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Approach to Hemoptysis

Definition and Classification

Any volume that threatens the airway is effectively "massive." - Washington Manual of Medical Therapeutics

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Step 1 - Confirm True Hemoptysis

• Pseudohemoptysis: blood from the upper airway (nose, pharynx, larynx) - inhaled and expectorated
• Hematemesis: vomited blood

• Fishman's Pulmonary Diseases and Disorders, p. 444

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Step 2 - Identify the Bleeding Source (Pathophysiology)

• Only 1% of pulmonary blood flow, but accounts for up to 88% of massive hemoptysis
• Disrupted by: tumor invasion, fungal invasion, foreign body, denuded mucosa (bronchiectasis)

• Sources: vasculitis, DAH, PE/infarction, severe mitral stenosis, AVM rupture, Rasmussen aneurysm (TB cavity eroding a pulmonary artery), pulmonary artery catheter trauma
• Washington Manual of Medical Therapeutics, p. 380

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Step 3 - Differential Diagnosis

Airway

• Acute/chronic bronchitis (most common cause in developed countries; 2-37% of cases)
• Bronchiectasis (1-37%; especially CF, post-TB)
• Bronchogenic carcinoma (2-24%; must rule out in smokers >40 years)
• Carcinoid tumor, endobronchial metastases (breast, colon, kidney, melanoma)
• Foreign body, broncholithiasis, bronchovascular fistula, pulmonary endometriosis (catamenial hemoptysis)

Parenchymal

• Tuberculosis (2-69%; leading cause globally; cavities → Rasmussen aneurysm)
• Pneumonia, lung abscess
• Fungal infections - aspergilloma (colonization of old TB cavity; massive hemoptysis as cavities erode bronchial/pulmonary vessels)
• Vasculitides - GPA (Wegener's), Goodpasture syndrome (anti-GBM), ANCA-positive vasculitis, SLE → diffuse alveolar hemorrhage

Vascular

• Pulmonary embolism with infarction (classically pleuritic pain + hemoptysis + small pleural effusion)
• Mitral stenosis (submucosal bronchial venous congestion; historically a classic cause of brisk bright-red hemoptysis)
• LV failure (pink, frothy sputum; heart failure cells/hemosiderin-laden macrophages)
• AVM, Dieulafoy disease of the bronchus (rare submucosal broncho-pulmonary arterial fistula)

Coagulopathic / Systemic

• Thrombocytopenia, DIC, anticoagulant therapy, hemophilia
• Cocaine and other inhaled agents

Idiopathic

• Up to 50% of cases remain unexplained; up to 4% of these are eventually diagnosed with malignancy

• Fishman's Pulmonary Diseases and Disorders, p. 443

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Step 4 - Initial Evaluation

History

• Volume (estimated), onset, duration, recurrence
• Age, smoking history (>40 pack-year smoking, age >40: risk factors for malignancy)
• Prior lung disease (TB, bronchiectasis, COPD, malignancy)
• Associated symptoms: fever/productive cough (infection), weight loss/hemoptysis >1 week (malignancy), pleuritic chest pain (PE), dyspnea, leg swelling
• Coagulopathy risk, anticoagulant/antiplatelet use
• Geographic exposure (TB, histoplasmosis, paragonimiasis)
• Menstrual timing (catamenial hemoptysis)

Physical Examination

• Vital signs + SpO2 first
• Lung: focal crackles, bronchial breath sounds, wheeze/stridor
• Heart: murmurs (mitral stenosis = opening snap + mid-diastolic rumble)
• Skin/mucous membranes: telangiectasias (HHT), purpura (vasculitis), clubbing (malignancy, bronchiectasis)
• Lymphadenopathy, cachexia (malignancy)

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Step 5 - Investigations

Bedside / Emergency (all patients)

Targeted Labs (based on clinical suspicion)

• Sputum: Gram stain/culture, AFB smear/culture, cytology
• Urinalysis + microscopy: pulmonary-renal syndromes
• Serology: ANCA (MPO, PR3), anti-GBM (Goodpasture), ANA, dsDNA, complement, cryoglobulins
• BNP/NT-proBNP: LV failure
• ECG/echo: structural heart disease

Imaging

• Chest CT (with/without contrast): Indicated if diagnosis uncertain after initial evaluation
  • CT angiography: best for vascular causes (AVM, aneurysm) and pre-embolization planning; identifies source with high sensitivity; may be better than bronchoscopy for etiology/source in stable patients
  • Detects up to 96% of CXR-occult malignancies
  • Limited for subtle mucosal lesions
• CT is not appropriate in hemodynamically unstable patients - proceed directly to bronchoscopy

Bronchoscopy

• Localizes/lateralizes bleeding source in >66% of cases
• Yield is highest when performed during or within 48 hours of active bleeding
• Indications:
  • Source unclear after imaging
  • Persistent or recurrent hemoptysis
  • Suspected airway abnormality
  • Risk factors for bronchogenic carcinoma (male sex, age >40, >40 pack-year, hemoptysis >1 week, volume >30 mL)
  • Obtaining biopsy if malignancy suspected
  • Pre-embolization localization
  • Evaluation for alveolar hemorrhage
• Washington Manual of Medical Therapeutics, p. 382

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Step 6 - Management

Algorithm

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Non-Massive Hemoptysis (conservative approach)

• Identify and treat the underlying cause
• Reversal of coagulopathy (correct platelets, INR)
• Antitussives (reduce irritation and minor mucosal trauma)
• Antibiotics (for infection, including TB, fungal disease, NTM)
• Steroids/immunosuppression (vasculitis, DAH, Goodpasture)
• Diuretics/inotropes (LV failure, mitral stenosis)
• Bronchoscopy if recurrent or cause unclear
• Follow-up CXR at 6-8 weeks for persistent infiltrate

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Massive Hemoptysis (emergency - multidisciplinary approach)

1. Immediate Stabilization

• Position: lateral decubitus with bleeding lung DOWN - prevents aspiration into the unaffected lung
• Airway protection: early intubation with a large-bore (>8 mm) endotracheal tube
  • Single-lumen mainstem intubation into the unaffected bronchus (selective ventilation)
  • Double-lumen tube under skilled supervision
• Supplemental oxygen, hemodynamic resuscitation
• Inhaled tranexamic acid (nebulized): emerging evidence supports reduction in expectorated volume, hospital stay, and recurrence rates (PMID 39841268)

2. Bronchoscopy

• Rigid bronchoscopy preferred in massive hemoptysis: better airway control, suctioning, and instrument access
• Flexible bronchoscopy also used, especially for localization
• Endobronchial interventions:
  • Direct tamponade with bronchoscope tip
  • Balloon tamponade (Fogarty/bronchial blocker balloon, left 1-2 days; monitor for mucosal ischemia)
  • Topical hemostatics: cold saline, topical epinephrine, vasopressin, thrombin, oxidized regenerated cellulose
  • Electrocautery / argon plasma coagulation (APC): for endobronchial lesions
  • Nd:YAG laser, endobronchial stent

3. Bronchial Artery Embolization (BAE)

• First-line definitive procedure for massive hemoptysis
• Success rate >75-90% acutely (up to >85% with careful localization)
• Most effective when CT angiography is used for pre-procedural planning
• Rebleeding rate: 20-50% at 1 year; usually responds to repeat embolization
• Rebleeding more common in: sarcoidosis, malignancy, aspergilloma
• Complications: post-embolization syndrome (pleuritic pain, fever, dysphagia, leukocytosis, 5-7 days, self-limited), bronchial/partial pulmonary infarction, and rarely ischemic myelopathy (spinal artery inadvertent embolization)
• Failure usually due to incomplete source vessel identification; post-embolization arteriography may reveal additional culprit vessels from intercostal/phrenic arteries

4. Surgery

• Indicated when bronchoscopic and embolization strategies fail
• Better outcomes when done electively (non-urgently) after embolization allows stabilization
• Emergency surgery carries high mortality
• Also indicated for: Aspergillus-related cavitary lesions (after granulocytopenia resolves), post-lobectomy hemothorax emptying into airways
• Fishman's Pulmonary Diseases and Disorders, p. 445-446; Harrison's Internal Medicine 22e, p. 635; Washington Manual, p. 383-384

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Special Situations

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Summary: The 3 Goals of Management

1. Stabilize airway and hemodynamics (position, intubate, oxygenate)
2. Diagnose cause and localize bleeding source (history, CXR, CT, bronchoscopy, arteriography)
3. Target therapy (treat underlying cause; BAE first-line for massive; surgery as salvage)

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Approach to Dyspnea

Definition

"Air hunger," "unable to get enough air," "can't take a deep breath," "chest tightness," "heavy breathing," "smothering" - all are valid descriptions. The specific quality matters clinically.

• Murray & Nadel's Textbook of Respiratory Medicine, p. 854

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Epidemiology and Importance

• Up to 25% of middle-aged and older adults suffer from dyspnea
• Present in 16% of non-critically ill hospitalized patients in the first 24 hours; 23% of ED admissions; 49% of critically ill patients
• Dyspnea is an independent predictor of mortality in cardiorespiratory disease
• Patients often gradually limit activity to avoid dyspnea, leading to deconditioning - which in turn worsens dyspnea: a vicious cycle

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Pathophysiology: 4 Mechanisms of Dyspnea

1. Abnormal Blood Gases (Chemoreceptor Stimulation)

• Hypercapnia is a more potent driver of dyspnea than hypoxemia
• Hypoxemia alone causes relatively low-intensity dyspnea
• A-(A-a)PO₂ gradient: if elevated (>0.3 × age), gas exchanger abnormality is contributing
• Sensation: "air hunger," urge to breathe, "I cannot get enough air"

2. Receptor Stimulation (Afferent Signals)

• Pulmonary C-fibers (juxtacapillary receptors): triggered by inflammation, inhaled chemicals/toxins, increased pulmonary capillary pressure (LV failure)
• Rapidly adapting stretch receptors (irritant receptors): triggered by lung deflation/atelectasis → intense need to take a deep breath; also respond to bronchospasm → "chest tightness"
• Slowly adapting stretch receptors: activated by large tidal volumes → may reduce air hunger (basis for pursed-lip breathing benefit)
• Pulmonary vascular pressure receptors: contribute to dyspnea in PE, pulmonary HTN, LV failure
• Metaboreceptors in skeletal muscle: stimulated by low oxygen delivery in exercise limitation and heart failure → "breathing more" quality

3. Increased Mechanical Load on the Respiratory System

• Increased airway resistance: COPD, asthma
• Decreased respiratory system compliance: ILD, pulmonary edema, obesity, kyphoscoliosis
• Sensation: "increased work or effort to breathe"

4. Neuromuscular Weakness

• System cannot handle even normal mechanical loads
• Guillain-Barré, myasthenia gravis, diaphragm paralysis, spinal cord injury
• Sensation: "increased effort" with rapid shallow breathing
• Murray & Nadel's Textbook of Respiratory Medicine, p. 855-859

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The Language of Dyspnea (Diagnostic Clues)

• Murray & Nadel's Textbook of Respiratory Medicine, Table 36.1

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Special Forms of Dyspnea

• Murray & Nadel's, p. 3487; Goldman-Cecil, p. 2519

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Differential Diagnosis

By Onset and Time Course

• Pulmonary embolism
• Acute myocardial infarction / ACS
• Acute pulmonary edema (LV failure, flash pulmonary edema)
• Tension pneumothorax
• Pericardial tamponade
• Acute severe asthma / status asthmaticus
• Anaphylaxis
• Upper airway obstruction (foreign body, angioedema, epiglottitis)
• Acute respiratory distress syndrome (ARDS)
• Severe hypertensive emergency
• Drug overdose (salicylates, opioids → respiratory failure)

• Pneumonia, pleural effusion
• Worsening heart failure or COPD exacerbation
• Pericardial effusion
• Anemia

• COPD, asthma, ILD
• Heart failure (LV or RV dysfunction)
• Pulmonary arterial hypertension
• Valvular heart disease (especially mitral or aortic)
• Obesity-hypoventilation syndrome
• Deconditioning
• Severe anemia
• Neuromuscular disease (ALS, myasthenia gravis, Guillain-Barré)
• Malignancy (endobronchial, pleural, mediastinal)
• Thyroid disease (hypothyroidism → pleural/pericardial effusion, hyperthyroidism → high-output state)
• Psychogenic / hyperventilation syndrome

By Organ System

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Diagnostic Approach

Step 1: Is This an Emergency? (Rule Out Life-Threatening Causes)

• SpO₂ <90%, stridor, accessory muscle use, cyanosis, altered mental status
• Hemodynamic instability, diaphoresis, unilateral absent breath sounds
• Signs of obstructive shock (elevated JVP + hypotension + clear lungs → tamponade/tension PTX)

Step 2: History

• Onset: sudden (PTX, PE, acute MI, foreign body) vs. gradual (CHF, COPD, ILD)
• Time course: acute, subacute, chronic, episodic (asthma), progressive
• Severity: exertional only? At rest? Functional impairment (MRC scale: how many stairs, flat ground distance, dressing, eating)
• Quality: "air hunger" vs. "tight chest" vs. "cannot breathe deeply" vs. "effort" - guides physiology
• Positional: orthopnea (CHF), platypnea (hepatopulmonary syndrome)
• Nocturnal: PND (CHF), nocturnal asthma
• Associated symptoms:
  • Chest pain → ACS, PE, pneumothorax, pericarditis
  • Cough/wheezing → asthma, COPD, heart failure
  • Fever/productive cough → pneumonia, bronchitis
  • Leg edema → heart failure, DVT/PE
  • Palpitations → arrhythmia, thyrotoxicosis
  • Weight loss → malignancy, COPD, cardiac cachexia
• Triggers: allergens/dust/exercise/cold air (asthma), occupational/environmental exposures (hypersensitivity pneumonitis, occupational asthma)
• Medical history: prior CHF, COPD, malignancy, PE/DVT, connective tissue disease, HIV
• Medications: beta-blockers (mask tachycardia; can trigger bronchospasm), ACE inhibitors (cough), amiodarone (pulmonary toxicity), methotrexate (pneumonitis), bleomycin (ILD)
• Social history: smoking (COPD, lung cancer), occupation, travel (PE risk), IV drug use (septic emboli, endocarditis)

Step 3: Physical Examination

• Murray & Nadel's Textbook of Respiratory Medicine, Table 36.2

Step 4: Initial Investigations (All Patients)

Step 5: Targeted Investigations (Based on Working Diagnosis)

CPET is particularly valuable when both cardiac and respiratory problems are present, or when no cause is found after standard evaluation.

• Murray & Nadel's Textbook of Respiratory Medicine, p. 860

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Management

Disease-Specific Treatment

• Asthma/COPD: bronchodilators (SABA, LAMA, ICS), pulmonary rehabilitation
• Heart failure: diuretics (furosemide), ACE inhibitors/ARBs, beta-blockers, SGLT2 inhibitors
• PE: anticoagulation, thrombolysis (massive PE), embolectomy
• Pneumonia: antibiotics, oxygen supplementation
• Pleural effusion/PTX: thoracentesis, chest drain
• Anemia: treat cause; transfusion for severe/symptomatic
• ILD: corticosteroids (some subtypes), antifibrotics (pirfenidone, nintedanib for IPF)
• Pulmonary HTN: PDE5 inhibitors, endothelin antagonists, prostacyclins

Symptomatic (Non-Disease-Specific) Treatment

Dyspnea in End-Stage / Palliative Setting

• Goals of care shift from prolonging life to maximizing comfort
• Low-dose oral/parenteral opioids are the most evidence-based pharmacologic intervention
• Coordination of pulmonary and palliative care improves breathlessness mastery and prolongs survival
• Fear of opioid-induced respiratory depression should not prevent their use at appropriate dyspnea-relief doses
• Murray & Nadel's Textbook of Respiratory Medicine, p. 862-863

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Quantifying Dyspnea: Validated Scales

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Summary Framework

DYSPNEA
  |
  ├─ EMERGENCY? (SpO₂, HR, BP, RR, appearance)
  |      YES → immediate stabilization (O₂, IV access, monitor)
  |                 → CXR, ECG, ABG, troponin, BNP, D-dimer
  |                 → Treat: PTX drain / pericardiocentesis / thrombolysis / diuretics / bronchodilators
  |
  ├─ HISTORY → onset / quality / position / triggers / associated symptoms
  |
  ├─ 4 MECHANISMS → blood gases / receptor stimulation / mechanical load / neuromuscular
  |
  ├─ INITIAL TESTS → SpO₂, CXR, ECG, CBC, BMP, BNP, ABG
  |
  ├─ TARGETED TESTS → echo / CT-PA / spirometry / HRCT / CPET
  |
  └─ TREATMENT → disease-specific + symptomatic (O₂, opioids, rehab, fan)

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1. Definition & Classification - CAP, HAP, VAP, aspiration, immunocompromised
2. Pathogens - typical, atypical, viral, HAP/VAP MDR organisms, special populations
3. Pathophysiology - routes of infection, 4 stages of lobar pneumonia (congestion → red hepatization → grey hepatization → resolution), host defense mechanisms
4. Clinical Features - typical vs atypical presentation, physical examination signs
5. Diagnosis - CXR patterns, sputum, blood cultures, urine antigens, procalcitonin, BAL
6. Severity Scoring - full CURB-65 criteria with score-based management, PSI/PORT, IDSA/ATS severe CAP major and minor criteria
7. Treatment - stratified outpatient/inpatient/ICU regimens, HAP/VAP, MRSA/Pseudomonas coverage, duration of therapy
8. Complications - empyema, lung abscess, ARDS, cardiac complications (seen in 20-25%)
9. Prevention - pneumococcal vaccine schedule, influenza, VAP bundle

1. Write out the revision notes as text for both Asthma and COPD (formatted, detailed, exam-ready)
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4. Answer specific questions about Asthma or COPD