HERMES Adult Respiratory Medicine cheat sheet

Asthma is defined by variable expiratory airflow limitation plus compatible respiratory symptoms; documenting reversibility (FEV1 rise >12% and >200 mL after 200-400 mcg salbutamol) or peak flow variability supports the diagnosis.

GINA treatment steps: as-needed low-dose ICS-formoterol (steps 1-2), daily low-dose ICS plus as-needed ICS-formoterol (step 3), medium-dose ICS-LABA maintenance (step 4), and specialist referral with add-on therapy at step 5.

SABA-only treatment is no longer recommended for any age group because of increased exacerbation and mortality risk; ICS-containing regimens are preferred even in mild asthma.

Acute severe asthma: oxygen to target SpO2 93-95%, repeated inhaled SABA with ipratropium, systemic corticosteroids within the first hour, and IV magnesium sulfate 2 g over 20 minutes for non-responders.

COPD diagnosis requires post-bronchodilator FEV1/FVC <0.70 in a patient with symptoms and relevant exposure; severity is graded by FEV1 percent predicted (GOLD 1 >=80%, GOLD 2 50-79%, GOLD 3 30-49%, GOLD 4 <30%).

GOLD ABE grouping uses exacerbation history and mMRC or CAT score; group A starts a bronchodilator, group B a LABA plus LAMA, and group E a LABA plus LAMA with ICS added when blood eosinophils are >=300 cells/microlitre.

Non-invasive ventilation for acute hypercapnic COPD exacerbation reduces intubation and mortality when pH is 7.25-7.35 with PaCO2 >45 mmHg; contraindications include vomiting, impaired consciousness, and facial trauma.

Bronchiectasis management centres on airway clearance, treating exacerbations with culture-directed antibiotics, and long-term macrolide therapy to reduce exacerbation frequency in selected patients without Pseudomonas aeruginosa.

Cystic fibrosis diagnosis rests on clinical features plus evidence of CFTR dysfunction: sweat chloride >60 mmol/L, two disease-causing CFTR mutations, or abnormal nasal potential difference.

Idiopathic pulmonary fibrosis is diagnosed by a usual interstitial pneumonia pattern on high-resolution CT (subpleural, basal-predominant reticulation, honeycombing, traction bronchiectasis) and absence of an alternative cause.

Antifibrotic therapy (pirfenidone or nintedanib) slows FEV1 and FVC decline in IPF; neither reverses fibrosis, and both require monitoring of liver enzymes and gastrointestinal tolerance.

Acute exacerbation of IPF is defined as new bilateral ground-glass or consolidation on CT within one month, with exclusion of infection, heart failure, and pulmonary embolism; mortality exceeds 50%.

Hypersensitivity pneumonitis requires antigen identification and avoidance; fibrotic (chronic) disease carries a worse prognosis, and corticosteroid benefit is uncertain in the fibrotic phenotype.

Sarcoidosis staging by chest radiograph: stage I bilateral hilar lymphadenopathy, stage II lymphadenopathy plus parenchymal infiltrates, stage III parenchymal infiltrates alone, stage IV fibrosis.

Connective tissue disease-associated ILD screening uses annual pulmonary function tests and HRCT in systemic sclerosis, rheumatoid arthritis, and inflammatory myopathies; FVC decline >10% predicts progression.

Pulmonary function in ILD typically shows a restrictive pattern (reduced TLC, FVC, DLCO) with preserved or increased FEV1/FVC ratio; a reduced DLCO often precedes spirometric change.

Bronchoalveolar lavage lymphocytosis >25-30% suggests hypersensitivity pneumonitis or sarcoidosis, while eosinophilia >25% suggests eosinophilic pneumonia; BAL cellularity is not diagnostic alone.

Lung transplantation referral for ILD is considered when DLCO <40% predicted, FVC <80% predicted, or there is desaturation on six-minute walk testing or hospitalisation for respiratory failure.

Cystic fibrosis newborn screening uses immunoreactive trypsinogen; positive screens proceed to DNA mutation panel and sweat chloride testing, with sweat chloride >60 mmol/L diagnostic.

Bronchiolitis in infants under 12 months is usually caused by respiratory syncytial virus; management is supportive, and routine bronchodilators, corticosteroids, and antibiotics are not recommended.

Croup (laryngotracheobronchitis) is treated with a single dose of oral dexamethasone 0.15-0.6 mg/kg; nebulised adrenaline is reserved for moderate-to-severe stridor at rest.

Preschool wheeze phenotypes: episodic viral wheeze and multiple-trigger wheeze; a therapeutic trial of inhaled corticosteroid for 8-12 weeks with reassessment helps distinguish responders.

Paediatric asthma severity is assessed by symptom frequency, reliever use, and activity limitation; spirometry with bronchodilator response supports diagnosis in children old enough to cooperate (usually >5 years).

Primary ciliary dyskinesia presents with neonatal respiratory distress, chronic wet cough, situs inversus in about half of cases, and low nasal nitric oxide; diagnosis uses high-speed video microscopy or genetics.

Foreign body aspiration should be suspected with sudden onset of cough or unilateral wheeze in a toddler; rigid bronchoscopy is both diagnostic and therapeutic.

Congenital diaphragmatic hernia causes respiratory distress and scaphoid abdomen in the newborn; management avoids immediate surgical repair and prioritises gentle ventilation to limit pulmonary hypertension.

Pulmonary hypertension is defined by mean pulmonary arterial pressure >20 mmHg at rest; precapillary disease adds pulmonary vascular resistance >=3 Wood units and pulmonary artery wedge pressure <=15 mmHg.

Pulmonary arterial hypertension (group 1) treatment risk-stratifies patients; low-risk patients may start dual oral therapy, while high-risk patients receive parenteral prostacyclin plus combination therapy.

Acute pulmonary embolism risk stratification uses haemodynamic stability first; unstable patients receive systemic thrombolysis or embolectomy, while stable patients are stratified by sPESI, RV function, and troponin.

Wells score and D-dimer are used to rule out pulmonary embolism in low-probability patients; a negative age-adjusted D-dimer in a low-risk patient safely excludes PE without imaging.

Chronic thromboembolic pulmonary hypertension requires at least three months of anticoagulation plus persistent perfusion defects on V/Q scan; pulmonary endarterectomy is the treatment of choice for accessible disease.

Hereditary haemorrhagic telangiectasia and portopulmonary hypertension are causes of group 1 PAH; screening echocardiography is recommended in systemic sclerosis because PAH is a leading cause of death.

Right heart catheterisation is mandatory to confirm pulmonary hypertension and to distinguish precapillary from postcapillary disease; echocardiography estimates but does not diagnose.

Calcium channel blockers are indicated only in idiopathic PAH patients who are vasoreactive on acute testing (about 10%); non-responders may deteriorate with these agents.

ARDS is defined by acute onset within one week, bilateral opacities not fully explained by effusion or collapse, and PaO2/FiO2 <=300 mmHg on PEEP >=5 cmH2O; severity is mild 200-300, moderate 100-200, severe <100.

Lung-protective ventilation in ARDS uses tidal volume 6 mL/kg predicted body weight, plateau pressure <=30 cmH2O, and driving pressure monitoring; prone positioning for 16 hours daily reduces mortality when PaO2/FiO2 <150.

Predicted body weight formulas: male 50 + 0.91 x (height in cm - 152.4); female 45.5 + 0.91 x (height in cm - 152.4).

Weaning from mechanical ventilation uses a spontaneous breathing trial; a rapid shallow breathing index (respiratory rate/tidal volume in litres) <105 predicts extubation success.

Non-invasive ventilation is first-line for acute hypercapnic exacerbation of COPD and for cardiogenic pulmonary oedema; it is generally avoided in undifferentiated shock or facial trauma.

Ventilator-associated pneumonia is suggested by new infiltrate plus fever, purulent secretions, or leukocytosis after 48 hours of ventilation; early empiric therapy is guided by local resistance patterns.

High-flow nasal oxygen provides heated humidified gas at up to 60 L/min with FiO2 up to 1.0; it reduces work of breathing and is used before considering intubation in acute hypoxaemic failure.

Sedation in critical care targets light levels (RASS -1 to 0) with daily interruption where safe; deep sedation is associated with longer ventilation and delirium.

Community-acquired pneumonia severity is assessed with CURB-65 (confusion, urea >7 mmol/L, respiratory rate >=30, blood pressure low, age >=65); score 0-1 supports outpatient care, >=2 consider admission.

Empiric CAP therapy in outpatients without comorbidity is amoxicillin or doxycycline; with comorbidity use amoxicillin-clavulanate plus macrolide or a respiratory fluoroquinolone.

Hospital-acquired and ventilator-associated pneumonia empiric therapy must cover Pseudomonas aeruginosa and MRSA when risk factors exist; de-escalate based on culture results.

Tuberculosis diagnosis uses sputum acid-fast bacilli smear, culture (gold standard), and nucleic acid amplification testing; drug susceptibility testing is mandatory on the initial isolate.

Latent tuberculosis treatment options include 4 months of rifampicin, 3 months of weekly isoniazid plus rifapentine, or 6-9 months of isoniazid; choice depends on interactions and liver risk.

Pneumocystis jirovecii pneumonia prophylaxis with co-trimoxazole is indicated when CD4 count <200 cells/microlitre; treatment doses are higher and adjunctive corticosteroids are used when PaO2 <70 mmHg.

Influenza pneumonia treatment with oseltamivir is most effective within 48 hours of symptom onset but should be given regardless of timing in hospitalised or severe cases.

Pleural infection requires diagnostic thoracentesis; pH <7.20, glucose <2.2 mmol/L, or loculation indicates need for chest drainage, and intrapleural fibrinolytics plus DNase may be used for complicated collections.

Obstructive sleep apnoea diagnosis uses the apnoea-hypopnoea index: mild 5-15, moderate 15-30, severe >30 events per hour on polysomnography or home sleep testing.

CPAP is first-line for moderate-to-severe OSA and for mild OSA with symptoms or cardiovascular comorbidity; adherence is defined as >=4 hours per night on >=70% of nights.

Central sleep apnoea in heart failure is treated by optimising cardiac therapy; adaptive servo-ventilation is contraindicated in heart failure with ejection fraction <45% due to increased mortality.

Obesity hypoventilation syndrome is defined by BMI >=30, daytime PaCO2 >45 mmHg, and sleep-disordered breathing without another cause; treatment is weight loss plus nocturnal non-invasive ventilation.

STOP-BANG screening scores >=3 indicate high OSA risk and warrant sleep testing; the components are snoring, tiredness, observed apnoea, pressure, BMI, age, neck circumference, and gender.

Obesity hypoventilation and OSA both raise perioperative risk; preoperative screening and postoperative monitoring are indicated for patients with known or suspected disease.

Narcolepsy type 1 is defined by excessive daytime sleepiness plus cataplexy or low CSF hypocretin-1; multiple sleep latency testing shows mean sleep latency <=8 minutes with >=2 sleep-onset REM periods.

Restless legs syndrome is diagnosed clinically with an urge to move the legs, worse in the evening, relieved by movement; iron deficiency should be checked and treated.

Lung cancer staging uses TNM 8th edition; stage IV disease includes any T with distant metastasis, and staging is completed with CT plus PET-CT and brain imaging where indicated.

Non-small cell lung cancer with resectable stage I-II disease is treated with surgical resection; mediastinal staging with endobronchial ultrasound is performed when nodes are enlarged or PET-avid.

Molecular testing in advanced non-squamous NSCLC must include EGFR, ALK, ROS1, BRAF, KRAS, MET, RET, and PD-L1 expression; targeted therapy is preferred over chemotherapy when a driver mutation is found.

Small cell lung cancer is staged as limited versus extensive; limited-stage disease is treated with concurrent chemoradiotherapy, and prophylactic cranial irradiation is considered in responders.

Malignant pleural mesothelioma is associated with asbestos exposure and typically presents with unilateral pleural thickening or effusion; diagnosis requires adequate tissue biopsy with immunohistochemistry.

Solitary pulmonary nodule risk is estimated by size, smoking history, and morphology; nodules >=8 mm generally require PET-CT or biopsy, while smaller nodules are followed with serial CT.

Superior vena cava syndrome in lung cancer is managed with urgent imaging, tissue diagnosis if possible, and radiotherapy or stenting; corticosteroids are used for cerebral oedema or airway compromise.

Paraneoplastic syndromes: squamous cell carcinoma secretes PTH-related peptide causing hypercalcaemia; small cell carcinoma causes SIADH and ectopic ACTH; carcinoid tumours cause flushing and diarrhoea.