CA/CM II PULMO

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Dullness

a) Relative intensity: Medium b) Relative pitch: Medium c) Relative duration: medium d) Example of location: Liver e) Pathologic examples: lobar pneumonia

Hyperresonance

a) Relative intensity: very loud b) Relative pitch: lower c) Relative duration: longer d) Example of location: usually none e) Pathologic examples: COPD, pneumothorax

Anteroposterior diameter

a) The shape of the chest, which is normally wider than it is deep. b) The ratio of the anteroposterior (AP) diameter to the lateral chest diameter is usually 0.7 to 0.75 up to 0.9 and increases with aging

a) Mediastinal crunch (Hamman's Sign)

a. A mediastinal crunch is a series of precordial crackles synchronous with the heartbeat, not with respiration. b. Best heard in the left lateral position, it arises from air entry into the mediastinum causing mediastinal emphysema (pneumomediastinum). c. It usually produces severe central chest pain and may be spontaneous. d. It has been reported in cases of tracheobronchial injury, blunt trauma, pulmonary disease, use of recreational drugs, childbirth, and rapid ascent from s cuba diving

Acute Bronchiolitis

· Pathophysiology: o Infection that impacts the smaller airways, Virus invades the terminal aspect of the bronchioles o Typically starts as an upper respiratory (rhinorrhea, sneezing, etc.) o Causes: RSV, rhinovirus, parainfluenza type 3, influenza, adenovirus, coronavirus · Epidemiology/Risks: o Children <2 (peak 3-6mo) but up to 5 , M>F o Most common cause for admission of infants <12 months old in US o Seasonal incidence: beginning late October, peaking Jan.-Feb., ending early April o Risks to catch: Climate linked to indoor crowding, Air pollutants, Environmental tobacco smioke o Prematurity, Low birth weight, Underlying medical condition o Risks for severe diseases: Premature (< 36 wks), Low birth weight, Age < 12 wks, Chronic pulmonary disease (dysplasia), Anatomic airway defects, Congenital heart disease, Immunodeficiency · Symptoms/PE: o Edema and inflammation of the airways in sm. Bronchi and bronchioles o Excessive mucous production from edema and sloughing epithelial cells o Obstruction of small airways causes atelectasis and symptoms o URI preceding, Persistent cough (sounds like a seal barking), Increased work of breathing o Tachypnea, fever, Intercostal retractions, nasal flaring, use of abd. muscles, grunting o Auscultory: wheezes and crackles o Minute to minute variation in clinical presentation (hallmark of disease) o Duration of symptoms and findings can be up to 2-3 weeks · Diagnostics: o Pulse ox / monitoring o Viral testing: RSV PCR / respiratory panel from nasal suctioning or sample o No need for chest x ray or labs · Treatment: o Non severe: § Nasal suctioning, Hydration and nutrition support, Self limiting disease, Follow up o Severe: § Nasal suctioning, Hydration and nutritional support, Bronchodilator ??? § Glucocorticoid steroids NOT if first episode § Supplemental oxygen (SPO2 < 90 %) § Mechanical ventilation (tiring and failing treatment, no improvement with O2) § ETT vs HFNC o Prevent: RSV antibody injections - palivizumab, Flu vaccine o Send home: § Resp rate < 60/min, age < 6 mos, resp rate <55/min age 6 - 11 mos, Resp rate <45/min age >12 mos § Caretaker able to suction nares, Patient stable on room air for 12 hours § Adequate oral intake/hydration, Home resources, Family education o Hospitalize: § Toxic appearance, lethargy, dehydration § Moderate to severe respiratory distress: Physical signs (retractions, etc), Resp. rate > 70 § Apnea, Hypoxemia § Unable to be cared for at home · Complications: o Apnea and respiratory failure, Hypoxemia o If ventilated- pneumothorax, pneumomediastinum o Dehydration o Aspiration pneumonia o Secondary bacterial infection

Chest X-ray

· Indication: o This is the most obtained x-ray study because it can indicate so much information about the heart, lungs, bony thorax, mediastinum, and great vessels. § Tumors, inflammation, fluid accumulation, air accumulation, heart size, calcifications, infection in lungs o Standard is two view PA and lateral chest XR · Contraindication: o Patients who are pregnant, unless the benefits outweigh the risk of radiation exposure to the fetus · Interpretations: o Views: § For a posteroanterior (PA) view (projection) the x-rays pass through the back of the body (posterior) to the front (anterior). § For an anteroposterior view, the x-rays pass through the body from front to back. For a lateral view, the x-rays enter from the side. § For oblique views, x-rays pass through the body at various angles. § Lordotic views, obtained with the patient recumbent, provide visualization of the apices (rounded upper portions) of the lungs and are usually used to detect tuberculosis. § Decubitus films are obtained with the patient in the recumbent lateral position, to demonstrate and localize fluid, which becomes dependent in the pleural space (pleural effusion). o Lung tumors (primary or metastatic): These are evident as soft-tissue masses in the lung fields. o Pneumonia: Increased opacity (lightness) in the lung field indicates pneumonia or atelectatic lung tissue. o Pulmonary edema: Increased opacity of the lung is indicative of pulmonary edema, most commonly from congestive heart failure. o Pleural effusion: Fluid in the chest wall is evident as increased opacity outside the lung fields; in particular, in the costophrenic margins. A lateral decubitus film will show layering out of free pleural fluid. Entrapped fluid, however, will not layer out. o Chronic obstructive pulmonary disease: Increased lung space is classic for COPD. o Pneumothorax: Air outside the lung space (pneumothorax) is always abnormal. If large enough, chest tube insertion is required to release the trapped air and re-expand the lung. o Atelectasis: Collapse of pulmonary alveoli is evident as white patches or lines in the lung fields. o Tuberculosis (TB): Usually in the upper lobes, chronic TB is generally associated with calcification. o Lung abscess: Lung abscess is evident as a lung mass with a hollow (radiolucent) center. Sometimes, fungus can grow inside an abscess. o Congenital lung diseases (hypoplasia): Congenital aplasia or hypoplasia of the lung tissue is evident by reduced lung tissue on the affected side. o Pleuritis: A thickened pleura indicates pleuritis, which is caused by a viral, bacterial, neoplastic, or other cause. o Foreign body in the chest, bronchus, or esophagus: Swallowed, aspirated, or penetrating (bullets) foreign bodies can be easily seen. · Complications: o Bedside radiography: most common in ED/ICU in critical patients. Images are lower quality, cost more § AP projection and slightly lordotic angulation of XR beam distort basal lung structures o Conditions (eg, severe pain or shortness of breath because of COPD) that prevent the patient from taking and holding a deep breath o Scarring from previous lung surgery (makes interpretation difficult) o Obesity (requires more x-rays to penetrate the body to provide a readable x-ray film) o Pacemaker, jewelry, body piercing, or undergarments/articles of clothing with metallic components can obstruct identification of radiographic findings. · Cost-effectiveness: cheaper, a few hundred

Ventilation/perfusion lung scan (V/Q scan)

· Used in people who have renal disease and cannot get a CT pulmonary angiography · Nuclear medicine scan that uses radioactive material to examine airflow (ventilation) and blood flow (perfusion) in the lungs to look for evidence pulmonary embolism (PE)

Bronchophony

(Consolidated airless lung) a. Ask the patient to say "ninety-nine." Normally the sounds transmitted through the chest wall are muffled and indistinct. b. Louder voice sounds are called bronchophony

Whispered pectoriloquy

(Consolidated airless lung) a. Ask the patient to whisper "ninety-nine" or "one-two-three." The whispered voice is normally heard faintly and indistinctly, if at all. b. Louder, clearer whispered sounds are called whispered pectoriloquy.

Egophony

(Normal air filled lung) a. Ask the patient to say "ee." You will normally hear a muffled long E sound. b. If "ee" sounds like "A" and has a nasal bleating quality, an E-to-A change, or egophony, is present.

a technically adequate chest radiograph

- Two views - Right patient, right study, right date - Be able to see all of what you are trying to see - Proper inspiration if necessary - count the number of ribs seen, should see 10 ribs (8-9 for hospitalized pts) - Penetration - able to see the thoracic spine through the heart shadow in an AP film, overpenetration (too dark), under penetration (too bright) - Rotation - position of the medial ends of each clavicle relative to spinous processes - Magnification - the closer an object is to the surface on which it is being imaged, heart appears larger on AP view - Angulation - looking for a completely horizontal picture, avoid apical lordotic view - Understand what view you are looking at

Drug Induced Lung Disease

Common causes- chemo, biologics, immunotherapies, amiodarone, nitrofurantoin o MTX, sulfasalazine, NSAIDs • MTX-induced pneumonitis- CXR show diffuse, b/l reticular opacities or mixed reticular and ground glass patterns. • TNF-alpha inhibitors- associated with incr risk of reactivation of TB and granulomatous lung disease/hilar adenopathy • Pneumonitis- • Tx- withdrawal of offending agents o Steroids, usually short term if more severe

normal and abnormal lung markings seen on x-ray

A - Airway B- Bone C- Cardiac D-Diaphragm E&F - equal (lung) fields G - Gastric bubble H - hilum (and mediastinum)

Thoracic kyphoscoliosis

Abnormal spinal curvatures and vertebral rotation deform the chest. Distortion of the underlying lungs may make interpretation of lung findings very difficult.

Traumatic flail chest

Multiple rib fractures may result in paradoxical movements of the thorax. As descent of the diaphragm decreases intrathoracic pressure, on inspiration, the injured area caves inward; on expiration, it moves outward.

Arterial Blood Gas: O2 Saturation

Alpha-1 antitrypsin Test

Indication: Serum alpha1-antitrypsin (AAT) determinations are obtained in patients with a family history of emphysema, because there is a familial tendency for a deficiency of this antienzyme Interpretation: Normal: 85-213 mg/dL or 0.85-2.13 g/L Increase: Acute and chronic inflammatory disorders, Stress, Infection, Thyroid infections Decrease: Early onset of emphysema (adults), Neonatal respiratory distress syndrome, Cirrhosis (children)

Arterial Blood Gas: O2 Content

ABG interpretation

Evaluate the pH: · If the pH is less than 7.4, acidosis is present. · If the pH is greater than 7.4, alkalosis is present. Next look at the PCO2: · If the PCO2 is high in a patient who has been said to have acidosis (by step 1), the patient has respiratory acidosis. · If the PCO2 is low in a patient who has been said to have acidosis (by step 1), the patient has metabolic acidosis (MA) and is compensating for that situation by blowing off CO2. · If the PCO2 is low in a patient who has been said to have alkalosis (by step 1), the patient has respiratory alkalosis. · If the PCO2 is high in a patient who has been said to have alkalosis (by step 1), the patient has metabolic alkalosis and is compensating for that situation by retaining CO2. Next look at the bicarbonate ion (HCO3-). · In patient 2A, HCO3- can be expected to be high in an attempt to compensate for the respiratory acidosis. · In patient 2B, HCO3- can be expected to be low as a reflection of the MA. · In patient 2C, HCO3- can be expected to be low to compensate for the respiratory alkalosis. · In patient 2D, HCO3- can be expected to be high as a reflection of the metabolic alkalosis.

Pulmonary function testing

Indication: 1. Preoperative evaluation of the lungs and pulmonary reserve. 2. Evaluation of response to bronchodilator therapy. 3. Differentiation between restrictive and obstructive forms of chronic pulmonary disease. 4. Determination of the diffusing capacity of the lungs (DL ). 5. Performance of inhalation tests in patients with inhalation allergies. Interpretation: Normal: Vary with patient age, sex, height, and weight

Arterial Blood Gas: HCO3-

Arterial Blood Gas: PCO2

Arterial Blood Gas: pH

Arterial Blood Gas: Base Excess

Arterial Blood Gas: Alveolar to Arterial O2 Difference

Arterial Blood Gas: PO2 (Arterial)

Indication: Measurement of arterial blood gasses (ABGs) provides valuable information in assessing and managing a patient's respiratory (ventilation) and metabolic (renal) acid-base and electrolyte homeostasis. It is also used to assess the adequacy of oxygenation. Interpretation: Critical: <40 Normal: 80-100 mm Hg The PO2 level is decreased in: -patients who are unable to oxygenate the arterial blood because of O2 diffusion difficulties (eg, pneumonia, shock lung, congestive failure) -patients in whom venous blood mixes prematurely with arterial blood (eg, congenital heart disease) -patients who have underventilated and overperfused pulmonary alveoli (pickwickian syndrome; ie, obese patients who cannot breathe properly when in the supine position or in patients with significant atelectasis). PO2 is one of the measures used to determine the effectiveness of O2 therapy.

Tuberculin skin testing

Indication: These tests are used to diagnose active TB infection in patients recently exposed to or suspected to have TB infection. Interpretation: positive: induration greater than or equal to 15 mm

Legionnaires Disease antibody

Indication: This test is indicated in patients suspected to have Legionnaires disease and who have negative cultures and smears identifying Legionella. Fulminating pneumonia caused by Legionella pneumophila, a tiny, gram-negative, rod-shaped bacterium Interpretation: Normal: No Legionella antibody titer

Carboxyhemoglobin Test

Indication: This test is used to detect CO poisoning. This test can also be used to evaluate patients with complaints of headache, irritability, nausea, vomiting, and vertigo, who may have been unknowingly exposed to CO. Its greatest use, however, is in patients exposed to smoke inhalation, exhaust fumes, and fires. Interpretation: Critical value: >30% Normal: Nonsmoker: <3% saturation of total hemoglobin Light smoker: 2%-5% Heavy smoker: 5%-10%

Thoracentesis and pleural fluid analysis, including differentiation between transudate and exudate

Indication: Thoracentesis is performed to determine the cause of an unexplained pleural effusion. It is also performed to relieve the intrathoracic pressure that accumulates with a large volume of fluid and inhibits respiration. Interpretation: Normal: Gross appearance: clear, serous, light yellow, 50 mL RBCs: none WBCs: <300/mL Protein: <4.1 g/dL Glucose: 70-100 mg/dL Amylase: 138-404 units/L Alkaline phosphatase: Adult male: 90-240 units/L Female <45 years: 76-196 units/L Female >45 years: 87-250 units/L Lactic dehydrogenase (LDH): similar to serum LDH Cytology: no malignant cells Bacteria/Fungi: None Carcinoembryonic antigen (CEA): <5 ng/mL

Angiotensin-converting enzyme Test

Indication: ACE is used to detect and monitor the clinical course of sarcoidosis (a granulomatous disease that affects many organs, especially the lungs). Furthermore, it is used to differentiate between sarcoidosis and other granulomatous diseases. It is also used to differentiate active and dormant sarcoid disease. Interpretation: Normal: 8-53 U/L Increase: Sarcoidosis

Bronchoscopy

Indication: Bronchoscopy permits endoscopic visualization of the larynx, trachea, and bronchi by either a flexible fiberoptic bronchoscope or a rigid bronchoscope. Reasons for these procedures are described below. Interpretation: Normal: Normal larynx, trachea, bronchi, and alveoli

Cystic fibrosis genetic testing

Indication: Genetic testing is used to identify a predisposition to disease, establish the presence of a disease, establish or refute paternity, or to provide forensic evidence used in criminal investigations. Cystic fibrosis (CF) is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Interpretation:Normal: no mutation A mutation in this gene alters the cell's capability to regulate the chloride (and therefore sodium) transport. As a result, the lungs and digestive tract of CF patients fill with thick mucus. As bacteria invade their mucus-filled lungs, CF patients experience frequent lung infection. As mucus blocks the pancreas, inefficient digestion results.

Polysomnography (sleep study)

Indication: Sleep studies are indicated in any person who snores excessively; experiences narcolepsy, excessive daytime sleeping, or insomnia; or has motor spasms while sleeping; and in patients with documented cardiac rhythm disturbances limited to sleep time. Interpretation: Normal: Respiratory disturbance index (RDI): fewer than five episodes of apnea per hour Normal progress through sleep stages No interruption in nasal or oral airflow End tidal CO2: 30-45 mm Hg Oximetry: ≥90%; no oxygen desaturation of >5% Minimal snoring sounds EKG: no disturbances in rate or rhythm No evidence of restlessness No apnea MSLT: onset of sleep >9 minutes

Carbon dioxide test

Indication: The CO2 content is a measure of CO2 in the blood. In the peripheral venous blood this is used to assist in evaluating the pH status of the patient and to assist in evaluation of electrolytes. Interpretation: Critical values: <10 mEq/L or >40 mEq/L Normal: 23-30 mEq/L or 23-30 mmol/L

Peak flow meter

Indication: measure how air flows from your lungs in one "fast blast." In other words, the meter measures your ability to push air out of your lungs. Interpretation: Normal: 400 and 700 litres per minute 80 to 100 percent of your usual or "normal" peak flow rate signals all clear. A reading in this zone means that your asthma is under reasonably good control. 50 to 80 percent of your usual or "normal" peak flow rate signals caution. It is a time for decisions. Your airways are narrowing and may require extra treatment. Less than 50 percent of your usual or "normal" peak flow rate signals a Medical Alert. Immediate decisions and actions need to be taken. Severe airway

Pulse oximetry

Indication:Oximetry is used to monitor arterial O2 saturation levels (SaO2) in patients at risk for hypoxemia. This includes patients who are undergoing surgery, cardiac stress testing, mechanical ventilation, heavy sedation, or lung function testing, or who have multiple trauma. It is also used as an indicator of partial pressure of oxygen (Po2) in patients who may experience hypoventilation, sleep apnea, or dyspnea. This test is commonly used to titrate O2 levels in hospitalized patients. Interpretation: Normal: >95% Critical value: <75%

Sputum culture

Indication:Sputum culture is indicated in any patient with a persistent productive cough, fever, hemoptysis, or a chest x-ray picture compatible with a pulmonary infection. This test is used to diagnose pneumonia, bronchiectasis, bronchitis, or pulmonary abscess. Bacterium, fungus, or virus can be cultured. Interpretation: Normal: Normal upper respiratory tract

D dimer

Indication:The D-dimer test is used to identify intravascular clotting Interpretation: Normal: <0.4 mcg/mL positive/elevated: significant formation and breakdown of blood clot in your body

Lung cancer screening

LD chest CT for high-risk pts o Early detection, increased cure rate, less invasive surgical interventions with better outcomes, fewer stage IV CA (70% stage I or II 🡪 better prognosis/survival rate) o Harms of screening- detection of benign modules and work up—96% false positives with increased radiation exposure, anxiety o Research may suggest screening every 2.5 yrs? o 30 PYH or quit within 15 yrs, cancer hx or risk 🡪 screening recommended

Funnel chest (pectus excavatum)

Note depression in the lower portion of the sternum. Compression of the heart and great vessels may cause murmurs.

TMN Staging

T = tumor ▪ TX = unable to assess—presence in washings/sputum but not visualized ▪ T0 = no evidence of primary tumor ▪ T1 = no local tissue invasion (Tis) • < 3 cm - lung visceral pleura—no invasion ▪ T2 = any of the following • > 3 cm but < 5 cm in greatest dimension • Involves main bronchus, regardless of distance to carina • Associated with atelectasis or obstructive pneumonitis that extends to hilum but does not involve the entire lung ▪ T3= > 5 cm but < 7 cm; invades chest wall, parietal pleura and phrenic nerve ▪ T4 = > 7 cm • Separate tumor in a different ipsilateral lobe that invades mediastinum, heart, great vessels, trachea, esophagus, vertebral body, carina o N = regional lymph nodes ▪ NX- nodes cannot be assessed ▪ N0- no regional node metastasis ▪ N1- METS in ipsilateral peribronchial and/or hilar nodes ▪ N2- METS in ipsilateral mediastinal and/or subcarinal nodes ▪N3- METS in contralateral mediastinal hilar nodes, ipsilateral/contralateral scalene or supraclavicular nodes o M = distant metastases—brain, adrenal, bone (frequently sx), liver most common ▪ MX- distant METS cannot be assessed ▪ M0- no distant METS ▪ M1- distant METS present • 1a- separate tumor in contralateral lobe; tumor with pleural or pericardial nodule or malignant effusion • 1b- single extrathoracic METS • 1c- multiple extrathoracic METS, one or more organs

Interstitial Lung Disease (ILD)

TAKE HOME: · ILD is a disease of the lung connective tissue · There are MANY causes, endogenous and exogenous · Sometimes it is idiopathic, IPF is the most common · Progressive Fibrosing ILD is treated with antifibrotics · Inflammatory ILD is treated with immunosuppression · Pathophysiology: o Interstitium: The tissue compartment in the lung sandwiched between the epithelial and endothelial basement membranes. o When the normally thin interstitium is altered, damaged, or destroyed by inflammation, hyperplasia, scar formation (fibrosis), necrosis, etc. o Can also involve the epithelium, endothelium, and alveolus, thus Diffuse Parenchymal Lung Disease (DPLD) is a more accurate description. o Connective tissue diseases associated: § Scleroderma, RA (UIP > NSIP), MCTD, Polymyositis/Dermatomyositis, Sjogren's, Typically NOT Lupus

PERC Rule for PE

The PERC rule can be applied to patients where the diagnosis of PE is being considered, but the patient is deemed low-risk. Age ≥50? If yes, +1 HR ≥100? If yes, +1 O₂ sat on room air <95%? If yes, +1 Unilateral leg swelling? If yes, +1 Hemoptysis? If yes, +1 Recent surgery or trauma? (Surgery or trauma ≤4 weeks ago requiring treatment with general anesthesia) If yes, +1 Prior PE or DVT? If yes, +1 Hormone use? (Oral contraceptives, hormone replacement or estrogenic hormones use in males or female patients) If yes, +1 Follow up with D-dimer - If positive --> CTA - If negative --> Stop Workup A PERC evaluation is considered positive if any one of the eight criteria are met.

Well's Criteria for PE

The Wells' Criteria risk stratifies patients for pulmonary embolism (PE) and provides an estimated pre-test probability. The physician can then chose what further testing is required for diagnosing pulmonary embolism (I.E. d-dimer or CT angiogram). Clinical signs and symptoms of DVT? If yes, +3 PE is #1 diagnosis OR equally likely? If yes +3 Heart rate > 100? If yes +1.5 Immobilization at least 3 days OR surgery in the previous 4 weeks? If yes+1.5 Previous, objectively diagnosed PE or DVT? If yes +1.5 Hemoptysis? If yes+1 Malignancy w/ treatment within 6 months or palliative? If yes +1 · Low risk < 2 --> Move on to PERC rule · Moderate risk (2-6) --> Get D-dimer; If positive, get a CTA --> If negative, stop work-up · High risk > 6 --> Get a CTA

Normal Chest Wall

The lateral diameter of the thorax in the normal adult is greater than its AP diameter. The ratio of its AP diameter to the lateral diameter is normally ∼0.7 up to 0.9 and increases with aging

Pigeon chest

The sternum is displaced anteriorly, increasing the AP diameter. The costal cartilages adjacent to the protruding sternum are depressed

Barrel chest

There is an increased AP diameter. This shape is normal during infancy, and often accompanies aging and chronic obstructive pulmonary disease

Alpha 1 antitrypsin

a genetic disorder that leads to panacinar emphysema, hepatomegaly, cirrhosis • " is a clinically under-recognized inherited disorder affecting the lungs, liver, and rarely, skin" (UTD) • 1 in 2,500 individuals—most often whites of European ancestry • SXS: manifestations of COPD, skin; panniculitis (unopposed enzyme action and protein breakdown within the skin.) • A1ATD-associated lung disease predominately occurs in adults and is caused principally by inadequate protease inhibition

Resonance

a) Relative intensity: Loud b) Relative Pitch: Low c) Relative duration: Long d) Example of location: Healthy lung e) Pathologic examples: simple chronic bronchitis

Pleural rub

a. A pleural rub is a discontinuous, low-frequency, grating sound that arises from inflammation and roughening of the visceral pleura as it slides against the parietal pleura. b. This nonmusical sound is biphasic, heard during inspiration and expiration, and often best heard in the axilla and base of the lungs

Crackles/rales

a. Crackles are discontinuous nonmusical sounds that can be early inspiratory (as in COPD), late inspiratory (as in pulmonary fibrosis), or biphasic (as in pneumonia). b. They are currently considered to result from a series of tiny explosions when small distal airways, deflated during expiration, pop open during inspiration. c. With few exceptions, recent acoustic studies indicate that the role of secretions as a cause of crackles is less likely

Rhonchi

a. considered by some to be a variant of wheezes, arising from the same mechanism, but lower in pitch. b. Unlike wheezes, rhonchi may disappear with coughing, so secretions may be involved

Wheezes

a. continuous musical sounds that occur during rapid airflow when bronchial airways are narrowed almost to the point of closure. b. Wheezes can be inspiratory, expiratory, or biphasic. c. They may be localized, due to a foreign body, mucous plug, or tumor, or heard throughout the lung. d. Although wheezes are typical of asthma, they can occur in a number of pulmonary diseases. e. Recent studies suggest that as the airways become more narrowed, wheezes become less audible, culminating finally in "the silent chest" of severe asthma requiring immediate intervention.

Stridor

a. continuous, high-frequency, high-pitched musical sound produced during airflow through a narrowing in the upper respiratory tract. b. Stridor is best heard over the neck during inspiration but can be biphasic. c. Causes of the underlying airway obstruction include tracheal stenosis from intubation, airway edema after device removal, epiglottitis, foreign body, and anaphylaxis. Immediate intervention is warranted.

Tactile fremitus

i. Fremitus refers to the palpable vibrations that are transmitted through the bronchopulmonary tree to the chest wall as the patient is speaking and is normally symmetric ii. Decreased or absent when the voice is higher pitched or soft or when the transmission of vibrations from the larynx to the surface of the chest is impeded by a thick chest wall, an obstructed bronchus, COPD, pleural effusion, fibrosis, air (pneumothorax), or an infiltrating tumor. i. Normal air filled lung: normal ii. Consolidated airless lung (lobar pneumonia): increase

Coarse Crackles

i. appear in early inspiration and last throughout expiration (biphasic), have a popping sound, are heard over any lung region, and do not vary with body position. ii. They have a longer duration and lower frequency than fine crackles, change or disappear with coughing, and are transmitted to the mouth. iii. Coarse crackles appear to result from "boluses of gas passing through airways as they open and close intermittently" iv. Examples include COPD, asthma, bronchiectasis, pneumonia (crackles may become finer and change from mid to late inspiratory during recovery), and heart failure.

Fine Crackles

i. softer, higher pitched, and more frequent per breath than coarse crackles. ii. They are heard from mid to late inspiration, especially in the dependent areas of the lung, and change according to body position. iii. They have a shorter duration and higher frequency than coarse crackles. iv. Fine crackles appear to be generated by the "sudden inspiratory opening of small airways held closed by surface forces during the previous expiration. v. Examples include pulmonary fibrosis (known for "Velcro rales") and interstitial lung diseases such as interstitial fibrosis and interstitial pneumonitis.

External respiration

refers to the processes that are involved in the diffusion between the lungs and pulmonary circulation, including the mechanical events that are involved to make that happen.

CHEMICAL TOXINS

may be inhaled or d/t gas vapor, includes smoke, carbon monoxide, can be d/t plastics

Allergies: Type I

o Allergic o Anaphylactic, immediate type hypersensitivity (IgE mediated) § IgE binds to antigen; mast cell and basophil activation results in allergic rxn (via T helper cells) § increase in vascular permeability, smooth muscle contraction, chemotactic activation of inflammatory cells o Clinical features: anaphylaxis, angioedema, bronchospasm, uticaria, pruritis, watery nasal discharge, mucous secretions, erythema, NVD, itching/tingling lips o Ex: bee stings, latex, certain medications (PCN) o Treatment: § epinephrine, O2/ventilator, vasopressors (dopamine), antihistamines, aminophylline to antagonize adenosine Rs, smooth muscle relaxation, glucocorticoids

Klebsiella pneumonia

o Aspiration pneumonia: ETOH, loss of gag reflex o Gram-neg bacilli o Virulence: Capsule, Endotoxin, Tissue damage o Necrosis & Scarring Even after infection cleared o Serious danger to older hospitalized patients, Mortality ~ 40% o Increasing concern re: trends in resistance Beta-lactamase (cephalosporin, carbapenem)

CO2

o CO2 is carried in the blood three different ways: § dissolved in the water of the RBC and plasma (7%) § bound to hemoglobin at a different site than O2 (23%) § in the plasma as the bicarbonate ion (HCO3-) o CO2 bound directly to Hb is called carbamino Hb because CO2 binds to free amino groups on each heme group o CO2 and water bind to form carbonic acid (remember that an acid is a substance that liberates H+ (a proton)) § in RBCs, this reaction is accelerated 5000 times by the enzyme carbonic anhydrase § Hydrogen ions in red blood cells then bind to hemoglobin, which buffers the acid - § Bicarbonate ions move quickly from the RBC into the plasma § There is a 1:1 exchange of bicarbonate ions with Cl-; called the chloride shift. § These reactions reverse in the lungs with CO2 unloading.

Tobacco Abuse/Smoking Cessation

o COPD and Cancer causers • Tobacco- nicotine, carcinogens, 4,000 substances, tar; smokeless tobacco also high risk • Cigars and pipes- 2 cigars per day = 8x risk of oral cancer, 4x risk of esophageal cancer (lower risk of lung cancer, heart disease, COPD compared to cigarettes) • Addiction—nicotine causes dependence, possible genetic role, physical and psychological dependence, most reducible risk factor for cardiovascular disease and cancer • Epidemiology- smoking rates: 28% men, 25% women, 38% HS seniors, 80% start by age 18 • Effects of tobacco o GENERAL- 1/5 premature deaths are d/t tobacco (shortens life expectancy by 10 years), 40% of smokers die prematurely unless able to quit, life expectancy increases 3-5 years if smoking is stopped by age 35 o CARDIO- increase in thrombus production, plaque instability, increase in MI, increase death rates, angina, stroked, PVD (90% of cases) ▪ 15 years after quitting, risk similar to non-smoker o LUNG- COPD/emphysema (90% of cases involve tobacco), chronic cough, spontaneous pneumothorax, bronchiolitis (interstitial lung disease including fibrosis, eosinophilic granuloma, pulmonary hemorrhage, desquamative interstitial pneumonia) 90% cases; most common lung cancer seen in non-smokers is adenocarcinoma o CANCER- 90% of lung ca pts are/were smokers; 13x increase in cancer in smokers than in non-smokers; 20+ cancers have been directly linked w/ smoking/tobacco ▪ Bladder ca—2 to 4x increase risk; 50% men, 40% women; breast, cervical, colorectal, esophageal (squamous), head and neck ▪ Myeloid leukemia, pancreatic cancer, renal cell cancer, uterine cancer REDUCED in tobacco use o Other complications- polycythemia, PUD, osteoporosis, cataracts, macular degeneration, wrinkling of skin, gallstones, impotence, decreased fertility o Pregnancy- premature rupture of membranes, placenta previa, abruptio placentae, preterm delivery ▪ Post-pregnancy 🡪 lower birth weights, reduced post-natal pulmonary function, increase in SIDS o IBD—risk of ulcerative colitis is 40% of that of non-smokers; 2x increase risk of Crohn's o Surgery- 1.5-4x increase complications o Second-hand smoke 🡪 1.5x increase in lung CA • Tx- tobacco history important—90% of people don't use programs o Pack years- number of years smoking x packs per day o 1) pre-contemplation 2) contemplation 3) determination 4) action 5) maintenance o Quit cold turkey- advantage- cost and success rates. Disadvantages—nicotine withdrawal, weight gain. o Pharm- nicotine replacement, anti-depressants, nicotine receptor blockers ▪ Nicotine replacement- deliver 25-40% levels of smoking • Lozenge- similar to gum, Nicorette; patch- 2x quit rates; spray; inhaler ▪ Antidepressants- Buproprion/Wellbutrin o Non-pharm- counseling, support groups; behavioral therapy—avoid triggers • Cessation- 1/3 smokers try to quit each year; 70-80% of smokers want to quit; 20-25% successfully quit each year but resumption is common o ASK about tobacco every visit o ADVISE smokers to quit o ASSESS readiness to quit o ASSIST smokers in quitting o ARRANGE follow up • Problems with quitting- cough, weight gain, withdrawal, cost. Counseling important for success

Hemophilus influenzae

o Causes secondary bacterial infection following URTI § Used to be a primary pathogen of children prior to hib vaccination § Consider in adults with underlying lung disorders, the elderly and immunosuppressed o Gram-neg coccobacillus o Anaerobic and Aerobic Growth § Aerobics Needs X and V Factors § Culture media needs to provide o Transmission by Droplets & Fomites o Virulence factors: Capsule (Except non-typical which has no capsule, Non-typical - CAP in Adults), Beta-lactamase (Breaks Beta-lactam ring of certain antibiotics), Endotoxin (LPS), IgA protease

Chemoreceptors

o Central: primary chemoreceptors in the central nervous system are near the surface of ventrolateral regions of the medulla that are associated with the arcuate nucleus § Measure pH § Lower pH = acidic = more CO2 = more ventilation to remove CO2 § Higher pH = basic = less CO2 = less ventilation to keep CO2 o Peripheral: located in the bifurcations of the carotid arteries (carotid bodies) and the aortic arch (aortic bodies) § Measure oxygen § Less oxygen = more ventilation § 12 breaths/minute

Allergies: Type II

o Cytotoxic o Cytotoxic reaction to antibody, antibody-mediated (IgG or IgM) § Antibody binds to antigen without complement § Result is cellular lysis/tissue injury o Clinical features: hemolytic anemia, interstitial nephritis o Ex: hemolytic reactions, Goodpasture Syndrome

Allergies: Type IV

o Delayed o Delayed or T cell mediated § An inflammatory response due to leukocytes § Cell mediated rather than being due to antibody o Clinical features: contact dermatitis o Ex: PPD test, poison ivy

DLCO/VA Test

o Diffusing capacity of the lungs is measured with a nontoxic mixture of carbon monoxide (CO) and helium (He) o CO diffuses rapidly through healthy membranes and is rapidly taken up by hemoglobin. § The concentrations are not high enough to block oxygenation of hemoglobin but high enough to be measured in expired air. § If diffusion barrier is normal DLCO, will be normal § If diffusion barrier is impaired DLCO will be reduced § Will not equilibrate in alveoli o Helium is used to measure TLC. It is inert and does not leave the alveoli. § This method looks at the concentration of an inert gas that does not cross the alveolar membrane. § First the gas concentration and volume of the bell of the spirometer are measured (C1 and V1). § Then the subject breaths from the bell until the gases in the lung and bell equilibrate. § The gas concentration (C2) will diminish proportionally to the difference in volume (V1 + V2, where V2 is the volume of the lungs and airways). § So, the lung volume (TLC) can now be calculated : C1 x V1 = C2 x (V1 + V2). o Increased: Active smoking (carboxyhemoglobin falsely elevates the DLCO), Polycythemia, Pulmonary hemorrhage, Left-to-right intracardiac shunt o Decreased: Poor inspiratory effort, Low lung volumes (restrictive defect), Abnormal vasculature (pulmonary hypertension), Missing lung units (emphysema), Thickened interstitium (ILD), Anemia o Reduction categories § Normal: 80-100% predicted § Mild: 60—80 % predicted § Moderate: 40-60% predicted § Severe: <40 % predicted

Dynamic airway compression

o During forced expiration, § initially the pressure pushes the air out of the lungs, · but then it compresses the airways, o limiting the outflow of air § leads to wheezing o when the pressure surrounding the airway exceeds the pressure within the airway lumen. o pressure within the airways is subatmospheric and the airways are surrounded by atmospheric pressure.

Dead air space

o During inspiration, the last gas into the lungs is trapped in the dead spaces and is not influenced by gas exchange in the alveoli o Therefore, the first gas out during expiration is similar to atmospheric gas, with high O2 content and low CO2 content o The last gas expired during expiration has lower O2 content and higher CO2 content, because it reflects the gas exchange in the alveoli

Pleural pressure

o Elastic pressures (Pel) are inward forces due to the elastic tissues (elastin, collagen) of the lung and the surface tension in the alveoli o These are counteracted by the outward forces of the chest wall (Pcw) o a suction in the pleural space (Ppl) because of the tight seals of the pleural membranes o End of expiration: § Chest wall and lung recoil pressures are in balance § PA = Pb = 0 cm H2O. Ppl = -5 cm H2O. o Inspiration: § Inspiration begins (diaphragm contracts) § lung recoil pressures increase · causing Ppl to decrease; o PA decreases so that PA < Pb (difference is -1 cm H20) § and air moves into the lungs . o End of inspiration § lungs are expanded and no longer moving outward § Ppl = -8 cm H2O and PA = Pb = 0 cm H2O o Expiration: § inward elastic recoil pressures dominate creating an inward pull and positive PA (PA > Pb) § air flows out of the lungs.

Staphylococcus aureus

o Especially common after influenza (Influenza virus markedly reduces tracheal mucus velocity ) o Gram-positive cocci in clusters o Virulence: Exotoxins, Beta-lactamase, Coagulase (thrombin coat), Protein A (binding), Some with mutant penicillin-binding proteins (MRSA)

Pseudomonas aeruginosa

o Gram negative aerobic bacillus o Commonly found in the environment - especially WATER o Virulence factors: LPS endotoxin, Exotoxins (A, S, U, elastase, alkaline protease, etc) o Drug resistance factors: Amp C Beta lactamase, Forms a biofilm o Common pathogen in VAP/HAP - most common gram (-) pathogen, Cystic fibrosis and Immunocompromised patients o Outbreaks seen in healthcare settings with unclean or faulty medical equipment, environmental reservoirs, cross contamination o Sx: Cough producing a purulent sputum, SOB, Fever, Chills , Confusion, Severe systemic toxicity (common), Onset sudden or gradual o Culture, x-ray,

Allergies Medications

o Histamine 1 and 2 blockers, non-sedating histamines o Nasal corticosteroids, ipratropium o Leukotriene receptor antagonists o Other decongestants, systemic corticosteroids, cromolyn o Allergy shots/desensitization

Allergies: Type V

o Idiopathic o SJS

Allergies: Type III

o Immune complex deposition o Immune complex/IgG/IgM mediated § if antibodies (immune complexes) not cleared by reticuloendothelial system § can deposit in tissues: blood vessels, tissues (kidneys) o Clinical features: serum sickness (flu-like sx), self-limiting o Ex: hypersensitivity pneumonitis, SLE, PAN

Oxygen Content and Oxygen Saturation

o It is important to distinguish between oxygen saturation and oxygen content o Saturation: § The % saturation of oxygen is a relative measurement and is the same regardless of the hemoglobin content of the blood § The % saturation of oxygen is dependent on the partial pressure of oxygen (PO2) o Content: § oxygen content is a calculation of the specific amount of oxygen that is carried by hemoglobin § is dependent on the specific amount of hemoglobin in the blood

Anaphylaxis

o Life-threatening, immediate reaction (seconds to minutes) o Due to histamine, leukotrienes, and prostaglandin D2 o Signs/Symptoms: o Respiratory distress (laryngeal edema/stridor, bronchospasm) o Vascular collapse/shock o Pruritis o N/V/D o Clinical diagnosis: ↑expiratory phase and STRIDOR o Treatment: o Epinephrine (EpiPen) o O2/ventilator if needed o IV fluids o Vasopressors if needed (dopamine) o Antihistamines o Aminophylline (smooth muscle relaxant, not used much) o Glucocorticoids

Ventilation

o Minute ventilation: amount of air that is breathed each minute § at rest, the average f is 12 breaths a minute; resting average VT (tidal volume) is 500 ml o Alveolar ventilation: volume of fresh or new air that goes into the alveoli each minute § calculated by subtracting out the dead air (dead air volume is VD; average 150 ml) from VT

Host defenses

o Nasal hairs filter particles > 10 microns o "Speed bumps": Nasal turbinates, Branching bronchi o Blocking mechanism: Epiglottic reflex, Cough o Normal FloraL Relatively constant, Binding sites occupied o Epithelial cells: Cilia (mucociliary escalator), Mucous (lysozyme, IgA antibodies)

Partial pressure of gases

o Partial pressure of a gas = the fraction of the gas in the air x barometric pressure (Pb) o Pb is approximately 760 mm Hg at sea level and less as the elevation of the location increases above sea level o In the airways, the gases are slightly diluted by water vapor, a value that is consistently 47 mm Hg, regardless of Pb § Thus, the partial Pressure of a gas in the lungs is calculated by first subtracting out the partial pressure of water vapor (47 mm Hg) from Pb o the PO2 (partial pressure of O2) is reduced by water vapor § In the alveolus, oxygen moves into the blood and CO2 moves out from the blood, so PO2 drops and PCO2 increases § In expired air, PO2 increases again and the PCO2 drops again, because the first air out is humidified atmospheric air in the anatomical dead space that mixes with the alveolar air.

Pulmonary nodules

o Pathophysiology: o Nodule = a single small round or oval, well-circumscribed <3cm (if >3cm mass) o Distinct margins, may have calcification, satellite lesions, central cavitation o 60% benign, 40% malignant, >75% of these are primary lung CA o 25% bronchogenic CA presents as SPN with >50% 5 yr survival o Epidemiology/Risks: o granulomatous infx (TB), tumors (benign or malignant), inflammation (RA, sarcoidosis), mediastinal tumors (thymoma) o Symptoms/PE: o asymptomatic mostly o rare: Hemoptysis, Cough, Clubbing, Endocrinopathy o Benign: Pt is young, Asymptomatic, <2 cm in diameter, Smooth margins on CT, Calcified o Malignant: Pt is >45 y/o, Symptomatic , >2 cm in diameter, Indistinct margins - spiculation, Eccentric or stippled calcification is indeterminate o Metastatic: Smooth / lobulated margins, Located peripherally, Tends to occur in lower lobe, Absence of satellite lesions, Uncommon to be "solitary" o Diagnostics: o CT for nodules < 1 cm and intermediate probability for malignancy o PET scan for > 1 cm and intermediate probability o Simple labs- CBC, CMP, UA o Excision/biopsy if metastatic o malignant pulmonary nodule- symptomatic, >45 yrs old, > 2cm, indistinct margins with spiculation, eccentric/stippled calcification is indeterminate o most are asx—could rarely present with hemoptysis, cough, clubbing, endocrinopathy o metastatic node- smooth/lobulated, located peripherally, tends to occur in lower lobe, absence of satellite lesions, uncommon to be solitary o Treatment: o Benign § Watchful waiting if · < 8 mm without documented growth, 8-30 mm low risk · Documented stable x2 yrs (subsequent serial XRs), Likely benign by CT/PET · Resect if : Otherwise or > 30 mm o Malignant: surgical resection, radiation, chemo (often w/ radiation). Cure is unlikely without resection

Small Cell Lung Cancer (Oat cell, SCLC)

o Pathophysiology: o Originates centrally in bronchial neuroendocrine cells epithelium, commonly near hilum o Seen in 15-20% of bronchogenic cases o Grows rapidly and submucosally one of the most aggressive o Malignant, metastasizes early, doubling time 30 days, cells compressed into oval shape (oat cell) o Epidemiology/Risks: smoking o Symptoms/PE: o paraneoplastic syndrome like SIADH, SVC syndrome, Cushing syndrome, Lamber-Eaton syndrome o Diagnostics: o CXR: may show centrally located mass. o CT-guided biopsy o histology will show dark blue cells with rosette formation o Open biopsy to take out tissue is gold standard o sputum cytology (central but usually not sufficient), bronchoscopy (central) o transthoracic needle bx (peripheral), pleural fluid analysis o Labs- CBC, lytes, Ca, AST/ALT, alkaline phosphatase, total bilirubin, creatinine, LDH not specific but often elevated (esp in brain cancer) o Staging: o Limited stage: tumor confined to the same side of chest, supraclavicular lymph nodes or borth with a 20% 2-year-survival rate o Extensive stage: anything beyond limited stage, with a 5% 2 year-survival rate o UNTREATED OVERALL SURVIVAL: 6-18 WEEKS o Treatment: o found with metastasis, good response to chemo/radiation o high relapse rate, reoccurrence has low prognosis o NO surgery/resections

Carcinoid tumors

o Pathophysiology: o Rare neuroendocrine tumors characterized by slow growth, highly differentiated, low-grade malignant neoplasm o Tend to occur as sessile (or occasionally as pedunculated) growths in central bronchi o Typical = well differentiated, low grade o Atypical (10%): more aggressive and more likely to metastasize, differentiate with biopsy o Epidemiology/Risks: <60y/o o Symptoms/PE: often asymptomatic o hemoptysis, cough, persistent wheezing, recurrent pneumonias, carcinoid syndrome (2%) with flushing, diarrhea, tachycardia, bronchoconstriction, hypotension o Diagnostics: Bronchoscopy, CT, typical vs. atypical differentiated by bx o Treatment: o steroids for carcinoid syndrome (emergent) o surgery w/ resection is only curative tx

Bronchogenic Carcinoma

o Pathophysiology: o arising from the epithelium of the bronchus or bronchiole o Great tendency for METS to brain, bone , liver, lymph nodes, adrenals o Includes: small cell and non-small cell carcinoma o Epidemiology/Risks: 99% of lung cancers o MC cause of cancer deaths in men & women; o 40-80y; 8% males, 6% females; o 13% of all cancers, 25% of all cancer deaths o Risk: SMOKING MOST COMMON, 2nd hand smoke, toxic exposures o Symptoms/PE: o asymptomatic (incidental) o cough, hemoptysis, vague, non-pleuritic chest pain, dyspnea anorexia, wt loss, anemia o recurrent/persistent pneumonia, exudative pleural effusion, Pancoast syndrome o Diagnostics: o CXR, CT o Open biopsy to take out tissue is gold standard o sputum cytology (central but usually not sufficient) o bronchoscopy (central), transthoracic needle bx (peripheral) o pleural fluid analysis o Labs- CBC, lytes, Ca, AST/ALT, alkaline phosphatase, total bilirubin, creatinine, LDH not specific but often elevated (esp in brain cancer) o Treatment: o Extremely variable based on patient, stage, tumor profile and clinical trials o 34% survival, Prognosis 5 yr survival = Only 18%

Mesothelioma

o Pathophysiology: o malignant tumor of the pleura (80%), peritoneum (20%), or both. o Epidemiology/Risks: o A complication of asbestos exposure. o 60 y/o, occurs 20-40 years of exposure or as little as 1-2 years o Symptoms/PE: o Chest pain, dyspnea, cough, hoarseness, high sweats, dysphagia, fatigue, weight loss o DOE followed by SOB, Pleuritic chest pain o pleural effusion almost always present (unilateral dullness to percussion at lung base, asymmetric chest wall expansion during respiration), decr breath sounds o Diagnostics: o CXR: pleural thickening, exudative effusion o CT: thoracentesis of pleural effusion, closed pleural biopsy o PET scan: for staging o Pleural bx via VATS o Treatment: o None to limit progression, Drain effusions o 5-16 months survival from onset of sx; 75% dead 1 yr from dx

Large Cell Lung CA

o Pathophysiology: 15-35% o Lacks glandular or squamous differentiation o very aggressive; rapid growth, early mets, DT 100 o found peripherally or centrally o Early metastasis, Doubling time approx 100 days, Cavitation common o Epidemiology/Risks: Smokers o Symptoms/PE: o cough, hemoptysis, vague, non-pleuritic chest pain, dyspnea o anorexia, wt loss, anemia o recurrent/persistent pneumonia, exudative pleural effusion o Pancoast syndrome o Diagnostics: CT, CXR, Labs o Treatment: varies

Squamous Cell Lung CA

o Pathophysiology: 25-35% o originates in basal cells of bronchial epithelium; central (large bronchi near hilum) § frequent projects in bronchi o rapid growth, late metastasizing, DT 100d o Epidemiology/Risks: smoking o Symptoms/PE: o Hemoptysis**, Hypercalcemia o "CCCP" § CENTRALLY located and may widen mediastinum § CAVITARY lesions, § HYPERCALCEMIA § PANCOAST syndrome o Diagnostics: o more amenable to sputum examination o Biopsy—keratinization and or intracellular desmosomes o Treatment: chemo, resection

Adenocarcinoma Lung CA

o Pathophysiology: 35-40% of NSCLC o arises from mucous glands of tracheobronchial tree; peripheral o moderate growth and mets rate, DT 180d o Commonly found in lung parenchyma § Cavitation common § Associated with pleural fibrosis/scarring o Epidemiology/Risks: o common in smokers, non-smokers, females o smoking strongest risk factors o Also, silica, asbestos, radon, heavy metal exposure o Symptoms/PE: Productive cough, dyspnea, hemoptysis, weight loss o Diagnostics: gland formation, mucin production o Treatment: surgical resection

Non-Small Cell Lung CA (NSCLC)

o Pathophysiology: 80-85% o Includes Adenocarcinoma 35%, squamous cell carcinoma 20%, large cell carcinoma 10% o Epidemiology/Risks: o Adenocarcinoma: smokers/nonsmokers, female o Squamous cell: males o Symptoms/PE: o Adenocarcinoma: gynecomastia o Squamous cell: hypercalcemia o Diagnostics: o Open biopsy to take out tissue is gold standard o sputum cytology (central but usually not sufficient), bronchoscopy (central) o transthoracic needle bx (peripheral), pleural fluid analysis o Labs- CBC, lytes, Ca, AST/ALT, alkaline phosphatase, total bilirubin, creatinine, LDH not specific but often elevated (esp in brain cancer) o Treatment: o Overall, 5 yr survival is 15% o surgery, radiation, chemo

Pulmonary Langerhans Cell Histiocytosis (LCH)

o Pathophysiology: AKA eosinophilic granuloma (EG) and histiocytosis X, Limited to lungs and bone and occasionally the hypothalamus o Epidemiology/risks: Near universal association with smoking, Uncommon o Presentation: § frequently asymptomatic § may present with spontaneous pneumothorax § dyspnea, dry cough, fatigue, weight loss § often in young smokers § occasionally presents with diabetes insipidus and cystic bone lesions o Diagnostic: § Characteristic staining for S-100 protein by Langerhans cells § HRCT: Multiple cysts mid/upper lung, Interstitial thickening. Ill-defined nodules § PFTs: restrictive pattern with decreased DLCO o Prognosis - variable o Treatment: smoking cessation, steroids for progressive disease

Lymphangioleiomyomatosis (LAM)

o Pathophysiology: Interstitial smooth muscle proliferation and formation of diffuse, small cysts o Epidemiology/risks: rare ILD, Women, childbearing age o Symptoms: Spontaneous pneumothorax, Progressive dyspnea, Significant airflow limitation, Chylous pleural effusion

Acute respiratory distress syndrome

o Pathophysiology: Life-threatening acute hypoxemic respiratory failure o episode of diffuse lung injury due to any of a number of causes (toxin, sepsis, trauma, transfusion, aspiration, drug overdose, surgery, acute interstitial pneumonia) o where fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. o Epidemiology/Risks: o seen in 10% of ICU pts o risks: older age, hx alcoholism, presence of metabolic acidosis, multiple comorbidities o Symptoms/PE: o rapid onset of dyspnea (severe), hypoxemia, respiratory/multi-organ failure o 3 stages § Exudative: first 7 days, onset in 12 hours to 7 days after the event/insult · Significant alveolar edema, lung collapse/atelectasis, decreased pulmonary compliance (stiff lung), resultant increased work-load of breathing and dyspnea · Microvascular occlusion decr perfusion of ventilated lung, (pulmonary dead space) · Large WBC response § Proliferative: day 7-21 · Clinical improvement, get off ventilator, improvement in hypoxemia · Lymphocytes predominate in pulmonary infiltrates § Fibrotic: 3-4 wks up to 6 months · Long term ventilator support and O2 · Interstitial fibrosis pattern or emphysematous changes with bullae formation o Diagnostics: must exclude many differentials o CXR: pulmonary infiltrates, bilateral unexplained by pleural effusion, collapsed nodules, CHG o Hypoxia Carrico Index- measure of hypoxia calculated as PaO2 in mmHg off ABG/FIO2 § ARDS less than 200; ALI 200-300; normal person around 380 o Mod-severe oxygen impairment (severe ARDS <100mmHg) o ∅ cardiogenic pulmonary edema (PCWP <18) o Treatment: o Treat insult condition, minimize complications § Prevent thromboembolic disease, prevent GI bleed, prevent skin breakdown § Prevent nosocomial infections, ensure adequate nutrition, good ICU care, proper ventilation o Proper ventilation o ICU care for ARDS pt- § Judicious fluid management—fluid restriction helpful. Decreases LA filling pressure and pulmonary edema o Pharmacology- steroid therapy, surfactant to prevent sticky lung

Rhinovirus

o Pathophysiology: cause of URTI o More than 100 serotypes, children main reservoir o Transmission: virus is deposited on nasal mucosa after inoculation into the nose or onto the conjunctival surface o Epidemiology/Risks: 5-40 y/o, 33-50% of common colds o Symptoms/PE: o Usually afrebrile with nasal discharge, congestion, cough, sore/scratchy throat o Sx longer in children and initial fever o Diagnostics: hx o Treatment: supportive: Acetaminophen, NSAIDS, antihistamine, decongestant,

Hyaline membrane disease (Respiratory Distress Syndrome)

o Pathophysiology: deficiency of pulmonary surfactant in immature lung due to pulmonary immaturity leading to alveolar collapse o type II alveolar cells are not producing surfactant large alveoli stay inflated and small ones cannot inflate. Lungs will collapse between breaths o lungs become stiff, non-compliant and hyaline membrane forms inside the alveoli which acts as a barrier to gas exchange leading to hypoxemia and CO2 retention o Epidemiology/Risks: most common respiratory disease in premature infants o White males, infants of mothers w DM, cold exposure, c-section deliveries o Symptoms/PE: Central cyanosis, retractions, grunting with expiration, atelectasis, tachypnea, nasal flaring o Diagnostics: o Signs of respiratory distress in the first 24 hours o CXR: ↓lung volume, diffuse ground glass appearance o Treatment: o supportive care: Incubator/warmer to prevent hypothermia and to increase O2 consumption. § O2 levels assessed through A-line or transcutaneous sensor. o Exogenous surfactant therapy is used to prevent and treat RDS o Prevention: steroids if risk of delivery before 34 wks gestation

Adenovirus

o Pathophysiology: family of viruses that cause febrile illness in young children o Associated with URI but also PNA o 60 serotypes, elicity strong immune response (host defense via cell mediated immunity) o Transmission: respiratory dropless, fecal-oral, resistant to lipid disinfectants but can be inactivated by heat/bleach/formaldehyde o Epidemiology/Risks: o Cause 5-10% of all febrile illnesses in infants and young children o Prevalent in daycares/crowded settings, swimming pools o Symptoms/PE: vary with age/immunocompetence o Febrile respiratory illness 5-7 days o Pharyngitis, coryza, OM, bronchiolitis, pneumonia, conjunctivitis o Diagnostics: o Viral cx, adenovirus specific antigen assays, PCR assay o Swabs via various routes (NP, throat, conjunctival, stool/rectal) o Treatment: o Self-limiting, supportive tx o Antiviral therapy for immunocompromised/severe disease (cidofovir)

Beryllium

o Pathophysiology: rare metal with toxicity in humans—causing granulomas throughout the body—primarily in the lung o Epidemiology/Risks: o Exposure: electronics, aerospace, ceramics, tool & dye manufacturing, fluorescent light bulbs o Symptoms/PE: o cough, dypsnea, chest pain, blood-tinged sputum, crackles, weight loss, arthralgias o Acute ARDS; subacute- pneumonitis o Can get cutaneous nodules if beryllium penetrates skin o Diagnostics: Latency period 3 months to 30 years o CXR: 50% normal but can see patchy airspace disease, hilar lymphadenopathy, ↑interstitial lung markings o Hx o positive BeLPT o PFT (early stage) will likely be normal but may show mild limitation and decreased DLCO o Lung biopsy: noncaseating granulomas and/or mononuclear cell infiltrates on lung biopsy o Treatment: o limit exposure. o Corticosteroid therapy (ICS in early disease) o supplemental O2/rehab if neede o later disease: prednisone 6-12 wks then taper

Lung volume

o Plethysmography, Done in the "body box" o Measures pressures and volume of gases o Uses Boyles Law to assess more complicated lung volumes....that can't be exhaled o Can be too large or too small o Are they restricted? § Yes: TLC < LLN (<5th percentile) § Mild: 65-80% predicted § Moderate: 45-65% predicted § Severe: <45% predicted o Supranormal Total Lung volume: § Associated with high Residual Volume as well § Hyperinflation (TLC) § Air trapping (RV

Airway resistance

o Poisuelles Law o Conducting zones: trachea, bronchi, bronchioles, terminal bronchioles o Transitional and respiratory zones: respiratory bronchioles, alveolar ducts, alveolar sac o Cross-sectional area (total combined diameters of a section of airway throughout its length) gets less as it goes from trachea alveolar sac o The greatest resistance is in the trachea, bronchi, and bronchioles o With an increase in lung, volume, Resistance ® decreases, because of traction § anatomically, all of the alveoli and airway tissues are connected, § when the lungs expand due to expansion of the chest cavity, the outer tissues of the lungs open wider and pull the inner tissues open wider (traction) § because of the inverse relationship of radius (r) and resistance, as r increases, R decreases § Resistance is LEAST at end of inspiration

Surface Tension

o Surfactant is secreted by type II alveolar cells and reduces the surface tension in the alveoli § Reduces surface tension by decreasing density of water molecules at air-water interface § Hydrophobic tails pulls the surfactant tail upward, resultant vector is minimal § Surfactants are detergents, polar molecules, and pulmonary surfactants are DPPC § in premature infants, less surfactant is secreted, and surface tension is elevated (infant respiratory distress syndrome) o Water molecules have a strong polarity (adhesive forces) and will pull towards each other. § Therefore, water will pull towards its core and away from the air, tending to form droplets, rather than spread out evenly over a surface o For surface tension, the alveolus is similar to a water droplet: § Because of fluids lining it, the alveolus will tend to draw to its core and get smaller. § The "resolved direction of tension" is smaller because the water molecules draw tightly together. § Law of Laplace: a smaller radius requires a greater pressure to open the alveoli. · smaller alveoli have greater pressures than larger ones, so air tends to move into the larger alveoli leading to collapse of alveoli (atelectasis) · Surfactant reduces the surface tension and stabilizes the pressures among alveoli by reducing the pressure required to keep the smaller alveoli open

Effects of Arterial PCO2 and pH

o Ultimately, the primary purpose of breathing is to maintain the appropriate levels of H+, O2, and CO2 in the tissues o These substances can be important controllers of breathing rate and depth o Changes in either pH or PCO2 have an effect on respiration o In the normal range, the slope of PCO2 is much steeper and over a wider range than the slope for pH o The influence of PO2 on breathing is only slight until the PO2 drops below 50-60 mm Hg o effects of increasing PCO2 on changes in respiration are augmented by decreasing PO2 o lower levels of PO2, the respiratory response is greater for an increase in PCO2 o increased sensitivity to changes in PCO2 at those levels of PO2

Encounter + Entry

o Usual Starting Point: Colonization of Upper Airway o Relocating to Lower Respiratory Tract via Inhalation (Lungs Function In Gas Exchange) or Aspiration/Microaspiration o Other Less Common Routes § Hematogenous (Entire Blood Supply Goes Through Lungs) § Spread from Contiguous Infection

Lung Sounds

o Velocity is greatest in narrow tubes or with the lowest total cross-sectional area. § in diseases (asthma, COPD) where the airways narrow (increased airway resistance), the velocity is greatest. § Normally, the velocity slows in the respiratory zone, which allows more time in the alveoli for exchange of gases. o Laminar flow is characterized by a "parabolic profile," § because there is greater friction of molecules on the sides of the tube, slowing them down more than those in the center § when listening with a stethoscope: laminar flow is silent o Turbulent flow occurs in tubes when the fluid is high velocity § fluid is characterized by swirls and eddies § when listening with a stethoscope: associated with vibration of airways and tissue, creating noises § where some of the molecules move sideways or backward impeding forward movement of others · Examples: o Wheezing is usually a sound of high velocity airflow causing turbulence in the airways. o Rales is caused by the sudden opening of collapsed alveoli, creating a sudden deceleration (like the popping open of a parachute).

LRTI results from?

o a defect in host defenses § Age: Decreased Mucociliary Clearance, Elastic Recoil, Cough and Humoral & Cell-Mediated Immunity § Aspiration: Lack of coordination of epiglottis closure (CNS Lesion, Loss of Consciousness), Cough reflex depressed (ETOH, Anesthesia, Medications) § Micro-aspiration: during sleep § ETOH: Increased colonization of upper RT, Decreased neutrophil mobilization, Vomitus aspiration causes pneumonitis § Smoking/Vaping: Impaired Mucociliary Elevator, Decrease Macrophage Activity § Environmental pollutants: Impaired Mucociliary Elevator, Direct irritants o specific virulence factors of microorganisms o an overwhelming inoculum

Compliance

o change the amount of pressure required to achieve a change in volume o less pressure is needed when lung volume is lower o more pressure is needed when lung volume is higher § when the lung approaches full inflation, the elastin and collagen fibers are uncoiled § more tension with expansion o high compliance ex: emphysema § the lung at rest has a greater volume (FRC) than normal, a change in transpulmonary pressure causes less change in volume than normal. § compared to normal, more work is required for breathing. o low compliance ex: pulmonary fibrosis

Diffusion

o diffusing capacity of the lung (DL; diffusion capacity) refers to the capabilities of the lung to transfer gases from the alveoli to the red blood cells o In exercise, several mechanisms increase DL, including § increased VT (tidal volume) (increasing A [surface area]) § increased perfusion of alveoli (increasing A [surface area]) § increased production of CO2 by the tissues (increasing ∆P for CO2) o Example: § Emphysema is associated with loss of alveoli, reducing A § Pulmonary fibrosis is associated with thickened membranes (increasing Thickness) and destruction of alveoli (reducing A) o Giving oxygen affects diffusion, not perfusion

2,3 DPG

o highly anionic compound that is concentrated in the concave center of red blood cells and binds to hemoglobin o Relaxed (R) conformation of hemoglobin has a greater affinity for oxygen than the tight (T) conformation. o 2,3 DPG binding to hemoglobin stabilizes the T conformation less affinity for O2. o Deoxygenated Hb has 100X greater affinity for 2,3 DPG than does oxygenated Hb.

Alveolar Gas equation

o used to approximate the partial pressure of oxygen in the alveolus o It is impractical to measure alveolar PO2, so PAO2 is often calculated using alveolar CO2 that is adjusted by the respiratory quotient (RQ), or respiratory exchange ratio (RER) o RQ depends on the type of food that is consumed (carbohydrate, fat, protein) and is typically less than 1, because the overall exchange of O2 and CO2 is not usually 1:1. § average RQ is usually ~0.8, since the human diet is normally a mixture o In determining the arterial PA § Pa oxygen difference, PaO2 is measured from arterial blood gas measurements and PAO2 is often estimated from the alveolar gas equation. o As alveolar ventilation rises, arterial PCO2 (PaCO2) goes down and vice versa

Internal respiration

occurs in the metabolizing tissues, where oxygen diffuses out of the blood and carbon dioxide diffuses out of the cells.

OCCUPATIONAL HEALTH CARCINOGENS

pollution (beryllium, chromium, formaldehyde, second-hand smoke, wood, radon)

Inflammatory cells:

§ Bacterial infection: Macrophages, Neutrophils (Recruited by cytokines) § Viral infection: Lymphocytes § Specific immunity § Cell-Mediated Immunity: Mycobacterium (ie. Tuberculosis), Legionella

COP (Cryptogenic organizing pneumonia)

§ Cryptogenic = COP · Idiopathic · Formerly called BOOP § Reactive response to insult · Infection, malignancy, inhalational injury § Cough, dyspnea, fever, chills, weight loss § Airspace consolidation, migratory § Tx: Oral steroids (6-12 months) § Looks like PNA § Air bronchograms, Bilateral

LIP (Lymphoid interstitial pneumonia)

§ Diffuse lymphocytic interstitial infiltrate § Cough, dyspnea, fever, chest pain § More common in women § May progress to lymphoma § Associated with underlying autoimmune disorders (Sjogren's, HIV) § CT: Patchy areas of ground glass attenuation, cysts and centrilobular nodules

RB-ILD (Respiratory bronchiolitis - interstitial lung disease)

§ ILD associated with the pathologic lesion of RB § RB: lesion in small airways of smokers § pigmented intraluminal macrophages within first- and second-order respiratory bronchioles § Cough, dyspnea § Improves with smoking cessation

Alveolar defense

§ IgA antibodies § Complement Cascade § Alveolar Macrophages § Cell-mediated Immunity § Lactoferrin § Surfactant A, B, C, DL Increase Macrophage Microcidal Activity

ILD Known Causes

§ Known causes: · Rheumatic Disease, HSP, Pneumoconiosis, Smoking Related · Drug reaction: o Common Offenders: Chemotherapy, Biologics, Immunotherapies, Amiodarone, Nitrofurantoin o Tx: withdrawal of offending agent! Steroids, usually short term

DIP (Desquamative interstitial pneumonia)

§ More extensive form of RB-ILD § Pigmented macrophages fill alveolar spaces § Cough, dyspnea § Improves with smoking cessation

Chlamydophilia,

§ No cell wall so no gram stain result § Pharyngitis+sinusitis § Obligate intracellular parasite: Can't make own ATP, Requires Cell Culture to Diagnose § Obligate anaerobe § Virulence factors: Endotoxin (LPS), grow in phagosome, Ciliostatic factor § Extracellular body is infectious

AIP (Acute interstitial pneumonia)

§ Rapidly progressive (weeks to months) § May have preceding URI symptoms (or not) § Severe dyspnea of rapid onset and progression § Hypoxemic respiratory failure/ARDS with bilateral airspace opacities § Diffuse alveolar damage/hyaline membranes on Path § Progress to organization/fibrosis § Tx: Supportive. Steroids +/- antibiotics

NSIP (Non-specific interstitial pneumonia)

§ The most common pattern seen in CTD-ILD § Scleroderma, PM/DM, and Sjogren's § Not RA (UIP > NSIP) § Drug toxicity § Infection § Idiopathic § Overlap: clinically, CT, and histologically · HP, COP, UIP/IPF, and RB-ILD § More favorable prognosis than UIP § Uniform lymphocytic interstitial inflammation § Typically responds to immunotherapy § CT findings: · + GGO · Subpleural sparing · Basal predominant · Homogeneous · +/- Fibrosis

Epithelial cells:

§ Upward Beating Cilia § Mucous · Mechanical trap organisms: Flow upward with beating cilia, Mucociliary escalator § Combat organism: Lysozyme, IgA antibodies § Alveolar normal flora (Once thought to be sterile)

Legionella pneumophilia

§ adolescents and young adult § Difficult to stain and difficult to grow on routine media § May need bronchoalveolar lavage or tissue biopsy for definitive § Diarrhea, CNS symptoms § Aerobic, Gram-neg bacilli § Found in water sources, Air conditioning, Plumbing, Hot tubs, Droplet infection § Host Factors Increase Risk (Advanced Age, Immunosuppressed, Chronic Pulmonary Disease, Cigarette Smoking, Alcoholism) § Virulence Factors (Endotoxin, Metallo-protease, Beta-lactamase, Exotoxins, Pili) § Intrinsic resistance to Beta-lactams

Mycoplasma

§ adolescents and young adult § pharyngitis + diarrhea, coryza, myringitis § No cell wall, no gram stain result § Aerobic, intra or extracellular § Smallest free-living organisms § Colonize mucosal respiratory surfaces, Bronchopneumonia results § Long incubation period § Virulence Factors: Can survive intracellularly, Sheer off cilia, Adhesin protein, Produce hydrogen peroxide

Benign VS Malignant

· Benign Tumor o Slow or very fast growing o Usually encapsulated o well demarcated NOT invasive or metastatic · Malignant Tumor o Composed of embryonic, primitive, or poorly differentiated cells o Disorganized growth o Nutritionally demanding o May develop anywhere in lung o Commonly originate in tracheobronchial mucosa (bronchogenic carcinoma)

O2 Affinity

· Factors that decrease the affinity of hemoglobin for oxygen include a reduction in blood pH, an increase in temperature, an increase in Pa co 2 , and an increase in the concentration of 2,3-diphosphoglyceric acid (2,3-DPG) · These factors facilitate unloading of oxygen into tissues, which is seen as a shift of the oxyhemoglobin dissociation curve to the right. · The oxygen-carrying capacity of hemoglobin is also affected by competitive inhibitors for binding sites, such as carbon monoxide. · Carbon monoxide has an affinity for hemoglobin that is 240 times greater than that of oxygen and preferentially binds to the hemoglobin molecule. However, this does not affect the amount of oxygen dissolved in the blood.

Chest computed tomography (CT)

· Get x-ray first and then get CT after · Used to evaluate and get better understanding of somebody's pneumonia, interstitial lung disease · If you have strong suspicion somebody has PE

Chest radiograph (x-ray)

· Helpful in diagnosis of pneumonia, pneumothorax, hemothorax, pulmonary nodules, widened mediastinum, free air, hiatal hernia, rib fractures, verification of tube/line placement

Sputum culture

· Indication: o Gram stain and culture o Can be used in bacterial pneumonia to help guide ABX choice o indicated for all pts with hospital acquired PNA o Sputum culture is indicated in any patient with a persistent productive cough, fever, hemoptysis, or a chest x-ray picture compatible with a pulmonary infection. This test is used to diagnose pneumonia, bronchiectasis, bronchitis, or pulmonary abscess. Bacterium, fungus, or virus can be cultured. · Contraindication: o Sputum for C&S should be collected before antimicrobial therapy is initiated, unless the test is being performed to evaluate the effectiveness of medications already being given. · Interpretations: o Growth of bacteria/virus/fungi · Complications: o Time: § Preliminary reports are usually available in 24 hours. § Cultures require at least 48 hours for completion. § Sputum cultures for fungus (eg, Pneumocystis) and Mycobacterium tuberculosis take 6 to 8 weeks. · Cost-effectiveness: $15-100

PET Scan

· Indication: o Image glycolytic pathway of tumor cells or other metabolically active tissues with affinity for glucose. o For intrathoracic tumors, solitary pulmonary nodules. Help stage intrathoracic tumors o PET scanning is used in many areas of medicine, most commonly for evaluation of the heart and brain. It is also commonly used in many aspects of oncology. o In PET scanning, radioactive chemicals are administered to the patient. These chemicals are used in the normal metabolic process of the cells of the particular organ being imaged. · Contraindication: o There are no absolute contraindications for a PET scan. This study may not be suitable for pregnant women. The benefit versus risk should be discussed with the nuclear medicine specialist. · Interpretations: o Visualization of tumors · Complications: o Recent use (within 24 hours) of caffeine, alcohol, or tobacco may affect test results. o Ingestion of a small- to moderate-sized meal can cause a marked uptake of 18F-FDG in the gut and muscles, thereby leaving little or no radionuclide to be taken up by tumor. This can cause a false-negative result. The cause of this uptake is due to hyperinsulinemia. o Anxiety can cause increased uptake in multiple areas (eg, neck, upper mediastinum) of the body. If the patient is anxious, sedatives can be administered 30 minutes before testing. However, these could interfere with PET scanning of the brain if cognitive activities will be used to measure changes in brain activity. o Warm blankets used before and during uptake time can decrease uptake. o Mild to moderate exercise can instigate marked uptake of 18F-FDG in the muscles thereby leaving little or no radionuclide to be taken up by tumor. This causes a false-negative result. o The liver and spleen avidly take up 18F-FDG. Therefore those organs are difficult to evaluate on PET imaging. o 18F-FDG is excreted by the urinary system. As a result, the bladder may obscure areas of increased uptake in the pelvis. o Uptake of 18F-FDG can occur in the lymph node basin draining the site of the FDG injection. If PET is being done to stage tumors that could metastasize to those lymph nodes, inject the 18F-FDG on the contralateral side. · Cost-effectiveness: expensive, a few thousand

Arterial Blood Gas analysis

· Indication: o Measurement of arterial blood gasses (ABGs) provides valuable information in assessing and managing a patient's respiratory (ventilation) and metabolic (renal) acid-base and electrolyte homeostasis. It is also used to assess the adequacy of oxygenation. · Contraindication: o There is no palpable pulse. o Cellulitis or open infection is present in the area considered for access. o The Allen test is negative, indicating that there is no ulnar artery. If the radial artery is used for access, thrombosis may occur and jeopardize the viability of the hand. o There is an AV fistula proximal to the site of proposed access. o The patient has a severe coagulopathy. · Interpretations: o CRITICAL: § pH: <7.25, >7.6 § PCO2: <20, >60 § HCO3-: <10, >40 § PO2 (arterial): <40 § O2 saturation: 75% or lower Base/Excess: ±3 mEq/L o pH: § Normal: 7.35-7.45 § In respiratory or metabolic alkalosis the pH is elevated; in respiratory or metabolic acidosis the pH is decreased. o PCO2: § Normal: 35-45 mm Hg § The Pco2 level is elevated in primary respiratory acidosis and decreased in primary respiratory alkalosis o HCO3-: § Normal: 21-28 mEq/L § As the HCO3- level increases, the pH also increases; therefore the relationship of bicarbonate to pH is directly proportional. § HCO3- is elevated in metabolic alkalosis and decreased in metabolic acidosis o PO2: § Normal: 80-100 mm Hg § The PO2 level is decreased in: · patients who are unable to oxygenate the arterial blood because of O2 diffusion difficulties (eg, pneumonia, shock lung, congestive failure) · patients in whom venous blood mixes prematurely with arterial blood (eg, congenital heart disease) · patients who have underventilated and overperfused pulmonary alveoli (pickwickian syndrome; ie, obese patients who cannot breathe properly when in the supine position or in patients with significant atelectasis). § PO2 is one of the measures used to determine the effectiveness of O2 therapy. o O2 SAT: § Normal: 95%-100% § O2 saturation is an indication of the percentage of hemoglobin saturated with O2. § As the Po2 level decreases, the percentage of hemoglobin saturation also decreases. o O2 Content: § Arterial: 15-22 vol % § Venous: 11-16 vol % § This is a calculated number that represents the amount of O2 in the blood. § Nearly all O2 in the blood is bound to hemoglobin. O2 content decreases with the same diseases that diminish PO2. o Base excess: § Normal: 0 ± 2 mEq/L § A negative-base excess (deficit) indicates metabolic acidosis (eg, lactic acidosis). A positive-base excess indicates metabolic alkalosis or compensation to prolonged respiratory acidosis. o Alveolar to Arterial O2 difference: § Normal: <10 mm Hg § If the A-a gradient is abnormally high, there is either a problem in diffusing O2 across the alveolar membrane (thickened edematous alveoli) or unoxygenated blood is mixing with the oxygenated blood. · Complications: o Occlusion of the artery used for access. It is preferable to avoid use of end arteries such as the brachial or femoral artery. o Penetration of other important structures anatomically juxtaposed to the artery (eg, nerve) · Cost-effectiveness: $100-250

Pulse Oximetry

· Indication: o Oximetry is used to monitor arterial O2 saturation levels (SaO2) in patients at risk for hypoxemia. o This includes patients who are undergoing surgery, cardiac stress testing, mechanical ventilation, heavy sedation, or lung function testing, or who have multiple trauma. o It is also used as an indicator of partial pressure of oxygen (Po2) in patients who may experience hypoventilation, sleep apnea, or dyspnea. o This test is commonly used to titrate O2 levels in hospitalized patients.Contraindication: · Interpretations: o Normal: >95 o Critical: <75 · Complications: o hyperoxemia can't be detected, can miss hypoxemia (esp in children), does not measure ventilation · Cost-effectiveness: cheap, $50 for a pulse oximeter

Pulmonary Function Testing

· Indication: o Preoperative evaluation of the lungs and pulmonary reserve. o Evaluation of response to bronchodilator therapy. o Differentiation between restrictive and obstructive forms of chronic pulmonary disease o Determination of the diffusing capacity of the lungs (DL ) o Performance of inhalation tests in patients with inhalation allergies. · Contraindication: o Patients who are in pain, because of the inability for deep inspiration and expiration Patients who are unable to cooperate because of age or mental incapability · Interpretations: o Spirometry: A spirometer is a machine that can measure air volumes. § Values greater than 80% of predicted values are considered normal. § Spirometry provides information about obstruction or restriction of airflow. § Spirometry supports the diagnosis of COPD and chronic restrictive pulmonary disease (CRPD). o Airflow measurement: This portion of the study adds a time element to spirometry. § The shape of the curve can be interpreted to identify and quantify airway obstruction. § If airflow rates are significantly diminished (<60% of normal) or if requested by the physician, the test can be repeated after bronchodilators are administered by nebulizer. § If the airflow rates improve by 20%, use of bronchodilators may be recommended for the patient. § Emphysema or restrictive lung disease usually does not improve with bronchodilator therapy. § Patients with an asthmatic component to COPD will benefit from bronchodilators. o Measurement of lung capacity: information about air trapping within the lung. o Gas exchange studies: measure the diffusing capacity of the lung (DL), that is, the amount of gas exchanged across the alveolar-capillary membrane per minute. § Gas exchange is abnormal in congestive heart failure, pneumonia, and other diseases that fill the alveoli with fluid or exudate. § Any disease that causes deposition of material in the interstitium of the lung (eg, acute respiratory distress syndrome [ARDS], collagen-vascular disease, Goodpasture syndrome, pulmonary fibrosis) will decrease gas exchange. o Forced vital capacity (FVC): § Amount of air that can be forcefully expelled from a maximally inflated lung position. § Less than expected values occur in obstructive and restrictive pulmonary diseases. o Forced expiratory volume in 1 second (FEV1): § Volume of air expelled during the first second of FVC. § In obstructive pulmonary disease, airways are narrowed and resistance to flow is high. Therefore not so much air can be expelled in 1 second, and FEV1 is less than the predicted value. § In restrictive lung disease, FEV1 is decreased because the amount of air originally inhaled is low, not because of airway resistance. Therefore the FEV1/FVC ratio should be measured. § In restrictive lung disease a normal value is 80%, and in obstructive lung disease this ratio is considerably less. The FEV1 value will reliably improve with bronchodilator therapy if a spastic component to obstructive pulmonary disease exists. o Maximal midexpiratory flow (MMEF) or forced midexpiratory flow: § Maximal rate of airflow through the pulmonary tree during forced expiration. § This test is independent of the patient's effort or cooperation. § MMEF volumes are lower than expected in obstructive pulmonary diseases and normal in restrictive pulmonary diseases. o Maximal volume ventilation (MVV) (formerly, maximal breathing capacity): § Maximal volume of air that a patient can breathe in and out during 1 minute. § It is less than the expected value in both restrictive and obstructive pulmonary disease. · Complications: o Light-headedness during the test, because of relative hyperventilation Fainting during FVC maneuver, because of Valsalva effect Asthmatic episode, precipitated by inhalation studies; bronchodilators may be necessary for immediate treatment · Cost-effectiveness: $300-900

Chest/Lung CT Scan

· Indication: o Standard with contrast o Advantage over XR- displays cross-sectional anatomy with higher contrast resolution. o Gold standard for PE o This test is used to more thoroughly evaluate suspected disease in the chest. Questionable or vague abnormalities on the routine chest x-ray can be more thoroughly evaluated with CT scanning of the chest. § tumors, nodules, hematomas, parenchymal coin lesions, cysts, abscesses, pleural effusion, and enlarged lymph nodes affecting the lungs and mediastinum. § Tumors and cysts of the pleura and fractures of the ribs can also be seen. · Contraindication: o Consider pt's ability to lay down flat for at least a couple of minutes at a time o Patients who are allergic to iodinated dye or shellfish o Patients who are claustrophobic o Patients who are pregnant, unless the benefits outweigh the risks o Patients whose vital signs are unstable o Patients who are very obese (usually over 300 pounds), because the CT table cannot support the weight · Interpretations: o SEE CHEST X-RAY · Complications: o Acute renal failure from dye infusion: Adequate hydration beforehand may reduce the likelihood of this complication o Hypoglycemia or acidosis may occur in patients who are taking metformin (Glucophage) and receive iodine dye. The metformin should be held on the day of testing to prevent this complication. · Cost-effectiveness: o More expensive than chest x-ray, ~500

Ventilation/perfusion scan

· Indication: o The lung scan is very helpful in making the diagnosis of pulmonary embolism (PE). It is easily and rapidly performed on patients who have sudden onset of noncardiac chest pain or shortness of breath. It is often performed on patients who have unexplained tachycardia or hypoxemia · Contraindication: o Patients who are pregnant unless the benefits outweigh the risk of fetal damage · Interpretations: o This nuclear medicine procedure is used to identify defects in blood perfusion of the lung in patients with suspected PE o A homogeneous uptake of particles that fills the entire pulmonary vasculature conclusively rules out PE. o If a defect in an otherwise smooth and diffusely homogeneous pattern is seen, a perfusion abnormality exists · Complications: o Patients with known pulmonary parenchymal or pleural problems (eg, pneumonia, emphysema, pleural effusion, tumors), which will give the picture of a perfusion defect and simulate PE · Cost-effectiveness: o $500-1500

Pulmonary angiography

· Indication: o Uses catheter and XR dye. o Perhaps higher risk than other tests (renal failure, allergy) to rule out PE o Gold standard for PE · Contraindication: o contrast allergy (can be overcome), kidney failure o patients with severe pulmonary hypertension. · Interpretations: o Visualization of blood clot, aneurysm, An artery abnormally connected to a vein, Heart and blood vessel problems present at birth, Foreign body in a blood vessel, stenosis · Complications: o Acute valvular damage o Ventricular perforation/rupture o Allergic reaction to the contrast dye o Bleeding due to puncture of a blood vessel Injury to nerves o Clot (embolus) in a blood vessel o An area of swelling due to buildup of blood (hematoma) Infection · Cost-effectiveness: o Varies, $400-2,000

O2 transport

· Most of the oxygen contained in the blood is bound to hemoglobin; a small fraction is dissolved and measured as the Pa o 2 . · The amount of oxygen dissolved is about 3 mL/L in arterial blood, whereas the amount of oxygen bound to hemoglobin is about 197 mL/L, assuming a normal hematocrit. · Each molecule of hemoglobin is capable of carrying four molecules of oxygen. · The shape of the oxyhemoglobin association curve reflects the cooperative binding of oxygen to hemoglobin · Inhaled oxygen enters the lungs and reaches the alveoli. · The layers of cells lining the alveoli and the surrounding capillaries are each only one cell thick and are in very close contact with each other. · This barrier between air and blood averages about 1 micron (1/10,000 of a centimeter, or 0.000039 inch) in thickness. · Oxygen passes quickly through this air-blood barrier into the blood in the capillaries. · Similarly, carbon dioxide passes from the blood into the alveoli and is then exhaled.

Shunting

• A shunt is a condition where circulation is adequate but oxygenation of the blood is inadequate. • A physiological shunt occurs when there is adequate circulation, but ventilation is very low or absent (V/Q approaches zero) • An anatomical shunt exists when the blood bypasses the lungs.

pneumothorax

· Pathophysiology: o Accumulation of air in the pleural space due to rupture of apical bleb o Types: § Primary/spontaneous: without trauma or primary lung disease § Secondary: Underlying lung disease w/o trauma § Traumatic: Occurs as a result of penetrating or non- penetrating trauma: § Tension pneumothorax: due to chest wound or pulmonary laceration, positive air pressure pushes lungs, trachea, great vessels & heart to the contralateral side, Immediately life-threatening § Chylothorax: results from thoracic duct damage with chyle (lymph) leakage from the lymphatic system into the pleural space § Hemothorax: a collection of blood in the space between the chest wall and the lung · Epidemiology/Risks: o Spontaneous (aka primary): thin tall males, 10-30 o Traumatic: iatrogenic (CPR, PEEP, thoracentesis), trauma (MVA) o Tension: trauma, mechanical ventilation, resuscitation o All: Smokers · Symptoms/PE: o acute onset of ipsilateral chest pain and dyspnea, o ↑hyperresonance to percussion, ↓fremitus, ↓breath sounds o unequal respiratory expansion, tachycardia, tachypnea o chest pain, usually pleuritic, unilateral, non- exertional and sudden onset -dyspnea o Tension clue: trachea not midline, ↑JVP, pulsus paradoxus, hypotension · Diagnostics: o CXR reveals presence of pleural air, loss of peripheral lung markings · Treatment: o Primary may spontaneously remit ±Needle aspiration ±Short-term chest tube ±Stapling of bleb (rare) o Tension: § Needle aspiration followed by chest tube § Typically requires mechanical ventilation or resuscitation in order to improve oxygenation and cardiac output

Pleural effusion (Transudate vs. Exudate)

· Pathophysiology: o Accumulation of significant volumes of fluid resultant from inflammation of structures adjacent to the pleural sac or lesions within the chest o Up to 25% associated with malignancy · Epidemiology/Risks: most commonly due to CHF and hepatic cirrhosis · Symptoms/PE: can be asx o Causes restriction of lung expansion SOB, also may have cough and pleuritic chest pain o CHF effusion clues = h/o CVD, R>L effusion, ↑BNP, fluid across diaphragm o Parapneumonic effusion clues = fever, cough, chest pain, ↑WBC o Malignant effusion clue = dyspnea out of proportion to effusion size · Diagnostics: o ↓tactile fremitus, egophony, ↓breath sounds, dullness to percussion ±pleural friction rub o Decreased chest wall expansion o CXR: meniscus sign, blunting of CP angles, lateral decubitus best (for smaller effusions and differentiate loculations and empyema from new effusions or scarring) o Guided thoracentesis and examination of the pleural fluid GOLD STANDARD § Exudate: local factor · associated with "leaky" capillaries due to infection, malignancy or trauma o in bacterial pneumonia, malignancy, viral infx, PE, parapneumonic effusion most common · Leads to accumulation of protein rich pleural fluid and cells · LIGHT's CRITERIA: if at least one of the following criteria is present, then the fluid is determined to be an exudate: o Pleural fluid protein to serum protein ratio greater than 0.5 o Pleural fluid LDH to serum LDH ratio greater than 0.6 o Pleural fluid LDH greater than two-thirds the upper limit for normal serum LD § Transudate: excess formation of fluid or decreased absorption; cause is systemic · (intact capillaries)—associated with increased hydrostatic or decreased oncotic pressure (CHF, atelectasis, renal or liver disease) · Leads to accumulation of protein poor pleural fluid · Treatment: o Tx underlying condition o Thoracentesis (dx/tx) o Chest tube drainage if empyema o Pleurodesis (thoracostomy w/ talc or other substance) if malignant/chronic

Pertussis (Whooping Cough)

· Pathophysiology: o Bordetella pertussis—gram negative bacillus w/ incubation 7-10 days average o Transmission via respiratory droplets (cough, sneeze, speak) · Epidemiology/Risks: peaks every 3-5 years, rare due to vaccination, unvaccinated children; most common <2 y/o · Symptoms/PE: o Classic: paroxysms of coughing, inspiratory whoop, post-tussive vomiting § Catarrhal stage (1-2 WEEKS) : · insidious onset of sneezing, runny nose, loss of appetite and malaise with a hacking cough that is most prominent at night—MOST INFECTIOUS STAGE · Fever uncommon, cough increases gradually and runny nose stays watery § Paroxysmal stage (10 WEEKS) : · spasms of rapid coughing fits followed by deep, high-pitched inspiration (WHOOP)—can be fatal for infants. · May gag/vomit/sweat, Cyanosis § Convalescent stage (UP TO 12 WEEKS): · decreases in frequency and severity of paroxysms, total cough duration 1 month o ANY COUGH LASTING > 2 weeks, consider (examine VAX status, R/O other causes) · Diagnostics: culture, PCR, lymphocytosis · Treatment: o w/in 3 weeks: abx (azithro/clarithro/tmp-smx) o after 3 weeks: supportive o hospitalization for observation if needed · prevent with vaccination and TDAP booster

Epiglottis

· Pathophysiology: o MEDICAL EMERGENCY DUE TO AIRWAY OBSTRUCTION o Now rare-- usually caused by group A streptococcus or Staphylococcus aureus or Haemophilus influenzae type b in unimmunized patients · Epidemiology/Risks: o kids aged 2-7 years, adults 45-65 years, 2x more common in males and adults w dm/cocaine use · Symptoms/PE: o TRIPOD POSITION-- sitting, head held forward, the mouth open, and the jaw thrust forward o distressed, dysphagia, inspiratory stridor, drooling, fever, cough is rare, respiratory distress; tachypnea, dyspnea, hot potato voice · Diagnostics: o Lateral x-ray reveals thickened and bulging epiglottis, thumbprint sign o Laryngoscaopy: cherry red epiglottis o Direct visualization of the epiglottis is diagnostic BUT MANIPULATION MAY INITIATE SUDDEN FATAL airway obstruction in children o Direct observation of the larynx should only be performed in the operating room with an anesthesiologist and a competent surgeon prepared to place an endotracheal tube or perform a tracheostomy if needed o CBC and epligottis cx · Treatment: o Maintain airway, keep patient calm, Intubation usually necessary o Steroid for airway edema o Abx: 2nd/3rd gen cephalosporin + vancomycin o Give rifampin to close contacts, Hib vaccine

Croup (laryngotrachobronchitis)

· Pathophysiology: o Most common infection/ inflammation of the middle respiratory tract o parainfluenza viruses (types 1, 2, 3, and 4) and respiratory syncytial virus (RSV) · Epidemiology/Risks: 6mo-3yrs · Symptoms/PE: o Stridor (harsh, high-pitched respiratory sound produced by turbulent airflow—inspiratory), o hoarseness ("seal barking"), fever, respiratory distress o URI (rhinorrhea) prior/during/after acute presentation o Significant upper airway obstruction, respiratory distress, death is rare · Diagnostics: mainly clinical, Front cervical xray: Steeple sign/wine bottle sign in 50% patients · Treatment: supportive o Mild (no stridor at rest, no distress) - supportive care, O2 if below 92%, dexamethasone o o Moderate (stridor at rest, mild/mod retractions) - dexamethasone, nebulized epi, observe 3-4 hrs before considering d/c o Severe Dexamethasone and nebulized epi; hospitalization

Cor pulmonale

· Pathophysiology: o Right ventricular hypertrophy or right-sided heart failure due to pulmonary HTN o PH-induced altered structure (hypertrophy or dilatation) and/or impaired function · Epidemiology/Risks: COPD, interstitial lung disease, sarcoidosis, OSA, high altitude , pulmonary htn · Symptoms/PE: Dyspnea, wheezing, wet cough, edema, cyanosis, ascites · Diagnostics: o ↑JVD o EKG: tall peaked T waves, R axis deviation o CXR/echo: RVH, pulmonary artery hypertrophy o RHC is gold standard for diagnosing pulmonary HTN · Treatment: o Mild-moderate: monitor o Severe pulm HTN: treat underlying condition (COPD, ILD, OSA) § Supplemental O2, smoking cessation, exercise, diuretics, eventual transplant § Diuretics, salt restriction

Silicosis

· Pathophysiology: o Silica dust inhalation calcification & fibrosis o development of mycobacterial infection and of collagen vascular disease · Epidemiology/Risks: o Exposure to "free" silica or silicon dioxide in sandstone, granite, quartz or slate occurs in the tunneling, mining, quarrying, foundry, sandblasting and ceramic industries · Symptoms/PE: o initially asymptomatic secondary to the long latency period but may progress despite removal from continued exposure o progressive dyspnea and respiratory failure, +/- rales, wheeze, cough o Acute Silicosis (Silico proteinosis): seen in tunnelers or sandblasters exposed to high dose (silica) with onset of respiratory symptoms (cough, dyspnea) within months o Caplan's syndrome: a combination of rheumatoid disease with large necrobiotic nodules associated with simple silicosis o Tuberculosis: frequent co-morbidity o Malignancy: higher incidence of bronchogenic carcinoma · Diagnostics: o Radiology § 10 to 20 year latency § Simple Silicosis: multiple small upper lobe nodules (1-10mm), rare calcifications § Complicated Silicosis: Large opacities or conglomerate nodular shadows (>10mm) with progressive fibrosis o Acute: after high intensity exposure, weeks to years o Chronic: after 10 or more years of low moderate exposure § Simple (nodular) or Complicated silicosis (Progressive Massive Fibrosis) § Accelerated: after moderate high exposure § Hilar adenopathy: common, may develop "egg shell calcification" o Accelerated: after moderate high exposure · Treatment: supportive, lung transplant in end-stage; if fibrosis anti-fibrotics

Obstructive sleep apnea

· Pathophysiology: o sleep disorder characterized by repetitive complete (apneas) or partial (hypopnea) upper airway collapse despite associated respiratory effort causing recurrent arousals and cyclical hypoxemia o During an obstructive apnea event, alterations in intrathoracic pressure cause sympathetic nervous activation and systemic and pulmonary arterial hypertension. o This can lead to chronic and sustained systemic and pulmonary hypertension, arrhythmias, and associated complications. · Epidemiology/Risks: obsesity, higher age, males · Symptoms/PE: o snoring, witnessed breathing pauses, restless or non-refreshing sleep, awakenings (with gasping or paroxysmal nocturnal dyspnea), insomnia, o excessive daytime sleepiness or fatigue, low visibility of posterior pharynx when patient opens mouth), o retrognathia or increased overjet (top incisor teeth ahead of bottom incisors), lateral peritonsillar narrowing, macroglossia, tonsillar hypertrophy, elongated or enlarged uvula, high-arched or narrow hard palate, nasal abnormalities (polyps, deviation of septum, turbinate hypertrophy), large neck circumference · Diagnostics: o In-lab polysomnography (PSG) is the "gold standard" diagnostic test for OSA and for excluding other nonobstructive causes for sleep disturbance (>15 events an hour) o Labs- polycythemia d/t chronic hypoxemia o Epsworth sleepiness scale—pt perception of fatigue and sleep · Treatment: o weight loss, avoidance of supine sleep, CPAP (but does not reduce cardiovascular events/death) o Can treat daytime somnolence with Solriamfetol o Tracheostomy considered definitive treatment for OSA

Pulmonary embolism

· Pathophysiology: o thrombi in systemic venous circulation or the R side of the heart, or from tumors that have invaded the venous circulation o 90% pulmonary emboli originate as clots in the deep veins (DVTS!) legs o revolve around Virchow's triad: hypercoagulable state, venous stasis, vascular intimal inflammation or injury · Epidemiology/Risks: o THIRD leading cause of death in hospitalized patients o Risks: prior DVT or PE, stasis, ↑CVP, hypercoagulability (fV), cancer & tx, OCP + smoking 7x risk · Symptoms/PE: difficult to recognize o pleuritic CP, dyspnea, apprehension, , hemoptysis, diaphoresis, tachycardia, crackles, o dyspnea, tachypnea, pleuritic chest pain, cough, and/or low grade fever o calf/thigh pain, syncope, leg swelling/erythema/tenderness o rales, decr breath sounds, JVD, accentuated pulmonic component of S2 · Diagnostics: o ABG: respiratory alkalosis (secondary to hyperventilation) o EKG: tachycardia and non-specific ST-T wave changes o CXR: non-specific abnormalities such as basilar atelectasis o Ventilation-perfusion lung scan: perfusion defects o D-dimer o Spiral/helical CTA (replaced V-P scan): gold standard o Pulmonary Embolism Rule-Out Criteria (PERC) § PERC includes 8 factors · age < 50 years, pulse rate < 100 beats/minute, oxygen saturation (SpO2) > 94%, no unilateral leg swelling, no hemoptysis, no surgery or trauma within 4 weeks, no previous DVT or PE, no oral hormone use § patients fulfilling all 8 criteria are considered negative for PE (pretest probability < 1%) § If any 1 of the 8 criteria in PERC is met, D-dimer assay is beneficial o Wells' Criteria risk stratifies patients for pulmonary embolism (PE) § Clinical sn/sm of DDVT, PE is #1 diagnosis or equally likely, heart rate >100, immobilation of 3 days or surgery in past month, previous objectively diagnosed PE/DVT, hemoptysis, malignancy with treatment within 6 mo or palliative. · Treatment: o ASAP- LMWH, fondaparinux, Xa inhibitors o 1st PE: anticoagulants o Prevention: early ambulation, stockings, mechanical compression devices, anticoags, statins

Bronchiectasis

· Pathophysiology: Abnormal, permanent dilation of the bronchi and destruction of bronchial walls, leading to impairment of mucociliary escalator leading to increased infx o may be congenital (50% CF) or tumors, FB's, recurrent lung infections · Epidemiology/Risks: Risks go up due to cystic fibrosis, RA · Symptoms/PE: purulent foul-smelling sputum, hemoptysis, cough, recurrent pneumonia, crackles, wheezing, rhonchi, clubbing · Diagnostics: o HRCT is MODALITY OF CHOICE (dilated tortuous airways) § tram-track lung markings (dilated airways seen in a horizontal orientation) § honeycombing** (presence of small cystic spaces with irregularly thickened walls composed of fibrous tissue) § signet ring sign (incr airway diameter is greater than adjacent vessel diameter) o PFT is gold standard § not fully reversible obstructive pattern (decr FEV1. FEV1/FVC <70% predicted, decr FVC). § Hyperinflation will lead to incr lung volumes (RV, TLC, RV/TLC, FRC) · Treatment: conservative (chest physiotherapy, mucolytics, bronchodilators) o ABX often needed/cycled o Surgical resection/transplantation may be needed o Treated similarly to COPD

Cystic fibrosis

· Pathophysiology: Autosomal recessive dz results in abnormal production of mucus by almost all exocrine glands causing obstruction of these glands and ducts o Increased risk of malignancies of GI tract, osteopenia and arthropathies · Epidemiology/Risks: o Most common life-limiting autosomal recessive disease in White people o absent or reduced function of the CFTR protein. CFTR is expressed at mucosal surfaces of aerodigestive tract, sweat gland, vas deferens and conducts flow of chloride, bicarb, thiocyanate. · Symptoms/PE: o excess sputum, decreased exercise intolerance, increased AP diameter o short stature, delayed sexual maturation, clubbing of digits, wrinkling of hands/feet, hypochloremic hypokalemic alkalosis, GERD, esophagitis o chronic productive cough/crackles on auscultation. o Mucus retention and airway inflammation may cause chronic wheezing. o Bronchiectasis can be seen on CT in 30% infants o Viral infections can cause exacerbation -fever uncommon o Bacterial infx—S. aureus and P. aeruginosa o Chronic sinus disease (lack of smell, sinus pain, polyps, congestion, d/c) o GI- meconium ileus, bowel obstruction, pancreatic insufficiency (maybe fat malabsorption), diarrhea, abd pain, oily stool o Reproductive issues- male infertility, females with cystic fibrosis have problems conceiving · Diagnostics: o elevated sweat chloride concentration (GOLD STANDARD) o 2 disease defining mutations/variants in the CFTR gene, and/or evidence of organ dysfunction (such as lung and/or gastrointestinal disorders), o apical crackles o bronchiectasis on CXR or CT, CXR o mucous plugging, small round opacities, focal atelectasis o PFTs show mixed obstructive and restrictive patterns o ABG with hypoxia or in chronic advanced dz; compensated respiratory acidosis · Treatment: o Median survival is 31 years o 2019—TRIKAFTA--FDA approves new breakthrough therapy for cystic fibrosis, for 6 y/o+ o standard supportive therapy: airway clearance, abx tx for infx

Pneumonia (Community)

· Pathophysiology: Infection of the lung parenchyma acquired outside of the hospital o "Professional Invaders" § Adhere to respiratory mucosa, Interfere with cilia, Resist respiratory macrophages, Cause damage to local tissues o Causes: S. pneuomonia most common, "Pneumococcus" § Gram + diplococci, colonizes nasopharynx, droplet/person-to-person trans. § Large, evade phagocytosis, inhibits complement, inhibits opsonizaton § Toxins (pneumolysin, neuraminidase, hylaurdinase, autolysin) § Complications: pleural effusion, empyema § Near- Full pulmonary remodeling after infection · Epidemiology/Risks: o 4.5 M outpatient and ER visits annually o Second most common cause of hospitalization, Most common cause of infection related death o Older Age, Chronic comorbidities, Viral respiratory tract infections (Influenza, COVID-19) o Impaired airway protection: allow for microaspirations of stomach or upper airway secretions o Alterations in consciousness (CVA, Drugs, alcohol, trauma, seizure) o Dysphagia/dysmotility (Esophageal lesions, GERD) · Symptoms/PE: o Acute onset o Cough, sputum production, dyspnea, pleuritic chest pain, Tachypnea (most sensitive?) o Fever, Chills, Tachycardia, Altered breath sounds & rales (Bronchophony/egophony) o Pts. aged 65 years or older § Less severe symptoms & signs § Afebrile, Altered mental state § Tachypnea = sensitive sign 45-70% elderly patients. · Diagnostics: o Chest x-ray gold standard, PA views § Confirm infiltrate § Determine pattern: lobular, patchy, interstitial, bilateral diffuse (wool), necrotizing, § Find co-existing conditions o CURB-65 for hospitilizations or not § 0-1 Criteria Met = Outpatient § 2 Criteria = Admit to General Medicine Flr § 3-5 Criteria = ICU Admission o Labs, cultures, antigen tests · Treatment: o Treatment is best w/ pathogen directed therapy o Essential with "critical pathogens": Legionella, Influenza, MRSA o Pathogen directed approach not always possible (Not essential with outpatients or not practical) o For abx treatment: the quicker the better, response in 1-3 days, § If start with IV, switch to PO once fever subsides § Antibiotics until at least 3 days after afebrile § Min 5-7 days o Empiric abx treatment o No comorbid factors (OUTPATIENT): Amoxicillin(rare) or Doxycycline, Macrolide if local pneumococcal resistance <25% o With comorbid factors (OUTPATIENT): § Option 1: · Amoxicillin/Clavulanate or Cephalosporin (Cefpodoxime, cefuroxime) AND · Macrolide or doxycycline (Azithromycin, clarithromycin) § Option 2: · Monotherapy with resp. fluoroquinolone (Levofloxacin/mofloxacin, Gemifloxacin) o Non severe pneumonia (IN PATIENT) § Standard Regime (Beta lactam + macrolide or resp. fluoroquinolone) § Prior MRSA (Standard regime PLUS vancomycin) § Prior P. aeruginosa (Standard PLUS P. aeruginosa coverage, piperacillin-tazobactam or imipenem or cefepime or ceftazadime or aztreonam) o Severe pneumonia (IN PATIENT) § Standard Regime (Beta lactam + macrolide or Beta-lactam + resp. fluoroquinolone) § Prior MRSA (Standard regime PLUS vancomycin) § Prior P. aeruginosa (Standard PLUS P. aeruginosa coverage, piperacillin-tazobactam or imipenem or cefepime or ceftazadime or aztreonam) o PREVENTION: § Pneumococcal Vaccine, Influenza Vaccine, Smoking Cessation § Vax: · Pneumovax 23-valent pneumococcal polysaccharide vaccine (PPSV23) o Age ³ 65 o Age < 65 if immunocompetent · Prevnar 13 13-valent pneumococcal conjugate vaccine (PCV13) o Routine administration in adults aged > 65 years o Need boosters

Legionnaires Disease

· Pathophysiology: Legionella, exposure to contaminated water droplets from cooling/ventilation systems · Epidemiology/Risks: older age, smoking, immunosuppression, pulmo/rena/cardio dz o known or potential exposure to a contaminated water source (eg, hot tubs, birthing pools, fountains) and exposure to soil or potting mix in areas where the incidence of L. longbeachae is high · Symptoms/PE: high fever, dry cough , dyspnea, systemic sxs (GI, altered mental status), N/V/D · Diagnostics: o CXR may show patchy infiltrates or lobar consolidation o slightly elevated to normal CBC o Gram stain with increased leukocytes but no bacteria; Legionella are intracellular organisms o urine legionella antigen o sputum culture, PCR · Treatment: o Treat like CAP, w/ abx a fluoroquinolone, macrolide, or tetracycline

Tuberculosis

· Pathophysiology: M. tuberculosis and other mycobacteria o Transmission: inhaling DROPLET NUCLEI via respiratory actions in people with active dz o Develops when immune system cannot keep tubercle bacilli under control § May develop very soon after infection or many years after infection o Probability that TB will be transmitted depends on: § Infectiousness of person with TB disease, Environment in which exposure occurred § Length of exposure, Virulence (strength) of the tubercle bacilli o The best way to stop transmission is to: Isolate infectious persons, Provide effective treatment to infectious persons ASAP o Tb Infection is also called LTBI (latent tuberculosis infection) § LTBI is Quiescent TB organisms that can reactivate, Reactivated TB is TB infection § Occurs when tubercle bacilli are in the body, but the immune system is keeping them under control § Detected by the Mantoux tuberculin skin test (TST) or by blood tests such as interferon-gamma release assays § People with LTBI are NOT infectious § About 10% of all people with normal immune systems who have LTBI will develop TB disease at some point in their lives, highest at 2 years after infx § People with LTBI can be given treatment to prevent them from developing TB disease § Detecting TB infection early and providing treatment helps prevent new cases of TB disease · Epidemiology/Risks: o one of the leading causes of death due to infectious disease in the world o Each year, 9 million people develop TB disease, 2 million people die of TB o Conditions that increase risk: DM, cancer, silicosis, immunocompromised, HIV, People infected with M. tuberculosis within past 2 years, children less than 4 years old, IV drugs o Individuals infected within the past 2 years are more likely to develop TB disease § Risk of developing disease in first 2 yrs-5%, Risk over entire lifetime is 10% o High-priority groups for LTBI treatment if positive IGRA or TST result of > 5 mm § Recent close contacts of people with infectious TB disease including under 4 y/o § HIV, , chest x-ray findings suggestive of previous TB disease, organ transplants § Other immunosuppressed patients · Symptoms/PE: COUGH, hemoptysis, fever, night sweats, anorexia, weight loss · Diagnostics: o Clinical specimens (e.g., sputum, urine, fluid samples from spine for TB meningitis) and culturing o nucleic acid amplification testing (NAAT), AFB smear o biopsies reveal CASEATING granulomas o Chest x-ray: Infiltrates (collections of fluid & cells in lung tissue +Cavities (hollow spaces w/in lung) o Bronchoscopy of lung to obtain pulmonary secretions or lung tissue o Gastric washing (for children): Tube is inserted through nose and into stomach to obtain gastric secretions that may contain sputum o LTBI: § Mantoux tuberculin skin test (TST) § Blood tests known as interferon-gamma release assays (IGRAs) · Advantage: Requires single patient visit, results in 24 hours, no booster phenomenon, Less likely to have incorrect reading compared to TST, BCG vaccination does not affect results · Disadvantage: Blood samples must be processed within 12 hours for some IGRAs, possible errors in running and interpreting test, limited data on its use in certain populations & on its use to determine who is at risk for developing TB disease o · Treatment: o LTBI is treated to prevent the development of TB disease § LTBI is treated with medication -6 months § INH 300mg for 6 months has been standard, § New data suggests Rifampin x 4 months best o High-priority groups for LTBI treatment if positive IGRA or TST result of > 5 mm § Recent close contacts of people with infectious TB disease including under 4 y/o § People living with HIV People with chest x-ray findings suggestive of previous TB disease § Patients with organ transplants § Other immunosuppressed patients o TB disease must be treated for at least 6 months; in some cases, treatment lasts longer § e.g., patients with cavities on chest x-ray and positive sputum cultures at 2 months should have treatment extended to 9 months § detecting TB infection early & High-priority groups for LTBI treatment if positive § providing treatment helps prevent new cases of TB disease § Initial Phase: · First 8 weeks of treatment, Most bacilli killed during this phase · 4 drugs used: Isoniazid (INH), Rifampin (RIF), Pyrazinamide (PZA), Ethambutol (EMB) § Continuation Phase: · After first 8 weeks of TB disease treatment, Bacilli remaining after initial phase are treated with at least 2 drugs § Relapse: · Occurs when treatment is not continued for long enough · Surviving bacilli may cause TB disease at a later time o Drug resistant TB: resistant to at least one TB treatment drug

COVID-19 (SARS CoV-2)

· Pathophysiology: SARS-COV-19 o Person-to-Person through respiratory droplets § Primary mode of transmission § 6 feet for prolonged period of time (30 minutes or more) § People who do not have symptoms may be able to spread the virus (asymptomatic or pre-symptomatic spread) o Contact with contaminated surfaces less common § May be possible to get infected by touching contaminated surfaces then touching your mouth or nose § Prevented through handwashing o Aerosol transmission - smaller sized droplet - common o Non Pharmaceutical interventions- § Distancing—how far is enough-(3ft-6ft-14ft) § Face coverings—controversies-types—Bangladesh study--effective § Hand Hygiene alcohol 60-70% § Avoid crowds(groups without distancing) § New data on Bars, restaurants, gyms- close contacts- MMWR o · Epidemiology/Risks: o Increase Age, underlying illness, minority = worse outcomes o Mortality rates—depends on host- underlying conditions · Symptoms/PE: o Asymptomatic infection 25-45% § Pre-symptomatics - 2 days prior to infection § Incubation -2 to 14 days( delta may be shorter 2-4 d), symptoms appear § Majority symptoms 5-7 days (Delta 2-4 days o Fever, Shaking chills(repeated), Cough, Muscle Pain, sore throat, headache, runny nose o Shortness of breath or difficulty breathing, Loss of taste and smell, N/V/D o Older adults and people with underlying medical conditions are at high risk for developing more serious complications (Severe disease-multisystem illness, Hospitalization and intubation) o Children often asymptomatic or mild symptoms (cough/malaise/fever) · Diagnostics: o Gold standard PCR, Antibodies for past infection, Antigen tests for present infection o Rapid tests being developed both antigen and PCR o Home Tests - now available § Sensitivity vs specificity predictive value · Treatment: o Remdesivir some efficacy in some trials(WHO opinion not effective) o Steroids- used in severely ill o Post acute plasma - no longer used o Monoclonal antibodies - treat early - new data on prevention o Anti - coagulation -hospitalized - low dose o Anti - inflammation agents o Ventilatory support - proning · Vaccine: o Covid IgM 7-10 days after infection—not durable o Covid IgG 21 days after infection -lasts at least 4 months o T Cell responses not well measured o Reinfection occurs -likely after 3-4 months in a few o Vaccines are unprecedented in development o Vaccine type § Weakened or inactive virus vaccines § Viral vector vaccines § Nucleic acid (mRNA) vaccines § Protein-based vaccines

Respiratory Syncytial Virus

· Pathophysiology: contagious respiratory illness caused by RSV o Causes bronchilotis (children) and pneumonia (elderly) o Eye/nose/mouth inoculation after contact with secretions/fomites · Epidemiology/Risks: o One of the most common causes of respiratory infection in infants and children worldwide o <2 y/o, peaks Jan/feb, LRTI in children/elderly, URTI in adults · Symptoms/PE: o rhinorrhea, sneezing, wheezing, low grade fever, nasal flaring, tachypnea, bronchiolitis, apnea · Diagnostics: RSV PCR/cx, CXR may show air trapping and peribronchial thickening · Treatment: supportive

Pneumoconiosis

· Pathophysiology: restrictive disease o Chronic fibrotic lung disease § Causes: inorganic dust (Asbestosis, Silicosis, Coal Miner's Lung) o Results from accumulation of dust in the lungs and the tissue reaction to its presence · Epidemiology/Risks: mining/tunneling/excavating, sand-blasting, cement, coal dust, metals/iron · Symptoms/PE: o asymptomatic sometimes o dyspnea, inspiratory crackles, clubbing and cyanosis, restrictive lung disease on PFTs o Asbestosis: (insulation, demolition, construction)CXR with linear opacities at bases and pleural plaques, interstitial fibrosis, thickened pleuraincreased risk for lung CA, mestothelioma o Coal workers pneumoconiosis: coal miningCXR with small opacities in the upper lung fields o Silicosis: mining, sand blasting, quarry and stone workCXR with nodular opacities in the upper lung fields, calcifications of hilar lymph nodes · Diagnostics: o Hx of exposure o Abnormal CXR consistent with exposure o Abnormal PFT consistent with interstitial lung disease o Detailed occupational history may be needed to determine active or passive exposure · Treatment: Supportive

Influenza

· Pathophysiology: contagious respiratory illness caused by influenza virus o Transmission via respiratory droplets, 2-8 hrs survival on surfaces o Drift = epidemics, A>B, Shift = pandemics, A only, § Influenza C causes mild illness, no epidemics o Incubation period 1-7 days, symptomatic 3-14 (average4 days), o hemagglutinin + neuraminidase proteins, self-limiting · Epidemiology/Risks: 5-20% of u.s population gets it every year o Infx rates highest among children but deaths/serious illness highest in >65 · Symptoms/PE: o Abrupt onset fever, chills, muscle aches, headache, fatigue, cough, pharyngitis, rhinitis o Gastrointestinal symptoms in children o Emergency signs (adults): difficulty breathing, pain/pressure in chest or abdomen, sudden dizziness, confusion, severe or persistent vomiting, flu-like sx improve but return w/ fever and worse cough o Emergency signs (children): Bluish or gray skin color, Not drinking enough fluids, Severe or persistent vomiting, Not waking up or not interacting, Irritable; child does not want to be helpd, Flu-like symptoms improve, but then return with fever and worse cough · Diagnostics: PCR (gold standard) and hx of sx, peak Dec-Mar · Treatment: o Antivirals within 48 hours onset of sx § +close contacts o Supportive o No aspirin in children · Prevention: vaccination (esp high risk) cleanliness, social distancing/masks o Contraindications for vax: § severe allergies to chicken eggs § previous severe allergic reaction to a influenza shot § People who have developed Guillain-Barre syndrome within 6 weeks of a previous influenza vaccine § Children less than 6 months § People who are currently ill with a fever (should wait until symptoms are gone and then get the shot) · Complications: pneumonia, sinusitis, AOM, bronchitis, Reye syndrome

(Pediatric) Foreign body aspiration

· Pathophysiology: foreign body o most FB in children are found in the bronchi, Laryngeal/tracheal FB less common o R LUNG more common due to it being wide, more vertical, shorter R main bronchus · Epidemiology/Risks: < 3 years, M> F, alcoholism, impaired cough/swallowing reflex, dementia, kids · Symptoms/PE: o About half are delayed in presentation (> 24 hours) o severe respiratory distress, cyanosis, and altered mental status have a true medical emergency that demands prompt recognition o STRIDOR, drooling, choking, tachypnea, hemoptysis o Classic triad has high specificity(not always present): wheezing, cough, diminished BS · Diagnostics: o Obtain PA and lateral chest x-rays if foreign body aspiration is suspected. o Most foreign bodies are radiolucent (X-ray may be normal within 24 hours of aspiration episode.) o Bronchoscopy may be used for both diagnosis and treatment of foreign body aspiration. · Treatment: o life support, and rigid bronchoscopic removal of the FB · Complications: aspiration pneuomonia, gastric aspioration may cause ARDS

Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)

· Pathophysiology: generalized lung inflammation of alveoli and bronchioles o Causes: organic dusts o An inflammatory reaction to specific antigens in organic dusts (Th1 and IgG mediated) · Epidemiology/Risks: exposures · Symptoms/PE: o fine inspiratory crackles , pulmonary HTN (dx echo) , clubbing later o Acute: § acute onset of dyspnea, productive cough, fever in response to large acute exposure § Flu-like, Sx within 4-8 hrs after exposure until a few days, typically resolve § inspiratory crackles o Subacute/Intermittent: § productive cough, dyspnea, pleuritis, hospitalization? within weeks and typically resolve. § No fever or chills § Biopsy shows non-caseating granulomas § CXR shows micronodular opacities in lower lung fields o Chronic: § slow gradual onset of dyspnea due to progressive fibrosis usually after long-term, low-level exposure § cough, weight loss, malaise, dyspnea · Diagnostics: o CXR: normal to honeycombing, poorly defined infiltrate, reticulonodular, "ground glass" appearance, apices typically spared o CT BEST—ground glass appearance, mosaic pattern of air trapping—micronodular pattern o PFT: restrictive (can be obstructive), decreased DLCO o Biopsy- inflammation, plasma cells, lymphocytes, granulomas o Labs- leukocytosis with LEFT SHIFT, + hypersensitivity panel · Treatment: avoid antigen, avoid dust, steroids may be used

Pulmonary hypertension

· Pathophysiology: hemodynamic state in which the pressure in the pulmonary artery is elevated above a mean of 20- 25 mmHg · Epidemiology/Risks: F>M 30-60; can be hereditary o Risk factors- genetic mutations, drug/toxin-induced, scleroderma, SLE, RA, HIV, congenital heart disease, states of hypoxemia o Most common is pulm HTN due to left-sided heart disease o Primary (idiopathic): most common in middle-aged/young women (BMPR2 gene defect o Secondary: pulm HTN d/t pulmonary disease, sleep apnea, PE, cardiac/metabolic/systemic disease · Symptoms/PE: o dyspnea is insidious and gradually progressive. o fatigue, LH, retrosternal chest pain, palpitations, exertional syncope. o In advanced disease (edema, HF) o ↑JVD, ↑RV impulse on palpation, Loud S2 -S4 gallop, tricuspid regurg murmurs · Diagnostics: o ECG: right axis deviation, RV ventricular enlargement, RA enlargement, ST and T wave changes across anterior precordium, "pruning" of vessels, interstitial/alveolar edema o CXR: enlarged proximal pulmonary arteries, reduction in retrosternal air space o Right heart catheter: gold standard, mean PAP ≥25 mmHg at rest (or >30 during exercise); vasoreactivity trial o Echo: ↑PAP, RVH, R atrial enlargement, tricuspid regurgitation · Treatment: o low level graded aerobic exercise but avoid physical exertion, sodium restricted diet o Primary: Calcium channel blockers if vaso-restrictive § Other options are Prostacyclins, phosphodiesterase-5 inhibitors, oxygen therapy o Heart-lung transplant is definitive management o Secondary: treat underlying disease

Pleurisy

· Pathophysiology: inflammation of parietal pleura resulting in sudden/intense chest p! on inhalation /exhalation · Epidemiology/Risks: o Prior pneumothorax, lupus, community acquired pneumonia, RA, TB, respiratory infx, pe, Cancer, · Symptoms/PE: o Chest pain on inhalation and exhalation, o pain may be described as "catching", "stabbing", may worsen with activity, sneezing, coughing o Cardiac causes pain may worsen when supine (pericarditis), radiates to shoulders (MI), tearing pain (aortic dissection) · Diagnostics: o RULE OUT PE, most common life-threatening cause o CXR (dependent on the underlying condition) o may also request CT, lung ultrasound o Pleural rub, Dullness on percussion, Distant breath sounds · Treatment: NSAIDs, Tx underlying cause

Atelectasis

· When a plug (from mucus or a foreign object) obstructs bronchial air flow, affected alveoli collapse and become airless. · Percussion note: dull over airless area · Trachea: May be shifted toward involved side · Breath sounds: Usually absent when bronchial plug persists. Exceptions include right upper lobe atelectasis, where adjacent tracheal sounds may be transmitted. · Adventitious sounds: none Tactile fremitus and transmitted voice sounds: Usually absent when the bronchial plug persists. In right upper lobe atelectasis may be increased

Pneumonia (Health Care Institution Associated, Nosocomial)

· Pathophysiology: micro aspirations most common route o HAP: Infection of the lung parenchyma acquired in the hospital (acquired ≥ 48 hours after admission) , often MRSA § admitted to an acute care hospital for 2 or more days within 90 days of infection (not hospitalized for pneumonia); § resided in a nursing home or long term care facility; § received IV antibiotics, chemotherapy, or wound care within 30 days of infection; § or attended a hospital or hemodialysis clinic o VAP: Infection of the lung parenchyma acquired via ventilator (≥ 48 hours after endotracheal intubation), often Staph aureus · Epidemiology/Risks: o Second most common cause of healthcare acquired infections (non-VAP, seeing decreasing rates) o For MDR HAP § IV antibiotics w/in 90 days, Colonization or prior MDR pathogen, Structural lung disease* § Treatment in a unit with >20% isolates are MRSA, or prevalence of MRSA is unknown** o For MDR VAP § IV antibiotic within 90 days, Septic shock at time of VAP, ARDS preceding VAP, > 5 days of hospitalization prior to VAP, Acute renal replacement therapy prior, Same as HAP o Increased mortality § Ventilatory support required, Septic Shock, IV antibiotics within 90 days, Structural lung disease, Comorbidities · Symptoms/PE: See CAP pneumonia · Diagnostics: o New lung infiltrate (CXR) that is of infectious nature o Sputum or bronchial specimen cultures and gram stains o Molecular testing for pathogens—more specific · Treatment: o Is sepsis present? Yes then initiate aggressive treatment o No multidrug resistance: § Cefepime, Piperacillin-tazobactam, Imipenem (Usually reserved for when broad spectrum is needed), Levoflxacin · Can change to PO when patient tolerating clinically improved · Less effective against gram neg bacilli o Yes multidrug resistance § One from the following · Piperacillin-tazobactam, Cefepime, Ceftazidime, Imipenem, Meropenem § Plus one of the following · Aminoglycoside, Gentamicin, Amikacin, Tobramycin, Fluoroquinolone with antipseudomonal coverage, Ciprofloxacin, Levofloxacin (best for Legionella) § Plus one of the following · Linezolid, Vancomycin (special dosing) o Conversion to PO abx when Hemodynamically stable, Clinical improvement, Tolerate po meds o 7 days o Lack of response or deteriorating? § Wrong drug, Wrong organism, Complication underneath o Prevention of VAP: prevent colonization (clean) and aspiration

Acute bronchitis

· Pathophysiology: obstructive lung disease o LRTI involving the large airways (bronchi), w/o pneumonia, that occurs in the absence of COPD o acute inflammation, self-limited 1-3 weeks o Causes (healthy adults) § Viral (60%): Influenza A&B, Parainfluenza, Coronavirus types 1 to 3, Rhinoviruses, RSV § Bacterial: Bordetella pertussis, Chlamydia pneumoniae, Mycoplasma pneumoniae o Causes (COPD) § H. flu, Moraxella, Pneumococcus · Epidemiology/Risks: o most common conditions in ambulatory clinics with 10% of annual visits, > 100 Mil visits per year o Peaks late fall and winter (with most of the respiratory viruses (URI type)) o Smoking predisposes people · Symptoms/PE: o Cough, 1 - 3 weeks, With or without sputum (color doesn't indicate pathogen) o Preceded by URI o Wheezing, rhonchi, and mild dyspnea (Decreased FEV1 in 40%) § Bronchial hyper-responsiveness cause of prolonged cough (up to 6 weeks out) o Clinical features specific to other cause § Paroxysmal cough (whooping) = pertussis § Fever and systemic symptoms or Physical findings of rub, consolidation = consider pneumonia · Diagnostics: o Consider x-ray when : Abnormal vital signs, Signs of consolidation on physical, Mental status or behavioral changes in those > 75, immunocompromised, Underlying lung disease, Dyspnea, hemoptysis, Dementia o Labs: influenza, COVID 19, Procalcitonin · Treatment: o Healthy adults: § No antibiotics (until > 2 wks) + Bronchodilator (Albuterol inhaler) for wheezing § OTC: guaifenesin, dextromethorphan, Tesslon § ? Corticosteroids (wheezing) no great evidence § NO NARCOTIC COUGH SYRUPS · Complications: o Pneumonia, Hypoxia, Chest wall pain, rib fractures (from cough)

Emphysema "PINK PUFFER"

· Pathophysiology: obstructive lung disease o a disease of terminal respiratory units: loss of alveolar sacs, alveolar septa, capillaries o cause: imbalance of anti-oxidants (cigarette smoke contains oxidants that inhibit the normal protective function of protease inhibitors) and protease inhibitors (normally hold protein destruction in check) o decr protective enzymes (alpha-1 antitrypsin) incr in damaging enzymes (elastase release from macrophages and neutrophils) cause ALVEOLAR CAPILLARY DESTRUCTION o Destruction of elastin and other connective tissue elements in the lungs by these proteases leads over time to the loss of elastic recoil (decreased elastin and collagen) · Epidemiology/Risks: smoking, air pollution, hazardous dust · Symptoms/PE: o SOB, quiet lungs, thin; recent weight loss, increased AP diameter o chronic DRY cough, hyperinflation, decr breath sounds o Hyperresonance from air trapping to percussion, wheezing. o Severe disease: pursed lip expiration to increase airway pressure and precent airway collapse § Semi-tripod position to improve breathing · Diagnostics: o CXR; hyperinflation (lungs dark), diaphragm flattened, parenchymal bullae, inc AP diameter o Can be centrilobular (common w/ smoking), or panlobular (antitrypsin deficiency) o PFT: gold standard, show obstructive pattern that isn't fully reversible § Obstructive- decr FEV1, FEV1/FVC <70%, decr FVC § Hyperinflation- incr RV, TLC, RV/TLC, FRC; decr DLCO in emphysema · Treatment: see chronic bronchitis

COPD

· Pathophysiology: obstructive lung disease o loose term that includes several obstructive disorders (chronic bronchitis/emphysema) § Frequently, patients present with symptoms of both conditions. o increase in airway resistance, especially in expiration o Small airway disease airway obstruction § Airway inflammation, airway fibrosis, luminal plugs leading to increased airway resistance and therefore airway obstruction o Parenchymal destruction airway obstruction § Loss of alveolar attachments, decrease of elastic recoil, air-trapping causing airflow obstruction · Epidemiology/Risks: o Smoking (90%), inhaled irritants (10%), , alpha-1 antitrypsin and indoor pollution o men > women ; 4th leading cause of death in the world o age, lower SES, , occupational dust and chemicals, pollution, nutrition, infections · Symptoms/PE: chronic productive cough, noisy lungs with rhonchi and wheezing, peripheral edema, overweight and cyanotic, pursed lip breathing · Diagnostics: o CXR; increased interstitial markings at bases, blebs o PFT: (required for diagnosis) high RVC/TLC/CO2, low FEV1/FVC+FEV1 o GOLD CLASSIFICATION § STAGE 1- MILD: FEV1 > 80% predicted § STAGE 2-MODERATE 50-80% of predicted FEV1 § STAGE 3- SEVERE 30-50% of predicted FEV1 § STAGE 4- VERY SEVERE less than 30% of predicted FEV1 OR FEV1 < 50% predicted plus chronic respiratory failure o LUNG VOLUMES § Normal TLC = 80-120% § >120% = hyperinflation § <80% = restriction § 70-80% = mild § 60-70% = moderate 50-60% = moderately severe § < 50% = severe o RV/TLC < 35% = normal § RV/TLC > 35% (or greater than predicted) = air trapping o DLCO § > 120% = elevated; 80-100% = normal; 60-80% = mild; 40-60% = mod; < 40% = severe § DLCO can help distinguish asthma from COPD · Treatment: o Relieve sx, prevent disease progress, improve health status, prevent/treat complications, prevent/treat exacerbations, reduce mortality o Education, lifestyle change o Anticholinergics: ipratropium, tiotropium and umeclindinium are the most effective bronchodilators in COPD o also SABA/LABA/ICS

Chronic bronchitis "Blue Bloaters"

· Pathophysiology: obstructive lung disease o subtype of COPD defined as a cough that lasts >3mo in each of 2 successive years o Exacerbations: Acute infections · Epidemiology/Risks: Smoking, air pollution, hazardous dust, · Symptoms/PE: o chronic cough, sputum production, dyspnea, prolonged expiration o crackles/rales, rhonchi, wheezing. o JVD, peripheral edema, CYANOSIS AND BLUE BLOATER · Diagnostics: o PFT: obstructive pattern, not fully reversible (decr FEV1, FEV1/FVC < 70% pred, decr FVC) § Hyperinflation- incr RV, TLC, RV/TLC, FRC; normal DLCO o CXR: pulm HTN (enlarged rt heart border), incr AP diameter, incr vascular markings o ECG: cor pulmonale o CBC: incr H&H; o ABG: resp acidosis (severe hypoxia and hypercapnia) o Severe V/Q mismatch · Treatment: o See COPD

Asthma (reactive airway disease)

· Pathophysiology: obstructive lung disease, IgE, mast-cell mediated o chronic inflammatory disorder of the airways with bronchial hyperresponsiveness producing symptoms related to limited airflow that can be reversed § Desquamation of airway epithelium, smooth muscle hyperplasia, and airway remodeling can lead to permanent lung impairment o triggers: allergens, medications (particularly aspirin and nonsteroidal anti-inflammatory drugs), and environmental factors such as tobacco smoke and occupational exposure § Viral URIs are the most important triggering factor for ages § Exercise, high humidity, cold/dry air · Epidemiology/Risks/Risks: o One of most common chronic diseases of kids, up to 10% of adults self-report asthma o 80 % of children with atopic dermatitis develop asthma and/or allergic rhinitis later in childhood o Genetic predisposition possible, genes mainly involve immune system, environmental influences, obesity, early puberty · Symptoms/PE: o difficulty breathing, feeling of tightness in the chest o Coughing, wheezing (usually expiratory, can be inspiratory) o Acute: tachypnea, hypoxia, accessory muscle use, retractions, and prolonged expiratory phase o Allergic salute, Nasal polyps o Halitosis due to chronic rhinitis, sinusitis, and mouth breathing o Atopy-associated asthma: pale/swollen turbinates, cobblestoning in pharynx and/or conjunctiva, eczema/atopic dermatitis · Diagnostics: o HX and wheezing on PE, reversible and inducible sx o PFT § FEV1/FVC reduced, <.7/LLN, FEV1 obstruction <80%, High CO2 § Scooped, concave appearance to expiratory portion of flow-volume loop § After 2-4 puffs albuterol, increase of FEV1 >12% is pos response o Bronchoprovocation testing - useful for patients with normal baseline spirometry or no variability in peak flow or only cough as symptom of asthma o Labs- total IgE, eosinophil count, skin testing or blood testing for allergens o CXR: hyperinflation, longstanding asthma, rule out other differentials o Monitor peak expiratory flow rate! · Treatment: Reduce impairment and optimize lung function o bronchodilators and anti-inflammatories; education and med adherence are important o STEP WISE THERAPY § Mild intermittent- PRN low dose ICS-LABA; exercise-induced: pre-medicate 10 min before activity § Mild persistent- daily low-dose ICS or PRN low dose ICS-LABA, consider montelukast § Moderate persistent- daily low-dose ICS or LABA or medium dose ICS, consider montelukast § Severe persistent- daily medium or high-dose ICS-LABA § May need tiotropium, anti-IgE, anti-IL5/5R, anti-IL4R, or LD oral corticosteroid 🡪 follow with pulm/allergy o Patient educations: avoid triggers, use inhalers correctly, recognize attack sx o Hospitalize: § PEF <50% predicted or SpO2 <90% § No improvement with rescue SABA inhaler, Cannot speak full sentences, only short phrases § Tachypnea >30, Tachycardia >120 (or pulsus paradoxus), Tripod position § Flaring nostrils and/or pursed lips with inspiration § Accessory muscle use and/or retractions § Cyanosis - late sign § Decreased breath sounds are more worrisome than wheezing! § Absent breath sounds = EMERGENCY · Complications: o secondary bacterial or viral lower respiratory infections, those associated with chronic use of inhaled or oral glucocorticosteroids, respiratory failure, and rarely death.

Asbestos

· Pathophysiology: progressive parenchymal fibrosis o Group of "combined" silicates that form fibrous-like minerals that are resistant to high temperatures with varying latency from time of exposure to clinical or radiologic expression · Epidemiology/Risks: o Exposure: in asbestos mining/processing industries and in secondary industries such as insulation, textile manufacturing, construction and ship building · Symptoms/PE: o Pleural - Most common manifestation of exposure, rarely results in pulmonary impairment § Bilateral pleural thickening or plaques, Calcifications of pleural plaques, Effusions o Parenchymal fibrosis (Asbestosis) § Mid to lower lung distribution, interstitial lung disease due to asbestos § results in progressive pulmonary impairment o dyspnea, cough, hypoxemia, crackles, clubbing, cor pulmonale · Diagnostics: o PFTs: restrictive with decreased DLCO o CXR: primarily affects lower lobes; pleural plaques, interstitial fibrosis (honeycomb) ± "shaggy heart sign" o CT: calcified pleural plaques (honeycomb) o Bx: may show linear asbestos bodies o Abestos fibers § Light microscopy (Ferruginous Bodies) § Iron stains need to be requested § Do not distinguish mineral at core § Chrysotile fibers cleared from lung · Treatment: anti-fibrotics, supportive · Prognosis: o Malignancy - >20 yr latency § Mesothelioma - (pleural and peritoneal) § Bronchogenic Carcinoma

Idiopathic pulmonary fibrosis (diffuse parenchymal lung disease)

· Pathophysiology: restrictive disease o infiltration of inflammatory cells and fluid, fibrosis (fibrous connective tissue), scarring, loss of capillaries and alveolar tissues and remodeling, isolated to lungs o increased lung recoil pressures and increased stiffness o increased diffusion distances, leading to decreased diffusion of gases o loss of surfactant · Epidemiology/Risks: o 1/200 interstitial lung disease, others caused by occupation/environment o Age 60-80, M>F, white o Hx smoking, genetic variants of a number of genes, exposure to metal and wood dust, and possibly gastroesophageal reflux and exposure to certain viruses · Symptoms/PE: o progressive exertional dyspnea, dry cough, fatigue, tachypnea, o clubbing; cyanosis; and bibasilar, inspiratory, dry ("velcro") crackles o fine mid-end inspiratory crackles overlying both lung bases, digital clubbing, and signs of R sided heart failure with advanced disease · Diagnostics: dx of exclusion o PFT: restrictive defect (reduced FVC and TLC) and decreased DLCO § Exertional hypoxemia on ExOx o High-resolution computed tomography (HRCT): § UIP pattern key components · Subpleural, basilar predominance · Reticular pattern with traction bronchiectasis · Subpleural honeycombing · NO ground glass, nodules, cysts, etc o Consider surgical lung biopsy to detect a usual interstitial pneumonia pattern if HRCT is not definitive · Treatment: o Co-morbidities: GERD, COPD, OSA, PH, Psych o Oxygen therapy o Antifibrotic agents (slow decline in FVC): Esbriet (pirfenidone), Ofev (nintedanib) o Lung transplantation o Acute exacerbations: Vaccinations (prevention) · Complications: o Average life expectancy 3-5 years from Dx o Increased incidence of: bronchogenic carcinoma, pulm HTN o Acute exacerbations: Often fatal, If survived can hasten decline

Sarcoidosis

· Pathophysiology: restrictive disease, Multisystem disease of unknown etiology o Characteristic non-caseating granulomas § Caseation: necrosis with conversion of damaged tissue into a soft cheesy substance § Granuloma: a mass or nodule of chronically inflamed tissue with granulations that is usually associated with an infective process · Epidemiology/Risks: o 70-90% of cases in 10 - 40 yr old, F>M o 3-4x more common in African Americans (more acute, severe disease than whites) · Symptoms/PE: 50% asymptomatic o 90% involves lungs § Bilateral hilar adenopathy § Pulmonary reticular opacities fibrosis o Constitutional symptoms - fever, anorexia, fatigue, malaise o Organ specific symptoms § Ophthalmologic (20%): uveitis § Cardiac (5%): heart block, PVCs , VT, cardiomyopathy § Dermatologic (30%): sarcoidal skin plaques, erythema nodosum, lupus pernio, scars § Hepatic/Splenic (25%): enlargement § Bone/Joint: migratory polyarthritis, poly/monoarticular arthritis, chronic arthritis § CNS (5%): facial nerve palsy, seizures, hypothalamus fnx § Renal: hypercalcemia, renal failure o Lofgren's Syndrome: acute onset with fever, arthralgia, hilar adenopathy and erythema nodosum - good prognosis o Uveoparotid Fever (Heerfordt's syndrome): fever, uveitis and parotiditis o cough, dyspnea of insidious onset, chest discomfort, skin (25% cases); erythema nodosum, lupus pernio, eyes (25% cases); dry eye (SICCA), anterior uveitis, parotiditis, LAD · Diagnostics: OF EXCLUSION! o Radiographic Findings: § Adenopathy: Bilateral hilar and/or mediastinal § Parenchymal: reticulonodular, alveolar, nodules § Granulomas may be calcified § Pleural effusion: very rare § Patterns: · Stage 0: normal · Stage1: Hilar/mediastinal adenopathy, nl parenchyma (good prognosis) · Stage 2: Adenopathy with parenchymal disease (<50% spontaneously resolve) · Stage 3: Diffuse parenchymal disease, No adenopathy (<25% spontaneously resolve) · Stage 4: Fibrotic/Honeycombed lung · Nodular o Bronchoalveolar lavage o Biopsy: non-caseating granulomas o Supportive labs: hyperCA, increased 1,25 VitD, High CD4/CD8 ratio, Lymphocytopenia, Elevated globulins o Negative w/u for TB, fungal, malignant processes o leukopenia, eosinophilia, hypercalcemia, hypercalciuria, angiotensin-converting enzyme levels elevated in up to 75% patients, bilateral hilar lymphadenopathy** or parenchymal lung involvement, occurring in 90% of cases, transbronchial bx of the lung or FN bx confirms dx · Treatment: o Oral corticosteroids are first line o Immunomodulatory therapy o Methotrexate, azathioprine, Plaquenil, Anti TNF, Remicade o Indications of treatment: § Progressive or symptomatic pulmonary disease § Ocular impairment § Cardiac or CNS sarcoidosis § Cutaneous lesions § Hypercalcemia/hypercalciuria with renal insufficiency · Prognosis- 65% recover completely, 20% permanent disability. Mortality 5-10%

Idiopathic Interstitial Pneumonia

· Pathophysiology: restrictive disease, SEE ILD · Epidemiology/Risks: SEE ILD · PE: o Rash, Telangiectasias, Sclerodactyly / Skin thickening o Mechanics hands, Gottron papules/sign o Periungual erythema/hypertrophy o Nail fold Capillaries o Digital ulcers /pulp loss o Synovitis, Muscle weakness o Parotid swelling · Symptoms: o Dyspnea, Crackles, Clubbing, Cyanosis o Asymptomatic (Sarcoid) o Exertional dyspnea, Cough (dry) o Symptoms of systemic disease · Diagnostics: o Pulmonary Function Testing: § Restrictive ventilatory defect · Decreased FVC with normal/ increased FEV1/FVC ratio · Decreased total lung capacity (TLC) § Decreased DLCO (gas diffusion capacity) § Arterial oxyhemoglobin desaturation with exercise o Radiographic Findings: § Increased interstitial markings § fine reticulation or coarse reticulation § reticulonodular, honeycombing § Fibrotic or Non-fibrotic (reversibility) § Associated Findings vary by etiology · Honeycombing - IPF · Ground Glass (inflammation) - CTD-ILD · Mediastinal / Hilar Adenopathy - Sarcoid · Consolidation - Organizing pneumonia · Mosaic pattern (air trapping) - HSP · Pleural Effusions - SLE · Nodules, Cysts o Chest CT, Echo (for pulmonary htn) o Labs: CBC, Ca/VitD, UA, ANA/Scl-70, RF/CCP, Myositis panel, SSA/SSB, HIV, HSP panel, ANCA · Treatment: o if progressive, fibrosing antifibrotics o if inflammatory give immunosuppressants

Oxyhemoglobin Dissociation Curve

· Relationship between oxygen carried in combination with hemoglobin and the PO2 of blood is described by this curve · X-axis- PO2 or dissolved oxygen. Reflects partial pressure of oxygen in the lungs. o PO2 ranges from 95-11 mmHg when breathing room air but can rise to 200 mmHg when O2-enriched air is breathed. · Y-axis- o LEFT depicts Hgb saturation or the amount of oxygen that is carried by hemoglobin. o RIGHT y axis depicts O2 content or total amount of oxygen that is being carried in the blood · S-shaped oxygen dissociation curve reflects the effect that O2 sat has on the conformation of the hemoglobin molecule and its affinity for O2. o Flat upper right represents binding of O2 to hemoglobin in the lungs. Occurs around 100 mmHg PO2, where hemoglobin is 98% saturated. o The steeper lower-left portion of the curve—between 40-60 mmHg represents the removal of O2 from hemoglobin as it moves through the tissue capillaries. § Reflects the fact that there is considerable transfer of O2 from hemoglobin to the tissues with only a small drop in PO2, ensuring a gradient for O2 to move into body cells. § Tissues normally remove 5mL O2 per dL blood is approx. 75% saturated as it returns to the right side of the heart. · Hemoglobin can be regarded as a buffer system that regulates the delivery of oxygen to tissues. In order to function as buffer, the affinity of hemoglobin · Right shift- indicates that the affinity of hemoglobin for oxygen is decreased and the PO2 that is available to the tissues at any level of hemoglobin saturation is increased. o Can be caused by increase in tissue metabolism, fever, acidosis or increase in PCO2. High altitude and conditions such as pulmonary insufficiency, heart failure, severe anemia can also cause curve to shift right o Anemia · Left shift- affinity of hemoglobin for O2 is increased and the PO2 that is available to the tissues at any given level of Hgb saturation is decreased. It occurs in situations associated with a decrease in tissue metabolism, such as alkalosis, decreased body temperature, decreased PCO2 levels. o Degree of shift determined by P50-partial pressure of O2 that is needed to achieve 50% saturation of hemoglobin. o CO poisoning · Total oxygen content is total amount of oxygen that is carried in the blood, including the dissolved oxygen and that carried by Hgb

CT pulmonary angiography

· Used to obtain an image of the pulmonary arteries with the maximum intensity of radio-opaque contrast in the pulmonary arteries · Useful to trace pulmonary embolism · Contrast is rough on the kidneys, so cannot do in somebody with renal disease

Consolidation

· What it is: Alveoli fill with fluid, as in pneumonia · Percussion note: Dull over the airless area · Trachea: Midline · Breath sounds: Bronchial over the involved area · Adventitious sounds: Late inspiratory crackles over the involved area · Tactile fremitus and transmitted voice sounds: Increased over the involved area, with egophony, bronchophony, and whispered pectoriloquy

Pleural effusion

· What it is: Fluid accumulates in the pleural space and separates air-filled lung from the chest wall, blocking the transmission of breath sounds. · Percussion note: Dull to flat over the fluid · Trachea: Shifted toward the unaffected side in a large effusion · Breath sounds: Decreased to absent, but bronchial breath sounds may be heard near top of large effusion. · Adventitious sounds: None, except a possible pleural rub · Tactile fremitus and transmitted voice sounds: Decreased to absent, but may be increased toward the top of a large effusion

Healthy lung

· What it is: The tracheobronchial tree and alveoli are open; pleurae are thin and close together; mobility of the chest wall is unimpaired. · Percussion note: Resonant · Trachea: Midline · Breath sounds: Vesicular, except perhaps bronchovesicular and bronchial sounds over the large bronchi and trachea, respectively · Adventitious sounds: None, except a few transient inspiratory crackles at the bases of the lungs · Tactile fremitus and transmitted voice sounds: normal

Pneumothorax

· What it is: When air leaks into the pleural space, usually unilaterally, the lung recoils away from the chest wall. Pleural air blocks transmission of sound. · Percussion note: Hyperresonant or tympanitic over the pleural air · Trachea: Shifted toward the unaffected side if tension pneumothorax · Breath sounds: Decreased to absent over the pleural air · Adventitious sounds: None, except a possible pleural rub · Tactile fremitus and transmitted voice sounds: Decreased to absent over the pleural air

ORGANIC DUSTS

• Cotton dust—sx worse early in week, chest tightness Monday, causes obstructive pattern • Grain—typically d/t grain storage exposure, clinically similar to tobacco-induced LD • Farmer's lung—mechanism d/t moldy hay spores can cause hypersensitivity pneumonitis; may be acute or chronic § Suberosis (moldy cork dust) § Byssinosis (cotton dust, flax and hemp) § Malt Worker's Lung (Aspergillus clavatus) § Maple Bark Disease (Cryptostroma) § Bagassosis (Thermoactinomyces sacchari) § Mushroom-Worker's Lung (Micropolyspora) § Bird Fancier's Lung (bird proteins/dander) § Farmer's Lung (thermophilic actinomycetes) § Hot Tub Lung (MAI/MAC)

Obstructive Lung Disease

• Obstructive diseases are associated with problems of airway resistance. • Resistance is reduced during both inspiration and expiration, but it is most impaired during expiration because of dynamic airway compression during forced efforts to get air out of the lungs • Problem with obstructed airflow • Inflamed, easily collapsible airways • Higher residual volume • Higher total lung capacity • MOST HELPFUL WITH PFT • Are they obstructed? • Yes: FEV1/FCV <70/LLN No: FEV1/FCV >70

Ventilation-Perfusion (V/Q) mismatch

• V/Q ratio is an expression of the matching of ventilation and perfusion • V/Q can be used to look at ventilation-perfusion matching for a region of the lung or for the whole lung • any factor that changes either ventilation or perfusion changes V/Q • normal V/Q of the whole lung is 0.8, partly due to gravitational effects • The weight of the lungs pulls tissue more at the apex (top) than at the bottom • Gravity causes greater volume and flow of blood at the bottom of the lung - • Therefore, as a result of gravity, both ventilation and perfusion are less at the top • normal ventilation and perfusion (normal V/Q) • blood and alveoli here reflect normally good diffusion and equilibration of gases • venous blood coming into lungs has low PO2 and high PCO2 • with rapid equilibration, blood PO2 increases and blood PCO2 drops and • PAO2 decreases, PACO2 increases • decreased ventilation (and decreased V/Q) • in this example, there is a total blockage of the respiratory unit (perfusion is normal); • therefore, alveolar ventilation is zero and • V/Q is zero • PAO2 and PACO2 resemble blood values, because diffusion is normal; • referred to as shunted blood or a physiological shunt • decreased perfusion (and increased V/Q) • ventilation here is normal, but there is no blood flow through the area • Q is zero, so V/Q is infinity (think extremely large!) in this area • PAO2 and PACO2 resemble the conducting airways (there is no gas exchange) • this scenario represents physiologic dead space

Restrictive Lung Disease

• inspiratory movement is restricted. These problems are usually associated with diseases of the interstitium • restricts lung expansion • increased lung connective tissue • inflammation of alveolar epithelium • thickened interstitium and membranes • ↓ TLC, RV, FVC, FEV1 • Anatomic reasons, drug adverse reactions, ILD, neuromuscular lung disorder

alveolar-arterial gradient for O2

• measure of the difference between the concentrations (partial pressures) of oxygen in the alveoli (PAO2) and systemic arterial blood (PaO2). • diagnose conditions of hypoxemia (low blood oxygen) by checking the integrity of the alveolar-capillary membranes (not enough oxygen in alveoli or not enough diffusion). • In conditions of low oxygen and normal membranes, the A-a gradient does not change significantly. • With diseased membranes, a V/Q abnormality, or a right-to-left shunt, the A-a gradient will increase showing diffusion problem, V/Q abnormalities, or a right-to- left shunt • normal V/Q mismatch, the normal A-a gradient is 5-10 mm Hg in young adults (nonsmokers). • The gradient changes with age increases about 1-2 mm Hg per decade of age. • A healthy 40 year old should have a gradient of less than 14-15 mm Hg); at 80, the gradient is expected to be about 24 mm Hg. • A-a gradient = (Pt age /4) + 4 • Positive A-A gradient >10 means there is sufficient alveolar oxygen but not enough arterial oxygen so there is a problem getting oxygen from alveolus to blood (diffusion) • Lung disease • Negative A-A gradient <10 means diffusion barrier is intact but it's not getting enough oxygen to the alveolus • High altitudes • Ventilation problem (neuromuscular weakness in MS, MG, obesity, sedation)

the posterior-anterior view

□ Comment on whether or not this is correct patient, correct date and correct study □ Assess for the technical adequacy of the film and make a comment about whether or not it is technically adequate 1. Penetration: Should be able to see the spine through the heart 2. Inspiration: Should see at least 8 to 9 posterior ribs 3. Rotation: Spinous processes should fall equidistant between the medial ends of the clavicles 4. Magnification: Heart will be magnified on AP/portable films 5. Angulation: Clavicle normally has an S shape, and medial end superimposes onto the 3rd or 4th rib □ Airway Comment on the trachea—is it patent? Narrowed? Midline? Can deviate to the right in adults due to the aortic arch □ Bone Comment about the bony structures—are there any fractures? Lytic lesions? Deformities? Extra or missing bones? Pay attention to clavicles, ribs, scapulae, thoracic vertebrae, and humeri □ Cardiac Comment on the size—is it less than half the transthoracic diameter? Comment on the borders—are they clear/well defined? □ Diaphragm Is the outline of the diaphragm clear and smooth? Are the costophrenic angles well defined? (Whiteness immediately above the diaphragm indicates pleural effusion or consolidation) Is there any air below either hemidiaphragm to indicate bowel perforation? (pneumoperitoneum) □ Lung fields Comment on whether or not the lucency of the right and left lung fields are equal/symmetrical? Are there any infiltrates/opacities? □ Gastric bubble Point out the air bubble below the left hemidiaphragm □ Hilum and mediastinum Hilum= pulmonary arteries, lymph nodes Mediastinum=an area outside of the lungs whose lateral margins are defined by the medial borders of each lung, anterior margin is the sternum and posterior margin is the spine Examples of mediastinal masses Mediastinal masses originate from thyroid, lymph nodes, descending aorta, etc.

lateral chest x-ray

□ Retrosternal space Clear space behind the sternum Often looks like a crescent shape □ Hilar region Assess for masses or other abnormalities □ Thoracic spine Normally the thoracic spine appears to get darker as you go from top to bottom because there is less dense tissue for the x-ray beam to transverse just above the diaphragm Pneumonia in the left lower lobe is an example of what might cause the bodies to be more white = spine sign □ Right and left hemidiaphragms and costophrenic sulci/angles Right hemidiaphragm is usually visible from its entire length from front to back and is slightly higher than the left Left hemidiaphragm is better/more sharply seen posteriorly but is silhouetted by the muscle of the heart anteriorly, its edge disappears anteriorly Posterior costophrenic sulci/angles are usually sharply outlined and acutely angled In conclusion: □ Brief statement of your overall findings □ Organized approach and ability to defend statements

CA/CM II PULMO

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