COUGH, HEMOPTYSIS

and DYSPNEA
COUGH:
COUGH is an explosive expiration that provides a normal
protective mechanism for clearing the tracheobronchial tree of
secretions and foreign material

MECHANISM:
Coughing may be initiated either VOLUNTARILY or REFLEXIVELY

As a defensive reflex, it has both AFFERENT and EFFERENT

pathways:
AFFERENT LIMB includes receptors within the sensory
distribution of the TRIGEMINAL, GLOSSOPHARYNGEAL, SUPERIOR
LARYNGEAL and VAGUS nerves
EFFERENT LIMB includes the RECURRENT LARYNGEAL NERVE
and the SPINAL NERVES
COUGH:
MECHANISM:
The cough starts with a deep inspiration followed by glottic
closure, relaxation of the diaphragm, and muscle contraction
against a closed glottis

The resulting markedly positive intrathoracic pressure causes

narrowing of the trachea

Once the glottis opens, the large pressure differential between

the airways and the atmosphere coupled with tracheal narrowing
produces rapid flow rates through the trachea

The shearing forces that develop aid in the elimination of mucus

and foreign materials
COUGH:
ETIOLOGY:
1. Cough can be initiated by a variety of IRRITANT TRIGGERS:
EXOGENOUS SOURCE - smoke, dust, fumes, foreign bodies
ENDOGENOUS ORIGIN upper airway secretions (postnasal drip),
gastric contents (gastroesophgeal reflux)

2. Any disorder resulting in inflammation, constriction, infiltration

or compression of airways can be associated with cough.
INFLAMMATION airway infections (viral or bacterial)
CONSTRICTION asthma
INFILTRATION neoplasm (bronchogenic carcinoma, carcinoid
tumor) or granulomas (endobronchial sarcoidosis or TB)
COMPRESSION extrinsic masses (lymph nodes, mediastinal
tumors, aortic aneurysm)
COUGH:
3. PARENCHYMAL LUNG DISEASES interstitial lung
disease, pneumonia, lung abscess

4. OTHERS:
Congestive heart failure (CHF) cough results as a
consequence of interstitial as well as peribronchial edema

Use of angiotensin-converting enzyme inhibitors (ACEI)

cough occurs in 5-20% of patients

onset is within 1week of starting the drug but can be delayed

for up to 6month due to accumulation of BRADYKININ or

SUBSTANCE P which are both degraded by ACE
COUGH:
CATEGORIES of COUGH ACCORDING to DURATION:
1. ACUTE COUGH < 3weeks
Most often due to upper respiratory infection (common cold, acute
bacterial sinusitis, pertussis)
More serious disorders (pneumonia, pulmonary embolus, CHF) can
also present acutely

2. CHRONIC COUGH - > 3 weeks

Chronic abstructive lung disease (COLD) or bronchogenic carcinoma
in a smoker
In a nonsmoker with normal CXR and is not taking ACEI, the most
common causes of chronic cough are
POSTNASAL DRIP
ASTHMA

GASTROESOPHAGEAL REFLUX
APPROACH to the PATIENT with
COUGH:
A detailed HISTORY frequently provides the most valuable clues for
etiology of the cough. Paricularly important questions include:
1. Is the cough ACUTE or CHRONIC?
2. At its onset, were there associated symptoms suggestive of a
respiratory infection?
3. Is it seasonal or associated with wheezing?
4. Is it associated with symptoms suggestive of postnasal drip (nasal
discharge, frequent throat clearing, a tickle in the throat) or
gastroesophageal reflux (heartburn or sensation of regurgitation)
5 . Is it associated with fever or sputum? If sputum is present, what
is its character?
6. Does the patient have any associated diseases or risk factors for
disease (cigarette smoking, HIV, environmental exposure)?
7. Is the patient taking an ACEI?
APPROACH to the PATIENT with
COUGH:
PHYSICAL EXAMINATION:
May point to a systemic or nonpulmonary cause of cough
(heart failure, primary nonpulmonary neoplasm, AIDS)

Examination of the oropharynx may provide suggestive

evidence for postnasal drip (oropharyngeal mucus or
erythema, or a cobblestone appearance to the mucosa)

Auscultation of the chest may demonstrate:

INSPIRATORY STRIDOR indicative of upper airway disease

RHONCHI or EXPIRATORY WHEEZING indicative of lower airway

disease
INSPIRATORY CRACKLES suggestive of a process involving the

pulmonary parenchyma (ILD, pneumonia, pulmonary edema)

APPROACH to the PATIENT with
COUGH:
CHEST RADIOGRAPHY:
Particularly helpful in suggesting or confirming the
cause of the cough

Important potential findings:

presence of an intrathoracic mass lesion

a localized pulmonary parenchyma infiltrate

a diffuse interstitial or alveolar disease

An area of honeycombing or cyst formation may

suggest bronchiectasis, while symmetric bilateral
hilar adenopathy may suggest sarcoidosis
APPROACH to the PATIENT with
COUGH:
PULMONARY FUNCTION TESTING:
Useful for assessing the functional abnormalities that accompany
certain disorders producing cough

Measurement of forced expiratory flow rates can demonstrate

reversible airflow obstruction characteristic of asthma

When asthma is considered but flow rates are normal,

bronchoprovocation testing with metacholine or cold-air inhalation
can demonstrate hyperreactivity of the airways to a
bronchoconstrictive stimulus

Measurement of lung volumes and diffusing capacity is useful for

demonstration of a restrictive pattern (diffuse interstitial lung
diseases)
APPROACH to the PATIENT with
COUGH:
SPUTUM EXAMINATION:
If sputum is produced, gross and microscopic examination provide
useful information

Purulent sputum: chronic bronchitis, bronchiectasis, pneumonia or

lung abscess

Bloody sputum: as above, endobronchial tumor

>3% eosinophils on staining of induced sputum in a patient w/o

asthma: eosinophilic bronchitis

Gram- and acid-fast stains and cultures may demonstrate a particular

infectious pathogen, while sputum cytology may provide a diagnosis
of a pulmonary malignancy
APPROACH to the PATIENT with
COUGH:
FIBEROPTIC BRONCHOSCOPY:
Procedure of choice for visualizing an endobronchial
tumor and collecting cytologic and histologic specimens

HIGH-RESOLUTION COMPUTED TOMOGRAPHY

(HRCT):
Can confirm the presence of interstitial disease and
frequently suggests a diagnosis based on the pattern of
disease
Procedure of choice for demonstrating dilated airways
and confirming the diagnosis of bronchiectasis
COMPLICATIONS of
COUGH:
Common complications of coughing:
chest and abdominal wall soreness
urinary incontinence
exhaustion

COUGH SYNCOPE :
paroxysms of coughing may precipitate syncope due to markedly
positive intrathoracic and alveolar pressures, diminished venous
return, and decreased cardiac output

Cough fractures of the ribs may occur in otherwise normal

patients, but their occurrence should raise the possibility of
pathologic fractures (multiple myeloma, osteoporosis, osteolytic
metastases)
TREATMENT of COUGH:
Definitive treatment of cough depends on determining the
underlying cause and then initiating specific therapy

Elimination of an exogenous inciting agent (cigarette smoke, ACEI) or

an endogenous trigger (postnasal drip, gastroesophageal reflux)
when such precipitants are identified

Other important management considerations:

Treatment of specific respiratory tract infections
Bronchodilators for reversible airflow obstruction
Inhaled glucocorticoids for eosinophilic bronchitis
Chest physiotherapy to enhance clearance of secretions
(bronchiectasis)
Treatment of endobronchial tumors or ILDs when such therapy is
available and appropriate
TREATMENT of COUGH:
CHRONIC, UNEXPLAINED COUGH:
Empirical approach to treatment is used for both diagnostic and
therapeutic purposes
Antihistamine-decongestant combination or nasal ipatropium
spray initially to treat unrecognized PND
If ineffective, this may be followed by treatment for asthma and
for GERD

SYMPTOMATIC or NONSPECIFIC THERAPHY of COUGH should

be considered when:
1. the cause of the cough is not known or specific treatment is
not possible
2. the cough performs no useful function or causes marked
discomfort
TREATMENT of COUGH:
An irritative, NONPRODUCTIVE COUGH may be
suppressed by an ANTITUSSIVE agent, which
increases the latency or threshold of the cough
center:
CODEINE 15mg qid
DEXTROMETHORPHAN (non-narcotic) 15mg qid

A cough PRODUCTIVE of significant quantities of

SPUTUM should not be suppressed, since retention of
sputum in the tracheobronchial tree may interfere
with the distribution of ventilation, alveolar aeration,
and the ability of the lung to resist infection
HEMOPTYSIS:
HEMOPTYSIS is defined as the expectoration
of blood from the respiratory tract

MASSIVE HEMOPTYSIS expectoration of

>100mL to >600mL over a 24-hr period
Can represent an acutely life-threatening
problem large amounts of blood can fill the
airways and the alveolar spaces, not only
seriously disturbing gas exchange but
potentially causing the patient to suffocate
HEMOPTYSIS:
ETIOLOGY:
Because blood originating from the
nasopharynx or the GIT can mimic blood
coming from the LRT, it is important to
determine initially that the blood is not coming
from one of these sites

Clues that the blood is originating from the GIT

include a dark red appearance and an acidic
pH, in contrast to the typical BRIGHT RED
APPEARANCE and ALKALINE pH of true
hemoptysis
DIFFERENTIAL DIAGNOSIS of
HEMOPTYSIS:
1. Source other than the LRT
Upper airway (nasopharyngeal) bleeding
GI bleeding

2. Tracheobronchial source
Neoplasm (bronchogenic carcinoma, endobronchial
metastatic tumor, Kaposis sarcoma, bronchial carcinoid)
Bronchitis (acute or chronic)

Bronchiectasis

Bronchiolithiasis

Airway trauma

Foreign body
DIFFERENTIAL DIAGNOSIS of
HEMOPTYSIS:
3. Pulmonary parenchymal source
Lung abscess
Pneumonia

Tuberculosis

Mycetoma (fungus ball)

Goodpastures syndrome

Idiopathic pulmonary hemosiderosis

Wegeners granulomatosis

Lupus pneumonitis

Lung contusion
DIFFERENTIAL DIAGNOSIS of
HEMOPTYSIS:
4. Primary vascular source
Arteriovenous malformation
Pulmonary embolism

Elevated pulmonary venous pressure (MS)

Pulmonary artery rupture secondary to balloon-tip

pulmonary artery catheter manipulation

5. Miscellaneous causes
Pulmonary endometriosis
Systemic coagulopathy

use of anticoagulants or thrombolytic agents

APPROACH to the PATIENT with
HEMOPTYSIS:
HISTORY:
Blood-streaking of mucopurulent or purulent sputum - bronchitis

Chronic production of sputum with a recent change in quality or

appearance acute exacerbation of chronic bronchitis

Blood-streaked purulent sputum with fever or chills pneumonia

Putrid-smelling sputum lung abscess

Chronic and copious sputum production bronchiectasis

Hemoptysis following the acute onset of pleuritic chest pain and

dyspnea pulmonary embolism
APPROACH to the PATIENT with
HEMOPTYSIS:
HISTORY OF PREVIOUS OR COEXISTING DISORDERS:
Renal disease Goodpastures syndrome, Wegeners granulomatosis

Lupus erthymatosus pulmonary hemorrhage from lupus pneumonitis

Previous malignancy recurrent lung cancer or endobronchial

metastasis from a nonpulmonary primary tumor

AIDS endobronchial or pulmonary parenchymal Kaposis sarcoma

Risk factors for bronchogenic carcinoma smoking, asbestos exposure

Previous bleeding disorders, treatment with anticoagulants, or use of

drugs that can be associated with thrombocytopenia
APPROACH to the PATIENT with
HEMOPTYSIS:
PHYSICAL EXAMINATION:
PULMONARY AUSCULTATION:
Pleural friction rub pulmonary embolism
Localized or diffuse crackles parenchymal bleeding or an underlying
parenchymal process associated with bleeding
Evidence of airflow obstruction chronic bronchitis
Prominent rhonchi w/ or w/o wheezing or crackles bronchiectasis

CARDIAC EXAMINATION:
may demonstrate findings of pulmonary arterial hypertension, MS or
heart failure

SKIN EXAMINATION:
may reveal Kaposis sarcoma, AVM of Osler-Rendu-Weber disease, or
lesions suggestive of SLE
APPROACH to the PATIENT with
HEMOPTYSIS:
DIAGNOSTIC EVALUATION:
CHEST RADIOGRAPH (often followed by CT scan) to look
for a mass lesion, findings suggestive of bronchiectasis,
or focal or diffuse parenchymal disease

Additional initial screening evaluation: CBC, a

coagulation profile, and assessment for renal disease
with a urinalysis and measurement of BUN and
creatinine levels

When sputum is present, Gram- and acid-fast stains

(along with corresponding cultures) is indicated
APPROACH to the PATIENT with
HEMOPTYSIS:
DIAGNOSTIC EVALUATION:
FIBEROPTIC BRONCHOSCOPY useful for
localizing the site of bleeding and for
visualization of endobronchial lesions
When bleeding is massive, RIGID
BRONCHOSCOPY is preferred because of better
airway control and greater suction capability

HRCT diagnostic procedure of choice in

patients with suspected bronchiectasis
ALGORITHM for the EVALUATION of
NON-MASSIVE HEMOPTYSIS:
TREATMENT of
HEMOPTYSIS:
The rapidity of bleeding and its effect on gas exchange
determine the urgency of management:

BLOOD STREAKING of sputum or production of small amounts

of pure blood establishing a diagnosis is the first priority

MASSIVE HEMOPTYSIS maintaining adequate gas exchange,

preventing blood from spilling into unaffected areas of the lung,
and avoiding asphyxiation are the highest priorities
Keeping the patient at rest and partially suppressing cough may help
the bleeding to subside
If the origin of the blood is known and is limited to one lung, the
bleeding lung should be placed in the dependent position, so that
blood is not aspirated into the unaffected lung
TREATMENT of
HEMOPTYSIS:
With massive bleeding, the need to control the airway and
maintain adequate gas exchange may necessitate ET
intubation and MV

In patients in danger of flooding the lung contralateral to

the side of hemorrhage despite proper positioning, isolation
of the right and left mainstem bronchi from each other can
be achieved by selectively intubating the nonbleeding lung
or by using specially-designed double-lumen ET tubes

Another option involves inserting a balloon catheter through

a bronchoscope by direct visualization and inflating the
balloon to occlude the bronchus leading to the bleeding site
TREATMENT of
HEMOPTYSIS:
Other available techniques for control of
significant bleeding:
laser phototherapy
electrocautery
embolotherapy
surgical resection of the involved area of lung
DYSPNEA:
DYSPNEA is defined as an abnormally uncomfortable awareness
of breathing

MECHANISMS of DYSPNEA:
Dyspnea is characterized by an excessive or abnormal activation of
the respiratory centers in the brainstem

The activation comes about from stimuli transmitted from or

through a variety of structures and pathways, including:
(1) INTRATHORACIC RECEPTORS via the vagal nerves
(2) AFFERENT SOMATIC NERVES, particularly from the respiratory muscles

and chest wall, but also from skeletal muscles and joints
(3) CHEMORECEPTORS in the brain, aortic and carotid bodies

(4) higher (CORTICAL) centers

(5) AFFERENT FIBERS in the phrenic nerves

LIKELY MECHANISMS of DYSPNEA in
SELECTED CONDITIONS:
ASTHMA: Increased sense of effort
Stimulation of irritant receptors in airways

NEUROMUSCULAR DISEASE: Increased sense of effort

COPD: Increased sense of effort

Hypoxia
Hypercapnea

MECHANICAL VENTILATION: Afferent mismatch

Factors associated with the underlying
condition

PULMONARY EMBOLISM: Stimulation of pressure receptors in pulmonary

vasculature or right atrium
DIFFERENTIAL DIAGNOSIS of
DYSPNEA:
1. OBSTRUCTIVE DISEASE of AIRWAYS:
A. EXTRATHORACIC
1. aspiration of food or a foreign body, or with

angioedema of the glottis

2. acute upper airway obstruction

3. chronic upper airway obstruction tumors, fibrotic

stenosis following tracheostomy or prolonged ET

intubation

B. INTRATHORACIC
1. acute intermittent obstruction asthma

2. chronic chronic bronchitis, bronchiectasis, emphysema

DIFFERENTIAL DIAGNOSIS of
DYSPNEA:
2. DIFFUSE PARENCHYMAL LUNG DISEASES:
Acute pneumonia
Sarcoidosis
Pneumoconiosis

3. PULMONARY VASCULAR OCCLUSIVE DISEASES:

Recurrent pulmonary emboli

4. DISEASES of the CHEST WALL or RESPIRATORY MUSCLES:

Kyphoscoliosis
Pectus excavatum
Ankylosing spondylitis
Neurologic or muscular disorders
DIFFERENTIAL DIAGNOSIS of
DYSPNEA:
5. HEART DISEASE:
EXERTIONAL DYSPNEA:
occurs most commonly as a consequence of an elevated pulmonary
capillary pressure
may be due to LV dysfunction, reduced LV compliance, and MS

The elevation of hydrostatic pressure in the pulmonary vascular

bed results in transudation of liquid into the interstitial space,
reducing the compliance of the lungs and stimulating
juxtacapillary receptors in the alveolar interstitial space

Pulmonary venous hypertension results in thickening of the walls

of small pulmonary vessels and an increase in perivascular cells
and fibrous tissue, causing a further reduction in compliance
DIFFERENTIAL DIAGNOSIS of
DYSPNEA:
5. HEART DISEASE:
The competition for space among vessels, airways, and increased
fluid within the interstitial space compromises the lumina of small
airways, increasing the airways resistance

Diminution of compliance and an increase in the airways resistance

increase the work of breathing

CONGESTIVE HEART FAILURE:

involves elevation of both pulmonary and systemic venous pressures and

may cause hydrothorax, interfering further with pulmonary function and

intensifying dyspnea
ORTHOPNEA, i.e., dyspnea in the supine position, is the result of the

alteration of gravitational forces when this position is assumed, which

elevates pulmonary venous and capllary pressures, thus increasing the
pulmonary closing volume and reducing vital capacity
PAROXYSMAL NOCTURNAL DYSPNEA
(PND):
Also known as CARDIAC ASTHMA

Characterized by attacks of severe SOB that generally

occur at night and usually awaken the patient from
sleep

The attack is precipitated by stimuli that aggravate

previously existing pulmonary congestion

The total blood volume is augmented at night because

of the reabsorption of edema from dependent portions
of the body during recumbency
PAROXYSMAL NOCTURNAL DYSPNEA
(PND):
DIFFERENTIAL DIAGNOSIS:
1. CHRONIC BRONCHITIS:
Characterized by mucus hypersecretion , and after a few

hours sleep, secretions can accumulate and produce

dyspnea and wheezing, both of which are relieved by
cough and expectoration of sputum

2. ASTHMA:
Asthma patients have circadian variations in their degree

of airway obstruction, and the obstruction becomes most

severe between 2 A.M. and 4 A.M. which can be sufficiently
severe that the patient awakens with a sense of
suffocation, extreme dyspnea and wheezing
CHEYNE-STOKES
RESPIRATION:
Also known as PERIODIC RESPIRATION or CYCLIC RESPIRATION

Characterized by diminished sensitivity of the respiratory center to arterial

PCO2

PHASES:
1. APNEIC PHASE- the arterial PO2 falls and the arterial PCO2 rises and the
changes in the arterial blood stimulate the depressed respiratory center
2. HYPERVENTILATION and HYPOCAPNIA, followed in turn by the recurrence of
apnea

Cheyne-Stokes respiration occurs most often in:

patients with cerebral AS and other cerebral lesions
the prolongation of the circulation time from the lung to the brain that occurs
in HF, particularly in patients with HTN and CAD, also appears to contribute to
this form of disordered breathing
DIFFERENTIATION between CARDIAC
and PULMONARY DYSPNEA:
In patients in whom the etiology of dyspnea is not clear, it is
desirable to carry out PFT, for these tests may be helpful in
determining whether dyspnea is produced by heart disease,
lung disease, abnormalities of the chest wall, or anxiety

Determination of the EJECTION FRACTION at rest and

during exercise by ECHOCARDIOGRAPHY or
RADIONUCLIDE VENTRICULOGRAPHY is helpful in the
differential diagnosis of dyspnea:
LV ejection fraction id depressed in LV failure
RV ejection fraction may be low at rest or may decline during exercise

in patients with severe lung disease

Both left and right venticular EF are normal at rest and during exercise

in dyspnea due to malingering or anxiety

DIFFERENTIATION between CARDIAC
and PULMONARY DYSPNEA:
EXERCISE TREADMILL TEST:
helps in the identification of the patient who is
malingering or whose dyspnea is secondary to anxiety

CARDIOPULMONARY TESTING:
the patients maximal functional exercise capacity is
assessed while measurements of the ECG, BP, oxygen
consumption, arterial saturation (oximetry), and
ventilation are carried out
useful in the differentiation between cardiac and
pulmonary dyspnea
PATTERNS of ABNORMALITY in
CARDIOPULMONARY EXERCISE TESTING:
CARDIOVASCULAR LIMITATION:
Heart rate >85% of predicted maximum
Low anaerobic threshold

Reduced maximal oxygen consumption

Drop in BP with exercise

Arrhythmias or ischemic changes on ECG

Does not achieve maximal predicted ventilation

Does not have significant desaturation

RESPIRATORY LIMITATION:
Achieves or exceeds maximal predicted ventilation
Significant desaturation (<90%)

Stable or increased dead space-to-TV ratio

Development of bronchospasm with falling FEV1

Does not achieve 85% of predcited maximal heart rate

No ischemic ECG changes

DYSPNEA in ANXIETY
STATES:
NEUROCIRCULATORY ASTHENIA:
When HYPERVENTILATION SYNDROME is present and
accompanied by chest pain and ECG changes, the chest pain
is often sharp, fleeting and in various loci, and the ECG
changes are most often seen during repolarization

Frequent sighing respirations and an irregular breathing

pattern point to a PSYCHOGENIC origin of the dyspnea

Anxiety and depression in association with heart or lung

disease can serve to intensify dyspnea symptoms beyond
what would be expected for a given degree of dysfunction