A Clinical Approach to Dyspnoea in the Emergency Department
Introduction: The Challenge of Breathlessness
Dyspnoea, the subjective feeling of being short of breath, is one of the most common and challenging presentations in the Emergency Department (ED). For the patient, it is a uniquely terrifying experience, a primal fear of "air hunger" that can induce significant anxiety and panic, further worsening the sensation (1). For the clinician, it represents a formidable diagnostic puzzle. The symptom is non-specific, stemming from a vast differential diagnosis that spans multiple organ systems, from the relatively benign, like anxiety, to the imminently life-threatening, such as a massive pulmonary embolism. The significant overlap in clinical presentation between cardiac, pulmonary, and other systemic causes demands a sharp, systematic approach to avoid diagnostic error.
The gravity of this symptom is underscored by its substantial impact on healthcare resources. In the Asia-Pacific region, including Malaysia, dyspnoea accounts for 5.2% of all ED visits, a figure that highlights its prevalence (5). These patients are often critically ill, comprising 11.4% of all ward admissions and a staggering 19.9%—nearly one in five—of all ICU admissions originating from the ED (5, 6). This establishes dyspnoea not just as a common complaint, but as a major driver of acute hospital workload and a key indicator of severe underlying pathology. Furthermore, a presentation with acute dyspnoea is a harbinger of significant morbidity and mortality. The overall in-hospital mortality rate for patients admitted with this symptom is approximately 5-6% (5). The severity of the symptom itself is a powerful prognostic marker, in some cases more so than objective tests. For instance, in patients with chronic heart failure, the degree of dyspnoea is a stronger predictor of mortality than angina (3). Given these high stakes, a structured, evidence-based framework is essential. This guide provides such a framework for the Malaysian junior doctor to evaluate, investigate, and manage the dyspnoeic patient effectively and safely.
The First 5 Minutes: Primary Survey and Red Flag Recognition
Your immediate priority is not to make a definitive diagnosis, but to assess the degree of physiological distress and identify any immediate life-threats that require urgent intervention. This process involves parallel assessment and action. A rapid primary survey (Airway, Breathing, Circulation) is critical to spot "red flags" that demand immediate resuscitation, often while the rest of the assessment continues.
⚠️ Red Flag Signs of Impending Collapse
Altered Mental Status: Confusion, agitation, or drowsiness are ominous signs. They suggest the brain is not receiving enough oxygen (severe hypoxia) or is being poisoned by excess carbon dioxide (hypercapnia), leading to CO2 narcosis. This is a sign that the body's compensatory mechanisms are failing (4).
Inability to Speak: If the patient can only speak in single words or short phrases between breaths, their work of breathing is so severe that it prevents normal phonation. This indicates a critical lack of respiratory reserve.
Obvious Signs of Distress: The use of accessory muscles (sternocleidomastoid, scalenes), tripod positioning (leaning forward on outstretched arms), or paradoxical abdominal breathing (the abdomen pulling in during inspiration) are all signs that the primary respiratory muscles, chiefly the diaphragm, are fatigued and failing. The body is recruiting every available muscle to maintain ventilation (4).
Cyanosis: A bluish discoloration of the lips or fingertips is a late and critical sign of severe hypoxemia. It signifies a significant amount of deoxygenated haemoglobin in the arterial blood and indicates profound respiratory failure.
Stridor: A high-pitched, monophonic inspiratory sound indicating severe, critical narrowing of the upper airway (e.g., larynx or trachea). This is an airway emergency that requires immediate expert intervention.
"Silent Chest": In a patient with a history of asthma, the absence of wheezing during a severe attack is a pre-arrest sign. It means airflow is so limited that it is insufficient to generate the turbulence that causes wheezing. The chest has gone quiet because air is no longer moving (4).
Haemodynamic Instability: Hypotension (SBP < 90 mmHg) or other signs of shock (tachycardia, cool peripheries) indicate that the respiratory problem is now causing circulatory collapse, either through direct mechanical effects (e.g., tension pneumothorax, massive PE) or profound hypoxia.
Severe Hypoxia: An oxygen saturation (SpO2) below 90% despite the administration of high-flow supplemental oxygen suggests a severe ventilation-perfusion (V/Q) mismatch or shunt that is not correctable with oxygen alone, indicating a need for advanced respiratory support.
If any of these are present, escalate for senior help immediately and begin resuscitation.
Pathophysiology: The "Neuromechanical Mismatch"
Dyspnoea is not simply a consequence of abnormal blood gases; it is a complex neurological sensation. It arises from a "neuromechanical uncoupling," a mismatch between the brain's demand for breathing (the efferent signal from the motor cortex) and the feedback it receives from the body's respiratory system about the actual mechanical act of breathing (the afferent signals from chemoreceptors and mechanoreceptors) (9). This disparity between the central respiratory drive and the resulting mechanical action is consciously perceived as the uncomfortable sensation of breathlessness. The quality of this sensation, as described by the patient, provides vital diagnostic clues to the underlying pathophysiology.
"Air Hunger" or "Feeling of Suffocation": This sensation reflects a powerful, unmet ventilatory drive, typically from intense chemoreceptor stimulation. In a Pulmonary Embolism (PE), a large ventilation-perfusion (V/Q) mismatch develops, meaning parts of the lung are ventilated but not perfused. This leads to hypoxemia and a powerful, centrally mediated "air hunger." Similarly, in Metabolic Acidosis (e.g., DKA), the body drives ventilation (Kussmaul breathing) to blow off CO2 and compensate for the acidosis, an effort the patient perceives as a desperate need for air (1).
"Chest Tightness": This constrictive, band-like sensation is strongly associated with bronchoconstriction. The narrowing of the airways activates vagal irritant receptors embedded in the airway walls, sending signals to the brain that are interpreted as tightness. This is the pathognomonic description of Asthma but can also be reported by patients with acute pulmonary oedema ("cardiac asthma"), where fluid accumulation in the bronchial walls causes a similar narrowing (9).
"Increased Work/Effort of Breathing": This is the conscious perception of the muscular effort required to move air. It arises from feedback from proprioceptors (stretch receptors) in the chest wall muscles and diaphragm. In conditions like COPD, severe airflow limitation and dynamic hyperinflation mean the patient must use significant force to overcome resistance and exhale, leading to a profound sense of effort. Similarly, in restrictive diseases like pulmonary fibrosis, the lungs are stiff and non-compliant, requiring immense effort for each breath (11).
Etiology: A Structured Differential Diagnosis
Organise potential causes by system to ensure that critical diagnoses are not missed. This structured approach prevents premature diagnostic closure. In the Asia-Pacific region, a core group of four conditions account for over two-thirds of all dyspnoea presentations: Lower Respiratory Tract Infection (LRTI), Heart Failure (HF), COPD, and Asthma (5).
Pulmonary
Causes originating from the lungs, airways, or pleura.
Obstructive: Asthma, COPD Exacerbation.
Infectious: Pneumonia, Acute Bronchitis.
Vascular: Pulmonary Embolism (PE). A classic cause of sudden-onset dyspnoea with pleuritic chest pain.
Parenchymal: Interstitial Lung Disease (ILD).
Pleural/Mechanical: Pneumothorax (air in the pleural space causing lung collapse), Pleural Effusion.
Cardiac
Causes related to the heart's function as a pump or its electrical system.
Pump Failure: Acute Decompensated Heart Failure (ADHF). The heart fails to effectively pump blood forward, leading to a backup of pressure and fluid in the lungs.
Ischaemia: Acute Coronary Syndrome (ACS), where dyspnoea can be the primary presenting symptom, an "anginal equivalent," especially in elderly or diabetic patients.
Mechanical Obstruction: Pericardial Tamponade (fluid in the pericardial sac compressing the heart), Acute Valvular Disease.
Electrical: Tachyarrhythmias or bradyarrhythmias that compromise cardiac output.
Upper Airway Obstruction (Immediate Life-Threats)
A mechanical blockage of the large airways.
Anaphylaxis / Angioedema.
Foreign Body Aspiration.
Epiglottitis.
Other Systemic Causes
Causes from outside the cardiopulmonary system.
Metabolic: Metabolic Acidosis (DKA, salicylate toxicity) causing compensatory Kussmaul breathing.
Haematologic: Severe Anaemia, where reduced oxygen-carrying capacity leads to tissue hypoxia on exertion.
Neuromuscular: Myasthenia Gravis, Guillain-Barré Syndrome, where weakness of the respiratory muscles leads to pump failure.
Psychogenic: Anxiety/Panic Disorder (a diagnosis of exclusion only after all organic causes are ruled out).
Focused Clinical Evaluation
Once immediate life-threats are being addressed, a focused history and physical exam can rapidly narrow the broad list of differentials.
Key Historical Clues
Onset: A truly sudden onset (over seconds to minutes) is highly suggestive of a vascular or mechanical catastrophe like a PE, pneumothorax, or acute myocardial infarction. A more gradual onset (over hours to days) is more typical of an infectious process like pneumonia or a decompensation of a chronic condition like heart failure or COPD (33).
Positional Symptoms:
Orthopnoea: Breathlessness on lying flat is a classic symptom of ADHF. When supine, fluid from the lower extremities and splanchnic circulation is redistributed to the central circulation, increasing pulmonary venous pressure and causing interstitial oedema (34).
Paroxysmal Nocturnal Dyspnoea (PND): Waking from sleep gasping for air is highly specific for ADHF. It shares the same mechanism as orthopnoea but represents a more severe form of fluid intolerance, often occurring after a few hours of sleep as interstitial fluid accumulates to a critical point (34).
Associated Symptoms:
Chest Pain: The character is critical. A sharp, stabbing, pleuritic pain (worse on inspiration) points towards inflammation of the pleura and suggests PE, pneumonia, or pneumothorax. A dull, heavy, crushing central pain suggests ACS (10).
Cough/Sputum: Purulent (yellow/green) sputum is characteristic of a bacterial infection like pneumonia or an acute exacerbation of COPD (AECOPD). Pink, frothy sputum is pathognomonic for severe acute pulmonary oedema, caused by the leakage of red blood cells and plasma fluid into the alveoli under high pressure (37). Haemoptysis (coughing up blood) is a red flag for PE (due to lung infarction), malignancy, or severe infection like tuberculosis.
Unilateral Leg Swelling: In a dyspnoeic patient, this is highly suggestive of a deep vein thrombosis (DVT) and should elevate the suspicion of PE to a very high level, as the leg is the most common source of the embolus (10).
Key Physical Examination Findings
Vital Signs: Pulsus paradoxus (an abnormally large drop in systolic blood pressure >10 mmHg during inspiration) is a specific sign of severe obstructive airway disease (asthma, COPD) or cardiac tamponade. It's caused by exaggerated interventricular dependence within a constrained space (either by hyperinflated lungs or pericardial fluid) (13).
Cardiovascular:
Raised JVP: A key and specific sign of right heart pressure overload and fluid overload, seen in ADHF. It directly reflects the pressure in the right atrium. The hepatojugular reflux (distension of the JVP on liver pressure) indicates the right ventricle cannot accommodate the increased venous return, and is highly specific for ADHF (35).
S3 Gallop: A low-pitched sound in early diastole ("ken-tuc-ky"), representing the tensing of the chordae tendineae during rapid ventricular filling into a stiff, non-compliant ventricle. It is a highly specific sign of heart failure (10).
Muffled Heart Sounds: Suggests that sound transmission is being dampened by fluid in the pericardial sac, raising suspicion for a pericardial effusion or tamponade.
Respiratory:
Wheezing: The high-pitched whistling sound of turbulent airflow through narrowed airways. It is the hallmark of asthma/COPD but can also be heard in ADHF ("cardiac asthma") due to fluid causing bronchial wall oedema and narrowing (10).
Crackles (Rales): Discontinuous "popping" sounds. Fine, bibasilar crackles are characteristic of the alveolar fluid in pulmonary oedema (ADHF), caused by the explosive opening of small airways previously closed by fluid. Coarser crackles may be heard in pneumonia as air moves through secretions (10).
Unilateral Absent Breath Sounds: A critical finding that strongly suggests a large pneumothorax (no lung to transmit sound) or a massive pleural effusion (fluid insulating the sound) (11).
Percussion: Dullness to percussion indicates underlying consolidation (pneumonia) or fluid (pleural effusion), which do not resonate. Hyper-resonance suggests trapped air under pressure, as in a pneumothorax.
Stepwise Investigative Approach
Investigations should not be a "shotgun" approach but must be guided by the clinical assessment to answer specific questions, moving from rapid bedside tests to more definitive studies.
First-Line (Bedside & Immediate)
ECG: Mandatory. It is a critical screening tool for life-threatening cardiac causes. It can reveal evidence of ACS (ST changes), arrhythmias, or signs of acute right heart strain highly suggestive of a significant PE (e.g., the classic S1Q3T3 pattern, new right bundle branch block, or T-wave inversions in the anterior leads V1-V4) (13).
Point-of-Care Ultrasound (POCUS): An invaluable tool that extends the physical exam. A brief, structured exam can answer critical questions in minutes.
Lungs: The presence of normal "lung sliding" (the shimmering of the pleural line with respiration) effectively rules out a pneumothorax at that location. The presence of diffuse, bilateral "B-lines" (vertical, comet-tail artifacts arising from the pleural line) is highly suggestive of an interstitial syndrome, most commonly cardiogenic pulmonary oedema (33).
Heart: A basic cardiac view can quickly assess for a large pericardial effusion, estimate global left ventricular function, and look for signs of right ventricular (RV) strain (a dilated RV that is larger than the LV), which dramatically increases the likelihood of PE (33).
Peak Expiratory Flow Rate (PEFR): In a cooperative patient with suspected obstructive airway disease (asthma or COPD), a PEFR measurement provides an objective measure of the severity of airflow obstruction. Serial measurements are invaluable for assessing the response to bronchodilator therapy (47).
Second-Line (Laboratory & Imaging)
Chest Radiograph (CXR): A portable CXR is a cornerstone of the workup. It is essential for identifying consolidation (pneumonia), signs of pulmonary oedema (cardiomegaly, upper lobe diversion, Kerley B lines, pleural effusions), a pneumothorax, or a large pleural effusion. However, a normal CXR is common in life-threatening conditions like PE, early heart failure, and asthma, so a clear CXR does not rule out serious pathology (13).
Arterial Blood Gas (ABG): This is indicated for patients with severe respiratory distress, suspected hypercapnic respiratory failure (e.g., a drowsy patient with known COPD), or when pulse oximetry is unreliable. It provides definitive information on oxygenation (PaO2), ventilation (PaCO2), and acid-base status, which is crucial for decisions regarding NIV or invasive ventilation. It allows classification of respiratory failure into Type 1 (hypoxic) or Type 2 (hypercapnic) (13).
Blood Tests:
BNP/NT-proBNP: These markers are released from the ventricles in response to myocardial stretch. They have a very high negative predictive value; a normal level makes a diagnosis of ADHF highly unlikely. An elevated level is supportive but not specific, as levels can also be raised in PE, renal failure, and sepsis (13).
D-dimer: This is a fibrin degradation product. Its use is very specific: to help rule out PE in patients who have a low-to-intermediate pre-test probability based on a clinical decision rule (e.g., Wells' score). It should not be ordered in high-probability patients, as a positive result is unhelpful and a negative result is not reliable enough to rule out disease in this group (27).
Troponin: Primarily ordered to rule out ACS. It is important to note that troponin can also be elevated due to myocardial strain from other severe conditions, including massive PE or severe sepsis, so an elevated level must be interpreted in context.
Third-Line (Definitive)
Computed Tomography Pulmonary Angiogram (CTPA): This is the gold-standard imaging modality for diagnosing pulmonary embolism. It requires a stable patient and adequate renal function to tolerate intravenous contrast (27).
Formal Echocardiography: Provides a comprehensive evaluation of cardiac structure, valvular function, and pressures. It is essential for the definitive diagnosis and management of heart failure and for assessing the haemodynamic impact of a PE (13).
Management: Resuscitation and Definitive Care
Management is a two-phase process: immediate resuscitation to stabilize physiology, followed by definitive, diagnosis-driven treatment.
Initial Emergency Management (The ABCs)
This physiology-based approach should be initiated immediately for any patient in significant distress, often before a definitive diagnosis is made.
A - Airway: Ensure a patent airway. Use simple manoeuvres or adjuncts. Be prepared for early endotracheal intubation if the airway is threatened by swelling, secretions, or a deteriorating GCS.
B - Breathing:
Oxygenation: Administer high-flow oxygen to maintain SpO2 92-96%. A critical exception, emphasized in Malaysian guidelines, is for patients with known or suspected COPD. In these individuals, who may be chronic CO2 retainers, high oxygen concentrations can worsen V/Q mismatch and suppress their hypoxic respiratory drive. Therefore, a lower target saturation of 88-92% should be aimed for, ideally using a controlled-delivery device like a Venturi mask (49, 55).
Ventilation: Support the work of breathing with Non-Invasive Ventilation (NIV) early.
CPAP: Highly effective for acute cardiogenic pulmonary oedema. It increases intrathoracic pressure, which reduces venous return (preload) and systemic vascular resistance (afterload), while also recruiting collapsed, fluid-filled alveoli to improve oxygenation (62).
BiPAP: The preferred mode for patients with hypercapnic respiratory failure, most notably in AECOPD. It provides a higher pressure during inspiration (IPAP) to assist ventilation and a lower pressure during expiration (EPAP) to prevent alveolar collapse. It is proven to reduce the need for intubation and mortality (55).
C - Circulation: Secure large-bore intravenous (IV) access promptly and place the patient on a continuous cardiac monitor. Treat hypotension based on the suspected cause (e.g., fluids in sepsis, vasopressors in cardiogenic shock).
Positioning: Sit the patient upright. This simple yet effective intervention uses gravity to improve lung expansion, reduce the pressure of abdominal contents on the diaphragm, and, in heart failure, decrease venous return to the heart (61).
Diagnosis-Specific Definitive Management
Acute Severe Asthma (MOH CPG 2017):
Core treatment: Rapid and repeated administration of inhaled short-acting β2-agonists (SABA, e.g., Salbutamol) and a short-acting muscarinic antagonist (SAMA, e.g., Ipratropium Bromide), plus early systemic corticosteroids (IV Hydrocortisone or Oral Prednisolone) to reduce airway inflammation (49).
For non-responders, IV Magnesium Sulphate (1.2-2g over 20 mins) can act as a bronchodilator by relaxing smooth muscle. Escalate to seniors/ICU early (49).
AECOPD (MOH CPG 2nd Ed):
Key interventions: Controlled oxygen (target 88-92%), inhaled bronchodilators, and systemic corticosteroids (55).
Antibiotics are indicated for patients meeting the Anthonisen criteria for a bacterial infection: an increase in sputum purulence plus one other symptom (increased dyspnoea or sputum volume) (55).
NIV (BiPAP) is strongly recommended for persistent acute hypercapnic respiratory failure (respiratory acidosis with a pH < 7.35).
Acute Decompensated Heart Failure (ADHF):
For the common "wet and warm" patient, use IV loop diuretics (Furosemide) to remove excess fluid and vasodilators (IV Glyceryl Trinitrate) to reduce both preload and afterload, thereby decreasing the workload on the failing heart (70).
Identify and treat the precipitant (mnemonic CHAMP: ACS, Hypertension Emergency, Arrhythmia, Acute Mechanical Cause, PE) (57).
Pulmonary Embolism (PE):
Anticoagulate immediately on high clinical suspicion (e.g., with Low Molecular Weight Heparin) unless there are absolute contraindications (27).
Massive PE (unstable): This is a true emergency. The definitive treatment is reperfusion therapy with systemic thrombolysis (e.g., alteplase) to dissolve the clot.
Submassive/Low-Risk PE (stable): For these patients, anticoagulation alone is the standard of care to prevent further clotting (27).
Palliative Management of Refractory Dyspnoea
For a significant subset of patients with end-stage COPD, heart failure, or advanced malignancy, the underlying disease is irreversible. The goal of treatment shifts from curative to palliative, focusing on the relief of suffering.
Non-Pharmacological (First-Line):
Fan Therapy: A handheld fan directed towards the cheeks and nose is a remarkably effective, evidence-based intervention. It stimulates cold receptors in the distribution of the trigeminal nerve, which is thought to centrally modulate and reduce the sensation of breathlessness (63).
Positioning: The upright, forward-leaning "tripod" position optimizes the mechanics of the diaphragm and accessory muscles, reducing the work of breathing.
Breathing Techniques: Pursed-lip breathing (inhaling through the nose and exhaling slowly through pursed lips) creates back-pressure that keeps airways open longer, reduces dynamic hyperinflation, and gives the patient a sense of control.
Pharmacological:
Low-Dose Opioids: Morphine is the gold-standard pharmacological treatment for refractory dyspnoea at the end of life. It does not improve respiratory mechanics but acts on μ-opioid receptors in the central nervous system to reduce the brain's perception of "air hunger." Doses should be started low (e.g., oral morphine solution 2.5 mg) and titrated slowly. It is crucial to overcome "opiophobia"; when used appropriately, it is a safe and humane treatment that does not hasten death (63).
Benzodiazepines: These drugs do not directly treat dyspnoea but can be a useful adjunct to treat the severe anxiety and panic component that often creates a vicious cycle of worsening breathlessness (74).
Conclusion: Key Take-Home Messages
Systematic, Not Scattered: Dyspnoea is a symptom, not a diagnosis. A chaotic approach is dangerous. Adhere to a structured primary survey (ABC), followed by a focused history and physical examination to build a logical differential diagnosis. This systematic process is your greatest defense against diagnostic error.
Recognise Red Flags: Your first and most important job is to keep the patient alive. Be hyper-vigilant for the signs of impending respiratory collapse. When these are present, act first and diagnose later.
Know Your Guidelines: The Malaysian Ministry of Health has produced excellent, evidence-based Clinical Practice Guidelines for the management of Asthma and COPD. These are your roadmap for managing two of the most common and high-risk causes of dyspnoea you will encounter.
Think Beyond the Lungs: Not all that wheezes is asthma, and not all dyspnoea is a primary lung problem. Always maintain a broad differential diagnosis that includes cardiac, vascular, and systemic etiologies to avoid premature diagnostic closure.
Don't Forget Palliation: For patients with advanced, irreversible disease, the goal must shift from cure to comfort. Learn to recognize when this shift is appropriate and master the simple, powerful interventions that can relieve the profound suffering of refractory breathlessness.
By internalizing these principles, the junior clinician can approach the dyspnoeic patient not with fear, but with a quiet confidence born of a structured, knowledgeable, and compassionate methodology.
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