How to Approach Dyspnea: A Practical Guide to Diagnosing Shortness of Breath

“Doctor, this patient is really struggling to breathe!”
Such a comment often marks the beginning of an urgent clinical encounter.
Dyspnea is a common and potentially life-threatening symptom encountered in both emergency and outpatient settings.
However, normal SpO₂ does not always guarantee safety—appearances can be deceiving.

This article explores the underlying causes of dyspnea from a symptom-based perspective, covering everything from acute versus chronic onset to differential diagnosis and treatment strategies including NPPV.
It also highlights practical tips for history-taking, physical examination, and time-efficient evaluation strategies that are frequently tested in OSCEs.
Whether you are a medical student or a junior resident, this is your go-to guide for confidently managing patients with shortness of breath.

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✅ What You Will Learn from This Article

• How to assess dyspnea in real-time: Learn a structured framework for taking history and performing physical exams using OPQRST and PAM HITS FOSS to differentiate between acute and chronic cases—and spot key signs like orthopnea and cyanosis.
• How to distinguish common causes of dyspnea: Understand the clinical clues for asthma, pneumonia, COPD, and hyperventilation syndrome using symptoms, auscultation, SpO₂, imaging, and ABG results.
• How to evaluate severity and choose appropriate interventions: Master decision-making strategies including red flag detection, NPPV indications, and early recognition of conditions like CO₂ narcosis and silent chest.

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🩺 Case Introduction: The Patient Who “Can’t Breathe”

🪪 Doorway Information

• Age/Gender: 65-year-old female
• Chief Complaint: “I feel short of breath.”
• Vital Signs: Temp 37.8°C, HR 112 bpm, RR 26/min, BP 118/64 mmHg, SpO₂ 93% (room air)
• First Impression: Sitting in a tripod position, speaking in short phrases, mild wheezing on auscultation

🗣 Patient’s Words

“It suddenly became hard to breathe last night… I couldn’t sleep unless I was sitting up. Lying down made my cough worse.”

So—how would you approach this patient from the very first moment? In the following sections, we’ll walk through a step-by-step strategy to analyze dyspnea based on this case, starting from initial impression to structured clinical reasoning.

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🤔 How to Think When You See Dyspnea: Is It Really the Lungs?

When a patient says, “I can’t breathe,” our instinct may be to think of lung disease—but that’s not always the case. Dyspnea is a complex symptom that can result from many different organ systems.

Here’s a broad overview of common causes:

• Pulmonary: Asthma, COPD, pneumonia, pneumothorax
• Cardiac: Heart failure, pulmonary embolism, acute myocardial infarction
• Metabolic/Hematologic: Acidosis, anemia, carbon monoxide poisoning
• Neuromuscular: ALS, myasthenia gravis, obesity hypoventilation syndrome (OHS)
• Psychogenic/Functional: Hyperventilation syndrome, panic disorder
• Chest wall/musculoskeletal: Rib fracture, costochondritis, slipping rib syndrome

So the first question to ask is: “Is the problem truly in the lungs?” Keeping an open differential is the crucial first step in approaching dyspnea.

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Step 1: Assess the Severity First

Before jumping to a diagnosis, evaluate the urgency. Look for signs that demand immediate intervention:

• SpO₂ < 92%
• RR > 25/min
• Inability to speak full sentences
• Tripod position, orthopnea, drowsiness (possible CO₂ narcosis)
• “Silent chest” or severe accessory muscle use

If any of these are present, oxygen therapy, arterial blood gas (ABG), or even NPPV may be urgently needed.

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Step 2: Structure Your Differential Thought Process

Once severity is assessed, start categorizing the possible causes:

• Is it primarily respiratory? Or could it be cardiac, neuromuscular, or psychogenic?
• Is it acute or chronic? (Did it start minutes ago? Or over months?)
• Is there chest pain or tenderness? Suggesting a chest wall etiology?

This mindset—avoiding tunnel vision on the lungs while scanning for life-threatening red flags—is the foundation of a strong clinical approach to dyspnea.

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📝 Step 1: History Taking for Dyspnea – OPQRST and PAM HITS FOSS

The first step in evaluating dyspnea is to clarify “what kind of breathlessness the patient is experiencing.”
Using the OPQRST and PAM HITS FOSS frameworks helps uncover key clues for narrowing the differential.

🔍 OPQRST – Symptom Characteristics

• Onset: Sudden (e.g., PE, pneumothorax) or gradual (e.g., pneumonia, heart failure)? During rest or exertion?
• Provocation/Palliation: Worse when lying flat (orthopnea)? Triggered by movement, speaking, or inhaling?
• Quality: “Can’t inhale,” “tightness,” “choking,” or “with chest pain”?
• Region/Radiation: Chest? Back? One-sided or diffuse?
• Severity: Can they talk in full sentences?
• Timing: Intermittent or constant? Worse at night or early morning?

Particularly, sudden onset dyspnea should prompt suspicion of PE, pneumothorax, asthma attack, or AMI.

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🩺 PAM HITS FOSS – Underlying Risks

• P: Past medical history – asthma, COPD, heart failure, anxiety
• A: Allergies – atopic history, risk of anaphylaxis
• M: Medications – beta-blockers (asthma trigger), chemotherapy (ILD)
• H: Hospitalizations – pneumonia, PE, recent surgery
• I: Injury – chest trauma, rib fracture
• T: Trauma/Surgery – pleural drainage, postoperative PE
• S: Surgeries – anesthesia complications, respiratory muscle weakness
• F: Family history – asthma, thrombophilia, inherited lung disease
• O: OB/GYN – pregnancy increases PE risk
• S: Sexual history – HIV risk (PJP)
• S: Social history – smoking, drug use, occupational dust, stress, sleep pattern

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💡 Column: Avoiding Miscommunication About “Breathlessness”

When a patient says, “I feel tight in my chest,” don’t immediately assume it’s chest pain. It could mean:

• “Can’t breathe well” = dyspnea
• “Feels stuck in the throat” = globus sensation or anxiety
• “Choking” = aspiration or dysphagia

Follow up with questions like:

• “Is it harder to breathe in or breathe out?”
• “Do you feel like you’re breathing fast?”

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🛠 Tips: 5 Clues You Don’t Want to Miss in the History

1. “Suddenly”: Think PE, pneumothorax, asthma exacerbation
2. “Worse lying down”: Orthopnea → Suggests heart failure
3. “Can’t take a deep breath”: Chest wall pain, rib fracture, herpes zoster
4. “Feeling faint”: Severe hypoxia or CO₂ narcosis
5. “Stress makes it worse”: Hyperventilation syndrome or psychogenic dyspnea

History-taking is not just about collecting data—it’s about catching red flags early and guiding efficient next steps.

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🩻 Step 2: Physical Examination for Dyspnea – What to Look, Listen, and Feel

Now that we’ve built a working differential from the history, the physical exam is your chance to test those hypotheses. Don’t just focus on the lungs—dyspnea may reveal itself through signs across the entire body.

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👀 General Appearance: First Impressions Can Be Lifesaving

• Posture: Tripod position, sitting upright = respiratory distress
• Speech: Inability to speak full sentences = moderate to severe dyspnea
• Facial expression or mental status: Somnolence, agitation, confusion = possible CO₂ narcosis
• Skin findings: Cyanosis, diaphoresis, rashes (e.g., herpes zoster)

These signs help determine whether oxygen therapy, NPPV, or even intubation is immediately needed.

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🫁 Lung Auscultation: It’s Not Just About “Clear or Not”

Be sure to evaluate:

• Wheezing: Asthma, COPD, anaphylaxis
• Crackles (rales): Pneumonia, heart failure, interstitial lung disease
• Stridor: Upper airway obstruction, laryngeal edema, foreign body
• Diminished or absent breath sounds: Pneumothorax, atelectasis, silent chest

Always check for asymmetry. Unilateral changes may indicate pneumothorax, foreign body, or lobar consolidation.

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🫀 Beyond the Lungs: Clues from the Neck, Legs, Chest, and Heart

• Neck veins: Jugular venous distension = heart failure, tension pneumothorax
• Lower limbs: Edema or signs of DVT → suspect PE
• Chest wall: Bruising or tenderness → rib fracture, herpes zoster
• Pulses and heart sounds: Tachycardia, muffled heart sounds, arrhythmia

A whole-body approach prevents missing non-pulmonary causes of dyspnea and helps triage severity.

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🛠 Tips: Interpreting What You Hear

• Silent chest ≠ normal: It may mean airflow is too limited to generate sound—an emergency in severe asthma
• Stridor + “choking gesture”: Possible upper airway obstruction
• Crackles + orthopnea: Think heart failure
• Unilateral decreased breath sounds: Rule out pneumothorax or atelectasis

The physical exam is your chance to rapidly rule in or rule out dangerous conditions.
Use your senses—and your clinical intuition—wisely.

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🧪 Step 3: Investigations & Imaging for Dyspnea – ABG, CXR, and Beyond

Once you’ve formed a working differential based on the history and physical exam, it’s time to order targeted investigations.
The goal isn’t to “run all the labs”—but rather, to ask: “What do I want to confirm or rule out with this test?”

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🔬 1. Blood Tests: Infection, Heart Failure, Clotting, and Metabolic Clues

• CRP/WBC: Infection (e.g., pneumonia)
• BNP: Suggestive of heart failure (adjust for age & renal function)
• D-dimer: PE screening in low-risk patients (use with pretest probability)
• Lactate: Indicates poor perfusion (e.g., sepsis, shock)
• Electrolytes & BUN/Cr: Assess acid-base status, dehydration, uremia

💡 Remember: SpO₂ can be normal even in severe anemia—always consider oxygen delivery (DO₂ = CaO₂ × CO × 10).

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🩸 2. Arterial Blood Gas (ABG): Direct Measurement of Oxygenation & Ventilation

• PaO₂ < 60 mmHg: Defines hypoxemic respiratory failure
• PaCO₂ > 45 mmHg: Suggests ventilatory failure (type II)
• pH: Helps identify acid-base imbalance (respiratory vs metabolic)

📘 Definition of Respiratory Failure

• Type I (Hypoxemic): PaO₂ < 60, PaCO₂ normal or low (e.g., pneumonia, PE)
• Type II (Hypercapnic): PaO₂ < 60, PaCO₂ elevated (e.g., COPD, neuromuscular)

🧠 Type II often needs NPPV and careful oxygen titration—beware of CO₂ narcosis.

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🖼 3. Chest X-ray (CXR): The Initial Imaging for Most Patients

• Infiltrates: Pneumonia, pulmonary edema (butterfly shadow)
• Hyperlucency: Pneumothorax, PE
• Opacification: Pleural effusion, atelectasis
• Cardiomegaly: Heart failure, pericardial effusion

Always compare both sides—unilateral abnormalities (e.g., effusion, pneumothorax) are key clues.

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🔍 4. Chest CT and Contrast-Enhanced CT

• CT Angiography: Definitive test for pulmonary embolism
• HRCT: Best for interstitial lung disease, PJP, drug-induced lung injury

⚠️ Before CT: Always review renal function and allergy history due to contrast risk.

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🫠 5. POCUS (Point-of-Care Ultrasound): Fast, Bedside, High-Yield

• B-lines: Suggest pulmonary edema, interstitial involvement
• Pleural effusion: Detect even small amounts
• IVC diameter: Assesses fluid status or right heart strain
• Cardiac echo: Evaluate EF, RV dilation, tamponade

🎯 When breath sounds are unclear, POCUS can be a game changer.

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🧠 Clinical Thinking: How to Choose Tests Wisely

• Ask: “What do I want to confirm or exclude with this test?”
• Use normal findings to rule out disease (e.g., low BNP → heart failure less likely)
• Interpret results in context: history, exam, and overall picture

By the end of this phase, you should have a refined diagnosis—or at least a clear direction for management.

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🧑‍⚕️ Case Review – Applying Steps 1–3 to the 65-Year-Old Patient

Now that we’ve walked through Steps 1 to 3, let’s apply them to our initial case of the 65-year-old woman with shortness of breath.

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📝 Step 1: History Taking

Doctor: “What brought you in today?”

Patient: “It suddenly became hard to breathe last night… I couldn’t sleep unless I was sitting up. I also started coughing, and lying down made it worse.”

Hmm… acute onset with orthopnea? Could be heart failure, an asthma exacerbation, or even pneumonia. The fact that her symptoms worsen when lying down makes me think of a circulatory cause too.

OPQRST Highlights:

• Onset: Sudden, began last night
• Provocation: Worsens when lying down, improves when sitting
• Quality: “Feels like I can’t get air in”
• Severity: Can’t talk in full sentences

PAM HITS FOSS Revealed:

• Past history: Hypertension, diabetes
• Medications: Beta-blocker noted
• Smoking: 20 pack-year history
• No history of asthma or known COPD

🔎 Summary:

• Fact: Acute dyspnea + orthopnea + fever + cough
• Problem: Moderate to severe dyspnea with positional dependence
• Hypotheses: Heart failure, pneumonia, PE, COPD/asthma exacerbation, hyperventilation syndrome

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🩺 Step 2: Physical Examination

Okay, she’s sitting forward, in tripod position. SpO₂ is 93%, RR is 26. She’s using accessory muscles—definitely working to breathe.

• Speech: Short phrases only
• Facial signs: Mouth breathing, visible distress
• Auscultation: Bilateral wheezing and coarse crackles
• Neck: Mild jugular venous distension
• Extremities: Mild leg edema

The wheezes could point to COPD or asthma, but those crackles make me wonder about fluid overload or infection. No silent chest—so at least airflow is preserved.

JVD and edema make heart failure plausible, but the beta-blocker and smoking history make me lean toward COPD exacerbation—possibly triggered by infection.

🧠 Combined Impression:

Likely COPD exacerbation + superimposed infection, possibly with elements of heart failure

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🧪 Step 3: Investigations

Her vitals and physical signs suggest we may be dealing with type II respiratory failure. Better get an ABG.

• ABG: PaO₂ 58 mmHg, PaCO₂ 48 mmHg → Type II respiratory failure
• BNP: 250 pg/mL → Possible heart strain
• CRP: 6.2 mg/dL → Evidence of infection
• CXR: Bilateral hilar infiltrates + signs of hyperinflation
• POCUS: IVC shows poor variability, echo shows preserved EF

CO₂ is up and pH might be borderline. Definitely need to think about NPPV. Diagnosis? Most likely an infectious COPD exacerbation causing type II respiratory failure. Heart failure may be contributing too.

✅ Conclusion:

Infectious COPD exacerbation with type II respiratory failure, possibly with mild fluid overload. NPPV should be considered early. Oxygen therapy must be carefully titrated to avoid worsening hypercapnia.

By carefully applying Steps 1 through 3, we’ve translated a vague complaint—“I can’t breathe”—into a working diagnosis and an initial management plan.

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🧑‍⚕️ When to Refer – Specialist Consultation and What You Can Do First

Not all patients with dyspnea need to be referred immediately. However, certain clinical findings indicate the need for prompt specialist evaluation—especially when respiratory failure or life-threatening conditions are suspected.

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🚨 When to Refer Immediately

• SpO₂ remains below 90% despite oxygen therapy
• Respiratory rate > 30/min, severe respiratory effort
• Altered mental status suggesting CO₂ narcosis (type II respiratory failure)
• “Silent chest” or extreme fatigue → impending respiratory collapse
• Suspected acute heart failure, pulmonary embolism, or unclear etiology with abnormal imaging

📦 Information to Prepare Before Referral:

• Vital signs: SpO₂, RR, FiO₂ or oxygen flow rate
• Imaging: Chest X-ray or CT findings
• ABG results: PaO₂, PaCO₂, pH, HCO₃⁻
• Past history: Including inhalers, steroids, recent infections
• Swallowing evaluation (e.g., VFSS), functional status, caregiver needs

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🧰 What You Can Do as a Primary Care or ER Doctor

💨 Managing Suspected Respiratory Failure

• Oxygen target: SpO₂ ≥ 95% in most cases
• In high CO₂ risk patients (e.g., COPD): Titrate slowly to SpO₂ 90–92%
• Consider NPPV early: Especially in type II failure with preserved consciousness

🍽 ABCDE Approach for Aspiration Pneumonia

• A – Airway: Evaluate for suction needs, aspiration risk
• B – Bacteria: Select antibiotics appropriately with help from NST
• C – Consciousness & Care: Oral care (OHAT score), consider dental referral
• D – Dysphagia: Bedside screening, VFSS with speech therapists if needed
• E – Eating & Environment: Nutritional team input, caregiver education

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🔍 Don’t Miss These Non-Respiratory Causes of Dyspnea

• Rib fracture, costochondritis, herpes zoster
• Paradoxical breathing: Neuromuscular disease or exhaustion
• Inspiratory stridor: Upper airway obstruction (e.g., anaphylaxis, foreign body)

Family physicians are uniquely positioned to recognize non-pulmonary causes of dyspnea and to coordinate early multidisciplinary care.

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🌬 Asthma, COPD, and ACO – Key Differences and Inhaler Strategies

In patients with dyspnea, distinguishing between asthma, COPD, and asthma-COPD overlap (ACO) is essential. These conditions may appear similar but require very different management strategies.

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🧬 Core Differences

• Asthma: Onset often in childhood or adolescence, associated with allergies, reversible airflow limitation, nighttime symptoms
• COPD: History of smoking (>25 pack-years increases risk), irreversible and progressive dyspnea on exertion
• ACO: Mixed features of both asthma and COPD, typically requires inhaled corticosteroids

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💊 Inhaler Choices and Stepwise Therapy

• Asthma: Start with ICS; escalate to ICS/LABA in moderate to severe cases. Use SABA as a reliever.
• COPD: Begin with LABA or LAMA. Consider ICS only if eosinophils are elevated or exacerbations are frequent.
• ACO: Combine ICS + LABA ± LAMA from the outset

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⚠️ Inhaler Contraindications and Cautions

• LAMA: Use with caution in patients with glaucoma or prostatic hyperplasia
• ICS: Risk of hoarseness and oral candidiasis → instruct patients to rinse mouth after use
• LABA: May cause palpitations or tremors in sensitive patients

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💡 Tip: SMART Therapy (Single Maintenance and Reliever Therapy)

Using a single inhaler like Symbicort (ICS + formoterol) both as maintenance and reliever reduces exacerbations and empowers patient self-management.
Number of daily uses can reflect symptom control.

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📈 Recognizing and Responding to Exacerbations

Definition: An acute worsening of symptoms requiring SABA or oral steroids

• Asthma Exacerbation:
  • Mild (SpO₂ > 95%): SABA alone
  • Moderate (SpO₂ 90–95%): SABA + ICS/LABA
  • Severe (SpO₂ < 90%, silent chest): IV steroids, consider NPPV or ICU transfer
• COPD Exacerbation – ABC Remedy:
  • A: Anticholinergics (SAMA or LAMA)
  • B: Beta-agonists (SABA or LABA)
  • C: Corticosteroids (short course of oral steroids)

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🧮 Pack-Year Matters

A smoking history of more than 25 pack-years significantly increases COPD risk, as supported by large cohort studies (e.g., NEJM, Lange et al.). Always quantify smoking exposure during history-taking.

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📚 NPPV Essentials – When and How to Use Non-Invasive Ventilation

NPPV (Non-invasive Positive Pressure Ventilation) supports ventilation without the need for endotracheal intubation. It’s a vital tool for managing respiratory failure—especially when oxygen alone isn’t enough.

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✅ Common Indications

• COPD exacerbation with type II respiratory failure: CO₂ retention + acidosis (pH ↓)
• Cardiogenic pulmonary edema: Improves oxygenation and reduces preload
• Hypoxemic respiratory failure in immunocompromised patients: Helps avoid intubation

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⛔ When to Avoid or Use with Caution

• Decreased consciousness or agitation (risk of aspiration or poor compliance)
• Excessive secretions, vomiting, or poor cough reflex
• Facial trauma, post-op facial surgery → poor mask fit

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🧪 Oxygen vs NPPV: What’s the Difference?

• Oxygen therapy: Raises FiO₂ (oxygen concentration)
• NPPV: Adds positive pressure to support alveolar ventilation and reduce work of breathing. Also helps eliminate CO₂.

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🧠 NPPV Modes and Their Clinical Uses

Mode	Description	Main Indications
BiPAP	Two levels: IPAP (inspiratory) and EPAP (expiratory)	COPD exacerbation, type II respiratory failure
CPAP	Continuous positive pressure throughout respiratory cycle	Cardiogenic pulmonary edema, OSA
Nasal High Flow	High-flow, humidified O₂ via nasal cannula (up to 60 L/min)	Hypoxemic respiratory failure, immunocompromised patients

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💡 Tips for Practical NPPV Use

• High CO₂ = BiPAP, Heart failure = CPAP, Mild hypoxia = High Flow
• Reassess ABG after 30–60 minutes to evaluate response
• Avoid excessive oxygen in CO₂-retaining patients (SpO₂ goal: 88–92%)

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🧪 Starting Settings for BiPAP

• IPAP: 10–15 cmH₂O
• EPAP: 4–6 cmH₂O
• Target SpO₂: 88–92%

If pH or PaCO₂ does not improve after several hours, consider intubation and invasive ventilation.

Understanding indications, contraindications, and early ABG monitoring will help you decide whether NPPV is appropriate—and avoid missing the window for escalation.

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🩺 Tips & Clinical Pearls for Assessing Dyspnea

🛠 Practical Tips – What Not to Miss

• Can the patient talk? – If they can only speak in single words or phrases, it’s at least moderate dyspnea.
• Organize your OPQRST findings: Pay close attention to onset, triggers, and posture.
• Auscultation tips: Listen for asymmetry, prolonged expiration, or stridor—don’t ignore “silent chest.”
• Red flags: Cyanosis, use of accessory muscles, orthopnea, paradoxical breathing
• SpO₂ can lie: Watch for CO₂ retention or silent hypoxia (e.g., in COVID-19)
• Don’t stop at CXR: If PE or interstitial lung disease is suspected, go further with CT
• Use POCUS wisely: Especially helpful when breath sounds are faint or absent

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💬 Clinical Pearl

“Dyspnea is to the lungs what chest pain is to the heart. It deserves the same urgency and systematic evaluation.”

― Dr. Louise Cullen, Emergency Physician, Australia

Dyspnea may seem nonspecific, but like chest pain, it can signal deadly conditions.
A structured approach will help you avoid anchoring bias and truly narrow the diagnosis.

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🗣️ OET Speaking Session – Dyspnea (Shortness of Breath)

👥 Scenario

You are a doctor in an emergency department. A 65-year-old woman presents with sudden onset of breathlessness since last night. She reports that she couldn’t sleep lying down and feels exhausted. She has a history of hypertension and a 20 pack-year smoking history.

You suspect an acute exacerbation of COPD possibly complicated by infection or mild heart failure. Her SpO₂ is 93% on room air. She is alert but visibly struggling to breathe.

🎯 Your Task

• Explain the possible causes of her breathlessness
• Discuss the need for further tests such as ABG and chest imaging
• Reassure her and respond to emotional concerns
• Explain the treatment plan including oxygen and possibly NPPV

💬 Sample Statements You Can Use

• “Your symptoms could be related to a flare-up of a chronic lung condition. We also want to make sure there’s no infection or heart issue involved.”
• “We’ll start by giving you some oxygen and do a few tests to check your lung function and blood gases.”
• “Your condition is stable, but we’ll continue to monitor you closely and may use a non-invasive breathing support mask if needed.”
• “Let us know if you feel more anxious or if your breathing becomes more difficult—we’re here to help.”

💬 Common Patient Cues & Sample Doctor Responses

🧠 Challenging Questions & Sample Doctor Responses

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✉️ OET Writing Task – Sample Referral Letter

Today’s Date

Dr. Rachel Lee
Respiratory Medicine
Central Medical Hospital

Re: Ms. Naomi Tanaka, 65 years old

Dear Dr. Lee,

I am referring Ms. Naomi Tanaka, a 65-year-old woman, for further assessment and management of acute dyspnea suspected to be an exacerbation of chronic obstructive pulmonary disease (COPD), possibly with superimposed infection and early features of heart failure.

She presented to our emergency department with sudden onset of breathlessness that began last night. She reports orthopnea and difficulty sleeping due to respiratory discomfort. Her vital signs were: Temp 37.8°C, RR 26, HR 112 bpm, BP 118/64 mmHg, and SpO₂ 93% on room air. She was alert but in moderate distress, using accessory muscles to breathe.

On auscultation, she had bilateral wheezes and coarse crackles. Her past medical history includes hypertension and type 2 diabetes. She has a 20 pack-year smoking history. She is currently on amlodipine and metformin. No known asthma or established COPD diagnosis is documented.

ABG showed type II respiratory failure (PaO₂ 58 mmHg, PaCO₂ 48 mmHg), and CXR revealed bilateral hilar infiltrates and hyperinflation. BNP was 250 pg/mL and CRP 6.2 mg/dL. She was started on oxygen therapy, inhaled bronchodilators, and empiric antibiotics. NPPV is being considered based on her gas exchange and respiratory effort.

I would appreciate your further evaluation and input regarding long-term diagnosis, treatment optimization, and the need for respiratory rehabilitation or outpatient follow-up.

Kind regards,

Dr. [Your Name]
Emergency Physician

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🧾 Summary & Take-Home Message

Dyspnea is a symptom that crosses organ systems and specialties. It can result from pulmonary, cardiac, neuromuscular, metabolic, or even psychiatric causes. That’s what makes it both challenging and clinically rich.

In this article, we emphasized that the key to diagnosing dyspnea is not simply having knowledge—but knowing how to apply it:

• 📝 History: Use OPQRST and PAM HITS FOSS to understand timing, severity, and risk factors.
• 🩺 Examination: Don’t just listen—observe posture, speech, effort, and look beyond the lungs.
• 🧪 Investigations: Use tests like ABG and imaging purposefully. Define what you want to confirm or exclude.

Above all, never forget to ask: “Is this really the lungs?”—because the most dangerous diagnosis is the one you didn’t think of.

We hope this guide empowers you to face dyspnea with confidence in any clinical setting—from the bedside to the OSCE.

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🔗 Related Articles

• How to Approach Fever – More Than Just a Cold?
• Chronic Cough – Diagnostic Strategies for Acute vs Chronic Cases
• Pleural Effusion – Infection, Malignancy, or Heart Failure?
• Hemoptysis – From History to CT Imaging
• Chest Pain – Clinical Reasoning with POCUS
• Syncope – How to Identify Transient Loss of Consciousness
• 【日本語版】呼吸困難の診かた｜急性・慢性の鑑別とNPPVの判断まで

🩺 Looking to practice realistic cases in English?
Check out our Mock Patient Scripts for Dyspnea—featuring 3 practical scenarios for OSCE and OET training.

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📚 References

1. Japanese Respiratory Society. Asthma Prevention and Management Guidelines 2021. Nankodo.
2. GOLD 2024 Report: Global Strategy for the Diagnosis, Management, and Prevention of COPD. https://goldcopd.org/
3. Ministry of Health, Labour and Welfare. Guidelines for Aspiration Pneumonia (2nd Edition). March 2020.
4. Itō K, et al. How to Assess Dyspnea. Journal of the Japanese Society of Internal Medicine. 2022;111(3):561–566.
5. Tanaka Y. Practical Use of NPPV and HFNC in Respiratory Medicine. Resp Med. 2020;37(5):471–479.
6. Pratter MR. Overview of Common Causes of Dyspnea. Respir Care. 2003;48(12):1204–1213.
7. Cullen L, Greenslade J. Dyspnea: A Red Flag Not to Ignore. Emerg Med Australasia. 2019;31(2):234–238.
8. Lange P, et al. Lung Function Trajectories Leading to Chronic Obstructive Pulmonary Disease. N Engl J Med. 2015;373:111–122.