Pulmonary Medicine Guide
Oxygen Supplementation: From Room Air to Mechanical Ventilation
Oxygen Delivery Hierarchy
Understand the spectrum of oxygen delivery systems from lowest to highest FiO2 capability:
Simple Oxygen Delivery Systems
Nasal Cannula (NC)
The most commonly used delivery system for stable patients:
FiO2 Rule of Thumb
Each liter of flow increases FiO2 by approximately 4% above room air (21%). Thus: 1 L/min = 25%, 2 L/min = 29%, 3 L/min = 33%, and so on.
- Flow rates: 1–6 L/minute
- FiO2 range: 24–44%
- Comfort: Well-tolerated; allows eating and communication
- Limitations: Cannot deliver FiO2 >44% reliably; flow >6 L/min causes nasal irritation without benefit
- Mechanism: Blends oxygen with room air at the nares
Simple Face Mask
Used when higher FiO2 needed but patient not in acute distress:
- Flow rates: 5–10 L/minute
- FiO2 range: 40–60%
- Advantages: Higher FiO2 than nasal cannula
- Disadvantages: Covers mouth; interferes with eating/speaking; patient must tolerate mask
Venturi Mask (Air-Entrainment Mask)
Delivers precise, predictable FiO2 using Bernoulli principle:
- Flow rates: 4–15 L/minute (depending on FiO2 set)
- FiO2 range: 24–50% (some models 24–60%)
- Advantage: Precise FiO2 delivery; useful in COPD where hypercapnia risk is high
- Disadvantage: Bulkier; more equipment required
Venturi setting guide:
| Color Adapter | FiO2 | Flow (L/min) |
|---|---|---|
| Blue | 24% | 3 |
| White | 28% | 4 |
| Yellow | 31% | 6 |
| Orange | 35% | 8 |
| Red | 40% | 15 |
Non-rebreather (NRB) Mask
Highest FiO2 achievable with spontaneous breathing:
- Flow rates: 10–15 L/minute (reservoir should remain ≥1/3 full)
- FiO2 range: 80–95%
- Use case: Acute hypoxemia, suspected severe hypoxia
- Mechanism: One-way valves prevent rebreathing of exhaled air; reservoir bag stores 100% oxygen
- Critical point: Ensure reservoir fills adequately with each breath; adjust flow to maintain this
High-Flow Nasal Cannula (HFNC)
Bridge between standard supplemental oxygen and non-invasive ventilation:
Physiologic Benefits
- Delivers heated, humidified oxygen at high flow rates
- Provides modest positive pressure support (PEEP approximately 3–4 cmH₂O)
- Washes out dead space, reducing rebreathing of CO₂
- Allows better nutrition and communication vs. face mask
Initial Settings and Titration
Starting parameters:
- FiO2: Start at 100%; titrate down every 15–30 minutes targeting SpO2 >90%
- Flow rate: 0.5 L/kg/min (e.g., 70 kg patient = 35 L/min)
- Can increase flow up to 2 L/kg/min if needed for distress or CO₂ retention
Titration approach:
- Begin at 100% FiO2
- If SpO2 >94%, reduce FiO2 by 10% every 15–30 min
- Adjust flow based on respiratory distress (increase if increased work of breathing)
- Monitor for improvement in respiratory rate, comfort, oxygen saturation
When HFNC Fails
Persistent hypoxemia or hypercapnia despite HFNC indicates need for escalation to non-invasive or invasive ventilation.
Non-Invasive Ventilation (NIV): BiPAP
Physiology and Indications
BiPAP (Bilevel Positive Airway Pressure) provides two levels of pressure:
- IPAP (Inspiratory Positive Airway Pressure): Applied during inspiration; supports work of breathing
- EPAP (Expiratory Positive Airway Pressure): Applied during expiration; maintains airway patency and oxygenation
Common indications: - COPD exacerbation (hypercapnic respiratory failure) - Cardiogenic pulmonary edema - Pneumonia with respiratory fatigue - Neuromuscular weakness causing hypoventilation
Initial Settings
A typical starting point for a patient in distress:
| Setting | Initial Value | Adjustment |
|---|---|---|
| IPAP | 10 cmH₂O | Increase by 2–4 cmH₂O if respiratory rate remains >30 or persistent CO₂ retention |
| EPAP | 5 cmH₂O | Increase if persistent hypoxemia or pulmonary edema; rarely >10 cmH₂O |
| FiO2 | 100% | Titrate down toward SpO2 goal |
| Backup respiratory rate | 12–16 bpm | Set slightly below patient's intrinsic rate |
Adjusting BiPAP for Clinical Response
Interpret the Problem
- Persistent high respiratory rate or CO₂ retention? → Increase IPAP to 12–16 cmH₂O
- Persistent hypoxemia? → Increase EPAP and FiO2 simultaneously
- Patient discomfort or inability to synchronize? → Lower initial pressures; increase gradually
Predictors of BiPAP Success
Strong indicators that BiPAP will be effective rather than delaying intubation:
- RR <30 at initiation (or drops below 30 within 1–2 hours)
- Tidal volume 6–8 mL/kg of ideal body weight
- Arterial pH rises ≥0.06 within first 2 hours
- PaCO₂ drops ≥8 mmHg within first 2 hours
- Patient comfort and synchronization with ventilator
Intubation Criteria
When to abandon NIV and proceed to mechanical ventilation:
| Criterion | Value |
|---|---|
| Hypercapnia | PaCO₂ >80 mmHg despite optimization |
| Severe acidemia | pH <7.25 despite BiPAP trial |
| Altered consciousness | GCS <8 (unable to protect airway) |
| Respiratory exhaustion | Severe distress, inability to cooperate |
| Acute deterioration | Decompensation during NIV trial |
COPD Exacerbation
Clinical Presentation
Acute worsening of baseline dyspnea, cough, and sputum production. Patients may also report:
- Increased sputum volume or change in character (purulent appearance suggests infection)
- Chest tightness or wheezing
- Orthopnea or worsening exercise tolerance
- Hemoptysis (suggests infection, malignancy, or PE)
Rule Out Other Causes
Acute dyspnea in a COPD patient is not always an exacerbation. Always consider pneumonia, pneumothorax, pulmonary embolism, acute coronary syndrome, and heart failure.
Initial Assessment and Diagnostics
| Test | Rationale |
|---|---|
| ABC | Assess airway patency, breathing effort, circulation |
| Chest X-ray | Identify infiltrate (pneumonia), pneumothorax, or other acute pathology |
| Arterial or venous blood gas | Assess CO₂ retention (hypercapnia), pH (acidemia), oxygenation |
| Complete blood count | Evaluate for leukocytosis (infection), anemia |
| Comprehensive metabolic panel | Renal function (affects medication clearance), electrolytes |
| Sputum culture | If purulent sputum; identify organism for antibiotic targeting |
| Procalcitonin | Adjunct to guide antibiotic initiation (elevated suggests bacterial infection) |
| ECG | Rule out acute coronary syndrome or arrhythmia |
Treatment Strategy
Bronchodilation
Rapid-acting beta-2 agonist + anticholinergic combination is the foundation:
- Albuterol 2.5 mg in 3 mL normal saline via nebulizer, delivered every 4 hours (or continuously if severe distress)
- Ipratropium 0.5 mg in 3 mL normal saline via nebulizer every 4 hours
- May combine into single nebulizer treatment for convenience
IV magnesium sulfate (2 g IV over 20 minutes) can augment bronchodilation in severe exacerbations.
Corticosteroids
Reduces airway inflammation and accelerates recovery:
- Oral prednisone 40 mg daily for 5 days (no taper necessary for short course)
- OR IV methylprednisolone 125 mg (IV methylpred ~1 mg = ~1.25 mg prednisone)
- Equivalent to approximately 100 mg IV methylprednisolone daily for 5 days
Antibiotics
Indicated if patient has one or more signs of bacterial infection:
- Purulent sputum
- Elevated temperature
- Elevated white blood cell count
- Infiltrate on chest X-ray
Antibiotic options:
| Agent | Dosing | Notes |
|---|---|---|
| Azithromycin | 500 mg daily × 3 days | Alternative day-1 loading: 500 mg then 250 mg daily × 4 more days |
| Doxycycline | 100 mg BID × 5–7 days | Avoid in renal failure; photosensitivity; good lung penetration |
| Respiratory fluoroquinolone (levofloxacin) | 750 mg daily × 5 days | Broad spectrum; good for atypical organisms; monitor QT interval |
| Amoxicillin-clavulanate | 875 mg BID × 5–7 days | If beta-lactam preferred; reasonable coverage |
Oxygen Therapy
Target SpO2: 88–92% in COPD exacerbation
Critical Concept
Many COPD patients have chronic CO₂ retention and depend on hypoxic respiratory drive. Excessive oxygen can suppress respiration and worsen hypercapnia. Monitor ABG/VBG closely and titrate conservatively.
- Start with nasal cannula 1–2 L/min
- Use Venturi mask (24–28% FiO2) if available to target precise FiO2
- Escalate to HFNC or BiPAP if inadequate response after 1–2 hours of therapy
Non-Invasive Ventilation
Consider early BiPAP if:
- Respiratory rate persistently >25
- Signs of accessory muscle use
- Hypercapnia (PaCO₂ >50) or acidemia (pH <7.35)
- Clinical deterioration despite bronchodilators and steroids
Monitoring
- Repeat blood gas at 30–60 minutes to assess response
- Reassess q1–2h initially; document respiratory rate, work of breathing, oxygen saturation
- Watch for signs requiring escalation to higher level of care (mechanical ventilation)
Pulmonary Embolism: Risk Assessment, Diagnosis, and Management
Risk Stratification
Wells Criteria for PE Probability
Clinically asymptomatic patients with low Wells score and normal D-dimer can be safely discharged without imaging:
| Clinical Finding | Points |
|---|---|
| Heart rate >100 | 1.5 |
| Clinical signs of DVT | 3 |
| PE is primary diagnosis | 3 |
| Hypoxemia (SpO₂ <90%) | 1.5 |
| Hemoptysis | 1 |
| Clinical signs of heart failure | 1.5 |
| Prior PE or DVT | 1.5 |
Score interpretation:
- ≤4 points = Low probability; D-dimer can rule out
- 4–6 points = Intermediate probability; recommend imaging
- >6 points = High probability; proceed directly to imaging
Diagnostic Workup
D-Dimer
- Highly sensitive but low specificity
- Use only in low-probability patients (Wells ≤4) to exclude PE
- Negative D-dimer essentially rules out PE
- Positive D-dimer requires imaging confirmation
Computed Tomography Pulmonary Angiography (CTPA)
The gold standard for PE diagnosis:
- Sensitivity ~95%; Specificity ~98%
- Requires iodinated contrast (avoid if contrast allergy or severe renal insufficiency)
- Risk of contrast-induced nephropathy in CKD
- Can assess RV size, RV:LV ratio (RV strain)
Ventilation-Perfusion Scan
Reserved for patients with contrast allergy or renal failure:
- High probability scan (segmental or larger perfusion defects without matched ventilation defect) = high likelihood PE
- Low probability scan = PE unlikely, can defer further testing
- Indeterminate results require additional testing
Lower Extremity Venous Ultrasound
- Detects deep vein thrombosis (DVT) as source of PE
- Can be used as initial test if DVT suspected clinically
- If proximal DVT found, treat as PE even without confirmation in pulmonary arterial tree
Echocardiography
Assess for RV strain and guide prognosis:
- RV dilation (RV:LV ratio >0.9) indicates hemodynamic impact
- RV dysfunction without hypotension suggests submassive PE
- Elevated troponin + RV strain indicates higher mortality risk
PE Risk Stratification and Treatment
Massive PE (Hemodynamically Unstable)
Presentation: Hypotension (SBP <90) or cardiogenic shock
Treatment priorities:
- Thrombolytic therapy (alteplase 15 mg bolus, then 50 mg infusion over 30 min, then 35 mg over 60 min)
- Parenteral anticoagulation (heparin drip)
- Vasopressor support if persistent hypotension
- Surgical embolectomy or catheter-directed thrombectomy if available and thrombolytics contraindicated
Time-Critical Intervention
Massive PE is immediately life-threatening. Mobilize ICU, cardiothoracic surgery, and interventional radiology.
Submassive PE (Hemodynamically Stable with RV Strain)
Presentation: Normal blood pressure but elevated troponin and/or RV dilation on echo
Treatment approach:
- Anticoagulation is primary therapy
- Thrombolytics can be considered if:
- Clinical deterioration
- Very elevated troponin/BNP
- Severe RV dysfunction
- Hemodynamic compromise develops
- Close monitoring in ICU or intermediate care
- Serial troponin and lactate to detect deterioration
Subsegmental or Low-Risk PE
Presentation: Small PE without RV strain or troponin elevation
Management:
- Anticoagulation if unprovoked or high-risk provocation
- Can observe without anticoagulation if transient provocation (surgery/immobility recently resolved)
- Outpatient follow-up and imaging surveillance may suffice
Anticoagulation and Duration
Initiation of Anticoagulation
First-line options:
| Agent | Dosing | Route | Transition |
|---|---|---|---|
| Unfractionated heparin (UFH) | 80 IU/kg bolus, then 18 IU/kg/hr infusion; adjust for aPTT 60–100 | IV | Transition to warfarin or DOAC |
| Enoxaparin (LMWH) | 1 mg/kg IV or SC Q12H; or 1.5 mg/kg SC daily | IV or SC | Transition to warfarin or DOAC |
| Fondaparinux | Weight-based SC once daily: <50 kg (5 mg), 50–100 kg (7.5 mg), >100 kg (10 mg) | SC | Transition to warfarin or DOAC |
| DOAC (rivaroxaban) | 15 mg daily × 21 days, then 20 mg daily | PO | No transition needed; continue indefinitely if unprovoked |
Long-term Anticoagulation Duration
| PE Type | Duration | Notes |
|---|---|---|
| Provoked (surgery, immobility, hospitalization) | 3–6 months | Shorter duration acceptable if transient provocation |
| Unprovoked (no clear risk factor) | ≥3 months; many continue indefinitely | Individualize based on bleeding risk and recurrence risk |
| Cancer-associated | Duration of cancer treatment + ≥3 months | Consider LMWH vs. DOAC; anticoagulate throughout chemotherapy |
| Antiphospholipid syndrome | Indefinite | High recurrence risk |
Shared Decision-Making
Discuss bleeding vs. recurrence risk with patient. After 3–6 months, reassess benefit of continuing anticoagulation.
Pleural Effusions: Classification and Management
Light's Criteria for Exudate vs. Transudate
Determining whether an effusion is exudative (pathologic) or transudative (mechanical) guides further workup:
An effusion is exudative if ONE OR MORE of the following are present:
| Criterion | Exudate Threshold |
|---|---|
| Protein ratio (pleural:serum) | >0.5 |
| LDH ratio (pleural:serum) | >0.6 |
| Absolute pleural LDH | >2/3 of upper limit of normal serum LDH |
Transudative Effusions
"Mechanical" effusions resulting from imbalance of hydrostatic and oncotic pressures:
| Cause | Pathophysiology |
|---|---|
| Congestive heart failure | Most common overall cause; elevated hydrostatic pressure |
| Cirrhosis | Ascites + portal hypertension → right heart failure |
| Nephrotic syndrome | Massive proteinuria → low serum albumin |
| Dialysis | Post-dialysis fluid shifts |
| Severe malnutrition | Reduced plasma oncotic pressure |
Management: Treat underlying condition (diuretics for CHF, lactulose for cirrhosis, etc.). Thoracentesis is diagnostic only if diagnosis uncertain.
Exudative Effusions
Pathologic processes affecting the pleura or underlying lung:
| Category | Specific Causes |
|---|---|
| Infection | Bacterial pneumonia, tuberculosis, fungal, empyema, parapneumonic |
| Malignancy | Lung, breast, lymphoma, metastatic disease; can be bloody |
| Pulmonary embolism | Often hemorrhagic; LDH elevated |
| Autoimmune | Systemic lupus erythematosus, rheumatoid arthritis, vasculitis |
| Pancreatitis | Acute pancreatitis → pancreaticpleural fistula |
| Renal failure | Uremic pleuritis |
| Post-cardiac surgery | Dressler syndrome (post-pericardiotomy syndrome) |
| Other | Esophageal rupture, aortic dissection, liver abscess |
Thoracentesis: Diagnostic and Therapeutic
Pleural fluid sampling provides diagnostic information and can provide symptomatic relief if effusion is large:
Fluids to Send and Testing
Always send pleural fluid for:
| Study | Information Obtained |
|---|---|
| Cell count and differential | WBC/RBC; neutrophil-predominant (infection/inflammation), lymphocyte-predominant (malignancy/TB), eosinophil-predominant (drug reaction, fungal) |
| Protein | Used in Light's criteria; also assessed for exudative classification |
| LDH | Used in Light's criteria for exudate determination |
| Glucose | Low glucose (<60) suggests empyema, rheumatoid pleuritis, or esophageal rupture |
| pH | pH <7.2 suggests complicated parapneumonic/empyema; pH <7.0 suggests esophageal rupture |
| Gram stain | Identifies bacteria; guides antibiotic selection |
| Bacterial culture | Grows causative organism if bacterial infection present |
| Acid-fast bacilli (AFB) culture | Diagnoses tuberculosis (low yield; still recommended) |
| Cytology | Identifies malignant cells in suspected malignancy |
Complicated Parapneumonic Effusion / Empyema
When to pursue chest tube drainage vs. antibiotics alone:
| Finding | Implication | Action |
|---|---|---|
| pH <7.2 | Loculated/walled-off infection | Chest tube or pigtail catheter needed |
| Glucose <60 | Walled-off infection | Chest tube or pigtail catheter needed |
| Positive Gram stain or culture | Documented bacteria | Chest tube or pigtail catheter needed |
| LDH >1000 | High inflammatory burden | Consider chest tube if pH/glucose also low |
| Uncomplicated parapneumonic (pH >7.2, glucose >60, negative Gram stain) | Will likely resolve with antibiotics | Antibiotics alone; recheck with imaging if inadequate response |
Hemoptysis: Evaluation and Management
Definition and Severity
Hemoptysis is expectoration of blood from the respiratory tract. Severity classification:
| Category | Volume | Urgency | Approach |
|---|---|---|---|
| Minor/mild | <30 mL per 24 hr | Outpatient workup | CXR, CT if abnormal; reassurance if normal |
| Moderate | 30–600 mL per 24 hr | Expedited workup | Same day CXR and specialist evaluation |
| Massive/life-threatening | >600 mL per 24 hr OR >100 mL/hr | EMERGENCY | ICU admission, airway protection, bronchoscopy, consider IR |
Massive Hemoptysis
Immediately place on continuous monitoring. Consider double-lumen endotracheal tube to protect airway and isolate bleeding lung. Prepare for interventional radiology or surgery.
Differential Diagnosis by Mechanism
| Mechanism | Examples |
|---|---|
| Mucosal inflammation | Acute bronchitis, upper respiratory infection, chronic bronchitis exacerbation |
| Structural airway disease | Bronchiectasis, bronchial adenoma, airway granuloma |
| Infection | Pneumonia (especially staph, fungal), lung abscess, tuberculosis |
| Malignancy | Lung cancer, metastases, lymphoma |
| Vascular causes | Pulmonary embolism, arteriovenous malformation, bleeding disorder |
| Cardiac | Acute decompensated heart failure (pink sputum), mitral stenosis |
| Vasculitis | Granulomatosis with polyangiitis, microscopic polyangiitis, Goodpasture syndrome |
Diagnostic Approach
Initial Evaluation
- History and physical exam — quantify volume, assess for fever/weight loss/risk factors
- Chest X-ray — identifies infiltrate, mass, cavitation, pneumothorax
- Complete blood count — assess hemoglobin/platelet counts
- Coagulation studies — PT, aPTT, fibrinogen if massive bleeding
- Sputum culture — if infectious cause suspected
- Sputum cytology — if malignancy suspected (low sensitivity; repeat if high clinical suspicion)
Advanced Imaging
- High-resolution CT chest — superior to CXR for detection of bronchiectasis, AVM, nodules, cavitation
- Bronchoscopy — therapeutic (tamponade, endobronchial coagulation, epinephrine instillation) and diagnostic (biopsy of lesion, specimen collection for culture); may localize source in massive hemorrhage
Interventional Radiology (IR)
- Bronchial artery angiography and embolization — definitive therapy for massive hemoptysis when bronchoscopy fails or bleeding source identified
- Success rate >90% for hemostasis
Management
Supportive Care
- NPO status until hemoptysis controlled and airway assessment complete
- IV access — 2 large-bore peripheral lines or central line in massive hemorrhage
- Type and crossmatch — have blood available if massive bleed
- Supplemental oxygen — maintain SpO2 >90%
- Monitoring — pulse oximetry, EKG, frequent vital signs
Positioning and Localization
- Position patient with bleeding lung dependent (bleeding side down)
- Bronchoscopy localizes exact site; note if left or right, what lobar/segmental distribution
Pharmacologic Therapy
| Agent | Dose | Indication | Mechanism |
|---|---|---|---|
| Epinephrine (1:1000) | 5–10 mL topically via bronchoscope | Acute hemoptysis during scope | Vasoconstriction |
| Tranexamic acid | 500 mg IV Q6H × 2–4 days | May reduce rebleeding | Antifibrinolytic |
| Aminocaproic acid | 4–5 g IV followed by 1 g/hr infusion | Alternative to tranexamic acid | Antifibrinolytic |
Endoscopic Therapy
When bronchoscopy identifies the bleeding source:
- Epinephrine injection into bleeding mucosa
- Argon plasma coagulation (APC) to cauterize visible vessel
- Cold saline irrigation to promote clot formation
- Packing or balloon tamponade (temporary) while awaiting IR intervention
Surgical Consultation
Indicated if:
- Bleeding fails to control with medical/IR therapy
- Anatomical lesion (e.g., cavitary TB) with massive recurrent hemorrhage
- Bronchiectasis confined to single lobe with refractory bleeding