this slide contains anatomy physiology of respiratory system,disease conditions, diagnostic tests and disease condition copd.

2. RESPIRATORY
SYSTEM
MS SEENA RACHEL GEORGE
I/MSC NURSING
BHCON

3. THE HUMAN RESPIRATORY SYSTEM
* It is the system, consisting of tubes and is
responsible for the exchange of gases in Humans by
filtering incoming air and transporting it into the
microscopic alveoli where gases are exchanged
* Your respiratory system provides the energy
needed by cells of the body to funtion according to
their designated tasks.

5. The organs of the
“Respiratory Tract”
can be divided into two groups
“STRUCTURALLY”
** The Upper Respiratory Tract**
* Nose
* Nasal cavity
* Sinuses
* Pharynx
** The Lower Respiratory Tract**
* Larynx
* Trachea
* Bronchial Tree
* Lungs

6. CONDUCTING PASSAGES
• NOSE - NASAL CAVITY &
PARANASAL SINUSES
• PHARYNX
• LARYNX – EPIGLOTTIS & VOCAL CORDS
• TRACHEA
• BRONCHI – BRONCHIAL TREE
• LUNGS –LOBES OF THE LUNGS ,
PLUERAL CAVITIES AND ALVEOLI

7. Nose (nasal cavity)
• Both olfactory and respiratory functions
• Inspired air is warmed or cooled
• Brought close to body temperature
• Also moistened by fluid derived from
transudation through epithelium and
secretions of glands and goblet cells

8. Warming and
humidification of inspired air
• Moist air is necessary
for integrity and proper
functioning of
ciliated epithelium
• Secretions have
bactericidal actions
• Stiff hairs trap dust and
foreign particles
• Resonator in voice and speech

9. Pharynx
• Nasal cavity opens posteriorly into
nasopharynx
• During swallowing, respiration is
Temporarily inhibited permitting
food to enter oropharynx
• Elevation of larynx and
closure of vocal cords
prevents entry of food into larynx

10. Larynx
• Lower part of pharynx and at upper end of
trachea
• Cartilagenous, cartilages being held
together ligaments
• Production of voice
• Achieved by forcible expulsion of air from
lungs, causing production of sound
• Contraction of adductor muscles and glottis

11. *It is an enlargement in the airway
superior to the trachea and inferior to the pharynx.
• It helps keep particles from entering the
trachea and also houses the vocal cords.
* It is composed of a framework of muscles
and cartilage bound by elastic tissue

12. The Epiglottis
* It is a large leaf-shaped piece of cartilage.
* A flap of cartilage that prevents food from
entering the trachea (or windpipe).
* During swallowing, there is elevation of the larynx

13. The Vocal Cords
* Inside the larynx, 2 pairs of folds of muscle and
connective tissues covered with mucous
membrane make up the vocal cords.
a. The upper pair is the false vocal cords.
b. The lower pair is the true vocal cords.
c. Changing tension on the vocal cords controls pitch,
while increasing the loudness depends upon
increasing the force of air vibrating the vocal cords.

14. * During normal breathing,
the vocal cords are relaxed and the
glottis is a triangular slit.
• During swallowing the false vocal
cords and epiglottis close off the glottis.

15. THE TRACHEA
• It is a tubular passage way for air,
located anterior to the esophagus
• It extends from the larynx
to the 5th thoracic vertebra
where it divides into the
right and left bronchi.

16. • The inner wall of the trachea is lined with
ciliated mucous membrane
with many goblet cells
that serve to trap incoming
particles.
• The tracheal wall is
supported by 20 incomplete
cartilaginous rings.

17. BRONCHI
* The Bronchi are the two main air passages
into the lungs.
* They are composed of the:
** “Right Primary Bronchus”
- leading to the right lung.
** “Left Primary Bronchus”
- leading to the left lung.

18. The Bronchial Tree
* The bronchial tree consists of branched tubes
leading from the trachea to the alveoli.
* The bronchial tree begins with the two
primary bronchi, each leading to a lung.
* The branches of the bronchial tree from the trachea
are right and left primary bronchi;
these further subdivide until bronchioles
give rise to alveolar ducts which terminate in alveoli.

20. LUNGS
• One on either side
• Large cone-shaped spongy structures
which occupy most of thoracic cavity
• Left lung is divided into 2 lobes and right
into 3
• Lined by pleura (visceral and parietal)

21. Terminal branches
• Bronchioles branch further
and the smallest
subdivisions being terminal
bronchiole
• It is estimated, no. of
divisions from tracheal
bifurcation to terminal
bronchiole is 16
• Total no. of divisions till
alveoli is 23

22. * The right lung has three lobes.
* The left lung has two lobes.
* Each lobe is composed of lobules
that contain air passages, alveoli,
nerves,
blood vessels, lymphatic vessels,
and connective tissues.

23. Pulmonary alveoli
• Alveoli are lined by a single layer
of flat epithelial
cells
• Alveolar type I cells are principal
lining
• Type II are cuboidal cells, secrete
surfactant
• Average width is 0.3 mm
• 300 million alveoli in human lung
Surfactant
• Formed from fatty acids by alveolar
type II cells
• Complex mixture of several
phospholipids,
proteins and ions
• Most important components are
phospholipid,
dipalmitoyl phosphatidyl choline (DDPC),
surfactant appoproteins and calcium

25. The Pleural Cavities
* A layer of serous membrane, between the
visceral pleura and the parietal pleura.
• It contains a lubricating fluid secreted
by the membranes that prevents
friction between the membranes
and allows their easy movement
on one another during breathing.

26. The Alveoli
* They are cup-shaped out pouching lined
by epithelium and supported by a thin elastic
basement membrane.
• With that you can imagine having bunch of grapes
with each grape indicating and alveolus.
* Alveolar sacs are 2 or more alveoli that
share a common opening.

27. STRUCTURE
nose / nasal cavity
pharynx (throat)
larynx
trachea (windpipe)
bronchi
bronchioles
alveoli
FUNCTION
warms, moistens, & filters air as it is inhaled
passageway for air, leads to trachea
the voice box, where vocal chords are located
tube from pharynx to bronchi
rings of cartilage provide structure, keeps the
windpipe "open"
trachea is lined with fine hairs called cilia which
filter air before it reaches the lungs
two branches at the end of the trachea, each
lead to a lung
a network of smaller branches leading from the
bronchi into the lung tissue & ultimately to air
sacs
the functional respiratory units in the lung
where gases (oxygen & carbon dioxide) are
exchanged (enter & exit the blood stream)
Summary of FUNCTIONS

28. LIST OF RESPIRATORY AND LUNG DISEASES
• Upper respiratory tract infections
• Lower respiratory tract infections.
• Asthma.
• Copd
• Inflammatory lung diseases

29. • Obstructive lung diseases.
• Restrictive lung diseases.
• Respiratory tumors
• Pleural cavity diseases.
• Pulmonary vascular diseases.

30. Diagnostic Test
• CHEST XRAY
• ABG ANALYSIS
• EXERCISE TESTING
• MEDIASTINOSCOPY & MEDIASTINOTOMY

31. • BRONCHOSCOPY
• CHEST IMAGING
• CHEST TUBE INSERTION

32. • NEEDLE BIOPSY OF THE PLEURA OR LUNG
• PULMONARY FUNCTION TEST (PFT)
• SUCTIONING
• THORACOCENTESIS
• THORACOSCOPY
• THORACOTOMY

34. COPD
• Also known as
 COLD (Chronic Obstructive Lung Disease )
 COAD (Chronic Obstructive Airway Disease)
 Smoker’s lung
 CAL (Chronic Airflow Limitation)
 CORD (Chronic Obstructive Respiratory Disease)

35. DEFINITION
Chronic obstructive pulmonary disease (COPD) is
a preventable and treatable disease characterized
by airflow limitation that is progressive, not fully
reversible and associated with an abnormal
inflammatory response of the lungs.

37. Chronic Bronchitis
• Chronic bronchitis is a
chronic inflammatory
condition in the lungs
• It causes a cough that
often brings up mucus, as
well as shortness of
breath,wheezing, and
chest tightness

38. Emphysema
• In emphysema, there is
over-inflation of the air
sacs (alveoli) in the
lungs, causing a
decrease in lung
function, and often,
breathlessness. It
involves destruction of
the lungs.

39. EPIDEMIOLOGY
• More common in older people, especially those
>65 years.
• Fifth leading cause of death and disability
worldwide.
• Death rates for males and females are roughly
equivalent.
• COPD mortality has also increased compared with
heart and cerebrovascular disease over the same
period.

40. Risk Factors
Exposures HostFactors
Environmental tobacco
smoke
Genetic predisposition
(AAT deficiency)
Occupational dusts and
chemicals
Airway
hyperresponsiveness
Air pollution Impaired lung growth

41. Risk Factors
• Exposures:
– Cigarette smoking
(tobacco exposure)
accounts for 85% to
90% of cases of COPD.
– Air pollution and
occupational exposures
result in inflammation
and cell injury which
leads to COPD.

42. Host Factors
• Host factor refers to the traits of an individual
person that affect susceptibility to disease.
– AAT deficiency accounts for less than 1% of COPD
cases.
– Airway hyperresponsiveness due to various
inhaled particles may cause an accelerated decline
in lung function.
– Impaired lung growth due to low birth weight,
prematurity at birth, or childhood illnesses.

43. Pathophysiology of COPD
1. Airway inflammation
2. Structural changes
3. Mucociliary dysfunction
- Chronic inflammatory cascade for COPD

46. ASSESSMENT
1. Clinical presentation:
– History
– Physical examination
2. Diagnostic testing:
– Pulmonary function testing
– Laboratories
– Imaging

47. Clinical Presentation
History
Physical
Examination
- Symptoms: Cough,
dyspnea, sputum,
wheezing
- Smoking history,
environmental and
occupational risk
factors
- Cyanosis of mucosal
membranes
- Barrel chest
- Increased resting
respiratory rate
- Shallow breathing
- Pursed lips during
expiration
- Use of accessory
respiratory muscles

48. ASSESSMENT
• General appearance
• Vital signs ,Heart rhythm,
• Pallor and cyanosis of nail beds and mucous membranes (late
stages of the disease)
• ABGs, SaO2, CBC, WBC, and chest x-ray results
• Assess/Monitor Client’s history (occupational history, smoking
history) Respiratory rate, symmetry, and effort Breath sounds
Activity tolerance level and dyspnea
• Nutrition and weight loss

49. • Monitor for signs and symptoms.
Chronic dyspnea, Chronic cough,
Hypoxemia, Hypercarbia (increased PaCO2),
Respiratory acidosis and
compensatory metabolic alkalosis.
• Crackles ,Rapid and shallow respirations.
• Use of accessory muscles

50. • Barrel chest or increased
chest diameter
• Hyper resonance on percussion
due to “trapped air” (emphysema)
• Asynchronous breathing
• Thin extremities and enlarged neck muscles
• Dependent edema secondary to right-sided heart failure
•

52. Diagnostic Testing
• Pulmonary function testing or
Spirometry
– Comprehensive assessment of lung
volumes and capacities
– Performed in all patients suspected
of COPD
– FEV1 defines the severity of
expiratory airflow obstruction and is
a predictor of mortality
• Bronchodilator reversibility:
– A large increase in post-
bronchodilator FEV1 supports the
diagnosis of asthma

54. Diagnostic Testing
• Laboratories:
–ABG Monitoring:
• Done for patients with severe COPD,
respiratory failure or a severe
exacerbation
–ATT levels (1.5 - 3.5 gram / liter):
• Measured in young patients who develop
COPD and have a strong family history.
• A serum value <15–20% of the normal
limits is highly suggestive of α1-
antitrypsin deficiency.

55. Diagnostic Testing
• Imaging:
– Chest radiographs
• Not sensitive for the diagnosis of
COPD
• Helpful in excluding other
diseases (pneumonia, cancer,
congestive heart failure, pleural
effusion & pneumothorax)
– Chest CT
• For patients with severe COPD for
lung volume reduction surgery
(LVRS) & lung transplantation.

56. COPD Management
• Goals of COPD Management:
– To relieve symptoms
– To improve quality of life
– To decrease the frequency & severity of acute attacks
– To slow the progression of disease
– To prolong survival

57. COPD Management
Nonpharmacologic
Treatment
Smoking cessation
Immunization
Long term oxygen
therapy
Pulmonary
rehabilitation
Pharmacologic
Treatment
Corticosteroids
Bronchodilators
AAT Replacement therapy

58. Smoking Cessation
• Only proven intervention to affect long term
decline in FEV1 & slow the progression of COPD
– Nicotine replacement therapy
• Transdermal patch
• Chewing gum
• Inhaler
• Nasal spray
• Lozenges
– Non-nicotine pharmacotherapy
• Bupropion
• Varenicline

59. Smoking Cessation
Product Sideeffects/Precautions
Nicotine replacement therapy Headache, insomnia, nightmares,
nausea, dizziness, blurred vision
Bupropion Headache, insomnia, nausea,
dizziness, xerostomia, hypertension,
seizure.
Avoid monoamine oxidase inhibitors
Varenicline Nausea, vomiting, headache,
insomnia, abnormal dreams
Worsening of underlying psychiatric
illness

60. Immunization
• Influenza vaccination
– Reduces the incidence of influenza-related acute
respiratory illness in COPD patients
– Patients with serious allergy to eggs should not be
given this vaccine.
– Brand available: Fluarix®
– An oral antiinfluenza agent (Oseltamivir) can be
given to such patients but its less effective and
causes more side effects.
– Available brand: Tamiflu®

61. Immunization
• Polyvalent pnuemococcal vaccine
– Recommended for all COPD patients
• 65 years and older
• Less than 65 years only if the FEV1 is less
than 40% predicted.
– Dosage: 0.5ml IM
– Available brand: Pneumovax® (0.5ml
pre-filled syringes)

62. Long-term Oxygen Therapy
• Should be started if
– Resting PaO2 is less than 55 mm
Hg
– Evidence of right-sided heart
failure, polycythemia, or
impaired neuropsychiatric
function with a PaO2 of less
than 60 mm Hg

63. Pulmonary Rehabilitation
• Improves symptoms and
quality of life
• Reduces frequency of
exacerbations
• Components include:
– Exercise training
– Nutritional counselling
– Psychosocial support

64. Pharmacologic Treatment
Bronchodilators
Long-acting
2-agonists
Anticholinergics
Methylxanthines
Short-acting
2-agonists
Anticholinergics

65. Short-acting 2-agonists
• Stimulate adenyl cyclase to
increase the formation of cAMP
which causes bronchodilation.
• Improve mucociliary clearance
MOA
• 4 to 6 hoursDuration of action
• Albuterol (Ventolin®),
levalbuterol, pirbuterol
Selective 2-
agonists
• Metaproterenol, isoetharine,
isoproterenol, epinephrine
Less selective 2-
agonists

66. Short-acting Anticholinergics
• Competitively inhibit cholinergic
receptors in bronchial smooth
muscle, block Ach, with the net
effect of reduction in cGMP, which
normally constrict bronchial smooth
muscle.
MOA
• 4 to 6 hours, slower onset of
action in comparison to -
agonists
Duration of
action
• Ipratropium (Atrovent®,
Atem®)
• Atropine
Examples

67. Long-acting 2-agonists
• Same as that of short-acting
2-agonistsMOA
• 12 hours
Duration
of action
• Salmeterol (Serevent®)
• Formoterol
• Arformoterol
Examples

68. Long-acting Anticholinergics
• Same as that of short-acting
anticholinergicsMOA
• Cause bronchodilation within 30
minutes, which persists for 24 hours,
allowing once daily dosing
Duration
of action
• TiotropiumExample

69. Combination Anticholinergics & 2-
agonists
• Combining bronchodilators
with different MOA allows
reduced doses to be
administored, reducing
side effects.
• Albuterol and Ipratropium
available as an MDI
Combivent®

70. Methylxanthines
• Produce bronchodilation by:
• Inhibition of PDE, increasing cAMP levels
• Inhibition of calcium ion influx into
smooth muscle
• Prostaglandin antagonism
• Stimulation of endogenous
catecholamines
• Inhibition of release of mediators from
mast cells and leukocytes
MOA
• 8-12 mcg/ml
Therapeutic
Serum Levels

71. Methylxanthines
• Minor side effects:
– dyspepsia, nausea, vomiting, diarrhea, headache, dizziness,
tachycardia
• Serious toxic effects:
– arrhythmias and seizures
• Considered in patients who donot respond well to
bronchodilators

72. Corticosteroids
• Mechanism of Action
– Reduction in capillary permeability to decrease mucus
– Inhibition of release of proteolytic enzymes from
leukocytes
– Inhibition of prostaglandins
• ICS: Beclomethasone (Bekson, Clenil-A, Clenil
Forte, Rinoclenil), flunisolide, budesonide,
fluticasone, mometasone
• Systemic CS: Prednisolone (Deltacortil),
Methylprednisolone, Prednisone

73. Corticosteroids
• Inhaled CS
–Considered for symptomatic stage III or IV
disease who experience repeated
exacerbation despite bronchodilator therapy
• Systemic CS
–Short term use for acute exacerbations
–Not used in chronic management because of
high risk of toxicity

74. Combination ICS & Bronchodilators
• Effective in reducing the rate of COPD exacerbations
• Reduces the number of total inhalations needed, more patient
compliance
• Available combination:
– Beclomethasone with salbutamol (Clenil Compositum®)
– Budesonide with formeterol
– Fluticasone with salmeterol

75. AAT Replacement Therapy
• Considered for patients with AAT deficiency
• Life time treatment
• Therapy consists of giving a concentrated form of AAT, derived
from human plasma.
• The recommended dosing regimen for replacing AAT is 60
mg/kg administered IV once a week.

76. Indacaterol
• Indacaterol is an ultra-long-acting beta-
adrenoceptor agonist
• Approved by FDA on July 1, 2011
• Requires once daily dosing, unlike other long-
acting
• In clinical trials, the most common adverse
events were runny nose, cough, sore throat,
headache, and nausea.
• Recommended dose is one capsule (75mcg) per
day.

77. Devices used in COPD
• Inhalers
• Small, handheld devices that
deliver a puff of medicine into the airways.
• Metered-dose inhalers (MDIs)
• Dry powder inhalers (DPIs) or
breath activated inhalers
• Inhalers with spacer devices

78. Metered-dose Inhalers
• Contains a liquid
medication delivered as
an aerosol spray.
• Quick to use, small, and
convenient to carry.
• Needs good co-
ordination to press the
canister, and breathe in
fully at the same time

79. Breath-activated inhalers
or DPI• It releases a puff of dry
powder instead of a
liquid mist
• Require less co-
ordination than the
standard MDI.
• Slightly bigger than the
standard MDI.
• Example: Rotahaler

80. Inhalers with spacer devices
• Spacer devices are used with
pressurised MDIs
• The spacer between the
inhaler and the mouth holds
the drug like a reservoir
when the inhaler is pressed.

81. Nebulizers
• Nebulisers are
machines that turn the
liquid medicines into a
fine mist, like an
aerosol.
• Useful in people who
are very breathless e.g.
In severe attack of
COPD
• They are not portable

82. Nanda Nursing Diagnosis for COPD
1. Ineffective airway clearance related to: bronchoconstriction, increased sputum production, ineffective
cough, fatigue / lack of energy, broncho pulmonary infection.
2. Ineffective breathing pattern related to: shortness of breath, mucus, bronchoconstriction, airway
irritants.
3. Impaired gas exchange related to: ventilation perfusion inequality.
4. Activity intolerance related to: imbalance between oxygen supply with demand.
5. Imbalanced Nutrition: less than body requirements related to: anorexia.

83. 6. Disturbed sleep pattern related to: discomfort, sleeping position.
7. (Bathing / Hygiene) Self-care deficit related to: fatigue secondary to
increased respiratory effort and ventilation and oxygenation insufficiency.
8. Anxiety related to: threat to self-concept, threat of death, purposes that
are not being met.
9. Ineffective individual coping related to: lack of socialization,
anxiety,depression, low activity levels and an inability to work.
10. Deficient Knowledge related to: lack of information, do not know the
source of information.

87. • Frequent sputum production is associated with disturbed
night's rest and impaired sleep quality in patients withCOPD.
In this study, we measured night's rest parameters measured
with an accelerometer and sleep quality in mild to very severe
patients with COPD. Furthermore, our aim was to investigate the
association between night's rest parameters and clinical variables
and the association between sleep quality and quality of life or
health status.
• . find an association between frequent sputum production and
disturbances during night's rest and sleep quality. Future
studies should investigate whether the treatment of mucus
hypersecretion leads to improved night's rest.

88. • Pneumonia in Childhood and Impaired Lung Function in Adults: A Longitudinal
Study.
Chan JY1, Stern DA2, Guerra S2, Wright AL2, Morgan WJ2, Martinez FD3.
Author information
• BACKGROUND:
Diminished lung function and increased prevalence of asthma have been reported in
children with a history of early lower respiratory illnesses (LRIs), including pneumonia.
Whether these associations persist up to adulthood has not been established.
• CONCLUSION
Early pneumonia is associated with asthma and impaired airway function, which is
partially reversible with bronchodilators and persists into adulthood. Early pneumonia
may be a major risk factor for adult chronic obstructive pulmonary disease.

90. References
• BMJ Best Practices
• American Thoracic Society COPD guidelines
• The Washington’s manual of medical therapeutics
• Pharmacotherapy : A pathophysiologic approach, Joseph T.
DiPiro
• Respiratory care pharmacology, Rau, Joseph