammation and abnormal lung structure
 Cigarette smoke either primary or secondary
 Use of fossil fuels for cooking or heating in a closed space/ air pollution
 Airway hyper responsive to environment
 Low socioeconomic class
 Childhood illnesses, measles, repeated infections dietary deficiencies (vit. C/E)
o Cigarette smoke activates inflammatory cells
 Decreases anti-proteases
 Increased mucus secretion
 Plasma leak
 Bronchoconstriction
 Activation of nuclear factor-Kb
 Tumor necrosis factor alpha and IL- beta which recruits neutrophils
Features of obstructive diseases
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Emphysema (primarily a destructive anatomical process)
o Expect permanent enlargement of the air sacs distal to terminal bronchioles
o If respiratory bronchiole is primarily affected think centrilobular (centriacinar) *smokers
o If entire air space its panacinar (panlobular) *alpha-1 anti-trypsin deficiency
o The “purely” emphysema patient
 Thin, mm wasting, pursed lip breathing, use accessory mm of ventilation (like
scalene)
 Flat often immobile diaphragm, distant breath sounds, hyper resonance to
percussion on PE
 Small heart and low BP
 Hallmarks hypoxemia and low stats at first
Chronic Bronchitis
o Persistent cough resulting in sputum production for more than 3 months in each of the
past 2 years
o Hyperplasia of the mucus glands in the bronchi and bronchioles
o Clinical hallmark is cough with marked sputum production
o Pure chronic bronchitis is a “blue bloater”
 Obese, peripheral edema, may have venous distention of the neck veins, cor
pulmonae
 Elevated hemoglobin and hemacrit- causes hyper-coaguable state
 May see some clubbing of the fingers
Physical findings of COPD
o Shortness of breath, +/- cough, increased respiratory rate, accessory mm use, emaciated
or bese, decrease exercise tolerance, peripheral edema
Bronchiectasis
o Abnormal and permanent dilation of bronchi, usually caused by infection
Cystic fibrosis
o Autosomal recessive disease with mutations effecting the CFTR protein
o Seen at birth with meconium, ileus, recurrent respiratiory infections and failure to thrive
o Not all bronchiectasis is CF but patients with CF will have some degree of bronchiectasis
o CFTR abnormality
 Accelerated Na+ absorption in CF reflects the absence of the CFTR inhibitory
effect on the Na+ channels in the airway epithelia
 Abnormal “dehydration” of airway secretions inhibits mucous clearance
and causes increase infections
Goals of therapy for obstructive airways disease
o Induce bronchodilation
o Decrease airway inflammation
beta agonists primarily used
o Improve mucociliary clearance
Therapeutic interventions
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Stop smoking, avoid airway irritants, bronchodialator, anticholinergic steroids, oral IV,
vaccinations with pneumococcal and influenza vaccinies, oxygen both in acute and
chronic, antibiotics for acute exacerbations
o Inhaled bronchodilators
 Relaxation airway smooth mm
 Decrease mast cell mediator release
 Increase mucociiary clearance
 Increase mucus secretion
Acute evaluation
o Remember ABC’s, IV, O2 and monitor
o Keep saturation above 90%
o Head to toe PE
o Chest x-ray, EKG, other blood tests
o Bedside spirometry
o Consultation, admission or send home
Chronic management of COPD
o Chronic bronchodilators and anticholinergics
o Mucolytic agents
o Chest physical therapy and OMT
o Home O2 at night or continuous
o Avoid pollutants and cigaretts
o Inhaled corticosteroids and oral steroids
o Lung resection, bullectomy
o Diet and exercise
o Chronic pulmonary rehabilitation
Obstructive pattern
o TLC, RV, FRC all increased
o FVC, FEV1, and FEV1/FVC ration is decreased
Restrictive pattern
o TLC,RV, FRC all decreased
o FCV, FEV1 are decreased but the ratio is increased to normal
Lung function
o Smokers show a decrease in the FEV1 of 45-60 ml/yr
o Those who smoke and develop COPD show loses of FEV1 70-120 ml/yr
o Ingeneral lung capacity will diminish somewhat as you get older
Non re-breather mask
o Should give pt Fio2 of 90-100% but it actually gives 55-80%
Lect. 8 Upper respiratory Diseases Dr. Sahhar
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Noisy breathing
o Occurs as a result of turbulent airflow arising anywhere from the nose to the bronchiole
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Stridor
 Is an externally audible harsh, vibratory sound of variable pitch produced by
airflow limitation in the larynx and extra thoracic portion of the trachea
o Wheeze
 An audible sound that is usually high pitch, continuous, and musical or whistling
in nature produced by airflow limitation in the intra thoracic portion of trachea
and bronchioles
Evaluation
o Location of stridor
 Supraglottic region- inspiratory stridor
 Glottis and subglottic- biphasic (inspiratory and expiratory)
 Intrathoracic trachea- expiratory stridor (wheeze)
 Bronchi/bronchioles- expiratory fine wheeze
o Frequency and duration
 Acute: symptoms < 3 weeks Chronic: symptoms > 4 weeks that never fully
resolve w/o treatment
 Recurrent: symptoms come back again after initial resolution, but the
intervening period bwt exacerbations should be free of symptoms
o Age of onset
 Congenital lesions- After birth w/n 3-4 months
 Acquired (typically)- later in life acquired (typically)
o Response to previous therapies
 Asthma- bronchodilators
 Laryngitis- racemic epinephrine
o Relation to position and activity
 Exercise/exertion- sym. Worse with asthma, laryngomalacia, fixed airway
obstruction
 Prone position- sym. Improve with laryngomalacia
 Sleep- sym wose with airway hypotonia, adenotonsillar hypertrophy
o Past medical and surgical hsty
 Endotracheal intubation- SG stenosis
o Severity
 Dyspnea and sleep apnea
 Feeding problems
 Poor weiht gain
 Asymptomatic (happy wheezer)
o Physical examination
 Determine the severity of respiratory distress “respiratory distress score”
Investigation
o AP and lat x-ray of soft tissues of neck
o Chest x-ray
o Esophagogram (barium swallow)
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Airway fluouroscopy
Ph probe
Pulmonary function test “TV flow loop”
Flexible fiberoptic bronchoscopy
Flexible fiberoptic laryngoscopy (nasopharyngoscopy) and bronchoscopy
 Gold standard and mainstay of diagnosis
Group “larynotracheobronchitis”
o Caused by viral infection (para-infl 1 and 3, RSV, influenza)
o Laryngeal and subglottic edema lead to SG narrowing
o Main symptoms of croup are
 Stridor
 Respiratory distress
 Barking cough
o Differentiate from epiglottis by presence of viral prodrome (runny- congested nose and
sneezing)
o Responds to adrenergic agonist (racemic epi) and steroids (dexmethazone)
o With croup you see the classic steeple sign on x-ray
Epiglottitis
o Medical emergency (sudden aw obstruction)
o H. influenza type-b (pre vaccines and unvaccinated) GAS or Staph A.
o Presentation: high fever, toxic, ill looking, sore throat, dyspnea, stridor (late sign),
difficulty swallowing, drooling, hyperextended neck
o Tripod position- sitting upright and leaning forward with chin up mouth open while
bracing on the arms
o Investigation- lateral x-ray “thumb sign” classic for epiglottitis
o Dx: cherry- red swollen epiglottis
o RX: et intubation (in OR by anesthesia) and antibiotics
Laryngomalacia
o Most common cause of congenital stridor 60-75%
o High pitched and fluttering in nature
o Stridor typically develops with in the first few weeks of life and progresses in severity
over a period of a few months
o Usually resolves spontaneously with in 12-24 mon
o Severe cases of stridor may be associated with sternal retraction, respiratory distress
and feeding difficulties
o It is exacerbated by exertion, crying, feeding, agitation or supine positioning
o Placing the infant in the prone position or on a side position and extending the neck may
relieve the stridor
o Classification/types
 Type 1: redundant supraglottic mucosa prolapse
 Type 2: shortened aryepiglottic folds
 Type 3: posterior displacement of the epiglottis
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Dx with flexible laryngoscopy (gold standard) and visualizing supraglottic structures
getting sucked into the glottis during inspiration
o Treatment
 Wait and watch
 Treat GERD
 Tracheostomy
 Surgery
o Omega- shaped epiglottis
Laryngeal web
o Congenital form
 Failure of recanalization of larynx
 Primarily glottis
 Thin or thick
 Congenital hoarseness
 Respirator distress at birth
o Acquired form
 Trauma to larynx
o Both show really narrow glottis
Vocal cord paralysis (A.K.A vocal fold immobility (VFI))
o 10-20% of all congenital laryngeal anomalies (second to laryngomalacia)
o Causes
 Birth trauma (stretching of the recurrent laryngeal nerve) associated with
difficult deliveries
 Central nervous system abnormalities
 Peripheral causes, such as cardiovascular and mediastinal problems, may
present as unilateral vocal cord paralysis (left side more common)
o Bilateral vocal cord paralysis typically presents with high pitched inspiratory stridor with
normal cry and possibly a mildly hoarse cry
 Presents immediately after birth and may be severe, req. emergent airway
intervention such as intubation and possible tracheotomy
o Unilateral vocal cord paralysis typically presents with a weak, breathy cry and feeding
difficulties
 This may manifest as aspiration, resulting from the inability of the vocal cords to
approximate to protect the airway
Vocal cord paresis
o Weakness of vocal cords
o Occure after traumatic or prolonged endotracheal intubation
o Direct injury or inflammation of vocal cords
o Limitation of vocal cord movement
Vocal cord dysfunction (A.K.A paradoxical vocal cod motion)
o Disordered movemtn of cocal cords
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Vocal cords involuntarily close during inspiration and sometimes expiration (more
problem with inspiration)
o Mistaken as asthma
o Respiratory distress with physical or emotional stress
o Dx with spirometry and laryngoscopy
o Treatment: calming technique and speech therapy
o Vocal cords are adducted instead of abducted
Congenital subglottic stenosis
o Narrowing of the laryngeal lumen in the cricoid region w no hsty of tintubation or
surgical traum
o Classification
 Membranous: more common and milder type
 Cartilaginous: less common and more severe
o Presentation
 Recurrent croup with viral infections
 Apnea, cyanosis, hoarseness of voice, failure to thrive,
 Misdiagnosed as asthma
o Diagnosis
 X-ray AP and lateral
 Bronchoscopy flexible or rigid
 Intubation with differeing size tubes and application of 20 cm of H2O pressure
to look for leaks
 Less than 3.5 mm diameter in newborn considered stenosis
o “myers and cotton” grading
 % of narrowed lumen
 Grade 1- 0-50%
 Grade 2- 51-70%
 Grade 3- 71-99%
 Grade 4- 100%
o Treatment
 Expectant observation (grade 1 and mild grade 2)
 Endoscopic dilation with or without CO2 laser
 Tracheostomy
 Open reconstruction
o See hour glass sign on x-ray
Lect. 6 and 7 restrictive lung diseases Dr. Kilgore
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Restrictive diseases
o There is an overall decrease in lung vol. due to
 Maj. Alteration of the lung parenchyma
 Diseases of the chest wall, pleura or neuromuscular apparatus
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Thus there may be diseases of the “rate controller” the “ventilator pump” or the “gas
exchanger”
o Physiologically restrictive lung diseases are defined by reduced total lung capacity,
vital capacity, and functional residual capacity, but with a preserved airflow
o Physiologically restrictive lung diseases are defined by reduced total lung capacity, vital
capacity and functional residual capacity but with preserved airflow the fev1/FVC will be
normal
o Increased elastic recoil reduces the ability to expand the lungs and increases ability to
empty air from lungs thus TLC and RV decrease
Categories of restrictive lung diseases
o Extrinsic (extra-parenchymal diseases)
 Causes the respiratory controller or the ventilator pump
 Any entity that may affect the CNS may ultimately effect the lungs (CNS
bleeds, CNS masses, encephalitis, meningitis, head trauma, strokes,
drugs)
 Processes can cause changes in the respiratory rate, depth of breathing
and can cause non cardiogenic pulmonary edema, hypoventilation,
aspiration, pneumonia, hypoxemia, resp failure and death
 Anything that affects the respiratory controller
o These patients may hypoventilation
o May aspirate and develop pneumonitis and edema
o May develop non cardiogenic pulmonary edema which leads to
an obstructive and or restrictive defect
o Bottom line protect the airway and ensure ventilation
 The ventilator pump
o Consists of airways, bones, mm, peripheral nerves, and the
pleura abnormalities or diseases of any or all of these entities
may lead to a restrictive abnormality of the respiratory system
 Extrinsic lung diseases
 Neuromuscular diseases
o ALS, polio, myasthenia gravis, spinal cord lesions, Gillian-barre,
bilateral diaphragm paralysis
 Non neuromuscular
o Obestity, chest wall trauma, dyphoscoliosis, pleural diseases,
pneumothorax
 By their very nature, severe kyphoscoliosis and massive obesity are
easily recognizable
 Pleural disorders are associated with decreased tactile feremitus,
dullness or hyperressonance upon percussion and decreased intensity
of breath sounds
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In cases of neuromuscular diseases, the PE findings may indicate
accessory mm usage, rapid shallow breathing, paradoxical breathing
and other features of systemic involvement
 External trauma may be evident and/or the patient may have minor
trauma but be massively obese that his/her respiratory function may be
compromised
 Final result= restrictive defect
o Intrinsic lung diseases
 Cause
 Inflammation and or scarring of lung tissue (interstitial lung dz)
 Fill the air spaces with exudate and debris (pneumonitis)
 THE GAS EXCHANGER, There is a multitude of diseases that effect this
area of the lung. You can expect changes in compliance, possible
hypoxemia at rest or with exercise, an abnormal diffusion capacity for
Carbon Monoxide, and at times a relentless progression of the disease
 Affect the airway
 Sarcoidosis
 Eosinophilic granuloma
 Bronchiolitis
 Lyphangioleiomyomatosis
 Hypersensitivity pneumonitis
 Affect the interstitium
 Asbestosis
 Idiopathic pulmonary fibrosis
 Sarcoidosis
 Connective tissue- related to ILD
 Affect the capillaries
 Good pastures syndrome
 Wegeners granulomatosis
 Microscopic polyangitis
Initial evaluation, stabilization and treatment
o Good history including occupational history, recent or past exposure to agents,
medications, underlying medical problems and thorough review of symptoms
o Duration of illness
 Acute disorders last days to weeks
 Subacute lasting weeks to months
 Chronic cases lasting months to years
o Smoking hsty, prior medication use, radiation exposure, occupational exposure, family
hsty, environmental exposure
How do I go about this
o Stable or unstable
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IV, o2, monitor, the basic ABC’s of any evaluation
Is it extrinsic or intrinsic restrictive disorder
What lab or radiographic test must I order
 CXR, CT MRI special lab test lung biopsy, bronchoscopy, or intubation,
ventilation Can I correct the problem with medication
o Extrinsic
 Treat the abnormality based on if it affects the respiratory controller or the
ventilator pump
 Prevent hypoxemia
 Appropriate monitoring of patient
 Frequent vital signs
 Appropriate labs including ECG
 X ray, CT, MRI
o Intrinsic disorder- the gas exchanger
 Besides the basic lab test and chest x ray do I need to proceed with more
extensive testing (bronchoscopy with biopsy or bronchoveolar lavage (BAL),
fluoroscopy, surgical lung biopsy, or PFT’s exercise testing?)
 Start with ABC’s IV, O2, monitor, acute or sub acute or chronic
 Labs ECG, CXR, CT, MRI
 Treatment, steroids, anti-inflammatory or chemo
Diffuse interstitial pulmonary fibrosis
o Pathology
 Thickening of interstitium
 Initially, infiltration with lymphocytes and plasma cells
 Later fibroblasts lay down thick collagen bundles
 Eventually alveolar architecture is destroyed- honey comb lungs
o Etiology is unk maybe immunological rxt
o Clinical features
 Uncommon disease, affects adults in late middle age
 Progressive exertional dyspnea, later at rest
 Non productive cough, dry in nature
 Velcro crackles through both lungs (inspiratory)
 Disease progresses insidiously, median survival 4-6 yrs
 Wheezing is an uncommon manifestation but can occur in patients with
lymphangitic carcinomatosis, chronic eosinophilic pneumonia, and respiratory
bronchiolitis
 Chest pain is rare
o Treatment
 Ea. Patient is individually assessed
 Pt are treated if they have symptoms or progressive dysfunction on pulmonary
function tests
 Corticosteroids (prednisone 1mg/kg is standard therapy)
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 Addition of Imuran may benefit survival and cyclophosphamide occasionally
 Ancillary therapies such as O2, rehabilitation, psychosocial aspects are helpful
Pneumoconiosis
o Restrictive, occupational lung disease caused by the inhalation of mineral dust. It results
in a pulmonary function study that reveals a chronic restrictive lung pattern and x rays
reveal pulmonary fibrosis
o Silicosis
 Exposure to crystalline free silica, acute silicosis causes pulmonary alveolar
proteinosis, chronic simple nodular silicosis to progressive massive fibrosis
 Pft normal ovstructive or restrictive pattern
 CXR eggshell nodal calcifications
o Asbestosis shipyard workers, insulators, fibrosis of lung and pleural disease, asbestos
bodies of long and short fibers, Mesothelioma- lung CA pleural plaques
restrictive PFT’s
o Berylliosis
 Rare metal acute and chronic form which is more of agranulomatous disease
and hard to differentiate from sarcoidosis, rx- corticosteroids, avoid further
exposure
o Coal workers pneumoconiosis
 Exposure to coal dust and graphite coal macue, chronic
 Cough; CXR diffuse small round opacities
 Caplan syndrome- coal dust exposure and RA
o One finds multi large sometimes cavitary nodules in association
with RA
 CXR
o Range from anthracosis (carbon deposited in lung macrophages
and lymphatic’s) to progressive massive fibrosis
o Fibrosis primarily in the upper zones of the lungs
o Sarcoidosis
 A disease characterized by the presence of granulomatous tissue. This is a
systemic disease which involves eyes, brain, heart, lungs, bones, and kidneys,
skin, liver, spleen.
 90% of patietns have lung involvement
 Pathology
 Non caseating granuloma composed of histocytes giant cells and
lymphocytes
 In advanced you see fibrotic changes
 Etiology is unk likely immunological
 Stages
 0- no obvious intrathoracic involvement
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1- bilateral hilar lymphadenopathy, often accompanied by arthritis,
uveitis, erythema nodosum
 2- pulmonary parenchyma is also involved, changes in upper/mid zones
 3- pulmonary infiltrates and fibrosis w/o adenopathy
 4- end stage fibrosis
 Pulmonary function is susally reserved in stages 0 and 1
 However higher stages are associated with pulmonary fibrosis and restrictive
lung defect
 Treartment and prognosis
 85% improve spontaneously 15% develop progressive fibrosis and
respiratory failure
 Treatment is often observational but in symptomatic pt use prednisone
Hypersensitivity pneumonitis (A.K.A extrinsic allergic alveolitis)
o In response to inhaled organic dust
 Ex. Farmers lung
o Exposure may be occupational or environmental
o Type 3 (immune complex mediated) and type 4 (delayed hypersensitivity)
hypersensitivity rxt
o May see loosely formed granulomas
o All this may lead to fibrosis
o Look for precipitation anti-bodies to specific antigens
o Dx by trans bronchial biopsy or open lung biopsy
o Rx avoid exposure and use corticosteroids
o Acute
 Dyspnea, fever malaise, chills and cough 4-6 hours after exposure and continue
24-48 hours after
 PE fine crackles and wheezes throughout the lungs
 CXR initially normal or may show ground glass appearance, non specific
infiltrates to mid and upper lung
 CT- very sensitive ground glass opacities and centrolobular nodulars
 ABG’s hypoxemia
 PFT’s may have obstructive and restrictive defect
Lect. 5 pneumothorax Dr. Myles
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Anatomy
o Pleural membranes form closed space- contains film of few mm of serous fluid
o Sensory nerve endings supply parietal pleura
Physiology
o Normally pressure in pleural space is negative with respect to alveolar pressure
Pneumothorax
o Accumulation of air in the pleural space
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Cause- open connection bwt the pleural space and outside air
 Open ptx- thoracic wall injury
 Closed ptx- alveolar injury/ tearing
o Mechanics
 Inspiration
 Air enters the pleural space
 Air accumulates- leads to collapse of ipsilateral lung
 Breathing also impaired in opposite lung
 Mediastinum shifts towards healthy lung and compresses it
 TV of healthy lung thus decreased
o Main physiologic consequences
 Decreases vital capacity
 Decrease in arterial P02 hypoxia
 Areas of low v/q ratio
 Anatomic shunting (R to L)
 Alveolar hypoventilation
Clinical presentation
o Sand s based on size of ptx and presence of underlying lung and systemic disease
o Symptoms of ptx
 Sudden onset of ipsilateral chest or shoulder pain
 Dyspnea- variable and cough
o Signs of ptx
 Mild resting tachycardia
 Tachypnea
 Unilateral decrease breath sounds (caution often normal with small ptx)
Differential diagnosis
o Acute coronary syndrome, pulmonary embolus, esophageal rupture, aortic dissection,
pericardial tampanode, herpes zoster, metastatic cancer
Diagnosis and initial treatment
o Usually suggested by the clinical exam
o Most important initial step – determine the pt stability
o Most important initial test- CXR
 Upright recommended exception in tension ptx
o Other components- 12 lead EKG, ABG not usually helpful
o Initial treatment
 O2, immediate decompression of pleural space if tension pneumothorax or
unstable, iv, pain control
CXR findings
o Diagnostic findings- thin visceral pleural line lying parallel to the chest wall separated by
a radiolucent band containing no lung marking
o Sizing of the ptx
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 Most guidelines base on size in cm rather than %
 Symptoms more important than size in determining namagement
Inspiratory/expiratory films
 Historically expiratory CXR thought to help optimize visualization
 However no more sensitive so not reg. used or recommended
CT scan
o Much more sensitive than CXR and more accurate in sizing
o Not routinely ordered in evaluation
Primary spontaneous pneumothorax
o Spontaneous ptx in pts w/o known pulmonary disorder
o Classic patient
 Body habitus usally <40 y/o
 Occurs at rest not related to physical exertion
o Other factors
 Cigarette smoking
 Marfans
o Clinical manifestation
 Chest pain and dyspnea
 Acute onset, ipsilateral
 Often pleuritic
 Mild and rarely life threatening
o PE findings
 Vital signs often normal
 Most common finding tachycardia
 Ipsilateral chest finds
 Decreased movement with respiratory cycle
 Hyperresonance to percussion
 Decreased breath sounds and fremitus
o Diagnosis
 Suggested by clinical history and PE
 CXR is most important test
o Recurrence
 Ipsilateral up to 40% most within 6-12 months
 Contralateral – 15%
o Risk factors
 Tall pts, those who continue to smoke, after one recurrence risk of another
increases to > 50%
Secondary spontaneous pneumothorax
o Has an underlying lung disease
o Most common risk factor is COPD
o Peak age is 60-65 males more commonly
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Presents with dyspnea and more severe symptoms; extreme shortness of breath out of
proportion (bc of underlying disease)
o Much higher mortality rate than PSP
o Clinical manifestations
 Main symptom- dyspnea
 Often severe and out of proportion
 Chest pain
 Hypoxia and hypotension may be severe
 Symptoms much greater than PSP
 Vital signs abnormal
o Diagnosis
 CXR most important
Iatrogenic pneumothorax
o Most commonly associated prcedures
 Ransthoracic needle aspiration/ biopsy
 Subclavian or IJ cathereterization (1-6%)
 Mechanical ventilation
 CPR
Treatment of primary and secondary pneumothorax
o 2 maj. Goals
 Eliminate air from the pleural space
 Decrease likelihood of occurance
o Approaches
 Observation, supplemental o2, simple aspiration, tube thoracostomy (all these
treat they do not prevent recurrence
 Tube thoracostomy with pleurodesis, thoracoscopy with over-sewing of blebs
and pleurodesis, open thoracotomy
o Observation
 Air in pleural space is gradually reabsorbed approx. 1.25% per 24 hours
 Must be small PSP to be eligible to observe
 Pt must also be stable
 SSP not generally recommended
 Watch 3-6 hours and repeat CXR and return 24-48 for f/u CXR
o Oxygen
 Supplemental o2 accelerates rate of pleural air absorption (approx. 4 times
faster)
o Simple aspiration
 Initial tx of choice for most pts with PSP (not really for SSP has a lower success
rate)
 If aspiration is unsuccessful, tube thoracostomy req.
o Tube thoracostomy
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Chest tube- rapid re-expansion of underlying lung
Indications
 Any ptx which patient is unstable, PSP, SSP
 Tube size
 14-22 for PSP or SSP
 32-36 if associated with hemothorax or trauma
 Location
 4th to 5th ICS at nipple level
 Mid to anterior axillary line
o Pleurodesis
 Creation of a fibrous adhesion bwt the visceral and parietal layers of the pleura,
thus obliteration the pleural space
o Video assisted thoracoscopic surgery (VATS)
 Utilized to prevent occurrence
 Facilitates elimination of blebs and pleurodesis
 Blebs eliminated by stapling or suturing
 Preferred to thoracotomy- shorter hospitalization
Management of pneumothorax
o Primary
 Small (<2-3 cm) observe and o2
 Large – large catheter or CT
 Surgical recurrence prevention after second PSP
o Secondary
 Decompression
 Generally tx with chest tube
 Surgical recurrence prevention after 1st SSP
Traumatic pneumothorax
o Open: penetrating chest wounds
o Closed: blunt trauma, often associated with rib fx
o Small open wounds
 Act as a one way valve air enters during inspiration and can’t leave in expiration
 May rapidly lead to tension ptx
o Large open wounds
 >2/3 of the area of trachea, air enters pleural cavity through chest wall, not the
tracheobronchial tree
 Significant ventilation impairment
 Covers immediately with an occlusive dressing taped on 3 sides (not 4 bc that
would create a tension ptx)
Tension pneumothorax
o Alveolar- pleural defect acts as one way valve, air enters but can’t exit
 Impairs venous return to heart
o
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Clinical findings
 Respiratory distress
 Diminished breath sounds
 Hyperresonance to percussion
 Hypotension, tachycardia, hypoxia
o This is a clinical diagnosis: do not wait for radiologic confirmation to treat
o Management
 Emergency
 Immediate needle decompression
 Insert 14-16 gauge IV catheter over rib at 2nd ICS mid clavicular line
Catamenial pneumothorax
o Spontaneous ptx occurring at time of menstruation
o Women 3-40 yo
o Endometrial tissue migrates to the rt diaphragm
Deep sulcus sign
o A deep lateral costophrenic angle in a supine pt is suggestive of ptx on that side
o May be only indication of ptx on a supine pt
Lect. 4 pulmonary function tests Dr. Go
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Why do PFT’s
o Detect presence/absence of lung dysfunction
o Quantify the severity of known lung disease
o Asses the change in lung function over time or following administration of or change in
prescription
o Assess the potential effects or response to environmental or occupation al exposure
o Assess the risk for surgical procedures known to affect the lung function
o Assess impairment/disability
Contraindications (all relative weigh the advantages)
o Hemoptysis of unk origin (coughing up blood)
o Pneumothorax
o Unstable cardiovascular status
o Aneurysms- thoracic, cerebral and abdominal
o Recent eye, thorax and abdomen surgery
o Presence of an acute process
PFT’s testing requirements
o Effort dependent test
o Careful instruction
o Pt cooperation
o Physical, cognitive impairment and age may limit the subjects ability to perform – 4 yrs
and older is a reasonable test
Components of PFT
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Spirometry
 Forced vital capacity maneuver
 FVC, FEV1, FEV1/FVC ratio, FEF 25-75%, PEF
 Slow capacity maneuver
 MVV
Forced vs. slow capacity
o Fvc- forced vital capacity- vol of air expired during a rapid forced expiration starting at
full inspiration (TLC total lung vol) and ending at RV
o SVC- slow vital capacity- max vol of air that can be slowly exhaled after a mx inspiration
and ending in a residual vol
o In COPD usually FVC is smaller than the SVC bc of air trapping from premature airway
closure during forceful maneuver
FEV1, FEV1/FVC ratio
o FEV1 is the forced expiratory vol in 1 second. This is compared to a population normal
based on age, height and gender
o FEV1/FVC ration compares the patients FEV1 to their FVC
o These parameters are important in differentiating whether pt has a restrictive or
obstructive disease
FEF 25-75%
o Forced expiratory flow in the mid portion of the FVC maneuver
o Not effort dependent and very reproducible
o Measures the smaller airway function
Flow vol. loops
o Top art is expiration and bottom is inspiration
Spirometry interpretation
o FVC
 80-120% is normal
 70-79% is mild reduction
 69-50% is moderate
 Anything below 50 is severe
o FEV1
 75% normal
 60-75% mild obstruction
 50-59% moderate
 49% severe
 <25 years old add 5% > 60 subtract 5%
o FEF 25-75%
 79% normal
 60-79% is mild obstruction
 40-59% is moderate
 <40% is severe
o FEV1/fVC
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Interpretation of absolute value
 80 or higher is normal below 79 is abnormal
Obstructive disorders
o FVC, FEV1, FEF 25-75% is decreased
o TLC is increased
Restrictive
o FVC, FEV1, FEF 25-75% and TLC are decreased
o FEV1/FVC is increased to normal
Blood plethysmography
o The body box- gold standard
o Measures thoracic gas vol. and airway resistance
o Assesses restrictive vs. obstructive defects
o Determines TGV and indirectly reflects FRC, RV, and RV/TLC ratio
o Airway resistance
Helium or nitrogen washout
o Another technique of determining the FRC
o Not as accurate for pts with COPD
o Multi breath test which can last upwards of 6-10 min
o Determines FRC, RV, RV/TLC ratio
Diffusion capacity- DLCO
o Single breath maneuver
o Measure the co transfer from inspired gas to pulmonary capillary blood
o Good for
 Evaluation and follow up of
 Idiopathic pulmonary fibrosis
 Bronchiolitis obliterans
 Drug reaction s
 Dust related (asbestos)
 Sarcoidosis
 Pulmonary involvement in systemic (RA and lupus)
Incentive Spirometry
o Device used to prevent atelectasis
o Indications
 Predisposing conditions that lead to atelectasis surgery of abdomen or chest or
pt undergoing surgery with underlying resp. conditions
 Presence of mild atelectasis
 Presence of restrictive lung defect associated with quadriplegia and or
dysfunctional diaphragm
o Contraindications
 Pt cooperation absent or inability to understand
 Vital capacity is < 10 ml/kg or inspiratory capacity is < 1/3 of the predicted
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Proper incentive spirometry maneuver
o Pt sitting upright if possible
o Pt breathes slowly from end tidal expiration to full vol.
o Holds breath at least 5 sec
o Exhales passively
o 10-20 maneuvers per hour
o Doing this in rapid succession will cause hyperventilation
Peak flow meters
o Measures peak expiratory flow
o Important tool in the management and prevention of asthma attacks
o Maneuver fillings to capacity, blow out forcefully
o Should be done BID, min 3X each; results should be reproducible take the best efforts
results
Personal Best Peak Flow Readings and when to worry
o ZoneReadingDescription Green Zone71 to 100 percent of the usual or normal peak flow
readings are clear. A peak flow reading in the green zone indicates that the asthma is
under good control. Yellow Zone 50 to 70 percent of the usual or normal peak flow
readings indicates caution. It may mean respiratory airways are narrowing and
additional medication may be required. Red Zone less than 50 percent of the usual or
normal peak flow readings indicates a medical emergency. Severe airway narrowing
may be occurring and immediate action needs to be taken. This would usually involve
contacting a doctor or hospital.
Lect. 3 ABG Dr. Rawlins
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BMP is basic metabolic profile
Normal
o Ph is 7.35 to 7.45
o HCO3 is 22-26
o Pco2 is 35-45
PH is approx. HCO3/Pco2
Normal acid base metabolism 3 phases
o Intracellular production of acids and bases as by products of metabolism
 Left- intracellular aerobic metabolism of carbs, fats, and proteins yields co2
(volatile acid) than is eliminated in the lungs
 Right- intracellular anaerobic metabolism of carbs in aerobic metabolism of fats
and proteins yields b-hydroxybutyric acid (keto acid) lactic acid, sulfuric acid,
phosphoric acid (non volatile acids)
o Intravascular transport of acids (or bases
o Elimination of acids (or bases) by the kidneys and co2 by the lungs
Over view of the acid production and regulation of the partial pressure of co2 and hco3(bicarbonate)
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Respiratory component processes volatile acids (co2)
Metabolic side processes non volatile
Any change in one side will affect the other bc of co2/hco3- equilibrium
 Pco2 is maintained at 40 mmHg by increase or decrease of respiratory rate
 Hco3- is maintained at 24 mEq/L by increase the reclamation and generation of
Hco3The buffer system
o Transporting acid and migrating Ph change
 Pk values of non volatile acids (HA) produced by cellular metabolism are much
lower than 7.4 (ph of blood) they are forced to dissociate in the blood H+ ions
and anions
 If allowed to accumulate in the blood ph would fall
 Body provides buffereing anion (B-) to bind the H+ ions and transport
them to the blood
 The predominant buffer in extracellular fluid is Hco3- so H2O and Co2 are
produced
 The co2 produced is transported as HCO3- by the RBC to then lungs where it is
converted back into co2 and exhaled
 Thus when non volatile acid is produced hco3- is consumed and co2 is produced
The respiratory component (elimination of co2 via the lungs)
o Most co2 produced is converted to hco3- and h+ by carbonic anhydrase
o When it hist the lungs it is converted back into co2 (by carbonic anhydrase) to co2 which
then diffuses into the alveolus and is exhaled by alveolar ventilation
o Alveolar ventilation is measured by the amt. of air that enters and leaves the alveoli in 1
min
 Normal pco2 = 40 mmHg
 Hypoventilation (hyercapnia) = pco2> 45
 Hyperventilation (hypocapnia) = pco2< 35
o Lungs are fast kidneys are slow (takes them hours for HCO3- to adjust)
The metabolic component
o The strong non volatile (HA) produced by intracellular metabolism dissociated into Aand H+
o The anions is transported to the kidneys where it is filtered and secreted in the urine
o When H+ ion is buffered by Hco3-and co2 is produced and eliminated the HCO3consumed must be replaced
 Kidneys do this generating new HCO3- and reclaiming HCO3Main pts of Henderson hasselbach equation
o The ph is positively related to (HCO3-)
o The ph is inversely related to the pCO2
o The ration of HCO3- to the pCO2 defines what ph will be
Common lab tests in acid base evaluation
o Arterial blood gas (ABG) meausres the ph and co2 calculates the HCO3
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o Serum anion gap measures the cations (Na+) to the anions (HCO3- and Cl-)
Metabolic acidosis
o Results from any disorder that decreases HCO3o In all metabolic acidosis a non volatile acid is added to the body either directly through
addition or indirectly though inappropriate wasting of HCO3- by kidney or GI
o 2 types elevated gap and normal gap
 Difference lies in the identity of the anion (A-) accompanying the H+ ion
 Elevated gap the A- is an unmeasured anion and the end result is exchange of
HCO3- for A- which increases AG
 Calculate serum anion gap= Na+ - (HCO3- +Cl-)
o Unmeasured anions create gap
 Methanol, uremia, diabetic ketoacidosis, paraldehyde ingestion, iron, isoniazide,
inhalants, lactic acidosis, ethylene glycol, ETOH, salicylates
o Non gapped metabolic acidosis
 A normal gap acidosis the A- is Cl- which is measured
 The bod adds HCl to make the end result a normal anion gap acidosis bc the
HCO3- exchange for Cl- so as to not increase the gap
o Differential
 Diarrhea, ureteral diversion, RTA, hyperlimentation, ammonium chloride/
acetazolamide, miscellaneous
Metabolic alkalosis
o Results in any process that causes increase in serum HCO3o Acid is removed by loss or inappropriate addition of HCO3o Metabolic alkalosis in euvolemia and normal renal function is almost impossible
 The body can maintain HCO3- as long as ECF is not depleted
 ECF (extra cellular fluid) stimulates angiotesion aldosterone- net increase in Na+
and HCO3 = contraction alkalosis
Respiratory acidosis
o Results from any process that causes a primary increase in pCO2
Respiratory alkalosis
o Results from any process that causes a primary decrease in Pco2
Compensation patterns
o Response to the primary pathological process
 Only a process with primary change should be termed acidosis/ alkalosis
 Metabolic acidosis/alkalosis the primary change is HCO3 The brain will adjust ventilator patterns which change the pCO2 in the
same direction as HCO3o Respiratory acidosis/ alkalosis primary change occurs in Pco2
 The renal tubular cells of kidneys sense ph and change to adjust HC3- which will
change in the same direction of Pco2
Things to Know for Radiology for CM
Radiographic progression of CHF
Know this slide: where are the atria (left)
If the person were to have Right middle lobe pneumonia: hard borders or not???
ancer
-dimer
Tension pneumothorax: contents shifted
Should see 5-6 posterior ribs normally
Posteroanterior view
Secondary reactive Tb in the upper apices
Bands = Atelectasis
Most common cause of post-