Based on expectoration: It is also classified into productive or dry cough depending on the presence

or absence of expectoration, respectively (Table 3C.1).

Flowchart 3C.1: Algorithm showing cough reflex.

Table 3C.1: Classification of cough based on etiology.

Cough Duration Respiratory causes Non-respiratory causes

Acute

cough

Less than 3 weeks Tracheobronchitis

Bronchopneumonia

Viral pneumonia

Acute-on-chronic bronchitis

Pulmonary embolism

Sudden onset:

Bronchial asthma

Asthmatic bronchitis Whooping cough

Foreign body

LVF

GERD

Subacute

cough

3–8 weeks Tuberculosis, pneumonia (bacterial, viral,

fungal)

B. pertussis

Bronchiectasis

Postviral tussive syndrome

GERD

Tourette’s syndrome

Intentional cough

Chronic

cough*

Lasting for more than

8 weeks

COPD, asthma

ILD

Tuberculosis

Lung cancer

Pneumoconiosis (asbestosis, silicosis,

anthracosis, etc.)

Mesothelioma of lung

Upper airway cough syndrome

Drug induced (ACE inhibitors, beta

blockers, NSAIDs)

Habit cough syndrome

*Chronic cigarette smoking is the most common cause of chronic cough.

(LVF: left ventricular failure; GERD: gastroesophageal reflux disease; COPD: chronic obstructive

pulmonary disease; ILD: interstitial lung disease; ACE: angiotensin converting enzyme; NSAIDs:

nonsteroidal anti-inflammatory drugs)

Table 3C.2: Different types of cough.

Types Features

Dry cough Pleural disorders, diseases of interstitium, mediastinal lesions

Productive

cough

Suppurative lung disease, airway diseases

Brassy/Gander

cough

Metallic sound due to compression of trachea by intrathoracic space occupying lesions or aortic aneurysms

also known as leopards growl

Bovine cough Loss of expulsive nature as in a tumor pressing on the recurrent laryngeal nerve

•

•

•

•

•

•

•

•

•

Paroxysmal

cough

Whooping cough, chronic bronchitis, foreign body, bronchial asthma

Barking cough Involvement of epiglottis, croup (laryngotracheobronchitis), hysteria

Spluttering

cough

Tracheoesophageal fistula, cough while swallowing

Hacking cough Heavy smokers, chronic pharyngitis or laryngitis

Otogenic cough Due to stimulation of Arnold’s nerve in the external auditory meatus (impacted wax/foreign body)

EXPECTORATION/SPUTUM

Sputum can be described under the following headings:

Quantity

Quality

Odor

Quantity

Normal 10–15 mL/24 hour

Bronchorrhea Production of more than 100 mL/day

Bronchiectasis

Lung abscess

Bronchoalveolar carcinoma

Organophosphorus poisoning

Quality

Mucoid Chronic bronchitis, bronchial asthma

Mucopurulent Infections

Purulent Lung abscess, bronchiectasis

Rust-colored purulent

sputum

Pneumococcal pneumonia

Currant-jelly and sticky

sputum

Klebsiella pneumoniae

Blood-tinged foamy

sputum

Pulmonary edema (pink frothy)

Greenish Pseudomonas

Granules—yellow/black Actinomycosis

Anchovy sauce (brown) Amebic abscess rupturing into lung

Black (melanoptysis) Carbon particles discolor the sputum gray (as in cigarette smokers) or black (as in coal miners or

with smoke inhalation)

Odor

Foul smelling sputum Anaerobic infection seen in lung abscess, bronchiectasis

Special Points

Chronic expectoration of large amounts of purulent and foul-smelling sputum is strongly suggestive of

bronchiectasis.

Sudden production of such sputum in a febrile patient indicates a lung abscess.

Table 3C.3: Causes of hemoptysis.

•

•

Structure

involved

Common causes Uncommon causes

Bronchial

disease

Bronchial carcinoma, bronchiectasis, acute and chronic bronchitis Bronchial adenoma, foreign body

Parenchymal

disease of

lung

Pulmonary tuberculosis (Rasmussen’s aneurysm—dilation of a pulmonary

artery in a tuberculous cavity), lung abscess, pneumonia (particularly

Klebsiella), fungal infections (aspergilloma and invasive aspergillosis),

pulmonary contusion/laceration (traumatic)

Parasites (e.g. hydatid disease,

flukes), trauma, actinomycosis, mycetoma

Vascular

diseases of the

lung

Pulmonary infarction Goodpasture’s syndrome,

polyarteritis nodosa, idiopathic

pulmonary hemosiderosis,

primary pulmonary hypertension

Cardiovascular

disease

Acute left ventricular failure Mitral stenosis, aortic aneurysm,

pulmonary thromboembolism

Hematological

disorders

Leukemia, hemophilia,

anticoagulants, hemorrhagic

diathesis

Three-layer sputum consisting of a foamy upper layer, mucous middle layer, and viscous purulent

bottom layer is pathognomonic of bronchiectasis.

Postural variation in sputum: Bronchiectasis, lung abscess.

HEMOPTYSIS

Definition: Hemoptysis is defined as coughing of blood originating from below the vocal cords.

Hemoptysis can range from blood-streaking of sputum to the presence of gross blood in the absence of

any accompanying sputum. The different causes of hemoptysis are given in Table 3C.3.

The clinical clues of hemoptysis, differences between true and false hemoptysis and differences

between hemoptysis and hematemesis are described in Table 3C.4 to Table 3C.6, respectively.

Table 3C.4: Clinical clues of hemoptysis.

Clinical clues Suggested diagnosis

Anticoagulant use Medication effect, coagulation disorder

Tobacco use Acute bronchitis, chronic bronchitis, pneumonia,

lung cancer

Dyspnea on exertion, fatigue, orthopnea, paroxysmal nocturnal dyspnea,

frothy pink sputum

Congestive heart failure, left ventricular failure

and mitral stenosis

Fever, productive cough Upper respiratory tract infection, acute bronchitis,

pneumonia, lung abscess

History of cancer (e.g. breast, colon, or kidney) Endobronchial metastasis from carcinoma

History of chronic lung disease, recurrent lower respiratory tract

infection, cough with copious purulent sputum

Bronchiectasis, lung abscess

Pleuritic chest pain, calf tenderness Pulmonary embolism or infarction

Toxic symptoms Tuberculosis

Weight loss Emphysema, lung cancer, tuberculosis,

bronchiectasis, lung abscess

Melena, alcoholism, chronic use of nonsteroidal anti-inflammatory drugs

(NSAIDs)

Gastritis, gastric or peptic ulcer, esophageal

varices

Association with menses Catamenial hemoptysis

Cachexia, clubbing, hoarseness Lung cancer, small cell carcinoma

■

■

■

■

■

Clubbing Lung cancer, bronchiectasis, lung abscess

Dullness to percussion, fever, crepitations Pneumonia

Table 3C.5: Differences between true and false hemoptysis.

True hemoptysis False hemoptysis

Below vocal cords Above vocal cords

Persists as blood tinged sputum Does not persist

May be mixed with sputum Not mixed with sputum

History of cardiopulmonary disease Obvious by ENT examination

Chest X-ray may be abnormal Normal chest X-ray

Table 3C.6: Differences between hemoptysis and hematemesis.

Hemoptysis Hematemesis

Coughing of blood. Cough precedes hemoptysis Vomiting of blood. Nausea and vomiting precedes hematemesis

History of cardiopulmonary disease History of gastrointestinal disease

Bright red in color Dark brown in color

Sputum remains blood stained after the attack for few days Usually followed by melena

Mixed with sputum Mixed with gastric contents

Blood is frothy due to admixture of air Airless and not frothy

Alkaline Acidic

Sputum contains hemosiderin laden macrophages No

Melena absent Melena present

Massive hemoptysis: Life-threatening (or) massive hemoptysis is defined as coughing of blood >150

mL/episode (or) > 600 mL/24 hour. Only 5% of hemoptysis is massive but mortality is 80%. Clinical

definition of massive hemoptysis is any bleeding that result in a threat to life because of airway or

hemodynamic compromise due to bleeding. The different causes of massive hemoptysis are given in

Box 3C.2.

DYSPNEA

Definition

“Dyspnea” is a term used to characterize a subjective experience of breathing discomfort that is

comprised of qualitatively distinct sensations that vary in intensity (undue awareness of unpleasant

breathing).

Box 3C.2: Causes of massive hemoptysis.

Pulmonary tuberculosis

Pulmonary infarction

Bronchiectasis

Bronchogenic carcinoma

Cystic fibrosis

■

■

■

■

Lung abscess

Necrotizing pneumonia

Mitral stenosis

Pulmonary arteriovenous malformation

Mechanism of Dyspnea

Chemoreceptors

Peripheral Carotid and aortic bodies (sensitive to changes pO2

, pCO2 and H

+

)

Central Medulla (sensitive only to changes in pCO2

, not pO2

, change in pH of cerebrospinal fluid)

Increased work of breathing

Airflow obstruction Bronchial asthma, chronic obstructive pulmonary disease (COPD), tracheal obstruction

Decreased pulmonary

compliance

Pulmonary edema, fibrosis, allergic alveolitis

Restricted chest

expansion

Ankylosing spondylitis, respiratory paralysis, kyphoscoliosis

Increased ventilatory drive

Increased physiological

dead space (V/Q mismatch)

Consolidation, collapse, pleural effusion (PE), pulmonary edema

Hyperventilation due to receptor stimulation

Chemoreceptors Acidosis, hypoxia (shock, pneumonia), hypercapnia

J receptors at

alveolocapillary junction

Pulmonary edema, pulmonary embolism, pulmonary congestion (activates Hering-Breuer reflex

which terminates inspiratory effort before full inspiration is achieved—rapid and shallow)

Muscle spindles in

intercostal muscles

Tension-length disparity

Central Exertion, anxiety, thyrotoxicosis, pheochromocytoma

Impaired respiratory muscle function

Diseases with impaired muscle function

Poliomyelitis, Guillain-Barre syndrome (GBS), myasthenia gravis

Table 3C.7: Differences between paroxysmal nocturnal dyspnea (PND) orthopnea.

Paroxysmal nocturnal dyspnea Orthopnea

Definition Episode of sudden onset of dyspnea 2–2.5 hours after sleep Dyspnea in recumbent posture

Timing Patient wakes up from rapid eye movement (REM) sleep Occurs soon after lying down

Method of

relief

Sits up with legs hanging down, stands up, air hunger, self

ventilates of comfort

Gets up, uses more pillows, sleeps in erect

posture

Mechanism Depressed respiratory center. Sympathetic overactivity during

REM → catecholamine surge resulting in tachycardia →

interstitial pulmonary congestion → respiratory center lags

behind → perceived as acute dyspnea. There is sudden

transient increase in PCWP

Shifting of venous blood (>400 mL) into pulmonary

circulation, V/Q mismatch, compression of

diaphragm, postural diastolic dysfunction. There is

a slow sustained rise in pulmonary capillary wedge

pressure (PCWP)

Associated

symptoms

Angina, perspiration, palpitation, rarely hemoptysis All the symptoms of congestive cardiac failure

(CCF)

Oxygen Transient hypoxia Normal

•

•

•

•

saturation

Differential

diagnosis

Night mares/panic attacks/nocturnal hypoglycemia/obstructive

sleep apnea (OSA)

COPD/gross obesity/acute asthma/gross ascites

Orthopnea

Dyspnea develops in recumbent position and is relieved by sitting up or by elevation of the head with

pillows.

The severity can be graded by the number of pillow used at night, e.g. three pillow orthopnea.

Pathophysiology of Orthopnea

Pulmonary congestion during recumbency (cannot be pumped out of LV) seen in congestive heart

failure (CHF), chronic obstructive pulmonary disease (COPD) and bronchial asthma.

Increased venous return.

Diaphragm elevation leading to decreased vital capacity.

Conditions Associated with Orthopnea

Orthopnea is classically seen in left heart failure but can also occur in constrictive pericarditis, COPD,

bilateral diaphragmatic palsy, asthma triggered by gastric reflux, and gross ascites.

Paroxysmal Nocturnal Dyspnea

Attacks of dyspnea occur at night and awaken the patient from sleep. The important differences

between orthopnea and PND are given in Table 3C.7.

Mechanism (Fig. 3C.1)

It is due to decreased responsiveness of respiratory center in brain during sleep and pulmonary

congestion (due to increased sympathetic activity during REM sleep), that occurs 2–3 hours after

onset of sleep.

•

•

•

•

•

•

•

•

•

•

•

•

•

•

Fig. 3C.1: Mechanism of paroxysmal nocturnal dyspnea (PND).

Absorption of edema fluid with increase in right ventricular output causing over filling of the lungs.

Takes 10–30 minutes for recovery after upright posture.

Specific sign of LV dysfunction and includes ischemic heart disease, aortic valve disease,

hypertension, cardiomyopathy.

It has low sensitivity (<30%) but 75% specificity to diagnose heart disease.

Differential Diagnosis for Paroxysmal Nocturnal Dyspnea

Left heart failure

Nocturnal episodes of asthma

Postnasal discharge with attendant severe cough

Sleep apnea with arousal

Nightmares

Nocturnal angina with dyspnea (angina equivalent)

Nocturnal aspiration in gastroesophageal reflux disease

Nocturnal episodes of recurrent minute pulmonary emboli

Nocturnal hypoglycemia.

Trepopnea

Aggravation of dyspnea when lying on one side and relieved by lying on opposite side.

Causes

Unilateral lung disease: Uninvolved normal lung receives more blood supply due to gravity.

•

•

•

•

•

•

Congestive heart failure: Lying on right side enhances venous return and sympathetic activity.

Lung tumor: Gravity induced compression of blood vessels or lung.

Platypnea

Dyspnea on sitting or standing and relieved by supine position.

Causes

Venous to arterial shunting (lung bases)

Intracardiac shunts (ASD, pneumonectomy)

Intrapulmonary right to left shunt [hepatopulmonary syndrome, pulmonary embolism (PE), COPD]

Acute respiratory distress syndrome (ARDS).

Bendopnea

A newly described symptom in patients with heart failure is mediated via a further increase in ventricular

filling pressures during bending in subjects whose sitting ventricular filling pressures are already high,

particularly in patients with low cardiac index (Fig. 3C.2).

Fig. 3C.2: A patient sits in a chair, bends at the waist, and touches his or her feet. Bendopnea is

considered present if dyspnea occurs within 30 seconds of bending.

Approach to dyspnea

Onset and duration

Minutes to hours (rapid onset) Pneumothorax, acute asthma, pulmonary embolism (PE), pulmonary

edema, foreign body

Hours to days (gradual onset) Pneumonia, pleural effusion, anemia, Guillain–Barre syndrome (GBS)

Months to years (slow onset) Pulmonary tuberculosis (PTB), COPD, carcinoma, fibrosing alveolitis

Severity

Medical Research Council (MRC) (Table 3C.8) Discussed below

Modified Medical Research Council (mMRC)

(Table 3C.9)

New York Heart Association (NYHA) (Table

3C.10)

1.

2.

3.

4.

5.

•

•

Aggravating and relieving factors

Improves on weekend/holidays Occupational asthma, extrinsic alveolitis

Recumbency/sleep Orthopnea/paroxysmal nocturnal dyspnea (PND)

Associated symptoms (Table 3C.11)

Pleuritic chest pain Pneumonia, pulmonary infarction, rib fracture, pneumothorax

Central non-pleuritic chest pain Myocardial infarction, massive pulmonary embolism

Cough or wheeze Asthma, pulmonary embolism, pneumothorax

Table 3C.8: Medical Research Council grading of breathlessness.

Note troubled by breathlessness except on strenuous exertion

Short of breath when hurrying on level ground or walking up slight hill

Walks slower than people of same age or stops after 15 minutes when walking at own pace on level

Stops after 100 yards (90 m) or after few minutes in level ground

Too breathless to leave house, dress or undress

Table 3C.9: Modified Medical Research Council grading of breathlessness.

Grade Description of breathlessness

Grade

0

I only get breathless with strenuous exercise

Grade

1

I get short of breath when hurrying on level ground or walking up a slight hill

Grade

2

On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when

walking at my own pace on the level

Grade

3

I stop for breath after walking about 100 yards or after a few minutes on level ground

Grade

4

I am too breathless to leave the house or

I am breathless when dressing

Pitfalls of mMRC Grading

The mMRC dyspnea scale quantifies disability attributable to breathlessness, and is useful for

characterizing baseline dyspnea in patients with respiratory diseases.

It describes baseline dyspnea, but does not accurately quantify response to treatment of COPD.

Table 3C.10: New York Heart Association (NYHA) classification of breathlessness.

NYHA

Class

Patients with cardiac disease

(Description of heart failure related symptoms)

Class I

(Mild)

Patients with cardiac disease but without resulting in limitation of physical activity. Ordinary physical activity does

not cause undue fatigue, palpitation, dyspnea or anginal pain

Class II

(Mild)

Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain

Class III

(Moderate)

Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less

than ordinary activity causes fatigue, palpitation, dyspnea or anginal pain

Class IV

(Severe)

Patients with cardiac disease resulting in the inability to carry on any physical activity without discomfort. Symptoms

of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken,

discomfort is increased

Table 3C.11: Causes of acute and chronic dyspnea.

Acute dyspnea Chronic dyspnea

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

■

■

■

■

■

■

■

■

■

■

•

•

•