Respiration by dr. mudassar

RESPIRATORY PHYSIOLOGY
DR.MUDASSAR ALI

THE RESPIRATORY SYSTEM
GAS LAWS
Dalton's Law (also called Dalton's Law of Partial Pressures)
Total pressure exerted by a gaseous mixture is equal to the
sum of partial pressures of each individual component in a
gas mixture. This law was observed by John Dalton in 1801
and is related to ideal gas laws.
Mathematically,pressure of a mixture of gases
can be defined as the summation
where P represents the partial pressure of each
component.

DALTON'S LAW
• This law simply says that if you add up all the partial
pressures of the components of a gas, they will sum to the
total pressure of the gas as a whole. It also defines partial
pressure as a component of the total pressure.

Boyles Law :P1V1 = P2V2
• This means that (if temperature is constant), if you have an enclosed
space and the volume changes, the pressure does, too, but in a
manner according to the original state.
• So if the thoracic cavity has a certain volume and pressure, when you
change the volume (for example, increase it for inspiration), the
pressure will change as well (in this example, decrease).
• Pressure is inversely proportional to volume at constant temperature.

CHARLES’S LAW
• At a constant volume pressure is directly proportional to
absolute temperature.
• AVOGADRO’S LAW.
Equal volume of different gases at the same temperature and
pressure have the same numbers of molecules.
IDEAL GAS LAW.
PV=nRT
It is combination of three laws.(charles’s+ boyle’s+ avogadro’s)

HENRY'S LAW
• This law says that each component of a gas will diffuse into
a liquid at a rate proportional to its partial pressure. So the
higher the pressure, the more of that gas that will enter the
liquid.

GRAHAM’S LAW
• The relative rates of diffusion of gases under the same
condition are inversely proportional to the square root of
densities of those gases.

HALDANE EFFECT
• This relates to the fact that Hb carries CO2 or H+ better
when it isn't also carrying O2.
• It also says the opposite (that Hb carries O2 better when it
doesn't also have to carry CO2 or H+).

BOHR EFFECT
• This says that oxygen unloading happens more readily
(where it is needed) when CO2 and hydrogen ion
concentration is higher.
• This does relate to the fact that Hb carries O2 better when
it doesn't also have to carry CO2 or H+, but that specific
detail is part of the Haldane effect

RESPIRATION
Transport of oxygen from the outside air to the cells within tissues and
the transport of carbon dioxide in the opposite direction.
(1) Pulmonary ventilation
(2) Diffusion of oxygen and carbon dioxide between the alveoli and the
blood
(3) Transport of oxygen and carbon dioxide in the blood and body fluids
to and from the body’s tissue cells
(4) Regulation of ventilation and other facets of respiration

Chapter 22, Respiratory System 11
Respiratory System
Figure 22.1

RESPIRATION INCLUDES TWO PROCESSES
1. External respiration
It is the absorption of 02 and removal of CO2 from the body
as a whole.
2. Internal respiration
It is the utilization of 02 and production of CO2 by cells and
the gaseous exchanges between the cells and their fluid
medium.

Chapter 22, Respiratory System 13
FOUR PROCESSES OF RESPIRATORY SYSTEM
• Respiration – four processes must happen
– PULMONARY VENTILATION – moving air into and out of the
lungs
– EXTERNAL RESPIRATION – gas exchange between the lungs
and the blood.
– TRANSPORT – transport of oxygen and carbon dioxide
between the lungs and tissues
– INTERNAL RESPIRATION – gas exchange between systemic
blood vessels and tissues.

FUNCTIONS OF RESPIRATORY SYSTEM
I. RESPIRATORY FUNCTIONS
a) Exchange of gases between atmosphere and blood.
b) Maintenance of pH of the body fluids.
c) Excretion of water vapor.
d) Excretion of certain volatile substance e.g. acetone.
e) Respiratory muscles are used during laughing, singing etc.

2. Non respiratory functions /endocrine function
a) Formation of surfactant.
b) Capillary endothelium of respiratory system secretes[ACE] which converts
angiotensin I to angiotensin II that plays role in long term regulation of
blood pressure.
c) Respiratory system plays a role in immune function by
i. Secreting immunoglobulin A (IgA).
ii. Exhibiting phagocytic activity due to presence of macrophages
in alveoli, these are known as pulmonary alveolar macrophages.
d) Respiratory system plays a role in allergic reactions because mast cells are
abundant in respiratory tract. Mast cells play role in allergic reactions by
releasing histamine, bradykinin, prostaglandins and serotonin.

• CONTROL OF RESPRIATION
• The respiratory control centers are located in the medulla oblongata
& pons of brain.
• BREATHIG RATE
• At rest normal human breathes 12 to 16 times a minute. About 500ml
of air per breath or 6 to 8 L/min is inspired & expired.
• This air mixes with the gas in alveoli by simple diffusion. In this
manner, 250ml of O2 enters the body per minute & 200ml of CO2 is
excreted.

ALVEOLI
• Alveoli are surrounded by pulmonary capillaries.300 million alveoli,total area of
alveolar walls in contact with capillaries in both lungs is 70 m2.Alveoli are lined by
two types of epithelial cells.
1. TYPE I CELLS
• Flat cells with large cytoplasmic extensions & are primary cells of alveoli, covering
approximately 95% of alveolar epithelial surface area.
2. TYPE II CELLS (GRANULAR PNEUMOCYTES)
• These cells make approximately 5% of the surface area, they constitute
approximately 60% of the epithelial cells in the alveoli. These cells secrete
surfactant & play role in alveolar repair.
3. Alveoli also contain specialized cells like pulmonary alveolar macrophages (PAMS
OR AMS), lymphocytes, plasma cells, neuroendocrine cells & mast cells.
Mast cells contain heparin, various lipids, histamine & various proteases that
participate in allergic reactions.

LEARNING OBJECTIVES
At the end of this chapter student should be able to know
 Mechanics of breathing
 Pulmonary pressures
 Lung compliance & role of surfactant
 Law of laplace & ARDS
 Dead space
 Lung volume & capacities
 Protective reflex

• Lungs can be expanded
and contracted in 2 ways
1) By downward and upward
movement of the
diaphragm to lengthen or
shorten the chest cavity
2) By elevation and
depression of the ribs to
increase and decrease the
anteroposterior diameter
of the chest cavity.

NORMAL QUIET BREATHING
• Diaphragm
• Nerve supply phrenic nerve , C 3,4,5
• During inspiration………………. Contraction of diaphragm
causes lower surface of lungs downward.
• During expiration …………… relaxation of diaphragm, elastic
recoil of lungs, chest wall and abdominal structures
compresses lungs and expels air.

BY ELEVATION & DEPRESSION OF RIBCAGE
• Increase or decrease
anteroposterior diameter
of chest cavity
1. Pump handle – Sternum
moves forward, ribs
moving up and away from
spine, Antero posterior
diameter increases
2. Bucket handle – ribs
moving outward,
transverse diameter
increase.

FORCEFUL INSPIRATION AND EXPIRATION
• Muscles of forceful inspiration
I. External intercostals
II. Sternocleidomastoid
III. Anterior serrati
IV. Scaleni
• Muscles of forceful expiration
• Abdominal recti
• Internal intercostals.

• Lungs are surrounded on each side by a double layer of
membranes called Pleura/ Pleural membranes.
• VISCERAL PLEURA: Attached to the lungs
• PARIETAL PLEURA: It is the outer layer & is attached to the
inner side of the thoracic wall.
• INTRAPLEURAL SPACE: Space between the visceral &
parietal layer of pleural membrane.
• PLEURAL FLUID / INTRAPLEURAL FLUID
• It is thin layer of fluid present between two layers of the pleural
membrane (visceral & parietal).
• This fluid lubricates movement of the lungs within the cavity.
• This fluid exerts pressure called intrapleural pressure & it is negative
pressure.

PLEURAL EFFUSION:
• Collection of large amount of free fluid in pelural space is
called pleural effusion.
• CASUES
1. Cardiac failure
2. Inflammation or infection of the pleural surface
3. Blockage of lymphatics, draining fluid from pleural cavity.
• PNEUMOTHORAX
Presence of air in pleural cavity is known as
pneumothorax. Air enters either through a rupture or a
hole in chest wall.

PRESSURE AND ITS CHANGES DURING RESPIRATION
• Pleural pressure is the pressure of the fluid in the thin
space between the lung pleura (visceral) and the chest wall
pleura (parietal). Normally, this is a slightly negative
pressure.
VALUES.
• -5 to -7.5 during inspiration.
• -2 during expiration.

ALVEOLAR PRESSURE
• Alveolar pressure is the pressure of the air inside the lung
alveoli. When no air is flowing into or out of the lungs, the
pressures in all parts of the respiratory tree is considered to
be zero.
VALUES.
• -1 cm of water during inspiration.
• +1cm of water during expiration.

TRANSPULMONARY PRESSURE.
• The difference between the alveolar pressure and the
pleural pressure is called the transpulmonary pressure.
• It is the pressure difference between inside the lungs
(alveolar pressure) minus the pressure just outside the
lungs (pleural pressure)

• PLEURAL PRESSURE
• ALVEOLAR PRESSURE
• TRANSPULMONARY
PRESSURE (Recoil
pressure)

LUNG COMPLIANCE
• Extent to which lungs expand for each
unit increase in transpulmonary
pressure is called the lung compliance.
• Compliance of both lungs = Average
200ml/cmH2O
COMPLIANCE= ∆v
___________
∆p

CHARACTERISTICS OF THE COMPLIANCE
DIAGRAM
(1) Elastic forces of lung tissue itself
(2) Elastic forces caused by surface tension of the fluid that lines inside
walls of alveoli & other lung air spaces.
3) Transpulmonary pressure.
.

Elastic forces of lung tissue are determined by
a) Elastin
b) Collagen
• In deflated lungs-------these fibers are Contracted & kinked.
• In expanded lungs------- these fibers are Stretched & unkinked

Elastic forces caused by surface tension of fluid that lines inside walls of
alveoli & other lung air spaces.
.
• Work against the elastic forces
of lung
1. Lung elastic tissue---1/3
2. Surface tension in alveloi--2/3

FACTORS AFFECTING COMPLIANCE
• DECREASED COMPLIANCE .
• Pulmonary edema, Fibrosis, Pneumothorax, Hydrothorax,
Pleural effusion , COPD, Scaring of lungs in T.B,
Thickening of pleura, Absence of surfactant in new born,
Deformaties of thorax like kyphosis.
• INCREASE COMPLIANCE.
• Increase with increasing elasticity.

Alveolar Surface Tension
PRINCIPLE OF SURFACE TENSION
Water forms a surface with air in alveoli,
called water air interface. Water
molecules on the surface of water have
strong attraction for one another and
always attempts to contract. This is what
holds raindrops together .
Now let us reverse these principles & see
what happens on the inner surfaces of
alveoli. Here, water surface is also
attempting to contract. This results in an
attempt to force the air out of the alveoli
through the bronchi. This causes alveoli
to try to collapse.
This force of the entire lungs is called the surface
tension elastic force

.
FACTORS PREVENTING THE LUNGS FROM COLLAPSE
• Surfactant
• Intrapleural pressure
1. Surfactant is a surface-active lipoprotein complex formed by type II
alveolar cells. Proteins & lipids that comprise surfactant have both a
hydrophilic region & hydrophobic region. Main lipid component of
surfactant, dipalmitoylphosphatidylcholine, reduces surface tension.
2. Pleural pressure is pressure in pleural space. When this pressure is
lower than the pressure of alveoli they tend to expand. This prevents
the elastic fibers & outside pressure from crushing the lungs. It is a
homeostatic mechanism.

SURFACTANT
• Surface active agent, reduces the surface tension so preventing the
full collapse of alveoli
• Secreted by alveoli type II cells
• Lipoprotein mixture in thin fluid layer on the interior of alveoli
• Surface tension inversely proportional to concentration of surfactant

COMPOSITION
• Surfactant apoproteins, Phospholipids, Calcium ions
Dipalmityolphasphatidylcholine.
• Dipalmitoyl component reduces the surface tension
• During inspiration water molecules move apart & expiration close to
each other
• FUNCTIONS OF SURFACTANT
1. Surfactant reduces tendency of alveoli to collapse by reducing
surface tension.

MECHANISM OF REDUCING SURFACE TENSION
• Dipalmityolphosphatidylcholine, along with less important
phospholipids responsible for reducing surface tension.
• It does this by not dissolving uniformly in fluid lining alveolar surface.
• Instead, part of molecule dissolves, while remainder spreads over the
surface of water in alveoli.
• In this way, surfactant weakens & disrupts the bond & cohesive forces
between water molecules & prevents collapse of alveoli.

2. Surfactant also causes stability of alveoli i.e. it maintains almost
uniform size of alveoli by reducing surface tension that tends to
collapse the alveoli.
3. Surfactant prevents pulmonary oedema (Pulmonary oedema is
excess collection of fluid in alveoli & interstitial space surrounding
alveoli).
• HOW PULMONARY OEDEMA DEVELOPS:
It develops in the absence of surfactant because surface tension pulls
fluid from capillaries surrounding the alveoli & leads to the
development of pulmonary oedema i.e. excess collection of fluid in
alveoli & interstitial space surrounding alveoli.

LAW OF LAPLACE
Pressure= 2 × Surface tension
____________
Radius of alveolus
Pressure 3mmHg
Respiratory distress syndrome of new born

INFANT RESPIRATORY DISTRESS SYNDROME (IRDS) ALSO KNOWN
AS HYALINE MEMBRANE DISEASE or ACUTE RESPIRATORY DISTRESS
SYNDROME
• Surfactant synthesis begins in 25th week of fetal development &
completes in 32 week. Surfactant is important at birth. Fetus makes
respiratory movements in utero but lungs remain collapsed until
birth.
• After birth, infant makes several strong inspiratory movements &
lunges expand. Surfactant prevents them from collapsing.
• Babies born prematurely without adequate development of
surfactant suffers from surfactant deficiency that is an important
casue of infant respiratory distress syndrome (IRDS, also known as
hyaline membrane disease).
• Surface tension in the lungs of these infants is high & alveoli are
collapsed in many areas called Atelectasis of alveoli.
• Additional factor in IRDS is retention of fluid in lung.

WORK OF BREATHING
• Inspiration - active process, so work is done
• Energy consumed (work done) during inspiration – 3-5% of total
energy used by body
• During exertion - ↑ ventilation – both inspiration & expiration –
active, energy utilized upto 50 times more

TYPES OF WORK OF BREATHING
1. COMPLAINCE WORK OR ELASTIC WORK:
that required to expand lungs against the lung & chest elastic forces
2. TISSUE RESISTANCE WORK:
that required to overcome the viscosity of lung & chest wall
structures
3. AIRWAY RESISTANCE WORK
that required to overcome airway resistance to movement of air
into lungs.

LUNG VOLUME AND CAPACITIES
• Four lung volume & four lung capacities
• All volume & capacities 10 – 20 % less in women & greater in
heavy built or athletes.
• More in standing & sitting position rather in lying

• VOLUMES
1. Tidal volume:
Volume of air inspired or
expired with each breath
500ml
2. Inspiratory Reserve
Volume:
Max extra volume of air
inspired over & above the
normal tidal volume
3000ml

3. Expiratory Reserve
Volume:
Max extra volume of air
expired after the end of
normal tidal expiration
1100ml
4. Residual Volume:
Volume of air remained in
the lungs after forceful
expiration
1200ml

Capacities
1. Inspiratory Capacity:
Tidal volume +Inspiratory
reserve volume
3500ml
2. Functional Residual
Capacity (FRC):
Expiratory reserve volume
+ residual volume
2300ml

3. VITAL CAPACITY :
Inspiratory reserve volume +
expiratory reserve
volume + tidal Volume
4600ml.
Maximum amount of air a
person expired after
maximum inspiration.
4. TOTAL LUNG CAPACITY:
Max volume of lung to
which it can expanded
greatest possible effort.
5800ml

MEASUREMENT OF LUNG VOLUMES AND
CAPACITIES
Spirometer
except
functional residual
capacity(FRC).
FRC measured by
helium dilution
method and
nitrogen washout
method.

• HELIUM DILUTION METHOD
Spirometer of known volume with Helium with known
concentration
After normal expiration, inspire through spirometer
FRC gases mixed with Helium & dilute it
DILUTION CALCULATED
CiHe
FRC = __________________ -1 x Vi-spir
CfHe
• CiHe = Initial conc. of Helium
• CfHE = Final conc. of Helium
• Vi-spir = Initial volume of spirometer

• So residual volume (RV)
can be determined as
RV = FRC-ERV
• TLC can be calculated
TLC= FRC + IC

• FEV1
The fraction of the vital capacity expired during the first
second of a forced expiration is referred to as FEV1 (formerly the
timed vital capacity).
• FORCED VITAL CAPACITY (FVC):
It is the largest amount of air that can be expired after a
maximal inspiratory effort.
CLINICAL:
FEV1 FVC ratio (FEV1/ FVC) is a useful tool in the diagnosis of
airway disease. In a healthy normal adult male, FVC is approximately
5.0 L, FEV1 is approximately 4.0 L, and thus, the normal calculated
FEV1/ FVC is 80%.
• Obstructive disorders result in a marked decrease in both FVC
and FEV1/ FVC(42%).
• Restrictive disorders result in loss of FVC without loss in FEV1/
FVC (90%).

MINUTE RESP. VOLUME
• Total volume of new air into respiratory passages
per minute
• TV x Resp. rate
• 500x12= 6000ml/min or 6L/min

DEAD SPACE
Part of respiratory tract which does not involve in exchange
of gases.
Physiological dead space=Anatomical dead space + Alveolar dead space
1. Anatomical dead space
The part of the respiratory tract which does not participate in
exchanging the gases (Nose - Bronchioles). 150ml
2. Alveolar dead space
Those alveoli which are not functional.

MEASURMENT OF DEAD SPACE VOLUME
VD = Gray area× VE
Pink area + Gray area
• VD is dead space air
• VE is the total volume of
expired air.

Measurement of Dead Space Volume.
• In making this measurement , subject suddenly takes a deep breath of
100% O2, which ﬁll the entire dead space with pure O2.
• Some oxygen also mixes with alveolar air but does not completely replace
this air.
• Then the person expires through a rapidly recording nitrogen meter, which
makes the record.
• First portion of the expired air comes from dead space regions of
respiratory passage, where the air has been completely replaced by O2.
• Therefore, in the early part of record, only O2 appears & nitrogen
concentration is zero.
• Then, when alveolar air begins to reach the nitrogen meter, nitrogen
concentration rises rapidly, because alveolar air containing large amounts of
nitrogen begins to mix with dead space air.

• After still more air has been expired, all the dead space air has been
washed from the passages & only alveolar air remains.
• Therefore, the recorded nitrogen concentration reaches a plateau
level equal to its concentration in alveoli.
• With a little thought, that gray area represents the air that has no
nitrogen in it; this area is a measure of volume of dead space air.
• For exact quantiﬁcation, following equation is used:
VD = Gray area× VE
Pink area + Gray area
• Let us assume, that the gray area on the graph is 30 cm², the pink
area is 70 cm² & total volume expired is 500 ml.

DEAD SPACE SLIGHTLY INCREASES
• With Age (in old age  elasticity of alveoli is less  fully
functional alveoli are less  physiological dead space
increases).
• In males (anatomical dead space is more)
• On Standing
• During deep inspiration (in young men) due to expansion of
airway containing no alveoli.
• When a person breathes from a long tube (during anesthesia
or artificial respiration).

DEAD SPACE SLIGHTLY DECREASES
• On tracheostomy (breathing through a hole made surgically
in trachea).
• Anatomical dead space may fall to 110 ml during
expiration, as expiration is accompanied by constriction of
airways.

• ALVEOLAR AIR
• Volume of air Which is available for exchange of gases in alveoli per breath
is called alveolar air.
• Alveolar Air = Tidal volume — Dead space air
500mL — 150mL = 350 ml
• ALVEOLAR VENTILATION
• The rate at which alveoli get ventilated per minute is called
alveolar ventilation.
VA = (VT - VD) × Freq
350ml x 12 (respiratory rate) = 4.2 L/min
Alveolar ventilation per minute is Rate of alveolar ventilation
• VA (alveolar ventilation per minute)
• Freq (frequency of respiration per minute)
• VT (tidal volume)
• VD (physiologic dead space)

UQ’S
Q1 a)Draw and label spirogram?
b)Define vital capacity.what is its normal value?
c)what is haldane’s effect?
Q2) a)What is FEV1/FVC ratio?Give its clinical significance?
b)Enumerate factors which decreases lung compliance?
c)Define dead space. How can you calculate it by bohr’s equation?
Q3)A premature infant delivered by C-section has marked difficulty in
breathing (Dyspnea),cyanosis and respiratory rate is 100/min.
a)What will be your diagnosis?
b)What is the physiological basis of this disorder?
c)How will you manage this patient?
Q4) a)Draw and label lung compliance diagram & pulmonary pressures graph?
b)Define FRC and how can you calculate FRC?

COUGH REFLEX
• Protective reflex
• Bronchi & trachea – very sensitive to foreign matter
• Irritant receptors – responsive to mechanical, chemical
irritants

1. Afferent impulses – vagus to cough center in medulla
2. 2.5 L inspired & glottis closed, vocal cords shut tightly
3. Abdominal muscle & other expiratory muscles contract
4. Lung pressure increases to 100mmHg
5. Vocal cords & glottis suddenly opens
6. Air exploded out and posterior nares closed
7. Velocity – 70 – 100 miles/hours (air expelled out)

SNEEZING REFLEX
• Like cough reflex
• Irritation in nose, mechanical or chemical
• Afferent impulses through trigeminal nerve to sneezing
center in medulla
• Uvula is depressed, so expelled air through nose & Mouth

HICCUP
• Characterized by short inspiration because of brief
contraction of diaphragm & inspiratory muscles
• Glottis closed – characteristic sensation and sound
• Short duration and repond to breath holding---- increase
pCO2
• Because of stimulation of nerve ending in GIT and
abdominal cavity

YAWNING
• Caused by the underventilation of alveoli →↓ PO2
• Induces deep inspiration
• Characterized by wide – opened month
• Prevent collapse of alveoli by increasing ventilation
• Also ↑ venous return

VOCALIZATION
SPOKEN SPEECH COMPONENTS:
1) Phonation (sound production in voice box / larynx
by vocal cord vibration).
2) Articulation (word formation).
3) Resonance.

• ARTICULATION
is word formation from sounds (tongue, lips, palate, teeth).
• RESONANCE
Resonating channels (sinuses, naso-pharynx, thoracic
cavity, nasal cavity).
Q) BRIEFLY EXPLAIN THE AUTONOMIC & LOCAL CONTROL OF
BRONCHIOLAR MUSCULATURE?

Nervous & Local Control of Bronchiolar
Musculature“Sympathetic” Dilation of Bronchioles.
• Direct control of bronchioles by sympathetic nerve fibers is relatively weak because
few fibers penetrate to central portions of lung.
• However, bronchial tree is very much exposed to nor epinephrine & epinephrine
released into blood by sympathetic stimulation of adrenal gland medullae. Both
hormones, especially epinephrine because of its greater stimulation of beta-
adrenergic receptors cause dilation of bronchial tree.
• Parasympathetic Constriction of Bronchioles. A few parasympathetic nerve fibers
derived from vagus nerves penetrate lung parenchyma. These nerves secrete
acetylcholine & when activated cause mild to moderate constriction of bronchioles.
• When a disease process such as asthma has already caused some bronchiolar
constriction, superimposed parasympathetic nervous stimulation often worsens
the condition. When this situation occurs, administration of drugs that block the
effects of acetylcholine, such as atropine, can sometimes relax the respiratory
passages enough to relieve the obstruction.

• Local secretory factors may cause bronchiolar constriction. Several substances
formed in lungs causing bronchiolar constriction. Two of the most important of
these are histamine & slow reactive substance of anaphylaxis.
• Both substances are released in lung tissues by mast cells during allergic reactions
& play role in causing airway obstruction.
• Irritants that cause parasympathetic constrictor reﬂexes of airways (smoke, dust,
sulfur dioxide & some acidic elements in smog) may act directly on lung tissues to
initiate local, non-nervous reactions that cause obstructive constriction of airways.
• Mucus lining respiratory passage & action of cilia to clear passage.
• All respiratory passages from nose to terminal bronchioles are moist by a layer of
mucus that coats the entire surface. Mucus is secreted partly by mucous goblet
cells in epithelial lining of passages & partly by small submucosal glands.

• In addition to keep surfaces moist, mucus traps small particles out of
inspired air. Mucus is removed from passages in following manner.
• Entire surface of respiratory passages, both in nose & in lower
passages the terminal bronchioles, is lined with ciliated epithelium,
with about 200 cilia on each epithelial cell.
• These cilia beat continually at a rate of 10-20 times per second & the
direction of their“power stroke” is always toward pharynx.
• Cilia in the lungs beat upward, whereas those in the nose beat
downward. This continual beating causes the coat of mucus to ﬂow
slowly, at a velocity of a few mm/min, toward the pharynx.
• Then mucus & its entrapped particles are either swallowed or
coughed to exterior.

PULMONARY CIRCULATION
DR. MUDASSAR ALI

LEARNING OBJECTIVE
At the end of this chapter student should know
• Characteristics of pulmonary circulation & Pulmonary
wedge pressure.
• Lung zones.
• Pulmonary edema & Pulmonary edema safety factor.
• Mechanism of dry alveoli.

PHYSIOLOGICALANATOMY OF PULMONARY
CIRCULATORY SYSTEM
• The pulmonary artery
• The pulmonary veins
• Bronchial arterial blood
• Lymphatic from the lungs
enter into right thoracic
lymph duct

PULMONARY CIRCULATORY SYSTEM
• In pulmonary circulation, deoxygenated blood from right
ventricle passes to lungs via pulmonary arteries.
• Blood is oxygenated in lungs that return to pulmonary veins
through pulmonary capillaries. Pulmonary veins drain
oxygenated blood to the left atrium.
BLOOD VOLUME OF THE LUNG
• 450 ml.
• 9 % of the total blood volume of entire circulatory system.
• Approximately 70 ml in the pulmonary capillaries.

CHARACTERISTICS OF PULMONARY CIRCULATION
1.Pressures in the pulmonary circulation:
• During systole, Systolic pulmonary arterial pressure is 25
mm Hg, Diastolic pulmonary arterial pressure is 8 mm Hg
and mean pulmonary arterial pressure is 15 mm Hg.
• Mean pulmonary capillary pressure is about 7 mm Hg.

Left Atrial and Pulmonary Venous Pressures
• Mean pressure in left atrium &
major pulmonary veins is 2
mm Hg varying from 1 mm Hg
to 5 mm Hg
• This pressure is measured
through wedge shaped
catheter. This pressure is called
the "pulmonary wedge
pressure," and is 5 mm Hg.
• 2 to 3 mm Hg greater than the
left atrial pressure

BRONCHIAL VESSELS
Bronchial arterial blood is oxygenated blood,incontrast to partially
deoxygenated blood in pulmonary arteries. It supplies supporting
tissues of lungs including connective tissue, septa,large and small
bronchi. After this, it empties into pulmonary veins and enters the left
atrium.
BRONCHIAL CIRCULATION:
It supplies oxygen to supporting structures,only 2% blood volume. One
third of Bronchial venous blood is drained into pulmonary vein which
goes to left side of heart remaining two third is drained into systemic
veins.
Left ventricular output is 2% greater than right ventricular output
because oxygenated blood of pulmonary circulation in left atrium is
mixed with deoxygenated blood of bronchial circulation.

4.LYMPHATICS
Lymph vessels present in all supportive tissues of lung beginning in
connective tissue spaces that surround bronchioles, hilum & mainly
into right thoracic duct.
Particulate entering alveoli is partly removed by way of these
channels and plasma protein leaking from lung capillaries is also
removed from lung tissues,thereby prevent pulmonary edema.
5.COMPLIANCE OF PULMONARY VESSELS
Pulmonary vessels are thin and distensible that gives pulmonary
arterial tree a large compliance, averaging 7 ml/mm Hg. This large
compliance allows pulmonary arteries to accommodate stroke
volume output of right ventricle

6) Lungs as a Blood Reservoir
Lungs as a Blood Reservoir (contribute 250 ml blood to systemic
circulation when needed eg.after hemorrhage
7) Cardiac Pathology Results in Shift of Blood Between the
Pulmonary and Systemic Circulatory Systems
Failure of left side of heart or increased resistance to blood flow
through mitral valve as a result of mitral stenosis or mitral
regurgitation causes blood to dam up in pulmonary circulation,
sometimes increasing pulmonary blood volume as much as 100
percent causing large increases in the pulmonary vascular pressures.

8) EFFECT OF HYPOXIA
(AUTOMATIC CONTROL OF PULMONARY BLOOD FLOW DISTRIBUTION)
• When the conc. of oxygen in the air of alveoli decreases below
normal (below 70%) adjacent blood vessels constrict within 3-10 min.
•
• Low oxygen conc. causes some vasoconstrictor substance to be
released from the lung tissue (type II alveolar cells). These substance
promotes constriction of arteries.
•
• This causes blood to flow through other areas of lungs that are
better aerated.
•
• This effect of low oxygen on pulmonary vascular resistance has an
important function to distribute blood where it is most effective.

9) Effect of Hydrostatic Pressure Gradients in Lungs on
Regional Pulmonary Blood Flow .
• Blood pressure in foot of a standing person can be 90 mmHg
greater than pressure at level of heart. This is caused by hydrostatic
pressure.
• Hydrostatic pressure is by the weight of blood itself in blood
vessels. The same effect occurs in lungs.
• Normally pulmonary arterial pressure in upper portion of lung of
standing person is 15 mm Hg less than pulmonary arterial pressure at
the level of heart. Pressure in lowest portion of lungs is 8 mmHg
greater from the heart.
• Such pressure differences have profound effects on blood flow
through the different areas of lungs.
• In each zone, patterns of blood flow are quite different.

Zones 1, 2, and 3 of Pulmonary Blood Flow
• Capillaries in alveolar walls are distended by blood pressure inside
them- but they are compressed by alveolar air pressure on their
outsides.
• Any time lung alveolar air pressure becomes greater than capillary
blood pressure,capillaries close & there is no blood flow. Under
different normal & pathological lung conditions,one may find any one
of three possible zones of blood flow.
• Zone 1. which is no blood flow during cardiac cycle,occurs either
pulmonary arterial pressure is too low or the alveolar pressure is too
high to allow flow
1.Breathing against a positive air pressure
2.After severe blood loss.

• Zone 2: intermittent blood flow only during peaks of pulmonary
arterial pressure because systolic pressure is greater than
alveolar air pressure,but diastolic pressure is less than alveolar
pressure.
• Zone 3: Continuous blood flows because alveolar capillary
pressure remains greater than alveolar air pressure during
entire cardiac cycle.
• When person is lying down, no part of lung is more than few
centimeters above the level of heart.In this case, blood flow in
normal person is entirely zone 3 blood flows including lung
apices.
• Zone I: Palv > Part >Pvein (no blood flow)
• Zone II: Part > Palv > Pvein (intermittent flow)
• Zone III: Part > Pvein> Palv (Continuos flow)

• Normally,lungs have only zones 2 and 3 blood flow—zone 2
(intermittent flow) in apices & zone 3 (continuous flow) in lower
areas.
• E.g when person is in upright position, pulmonary arterial pressure at
lung apex is 15mmHg less than pressure at level of heart.
Therefore,apical systolic pressure is 1OmmHg (25mmHg at heart level
minus 15mm Hg hydrostatic pressure difference).This 10mm Hg apical
blood pressure is greater than zero alveolar air pressure, so blood
flows through pulmonary apical capillaries during cardiac systole.
• During diastole,8mmHg diastolic pressure at level of heart is not
sufficient to push blood up the 15mm Hg hydrostatic pressure
gradient required to cause diastolic capillary flow.

Capillary Exchange of Fluid in the Lungs, and
Pulmonary Interstitial Fluid Dynamics

MECHANISM FOR KEEPING ALVEOLI “DRY.”
MEAN FILTRATION PRESSURE &ITS IMPORTANCE
• Pulmonary capillaries & pulmonary lymphatic system maintain slight -
ve pressure in interstitial spaces.
• It is clear that whenever extra fluid appears in alveoli, it will simply
sucked mechanically into lung interstitium through small openings
between the alveolar epithelial cells.
• Excess fluid is either carried away through pulmonary lymphatics or
absorbed into the pulmonary capillaries.
• Under normal conditions, alveoli are kept “dry,” except for a small
amount of fluid that seeps from the epithelium onto the lining
surfaces of alveoli to keep them moist.

Pulmonary Edema Safety Factor
• Normally, plasma colloid osmotic pressure is 28 mmHg,this pressure
opposes movement of fluid from pulmonary capillaries.
• Pulmonary capillary hydrostatic pressure is 7 mmHg and this
pressure is major force that cause movement of fluid outward from
capillaries into pulmonary interstitium.
• If this pressure rises to more than plasma colloid osmotic pressure
then pulmonary oedema develops.
• When pulmonary capillary hydrostatic pressure does not rises above
28 mmHg, pulmonary oedema does not develop.
• Therefore, 28-7 mmHg =21 mmHg This 21 mmHg pressure difference
is called pulmonary oedema safety factor against pulmonary oedema.

SAFETY FACTOR IN CHRONIC CONDITIONS
• When pulmonary capillary pressure remains elevated chronically (for
at least 2 weeks),lungs become even more resistant to pulmonary
edema because lymph vessels expand greatly, increasing their
capability of carrying fluid away from interstitial spaces perhaps as
much as 10-fold.
• Therefore,patients with chronic mitral stenosis,pulmonary capillary
pressures of 40 to 45 mmHg have been measured without
development of lethal pulmonary edema.

PULMONARY EDEMA
• Excess collection of fluid in alveoli & interstitial space surrounding
alveoli is called Pulmonary edema.
• Pulmonary edema occurs in same way that edema occurs elsewhere
in body. Any factor that causes pulmonary interstitial fluid pressure to
rise from –ve range into +ve range will cause rapid filling of
pulmonary interstitial spaces & alveoli with large amounts of free
fluid.

• CAUSES
The most common causes of pulmonary edema are as follows:
1. Left-sided heart failure or mitral valve disease 2.ARDS
3. Ischemic heart disease/ Myocardial infarction 4.Fluidoverload
5. Damage to the pulmonary blood capillary membranes caused by
infections such as pneumonia.
These causes rapid leakage of both plasma proteins and fluid out of
capillaries.
• SYMPTOMS
1) Breathlessness (dyspnea) 2) Orthopnea (dyspnea on lying)
3) Pink frothy sputum
• SIGN
1) Distressed, pale, and Sweaty 2) Increased pulse 3) Pink frothy
sputum
4) JVP raised (jugular venous pulse) 5) Fine lung crackles/wheeze
6) Gallop rhythm

• DIAGNOSIS
1. X-Ray chest PA view to see pneumonia or pleural effusion
or signs of pulmonary edema.
2. ECG (Electrocardiogram) to see myocardial infarction
3. Serum electrolytes especially Na+ and K+
• TREATMENT
1. 100 % oxygen therapy
2. Inj. Diamorphine (It causes dilatation of the bronchioles)
3. Inj. Furosemide (It removes excess fluid collection

RAPIDITY OF DEATH IN ACUTE PULMONARY EDEMA
• When pulmonary capillary pressure rises even slightly above the
safety factor level, lethal pulmonary edema can occur within hours or
even within 20 to 30 minutes if the capillary pressure rises 25 to 30
mm Hg above the safety factor level.
Thus, in acute left-Sided heart failure in which
pulmonary capillary pressure occasionally does rise to 50 mm Hg,
death frequently ensues in less than 30 minutes from acute
pulmonary edema.

Pleural Cavity
• The pleural space—the
space between the parietal
& visceral pleurae—is
called a potential space
• A thin layer of mucoid
fluid lies between the
parietal & visceral pleurae.

PLEURAL EFFUSION
• Blockage of lymphatic
• Cardiac failure
• Greatly reduced plasma
colloid osmotic pressure
• Infection or any other
cause of inflammation

LEARNING OBJECTIVES
• Diffusion capacity
• Layers of respiratory membranes and factors affecting rate
of diffusion.
• Ventilation perfusion ratio & Physiological shunt

Diffusion
• Random movement of molecules of gas by
their own kinetic energy
• Net diffusion from higher conc. to lower conc
• Molecules try to equilibrate in all empty
places

Partial Pressure
• The pressure exerted by the gas molecules on a
surface
In atmospheric air
• PO2 160mmHg
• PCO 2 0.3mmHg
• PN2 600mmHg

Pressure of gases dissolved in water & tissues
• Partial pressure in fluid develop same way as in air
• Partial pressure= conc. of dissolved gas/solubility coefficient
HENRY’S LAW
• Solubility coefficients of different gases
O2=0.024 CO2=O.57 CO=0.018 N2=0.012 H=0.008
• Water solubility of CO2 20 times more than that of O2
• Partial pressure of carbon dioxide is less than one twentieth that
exerted by oxygen.

Water Vapor Pressure
• In airway passage air gets humidified, water vapors mixed
up with inspired air
• At body temp. 370C pH2O =47mm Hg
• pH2O directly proportional to temperature
• In fever pH2O is more

Rate of diffusion
D=Δ P×A×S/d×√MW
Δ P=Partial pressure difference A=cross-sectional area S=solubility
of gas d= distance
√MW=molecular weight
• Diffusion coefficient=S/ √MW
• Two gases at same partial pressure, rate of diffusion proportional to
diffusion coefficient

Respiratory Unit
• Respiratory Lobule
1. Respiratory bronchiole
2. Alveolar ducts
3. Atria
4. Alveoli

• 300 millions alveoli
• Diameter 0.2 milliliter
• Sheet of flowing blood

Respiratory Membrane or Pulmonary Membrane
Membranes of all the
terminal portions of the
lungs

Factors That Affect the Rate of Gas Diffusion
Through the Respiratory Membrane
1. Thickness of membrane
2. Surface area of membrane
3. Diffusion coefficient
4. Partial pressure difference of
the gas
1. Edema & Fibrosis
2. Emphysema
3. Solubility of gas/ √ Mol. Weight
4. partial pressure of gas in the
alveoli and partial pressure of
the gas in the pulmonary
capillary blood

Diffusion Capacity
Volume of a gas that will diffuse through the membrane each minute for
a partial pressure difference of 1 mmHg
• Diffusing capacity for oxygen
21 ml/min/mm Hg at rest
65 ml/min/mm Hg during exercise
• Diffusing capacity for carbon dioxide 20 times more than O2
400 to 450 ml/min/mm Hg at rest
1200 to 1300 ml/min/mm Hg during exercise

Measurement of Diffusing Capacity
1. Alveolar Po2
2. Po2 in the pulmonary capillary blood
3. Rate of oxygen uptake by the blood
DC of CO= Volume of CO absorbed
pCO
 DC of CO is measured by CO method
 DC of O2 = DC of CO × 1.23
= 17× 1.23= 21ml/min/mmHg

CO Method
• A small amount of CO is breathed into alveoli & partial pressure of CO
in alveoli is measured from alveolar air samples.
• CO pressure in blood is essentially zero, because hemoglobin (high
affinity with Hb250x more than O2)combines with this gas so rapidly
that its pressure never has time to build up.
• Therefore, the pressure difference of CO across the respiratory
membrane is equal to its partial pressure in the alveolar air sample.
• Then, by measuring the volume of CO absorbed in a short period &
dividing this by the alveolar CO partial pressure, one can determine
accurately CO diffusion capacity.

Humdified air
Po2 149
Pco2 0.3
Venous blood
Po2 40
Pco2 45
Alveolar air
Po2 104
Pco2 40

Ventilation – Perfusion Ratio
The imbalance between alveolar ventilation & alveolar
blood flow
• Va Alveolar ventilation
• Q Blood flow
• Va/Q
• When the ventilation(Va) is zero, yet there is still
perfusion (Q) of the alveolus, Va/Q is zero
• When there is adequate ventilation (Va) but zero
perfusion (Q),Va/Q is infinity.

Normal ventilation Perfusion ratio
• Normal alveoler ventilation /min=4.2L
• Normal perfusion/min(Cardiac output)=5L
• Normal ventilation Perfusion ratio=4.2/5=0.84-1
• All parts of lung do not receive equal amount of blood.
• At apex of the lung :excessive ventilation less perfusion so
Vent/perfusion ratio is more. This makes this part of lung more
susceptible to tuberculosis. Excessive O2 favours growth of bacteria.
• At the base of the lung: Less ventilation more perfusion.

Physiological Shunt
• When Va/Q is below normal
• Shunted blood
• Bronchial vessels
• The total quantitative amount of shunted blood per minute is called
the physiologic shunt
• The greater the physiologic shunt, the greater the amount of blood
that fails to be oxygenated as it passes through the lungs.
• Lower part of lung Va/Q is 0.6 times below normal

Physiological Dead Space
• When Va/Q is ∞
• Alveolar wasted ventilation or alveolar dead space
• Anatomical dead space
• The sum of these two types of wasted ventilation is called the
physiologic dead space
• When the physiologic dead space is great, much of the work of
ventilation is wasted effort because so much of the ventilating air
never reaches the blood
• Upper part of Lung Va/Q 2.5 times more than normal

Transport of Oxygen & Carbon Dioxide
in Blood and Tissue Fluids
DR. MUDASSAR ALI

LEARNING OBJECTIVE
• Transport of oxygen (Hb-O2 dissociation curve)
• P50 and Bohr’s effect
• Causes of left and right shift of curve
• Transport of carbon dioxide
• Chloride shift and haldane effect

Transport of O2 from Lungs to Body
Tissues
• Diffusion of O2 from alveoli into pulmonary capillary blood
is due to greater oxygen partial pressure (PO2) in alveoli
than pulmonary capillary blood.
• In other body tissues, a higher PO2 in capillary blood than in
the tissues causes oxygen to diffuse into the surrounding
cells.

Diffusion of O2 from Alveoli to Pulmonary Capillary
Blood
• PO2 in alveolus averages 104 mm Hg, whereas PO2 of
venous blood entering the pulmonary capillary at its
arterial end averages only 40 mm Hg because a large
amount of oxygen was removed from this blood as it
passed through the peripheral tissues.
• Initial pressure difference that causes oxygen to diffuse
into the pulmonary capillary is 104 - 40, or 64 mm Hg.

Transport of Oxygen from Lungs to
Body Tissues

Transport of Oxygen in the Arterial Blood
• 98% of the blood that enters the left atrium from the lungs has just
passed through the alveolar capillaries & has become oxygenated up
to a PO2 of about 104 mm Hg.
• Remaining 2 % of the blood has passed from the aorta through the
bronchial circulation, which supplies mainly the deep tissues of the
lungs and is not exposed to lung air. This blood flow is called "shunt
flow," meaning that blood is shunted past the gas exchange areas

• On leaving the lungs, the PO2 of shunt blood is about that of normal
systemic venous blood, 40 mm Hg.
• When this blood combines in pulmonary veins with the oxygenated
blood from the alveolar capillaries, this so-called venous admixture
of blood
• This causes PO2 of blood entering the left heart & pumped into aorta
to fall to about 95 mm Hg.

Role of Hemoglobin in Oxygen Transport
97 % oxygen in chemical combination with
hemoglobin in the red blood cells.
3 % is transported in dissolved state in the water of
the plasma & blood cells.

Structure of hemoglobin molecule
4 Heme groups
2 alpha chains 2 beta chains
Oxy-Hb = Hb4O8
4 subunits which can bind 8 atoms or 4 molecules of oxygen.
This is a reversible process.

Oxygen-Hemoglobin Dissociation Curve.

• Oxygen–hemoglobin dissociation curve, also called the
oxyhemoglobin dissociation curve or oxygen dissociation curve
(ODC), is a curve that plots the proportion of hemoglobin in
its saturated form on vertical axis against the prevailing
oxygen tension on horizontal axis.
• O2- hemoglobin dissociation curve, which demonstrates a
progressive increase in the percentage of hemoglobin bound with O2
as blood Po2 increases, called the percent saturation of hemoglobin.
Because the blood leaving the lungs and entering the systemic
arteries usually has a Po2 of about 95 mm Hg, it can be seen from the
dissociation curve that the usual O2 saturation of systemic arterial
blood averages 97%.
• Conversely, in normal venous blood returning from the peripheral
tissues, the Po2 is about 40 mm Hg, and the saturation of hemoglobin
averages 75%.

Factors That Shift the Oxygen Hemoglobin
Dissociation Curve

P50
P50 at which Hb is 50 % saturated
Po2 26.7 mm Hg.
If a compound has lower P50
It has high affinity for oxygen.
Myoglobin is in muscle & acts
as oxygen reservoir in muscle,
as it can bind more oxygen at
low partial pressure of oxygen.
If a compound has higher P50
It has low affinity for oxygen.

Per Cent Saturation Of Hemoglobin.
15 grams of hemoglobin in each 100 ml of blood
Each gram of hemoglobin can bind with a
maximum of 1.34 mlof oxygen
20 ml of oxygen if the hemoglobin is 100 per cent
saturated.
20 volumes percent

• 97 % saturated is about 19.4 ml
per 100 milliliters of blood.
• On passing through the tissue
capillaries, this amount is
reduced, on average, to 14.4 ml
(Po2 of 40 mm Hg, 75 per cent
saturated hemoglobin).
• Thus, under normal conditions,
about 5 ml of oxygen are
transported from the lungs to
the tissues by each 100
milliliters of blood flow.

Utilization Coefficient
• The percentage of blood that gives up its oxygen as
it passes through the tissue capillaries is called the
utilization coefficient.
• The normal value for this is about 25%

Factors That Shift Oxygen-Hemoglobin
Dissociation Curve

Bohr Effect
Shift of the oxygen hemoglobin dissociation curve to the right
in response to increases in blood carbon dioxide and
hydrogen ions
Tissues
CO2 blood H2CO3 ,hydrogen ion
Lungs
CO2 diffuses from the blood into the alveoli. Reduces the
blood PCO2 and hydrogen ion
Shifting the O2-hemoglobin dissociation curve to the left .

Hemoglobin Helps Maintain Nearly Constant
PO2 in the Tissues.
• Normal 5 ml of O2 to be released per 100 ml of blood flow
• PO2 must fall to about 40 mm Hg.
• Tissue PO2 normally cannot rise above this 40 mm Hg level

Transport of Oxygen in Dissolved State
Po2 of 95 mm Hg
• 0.29 ml of oxygen is dissolved in every 100 ml
Po2 of 40 mm Hg
• 0.12 ml of oxygen remains dissolved.
0.17 milliliter of oxygen is normally transported in the
dissolved state to the tissues by each 100 ml of arterial
blood flow.

Transport of
Co2 in Blood
• carbon dioxide can usually be
transported in far greater quantities
than oxygen .
• carbon dioxide in blood has a lot to do
with the ACID-BASE BALANCE of the
body fluids.
• Normaly 4 ml of carbon dioxide is
transported from the tissues to the
lungs in each 100 ml of blood .
4 ml/100ml of blood
150

Forms in Which Co2 Is Transported
• Transport of Carbon Dioxide in the Dissolved State
• Transport of Carbon Dioxide in the Form of Bicarbonate Ion
• Transport of co2 in combination with hemoglobin and plasma
proteins-------Carbaminohemoglobin
151

Transport of Carbon Dioxide in Blood

• Reaction of Carbon Dioxide with Water in Red Blood Cells-Effect of
Carbonic Anhydrase
• CO2+H2O H2CO3
Carbonic anhydrase, catalyzes ( about 5000-fold).
Therefore, instead of requiring many seconds or minutes to occur, as is
true in the plasma, the reaction occurs so rapidly in red blood cells that
it reaches almost complete equilibrium within a very small fraction of a
second.
• This allows tremendous amounts of carbon dioxide to react with red
blood cell water even before the blood leaves the tissue capillaries.
153

• Dissociation of Carbonic Acid into Bicarbonate & Hydrogen Ions
In another fraction of a second, carbonic acid formed in red cells
(H2CO3) dissociates into hydrogen & bicarbonate ions .
H2CO3 H+ + HCO3-
 Most of the H+ ions then combine with hemoglobin in red blood
cells because hemoglobin protein is a powerful acid-base buffer.
 Many of ions diffuse from the red cells into plasma, while chloride
ions diffuse into the red cells to take their place. This is made
possible by the presence of a special bicarbonate-chloride carrier
protein in the red cell membrane that shuttles these two ions in
opposite directions at rapid velocities.
 hus, the chloride content of venous red blood cells is greater than
that of arterial red cells, a phenomenon called the Chloride shift.
154

• Reversible combination of carbon dioxide with water in red blood
cells accounts for about 70 % of the carbon dioxide transported from
the tissues to the lungs.
• This means of transporting carbon dioxide is most important.
• When a carbonic anhydrase inhibitor (acetazolamide) is administered
to an animal to block the action of carbonic anhydrase in the red
blood cells, carbon dioxide transport from the tissues becomes so
poor that the tissue Pco2 can be made to rise to 80 mm Hg instead of
the normal 45 mm Hg.
155

Transport of Co2 in Combination with Hemoglobin &
Plasma Proteins-Carbaminohemoglobin
• Co2 reacts directly with amine radicals of hemoglobin
molecule to form the compound carbaminohemoglobin
(CO2Hgb).
• This combination of carbon dioxide & hemoglobin is a
reversible reaction that occurs with a loose bond, so Co2 is
easily released into alveoli, where Pco2 is lower than in
pulmonary capillaries.

HALDANE EFFECT
When Oxygen Binds with Hemoglobin, Carbon Dioxide Is Released (the
Haldane Effect) to Increase CO2 Transport
• An increase in CO2 in the blood causes oxygen to be displaced from
the hemoglobin ( Bohr effect), which is an important factor in
increasing O2 transport.
157

Haldane Effect
Binding of oxygen with hemoglobin tends to displace
carbon dioxide from the blood
Combination of oxygen with hemoglobin in the lungs causes the
hemoglobin to become a stronger Acid
(1) The more highly acidic hemoglobin has less tendency to
combine with carbon dioxide to form carbaminohemoglobin,
thus displacing much of the carbon dioxide that is present in the
carbamino form from the blood.
(2) The increased acidity of the hemoglobin also causes it to
release an excess of hydrogen ions & these bind with
bicarbonate ions to form carbonic acid; this then dissociates
into water and carbon dioxide, & carbon dioxide is released
from the blood into the alveoli & finally into the air.

REGULATION OF RESPIRATION
DR. MUDASSAR ALI

Learning objective
• Nervous regulation of respiration
• Chemical regulation of respiration
• Periodic breathing
• Apnea
• Regulation of respiration during exercise

• Located bilaterally in Pons and
Medulla oblongata
• Composed of
1. Pre-Botzinger complex
2. Dorsal Respiratory Group (DRG)
3. Ventral Respiratory Group (VRG)
4. Pneumotaxic center
5. Apneustic center

Pre-Botzinger complex (pre-BOTC)
• A collection of pace-maker cells at the upper end of
Dorsal Respiratory Group (DRG)
• Synaptic connection with DRG
• Located between nucleus ambiguus & lateral
reticular nucleus
• Discharge rhythmic respiratory signals

Dorsal Respiratory Group
• Extends most of the length of M. oblongata
• Neurons located in nucleus of tractus solitarius &
additional neurons in reticular substance of medulla
• In Nucleus tractus solitarius terminations of vagus &
glossopharyngeal nerve
• Both nerves – afferent nerves for resp. signals to center

• Ramp signals to inspiratory muscles, Rhythmic cycle

• Ramp signals controlled by
(a) Pneumotaxic center
(b) Stretch receptors in the
lungs
Significance
• No gasping
• Smooth inflation of lungs
Full cycle of respiration
5 seconds
• 2sec inspiration
• 3 sec expiration

• Fibers from respiratory
center (DRG) onto the
motor neurons in spinal
cord between C3 & C5 to
form phrenic nerve
• Complete lesion of spinal
cord above C3 will stop the
breathing
• Lesion after C5 will not
affect the respiration

Pneumotaxic Center
• Upper part of Pons
• Two nuclei – nucleus parabrachialis & nucleus Kolliker fuse
• SWITCHING OFF Ramp Signal
• Controls rate & duration of Inspiratory ramp signals
• Strong stimulation may reduce Inspiratory phase to 0.5 sec
respiratory rate ↑ to 30 – 40/min
• Weak stimulation may ↑ Inspiratory phase to 5sec or more
respiratory rate ↓ to 3-5/ min

Ventral Respiratory Group
• Ventral part of medulla
• Two nuclei (1) Nucleus Ambiguus rostrally (2) Nucleus
Retroambiguus caudally
• Both types of neurons – INSPIRATORY & EXPIRATORY
• Center remain inactive during quite breathing
• Active only in increased pulmonary ventilation, during which signal
from DRG spill over to VRG
• Stimulation of accessory inspiratory muscles & expiratory muscles

Apneustic Center
• Located in lower part of pons
• Prevent inspiratory neurons from being switched off → prolonged
inspiration
• Shortens expiration
• Such Respiration called – apneusis
• Work in association with pneumotaxic center though role not well-
known

Hering-Breuer Inflation Reflex
• Muscular portions of the walls of bronchi & bronchioles throughout
the lungs have stretch receptors
• Transmit signals through the vagi into the dorsal respiratory group of
neurons when the lungs become overstretched.
• Switches Off the inspiratory ramp & thus stops further inspiration
• These signals affect inspiration in much the same way as signals from
the pneumotaxic center
• It also increases rate of respiration

• This reflex is activated when tidal volume increases
to more than three times normal
• Therefore, this reflex appears to be mainly a
protective mechanism for preventing excess lung
inflation

Lung “J Receptors.”
• In the alveolar walls in juxtaposition to the pulmonary
capillaries
• Stimulated especially when the pulmonary capillaries
become engorged with blood or
• When pulmonary edema occurs in such conditions as
congestive heart failure.
• Their excitation may give the person a feeling of dyspnea.

CHEMICAL CONTROL OF
RESPIRATION
• Excess CO2
• Excess Hydrogen ion
• Decreased Oxygen
Stimulates Respiration

Central chemosensitive area
Stimulated by CO2 & H+
Oxygen have no effect
Peripheral chemoreceptors
Stimulated by O2
CO2 & H+ has little effect

Location of Chemosenstive area
• Located bilaterally beneath
the ventral surface of
medulla
• Hydrogen ions are only the
main direct stimulus for
these group of neurons

Decreased Stimulatory Effect of Carbon Dioxide After the First 1 to
2 Days
•
• Renal readjustment of hydrogen ion by increasing the blood
bicarbonate, which binds with hydrogen ions in blood &
cerebrospinal fluid to reduce their concentrations
• CO2 has a potent acute effect on controlling respiratory
drive but only a weak chronic effect after a few days of
adaptation.

Acclimatization
• Mountain climbers have found that when they ascend a
mountain slowly
• Over a period of days rather than a period of hours
• They breathe much more deeply & therefore can withstand
far lower atmospheric oxygen concentrations than when
they ascend rapidly

• The reason is within 2 to 3 days, the respiratory center in
brain stem loses about four fifths of its sensitivity to
changes in Pco2 and hydrogen ions.
• Therefore, the excess ventilatory blow-off of carbon dioxide
that normally would inhibit an increase in respiration fails to
occur
• Low oxygen can drive the respiratory system to a much
higher level of alveolar ventilation than under acute
condition
• The alveolar ventilation often increases 400 to 500 per cent
after 2 to 3 days of low oxygen

Peripheral Chemoreceptor
• Both bodies are supplied by
special minute arteries
direct from the arterial trunk
• Carotid bodies through
Hering N to Glossopharyngeal
N Aortic Bodies through
Vagus N to DRG

Stimulation of Chemoreceptors by Decreased
Arterial Oxygen

Effect of Carbon Dioxide & Hydrogen Ion Concentration
on
Chemoreceptor Activity
They have a weak effect but stimulation by way of the
peripheral chemoreceptors occurs as much as five times as
rapidly as central stimulation

PERIODIC BREATHG
Abnormal or uneven respiratory rhythm is called periodic
breathing.
EXPLANATION.
In this condition,person breathes deeply for a
short interval & then breathes slightly or not at all for an
additional interval, with the cycle repeating itself over &
over.
EXAMPLES OR TYPES OF PERIODIC BREATHING.
1. Cheyne-stokes breathing.
2. Biot’s breathing.
PERIODIC BREATHING

Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by
progressively deeper, and sometimes faster, breathing followed by a gradual decrease
that results in a temporary stop in breathing called an apnea. The pattern repeats,
with each cycle usually taking 30 seconds to 2 minutes.

CHEYNE STOKES BREATHING
• It is characterized by slowly waxing and waning respiration
occurring about every 40 to 60 seconds.
EXPLANATION.
To begin with breathing is shallow. Amplitude
of respiration increase gradually & reaches maximum then
it decreases and reaches minimum and is followed by
apnea. It is called waxing & waning of breathing.

CAUSES FOR WAXING & WANING.
• When person over breathes it blows off much CO2 from pulmonary
blood while at same time blood O2 increases.
• It take several seconds before changed pulmonary blood can be
transported to brain & inhibits excess ventilation.
• By this time person has already overventilated for an extra few
seconds.
• When overventilated blood finally reaches brain respiratory center
becomes depressed. Opposite cycle begins that is CO2 increases & O2
decreases in alveoli due to decreased ventilation.
• Again it takes few seconds before brain can respond to these
changes. When brain does respond person breathes more once again
& cycle repeats.

• Cheyne stokes breathing occurs in both physiological &
pathological condition.
Physiologically.
Hyperventilation, High altitude, exercise, newborns.
Pathologically.
Cardiac diseases(cardiac failure),Brain damage, premature
infants, raised intracranial pressure.

BIOT’S BREATHING
• It is characterized by period of apnea & hyperapnea but
there is no waxing & waning. After apneic period,
hyperpnea occurs abruptly.
• It does not occur physiologically only occur in pathological
condition(lesions or injuries to brain).

APNEA
Apnea means cessation of breathing and if it is prolonged
can lead to death.
CONDITIONS WHEN APNEA OCCUR
voluntary. Deglutition.
Adrenaline. Apnea after hyperventilation.
• SLEEP APNEA
• Absence of spontaneous breathing
• Occur during normal sleep
Apnea time.(breath holding time)
40-60 seconds in normal person.

CLASSIFICATION
• Obstructive, Central & Mixed.
• During sleep muscles relax but airway passage remains
open enough to permit adequate airflow.

OBSTRUCTIVE SLEEP APNEA
• It is caused by blockage of upper airway , pharynx normally
keep passage open to allow air to flow into lungs during
inspiration.
• Some individuals have an especially narrow passage &
relaxation muscles during sleep causes pharynx to
completely close so air cannot flow into lungs.
• Mixed apnea (combination of central & obstructive)
abnormal control of breathing due to immature or
underdeveloped brain & respiratory system.

CENTRAL APNEA
• Characteristic feature is snoring.
• Sleep apneas can be caused by obstruction of upper
airways especially pharynx(excess tissue growth in
airway like enlarged tonsils (obstructive) or by impaired
CNS respiratoy drive.(central apnea)
• Damage to the central respiratory centers or
abnormalities of the respiratory neuromuscular apparatus.
• Strokes

Regulation of Respiration During
Exercise

CHANGES IN RESPIRATORY SYSTEM
• Pco2 increase, Po2 decrease, Lactic acid produced.
• Adrenal gland activated (adrenaline,nor-adrenaline) produced.
• Body pH change to acidic side,Body temperature increase.
• Impulse from exercising muscle & joints goes to respiratory centres &
stimulate to produce hyperpnea.
• R.R increase upto 16-50/min.
• Tidal volume increase in athletes rise upto 3000 ml.
• Pulmonary ventilation increase.(Normal 5-8 L) during exercise goes
upto 120 L.

RESPIRATORY INSUFFICIENCY
Dr. Mudassar Ali

LEARNING OBJECTIVE
At the end of this chapter students should be able to know
• FEV1/FVC ratio
• Obstructive and restrictive lung disease (emphysema,
asthma, Atelectesis, Pneumonia)
• Cyanosis, Hypoxia & its types
• CO poisoning & Hyperbaric oxygen therapy
• Oxygen toxicity & O2 debt
• Artificial respiration

• FEV1
The fraction of the vital capacity expired during the first
second of a forced expiration is referred to as FEV1 (formerly the
timed vital capacity).
• FORCED VITAL CAPACITY (FVC):
It is the largest amount of air that can be expired after a
maximal inspiratory effort.
CLINICAL:
FEV1 FVC ratio (FEV1/ FVC) is a useful in diagnosis of airway
disease. In healthy adult male, FVC is approximately 5.0 L, FEV1 is 4.0
L, and thus, the normal calculated FEV1/ FVC is 80%.
• Obstructive disorders result in a marked decrease in both FVC
and FEV1/ FVC(42%).
• Restrictive disorders result in loss of FVC without loss in FEV1/
FVC (90%).

OBSTRUCTIVE LUNG DISEASES
It is abnormal respiratory condition in which person feels difficulty to
push air outside the lung (expiration).
Obstructive disease is characterized by increase in airway resistance,that
is measured as decrease in expiratory flow rate.
Asthma,chronic bronchitis,emphysema & bronchiectasis.
RESTRICTIVE LUNG DISEASES
It is abnormal condition in which person feels difficulty to get air into
lungs(inspiration).
Fibrosis, ARDS, Tuberculosis,Silicosis,Kyphosis,pneumoconiosis & chest
wall disorders

VARIABLES OBSTRUCTIVE DISEASES
(EMPHYSEMA)
RESTRICTIVE DISEASES
(FIBROSIS)
TLC INCREASE DECREASE
RV INCREASE DECREASE
FEV1 DECREASE DECREASE
FVC DECREASE DECREASE
FRC INCREASE DECREASE
FEV1/FVC DECREASE INCREASE
RV/TLC < 25% INCREASE DUE TO INCREASE
IN RV
NORMAL OR INCREASE DUE
TO DECREASE TLC.

PEAK EXPIRATORY FLOW RATE.
.
Maximum rate at which air can be expired after a deep
inspiration is called PEFR. VALUE 400 LITERS/MIN
PEFR is measured by using Wright peak flow meter.
SIGNIFICANCE.
For assessing respiratory diseases especially to differentiate
obstructive and restrictive diseases.
In restrictive diseases PEFR is 200 liters/min.
In obstructive diseases PEFR is 100 liters/min.

CHRONIC PULMONARY EMPHYSEMA
• CAUSE
Excessive cigrate smoking
• SEQUENCE OF EVENTS:
Chronic infection----------- paralysis of cilia------- Excessive
mucus accumulation----- inhibition of alveolar macrophages
chronic obstruction of smaller bronchioles---------entrapment
of air in the alveoli and overstretching them ----- destruction
of as much as 50 to 80 per cent of the alveolar walls.

ABNORMALITIES OF EMPHYSEMA
• Increased air way resistance
leads to increased work of
breathing
• Loss of alveolar walls leads to
decreased diffusing capacity
• Abnormal ventilation
perfusion ratio in same lung
Physiological shunt
Physiological dead space

PNEUMONIA
• pneumonia includes any
inflammatory condition of
lung in which some or
alveoli are filled with fluid
and blood cells
• A common type of
pneumonia is bacterial
pneumonia, caused by
pneumococci.

• Involvement of entire lobe is
called LOBAR PNEUMONIA
• Involvement of alveoli
contiguous to bronchi is called
BRONCHOPNEUMONIA

• This disease begins with
infection in the alveoli
pulmonary membrane
becomes inflamed and highly
porous
• Consolidation of lung occurs
i.e, alveoli are filled with blood
cells and fluids

ABNORMALITIES
1) Decrease total surface area of respiratory
membrane
2) Decrease V/Q ratio
Result: hypoxemia and hypercapnia

PNEUMOTHORAX
– “Pneumo”- gas
“Thorax” – chest cavity
– Air entering pleural space
directly through chest wall

TYPES OF PNEUMOTHORAX
• Spontaneous Pneumothorax
– Primary -rupture of subpleural
bleb
– Secondary - underlying
lung/pleural disease
• emphysema
• Chronic bronchitis, asthma, TB, …

• Traumatic Pneumothorax
– Open
• Chest wall is penetrated :
outside air enters pleural space
– Closed
• Chest wall is intact Ex.
Fractured rib

TYPES OF PNEUMOTHORAX
• Tension Pneumothorax
– “Ball-valve mechanism”
– Injury to pleura creates a tissue flap that
opens on inspiration and closes on
expiration

• Asymmetric chest expansion
• Deviated trachea
• Diminished breath sounds
unilaterally
• Dyspnea
• Pleuritic chest pain
– Nerve endings at pleural capsule

Bronchial asthma
• Respiratory disease characterized by difficult breathing with
wheezing.(whistling sounds).
• It is due to bronchiolar conctriction caused by spastic contraction of
smooth muscles in bronchioles leading to airway obstruction.
• CAUSES:
1.Pulmonary edema and congestion of lungs caused by left ventricular
failure.(cardiac asthma)
2.Inflammation. 3.Hypersensitivity.
• LABS
• Tidal volume,vital capacity,FEV1,Alveolar ventilation decrease.
• Residual volume and FRC increase.
Carbondioxide accumulates resulting in acidosis,dyspnea and cyanosis.

ABNORMALITIES IN RESPIRATION
• HYPERCAPNIA
means excess carbon dioxide in body fluids. It is caused by
hypoventilation or circulatory deficiency.
• HYPOCAPNIA
means decreased carbon dioxide in body fluids and is caused
by hyperventilation.
In voluntary hyperventilation arterial PCO2 falls from 40 to 15 mmHg
while alveolar PO2 rises 120 to 140 mmHg.
• ASPHYXIA
condition characterized by combination of hypoxia and
hypercapnea due to airways obstruction.
This occur in strangulation,hanging,drowning.

ATELECTASIS
• Atelectasis means collapse of the alveoli. It can occur in localized
areas of a lung or in an entire lung.
• Common causes
(1) Total obstruction of the airway
(2) Lack of surfactant in the fluids lining the alveoli.
• Air way obstruction causes lung collapse. The airway obstruction
results from
(1) Blockage of many small bronchi with mucus
(2) Obstruction of a major bronchus by either a large mucus plug or
some solid object such as a tumor.

CYANOSIS
Cyanosis means blueness of skin and its cause is excessive amounts
of deoxygenated hemoglobin in skin blood vessels, especially in the
capillaries.
• TYPES OF CYANOSIS
Two types (Peripheral & Central)
• Cyanosis appears whenever arterial blood contains more than 5 g of
deoxygenated hemoglobin in 100 ml of blood.
• A person with anemia never becomes cyanotic because there is not
enough hemoglobin(5 g to be deoxygenated in 100 ml of arterial
blood)
• In polycythemia,excess hemoglobin available that become
deoxygenated leads to cyanosis.

DYSPNEA (difficulty in breathing)
• It is defined as difficult or labored breathing in which the
subject is conscious of shortness of breath.
• HYPERPNEA
• General term for an increase in the rate or depth of
breathing regardless of the patient’s subjective sensations.
• TACHYPNEA
• It is rapid, shallow breathing.
• In general, normal individual is not conscious of respiration
until ventilation is double and breathing is not
uncomfortable until ventilation is tripled.

HYPOXIA
Is defined as the O2 deficiency at tissue level.
CLASSIFICATION
Hypoxia has been divided into four types.
1) Hypoxic hypoxia.
2) Anemic hypoxia.
3) Stagnant or ischemic hypoxia.
4) Histotoxic hypoxia

HYPOXIC HYPOXIA
is a type of hypoxia in which PO2 of arterial blood is reduced it
results from inadequate oxygenation of blood in lungs because of
A) Deficiency of oxygen in atmosphere (at high altitude)
B) Hypoventilation due to lung collapse or neuromuscular disorders like
myasthenia gravis.
C) Impaired function of respiratory membrane resulting from pulmonary
oedema, fibrosis of lungs & ventilation perfusion imbalance.

ANEMIC HYPOXIA
It is type of hypoxia in which arterial PO2 is normal but
amount of hemoglobin available to carry O2 is reduced.
This type of hypoxia is seen in
A) In anemia because Hemoglobin level is low.
B)Carbon mono-oxide poisning .

STAGNANT OR ISCHEMIC HYPOXIA
It is type of hypoxia in which blood flow to tissue is so low that
adequate O2 is not delivered to it despite a normal PO2 and
hemoglobin concentration.
This type of hypoxia is seen in
a) Ischemic heart disease
b) Severe cold (it produces vasoconstriction leading to decreased
blood flow to skin)
Raynaud’s disease (also produces vasoconstriction)

HISTOTOXIC HYPOXIA
It is type of hypoxia in which amount of O2 delivered to
tissue is adeqate but because of action of toxic agent, tissue cells
cannot make use of O2 supplied to them.
This hypoxia is seen in cyanide poisoning & vitamin deficiency.

EFFECTS OF HYPOXIA ON CELLS AND TISSUES
1. EFFECTS ON CELLS(blood): Hypoxia causes production of
angiogenic factors & erythropoietin.
2.EFFECTS ON BRAIN: In hypoxic hypoxia and other forms of
hypoxia,brain affected first.
• Sudden drop of inspired Po2 to less than 20 mmHg causes loss of
consciousness in 10 to 20 s and death in 4 to 5 min.
• Less severe hypoxia causes mental aberrations like impaired
judgment, drowsiness, dulled pain sensibility, excitement,
disorientation, loss of time sense, tachycardia & headache.

• ON G.I.T
loss of apetite,nausea,vomiting.mouth becomes dry.
• ON KIDNEY
increased secretion of erytropoitin from JG cells.
• ON CVS
Intially heart rate,cardiac output and blood pressure increase
due to reflex stimulation but later heart rate. Blood pressure and
cardiac output decrease.
• RESPIRATION
Intially respiratory rate increased due to reflex through
chemoreceptors but finally it decrease due to failure of respiratory
centers.

TREATMENT OF HYPOXIA
• O2 is of great benefit in hypoxic hypoxia.
• Pure oxygen and oxygen combined with other gas.
• Oxygen therapy carried out by
placing patient head in tent containing oxygen.
breath oxygen either from a mask or intranasal tube.
• Treatment regimens that deliver less than 100% O2 are of value both
acutely and chronically.

• Administration of oxygen rich gas mixtures is of very limited value in
anemic and histotoxic hypoxia.
• Anemic hypoxia is treated by giving oxygen at high pressure called
Hyperbaric O2 therapy.
• Treatment of cause.

HYPERBARIC O2 THERAPY
• Hyperbaric O2 therapy (i.e. administration of oxygen at high
pressure) in closed tanks is used to treat diseases in which improved
oxygenation of tissues cannot be achieved in other ways.
• It is of demonstrated value in CO poisoning, radiation induced tissue
injury, Gas gangrene, blood loss anemia, Diabetic leg ulcers & other
wounds that are slow to heal
• It is also primary treatment for decompression sickness & air
embolism.

OXYGEN (O2) TOXICITY
• It is interesting that while O2 is necessary for life in aerobic
organisms it is also toxic.
• Increased O2 content in tissues beyond critical level is called
oxygen poisoning or toxicity.It occurs because of breathing pure O2
with high pressure.
• Toxicity is due to production of reactive oxygen species including
superoxide and H2O2.
• When 80-100% O2 is administered to humans for 8h or more
respiratory passages become irritated causing

1. Substernal distress 2.Nasal congestion
3. Sore throat 4. Coughing
5. Some infants treated with O2 for RDS develop chronic
condition characterized by lung cysts and densities
(bronchopulmonary dysplasia) & retinopathy of
prematurity(retrolental fibroplasia)
formation of opaque vascular tissue in eyes which lead to
serious visual defects.
6. Convulsions, coma & death.

Oxygen debt
Body normally contains about 2 liters of stored oxygen that can be used
for aerobic metabolism even without breathing any new oxygen. This
stored oxygen consists of
1) 0.5 liter in air of lungs
2) 0.25 liter dissolved in body fluids
3) 1 liter combined with hemoglobin.
4) 0.3 liter stored in muscle fibers combined mainly with myoglobin.

• In heavy exercise almost all stored oxygen is used within a minute or
so for aerobic metabolism.
• After exercise is over this stored oxygen must be replenished by
breathing extra amounts of oxygen.
• In addition about 9 liters more oxygen must be consumed to provide
for reconstituting both phosphagen system and lactic acid system.
• All this extra oxygen that must be repaid i.e. about 11.5 liters is
called oxygen debt.

CO POISONING
SOURCES
• Gasoline engine,coal mines,gases from guns,deep wells,underground
drainage system.
TOXIC EFFECT
• It combine with hemoglobin to form carboxyhemoglobin which
cannot take up oxygen. As a result anemic hypoxia occurs.
• Hemoglobin has 200 time more affinity for CO then O2.
• Presence of carboxyhemoglobin decrease release of O2 from
hemoglobin as a result the oxygen –Hb curve shift to left

• SYMPTOMS (depends on concentration of CO)
• Headache & nausea (mild symptoms)
• Convulsion,cardiopulmonary arrest,comma
• If saturation with Hb above 50%.. death accur
TREATMENT
• Termination of exposure
• Provide adequate ventillation and artificial respiration
• Administration of 100 % oxygen

ACID BASE BALANCE AND GAS TRANSPORT
• Under normal conditions cellular metabolism accurs which result in
formation of carbondioxide & hydrogen ions.
• Carbondioxide is excreted through lungs and hydrogen excreted
through kidneys.
• Formation and excretion of these products result in normal pH.
• Any abnormality in formation & excretion results in conditions like
acidosis and alkalosis.

• pH normal = 7.40
• Acidosis :
The decrease in pH below the normal is acidosis
• Alkalosis :
An increase in pH above normal is termed as alkalosis

BUFFERING SYSTEM
• The buffering system maintains the normal pH.
• Acid and base shifts in blood are largely controlled by the
three main buffers
1. Proteins
2. Hemoglobin
3. The carbonic acid- bicarbonate system

RESPIRATORY ALKALOSIS
• Any short-term increase in ventilation that lowers
PCO2(35mmHg).
• Physiological: ascend to high altitude
• Pathological: obstructive diseases
(asthma,COPD)

RESPIRATORY ACIDOSIS
• Any short term rise in arterial PCO2(above40mmhg) due to
decreased ventilation is called respiratory acidosis.
• CAUSES
• Obstruction in respiratory passage like COPD, asthma.
• Infections(pneumonia)
• Pulmonary embolism

ARTIFICIAL RESPIRATION
• REST OF BREATHING .
• Accident ,drowning ,gas poisoning, electric shock,
anesthesia.
• O2 TO BRAIN (CORTEX)
• Lack of O2 for 5 min →→irreversible injury.

• MANUAL METHOD.
MOUTH TO MOUTH BREATHING.
• 12-14/min.
• Tidal volume twice the normal.
• Co2 from expired air stimulate respiratory centers.
• MECHANICAL METHODS.
• Drinker method (tank respirator or iron tank method.)
• Ventillator method (volume ventilator,pressure ventilator)

UQ’s
 What is the effect of CO poisoning on the oxygen Hb dissociation curve. Explain
with the help of graph.
 Define and describe the mechanism of cyanosis in different clinical conditions.
 Define hypoxia. Enumerate its types and describe the physiological mechanism of
anemic hypoxia.
 Define the following
Eupnea
Asphyxia
Hypercapnia
Respiratory acidosis
Apnea
 Enumerate buffer system.Enlist characteristic features of hypoxia on acute ascent
at high altitude.
 Define periodic breathing and explain the mechanism of chyne stroke breathing.

• Enumerate methods of artificial respiration?
• Enumerate causes and effect of Atelactasis?
• How Cheyne stokes breathing occur in patient with
cardiac failure?

HIGH ALTITUDE & SPACE PHYSIOLOGY
Dr. Mudassar Ali

LEARNING OBJECTIVES
• Acclimatization
• Changes in the body at high altitude(Immediate & delayed
effects of hypoxia)
• Acute & chronic mountain sickness
• Effects of centrifugal accelaratory forces

• At high altitudes the barometric pressure is low.
• However amount of oxygen present is same as at sea level.
• Due to low barometric pressures partial pressure of oxygen is
proportionally reduced, this leads to hypoxia.

OXYGEN HB SATURATION AT DIFFERENT ALTITUDES

CHANGES IN THE BODY AT HIGH ALTITUDE
 HYPOXIA
1. Immediate effects
2. Delayed effects
 EFFECTS OF EXPANSION OF GASES
 EFFECTS OF FALL IN ATMOSPHERIC TEMPERATURE

IMMEDIATE EFFECTS OF HYPOXIA
• Erythropoietin released , Increased RBC count.
• Increased oxygen carrying capacity of blood.
• Increased heart rate , Increased blood pressure.
• Resp. rate increased.
• Loss of appetite, nausea & dry mouth.
• Symptoms of alcoholic intoxication.

DELAYED EFFECTS OF HYPOXIA
• Person becomes highly irritable
• Vomiting, Breathlessness
• Pulmonary edema , Headache, Depression
• Lack of sleep , Weakness , Fatigue
• Cerebral edema

EFFECTS OF EXPANSION OF GASES
• Volume of gases increases as barometric pressure decreases.
• Expansion of gases in GIT may causes painful distention of
stomach & intestine.
• Rapid ascent from sea level cause decompression sickness.

EFFECTS OF FALL IN ATMOSPHERIC
TEMPERATURE
• Environmental temperature falls gradually at high altitudes.
• Injury due to cold or frost bite occurs if the body is not
adequately protected by warm clothing

ACCLIMATIZATION
• While staying at high altitudes for several days to several
weeks, a person slowly gets adapted or adjusted to the low
oxygen tension so that hypoxia causes lesser effects.
THE ADAPTATION OR ADJUSTMENT TO THE HIGH ALTITUDE
ARE COLLECTIVELY KNOWN AS ACCLIMATIZATION.

CHANGES DURING ACCLIMATIZATION
• Increase in pulmonary ventillation
• Increase number of RBCS
• Increased diffusing capacity of lungs
• Increased vascularity of peripheral tissues
• Increased heart rate & cardiac output
• Shifting of oxyhemoglobin curve to right
• Increased ability of tissue cells to use oxygen despite low p02

• INCREASE IN PULMONARY VENTILLATION
• Immediate exposure to low po2 stimulates arterial chemoreceptors
& this increases alveolar ventilation to a maximum of about 1.65
times.
• If person remains at high altitude for several days, chemoreceptors
increases ventillation about 5 times normal.
• Increased ventillation mainly reduces bicarbonate ions in CSF & brain
tissues
• COMPENSATION BY KIDNEYS FOR RESPIRATORY ALKALOSIS
• Kidney respond by reducing hydrogen ion secretion & increasing
bicarbonate excretion

INCREASE NUMBER OF RBCs
• Hypoxia as a principal stimulus increase in RBC production by
increasing the rate of erythropoietin release.
• Hematocrit rises slowly to about 60 & whole blood Hb concentration
rises from normal 15 to 20 g/dl

INCREASED DIFFUSING CAPACITY OF
LUNGS
• Diffusing capacity for O2 can increase as much as three fold at high
altitude than normal .
• Part of increase results from;
1. Increased pulmonary capillary blood volume, which expands the
capillaries & increases surface area through which oxygen can
diffuse.
2. An increase in lung air volume, which expands the surface area of
alveolar capillary.
3. An increase in pulmonary arterial blood pressure, this forces blood
into greater number of alveolar capillaries

INCREASED VASCULARITY OF THE
PERIPHERAL TISSUES
• Another circulatory adaptation is growth of increased
number of systemic circulatory capillaries in the non
pulmonary tissues, which is called increased tissue
capillarity.

MOUNTAIN SICKNESS
IT IS CONDITION CHARACTERIZED BY THE ILL EFFECTS OF
HYPOXIA AT HIGH ALTITUDE.
• This is commonly developed to the persons going to high
altitude for the first time.

ACUTE MOUNTAIN SICKNESS
ACUTE CEREBRAL EDEMA
• LOCAL VASODILATION OF CEREBRAL VESSELS
• INCREASE BLOOD FLOW
• INCREASED CAPILLARY PRESSURE
• FLUID LEAK INTO SPACES
• DISORIENTATION

ACUTE PULMONARY EDEMA
• SEVERE HYPOXIA LEADS TO PULMONARY
• VASOCONSTRICTION AT FEW AREAS
• SO THE BLOOD IS PUSHED TO UN CONSTRICTED AREAS
• CAPILLARY PRESSURE RISES
• LOCAL EDEMA
• PULMONARY DYSFUNCTION

CHRONIC MOUNTAIN SICKNESS
• Increase in hematocrit.
• Increase in pulmonary arterial pressure.
• Right side of heart becomes enlarged.
• Peripheral arterial pressure begins to fall.
• Congestive heart failure.
• Death.

AVIATION AND SPACE PHYSIOLOGY
• Acceleration and deceleration during the flight.
• Centrifugal accelaratory forces.
• Gravity and anti gravity forces.

EFFECTS OF CENTRIFUGAL ACCELARATORY FORCES
1. Decreased cardiac out put.
2. Decreased stroke volume.
3. Blackout of vision.
4. Rupture of cerebral vessels.
5. Blindness.

WEIGHTLESSNESS (MICROGRAVITY)
• SYMPTOMS:
1. Motion sickness.
2. Abnormal hydrostatic pressures.
3. No strength of muscles.
4. Decrease in blood volume.
5. Decrease RBC.
6. Loss of bone mass.

TREATMENT
1. Exercise
2. The application of intermittent artificial gravity caused by
short periods of centrifugal acceleration of the astronauts
while they sit in specially designed short arm centifuges
that creat forces upto 2 to 3G

DEEP SEA PHYSIOLOGY.
Dr. Mudassar Ali

LEARNING OBJECTIVE
• Hyperbarism & Nitrogen narcosis
• Decompression sickness
• SCUBA

Physiology of deep-sea diving and other hyperbaric
conditions
HYPERBARISM:
• When human beings descend beneath the sea, pressure around
them increases tremendously.
• To keep lungs from collapsing, air must be supplied at high pressure
to keep them inflated. This exposes blood in lungs to extremely high
alveolar gas pressure, a condition called hyperbarism.
• Beyond certain limits, these pressures cause tremendous alterations
in body physiology and can be lethal.

RELATIONSHIP OF PRESSURE TO SEA DEPTH
• A column of seawater 33 feet (10.1 meters) deep exerts same
pressure at its bottom as pressure of atmosphere above sea.
• Therefore, a person 33 feet beneath the ocean surface is exposed to
2 atmospheres pressure, 1 atmosphere of pressure caused by weight
of air above water and second atmosphere by weight of water itself.
At 66 feet pressure is 3 atmospheres, and so forth.

EFFECT OF SEA DEPTH ON THE VOLUME OF GASES–
BOYLE’S LAW
– Another effect of depth is compression of gases to smaller and
smaller volumes. lower part of figure shows a bell jar at sea level
containing 1L of air. At 33 feet beneath the sea, where the
pressure is 2 atmospheres, volume has been compressed to only
½ L, and at 8 atmospheres (233 feet) to one-eighth liter.
– Thus, volume to which a given quantity of gas is compressed is
inversely proportional to the pressure.
This principle is called Boyle’s law.

EFFECT OF HIGH PARTIAL PRESSURES OF
INDIVIDUAL GASES ON THE BODY
Individual gases to which a diver is exposed when breathing
air are nitrogen, O2 and CO2 each of these at times can
cause significant physiologic effects at high pressures.

NITROGEN NARCOSIS AT HIGH NITROGEN
PRESSURES
About four fifths of air is nitrogen. At sea-level pressure, N2 has no
significant effect on body function. At high pressures it can cause varying
degrees of narcosis.
When diver remains beneath sea for an hour or more and is breathing
compressed air, the depth at which first symptoms of narcosis appear is
about 120 feet.
At 150 to 200 feet, diver becomes drowsy. At 200 to 250 feet, diver often
becomes too clumsy to perform the work required.
Beyond 250 feet (8.5 atmospheres pressure), diver usually becomes
almost useless as a result of nitrogen narcosis if he or she remains at
these depths too long.

NARCOTIC EFFECTS OF NITROGEN AND ALCOHOL
Nitrogen narcosis has characteristics similar to those of alcohol
intoxication, and for this reason it has frequently been called
“raptures of the depths.”
MECHANISM:
Mechanism of narcotic effect is believed to be the same as that of
most other gas anesthetics. It dissolves in fatty substances in
neuronal membranes & because of its physical effect on altering ionic
conductance through the membranes, reduces neuronal excitability.

DECOMPRESSION SICKNESS
• Disorder that occurs when person returns rapidly to normal
surroundings(atmosphereic pressure) from area of high
atmospheric pressure like deep sea.
• It is also known as Dysbarism, Caisson disease or sickness,
Bends or Diver’s palasy.

MECHANISM OF DECOMPRESSION SICKNESS
• Normally, nitrogen is not metabolized by the body, it remains
dissolved in body tissues until nitrogen pressure in lungs in decreased
back to some lower level, at which time the nitrogen can be removed
by the reverse respiratory process.
• However, this removal often takes hours to occur and is the source
of multiple problems collectively called decompression sickness.

VOLUME OF NITROGEN DISSOLVED IN BODY FLUIDS
AT DIFFERENT DEPTHS
At sea level, almost 1 L of N2 is dissolved in entire body. Slightly
less than one half of this is dissolved in the water of body and a little
more than one half in the fat of body. This is true because nitrogen is
five times as soluble in fat as in water.
After the diver has become saturated with nitrogen, the sea-level
volume of nitrogen dissolved in the body at different depths is as
follows:

NITROGEN ELIMINATION FROM THE BODY
• If a diver is brought to the surface slowly, enough of the dissolved
nitrogen can usually be eliminated by expiration through lungs to
prevent decompression sickness.
• About two thirds of the total nitrogen is liberated in 1 hour and
about 90 per cent in 6 hours.

DECOMPRESSION SICKNESS OR CAISSON
DISEASE
If a diver has been beneath the sea long enough that
large amounts of nitrogen have dissolved in his or her body
and the diver then suddenly comes back to the surface of
the sea, significant quantities of nitrogen bubbles can
develop in the body fluids either intracellularly or
extracellularly and can cause minor or serious damage in
almost any area of the body, depending on the number and
sizes of bubbles formed; this is called decompression
sickness.

REASON OF SYMPTOMS OF DECOMPRESSION
SICKNESS (“BENDS”)
• The symptoms of decompression sickness are caused by
gas bubbles blocking many blood vessels in different
tissues.
• At first, only smallest vessels are blocked by minute
bubbles but as bubbles coalesce, progressively larger
vessels are affected. Tissue ischemia and sometimes tissue
death are the result.

SYMPTOMS
1) Pain in joints and muscles of legs and arms, affecting 85 to 90 % of those
persons who develops decompression sickness. Joint pain accounts for
term “bends” that is applied to this condition.
2) Nervous system symptoms ranging from dizziness (5 % to paralysis or
collapse and unconsciousness in as many as 3 %). Paralysis may be
temporary, but sometime permanent.
3) 2 % people with decompression sickness develop “the choke,” caused by
massive numbers of micro-bubbles plugging lung capillaries. This is
characterized by serious shortness of breath followed pulmonary edema
and occasionally death.

TREATMENT OF DECOMPRESSION SICKNESS
• Treatment is tank decompression. Treatment is to put the
diver into a pressurized tank and then to lower the
pressure gradually back to normal atmospheric pressure.
• Tank decompression is even more important for treating
people in whom symptoms of decompression sickness
develop minutes or even hours after they have returned to
the surface.

PREVENTION
• Decompression sickness is prevented by taking proper
precautionary measures.
• While returning to sea level the ascent should be very slow.
• Stepwise ascent allows nitrogen to come back to the blood
without forming bubbles.

SCUBA (SELF-CONTAINED UNDERWATER BREATHING
APPARATUS) DIVING
Before 1940s all diving was done using diving helmet
connected to a hose through which air was pumped to the
diver from surface. In 1943, French explorer Jacques
Cousteau popularized a self-contained underwater
breathing apparatus known as the SCUBA apparatus.
The type of SCUBA apparatus used in more than 99 percent
of all sports and commercial diving is the open-circuit
demand system.

The system consists of the following
components
1) One or more tanks of
compressed air or some other
breathing mixture.
2) A first-stage “reducing” valve for
reducing high pressure form
tanks to low pressure.
3) A Combinaiton inhalation
“demand” valve and exhalation
valve that allows air to be pulled
into lungs with slight negative
pressure of breathing and then
exhaled into sea at a pressure
level slightly positive to the
surrounding water pressure.
4) A mask and tube system with
small “dead space.”

PROBLEMS OF SCUBA DIVING
• Important problem in use of self-contained underwater breathing
apparatus is the limited amount of time one can remain beneath the
sea surface; for instance, only a few minutes are possible at a 200-
foot depth.
• Reason for this is that tremendous airflow from the tanks is
required to wash CO2 out of lungs. greater the depth, greater the
airflow in terms of quantity of air per minute that is required,
because the volumes have been compressed to small sizes.

SPECIAL PHYSIOLOGIC PROBLEMS IN SUBMARINES
ESCAPE FROM SUBMARINES:
Same problems encountered in deep-sea diving are often met in
relation to submarines, especially when it is necessary to escape form a
submerged submarine. Escape is possible from as deep as 300 feet
without using any apparatus. However, proper use of rebreathing
device, especially when using helium, theoretically can allow escape
from as deep as 600 feet or perhaps more.
One of the major problems of escape is prevention of air embolism.
As person ascends, gases in lungs expand and sometimes rupture a
pulmonary blood vessel forcing gases to enter the vessel and cause air
embolism of circulation. Therefore, as person ascends, he or she must
make a special effort to exhale continually.

HEALTH PROBLEMS IN SUBMARINE INTERNAL
ENVIRONMENT
Except for escape, submarine medicine generally centers on
several engineering problems to keep hazards out of the
internal environment.
First:
In atomic submarines, there exists the problem of radiation
hazards, but with appropriate shielding, amount of radiation
received by crew submerged beneath sea has been less than
normal radiation received above the surface of sea from cosmic
rays.

Second:
• Poisonous gases on occasion escape into the atmosphere
of submarine & must be controlled rapidly.
• For instance during several weeks submergence,
cigarette smoking by the crew can liberate enough carbon
monoxide, if not removed rapidly cause CO poisoning.

Respiration by dr. mudassar

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