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“Why can’t I breathe?” An account of a real patient presenting with breathlessness

January 8 2024

One of my biggest fears is not being able to breathe. The thought of losing my breath and unable to get it back fills me with dread. So when I see a patient struggling to breathe, it’s all action-stations for me to help them as soon and as much as able.The following story is the admission of such a patient. A brief description of the assessment, investigations and treatment to manage this horrendous symptom of lung cancer are included, with a focus on dyspnoea causes.

What’s the story?

Robert (pseudonym) is a 74-year-old male recently diagnosed with metastatic lung cancer. The staging PET scan reported a large left lower lobe and mediastinal mass with pleural and pericardial effusions. He presents today with worsening breathlessness and bilateral ankle oedema. He reports breathing is worse on exertion and when lying flat (orthopnoea) and he has developed a cough which is worse at night. He describes heart palpitations and has reduced exercise tolerance. 

On entering his room, I see that he is sitting forward in his chair with hands clenched on the arms. He is displaying pursed lip breathing and puffing his cheeks out on expiration. He constantly shuffles and appears uncomfortable. He speaks in short sentences, verbalising concern around his condition. I can see the distress in his eyes. “Why can’t I breathe?”

Roberts observations are within normal limits, however, he is borderline hypotensive, tachycardic and tachypnoeic. He has lost four kilograms of weight over the last three weeks, admitting a reduced appetite and oral intake. He denies any pain.  

Physical examination shows bilateral pitting oedema to calf level, but no associated pain. He describes a dry, irritating, non-productive cough. There is no finger clubbing or cyanosis. His skin is dry and cool with no discolouration or broken areas. His oral cavity is pink but mucous membranes appear dry.

Respiratory assessment demonstrates dull percussion over the left lung base, reduced air entry on auscultation of left lung base and an observed uneven rise of chest during inspiration. Cardiac assessment shows Korotkoff sounds on expiration at 95mmHg, on inspiration at 88-89mmHg meaning a fall of less than 10mmHg and no pulsus paradoxus evident.  

Admission blood tests reveal a raised LDH and CXR reports a left basal consolidation, large left pleural effusion and enlarged heart size.  

What’s happening?

Breathing is an unconscious action controlled in the brainstem instructing the respiratory muscles to contract and relax as a response to sensory stimuli.1 Mechanoreceptors, baroreceptors, chemoreceptors and lung stretch receptors stimulate afferent (sensory) impulses to the medulla which processes the information, triggering efferent (motor) signals via the phrenic and thoracic spinal nerves to regulate physical breathing.1,2 These pathways work in synergy to maintain homeostasis and keep regulation of ventilation, airway pressures, pH balance, oxygen levels and air flow.2

Dyspnoea is a subjective experience of breathing discomfort and occurs when the demand to breathe is not met by the ability to do so.3 Particular conditions affecting the respiratory system will stimulate the brain to increase respiratory effort countering the alteration, but also causing dyspnea.3 The sensory cortex is also stimulated which perceives the sensation of increased muscular effort and causes breathlessness.3 This signaling to increase the work of breathing can be caused by a number of conditions involving the cardiac, respiratory, haematological, metabolic, psychogenic or neurological systems.3

With Roberts presentation, history and examination, it is likely that the dyspnoea is due to his pleural effusion, mediastinal lymph node mass and large tumour invading into the parietal pleura and pericardium. Mediastinal masses block the drainage of fluid from pleural and pericardial cavities, whilst invasion of cancer cells into the spaces secrete mediators that increase vascular permeability and plasma leakage causing enhanced fluid production leading to effusions and inflammation.4 The pleural fluid causes reduction in chest wall and diaphragm compliance and reduced lung volume, triggering the dyspnoea pathway.5 His respiratory examination suggested a left sided effusion, also evident on CXR.

The CXR also showed an increased heart size. This and other symptoms (dyspnea, orthopnoea, cough, fatigue, lower limb oedema, palpitations, borderline tachycardia and hypotension) are suggestive of a pericardial effusion.6 Pressure exerted on the heart due to fluid accumulation triggers the brain to increase respirations to overcome the load and increase ventilatory requirements, resulting in dyspnea.2

Another possibility is a PE, which cancer patients have a higher risk of developing as cancer cells activate the clotting cascade either by thromboplastin activation or by stimulation of monocytes and macrophages promoting the conversion of prothrombin to thrombin, thus causing a clot or thrombus.7 Dyspnoea occurs due to gas exchange abnormalities, hypoxemia and increased arterial pressure from detection of pulmonary artery embolic obstruction, triggering the motor response to increase respirations.8 However, Robert has no chest pain and his lower leg oedema is bilateral with most VTE presentations being unilateral, making PE a less likely differential.8

What’s next?

Further imaging is planned to characterise the location and extent of effusions for drainage consideration. Bilateral leg dopplers and a CTPA are ordered to investigate for a PE/DVT.

Robert is closely monitored and symptoms supported with supplemental oxygen, breathing exercises and positional relief. Pharmacological interventions are considered, but Robert is reluctant to try them at this point. There is a possibility that Robert will require a pleural and pericardial drainage. He is educated on these procedures and the possibility of an ICU stay post procedure.

He is anxious about his presenting condition, concerned that it will delay starting his anti-cancer treatment. Psychological support and reassurance is provided to him that we will do our best to relieve his discomfort and improve his situation, which also contributes to some dyspnoea relief. Ongoing breathlessness may affect Robert’s quality of life and be distressing if chronic. The involvement of the palliative care team and GP to help with symptom management and provide psychosocial community support is vital for Robert. Starting his treatment will be important to treat the malignancy, potentially reduce the risk of further effusions and give Robert peace of mind that we are treating his cancer and helping to achieve his goal to “see one more Christmas”.


  1. Mahler, D., & O’Donnell, D. (2014). Neurobiology of dyspnea: An overview. In D. Mahler & D. O’Donnell (Eds.), Dyspnea: Mechanisms, measurement and management (3rd ed., pp. 3-10). Boca Raton, USA: CRC Press. 
  2. Williams, C. (2006). Dyspnea. The Cancer Journal, 12(5), 365-373. 
  3. Coccia, C., Palkowski, G., Schweitzer, B., Motsohi, T., & Ntusi, N. (2016). Dyspnoea: Pathophysiology and a clinical approach. South African Medical Journal, 106(1), 32-36. doi: 10.7196/samj.2016.v106i1.10324 
  4. Spella, M., Giannou, A., & Stathopoulos, G. (2015). Switching off malignant pleural effusion formation—fantasy or future? Journal of Thoracic Disease, 7(6), 1009-1020. doi: 10.3978/j.issn.2072-1439.2015.05.20 
  5. Michael, C. (2012). Lung carcinoma. In B. Davidson, P. Firat & C. Michael, Serous effusions: Etiology, diagnosis, prognosis and therapy (pp. 27-46). London: Springer. 
  6. Burazor, I., Imazio, M., Markel, G., & Adler, Y. (2013). Malignant pericardial effusion. Cardiology, 124, 224-232. doi: 10.1159/000348559 
  7. Perrier, A., & Righini, M. (2016). Diagnosis of acute pulmonary thromboembolism. In A. Peacock, R. Naeije & L. Rubin (Eds.), Pulmonary circulation: Diseases and their treatment (4th ed., pp. 574-586). Boca Raton, USA: CRC Press. 
  8. Turetz, M., Sideris, A., Friedman, O., Triphathi, N., & Horowitz, J. (2018). Epidemiology, pathophysiology, and natural history of pulmonary embolism. Seminars in Interventional Radiology, 35(02), 92-98. doi: 10.1055/s-0038-1642036 

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ANZ-LCNF acknowledges and respects traditional owners and Aboriginal and Torres Strait Islander Elders past and present, on whose land we work to support the provision of safe and quality thoracic oncology nursing care.

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