Pulmonary function testing (PFT)
Pulmonary function tests (PFTs) measure different lung volumes and other functional metrics of pulmonary function. They can be used to diagnose ventilatory disorders and differentiate between obstructive and restrictive lung diseases. Obstructive lung disease = Increased resistance to air flow caused by narrowing of airways- COPD (chronic bronchitis, emphysema)- Bronchial asthma- Bronchiectasis, cystic fibrosis- FEV1 ↓ (< 80% of the predicted value)- FEV1/FVC ↓ (< 70% of the predicted value)- Vital capacity ↓- Residual volume ↑- Total lung capacity: Normal or ↑- Spirometer tracing: Air trapping: a "scalloping" of the expiratory limb in conditions such as emphysema or in patients who have undergone a pneumectomy. Restrictive lung disease = Impaired ability of the lungs to expand (as a result of reduced lung compliance)- Interstitial lung disease (e.g., sarcoidosis, pneumoconioses, idiopathic pulmonary fibrosis)- Alveolar (e.g., pneumonia, pulmonary edema or hemorrhage)- Diseases of the pleura and pleural cavity (e.g., chronic pleural effusion, pleural adhesions, pneumothorax)- Deformities of the thorax/mechanical limitation (e.g., kyphoscoliosis, ankylosing spondylitis, obesity, ascites, pregnancy)- Respiratory muscle weakness (e.g., phrenic nerve palsy, myasthenia gravis, ALS, myopathies)- FEV1: ormal or ↓- FEV1/FVC: ormal or ↑- Vital capacity ↓- Residual volume: Normal or ↓- Total lung capacity ↓
Bronchial challenge tests
The following tests help distinguish bronchial asthma from other causes of obstructive lung disease. Methacholine challenge test (bronchoprovocation test)- Indication: This test is used to determine if airway hyperresponsiveness is present.- Description: Lung function tests are performed before and after the administration of methacholine. - Interpretation: A doubling of airway resistance with a reduction of FEV1 of at least 20% points to a diagnosis of airway hyperresponsiveness (e.g., bronchial asthma).Because the methacholine challenge test can trigger a life-threatening asthma attack, medications that reverse bronchospasm (e.g., epinephrine, atropine) should be kept at hand during the test! Bronchodilator reversibilty test (post-bronchodilator test)- Indication: This test allows reversible airway obstruction to be differentiated from irreversible obstruction.- Description: To perform this test, FEV1 and airway resistance are measured before and 10 minutes after the inhalation of a fast-acting bronchodilator (e.g., albuterol, ipratropium bromide).- Interpretation: An increase in FEV1 by 200 mL or 12% of the initial value indicates reversible airway obstruction (bronchial asthma).
Asthma
Asthma is a chronic inflammatory disease of the respiratory system characterized by bronchial hyperresponsiveness, episodic exacerbations (asthma attacks), and reversible airflow obstruction. Epidemiology:- Prevalence: 5-10% of the US population- More common in black than white patients Triggers:- Allergic asthma (extrinsic asthma)→ Cardinal risk factor: atopy→ Environmental allergens: pollen (seasonal), dust mites, domestic animals, mold spores→ Allergic occupational asthma: from exposure to allergens in the workplace (e.g., flour dust) - Nonallergic asthma (intrinsic asthma)→ Viral respiratory tract infections (one of the most common stimuli, especially in children)→ Cold air→ Physical exertion (exercise-induced asthma)→ Gastroesophageal reflux disease (GERD): often exists concurrently with asthma → Chronic sinusitis or rhinitis→ Medication: aspirin/NSAIDS (aspirin-induced asthma), beta-blockers→ Stress→ Irritant-induced asthma (e.g., from exposure to solvents, ozone, tobacco or wood smoke, cleaning agents) Mild to moderate signs and symptoms:- Persistent, dry cough that worsens at night, with exercise, or on exposure to triggers/irritants (e.g., cold air, allergens, smoke)- End-expiratory wheezes- Dyspnea- Chest tightness- Chronic allergic rhinitis with nasal congestion Severe signs and symptoms- Severe dyspnea- Pulsus paradoxus- Hypoxemia- Accessory muscle use- Increased risk of pulmonary infection (in chronic asthma) Cough variant asthma:- A form of asthma in which the predominant symptom is chronic, dry cough- Other characteristic symptoms of asthma (e.g., wheezes, congestion, dyspnea) are absent. Diagnostics:- Pulmonary function testing (spirometry) → First-line diagnostic test for confirmation of the diagnosis in patients ≥ 5 years of age. → Shows signs of obstructive lung disease with increased airway resistance → ↓ FEV1, ↓ Tiffeneau index (FEV1/FVC ratio)→ Obstruction is reversible with bronchodilators → diagnostic confirmation via post-bronchodilator test - Methacholine challenge test (bronchoprovocation test)→ Second-line diagnostic test if pulmonary function testing is nondiagnostic→ Evidence of bronchial hyperresponsiveness after inhalation of methacholine→ Positive if FEV1 reduced ≥ 20%- Chest x-ray → Usually only indicated in patients with severe asthma to exclude differential diagnoses (e.g., pneumonia, pneumothorax)- Pulse oximetry and blood gas analysis (ABG)→ Blood gas analysis should be performed if oxygen saturation (SpO2) is < 94%.→ Initially: ↓ pCO2, ↑ pH, ↓ pO2 leading to type 1 respiratory failure→ Ultimately: severe respiratory distress: ↑ pCO2, ↓ pH, and ↓↓ pO2 leading to type 2 respiratory failure Mild intermittent asthma:- Symptoms (e.g., dyspnea, wheezing, cough): ≤ 2 days/week- Nighttime symptoms: Rare- FEV1: > 80% Mild persistent:- Symptoms (e.g., dyspnea, wheezing, cough): > 2 days/week- Nighttime symptoms: 3-4 times/month- FEV1: > 80% Moderate persistent:- Symptoms (e.g., dyspnea, wheezing, cough): Daily - Nighttime symptoms: 1-2 times/week- FEV1: 60-80% Severe persistent:- Symptoms (e.g., dyspnea, wheezing, cough): Throughout the day- Nighttime symptoms: Often (most nights)- FEV1: < 60% Treatment:- Short-acting beta-2 agonists (SABA): Albuterol, Terbutaline- Long-acting beta-2 agonists (LABA): Salmeterol, Formoterol- Inhaled corticosteroids (ICS): Beclomethasone, Fluticasone, Budesonide, Ciclesonide, Mometasone, Triamcinolone- Leukotriene pathway modifiers: Montelukast, Zafirlukast, Zileuton- Short-acting muscarinic antagonists (SAMA): ipratropium bromide- Long-acting muscarinic antagonists (LAMA): tiotropium bromide- Biological agents: Omalizumab, Mepolizumab- Mast cell stabilizers: Cromolyn sodium, Nedocromil sodium
Status asthmaticus
Clinical features:- Initially: orthopnea, tachypnea, tachycardia, and cyanosis- Signs of imminent respiratory arrest→ Drowsiness/confusion→ Paradoxical thoracoabdominal movement→ Bradycardia→ Absent wheezing→ Pulsus paradoxus Diagnosis: - ABG (i.e., to identify hypercapnia and hypoxemia) - CBC- BMP- Peak expiratory flow measurement - Chest x-ray - ECG (in older patients) Hospitalization:- PEF or FEV1: 50-70% of the predicted value- PEF or FEV1 < 50% of the predicted value → admitted in the ICU Medications:- Short-acting beta-2 agonist (SABA)- Short-acting muscarinic antagonists (SAMA) like ipratropium bromide- Oral corticosteroid- Intravenous magnesium sulfate- Oxygenation and ventilation→ Supplemental oxygen and/or helium-oxygen mixture (heliox)→ Bilevel positive airway pressure (BiPAP) Indications for intubation:- Use of accessory muscles- Decreased oxygen saturation- Inability to speak in full sentences- Inadequate response to initial therapy- Normalizing PCO2 or pH
COPD
A chronic pulmonary disease characterized by persistent respiratory symptoms and airflow limitation (postbronchodilator FEV1/FVC < 0.70), which is caused by a mixture of small airway obstruction and parenchymal destruction.- Chronic bronchitis: productive cough (cough with expectoration) for at least 3 months each year for 2 consecutive years- Emphysema: permanent dilatation of pulmonary air spaces distal to the terminal bronchioles, caused by the destruction of the alveolar walls and the pulmonary capillaries required for gas exchange. Epidemiology:- Sex: 3:2 male/female ratio - The third most common cause of death worldwide- Prevalence: 6% Etiology:- Tobacco use (90% of cases) → Smoking is the major risk factor for COPD, but those who have quit ≥ 10 years ago are not at increased risk.- Nonorganic dust: such as industrial bronchitis in coal miners- Organic dust: ↑ incidence of COPD in areas where biomass fuel (e.g., wood, animal dung) is regularly burned indoors- Recurrent pulmonary infections and tuberculosis- Premature birth - Endogenous factors: α1-Antitrypsin deficiency, antibody deficiency syndrome (e.g., IgA deficiency), primary ciliary dyskinesia (e.g., Kartagener syndrome) GOLD 1 (Class I): FEV1 ≥ 80%GOLD 2 (Class II): 50% ≤ FEV1 < 80%GOLD 3 (Class III): 30% ≤ FEV1 < 50%GOLD 4 (Class IV): FEV1 < 30% Clinical features:- Chronic cough with expectoration (expectoration typically occurs in the morning)- Dyspnea and tachypnea- Pursed-lip breathing - End-expiratory wheezing, crackles, muffled breath sounds, and/or coarse rhonchi on auscultation- Tachycardia- Cyanosis- Often weight loss and cachexia Nail clubbing is not a finding specific to COPD; its presence usually suggests comorbidities such as bronchiectasis, pulmonary fibrosis, or lung cancer. Spirometry and/or body plethysmography :- FEV1/FVC < 70% (Tiffeneau-Pinelli index) - Decreased FEV1: used to classify COPD according to GOLD - TLC: Chronic bronchitis: normal; Emphysema: increased- Increased intrathoracic gas volume- DLCO: Chronic bronchitis: normal; Emphysema: decreased Post-bronchodilator test: Assesses reversibility of bronchoconstriction - FEV1/FVC < 0.7 is diagnostic of COPD- FEV1 < 12% (irreversible bronchoconstriction): COPD is more likely than asthma. - Pulse oximetry: assess O2 saturation- BGA: only indicated when O2 is < 92% or if the patient is severely ill (e.g., altered mental status, acute exacerbation) General treatment:- Cessation of tobacco use (single most effective step to slow the decline in lung function)- Vaccinations→ Age 19-64 years: Administer PPSV23.→ Age ≥ 65 yearsa) Vaccinated: Administer PPSV23 (should be at least 5 years after the previous PPSV23 dose and at least 1 year after PCV13).b) Not vaccinated or unknown vaccination history: Administer PCV13 followed by PPSV23→ Influenza (annual): reduces serious illness and death in COPD patients- Pulmonary rehabilitation (indicated in patients with GOLD B, C, and D) Medical treatment:- Long-acting parasympatholytics (long-acting muscarinic antagonists, LAMAs): tiotropium bromide- Long-acting β2-agonists (LABAs): salmeterol, formoterol- Short-acting parasympatholytics (short-acting muscarinic agonists, SAMAs): ipratropium bromide- Short-acting β2-agonists (SABAs): salbutamol, fenoterol- Inhaled corticosteroids (ICS): budesonide, fluticasone, beclomethasone- PDE type 4 inhibitors: roflumilast Long-term oxygen therapy (LTOT) indicated in the case of:- PaO2 ≤ 55 mm Hg or SaO2 ≤ 88 % at rest → Increases the chance of survival in patients with COPD→ Supplemental O2 can worsen hypercapnia→ The target oxygen saturations is 90-93%.- PaO2 between 55 and 60 mmHg or SaO2 of 88 mmHg if there is evidence of pulmonary hypertension, congestive cardiac failure, or polycythemia
Acute exacerbation of chronic obstructive pulmonary disease (AECOPD)
Etiology:- 80% of cases are caused by infection (especially in winter and fall).→ Most commonly Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae and viruses such as influenza- Congestive heart failure and pulmonary embolism- Can be triggered by drugs (e.g., beta blockers), allergens, air pollution, stress- Associated with former antibiotic use, advanced age, advanced COPD stage, and peripheral eosinophilia Clinical features:- Worsening of respiratory symptoms (cough, expectoration, dyspnea)- Wheezing, tachypnea- Fever accompanied by chills- Previous treatment has not relieved symptoms.- Patients with severe AECOPD present with:→ Respiratory failure→ Retractions → Thoracoabdominal asynchrony → Severe hypoxemia/respiratory acidosis→ Altered mental status→ Central cyanosis Diagnostics:- CXR to determine etiology of COPD exacerbation (e.g., features of pneumonia, congestive heart failure)- Arterial blood gas findings/pulse oximetry: hypercarbia, hypoxemia, and acidosis Treatment:- Oxygen supplementation: if O2 < 92%, but be mindful that inappropriate O2 therapy poses a risk of life-threatening hypercapnia (CO2 narcosis)- Beta agonists: inhaled SABA (e.g., albuterol, levalbuterol) PLUS- Anticholinergics: SAMA (e.g., ipratropium bromide)- Systemic glucocorticoids: prednisolone (oral) or methylprednisolone (IV) in severe treatment-refractory exacerbations- Antibiotic treatment is indicated for patients with ≥ 2 of the following cardinal symptoms:→ Increased dyspnea→ Increased cough→ Increased sputum production
Hypoxia and hypoxemia
Hypoxia is a state deficient O2 supply to the body or its organs. Hypoxemia is a ↓ Pao2. Both conditions can be caused by a number of processes. 1. Determine if there is an alveolar-arterial (A-a) oxygen gradient.a. No gradient: Consider a low Fio2 state or high altitude. Corrects with supplemental O2.b. Positive gradient:- Shunt-pathology: Does not correct with supplemental O2. Causes may be pulmonary or extrapulmonary.→ Pulmonary process: Alveolar collapse (atelectasis), lobar pneumonia, ARDS.→ Extrapulmonary processes: PDA, patent foramen ovale.- Ventilation-perfusion (V/Q) mismatch: Corrects with supplemental O2. Causes include asthma, COPD, pneumonia, interstitial lung disease, and pulmonary embolism. 2. Hypoxia can also be accompanied by hypercarbia (↑ Paco2). Causes include:- ↓ respiratory drive from CNS depression (opiates, stroke) or central sleep apnea.- Neuromuscular disease (normal A-a gradient)- COPD or obstructive lung disease (generally ↓ A-a gradient) Treatment:- Always treat hypoxic patients with adequate amounts of O2 to maintain saturations > 90% or a Pao2 of > 60 mmHg.
Pleural effusion
Pleural effusion is an accumulation of fluid in the pleural cavity between the lining of the lungsand the thoracic cavity (i.e., the visceral and parietal pleurae). Transudative pleural effusion:- Congestive heart failure- Hepatic cirrhosis- Nephrotic syndrome- Protein-losing enteropathy- Chronic kidney disease Exudative pleural effusion- Infection: Pneumonia (parapneumonic effusion), Tuberculosis, Pleural empyema- Malignancies: E.g., lung cancer, metastatic breast cancer, lymphoma, mesothelioma- Pulmonary embolism - Autoimmune disease: Vasculitis, SLE, Rheumatoid arthritis, Sarcoidosis- Pancreatitis- Hemothorax- Chylothorax Clinical features:- Patients with a small pleural effusion (< 300 mL) are often asymptomatic. - Dyspnea - Pleuritic chest pain - Dry, nonproductive cough - Symptoms of the underlying disease (e.g., fever in empyema, cachexia in cases of malignancy, symptoms of left-sided heart failure)- Inspection: Asymmetric expansion and unilateral lagging on the affected side- Palpation: Reduced tactile fremitus due to fluid in the pleural space- Auscultation: Faint or absent breath sounds over the area of effusion, Pleural friction rub - Percussion: dullness over the area of effusion Diagnostics:- Imaging: Chest x-ray, ultrasound, chest CT- Thoracocentesis indications:→ Any new unilateral effusion > 1 cm on x-ray in an undiagnosed patient → History of malignant tumor with effusion > 1 cm on x-ray→ Large effusion with dyspnea and/or cardiac decompensation Light's criteria:- Pleural fluid protein:serum protein ratio: ≤ 0.5 vs. > 0.5- Pleural fluid LDH:serum LDH ratio: ≤ 0.6 vs. > 0.6 - Pleural fluid LDH (lactate dehydrogenase): < ⅔ the upper limit of normal serum LDH vs. > ⅔ the upper limit of normal serum LDH→ Very high LDH levels (e.g., > 1000 IU/L) suggest empyema, malignancy, or rheumatoid effusion. Treatment:- Treat underlying condition (e.g., loop diuretics for acute congestive heart failure, antibiotics for pneumonia).- Therapeutic thoracentesis to remove fluid- Tube thoracostomy: for recurrent pleural effusion or urgent drainage of infected and/or loculated effusions- Video-assisted thoracoscopic surgery (VATS)- Pleurodesis: chemical or surgical obliteration of the pleural space- Indwelling pleural catheter: especially for recurrent, malignant pleural effusionsA chest x-ray should be performed after each of these procedures in order to rule out iatrogenic pneumothorax!
Pneumothorax
Epidemiology:- Primary spontaneous pneumothorax→ Sex: ♂ > ♀ (approx. 6:1)→ Peak incidence: 20-30 years- Secondary spontaneous pneumothorax→ Peak incidence: 60-65 years Primary pneumothoray: Ruptured subpleural apical blebs- Risk factors: → Family history→ Male gender→ Asthenic body habitus (slim, tall stature) (e.g., in Marfan syndrome)→ Smoking: 90% of cases; up to 20-fold increase in risk → Homocystinuria Secondary (pneumothorax as a complication of underlying lung disease)→ Catamenial pneumothorax (extremely rare; thoracic endometriosis)→ Pulmonary tuberculosis→ Cystic fibrosis → bronchiectasis with obstructive emphysema and bleb or cyst rupture→ Pneumocystis pneumonia → alveolitis, rupture of a cavity→ COPD (smoking) → rupture of bullae in emphysema Clinical features:- Sudden, severe, and/or stabbing, ipsilateral pleuritic chest pain and dyspnea- Reduced, or absent breath sounds, hyperresonant percussion, decreased fremitus on the ipsilateral sideSubcutaneous emphysema - Additionally in tension pneumothorax:→ Severe acute respiratory distress: cyanosis, restlessness, diaphoresis→ Reduced chest expansion on the ipsilateral side→ Distended neck veins and hemodynamic instability (tachycardia, hypotension, pulsus paradoxus) → Secondary injuries (e.g., open or closed wounds) Diagnostics:- Suspected pneumothorax is confirmed by chest x-ray. Immediate x-ray or an extended focused assessment with sonography for trauma (eFAST) in adults with severe respiratory compromise and children- CT may provide detailed information about the underlying cause (e.g., bullae in spontaneous pneumothorax).- Tension pneumothorax is primarily a clinical diagnosis and prolonged diagnostic studies should be avoided to initiate immediate treatment.- Arterial blood gas analysis (ABG): To detect respiratory acidosis- Chest x-ray (confirmatory test)→ Ipsilateral pleural line with reduced/absent lung markings → Sudden change in radiolucency → Deep sulcus sign: dark and deep costophrenic angle on the affected side → If pulmonary disease is present: airway or parenchymal lesions- ECG: For all patients with anterior chest trauma Treatment:- If small (≤ 2 to 3 cm between the lung and chest wall on a chest x-ray) and asymptomatic: Usually resolve spontaneously within a few days (∼ 10 days)→ Supplemental oxygen (4-6 L/min) via nasal cannula or mask with reservoir→ Serial follow-up with repeat CXR- If small and symptomatic (but hemodynamically stable) or large (> 3 cm between the lung and chest wall on chest x-ray) primary pneumothorax, iatrogenic, traumatic, or secondary pneumothorax → Immediate supplemental oxygen (4-6 L/min) via nasal cannula or mask with reservoir→ Upright positioning → Symptomatic treatment→ Tube thoracostomy - Open pneumothorax:→ Simple partially occlusive dressings taped at 3 out of 4 sides of the lesion→ Followed by thoracostomy→ Observe for development of tension pneumothorax- Tension pneumothorax:→ Emergency chest decompression via chest tube placement if immediately available → Otherwise perform emergency needle thoracostomy, followed by chest tube placement Chest tube placement:- Bülau drain: 4th intercostal space (nipple line) in between anterior and median axillary line (safe triangle; midaxillary line) Needle thoracostomy:- Immediate insertion of a large-bore needle into the 2nd intercostal space along the midclavicular line (followed by insertion of a chest tube)
Pulmonary embolism
Etiology:- Deep vein thrombosis (most common cause)→ Risk factors: obesity, hypomobility or immobility, malignancy, pregnancy, dehydration, hypercoagulability, use of contraceptives, previous DVT - Fat embolism during major surgical interventions (e.g., endoprosthesis replacement, osteosynthesis)- Others: air embolism, amniotic fluid embolism, tissue embolism, cement embolism, bacterial embolism, tumor embolism Clinical features:- Acute onset of symptoms, often triggered by a specific event (e.g., on rising in the morning, sudden physical strain/exercise)- Dyspnea and tachypnea (> 50% of cases) - Sudden chest pain (∼ 50% of cases), worse with inspiration- Cough and hemoptysis- Possibly decreased breath sounds, dullness on percussion, split-second heart sound audible in some cases - Tachycardia (∼ 25% of cases), hypotension- Jugular venous distension - Low-grade fever- Syncope and shock with circulatory collapse in massive PE (e.g., due to a saddle thrombus)- Symptoms of DVT: unilaterally painful leg swelling Initial management according to modified Wells criteria:- Hemodynamically stable patients (systolic BP > 90 mmHg) with high probability of PE (Wells score > 4) → CTA for definitive diagnosis→ Unless strongly contraindicated (e.g., high risk of bleeding, recent surgery), start empiric anticoagulation before conducting a CTA → If too unstable for CTA → perform bedside echocardiography obtain a presumptive diagnosis of PE (right ventricle enlargement/hypokinesis or visualization of clot) prior to empiric thrombolysis. - In patients with a low or medium probability of PE (Wells score ≤ 4) → measure D-dimer levels (+ ABG evaluation + CXR)→ If positive (D-dimers ≥ 500 ng/mL) → CTA → evidence/exclusion of PE→ If negative → PE unlikely → consider other causes of symptoms - Arterial blood gas (ABG) test: → Respiratory alkalosis: ↓ paO2 < 80 mmHg, ↓ paCO2, ↑ pH→ ↑ Alveolar-arterial (A-a) gradient: compares the oxygenation status of alveoli to arterial blood → ↓ O2 saturation Acute management- General measures→ 45° reclining sitting posture→ Oxygen supplementation and intubation if respiratory failure→ IV fluids and/or vasopressors in patients with hypotension→ Analgesics and sedatives- Non-life-threatening pulmonary embolism: therapeutic anticoagulation→ Empiric anticoagulation in patients with no absolute contraindication until definitive diagnosis has been made 1. Initial anticoagulation (0-10 days):- Low molecular weight heparin (LMWH) or fondaparinux in stable patients without renal insufficiency, especially in cancer patients - Unfractionated heparin (UFH) in patients with renal failure and those who may still require thrombolysis 2. Long-term anticoagulation and prophylaxis (3-6 months)- Anticoagulation treatment is indicated for a minimum of three months after PE. The following agents may be used:→ Warfarin (target INR 2-3)→ LMWH→ Direct oral anticoagulants (rivaroxaban, apixaban, edoxaban, dabigatran) - Patients with a hypercoagulable state with DVT or PE: heparin followed by 3-6 months of warfarin for the first event, 6-12 months for the second, and lifelong anticoagulation for further eventsMassive, life-threatening pulmonary embolism: recanalization- Thrombolytic therapy. Indications:→ In cases of massive PE causing right heart failure→ In hemodynamically unstable patients requiring resuscitation→ Alternative to PTCA for patients with STEMI if PTCA cannot be performed within 90-120 minutes → Procedure: fibrinolysis, preferably with recombinant tissue-type plasminogen activator (tPA), e.g., alteplase- Embolectomy: Treatment of last resort when thrombolysis is contraindicated or unsuccessful
Acute respiratory distress syndrome (ARDS)
Etiology:- Sepsis (most common cause) E.g., secondary to trauma, infection or peritonitis- Trauma- Shock- Massive transfusion (See “TRALI” for details)- Acute pancreatitis- Hematopoietic stem cell transplantation- Medication (e.g., salicylic acid, tricyclic antidepressants, bleomycin)- Recreational drug overdose (e.g., cocaine)- Pneumonia- Aspiration- Inhaled toxins- Pulmonary contusion- Inhalation injury (e.g., inhalation of hyperbaric oxygen)- Near drowning- Fat embolism (e.g., through blunt trauma)- Amniotic fluid embolism (e.g., during labor)- Lung transplantation Clinical features:- Acute onset- Tachypnea and tachycardia- Cyanosis, dyspnea, and diffuse crackles- Fever, cough, and chest pain may also be present.- Most patients begin to improve after the first 1-3 weeks and symptoms usually resolve fully.- Some develop pulmonary fibrosis with prolonged resolution of symptoms and extended ventilator dependence. Diagnostics:- Arterial blood gas→ Initially, hypoxemic respiratory failure with ↓ PaO2 and respiratory alkalosis → PaO2/FiO2 ≤ 300 mm Hg→ Hypercapnic respiratory failure develops with disease progression.- Chest x-ray → Diffuse bilateral infiltrates (perihilar bat wing or butterfly distribution of infiltrates)→ Air bronchogram → Atelectasis→ Pleural effusionsARDS is a likely diagnosis in the presence of both typical causes and therapy-resistant hypoxemia. The diagnosis is further supported by characteristic findings on chest x-raythat are not explained by underlying cardiac disease. Treatment approach:- The primary objective is achieving sufficient oxygen saturation (while avoiding oxygen toxicity). - Treat the underlying cause (e.g., sepsis). - Sedation (benzodiazepines, opioids)- If oxygenation is insufficient:→ Noninvasive oxygenation (e.g., via masks and nasal tubes) can usually deliver a FiO2 of ∼ 70%.→ Endotracheal intubation and lung protective ventilation can usually provide a FiO2 of 100% and should be administered early on in most patients. Lung protective ventilation:- Description: Pressure-controlled ventilation with a low tidal volume and low peak inspiratory pressure to avoid further pulmonary damage. However, increasing the positive end-expiratory pressure (PEEP) is often necessary during treatment. With this type of ventilation, higher levels of CO2 can be tolerated (permissive hypercapnia). - Standard tidal volume ≅ 6 mL/kg body weight- FiO2 < 0.5 (< 50% in the gas mixture) to avoid oxygen toxicity- PEEP and FiO2 can be adjusted to recruit collapsed alveoli and guarantee sufficient oxygen saturation.- Goal: SaO2 > 90% (or PaO2 > 55 mm Hg) Complications: Can progress to interstitial fibrosis and restrictive lung disease.
Sarcoidosis
Sarcoidosis is a multisystem disorder characterized by noncaseating granulomatous inflammation. Epidemiology:- Bimodal distribution: 25-35 years old with a second peak for females 45-65 years old- Sex: ♀ > ♂ (2:1)- Prevalence: 10 times higher among African Americans than whites in the US. African Americans are also more likely to have chronic and more severe disease courses. Acute sarcoidosis (approx. ⅓ of cases):- Typically has a sudden onset and remits spontaneously within approx. 2 years- Progression to chronic sarcoidosis is rare.- General: fever, malaise, lack of appetite, weight loss- Pulmonary: dyspnea, cough, chest pain- Extrapulmonary: arthritis, anterior uveitis, erythema nodosum Chronic sarcoidosis (approx. ⅔ of cases):- Gradual disease course; may be recurrent or progressive- Pulmonary (most common)- Often asymptomatic in the early stages- Dry cough, exertional dyspnea- Mild rales on pulmonary auscultation- Extrapulmonary → Peripheral lymph nodes are the most frequent site of extrapulmonary manifestation (40%). → Eyes (25%): granulomatous uveitis; blurred vision (ocular sarcoidosis) → Skin (25%): Lupus pernio: pathognomonic, extensive, purple skin lesions (violaceous skin plaques) on the nose, cheeks, chin, and/or ears; also referred to as epithelioid granulomas of the dermis → Scar sarcoidosis: inflamed, purple skin infiltration and elevation of old scars or tattoos - Other manifestations→ Musculoskeletal; bone lesions→ Nervous system (neurosarcoidosis): cranial nerve palsy (7th cranial nerve palsy is the most common), diabetes insipidus, meningitis, hypopituitarism→ Heart, Liver, Kidneys, Spleen Lofgren syndrome: Highly acute clinical presentation with fever and the following triad of symptoms1. Migratory polyarthritis: symmetrical arthritis that primarily affects the ankles2. Erythema nodosum: primarily affects the extensor surface of the lower legs3. Bilateral hilar lymphadenopathy Heerfordt syndrome: Chronic clinical presentation with fever and the following triad of symptoms1. Parotitis2. Uveitis (iridocyclitis)3. Facial palsy Diagnostics:- Chest x-ray: Best initial test- Acute sarcoidosis: ↑ Inflammatory markers; Findings typical for sarcoidosis are absent (e.g., ↑ ACE, ↑ IgG, ↑ calcium)- ↑ Calcium due to elevated levels of 1,25-(OH)2-vitamin D3- ↓ CD4+ T cells: T helper cells are consumed during granuloma formation → CD4+ levels are low in serum and high in bronchoalveolar lavage.- ↑ IgG (approx. 50% of patients)- ↑ Angiotensin-converting enzyme (ACE) blood levels; may be used to monitor disease activity and therapy - ↑ Inflammatory markers, possible lymphopenia- Urine analysis: hypercalciuria- Bronchoscopy: Biopsy: the gold standard for diagnosis Treatment:- Isolated pulmonary sarcoidosis: In most cases, no treatment is required. The disease is often asymptomatic, non‑progressive, and has a high rate of spontaneous remission.- Symptomatic or extrapulmonary sarcoidosis→ First line: glucocorticoids→ Second line: alternative immunosuppressive therapy (e.g., methotrexate or azathioprine), possibly in combination with glucocorticoids→ Antimalarial drugs (e.g., chloroquine, hydroxychloroquine) → Last resort in severe pulmonary disease: lung transplantation→ NSAIDs are always indicated for symptom relief. Complications:- Patients with sarcoidosis have an increased risk of malignant changes (esp. within the lungsand lymph nodes).- Bronchiectasis- Lung fibrosis: Irreversible fibrotic remodeling together with compression of large pulmonary arteries due to bilateral hilar lymphadenopathy may increase pulmonary vascular resistance, resulting in pulmonary hypertension (PH). - Chronic renal failure
Obstructive sleep apnea (OSA)
Risk factors:- Obesity, especially around the neck (short, wide “bull neck”)- Structural abnormalities that impair respiratory flow: adenotonsillar hyperplasia (especially in children), nasal septum deviation, previous upper airway surgery, enlarged uvula, tongue, or soft palate (especially in adults), overbite with a small chin, hypertrophied pharyngeal muscles, nasal polyps- Alcohol consumption before sleep- Intake of sedatives and/or beta-blockers before sleep- Smoking- Family history- Acromegaly- Hypothyroidism Clinical features:- Restless sleep with waking, gasping, or choking- Loud, irregular snoring with apneic episodes (third-party reports)- Excessive daytime sleepiness (e.g., patient falls asleep, microsleep during meetings or while watching TV)- Impaired cognitive function (e.g., impaired concentration, memory loss)- Depression, decreased libido Diagnostics:- Initial assessment: standardized questionnaires and third-party reports (interview sleeping partner regarding snoring and respiratory interruptions)- Polysomnography: first-line method; a test that records physiologic variables during sleep (including sleep stages, respiratory flow, respiratory pauses, and oxygen saturation); it may also help to identify the type of sleep disorder and associated conditions (e.g., seizures) - Home sleep apnea testing (less sensitive): ambulatory screening method based on the use of a device for monitoring cardiorespiratory parameters during the night. Indicated in patients with a high pretest probability of moderate to severe OSA or when in-laboratory polysomnography is not feasible. Treatment:- Mild to moderate OSA (mild symptoms and < 20 apneic episodes)→ Weight loss → Reduce and/or avoid risk factors: alcohol, nicotine, sedatives (e.g., benzodiazepines)→ Sleep hygiene: regular and sufficient sleep→ Lateral as opposed to supine sleeping position→ Blood pressure control→ Oral appliances - Severe OSA (> 20 apneic episodes and alterations in arterial oxygen saturation)→ Surgery (uvulopalatopharyngoplasty): Resection of the uvula and redundant retrolingual, soft palate, and tonsillar tissue → Bilevel positive airway pressure (BPAP) → Continuous positive airway pressure (CPAP)
Obesity hypoventilation syndrome (Pickwickian syndrome)
A breathing disorder that only affects morbidly obese individuals; frequently accompanied by OSA, it is characterized by diurnal hypercapnia Etiology: morbid obesity (BMI ≥ 30 kg/m2) Risk factors: identical to those of obesity Pathophysiology: obesity reduces inspiratory muscle strength and restricts respiratory excursions → alveolar hypoventilation, sleep-disordered breathing (e.g., OSA), and failure of ventilatory compensatory mechanisms → decreased PaO2 and increased PaCO2 during sleep (PaCO2 retention extends to the waking hours) Clinical features:- Same symptoms as those of OSA- Headaches and severe sleepiness Diagnostic criteria:- BMI ≥ 30 kg/m2- Arterial blood gasses showing diurnal hypercapnia (PaCO2 > 45 mm Hg) that cannot not be explained by another condition - Polysomnography shows hypoventilation during sleep with or without obstructive apnea events. Treatment:- Weight loss- Nasal intermittent positive pressure ventilation
Central sleep apnea (CSA)
Breathing-related sleep disorder characterized by repetitive cessation or decrease of respiratory effort during sleep due to impaired function of the respiratory center. Airway obstruction is absent. Etiology: idiopathic or caused by an underlying disorder Risk factors:- Age > 65 years- Male sex- Heart failure - Central nervous system disease (e.g., trauma, brainstem tumor, stroke) - Certain drugs (e.g., chronic opioid use) Pathophysiology: lack of stimulation to the respiratory center with patent upper airways→ periodic lack of respiratory muscle innervation → interruption of thoracic and/or abdominal respiratory movements Clinical features:- Morning headaches- Repeated waking at night- Daytime sleepiness- Snoring - Association with OSA is very common- Possibly Cheyne-Stokes breathing (especially in patients with heart failure) Diagnosis:- Based on clinical history (e.g., underlying conditions such as heart failure or stroke)- Polysomnography Treatment:- Treat underlying disorder (if present)- CPAP
Solitary pulmonary nodule
Benign lesions (e.g., histoplasmosis, cocidioidomycosis, TB, hamartoma):- No growth on serial imaging 2 years apart- A diffuse, dense and central, popcorn-like, or concentric "target" calcification pattern- Occurence in patients who are lifelong nonsmokers, are < 30 years of age, and have no history of malignancy Malignant lesions (i.e., lung cancer or metastases):- Size > 2 cm- Spiculation (i.e., ragged edges)- Sunburst pattern- Upper lobe location- Occurence in patients who are smokers, are > 40 years of age, or have a prior diganosis of cancer
Recommendations for lung cancer screening
Recommended test : Low-dose chest CT scan Recommended interval: Yearly Age for screening: 55-80 Eligibility:- Patient has ≥30-pack-year smoking historyAND- Patient is a current smoker or quit smoking within the last 15 years Termination of screening :- Age >80 OR- Patient successfully quit smoking for ≥15 years OR- Patient has other medical conditions that significantly limit life expectancy or ability/willingness to undergo lung cancer surgery
Allergic bronchopulmonary aspergillosis (ABPA)
Chronic exposure to Aspergillus can lead to allergic bronchopulmonary aspergillosis (ABPA) Lungs:- Asthmatic symptoms (e.g., shortness of breath, wheezing)- Productive cough with brown bronchial mucous casts- Sinusitis without tissue infiltration- Fungus ball in the paranasal sinuses with symptoms of chronic rhinosinusitis- May progress in immunocompromised patients (see invasive aspergillosis)- Nonspecific symptoms: weight loss, chronic fatigue; irritation of the skin, mucus membranes, and eyes Diagnostics:- History of asthma or cystic fibrosis- Positive Aspergillus antigen skin test OR ↑ IgE levels- Laboratory tests: ↑ ESR and eosinophilia- Tissue biopsy followed by histopathology and culture → Positive findings (e.g. presence of monomorphic, septate hyphae that branch at acute angles, as seen on silver or PAS stained samples) confirm the diagnosis of aspergillosis infection.- X-ray and CT: parenchymal opacities; features of bronchiectasis Treatment:- Avoid aspergillus exposure- Glucocorticoids - Consider adding itraconazole- In addition, in the presence of sinusitis: Endoscopic drainage; Surgical resection of nasal polyps
Solitary pulmonary nodules – Malignancy probability
Factors increasing malignant probability:- Large size*- Advanced patient age- Female sex- Active or previous smoking- Family or personal history of lung cancer- Upper lobe location- Spiculated radiographic appearance *Size >2 cm independently correlates with >50% malignant probability.
Pulmonary contusion
Clinical features:- Dyspnea, tachypnea- Tachycardia- Hypoxia and hypoxemia (may worsen after fluid administration as pulmonary edema worsens)- Chest pain Diagnostics:- Chest x-ray: patchy alveolar infiltrates; diffuse opacity or 'white out'- CT if x-ray is inconclusive Treatment:- Monitor blood gases- Intubation: usually not necessary Complications:- Pneumonia- ARDS
Acute bronchitis
Etiology: Preceding respiratory illness (90% viral) Clinical presentation:- Cough for > 5 days to 3 weeks (± purulent sputum)- Absent systemic findings (eg, fever, chills)- Wheezing or rhonchi, chest wall tenderness Diagnosis & treatment:- Clinical diagnosis, CXR only when pneumonia suspected- Symptomatic treatment (eg, NSAIDs &/or bronchodilators)- Antibiotics not recommended
Management of choking
Partial obsturction: Coughing, gagging → Allow spontaneous coughing Complete obstruction:- Hands clutched at throught- Inability to talk- Difficult breathing- Unable to cough- Cyanosis→ Age < 1 year → Turn the child head down and administer 5 back blows/turn the child face up and administer 5 chest thrusts→ Age > 1 year → Lean the patient forward and perform abdominal thrusts
Recommendations for lung cancer screening
Recommended test: Low-dose chest CT scan Recommended interval: Yearly Age for screening: 55-80 Eligibility:- Patient has ≥ 30-pack-year smoking historyAND- Patient is a current smoker or quit smoking within the last 15 years Termination of screening:- Age > 80 OR- Patient successfully quit smoking for ≥15 years OR- Patient has other medical conditions that significantly limit life expectancy or ability/willingness to undergo lung cancer surgery
Aspiration pneumonia
Definition: Aspiration is the inhalation of foreign material into the respiratory tract. It most commonly occurs after instrumentation of the upper airways or esophagus (e.g., upper GI endoscopy) or secondary to vomiting and regurgitation of gastric contents.- Aspiration pneumonitis: Aspiration of gastric acid that initially causes tracheobronchitis, with rapid progression to chemical pneumonitis Risk factors - Altered consciousness: alcohol, sedation, general anesthesia, stroke- Apoplexy and neurodegenerative conditions - Gastroesophageal reflux disease, esophageal motility disorders- Congenital defects (e.g., tracheoesophageal fistula) Pathogens: mixed infections with anaerobic organisms are common (e.g., Klebsiella spp.) Clinical findings:- Immediate symptoms: bronchospasms, crackles on auscultation, hypoxemia with cyanosis- Late symptoms: fever, shortness of breath, cough with foul-smelling sputum Diagnosis:- Arterial blood gas analysis (↓ PaO2, pH < 7.35, PaCO2 > 45 mm Hg)- Radiologic imaging: The lung region in which the infiltrates are seen depends on the patient's position on aspiration. → Supine position: superior segment of the right lower lobe (most common site of aspiration)→ Standing/sitting: posterior basal segment of the right lower lobe→ Right lateral decubitus position: posterior segment of the right upper lobe or right middle lobe Management:- If secondary to extubation: Immediate (re)intubation with administration of 100% O2- Endotracheal suction with microbiological analysis of bronchial secretions- Antibiotic treatment that covers anaerobes (e.g., ampicillin-sulbactam, carbapenems, or clindamycin) - Regular monitoring: arterial blood gas, radiologic imaging Prevention: Optimize treatment and/or prophylaxis of underlying causes to reduce the risk of aspiration (e.g., elevation of the head of the bed).
Rib fracture
Etiology: mostly blunt trauma, pathologic fractures, nonaccidental trauma (child abuse) Clinical features:- Pain on inspiration- Focal chest wall tenderness- Crepitus- Chest wall deformity- Flail chest: multiple (≥ 3) rib fractures in 2 or more places, resulting in a floating section of ribs and soft tissue within the chest wall→ Paradoxical movement: the floating segment moves inward during inspiration and outward during expiration - Respiratory distress, tachypnea, and shallow breaths Diagnostics- Chest x-ray (AP and lateral view): fracture lines, displaced fractures- Possible CT if complications are suspected Complications:- Pneumothorax- Hemothorax - Especially in the elderly: pain → splinting and hypoventilation → atelectasis and/or pneumonia- Pulmonary contusion - Respiratory failure- Fracture of the lower ribs → abdominal organ injury Treatment:- Usually no surgery necessary- Analgesia: NSAIDs, Opiates, Local nerve block or epidural catheter- Intubation with positive pressure ventilation in severe flail chest (bridge to surgery)- In case of pneumothorax or hemothorax: thoracic drainage and thoracic surgical intervention Indications for surgery:- Significant chest wall deformity- Severe flail chest- Nonunion
ARDS definition
1. Acute (< 1 week) 2. P:F ratio < 300 with > 5 cmH2O PEEP 3. Bilateral opacities on CXR or chest CTM 4. Must not be fully explained by cardiac failure/fluid overload
RSBI score
Used to assess whether it is time to extubate RR/tidal volume < 105 predicative of successful extubation > 105 more likely to fail extubation
Cuff leak
Marker of laryngeal edema Causes:- Traumatic intubation- Oversized endotracheal tube- Prolonged intubation Goals:1. Audible cuff leak2. Volume > 110 mL on the ventilator Treatment: Steroids for 24 hours
Pulmonary hypertension – Treatment
Treatment of the underlying cause Additional treatment:- Diuretics - Physical exercise - Oxygen therapy Pulmonary vasodilator therapy - Calcium channel blockers (if responsive to NO)- Long-acting synthetic prostacyclin (epoprostenol) or prostacyclin analogs (e.g., iloprost, treprostinil)- Endothelin receptor antagonists (e.g., bosentan, macitentan, and ambrisentan)- Phosphodiesterase 5 inhibitors (e.g., sildenafil) Patients who are refractory to medical treatment:- Atrial septostomy (right-to-left shunt) or- Heart-lung/bilateral lung transplantation
