HUMAN SYSTEM ANATOMY &

PHYSIOLOGY I

RESPIRATORY SYSTEM 2

ALVEOLAR VENTILATION, GAS TRANSPORT &

REGULATION

DR WAN SAFWANI WAN KAMARUL ZAMAN

 PULMONARY VENTILATION

• Exchange of gas at alveolus known as alveolus ventilation. Not

all the air breath in will exchange in alveolus as inspired gas
do filled the air-way (mouth, trachea, bronchus & bronchiole).
Air that fill these space also know as anatomical death space)

• Anatomical death space can be increase when less elastic

tissue due aging.

• Alveolus ventilation is define as amount of gas enter the

alveolus in one minute ( tidal volume X frequency of
respiration L / minute)
 PRESSURE RELATIONSHIPS IN THORACIC
CAVITY
INTRAPULMONARY PRESSURE
• Intra-alveolar pressure (Ppul)
• Pressure in alveoli
• Rise & falls with phases of breathing
• Equalizes with atmospheric pressure.

INTRAPLEURAL PRESSURE
• Pressure in pleural cavity (Pip)
• Fluctuates with breathing phases
• 4 mm Hg less than Ppul – Pip is always negative relative to Ppul
 PRESSURE RELATIONSHIPS IN THORACIC CAVITY
2 opposing forces – to pull lungs away from thorax wall & cause lung
collapse:

1) Lungs tendency to recoil – elasticity assume smallest size

possible
2) Surface tension of alveolar fluid – to draw alveoli to smallest
dimension

BUT….

These are opposed by natural elasticity of chest wall – pull thorax

outward & enlarge lungs

The net result between these forces – negative Pip

 PRESSURE RELATIONSHIPS IN THORACIC
CAVITY
So…the amount of pleural
fluid in pleural cavity must
remain minimal for negative
Pip to be maintained

If not…immediate lung
collapse

Transpulmonary pressure –
difference between Ppul & Pip
keeps air spaces in lungs
open
 PHYSICAL FACTORS INFLUENCING PULMONARY
VENTILATION

1) Airway resistance

• The friction encountered by

air in the airways

• Gas flow is reduced as airway

resistance increases.
 PHYSICAL FACTORS INFLUENCING PULMONARY
VENTILATION

2) Lung compliance

• Degree of change in transpulmonary pressure required to

cause a change in lung volume.

• Reflects the distensibility of lung tissue and alveolar surface

tension.

• Measure of change in lung volume that occurs with a given

change in transpulmonary pressure.

• The higher the compliance the easier to expand the lungs

 PHYSICAL FACTORS INFLUENCING PULMONARY
VENTILATION
3) Alveolar surface tension

• Due to water in the alveoli acts to draw the walls of the alveoli
together
• Presenting a force that must be overcome in order to expand
the lungs.
• Reduce by surfactant produced by type II alveolar cells –
decreases cohesiveness of water molecule.
• Without surfactant – alveoli can collapse between breaths.
• Pulmonary Surfactant is a phospholipids & protein (know as
phophatidil choline) that produce maximum at 34-36 of
pregnancy. Thus baby born premature may die of hyaline
membrane disease / Respiratory Distress Syndrome.
 RESPIRATORY VOLUMES
4 respiratory volumes:

• Tidal volume is the amount of air that moves in and out of the
lungs with each breath during quiet breathing.

• The inspiratory reserve volume is the amount of air that can be

forcibly inspired beyond the tidal volume.

• The expiratory reserve volume is the amount of air that can be

evacuated from the lungs after tidal expiration.

• Residual volume is the amount of air that remains in the lungs

after maximal forced expiration.
 RESPIRATORY CAPACITIES
• Inspiratory capacity is the sum of tidal volume and inspiratory reserve
volume, and represents the total amount of air that can be inspired after
a tidal expiration.

• Functional residual capacity is the combined residual volume and

expiratory reserve volume, and represents the amount of air that
remains in the lungs after a tidal expiration.

• Vital capacity is the sum of tidal volume, inspiratory reserve and

expiratory reserve volumes, and is the total amount of exchangeable air.

• Total lung capacity is the sum of all lung volumes.

• The anatomical dead space is the volume of the conducting zone

conduits, which is a volume that never contributes to gas exchange in the
lungs.
 SPIROMETER
• Test for lung function

• Common parameters: Vital

capacity (VC), Forced vital
capacity (FVC), Forced
expiratory volume (FEV)

• Diagnose & manage asthma,

COPD & to distinguish
respiratory from cardiac
disease as the cause
 HYOPOVENTILATION

Define as condition the exchange of O2 in blood is less as

the result of increase alveolus ventilation (PAO2 < 104
mmHg & PACO2 >40 mmHg).

Alveolus Hypoventilation when breath in normal

atmosphere air will causes hypoxemia (PaO2 < 97 mmHg)
& increase accumulation of CO2. Thus need to treat with
100% O2.
 HYPERVENTILATION

Alveolus ventilation excess that lead to increase PaO 2 & PaCo2

than normal.
Condition or factor that causes:
1. High altitude.
2. Worry ness & hysteria.
3. Acidosis metabolite.
4. Brain infection such as meningitis.
5. Fever & ventilator machine
6. hormones adrenalin, tyrosine & progesterone.
GAS EXCHANGE
 EXTERNAL RESPIRATION: PULMONARY GAS
EXCHANGES
• Dark red blood flow through pulmonary circuit scarlet when
return to heart

• Colour change due to oxygen uptake & binding of hemoglobin to

RBCs.

• Unloading of carbon dioxide

• 3 factors influence movement of oxygen & carbon dioxide across

respiratory membrane:
1) Partial pressure gradients & gas solubilities
2) Matching of alveolar ventilation & pulmonary blood perfusion
3) Structural characterisitics of respiratory membrane
PARTIAL PRESSURE GRADIENTS & GAS SOLUBILITIES
• PO2 of venous blood in pulmonary
arteries is 40 mm Hg

• PO2 in alveoli is 104 mm Hg

• So….steep oxygen partial pressure

exists

• Oxygen diffuses rapidly from alveoli

into pulmonary capillary blood until
equilibrium occurs

• CO2 diffuses in opposite direction

until equilibrium at 40 mm Hg
 VENTILATION-PERFUSION COUPLING

• Local autoregulatory mechanism

respond to alveolar condition.

• Ensures a close match between

the amount of gas reaching the
alveoli and the blood flow in the
pulmonary capillaries.
THICKNESS & SURFACE AREA OF RESPIRATORY
MEMBRANE

• The respiratory membrane is normally very

thin, 0.5 μm to 1 μm thick

• Presents a huge surface area for efficient gas

exchange.
 INTERNAL RESPIRATION: CAPILLARY GAS
EXCHANGE IN BODY TISSUES

• The diffusion gradients for oxygen and carbon

dioxide are reversed from those for external
respiration and pulmonary gas exchange.

• The partial pressure of oxygen in the tissues is

always lower than the blood, so oxygen diffuses
readily into the tissues, while a similar but less
dramatic gradient exists in the reverse direction
for carbon dioxide into blood.
TRANSPORT OF
RESPIRATORY
GASES BY BLOOD
 OXYGEN TRANSPORT
• Oxygen is poorly soluble in the blood, only 1.5%
is dissolved in plasma, while the remaining
98.5% must be carried on hemoglobin.

• Up to four oxygen molecules can be reversibly

bound to a molecule of hemoglobin—one
oxygen on each iron.

• Oxyhemoglobin (HbO2), deoxyhemoglobin, or

reduced hemoglobin (HHb). Oxygenation of
hemoglobin occurs in the lungs and oxygen
unloading occurs in the tissues.

• The affinity of hemoglobin for oxygen increases

with each successive oxygen that is bound and
decreases with each oxygen released, making The PO2 gradient required to unload one
oxygen loading and unloading very efficient. oxygen from fully saturated HbO2 is 60 mm Hg.

• At higher plasma partial pressures of oxygen, The PO2 gradient required to unload one
hemoglobin unloads little oxygen, but if plasma oxygen from partially saturated HbO2 is
partial pressure falls dramatically, i.e. during substantially less, and decreases with
vigorous exercise, much more oxygen can be each successive oxygen removed.
 OTHER FACTORS INFLUENCING HEMOGLOBIN
SATURATION
Temperature
• Increased temperature, a by-product of increased
metabolic activity, pushes Hb from its high affinity
structure toward its low affinity structure, from
which oxygen unloads more easily.
• Increased temperature also increases the metabolic
rate of RBCs, increasing the production of BPG,
which also facilitates oxygen unloading from HbO2.
 OTHER FACTORS INFLUENCING HEMOGLOBIN
SATURATION
pH

• Lower pH (increased H+ concentration) favors oxygen unloading from HbO2 because H+

ion binding to the protein portion of Hb stabilizes the low affinity structure of Hb.

• Oxygen saturation of HbO2inhibits H+ ion binding to Hb but metabolically active tissues

generate enough H+ ions to overcome the inhibition .

• As H+ ions bind to Hb, the affinity for O2 decreases; as O2 is released from Hb H+ ions can
more easily bind, which further facilitates the release of O 2.

• In the lungs the increased PO2 favors oxygen binding to HHb, which drives H+ ions off Hb
and into solution and increases the affinity of Hb for O2; the complete oxygen saturation
of HbO2 achieved in the lungs stabilizes the high affinity structure of Hb.

• This interaction, which facilitates oxygen unloading where it is needed and oxygen
loading where it is plentiful, is known as the Bohr effect.
 OTHER FACTORS INFLUENCING HEMOGLOBIN
SATURATION

PCO2
• Increased blood PCO2, the result of metabolic activity of
tissues, decreases the affinity of Hb for oxygen and
facilitates oxygen unloading.

BPG (Bisphosphoglycerate)
• A by product of glycolysis in RBCs, BPG binds to Hb and
stabilizes the low affinity structure.
 CARBON DIOXIDE
TRANSPORT
• Carbon dioxide is transported
in the blood in 3 ways:
1) 7–10% is dissolved in plasma
2) 20% is carried on hemoglobin
bound to globins
3) 70% exists as bicarbonate, an
important buffer of blood
pH.
• The Haldane effect
encourages CO2 exchange in
the lungs and tissues: when
plasma partial pressure of
oxygen and oxygen saturation
of hemoglobin decrease,
more CO2 can be carried in
the blood.
• Carbonic acid-bicarbonate
buffer system – resisting
shifts in blood pH
 HYPOXIA

Define as an inadequate oxygen supply to the body tissues.

1.   Hypoxia Hypoxic  commonly found in clinic due to  PO2 in

inspired air, Hypoventilation & oxidation in blood is insufficient).
2.   Hypoxia Anemia  Due to concentration of HB  , abnormal Hb
(megablastic Hb) & failure of Hb to bind oxygen (CO poisonous)
3.   Hypoxia stagnant  Hypoxia ischemic due to slow blood flow &
blockade of arterial blood flow (congestive heart failure &
hipovolemia shock).
4.Hypoxia Histotoxic  PO2 normal but inability Hb to bind O2
(cyanide poison)
 NEURAL
CONTROL OF
RESPIRATION
 MEDULLARY RESPIRATORY CENTERS
• 2 areas of medulla oblongata
1) dorsal respiratory group (DRG)
dorsally at root of cranial nerve
2) ventral respiratory group (VRG)
extend in ventral brain stem from
spinal cord to pons medulla junction.

• VRG – rhythm-generating & integrative

center.
• Inspiration – impulse runs along
phrenic & intercostal nerves
• Expiration – impulse stops & relaxation
of muscles & recoil of lungs.

• DRG – integrates input from peripheral

& chemoreceptors – send info to VRG
 PONTINE RESPIRATORY CENTERS

• Influence & modify activity

of medullary neurons
• Transmit impulses to VRG
• During certain activities:
sleep, exercise
 FACTORS INFLUENCING BREATHING RATE &
DEPTH
CHEMICAL FACTORS
• Levels of CO2, O2 and H+ - changes in CO2 is most important
• Sensors – chemoreceptors at 2 sites:
1) central chemoreceptors – bilaterally in ventrolateral medulla
2) peripheral chemoreceptors – aortic arch & carotid arteries

1) Influence of PCO2
• CO2 is hydrated in CSF – liberate H+ - detected
• Increase breathing rate & depth – enhance alveolar ventilation
• To flush out CO2 – to restore normal level

2) Influence PO2
• Slight influence – limited to enhancing peripheral receptors to increase PCO2
• To be major stimulus – drop below to at least 60mmHg.
• O2 reservoir – bound to hemoglobin.
 FACTORS INFLUENCING BREATHING RATE
& DEPTH
3) Influence of Arterial pH
• Ventilation occurs is mediated through peripheral
chemoreceptors
• Drop in blood pH – CO2 retention & metabolic causes
• Declines in pH – elimination of CO2
• So, respiratory & depth increase

HIGHER BRAIN CENTERS

• Hypothalamus
• Corticol controls – voluntary control through cerebral cortex
 LOVE YOUR LUNGS…

Emphysema – permenant enlargement of alveoli accompanied by destruction of

alveolar walls leading to lost of elasticity
THINK TWICE BEFORE YOU START SMOKING !!