Today i have lecture in my ward on the topic of symptomatology of resp

Today i have lecture in my ward on the topic of symptomatology of respiratory system. Explain the different symptomatology and how do we differentiate it from symptoms of other system

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respiratory symptoms AND differential diagnosis

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Merck Manual professional symptoms respiratory disorders cough dyspnea hemoptysis chest pain wheeze stridor

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https://www.merckmanuals.com/professional/pulmonary-disorder…

Symptomatology of the respiratory system

The principal respiratory complaints are cough, sputum production, dyspnea, wheeze, stridor, chest pain, and hemoptysis. In clinical practice, the two most common are cough and breathlessness. - Fishman’s Pulmonary Diseases and Disorders, p. 394

A respiratory symptom is not automatically caused by lung disease. The key is to characterize it carefully, look for associated respiratory signs, and actively exclude cardiac, upper-airway, gastrointestinal, hematologic, and psychogenic causes.

1. Cough

Definition: A protective expiratory reflex that clears secretions or foreign material from the airways.

Ask about

Duration: acute (<3 weeks), subacute (3-8 weeks), chronic (>8 weeks)
Dry or productive
Timing: nocturnal, early morning, seasonal, post-meal, with exertion
Triggers: cold air, dust, smoke, lying flat, exercise
Associated symptoms: fever, nasal symptoms, wheeze, reflux, weight loss, hemoptysis

Respiratory causes

Acute respiratory infection, pneumonia
Asthma or COPD
Bronchiectasis
Tuberculosis
Interstitial lung disease
Lung cancer
Postnasal drip / upper-airway cough syndrome

Differentiation from other systems

Alternative system	Clues favoring it rather than primary lower respiratory disease
ENT / upper airway	Nasal blockage, sneezing, throat clearing, postnasal drip, sinus pain
Gastrointestinal	Cough after meals or when lying down, heartburn, sour regurgitation, hoarseness: consider GERD
Cardiovascular	Nocturnal cough with orthopnea, paroxysmal nocturnal dyspnea, leg edema: consider left heart failure
Drug-related	Dry persistent cough after starting an ACE inhibitor
Psychogenic / habit cough	Often absent during sleep, variable and distractible, diagnosis only after organic disease is excluded

Sputum helps localize the problem

Mucoid or white: viral illness, asthma, chronic bronchitis
Yellow/green: airway inflammation or infection, but does not by itself prove bacterial infection
Copious purulent, foul-smelling: bronchiectasis, lung abscess, anaerobic infection
Rust-colored: classically pneumococcal pneumonia
Pink frothy: pulmonary edema
Blood-streaked: airway inflammation, TB, malignancy, pulmonary embolism, etc.

2. Dyspnea (shortness of breath)

Definition: Subjective uncomfortable awareness of breathing or breathing effort.

Ask the patient to describe it in their own words:

“Cannot get enough air”
“Chest tightness”
“Breathing takes effort”
“Cannot breathe when lying flat”

Respiratory patterns

Acute dyspnea: asthma exacerbation, COPD exacerbation, pneumonia, pneumothorax, pulmonary embolism, upper-airway obstruction, acute respiratory distress.
Chronic/progressive dyspnea: COPD, asthma, interstitial lung disease, pleural effusion, pulmonary hypertension, lung cancer.
Exertional dyspnea: COPD, interstitial disease, pulmonary vascular disease, anemia, heart disease, deconditioning.
Episodic dyspnea with wheeze/chest tightness: asthma is likely, though not the only possibility.

Differentiate respiratory from cardiac dyspnea

Feature	More suggestive of respiratory disease	More suggestive of cardiac disease
Associated symptoms	Cough, sputum, wheeze, pleuritic pain, fever	Orthopnea, paroxysmal nocturnal dyspnea, ankle swelling, palpitations
Examination	Wheeze, prolonged expiration, asymmetric breath sounds, focal crackles, hyperinflation	Raised JVP, peripheral edema, S3, basal crackles, displaced apex beat
Typical examples	Asthma, COPD, pneumonia, PE, pneumothorax, ILD	Left ventricular failure, ischemia, valvular disease
Response to posture	Not characteristic, except severe disease	Worse lying flat in heart failure; sitting forward may relieve symptoms

Important caveat: wheeze can occur in heart failure, sometimes called “cardiac asthma.” Therefore, wheeze alone does not establish asthma or COPD. Merck’s dyspnea review also highlights heart failure, anemia, and upper-airway disorders as important non-pulmonary causes.

Other non-respiratory causes:

Anemia: fatigue, pallor, tachycardia, little or no chest examination abnormality
Metabolic acidosis: deep rapid breathing, for example diabetic ketoacidosis, sepsis, renal failure
Anxiety/panic: episodic dyspnea, tingling around mouth/fingers, tremor; never label it anxiety before excluding dangerous disease
Neuromuscular weakness: weak cough, difficulty lying flat, reduced vital capacity

3. Wheeze

Definition: A continuous musical, usually expiratory sound caused by narrowed intrathoracic airways.

Typical respiratory causes

Asthma
COPD
Acute bronchitis/bronchiolitis
Anaphylaxis
Endobronchial lesion or foreign body if localized/unilateral

Clinical clues

Diffuse bilateral expiratory wheeze: asthma/COPD more likely
Localized or monophonic wheeze: focal bronchial obstruction, tumor, foreign body
“Silent chest” in a severely breathless patient: critical airflow obstruction, an emergency

Differentiate from

Cardiac failure: wheeze plus orthopnea, edema, raised JVP, crackles
Upper-airway obstruction: usually stridor rather than wheeze
Vocal cord dysfunction: episodic breathlessness, throat tightness, inspiratory noise, often normal oxygenation and spirometry between episodes

Wheezes tend to be worse on expiration and arise from small-airway narrowing, while stridor is louder over the larynx and should raise concern for upper-airway obstruction. Merck’s pulmonary evaluation guide

4. Stridor

Definition: A harsh, high-pitched sound due to large-airway obstruction, usually at the larynx or extrathoracic trachea.

Inspiratory stridor: extrathoracic upper-airway obstruction, such as laryngeal edema, epiglottitis, foreign body, vocal cord dysfunction.
Expiratory stridor: intrathoracic tracheal obstruction.
Biphasic stridor: fixed obstruction at the glottis, subglottis, or cervical trachea.

How to distinguish it from wheeze

Stridor: loudest over neck/larynx, predominantly inspiratory, may be audible without a stethoscope.
Wheeze: musical, generally expiratory, louder over the chest.

Clinical importance: Acute stridor with respiratory distress, cyanosis, drooling, altered voice, or inability to speak is an airway emergency. Large-airway disease commonly causes cough, sputum, dyspnea, hemoptysis and wheeze, but acute stridor signals possible life-threatening tracheal obstruction. - Murray & Nadel’s Textbook of Respiratory Medicine, p. 1634

5. Chest pain

First decide whether pain is pleuritic or non-pleuritic.

Pleuritic chest pain

Sharp pain, worsened by deep inspiration, coughing, or movement.

Respiratory/pleural causes

Pleurisy due to pneumonia or viral infection
Pulmonary embolism
Pneumothorax
Pleural effusion
Pleural malignancy

Associated findings

Fever and productive cough: pneumonia
Sudden pain plus acute dyspnea and reduced unilateral breath sounds: pneumothorax
Sudden pleuritic pain, dyspnea, tachycardia, hemoptysis, risk factors for thrombosis: pulmonary embolism

Differentiate from other chest pain

Pattern	Likely system/cause
Central heavy/pressure-like pain with exertion, radiating to arm/jaw, sweating/nausea	Myocardial ischemia
Burning retrosternal pain after meals or when supine, acid regurgitation	GERD
Pain reproducible on palpation or movement	Musculoskeletal chest wall pain
Tearing pain radiating to back, unequal pulses	Aortic dissection, emergency
Sharp positional pain relieved by leaning forward	Pericarditis

Do not assume “pleuritic” means benign. Pulmonary embolism, pneumothorax, and pneumonia can all be serious.

6. Hemoptysis

Definition: Expectoration of blood originating below the vocal cords.

Common respiratory causes

Acute bronchitis
Bronchiectasis
Tuberculosis
Pneumonia
Lung cancer
Pulmonary embolism
Vasculitis or diffuse alveolar hemorrhage

Differentiate hemoptysis from hematemesis and pseudohemoptysis

Feature	Hemoptysis	Hematemesis	Pseudohemoptysis
Source	Lower respiratory tract	Gastrointestinal tract	Nose, mouth, pharynx
Preceded by	Cough	Nausea/retching	Epistaxis, gum bleed, throat symptoms
Appearance	Bright red, frothy, mixed with sputum	Dark red or “coffee-ground,” mixed with food	Blood seen in mouth/nose
pH	Usually alkaline	Usually acidic	Variable
Associated signs	Dyspnea, chest symptoms, lung findings	Melena, abdominal symptoms, liver disease	Nasal/oral lesion

Any significant hemoptysis requires assessment of airway stability and circulation. Massive or ongoing bleeding can obstruct the airway even before blood loss causes shock.

7. Cyanosis

Definition: Bluish discoloration due to increased deoxygenated hemoglobin.

Central cyanosis: tongue and mucous membranes are blue. Seen in severe hypoxemia, right-to-left cardiac shunt, severe lung disease.
Peripheral cyanosis: cold blue fingers/toes with a relatively pink tongue. Seen in low peripheral flow, shock, cold exposure, heart failure.

Differentiation

Central cyanosis can be respiratory or cardiac.
Pulse oximetry, arterial blood gas where indicated, and cardiovascular examination help distinguish causes.
A patient with cyanosis and sudden dyspnea should be treated as potentially unstable.

8. Fever, weight loss, night sweats, and fatigue

These are systemic symptoms, not specifically respiratory, but their combination with respiratory symptoms is highly informative.

Associated feature	Respiratory diagnostic implication
Fever + acute cough + purulent sputum + pleuritic pain	Pneumonia
Weight loss + chronic cough + hemoptysis	TB or lung malignancy
Night sweats + fever + chronic cough	TB, lymphoma, chronic infection
Fatigue + dyspnea but normal chest findings	Consider anemia, cardiac disease, endocrine or systemic illness

Practical ward approach: symptom clusters

Obstructive airway pattern

Cough + wheeze + chest tightness + prolonged expiration
Think: asthma, COPD.
Check: smoking history, variability, triggers, nocturnal symptoms, response to bronchodilator.

Infective/consolidation pattern

Fever + productive cough + pleuritic pain + breathlessness
Think: pneumonia.
Look for: tachypnea, focal crackles, bronchial breathing, dullness, increased vocal resonance.

Pleural pattern

Sharp pleuritic pain + reduced movement/breath sounds on one side
Think: pneumothorax, pleural effusion, pleurisy.
Percussion helps: hyperresonance suggests pneumothorax, stony dullness suggests large effusion.

Pulmonary vascular pattern

Sudden dyspnea + pleuritic pain ± hemoptysis/syncope
Think: pulmonary embolism.
Ask about: recent surgery, immobilization, cancer, prior VTE, pregnancy/postpartum state, estrogen use.

Upper-airway pattern

Voice change + throat discomfort + inspiratory noise/stridor
Think: laryngeal or tracheal obstruction, not ordinary asthma.

Cardiac mimic pattern

Dyspnea + orthopnea + PND + edema + raised JVP
Think: left-sided heart failure, even if wheeze is present.

Red flags to state in your lecture

Urgent assessment is needed for:

Severe breathlessness, inability to speak full sentences, exhaustion, confusion, or cyanosis
Acute stridor
Silent chest in a wheezing patient
Sudden unilateral pleuritic chest pain with reduced breath sounds
Suspected pulmonary embolism
Hemoptysis that is large-volume, recurrent, or accompanied by hypoxia/hemodynamic instability
Chest pain suggestive of acute coronary syndrome or aortic dissection
Fever with hypotension, hypoxia, or altered mental status

One-line summary

Respiratory symptoms are recognized by their relation to breathing, cough, sputum, airway sounds, pleuritic pain, and objective chest findings, but every key symptom has important mimics, especially heart failure/ischemia, GERD, upper-airway disease, anemia, and anxiety.

Also mention the clinal pathology for the symptoms

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dyspnea mechanisms AND cough pathophysiology

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Merck Manual pathophysiology cough dyspnea hemoptysis pleuritic chest pain wheeze stridor

Clinical pathophysiology of major respiratory symptoms

Use this section after describing each symptom in your lecture. It answers: “What pathological process produces this symptom?”

Symptom	Clinical pathophysiology	Typical clinical correlation
Cough	Irritation/inflammation of cough receptors in the larynx, trachea, carina, and large bronchi activates a vagal afferent reflex. The cough centre coordinates deep inspiration, glottic closure, contraction of expiratory muscles, then forceful expiration. Cough clears mucus, inhaled particles, and aspirated material.	Dry cough: airway irritation, viral infection, asthma, interstitial lung disease, ACE inhibitor, tumor. Productive cough: excess mucus/pus in bronchitis, pneumonia, bronchiectasis. Weak cough: neuromuscular weakness or severe fatigue.
Sputum production	Goblet-cell hyperplasia and hypertrophy of submucosal mucus glands produce excess mucus. In infection, neutrophils, cellular debris, and microorganisms make sputum purulent. Bronchiectasis causes retained secretions because permanently dilated bronchi clear mucus poorly.	Chronic morning mucoid sputum suggests chronic bronchitis. Copious purulent sputum, especially in the morning or with positional change, suggests bronchiectasis or lung abscess.
Dyspnea	Dyspnea is the conscious perception of excessive respiratory drive or effort. It occurs when there is mismatch between the brain's drive to breathe and the ability of the lungs, airways, chest wall, respiratory muscles, or circulation to meet that demand. Mechanisms include increased airway resistance, reduced lung compliance, hypoxemia, hypercapnia, increased dead space, respiratory-muscle load, and pulmonary vascular receptor stimulation.	Asthma/COPD: increased airway resistance and air trapping. Interstitial lung disease/pulmonary edema: stiff lungs, reduced compliance. PE: increased dead space and pulmonary vascular obstruction. Anemia: reduced oxygen-carrying capacity. Heart failure: pulmonary congestion plus reduced cardiac output.
Wheeze	Airflow through narrowed intrathoracic airways causes oscillation of airway walls and produces a musical sound, usually on expiration. Narrowing may result from bronchospasm, mucosal edema, mucus plugging, or dynamic airway collapse.	Diffuse expiratory wheeze: asthma/COPD. Localized monophonic wheeze: focal obstruction such as tumor, foreign body, or bronchial stenosis. A nearly silent chest in a very breathless patient indicates critically reduced airflow.
Stridor	Turbulent airflow through a narrowed large upper airway, usually larynx or extrathoracic trachea. Negative pressure during inspiration worsens dynamic narrowing outside the thorax, hence inspiratory stridor.	Inspiratory: laryngeal edema, foreign body, epiglottitis, vocal-cord dysfunction. Biphasic: fixed subglottic/tracheal lesion. It is louder over the neck than chest wheeze and can indicate impending airway obstruction.
Hemoptysis	Blood enters the tracheobronchial tree and is expectorated. Most clinically important hemoptysis arises from the high-pressure bronchial arterial circulation, rather than the pulmonary arterial circulation. It results from inflamed, fragile, neovascular, eroded, or infarcted vessels.	Bronchitis and bronchiectasis: inflamed/neovascular bronchial vessels. TB and cancer: tissue destruction or vascular erosion. PE: pulmonary infarction. Diffuse alveolar hemorrhage: capillary inflammation, often vasculitis. Merck’s hemoptysis review explains this bronchial-circulation predominance.
Pleuritic chest pain	The lung parenchyma itself has few pain fibers. Pain occurs when inflammation, infection, infarction, air, or tumor irritates the parietal pleura, which is pain-sensitive. Pleural movement during inspiration and coughing stretches inflamed pleura, causing sharp pain.	Pneumonia with pleurisy, pulmonary embolism with peripheral infarction, pneumothorax, pleural effusion, and pleural malignancy. Pain is sharp and worsens on deep breathing or cough.
Chest tightness	Usually caused by bronchial smooth-muscle constriction, mucosal edema, and dynamic hyperinflation. The patient experiences increased breathing effort and stretching of chest-wall muscles.	Typical of asthma, but can also occur in COPD. Exertional pressure-like tightness must also raise concern for myocardial ischemia.
Cyanosis	Visible blue discoloration occurs when there is an increased concentration of deoxygenated hemoglobin in capillary blood. It may be central from arterial hypoxemia or peripheral from slow peripheral flow and increased oxygen extraction.	Central cyanosis: tongue and mucosa involved, seen in severe hypoxemia, severe lung disease, or right-to-left cardiac shunt. Peripheral cyanosis: extremities cold/blue but tongue relatively pink, seen in shock, cold exposure, or heart failure.
Fever	Cytokines, especially IL-1, IL-6, and TNF, reset the hypothalamic temperature set point via prostaglandin E2. In respiratory disease, this commonly reflects infection or inflammatory disease.	Fever with cough, sputum, tachypnea, focal crackles, and consolidation suggests pneumonia. Fever is not specific to respiratory disease.
Clubbing	The exact mechanism is incompletely understood. Megakaryocytes/platelet clumps may bypass pulmonary filtration and reach systemic circulation, releasing growth factors such as platelet-derived growth factor and VEGF in the fingertips, producing connective-tissue and vascular proliferation.	Seen in bronchiectasis, lung abscess, cystic fibrosis, interstitial lung disease, and lung cancer. It may also occur in cyanotic congenital heart disease, infective endocarditis, inflammatory bowel disease, and cirrhosis.

Key mechanisms to say during a ward presentation

Airway narrowing produces wheeze, cough, prolonged expiration, and dyspnea.
Causes include bronchospasm, edema, mucus, tumor, or a foreign body.
Alveolar filling with exudate, transudate, blood, or cells produces impaired gas exchange and thus dyspnea/hypoxemia.
Examples: pneumonia, pulmonary edema, alveolar hemorrhage.
Reduced lung compliance makes lungs stiff, increasing the work of breathing and causing dyspnea.
Examples: interstitial lung disease, pulmonary edema, ARDS.
Pleural inflammation produces sharp pleuritic pain, because the parietal pleura is pain-sensitive.
Examples: pleurisy, pulmonary embolism, pneumothorax.
Pulmonary vascular obstruction produces sudden dyspnea, tachycardia, pleuritic pain, and sometimes hemoptysis through increased dead space and, when infarction occurs, pleural irritation.
The classic condition is pulmonary embolism.
Upper-airway narrowing produces stridor, while lower-airway narrowing produces wheeze. This is a high-yield distinction.
High-pressure bronchial-vessel bleeding generally produces hemoptysis.
This explains why bronchiectasis, TB, and malignancy may cause substantial bleeding.

Short viva-style answer

Respiratory symptoms result from pathology in the airways, alveoli, pleura, pulmonary vessels, or respiratory muscles. Airway inflammation and narrowing cause cough, wheeze and obstructive dyspnea; alveolar or interstitial disease causes impaired gas exchange and restrictive dyspnea; pleural inflammation causes pleuritic pain; pulmonary vascular disease causes sudden dyspnea and sometimes hemoptysis; and upper-airway obstruction causes stridor. The main non-respiratory mimics are cardiac failure/ischemia, GERD, ENT disease, anemia, metabolic acidosis, and anxiety.

The common large-airway symptom cluster is cough, sputum, dyspnea, hemoptysis, and wheeze, though these symptoms are not specific and require clinical correlation. - Murray & Nadel’s Textbook of Respiratory Medicine, p. 1634. The clinical approach chapter emphasizes that cough and breathlessness are the commonest respiratory presentations. - Fishman’s Pulmonary Diseases and Disorders, p. 394.

Now combine both responses to form one answer. Keep it precise and concise

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Symptomatology of the Respiratory System

The common respiratory symptoms are cough, sputum production, dyspnea, wheeze, stridor, chest pain, hemoptysis, and sometimes cyanosis and constitutional symptoms. The core clinical task is to identify the underlying anatomical site: airway, lung parenchyma/alveoli, pleura, pulmonary vessels, or upper airway, while excluding mimics from the heart, gastrointestinal tract, ENT, and systemic disorders.

Symptom	Clinical pathology / mechanism	Key respiratory causes	Differentiation from other systems
Cough	Stimulation of cough receptors in larynx, trachea, carina, and large bronchi triggers a vagal reflex to expel irritants or secretions.	URTI, asthma, COPD, pneumonia, TB, bronchiectasis, lung cancer.	GERD: after meals/lying down, heartburn. Postnasal drip: throat clearing, nasal symptoms. Heart failure: cough worse supine with orthopnea/edema. ACE inhibitor: persistent dry cough.
Sputum	Excess mucus from goblet-cell and submucosal-gland activity; pus reflects neutrophils and inflammatory debris.	Chronic bronchitis, pneumonia, bronchiectasis, lung abscess.	Purulent sputum suggests airway infection/inflammation but does not alone prove bacterial infection. Copious, foul sputum suggests bronchiectasis or abscess. Pink frothy sputum suggests pulmonary edema.
Dyspnea	Mismatch between respiratory drive and the ability of lungs, airways, chest wall, muscles, or circulation to meet ventilatory demand. Mechanisms: airway resistance, stiff lungs, hypoxemia, hypercapnia, dead-space ventilation, and respiratory-muscle loading.	Asthma/COPD, pneumonia, ILD, pneumothorax, pleural effusion, pulmonary embolism.	Heart failure: orthopnea, PND, raised JVP, edema. Anemia: pallor and tachycardia with often normal chest findings. Metabolic acidosis: deep rapid breathing. Anxiety: episodic symptoms only after organic disease is excluded.
Wheeze	Oscillation of narrowed intrathoracic airway walls during airflow, usually expiration. Narrowing results from bronchospasm, mucosal edema, mucus, or obstruction.	Asthma, COPD, bronchiolitis, anaphylaxis.	Localized wheeze: tumor or foreign body. Cardiac asthma: wheeze with edema, raised JVP, basal crackles.
Stridor	Turbulent flow through narrowed larynx or trachea. Inspiratory stridor occurs mainly with extrathoracic upper-airway obstruction.	Foreign body, laryngeal edema, epiglottitis, vocal-cord dysfunction, tracheal stenosis.	Louder over the neck, predominantly inspiratory and harsher than wheeze. Acute stridor is an airway emergency.
Pleuritic chest pain	Inflammation or irritation of pain-sensitive parietal pleura. Lung tissue itself is relatively insensitive to pain.	Pneumonia with pleurisy, pulmonary embolism, pneumothorax, pleural effusion.	MI: central pressure/heaviness, often exertional, radiation to jaw/arm. GERD: burning after meals/lying flat. Musculoskeletal pain: reproducible on palpation/movement.
Hemoptysis	Bleeding into the tracheobronchial tree, most often from high-pressure bronchial arteries; due to inflammation, neovascularization, tissue destruction, or vessel erosion.	Bronchitis, bronchiectasis, TB, lung cancer, pulmonary embolism, vasculitis.	Hematemesis: nausea/retching, coffee-ground/dark blood, melena. Pseudohemoptysis: blood from nose, gums, or pharynx.
Cyanosis	Increased deoxygenated hemoglobin. Central cyanosis indicates arterial desaturation; peripheral cyanosis reflects slow peripheral circulation/increased extraction.	Severe hypoxemic lung disease, respiratory failure, pulmonary embolism.	Central: tongue and mucosa blue, also seen with right-to-left cardiac shunt. Peripheral: cold blue extremities with relatively pink tongue, seen in shock/heart failure/cold exposure.
Fever, weight loss, night sweats	Cytokine-mediated systemic inflammatory response.	Pneumonia, TB, lung abscess, malignancy.	Not specific to respiratory disease. Combine with cough, sputum, chest signs, exposure history, and imaging.
Clubbing	Likely platelet/megakaryocyte-derived growth-factor release in fingertips, causing vascular and connective-tissue proliferation.	Bronchiectasis, lung abscess, cystic fibrosis, ILD, lung cancer.	Also occurs in cyanotic congenital heart disease, infective endocarditis, cirrhosis, and inflammatory bowel disease.

High-yield clinical patterns

Obstructive airway disease: cough, wheeze, chest tightness, prolonged expiration, dyspnea
- Think asthma or COPD.
Pneumonia/consolidation: fever, productive cough, pleuritic pain, dyspnea
- Look for focal crackles, bronchial breathing, dull percussion note, increased vocal resonance.
Pleural disease: sharp pain aggravated by breathing, reduced unilateral air entry
- Hyperresonance suggests pneumothorax; stony dullness suggests pleural effusion.
Pulmonary embolism: sudden dyspnea, pleuritic pain, tachycardia, possible hemoptysis or syncope.
Upper-airway obstruction: hoarseness, throat symptoms, inspiratory stridor
- Differentiate from asthma, which causes mainly expiratory wheeze.
Heart failure mimic: dyspnea with orthopnea, PND, edema, raised JVP, basal crackles, sometimes wheeze.

Important red flags

Severe breathlessness, cyanosis, confusion, exhaustion, or inability to speak full sentences
Acute stridor
Silent chest in a wheezing patient
Sudden pleuritic pain with dyspnea or unilateral reduced breath sounds
Significant or recurrent hemoptysis
Chest pain suggestive of myocardial ischemia or aortic dissection

Summary: Airway pathology causes cough, wheeze, and stridor; alveolar/interstitial pathology causes hypoxemia and dyspnea; pleural pathology causes pleuritic pain; pulmonary vascular pathology causes sudden dyspnea and sometimes hemoptysis. Always distinguish these from cardiac failure/ischemia, GERD, upper-airway disease, anemia, and systemic causes.

The classic large-airway symptom group is cough, sputum production, dyspnea, hemoptysis, and wheeze. - Murray & Nadel’s Textbook of Respiratory Medicine, p. 1634.

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