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Pulmonary Medicine Review: Respiratory Exam, Diagnostics, and Disease States

Respiratory assessment and examination

  • Abnormal breathing effort or patterns offer clues to pathology (e.g., Cheyne-Stokes, Biot, ataxic breathing).

  • These patterns often indicate changes in neurologic control of respiratory drive and are common in advanced metabolic states, end-of-life, or severe neurologic injury.

  • Look for use of accessory muscles (sternocleidomastoids, intercostals), marked retractions, and overall work of breathing.

  • Audible upper-airway noises (stridor, snoring, gurgling, gasping) suggest upper airway narrowing; noises arise from airflow through constricted passages.

  • Inspiratory gasp (whooping sound) is classic for pertussis and explains the name “whoop.”

  • Retractions and accessory muscle use indicate increased diaphragmatic effort and outward thoracic cavity movement for lung expansion.

  • Chest deformities and chest-wall abnormalities can develop with chronic or congenital conditions; assess front-to-back AP diameter (barrel chest in emphysema).

  • Chest wall deformities examples: pectus excavatum and pectus carinatum (perinatum in transcript).

  • Severe deformities can contribute to pulmonary and cardiovascular issues; include these in differential diagnoses.

  • Trauma can cause chest-wall abnormalities; palpate for crepitus and segmental movement that is not synchronized with the chest wall (paradoxical movement/sucking sound).

  • Tracheal position: midline trachea is normal; tracheal deviation is a late, severe finding (seen with large pneumothorax or cardiac tamponade).

Auscultation and breath sounds

  • Breath sounds are generated by airflow against bronchial walls; larger airways yield louder sounds.

  • Vesicular breath sounds: normal, low-pitched, heard in most lung fields.

  • Tracheal breath sounds: high-pitched and loud over large airways.

  • Density changes/displacements (fluid, air in bullae, pleural effusion) reduce normal sounds; terminal-airway obstruction can shift sounds toward bronchial sounds.

  • Adventitious sounds to identify in exam/questions:

    • Crackles (rails): high-pitched popping sounds from alveolar units opening; common with pulmonary edema, CHF, cirrhosis, and interstitial fluid accumulation.

    • Wheezes: high-pitched musical sounds from narrowed airways; often bronchospasm (e.g., asthma).

    • Rhonchi: low-pitched “snoring”/gurgling sounds from mucus obstruction; seen with mucus production (CF, pneumonia).

    • Pleural friction rub: fine, grating sounds like walking on snow; due to pleural surface irritation.

Percussion and fremitus

  • Percussion is like tapping a drum to assess air vs fluid vs solid tissue:

    • Normal: resonant (air-filled).

    • Dull: fluid or inflammation in the area.

    • Hyperresonant: increased airspaces (e.g., COPD, emphysema, pneumothorax).

  • Tactile fremitus:

    • Increased fremitus with increased tissue density (consolidation).

    • Decreased fremitus with increased air in the chest (emphysema; hyperinflation).

    • A common mnemonic in practice is “99” vs “111” to compare vibration transmission (some instructors prefer 99; others prefer 111).

Pulmonary function tests (PFTs) and spirometry

  • Primary PFT tool: spirometry; provides objective measures over time or in response to therapy.

  • Challenges: requires patient cooperation and following directions; difficult in children ≤4 years.

  • Additional PFT measures and tests include: DLCO (diffusion capacity for CO), six-minute walk test, bronchoprovocation testing.

  • Key spirometry metrics:

    • FVC: Forced Vital Capacity — total volume exhaled.

    • FEV1: Forced Expiratory Volume in 1 second — air moved in the first second of exhalation.

    • FEV1/FVC ratio: often used to distinguish obstructive vs restrictive disease.

    • Typical target values: FEV1/FVC ext{ ratio}
      ightarrow ext{ often } rac{FEV1}{FVC} \, ext{percentage} ext{ around } 80 ext{%}; many vignette answers use thresholds around 75–80% (commonly 75 or above).

  • Diagnostic interpretation:

    • Obstructive disease: reduced FEV1 with reduced FEV1/FVC ratio; volumes may be preserved or reduced depending on stage.

    • Restrictive disease: reduced FVC with normal or increased FEV1/FVC ratio.

  • Common indications for spirometry:

    • Presenting symptoms suggesting pulmonary disease (exertional dyspnea, nighttime cough).

    • Risk factors (heavy smoker, strong family history of asthma).

    • Preoperative assessment (DLCO and PFTs to predict postoperative function).

    • Monitoring disease control and therapy response (e.g., after initiating inhaled corticosteroids).

  • Pre- and post-bronchodilator testing:

    • Look for bronchodilator response (e.g., increase in FEV1 by >12% and >200 mL post-bronchodilator) to help diagnose reversible obstruction.

  • Other diagnostic notes:

    • Allergy testing and FeNO (fractional exhaled nitric oxide) data helpful in allergic asthma.

    • Imaging (chest X-ray, high-resolution CT) used for screening, to assess chronic changes, and to exclude other etiologies.

Arterial blood gases (ABG) and acid-base interpretation

  • Core ABG components: pH, PaCO2, and bicarbonate (HCO3-).

  • Normal reference ranges (useful quick mental model):

    • pH: 7.35 o 7.45

    • PaCO_2: 35 o 45 ext{ mmHg}

    • HCO_3^-: 22 o 26 ext{ mEq/L}

  • Quick memory aid: pH normal around 7.40; pCO2 normal around 40; bicarbonate normal around 24.

  • Respiratory disorders (acute vs chronic) interpret by the direction of pCO2 and pH:

    • Respiratory acidosis: low pH with high PaCO2.

    • Respiratory alkalosis: high pH with low PaCO2.

  • Metabolic disorders:

    • Metabolic acidosis: low pH with low HCO3-.

    • Metabolic alkalosis: high pH with high HCO3-.

  • Compensation concepts:

    • Primary respiratory disorder compensation: kidneys alter bicarbonate to compensate (buffer system).

    • Steps to analyze ABG:

    • Step 1: Look at pH to determine acidosis vs alkalosis.

    • Step 2: Check PaCO2 (respiratory acid) vs HCO3- (metabolic base) to identify primary process.

    • Step 3: If pH is abnormal, assess whether CO2 and HCO3- move in opposite directions (respiratory origin) or in same direction (metabolic origin).

    • Step 4: Evaluate compensation:

      • Partial compensation: pH not normalized; abnormal CO2 and HCO3- with opposite directions (respiratory primary) or same direction (metabolic primary).

      • Full (complete) compensation: pH near normal while CO2 and HCO3- remain abnormal; kidneys have adjusted to restore pH towards normal.

  • Respiratory compensation is typically faster than metabolic compensation; metabolic compensation (bicarbonate adjustment) takes longer.

  • Practical ABG approach:

    • If pH is low and PaCO2 is high, likely primary respiratory acidosis.

    • If pH is high and PaCO2 is low, likely primary respiratory alkalosis.

    • If pH is low with low HCO3-, metabolic acidosis; if pCO2 is high, there may be concurrent respiratory acidosis.

Major obstructive airway diseases

Asthma

  • Heterogeneous syndrome with bronchospasm and airway inflammation; airway edema and hyperresponsiveness.

  • Triggers: allergies, infections, irritants, occupational exposures; including aspirin-exacerbated respiratory disease (Samter's triad: asthma, nasal polyps, NSAID sensitivity).

  • Exercise-induced bronchoconstriction (EIB) due to catecholamine flux; typically treated with albuterol; inhaled corticosteroids (ICS) are not the primary initial therapy for EIB alone.

  • Phenotypes/classification (retrospective): intermittent, persistent, severe (brittle) asthma; severity assessed by symptom frequency, nighttime awakenings, exacerbations, and inhaler use.

  • Acute exacerbation progression: early response to rescue inhaler; late phase with mucosal inflammation if untreated.

  • HPI and exam clues: dyspnea, cough, chest tightness, fatigue; wheezing; prolonged expiratory phase; accessory muscle use; tachypnea; speaking difficulty (two-word or one-word sentences) due to breathlessness.

  • Red flags: fatigue with diminished effort; quiet breath sounds suggesting severe inflammation and impending respiratory failure.

  • Workup in acute asthma: spirometry with bronchodilator response (pre- and post-bronchodilator FEV1 and FEV1/FVC; improvement criteria: >12% and >200 mL); bronchoprovocation testing with methacholine if baseline spirometry is inconclusive; FeNO and IgE testing for allergic components; chest X-ray primarily to exclude other causes; asthma action plan (green/yellow/red traffic-light system).

  • Age-specific management:

    • <4 years: presumed asthma; rescue albuterol; consider low-dose ICS; escalate to medium-dose ICS as needed; red-stage may require high-dose ICS or oral steroids; PRN albuterol; montelukast as add-on; environmental control; immunotherapy in select cases.

    • 5–11 years: start with ICS (low dose) ± add-ons; consider oral steroids for exacerbations; consider leukotriene receptor antagonists; step-up therapy based on control.

    • >12 years (adults): minimize reliance on frequent short-acting beta-agonists (SABA); maintain ICS as baseline; consider LABA/LAMA combinations; triple therapy (ICS + LABA + LAMA) for persistent disease; add montelukast; consider biologics for moderate-to-severe allergic or eosinophilic asthma (anti-IgE, anti-IL4R, IL5/IL5R pathways, etc.).

  • Acute asthma management: short course systemic steroids (e.g., prednisone 40–60 mg for adults for 3–5 days, or appropriate pediatric dosing), inhaled bronchodilators (albuterol), DuoNeb (albuterol + ipratropium), magnesium for smooth-muscle relaxation, oxygen if hypoxic, noninvasive ventilation if needed, and intubation as a last resort in refractory cases.

  • Important therapeutic notes: minimize systemic steroids due to long-term risks; use environmental control and trigger avoidance; establish an action plan and ensure patient education about med use.

  • Immunotherapies and biologics: anti-IgE (omalizumab) for allergic asthma; anti-IL-4/IL-13 (dupilumab) for eosinophilic asthma; TSLP inhibitors (e.g., tezepelumab) for broader eosinophilic/allergic components; other agents target specific pathways (IL-5/IL-5R).

Chronic Obstructive Pulmonary Disease (COPD)

  • COPD umbrella term including chronic bronchitis, emphysema, and COPD with asthma overlap (A CO more overlap as disease evolves).

  • Chronic bronchitis: productive cough for at least 3 months in two consecutive years; mucus hypersecretion.

  • Emphysema: destruction of alveolar walls and enlargement of airspaces; air trapping; less mucus production.

  • COPD is largely not reversible; tissue destruction is largely irreversible.

  • COPD phenotypes and risk factors:

    • COPD-C: cigarette smoke, vaping, secondhand smoke, smoke exposure.

    • COPD-P: pollution or occupational exposure.

    • COPD-G: alpha-1 antitrypsin deficiency (younger patients with emphysema-like changes).

    • COPD-D: development (infection-related changes).

    • COPD-A: overlap with asthma.

  • Clinical phenotypes: pink puffers (emphysema) vs blue bloaters (chronic bronchitis).

    • Pink puffers: emphysema, dyspnea with minimal sputum, weight loss, pursed-lip breathing.

    • Blue bloaters: chronic bronchitis, cyanosis, productive cough, obesity, edema, sometimes cor pulmonale.

  • Diagnosis and assessment:

    • Symptoms: chronic cough, dyspnea, exertional dyspnea, sputum production.

    • Physical exam: prolonged expiration, decreased tactile fremitus, hyperresonant to percussion in emphysema, sometimes dull basally due to atelectasis.

    • Complications of advanced COPD: cyanosis, cor pulmonale (right-heart failure), JVD, hepatomegaly, tripod positioning, respiratory failure.

    • Clinical tools: MMRC dyspnea scale; COPD assessment test (CAT).

    • Spirometry: pre-bronchodilator FEV1 < 80% predicted and FEV1/FVC < 0.75 often present; bronchodilator response limited in established COPD.

    • Imaging: chest X-ray and high-resolution CT for bullae, hyperinflation, and volume loss; signs include hyperinflation, flattened diaphragms, vertical heart, decreased lung markings, possible bullae.

  • Gold classification and staging: based on FEV1, with additional ABCDE (exacerbations/hospitalizations) considerations:

    • GOLD 1 (mild) FEV1 ≥ 80%

    • GOLD 2 (moderate) 50% ≤ FEV1 < 80%

    • GOLD 3 (severe) 30% ≤ FEV1 < 50%

    • GOLD 4 (very severe) FEV1 < 30%

    • Exacerbation history (ABE): A (0–1 exacerbations, no hospitalization), B (more symptoms but not hospitalized), C and D (exacerbations with hospitalizations).

  • Gold standard management: address underlying cause (smoking cessation; vaccinations against influenza, pneumococcus, Tdap; pulmonary rehab; airway clearance and mucus management; tough cough training; palliative care when end-stage); consider oxygen therapy for hypoxemia; consider surgical approaches like lobectomy or bullectomy for localized disease; endobronchial valves for targeted airspace management; palliative measures when appropriate.

  • Pharmacologic COPD treatment: long-acting muscarinic antagonists (LAMA), long-acting beta-agonists (LABA), bronchodilator combinations (e.g., LABA/LAMA; triple therapies like ICS/LABA/LAMA);

    • Antibiotics for acute exacerbations depending on suspected etiology (e.g., azithromycin for anti-inflammatory and antibiotic effects; Augmentin, levofloxacin, cefdinir, ceftriaxone, etc.), with Pseudomonas risk guiding whether to use anti-pseudomonal coverage (e.g., piperacillin-tiperacillin, cefepime); avoid routine long-term macrolide prophylaxis due to resistance concerns.

    • Mucoregulators and hydration for mucus clearance; alpha-1 antitrypsin augmentation for deficiency.

    • Noninvasive ventilation (BiPAP/CPAP) preferred over invasive ventilation for acute COPD exacerbations when feasible.

  • Screening and prevention: USPSTF recommends low-dose CT for high-risk adults 50–80 with a smoking history; annual scans for high-risk individuals; discontinue screening based on life expectancy and compliance.

  • Comorbidities and prognosis: pneumonia risk high; DVT/PE risk rises with reduced mobility; pulmonary rehab improves mortality and morbidity; oxygen therapy improves survival in hypoxemic COPD.

Cystic Fibrosis (CF)

  • Etiology: CFTR gene mutation leading to defective chloride/sodium transport; thick, tenacious secretions in multiple organs; saltier sweat; pancreas and reproductive tracts affected; autosomal recessive (two abnormal alleles required).

  • Demographics: more common in Caucasians; life expectancy extended recently due to gene therapies and multidisciplinary care; newborn screening is important for early detection.

  • Genetic risk: if both parents are carriers (one mutant allele each), offspring have a 25% chance of affected, 50% carrier, 25% unaffected.

  • Diagnostic tests: elevated sweat chloride test; nasal potential difference; stool fat tests; pancreatic enzyme evaluation; genetic testing for CFTR mutations.

  • Clinical presentation: in infants, meconium ileus, failure to thrive, respiratory symptoms; persistent sinus/nasopharyngeal disease; pancreatic insufficiency leading to malabsorption; recurrent infections; possible pancreatitis and iron deficiency; infertility due to congenital bilateral absence of the vas deferens in many males.

  • Management: referral to CF center; multidisciplinary care including pulmonology, GI, nutrition; chest physiotherapy and airway clearance techniques; mucolytics; chest therapies; vaccines; CFTR modulators (targeted therapies); pulmonary rehab; nutrition and pancreatic enzyme replacement; transplant considerations in advanced disease.

Restrictive lung diseases

  • Restrictive disorders affect lung tissue/parenchyma rather than airways; FEV1 can be reduced with a relatively preserved or normal FEV1/FVC ratio.

  • Analogy: tissue behaves like a sponge that has dried out and stiffened; expansion and recoil are impaired.

  • Diagnosis and approach:

    • Usually diagnosed by exclusion; rule out obstructive disease first.

    • Causes include connective tissue diseases, radiation injury, medication toxicity (e.g., amiodarone), hypersensitivity pneumonitis, pneumoconioses (asbestosis, silicosis, berylliosis), sarcoidosis, and other multisystem diseases.

    • Imaging helps define fibrosis or interstitial involvement; bronchoalveolar lavage and biopsy may be required for diagnosis.

    • Complications include cor pulmonale due to chronic hypoxemia and pulmonary hypertension.

  • Examples of restrictive etiologies:

    • Pneumoconiosis (asbestosis, silicosis, coal workers’ lung, berylliosis) with exposure histories.

    • Sarcoidosis: noncaseating granulomas; typical in young Black females in the U.S.; may be asymptomatic early; symptoms include cough, dyspnea, fever, arthralgia; may have uveitis; elevated ACE; hypercalcemia; hilar lymphadenopathy on CXR; diagnosed by biopsy; limited treatment options; can progress to fibrosis.

Pulmonary nodules and cancer

  • Pulmonary nodules are often incidental findings; most are benign (vascular lesions or granulomas).

  • Risk factors for malignant nodules: age >65, smoking, prior chest radiation; benign nodules tend to be smooth and round; suspicious nodules may be spiculated or irregular.

  • Follow-up and workup:

    • Small, low-risk nodules: surveillance with annual CT (or semiannual depending on risk).

    • Nodules that double in size quickly (e.g., within 2 months) or grow too slowly (>2 years) are more likely benign or malignant depending on context.

    • Larger, suspicious lesions: CT-guided biopsy, bronchoscopy, PET scanning for staging; consider mediastinal lymph node sampling.

  • Neoplasms and subtypes:

    • Carcinoid tumors: often in younger patients; not strongly linked to smoking; often slow-growing; may present with paraneoplastic syndromes (carcinoid syndrome: flushing, diarrhea, wheezing); relatively favorable 5-year survival after resection.

    • Non-small cell lung cancer (NSCLC): most common primary lung cancer; subtypes include adenocarcinoma (peripheral, often in COPD/emphysema), squamous cell (central, near bronchi, possible endobronchial mass), and large cell (peripheral, poorly differentiated).

    • Small cell lung cancer (SCLC): two types: oat cell and combined; strongly associated with paraneoplastic syndromes (e.g., SIADH, Cushing); most aggressive with poorer prognosis; not typically amenable to surgical resection.

  • Staging and treatment: TNM staging guides prognosis and therapy; many NSCLC patients undergo resection in early-stage disease; adjuvant chemotherapy, radiotherapy, and immunotherapy vary by stage; SCLC typically treated with chemotherapy (limited vs extensive) rather than surgical resection; 5-year survival varies by stage and histology (high for resectable NSCLC with good outcome; limited statistics for SCLC).

  • Metastatic disease: intrathoracic and extrathoracic metastases common (bone, brain, liver, adrenal glands); brain metastases more common with certain histologies (SCLC, adenocarcinoma); treatment includes multidisciplinary tumor boards, systemic therapy, targeted therapy, and palliative care when appropriate.

Infections and inflammatory diseases

Influenza

  • Etiology: influenza A or B; transmission via respiratory secretions; prevention includes vaccination and infection-control practices.

  • Clinical course: uncomplicated influenza presents with flu-like symptoms (myalgias, headache, fever, malaise) typically within ~12 hours of onset.

  • Complications: progression includes worsening respiratory symptoms and potential respiratory failure; severe cases may require advanced support (e.g., ECMO in extreme lung injury).

  • Diagnostics: primarily clinical; rapid antigen tests or PCR are available depending on setting.

  • Treatment and prevention: mostly supportive; antiviral therapies (e.g., oseltamivir) within appropriate window; vaccination is key for prevention.

Acute viral bronchitis

  • Etiology: self-limited lower respiratory infection that begins with URI and descends to lower airway.

  • Symptoms: persistent cough (>5 days), sputum typically clear (can be purulent), mild dyspnea, normal vital signs; fever if concurrent infection.

  • Imaging: chest X-ray often normal; rule out pneumonia if symptoms worsen.

  • Management: no antibiotics for true viral bronchitis; supportive care with bronchodilators as needed; cough suppression as needed; hydration and rest; avoid unnecessary antibiotics.

Community-acquired pneumonia (CAP)

  • Definition: pneumonia acquired outside hospital settings.

  • Risk factors: elderly, comorbidities (COPD, heart failure, CKD, diabetes), impaired airway protection, crowded living conditions.

  • Common pathogens: Streptococcus pneumoniae, Haemophilus influenzae; MRSA and Gram-negative organisms can occur; Legionella and atypicals (Mycoplasma, Chlamydophila) for atypical presentations.

  • Presentation: cough, sputum production, dyspnea, chest pain, fever; B symptoms (fever, night sweats, weight loss) can occur; elderly may present with hypothermia or nonclassic symptoms; pleural involvement possible (pleural effusion or empyema).

  • Diagnostics: chest X-ray to localize and differentiate lobar vs interstitial patterns; sputum Gram stain and culture; urinary antigen testing for S. pneumoniae and Legionella; PCR for viral pathogens.

  • Severity assessment and disposition: pneumonia severity indices like PSI or CURB-65 help decide inpatient vs outpatient management.

  • Treatment basics: 5–7 days of antibiotics; outpatient regimens include amoxicillin, doxycycline, or azithromycin (adjusted for comorbidities and risk factors); stronger regimens (Augmentin plus macrolide or doxycycline; respiratory fluoroquinolones like levofloxacin or moxifloxacin) for patients with comorbidities; pseudomonas risk requires anti-pseudomonal coverage; biomarker-guided therapy not detailed in this transcript.

  • Prevention: vaccination and infection control; follow-up imaging (4–6 weeks) to ensure resolution if initially treated as outpatient.

Tuberculosis (TB)

  • Global burden: TB remains a significant infectious disease worldwide; transmission only with active TB and via droplets; TB is reportable to public health authorities.

  • Etiology: Mycobacterium tuberculosis; slow-growing, acid-fast bacillus.

  • Disease states: primary TB (initial infection, ~10% progress to disease); latent TB (asymptomatic, noninfectious but can reactivate); reactivation risk factors include HIV, immunosuppression, malnutrition, extremes of age, close contact with active TB, immigration from TB-endemic regions.

  • Clinical features: cough, dyspnea, chest pain, hemoptysis; B symptoms (fever, night sweats, weight loss); nonpulmonary TB possible (scrofula, Pott disease, miliary TB).

  • Diagnostics:

    • PPD (Mantoux) with wheel size thresholds depending on risk factors; false positives can occur with prior BCG vaccination.

    • Interferon-gamma release assays (IGRAs; e.g., QuantiFERON Gold) do not differentiate latent vs active TB but do not have cross-reactivity with BCG.

    • Chest X-ray findings: upper lobe infiltrates, cavitation, pleural effusions in active TB; miliary TB shows a “millet seed” appearance.

    • Sputum culture with acid-fast bacilli smear and PCR; tissue biopsy for granulomatous disease confirmation.

  • Latent TB treatment regimens (preferred when TB is latent):

    • Isoniazid + rifapentine weekly for 3 months; isoniazid + rifapentine daily for 3 months; rifampin alone for 4 months; isoniazid alone for 9 months.

  • Active TB therapy (intensive + continuation phases):

    • Intensive phase (approx. 2 months): four first-line meds (isoniazid, rifampin, pyrazinamide, ethambutol).

    • Continuation phase: isoniazid and rifampin for several additional months (typical total therapy is 6 months, but longer therapy may be required depending on disease and resistance patterns).

    • Hepatic monitoring is important due to hepatotoxic potential of rifampin and isoniazid.

Pleural diseases and pleural space pathology

  • Pleural effusion: abnormal accumulation of fluid in the pleural space; small effusions are often asymptomatic; larger effusions cause dyspnea and chest discomfort.

  • Pleural fluid analysis (Light’s criteria): determine transudate vs exudate using protein and LDH levels; transudates typically due to systemic factors (heart failure, cirrhosis, nephrotic syndrome, pulmonary embolism) with low protein/LDH; exudates due to local factors (infection, malignancy, inflammation) with higher protein/LDH.

  • Pleural fluid findings:

    • Pleural fluid ND, protein, LDH levels help classify; cell counts and differential; glucose and cytology for infection or malignancy.

  • Transudates vs exudates management:

    • Transudative effusions: address the underlying cause (e.g., heart failure, renal disease); therapeutic thoracentesis to relieve dyspnea; recurrent effusions may require ongoing drainage or other therapies.

    • Exudative effusions: treat underlying disease (antibiotics for infection, drainage for empyema, cancer therapy for malignancy);

    • Empyema requires antibiotics and possible intrathoracic therapy or surgical washout.

  • Other pleural conditions:

    • Hemothorax: blood in pleural space.

    • Chylothorax: milky chyle in pleural space from lymphatic disruption; management includes addressing lymphatic leakage.

    • Use of chest tubes and thoracostomy tubes with water seal; drainage can be intermittent depending on fluid/mechanism.

Pneumothorax

  • Pneumothorax: air in pleural space causing lung collapse; clinical signs include sudden pleuritic chest pain and dyspnea; decreased breath sounds, hyperresonance.

  • Types:

    • Simple (spontaneous) pneumothorax: often in tall, thin young men with spontaneous airspace rupture; underlying lung disease increases risk (emphysema, COPD); cigarette smoking is a risk factor.

    • Secondary or secondary spontaneous pneumothorax (with underlying lung disease): COPD, emphysema, asthma.

    • Iatrogenic pneumothorax: from procedures such as central line placement, biopsy, or mechanical ventilation.

    • Tension pneumothorax: progressive air accumulation causing mediastinal shift, decreased venous return, hypotension—emergency management.

  • Management:

    • Small, apical pneumothorax: observation and oxygen; possible small-bore chest tube or pigtail catheter if symptomatic.

    • Large pneumothorax or symptomatic patient: chest tube drainage; needle decompression in extreme or unstable cases (anterior or lateral approaches when necessary).

    • Treat underlying cause; counsel on recurrence risk and activity restrictions (avoid scuba diving and high-altitude exposure for at least 6 months post-event).

    • Chest tube removal when air leak ceases and radiographic resolution is observed.

Obstructive sleep apnea (OSA) and related disorders

  • Obstructive sleep apnea (OSA): repetitive upper airway collapse during sleep, with apneas and hypopneas; brain arousal leads to rebound airway opening.

  • Symptoms: daytime somnolence, nocturnal gasps or choking episodes; partner/family members often identify symptoms.

  • Diagnostic tools: STOP-Bang questionnaire; Epworth Sleepiness Scale (ESS); polysomnography (sleep study); home sleep tests when available.

  • Treatments:

    • CPAP (continuous positive airway pressure) as first-line for most patients; maintains airway patency during sleep.

    • Dental devices that advance the jaw to prevent airway collapse.

    • Inspire device (hypoglossal nerve stimulator) in select patients; programmable with titration to maintain airway patency.

  • Associated conditions and risks: systemic hypertension, atrial fibrillation, left ventricular hypertrophy, pulmonary hypertension, depression; sleep-disordered breathing can contribute to systemic complications.

  • Obesity hypoventilation syndrome (OHS): overlap with OSA; characterized by diurnal hypercapnia (elevated CO2) and hypoxemia due to obesity-related hypoventilation; often presents with chronic hypercapnia and restrictive physiology; treatment includes weight reduction strategies, noninvasive ventilation, and occasionally tracheostomy in severe cases; differentiate from central sleep apnea.

  • Distinctions:

    • Obesity hypoventilation syndrome (OHS) involves diurnal hypercapnia due to hypoventilation and obesity; obstructive sleep apnea is nocturnal due to airway collapse.

    • Central sleep apnea is due to brain signaling impairment, not airway mechanics.

Pulmonary hypertension and cor pulmonale

  • Pulmonary hypertension (PH) has multiple etiologies: pulmonary arterial hypertension (idiopathic), pulmonary venous hypertension (left heart disease), respiratory-associated PH (COPD/emphysema), chronic thromboembolic PH, and mixed etiologies.

  • Diagnosis: echocardiography to evaluate right heart pressures; right heart catheterization with measurement of wedge pressure (>25 mmHg suggests elevated left-sided pressures) for definitive PH; right-axis deviation and signs of right heart strain on EKG; evidence of right atrial enlargement and right ventricular hypertrophy on EKG.

  • Cor pulmonale: right heart hypertrophy and failure due to lung disease and increased pulmonary pressures; signs include JVD, hepatomegaly, hepatojugular reflux, and tripod posture to relieve dyspnea; progression to right-sided heart failure.

Acute respiratory distress syndrome (ARDS)

  • ARDS is a severe inflammatory response causing diffuse, noncardiogenic pulmonary edema.

  • History often includes a triggering event (infection, trauma, head injury).

  • Chest imaging: batwing or diffuse bilateral infiltrates; not due to cardiogenic edema.

  • Management: supportive care with oxygenation and ventilation support; address underlying cause; in severe cases, VV- or VA-ECMO may serve as a bridge to recovery.

Acute allergic reactions and anaphylaxis

  • Acute allergic reactions can be localized (hives, edema, GI symptoms) without systemic involvement.

  • Anaphylaxis involves rapid, systemic progression with widespread edema, hypotension, bronchospasm, and potential shock.

  • Immediate management: remove offending allergen, administer epinephrine promptly (intramuscular EpiPen dosing; IV dosing in controlled settings with careful monitoring or infusion in severe cases), secure airway, administer antihistamines, corticosteroids; consider glucagon if on non-selective beta-blockers; ensure patient carries epinephrine for emergencies; refer to allergy/immunology for trigger testing.

Vascular events: DVT and pulmonary embolism (PE)

  • Deep vein thrombosis (DVT): classic signs include erythema, swelling, warmth, tenderness; a palpable cord may be present; Homan’s sign is unreliable.

  • Risk factors (Virchow’s triad): hypercoagulability (hereditary deficiencies, cancer, pregnancy, certain drugs), stasis (immobility, low EF), endothelial injury (surgery, trauma).

  • Diagnosis: Wells score; D-dimer as a screening test (positive D-dimer requires imaging); compression ultrasound to detect clot; high suspicion may lead to CTA chest.

  • Pulmonary embolism (PE): presentation includes dyspnea, chest pain, possible hemoptysis; prior DVT may be present.

  • Diagnostic imaging: CT pulmonary angiography (CTA) with contrast showing intraluminal filling defect; V/Q scan as alternative when contrast is contraindicated; gold standard diagnostic visualization is pulmonary angiography (rarely used acutely).

  • EKG findings: S1Q3T3 pattern can be seen in PE; chest X-ray may show elevated hemidiaphragm or Hampton’s hump; Westermark sign (localized oligemia) may be observed.

  • Treatment:

    • Anticoagulation: heparin or LMWH transitioning to warfarin; DOACs (e.g., rivaroxaban, apixaban, edoxaban) for many patients; in pregnancy or cancer, LMWH preferred.

    • Recurrent PE or failure of anticoagulation may warrant IVC filter placement or vascular interventions (catheter-directed thrombolysis or thrombectomy).

    • Supportive care and DVT/PE prophylaxis with compression stockings; early mobilization when feasible.

Acute respiratory infections and emergencies recap

  • Quick reference to common respiratory emergencies and their initial management:

    • Asthma exacerbation: rescue bronchodilators; systemic steroids; consider inhaled corticosteroids; RAC/biologic options for refractory cases; monitor for red flags indicating respiratory failure.

    • COPD exacerbation: increase in cough, sputum production, dyspnea; treat with bronchodilators (short-acting to start), systemic steroids, antibiotics if bacterial infection suspected, oxygen to maintain sats ~90–92%, noninvasive ventilation when appropriate, consider empiric anti-pseudomonal coverage in severe cases; vaccination and pulmonary rehab.

    • Pneumonia: identify causative organisms; treat based on risk factors and community vs hospital setting; consider Gram stain/culture, urinary antigens, and PCR testing; guidelines-driven antibiotic therapy and follow-up imaging.

    • TB: differentiate latent vs active; manage with RIPE regimen in active disease; monitor liver function; ensure public-health follow-up; use isolation with negative-pressure rooms for active TB.

    • Pleural disease: differentiate transudative vs exudative effusions; treat underlying cause; therapeutic thoracentesis and chest tubes as needed; manage empyema with antibiotics and possible surgical intervention.

    • ARDS: recognize noncardiogenic edema pattern; supportive care with oxygen and ventilation; ECMO as a bridge in select severe cases.

Quick takeaway framework for exam scenarios

  • Start with clinical presentation: pattern of breathing, audible sounds, chest exam, trauma/iatrogenic history, exposure history, smoking history.

  • Use PFTs and ABG to classify obstructive vs restrictive processes and to quantify severity and compensatory status.

  • Distinguish reversible (asthma) from nonreversible (advanced COPD, fibrotic restrictive diseases) conditions when explaining prognosis and treatment options.

  • Consider differential diagnoses at each vignette and use stepwise testing (spirometry, imaging, labs) to confirm.

  • Emphasize safety-net approaches in emergencies: oxygenation targets, airway management, and rapid escalation to advanced therapies when needed.

  • Remember the role of vaccination, smoking cessation, and pulmonary rehab across chronic lung diseases to reduce morbidity and mortality.

ext{Key reference values:} \ pH \,= \,7.35 ext{ to } 7.45, \ PaCO2 \,= \,35 \, to \, 45 \, mmHg, \ HCO3^- \,= \, 22 \, to \, 26 \, mEq/L \text{ABG rules:} \ ext{Respiratory disorders: pH and PaCO}2 ext{ move in opposite directions; Metabolic disorders: pH and HCO}3^- ext{ move in same direction.} }