COUGH, DYSPNEA AND

HEMOPTYSIS
• COUGH
Definition:
• Cough is an protective mechanism that
ensures the removal of mucus, noxious substances,
and infectious organisms from the larynx, trachea,
and large bronchi .

• Cough is an explosive expiration that provides a

normal protective mechanism for clearing the
tracheobronchial tree of secretions and foreign
material.
 MECHANISM OF COUGH
• Coughing may be initiated either voluntarily or
reflexively.

• As a defensive reflex it has both afferent and efferent

pathways .
• Cough receptors:
– They are located in different parts of the
respiratory system such as larynx , pharynx ,
trachea, bronchi
– consists of rapidly adapting receptors and C-fibers
– When they are exposed to irritating substances,
they are stimulated
• Afferent pathway
– Impulses are transmitted along the
glossopharyngeal nerves to the cough center
• Cough center
– It is located in the nucleus of tractus solitarius in
the medulla oblongata.
– It receives impulses from the cough receptors and
initiates cough.

• Efferent pathway
The efferent messages of the cough reflex
travel down the vagus to the larynx and by the spinal
nerves to diaphragmatic,thoracic, abdominal and
pelvic muscles, all of which contract during a cough.
• Sequence of events in cough
– There is an initial deep inspiration
– Then the glottis and vocal cord closes
– The diaphragm relaxes
– The abdominal muscles and intercostal muscles
contract
– The pressure within the lungs builds up – upto
100mm of Hg
– The glottis and vocal cords open resulting in a rapid
release of air under pressure – speeds of upto 100
miles/hour
– The sound produced is due to the turbulent flow of air
– It helps to remove any irritant substances from the
respiratory system
• Acute cough (<3 weeks)
Is most often due to upper respiratory infection
(common cold, acute bacterial sinusitis, and
pertussis), pneumonia, pulmonary embolus, and
congestive heart failure, can also present with acute
cough.

• Sub acute cough (between 3 and 8 weeks)

Is commonly post-infectious, resulting from
persistent airway inflammation and/or postnasal drip
following viral infection, pertussis, or infection with
Mycoplasma or Chlamydia.
• Chronic cough (>8 weeks)
Asthma, COPD or bronchogenic carcinoma,
Eosinophilic Bronchitis , Post Nasal Drip , ACEI
induced , Smoking.
 Approach to the Patient
• A detailed history
• Physical examination
• Chest radiography
• Pulmonary function testing
• Gross and microscopic examination of sputum
• High-resolution computed tomography (HRCT)
• Fiberoptic bronchoscopy
 Cough: Treatment
• Definitive treatment of cough depends on
determining the underlying cause and then
initiating specific therapy.

• Elimination of an exogenous inciting agent

(cigarette smoke, ACE inhibitors) or an endogenous
trigger (postnasal drip, gastro esophageal reflux).

• Empirical approach to treatment is with an

antihistamine-decongestant combination, nasal
glucocorticoids, or nasal ipratropium spray to treat
unrecognized postnasal drip
• GERD
 Antacids, histamine type-2 (H2) receptor
antagonists, and proton-pump inhibitors are
used to neutralize or decrease production of
gastric acid
 dietary changes,
 elevation of the head and torso during sleep.
• Chronic idiopathic cough
 Narcotic cough suppressants like codeine ,
hyrocodone which increases the latency or threshold
of the cough center.
 Dextromethorphan is a non narcotic over-the-
counter, centrally acting cough suppressant with
fewer side effects and less efficacy compared to the
narcotic cough suppressants.
•
 DYSPNEA
• Definition
Dyspnea is defined as the uncomfortable
or abnormal awareness of one’s own
breathing in the context of what is normal for
a person according to his/her level of fitness
and exertional threshold of breathlesness.
• PATHOPHYSIOLOGY
Dyspnea results when there is an imbalance between
the need to breathe and the perceived ability to breathe.
Receptors involved:
 J receptors:situated at the alveolocapillary
junction.Stimulated by pulmonary congestion,edema and
microemboli.
 Stetch receptors in the thoracic cage and lung
 Chemoreceptors in the carotid arteries ,aorta and
and medulla ,stimulated by hypoxia, hypercarbia and
acidosis.
 Receptors in respiratory muscles
•
•
• Treatment: Dyspnea
• The first goal is to correct the underlying problem
responsible for the symptom.
• Mehanical or non invasive ventilation can be life
saving
• If this is not possible, one attempts to lessen the
intensity of the symptom and its effect on the
patient's quality of life.
• Supplemental O2 should be administered if the
resting O2 saturation is ≤ 89% or if the patient's
saturation drops to these levels with activity.
• For patients with COPD, pulmonary
rehabilitation programs have demonstrated
positive effects on dyspnea, exercise capacity,
and rates of hospitalization.
 HEMOPTYSIS
• Hemoptysis is the expectoration of blood from the
respiratory tract
• It can arise from any part of the respiratory tract,
from the alveoli to the glottis.
• It is important, however, to distinguish hemoptysis
from and hematemesis
• Hemoptysis can range from blood-tinged sputum to
life-threatening large volumes of bright red blood
• Massive haemoptysis has been arbitrarily
defined as a loss of more than 500ml of blood
over 24 hours or more than 150 ml per hour.
• It is a life-threatening medical emergency.
• HEMOPTYSIS can arise from the bronchial or
pulmonary circulation.
• Bronchial Circulation:
• Is the source of bleeding in the majority of
cases of hemoptysis and it also represents the
source of most episodes of massive
hemoptysis, because it arises from aorta and
is under systemic pressure.
Mechanisms by which massive hemoptysis is produced 
: include the following
1/ Chronic parenchyma inflammation leading to erosion of
bronchial and vascular walls ,enlargement and proliferation
of bronchial vessels, and formation of anastamoses
between bronchial and pulmonary circulation and
formation of bronchiectasis or lung abscesses.
2/ Various vascular alteration, such as aneurismal
formation, vasculitis and embolism.
Erosion of a calcified lymph node into the /3 
tracheobronchial tree. 4/
.vascular invasion by tumor
• Haemoptysis Hematemesis
• No nausea or vomiting Nausea and vomiting
• Concurrent lung disease Concurrent gastric or
hepatic disease

Sputum has a clotted appearance Typical coffee ground

apperance
• Haemoptysis is bright red Haematemesis is
brown to black
• Alkaline pH Acidic pH

• Mixed with macrophages and neutrophils Mixed with food

particles
• APPROACH
 History:
Nature of hemoptysis:whether blood-tinged,
purulent secretions; pink, frothy sputum; or frank blood
Quantity
 Physical examination:
vital signs and oxygen saturation
Clubbing of the digits may suggest underlying
lung diseases such as bronchogenic carcinoma or
bronchiectasis, lung abcess.
• INVESTIGATIONS
CHEST X RAY
CT CHEST
Laboratory studies : complete blood count to
assess both the hematocrit as well as platelet
count and coagulation studies.
Renal function and urinalysis should be
assessed because of the possibility of
pulmonary-renal syndromes presenting with
hemoptysis.
• Acute renal insufficiency, or red blood cells or red
blood cell casts on urinalysis should increase
suspicion for small-vessel vasculitis, and studies such
as antineutrophil cytoplasmic antibody (ANCA),
antiglomerular basement membrane antibody (anti-
GBM), and antinuclear antibody (ANA), should be
considered.
• Sputum for Gram and acid-fast stains as well as
culture should be obtained.
• If all of these studies are unrevealing,
bronchoscopy should be considered.
• TREATMENT
 Based on its etiology. Treatment of underlying
cause
 Large-volume, life-threatening hemoptysis
generally requires immediate intervention regardless
of the cause.
 establish a patent airway usually by
endotracheal intubation and subsequent mechanical
ventilation
 site of the bleeding can be identified either by chest
imaging or bronchoscopy
• Patients should be placed with the bleeding lung in a
dependent position (i.e., bleeding-side down) and, if
possible, dual lumen endotracheal tubes or an airway
blocker should be placed in the proximal airway of
the bleeding lung
• If the bleeding does not stop with therapies of the
underlying cause and passage of time, severe
hemoptysis from bronchial arteries can be treated
with angiographic embolization of the culprit
bronchial artery.
• In extreme conditions, surgical resection of the
affected region of lung is considered.