How to read this week
Week 5 is two different weeks wearing one name. Half of it is infection and inflammation — pneumonia, TB, ARDS, the interstitial diseases. The other half is vascular and structural catastrophe — pulmonary hypertension, embolism, pleural effusion, pneumothorax. They share one theme: the chest X-ray shows the aftermath, not the cause.
Infection & inflammation
- Pneumonia — CAP, HAP, VAP
- Tuberculosis
- ARDS / acute lung injury
- Idiopathic pulmonary fibrosis
- Sarcoidosis
- Cardiogenic pulmonary edema
Diagnostic currency: cultures, smears, and the CXR.
Vascular & structural
- Pulmonary hypertension — WHO groups I–V
- Pulmonary embolism
- Pulmonary vasculitis
- Pleural effusion & pleuritis
- Pneumothorax
- Chest wall disorders
Diagnostic currency: right-heart catheterization, CT angiography, and thoracentesis.
Your reading map
| Ch. | Title | What it actually contains |
|---|---|---|
| 27 | Restrictive (Inflammatory) Lung Diseases & CHF/Pulmonary Edema | Pneumonia · Tuberculosis · ARDS/ALI · Idiopathic pulmonary fibrosis · Sarcoidosis · Cardiogenic pulmonary edema |
| 32 | Lower Respiratory Tract Infections | COPD exacerbation · CAP · HAP · VAP · Seasonal influenza, plus the empiric antimicrobial tables Tables 32.1 (CAP) and 32.2 (HAP/VAP) |
| 28 | Pulmonary Hypertension & Pulmonary Vascular Disorders | PH and the WHO groups · PAH pharmacotherapy (Table 28.1) · Pulmonary embolism · Pulmonary vasculitis · Geriatric implications |
| 31 | Pneumothorax | Spontaneous · traumatic · iatrogenic · tension — and the chest-tube rules |
| 29 | Chest Wall & Secondary Pleural Disorders | Spine and rib disorders · Pleuritis · Pleural effusion and Light's criteria · Gerontologic considerations |
Infection is treated with a drug and a duration. Vascular catastrophe is treated with a drug and a clock. Pneumonia gets an antibiotic course measured in days; a pulmonary embolus gets an anticoagulant measured in months; a tension pneumothorax gets a needle measured in seconds.
The numbers worth carrying in
Pneumonia
An acute febrile inflammatory disorder of the lung — a lower respiratory tract infection with an infiltrate on chest X-ray. The infiltrate may lag behind the symptoms by 24–48 hours, which is why a repeat film at that point is justified.
What makes the diagnosis
- Cough, fever, purulent sputum, leukocytosis
- Decline in oxygenation
- Radiographic infiltrate — required
May be bacterial, viral, fungal, or parasitic.
Who gets into trouble
- Age > 65
- Chronic comorbidities
- Viral respiratory infection
- Impaired airway protection
- Smoking
- Recent antibiotic use
- Immunocompromise — HIV, chemotherapy, transplant
What drives mortality
- Congestive heart failure
- Diabetes mellitus
- Chronic liver and renal disease
- COPD
The very young and the very old die disproportionately.
Typical vs. atypical
Classic findings
- Fever
- Chills
- Leukocytosis
- Cough, with or without sputum
- Sputum production
- Increased fremitus
Variable presentation
- Fever may be high
- Leukocytosis may be absent — or show a left shift with band forms
- Cough is often dry
- Headache, sore throat
- Excessive sweating, chest soreness
- More often diffuse on film; may involve multiple segments or both lungs
Both forms show an infiltrate on chest X-ray. Time of year, known epidemics, and comorbid conditions help define which type you're facing.
The three clinical categories
Community-acquired
Acquired in the community setting — or within 48 hours of hospital admission.
Most common organisms:
- S. pneumoniae — most common bacterial cause in adults
- H. influenzae
- M. pneumoniae
- C. pneumoniae
- Respiratory viruses
Hospital-acquired
Occurs 48 hours or more after admission, not incubating at the time of admission. Includes VAP and healthcare-associated pneumonia.
Most common: Staphylococcus aureus, S. pneumoniae, H. influenzae.
Ventilator-acquired
Arises more than 48–72 hours after endotracheal intubation.
Most common organism: Pseudomonas.
- Aspiration — altered mental status or dysphagia from stroke or neuromuscular disease (e.g., Parkinson disease)
- Obstructive lesions — tumor, retained bronchopulmonary secretions
- Inhalation injury — hypersensitivity pneumonia, near drowning
Evaluation
Highest sensitivity — rules out when absent
- Fever ≥ 38 °C with chills/shivering
- Pleuritic chest pain
- Cough productive of mucopurulent sputum
- Dyspnea
- Tachypnea — especially over age 65
Highest specificity — rules in when present
- Asymmetric breath sounds
- Pleural rubs
- Egophony
- Increased tactile fremitus
- CBC with differential WBC count
- Blood cultures
- Gram stain and culture of sputum
- ABGs and/or pulse oximetry
- Procalcitonin, when available — may aid in diagnosing bacterial pneumonia and guide duration of therapy
- Chest X-ray — searching for a new infiltrate
On exam, look for tachypnea, tachycardia, fever, discomfort, rales ("crackles") over the affected area, and mental status changes or confusion.
Treatment principles
- Start empiric antimicrobial therapy with cultures pending — the regimens live in the next section and in Chapter 32.
- Revise therapy as culture data returns and as the patient improves. In general, use the narrowest-spectrum agent to which the known organism is expected to respond.
- Cover anaerobes in known or suspected aspiration.
- Treat coexisting illness simultaneously — COPD, CHF, diabetes, dehydration.
- Not everyone needs admission. Young adults in particular may be managed as outpatients.
Guided by three things:
- The possibility of rapidly progressive disease
- The patient's overall status and coexisting problems
- The patient's ability to reliably self-administer medication
If in doubt, it is reasonable to observe in the hospital during initial therapy and reassess early response.
Prevention
Yearly, for everyone 6 months and older
No preference for vaccine presentation when multiple types are available within an approved age range. Some patients are revaccinated within a season if they:
- Are immunocompromised
- Have severe underlying COPD or heart disease
PCV13 and PPSV23
- PCV13 — conjugate vaccine for infants, children, and adults older than 19 at high risk
- PPSV23 — polysaccharide vaccine for adults older than 65, and those older than 2 at high risk
- If giving both: start with PCV13, give PPSV23 at least 8 weeks later
Careful — the reading contradicts itself here. Chapter 27 says "at least 8 weeks"; Chapter 32 says "at least 1 year." Know both; the exam may follow either. - If PPSV23 already given, PCV13 comes at least 1 year later
Guidelines change frequently — check the CDC schedule.
Tuberculosis
Mycobacterium tuberculosis. Rates of new infection are increasing — especially among the homeless and those in crowded conditions such as nursing homes and prisons — and the rise has coincided with more patients living with HIV and AIDS. Multidrug-resistant TB is defined as resistance to isoniazid and rifampin.
Patient isolation during initial evaluation and treatment, according to OSHA standards, is mandatory. This is not a judgment call.
Clinical findings
What the patient reports
- Most patients are asymptomatic
- Fever
- Cough — generally productive of purulent sputum that may contain blood
- Weight loss
- Night sweats that may require changing the bed linen
What you find
- Body temperature elevation
- Cachexia
- Rales over affected areas — apical posttussive rales for apical disease
What the workup shows
- Normal CBC
- Low serum cortisol if disseminated disease has destroyed the adrenal cortices
- Acid-fast smears often positive — but treat empirically if findings suggest TB without a positive smear
- Culture usually positive within 6 weeks
Chest X-ray
- Infiltrate — especially in the upper lobes or the superior segments of the lower lobes; can appear anywhere
- Cavity within the lungs
Reading a PPD
The test is read 48 hours after intradermal injection of 0.1 mL purified protein derivative. Measure the indurated area — the largest diameter, not including flat erythema. A positive PPD indicates exposure, not necessarily active infection.
PPD induration — the three thresholds
The cut-off that counts as "positive" drops as the patient's risk rises. Hover a bar for its value.
A serum test used for diagnosis of TB — either latent or active — instead of the PPD. Its advantage: it is not affected by prior bacille Calmette-Guérin vaccination.
Treatment
Four-drug therapy is the backbone for suspected or active disease, or smear-positive disease pending culture return.
| Drug | Dose | Watch for |
|---|---|---|
| Isoniazid (INH) | 300 mg PO daily — or 5 mg/kg, maximum 300 mg/day Given with pyridoxine 25–50 mg PO daily | Peripheral neuropathy — prevented by pyridoxine (vitamin B6) |
| Rifampin Rifadin / Rimactane | 600 mg PO each day — or 10 mg/kg daily, maximum 600 mg/dose | — |
| Ethambutol Myambutol | Generally 15–25 mg/kg PO daily, maximum 2.5 g/dose Precede with screening of color vision. Weight-based alternative per the drug-susceptible TB guidelines: 40–55 kg → 800 mg; 56–75 kg → 1200 mg; 76–90 kg → 1600 mg, all PO daily. | Red/green color blindness and changes in visual acuity |
| Pyrazinamide | 15–30 mg/kg in 3 divided doses daily, maximum 2 g/dose | — |
Duration: usually 6–9 months — 6 months for most patients, 9 months for HIV-positive patients and pregnant women. Modify the regimen if susceptibility studies show resistance to first-line drugs.
The preferred TB regimen on a timeline
Intensive phase, then continuation. The standard course is 26 weeks; HIV-positive patients and pregnant women extend the continuation phase.
- Preferred standard: INH + RIF + PZA + EMB daily for 56 doses (8 weeks), then INH + RIF for 126 doses (18 weeks).
- INH + RIF + PZA + EMB daily for 8 weeks, then INH + RIF 3 times weekly for 16 weeks — especially if susceptibility to INH/rifampin is noted.
- INH + RIF + PZA + EMB daily for 2 weeks, then the same agents 2 times weekly for 6 weeks, then INH + RIF 2 times weekly for 16 weeks — if susceptible.
- Thrice-weekly INH + RIF + PZA + EMB for 24 doses (8 weeks), then thrice-weekly INH + RIF for 54 doses (18 weeks).
- Patients with advanced HIV (CD4 < 100/mcL) should be treated with daily or three-times-weekly therapy in both the initial and continuation phases.
For nonadherent patients, directly observed treatment may be initiated at 3 times per week, usually after 2 weeks of observed therapy — often in hospital.
Consider for
- Asymptomatic, positive PPD, normal chest X-ray
- Exposed to active TB with a negative PPD
- Undergoing immunosuppressive therapy for other reasons
- HIV infected
Management
- INH 300 mg PO daily. Controversy exists over 6 months versus up to 1 year; the standard regimen is 9 months — also the preferred duration for HIV-positive patients and pregnant women.
- Pyridoxine 25–50 mg PO daily may be given during INH therapy to prevent neuropathy.
ARDS & Acute Lung Injury
Any of the numerous causes of acute systemic inflammation can set the lung alight. The classic finding is refractory hypoxemia — and the two most common precipitants are pneumonia and sepsis.
Pneumonia & sepsis
The typical or usual causes of ARDS. Bacteremia and other severe systemic infections also qualify.
Massive trauma or injury
Including burns and smoke inhalation. Increased intracranial pressure — especially after trauma or intracranial bleeding — is another trigger.
Pancreatitis
Inflammation without infection can be enough to initiate the syndrome.
Shock — any cause
Cardiopulmonary bypass is a further recognised precipitant.
Aspiration
Aspiration of fluid, including gastrointestinal contents and near drowning.
The PaO₂/FiO₂ ratio — where ALI ends and ARDS begins
Two thresholds on one scale. Hover a zone for its definition.
Clinical findings
- Severe respiratory distress occurring during the course of one of the inciting events
- Often requires early mechanical ventilatory assistance — refractory hypoxemia is classic
- Symptoms: breathlessness, agitation, confusion, obtundation as oxygen delivery and uptake fall
- Other organ failure — kidneys, liver, bone marrow (reduced platelets), multisystem organ failure
- Lungs often sound clearer than the chest X-ray suggests
X-ray and CT
- Chest X-ray often shows evolving bilateral infiltrates — "whited out"
- CT chest shows the heterogeneous nature of the opacities
What to order
- ABG with PaO₂/FiO₂ ratio
- CBC with differential and platelet count
- Coagulation studies — PT, PTT, fibrinogen, fibrin degradation products
- Renal and liver function
- Urinalysis
- Blood and urine cultures; sputum culture and Gram stain
Treatment
Identification and prompt treatment of the underlying cause. In sepsis-associated ARDS, good outcomes require early resuscitation, appropriate antibiotics, and source control.
Assess and secure
- Assess adequacy of ventilation and the work of spontaneous breathing
- Intubate if ventilation is significantly compromised — especially with altered mentation
Ventilate
- Institute mechanical ventilation if work of breathing is not being met — patient fatigue, elevated PaCO₂
- Or if hypoxemia is not correctable with an FiO₂ of 0.5
Resuscitate
- Vigorous fluid resuscitation if hypotension is present
- Regulated by hemodynamic parameters, especially left ventricular ejection fraction
- Mechanical ventilation often requires positive end-expiratory pressure (PEEP).
- Monitor peak and plateau pressures to prevent barotrauma. Persistent breath-to-breath peak pressures greater than 45 cm H₂O are a risk factor.
- To prevent barotrauma:
- Reduced tidal volumes — typically 6 mL/kg
- Pressure-cycled ventilation
- In severe ARDS, high-frequency oscillatory ventilation may be the only way to oxygenate and ventilate
- Permissive hypercapnia, with bicarbonate repletion to avoid excessive acidosis
- The patient should be sedated for comfort.
- Nutritional support started early — use the enteral route (TPN with caution if enteral is unavailable). Most patients require nearly twice their usual daily caloric requirements.
The risk of pneumothorax or pneumomediastinum is high with ARDS. Sudden increases in ventilating pressure with desaturation indicate the need for an immediate repeat chest X-ray and possible chest tube insertion. Repeated physical and radiographic assessment may be needed to rule out barotrauma.
The Interstitial Diseases
Two scarring diseases with one shared signature: a restrictive ventilatory defect on pulmonary function testing, a reduced diffusing capacity, and "Velcro crackles" on auscultation.
Idiopathic pulmonary fibrosis
Etiology unknown; strongly linked to cigarette smoking. The most common cause of interstitial lung disease among elderly patients, and more common in men.
Symptoms: progressive dyspnea (slow or rapid) and nonproductive cough.
Noncaseating granulomas
Characterised pathologically by noncaseating granulomas and interstitial lung disease, with systemic manifestations: lymphadenopathy, cardiac involvement, iritis, cutaneous lesions, arthritis, GI involvement.
More common among females, North Americans, African Americans, and northern European Caucasians. Typical onset ages 20–40.
- Inhalation exposure — inorganic dusts (silica, asbestos), organic dusts (silos — hypersensitivity pneumonia), fumes (chlorine, sulfur dioxide)
- Drugs — chemotherapeutic agents (bleomycin), antibiotics (nitrofurantoin, sulfa), gold salts, amiodarone
- Autoimmune disorders
- Chronic lung infection — tuberculosis, deep fungal infection (histoplasmosis, coccidioidomycosis)
- Radiation to lung parenchyma
- In patients with prior malignancy — exclude lymphangitic spread of tumor
Sarcoidosis staging
The five stages on chest X-ray
Used to stage pulmonary involvement. Hover each stage.
Shared findings
- CXR and high-resolution CT — interstitial infiltrates, nodules, cystic ("honeycombing") changes, especially in the lower lobes
- PFTs — restrictive ventilatory defect; DLCO commonly reduced
- ABG and pulse oximetry — hypoxemia as disease progresses; CO₂ retention indicates severe disease
- Tissue: fiber-optic bronchoscopy with transbronchial biopsy first; bronchoalveolar lavage at the same time; thoracoscopic lung biopsy if more assurance is needed
Don't miss these
- PPD testing should be done in both
- Complement fixation serology for deep fungi — histoplasmosis, coccidioidomycosis, blastomycosis
- Sarcoidosis is associated with hypercalcemia — check calcium
- Sarcoidosis blood panel: CBC, calcium, LFTs, BUN, creatinine; plus EKG, urinalysis, PPD, ophthalmologic exam
- Vaccinate IPF patients against influenza and pneumococcus — these infections are poorly tolerated
Treatment
IPF — no cure
- No procedure or medication can remove the scarring
- Pirfenidone (Esbriet) and nintedanib (Ofev) slow progression
- Oxygen support to maximise blood oxygen levels
- Lung rehabilitation — helps exercise with less dyspnea
- Noninvasive positive airway pressure by mask may benefit selected patients
- Lung transplant for advanced disease
- Prognosis is often poor; counsel on palliative care and end-of-life issues
Sarcoidosis — individualized
- No cure; treatment based on symptoms and severity of organ involvement
- Refer to specialists for the organs involved
- Alternatives are indicated only when sarcoidosis does not respond to oral corticosteroids, when there is intolerance or contraindication, or when the steroid dose must be reduced
- Options: methotrexate, hydroxychloroquine, azathioprine, cyclophosphamide, infliximab, adalimumab, leflunomide
CHF & Cardiogenic Pulmonary Edema
The heart fails, the lung floods. Clinical manifestations come from restrictive ventilatory defects within the lung parenchyma that begin mild and later become severe.
Etiology
Ischemia
Coronary artery disease with myocardial ischemia and infarction — aggravated by obesity, limited exercise, dyslipidemia, and cigarette smoking.
Rhythm & pressure
- Arrhythmias — tachycardia especially, and bradycardia
- Hypertension
- Valvular dysfunction
Everything else
- Thyroid dysfunction — hyper- or hypothyroidism
- Diabetes mellitus
- Viral myocarditis
- Idiopathic cardiomyopathy
- Renal failure
- Drug therapy — especially certain chemotherapeutic agents
Symptoms & the NYHA scale
Watch the progression: exertional dyspnea → orthopnea → paroxysmal nocturnal dyspnea. Frank respiratory failure may follow. A dry cough is common. The time course may be slow or abrupt.
NYHA functional classification
The higher the class, the less the patient can do. Hover a bar.
Signs of fluid retention
- Edema and jugular venous distention
- Rales
- Tachycardia or bradycardia
- Inability to tolerate lying flat — orthopnea
- Tachypnea
- Pleural effusions
- Ascites when CHF is advanced
What to look for
- Vascular redistribution to upper lung fields
- Interstitial edema
- Kerley B lines
- Pleural effusions — usually bilateral or on the right
- Cardiomegaly
- EKG — assess for ischemia or infarction; determine rhythm
- Oxygenation — ABG and pulse oximetry, to ensure adequate oxygenation and assess CO₂ retention
- CBC — to rule out anemia
- Chemistries — TSH (if abnormal, check free T3/T4 to separate true disease from euthyroid sick state), renal function (BUN, creatinine), liver function, electrolytes including magnesium
- Cardiac enzymes — especially if recent MI or unstable angina is suspected
- Echocardiography — systolic function (rate of demise matters more than the actual ejection fraction), valvular function, global and segmental dyskinesia, diastology, right heart pressures to detect pulmonary hypertension
- Pulmonary function studies — not useful during acute pulmonary edema, but when stable they can demonstrate a restrictive defect (reduced vital capacity) and evaluate coexisting COPD
- Pulmonary artery catheterization — occasionally needed to document severity, especially with hypotension. In general, insertion is not necessary in treating CHF.
When hypotension is present, aggressive fluid therapy could further aggravate CHF. Catheterization can determine cardiac output, cardiac index, systemic vascular resistance, and pulmonary capillary wedge pressure — but it is not routine.
Treatment
Correct the cause of the CHF if known, especially ischemia. Guide fluid administration with bedside ultrasound measurement of the inferior vena cava (IVC), along with clinical indicators of volume status. Nitrates may be indicated — but may or may not be appropriate depending on the cause (e.g., arrhythmia, valvular heart disease).
- Sublingual or intravenous nitroglycerin
- Nitroglycerin patches such as Nitro-Dur 0.4 mg, applied daily
- Oral, long-acting nitrates such as isosorbide
- Supplement oxygen, usually via nasal cannula at low flow rates (e.g., 2 L/min).
- In frank pulmonary edema, oxygen should be supplied in higher amounts — use mask delivery PRN.
- If the patient cannot sustain the work of breathing during an acute episode, attempt noninvasive positive pressure ventilation via CPAP, followed by intubation and mechanical ventilation if necessary. This redistributes edema out of the lungs and back into the vascular space, and offloads the work of breathing.
- Eliminate cardiac depressants. Nondihydropyridine calcium channel blockers (diltiazem, verapamil). Remove β-blockers for acute decompensation and resume when clinically stable.
- Inotropic support in acute decompensation — dobutamine and milrinone.
Note: inotropes should only be started when there is hypotension and evidence of reduced organ perfusion. In these cases dobutamine is usually first-line. - Decrease afterload with an ACE inhibitor or angiotensin II receptor blocker (ARB) as blood pressure tolerates.
- Decrease preload with appropriate diuretics. If the patient has chest pain, morphine may be used as well.
- β-adrenergic antagonists to help regulate catecholamines — if blood pressure and heart rate will tolerate.
- Together these reduce interstitial edema and ventilatory restriction, improving respiratory symptoms. Aggressiveness must be proportionate to the severity of interstitial edema and respiratory distress.
Organism-Directed Regimens
Antimicrobial therapy for lower respiratory tract infections runs on two questions: where did the patient get it, and what am I worried about. Filter below to the scenario you need.
Renal dosing is the hidden variable. Vancomycin and the aminoglycosides repeat one instruction in the source: consult a pharmacist for pharmacokinetic modeling to reach therapeutic levels and avoid toxicity.
Previously healthy
No MDR S. pneumoniae risk factors.
- Azithromycin 500 mg initial dose day 1, then 250 mg Q24h days 2–5, or 500 mg Q24h No renal adjustment needed, but caution if CrCl < 10 mL/min; hepatically eliminated
- OR Doxycycline 100 mg Q12h No adjustment needed
Comorbid conditions or MDR risk
Heart disease, lung disease, diabetes, alcoholism, malignancy, immunosuppression, risk of MDR S. pneumoniae, or antibiotics within the past 3 months.
- Moxifloxacin 400 mg Q24h No adjustment needed
- Levofloxacin 750 mg Q24h CrCl 20–49: 750 mg Q48h; CrCl 10–19 or ESRD: 750 mg then 500 mg Q48h
- Gemifloxacin 320 mg Q24h CrCl ≤ 40 or ESRD: 160 mg Q24h, after dialysis on dialysis days
- OR Amoxicillin-clavulanate 875 mg Q12h plus azithromycin or doxycycline
Hospitalised, not ICU
- Ceftriaxone 1–2 g IV Q24h or ertapenem 1 g IV Q24h
- plus azithromycin 500 mg IV/PO Q24h or doxycycline 100 mg IV/PO Q12h Doxycycline can be used as an alternative to a macrolide
ICU — β-lactam backbone
β-lactam plus azithromycin or a respiratory fluoroquinolone. Options include ampicillin-sulbactam 3 g IV Q6h, ertapenem 1 g IV Q24h, or ceftriaxone 1–2 g IV Q24h.
If penicillin or azithromycin allergy: levofloxacin 750 mg IV/PO Q24h or moxifloxacin 400 mg IV/PO Q24h.
P. aeruginosa coverage
- Piperacillin-tazobactam 4.5 g IV Q6h
- Cefepime 2 g IV Q8h
- Imipenem 500 mg IV Q6h
- Meropenem 1 g IV Q8h
Community-acquired MRSA
- Vancomycin load 15–20 mg/kg/dose IV (max 2 g), then 15 mg/kg/dose Q8–12h if renal function > 90 mL/min, to reach target trough 15–20 mcg/mL. Check trough after every 3rd dose.
- Linezolid 600 mg IV or PO Q12h ESRD: no adjustment, but give after HD on dialysis days
No MRSA risk factors
- Piperacillin-tazobactam 4.5 g IV Q6h
- Cefepime 2 g IV Q8h
- Levofloxacin 750 mg IV/PO Q24h
- Imipenem 500 mg IV Q6h
- Meropenem 1 g IV Q8h
Treat MSSA empirically with piperacillin-tazobactam, cefepime, levofloxacin, imipenem, or meropenem.
High risk for MRSA
History of MRSA; recent hospitalisation in a unit where > 20% of S. aureus isolates are methicillin resistant; IV antibiotics in the last 90 days; or high mortality risk (multiorgan failure, mechanical ventilation).
- Vancomycin load 25 mg/kg/dose IV (max 2 g), then 15 mg/kg/dose Q8–12h if renal function > 90 mL/min, target trough 15–20 mcg/mL
- Linezolid 600 mg IV or PO Q12h
Anti-pseudomonal coverage
- Piperacillin-tazobactam 4.5 g IV Q6h · Cefepime 2 g IV Q8h · Ceftazidime 2 g IV Q8h
- Levofloxacin 750 mg IV/PO Q24h · Ciprofloxacin 400 mg IV Q8h
- Imipenem 500 mg IV Q6h · Meropenem 1 g IV Q8h · Aztreonam 2 g IV Q8h
- Aminoglycosides — amikacin 15–20 mg/kg IV Q24h; gentamicin 5–7 mg/kg IV Q24h; tobramycin 5–7 mg/kg IV Q24h
Use a second agent for Gram-negative anti-pseudomonal coverage only with history of MDR infection, severe critical illness (ARDS/pneumonia, septic shock), or severe immunocompromise. Avoid dual β-lactams.
When to give antibiotics
Only if exacerbation and/or acute infection is suspected — increased dyspnea, sputum production, sputum purulence, and increased coughing.
- First choice: amoxicillin-clavulanate or azithromycin
- Hypersensitivity or resistance, including pseudomonas risk: a macrolide (azithromycin) or a respiratory fluoroquinolone (levofloxacin)
- Add concomitant oral corticosteroids
Most common organisms: H. influenzae ≈ 45%, S. pneumoniae ≈ 30%, M. catarrhalis ≈ 20%, and E. coli/Klebsiella/Enterobacter/P. aeruginosa ≈ 5%.
Start within 48 hours
- Oseltamivir 75 mg PO BID × 5 days
- Zanamivir inhaled 10 mg BID × 5 days
- Baloxavir 80 mg PO single dose if > 80 kg (40 mg if 40–79 kg)
- Peramivir 600 mg IV × 1 dose
Consider longer treatment for immunocompromised patients or severe respiratory disease (ARDS, pneumonia). Treat empirically for bacterial coinfection in severe disease. RT-PCR on a nasopharyngeal specimen has the highest sensitivity and specificity in the shortest time.
Before stopping therapy, the patient must be:
- Afebrile for 48–72 hours
- Hemodynamically normal — HR < 100, systolic BP > 90, RR < 24, SpO₂ > 90% on room air
- Tolerating an oral diet
- With preserved mentation
- Prefer treatment based on respiratory cultures rather than empiric treatment. Consider MRSA nasal PCR screening to reduce overuse of empiric vancomycin.
- Inflammatory biomarkers such as procalcitonin or CRP should not be used to initiate therapy — clinical criteria guide that decision. They can help decide when to stop therapy.
- Use your hospital antibiogram specific to ICU patients when choosing empiric coverage.
- Cover S. aureus, P. aeruginosa, and other Gram-negative bacilli.
- VAP diagnosis: prefer less-invasive sampling (tracheal suctioning) over more-invasive (bronchial wash).
- VAP MRSA risk factors: IV antibiotics in the last 90 days, septic shock, ARDS, hospital stay > 5 days, or renal failure; history of antimicrobial resistance; or a unit where > 20% of S. aureus isolates are methicillin resistant — or where prevalence is unknown.
- Double-cover P. aeruginosa in units with > 10% Gram-negative resistance isolates, or if the patient has a history of Gram-negative resistance. Otherwise single coverage.
- Avoid aminoglycosides if adequate Gram-negative coverage is attainable with alternative agents.
- De-escalate based on susceptibility testing, including MDR organisms and ESBL Gram-negative bacilli.
Pulmonary Hypertension
Pulmonary hypertension (PH) is not the same as pulmonary arterial hypertension (PAH). PAH is a specific subgroup of PH. The WHO grouped them into five groups to keep the difference straight.
Three mechanisms
Increased vascular resistance
- Vasoconstriction — hypoxemia and acidosis
- Loss of vasculature — emphysema, lung resection
- Occlusion — pulmonary embolism
- Relative stenosis — vasculitis
Increased venous pressure
- Left ventricular failure or hypertrophy
- Right ventricular hypertrophy — e.g., due to PE
- Valvular disease — mitral stenosis, aortic stenosis
- Constrictive pericarditis
Increased blood flow
- Left-to-right shunt
- Polycythemia — primary or secondary, e.g. from hypoxemia
PH develops without a known cause (primary/idiopathic) or as the result of other diseases (secondary).
The WHO groups
PAH (or primary)
- Idiopathic PAH — seen most often in young women
- Familial or heritable PAH
- Associated PAH — collagen vascular disease (scleroderma), congenital shunts between systemic and pulmonary circulation, portal hypertension, HIV infection, drugs, toxins
- Chronic thromboembolic PH (CTEPH)
Associated with left heart disease
- Left ventricular systolic or diastolic dysfunction
- Valvular disease — e.g., mitral stenosis
- Congenital/acquired left heart inflow/outflow tract obstruction
- Congenital cardiomyopathies
Lung disease and/or hypoxemia
- COPD, interstitial lung disease
- Sleep-disordered breathing, alveolar hypoventilation
- Chronic exposure to high altitude
- Developmental lung abnormalities
CTEPH
- PE in the proximal or distal pulmonary arteries
- Embolization of other matter — tumor cells or parasites
Miscellaneous, hematologic, systemic
- Myeloproliferative disorders
- Sarcoidosis
- Sickle cell disease
What you see
- Dyspnea on exertion
- Those related to the cause of the PH
- Substernal discomfort
- Fatigue
- Dizziness, near or true syncope
- Palpitations
Exam: splitting of the second heart sound with an increased pulmonic component (P₂), peripheral edema from RV failure, ascites, RV heave, holosystolic murmur, elevated JVP.
Gold standard & the rest
- Right-heart catheterization — measure pulmonary artery pressure (> 25 mmHg) and left atrial pressure (< 18 mmHg suggests WHO group 1)
- Vasodilator study — acute vasodilator challenge
- BNP/proBNP to assess cardiac strain and monitor therapy; D-dimer if PE suspected
- Echocardiography with bubble study; EKG shows RV hypertrophy, right axis deviation, ± right bundle branch block
- CXR — enlarged proximal pulmonary arteries, narrowing in the medial third
- Lower-extremity Doppler, V/Q scan, CT angiography
Heart failure with preserved ejection fraction is a commonly under-recognized cause of PH in the elderly. Older patients are very unlikely to have PAH — more likely pulmonary venous hypertension from left ventricular systolic or diastolic failure, aortic or mitral valve disease, or left atrial noncompliance.
Treatment
All WHO groups may benefit
- Oxygen — shown to reduce peripheral vascular resistance, but long-term therapy has not been shown beneficial. May be recommended with COPD, low arterial oxygen pressure, symptomatic benefit, and correctable desaturation on exercise.
- Exercise — recommended for all; cardiopulmonary rehabilitation improves functional status, exercise capacity, and quality of life.
- Loop diuretics for decompensated right-heart failure with fluid retention, ascites, and peripheral edema.
- Anticoagulation recommended for PAH.
- Digoxin may improve cardiac output in idiopathic PAH and slow ventricular rate in arterial tachyarrhythmias — evidence for chronic use is lacking.
Also
- Treat the underlying disorders contributing to hypoxemia — COPD, CHF, obstructive sleep apnea
- Supplemental oxygen during the night
- If polycythemia is severe with hematocrit above 60%, consider therapeutic phlebotomy to yield a hematocrit of approximately 55%
- Maintain immunization against influenza and pneumococcal pneumonia
- Treatment depends on underlying etiology, WHO functional class, and severity of symptoms.
- Current therapies work by causing or targeting pulmonary artery vasodilation through various mechanisms.
- None of the targeted therapies has been shown to slow pathological progression.
- Depending on severity, two or more drugs from different classes are usually needed.
- Oral drugs, as monotherapy or in combination, are recommended for less severe disease; parenteral prostacyclins are usually used as combination therapy for more severe disease.
- Sequential therapy — start with monotherapy, add a second or third drug based on inadequate response or deterioration.
- Initial or upfront combination therapy is used when there are increased mortality risks or concurrent severe medical illness based on WHO functional class.
Table 28.1 — by WHO functional class
Calcium channel blockers
- Amlodipine (Norvasc) PO 20–30 mg/day
- Nifedipine ER (Procardia XL) PO 120–240 mg/day
- Diltiazem ER (Cardizem LA) PO 240–960 mg/day
A trial of CCBs is only recommended for patients with a positive response to vasoreactivity testing. CCB therapy can lose effectiveness over time.
Endothelin receptor antagonists
- Ambrisentan (Letairis) PO 5–10 mg/day
- Bosentan (Tracleer) PO — < 40 kg max 125 mg/day; > 40 kg max 250 mg/day
- Macitentan (Opsumit) PO 10 mg/day
Teratogenic — limited distribution through REMS programs and only available through specialty pharmacies. Not recommended with moderate-to-severe liver disease; monitor LFTs at baseline and as clinically indicated.
Prostacyclin analogues
- Epoprostenol (Flolan, Veletri) IV — start 1–2 ng/kg/min, titrate every 15 min to target 25–40 ng/kg/min
- Iloprost (Ventavis) INH 2.5–5 mcg inhaled 6–9 times/day (≥ 2 h apart), max 45 mcg/day
- Treprostinil (Remodulin, Tyvaso, Orenitram) IV/SC start 1.25 ng/kg/min, titrate by 1.25 ng/kg/min weekly for 4 weeks, then 2.5 ng/kg/min per week up to 40 ng/kg/min
May cause bleeding due to platelet aggregation inhibition. All prostacyclin-related drugs are only available through specialty pharmacies.
Prostacyclin receptor agonist
- Selexipag (Uptravi) PO max 3,200 mcg/day
Bleeding risk from platelet aggregation inhibition; specialty pharmacy only; many drug–drug interactions.
Phosphodiesterase 5 inhibitors
- Sildenafil (Revatio) PO max 60 mg/day
- Tadalafil (Adcirca) PO max 40 mg/day
Avoid with nitrates.
Guanylate cyclase inhibitor
- Riociguat (Adempas) PO max 2.5 mg TID
Contraindicated with nitrates or PDE-5 inhibitors. Smokers may require higher dosages. Teratogenic — REMS-restricted, specialty pharmacy only.
Pulmonary Embolism
A clot — or other undissolved solid, liquid, or gaseous material — travels to the lung via the venous system and lodges in the pulmonary arterial circulation, interrupting blood flow. Death occurs as a result of right ventricular failure.
The extent of injury
Determined by the size of the embolus — considered massive if more than 50% of flow is obstructed.
Accurate diagnosis is the key to reducing associated mortality.
Why clots form
- Venous stasis — DVT of the lower extremities and pelvis leads to 70% of pulmonary emboli. Prolonged immobility, surgery under general anesthesia > 30 min, CHF, dehydration, obesity, advanced age.
- Vessel wall injury — surgery, fractured hip or pelvis
- Hypercoagulability — estrogen, malignancy
Plus genetic predisposition.
Not everything is a clot
- Fat — orthopedic trauma, especially marrow-containing bone, and surgery
- Air — e.g., from a central line
- Tumor fragments
- Amniotic fluid
- Septic debris — indwelling venous access device
- Sudden, marked dyspnea in a susceptible patient
- Altered consciousness
- Body temperature elevation > 102 °F
- Petechiae over the thorax, shoulders, and axillae
Signs & symptoms
What the patient reports
- Dyspnea — insidious or sudden, the most common symptom
- Apprehension, anxiety, and a perception of "impending doom"
- Substernal discomfort
- Pleuritic pain with PE with infarction
- Hemoptysis with pulmonary infarction
- Syncope
What you find — none to collapse
- Tachycardia; tachypnea and dyspnea
- Initially elevated blood pressure
- Diaphoresis
- Chest pain — dull, central, pleuritic with infarction
- Decreased cardiac output; hypotension and shock
- Signs of RV overload — jugular venous distention, increased intensity of the second heart sound
- Peripheral phlebitis
Diagnostics
- ABG — acute respiratory alkalosis and variable degrees of hypoxemia
- EKG — nonspecific changes. Most common is sinus tachycardia; atrial fibrillation also common.
- Chest X-ray — normal, or with small infiltrates and/or effusion
- Ventilation/perfusion lung scan
- High probability → treat with anticoagulants
- Indeterminate or low probability with high clinical suspicion → consider pulmonary angiography
- If the chest X-ray is abnormal or COPD is present, lung scanning may be misinterpreted — consider CTA
- Pulmonary angiography — remains the accepted gold standard for detecting pulmonary emboli
- Venous Doppler of the lower extremities — may reveal DVT, which requires anticoagulation in part obviating evaluation of PE
- Spiral-cut, high-resolution CT of the chest — reliably shows central PE
Management
| Agent | Dose | Notes |
|---|---|---|
| Unfractionated heparin | Initial bolus 80 units/kg, then continuous infusion of 18 units/kg/hr | Goal: anti-factor Xa activity of 0.3–0.7 international units/mL. PTT goal is institution-specific and instrument/reagent dependent. Some hospitals draw PTT or anti-factor Xa every 6 hr. |
| Enoxaparin (Lovenox) | 1 mg/kg subQ every 12 hr | Acceptable alternative to heparin. Lower risk of bleeding and of heparin-induced thrombocytopenia. Anti-factor Xa requires monitoring in pregnancy, obesity (BMI > 30 kg/m² or 98 kg), renal failure, and bleeding/high bleeding risk. |
| Argatroban direct thrombin inhibitor | Non-ICU: 2 mcg/kg/min continuous IV infusion ICU/critically ill with organ dysfunction: 0.2–0.5 mcg/kg/min |
Goal: PTT of 1.5–3 times the patient's baseline PTT |
| Fondaparinux (Arixtra) | < 50 kg: 5 mg subQ once daily 50–100 kg: 7.5 mg subQ once daily > 100 kg: 10 mg subQ once daily |
Weight-banded dosing |
| Agent | Dose | Reversal & cautions |
|---|---|---|
| Dabigatran (Pradaxa) | 150 mg PO BID | Idarucizumab (Praxbind) — for life-threatening conditions such as intracranial hemorrhage, GI bleeding, and trauma. |
| Rivaroxaban (Xarelto) | 15 mg PO BID with food for 21 days, then 20 mg PO once daily with food | Andexanet alfa (Andexxa). Avoid if CrCl < 30 mL/min. |
| Apixaban (Eliquis) | 10 mg PO BID for the first 7 days, then 5 mg PO BID | Andexanet alfa. |
| Edoxaban (Savaysa) | 60 mg PO per day 30 mg PO per day if CrCl 15–50 mL/min, weight < 60 kg, or on certain P-gp inhibitors |
— |
| Warfarin (Coumadin) | Usual first dose 5 mg PO per day | Continue heparin until therapeutic. Adequate effect when INR is 2–2.5 for at least 2–3 days. Monitor INR after the initial daily dose. |
Factor Xa inhibitors reach therapeutic effect rapidly — bridging with heparin is unnecessary. Renal function, liver function, age, and weight must be considered and monitored every 3–6 months, with dosages adjusted accordingly.
Length of treatment: 3–6 months for the initial episode of PE; for recurrent or unprovoked PE, treat 6–12 months or longer, or consider an indwelling vena cava filter to protect against massive embolization in patients with ongoing risk factors.
- Fibrinolytic therapy — note contraindications before instituting. May be appropriate for massive proximal PE with persistent systemic hypotension and signs of right heart strain, and in patients with very little cardiopulmonary reserve.
- Alteplase (recombinant tPA): 100 mg IV infused over 2 hours.
- After fibrinolytic therapy is completed, begin heparin or enoxaparin when the PTT is < 2 times control.
- Hemodynamic support may be needed for massive emboli with hypotension.
- Surgical embolectomy — reserved for massive emboli in central pulmonary arteries where the clot is creating hypotension and shock.
- Inferior vena cava interruption ("umbrella" device, Greenfield filter) — indicated when the risk of further emboli is perceived to be high, or when there is an absolute risk to anticoagulation.
- Supplemental oxygen to keep oxygen saturation above 90%.
Pulmonary vasculitis
Triad you must recognize
Necrotizing granulomas of the respiratory tract (upper and lower), pulmonary microangiitis, and glomerulonephritis.
- Associated with hemoptysis, dyspnea, cough, pulmonary infiltrates
- Antineutrophilic cytoplasmic antibodies (ANCA) are often positive
- Treatment: prednisone 1 mg/kg/day or cyclophosphamide 2 mg/kg/day, with reasonable chance of remission within 1 year
- Two components: induction of remission, then maintenance to prevent relapse
- Induction options: prednisone 1 mg/kg/day (max 60–80 mg/day); oral cyclophosphamide 1.5–2 mg/kg/day; IV cyclophosphamide 0.5 g/m² every 2 weeks for 3–6 months; rituximab 375 mg/m² weekly for 4 weeks; methotrexate 20–25 mg PO weekly
- Maintenance: methotrexate or azathioprine 2 mg/kg/day
- Prophylaxis against PCP/PJP during induction may be necessary
Systemic granulomatous angiitis
- Involves lung, brain, skin (especially), and rarely the upper respiratory tract and kidneys
- Associated with the eventual development of lymphoma in many cases
- Treatment generally follows that for diffuse large B-cell lymphoma
- Choice based on symptoms, history of an inciting medication, extent of extrapulmonary involvement, and histopathologic grade
- If a medication is implicated, discontinue it and observe for changes in disease extent
- Refer to hematology oncology
Pleura & Chest Wall
The space between the lung and the chest wall, and the cage around it. Two emergencies live here: the tension pneumothorax, and the empyema that antibiotics alone will not cure.
Pneumothorax
Air in the pleural space, resulting from perforation of the chest wall or pleura, causing the lung to collapse.
Disruption of the visceral pleura
Air enters the pleural space from the lung. Occurs in individuals with or without underlying lung disease.
Look for it with COPD, tuberculosis, sarcoidosis, pulmonary fibrosis, bronchogenic carcinoma, or rupture of a subpleural bleb.
Penetrating chest trauma
The parietal pleura is disrupted. Air enters from the atmosphere during inspiration and exits during expiration — which decreases the likelihood of mediastinal tension and shift.
Blunt chest trauma
Usually due to rib fractures. The visceral pleura is disrupted and air enters the pleural space from the lung.
Complication of a procedure
Disruption of the visceral pleura as a complication of an invasive thoracic procedure — and also after procedures involving the neck or abdomen. Includes IV access device insertion, needle biopsy of liver or lung, and thoracentesis.
Air in, no air out
Following a spontaneous or traumatic pneumothorax, air enters the pleural space but is unable to exit. As pressure rises, the lung collapses, the mediastinum shifts to the opposite side, and venous return to the right heart is impaired — decreasing cardiac output and causing hypotension.
Tension pneumothorax is a medical emergency.
Subjective findings
- Possible sudden onset of dyspnea and shortness of breath (air hunger)
- Pleuritic chest pain — may be sharp and severe
- Apprehension and agitation
Physical findings
- Splinting and decreased inspiratory expansion of the involved hemithorax
- Bulging of the intercostal spaces on the affected side during exhalation
- Decreased breath sounds and fremitus with hyperresonant percussion
- Tracheal deviation toward the unaffected side — a late sign
- Subcutaneous emphysema
- Possible Hamman sign — mediastinal crepitus on auscultation
- On the ventilator: high peak inspiratory pressure with decreased compliance
Pneumothorax is established by demonstrating a white visceral pleural line — the interface between lung and pleural air. Increased translucency confirms the degree of collapse. Recognizing small pneumothoraces, particularly in mechanically ventilated patients, is crucial to preventing tension pneumothorax. ABGs typically show mild to moderate hypoxemia and hypercapnia.
- Immediate decompression with a 14- to 16-gauge needle into the second intercostal space, midclavicular line of the affected side.
- Must follow with chest tube insertion at the fourth or fifth intercostal space, midaxillary line, to closed water-seal drainage.
- Spontaneous pneumothorax — depends on size and underlying lung disease.
- If small: supplemental oxygen with a 100% non-rebreather mask and observe; repeat chest X-ray frequently.
- If collapse is greater than 20%: insert a chest tube at the fourth or fifth intercostal space, midaxillary line, to water-seal drainage.
- Traumatic pneumothorax — prompt chest tube insertion at the fourth or fifth intercostal space, midaxillary line, with closed chest drainage.
- Negative pressure (suction to the drainage apparatus) — use when the water seal fails to re-expand the lung after 24–48 hours, or when persistent pneumothorax perpetuates hypoxemia and/or hypercapnia.
Pleural effusion
Increased amounts of fluid within the pleural space. The first question is what kind of fluid.
Pressure problem
Due to increased hydrostatic or decreased oncotic pressure.
Causes: congestive heart failure, cirrhosis, hypoalbuminemia.
Permeability problem
Due to increased production of fluid from abnormal capillary permeability, or decreased lymphatic clearance from the pleural space.
Causes: malignancy, rheumatoid arthritis, vasculitis, lupus.
Infection and pus
Requires chest tube insertion and probable surgical intervention.
Antimicrobials alone are not curative when empyema is present. Select all antimicrobials on pleural fluid culture results, including sensitivity data.
Blood in the pleural space
If the fluid is bloody, insertion of a chest tube is often required.
Thoracic duct injury
Injury of the thoracic ducts with accumulation of chyle in the pleural space.
Next to a pneumonia
Pleural effusions that form in the pleural space adjacent to a pneumonia.
How much fluid does it take to see it?
Chest X-ray detection thresholds by view. Hover a bar for its value.
What you find
- Dyspnea
- Pleuritic chest pain
- Tachypnea
- Dullness on percussion with diminished or absent breath sounds over the affected area
- Pleural friction rub
- Fever, especially if the fluid is infected
CXR: blunting of the costophrenic angles — a linear shadow ascending vertically and clinging to the ribs in a meniscus pattern. Fluid may layer out on decubitus films, or loculate along the lateral chest wall (confirmed by ultrasound or CT).
Exudate if one or more
- Pleural fluid protein : serum protein > 0.5
- Pleural fluid LDH : serum LDH > 0.6
- Pleural fluid LDH more than two-thirds the upper limit of normal serum LDH
A transudate typically has a serum glucose equal to pleural fluid glucose and a pH between 7.40 and 7.55.
Thoracentesis is indicated when
- You need to identify the cause — infectious, malignancy, chylothorax
- The patient is dyspneic — the procedure is therapeutic, and can be diagnostic when fluid is sent for laboratory evaluation
Laboratory evaluation of pleural fluid
- Cell count and differential including WBC
- Chemistries — serum and pleural fluid levels of total protein, glucose, LDH, amylase, triglycerides
- Gram stain and cultures — bacteria (aerobic and anaerobic), acid-fast bacilli, fungi
- Fluid pH — tends to be low in empyema due to tuberculosis or anaerobic pathogens, and in rheumatoid involvement of the pleura
- Cytology — to assess for metastatic cancer to the pleura
Management ladder
- Observation if asymptomatic, with serial chest X-rays.
- If the risk of infection is small and the effusion is likely due to CHF: initiate diuresis and follow with serial chest X-rays to assess resolution.
- Thoracentesis as above.
- If bloody → chest tube. Empyema → chest tube and probable surgery.
- Repeated thoracentesis is acceptable for malignant effusions that reaccumulate — especially when needed infrequently.
- Pleurodesis — malignant effusions drained by chest tube may be sclerosed to prevent recurrence. A sclerosing agent is introduced through the chest tube (slurry) or by thoracoscopic surgical procedure (talc poudrage) after drainage is complete.
Pleuritis
Also called pleurisy — inflammation of the lung pleura causing pain. The pain is typically localized, sharp, and fleeting, and made worse by coughing, sneezing, and deep breathing. Etiologies include autoimmune disease, viral infections, pneumonia, lung cancer, and certain medications. Treatment depends on the cause.
Chest wall disorders
Scoliosis, kyphosis, ankylosing spondylitis
- Congenital scoliosis — S-shaped curvature; may induce a restrictive ventilatory defect. Risk of respiratory failure rises if the curvature is severe or superimposed chest disease makes breathing difficult.
- Kyphosis — accentuated dorsal curve; may coexist with scoliosis. Acquired kyphosis results from osteoporosis and vertebral collapse with pain — and treating that pain may introduce the additional risk of ventilatory compromise.
- Ankylosing spondylitis — chronic inflammatory disease of the axial skeleton joints; pain and progressive stiffening, with chest expansion becoming limited as it progresses.
Fractures and costochondritis
- Rib or sternal fracture can occur spontaneously or from trauma or surgery. Chest wall instability with flailing outward during inspiration limits movement, especially with multiple fractures — causing hypoventilation and poor secretion clearance.
- Pain medication may facilitate breathing, but excessive analgesia may lead to hypoventilation and ventilatory failure.
- Milder injuries may be stabilized with chest wall binders; significant impairment may require positive pressure ventilation to stabilize the wall.
- Sternal dehiscence after open heart surgery or mediastinal procedures can similarly compromise respiration.
- Costochondritis — may be confused with serious chest conditions; more common in young women; tenderness over the area; NSAIDs and heat help.
- Costosternal junction inflammation can also come from autoimmune arthritis (rheumatoid disease, SLE) or Tietze syndrome.
- Chest wall muscle compliance decreases with age — ribs become ossified (less flexible) and joints stiffen.
- Respiratory muscle strength and endurance decrease with aging.
- Antibiotic doses may need to be reduced in the elderly due to altered renal function or predisposition to medication side effects.
- The incidence of lung cancer increases with age — malignancy must be on the differential for pleural effusion in the elderly patient.
What to lock in
If this week supports one study habit, it is to anchor each condition to its decisive first move. These are the high-yield contrasts to carry forward.
PPD thresholds
5 / 10 / 15 mm — the cut-off falls as risk rises. Measure induration, not erythema, at 48 hours. A positive PPD means exposure, not active disease.
ALI vs. ARDS
One number separates them: PaO₂/FiO₂. Below 300 is acute lung injury; below 200 is ARDS. Refractory hypoxemia is the classic finding.
Pneumonia therapy
Culture first, then empiric therapy, then narrow. Revise as culture data returns; use the narrowest spectrum that covers the known organism. CAP 5–7 days; HAP/VAP 7 days.
Pleural effusion workup
Image → tap → analyze → treat. Observation if asymptomatic; diurese if CHF is likely; thoracentesis to identify the cause or relieve dyspnea; chest tube if bloody or empyema.
Tension pneumothorax
Needle first, chest tube second. 14–16 gauge, second intercostal space, midclavicular line — then a chest tube at the fourth or fifth intercostal space, midaxillary line. Never wait for the film.
Massive PE
> 50% of flow obstructed. Death comes from right ventricular failure. Persistent hypotension plus right heart strain is the trigger for fibrinolytics — alteplase 100 mg IV over 2 hours.
Light's criteria
Exudate if any one: protein ratio > 0.5, LDH ratio > 0.6, or pleural LDH > ⅔ the upper limit of normal.
The PH gold standard
Right-heart catheterization. PAP > 25 mmHg with LAP < 18 mmHg points to WHO group 1.
The antibiotic that needs a pharmacist
Vancomycin and the aminoglycosides. Target a vancomycin trough of 15–20 mcg/mL. Aminoglycosides are dosed once daily — amikacin 15–20 mg/kg, gentamicin or tobramycin 5–7 mg/kg IV Q24h. Consult a pharmacist for pharmacokinetic modeling on every order.
Find the organism before you treat it, find the clot before it kills, and find the air before it shifts.
Rapid-fire review
Answer out loud first, then reveal. Twelve questions covering all five chapters.
A patient has pneumonia symptoms but a normal chest X-ray on day 1. When do you repeat it, and why?
In 24–48 hours. The appearance of the infiltrate may lag behind the appearance of symptoms by 24–48 hours, so an early normal film does not exclude pneumonia.
Which physical exam findings have the highest specificity for pneumonia?
Asymmetric breath sounds, pleural rubs, egophony, and increased tactile fremitus. (The highest-sensitivity findings are fever ≥ 38 °C with chills, pleuritic chest pain, productive cough, dyspnea, and tachypnea.)
Differentiate HAP from VAP, including the most common organism for each.
HAP occurs 48 hours or more after admission (not incubating on admission) — most common organisms are S. aureus, S. pneumoniae, and H. influenzae. VAP arises more than 48–72 hours after endotracheal intubation — and Pseudomonas is the most common organism.
State the four first-line TB drugs, their doses, and the toxicity that requires screening before one of them.
Isoniazid 300 mg PO daily (with pyridoxine 25–50 mg daily to prevent peripheral neuropathy) · Rifampin 600 mg PO daily · Ethambutol 15–25 mg/kg PO daily — screen color vision first, because it can cause red/green color blindness and visual acuity changes · Pyrazinamide 15–30 mg/kg in 3 divided doses daily. Duration is 6–9 months (9 for HIV-positive patients and pregnant women).
What PaO₂/FiO₂ values define ALI and ARDS?
Less than 300 = ALI. Less than 200 = ARDS. The classic finding is refractory hypoxemia, and the lungs often sound clearer than the chest X-ray would suggest.
Your ARDS patient on the ventilator suddenly desaturates with rising ventilating pressures. What do you do?
Suspect barotrauma — pneumothorax or pneumomediastinum. Get an immediate repeat chest X-ray and prepare for possible chest tube insertion. Peak pressures persistently > 45 cm H₂O are the risk factor; tidal volumes are typically reduced to 6 mL/kg.
Name the five chest X-ray stages of sarcoidosis.
Stage 0 normal · Stage I bilateral hilar lymphadenopathy (BHL) · Stage II BHL plus pulmonary infiltrates · Stage III pulmonary infiltrates without BHL · Stage IV pulmonary fibrosis. Also remember: sarcoidosis is associated with hypercalcemia.
Which NYHA class describes a patient comfortable only at rest?
NYHA 3 — marked limitation with activity, comfortable only at rest. NYHA 4 is symptoms with any activity and occasionally at rest, with the patient on complete rest.
A patient with CHF is hypotensive. When should you start an inotrope, and which one first?
Only when there is hypotension AND evidence of reduced organ perfusion. In those cases dobutamine is usually first-line (milrinone is the alternative). Also remove β-blockers for acute decompensation and resume when stable.
A 60 kg patient has a massive PE with persistent hypotension and right heart strain. What is the thrombolytic dose?
Alteplase (recombinant tPA) 100 mg IV infused over 2 hours. Check contraindications before instituting therapy. Afterwards, begin heparin or enoxaparin when the PTT is < 2 times control.
State Light's criteria. Then: what glucose and pH would you expect in a transudate?
An exudate has one or more of: pleural fluid protein : serum protein > 0.5; pleural fluid LDH : serum LDH > 0.6; pleural fluid LDH more than two-thirds the upper limit of normal serum LDH. A transudate typically has a serum glucose equal to pleural fluid glucose, and a pH between 7.40 and 7.55.
Walk through the management of a tension pneumothorax, in order.
1. Immediate decompression with a 14- to 16-gauge needle into the second intercostal space, midclavicular line of the affected side. 2. This must be followed by chest tube insertion at the fourth or fifth intercostal space, midaxillary line, to closed water-seal drainage. Do not wait for imaging.
Sources
Every statement above comes from the assigned Week 5 reading — five chapters of Practice Considerations for Adult-Gerontology Acute Care Nurse Practitioners.
Chapters
Inocencio, B., & Fellin, R. (2021). Restrictive (inflammatory) lung diseases and congestive heart failure/pulmonary edema. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 27).
Harse, A. C., & Fellin, R. (2021). Lower respiratory tract infections. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 32).
Lakin, T. M., Hoy, H. M., & Fellin, R. (2021). Pulmonary hypertension and pulmonary vascular disorders. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 28).
Akintade, B. (2021). Pneumothorax. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 31).
Coates, J. (2021). Chest wall and secondary pleural disorders. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 29).
Selected sources cited in the reading
Kalil, A. C., Metersky, M. L., Klompas, M., Muscedere, J., Sweeney, D. A., Palmer, L. B., . . . Brozek, J. L. (2016). Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clinical Infectious Diseases, 63(5), e61–e111.
Mandell, L. A., Wunderink, R. G., Anzueto, A., Bartlett, J. G., Campbell, G. D., Dean, N. C., . . . Whitney, C. G. (2007). Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clinical Infectious Diseases, 44(Suppl. 2), S27–S72.
Thompson, B. T., Chambers, R. C., & Liu, K. D. (2017). Acute respiratory distress syndrome. New England Journal of Medicine, 377, 562–572.
Klinger, J. R., Elliott, C. G., Levine, D. J., Bossone, E., Duvall, L., Fagan, K., . . . Badesch, D. B. (2019). Therapy for pulmonary arterial hypertension in adults: Update of the CHEST guideline and expert panel report. Chest, 155(3), 565–586.
Uyeki, T. M., Bernstein, H. H., Bradley, J. S., Englund, J. A., File, T. M., Fry, A. M., . . . Pavia, A. T. (2018). Clinical practice guidelines by the Infectious Diseases Society of America: 2018 update on diagnosis, treatment, chemoprophylaxis, and institutional outbreak management of seasonal influenza. Clinical Infectious Diseases, 68(6), 1–47.
Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Drazner, M. H., . . . Wilkoff, B. L. (2017). 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guidelines for the management of heart failure. Journal of the American College of Cardiology, 136(6), 776–803.