Detail the differential diagnosis for patients with chronic dyspnea.

Evaluate patients with chronic dyspnea, distinguishing between cardiac, pulmonary, pulmonary-vascular, and neuromuscular causes.

Describe the changes in lung function that are associated with obstructive and restrictive lung diseases.

Compare community-acquired, health care-associated, hospital-acquired, and ventilator-associated pneumonias, with regard to etiology, common pathogens, and approach to management.

Discuss the importance of initial antibiotic therapy for patients with pneumonia and the factors to consider when selecting antibiotics.

How to Evaluate the Breathless Patient

Dyspnea: unpleasant sensation associated with breathing; patients describe in different terms (eg, shortness of breath, difficulty breathing, suffocation, tightness)

Causes of dyspnea: cardiac—eg, congestive heart failure (CHF) and arrhythmias; vascular density of lungs increases, reducing compliance; pulmonary—airway and parenchymal diseases result in impaired lung expansion and decreased vagal input from lungs; pleural effusions may expand chest wall and suppress vagal input; pulmonary vascular disease—eg, emboli and pulmonary hypertension; others—anemia associated with decreased drive to breathe; neuromuscular disease may affect breathing

Breathing reserve: ventilation capacity 60 to 100 L/min; pulmonary function often significantly impaired before symptoms emerge

Descriptor clues: patients with pulmonary etiology often complain of shortness of breath; those with cardiac etiology tend to complain of fatigue; duration of symptoms—pulmonary etiologies generally associated with faster recovery than cardiac etiologies

Cardiac causes of dyspnea: history often includes angina, but some patients report only dyspnea upon exertion; physical examination may not reveal abnormal findings, so history and risk factors important; CHF—patient may have weight gain, orthopnea, or nocturnal symptoms; findings on physical examination include elevated jugular venous pressure (JVP), third heart sound (S3 ) and crackles on auscultation, and leg edema; arrhythmias—often described as palpitations; ask about pulse (tachycardia); examination may be normal; stress testing—echocardiography often useful; difficult to detect arrhythmias with periodic monitoring; B-type natriuretic peptide (BNP)—normal level <100 pg/mL; even moderate elevations may indicate CHF

Pulmonary causes: asthma vs chronic obstructive pulmonary disease (COPD)—diagnosis partly based on risk factors (eg, smoking); bronchiectasis—sometimes misdiagnosed as chronic bronchitis; patients typically have increased production of sputum (purulent); interstitial lung disease (ILD)—patients may initially complain of irritating cough (sometimes misdiagnosed as acid reflux); bilateral dry crackles on auscultation; pleural effusions—chest pain often not present; studies—chest x-ray (CXR); lung function tests; diffusion capacity and lung volume tests if ILD suspected

Pulmonary vascular causes: acute pulmonary embolism (PE)—symptom onset often sudden; chronic thromboembolic disease—insidious onset; risk factors include hypercoagulability; symptoms often subtle (eg, intermittent chest pain, tachycardia); pulmonary hypertension—signs and symptoms similar to those of CHF, including elevated JVP; prominent pulmonary valve closure sound (P2) and cardiac heave may be present; studies—CXR useful, but often inconclusive; computed tomography (CT) with contrast; perfusion scan if chronic thromboembolic disease suspected; echocardiography if pulmonary hypertension suspected

Other causes: anemia—etiology often identifiable; neuromuscular weakness—often left out of differential diagnosis, unless patient has other obvious weakness; hoarse voice or inability to take deep breath should increase index of suspicion

Initial evaluation: begin with CXR and spirometry (unless CHF strongly suspected); if inconclusive, order high-resolution CT (HRCT) or echocardiography; consider stress testing for difficult cases; absence of abnormal findings—CXR may be clear in patients with coronary artery disease (CAD), CHF (especially compensated diastolic CHF), obstructive lung disease (eg, asthma, mild COPD), some restrictive lung disease (eg, early ILD; HRCT recommended if crackles heard on auscultation), and mild to moderate pulmonary hypertension and PE

Spirometry: measures volume and velocity of exhaled air; forced expiratory volume at 1 sec (FEV1 ) normally ≈70% of forced vital capacity (total amount of air exhaled); obstructive airway disease—forced vital capacity approaches normal, but velocity low; restrictive lung disease—normal velocity, but decreased forced vital capacity

Obstructive lung disease: asthma; COPD; chronic bronchitis; emphysema; bronchiectasis; bronchomalacia; airway tumors (rare); bronchiolitis

Restrictive lung disease: ILDs; diseases that affect alveolar filling (eg, pneumonia, pulmonary edema); large lesions (eg, lung cancer, enlarged heart, mediastinal masses); diseases of chest wall and pleura, including pleural effusion, kyphoscoliosis, and obesity

Lung volumes: lungs—small change in pressure results in large change in volume, until lungs near maximal expansion; chest wall—expands to increase volume of chest cavity; compliance increases with age; determinants of total lung capacity (TLC)—compliance of chest wall and lungs; muscle strength; determinants of residual volume (RV)—chest wall compliance; muscle strength; airway closure; determinants of functional residual capacity (FRC)—compliance of chest wall and lungs

Changes with disease states: obstructive disease—airway closure results in increased RV; later, morphologic changes result in increased FRC and TLC; restrictive disease—early changes result in decreased RV; reduced compliance results in decreased FRC and TLC; muscle weakness—normal FRC; insufficient pressure generated, so TLC decreases and RV increases; measuring maximum inspiratory and expiratory pressures useful; although effect on vital capacity and flow similar to that seen with restrictive disease, etiology different; obesity—normal TLC and RV; decreased FRC; excess weight increases pressure on lungs, making inspiration more difficult

Interstitial lung diseases: HRCT—recommended when restrictive disease suspected; good sensitivity for identifying ILDs; identifies edema; correlates with disease activity; known etiology—exposure to inorganic and organic dusts; hypersensitivity pneumonitis and allergic alveolitis (ask about pets, especially birds); Pseudomonas infection (ask about hot tub use); drug-induced ILD; cancer and lymphangitic spread; radiation; some infections; unknown etiology—idiopathic pulmonary fibrosis; other conditions—vasculitic syndromes; sarcoidosis; often require biopsy

Diffusion capacity: gas exchange in lungs occurs by passive diffusion; diffusion abnormalities rarely cause hypoxemia; “transfer factor” may be more precise term (incorporates factors other than diffusion); measurement—lung diffusion capacity for carbon monoxide (DL CO); interpretation—wide range of normal values; increased DL CO occurs with increased blood volume, presence of blood in airspace, increased pulmonary blood flow, and airway edema; decreased DL CO occurs with emphysema, bronchiectasis, and pulmonary hypertension (may be only abnormality); exercise-induced hypoxemia likely in patients with DL CO <40% of predicted; useful for diagnosing ILD and pulmonary vascular disease

Pulmonary hypertension: echocardiography for estimating right ventricular systolic pressure; if inconclusive, right heart catheterization recommended; mean pulmonary arterial pressure—\>25 mm Hg; increases with advanced disease (to ≥60 mm Hg in many patients); etiology—primary pulmonary arterial hypertension; CHF most common cause (results in pulmonary venous hypertension); pulmonary disorders; other disorders that directly affect pulmonary vasculature (eg, scleroderma, sarcoidosis)

Role of dynamic testing: when static testing inconclusive and for patients with disproportionately severe symptoms (relative to findings from static tests); used for simultaneous assessment of cardiovascular and ventilatory functions; options— treadmill; bicycle (preferred by speaker); exercise intolerance—breathlessness, pain, and/or fatigue with exertion (experienced even by trained athletes, but at higher intensity of exercise)

Maximal oxygen consumption (VO2max): considered within normal range when patient reaches 90% of predicted VO2max ; early exercise intolerance—eg, 60% of predicted VO2max ; important to identify etiology (eg, cardiac vs pulmonary limitation)

Closing comments: importance of history—distance patient can walk on flat surface (and time it takes); ability to climb flight of stairs; triggers for dyspnea; early diagnosis important

Pneumonia: Diagnosis and Management

Infection: primarily occurs by aspiration; criteria—impairment of local immune function; inoculation with sufficient number of organisms (decreases with increasing virulence); aspiration—commonly occurs during sleep; increases with central nervous system (CNS) impairment; small volume of aspirate (from oropharyngeal space) contains large number of organisms

Classification: community-acquired pneumonia (CAP); hospital-acquired pneumonia (HAP; occurs \>48 hr after admission); ventilator-associated pneumonia (VAP; occurs \>48 hr after placement on mechanical ventilatory support); health care-associated pneumonia (HCAP; patients have risk factors, including recent hospitalization, antibiotic therapy, or hemodialysis, or residence in long-term care facility); clinical relevance—initial therapy empiric; knowing likely pathogens helps direct choice of antibiotics; example—study found gram-negative bacilli present in mouth in ≈10% of healthy individuals (including hospital staff), ≈35% of moderately-ill patients, and \>70% of patients in intensive care unit (ICU); altered immune function allows establishment of organisms different from those seen in CAP

Prediction rule: Fine et al (1997) looked at factors predictive of death in patients with pneumonia; 5 levels of risk; best predictors—age \>50 yr; coexisting medical conditions (neoplastic disease; CHF; cerebrovascular disease; renal or liver disease); certain abnormalities on physical examination (altered mental status; tachycardia; tachypnea; decreased blood pressure; hypothermia or hyperthermia); risk factors assigned points; risk increases with increasing number of points; category-5 (highest risk) patients have ≈30% risk of dying; hospitalization—some physicians use prediction rule to make decisions about hospitalization, but speaker cautions against this; decision to admit patient may take other factors (including social circumstances) into account

Quality indicators (QIs): established by Centers for Medicare and Medicaid Services (CMS); not always supported by evidence; initiation of antibiotics—initial QI required initiation within 4 hr of presentation (later changed to 8 hr because of increased use of antibiotics without evidence of benefit); blood culture within first 24 hr— shown to be of no utility unless patient septic; QI rescinded; other QIs—appropriate selection of antibiotics; vaccination; counseling for smoking cessation; O2 assessment

Risk factors and pathogens: alcoholism—increases risk for drug-resistant pneumococcus, anaerobes, and mycobacteria; smoking—increases risk for pneumococcus, Haemophilus influenzae, and Moraxella catarrhalis; poor hygiene— increases risk for anaerobes; general health—Streptococcus pneumoniae most common pathogen across groups; Mycoplasma, Chlamydia, H influenzae, and viruses common in younger, healthier patients; Staphylococcus aureus becomes more common with worsening health status; Legionella important in hospitalized patients (especially patients in ICU); risk factors for Pseudomonas—bronchiectasis; history of corticosteroid use; malnutrition; recent history of broad-spectrum antibiotics

Treatment recommendations: outpatients—macrolide or fluoroquinolone monotherapy; other agents (eg, doxycycline) acceptable; hospitalized (non-ICU) patients—fluoroquinolone monotherapy or combination of β-lactam plus macrolide; coverage of atypical organisms important; ICU patients—combination of β-lactam plus macrolide or fluoroquinolone (no studies looking at fluoroquinolone monotherapy)

Noninfectious causes of fever and pulmonary infiltrates: pulmonary emboli; acute lung injury (caused by, eg, drug reaction, pancreatitis); acute chest syndrome (in patients with sickle cell anemia); lupus pneumonitis; acute myocardial infarction with CHF; alveolar hemorrhage syndromes; acute eosinophilic pneumonia

Diagnosis: study shows diagnosis (of VAP) made in <25% of cases (as low as 10% in some subpopulations); validated clinical criteria—fever; leukocytosis; purulent tracheal secretions; new infiltrate; basing diagnosis on presence of one of these results in high sensitivity but very low specificity (≈3%); requiring all 4 criteria for diagnosis dramatically improves specificity but decreases sensitivity to ≈6%; diagnosis reasonable for patients with “2.5” of 4 criteria; culture results— reasonable cutoff for diagnosis, 105 to 106 CFU/mL when sample taken from endotracheal space or 103 CFU/mL when sample taken by alveolar lavage; pathogens—culture from purulent tracheal secretions generally identifies same pathogens as culture from infiltrate; neutrophils—low likelihood of pneumonia if neutrophils <50% on lavage

Initial antibiotic therapy for all HAP: mortality rate increases 4-fold if initial antibiotic does not cover infecting organism; broad-spectrum antibiotics—better coverage but increased risk of developing resistance; empiric therapy for HAP—must cover Pseudomonas aeruginosa and S aureus (often methicillin-resistant [MRSA]), but these pathogens commonly missed; Acinetobacter also commonly missed, but less common cause of pneumonia; double-coverage—used when resistance suspected; no in vivo evidence of synergy in management of pneumonia; risk factors for multidrug-resistant (MDR) pathogens—recent antimicrobial therapy; current hospitalization of ≥5 days; high prevalence of MDR pathogens in hospital; patient has risk factors for HCAP; strategy at speaker’s institution—begin with β-lactam plus fluoroquinolone or aminoglycoside plus linezolid or vancomycin (to cover MRSA); tailor treatment based on patient factors (eg, allergies, comorbidities, and potential drug interactions)

Duration of therapy: study showed patients with VAP recover in ≈5 days; randomized study compared 8-day and 15-day courses of antibiotic therapy in patients with VAP; no differences in major end points, including mortality and recurrence; reduced risk for resistance with shorter course; Pseudomonas—higher likelihood of recurrence with short course; associated with chronic airway infection and unlikely to resolve until endotracheal tube removed; treat VAP for 8 days, and if recurrence occurs, long-term aerosolized antibiotics recommended

Prevention of nosocomial infection: vaccinate patients; remove catheters as quickly as possible; diagnose and treat infection effectively and discontinue if infection not proven after 2 days; use antimicrobial agents wisely; enforce hand hygiene practices to prevent transmission