applied physiology

1. APPLIED PHYSIOLOGY OF RESPIRATORY
SYSTEM
DR PRIYANKA.P.S
1STYRPG SCHOLAR
PANCHAKARMAdept
Alvasayurvedamedicalcollege
Co guide-
dr rohinipurohith

3. contents
 Respiration
 Types of respiration
 Respiratory passages
 Respiratory and non respiratory functions
 Pulmonary circulation
 Mechanics of respiration
 Pulmonary volume and capacities
 Variations of vital capacities
 Measurement of lung volumes and capacities
 Obstructive and restrictive respiratory disorders
 Ventilation
 Dead space
 Regulation of respiration
 Respiratory disturbnces

4. WHAT IS RESPIRATION
• Respiration is the process by which oxygen is
taken in and carbon dioxide is given out.
TYPES OF RESPIRATION
 External respiration
 Internal respiration

5. RESPIRATORY PASSAGES

6. SCHEMATICVIEW OF RESPIRATION

7. RESPIRATORY FUNCTIONS
1. Pulmonary Ventilation
2. Diffusion of O2 and CO2 between
the alveoli & the blood
3. Transportation of O2 & CO2 in
the blood & body fluids to & fro
from the body’s tissue cells
4. Regulation of Ventilation.

8. NON RESPIRATORY FUNCTIONS
OLFACTION
DEFENSE
MECHANISM
ANTI
COAGULANT
FUNCTION
SECRETION OF
ANGIOTENION
CONVERTING
ENZYME
MAINTENCE
OF WATER
BALANCE
VOCALIZATION
PREVENTION OF
DUST PARTICLES
REGULATION
OF BODY
TEMPERATURE
SYNTHESIS
OF
HORMONAL
SUBSTANCES

9. PULMONARY CIRCULATION

10. Cinical significance of pulmonary circulation
• Pulmonary hypertension
• Pulmonary embolus
• Pulmonary shunt
• Cardiac shunt

11. MECHANICS OF RESPIRATION
Muscles of Respiration
i. Primary Inspiratory:
Diaphragm,external intercostal
ii. Accessory Inspiratory: Sternomastoid, Scaleni,
Anterior Serrati, Elevators of Scapula & Pectoralis
major and minor
iii. Primary Expiratory: Internal Intercostal muscles
iv. Accessory expiratory: Abdominal muscles - abdominal rectii,
transversus abdominis, internal oblique

12. Inspiration
1. Diaphragm muscle contracts, increasing thoracic cavity size in the superior inferior dimension
2. External intercostal muscles contract, expanding lateral& anterior-posterior dimension
3. INCREASED volume (about 0.5 liter),
DECREASED pulmonary pressure (-1 mm Hg),air rushes into lungs to fill alveoli
Deep/forced inspirations as during exercise and pulmonary disease
scalenes, sternocleidomastoid,pectorals are used for more volume and expansion of thorax.

13. Expiration
1. Quiet expiration (exhalation) - simple elasticity of the lungs
DECREASES volume INCREASED pulmonary pressure ->
movement of air out of the lungs
2. Forced expiration - contraction of abdominal wall muscles
(i.e. obliques & transversus abdominus)further DECREASES
volume beyound relaxed point ----> further INCREASE in
pulmonary pressure ---> more air moves out.

14. MOVEMENTS OF LUNGS
Factors holding lungs against the thorax wall:
i. Surface tension holding the "visceral" and "parietal" pleura together.
ii. Intrapulmonary pressure is always slightly greater than
intrapleural pressure by 4 mm Hg.
iii. Atmospheric pressure acting on the lungs.
a) Atelectasis (collapsed lung) - hole in pleural "balloon"
causes equalization of pressure and collapse of the lung.
b) Pneumothorax - abnormal air in the intrapleural space,
can lead to collapsed lung.

15. compliance
• Ease with which lungs
can be stretched
• Determined by:
• Elastic forces of lung
tissue
• Alveolar surface tension
• Types:
• Static compliance
• Dynamic compliance
LOW COMPLIANCE
Kyphosis,scoliosis
Pulmonary fibrosis
Paralysis of RM,
Pleural effusion
Hydrothorax
Pneumothorax
HIGH COMPLIANCE
Emphysema
Old age

16. PULMONARY VOLUMES,CAPACITIES AND
FUNCTION TESTS
• Pft’s are used in assessing the functional status of
the respiratory system both in physiological and
pathological conditions.
• Carried out using spirometer
• The air in lung is classified into :
 Lung volumes
 Lung capacities

17. • LUNG VOLUMES- are the static volumes of air
breathed by an individual.
TIDAL VOLUME
INSPIRATORY RESERVE VOLUME
EXPIRATORY RESERVE VOLUME
RESIDUALVOLUME

18. Expiratory reserve volume- additional volume of air that can be
expired forcefully ,after normal expiration
Residual volume-volume of air remaining in the lungs even
after expiration
Tidal volume- volume of air breathed in and out of lungs in
single quiet normal respiration
Inspiratory Reserve Volume-Additional volume of air that can
be inspired forcefully after the end of normal inspiration

19. LUNG CAPACITIES
INSPIRATORY CAPACITY
VITALCAPACITY
FUNCTIONALRESIDUAL CAPACITY
TOTAL LUNGCAPACITY

20. INSPIRATORY
CAPACITY IS THE
MAXIMUM
VOLUME OF AIR
THAT IS INSPIRED
AFTER NORMAL
EXPIRATION,
INCLUDES –
IC=TV+IRV
500+3300=3800
ML
VITAL CAPACITY IS
THE MAXIMUM
VOLUME OF AIR
THAT CAN BE
EXPELLED OUT
FORCEFULLY AFTER
A DEEP
INSPIRATION-
VC=IRV+TV+ERV
3300+500+1000=4
800 ML
FUNCTIONAL
RESIDUAL
CAPACITY,VOLUME
OF AIR REMAINING
IN THE LUNGS
AFTER NORMAL
EXPIRATION
(AFTER NORMAL
TIDAL EXPRATION).
FRC=ERV+RV
1000+1200=2200
ML
TOTAL LUNG
CAPACITY IS THE
VOLUME OF AIR
PRESENT IN THE
LUNGS AFTER A
DEEP
INSPIRATION.IT
INCLUDES
,TLC=IRV+TV+ERV+
RV
3300+500+1000+
1200=6000 ML

22. VARIATIONS OF VITAL CAPACITIES
• PHYSIOLOGICALVARIATIONS
• VC less than in males, more heavy built, more in standing position, athletes,
increased in persons who play musical instruments.
• PATHOLOGICALVARIATIONS
• Vital capacity is greatly reduced in
• Asthma
• Emphysema
• Weakness or paralysis of respiratory muscle
• Pulmonary congestion
• Pneumonia
• Pneumothorax
• Hemothorax
• Pyothorax
• Hydrothorax
• Pulmonary edema
• Pulmonary tuberculosis

23. Measurement of lung volumes and capacities
SPHIROMETER
PLETHYSMOGRAPH

24. PEAK EXPIRATORY FLOW RATE(PEFR)
PEFR is the maximum rate at which the air can be
expired after a deep inspiration.
SIGNIFICANCE OF DETERMINING PEFR:
Reduction is more significant in the obstructive
diseases than in the restrictive diseases
 PEFR is 200 litres/minute- restrictive diseases.
100 litres/min-obstructive diseases.

25. RESTRICTIVE RESPIRATORY
DISEASES
STRUCTURES INVOLVED
POLIOMYELITISIS CNS
MYASTHENIA GRAVIS CNS AND THORACIC CAVITY
FLAIL CHEST (BROKEN
RIBS)
THORACIC CAVITY
PARALYSIS OF
DIAPHRAGM
CNS
SPINAL CORD DISEASES CNS
PLEURAL EFFUSION THORACIC CAVITY

26. OBSTRUCTIVERESPIRATORY
DISEASES
STRUCTURESINVOLVED
ASTHMA
CHRONIC BRONCHITIS
EMPHYSEMA
CYSTIC FIBROSIS
LOWER RESPIRATORY TRACT
LARYNGOTRACHEO BRONCHITIS
EPIGLOTTITIS
TUMORS
SEVERE COUGH AND COLD WITH
PHLEGM
UPPER RESPIRATORY TRACT

27. VENTILATION
PULMONARYVENTILATION
•Cyclic process by which fresh air
enters the lungs and an equal
volume of air leaves the lungs
•Pv=tidal volume*respiratory rate
•500 ml*12/min
•6,000 ml/minute,
•high volumes in tall people, high
altitude, low volumes in pregnancy,
smokers
ALVEOLARVENTILATION
•The amount of air utilized for
gaseous exchange every minute.
•Normal value -4200ml

28. DEAD SPACE
Dead space is defined as the part of
the respiratory tract where gaseous
exchange does not take place.
The air present in the dead space is
called as dead space air.
Parts which form the dead space are
nose, pharynx,trachea, bronchi,
terminal brochioles.

29. TYPES OF DEAD SPACE
Anatomical
dead space Physiological
dead space
volume of normal dead
space is 150 ml

30. REGULATIONOF RESPIRATION
Nervous Mechanism
A. Medullary Respiratory
Inspiratory Center (Dorsal Respiratory Group –
rhythmic breathing
• Phrenic nerve, Intercostal nerves , diaphragm +
external intercostals
• Expiratory Center (Ventral Respiratory Group –
forced expiration)
• Phrenic nerve, Intercostal nerves, Internal
intercostals + abdominalis (expiration)

31. Pons Respiratory Centre
1. Pneumotaxic center - slightly inhibits medulla,
causes
• shorter, shallower, quicker breaths
2. Apneustic center –
• stimulates the medulla,
• causes longer, deeper slower breaths

32. • Control of Rate & Depth of Breathing
1. Breathing rate - stimulation/inhibition of medulla.
2. Breathing depth - activation of inspiratory muscles.
3. Hering-Breuer Reflex - stretch of visceral pleura
that lungs have expanded (vagal nerve).
4. Hypothalamic Control - emotion + pain to the
medulla
5. Cortex Controls (Voluntary Breathing) - can override
medulla as during singing and talking

33. DISTURBANCE OF RESPIRATION
Apnea
Hyperventilation
Hypoventilation
Hypoxia
Oxygen toxicity
Hypercapnea
Hypocapnea
Asphyxia
Dysponea
Periodic breathing
cyanosis
Carbon monoxide
poisoning
Atelectasis
Pneumothorax
Pneumonia
Bronchial asthma
Pulmonary edema
Pleural effusion
Pulmonary tuberculosis
Emphysema

34. Tachypnea- the increase in rate of respiration
Bradypnea-the decrease in rate of respiration
Polypnea-rapid or shallow breathing
Apnea- temporary arrest of breathing
Hyperpnea- increase in pulmonary ventilation due to increase in rate of
force of respiration, occurs after exercise, fever etc
Hyperventilation – abnormal increase in rate and force of respiration which
often leads to dizziness, chest pain
Dysnea –difficulty in breathing
Periodic breathing: the abnormal respiratory rhythm

35. APNEA
Temporary
cessation of
breathing
Apnea time-
40-60 sec
Conditions
voluntary
effort
Apnea after
hyperventilati
on
Deglutition
apnea
Vagal apnea
Adrenaline
apnea
Clinical
classification
1.Obstructive
apnea
Sleep apnea
2.Central
apnea
3.Mixed
apnea

36. HYPERVENTILATION and hypoventilation
• Increased pulmonary ventilation due to forced
breathing is hyper ventilation
• Conditions-exercise,
• Effects- chyne stokes breathing
• Decrease in the pulmonary ventilation by decrease in
rate or force of breathing is hypoventilation
• Conditions-when respiratory centers are supressed, or
by administration of some drugs, partial paralysis of
respiratory muscles
• Effects-development of hypoxia and hypercapnea
leading to dysponea, severe conditions results in
lethargy , coma and death.

37. HYPOXIA
Reduced availability of oxygen to the tissues
Classification
1.Oxygen tension in the blood
2.Oxygen carrying capacity of blood
3.Velocity of blood flow
4.Utilisation of oxygen by the cells
a.hypoxic hypoxia
b.anemic hypoxia
c.stagnant hypoxia
d. histo toxic hypoxia

38. a.Hypoxic hypoxia:- means the decreased oxygen content
in the blood. (arterial hypoxia)
Causes
1.Low oxygen tension in the inspired air
2.Respiratory disorders associaed with decreased
pulmonary ventilation
3.Respiratory disorders associated with inadequate
oxygenation in lungs
4.Cardiac disorders in which enough blood is not pumped
to transport oxygen

39. a.Low oxygen tension in inspired air
1.High altitude
2.While breathing air in closed space
3.While breathing gas mixture containing
low partial pressure of oxygen

40. B.decrease in
pulmonary
ventilation
Obstruction of
respiratory
passage in
asthma
Nervous and
mechanical
hindrance to
respiratory
movements as
in
poliomyelitis.
Depression of
respiratory
centres in
brain tumours
pneumothora
x

41. 1.Impaired alveolar diffusion as
in emphysema
2.Presence of non functioning
alveoli as in fibrosis
3.Filling of alveoli with fluid as
in pulmonary
edema,pneumonia,pulmonary
hemorhhage,
4.Collapse of lungs as in
bronchiolar obstruction
5.Lack of surfactant
6.Abnormal pleural cavity such
as pneumothorax,
hydrothorax,hemothorax,
pyothorax
7.Increased venous admixture
as in the case of bronchiectasis
C.Respiratory disorders
associated with
inadequate oxygenation of
blood in lungs.

42. ANEMIC
HYPOXIA
INABILITY OF BLOOD TO
CARRY ENOUGH
AMOUNT OF OXYGEN ,
THE O2 AVAILABILTY IS
NORMAL BUT BLOOD IS
NOT ABLE TO TAKE UP
SUFICIENT OXYGEN
CAUSES
ANEMIA
1.DECREASED NUMBER OF RBCS
2.FORMATION OF ALTERED HB
3. DECREASED HB CONTENT IN
THE BLOOD
4.COMBINATION OF HB WITH
GASES OTHER THAN OXYGEN
AND CARBON DIOXIDE

43. SJKKL
CONGESTIVE
CARDIAC
FAILURE
HEMORRHAGE
SURGICAL
SHOCK
THROMBOSIS
EMBOLISM
DECREASED VELOCITY
OF BLOOD FLOW
STAGNANT HYPOXIA

44. OXYGENTOXICITY(POISONING)
• O2 toxicity is the increased o2 content in tissues beyound
certain critical level.
• It occurs by breathing pure o2 with high pressure of 2-3
atmospheres(hyperbaric oxygen)
• In this condition an excess amount of o2 is transported in
plasma as dissolved form because , the o2 carrying
capacity of hb is limited to 1.34ml/g
• EFFECTS OF O2 TOXICITY
• Lung tissues are affected first with tracheo bronchial
irritation and pulmonary edema.
• The metabolic rate increases in all the body tissues and the
tissues are burned out by excess heat.
• When brain is affected ,first hyper irritability occurs later it
is followed by increase muscular twitching,ringing in ears
and dizziness.
• Finally the toxicity results in convulsions, coma and death.

45. HYPERCAPNEA
• Increased carbon dioxide content of blood
• condition which leads to blockage of respiratory
pathway such as asphyxia,while breathing air
containing excess co2 content
• Effect on respiration: Respiratory centres are
stimulated excessively. It leads to dyspnea
• Effect on blood:the pH of the blood reduces and
the blood becomes acidic
• Effect on CVS:it is associated with tachycardia
and increased BP.
• Effect on CNS: it effect CNS and resulting in
Headache,Depression and laziness followed by
muscular rigidity ,fine tremors and generalized
convulsions . Finally, giddiness and loss of
consciousness occur

46. HYPOCAPNEA
• It is the decreased CO2 content in blood
• It occurs in conditions as so: with hypoventilation
• Effects on respiration: the respiratory centres are
depressed leading to decreased respiratory rate
and force of respiration
• Effects on blood: the pH of blood increases
leading to respiratory alkalosis.
• Effects on CNS: dizziness, mental confusion,
muscular twitching, loss of consciousness etc, are
the common features

47. ASPHYXIA
• Asphyxia is the condition characterized by combination
of hypoxia and hypercapnea due to obstruction of air
passage.
• It develops in condition characterized by acute
obstruction of air passage such as:
• Strangulation
• Hanging
• Drowning etc
• The effects of hypoxia develop in 3 stages
hyperapnea convulsions collapse

48. dysponea
• Dysponea means difficulty in breathing
• Also defined as a consiousness of necessity for increased
respiratory effort.
• Conditions:
• During severe muscular exercise-(physiologically)
• Pathological conditions:
• Respiratory disorders
• Cardiac disorders
• Metabolic disorders
• CYANOSIS:
• Defined as diffused bluish discolouration of skin and mucous
membrane.
• It is due to the presence of large amount of reduced hb in the
blood.
• Conditions- poisoning, polycytheamia

49. CARBONMONOXIDE POISONING
 Toxic effects of CO:
 it displaces O2 from Hb by binding with same site in Hb
for O2.
 So O2 transport & O2 carring capacity of blood are
decreased.
• Symptoms:
 while breathing air with 1% of CO, saturation of Hb with
CO becomes 15-20%. Mild symptoms like headache &
nausea appear
 If above 1% the saturation becomes 30-40%. It causes
convulsions, cardiorespiratory arrest, loss of
consciousness & coma
 When Hb saturation is above 50%, death occurs.

50. COUGH
ORIGIN COMMON CAUSE CLINICAL FEATURES
PHARYNX POST NASAL DRIP H/OOF CHRONIC RHINITIS
LARYNX LARYNGITIS ,TUMOUR,
WHOOPING COUGH,
CROUP
VOICE OR SWALLOWING
ALTERED,HARSH OR
PAINFUL COUGH,
PAROXYSMS OF COUGH,
OFTEN ASSOCIATED WITH
STRIDOR
TRACHEA TRACHEITIS RAW RETROSTERNAL PAIN
WITH COUGH
BRONCHI ACUTE BRONCHITIS AND
COPD, ASTHMA
DRY OR PRODUCTIVE
WORSE IN MORNINGS,
USUALLY DRY, WORSE AT
NIGHT

51. BRONCHIAL CARCINOMA
EOSINOHILIC BRONCHITIS,
FEATURES SIMILAR TO
ASTHMA,BUT NO AHR,
PERSISTENT COUGH
OFTEN WITH
HAEMOPTYSIS
LUNG PARENCHYMA TB
PNEUMONIA,
BRONCHIECTASIS
PULMONARY EDEMA
INTERSTITIAL FIBROSIS
PRODUCTIVE OFTEN WITH
HEMOPTYSIS,
DRY INITIALLY
PRODUCTIVE LATER
PRODUCTIVE , CHANGES
IN POSTURE INDUCE
SPHUTUM PRODUCTION,
OFTEN AT NIGHT MAY BE
PRODUCTIVE OF
PINK,FROATHY SPHUTUM)
DRY , IRRITANT
DISTRESSING

52. ATELECTASIS
• It refers to partial / complete collapse of lungs
Causes :
• Deficiency of surfactant.It causes collapse of lungs due
to increased surface tension, which leads to respiratory
distress syndrome
• Obstruction of a bronchus.In this condition, the alveoli
attached to the bronchus / bronchiole are collapsed
• Pneumothorax, hydrothorax, hemothorax, pyothorax
in the pleural space.
Effects:
• Decreased partial pressure of O2 leading to dyspnoea

54. PNEUMONIA
It is the inflammation of lung tissues followed by the
accumulation of blood cells, fibrin & exudates in the alveoli
The affected part of lungs becomes consolidated.
Causes:
The inflammation of lung is caused by:
Bacterial /viral infection
Inhaling noxious chemical substance
BACTERIAL, VIRAL , MYCOPLASMA, ASPIRATION, FUNGAL
COMMUNITY ACQUIRED, HOSPITAL
ACQUIRED,PNEUMOCOCCAL, BRONCHIAL, LOBAR,
LEGIONELLA, BILATERAL, EOSINOPHILIC, LIPOID,
HYPOSTATIC,INTERSTITIAL

55. Effects of pneumonia
Fever
Compression of
chest & chest
pain
Shallow
breathing
Cyanosis
Insomnia
delirium

57. Bronchial asthma
Asthma is defined as a chronic inflammatory
disease of airways.
This is the respiratory disease characterised by
difficult breathing with wheezing
It is due to bronchiolar constriction caused by
spastic contraction of smooth muscles in
bronchioles leading to obstruction of air
passage
The obstruction is further exaggerated by the
edema of mucous membrane & accumulation
of mucus in the lumen of bronchioles

58. Causes of bronchial asthma
Inflammation of air passage
Hypersensitivity of afferent glossopharyngeal & vagal
ending in larynx &afferent trigeminal endings in nose
Pulmonary oedema & congestion of lungs caused by
left ventricular failure

60. Pulmonary edema
It is the
accumulation
of serous fluid
in the alveoli &
the interstitial
tissues of lungs
Causes
• Increased
pulmonary
capillary pressure
due to left
ventricular
failure
• Pneumonia
• Breathing
harmful
chemicals like
chlorine/ sulphur
dioxide
Effects
• Severe
dyspnoea, cough
with frothy
blood stained
expectoration
,cyanosis
• The chronic
interstitial
oedema leads to
Asthma
• The alveolar
oedema is fatal &
cause sudden
death due to
suffocation

62. Pleural effusion
This is the accumulation of large amount of fluid in the
pleural cavity
Causes
Blockage of lymphatic drainage
Excessive transudation of fluid from pulmonary capillaries
due to increased pulmonary capillary pressure caused by
left ventricular failure
Inflammation of pleural membrane which damages the
capillary membrane allowing leakage of fluid & plasma
protein into the pleural cavity
Features
It causes atelectasis leading to dysponea & other
respiratory disturbances

64. Pulmonary tuberculosis
TB is the
disease
caused by
mycobacteri
um
tuberculosis
This
disease
can effect
any organ
in the
body
The lungs
are
effected
more
commonl
y
The infected
tissue is
invaded by
macrophages
& later it
becomes
fibrous
The
effected
tissue is
called
tubercle

65. Features of tuberculosis
Initially, the alveoli in the affected part
become non-functioning
It is due to thickness of respiratory
membrane
If a large part of lung is involved , the
diffusing capacity is very much reduced
In severe conditions, the destruction of
the lung tissue is followed by formation
of large abscess cavities

67. EMPHYSEMA
• This is one of the obstructive respiratory disease
• Here the lung tissues are extensively damaged
• The damaged lung tissues results in loss of
alveolar walls ,Because of this the elastic recoil of
lungs is also lost
• Causes
• Cigarette smoking
• Exposure to oxidant gases
• Untreated bronchitis

68. DEVELOPMENT OF EMPHYSEMA
Destruction of elastic tissue occurs
The destruction of alveolar mucus membrane
Because of this, the mucus cannot be removed from the respiratory passage
The cilia of respiratory epithelial cells are partially paralyzed & movement is very
much reduced
It increases the mucus secretion from the respiratory epithelial cells causing
obstruction of air passage
Smoke /oxidant gases irritate the bronchi& bronchioles leading to chronic infection

69. Effects of emphysema

70. BRONCHITIS
• It is the inflammation of mucus membrane in the
bronchial tubes.
• It typically causes bronchospasm & cough
• Symptoms include coughing up mucus,
wheezing,shortness of breath & chest discomfort
• It is divided into two types: ACUTE& CHRONIC
• Acute usually has a cough that last for three weeks.
• The 90% of cause is viral infection
• Chronic is a productive cough that last for 3 months -2
years
• Most people with CB have COPD
• SMOKING IS the common cause

72. COPD
• It is also known as chronic obstructive lung disease
(COLD)&COAD
• It is characterized by chronically poor airflow
• Main symptoms include shortness of breath, cough&
sputum production
• Most people with chronic bronchits have COPD
• Tobacco smoking is the most common cause globally , air
pollution & genetics
• Long term exposure leads inflammatory response in lungs
resulting in narrowing of small airways & breakdown of
lung tissue, known as emphysema and small airways
disease(obstructive bronchiolitis)
• COPD is often mix of these two diseases