Pulmonary Review

From Iusmicm

Contents

[edit] Introduction

[edit] Approach to Shortness of Breath

[edit] Lung

  • Interstitial Lung Disease, What is it?
  • Lung Nodules/Cancer (#1 cause of cancer death)
    • What types are there?
    • How are they distinguished from one another?
  • Pneumonia
    • Types, risk factors, treatment
  • Atelectasis (collapse of the lung)
    • Shallow breathing,
    • Surfactant problems
    • Obstruction of airway (mucus, tumor)

[edit] Vascular

  • Pulmonary Hypertension
    • How do we diagnose it?
    • How do we define it?
    • What causes it?
  • Pulmonary Embolism
    • How do we diagnose it?
    • How do we treat it?

[edit] Airway

  • Airway obstruction “COPD”
    • Asthma
    • Emphysema
    • Chronic Bronchitis
  • How do we diagnose it?
  • How do we treat it?
  • How do we distinguish these from one another?

[edit] Mechanical

  • Neurologic ventilatory problems
    • How do we diagnose and treat them?
  • Pleural problems
    • What is the purpose of the pleura?
    • How do we define pleural effusions?

[edit] Miscellaneous

  • Peds (Dr. Howenstine)
    • Recognize common pediatric respiratory problems
  • Respiratory Failure (Dr. Carlos)
    • What are our options for the failing patient?
    • When and how do we intubate patients?
    • Exam prep
  • Case Conference
    • Putting it all together…real life cases.


[edit] History and Physical Exam

  • “One of the essential qualities of the clinician is interest in humanity, for the secret in the care of the patient is in caring for the patient.”


[edit] Know the key details of the pulmonary history and physical exam

  • History:
    • Shortness of breath: When, where, how long, triggers, relievers
    • Cough: Mucus?, blood?, timing?
    • Associated conditions:
      • Chest pain, dizziness, leg swelling, dysphagia
    • Social History:
      • Pets (birds, rodents, lizards, farm animals)
      • Occupation (silica, asbestosis, fumes, metals)
      • Travel
        • Tuberculosis (remember vets ~ Vietnam)
        • Long flights = immobility (DVT, PE)
      • Smoking
        • Calculate pack/years, quit? when?
        • Ex. smoked 2ppd x 15 years = 30 pk/year history
        • Remember 2nd hand exposures!
    • Family History:
      • Tuberculosis (exposure)
      • Lung Cancer (? Genetic)
      • Rheumatic diseases
      • COPD/Emphysema
      • Alpha-1-antitrypsin (< 50 yrs old)
  • Physical:
    • Inspection:
      • Nasal flaring, pursed lips, sentences, abd breathing
      • Accessory muscles (scalene, SCM contract)
      • Kyphoscoliosis, clubbing, edema
    • Palpation
      • Tactile fremitus (consolidation increases), effusion decreases
      • Trachea
    • Percussion (use your wrist!)
      • Side to side, hyper or hypo
    • Auscultation
      • Egophony (“eeee” --- “aaaa” = consolidation)
      • Listen here
      • Dullness + crackles + increased breath sounds + increased fremitus = consolidation
      • Dullness + decreased breath sounds + decreased fremitus = effusion
      • Dullness + absent breath sounds = atelectasis


[edit] Interpret basic acid-base disorders

  • ABG gives you: pH, pCO2, and pO2
  • Anion gap can be calculated = Na - Cl + CO2
    • Requires CO2 value from serum chemistries


  • pH interpretation of ABG:
    • acute: decrease of pH by 0.08 generally indicates an increase of PaCO2 of 10 (and vice versa)
    • chronic: decrease of pH by 0.03 generally indicates an increase of PaCO2 of 10 (and vice versa)
      • includes a 5 pt bicarb rise for every 10 mm pCO2 rise
    • see table
Disorder PaCO2 pH HCO3 Anion Gap Common Causes
Metabolic acidosis low low up or down MULEPAKS (AG high), HARDUP (AG normal)
Metabolic Alkalosis high high contraction alkalosis, diuretics, corticoisteroids, gastric suctioning, vomiting, hypderaldosterone (Cushing's, Bartter's syndrome, severe K depletion)
Respiratory acidosis high low CNS depression, chest bellows dysfxn (Guillan-Barre, MG), lung or upper airway disease (COPD, asthma, pulm edema)
Respiratory alkalosis low high hypoxemia, altitude, anxiety, sepsis, pneumonia, mild asthma, early pulm edema, PE


[edit] ABG Interpretation

  • ABG gives you pH, pCO2, and pO2.
    • pCO2 tells you about ventilatory problems.
    • pO2 tells you about oxygenation problems.

[edit] Oxygenation Failure

  • Oxygenation failure is defined as an elevated A-a gradient.
    • A-a gradient: difference between alveolar oxygen and arterial oxygen = PiO2 - (pCO2 / R) - pO2
      • PiO2: pressure of oxygen in the inspired air; room air is 21% at 760 barometric pressure so around 150; can be diff on a ventilator.
      • pCO2: pressure of CO2 in the blood; from the ABG
      • R: respiratory quotient; assume 08
      • pO2: pressure of oxygen in the arterial blood; from ABG
    • Normal A-a gradient = (pt age / 4) + 4


  • To quantify the oxygenation problem (once we have calculated an elevated A-a gradient), we compare SaO2 to PaO2 and PaO2 to FiO2.
    • SaO2 = oxygen saturation; obtained via pulse oximetry
    • PaO2 = dissolved oxygen; obtained via ABG
    • FiO2 = inspired oxygen; assumed to be 21% on room air but can be whatever you set on a mask / cannula


  • SaO2 : PaO2: a measure of oxygen on hemoglobin to oxygen in the blood
    • high ratio means that....


  • PaO2:FiO2 = a measure of blood oxygen to alveolar oxygne.
    • A normal PaO2:FiO2 is calculated via the A-a gradient: A-a = FiO2 - (pCO2 / R) - pO2, so FiO2 / pO2 =
    • The worse the oxygenation issue, the lower the ratio.
    • That is, the worse the ability of the lungs to move oxygen from the alveolar air to the blood, the lower the PaO2 relative to a (practically) stable FiO2.


[edit] Diagnose pneumothorax, pleural effusion, and atelectasis on exam or xray (know what to look for!)

  • Pneumothorax
    • hypodense areas, lack of blood vessels, trachea deviates away from lesion
    • chest tube w/ suction to pull air off


  • Pleural effusion
    • poor phrenic angles, uni/bi lateral density, decubitus view (free, loculated, fluid air level)
    • trachea deviates away from lesion
    • hemithorax on lesion side increases
    • dullness, decreased breath sounds on lesion side
    • decreased fremitus on lesion side
    • thoracentesis


  • Atelectasis
    • trachea shifts toward side with atelectasis
    • hemithorax decreases on lesioned side
    • clear mucus plug with bronchoscopy

[edit] Know how to treat a pneumothorax, atelectasis secondary to mucus plug, and pleural effusion

  • see above

[edit] Know basic bronchoscopic indications

  • Indications for bronchoscopy:
    • Bronchoalveolar lavage (cultures, cell counts)
    • Evaluate for bleeding or obstruction or burn
    • Clear out mucus plugs “a snot bronch”
    • Biopsy of lung lesion
    • Biopsy of lymph node (EBUS)
      • Mediastinal staging of cancer
      • Diagnosis of sarcoidosis, histoplasmosis, cancer


[edit] Know the objective findings in vocal cord dysfunction syndrome

  • Findings in vocal cord dysfunction:
    • Adduction during inspiration (wheeze / stridor)
    • Variable extrathoracic obstruction (cords close on inspiration)


[edit] Pulm Function Testing

  • What can PFTs measure?
    • Air flow (spirometry), lung volumes, gas exchange (diffusing capacity)
    • Cannot diagnose any one disease, only determines a pattern of function.


[edit] What are functional patterns?

  • Obstructive: collapsible, narrow airways causing prolonged expiratory times
    • Asthma, emphysema, chronic bronchitis, CF, bronchiectasis
  • Restrictive: "small lungs" (2-2: fibrosis, mechanical restriction, neuromuscular dysfxn)
    • Parenchymal: idiopathic pulmonary fibrosis, pneumoconiosis, sarcoidosis
    • Restrictive bellows: nm disease (ALS, MD), chest wall abnormalities (obesity, kyphoscoliosis)
  • Gas exchange abnormalities
  • Note that both obstructive and restrictive patterns result in decreased FEV1
    • However, the FVC is decreased in restriction such that the ratio doesn't change much.
    • The FVC is normal in obstruction such that the FEV1/FVC ratio is lower.

[edit] Spirometry

  • Spirometry:
    • most reproducible value is FEV1.
    • provides the flow volume loop; always look at the flow volume curve when interpreting PFTs

[edit] Lung Volumes

  • Lung volume tests:
    • Dilution test and body plethysmography.
    • Plethysmograph uses Boyle's law (p1 x v1 = p2 x v2) in an airtight box
      • Most accurate
      • Test of choice for severe obstructive disease
    • Dilution test uses (someone's) law (c1 x v1 = c2 x v2) with a known concentration of inspired, inert gas.
      • Easier and cheaper
      • Less accurate b/c of areas of lung with "trapped gas"

[edit] Diffusing capacity

  • Gas exchange = Diffusing capacity
    • Gas exchange is a fxn of area available and capillary blood flow
    • Destroyed alveoli (emphysema) or thickening (fibrosis) will decrease the DLCO
    • DLCO = Single breath carbon monoxide test
      • Most common
      • Inhale CO, hold for 10, exhale, subtract output from input, calculate diffusion rate.
      • must be corrected for hemoglobin

[edit] Interpretation

  • Acceptibility: smooth, continuous curve; good start; good finish
  • Reproducibility: 3 maneuvers, largest FVC and FEV1 are within 200 ml of each other; see tech comments
  • Examine the loop:
    • early expiration drop-off: epiglottis closed
    • all over the place: variable effort
    • serated: coughing expiration, usable
    • Normals: FVC: > 80, FEV1: >80, TLC: >80, DLCO: 80-140, FEV1/FVC: >70
    • See workflow in slides


  • MIP, MEP: reduced in neuromuscular disease.
  • Methacholine testing: if it changes by >20% at low concentrations, asthma


  • Gems:
    • if decreased diffusing capacity is the only thing changed, think pulmonary vasculature problem
    • if elevated diffusing capacity, think asthma, pulmonary vascular congestion, or alveolar hemorrhage
    • if a bronchodilator reverses a low FVC and low FEV1 (which normally indicates restriction), think pseudorestriction


[edit] Peds Pulmonary

[edit] PE Terms

  • Wheezing:
    • Continuous musical sound
    • Expiratory in nature
    • Short inspiratory and prolonged expiratory phases
    • Usually produced by intrathoracic obstruction that worsens on expiration
    • Monophonic wheeze- obstruction by a central airway
    • Polyphonic wheeze- reflects peripheral airway obstruction
  • Stridor:
    • Musical, monophonic, often a high pitched sound
    • Inspiratory in nature
    • Usually produced by extrathoracic obstruction
      • Dynamic or fixed
    • Severe obstruction suggested by: prolongation of inspiratory phase or presence in both inspiratory and expiratory

[edit] Cases

  • Croup: seal bark, steeple sign
    • humidified oxygen, fluids, aerosolized epi, corticosteroids, heliox
    • Etiology: viral: parainfluenza, RSV, or influenza
    • cxr not usually useful
    • many develop second case


  • Pappillomatosis: just proximal to the vocal cords


  • Bronchiolitis
    • increased resp rate, wheeze, reduced oral intake, fussy
    • tx: oxygen, hydration, aerosolized meds (albuterol, epi), corticosteroids
    • get better of weeks,
    • increased lower resp infections for 1-2 years


  • Laryngomalacia
    • 3 mo old
    • noisy breathing, worse with feeding and when supine
    • no apnea or color change
    • frequent vomiting or spitting up
    • active, alert, NAD (no acute distress)
    • variable inspiratory stridor
    • no hoarseness
    • soft systolic murmur
    • cxr, bronchoscopy, sleep study, gastro-reflux eval
    • ddx: laryngomalacia, vascular ring, laryngeal / subglottic lesions
    • tx: not given
    • progx: worse for first months, improves at 6-18 mo


  • Cystic Fibrosis
    • 4 mo, 3 mo hx of cough and intermitten wheeze
    • voracious appetite, little weight gain, occasional emesis
    • 6-7 loose, malodorous stools / day
    • active, alert, thin
    • mild tachypnea
    • mild nasal crusting, clear rhinorrhea
    • few intercostal retractions, bilateral coarse polyphonic expiratory wheeze (periph obst)
    • protuberant abdomen, liver palp 3cm below rcm
    • well perfused, mild macular skin rash
    • cxr (wide mediastinum), electrolytes, sweat chloride test, fecal elastase, throat / sputum culture, dietary consultation
    • tx: dx early, resp care, nutritional supplements


[edit] Pneumonia

[edit] Concepts

  • Time of onset informs the likely causative agent:
    • 0-2 days: bacterial
    • 0-2 days: mycoplasma, viral, legionella, pneumocystis, fungal
    • chronic: anaerobic, mycobacterial, fungal, nocardia, actinomycosis


  • Distribution informs the likely causative agent:
    • Lobar: bacterial, anaerobes
    • Diffuse: viral, pneumocystis, mycoplasma, fungal
    • Nodular / cavitary: mycobacterial, fungal, anaerobes


  • Using pneumonia guidelines: decreased mortality, decreased hospital admissions, shortened stay at hospital, decreased ICU visits, reduced cost.

[edit] Details

  • Workup for the pt with pneumonia:
    • H&P
    • CBC, electrolytes, glucose, BUN / Cr, LFTs
    • ABG, puls oximetry
    • Chest radiograph
    • Sputum gram stain, sputum culture (2 days)
    • Blood culture x2 (hospitalized pts, only)
      • Legionella (DFA, urine antigen)
      • Fungi (Histo CF titers, histo urine antigen, fungal gel diffusion)
      • Mycoplasma (cold agglutinins, sputum DFA)
      • Respiratory viral titers
    • Thoracentesis


  • Criteria for admitting pneumonia pts:
    • Age > 65
    • Comorbid conditions: COPD, DM, CRI, CHF, liver disease, possible aspiration, altered mental status, post splenectomy, alcohol abuse, malnutrition, DIC, renal dysfxn
    • PE: RR > 30, sBP < 90, dBP < 60, pulse > 125, temp < 35, temp > 40
    • Labs: WBC < 4k or > 30k, pO2 < 60, pCO2 > 50, HgB < 9.0, pH < 7.35, high BUN, high creatinine
    • CXR: multilobar, cavitation, pleural effusion
    • CURB-65: confusion, BUN (> 20), RR (> 30), Blood pressure (s < 90, d < 60), 65 (age)
      • CURB-65 is scored: 0-1 is outpt, 2 is wards, 3-5 is ICU
    • "Severe" if: 1 major or 3 minor
      • Major: resp failure, septic shock (need for vasopressors)
      • Minor: rr, multilobar, confusion, BUN, WBC, platelets low, temp low, hypotension requiring fluids


  • Risk factors for penicillin-resistant penumococci infection:
    • 2 > Age > 65
    • beta-lactam therapy within last 3 mo
    • alcoholism
    • immune suppression
    • multiple medical comorbidities
    • exposure to children in day care center


  • Risk factors for enteric gram negative organisms infection:
    • nursing home
    • recent abx tx
    • multiple medical comorbidities
    • underlying cardiopulm disease


  • Risk factors for pseudomonas aerugenosa
    • structural lung disease
    • corticosteroid tx
    • abx for > 7 days
    • malnutrition / alcoholism


  • Pneumonia tx:
    • best predictor of outcome is whether appropriate abx were started upon admission (< 6 hr)
    • Specify abx as you get gram / cultures back
    • Immune competent top causes: s. pneumonia, atypicals (legionella, chlamydia, mycoplasma, h. influenzae
    • Immune compromised top causes: s. pneumonia, gram-neg bacilli, h. influenze
    • MRSA: vancomycin or linezolid
    • Switch to oral and d/c when stabilized; generally 7-10 days; add time for atypicals and even more for legionella
    • Tracheal aspirates are insensitive but have a good negative predictive value.
    • Invasive procedures to identify pathogen do not decrease mortality.


Category Description Agents Tx
I Outpt, no cardiopulm disease, no modifying factors S. pneumonaiae, m. pneumoniae, resp viruses, c. pneumoniae, h. influenzae advanced generation macrolide OR doxycycline
II Outpt, cardiopulmonary disease or modifying factors present S. pneumonaiae, m. pneumoniae, c. pneumoniae, resp viruses, enteric GNR, mixed infections (Beta lactam PLUS macrolid / doxycycline) OR fluoroquinolone
III Inpt, non-ICU S. pneumonaiae, m. pneumoniae, c. pneumoniae, H. influenzae, Legionella, Aspiration, Resp viruses, enteric GNR, mixed infections (IV beta lactam PLUS macrolide) OR IV fluoroquinolone
IVa S. pneumonaiae, Legionella, H. influenzae, aerobic GNR, S. aureus, m. pneumoniae, Resp viruses (IV beta-lactam PLUS macrolide) OR IV fluoroquinolone
IVb Risk factors for pseudomonas aerugenosa P. aerugenosa, S. pneumonaiae, Legionella, H. influenzae, aerobic GNR, S. aureus, m. pneumoniae, Resp viruses IV antipseudomonal beta lactam PLUS ( (IV ciprofloxacin / aminoglycoside PLUS IV macrolide) OR IV fluoroquinolone) )


  • Pneumonia resolution (order): fever, leukocytosis, rales, cxr (8-10 weeks!)
  • Pts that fail to respond: bronchoscopy, chest CT, open lung biopsy

[edit] Vaccination Recommendations

  • Pneumovax: >65 yo, smokers, cardiopulm disease, DM, etoh abuse, asplenia, suppressed, long term care facility; 1 time after 5 years
  • Inactivated influenza: age > 50, health care peeps, same high risk as pneumovax (plus contacts), annually
  • Attenuated influenzae: 5 < age < 49, health care peeps, NOT IN HIGH RISKERS, annually


[edit] Pulmonary Hypertension

[edit] What are the definitions of PAH?

  • Pulm HTN (PH): mPAP (mean pulmonary artery pressure) >= 25 mmHg at rest
  • Pulm Art HTN (PAH):
    • mPAP >= 25 mmHg at rest AND PCWP (pulm capillary wedge pressure = left atrial pressure) <= 15 mmHg AND PVR (pulmonary vascular resistance) >= 3 Wood units
      • note that the PCWP being <= 15 rules out left heart failure as PCWP is a measure of left atrial pressure
    • much rarer than PH
    • more severe than PH
    • more pronounced vascular remodeling
    • only type with plexiform lesions


  • PAH contains many subtypes based on etiology.
  • There are four other types of pulm HTN:
    • These four require only a mPAP >=25 mmHg
  1. due to left heart disease
  2. due to lung disease
  3. due to chronic thromboemboli
  4. unclear or multifactorial cause

[edit] Why would the pulmonary artery pressure increase?

  • Vasoconstriction, Vascular Remodeling, In-situ thrombosis
  • Dysfxn of one of three pathways that affect vasodilation / vasoconstriction: endothelin pathway, NO pathway, prostacyclin pathway
  • Pulm vascular changes include: intimal thickening, vasoconstriction, formation of plexi (PAH, only)

[edit] What are the S&S of Pulm HTN?

  • Symptoms: dyspnea, angina, syncope, edema
    • NOT associated with PH or PAH: cough, hemoptysis, wheezing, stridor
  • Syncope is a symptoms that indicates the PH / PAH is severe = Class IV.


  • Signs: loud S2, tricuspid regurg, right vent heave, S4
  • PE: jugular venous distension, ascites, hepatomegaly, lower extremity edema, cyanosis, right to left shunt


  • PH / PAH 2-2 connective tissue disorders: skin changes, alopecia, arthralgias, arthritis
  • PH / PAH 2-2 congential heart disease: murmurs, gallops, cyanosis
  • PH / PAH 2-2 portopulmonary HTN: spide naevi, telangiectasia, gynecomasita, testicular atrophy, ascies, hepatomegaly, nodular liver

[edit] Risk factors for pulmonary HTN

  • Collage vascular disease, congenital heart disease, portal HTN, HIV, drugs, toxins, pregnancy

[edit] How does one workup PH / PAH?

  • CBC: due to infection?, due to scleroderma / SLE, HIV?
  • , BMP, LFTs
  • Echo: due to left heart failure?, do to congestive heart failure?
  • V/Q scan: due to chronic PE?
    • Pulm angiogram to confirm PE
  • PFTs: due to lung disease? due to hypoxemia?
  • 6-minute walk test: how limiting is PH / PAH?
  • Right heart cathetrization: dermines the cause, grades the severity
    • RH cath gives: pressures, vascular resistance, and cardiac output can be measured
    • RH cath gives: oxygen sats in vena cava, right atrium, right ventr, and pulm artery
    • does oxygen increase from right atrium to right ventricle? -> ASD or VSD
    • is venous oxygen sat <70% -> tissue hypoperfusion
    • RH cath testing: give vasodilator; with strong (>10 mmHg to <40 mmHg) response, pt can be tx with calcium channel blockers alone


  • Classifying PH / PAH with the following factors:
    • clinical evidence of RH failure
    • Progression
    • WHO class
    • 6 minute walk distance
    • BNP
    • echocardiographic findings
    • hemodynamics

[edit] What are the treatment options for PH / PAH?

  • All pts:
    • o2,
    • diuretics,
    • digitalis,
    • avoid pulm stressors (prego / lifting / high altitude / cold medications / air travel),
    • low salt diet,
    • ligh exercise
    • immunizations
    • anticoagulate with warfarin: for pts with idiopathic, familial, anorexigenic, or thromboemboli PH


  • PH: treat underlying disease
    • Recall that all the non PAH cases of PH were "2-2 ..."


  • PAH:
    • RH cath with vasodilator challenge:
      • Positive response: just calcium blockers:
        • Diltiazem, nifedipine, amlodipine
        • Avoid verapamil
        • Tolerance occurs, monitor closely
      • Negative response: PAH specific meds
        • Prostacyclin analogs: the only drug shown to increase survival
        • Endothelin-1 receptor antagonists
        • Phosphodiesterase 5-inhibitors


[edit] Pulmonary Embolism

[edit] Risk factors for DVT / PE?

  • Factor V mutation: resistance to activated protein C
  • Homocysteinemia
  • Prothrombin 20210A mutation
  • Antithrombin III deficiency
  • Protein C or S deficiency


  • Sx:
    • high risk: age > 40, extensive pelvic or abd sx, major orthopedic sx of lower limbs
      • give full dose anticoags (LMWH, fondaparinux, or warfarin), use pneumatic leg pressure
    • moderate risk: age > 40, sx > 30 min
      • give anticoags, penumatic leg pressure
    • low: sx < 30
      • no specific prophylaxis

[edit] How do PEs present?

  • 25-40% present as tachypnea and tachycardia that cannot otherwise be explained.
  • In the pt with pulmonary comorbidities, a PE results in complete infarct (as opposed to incomplete infarction) such that they experience pleuritic pain, hemoptysis and demonstrate pulmonary infiltrates.

[edit] How does one diagnose a PE?

  • Three ways to dx a PE: direct viz of arterial bed, proof of DVT, or serologic evidence of clotting.


  • Visualizing arterial bed: Pulmonary angiogram is the gold standard to dx PE.
    • Other direct visualizations of the arterial tree are options, too.
    • Practically, sprial CT is how PEs are diagnosed.
      • Fast, can define anatomy and see other causes of presentation if PE not present.
      • Negative CT has a very high negative predictive value: 99.1%
      • Try to avoid in renal dysfxn pts; give prophylactic bicarb infusion if you must use contrast.
    • Chest MRI
    • Echo
    • Vent / Perfs scan


  • Evaluate the lower extremity for DVT:
    • Venogram: gold standard
    • Impedence plethysmography
    • Compression US: easy, cheap, capable
    • MRI


  • Measure for clotting:
    • D-dimer: two tests, many "normals", make sure you know the normal range for your local path lab
    • Use D-dimer to differentiate how to handle each risk group (low, medium, high; see Wells / Geneva criteria).
    • D-dimer is SENSITIVE, so use it to rule PE out.


  • There are other, supporting labs but NONE OF THESE RULE PE IN OR OUT:
    • Blood gas abnormalities are common but neither sensitive or specific to PE: hypoxia, increased A-a gradient, hypocapnea, respiratory alkalosis.
      • This hypoxia makes sense b/c with hemorrhage, pulmonary arterial blood (deoxygenated) will gain access to the pulm venous (oxygenated) stream, thus lowering the oxygen.
    • ECG may show S1Q3, RBBB, or new onset atrial fibrillation
    • CXR: 40% have normal CXR
      • elevation of ipsilateral hemidiaphragm
      • Hamptoms hump: hump at the base, running medially from the lateral pleural line, like a tall, skinny triangle
      • Westermark sign


  • Assess the risk of PE using the Wells criteria or the Geneva score.
    • Most people use the Wells Critieria to determine probability b/c it is based only on clinical parameters and therefore easy and quick.
    • The Geneva score can be used to predict probability, too; it requires blood gasses.
    • Note that D-dimer is NOT used to predict probability in the Geneva score.

[edit] How do we treat PEs?

  • We only really treat PE with "significant cardiopulm compromise."


  • Get baseline PT, PTT, and platelet count
  • Heparin bolus, then drip
    • Get heparin onboard early (as it will take a bit to get warfarin up to speed)
    • Use heparin over LMWH if you need to do procedures (can't reverse LMWH)
    • Use LMWH whenever you can b/c less hemorrhage
  • Upon official dx, second heparin bolus
    • Use as much heparin as it takes to get the PTT to "therapeutic" levels within 24 hours so the pt doesn't have a repeat event.
    • Use hirdins, too, if you need to.
  • Start warfarin


  • For transient, reversible risk factor that caused PE, treat for 3 months.
  • For "idiopathic" tx for 1 year, retest d-dimer after 30 days, tx again if elevated.
  • For recurrent risk factors, tx for life.


  • Thrombolytics do not decrease death!
    • Here, we are to understand this as heparin + thrombolytic (alteplase) as being no better for mortality but better at other adverse events.


  • Use IVC filters when pt cannot be anticoagulated.


[edit] Obstructive Airways Diseases

[edit] Basic pathophysiology

  • Emphysema: neutrophil elastase destroys alveoli and elastic recoil, hyperinflation ensues (irreversible)
    • a destruction w/o fibrosis
  • Chronic bronchitis: mucus hypersecretion (2/2 irritation) resulting in physical obstruction and cough
    • Defined as productive cough for > 3 months in 2 consecutive years.
  • Asthma: airway inflammation, bronchial hyperresponsiveness leads to constriction and air trapping (reversible)
    • The inflammation is slowly reversible; the hyperresponsive airway is rapidly reversible.
    • Think TNF and IL4.

[edit] Symptomatology

  • Hyperinflation, wheezing
  • Deaths: Pts that pass out at home. Asthma is a disease of not getting air out! Starts as hyperventilation, hard work getting air in. Ends with fatigue so bad that there is zero effort in breathing.

[edit] Diagnostic studies

  • PFTs (with reversability test via bronchodilator)
    • Emphysema: irreversible
    • Asthma: reversable
  • Can do an inducible test too with methacholine or eucapnic hyperventilation
    • Asthma gets worse, emphysema doesnt
    • Drop in FEV1 > 20% (at low doses)


  • PFT in general:
    • Emphysema: low diffusing capapcity


  • Peak flow rates:
    • Send home with pt to keep in purse; helps get pt to hospital when they aren't sure if their attack is serious or not.
    • Helps pt see that working outside (generated dip) is bad for asthma. Perhaps change lifestyle in some way?

[edit] Classifications (asthma & emphysema)

  • Emphysema classification:
    • At risk (normal spirometry), mild (FEV1 >80% predicted), moderate (<80%), severe (<50%), and very severe (,30%).


  • Asthma classification
    • Intermittent, mild persistent, moderate persistent, severe persistent
    • Intermittent: symptoms <= 2 d/we, awakened <= 2 d / mo, beta-agonist <= 2 d / we, normal FEV1 between attacks
      • Tx: rescue beta agonist
    • Mild persistent: symptoms < 7 d/we, awakened 3-4 d/mo, beta-agonist use < 7 d/we,
      • Tx: rescue beta agonist, controller of inhaled corticosteroids or leukotriene modifier
    • Moderate persistent: symptoms 7 d/we, awakened > 4 d / mo, beta-agonist use >= 7 d/we
      • Tx: rescue beta agonist, controller of medium dose inhaled corticosteroids, long acting beta agonist, +/- leukotriene modifier
    • Severe persistent: symptoms continuously, awakened >= 7 d/we, beta-agonist use > 1 hr / d
      • Tx: rescue beta agonist, controller of high dose inhaled corticosteroids, long acting beta agonist, +/- oral steroids or anti IgE
    • Not super important to keep in mind. Define on initial presentation, though. May educate tx.

[edit] Treatment strategies (asthma & emphysema)

  • Emphysema:
    • Class 0: avoid risk factors, get influenza vaccine
    • Class 1: avoid risk factors, get influenza vaccine, short acting vasodilator
    • Class 2: avoid risk factors, get influenza vaccine, short acting vasodilator, rehabilitation, long acting bronchodilator
    • Class 3: avoid risk factors, get influenza vaccine, short acting vasodilator, rehabilitation, long acting bronchodilator, inhaled glucocorticoids
    • Class 4: avoid risk factors, get influenza vaccine, short acting vasodilator, rehabilitation, long acting bronchodilator, inhaled glucocorticoids, oxygen, sx


  • Asthma:
    • Intermittent: rescue beta agonist
    • Mild persistent: rescue beta agonist, controller of inhaled corticosteroids or leukotriene modifier
    • Moderate persistent: rescue beta agonist, controller of medium dose inhaled corticosteroids, long acting beta agonist, +/- leukotriene modifier
    • Severe persistent: rescue beta agonist, controller of high dose inhaled corticosteroids, long acting beta agonist, +/- oral steroids or anti IgE

[edit] Factors indicating poor prognosis (emphysema)

  • Factors Associated With Poor Prognosis:
    • Airways responsiveness
    • Cigarette smoking
    • Low BMI or weight loss
    • HIV infection
    • Airway bacterial load
    • Decreased exercise capacity
    • Hypercapnea

[edit] Management goals (asthma)

  • Goals of Asthma Management:
    • Prevent troublesome symptoms
    • Require infrequent use of rescue meds
    • Maintain normal activity levels
    • Prevent recurrent exacerbations and minimize Emergency Department visits or hospitalizations
    • Prevent loss of lung function; for youths, prevent becoming a chronic problem
    • Provide optimal pharmacotherapy with minimal or no adverse effects


[edit] The Pleura & Neurologic Disorders

[edit] Recall the anatomy and physiology of the normal pleural space

  • Lymphatics are in direct communication with pleural space via stomas.
  • There are only sensory fibers in the parietal pleura, that is, the one toward the outside.
  • Chest tubes go in at T8 on the posterolateral aspect.
  • The pressure is always negative in the pleural space: -4 to -8 (expiration to inspiration)

[edit] List the signs and symptoms of pleural effusion and pneumothorax

[edit] Pleural Effusion

  • Definition: Excess fluid in the pleural space
  • Symptoms:
    • Asymptomatic OR
    • Pain
    • Dyspnea
    • Cough
    • Fever
  • Signs:
    • Absent or diminished breath sounds
    • Dullness to percussion (shifting dullness)
    • Diminished or absent tactile fremitus over effusion
  • CXR: H-word sign, rides up the lateral wall


[edit] Pneumothorax

  • Definition: air/gas in the pleural space
  • Symptoms:
    • Asymptomatic OR
    • Pleuritic chest pain
    • Cough
  • Signs:
    • Diminished or absent breath sounds on affected side
    • Tactile fremitus is diminished or absent
    • Hyper-resonance to percussion
  • CXR: If large enough, tracheal deviation AWAY from pneumothorax


[edit] Identify pathophysiologic causes of an effusion or pneumothorax

[edit] Pleural Effusion

  • See exudates and transudates and recall that fluid flow is a function of oncotic pressures and hydrostatic pressures.

[edit] Pneumothorax

  • Pathophysiology of Pneumothorax:
    • Because pressure within the intrapleural space is negative (-4 to -8 cm H2O), any communication between the air-filled lung parenchyma and pleural space will result in accumulation of air within the pleural space until the pressures are equalized
    • Result is collapse of the lung and hyperexpansion of the hemi-thorax, leading to impairment


[edit] Differentiate a transudative from an exudative effusion

  • Transudates are systemic and due to fluid issues (like hydrostatic or oncotic changes).
  • Exudates are local and due to changes in the tubes (like vessles or lymphatics).


  • Transudate ddx:
    • systemic; due to pathology of the liquid
    • think of all the organs that handle maintenance of the fluid: liver, heart, kidney
    • Increased hydrostatic pressure: CHF, renal failure
    • Decreased oncotic pressure: cirrhosis, nephrotic syndrome, hypoalbuminemia (malnutrition, etc)


  • Exudate ddx:
    • local issue, pathology of the tubes
    • Think of all the things that can go wrong with tubes: plugged (infection, thrombus), degenerative (collagen, neoplasms), inflammatory reaction (infection, tb, vasculitis, drugs)


  • Light's criteria determines if the fluid drained off an effusion is an exudate.
  • The fluid is an exudate if it has any one of the following three criteria:
    • fluid protein / serum protein > 0.5
    • fluid LDH / serum LDH > 0.6
    • fluid LDH > 2/3 the normal upper limit for serum
  • NB: the first two (protein and LDH ratios) require getting serum studies done!

[edit] Identify the characteristics of pleural fluid analysis in common pleural diseases

  • Empyema: Pus, putrid odor ,culture
  • Malignancy: Positive cytology
  • Lupus pleuritis: Positive LE cells, ANA > 1:160
  • Tuberculosis: AFB culture, ↑ ADA
  • Esophageal rupture: pH <6, ↑amylase
  • Pancreatitis: PF /serum amylase > 1
  • Chylothorax: Milky, triglycerides > 110mg/dL, chylomicrons
  • Hemothorax: Hematocrit PF / blood >0.5
  • Urinothorax: Creatinine PF / blood >1.0. ammonia odor
  • Peritoneal dialysis: Protein < 1 g/dL, glucose > 300-400 mg/dL
  • Amebic liver abscess: Anchovy colored
  • Rheumatoid arthritis: Glucose <30mg/dL


  • empyema: collection of pus in a body cavity
  • Parapneumonic effusion: any effusion associated with infectious pneumonia, lung abscess, or bronchiectasis
    • can have little or lots of fluid
    • translucent to straw-colored to pus
    • An empyema has a positive stain or culture whereas complicated PPE is usually negative.
      • Tx both with antibiotics and drainage.
      • Both are usually exudative.


  • Neoplastic disease
    • Almost always an exudate, can even be bloody
    • Dx usually by cytology
      • Sensitivity 90% with three samplings
    • Usually metastatic disease
    • Mesothelioma is the most common malignancy with pleural effusion

[edit] Identify the pulmonary function abnormalities associated with neuromuscular weakness

  • NM Disease present as restrictive patterns
  • Spirometry: decreased FVC
  • Lung volumes:
    • Decreased total lung capacity
    • increased residual volume
  • Diffusing capacity: preserved (except in rare cases, decreased)


  • Generally, there is hypoventilation in NM diseases, therefore, ABG abnormalities include:
    • increased pCO2 early and decreased pO2 late
      • recall that CO2 is ventilation limited but O2 is diffusion limited

[edit] List those neuromuscular diseases associated with respiratory failure

  • NM Diseases with associated pulmonary dysfxn: ALS, Guillan-Barre Syndrome, Myasthenia gravis, polymyositis, botulism, tetanus, duchenne's md.
  • These fail in four ways:
    • Mechanical obstruction of the airways
    • Atelectasis from hypoventilation
    • Aspiration pneumonia
    • Reducing the margin of error and allowing acute illness to overtake the pt


[edit] Interstitial Lung Disease and SPNs

[edit] Interstitial Lung Disease (ILD)

[edit] Recognize the scope and complexity of interstitial lung diseases (ILD)

  • Why is ILD so confusing?
    • Extensive number of diseases
    • Very similar presentation
    • No clear diagnostic algorithm
    • Histologic and radiographic patterns are rarely unique
    • When in doubt (which is often):
      • Go back for more history
      • Get more tissue
      • Just wait awhile, it will declare itself


  • List six broad categories of ILD
    • environmental
    • autoimmune
    • drugs
    • idiopathic
    • miscellaneous
    • infectious


  • Many diseases involved:
    • Slceroderma
    • Polymyositis-dermatomyositis
    • SLE
    • Mixed connective tissue disease
    • Ankylosing spondylitis
    • Behcet's
    • Sjogren's syndrome
    • Pleurisy
    • Sarcoid
    • Diffuse alveolar hemorrhage


  • Accept the difficulty in making the correct diagnosis (algorithms and pattern recognition)
    • Good diagnostic algorithms DO NOT EXIST, use your pattern recognition, pearls, clues, epidemiology, and get a tissue sample


  • Pneumonitis = organics (think bugs in a silo making gas, breathed in causing rxn)
  • Pneumoconiosis = inoraganics
    • Asbestosis
    • Silicosis

[edit] Review the relative value of various types of clinical information related to ILD

    • Super useful: knowing about ILD, getting a good history
    • Useful: CT scan, pathology
    • Interesting: blood test, CXR
    • Least helpful: physical examination

[edit] What does ILD look like on presentation?

  • Symptoms: cough, progessive dyspnea
    • DOE = dyspnea on exertion
    • Pleuritic pain: uncommon except with RA, SLE, drug-induced, and sarcoid
    • Hemoptysis: uncommon except with diffuse alveolar hemorrhage
  • Signs: crackles, clubbing, right heart failure
    • RA: proximal two joints of hands
  • PFTs: restrictive pattern, decreased DLCO, oxygen desaturation

[edit] XRAY and CT patterns

  • Nomenclature
    • assessment terminology is not as useful as descriptive terminology
    • reticular, linear, nodular, fluffly, ground glass
  • Get old images!
  • It is about pattern recognition

[edit] Biopsying: How, When, If

  • Surgical biopsy will always get you the histological sample you need for diagnosis, however, it is super invasive.
  • Transbronchial biopsy (TBBx) can get the sample one needs in about 1/3 of the cases for which one needs a biopsy.

[edit] Introduce a framework for categorizing ILD

[edit] Pulmonary Nodules

  • Nodule: a radiologically visible lesion that is within and surrounded on all sides by pulmonary parenchyma
    • Size limits: up to 3 – 4 cm diameter (above which is a mass)

[edit] Outline a reasonable diagnostic approach

  • Typically the Pulmonologist’s job
  • Are there old images?
  • Is the pt symptomatic?
  • Urgency?
  • Get images: size, shape, presence of calcium, and number (count), density
    • CT > CXR
    • See a SPN
      • Chances of it being malignant:
        • > 60 yo: > 50%
        • > 3 cm: 80-90%
        • < 2 cm: 20%
  • Look for associated findings (clubbing, etc.)


  • Option 1: Observation
    • benign lesions change size very rapidly or very slowly
    • hard to know if a small lesion is growing (volume, not diameter)
    • PET cannot see lesions < 1 cm


  • Option 2: Remove it
    • Should be done when lung fxn can handle it and "odds" are in "favor" of nodule being malignant


  • Option 3: Less invasive approach
    • Fiberoptic bronchoscopy: central lesions, able to sample lymph nodes
    • CT-guided FNA: peripheral lesions, 20-30% pneumothorax rate


  • Getting tissue:
    • Bronchoscopy
    • CT-guided FNA
    • Surgical Resection

[edit] Recognize when an urgent diagnosis is necessary

  • Noduels are often a sign of Scary stuff:
    • Cancer
      • Curative treatment available? URGENT !!
      • No curative treatment? Still scary but less urgent
    • Early sign of a chronic disease
    • Active infection
  • Not scary: Old scar tissue from:
    • Pneumonia
    • Self-limited fungal disease
    • Trauma
    • Something that really isn’t a nodule

[edit] Recognize the relative value of different sources of clinical information

[edit] Accept the difficulty in making the correct diagnosis (algorithms and pattern recognition)

[edit] Share a few examples

[edit] Hamartoma

  • Get the Size, shape, presence of calcium, and number (count), density
    • many different densities: probably a hamartoma
  • Look for associated findings (clubbing, etc.)
    • emphysema (seen on CT as blebs)
    • bronchial carcinoma (seen as a stellate bronchus on CT)

[edit] Treatment of Respiratory Failure

[edit] Be able to calculate the A-a gradient given an ABG and FiO2

  • A-a gradient is the difference between alveolar and arterial oxygen.
  • Provides a measure of gas exchange efficiency.
  • Normal A-a gradient is (age / 4) + 4
  • A-a = PiO2 - (pCO2 / R) - pO2
    • PiO2 = pressure of inspired oxygen
      • Room air is 150 = (atmospheric pressure - correction for humidity) * percent of air made of oxygen = (760-47)*0.21 = 150
      • Use this to calculate the PiO2 when a pt is on supplemental oxygen; substitute their oxygen percentage for 0.21.
    • pCO2 = arterial CO2; from ABG
    • R = respiratory quotent; assumbed to be 0.8; how much carbon dioxide is produced for each molecule of O consumed
    • pO2 = arterial oxyge; from ABG


  • A-a increases with FiO2, age, any failure to oxygenate (including shunting and V/Q mismatch).

[edit] Define Shunt & V/Q Mismatch (increased and decreased)

  • Shunt occurs when venous blood mixes with arterial blood bypassing oxygenation.
    • Extra pulmonary shunt: right to left cardiac shunts like tetraology of Fallot
    • Intra pulmonary shunt: blood is transported through the lungs without taking part in gas exchange; as in Atelectasis, Pneumonia, Hepatopulmonary syndrome, AVM


  • Ventilation-Perfusion (V/Q) mismatch: a combination of shunt and dead space
    • Decreased V/Q: areas in the lung that are better perfused then ventilated (aka “shunt”)
    • Increased V/Q: areas that are better ventilated then perfused (dead space)
  • V/Q mismatch: occurs in normal lungs based on lung zones (lower lung zones are better perfused)
  • Mismatch is exacerbated in most causes of respiratory failure:
    • Emphysema (decreased V/Q b/c non-functioning alveoli don't get ventilated)
    • Fibrosis (decreased V/Q b/c poor diffusion of air)
    • Secretions (decreased V/Q b/c blocks diffusion of air)
    • Pulmonary embolism (increased V/Q b/c blocks blood flow)

[edit] Know what influences the Oxygen dissociation curve to the right and left

  • Left shift: Things that cause Hb to more tightly bind oxygen:
    • alkalosis,
    • hypothermia
    • low pCO2
    • low 2,3-DPG
  • Right shift: Things that cause Hb to release oxygen more readily:
    • working muscle stuff...
    • higher temperatures
    • high pCO2
    • acidosis
    • high 2,3-DPG

[edit] Learn the types and FiO2’s of various supplemental oxygen devices

  • Nasal prongs:
    • 1 liter = 4% FiO2
    • Max: 40-44%
  • Simple Face mask:
    • Max: 55% FiO2 max
  • Venturi mask:
    • Color coded: 24-50% FiO2
  • Non-rebreather Mask:
    • Reservoir, valve, tight seal
    • 90% FiO2 max
    • AE: microatelectasis

[edit] Understand the types and indications for Non-invasive positive pressure ventilation

  • CPAP = continuous positive airway pressure
    • Useful for tx of pulmonary edema and obstructive sleep apnea.


  • BiPAP = bilevel positive airway pressure
    • Gives inspiratory pressure and expiratory pressure
    • Inspiratory pressure augments pt's own tidal volume, thus improving ventilation
    • Helps pt blow off CO2.


  • Intubate over NIPPV if:
    • Altered mental status (no gag reflex)
    • Facial deformity or trauma
    • Stridor or burns or obstruction of airway
    • Cardiac or respiratory arrest
    • Unable to clear sputum

[edit] Understand the procedure of endotracheal intubation and indications for mechanical ventilation

  • Indications for intubation:
    • Respiratory failure
    • Hypoxic (pneumonia, PE, aspiration, etc…)
    • Ventilatory (overdose, stroke, emphysema, etc…)
    • Airway (seizure, stroke, overdose, etc...)

[edit] Learn basic mechanical ventilation (not covered on exam)

[edit] Review for the Pulmonary Exam

[edit] Pulmonary & Critical Care Case Conference

  • Introduce you to “real-world” clinical medicine through actual case studies
  • Cases not on exam
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