Human respiration

1. HUMAN RESPIRATION

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Breathing Respiration
1.Intake of fresh air and
removal of foul air
Oxidation of foodto form carbon
dioxide, water and energy
2.Physical process Biochemical process
3.No energy is released
rather used
Energy is released in the form of
ATP
4.Extra cellular process Intra cellular process
5.No enzymes involved Large no of enzymes are involved
6.Confined to certain organsOccurs in all the cells of the body

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Types of Respiration
1. Anaerobic Respiration :
When nutrients are oxidized without the use of O2 .
In yeast glucose forms ethyl alcohol and CO2.
In bacteria and muscles glucose is converted to lactic acid
Endoparasitesare anaerobic in nature
2. Aerobic Respiration :
When nutrients are oxidized with the use of O2 either from air or from water .
i) External respiration : Exchange of gases between Blood and air
ii) Transport of gases to the tissues
iii) Internal respiration : Exchange of gases between blood and tissues
iv) Cellular respiration : Oxidation of nutrients in the cell and release of energy.

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Mechanisms of breathing vary among different groups of animals mainly on their habitats
and levels of organisation.
Lower invertebrates
Sponges, coelenterates, flatworms, etc., exchange O
2,by simple diffusion over their entire
body surface.
Earthwormsuse their moist cuticleand insectshave a network of tubes (tracheal tubes)to
transport atmospheric air within the body
Special vascularised structures called gillsare used by most of the aquatic arthropodsand
molluscs
Vascularised bags called lungsare used by the terrestrial molluscsfor the exchange of
gases.
Vertebrates
Fishesuse gills
Reptiles, birds andmammalsrespire through lungs.
Amphibianslike frogs can respire through their moist skinalso

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Human Respiratory System
1.Respiratory pathway :
a) Nostrils and Nasal
chamber
b) Pharynx
c) Larynx
d) Trachea
e) Bronchi
f) Bronchioles
g) Alveoli
1.Respiratory Organ :
a) Lungs

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NOSTRILS:
•Nostrils are the external openingsof thenose.
These are also called external nares.
Similarly a pair of internal openingsis present.
They open into pharynx. These are called internal
nares
NASALCHAMBERS:
•Thespacebetweentheexternalandinternal
naresisknownasnasalchamber.
•Internally,eachoneislinedbyamucous
membrane.
•Ciliatedepitheliumispresentinnasalchamber.
•Itisdividedintorightandleftpartsbya
cartilageknownasmesethmoid.
Nose

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Eachnasalchamberisfurtherdividedinto
threeregions:
Vestibule:
Thisistheanteriormostpartofthe
nasalchamber.
Ithashairtotrapdustparticlesand
preventthemfromgoinginside.
Respiratorypart:
Thisisthepartrichlysupplied
withcapillaries.
Itwarmstheairandmakesitmoist.
Sensory part:
This is lined by sensory epithelium for
detection of smell.

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Pharynx
•Nasal chamber opens into the pharynx.
•It is a short, vertical tube measuring about 12
cm.inlength.
•The respiratory and thefood passages cross
each other in the pharynx by two separate
passages.
•Its upper part is known asnaso-pharynx
which helps in conduction of airand the lower
part is called laryngo-pharynx or oro-pharynx
conducting foodto oesophagus.
In the pharynx, there are tonsils which are
made up of lymphatic tissue. They kill bacteria
trapped in the mucous

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Larynx
•Itisthesoundproducingorgan,hencealso
calledthesoundbox.
•Inmales,thelarynxincreasesinsizeatthe
timeofpuberty.Hence,itiscalledAdam's
appleandcanbenoticedintheneckregion
•.
•Fromthepharynx,airentersthelarynx
throughanopeningcalledglottis.
•Theglottisisguardedbyaflapcalled
epiglottis.Itpreventstheentryoffood
particlesintotherespiratorypassage
•Alongthesidesoftheglottisaretwofoldsof
elastictissuecalledvocalcords.Theseare
responsibleforproducingsound.

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Trachea
•It is also known as wind pipe.
•It is about 12 cm. longand 2.5 cm. wide.
•It lies in front of the oesophagusand extends
downward into the neck.
•The wall of the trachea is made up of fibrous
muscular tissue supported by'C'-shaped
cartilage rings. These are 16-20 in number.
They make the trachea rigid.
•The trachea is internally lined withciliated
epithelium and mucous glands.
•If any foreign particle enters, it is
immediately expelled out by coughing action.
Dust particles get trapped by the mucous. By
ciliarymovement, they are swept towards the
larynx and finally they enter the oesophagus

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Bronchi & Bronchioles
•Thedistalendofthetracheaisdividedinto
twobronchibehindthesternum.
•
•Eachbronchusissupportedbyacomplete
ringofcartilage.
•Itentersintothelungofitsrespectiveside.
•Onenteringthelung,eachbronchusfurther
dividesintosecondaryandthentertiary
bronchi.
•Tertiarybronchidivideintomanyminute
bronchioles.
•Wallofeachbronchioledoesnothave
cartilagerings.
•Eachbronchioleendsintoaballoon-like
alveolus.
•Thesealveolimakethelungsspongyand
elastic.

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These are the principal respiratory
organs, located in the thoracic cavity.
Lungs are paired, hollow, elastic organs.
Each lung is enclosed inpleural sac.
Pleural sac is made up of two
membranes ,outer parietal andinner
visceral. The enclosed cavity is called
the pleural cavity. It is filled with a
pleural fluid, which lubricates the
pleura and prevents the friction when
the pleural membranes slide over each
other.
Lungs are pink in colour, soft, elastic
and distensible.
They are highly vascular(richly
supplied with blood capillaries).
Lungs

13. Eachsachasabouttwentyalveoli
whichlooklikegrapes.Theyare
coveredwithanetworkofcapillaries
fromthepulmonaryarteryandvein.
Thealveolihaveverythin(0.0001mm)
wallcomposedofsimplenon-ciliated,
squamousepithelium.Ithascollagen
andelastinfibres.Thismakesthe
alveoliveryflexible.
Eachalveolusisabout0.1mmin
diameter.
Thehumanlunghasabout750million
alveoli,whichincreasesurfaceareafor
exchangeofgases.Thetotalarea
coveredbythemisabout50timesthe
surfaceareaofskin.
Alveoliaresuppliedbyanetworkof
pulmonarycapillaries.

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Mechanism of Breathing

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INSPIRATION:
•Itisanactiveprocessbroughtaboutbyribs,intercostalmuscles,sternum
anddiaphragm.
•Theintercostalmusclescontract,pullingtheribsoutwardandincreasethe
spaceinthethoraciccavity.
•
•Thelowerpartofthebreastbone(sternum)isalsoraised.
•Thediaphragmcontractsandbecomesalmostflat
•.
•Volumeofthethoraciccavityisfurtherincreased,pressureonthelungs
decreases.Thelungsexpandandtheirvolumeincreases.Atmosphericair
rushesintothelungsthroughtherespiratorypassagetomakethepressure
equal.Thustheairentersthelungs.

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EXPIRATION:
It is a passive process.
The inter-costal muscles relax pulling the ribs inwards.
The diaphragm relaxesand again becomes dome shaped.
Thus collective contraction of intercostalmuscle and diaphragm reduces the
volume of the thoracic cavity. The pressure on the lungs increases. The
lungs get compressedand the airin the lungs, rushes outthrough the
external nares.
Alternate inspiration and expiration together form the respiratory cycle.
It occurs16-20 times per minutein man.
Breathing is under the control of the medulla oblongataof the brain

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RESPIRATORY QUOTIENT (RQ)
The ratio of the volof CO2 / O2 used in unit time is called respiratory quotient
It varies for different substrates used for respiration
GLUCOSE has RQ = 1
FAT has RQ = 0.7
PROTEIN has RQ = 0.85
ORGANIC ACIDS has RQ = 1.3 or 1.4
In ANAEROBIC respiration RQ = infinity
RQ is determined by means of Ganong’srespirometer

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1. External respiration
•It includes the respiratory processes which take place in the lungs
O2 fromthe lungsdiffuses inthe lung capillariesand
CO
2
from the lung capillariesdiffuses into lungs
TRANSPORT OF GASES
The transport of respiratory (O
2and CO
2) gases takes place in the following events:
1.External respiration
2.Internal respiration
3.Cellular respiration
External respiration includes three events:
a. Exchange of gases
b. Formation of oxy-haemoglobin
c. Release of carbon-di-oxide:

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1.Exchange of gases
•Concentrationofoxygenishigherinthe
inspiredairthaninthealveolarbloodand
theconcentrationofcarbon-dioxideis
higherinthealveolarbloodthaninthe
inspiredair.
•Thisresultsintheexchangeofoxygen
fromtheairintothebloodandcarbon-
dioxidefrombloodintotheairwhichis
exhaledout.

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2.Formation of oxy-haemoglobin
The absorbed oxygencombines with the
haemoglobinof RBC's.
Haemoglobin is a respiratory protein
pigment. It forms the unstable
oxy-haemoglobin.
Haemoglobin+ Oxygen = Oxy-Hb
Hb+ 4 O
2 Hb(4O
2)
15 gmsof Hbis present in 100 ml of blood
1 gm of Hbcan carry 1.34 ml of O
2
Thus 100 ml of blood (15 gm of Hb) can carry approx
20 ml of O
2

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3. Release of carbon-dioxide
Carbon-dioxidefrom the blood is released
outside into the air.
CO
2is brought by the blood from the tissue
cells in the form of sodium and potassium
bicarbonates in the blood plasma.
Some amount of CO
2is also brought by
haemoglobin in the form of carbamino-
haemoglobin.
CO
2brought in all these forms is released.

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2. Internal respiration
•Itincludestherespiratoryprocesses
whichtakeplaceinthetissuecells.
•Oxygenbroughtbythebloodisgivento
thetissuecellsandcarbon-dioxidefrom
thetissues,ispassedintotheblood.
•Whenthebloodreachesthetissuecells,
theunstableoxy-Haemoglobinbreaks
downtoformhaemoglobinandoxygen.

24. O
2–HbDissociation Curve

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The ultimate purpose of respiration is torelease energy. This is carried out in the cells
by oxidation of food.
It results in the formation ofATP molecules. Energy is stored in this form. This energy is
used to carry out vital life processes
So ,ATP is called energy currency of cell.
ATP is formed as the main product using mitochondria, while by-products are CO
2and
water vapour which are transported by the blood to the lungs.
Energy released as heatto certain extent is used to maintain the body temperature.
3. Cellular respiration

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PULMONARY AIRVOLUMESAND
CAPACITIES:
•Thequantitiesofairthelungscanreceive,holdor
expelunderdifferentconditionsarecalled
pulmonaryorlungvolumes.
•Pulmonarycapacityreferstoacombinationoftwo
ormorepulmonaryvolumes
•.
SPIROMETRY istheprocessofrecordingthe
changesinthevolumeofairintoandoutoflungsand
theinstrumentusedforthispurposeiscalled
SPIROMETER
Thegraphshowingthechangesinthepulmonary
volumesandpulmonarycapacitiesunderdifferent
conditionsofbreathingiscalledaSPIROGRAM.

27. PULMONARY AIRVOLUMESANDCAPACITIES
(TV + IRV)
(RV + ERV)
(TV + IRV + ERV)

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•Itisthevolumeofairinspiredorexpired(both)witheachnormalbreath(effortless).It
amountstoabout500mlintheaverageadultman.
•Ofthe500mlofinspiredair,only350mloffreshairreachesthelungalveoliandiscalled
alveolarvolumewhileabout150mloftheinspiredairremainsintherespiratorytract
fromthenasalchamberstoterminalbronchioleswhichisoftencalledanatomicaldead
spaceandiscalleddeadspacevolume.
•Physiologicaldeadspaceincludesanatomicaldeadspaceandthespaceinthenon-
functionalalveoli.Itisnotusefulforthegasexchangeprocessasnogasexchange
occursinthedeadspace.
•Duringexercise,tidalvolumeisabout4-10timeshigherthannormal.
TIDALVOLUME(TV)

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It is the extra volume of air which can be inspired by forced inhalation beyond
the normal tidal volume.
It is about 2500-3000 ml.
It is the deepest possible inspiration
INSPIRATORY
RESERVEVOLUME(IRV)
It is the amount of air that can beexpired by forceful expiration after the end of
a normal tidal expiration.
It is about 1000 –1100 ml.
EXPIRATORY
RESERVEVOLUME(IRV)
It is the volume ofair left behind in the lung alveoli and respiratory passage
even after the most forceful expiration.
It is about 1500 ml.
This volume can never be expelled outby respiration.
RESIDUALVOLUME(IRV)

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It is the amount of air that a person caninhale to the maximum level.
It is the sumof the inspiratoryreserve volume(IRV) and the tidal volume (TV)and
is about 3500 ml. (Range 3 –3.5 L)
IC = IRV + TV
INSPIRATORYCAPACITY(IRV)
It is amount of air left in the lungs after normal expiration.
It is equal to the sum of expiratory reserve volume and the residual volume.
It is about 2500 ml. (2.5 Litres)
FRC = ERV + RV= 1000 + 1500= 2500 ml
FUNCTIONAL
RESIDUALCAPACITY(IRV)
It is themaximum amount of air that can be expelled from the lungs byforced
exhalation after a forced inhalation.
It is equal to the sum of tidal volume, inspiratoryreserve volume and expiratory
reserve volume.
Vital Capacity of lung = TV + IRV + ERV = 500 + 3000 + 1100= 4600 ml
Range of vital capacity = 3.5 –4.5 Litres in a normal adult person.
VC is higher in athletes, mountain dwellers, men and young ones
VC is lower in non-athletes, plain dwellers, women,oldand cigarette smokers
VITALCAPACITY(VC)

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It is the amount of air in the lungs and the respiratory passage after a maximum
inhalation effort.
It is equal to the sum of vital capacity and the residual volume.
TLC= VC + RV= 3.5 –4.5 L + 1.5 L= 5 –6 litres(Average 5800 ml)
TOTALLUNGCAPACITY(TLC)

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Haemoglobinhas about 250 timesmore affinityfor carbon monoxidethan for
oxygen.
In the presence of carbon monoxide, it readily combines to form a stable
compound called carboxy-haemoglobin.
The oxygen combining capacity with Hbdecreases and as a result tissue suffers
from oxygen starvation.
It leads to asphyxiationand in extreme cases to death.
Treatment: The person needs to be administered with pure oxygen-carbon
dioxide mixtureto have a very high O
2level to dissociate carbon monoxide from
haemoglobin.
Causes:
Carbon monoxide poisoning occurs often in closed roomwith open stove
burnersor furnacesor in garageshaving running automobile engines.
CARBONMONOXIDEPOISONING

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CONTROLOFRESPIRATION
Respiration has 2 control mechanisms :
Nervous and Chemical regulation
NERVOUS :
The respiratory center in medulla and pons
consist of
1) Dorsal respiratory group :
Located in the dorsal portion of medulla
Mainly causes Inspiration
2) Ventral respiratory group :
Located in the ventrolateral portion of
medulla
Causes Inspiration or expiration
3) Pneumotaxiccentre:
Located in the dorsal portion of pons
Mainly limits Inspiration

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CONTROLOFRESPIRATION

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CHEMICAL :
Chemoreceptors are located in the carotid
and aortic bodies
Afferent nerve fibresof carotid bodies pass
through Glossopharyngeal nerve to the dorsal
respiratory area
Afferent nerve fibresof aortic bodies pass
through vagusnerve to the dorsal respiratory
area
Excess CO
2and H
+
stimulate the respiratory
center and accordingly alter the inspiratory
and expiratory signals to the respiratory
muscles
Increased CO
2lowers the pH resulting in
acidosis

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RESPIRATORYDISORDERS
-inflammatory disease of the air ways
-reversible over-reactivity of the airway smooth muscle.
-The mucous membraneand muscle layersof the bronchi become thickenedand the
mucous glands enlarge reducing airflowin the lower respiratory tract.
-During an asthmatic attack, spasmodic contraction of bronchial muscle -(Bronchospasm)
constricts the airway and there isexcessive secretion of thick sticky mucus, which further
narrows the airway.
-Inspiration is normal but only partial expiration is achieved so that lungs become hyper-
inflatedand there is severe dyspnoea(difficulty in breathing, a.k.a. air hunger) and
wheezing.
-The duration of attacks usually varies from a few minutes to hours (status asthmaticus).
In severe attacks the bronchi may be obstructed by mucus plugs, leading to acute
respiratory failure, hypoxia(deficiency in the amount of oxygen reaching body tissues)
and possibly death.
Non -specific factors
Cold air, Cigarette smoking,
Air pollution, Upper respiratory tract infection,
Emotional stress and Strenuous exercise.
ASTHMA

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PHARYNGITIS:
The inflammationof the upper respiratory
tractcan be caused by inhaling different micro-
organisms.
Streptococcus pyogenesare common cause of
inflammation of palatine tonsils and walls of
pharynx.
Pharyngitis usually accompanies common
cold.

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LARYNGITIS:
It is an inflammation of larynxdue to viral or
bacterial infection.
It occurs in all the ages but more common in
children.
Symptoms:
The voice becomes huskyinitially.
Severe infection may lead to aphasia.
There is a feeling of rawnessin the throat.
Stridormay be present in children.
Coughof an irritating type may be present.
Cause:
Vocal misuse or overuse are common causes
of acute laryngitis

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ALLERGRIC RHINITIS (HAY FEVER):
In this condition, atopic (immediate)
hypersensitivity develops toforeign proteins
(antigens)e.g. pollen, mites in pillow feathers,
animal dander.
The acute inflammationof nasal mucosaand
conjunctioncauses rhinorrhoea(excessive
watery exudate from the nose), rednessof the
eyes and excessivesecretion of tears.
Atopic hypersensitivity tends to run in families
but no genetic factor has yet been identified.
Other forms of atopic hypersensitivity include:
Childhood onset asthma,
Eczemain infants and young children and
Food allergies

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PNEUMONIA:
Infection of the alveoli.
protective processes fail to prevent microbes reaching lungs.
Causes:
IMPAIRED COUGHING:
Coughing is aneffective cleaning mechanism, but if it is impairedif the person is
unconscious, damageto respiratory musclesor the nervessupplying them, or painful
coughing, then respiratory secretionsmay accumulateand become infected.
Ciliaryaction may be impairedor the epithelium destroyedby tobacco smoking, inhaling
noxious gases, infection etc.
Depressed macrophage (W.B.Cs) activitymay be caused by tobacco smoking, alcohol, and
anoxia(a condition characterized by an absence of oxygen supply to an organ or a tissue).
Other factors:
These include reduced resistance, leucopoenia (decreased W.B.C count) and chronic
diseases like cardiac failure, cancer, chronic renal failure.

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SOME PATHOGENS ASSOCIATED WITH
PNEUMONIA:
Streptococcus pneumoniae:
This is the commonest causative organismin
pneumonia, particularly Lobar Pneumonia
(acute bacterial pneumonia).
Mycoplasma:
It is the second commonest causative
organism, and affects mainly children and
young adults.
Other organisms:
Some viruses, protozoa and fungi may cause
pneumonia in people whose general resistance
is lowered or whose immune system is
depressed by HIV, immunosuppressant drugs
etc.

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OCCUPATIONAL LUNG DISEASES
This group of lung diseases is caused by inhaling atmospheric pollutants at work place
.
To cause disease, particlesmust be so small that they are carried in inspired air to the
level of therespiratory bronchioles and alveoli, where they can only be cleared by
phagocytosis.
Larger particlesare trapped by mucusin upper part of the respiratory tract and
expelled by ciliaryactionand coughing.
Recognition of the damaging effects of these substances has led to legislation that
limits workers exposure to these pollutants.

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SILICOSIS:
This may be caused by long-term exposure todust containing silicon compounds.
High-risk industries are quarrying, granite, slate, sandstone-mining, stone masonry, sand
blasting and glass and pottery work.
Inhaled silica particles accumulate in thealveoli.
The particles are ingested by macrophages, and are actively toxic to these cells.
The inflammatory reaction is triggeredwhen the macrophages destroy the particles and this
result in significant fibrosis.
Silicosis appears to predispose to the development oftuberculosis, which rapidly progresses
to tubercular bronchopneumoniaand possibly military TB(a form varying in severity, in
which minute tubercles form in different organs due to dissemination of bacilli through the
body by the blood stream).
Gradual destruction of lung tissue leads to progressive reduction in pulmonary function,
pulmonary hypertension and heart failure.

46. ASBESTOSIS:
Asbestosis is caused by inhalingasbestos
fibres, usually develops after 10 to 20 years
exposure, but sometimes after only 2 years.
Asbestos miners and workers involved in
making and using some products containing
asbestos are at risk.
There are different types of asbestos, but blue
asbestosis is associated with the most serious
disease.

47. Eupnea–normal breathing
Hypopnea –Slow breathing
Hyperpnoea –rapid breathing
Apnoea–No breathing
Dyspnoea–Difficult breathing
Tachypnoea–Rapid shallow breathing
Orthopnoea–Inability to breathe in horizontal position
Asphyxia –Combination of hypoxia and hypercapnea
Hypercapnea–Increased CO2 content of blood
Hypocapnea–Decreased CO2 content of blood
SOME RESPIRATORY TERMS

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