presentation on cough and dyspnea

1. Moderator-Dr.Balbir Malhotra
Presentor-Dr.Amit Goyal

2. COUGH – it is a sudden and variable expiratory
thrust of air from the lungs through the air
passages associated with phonation, which
momentarily interrupts the physiological pattern
of breathing
Without an effective cough reflex, there is a risk
of retaining airway secretions and aspirated
material predisposing to infection， atelectasis，
and respiratory compromise

3. 1. Rapid inspiration
2. Closure of the glottis
3. Contraction of the abdominal and expiratory thoracic muscles
4. Abrupt increase in pleural and intrapulmonary
pressures
5. Opening of glottis and expulsion of burst of air from
mouth
MECHANISM:

4. PHASES OF COUGH:
INSPIRATORY
COMPRESSIVE
EXPULSIVE
RECOVERY

6. PATHOPHYSIOLOGY OF COUGH

7. Cough reflex initiated by chemical/mechanical
stimuli
This is carried by the afferents which are type c
and type 1 fibers and innervate pharynx, larynx
,large airways , terminal bronchiole and lung
parenchyma
Afferents travel via vagus and superior laryngeal
nerve
NTS in brain stem is the cough center
Efferents travel via vagus, phrenic, spinal motor
nerves to the larynx, trachea, bronchi,
diaphragm producing cough

9.  Cough receptors- rapid acting receptors (RAR),
slow acting receptors (SAR), C fibers, and other
cough receptors are Mechanosensitive and
chemosensitive.
 Impulses from these receptors are all carried by
the vagus nerve

10. •The receptors have nerve terminals under or within the
epithelium concentrated at points of airway branching.
•They are polymodal and respond to a wide variety of
chemical n mechanical irritants, & by many inflammatory n
immunologic mediators like histamine, bradykinin, PGs n
substance-P.

11.  There occurs increase in sensitivity of RARs n C-fibers by
allergen challenge, viral infections, cigarette smoke and a
variety of inflammatory mediators.
 RARs can also be sensitized by mucus in the airways,
underlying smooth muscle contraction n mucosal edema.

12. Voluntarily a person is capable of
suppressing the reflex cough for some time
Cough can also be voluntarily induces (motor
and pre motor areas of brain)
Neuro transmitters involved in voluntary
control of cough are seratonin, gaba,
dopamine, nmda(N-methyl-D-aspartate ) etc
The central nervous pathways for cough show
interactions and plasticity

13. Efforts should be made to identify the cause
of cough
A cough lasting than more than 3 wks
require a detailed evaluation
Cough associated with or without sputum is
more important than the amount of sputum
and the presence or absence of sputum
should not be taken as a strict criterion for
diagnosis

14. Considerations at 1st visit
 Determine the severity
 Assess the cause
 Plan investigation and treatment

15. APPROACH TO
THE PATIENT OF
COUGH

16. Cough: onset,
duration,
character,
nature, triggers
Sputum-volume & character
Postural variations
Diurnal variations
Smoking, occupation
Drug history(ACE inhibitors)
And any ass.factors

17. HISTORY
 Onset-Acute <3 weeks
SubAcute 3-8 weeks
Chronic >8 weeks
.Character- BRASSY
WHOOPING
BOVINE
.Nature- Dry or Productive
Productive maybe –Mucoid
-Mucopurulent
-Purulent
Chronic bronchitis
Bronchietasis
Pneumonia and lung abcess

18. Sputum
 Rust coloured sputum - pneumococcal pneumonia
 Red currant jelly - klebsiella infection
 Foul smelling s/o anaerobic infection
 Pink frothy sputum - pulmonary oedema
 Black coloured sputum(melanoptysis) - coal workers’
pneumoconiosis
 Anchovy sauce sputum - ruptured amoebic liver abscess

19. ACUTE (<3 WKS)
 Tracheobronchitis
 Bronchopneumonia
 Viral pneumonia
 Acute-on-chronic bronchitis
 Pertussis
 Pulmonary embolism
 Foreign body aspiration
 Sudden onset – bronchial asthma ,asthmatic
bronchitis , whooping cough, foreign body
,LVF with PE

20. SUBACUTE (3-8 wks )
 trachiobronchitis ,
 pertussis ,
 post viral tussive syndrome

21. CHRONIC > 8 wks
• Upper airway cough syndrome
• Asthma
• Gastro oesophageal reflux disorder
• Post viral cough
• Chronic bronchitis
• Bronchiectasis, cystic fibrosis
• Ace inhibitor induced Cough
• Environmental irritants.

22. • Infections – Mycoplasma,
Chlamydia Bordetella
• Granulomatous disease –TB ,
Sarcoidosis.
• Neoplasms – Bronchogenic
carcinoma,Carcinoid tumor
• ILD

23. Micro aspirations
Zenker’s diverticulum
CVS – Disorders of pericardium, CCF,
Vasculitis
Tourette syndrome
Habitual or psychogenic cough.
Asymptomatic enlarged tonsils

24. Based on expectoration
• Dry cough: pleural disorders , diseases of
interstitium, mediastinal lesions
• Productive cough: suppurative lung disease,
airway diseases

25. Brassy/Gander cough –metallic sound d/t
compression of trachea by intra thoracic
space occupying lesions or aortic aneurysms
also known as leopards growl
Bovine cough –loss of expulsive nature as in a
tumour pressing on the recurrent laryngeal
nerve
Paroxysmal cough – chronic bronchitis,
foreign body , bronchial asthma

26. Barking cough – involvement of
epiglottis , croup( laryngo
trachiobronchitis) , hysteria
Whooping cough – pertussis
Spluttering cough- s/I T-E fistula ,
cough while swallowing

27. Lobar pneumonia – the cough is initially dry
a/w chest pain later becomes productive
Chronic bronchitis – productive cough for
most days of 3 months for 2 consecutiveyrs
Bronchiectasis – copious amt of foul smelling
sputum more on lying down
Gastro esophageal reflux disorder -
Nonproductive cough often following meals
with or without symptoms of GERD

28. Left ventricular failure - Cough intensifies
while supine, along with aggravation of
dyspnea
Angiotensin-converting enzyme (ACE)
inhibitors Nonproductive cough, more
common in women, may occur at any time ,
neurokinin 1 receptor polymorphism

29. INVESTIGATIONS
 CHEST X-RAY: Findings may include
 intrathoracic mass lesion,
 localised pulmonary parenchymal opacification or diffuse
interstitial or alveolar disease.
 Honeycombing or cyst formation may suggest
bronchiectasis
 symmetrical bilateral lymphadenopathy may suggest
sarcoidosis.
 PFT: To differentiate between restrictive and
obstructive diseases.
 HRCT

30. INVESTIGATIONS
SPUTUM EXAMINATION:
- volume
- colour
- odor
-consistency
- gram staining n culture
-acid fast staining
-cytology for malignancy
*>3% eosinophils in sputum of a patient without
asthma suggests the possibility of
EOSINOPHILIC BRONCHITIS.

31. INVESTIGATIONS
 OTHER INV:
 24 hr pH monitoring/endoscopy: to r/o GERD
 Fibreoptic bronchoscopy : to r/o endobronchial tumours n
collect biopsies.
 CT scan of sinuses, Allergy tests : for PND
 ECG / echocardiography : to r/o cardiac cause

32. Cough lasting less than 3 wks
Usually it is due to viral and bacterial
infections of upper respiratory tract
Usually the cough resolves within 2 wks
Other symptoms that can be associated
with cough are post nasal discharge ,
nasal obstruction, nasal discharge

33. CHRONIC COUGH
 Although there are numerous causes for cough,the
most common causes of chronic cough and sputum
(defined as lasting longer than 8 weeks) are
 Postnasal drip/ Upper airway cough
syndrome(UACS)
 Gastroesophageal reflux disease (GERD)
 Asthma.
 Non asthmatic eosinophilic
bronchitis(NSEB)

34. CHRONIC COUGH
Postnasal Drip (Rhinosinusitis, Upper Respiratory
Tract Syndrome):
 most common cause of chronic cough.
 Postnasal drip (“nasal catarrh”) is characterized by a
sensation of nasal secretions or of a “drip” at the back of the
throat, accompanied very often by frequent need to clear the
throat (“throat-clearing”).
 nasal quality to the voice
 Physical examination of the pharynx - a “cobblestoning”
appearance of the mucosa and draining secretions may be
observed.
 Computed tomography of the sinuses may reveal mucosal
thickening or sinus opacification and air-fluid levels.

35. TREATMENT:
 Topical administration of corticosteroid drops in the head-
down position is the best treatment, often with the
concomitant use of antihistamines.
 severe symptoms- short course of oral steroids, followed by
topical therapy.
 A topical anticholinergic spray to the nose (such as
ipratropium bromide).
 Antibiotic therapy is necessary in the presence of acute
sinusitis involving bacterial infection with the presence of
mucopurulent secretions that has persisted for at least 10
days.

36. CHRONIC COUGH
Asthma & Associated Eosinophilic
Conditions:
Asthma may present predominantly with cough,
often nocturnal,reversible airflow limitation
and bronchial hyperresponsiveness.
 This condition of “cough-variant” asthma is a
common type of asthma in children.
Eosinophilic bronchitis is characterized by
cough without asthma symptoms or bronchial
hyperresponsiveness but with eosinophilia in
sputum.

37. Cont.
 A predominance of eosinophils in induced sputum
and bronchial biopsies, together with a thickened
basement membrane and bronchial
hyperresponsiveness,is present in cough-variant
asthma.
 In eosinophilic bronchitis, conversely, cough
responsiveness to capsaicin is increased without
bronchial hyperresponsiveness,but the
immunopathologic abnormalities are similar to those
of asthma

38. CHRONIC COUGH
Gastroesophageal Reflux:
 GER may lead to symptoms of physical
complications such as heartburn,chest pain, a sour
taste, or regurgitation, and also a chronic
persistent cough.
 Coughing itself may precipitate reflux,setting a
vicious circle of acid inducing–cough that in turn
induces acid reflux.
 laryngeal symptoms may be present with
dysphonia,hoarseness, and sore throat; often,
posterior vocal cord laryngeal inflammation is
visible.
 antireflux treatment with a proton pump inhibitor
or a histamine H2-antagonist

39. Cough variant Asthma
Upper airway cough syndrome
Aspiration
Habitual cough
Foreign body
Drugs Angiotensin converting enzyme inhibitors
Chronic bronchitis

40. Chronic idiopathic cough,
narcotic cough suppressants， such as
codeine or hydrocodone
Dexomethorphan can also be used
Case series have reported benefit from off-
label use of gabapentin or amitryptyline for
chronic idiopathic cough.

41. In paediatric age group cough more than 4
wks is considered chronic
 Most common cause of chronic cough in
infants is aspiration and congenital heart
defects
 2-5 yrs – foreign body inhalation , hyper
reactive airways
 Adolescents – hyper reactive airways,
infections

42. RESPIRATORY
Pneumothorax
Subcutaneous emphysema
Pneumomediastinum
Pneumoperitoneum
Laryngeal damage
CARDIOVASCULAR
Cardiac dysrhythmias
Loss of consciousness or cough syncope
Subconjunctival hemorrhage

43. CENTRAL NERVOUSSYSTEM
Syncope Headaches
Cerebral air embolism
MUSCULOSKELETAL
Intercostal muscle pain
Rupture of rectus abdominis muscle
Increase in serum creatine phosphokinase
Cervical disc prolapse

44. GASTROINTESTINAL
Esophageal perforation
OTHER
Social embarrassment
Depression Urinary incontinence
Disruption of surgical wounds
Petechiae Purpura

46. Treating the Specific Underlying Cause
 Cough-Variant asthma
 Eosinophilic bronchitis
 Allergic rhinitis and postnasal
drip
 Gastro esophageal reflux
 Bronchodilators and inhaled
corticosteriods
 Inhaled corticosteroids
Leukotriene inhibitors
Topical nasal steroids
Antihistamines
 Topical nasal anticholinergics
(with antibiotics, if
indicated)
 Histamine H2 antagonist or
proton pump inhibitor

47. Treating the Specific Underlying Cause
 Angiotensin-converting
enzyme inhibitor
 Chronic bronchitis/COPD
 Bronchiectasis
 Infective Traheobronchitis
 Discontinue and replace
with alternative drug such as
angiotensin II receptor
antagonist
 Smoking cessation
Treat for COPD
 Postural drainage, Treat
infective exacerbation and
airflow obstruction.
 Appropriate antibiotic
therapy.
Treat any postnasal drip.

48. TREATMENT OPTIONS FOR COUGH
Antitussives
Antihistamines
Bronchodilators
Pharyngeal demulcents
Expectorants and mucolytics

49. ANTITUSSIVE AGENT
• Morphine
•Dihydro-
morphinone
• Codeine
• pholcode
ine
• Dexomet
horphan
• noscapin
e
,
• Diphenhydram
ine
• Benzonatate
• Triprolidine

50. Depression of
medullary centres or
associated higher
centres.
Increased threshold
of cough centre

51. An opium alkaloid.
It is more selective for cough centre.
Suppresses cough for about 6 hours.
The antitussive action is blocked by
naloxone.
Cough suppression occur with low doses of
opioids than those needed for
analgesia.(sub-analgesic dose 15 mg)
Abuse liability is low, but present.
Adverse Effects
•Constipation.
•Respiratory depression & drowsiness

52. raises threshold for cough & depresses
cough centre in medulla.
It has been found to enhance the
analgesic action of morphine & other μ
receptors agonists
As effective as codeine, does not depress
mucociliary function of the airway
mucosa.

53. Devoid of addicting actions.
Produces less constipation than codeine
Antitussive action for 6 hours.
it does not act through opioids
receptors.
Side effects:
Dizziness, nausea, drowsiness & ataxia.

54. Demulcents. promotes salivation & inhibit
impulses from inflamed mucosa
Linctus Thick liquid preparation
containing sucrose and medicinal
substance
Throat lozenges:They have lubricating
and soothing effect on irritated tissue of
throat may contain benzocaine or
dextromethorphan.
-They suppress cough reflex by decreasing the input of
stimuli from cough receptors in respiratory passages

55. Drugs which render sputum less visous
Inhalational:
• Acetylcysteine,
Oral :
•Acetylcysteine,
•Bromohexine,
•Carbocysteine,
• Methylcysteine.
Clinical Uses
Acute & chronic bronchitis.
Bronchial asthma

56. Drugs which ↑ bronchial secretions or
reduces its viscosity facilitating its removal
by coughing
Ipecacuanha
Ammonium chloride
Ammonium bicarbonate.
Terepin hydrate
Potassium Iodide
Guaiphenesin
Sodium or Potassium citrate

58. DEFINITION“A subjective experience of breathing discomfort
that is comprised of qualitatively distinct sensations
that vary in intensity.
The experience derives from interactions among
multiple physiological, psychological, social and
environmental factors and may induce secondary
physiological and behavioural responses.”

59. DYSPNEA…. breathing is difficult, laboured or uncomfortable
 subjective
 awareness of need for increased respiratory effort
 ventilatory demands > ventilatory capacity

60. Pathophysiology of Dyspnea
 Dyspnea results when there is an imbalance between
the perceived need to breathe and the perceived ability
to breathe.
 CO2 build up and oxygen deprivation were the critical
factors that result in dyspnea.
 Elevation in CO2 levels appear to stimulate dyspnea
more than do low oxygen levels

61.  Respiratory effort is believed to originate as a signal
transmitted from the motor cortex simultaneously to
the sensory cortex and to the motor command to
ventilatory muscles. The brain stem may also
contribute to the sense of effort.
 The perception of air hunger is believed to arise, in
part, from increased respiratory activity within the
brain stem,
 sensation of chest tightness probably results from
stimulation of vagal irritant receptors

62. MECHANISMS OF DYSPNEA
 Mechanical interference with
ventilation
 Weakness of the respiratory pump
 Increased respiratory drive
 Increased wasted ventilation
 Psychological dysfunction

63. MECHANICAL INTERFERENCE
 Obstruction to airflow- asthma, endobronchial
tumour
 Stiff lungs – interstitial fibrosis, LVF
 Resistance to expansion of chest
wall/diaphragm/kyphoscoliosis,
 obesity, abdominal mass

64. pump
 Absolute - neuromuscular diseases
 Relative - muscle at a mechanical disadvantage (Eg
hyperinflation, pneumothorax, effusion)
Increased respiratory drive
 hypoxemia of any cause
 Metabolic acidosis
 Stimulation of intrapulmonary receptors

65. Increased wasted ventilation
 Capillary obstruction (emphysema, ILD)
 Large vessel obstruction (PE, vasculitis)
Psychological dysfunction
 Anxiety
 Depression
 Somatization
 Alleged respiratory injury

66. CAUSES OF DYSPNEA
Acute
Pulmonary edema
Asthma
Injury to chest wall and intrathoracic structures
Spontaneous pneumothorax
Pulmonary embolism
Pneumonia
Adult respiratory distress syndrome
Pleural effusion
Pulmonary hemorrhage
Foreign body aspiration
Vocal cord dysfunction
Pulmonary vascular disease
Psychogenic dyspnea
Anemia, severe
Postintubation tracheal stenosis
Hypersensitivity disorders
Chronic, progressive
Chronic obstructive pulmonary disease
Left ventricular failure
Diffuse interstitial fibrosis
Asthma
Pleural effusions
Pulmonary thromboembolic disease

67. DYSPNEA AS DESCRIBED BY THE
PATIENT
Chest tightness- MI, asthma
Suffocation or air hunger-
Pulmonary edema
Inability to take enough air-COPD
Breathlessness experienced during
rest mostly and not during work-
psychogenic in origin.

69. Modified Borg Category
Scale

70. NEW YORK HEART ASSOCIATION GRADING
 GRADE I No limitations. Ordinary physical activity does not cause
undue fatigue, dyspnea or palpitations (asymptomatic left ventricular
dysfunction)
 GRADE II Slight limitation of physical activity. Such patients are
comfortable at rest. Ordinary physical activity results in fatigue, palpitations,
dyspnea or angina pectoris (symptomatically ‘mild’ heart failure)
 GRADE III Marked limitation of physical activity. Less than ordinary
physical activity will lead to symptoms (symptomatically ‘moderate’ heart
failure)
 GRADE IV Symptoms of congestive cardiac failure are present even
at rest. With any physical activity increased discomfort is experienced
(symptomatically ‘severe’ heart failure)

71. American Thoracic Society Shortness of
Breath Scale

72. MECHANICS OF DYSPNEA
 Dyspnea can occur either when there is an increase in
work of breathing or energy cost of breathing.
 Work of breathing can be thought to be made up of three
components—elastic component(increased in pulmonary
congestion), resistive component (increased in COPD) and
inertial component.

73. Dyspnea in COPD
 In normal individuals, during expiration, exhalation of air
is assisted by elastic recoil of the lung and is opposed by
airway resistance
 In COPD due to progressive loss of elastic recoil of lung
and increase in airway resistance there is incomplete
exhalation of air from the lung and there is increasing
amount of air trapping– lungs are in a state of
hyperinflation
 Due to hyperinflation of the lungs the respiratory muscles
face a number of mechanical disadvantages– thereby
increasing the work of breathing as well as 02 cost of
breathing .

74. DYSPNEA IN RESTRICTIVE LUNG DISEASES
 In patients with widespread pulmonary fibrosis the
minute ventilation is largely maintained by increase in
respiratory rate and this increases the work and energy
cost of breathing– dyspnea.

75. HEART DISEASE
Exertional dyspnea occurs most commonly as a consequence of
an elevated pulmonary capillary pressure, which in turn may
be due
 to left ventricular dysfunction
 Reduced left ventricular compliance
 Mitral stenosis

76. Mechanism of Dyspnea in Heart Disease
Elevation of hydrostatic pressure in the pulmonary
vascular bed
Upsetting of STARLING EQUILIBRUM
Resulting transudation of liquid into the interstitial
space
Reduction of the compliance of lungs and
stimulation of J (juxtacapillary) Receptors in the
alveolar interstial space

77. ORTHOPNEA
i.e. dyspnea in the supine position
Alteration of gravitational forces when supine position is
assumed
Elevates pulmonary venous and capillary pressure
Increases pulmonary closing volume and reduce the vital
capacity

78. OTHER VARIANTS
 TREPOPNEA
Dyspnea occurs only in lateral decubitus position,
most often in heart disease
 PLATYPNEA
Dyspnea that occurs only in upright position usually
due to alterations in ventilation-perfusion
relationships
 Causes
 Left atrial thrombus
 Left atrial tumours
 Pulmonary ateriovenous fistula

79. PAROXYSOMAL NOCTURNAL DYSPNEA/
CARDIAC ASTHMA
 Attacks of severe shortness of breath that generally occur at
night and usually awaken the patient from night
 PND is caused by depression of the respiratory center during
sleep which may reduce arterial O2 tension.
 Precipitated by stimuli that aggravate pulmonary congestion;
the total blood volume is augmented at night because of the
resorption of edema from dependent parts of the body during
recumbency
 A sleeping patient can tolerate relatively severe pulmonary
engorgement and may awaken only when actual pulmonary
edema and bronchospasm have developed, with the feeling
of suffocation and wheezing respirations

80. Asthma
Circadian variations in degree of obstruction
Most severe between 2 AM and 4 AM
Patients awaken with sense of suffocation, extreme
dyspnea and obstruction
Predominantly inflammatory but inhaled
bronchodilators usually improve symptom quickly

81. DIFFUSE PARENCHYMAL LUNG DISEASE
 Includes
 Acute disorders like pneumonia
 Chronic disorders such as sarcoidosis and various pneumoconiosis
 Patients are often tachypneic with arterial Pco2 and Po2 values
below normal
 Lung volumes are decreased and lungs are stiffer, i.e. less
compliant, than normal.

82. dyspnea
HISTORY
1) Age of onset–
 congenital-TE Fistula, laryngeal web, vascular ring,
 early and late infancy- congenital infections like CMV,
rubella leading to interstitial pneumonia,CHD
 preschool and school age-foreign body, , whooping
cough and asthma,
 adults- COPD,
 old age-cardiac cause.

83. 2) MODES OF ONSET, DURATION & PROGRESSION
Minutes to
Hours
Hours to
Days
Months to
Years
Pneumothorax
Acute asthma
Pulmonary
edema
Pulmonary
embol.
Foreign body
inhalation
Pneumonia
Pleural
Effusion
Anemia
LVF
Pulmonary
embolism
Pulmonary TB
COPD
Bronchial Ca
Fibrosing
Alveolitis
Chest wall
deformity and
Progressive
myopathies.

84. 3)Variability-
Diurnal—
 Asthma
 2-4A.M.,
 , after a bout of laughing(asthma)
 after exercise
 Cardiac –
 PND
 After exertion
 on the first working day after a holiday - occupational
lung disease.
Seasonal-Increased during season changes
(asthma).

85. ACUTE DYSPNEA: DIAGNOSTIC VALUE OF ASSOCIATED SYMPTOMS
 With chest pain
 If lateralised & pleuritic consider
 Pneumonia
 Pulmonary Infarction
 Rib fracture
 Pneumothorax
 If central & non pleuritic
 Myocardial Infarction
 Massive Pulmonary Embolism
 Without chest pain, cough or
wheeze
 Pulmonary Embolism
 Tension Pneumothorax
 Hypovolemic Shock
 Metabolic Acidosis
 Without chest pain but with
cough and wheeze
 Asthma
 Pulmonary Edema
 Pneumothorax

86. 5) AGGRAVATING AND RELEIVING FACTORS
Increased in supine position- LVF .
Increased in upright position- A-V mal. at the lung base,
Lt. atrial thrombus, Lt. atrial tumor, hepato-
pulmonary syndrome .
Increased in lateral position- cardiac disease
Increasing with exertion- cardiac cause
Increased at rest- psychogenic origin

87. 6) Severity of dyspnea .
7) Occupation history– asbestos related lung
diseases(asbestosis), chronic beryllium disease,
occupational asthma(with latency or without
latency), coal worker’s pneumoconiosis, extrinsic
allergic alveolitis (hypersensitive pneumonitis- due
to exposure to organic material).

88. 8) Family history of allergy, collagen vascular
disease.
9)Addiction history– smoking history, cocaine,
opiate overdose
10) Exposure to indoor pollutants
11)Treatment history—radiation(radiation
pneumonitis developing 6 weeks to 6 months
after radiation) , drugs( amiodarone,
nitrofurantoin, busalfan, adenosine ,
anorexigens, etc ) .

89. INVESTIGATIONS—

90. INVESTIGATIONS
Tests Some possible
abnormalities
Some possible
diagnoses
Plain chest radiograph Cardiac enlargement
Vascular enlargement
Abnormal interstitial
markings
Pleural effusions
Hyperinflation
Nodule/masses
CHF
Infection
COPD
Neoplastic disease
Pulmonary function tests
Spirometry
Diffusing capacity
Inspiratory &
expiratory maneuvers
Obstructive ventilatory
defect(decreased
FEV1/FVC ratio)
Restrictive ventilatory
defect
Decreased
Increased
Decreased values
Asthma
COPD
ILD
ILD
Pulmonary vascular
disease
Alveolar hemorrhage
Respiratory muscle
weakness

91. Tests Some possible
abnormalities
Some possible
diagnoses
Computed
tomography
Abnormal interstitial
markings
Cystic changes
Lymphadenopathy
Vascular filling
defects
Ground-glass
opacities
ILD
CHF
Atelectasis
Pulmonary embolism
Neoplastic disease
Blood tests Elevated WBC count
Anemia
BNP
Creatine
HCO3
ABG
Infection
Anemia
Heart failure
Acidoses(respiratory
or metabolic)
Alkaloses(respiratory)

92. SYMPTOMATIC MANAGEMRNT OF DYSPNEA
REDUCE SENSE OF EFFORT AND IMPROVE RESPIRATORY
MUSCLE FUNCTION
 Energy conservation (e.g., pacing)
 Breathing strategies (e.g., pursed-lip breathing)
 Position (e.g., leaning forward)
 Correct obesity or malnutrition
 Inspiratory muscle exercise
 Respiratory muscle rest (e.g., cuirass, nasal
ventilation,transtracheal oxygen)
 Medications (e.g., theophylline)
 Quit smoking immediately
DECREASE RESPIRATORY DRIVE
 Oxygen
 Opiates and sedatives
 Exercise conditioning
 Vagal nerve section

93. ALTER CENTRAL NERVOUS SYSTEM FUNCTION
 Education
 Psychological interventions (e.g., coping strategies,
 psychotherapy, group support)
 Opiates and sedatives
USE EXERCISE TRAINING ALONE OR WITH
PULMONARY
REHABILITATION
 Enhance self-esteem and self-confidence in ability to
perform
 Improve efficiency of movement
 Desensitization to dyspnea (e.g., from repeated exercise)

94. THANK YOU