Respiratory Physiology

• Gas transport, Factors affecting transport of respiratory

gases through blood.
• oxy-hemoglobin curve, Bohr effect, reverse Bohr effect,
Haldane effect.
• neural (voluntary and automatic) and chemical control
(mention the role of carotid and aortic bodies) of
respiration.
• smoking and its physiological effects, carbon monoxide
poisoning, oxygen toxicity, nitrogen narcosis.
• dysbarism, oxygen therapy, artificial respiration.
• respiratory disorders –hypoxia, hypocapnia,
hypercapnia, asphyxia.
• Parts of respiratory system
Air passages – nose, pharynx, larynx,
trachea(wind pipe),
2bronchi…..10 bronchi, 20 bronchi,
30 bronchi, terminal bronchiole,
respiratory bronchiole, alveolar
ducts, alveoli.
Trachea & 10 bronchi supported by C
shaped cartilages.
Part from trachea-up to respiratory
bronchioles….conducting zone
Resp. bronchioles onwards…
respiratory zone
Lungs&
Associated organs…
 Functional unit of lungs - Alveoli
• Region for Gas exchange
• it’s wall consists of diff. types of cells
Type I cells – flat, permits gas exchange
Phagocytes
Type II cells – secrete detergent like lipoprotein,
surfactants..reduces surface tension of alveoli.
300 million alveoli ..provides SA of 70m2
 Lungs
• Covered by a double membrane – pleura
• Parietal pleura & visceral pleura…pleural cavity..pleural
fluid (acts as a lubricant…reducing the friction between
the lungs & chest wall).
 ???? Gas exchange occurs
In lungs
O2 diffuses from alveolar air → pulmonary blood
CO2 diffuses ……… …………….. ←
Po2 in alveolar air=100 mmHg
Po2 in pulmonary blood = 40 mmHg..P difference…help diffusion.
Pco2 in blood reaching alveoli = 46mmHg
Pco2 in alveoli = 40 mmHg………..
In tissues
Po2 in blood reaching tissues = 95 mmHg
Po2 in cells = 40 mmHg
Pco2 in cells = 46 mmHg
Pco2 in blood reaching cells = 40 mmHg…………o2 diffuses
into cells & co2 leaves the cell.
 Hb & other respiratory pigments

RBC,carries 4 oxygen molecules, conjugated protein – haem &

globin part
Haem – gives red color, it’s a protoporphyrin III (4 pyrrole
groups linked together by methine groups ,=CH-) compound
having Fe at d centre.
Globin part – 4 types of pp chains…..α141aa, β146aa, ɣ&
delta,146aa but its sequence differs.
HbA – 98%..2α, 2β
HbA2 – 2%..2α , 2delta.
Abnormal Hb – SHb….6th position Glu → Val
2. Myoglobin
Skeletal & cardiac muscles
1 haem,1 globin chain…greater affinity for O2, temporary O2
storage
3. Haemocyanin
Contains Cu instead of Fe…blood plasma of molluscs &
arthropods.carries O2 mole/2Cu atoms.less efficient
than Hb.blue color in oxygenated state…
4.Haemerythrin
Contains Fe,reddish violet, in polychaetes, sipunculids…1
O2 /3 Fe atoms
5. Chlorocruorin
Contains Fe ,found in plasma of polychaete, green color in
dilute solutions,
6. Erythrocruorin
Large Hb in plasma of annelid worms & molluscs.it may
contains 108 pp chains each contains 1 haem
 Transport of O2 by Hb
1Hb carries 4 O2 molecules.
Hb +4 O2 → Hb (O2)4…oxyhaemoglobin

Binds loosely & reversibly…affinity of O2 towards Hb is

called…oxyphoretic property.
Fe remains in d ferrous state…ie, oxygenation

If oxidation d product will b methaemoglobin..Fe is in ferric

state……….its a stable compound

Formation & dissociation of oxyHb, depends on partial pressure

of O2 in d medium.
In lungs P O2 is high…….O2+Hb → oxy Hb
In tissues P O2 is low oxy Hb → O2+ reduced Hb
 Oxygen dissociation curve ( ODC) of Hb
Graph shows d relationship between P O2 & % of saturation of
Hb ( % of Hb bound with O2).

P O2 - X axis, % of saturation- Y axis.

S shaped graph

flat portion – 70-100 mm Hg

Steep slope – 10-60 mmHg

The graph shows that…..

At 100mmHg- % of satu..of Hb is 97
At 60 mmHg - % of satu…is 90…..this
property has some benefits ….even
If d PO2 is 60, % of saturation will b high
People do not show any hypoxic symptoms, if d partial P of o2
is not below 60 mmHg…. Pulmonary diseases,
 Factors affecting % of saturation of Hb
1. P CO2, PH
Bohr Effect : P CO2↑/PH↓ - ODC is shifted to d Right
Indicates less affinity of Hb for O2, less Hb is oxygenated
First described by Christian Bohr.
Significance of Bohr effect……
In tissue capillaries…When co2 ↑..acidity ↑/PH ↓it
promotes dissociation of oxyhaemoglobin…thus
facilitates delivery of O2 to d tissues.
Ie….In tissues PH affects binding of O2 to Hb even if
the PO2 is 40.
While, in the lungs PH does not affect binding of O2
to Hb. P O2 in lungs is 100 mmHg. Binding occurs
normally.
2. Temperature
T↑ - oxyHb ↓,……………..curve shifted to right.
Help rapid release of o2 to the tissues????metabolism ..heat ↑

3. 2,3 DPG
When produced in RBCs … it combines with the β chain of
Hb..↓affinity of Hb for O2….so tissues get more O2.

Properties of HbF
Less affinity to DPG…it binds feebly with ɣ chain(not β)

It has high affinity for O2….The ODC is shifted to left when compared
to HbA….ie at a particular PP more o2 binds with HbF than HbA.
 Transport of CO2
Transported mainly in 3 forms
1. In dissolved form in plasma5% - CO2+H2O → H2CO3 carbonic
acid…absence of carbonic anhydrase
2. As carbamino compounds in RBC – CO2+NH2-Hb →HbNH-COOH
(carbamino Hb)
• A small amount CO2+plasma proteins → carbamino proteins
3. As bicarbonates in RBC 70% - same reaction in presence of
carbonic anhydrase
 Haldane Effect
• First described by ..John Scott Haldane

• Deoxygenation of Hb increases its ability to bind with CO2 and

form carbaminoHb, with the help of aa especially Arginine &
Lysine at d N terminus

• This allows transport of CO2 on the empty Hb.

 Respiratory Problems
1. Hypoxia
• Oxygen deficiency at tissue level – adequate O2 is not delivered to
the tissues.
• 4 types –
1.Arterial hypoxia – due to low arterial PO2
Reasons –
deficiency of O2 in the inspired air…..high altitudes.
Hypoventilation….obstruction in d air passage/neuro muscular
diseases.
Reduced respiratory membrane diffusion..pulmonary diseases
2.Anaemic hypoxia – less functional Hb
Reduction in no. of RBC / low Hb content / abnormal Hb / failure of
Hb to combine with O2.
3.Stagnant hypoxia – blood flow to the tissues is decreased
Heart failure..pumping affected / haemorrhage / local thrombosis
4.Histotoxic hypoxia – adequate amt of O2 …tissues fail to utilyze O2
Cyanide poisoning…blocks the activity of cytochrome oxidase

2. Hypocapnia/hypocarbia – deficiency of CO2 in d arterial blood

Arterial P CO2 ↓ ie, 35 – 15 mmHg
Alveolar hypocapnia( ↓PCO2 in alveoli) → arterial hypocapnia.
Chronic hyperventilation (breath rate 18 breaths/min) → ’’
Commonly seen in persons with heart diseases,diabetes,cancer
Symptoms
Chronic coughing, nasal congestion, dizziness, headache, muscle
cramps, bronchospasm, cold extremities, mouth breathing, visual
blackout, angina pain.
3. Hypercapnia – high conc. of CO2 in blood due to hypoventillation
Obstruction of airways/ weakness of respiratory muscles/depression of
respiratory centre/ drug overdose/brainstem lesions,damage /
asthma/COPD/ obstructive sleep apnoea.
Symptoms
Symptoms, early stage- Headache/drowsiness
Severe –flushed skin/ dizziness/ rapid breathing/ increased blood
pressure & heart rate, muscle twitches…
4. Asphyxia
Breathlessness
Reason – retention of excess CO2 & lack of O2 when occur
simultaneously
Body’s response : to expel excess CO2 …
Rate & depth of respiration ↑…violent action of respiratory muscles
Heart rate & blood pressure↑sharply.
Salivation, vomiting, defecation may occur..then everything ↓leads to
death.
 Neural & Chemical control of Respiration
• Voluntary /involuntary
• Voluntary control
Cerebral cortex→→ respiratory motor neurons→→ lungs
• Involuntary control
• RespiratoryCentres in the brain – in the Medulla & pons
• Medullary centres – DRG/IC & VRG/EC
• Pontine centres -
PC, pneumotaxic centre & AP, Apneustic centre
 PC controls duration & rate of inspiration
lungs expand….
PC
strech receptors send impulse via
Respiratory Vagus nerve
motor neurons

EC/V
Inspiratory rmn IC/D inhibits RG
RG
muscles(Dia, Ex inter)

• Strech receptors ..on the wall of bronchi & bronchioles

• Transmission of impulse from PC to EC to IC …Hering-Breuer
reflex……to protect lungs from excessive inflation.
 Chemical control of respiration
• When arterial blood’s PO2/PCO2 / H+ conc.
changes…..automatically rate & depth of respiration changes.????
• Changes r detected by 2 types of receptors
1.Peripheral chemo receptors,PCR- 2
a. Aortic bodies –
located in d arch of aorta in d thorax &
connected to medulla .. vagus nerve

b. Carotid bodies – HEART

in d neck region near the bifurcation of d common carotid artery.
connected to medulla .. glossopharyngeal nerve.
PCR.. Stimulated when d arterial PO2 ↓, also by PCO2 & H+
Send impulses to d medullary inspiratory neurons…..↑ventilation
2. Central chemo receptors ( Text- diagram ….CR)

• Located near d respiratory centre in d medulla.

• Maintains normal level of PCO2
• Excited by high conc. of H+/ CO2

(CO2 + H2O→H2CO3→ H+ + HCO3-)

High conc. of H+ in CSF & extracellular fluid of brain…..Increases

ventilation…..helps to expel excess CO2
 Effects of smoking
• Cigarette smoke contains
Carcinogens – benzopyrene, poly nuclear hydrocarbons, nitrosamines.
Nicotine , CO, HCN, nitrogen oxides, Arsenic etc.
Effects of Nicotine
– stimulates nervous system …leads to addiction.
- circulatory system …↑heart rate & blood pressure, constricts
blood vessels in d skin, Buerger’s disease, gangrene( death&decay)
of toes & fingers, ↑cholesterol level …atherosclerosis, coronary
occlusion & heart attack.
-Respiratory system …ciliotoxins damage cilia & phagocytes in d
airway. Leads to airway obstruction & lung infection. lung diseases-
emphysema( reduces gas exchange) & chronic bronchitis (mucous), reduces
vital capacity. Cancer- lungs,larynx, oral cavity.
- general effects.. free radicals in smoke damages biomolecules,
people may not respond to drugs … bcz of d activation of enzymes
drugs r quickly metabolized.
 CO poisoning
• Colorless, odourless, tasteless gas
Main source - Produced by incomplete combustion of C containing
substances like coal, wood, oil/petrol.
Other sources – stoves, ovens, furnaces, exhaust fumes of
automobiles
• It has high affinity, 210 times greater than, for Hb than O2.
CO + Hb → carboxyHb
Result – less Hb is available for binding with O2….. Hypoxia
• ODC is shifted to left …
• Severity – even 0.1 % is lethal.
Symptoms
Cherry red color of skin & mucous membranes, headache, nausea,
vomiting, progressive brain damage, ……death
 Oxygen Toxicity
• breathing molecular O2 at increased PO2.
• Effect : Produces superoxide anion….. Damages cell membranes by
lipid peroxidation….Cells of CNS, eyes, lungs.
• O2 toxicity of the CNS - Paul Bert effect.
• .....respiratory organs - Lorrain Smith effect.
• Scuba divers, patients of hyperbaric O2 therapy….
???????? Hyperoxia
• Breathing elevated conc. of O2
• Tissue damages…....depends on… type of exposure
• high conc. & Short period, High Pressure – CNS affected
• Elevated conc. of O2 ..Normal pressure, longer period – pulmonary
& ocular toxicity.
Symptoms of hyperoxia
Disorientation, breathing problems, retinal detachment, visual defects
 Nitrogen Narcosis
• Breathing nitrogen under pressure.
• Most divers experience symptoms of nitrogen narcosis at depths
greater than 100 feet, but symptoms may occur in depths as little
as 33 feet. For this reason, use of compressed air deeper than 120
feet is not recommended.
• Ascent reverses the symptoms of nitrogen narcosis.
• Factors that increase the risk of narcosis include cold
temperatures, rapid descent, anxiety,alcohol, sedatives, fatigue, and
excess carbondioxide.
Nitrogen Narcosis Symptoms
• light-headedness, inattention, difficulty in concentrating, poor
judgment,anxiety, decreased coordination, hallucinations, and
Coma
 Dysbarism/Decompression sickness
• occurs when a person returns rapidly to atm. Pressure after he is
exposed to high barometric pressure.
• Seen in SCUBA divers, caisson workers, those who travel btwn
different altitudes.
• ………?????? if divers comeback to the sea level rapidly.
In d ocean P at 40m depth is 5 times more than d P at d sea level
A small part of air is dissolved in d blood & tissues …
• under high pressure more air dissolves in blood ….
• If we move slowly to d sea level (Npressure), extra gas comes out
slowly……as small bubbles
• But, if we rises rapidly……. Gas comes out quickly ….as large
bubbles… may cause vascular blockage or damage to brain cells.
 Oxygen Therapy
• Administration of O2 to increase the supply of oxygen to the lungs
and thereby increasing d availability of O2 to d tissues.
• Room air contains – 21% oxygen
• By using nasal cannula – increase fraction to 30-35%.
• Tight- fitting face mask/ incubator – 100% can be obtained.
• Hyperbaric O2 therapy – O2 is delivered at high pressure

• Hypoxaema (low level of oxygen in the blood due to injury/ illness).

• Patients with Chronic Obstructive Pulmonary Diseases, COPD
• Pre-hospital envt – major trauma, resuscitation, anaphylaxis (allergic
reaction), major hemorrhage, shock, active convulsions (sudden violent
irregular movement of the body caused by involuntary contraction of muscles ),
hypothermia.
Artificial Respiration
Schafer’s Method