Pulmonary Review
From Iusmicm
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==Interstitial Lung Disease and SPNs== | ==Interstitial Lung Disease and SPNs== | ||
+ | ===Interstitial Lung Disease (ILD)=== | ||
+ | |||
+ | ====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 | ||
+ | |||
+ | ====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 | ||
+ | |||
+ | ====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 | ||
+ | |||
+ | ====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 | ||
+ | |||
+ | ====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. | ||
+ | |||
+ | ====Introduce a framework for categorizing ILD==== | ||
+ | |||
+ | ===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) | ||
+ | |||
+ | ====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 | ||
+ | |||
+ | ====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 | ||
+ | |||
+ | ====Recognize the relative value of different sources of clinical information==== | ||
+ | |||
+ | ====Accept the difficulty in making the correct diagnosis (algorithms and pattern recognition)==== | ||
+ | |||
+ | ===Share a few examples=== | ||
+ | |||
+ | ====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) | ||
==Treatment of Respiratory Failure== | ==Treatment of Respiratory Failure== | ||
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+ | ===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). | ||
+ | |||
+ | ===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) | ||
+ | |||
+ | ===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 | ||
+ | |||
+ | ===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 | ||
+ | |||
+ | ===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 | ||
+ | |||
+ | ===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...) | ||
+ | |||
+ | ===Learn basic mechanical ventilation (not covered on exam)=== | ||
+ | |||
+ | ===Review for the Pulmonary Exam=== | ||
==Pulmonary & Critical Care Case Conference== | ==Pulmonary & Critical Care Case Conference== | ||
*Introduce you to “real-world” clinical medicine through actual case studies | *Introduce you to “real-world” clinical medicine through actual case studies | ||
*Cases not on exam | *Cases not on exam |
Current revision as of 01:36, 7 March 2012
[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
- Inspection:
[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
- A-a gradient: difference between alveolar oxygen and arterial oxygen = PiO2 - (pCO2 / R) - pO2
- 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
- mPAP >= 25 mmHg at rest AND PCWP (pulm capillary wedge pressure = left atrial pressure) <= 15 mmHg AND PVR (pulmonary vascular resistance) >= 3 Wood units
- PAH contains many subtypes based on etiology.
- There are four other types of pulm HTN:
- These four require only a mPAP >=25 mmHg
- due to left heart disease
- due to lung disease
- due to chronic thromboemboli
- 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
- Positive response: just calcium blockers:
- RH cath with vasodilator challenge:
[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
- high risk: age > 40, extensive pelvic or abd sx, major orthopedic sx of lower limbs
[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
- Blood gas abnormalities are common but neither sensitive or specific to PE: hypoxia, increased A-a gradient, hypocapnea, respiratory alkalosis.
- 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
- increased pCO2 early and decreased pO2 late
[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%
- Chances of it being malignant:
- 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
- Cancer
- 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
- PiO2 = pressure of inspired oxygen
- 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