ABIM Pulmonary cheat sheet

Post-bronchodilator FEV1/FVC below 0.70 defines persistent airflow obstruction and supports a diagnosis of COPD in a patient with compatible symptoms and exposures.

GOLD airflow limitation grades use FEV1 percent predicted: GOLD 1 is 80 or higher, GOLD 2 is 50 to 79, GOLD 3 is 30 to 49, and GOLD 4 is below 30.

Asthma reversibility is an FEV1 increase of at least 12 percent and at least 200 mL after a short-acting bronchodilator.

In COPD patients at risk for hypercapnia, supplemental oxygen is titrated to SpO2 88 to 92 percent.

Smoking cessation is the only intervention proven to slow the long-term decline in FEV1 in COPD.

Alpha-1 antitrypsin deficiency is suggested by early-onset emphysema, basilar-predominant emphysema, family history, or unexplained liver disease; serum alpha-1 antitrypsin level is the initial test.

In asthma, a long-acting beta-agonist is not used without an inhaled corticosteroid; inhaled corticosteroids are the main controller therapy.

For most symptomatic COPD patients, initial therapy is a long-acting muscarinic antagonist plus a long-acting beta-agonist; inhaled corticosteroid is added for exacerbations with blood eosinophils of 300 or higher.

Usual interstitial pneumonia on high-resolution CT shows peripheral and basal-predominant reticulation, honeycombing, and traction bronchiectasis with little ground-glass opacity.

Idiopathic pulmonary fibrosis is treated with nintedanib or pirfenidone to slow FVC decline; immunosuppressive regimens are harmful.

Sarcoidosis is characterized by noncaseating granulomas, bilateral hilar lymphadenopathy, and bronchoalveolar lavage CD4/CD8 ratio above 3.5.

Hypersensitivity pneumonitis is suggested by an exposure history, BAL lymphocytosis, centrilobular nodules, and air trapping.

Connective tissue disease-associated interstitial lung disease commonly shows a nonspecific interstitial pneumonia pattern, especially in scleroderma, rheumatoid arthritis, and inflammatory myopathy.

BAL lymphocytosis above 15 percent suggests hypersensitivity pneumonitis, sarcoidosis, or nonspecific interstitial pneumonia.

Acute exacerbation of idiopathic pulmonary fibrosis is new bilateral ground-glass opacity within one month after excluding infection and other causes.

In interstitial lung disease, a reduced DLCO often out of proportion to restriction indicates pulmonary vascular involvement or emphysema combined with fibrosis.

Pulmonary embolism evaluation uses the Wells score or PERC rule, D-dimer in low or intermediate probability, and CT pulmonary angiography for high probability or positive D-dimer.

Massive pulmonary embolism with sustained hypotension or shock is treated with systemic thrombolysis or surgical or catheter embolectomy.

Submassive pulmonary embolism has right ventricular dysfunction plus elevated troponin or BNP without hypotension; anticoagulation and close monitoring are standard.

Chronic thromboembolic pulmonary hypertension is evaluated with a ventilation-perfusion scan in patients with persistent dyspnea more than three months after anticoagulation.

Pulmonary arterial hypertension is defined by mean pulmonary artery pressure above 20 mm Hg, pulmonary vascular resistance at least 3 Wood units, and pulmonary artery wedge pressure 15 mm Hg or less.

Group 1 pulmonary arterial hypertension includes idiopathic disease, BMPR2 mutation, anorexigen exposure, connective tissue disease, HIV, portal hypertension, and congenital heart disease.

Vasoreactivity testing uses inhaled nitric oxide; calcium channel blockers are used only in patients with a positive vasoreactivity test.

Pregnancy is contraindicated in pulmonary arterial hypertension because maternal mortality is high.

Berlin criteria for acute respiratory distress syndrome require onset within one week, bilateral opacities not explained by heart failure, and PaO2/FiO2 of 300 or less on PEEP at least 5 cm H2O.

ARDS severity by PaO2/FiO2 on PEEP at least 5: mild 200 to 300, moderate 100 to 200, and severe below 100.

Lung-protective ventilation uses tidal volume 6 mL/kg predicted body weight and plateau pressure 30 cm H2O or less.

Prone positioning reduces mortality in moderate to severe ARDS, typically when PaO2/FiO2 is below 150.

Noninvasive ventilation reduces intubation and mortality in COPD exacerbation with respiratory acidosis, typically pH 7.25 to 7.35 with hypercapnia.

Type 2 respiratory failure is hypoxemia with PaO2 below 60 mm Hg plus hypercapnia with PaCO2 above 50 mm Hg.

Sepsis-associated hypoperfusion is treated initially with at least 30 mL/kg of intravenous crystalloid.

A spontaneous breathing trial assesses readiness for extubation after the cause of respiratory failure has improved.

Obstructive sleep apnea is diagnosed when the apnea-hypopnea index is at least 5 with compatible symptoms or at least 15 regardless of symptoms.

An apnea is cessation of airflow for at least 10 seconds; a hypopnea is at least 30 percent airflow reduction with arousal or desaturation.

STOP-BANG scores snoring, tiredness, observed apnea, pressure, BMI, age, neck circumference, and gender for OSA risk.

Obesity hypoventilation syndrome requires BMI at least 30, awake PaCO2 above 45 mm Hg, and sleep-disordered breathing after excluding other hypoventilation causes.

Adaptive servo-ventilation is contraindicated in heart failure with ejection fraction 45 percent or less because it increases mortality in central sleep apnea.

Narcolepsy is supported by a mean sleep latency of 8 minutes or less and at least two sleep-onset REM periods on multiple sleep latency testing.

Positive airway pressure titration identifies the pressure that eliminates apneas, hypopneas, and desaturations in the supine and lateral positions.

Restless legs syndrome is an urge to move the legs, worse at rest and in the evening, relieved by movement.

CURB-65 scores confusion, urea above 7 mmol/L, respiratory rate at least 30, low blood pressure, and age 65 or older to stratify community-acquired pneumonia.

Suspected pulmonary tuberculosis requires airborne isolation, acid-fast bacilli smears, nucleic acid amplification testing, and culture.

Active tuberculosis is treated with rifampin, isoniazid, pyrazinamide, and ethambutol during the intensive phase, with regimen duration guided by culture conversion and resistance.

Latent tuberculosis is treated with four months of daily rifampin or nine months of daily isoniazid; alternatives depend on resistance, age, and liver disease.

Pneumocystis jirovecii prophylaxis with trimethoprim-sulfamethoxazole begins when the CD4 count falls below 200 cells per microliter in HIV infection.

Pleural fluid that is frank pus or has pH below 7.20, glucose below 60 mg/dL, or LDH above 1000 IU/L indicates empyema and requires drainage.

Invasive pulmonary aspergillosis is supported by serum galactomannan and a CT halo sign in neutropenic or immunosuppressed patients.

Hospital-acquired pneumonia and ventilator-associated pneumonia require coverage for MRSA and Pseudomonas aeruginosa when risk factors are present.

Small cell lung cancer is staged as limited or extensive and treated with platinum plus etoposide, with radiation for limited-stage disease.

Early-stage non-small cell lung cancer, stage I to II, is treated primarily with surgical resection.

Unresectable stage III non-small cell lung cancer is treated with concurrent chemoradiation followed by consolidation durvalumab.

Advanced non-small cell lung cancer is tested for EGFR, ALK, ROS1, BRAF, KRAS, and PD-L1 before systemic therapy.

Activating EGFR mutations are treated with an EGFR tyrosine kinase inhibitor such as osimertinib; ALK rearrangements are treated with an ALK inhibitor.

Small cell lung cancer commonly causes SIADH and hyponatremia; squamous cell carcinoma commonly causes hypercalcemia.

Pancoast tumors cause shoulder and arm pain, Horner syndrome, and weakness of the intrinsic hand muscles.

Solitary pulmonary nodule follow-up by Fleischner criteria depends on nodule size, morphology, and patient cancer risk.

Mesothelioma is associated with asbestos exposure and presents with unilateral pleural thickening or effusion.

Light criteria classify an exudate when pleural fluid protein ratio exceeds 0.5, LDH ratio exceeds 0.6, or pleural LDH exceeds two-thirds the upper limit of normal serum LDH.

Transudative effusions are caused by heart failure, cirrhosis, and nephrotic syndrome; diuresis can convert a transudate into an exudate by raising pleural protein.

Empyema is treated with antibiotic therapy plus chest tube drainage; fibrinolytics or surgery are used when drainage is inadequate.

Malignant pleural effusion is diagnosed by cytology, cell block, or pleural biopsy; pleurodesis or an indwelling pleural catheter palliates recurrent effusion.

Tension pneumothorax is a clinical diagnosis requiring immediate needle decompression followed by tube thoracostomy without waiting for radiography.

Pleural fluid triglyceride above 110 mg/dL supports chylothorax, usually from thoracic duct disruption by trauma, surgery, lymphoma, or malignancy.

Pleural fluid adenosine deaminase above 40 IU/L supports tuberculous pleuritis, especially in high-prevalence settings.

Hepatic hydrothorax is a transudative effusion, usually right-sided, caused by portal hypertension and diaphragmatic defects.

Asbestosis causes lower-lobe-predominant interstitial fibrosis and often pleural plaques; asbestos exposure also increases risk of mesothelioma and lung cancer with a long latency.

Silicosis produces upper-lobe-predominant nodules and eggshell calcification of hilar lymph nodes and increases susceptibility to tuberculosis.

Chronic beryllium disease causes noncaseating granulomas and interstitial lung disease; the beryllium lymphocyte proliferation test supports sensitization.

Hypersensitivity pneumonitis from farmer's lung or bird fancier's lung produces centrilobular nodules, ground-glass opacity, and air trapping.

Coal worker pneumoconiosis causes upper-lobe nodules and, with progressive massive fibrosis, larger conglomerate opacities.

Byssinosis causes Monday-morning chest tightness and reversible airflow obstruction in textile workers exposed to cotton dust.

Radon exposure is the second leading cause of lung cancer after smoking and is highest in certain geographic regions.

Metal fume fever is an acute influenza-like illness after welding or galvanized metal exposure, with tolerance developing after repeated exposure.

Amyotrophic lateral sclerosis causes progressive restrictive respiratory failure; noninvasive ventilation improves survival when forced vital capacity falls below 50 percent or nocturnal hypoventilation develops.

Myasthenic crisis causes neuromuscular respiratory failure with weak cough and falling vital capacity; treatment is plasma exchange or intravenous immunoglobulin, with avoidance of aminoglycosides.

Guillain-Barre syndrome causes ascending weakness and respiratory failure; vital capacity and negative inspiratory force are monitored serially.

Duchenne muscular dystrophy causes restrictive lung disease and nocturnal hypoventilation; cough assistance and noninvasive ventilation are used as vital capacity declines.

Severe kyphoscoliosis produces restrictive physiology with reduced vital capacity and total lung capacity and often preserved DLCO until late disease.

Obesity hypoventilation syndrome is defined by BMI at least 30, awake PaCO2 above 45 mm Hg, and sleep-disordered breathing after excluding other causes.

Neuromuscular and chest wall disorders reduce vital capacity and total lung capacity with normal or only mildly reduced DLCO.

Paradoxical inward abdominal movement during inspiration suggests diaphragm weakness and impending respiratory failure.