Initial Management of Acute Dyspnea in COPD, Asthma, or Heart Failure
Immediately assess hemodynamic stability and respiratory status, then initiate controlled oxygen therapy targeting SpO2 88-92% in COPD patients (not >90% until blood gases confirm no hypercapnia risk), while simultaneously administering disease-specific pharmacotherapy: short-acting bronchodilators for COPD/asthma exacerbations and IV furosemide for heart failure, with early consideration of non-invasive ventilation if respiratory rate >25 breaths/min or SpO2 <90% despite initial interventions. 1
Immediate Triage and Monitoring
Triage patients with persistent dyspnea or hemodynamic instability to a location where immediate resuscitative support is available (ICU/CCU for high-risk patients with persistent significant dyspnea, hemodynamic instability, or recurrent arrhythmias). 1
Monitor transcutaneous oxygen saturation (SpO2) continuously from arrival. 1, 2
Obtain arterial blood gas analysis with pH, PaCO2, and lactate measurement within the first hour, especially in patients with COPD history or acute pulmonary edema, as this guides oxygen therapy and identifies hypercapnic respiratory failure. 1, 3 Venous blood gas is acceptable for pH and CO2 assessment in most cases except cardiogenic shock where arterial sampling is preferable. 1
Oxygen Therapy Protocol
Initiate controlled oxygen at 28% via Venturi mask or 2 L/min via nasal cannula in COPD patients until arterial blood gases are obtained—do not exceed this initial dose as hyperoxygenation increases ventilation-perfusion mismatch and can suppress ventilation leading to hypercapnia. 1, 3
Target SpO2 of 88-92% in COPD patients to avoid CO2 retention while correcting hypoxemia. 1, 2, 3
In heart failure without COPD, administer oxygen only if SpO2 <90% or PaO2 <60 mmHg (8.0 kPa), as oxygen causes vasoconstriction and reduces cardiac output in non-hypoxemic patients. 1, 2
Recheck arterial blood gases within 60 minutes of initiating oxygen and after any FiO2 changes. 3
Avoid hyperoxia in all patients—the fraction of inspired oxygen should be titrated according to SpO2 monitoring. 1
Disease-Specific Pharmacotherapy
For COPD Exacerbations:
Administer short-acting inhaled β2-agonists (albuterol) with or without short-acting anticholinergics (ipratropium 500 mcg) via nebulizer immediately as the initial bronchodilator therapy. 1, 3 Metered dose inhalers with spacers are equally effective but nebulizers may be easier for sicker patients. 1
Initiate systemic corticosteroids (prednisone 40 mg daily for 5 days) as they shorten recovery time, improve FEV1 and oxygenation, and reduce risk of early relapse. 1 Oral prednisolone is equally effective to intravenous administration. 1
Start empiric antibiotics if the patient has increased dyspnea, sputum volume, AND sputum purulence (or two cardinal symptoms if purulence is one of them), or if mechanical ventilation is required. 1, 3 Recommended duration is 5-7 days with choice based on local resistance patterns (aminopenicillin with clavulanic acid, macrolide, or tetracycline). 1
For Heart Failure:
Administer IV furosemide 40-80 mg as a slow injection (over 1-2 minutes) immediately in patients with acute heart failure and pulmonary edema. 4 If inadequate response within 1 hour, increase to 80 mg IV slowly. 4
Monitor urine output, renal function, and electrolytes every 4-6 hours during aggressive diuresis. 3
Consider vasodilators in hypertensive patients (systolic BP >140 mmHg) with acute heart failure to reduce afterload. 1
For Asthma Exacerbations:
Administer short-acting inhaled β2-agonists (albuterol) as first-line therapy via nebulizer or metered dose inhaler with spacer. 5
Add systemic corticosteroids early in moderate to severe exacerbations. 1
Non-Invasive Ventilation Criteria
Initiate non-invasive positive pressure ventilation (CPAP or BiPAP) as soon as possible in patients with respiratory distress defined as respiratory rate >25 breaths/min AND SpO2 <90%, as this decreases respiratory distress and reduces mechanical intubation rates. 1, 2
Use BiPAP (bi-level positive pressure ventilation) preferentially in COPD patients with hypercapnia (PaCO2 >45 mmHg with pH 7.25-7.35) as inspiratory pressure support improves minute ventilation. 1
Monitor blood pressure regularly during NIV as it can reduce blood pressure and should be used with caution in hypotensive patients. 1, 2
Reassess with arterial blood gas analysis at 1-2 hours after initiating NIV—if PaCO2 and pH have deteriorated on optimal settings, consider intubation. 1 If no improvement by 4-6 hours, institute alternative management (intubation). 1
Intubation Criteria
Proceed to endotracheal intubation if respiratory failure with hypoxemia (PaO2 <60 mmHg), hypercapnia (PaCO2 >50 mmHg), and acidosis (pH <7.35) cannot be managed non-invasively. 1, 2
Patients with pH <7.25 (H+ >56 nmol/l) respond less well to NIV and should be managed in HDU/ICU with preparation for intubation. 1, 3
Critical Diagnostic Differentiation
Obtain chest X-ray immediately to differentiate pulmonary edema (pulmonary venous congestion, cardiomegaly, interstitial/alveolar edema) from pneumonia or COPD exacerbation, though 20% may be normal limiting sensitivity. 1, 3
Consider B-type natriuretic peptide (BNP) measurement in patients with history of COPD or asthma presenting with dyspnea, as approximately 20% have undiagnosed heart failure. 6 At a cutpoint of 100 pg/mL, BNP has 93% sensitivity and 78% specificity for identifying new-onset heart failure in this population. 6
Perform bedside thoracic ultrasound for B-lines (indicating pulmonary edema) if expertise is available, as this may be more informative than chest X-ray with significant time savings. 1
Obtain ECG and cardiac biomarkers (troponin) to exclude acute coronary syndrome as a precipitant. 1, 3
Common Pitfalls to Avoid
Do not withhold beta-blockers in COPD patients with heart failure—COPD is not a contraindication, and beta-blocker use reduces mortality by 31% in this population. 7 However, concurrent COPD reduces beta-blocker prescription threefold in clinical practice. 7
Do not use routine oxygen in non-hypoxemic heart failure patients as it causes vasoconstriction and reduction in cardiac output. 1, 2
Do not use intravenous methylxanthines for COPD exacerbations due to increased side effects without proven benefit. 1
Do not mix furosemide with acidic solutions (labetalol, ciprofloxacin, amrinone, milrinone) in the same IV line as precipitation will occur. 4
Recognize that emergency physicians identify only 37% of new heart failure cases in patients with COPD/asthma history, highlighting the need for objective testing (BNP, echocardiography). 6