American Board of Internal Medicine Certification (ABIM Board Certification) Pulmonary & Critical Care Medicine Syllabus

What are the classic chest imaging and biopsy findings of pulmonary sarcoidosis?

Bilateral hilar lymphadenopathy with reticulonodular opacities (often upper-lobe); biopsy shows non-caseating granulomas. Stage I = hilar adenopathy alone; Stage IV = fibrosis.

Name two acute sarcoidosis syndromes and the first-line systemic therapy for symptomatic disease.

Lofgren syndrome (erythema nodosum, hilar adenopathy, arthralgia/fever - good prognosis) and Heerfordt syndrome (uveoparotid fever, facial palsy). First-line systemic therapy is corticosteroids.

Why must hypercalcemia be monitored in sarcoidosis?

Granulomas express 1-alpha-hydroxylase, increasing conversion of 25-OH vitamin D to active 1,25-(OH)2 vitamin D, causing hypercalcemia, hypercalciuria, and nephrolithiasis.

Which connective tissue diseases are most commonly associated with ILD, and which serologies suggest it?

Systemic sclerosis (most common, often NSIP pattern), rheumatoid arthritis (often UIP), polymyositis/dermatomyositis, Sjogren, and MCTD. Antibodies: anti-Scl-70, anti-Jo-1 (antisynthetase), anti-MDA5, anti-CCP.

What is the most common histologic ILD pattern in connective tissue disease (vs IPF)?

Nonspecific interstitial pneumonia (NSIP), which is more steroid/immunosuppressant-responsive and has a better prognosis than the UIP pattern seen in IPF.

What is the Wells score used for, and what does a low pretest probability with a negative D-dimer indicate?

Wells score estimates pretest probability of pulmonary embolism; a low/unlikely probability plus a negative high-sensitivity D-dimer reliably excludes PE without imaging.

What is the PERC rule for pulmonary embolism?

In patients with low clinical suspicion, if all 8 PERC criteria are negative (age <50, HR <100, SaO2 >=95%, no hemoptysis, no estrogen use, no prior DVT/PE, no unilateral leg swelling, no recent surgery/trauma), PE can be excluded without D-dimer testing.

How are pulmonary emboli risk-stratified into massive, submassive, and low-risk categories?

Massive (high-risk): hypotension/shock (SBP <90). Submassive (intermediate): normotensive but with RV dysfunction (echo/CT) and/or elevated troponin/BNP. Low-risk: normotensive, no RV strain, normal biomarkers.

When is systemic thrombolysis indicated in acute PE?

In massive (high-risk) PE with hemodynamic instability/hypotension, provided no contraindication to bleeding; selected deteriorating submassive PE may be considered (catheter-directed therapy is an alternative).

List the 5 WHO groups of pulmonary hypertension.

Group 1: pulmonary arterial hypertension (PAH). Group 2: due to left heart disease. Group 3: due to lung disease/hypoxia. Group 4: chronic thromboembolic (CTEPH). Group 5: multifactorial/unclear mechanisms.

What is the hemodynamic definition of pulmonary hypertension (current criteria)?

Mean pulmonary artery pressure >20 mmHg at rest by right heart catheterization. Pre-capillary PH adds PVR >2 Wood units and PAWP <=15 mmHg.

How do you distinguish pre-capillary from post-capillary pulmonary hypertension?

Pre-capillary (Groups 1,3,4): PAWP <=15 mmHg with elevated PVR. Post-capillary (Group 2): PAWP >15 mmHg (elevated left-sided filling pressures).

State Light's criteria for an exudative pleural effusion.

Exudate if ANY one is met: pleural/serum protein ratio >0.5; pleural/serum LDH ratio >0.6; or pleural fluid LDH >2/3 the upper limit of normal serum LDH.

What pleural fluid findings suggest the need for chest tube drainage in a parapneumonic effusion (complicated effusion/empyema)?

Pleural fluid pH <7.2, glucose <60 mg/dL, positive Gram stain/culture, or frank pus (empyema) indicate a complicated effusion requiring drainage.

What pleural fluid characteristics suggest a transudate, and name two common causes.

Fails all Light's criteria (low protein/LDH), typically clear; common causes are heart failure and cirrhosis (hepatic hydrothorax); also nephrotic syndrome.

What does a markedly elevated pleural fluid lymphocyte count plus high adenosine deaminase suggest?

Tuberculous pleuritis (lymphocyte-predominant exudate with ADA >40 U/L); malignancy and lymphoma can also cause lymphocytic effusions.

What is the initial management of a primary spontaneous pneumothorax that is small and the patient stable?

Observation with supplemental oxygen (oxygen speeds pleural air resorption); needle aspiration or small-bore catheter is an option. Large/symptomatic pneumothorax requires aspiration or chest tube.

How is a tension pneumothorax recognized and immediately treated?

Hypotension, distended neck veins, tracheal deviation away, absent breath sounds, hyperresonance; treat immediately with needle decompression (2nd intercostal space midclavicular line or 4th/5th anterior axillary) followed by chest tube - do NOT wait for imaging.

State the Berlin definition diagnostic criteria for ARDS.

Acute onset within 1 week; bilateral opacities on imaging not fully explained by effusions/collapse; respiratory failure not fully explained by cardiac failure/fluid overload; and hypoxemia by PaO2/FiO2 ratio with PEEP/CPAP >=5.

How is ARDS severity graded by PaO2/FiO2 ratio (with PEEP >=5)?

Mild: 200-300 mmHg; Moderate: 100-200 mmHg; Severe: <=100 mmHg.

What are the core lung-protective ventilation targets in ARDS?

Low tidal volume 6 mL/kg predicted body weight, plateau pressure <=30 cmH2O, driving pressure <15, permissive hypercapnia, and adequate PEEP; this strategy reduces mortality (ARDSNet).

Which adjunct therapy reduces mortality in severe ARDS (P/F <150)?

Early prone positioning (e.g., 16 hours/day) improves oxygenation and reduces mortality; neuromuscular blockade may be used in selected severe cases.

Differentiate hypoxemic (type 1) from hypercapnic (type 2) respiratory failure.

Type 1 (hypoxemic): low PaO2 with normal/low PaCO2, due to V/Q mismatch or shunt (e.g., pneumonia, ARDS, edema). Type 2 (hypercapnic): elevated PaCO2 with hypoxemia, due to alveolar hypoventilation (e.g., COPD, neuromuscular disease, drug overdose).

What is the alveolar gas equation and the normal A-a gradient?

PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2/R); at sea level on room air ~150 - (PaCO2/0.8). Normal A-a gradient is ~5-15 mmHg, increasing with age (estimate = age/4 + 4).

A patient has hypoxemia with a NORMAL A-a gradient. What are the two causes?

Hypoventilation and low inspired oxygen (high altitude). A widened A-a gradient instead indicates V/Q mismatch, shunt, or diffusion limitation.

What are the two best-established indications for noninvasive positive pressure ventilation (NIPPV)?

Acute hypercapnic respiratory failure from COPD exacerbation (respiratory acidosis pH <7.35) and cardiogenic pulmonary edema; both reduce intubation rates and mortality.

List contraindications to noninvasive ventilation.

Cardiac/respiratory arrest, inability to protect airway/impaired consciousness, excessive secretions, facial trauma/surgery, hemodynamic instability/shock, and high aspiration risk or uncooperative patient.

On a mechanical ventilator, which settings primarily control oxygenation vs ventilation (CO2 removal)?

Oxygenation is controlled by FiO2 and PEEP; ventilation (CO2 clearance) is controlled by respiratory rate and tidal volume (minute ventilation).

What criteria suggest a patient is ready for a spontaneous breathing trial (SBT) and likely successful extubation?

Resolution/improvement of underlying cause, adequate oxygenation (P/F >150, PEEP <=5-8, FiO2 <=0.4-0.5), hemodynamic stability off/minimal pressors, and a rapid shallow breathing index (RR/Vt) <105.

Define sepsis and septic shock per Sepsis-3.

Sepsis = life-threatening organ dysfunction (acute SOFA increase >=2) due to a dysregulated host response to infection. Septic shock = sepsis requiring vasopressors to maintain MAP >=65 mmHg AND lactate >2 mmol/L despite adequate fluid resuscitation.

What are the key components of the initial 'hour-1' sepsis bundle?

Measure lactate (remeasure if >2), obtain blood cultures before antibiotics, give broad-spectrum antibiotics, begin 30 mL/kg crystalloid for hypotension or lactate >=4, and add vasopressors to keep MAP >=65 if hypotensive during/after fluids.

What is the first-line vasopressor in septic shock, and what is added if MAP remains low?

Norepinephrine is first-line; vasopressin (and/or epinephrine) is added next, and consider stress-dose hydrocortisone in refractory shock requiring escalating vasopressors.

Compare the hemodynamic profiles (CO, SVR, PCWP/preload) of the four shock types.

Hypovolemic: low CO, high SVR, low preload. Cardiogenic: low CO, high SVR, high PCWP. Obstructive: low CO, high SVR, variable filling (high CVP). Distributive (septic): high/normal CO, low SVR, low/normal preload.

Interpret a single arterial blood gas: pH 7.20, PaCO2 60, HCO3 24. What is the disorder?

Acute respiratory acidosis (low pH, high PaCO2 with minimal HCO3 compensation). Acutely, HCO3 rises ~1 mEq/L per 10 mmHg rise in PaCO2.

How do you calculate the anion gap and what does an elevated anion gap metabolic acidosis suggest (mnemonic)?

Anion gap = Na - (Cl + HCO3), normal ~8-12. Elevated gap causes (GOLD MARK or MUDPILES): glycols, oxoproline, L-lactate, D-lactate, methanol, aspirin, renal failure, ketoacidosis (and uremia, DKA, propylene glycol, iron/INH, lactate, ethylene glycol, salicylates).

What is Winter's formula and what does it assess?

Expected PaCO2 = 1.5 x HCO3 + 8 (+/- 2). It checks for appropriate respiratory compensation in metabolic acidosis; a higher PaCO2 indicates a concurrent respiratory acidosis, a lower one a respiratory alkalosis.

How is obstructive sleep apnea diagnosed and graded by the apnea-hypopnea index (AHI)?

Diagnosed by polysomnography (or home sleep apnea test). AHI 5-14 = mild, 15-29 = moderate, >=30 = severe (AHI = number of apneas + hypopneas per hour of sleep).

What is the first-line treatment for moderate-to-severe obstructive sleep apnea, and what cardiovascular conditions is OSA associated with?

Continuous positive airway pressure (CPAP) is first-line; OSA is associated with hypertension (especially resistant), atrial fibrillation, heart failure, pulmonary hypertension, stroke, and increased perioperative risk.

How does obesity hypoventilation syndrome differ from obstructive sleep apnea?

OHS is defined by obesity (BMI >=30) with awake daytime hypercapnia (PaCO2 >45 mmHg) not explained by other causes; it is chronic hypercapnic respiratory failure, whereas OSA is primarily upper-airway obstruction without mandatory daytime hypercapnia.

What is central sleep apnea and a classic pattern seen in heart failure?

Cessation of airflow due to loss of ventilatory drive (no respiratory effort), unlike obstructive apnea. Cheyne-Stokes respiration (crescendo-decrescendo breathing with central apneas) is classically seen in heart failure and after stroke.