RESPIRATORY PHYSIOLOGY I - VISCERAL PLEURA: tightly adherent to the lung

itself
- PARIETAL PLEURA: attached inside the chest
LUNGS wall/ thoracic cavity

Functions: NOSE
1. Gas exchange - Very important because it is where air enters
- Transport of gas from the atmosphere towards - Although we can breathe through our mouth, it is
the lungs, to the blood, to the different tissues. better if we breathe through our nose because:
- Elimination of CO2 - it humidifies the air
2. Host defense - entraps of clear particles more than 10m in size
- It secretes several inflammatory mediators, (protective function: it acts as protective barrier)
immunoglobulins. - sense of smell (olfactory sense)
3. Metabolic organ - 50% of the total resistance of the airway
- It secretes several hormones - Host defense
- Ex. Dopamine, Serotonin, Angiotensin - Secretes several inflammatory mediators,
immunoglobulins.
Volume: 4 Liters
Surface Area: 85 m2 PARANASAL SINUSES
Demonstrates functional unity - Frontal, Sphenoid, Ethmoid, Maxillary
Weight (Adults): approximately 1 kg - It lightens the skull
- For voice resonance
- In SINUSITIS, changes in voice may be evident.

LARYNX

- Opening from the oropharynx towards the

trachea
- Formed by:
- Epiglottis
- Arytenoids
- Vocal cords
RIGHT LUNG - Also acts as a gate/door towards the airway
- Divided into 3 LOBES (upper, middle, lower) - During swallowing, epiglottis closes (covers the
- 2 interlobular fissures: HORIZONTAL FISSURE larynx) so that the food will not enter the airway;
and OBLIQUE FISSURE

LEFT LUNG
- Divided into 2 LOBES (upper, lower)
- Divided by OBLIQUE FISSURE
- It has the LINGULA (part of the lungs where the 1
heart lies)

The lungs are covered by a thin membrane called

PLEURA.

JOHN LERY T. MENIANO I-C

LOWER AIRWAY - As it goes further down, it becomes the
BRONCHIOLES.

LOWER AIRWAY
- Undergoes dichotomous branching (divides
into twos)
- This tubular structure is composed of cartilage
and muscle
- Bronchi and bronchioles differ in:
- Size
- Cartilage
- Epithelium
- Blood supply

- Further down the line, once the bronchioles

- Any structures found BELOW the LARYNX is attach to the alveoli or the alveolar ducts, it now
considered LOWER RESIPIRATORY TRACT; forms the respiratory unit.
- ABOVE the LARYXNX is UPPER
RESIPIRATORY TRACT. RESPIRATORY UNIT (Gas Exchange Unit)
- The demarcation is the LARYNX. - It is where gas exchange occurs.
Composed of:
- Respiratory bronchioles
TRACHEA - Alveolar ducts
- Alveoli

- Those that are not attached to the alveoli or the

alveolar ducts, is called the conducting unit.
- Ex. trachea, main stem bronchus

CONDUCTING UNIT (Anatomic Dead Space)

- Only conducts air from the upper airways
towards the alveoli.
- Dead space because there is no gas exchanges
that occurs.
- 150 ml in adults

- Divides into several bronchi. TRACHEA divides 16x 2

- RIGHT and LEFT MAINSTEM bronchus After the 16th division, it becomes the
divides into SECONDARY bronchus RESPIRATORY UNIT.
TERTIARY bronchus It is now attached to the Respiratory Bronchioles
and Alveolar Ducts

JOHN LERY T. MENIANO I-C


the trachea down to the respiratory bronchus are
known as the CONDUCTING airways.
ALVEOLI
- Cartilage
- Neuroendocrine cells
- KULTSCHITZKY CELLS: secretes DOPAMINE
and SEROTONIN
- Responsible for the metabolic function of the
lungs, because it secretes dopamine and
serotonin.
BLOOD SUPPLY
1. PULMONARY CIRCULATION
- Pulmonary Artery: the ONLY artery that carries
UNOXYGENATED blood.
- Pulmonary Vein: carries OXYGENATED blood;
the blood vessel that comes from the lungs.
- Largest vascular bed in the body (70-80 m2)
- Dense capillary network
- At REST: each capillary has a volume is 70 ml
- During EXERCISE: it can span and open up, and
the volume can increase up to 200 ml.

2. BRONCHIAL CIRCULATION
- It is where gas exchange occurs. - 2 Bronchial Arteries
- Polygonal in shape. - Supplies the bronchi, bronchioles, blood vessels,
- Type 1 and Type 2 cells. nerves, lymph nodes and visceral pleura.
- TYPE1 CELLS - 1/3 of the blood returns to the atrium
- 96-98% of the surface area - Rest of the blood to the left atrium via the
- Thin cytoplasm pulmonary veins.
- Basement membrane fused with the capillary
endothelium INNERVATION
- When we breathe, our breathing is AUTOMATIC
TYPE2 CELLS and UNDER CNS CONTROL
Small and cuboidal - Autonomic Nervous system
Although they are more numerous that Type1 -
cells, they only cover around 2-4% of surface Parasympathetic stimulation:
area because they are small and cuboidal. BRONCHOCONSTRICTION

FUNCTIONS: Sympathetic stimulation:

Synthesize pulmonary surfactant BRONCHORELAXATION/DILATION
Repair of alveolar structures
Non-Adrenergic, Non-cholinergic Inhibitory:
Gas exchange occurs in the alveoli through a BRONCHODILATION
dense meshlike network of capillaries and alveoli
called ALVEOLAR-CAPILLARY NETWORK Non- Adrenergic, Non-cholinergic Stimulatory:
BRONCHOCONSTRICTION
The barrier between gas in the alveoli and the red
blood cell is only 1-2 m in thickness. CENTRAL CONTROL OF RESPIRATION
- It is like a white polygon provided with several - Automatic, rhythmic, and centrally regulated
RBCs; basement membrane, septum is not visible - VOLUNTARY control
because it is very thin. - But when you hold your breath, you can just hold
it for a period of time.
- LUNG INTERSTITIUM - BRAINSTEM: main control center
- Composed of connective tissues, primarily 3
fibroblast. MUSCLES OF RESPIRATION
- FIBROBLAST 1. At INSPIRATION
- COLLAGEN- limits lung distensibility - Principal Muscles:
- ELASTIN- for elastic recoil of the lung A. DIAPHRAGM

JOHN LERY T. MENIANO I-C

B. EXTERNAL INTERCOSTALS
- Accessory Muscles:
A. STERNOCLEIDOMASTOID
B. SCALENE MUSCLES
2. At EXPIRATION
- In ordinary quiet respiration, EXPIRATION is
purely PASSIVE. It is accomplished when the
muscles of inspiration relax.
- In forced expiration:
a. Rectus abdominis, oblique and transverse
muscles
b. Internal intercostals
Figure 371 shows the mechanism by which the
external and internal intercostals act to cause
inspiration and expiration. To the left, the ribs
duringexpiration are angled downward, and the
externalintercostals are elongated forward and
downward. As they contract, they pull the upper
ribs forward in relationto the lower ribs, and this
causes leverage on theribs to raise them upward,
thereby causing inspiration.
The internal intercostals function exactly in the
opposite manner, functioning as expiratory
muscles becausethey angle between the ribs in
the opposite directionand cause opposite
leverage. (Guyton and Hall , 2011)
MUCOCILIARY CLEARANCE SYSTEM
1. PERICILIARY FLUID
Secreted by the pseudostratified columnar
epithelium
2. MUCUS GLANDS
- Secreted by mucus and serous cells
Functions:
- To remove particles and particulate in the lungs
(protective function)
PULMONARY SURFACTANT
Secreted by Type2 pneumocytes
80% phospholipids: Dipalmitoyl Phosphatidyl
Choline (DPPC); ex.Lecithin
8% proteins
8% Neutral Lipids (cholesterol)
4 Surfactant Proteins: SP-A, B, C, D
Function: reduces surface tension inside the
lungs
SP-A
hydrophilic collectin,
Type II epithelial cells and clara cells
Required in the formation of tubular myelin
SP-B
Hydrophobic protein
Protein clipped from Type II cell
Optimize rapid absorption and spreading
of phospholipids
SP-C
Hydrophobic
Develops Airway during early gestation
Spreading of Phospholipids
SP-D
Hydrophilic
Type II Cells and Clara cells
Important in Host defense
Surfactant reuptake
Regulation of Surfactant pool
Induced Glucocorticoids and inflammation
Surface Tension: a force caused by water
molecules at the air liquid interface)
- Example: Raindrops. When it rains, the raindrop 4
reacts with the air; it forms surface tension
because the water molecules tend to adhere to
one another, forming a raindrop. That force that
JOHN LERY T. MENIANO I-C
makes them adhere to one another is the surface
tension.
- Inside the lungs, since it has fluids, surface
tension is present; and there is a high surface
tension if there is no pulmonary surfactant.

LAPLACE LAW

P= 2T P= pressure
r T= tension
r= radius
- The SMALLER the RADIUS (sphere), the
HIGHERER the TENSION is.
- It has a tendency to collapse towards the
X-ray picture: normal vs. collapsed lungs
LARGER sphere (radius).
white out lung

MECHANICS OF BREATHING
- How the lungs and the chest wall act together in
order for the air to enter the lungs.

BOYLES LAW
- At constant temperature, the volume of gas is
inversely proportional to pressure.
- Decreasing volume increases collisions and
increases pressure

K =PV
- It is true with the ALVEOLI. If there is a high P1V1 = P2V2
surface tension in one of the alveoli, it has a
tendency to collapse to the other alveoli.
- If all the alveoli have high surface tension, then
the lungs will collapse.
- Pulmonary surfactant reduces/decreases surface
tension; it makes the alveoli stable

PULMONARY SURFACTANT DEFICIENCY

- Respiratory Distress Syndrome (RDS)
- in the NEWBORN
- especially those who are delivered prematurely
(<36 wks) V= P ; V = P
- Pulmonary surfactant is not that mature, leading
to RDS.
- But some may already have mature surfactants
they can tolerate breathing. Imagine a sealed container which has a moving
piston. Inside the container are gas molecules that
- Severe lung injury (Pneumonia, Toxic gas are constantly moving. If you have a larger volume
inhalation) or larger area, the gas molecules will have less
5
- Can destroy surfactant, leading to RDS. collision because of the large area. The collision
- Toxic gas destroys the lung epithelium and forms the pressure. Since there is less collision,
surfactant, increasing surface tension inside the the pressure produced is also less.
lungs.

JOHN LERY T. MENIANO I-C

- When the volume is decreased, the area
becomes less and the molecules will have TWO STRUCTURE THREE COMPARTMENT
increased collision with each other, producing MODEL
more pressure. - If the lungs are removed from the chest wall
LUNGS
MUSCLES OF RESPIRATION [Manual: Resp4] - The lungs have the tendency to recoil inwards
At INSPIRATION- an ACTIVE process and collapse because of its structure.
- Principal Muscles:
A. DIAPHRAGM CHEST WALL
- major muscle for inspiration - Because of its structure (muscles, ribs), it has a
- a thin, dome-shaped muscle tendency to recoil outwards
- supplied by 2 PHRENIC NERVES from C3- C5
- When it contracts, it increases the vertical LUNGS AND CHEST WALL
dimension of the thorax and the transverse Oppose each others action
diameter. - When inside the chest wall, the chest wall will
During contraction, it pushes down the pull the lungs outwards, opening up the lungs; and
abdominal organs, increasing the vertical since the lungs are very elastic structure, it
diameter of the chest wall. prevents the chest wall from over expanding.
- As it contracts, it also pushes the ribs outwards, Lungs- visceral pleura; Chest wall- parietal pleura
increasing the transverse diameter of the thorax. = they are in close relationship with one other
- When the transverse and vertical diameter of the separated only by a very thin fluid known as
thorax is increased, volume of the thorax is also pleural fluid.
increased. - This opposing interaction between the parietal
and visceral pleura produces the
B. EXTERNAL INTERCOSTALS INTRATHORACIC/ INTRAPLEURAL
- Connects adjacent ribs PRESSURE.
- During inhalation, it moves the ribs upward and
forward
- It INCREASES antero-postero-lateral (AP-L)
diameter, increasing the volume of the lungs.
- Supplied by INTERCOSTAL NERVES
C. Levatores Constarum
D. Serruti Postini Superiores

- Accessory Muscles:
A. STERNOCLEIDOMASTOID
B. SCALENE MUSCLES
C. Pectoralis major, minor
D. Serratus anterior
E. Muscles that fix the shoulder girdle: levator
scapula, trapezius, rhomboids

At EXPIRATION- a PASSIVE process

- In ordinary/ normal quiet respiration,
EXPIRATION is purely PASSIVE. It is
accomplished when the muscles of inspiration
(diaphragm) relax.
- When it relaxes, it decreases the diameter of the
chest wall, decreasing its volume expiration
- In forced expiration: use of abdominal muscles
a. Rectus abdominis 6
b. Internal and external obliques
c. Transversus abdominis
d. Internal intercostals

JOHN LERY T. MENIANO I-C


INTRATHORACIC/ INTRAPLEURAL PRESSURE
- Created by the interaction of lungs and thorax
- -3 to -5 cmH2O (-4 to -6 cmH2O) =below
atmospheric pressure which is 0 cmH2O (760
mmHg)
INTRAPULMONIC/INTRA-ALVEOLAR
PRESSURE
Pressure inside the alveoli
- At the end of expiration, before the start of
inspiration, the intrapulmonic/intraalveolar
pressure is equal to atmospheric pressure.
- 0 cmH2O (760 mmHg)
TRANSMURAL PRESSURE
- Pressure changes across the lung and chest wall
- TRANSPULMONARY PRESSURE =
ALVEOLAR PRESSURE PLEURAL
PRESSURE
- VOLUME: the air that goes inside the alveoli
- Once the diaphragm contracts, VOLUME of the
CHEST WALL INCREASES.
- INTRAPLEURAL PRESSURE will DECREASE
- Subatmospheric (negative)
- INTRA-ALVEOLAR PRESSURE will DECREASE
- Once the glottis opens, the air now from the
atmosphere will rush in towards the lungs.
- As you decrease the pleural and alveolar
pressure, there is now flow of air inside the airway
and lungs.
- During mid-inspiration, the air that goes inside
the lungs will now begin to create/ increase the
intra-alveolar pressure because of the added air
inside the alveoli. It now begins to rise.
- Once it reaches zero (atmospheric pressure),
flow of air will now stop because there is no more
pressure gradient.
- Then, the muscles of inspiration (diaphragm) will
now relax, reducing the diameter thoracic cavity,
decreasing the volume, and further increases the
pressure inside the alveoli EXPIRATION.
COMPLIANCE: Static Lung Mechanics
- Measure of distensibility of matter and specifies
the ease with which matter can be stretched or
distorted.
- Or in other words, it measures the expandibility
of the lungs and thoracic wall
- Ex. stretching a rubber band
- The ease of stretching the rubber band is
COMPLIANCE.
- ability to return to its original state is 7
ELASTICITY
C = V V= change in volume
P P= change in pressure
JOHN LERY T. MENIANO I-C

- INVERSE of ELASTANCE
- ELASTICITY: ability to oppose stretch or
distortion and ability to return to its original shape
after distortion of an external force
3 Main Factors:
a. Elastic Fibers
- Elastin in the lung interstitium
- The geometry of the lung itself contributes its
own elasticity; nylon stocking LOWEST.
- When it is stretched, there comes a point where
it is already difficult to stretch.
- And when it is stretched, it is like polygonal in
structure.
- This contributes to the elasticity of the lungs.
b. Pulmonary Surfactant
- Decreases surface tension, making the lungs
easier to expand.
- Makes the lungs dry, lessening its surface
tension
c. Interdependence of alveolar sacs
- Polygonal in shape; attached to one another
- When one alveoli expands, it will be pulled by the
other alveoli; they are pulling each other
- Ex. basketball net. When you pull one side of the
net to open it, it will pull the others because of its
geometric configuration.
It is very difficult to measure compliance; it is not
done regularly; Intrapleural Catheter
INSPIRATORY curve and EXPIRATORY curve
are not equal =HYSTERESIS
The volume during expiration is greater than
during inspiration.
As pressure is increased, it is NOT directly
proportional to the volume that goes inside the
lungs; the graph is not linear.
Ex. Rubber balloon. Initially (at around 10
cmH2O), it is very difficult to inflate because the
lungs are somehow stiff. Then as it is continuously
inflated, it suddenly becomes easier to inflate
(between -10 -20 cmH2O). Just like in the lungs.
Until such time you can no longer inflate, thats the
time you will start expiration.
The compliance of the lungs is GREATER during
MID- INSPIRATION.
- During late inspiration, because of the pressure
built up inside the lungs, and during the beginning
of inspiration, the compliance of the lungs is at its
In EMPHYSEMA, elastic structures are destroyed,
hence it cannot return to its original form.
- That is why in a little increase in pressure, the
volume is very HIGH.
In FIBROSIS, the lungs are very stiff. So even at
high pressure, the volume is very LOW.
COMPLIANCE= STATIC Lung Mechanics (No air
inside)
DYNAMIC Lung Mechanics (Movement of air)
DYNAMIC LUNG MECHANICS
Factors of speed of airflow in the airways:
A. PATTERN OF GAS FLOW
1. LAMINAR
- Gas flows in parallel with the tubes
- Occurs during LOW-PRESSURE/ quiet breathing
2. TRANSITIONAL
- In large airways, the flow is still laminar (pressure
is low), but at the branching points, that is where
transitional flow occurs.
- There is disturbance of flow at the corners. 8
- It is not purely laminar.
JOHN LERY T. MENIANO I-C
 CASE: Bronchiolitis
- Inflammation of bronchioles.
- Radius of the tubes decreases, increasing the
resistance.
- If there is very high resistance, air cannot go
inside the lungs.
3. TURBULENT
CASE: Asthma
- Occurs when there is high flow/ HIGH - There is bronchoconstriction (airways become
PRESSURE smaller)
- Ex. during exercise, flow of air is turbulent - radius = resistance = flow of air

REYNOLDS NUMBER

POISEUILLE EQUATION FOR LAMINAR

FLOW - The flow is TURBULENT if the Reynolds
number is > 2,000

B. AIRWAY RESISTANCE

pressure, radius = flow

viscosity, length = flow
V= flow
P= pressure difference
r= radius
n= viscosity
l= length of tubes
- The FLOW is DIRECTLY PROPORTIONAL to
PRESSURE.
- The higher the pressure, the greater the flow.
- The bigger the radius, the higher the flow.
- The lower the viscosity and the shorter the tubes,
the higher the flow.

RESISTANCE
- Point of HIGHEST RESISTANCE is at the
segmental bronchi or the MEDIUM-SIZED
AIRWAYS.
- The smaller tubes (bronchioles) work in parallel,
so the resistance is decreased.
viscosity, length = resistance - Ex. 3 + 3 + 3 = 9 (SERIES)
radius = resistance 1/3 + 1/3 + 1/3 = 1 (PARALLEL)
- That is why smaller airways have smaller 9
- Resistance is the inverse of flow. resistance than medium-sized airways.
- The higher the viscosity and the longer the tube, - During normal quiet breathing, the point of
the greater the resistance. highest resistance is at the medium sized airways.
- The smaller the radius, the higher the resistance.

JOHN LERY T. MENIANO I-C

- During EXERCISE, some books say that the AIR IN THE LUNGS
highest resistance is at the largest airways.
- Because during exercise, there is increased flow,
making it turbulent, making it the highest point of
resistance.

[BERNE & LEVY]

- From Poiseuille's equation, one might conclude
that the major site of airway resistance is in the
smallest airways. In fact, however, the major site
of resistance along the bronchial tree is the large
bronchi.
- The smallest airways contribute very little to the
overall total resistance of the bronchial tree. The
reason for this is twofold.
- First, airflow velocity decreases substantially as
the effective cross-sectional area increases (i.e.,
flow becomes laminar).
- Second and most important, the airway
generations exist in parallel rather than in series.
The resistance of airways in parallel is the inverse Tidal Volume (TV)
of the sum of the individual resistances; therefore, - Volume of air inspired and expired during normal
the overall resistance of the small airways is very quiet breathing. (500ml)
small.
Inspiratory Reserve Volume (IRV)
Factors for Airway Resistance
- Extra volume of air that can be inspired beyond
1. Lung Volume tidal volume. (3200ml)
- GREATER VOLUME = LOWER RESISTANCE
- Alveoli. Bronchioles are located in between the Expiratory Reserve Volume (ERV)
alveoli. - Extra volume of air after a forceful expiration and
- Once you inhale/ expand the lungs/ increase the tidal expiration. (1100ml)
volume:
- Alveoli will try to pull each other because of their Residual Volume (RV)
interdependence. - Volume of air left in the lungs after forceful
- Since the bronchioles are located in between, the expiration. (1200ml)
walls of the bronchioles will also be pulled open. - Cannot be measured by the spirometer
- When they collapse, the alveoli will also close. *Addition of volumes = CAPACITY
2. Neurohumoral Regulation Total Lung Capacity (TLC)
- Maximum volume that each lung can be
expanded with greatest possible effort.
CASE: Asthma - TLC = IRV + TV+ ERV + RV
- Bronchodilators are given
- 2 agonists (stimulates sympathetic system) Vital Capacity (VC)
- Maximum amount of air that can be expelled
after maximal inspiration.
- It is the volume from maximal inspiration towards
the forceful expiration.
- VC = IRV + TV + ERV

Inspiratory Capacity (IC) 10

- Amount of air that can be maximally inspired
after the tidal inspiration.
- IC = TV + IRV

JOHN LERY T. MENIANO I-C

Functional Residual Capacity (FRC)
- Amount of air remaining in the lungs at the end of
normal expiration.
- FRC= ERV + RV

- Cannot be measured also by the spirometer

because of the residual volume.

Timed Vital Capacity/ Forced Expiratory

Volume in 1 Second (FEV1)
- Amount of air expired by forceful expiration in 1
second.
- 80-85% of Vital Capacity

3 Most Important Volumes and Capacities:

1. Tidal Volume (TV)
- The normal quiet breathing

2. Residual Volume (RV)

- Provides air to aerate lungs in between breathing
- Because when it is totally collapsed, it is very
difficult to inflate.

3. Vital Capacity (VC)

- Factors affecting vital capacity:
a. Position
b. Strength of muscles
c. Compliance

WORK OF BREATHING
Work = pressure x change in volume

- Required to overcome elastic and flow resistive

properties of the lungs.
- Changes in the mechanical properties of the lung
or chest wall or both INCREASES work.
- Ex. Fibrotic Lungs (lungs are stiff). There is
increase in the work of muscles which may lead to
fatigue.
- Ex. Asthma, Bronchiolitis. There is increased
resistance. In order to increase the flow, work
should also be increased.
- Increased work may lead to fatigue respiratory
failure

11

JOHN LERY T. MENIANO I-C

RESPIRATORY PHYSIOLOGY II
Ventilation
Process of transporting air from the atmosphere
into the alveoli and lungs
Diagram of airway
Conducting zone - Trachea to terminal
bronchioles; 16 divisions
Anatomic dead space = 150mL
Respiratory Zone - airways attached to alveoli;
gas exchange
Total cross sectional area and airway
generation
Graphs showing the airway generation and the
total cross section areas.
From the trachea down to terminal bronchioles
(conducting zone).
The total cross area is about the same.
When it reaches the respiratory zone, the total
cross area increases.
Because you have two zones, you have two
ways to move the air
Convection
Conducting zone
Force that pushes the water down
Forward velocity
Once it reaches respiratory zone, forward
velocity
decreases because of the large cross sectional
area
Diffusion
Respiratory zone
Total (Pulmonary) Ventilation
Total amount of air that enters the lungs
Measure by collecting all the expired gas over a
given time
Tidal volume = volume of air you breath in and out
during normal quiet breathing (tidal breathing); 12
normal is 500mL (average) for adult
Example 500mL * 15 = 7,500 mL/min total
ventilation
JOHN LERY T. MENIANO I-C
 Not all participates in gas exchange because
some are located in the anatomic dead space
Alveolar Ventilation
Volume of air that reaches the alveoli
500mL - 150mL * 15 = 5,250 mL/min alveolar
ventilation
Anatomic Vs. Physiologic Dead space
Good gas exchange depends on pulmonary
blood flow or perfusion.
So ventilation should be equal to that of blood
flow, BUT WAIT, each capillary has only 70mL at
rest (200mL during exercise), so there is abig
discrepancy between ventilation and blood flow.
Pulmonary circulation is the only vascular bed Example
that receives the wholecardiac output. CO from
the heart to pulmonary circulation is about 5L.If
you look at the ventilation and blood flow, it is
around 5L, too,so theyre about equal. Ventilation
and pulmonary perfusion is almostequal allowing
good gas exchange and blood flow.
Alveolar Ventilation rate
Example
TV = 600mL
RR = 20/min
Dead space = 150mL
What is the rate of your alveolar ventilation,
9,000mL/min
Measurement of Alveolar Ventilation
Alveolar ventilation is directly proportional to
Vco2 (volume of
exhaled CO) per unit of time
Alveolar ventilation is inversely proportional to
Pco2 (partial pressure
of CO) in the blood
CNS injury - had hypoventilation accumulation
of CO increased pCO acidosis increase
in ventilation like
ambubaging (manual bag breathing) to eliminate
CO
Increase ventilation decrease pCO
Arterial CO is almost equal to alveolar CO
Double the ventilation and the pCO is halved; if
you decreaseventilation by half you double the
pCO
Regional differences in ventilation
Most dependent area has greater ventilation
Upright position - base of lungs
Supine position - posterior part of the
lungs, because of the gravity
13
Example
Apex, V=2, Q=1, V/Q = 2
Base, V=1, Q=2, V/Q = 0.5
JOHN LERY T. MENIANO I-C
 CNS injuries (hypo, hyper ventilation)
Variations in the V/Q ratio Hypoxemia stimulated aortic and carotid
V/Q mismatch = hypoxemia bodies respond to changes in blood O
V/Q = zero levels
Acidosis (metabolic acidosis - decreased
No alveolar ventilation HCO compensation by decreasing pCO,
Might be because of blockage (a mucous increasing pH tachypnea especially if
plug), foreign body aspiration that completely prolonged
blocks trachea
Lungs under atelectasis Problem in the lungs, kidneys will
compensate. Problem in the kidneys,
Low V/Q ratio lungs will compensate
Most of the small bronchioles are obstructed Hypotension
Mucous plugging caused by infection
decreases V/Q ratio
Partial obstruction decrease ventilation, Transport of Gases
continuous blood flow
Gay Lussac or Charles Law
V/Q = infinity
No capillary blood flow If the pressure of a given quantity of a gas remains
Blood flow is blocked, ventilation is continuous constant thevolume of a gas increases in directly
Cardiovascular anomalies proportional to its absolute temperature

High V/Q Temperature and volume changes

Some of the capillaries are destroyed with
continued ventilation Increase temperature increase molecular
Increasing ventilation, decreased perfusion activity increase volume

Hypoventilation
Decreased or insufficient volume of air that Ideal gas law
enters the alveoli

Effects
Poor oxygenation of blood
CO retention Those variables:
Respiratory acidosis
n = quantity of gas
Causes R = constant
CNS infection/injury T = temperature
Immerse in very cold water P = pressure in mmHg
Decreased temperature hypoventilation V = volume (liters)
because of pooroxygenation Combination of Boyles and Charles Law
Anesthetize
Vapor Pressure of Water

Hyperventilation All gaseous mixtures are saturated

Increase in ventilation in excess of what is with water vapor
required Vapor pressure and HO depends on
the temperature of water and gases
Effects Higher temperature = greater
Low pCO molecular activity
Respiratory alkalosis Water vapor pressure at 37C (sea 14
level) = 47mmHg
Causes
Anxiety (like thinking about those damn Solution of Gases in Water
shiftings)

JOHN LERY T. MENIANO I-C

Factors affecting solubility of gas in water at
equilibrium
Pressure of the gas surrounding the water
Solubility coefficient of the gas in water at
its temperature
The greater solubility coefficient, the gas is
more soluble
than others
body will absorb it and will go to the
pneumothorax
pressure of O in the pneumothorax will
increase
N and CO will decrease excess O in the
pneumothorax will be absorbed by the body
Diffusion

Movement of air across respiratory membrane

towards the capillaries

Example of solubility coefficient of gases at 37C Diffusion of Gases

O = 0.024 From area of high concentration to a
CO = 0.57; more soluble low concentration
N = 0.012 From high pressure to low pressure
He = 0.008 Pressure gradient or diffusion gradient
- difference between twopressures

Partial Pressure of Gases

Daltons Law

The total pressure exerted by a gas mixture is

equal to the sum
of the pressures of the individual gases (plus Respiratory Membrane
water vapor)
Major component:
Pb = 760mmHg (sea level) = pHO (47mmHg)
+ pO Fluid lining of the alveolus with the
(149.2mmHg) + pN (563.5mmHg) + pCO surfactant
(0.3mmHg) Alveolar epithelium
Epithelial basement membrane (BM)
Interstitial space between alveolus and
Pneumothorax capillary
Capillary BM
Air in the thoracic cavity. Capillary endothelial membrane
Large amount of air tension pneumothorax 0.3 m - size of respiratory epithelium
pushes
lungs to the contralateral side as well as the
mediastinal Ficks Law
structure.

Removing the air - definitive treatment for

pneumothorax expands lungs

Not all pneumothorax are caused by puncture in

the
chest wall: Continuous coughing rupture the
perivascular sheath air will go out of the pleura
15
(minimal amount of air)

Minimal or moderate amount of air gives 100%

O

JOHN LERY T. MENIANO I-C

 20x faster than O
Average adult at rest - 400-500mL/min

Volume of gas per given minute or diffusion is

directly proportional to

A=Area
Surface area of lungs/alveoli = 80m
Increase area, increase diffusion of gas
T = thickness (respiratory membrane) is inversely
proportional to diffusion

When the thickness is thin = greater diffusion

Thick = lesser diffusion
During cases of pneumonia
Impaired diffusion of gas
Decrease O level in blood

Fibrosis
Interstitial space thicken affects diffusion
Low O = hypoxemic
(P1-P2) is pressure difference/pressure
gradient; the greater thedifference, the greater the
diffusion
D is the diffusion coefficient, square root of MW;
which is directlyproportional to solubility coefficient
Uptake of O
RBC, when they go the the lungs (0.75 of a
second), during the firstthird (0.25 of a second) the
blood is already saturated with O
Indication: during exercise, blood flow to the
lungs will decrease to around 0.25 of a second. If
normal lungs, before 0.25, blood is already
saturated with O

The higher the solubility coefficient, the greater the

diffusion Interstitial lung disease or when respiratory
CO diffuses more than O membrane is thickened slow diffusion
Square root of the molecule weight is inversely
proportional to Abnormal: saturated at the end of transit time
diffusion, so the bigger the MW the lower the
diffusion If decrease transit time blood will go out of
the lungs still notsaturated with O
Factors influencing Diffusion With chronic pulmonary disease, patients
Thickness of membrane prefer to sit and lie down because they cannot
Surface area of membrane tolerate to walk, climb stairs, exercise, or exert
effort
Diffusion coefficient
Pressure gradient
High altitude O pressure decreases at around
Capillary blood volume 50 diffusion slows down deprived O
Capillary diameter
O and CO diffusion
Diffusing capacity of the Respiratory
Membrane Pulmonary artery carries unoxygenated blood
Pressure of O in unoxygenated blood is
Volume of gas will diffuse each minute for a around 45mmHg
pressure gradient of 1mmHg 16
When it enters the lungs, O will diffuse towards
Diffusing capacity of oxygen the blood (via
Average adult - 21mL
pressure gradient).
Diffusing capacity of CO

JOHN LERY T. MENIANO I-C

As the O in the blood travels, the pressure is
around 95-98mmHg

When it reaches the tissues, the partial pressure

of O in the tissuesis around 40mmHg with a
pressure difference of ~55mHg whichmeans that
O will diffuse towards the tissues.

CO in the tissues as the blood enters the

tissues, exposed to CO increase pCO O
dissociation curve will shift to the right activity of
O to the blood decreases decrease affinity of
O to theblood release of O in the tissues
(Bohr effect)

Unoxygenated blood (carrying CO with a

pressure of 45mmHg), willadditionally bind CO in
pressures of 46mmHg from other tissues.

The blood will go back to the lungs where

pressure of CO in the lungs is 40mmHg, once
it reaches the lungs, CO will be eliminated

Unlike O, CO has no pressure difference, if

there is such, it isslight (5mmHg pressure
difference between blood and lungs).

CO can be transferred and be eliminated in the

lungs because COhas greater solubility
coefficient (it diffuses fasters than O)
Even if there is no pressure difference at all, CO
can still diffuse tothe blood and be carried in the
lungs and be eliminated

17

JOHN LERY T. MENIANO I-C

RESPIRATORY PHYSIOLOGY III
BLOOD FLOW MECHANICS
Blood flow begins at the pulmonary artery
Pulmonary artery accompanies the
bronchus and they divide together until
they reach the terminal bronchioles
Once they reach the terminal bronchioles,
they become the pulmonary capillaries
Pulmonary vein surrounds your pulmonary
vessels and as these vessels coalesce,
the pulmonary vein is formed
Pressures between the pulmonary and
systemic circulation:
Systemic pressure is at least ten times higher than
the pulmonary pressure
Because the pulmonary blood vessels
have thinner walls with more smooth
muscles unlike in systemic circulation
where the vessels are thicker and more
muscular
Systemic circulation also has arterioles which
contain a large amount of smooth muscles
When you're running or exercising, you need more
blood in the lower extremities such as the legs and
these arterioles regulate blood flow to these parts
Pulmonary circulation is the only vascular
bed which receives the entire cardiac
output so the pressure must be low
enough to allow easier transport of blood
from the ventricles or else the right part of
the heart will have a difficult time in
pushing blood towards the pulmonary
circulation
Pulmonary vessels
Surrounded by gas
Contained inside the alveoli
Gas affects the blood vessels (alveolar
pressure affects pulmonary vessels)
2 types of pulmonary vessels exist:
Alveolar vessels, which are located at the
septum, and once the alveolar pressure increases,
it will compress the alveolar vessels. So
effectively, they are affected by the pressures
surrounding them.
Extra-alveolar vessels, which are exposed to a
pressure less than alveolar, and are pulled open
by the radial traction of the surrounding
parenchyma, increasing its calibre
Pulmonary Vascular Resistance
Vascular resistance = (input pressure - output
pressure) / blood flow
If you increase the pressure, resistance increases
Increase the resistance, blood flow will decrease.
This is true only for the systemic circulation
In pulmonary circulation this is not true due to thin-
walled property and lack of smooth muscles
Recruitment and Distension
If you increase the pressure through recruitment,
the resistance decreases and some of the
pulmonary vessels will open up
Just like your small airways, these capillaries work
in parallel and somehow function as one big tube
As you recruit more vessels, resistance further
decreases
In distension, when the pressure increases,
instead of opening up the other vessels, they
dilate the existing vessels, increasing the caliber
and resistance also decreases
These two mechanisms (recruitment and
distension) work hand-in-hand
During inspiration, there is no plugging of the
vessels so resistance is still high. But once you
inhale, extra-alveolar vessels will pull the walls of
the blood vessels through traction
If you increase the lung volume, you decrease the
resistance
Even if the capillaries are thin-walled, they are still
elastic. There will come a time where the
maximum elasticity is reached and the resistance
again decreases.
Measurement of blood flow
Fick's principle governs blood flow:
Oxygen consumption per minute is equal to the
amount of oxygen taken up by the blood in the 18
lungs per minute
Distribution of blood flow
Organs with greater areas have greater blood flow
The base of a structure has greater blood flow
JOHN LERY T. MENIANO I-C
Similar to ventilation, the most dependent portion
has the greatest ventilation
Chiefly due to gravity
Different Zones of Perfusion
Zone 1: No blood flow during all portions of the
cardiac cycle because the local alveolar capillary
pressure in that area of the lung never rises higher
than the alveolar air pressure during any part of
the cardiac cycle. (Alveolar Air Pressure >
Arterial Pressure)
Zone 1 Blood Flow Occurs Only Under
Abnormal Conditions.
Zone 1 blood flow, which is blood flow at
no time during the cardiac cycle, occurs
when either the pulmonary systolic arterial
pressure is too low or the alveolar
pressure is too high to allow flow. For
instance, if an upright person is breathing
against a positive air pressure so that the
intra-alveolar air pressure is at least 10
mm Hg greater than normal but the
pulmonary systolic blood pressure is
normal, one would expect zone 1 blood
flowno blood flowin the lung apices.
Another instance in which zone 1 blood
flow occurs is in an upright person whose
pulmonary systolic arterial pressure is
exceedingly low, as might occur after
severe blood loss. (Guyton and Hall,
2011).
Zone 2: Intermittent blood flow only during the
pulmonary arterial pressure peaks because the
systolic
pressure is then greater than the alveolar air
pressure,
but the diastolic pressure is less than the alveolar
air pressure.
Zone 3: Continuous blood flow because the
alveolar
capillary pressure remains greater than alveolar
air
pressure during the entire cardiac cycle.
Active control of circulation
Decrease alveolar PO2
Pneumonia, atelectasis: For instance, a part of
your lungs becomes atelectatic. The lungs will
collapse due to absence of oxygen (hypoxic
pulmonary vasoconstriction)
Blood flow now will be going to the normal or
healthy part of your lungs, so you will still have a
normal V/Q ratio. This is a protective function of
the lungs. If ventilation-perfusion occurs at the
damaged or atelectatic part of the lungs, there will
be V/Q mismatching, perfusion will be higher than
ventilation (not good!)
Inversely, if you increase PO2, vasodilatation will
occur.
This is important during fetal life because during
the first breath of the baby, the lungs will now
open up, oxygen will rush in, alveolar PO2 will
increase, pulmonary vasculatures will dilate and
begin pulmonary circulation. If this does not occur,
high pulmonary pressures will lead to deleterious
effects.
Chemical mediators (absence of these will
result to V/Q mismatching):
Catecholamines
Histamine 19
Angiotensin
Prostaglandins
JOHN LERY T. MENIANO I-C
Pulmonary vascular endothelium HgbS (sickle hemoglobin, Val in the beta chains,
Secretes endothelin shrinked hemoglobin results to hypoxemia).
Vasoconstriction
Combination of O2 with Hb
Nitric oxide Oxygen-hemoglobin dissociation curve
Increase in [BPG] during hypoxia
Causes vasodilatation by synthesis of cyclic GMP Factors may shift the curve to the right or left
NO: normal level is 20 ppm
Toxic at high doses!
In cases of chronic lung disease, chronic
hypoxemia and hypoxia, chronic pulmonary
hypertension, chronic pulmonary vasconstriction,
NO is administered (particularly in Europe)

Metabolic functions of hormones and their

fates:
Peptides:
Angiotensin I converted to Angiotensin II by ACE
Angiotensin II unaffected
Vasopressin unaffected
Bradykinin up to 80% inactivated

Amines:
Serotonin almost completely removed
Norepinephrine up to 30% removed
Histamine and Dopamine unaffected
Arachidonic acid metabolites: Transport of CO2 in the blood
Prostaglandins E2 and F almost completely
removed Same as oxygen, can be dissolved in the plasma
Prostaglandin A2 unaffected Carbaminohemoglobin CO2 bound to Hgb
Prostacyclin (PGI2) unaffected Cabonic anhydrase converts CO2 and water to
Leukotrienes almost completely removed carbonic acid
Majority of carbon dioxide is transported as
Filtration action for the blood bicarbonate
As blood flows to these capillary networks, it is Chloride shift (Hamburger shift) movement of Cl-
somehow filtered ion from the plasma towards the inside via
diffusion
Transport of oxygen in the blood
2 forms of O2 in the blood
Combined in the plasma (dissolved state) : 1-3 L
Combined with Hgb as HbO2
Concentration of Hgb: 14-15 g/100mL of blood
1 Hgb molecule: 4 O2 molecules
1 gram of Hgb: 1.34 mL of O2

Combined or Dissolved
Henry's Law
The amount of dissolved gas is proportional to the
partial pressure
0.003 mL O2 / 100 mL of blood or 0.003 vol%
100 mmHg of O2 : 0.3 mL / 100 mL of blood
Oxyhemoglobin 20
HgbA (adults) optimal form of Hgb
HgbF (fetal hemoglobin, high affinity for oxygen so
fetuses cannot utilize oxygen because it is tightly
bound to hemoglobin)

JOHN LERY T. MENIANO I-C

CO2 and O2 have different binding sites: Control system
Bohr and Haldane effect Voluntary system
Cerebral cortex
Corticospinal tract
Automatic system
Pons and medulla
Respiratory motor neurons in the lateral and
ventral portions of SC

Central controller
Medullary respiratory center
Dorsal inspiratory area
Rhythm of ventilation
Inhibited by impulses from pneumotaxic center
Vagal and glossopharyngeal nerves
Ventral expiratory area
Normally inactive
Apneustic center
Tissues: Bohr effect Lower pons
Lungs: Haldane effect If transacted inspiratory gasps or Apneustic
Significance: Most of the CO2 are taken by the Seen in severe brain injury
RBC Pneumotaxic center
Upper pons
Inhibits respiration
CO2 Dissociation Curve: Regulates respiratory volume
CO2 may be carried as dissolved, bicarbonate, fine tuning
and carmabinohemoglobin forms CO2 dissociation
curve is steeper and more linear than O2 Sensory receptors
dissociation curve CO2 curve is right-shifted by Central chemoreceptors
increases in SO2 Ventral surface of the medulla near the 9th and
10th CN
Regulation of Respiration Changes in H ion in CSF

Governed by the:
Condition of CSF
Local blood flow
Local metabolism
Peripheral chemoreceptors
Carotid bodies
Aortic bodies
Responds to:
Decrease PaO2 & pH
Increase in PaCO2 (less important than
central receptors)

Lung and other receptors

Pulmonary stretch (inflation and deflation)
Basic elements of respiratory control receptors
Central controller (pons, medulla, other parts of Within the smooth muscles
the brain) Inflation of the lung: slowing of RR 21
Effectors (output, Deflation: initiate respiratory activity
(missing) Hering-Breuer reflex

JOHN LERY T. MENIANO I-C

Irritant receptors Functions of the respiratory center
Between epithelial cells Coordinates activity of respiratory muscles
Stimulated by: Regulates frequency of respiration
Noxious gases Regulates strength of respiration
Cigarette smoke Controls rate and depth of breathing
Dust and cold air
Nervous stimuli of respiration
Vagus nerve Cortical origin
Bronchoconstriction and hyperpnea Voluntary control
Breath holding is possible but notindefinite
J-receptors Increased levels of PaCO2 stimulates
Alveolar walls close to capillaries respiratory center
Juxta-capillary or J-nerve
Neurogenic stimuli of visceral origin
Stimulated by: Cough reflex
Engorgement of the pulmonary capillaries Cessation of respiration, closure of the
Increases in interstitial fluid in the alveolar glottis and bronchoconstriction
wall Swallowing reflex
Hering-Breuer reflex
Other receptors outside the lungs Thoracic chemoreflexes (Bezold-Jarisch
Nose and upper airway receptors reflex)
Hypoventilation, hypotension, bradycardia
Nose
Nasopharynx
Neurogenic stimuli of somatic origin
Larynx Reflexes from joint
Trachea Back and forth motion of a limb
Increased ventilation in exercise
Responses: Effect of pain
Sneezing Effect of temperature
Coughing Increase in temperature increases
Bronchoconstriction ventilation
Warming of medullary centers
Joint and muscle receptors
Proprioceptors can stimulate respiratory Chemical stimuli of respiration
centers
Increase in PaCO2
Gamma system
Intercostal muscles and diaphragm Most important factor for control of ventilation
Main stimulus is from centralchemoreceptors
Arterial baroreceptors Additional stimulus from peripheral receptors
BP causes reflex hyperventilation
Severe cases lead to apnea through the Decrease in PaO2
carotid and aortic sinuses Stimulates aortic and carotid bodies
Pain and thermoreceptors No effect on central chemoreceptors
Causes apnea followed by Prolonged hypoxemia may cause MILD cerebral
hyperventilation acidosis stimulating ventilation
Increased temperature leads to
hyperventilation Response to pH or increase in [H+]
Hypothalamic thermostat Decreased pH, increased [H+]
stimulatesventilation
Site is peripheral receptors
Severe acidoses BBB becomes partly permeable 22
to [H+]
Maximal stimulation of chemoreceptors by lack of
O2 is only 65%

JOHN LERY T. MENIANO I-C

Increased CO2 and [H+] are more powerful stimuli Inspiratory center stimulates inspiratory muscles
CO2 can increase ventilation by 900% and
acidosis by 400% Inspiration resumes
Maximum increase in ventilation is reached when
PaCO2 is 9%
Coma at 20-30% Respiratory Changes in Health
Anesthesized at 30-40
Death at 40-50% Forced Expiration

Hering-Breuer Reflex

Components:
Sensory receptors stretch and deflation
Sensory afferent neurons vagus nerve
Respiratory center (DRG)
Efferent neurons phrenic and intercostal nerves
Effectors inspiratory muscles

Inspiration
Stimulates inflation receptors

Inhibitory impulses through vagus nerves
Inhibition of respiratory center cuts impulses to
respiratory muscles

Expiration stimulates deflation receptors Effects of Exercise
Excitatory impulses through the vagus Increase demand for O2
Excitation of the respiratory center Increase CO2 production
Increase respiratory rate
Contraction of inspiratory muscles Motor cortex sends impulses to respiratory center
Body movements stimulates proprioceptors
Double Vagotomy Increased body temperature stimulates respiratory
center
Abolishes Hering-Breuer reflex Increased CO2 stimulates respiratory center
Results to slower and deeper breathing
Still rhythmic due to the activity of pneumotaxic Increase diffusing capacity of O2
center
Inhibits respiration and allows expiration Increases 3 times
Opening of dormant capillaries increases area of
Mechanisms of rhythmicity after double diffusing membrane
vagotomy: Dilatation of pulmonary capillaries
Opening up of previously collapsed alveoli
Active Dorsal Respiratory Group (DRG) Blood is fully saturated with O2 despite rapid flow
Stimulates inspiratory muscles and pneumotaxic
center

Pneumotaxic center stimulates expiratory center
Inhibits inspiratory center

Cuts off impulses to inspiratory muscles and
pneumotaxic center
23
Pneumotaxic center ceases to stimulate the
expiratory center

No inhibition of inspiratory center

JOHN LERY T. MENIANO I-C

More O2 is given off per 100 mL of blood
Muscles utilize O2 fast
Decrease interstitial PO2 to as low as 15mmHg
Increase pressure gradient
O2 diffuses approximately 15 mL/ 100 mL of blood

High-altitude

Acute mountain sickness

Headache
Fatigue
Dizziness
Palpitations
Insomnia
Loss of appetite

Oxygen toxicity
Pulmonary edema
Decreased vital capacity secondary to atelectasis
Premature babies retrolental fibroplasia

Absorption Atelectasis
Decompression Sickness
Caused by the formation of N2 bubbles during
ascent from a deep dive
May result in pain bends and neurological
disturbances
Can be prevented by a slow, staged ascent
Incidence is reduced by breathing a helium-
oxygen mixture

24

JOHN LERY T. MENIANO I-C

Hypoxia Cheyne-Stokes Breathing

Decreased O2 or inadequate O2 to the tissues

4 types:
Hypoxic hypoxia/hypoxemia low PO2 in the
blood
Low PO2 and Low O2 content
Deficiency of oxygen in the atmosphere
Hypoventilation
Uneven distribution of alveolar gas and/or
pulmonary blood flow
Diffusion impairment
Venous to arterial shunt
Anemic hypoxia low carrying capacity of blood
for O2
Normal PO2 and Low O2 content
Anemia, deificient hemoglobin
Carbon monoxide poisoning
Circulatory (ischemic) hypoxia low blood flow
Normal PO2 and Normal O2 content
General or localized circulatory
insufficiency
Tissue edema Apnea
Abnormal tissue demands Absence of spontaneous breathing
Histotoxic hypoxia/anoxia inability of cells to
utilizeO2 Peripheral

Normal PO2 and Normal O2 content

Poisoning of cellular enzymes so they Central
cannot use the available oxygen (e.g.
cyanide poisoning)
centers
Terminologies:
Apnea cessation or absence of spontaneous
breathing Acid-Base Balance
Dyspnea difficult breathing Decrease rate of ventilation = increase
Hyperpnea increase in depth of breathing CO2, carbonic acid and [H+]
Tachypnea rapid breathing Excessive ventilation = decrease CO2,
Orthopnea dyspnea when lying down [H+]
Cyanosis bluish discoloration of skin; if > 5 High [H+] in metabolic acidosis increases
grams % of deoxygenated blood ventilation thus decreasing CO2 and [H+]
Asyphxia anoxia combined with increase PCO2 High pH decreases ventilation >
in the blood and tissues accumulation of CO2 increasing [H+]
Normal blood pH is 7.35 7.45
Periodic Breathing
Deep breathing followed by apnea
Cheyne-Stokes breathing
Due to:
Delay in the transport of blood to the brain
Severe cardiac failure

Increased negative feedback gain 25

JOHN LERY T. MENIANO I-C

1. Look at the pH number on your
results. The pH level in a healthy
human should be between 7.35 to 7.45.
Your body is constantly striving to keep
pH in balance.
If the pH level is below 7.35, then the
condition of acidosis is present,
indicating a buildup of carbonic acid in
the blood
If the pH level is above 7.45, then the
condition of alkalosis is present, which
indicates a buildup bicarbonate (bases)
in the blood.
2. Examine the PCO2 number on your
report. This number is the amount of
carbon dioxide in the blood. It is the
respiratory component in acid-base
balance. It is measured in millimeters of
mercury (mmHg). The normal level for
PCO2 is between 35 to 45 mmHg.
The condition of respiratory alkalosis is
present if the PCO2 number is below 35
mmHg. This means there is too little
carbon dioxide in the blood. A person
with this condition can be breathing very
fast (hyperventilating).
The condition of respiratory acidosis is
present if the PCO2 number is above 45
mmHg. There is too much carbon
dioxide in the blood. A person with this
condition can be confused or restless
and have a low heart rate.
3. Check your blood gas report for the
bicarbonate (HCO3) level. It is the
renal component in the acid-base
balance. The normal level for these ions
is between 24 to 26 MilliEQuivalents Per
Liter (mEq/L)
An HCO3 level is below 22 mEq/L
indicates metabolic acidosis. The body
cannot produce enough bicarbonates to
keep up with the carbonic acid in the
blood. It can be caused by many
conditions including dehydration and
kidney disease.
An HCO3 level above 26 mEq/L
indicates metabolic alkalosis. There are
too many bicarbonates in the blood. A
common cause is hyperventilation, but it
is also seen in many other conditions
including Cushing's disease and long
term steroid therapy.
4. Determine whether there is
compensation for the pH imbalance.
Generally, the pulmonary and renal
systems compensate for each other to
return the pH to normal. The lungs will
compensate for metabolic instability by
changing CO2 excretion and the
kidneys will compensate for the
respiratory instability by altering
bicarbonate retention and H+ secretion.
To look for compensation in respiratory
acidosis ( pH, CO2), look at the
HCO3 values. There is compensation
when the HCO3 level is increased
(excess hydrogen is excreted in the
urine in exchange for bicarbonate ions,
therefore making the blood more
alkaline). However, in respiratory
alkalosis (pH, CO2), there is
compensation when the HCO3 level is
decreased (the renal excretion of
bicarbonate increases to retain the
hydrogen ions, therefore, making the
blood more acidic).
To look for compensation in metabolic
acidosis (pH, HCO3), look at the
PaCO2 levels. There is compensation
when the PaCO2 level is decreased
(due to hyperventilation, thereby raising
the blood's pH value, making it more
alkaline.) However, in metabolic
alkalosis (pH, HCO3), there is
compensation when the PaCO2 level is
increased (due to hypoventilation,
therefore decreasing the blood's pH
value, making it more acidic)
5. Inspect the PO2 number in your
blood gas test results. This is the
amount of oxygen that is dissolved in
the blood. The normal PO2 level should
be between 80 to 100 mmHg. If they are
below limits, there is evidence of
hypoxemia, therefore, no compensation
is done to restore the pH balance.
6. Finally, evaluate the diagnosis of
your ABG reading
26
I CAN DO ALL THINGS THROUGH CHRIST WHO
STRENGTHENS ME. (Philippians 4:13)
THE TESTING OF YOUR FAITH PRODUCES
PERSEVERANCE. (James 1:3)
JOHN LERY T. MENIANO I-C