Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• The Intersection of COPD and Heart Failure: Diagnostic Overlap

  Chronic obstructive pulmonary disease and heart failure frequently produce the same presenting symptoms: breathlessness, reduced exercise tolerance, fatigue, cough and poor sleep. In older adults, the two conditions often coexist, making it difficult to identify which disease is driving a change in health. A patient may be treated for a flare of airway disease when pulmonary congestion is the greater concern, or receive cardiac treatment while persistent airflow limitation remains overlooked.

  This diagnostic overlap matters across Australian healthcare settings, from metropolitan respiratory clinics in Sydney and Melbourne to regional hospitals and remote general practices. Careful history-taking, physical examination and targeted testing can separate overlapping syndromes while recognising that COPD and heart failure may need treatment at the same time.

  Why Symptoms Converge

  COPD causes persistent airflow obstruction, air trapping and impaired gas exchange. Heart failure reduces the heart’s ability to maintain adequate circulation, often leading to raised filling pressures and fluid accumulation in the lungs. Both mechanisms increase the work of breathing and limit oxygen delivery during activity.

  Breathlessness that develops gradually is especially difficult to interpret. Wheeze may occur with pulmonary oedema as well as bronchial obstruction, while cough can reflect airway irritation, infection or pulmonary congestion. Fatigue may arise from hypoxia, poor sleep, reduced cardiac output, deconditioning or medication effects.

  Shared Risk And Disease Biology

  Smoking remains a major risk factor for COPD and also contributes to coronary artery disease, the commonest cause of heart failure in many older adults. Ageing, hypertension, diabetes, obesity and chronic kidney disease further increase the likelihood of both diagnoses. A patient with a long smoking history may therefore have substantial cardiovascular disease even when respiratory symptoms appear dominant.

  Environmental exposures can add complexity. Bushfire smoke affecting communities in New South Wales, Victoria and South Australia may worsen airway symptoms in people with COPD, while heatwaves can increase cardiovascular strain and dehydration. Occupational dust exposure, indoor air pollution and recurrent respiratory infections may also accelerate decline.

  Reading Breathlessness And Examination

  The timing and pattern of symptoms provide useful clues. Orthopnoea, waking at night gasping, rapid weight gain and ankle swelling support fluid overload, although peripheral oedema can also result from pulmonary hypertension, venous disease or some medicines. Breathlessness with wheeze, prolonged expiration and increased sputum volume may point towards COPD, particularly when it resembles previous exacerbations.

  Physical signs should be interpreted as a group rather than in isolation. Raised jugular venous pressure, a third heart sound, cool extremities and basal crackles increase concern about heart failure, but crackles may be absent in chronic congestion. Hyperinflation, diminished breath sounds and pursed-lip breathing support COPD, yet severe emphysema can make cardiac sounds difficult to hear.

  Testing Beyond A Single Diagnosis

  Spirometry confirms persistent airflow obstruction when the patient is clinically stable, while bronchodilator response can help describe the pattern without reliably excluding coexisting heart failure. Oxygen saturation, full blood count, renal function, electrolytes and an electrocardiogram are practical first-line investigations. Anaemia, arrhythmia and renal impairment can intensify symptoms from either condition.

  Natriuretic peptides can support or weaken the suspicion of heart failure, but results require context. Levels may rise with atrial fibrillation, kidney disease, pulmonary hypertension and older age, and can be lower in obesity. A normal or low result makes significant congestion less likely in many settings, whereas an elevated result should prompt clinical correlation rather than automatic diagnosis.

  Clinical Clues Worth Separating

  A structured assessment helps clinicians avoid anchoring on the patient’s established diagnosis. In Australian general practice, this is particularly important when Medicare-funded consultations, limited rural imaging access or delayed specialist review encourage decisions based on a small initial dataset.

  Useful features supporting a cardiac contribution include:

  • Orthopnoea or paroxysmal nocturnal breathlessness
  • Recent weight gain, oedema or reduced urine output
  • Atrial fibrillation, ischaemic disease or uncontrolled hypertension
  • Raised natriuretic peptide or congestion on imaging

  Features supporting a predominantly pulmonary contribution include:

  • Increased sputum purulence or volume
  • Prolonged expiration and persistent airflow limitation
  • A clear exposure or infection trigger
  • Symptom improvement after appropriate bronchodilator therapy

  Neither list excludes the other diagnosis. A patient can have infectious COPD exacerbation alongside left ventricular dysfunction, and diuretics can improve congestion without correcting airflow obstruction.

  Imaging And Functional Evidence

  Chest radiography may show hyperinflation, enlarged cardiac shadows, vascular redistribution or pleural effusions, although a normal film does not exclude early heart failure. Lung ultrasound can identify B-lines and pleural fluid, while echocardiography evaluates ejection fraction, valve disease, right-sided pressures and diastolic function. Access varies between metropolitan and regional Australia, so test selection often depends on urgency and local capability.

  Exercise assessment adds another layer. A six-minute walk test, functional history or formal cardiopulmonary exercise testing can reveal whether limitation is mainly ventilatory, circulatory or mixed. Diffusing capacity and lung volumes can clarify emphysema and hyperinflation, while ECG rhythm assessment may uncover atrial fibrillation as a reversible contributor to reduced exercise tolerance.

  Treatment Decisions Across Conditions

  Treatment should address the active mechanism without assuming that one diagnosis explains everything. COPD management may include inhaled bronchodilators, pulmonary rehabilitation, vaccination, smoking cessation support and a written exacerbation plan. Heart failure care may involve diuretics, guideline-directed therapies, blood pressure control and management of ischaemia or arrhythmia.

  Medication review is essential. Some beta-blockers are appropriate and valuable in heart failure, while cardioselective agents are generally considered when clinically indicated in people with COPD. Diuretics can relieve congestion but may disturb renal function and electrolytes. Inhaled therapies can improve respiratory symptoms, yet excessive reliance on short-acting medicines may obscure deteriorating cardiac status.

  What Clinicians Should Remember

  The safest approach is to reassess the working diagnosis whenever breathlessness changes character, treatment response is incomplete or new signs appear. Repeated weight measurements, symptom diaries, spirometry when stable, cardiac imaging and coordinated GP, respiratory and cardiology follow-up can reveal the contribution of each disease over time. This is especially valuable for patients moving between tertiary hospitals in Brisbane or Perth, local practices and community services.

  COPD and heart failure are frequently partners rather than competing explanations. Their symptoms overlap, their risk factors intersect and their treatments can influence one another. The key point to remember is that unexplained breathlessness deserves a dual assessment: look for airflow obstruction and cardiac congestion together, then treat the patient’s combined physiology rather than a label alone.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)