Glossary of Pleural Pulmonary
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- What is pleural effusion?
- Pleural effusion is an abnormal accummulation of fluid in the pleural space.
- Is pleural effusion detectable on a plain chest film?
- Yes, pleural effusion is often detectable on a plain chest film.
- What reabsorbs the aqueous phase of pleural fluid?
- The visceral pleural capillaries.
- What reabsorbs the protein phase of pleural fluid?
- The parietal pleural lymphatics.
- What is the rate of formation of pleural fluid on the parietal pleural surface?
- 0.1 ml/kg/hr
- What are the 5 major types of pleural effusion?
- 1. exudate
- What are the 3 possible features of exudate (must have 1)?
- 1. > 1/2 the protein content of the patient's serum
2. > 6/10 the lactate dehydrogenase (LDH) content of the patient's serum
3. LDH content > 2/3 the upper limit of "normal" serum
- What are the two most common causes of exudate?
- Cancer and pneumonia.
- Is exudate a passive or active metabolic/cellular process?
- Exudate is an active process.
- Is transudate pleural effusion an active or passive process?
- It is a passive movement of fluid.
- What are the 3 physiologic phenomena that result in transudate?
- 1. increased vascular hydrostatic pressure
2. decreased plasma oncotic pressure (osmotic pressure/suction re protein)
3. increased negative intrapleural pressure
- Name 5 causes of transudate.
- 1. CHF congestive heart failure
2. nephrotic syndrome
3. constrictive pericarditis
4. acute atelectasis
5. pulmonary embolism
- What is the most common cause of transudate?
- CHF (syndrome) causes 90% cases. LVF causes ressure to increase in the pulmonary vessels --> increased hydrostatic pressure
- How does nephrotic syndrome cause transudate?
- It causes decreased plasma oncotic pressure
- How does constrictive percarditis cause transudate?
- noncompliant pericardium restricts ventricular filling and mimics CHF.
- How does acute atelectasis cause transudate?
- It causes increased negative intrapleural pressure. Some alveoli collapse, showing up as whitish area.
- How does pulmonary embolism cause transudate?
- It causes increased pulmonary vascular resistance which causes increased hydrostatic pressure.
- Where does fluid start to collect and when does it show?
- In the costal-phrenic angle. It starts to show up when 200 ml has collected
- Is empyema a form of exudate or transudate?
- Empyema is a form of exudate.
- Why is empyema fluid turbid or purulent?
- Because of infection in the pleural space.
- What is hemothorax?
- Hemothorax is gross blood in the pleural space.
- What is the main cause of a hemothorax?
- Hemothorax is usually due to chest trauma.
- What is chylothorax?
- It is the leakage of lymphatic fluid (cholesterol) into the pleural space.
- What are 2 common causes of chylothorax?
- 1. Tuberculous pleuritis
2. Rheumatoid ??
- What kind of effusion is indicated by pleuritic chest pain (pain w/breathing NOT due to fractured rib)?
- Effusion is usually exudative.
- What are the signs/symptoms of small effusions?
- Usually asymptomatic. No physical findings if < 200 ml.
- What are the signs/symptoms of large effusions?
- - dyspnea
- lung compression
- dullness to percussion
- displacement of trachea (if massive effusion)
- increased fremitus
- What is fremitus?
- Palpable vibration.
- What do you see on an x-ray of pleural effusion?
- - blunting of costophrenic sulcus (angle) due to fluid accumulation
- thickening of interlobal and/or interlobular lung fissures
- loculated fluid (white shadow w/broad base toward the chest wall and point toward the lung
- crescentic line or meniscus (white opacification; if not all the way to apex, upper edge is curved)
- What test to you use to confirm pleural effusion?
- What is thoracentesis?
- Aspiration of fluid w/syringe and needle.
Should be done below the level of the effusion and immediately above the rib.
- What is the treatment for transudative PE?
- Treat the underlying condition unless the PE is compressing the lung or causing tracheal/mediastinal shift -- then place chest tube for drainage.
- How many primary bronchi are there?
- What branches are bronchioles?
- 12th - 16th
- What branches are terminal bronchioles?
- 17th - 24th
- Where are the alveolar ducts, sacs, and alveoli found?
- At the ends of the terminal bronchioles
- How far down is the respiratory "dead space"?
- Down to the 16th branch
- What is respiratory dead space?
- Air in the passageways that is not being exchanged.
Approx. 150 ml of every breath.
- Where does the diffusion of oxygen take place?
- From the terminal bronchi to the alveoli
- What is the acinus?
- It is everything distal to the terminal bronchioles
- How are capillaries arranged in the lungs?
- They run in sheets between and among the alveoli
- What nerve innervates the diaphragm?
- The phrenic nerve, C4.
- What is the primary respiratory muscle?
- The diaphragm
- How do the external intercostal muscles aid in respiration?
- They cause elevation of the ribcage for inspiration
- What are the accessory inspiratory muscles?
- - scalenes: hook onto ribs 1 & 2; orig from transverse processes of the cervical region; innervated by cerv plexus (C1-4)
- SCM: pulls on sternum and middle 3rd of clavicle; orig on mastoid process
- When are the accessory inspiratory muscles used?
- During very labored breathing and to turn the head.
- What muscles are used for expiration?
- - diaphragm (relaxes)
- abdominal muscles: pull lower ribs down
- internal intercostals: pull down ribs and compress thorax
- What is a thoracostomy?
- It is an incision made for drainage (when patient has pneumothorax or fluid in pleural space)
Should be just above upper surface of rib so as not to cut nerve, veins just underneath
- What instrument is used to measure lung volumes?
- What is resting tidal volume?
- TV; amount of air inhaled/exhaled when breathing normally
approx. 500 ml
- What is Inspiratory Reserve Volume?
- IRV: amount of air that can be taken in in addition to normal breath
- What is Expiratory Reserve Volume?
- ERV: amount of air that can be expelled after inhaling all the way
- What is Residual Volume?
- RV: amount of air left in lungs after expelling as much air as possible
approx 1000ml ??
- What is Functional Residual Capacity?
- FRC: = ERV + RV
- What is Vital Capacity?
- VC: The maximal amount of air that can be moved
= IRV + TV + ERV
- What is Forced Vital Capacity?
- FVC: the maximum volume of air which can be forcibly expelled after inhaling as deeply as possible
- Is slow VC (vital capacity) greater or less than FVC (forced vital capacity)?
- Slow VC is often greater than FVC.
- What is an obstructive disease?
- Patients have difficulty getting air out due to loss of collagen & elastin from bronchioles, and their lungs collapse during exhalation. Passages also narrowed by excess mucus.
- Does excess mucus secretion (asthma, chronic bronchitis) cause difficulty breathing in or out?
- It causes difficulty breathing in.
- What are signs of OBSTRUCTIVE lung diseases?
- - small and terminal bronchioles collapse
- FVC often decreased (> 6 sec)
- Are emphysema, asthma, chronic bronchitis restrictive or obstructive diseases?
- They are obstructive.
- What is a RESTRICTIVE lung disease?
- Patient has difficulty getting air in due to DECREASED LUNG COMPLIANCE and INCREASED, FOOTBALL-LIKE elasticity
- lung becomes fibrosed
- VC is smaller
- Are chest x-rays usually taken as inspiratory or expiratory films?
To accurately assess heart size.
- Is pressure in intrapleural "space" positive or negative?
- Negative pressure.
Chest wall pulls outward; lungs pull inward (recoil)
- What two elements are responsible for LUNG RECOIL?
- 1. collective surface tension w/in all alveoli
2. elasticity of lung
- At FRC, Functional Residual Capacity, how much is the chest expanded (%)?
- What is surface tension?
- Collection of molecular forces that occurs wherever a gas/fluid interface exists.
- What is surfactant?
- - Fluid that decreases surface tension to keep lungs from collapsing
- What cells produce surfactant?
- Type 2 epithelial cells w/in the alveoli
- What is the Law of LaPlace?
- P = 2T / r
Pressure (in bubble/alveolus) = 2 x tension of fluid / radius of bubble
- Why is air pressure greater in smaller alveoli?
- Law of LaPlace - Surface tension of fluid in alveolus shrinks the alveolus and is greater in the smaller alv. Thus, air pressure P in smaller alv is greater.
Smaller the alveolus, greater the surface tension, greater the wall tension, harder to inflate when one inhales
W/o surfactant, small alveoli would inflate much less than large ones during normal inspiration
- What is the effect of surfactant on surface tension T of alveoli?
- Surfactant decreases T better, the smaller the alveolus. This tends to even out T in all alveoli so they inflate more equally.
- What is lung compliance?
- Change in volume vs. change in pressure
- What is the cause of PRIMARY pulmonary hypertension?
- The cause is unknown.
- Who is most likely candidate for the rare primary pulmonary HTN?
- Young to middle-aged women.
- What are syptoms of primary pulmonary hypertension?
- - progressive dyspnea
- narrowing of pulm arteries
- What are common causes of secondary pulmonary hypertension?
- - vasoconstriction (chronic hypoxia)
- loss of pulmonary vessels
- vascular obstruction
- increased pulmonary venous pressure
- increased blood viscosity - from polycythemia
- What are the symptoms/signs of pulmonary HTN?
- - dyspnea
- chest pain on exertion
- syncope on exertion
- What is syncope?
- Brief lapse in consciousness caused by transient cerebral hypoxia. Fainting.
- What are the heart sounds associated with pulmonary hypertension?
- Narrow splitting of S2 with a loud P2 -- instead of the normal A2-P2, inspiratory or physiologic splitting.
- What are the lab findings for pulmonary HTN?
- - hypoxemia (deficiency in [O2] in arterial blood.
- polycythemia in many cases
- right atrial enlargement
- right ventricular strain
- right ventricular hypertrophy
- What will a V/Q scan show for pulmonary HTN?
- May show unmatched defects if HTN is due to recurrent pulmonary emboli
- What will show up on PFT's for pulmonary HTN?
- Nothing unusual
- What is the treatment for pulmonary?
- - no effective treatment
- periodic phlebotomy if polycythemia and hematocrit > 60%
- prostacyclin (Epoprostenol) - a potent pulmonary vasodilator
- What is phlebotomy?
- Incision of vein for the letting of blood. Chief treatment for polycythemia vera.
- What is polycythemia?
- Increase in # of erythrocytes in the blood that may be primary or secondary to pulmonary disease, heart disease, or prolonged exposure to high altitudes. May be idiopathic.
- What are the characteristics of asthma?
- Inflammatory lung disease:
- airway inflammation w/o infection
- incrsd airway reactivity (bronchospasm, mucus) to variety of stimuli
- airway obstruction & acute dyspnea due to bronchospasm & mucus production
- What is dyspnea?
- Distressful sensation of uncomfortable breathing
- What is the treatment for exudative pleural effusion?
- Tube thoracostomy (chest tube), typically in 5th or 6th interspace at midaxillary line
- If exudative pleural effusion is purulent and left untreated, what can result?
- Progression to fibropurulent, organized stage. Formation of a peel which can encase part of the lung.
- What is a peel?
- Fibroblasts migrate into the pleural space from both the visceral and parietal pleura and organize the pleural loculations into a thick, inelastic membrane called a pleural peel.
- What are the signs/symptoms of an asthma attack?
- Airway narrowing and acute dyspnea due to:
- bronchial edema
- incrsd bronchial mucus
- What are the 2 major categories of asthma?
- 1. extrinsic (allergy/immune rxn)
2. instrinsic, aka cryptogenic asthma (non-immune/allergic)
- What are the 3 types of extrinsic asthma?
- 1. atopic (allergic)
3. allergic bronchopulmonary aspergillosis
- Which is the most common type of extrinsic asthma?
- Atopic. Often associated w/other atopic manifestations (rhinitis, exzema, urticaria). Incrsd serum IgE and glood eosinophil count
- What causes allergic bronchopulmonary aspergillosis?
- Allergic response to colonies of aspergillus fungus in airways; incrsd serum IgE.
- What is cryptogenic (asthma)?
- Cryptogenic = "hidden"; pertaining to a disease of unknown cause
- What are some stimuli that trigger intrinsic/cryptogenic asthma bronchospasms?
- - exercise
- cold exposure
- inhaled irritants
- pul infxn, esp. viral
- Why is it often difficult to distinguish betwn intrinsic and extrinsic asthma?
- Patients w/allergic (extrinsic) asthma are often susceptible to attacks due to intrinsic triggers
- What is the pathogenesis of asthma?
- exaggerated bronchoconstrictor response, i.e., incrsd airway reactivity
- How can exaggerated bronchoconstrictor response in asthma be demonstrated?
- By a patient's response to inhalation of histamine or methacholine (FEV1 goes down by 20%)
- What is the histologic substrate of asthmatic hyper-reactivity?
- Episodic or persistent bronchial inflammation
- In allergic asthma, how is persistent inflammation manifested in the bronchial tissue?
- By inflammatory cells:
- What type of hypersensitivity rxn causes the inflammation of allergic (extrins) asthma?
- Type 1 Hypersensitivity reaction: mast cell degranulation & activation --> release of 1° and 2° chemical mediators of inflammation
- What are suggested causes of intrinsic asthma bronchial inflammation?
- - viral URI's
- common air pollutants, e.g., SO2 and NO2
- What are common signs & symptoms of asthma?
- - mild coughing & wheezing
- nocturnal cough in kids (1st clue)
- later punctuated by asthma "attack"
- Describe basic asthma attack.
- - respiratory distress w/accessory muscle use
- tachypnea & tachycardia
- audible wheeze on expiration or insp & exp
- possible coarse rhonchi
- prolonged exp phase
- dry, tight sounding cough
- Describe severe asthma attack.
- - wheeze may disappear
- can speak only few words at time
- central cyanosis (blue lips, tongue, buccal mucosa
- possible confusion/lethargy --> respiratory failure w/CO2 narcosis
- Abnormal sound heard on auscultation of an airway obstructed by thick secretions, muscular spasm, neoplasm, or external pressure. Continuous rumbling.
- CO2 narcosis?
- Depression of CNS, including respiratory center, due to excessive CO2.
- How do you reliably assess asthma attack severity?
- - degree of dyspnea
- use of accessory muscles
- difficulty speaking
- Describe hyperventilation during asthma attack.
- From hypoxemia, due to dcrsd V/Q ratio caused by airway obstruction. Dcrsd pCO2 early in attack.
- Describe air-trapping in asthma attack.
- - incrsd residual volume --> hyperinflation of lungs, worse hypoxemia (dcrsd pO2)
- incrsd pCO2 --> resp acidosis
- FVC and FEV1 decrease progressively
- Describe chest x-ray of asthma attack.
- Show hyperinflation (like emphysema)
- How does the degree of eosinophilia relate to severity of asthma attack?
- Eosinophilia correlates to severity.
- How does the presence, absence, or prominence of wheezing correlate w/severity of asthma attack?
- Wheezing does not correlate well.
- What does eosinophilia in a patient indicate?
- - atopy (allergy), including allergic asthma
- infection by parasite(s)
- What is PEF?
- peak expiratory flow - maximum flow generated during expiration performed with maximal force and started after a full inspiration; it is not effort-dependent
- How is asthma treated?
- - inhaled steroids to block inflammation
- oral steroids to block inflam during exacerbations
- leukotriene antagonists
- mast cell stabilizers to block histamine component of inflam
- What are 3 bronchodilators used for asthma and when are they used?
- 1. inhaled beta2 adrenergic agonists - resuce from symptoms
2. inhaled anticholinergics - rescue
3. oral xanthines - maintenance (opens airways)
- What controls how much blood goes to the lungs?
- ANS autonomic nervous system, symp and parasymp, and hypoxia
- How do local pulmonary arterioles react to hypoxemia due to underventilated aveoli?
- They constrict. Opposite of skeletal muscle arteries that dilate when muscles lack O2.
- What is hypoxia?
- Inadequate O2 tension at the cellular level. Area of lung not well ventilated.
- What is hypoxemia?
- An abnormal deficiency in the [O2] in arterial blood.
- What is the most important control of pulmonary vascular resistance?
- What is the consequence of chronic hypoxia?
- Under ventilation -> continuous local arteriole constriction -> incrs in total pulm vascular resistance -> RV has to work harder to push blood thru lungs
- How does hypoxia affect V/Q Ventilation/Perfusion ratio?
- Hypoxia causes vasoconstriction in local area, maintaining good V/Q ratio
- What is atelectasis?
- Collapse of the alveoli in a lung segment
- What are the 4 main categories of atelectasis?
- 1. resorption
4. diffuse microatelectasis
- How does resorption atelectasis work?
- Obstruction in airway -> no ventilation -> air in alveoli get absorbed.
Typical obstructions: mucus, mucopurulent plug, FB, tumor, enlarged lymph nodes (TB)
- What happens in compression atelectasis?
- Something pushes lung tissue out of normal place:
pleural effusion, tumor, emphysematous bullae, cardiomegaly, elevated diaphragm in patients (bedridden or w/ascites)
- What causes contraction atelectasis?
- Local or generalized fibrosis in lung or pleura.
- What is another name for cicatrization atelectasis?
- Contraction atelectasis
- What is diffuse microatelectasis?
- Generalized loss of lung expansion due to inadequate surfactant
- What causes diffuse microatelectasis?
- - O2 toxicity - breathing high % O2 too long - wears out surfactant
- neonatal or adult resp distress syndrome
- infection, which may cause adult resp distress syndrome
- What is bronchiectasis?
- Form of obstruct. disease. Pathologic expansion of bronchi and/or bronchioles resulting from chronic necrotizing infections caused by various consitions which destroy bronchial smooth muscle and elastic tissue. Not 1° disease, but 2° to infx or other condition.
- What are signs/symptoms of bronchiectasis?
- - Cough
- expectoration of copious purulent, sometime fetid sputum
- flecks of blood in sputum, if not frank hemoptysis
- What are 4 conditions that dispose to bronchiectasis?
- 1. bronchial obstruction - tumor, FB, mucus impaction
2. cystic fibrosis
3. HIV or other immunodeficiency states (immunoglobin deficiencies
4. pneumonia, bacterial, incompletely unresolved
- How does bronchial obstruction lead to bronchiectasis?
- Obstruction -> infx -> bronchiectasis local to affected lung segment.
Also complication of asthma and chronic bronchitis, recurrent infx.
- What is CF, cystic fibrosis?
- Inherited disorder of exocrine glands, esp resp and GI tracts.
Causes viscid mucus -> recurrent infx -> severe bronchiectasis.
- What TRIAD of conditions does CF cause?
- 1. COPD (bronchiectasis)
2. exocrine pancreatic insufficiency
3. high sweat chloride content BOARD
- What are the 2 critical factors in pathogenesis of bronchiectasis?
- 1. obstruction -> dcrsd NL clearance mech -> 2° infx
2. chronic or recurrent infx -> obstr secretion -> worse infx/inflam
- What part of lungs does bronchiectasis most affect?
- Lower lobes, vertical airways
- How much to bronchiectasis affected airways expand?
- 4 x normal diameter
- What flora can be cultured from bronchiectasis?
- MIXED flora: staph, strep, pneumococci, H. flu, Pseudomonas
- Can bronchiectasis lead to lung abscesses?
- Yes, it often leads to lung abcesses eventually.
- What does CT scan show for bronchiectasis?
- Dilated airways
- What does CXR show for bronchiectasis?
- Incrsd bronchovascular markings from 1) peribronchial fibrosis and 2) intrabronchial secretions
- What do labs cause suspicion of CF?
- - CXR abnormalities mostly apical or upper lobe
- sweat chloride test
- What diseases/disorders cause finger clubbing?
- bronchiectasis, smoking, lung CA, acute bacterial endocarditis
- How does bronchiectasis lead to cor pulmonale?
- Severe, widespread bronchiectasis -> obstrctv ventilatory defects -> hypercapnia/hypoxemia -> pul HTN -> cor pulmonale
- What is treatment for bronchiectasis?
- - antibiotics ABX to control infx
- beta 2 agonists to max ventilation in non-bronchiectatic airways
- O2 therapy
- What is cor pulmonale?
- Enlargement of heart's right ventricle caused by primary lung disease
- What is COPD, chronic obstructive pulmonary disease?
- Denotes 2 conditions:
2. chronic bronchitis
- Why do emphysema and chronic bronchitis often co-exist?
- 80% of COPD due to
- tobacco smoke, irritant chemical -> chronic cough & mucus secretions, CHRONIC BRONCHITIS
- destruct of acinar walls, perm enlargement of acinar airspaces, EMPHYSEMA
- What is emphysema?
- perm enlargement of airspaces distal to term bronchioles (acinus) due to inflam-induced destruction of the walls of
- resp bronchioles
- alveolar ducts
- Is emphysema always symptomatic?
- No. 1/2 time Asymptomatic
- Is emphysema associated w/smoking.
- What structures comprise an acinus?
- - resp bronchioles
- alveolar ducts
- How many acini comprise a lobule?
- 3 or more acini = lobule
- What are the 3 histological types of emphysema?
- 1. centriacinar
3. distal acinar
- Describe centriacinar emphysema.
- - enlarged bronchioles
- distal alveoli spared
- more common at lung apex
- due to smoking
- Describe panacinar emphysema.
- - entire acinus enlarged
- more common at lung base
- due to genetic alpha-1 antitypsinase deficiency
- Describe distal acinar emphysema.
- - far periph acini, close to lung pleura, are enlarged
- What is thought to cause spontaneous pneumothorax in young, tall, thin adult smokers?
- Distal acinar emphysema
- What is the mechanism for emphysema-induced pneumothorax?
- Enlarged acini burst, release air, cause separation of visceral from parietal pleura - + gravity -> pneumothorax. In tall, thin person, little abdom fat pushing abdom viscera up agnst diaphragm/lungs -> more downward gravity traction on lung
- Are histological divs of emphysema clinically important?
- No. They all amount to deterioration of lung function as COPD.
- What are signs/symptoms of emphysema?
- - progressive dyspnea
- airway obstructn -> long exp phase; pursed lip breathing (Pink Puffer)
- airway obtructn -> chng in chest A/P ratio; dcrsd diaphragmatic excursion; dcrsd vesicular breath sounds; distant heart sounds
- loss of alveolar capillaries -> incrsd pul vasc resist -> right heart failure
- What is diaphragmatic excursion?
- How far the diaphragm moves
- What are weight changes associated w/emphysema and chronic bronchitis?
- emphysema - weight LOSS
chronic bronchitis - weight GAIN
- In emphysema, what enzyme activity leads to acinar wall destruction?
- excess lung protease and/or elastase activity, unopposed by anti-protease activity
- In emphysema, how does acinar wall destruction lead to hyperinflation of lungs? AIRSPACE ENLARGEMENT
- 1. acinar wall destruct ->
dcrsd surface area for gas exchg
loss of struct integrity of acinar walls ->
obstructive collapse on exhale ->
air trapping & CO2 retention ->
- In emphysema, how does acinar wall destruction lead to hyperinflation of lungs? LOSS of ALVEOLI
- loss of alveoli ->
incrsd lung compliance & dcrsd lung recoil ->
hyperinflation of lungs
- What disorder causes acinar wall destruction:
- airspace enlargement &loss of alveoli leading to lung hyperinflation
- loss of alveolar capillaries?
- What do labs indicate for emphysema?
- - dcrsd FEV1, nr NL slow FVC (FEV1/FVC ration < 75%)
- dcrsd FEF 25-75%
- incrsd arterial pCO2 (above 50 mmHg)
- What is clinical course of emphysema?
- - progressive dyspnea (1st exertion, later resting
- severe weight loss
- chronic hypoxemia -> constrct of pul arterioles -> pul HTN -> RV fail (Cor Pulmonale) NOT due to LV fail
- death from pul fail: hypoxemia, resp acidosis, coma
- What are 4 treatments for emphysema?
- 1. stop smoking
2. bronchodilators: anticholinergic and beta-2 agonist inhalers
3. inhaled steroids - more for concurrent episodic asthma, URI, etc.
4. O2 supplementation in severe COPD to achieve certain arterial pO2, but not too much, to MAINTAIN HYPOXIC DRIVE
- What is hypoxic drive?
- Stimulation of respiration by low PaO2, mediated thru carotid and aortic bodies
- What conditions define chronic bronchitis?
- - mucus-producing cough most days
- cough 3 mos/yr for 2 successive yrs w/o other underlying disease to explain cough -> "Blue Bloater"
- inflam - scarred lining of bronch tubes - excess mucus - thick bronchial tube lining - irritating cough - hampered air flow - scarred lungs - infx breeding place
- What are treatments for chronic bronchitis?
- - stop smoking
- avoid air pollution
- inhaled bronchodilator
- What are signs/symptoms of atelectasis?
- - dyspnea, cyanosis
- tracheal deviation
- uneven chest expansion
- dcrsd breath sounds
- dullness to percussion (vs. pneumothorax causes hyperresonance or tympany)
- What is prophylaxis for atelectasis?
- - surgery
- encourage ventilation by incentive spirometry, coughing, early ambulation
- What is pneumothorax?
- Separation of the visceral and arietal pleurae by a volume of air. Affected lung segment collapses under surface tension-induced recoil of its collective alveoli.
- What are the 4 major categories of pneumothorax?
- 1° spontaneous PTX: absence of underlying lung disease
2° spontaneous PTX: complication of lung disease (emphysema, asthma)
traumatic PTX: blunt or penetrating trauma, iatrogenic causes
tension PTX: air inhaled in thorax, can't exit; positive interpleural press > ambient press; due to trauma, CPR, mech ventilation
- What are the symptoms of essential of diagnosis?
- Acute onset of ipsilateral chest pain & dyspnea
- What are the objective finding of diagnosis?
- - in mild cases, minimal
unilateral chest expansion
trach & mediastinal shift toward opposite side
dcrsd breath sounds & fremitus
percussion hyperresonance or tympany
CXR shows visceral-pleural line or area w/marked absence of pul vasculature
- Describe 1° PTX.
- - often tall, thin boys, young men
- maybe due to rupture of subpleural apical blebs due to high neg pleural pressure
- smoking increases risk
- What is a bleb?
- An accumulation of fluid under the skin.
- Describe 2° PTX.
- - assoc w/other lung diseases, e.g., pneumonia, TB, CF, asthma, COPD
- catamenial PTX
- What is catamenial PTX?
- a 2° PTX associated w/onset of menses and with intrthoracic endometriosis
- What is pulmonary barotrauma and what does it cause?
- Important contemp cause of PTX in patient on mech ventilation.
Often seen in ARDS patients w/hi pos inspir press or PEEP
- What is PEEP?
- positive end-expiratory pressure
- What are general signs/symptoms of PTX
- - chest pain, min-to-severe, on affected side
- possibly mild tachycardia
- if large, dcrsd breath sounds and fremitus; asymmetric chest expansion
- hyperresonance or tympany
- What are more specific signs/symptoms of TENSION PTX?
- - severe dyspnea & marked tachycardia
- trach or mediastinal shift (?chest trauma open to ambient air
- widespread percussion hyperresonance or tympany
- What do labs show for PTX?
- - ABG show hypoxemia (low pO2) & acute resp alkalosis from hyperventilation
- see visceral pleural line on expiratory film
- pleural effusion, i.e., blunting of costophrenic angle
- shift of trach TOWARD NL PTX
- shift of trach away from TENSION PTX
- What is ddx, differential diagnosis, for PTX?
- Given acute onset of dyspnea and/or chest pain:
- What are possible complications of PTX?
- - subcutaneous emphysema
- pneumomediastinum on CXR: suspect rupture of esophagus or bronchus as cause of PTX
- What is pneumomediastinum?
- Gas or air in mediastinal tissues.
- What is the treatment for a small PTX?
- - observe, may self resolve
- O2 supplement may incr rate of air reabsorption
- thoracostomy (chest tube), small bore
- serial CXR's q24 hr to follow progress
- What is the treatment for a large PTX?
- - admit to hospital
- thoracostomy until lung expands on serial CXR's
- What is average recurrence rate of PTX? Recurrence rate for smokers?
- 30% for average
50% for smokers
- What is restrictive lung disease?
- Characterized by dcrsd lung compliance -> incrsd inspiratory effort and smaller static and dynamic lung volumes
- What are the 2 major categories of restrictive lung disease?
- 1. extrapulmonary causes
2. parenchymal diseases
- What are the extrapulmonary cause of rest lung disease?
- - conditions that cause chest wall deformities, e.g., MD, kyphoscoliosis
- obesity hypoventilation syndrome, pickwickian
- What is another name for parenchymal restrictive lung disease?
- Interstitial lung disease.
- What are the 5 subdivisions of parenchymal disease?
- 1. primary pulmonary disease - idiopathic pulmonary fibrosis
2. systemic disease
3. environmental & occupational
5. drug induced
- What are systemic diseases that may cause restrictive lung disease?
- - hyaline membrane disease (kids)
- ARDS adult resp distress syn
- sarcoidosis, amyloidosis
- autoimmune: rheumatoid, SLE, systemic sclerosis, dermato/polymyositis
- pulmonary edema & pulmonary venous hypertension
- What is a "blue bloater"?
- COPD patients suffering primarily from chronic bronchitis. Derived from bluish color of lips and skin
- What are environmental and occupational causes of parenchymal disease (RLD)?
- - pneumonconioses (non-neoplastic lung reactions to inhaled inorganic dusts, e.g., asbestos, silica
- organic dusts
- toxic gases
- ionizing radiation
- What are infectious causes of parenchymal disease (RLD)?
Pneumocystis carinii - most frequently seen in AIDS patients
- Parenchymal restrictive lung disease:
2. affects alveolar epith cells or alveolar cap endothelium
3. affects interstitium
4a. interstitial fibrosis -> more damage to alveoli, caps -> hypoxia -> pul HTN -> cor pulmonale = RVH & RVF due to lung disease which causes pul HTN - not pul HTN for LVF
4b. intersitial fluid -> stiff lung -> incrsd effort-dyspnea
- Parenchymal restrictive lung disease: Idiopathic pulmonary fibrosis
- Findings similar to RLD cause by other etiologies which must be ruled out first.
Unknown antigen -> injury to type 1 alveolar cells and activation of fibroblasts > fibrosis of alveolar septa and arteriolar intima
- What is the clinical course of idiopathic pulmonary fibrosis (parenchymal RLD)?
- - fibrosis & pul edema >
decrsd ventilation >
- dcrsd vent and pul arteriolar fibrosis >
pul arteriolar vasoconstriction >
pul HTN >
cor pulmonale & death
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