PULMONARY

PHYSIOLOGY
The primary function of the respiratory system
is the continuous absorption of oxygen and the
excretion of carbon dioxide
The respiratory system and cardiovascular
system must work hand in hand in order to
maintain internal stability
Any change in the respiratory homeostasis must
result in one of the following:
1. change in arterial blood gas values
2. cardiopulmonary system increase work to
maintain homeostatic balance; blood gas
remains unchanged
 Degree of abnormality in the arterial blood gas
values is determined by the balance between
the severity of disease and degree of
compensation by the cardiopulmonary system

RESPIRATION
-biologic process of oxygen and carbon
dioxide exchanging across permeable
membranes
-EXTERNAL, INTERNAL, CELLULAR
EXTERNAL RESPIRATION
 pertains to the exchange between the gas of
the atmosphere and the pulmonary capillary
blood

 Most efficient gas exchange occurs when there

is an existing perfect match between all lung
ventilation and pulmonary blood flow
 REGIONAL DIFFERENCES IN VENTILATION
In a patient standing erect, intrapleural pressure is
more negative at the apex than the base
-the intrapleural negativity is less at the base
-gravity dependent
 Regional differences in ventilation refer to the
volume changes in relation to resting volume
-base of the lung has smaller resting volume, thus
creating a large volume change
-more of inspired tidal volume will distribute to the
basilar alveoli

Therefore, basilar ventilation is greater.

-depending on the body position
 REGIONAL DIFFERENCES IN
PERFUSION
Normal distribution of blood flow is dependent on
gravity and cardiac output
Best determined by the amount of blood ejected
by the right ventricle per minute (cardiac output)
Gravity dependent area: increased arterial
pressure compared to alveolar pressure
 ZONE 1: no flow; less gravity dependent area
ZONE 2: intermittent flow
ZONE 3: constant flow; more gravity
dependent area

 The greater the cardiac output=the greater the

pulmonary artery pressure=zones 2 and 3
extends upward
 V/Q RELATIONSHIP
Gas exchange unit is composed of an alveolus and
its associated pulmonary capillary
Four relationships of the respiratory unit:

1. Normal unit: ventilation and perfusion are equal

2. Deadspace unit: alveoli is ventilated with no
blood flow through the capillary
3. Shunt unit: alveolus is not ventilated with blood
flow on the adjacent capillary
4. Silent unit: alveolus is not ventilated with no
blood flow on the capillary
VENTILATION-PERFUSION DIFFERENCES IN THE LUNGS

APEX BASE
Alveoli Larger, more Smaller, less
expanded, stiffer, expanded, more
less compliant compliant
Effect of gravity Vessels less Vessels distended
distended
PaCO2 <40 mmHg >40 mmHg
PaO2 >100 mmHg <100 mmHg
pH >7.4 <7.4
Blood Flow Less More
Ventilation Less More
V/Q ratio Overventilated Underventilated
INTERNAL RESPIRATION

 exchange of gasses between the blood and the

tissues (cells)
 Dependent on:
1. metabolism
2. regional perfusion
3. arterial blood gasses
PICTURES
CELLULAR RESPIRATION

 Biochemical reactions essential for cellular

activation
 Requires energy
 Tissue hypoxia
- when cellular oxygen tensions are below
the level required to meet metabolic
demands
-if there is less oxygen for metabolic activity,
nonoxidative biochemical pathways
(anearobic) are used resulting to production
of carbon dioxide and other metabolites
Categories of tissue hypoxia:
1. Hypoxemic hypoxia
-secondary to inadequate arterial oxygenation

2. Anemic hypoxia
-secondary to inadequate hemoglobin content

3. Circulatory hypoxia
-secondary to inadequate perfusion

4. Histotoxic hypoxia
- secondary to an inability of the cells to use
oxygen
DYSOXIA

 characterizes abnormal utilization of

oxygen at the cellular level
 may result from either intrinsic
mitochondrial dysfunction or
exogenous poisons
 LUNG VOLUMES AND
CAPACITIES
TIDAL VOLUME (VT) 500 mL
-volume of air that goes in and out of the lungs

INSPIRATORY RESERVE VOLUME (IRV) 3500 mL

-volume of air that can be inhaled after a normal
inspiration

EXPIRATORY RESERVE VOLUME (ERV) 1500 mL

-volume of air that can be exhaled from the resting
end expiratory level

RESIDUAL VOLUME (RV) 1200 mL

-volume of air that remains in the lungs after a
maximum exhalation
INSPIRATORY CAPACITY (IC)
-maximum volume of air that can be inhaled from
the normal resting end expiratory level

FUNCTIONAL RESIDUAL CAPACITY (FRC)

-volume of air remaining in the lungs at a resting
end-expiratory level
-considered to be the neutral or equilibrium point for the
respiratory system (glottis open, respiratory muscles are
relaxed)

VITAL CAPACITY (VC)

-maximum volume of air that can be exhaled after a
maximum inspiration

TOTAL LUNG CAPACITY (TLC)

-amount of air contained in the lungs after a
maximum inspiration
 OBSTRUCTIVE RESTRICTIVE
 Increased resistance to  Decreased volumes and
airflow caused by obstruction capacity
of the airways

 FEV1 ratio is decreased  Decreased TLC and FVC

 Examples:  Examples:
-asthma CHESTWALL
-Chronic bronchitis -obesity
-Emphysema -kyphoscoliosis
-Bronchiectasis INTERSTITIAL
-Cystic fibrosis -ARDS
-pneumoconiosis
-Pulmonary fibrosis
 VENTILATION
Total Ventilation
 The total amount of air that goes in and out of the
lungs in one minute

 VE = VT x f

 VA = (VT – VD) x f
 VENTILATION
Conducting Airways (Anatomic Deadspace)
 Approximately 150 mL or, person’s weight in
pounds
 Area in the respiratory system that contains air
but does not undergo gas exchange (with CO2)
 Anatomic Deadspace: start of conducting
airways until the level of terminal bronchioles
 Alveolar Deadspace: alveoli containing air but
without blood flow within the surrounding
capillaries (no gas exchange)
 MUSCLES OF VENTILATION
Muscles for Ventilation
 Diaphragm
 Intercostal muscles (parasternal muscles,
adjacent to the sternum)
 Internal Intercostals
 External Intercostals
 Scalene
-stabilizes the upper ribcage
DIAPHRAGM
 Primary muscle for ventilation
 Intrathoracic pressure: creates a more
negative pressure, contracts and descends
during inspiration
 Points of attachment:
 Costal portion
-arises from the sternum, costal
cartilages and ribs
 Crural portion
-arises from the vertebral bodies
  Zone of apposition
-vertical fibers of the diaphragm
which lie closer to the inner wall of
the lower rib cage

 Holes of the diaphragm:

T8: Inferior vena cava
T10: Esophagus & Vagus
T12: Aorta, Azygos, Thoracic Duct

 In an upright position, R hemidiaphragm is

higher (8-9th TV; 5th rib) compared to the left
(9-10th TV; 6th rib) because of the liver
TIDAL BREATHING

 Diaphragm: major muscle for inspiration

 Intra-abdominal pressure increases
 Intrathoracic pressure decreases leading to
gush of air inside the lungs
 During inspiration, the muscle fibers of the
diaphragm are tensioned the dome is pulled
down 1 to 2 cm
 During inspiration, enlargement of the
thoracic cavity and compression of the
abdominal contents occur
Movement during Tidal Breathing

Pump Handle A/P diameter T1-T6

motion Transverse

Bucket Handle Lateral/Transverse T7-T10

motion

Caliper motion Lateral/Transverse T11-T12

Piston motion Superior & Inferior

 COPD patients during tidal breathing???
 COPD patients have increased lung volumes causing
the diaphragm to flat
 Contraction of a flattened diaphragm can result in
tension in the lower ribs causing them to be pulled
inward thus compression of the thoracic activity
 To enlarge the thorax, accessory muscles are
recruited by patients having increased lung volumes

COPD
-flat diaphragm
-wide intercostal spaces
-increased volumes with decreased flows
-xray: hyperlucent
COMPLIANCE

 Measurement of the distensibility of a

structure
 Change in volume per unit of pressure

 Spinal Cord Injury?

 Obstructive Pulmonary Disease?
 Restrictive Pulmonary Disease?
LUNG MECHANICS
 Inspiration
 Expiration

INSPIRATION
 movement of air into the lungs
 muscles involved are the diaphragm and
those that elevate the ribs and sternum
 As the diaphragm and other muscles of
inspiration contract and the rib cage rises
and thoracic volume increases
EXPIRATION

 movement of air out of the lungs

 Muscles actively involved are those
that depress the ribs and sternum
(usually only with forceful expiration)
 Largely a passive process
 Muscles of inspiration relax, the rib
cage descends due to gravity and the
thoracic cavity volume decreases
Pressure Changes and Airflow

Influencing Pulmonary Ventilation:

 Air flows from areas of higher to lower

pressure
– If pressure is higher at one end of a tube (P1)
than at the other (P2), air will flow down its
pressure gradient
 Pressure Differences (Breathing)
1. Pao
• pressure at the opening of the airway
• always in 0 (unless + or – pressure is applied in the
airway)
2. Pbs
• pressure at the body surface
• usually 0
3. Palv
• alveolar pressure
• also called the intrapulmonary pressure
• pressure may vary during breathing cycle
• Pressure of thin film fluid between the lung and the
chest wall
 • Negative pressure in this area expands the lungs
(decreasing values but force to expand the lungs
is increasing
• At FRC level, glottis is open, muscles are relaxed,
no air movement:
Intrapleural pressure: -5cmH2O
Recoil force: 5 cmH2O
Alveolar pressure: 0

4. Ppl
• Pleural pressure
• in negative subatmospheric pressure
• usually -5cmH2O
• varies during breathing cycle
Pressure Gradient
-difference between 2 pressures
 Transrespiratory (Palv – Pbs)
 Transpulmonary (Palv – Ppl)
 Causes gas to flow into and out of the alveoli
 Pressure difference maintains alveolar inflation
 Measures of the elastic forces in the lungs that tend to
collapse the lungs at each point of expansion (recoil
pressure)

 Transthoracic (Ppl – Pbs)

 Difference in pressure between the pleural space and the
body surface
 Pressure across the chest wall
 Represents the total pressure necessary to expand or
contract the lungs and the chest wall together
A. Inspiration
BEFORE INSPIRATION
• At FRC level (neutral)
• Intrapleural pressure= -5 cmH2O
• Recoil force= 5 cmH2O
• Alveolar pressure= 0

DURING INSPIRATION
• Inspiratory muscles contract
• Intrapleural pressure becomes more negative
• Recoil force becomes more positive
• Alveolar pressure changes from 0 to -1 cmH2O
• Air enters the lungs
END OF INSPIRATION

• Intrapleural pressure changes from -5cmH2O to

-8 cmH2O
• Recoil force changes from 5 cmH2O to 8 cmH2O
• Alveolar pressure goes back to 0 (lungs stops
expanding)
• No lung movement because intrapleural
pressure is equal but opposite to recoil force
and alveolar pressure is back to zero
B. Expiration
• Inspiratory muscles relax
• Intrapleural pressure goes back from -8 cmH2O
to -5 cmH2O)
• Recoil force goes back from 8 cmH2O to 5
cmH2O
• Alveolar pressure from 0 cmH2O at the end of
inspiration becomes +1 cmH2o until it becomes
0 cmH2O again
• FRC level is achieved once again
Alveoli Airflow

Fig. 20.11
RECOIL FORCE
• Directly proportional to lung volume under
normal conditions
• The force that collapses the lungs
• Components of lung recoil:
1. Tissue (elastic and collagen fibers)
-greater stretch means greater recoil
2. Surface tension
-force that will compress the alveoli
-acts to collapse the alveoi
-greatest component of recoil
-increase surface tensionincrease recoil
force
SURFACTANT
 Lowers surface tension in the lungs; increases
lung compliance
 Produced by alveolar type II cells
 Pulmonary surfactant’s ability to lower surface
tension decreases as surface area increases
 When surface area increases, the ability of
pulmonary surfactant to lower surface tension
increases
PROSTAGLANDINS (PGE2)
 Secreted to suppress proliferation of lung
fibroblasts, production of collagen decreaseing
pulmonary fibrosis
HISTAMINE
 Increases bronchoconstriction

ANGIOTENSIN CONVERTING ENZYME

 Abundant on the endothelial surface of lung vessels
 A vasoconstrictive substance which results to increase in
blood pressure and aldosteronepromotes sodium
retension, blood volume and sodium reabsorption
increases
KALLIKREIN
 Activates bradykinin
-END-