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RESPIRATORY PHYSIOLOGY
Jessamine C. Dacanay, MD, FPCP, DPCCP
Respiration
 Inspiration  active process; needs effort to do so
 Expiration  passive process
The Muscles of Inspiration
 Diaphragm – most important muscle of inspiration and
when it contracts, the abdomen is pushed down while
the ribs are pushed upward and outward to increase the
volume of the chest cavity.
 Scalene muscles – functions to lift the rib cage and the
sternum during inspiration even at quiet breathing.
Accessory Muscles for inspiration
 External intercostals – found in between the ribs, not
used during normal quiet breathing only for labored
breathing or exercise.
 Sternocleidomastoid
 Trapezius
 Pectoralis muscles
 Erector spinae
 Serratus
Muscles for expiration
 Expiration is normally passive; no muscle contraction
 Because the lung/chest wall is elastic, it returns to resting
position after inspiration
 Used during exercise, increased airway resistance (e.g.,
asthma)
 Abdominal muscles- internal oblique, ext oblique,
transversus abdominis, rectus abdominis
o Compress the abdominal cavity, push
diaphragm up, & push air out of lungs
 Internal intercostal muscles – in between the ribs and
pull the ribs down and inward
EVENTS DURING NORMAL TIDAL BREATHING
During Inspiration
1. Inspiratory muscles contract and cause the volume of the
thorax to increase
– Because lung volume increases, alveolar pressure
decreases below atmospheric pressure (becomes
negative)
– This pressure gradient causes airflow into the lungs;
it will continue to flow until the pressure gradient
between atmosphere & alveolar dissipates
2. Intrapleural pressure becomes more negative
– Lung volume increases during inspiration, the
elastic recoil strength of the lung also increases
intrapleural pressure becomes more negative than
at rest
3. Lung volume increases
PULMO – RESPIRATORY PHYSIOLOGY (DR. DACANAY)
Inspiratory muscles will contract and cause an increase in
the size of the thorax which causes the decreases in intrapleural
pressure.
Intrapleural pressure – pressure between the visceral and
parietal pleura.
If the pressure between the two pleura decrease, the
pressure is transmitted to the individual alveoli, the increase
pressure will reach the alveoli until such point that the alveolar
pressure will also decrease. The alveoli will expand at the same
time as the increase in volume of the thorax and this will cause
entry of air into the lungs because the pressure inside the alveoli
is more negative than the atmosphere as air pressure travels
from a high to low pressure.
During expiration
1. Alveolar pressure becomes greater than atmospheric
pressure
– Alveolar pressure becomes greater (positive) bec
alveolar gas is compressed by elastic recoil of the
lung
– Pressure gradient is now reversed, & air flows out of
the lungs
2. Intrapleural pressure returns to resting value
– During forced expiration, intrapleural pressure
becomes positive  compresses the airways, makes
expiration more difficult
– In COPD slow expiration with “pursed lips” to
prevent airway collapse
On expiration, the diaphragm relaxes and this will return
the thorax to its original volume. As this happens, the intrapleural
pressure also returns to the resting value. Take note that during
the forced expiration, the intrapleural pressure may become
positive. On forced expiration, the intrapleural pressure becomes
positive, it will cause the pressure in the pleura and the chest to
become higher than the atmospheric pressure, compressing the
airways.
That’s why COPD patients are instructed to breathe slowly
through pursed lip breathing to slow down expiration to prevent
increase in pressure on the chest.
3. The alveolar pressure is greater than the atmospheric
pressure
Since the size of the chest wall cavity decreases, the size of the
alveoli also decreases. This will cause the pressure inside the
alveoli to become higher than the pressure of the environment.
Therefore, the gradient escapes from the alveolus.
Summary of the Events involved in Normal Tidal Breathing
Inspiration
1. Brain initiates inspiratory effort.
2. Nerves carry the inspiratory command to the
inspiratory muscles.
3. Diaphragm (and/or external intercostals muscles)
contracts.
4. Thoracic volume increases as the chest wall expands.
5. Intrapleural pressure becomes more negative
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6. Alveolar transmural pressure gradient increases.
7. Alveoli expand (according to their individual
compliance curves) in response to the increased
transmural pressure gradient. This increases alveolar
elastic recoil.
8. Alveolar pressure falls below atmospheric pressure as
the alveolar volume increases, this establishing a
pressure gradient for airflow.
9. Air flows into the alveoli until alveolar pressure
equilibrates with atmospheric pressure.
*Nos. 4-8 occur simultaneously
Expiration (Passive)
1. Brain ceases inspiratory command.
2. Inspiratory muscles relax.
3. Thoracic volume decreases, causing intrapleural
pressure to become less negative and decreasing the
alveolar transmural pressure gradient.
4. Decreased alveolar transmural pressure gradient allows
the increased alveolar elastic recoil to return the alveoli
to their preinspiratory volumes.
5. Decreased alveolar volume increases alveolar pressure
above atmospheric pressure, thus establishing a
pressure gradient for airflow.
6. Air flows out of the alveoli until alveolar pressure
equilibrates with atmospheric pressure.
*nos. 3 and 5 occurs simultaneously
Pressure-Volume Relationships during respiratory cycle
Figure 1. Pressure-volume curve during the breathing cycle
Figure 1 shows us the increase in tidal volume (chest wall volume)
on inspiration and a decrease during expiration. At the same time,
the intrapleural pressure (area between the visceral pleura and
parietal pleura) becomes more negative on inspiration and less
negative on expiration. Airflow and the alveolar pressure is
negative on inspiration and positive on expiration. Alveolar
pressure starts at ) during resting and becomes negative relative
to the environment as we inhale. Inspiration stops when alveolar
pressure is again 0, proceeds instantaneously with expiration.
PULMO – RESPIRATORY PHYSIOLOGY (DR. DACANAY)
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Figure 2. Lung volumes on the Spirometer
Tidal volume- normal breathing volume; 500ml
Inspiratory Reserve Volume (IRV)- volume after maximum
possible inspiration.
Expiratory Reserve Volume (ERV)- volume after maximum
possible expiration.
Residual volume (RV)- volume of air inside the lungs that
cannot be utilized or expired.
Inspiratory capacity (IC)= Tidal volume + IRV
Vital Capacity= ERV+ IC or ERV+ Tidal Volume +IRV
Functional Residual Capacity (FRC)= ERV + RV
Total Lung Capacity (TLC)= IC+ FRC = 6.0 L
Mechanics of Breathing
Compliance
 The elastic recoil of the lungs, chest wall, and
respiratory system can be quantified in a number of
ways
 Measurement of elastic recoil pressure at two volumes
 The difference between these pressures (∆P) and
volumes (∆V) can then be used to calculate the
compliance (C)
 Distensibility (stretchability)
 Ease with which the lungs can expand
 Used to quantify elastic recoil
 Change in lung volume per change in transpulmonary
pressure
 C = DV/DP
 Compliance is reduced by factors that produce
resistance to distension
Compliance simply states the ease of stretching or distended. For
instance, a balloon’s capacity to inflate is its compliance. As one
exerts pressure by blowing into the balloon, the volume inside
the balloon also increases.
Elasticity.
 Opposite to compliance
 The tendency to oppose distensibility or stretching and
resist in changing shape.
 Ability to return to original configuration or shape.
The Lung Mechanics of Breathing
 When the lungs are inflated above their resting volume,
they have elastic recoil.
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 These result from the tension in the fibrous structures Factors that affect Hysteresis
and the surface tension in the alveolo-air liquid
interface  Elastic properties of the tissue
 It acts like an inflated balloon  Surface forces
 These tension determines the internal configuration  Properties of the surface material lining
and distribution of the volume and ventilation inside
the lungs
 Elastic recoil thus influence the flow of air, blood and
interstitial fluid in the lungs

COMPLIANCE OF THE LUNG

 It is the slope between two points of the pressure-

volume curve (Figure 3) . Highly compliant lung would
have a steeper pressure-volume curve.
 Always remember that compliance is prevented by the
fibrous CT and the surfactants otherwise, the absence of
thw two will cause overly distended lungs. Figure 4. Compliance curves of the emphysema and fibrosis of
the lungs.

I. ELASTIC PROPERTIES OF THE LUNG

Emphysema - ↓ elastic fibers to resist inflation of the lungs,

therefore the lung is very compliant.

Fibrosis – compliance is low due to increased connective tissue

Causes of increased and decreased lung compliance

↓ compliance ↑ compliance
-High expanding pressure -Emphysema
Figure 3. Pressure-Volume Curve. Note the two points of the -Increase pulmonary venous -Aging
slope also interpreted as the compliance of the lung. pressures (ex. Edematous
lungs)
Blue and Green boxes  imagine the lungs are like balloons that -Lack of surfactant
are difficult to inflate during the first time and also at the time it -Fibrosis
becomes almost full because of the elastic recoil forces. At this
point you exert high pressure but the volume increases quite
slow. But at midbreath, it is easier to make the lung expand d/t II. SURFACE TENSION
increased compliance.
 Results from the forces between molecules of liquid lining
At initial and last phase of the curve: the alveoli

C = V/P  Because of their surface tension, alveoli have a tendency to

collapse
C= ↓V/↑P = low compliance
Laplace’s Law
At the middle of the curve (mid breath)
 Pressure tending to collapse is directly proportional to
C = V/P surface tension & inversely proportional to alveolar radius
C= ↑V/↓P = high compliance  lungs are easily distensible P=2T/r
Hysteresis P-collapsing pressure or pressure required to keep alveolus open
 In an air filled lungs, elastic recoil pressure at a given (dynes/cm2)
lung volume is higher on inflation than on deflation on T-surface tension (dynes/cm)
the same volume. This phenomenon is called hysteresis r- Radius of the alveolus (cm)
 Inflation of the lung (inspiration) follows a different (Remember: smaller radius have more tendency to collapse than
curve than deflation (expiration)HYSTERESIS the larger airways)

– In middle range of pressures, compliance is greater,

and lungs are more distensible

– At high expanding pressures, compliance is lower,

and lungs are less distensible and curve flattens

PULMO – RESPIRATORY PHYSIOLOGY (DR. DACANAY) CASTILLO, N.P. 3F

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III. SURFACTANT Flow Resistance

 Produced by type II pneumocytes  Resistance = pressure/ flow

 Consists primarily of dipalmitoyl phosphatidyl choline
 Lines the alveoli, reduces surface tension, thus prevents R = (P1 - P2) = 8 ηl
small alveoli from collapsing & increases compliance V πr4
 Critical importance of TUBE RADIUS!
 If the radius is decreased to ½, the resistance increases 16-
Example: FOLD!
 Doubling the length only doubles resistance
Neonatal respiratory distress syndrome

 Lack of surfactant Increase in

parallel airways
 Atelectasis during expiration, difficulty reinflating lungs means increase in
(dec compliance)  hypoxemia (V/Q mismatch) length  ↑ airway
resistance

↑crosssectional
area by extensive
branching = ↓
resistance

Figure 7. Airway resistance across respiratory airways

Figure 6. Mechanical interdependence of the alveoli is
Factors that change airway resistance:
another factor that prevents the collapse of the alveoli. If an
alveolus start to collapse, the surrounding alveoli are stretched
1. Contraction or relaxation of bronchial smooth
and then recoil exerting expanding forces in the collapsing muscles
alveolus to open it.
Contraction (↑ resistance to Relaxation (↓ resistance to
airflow) airflow)
AIRWAY RESISTANCE Parasympa Acetylcholine Sympathetic
stimulation stimulation
Airflow (Q) SRS of serotonin Sympathetic Isoproterenol
anaphylaxis agonists beta agonists
• Driven by, & directly proportional to, the pressure difference (asthma) Nitric oxide
between the mouth (or nose) & the alveoli. Leukotrienes Thromboxane
• Inversely proportional to airway resistance A2
• The higher the resistance, the lower the flow
Q= ∆P/R 2. Lung volume
Q-airflow (ml/min or L/min)  Affects airway resistance bec of radial traction exerted
on the airways by surrounding lung tissue
∆P- pressure gradient (mmHg or cmH2O)
 High lung volumes are associated with more traction
R- airway resistance (cm/H2)/L/sec) decreased airway resistance
 B. asthma= may learn to breathe at higher lung volumes
Airway resistance to offset high airway resistance
 Low lung volumes are associated with less traction
 Described by POISEUILLE’S LAW: increased airway resistance

R=8ηl/∏r4 3. Viscosity or density of inspired gas

R- resistance
 changes resistance to airflow
η- viscosity of inspired gas
 Deep sea dive
l-length of the airway
r- radius of airway  density & resistance to airflow are increased
 Breathing a low-density gas such as helium reduces
 Inverse relationship between resistance & the size (radius) resistance to airflow
of the airway
4. Sites of airway resistance
(For the formulas, please know the relationship of the variables
from one another)  major site of airway resistance is the medium-sized
bronchi

PULMO – RESPIRATORY PHYSIOLOGY (DR. DACANAY) CASTILLO, N.P. 3F


 smallest airways would seem to offer highest
resistance, but they do not bec of their parallel
arrangement
PULMONARY CIRCULATION
• Pressures
 Lower than systemic circulation
• Resistance
 Also much lower than systemic circulation
• Cardiac output (CO)
 Equals cardiac output through systemic
circulation
 The low pressure of pulmonary circulation is
sufficient to pump these high levels of CO bec
pulmonary resistance is proportionately low
Distribution of pulmonary blood flow
 Uneven distribution of blood flow and is explained by
effects of gravity
 In supine position, blood flow is nearly uniform
throughout the lung.
 In standing position, blood flow is lowest at
apex (zone 1) and highest at base (zone 3)
Zones of the lungs
Zone 1- blood flow is lowest
 Alveolar pressure(Pa)>arterial pressure(PA)>venous
pressure(Pv)
 The high Pa collapses the capillaries & causes
reduced blood flow
 Clinical scenario: 1. Hemorrhage; 2. Positive
pressure ventilation
Zone 2-blood flow is medium
 PA>Pa>Pv
PULMO – RESPIRATORY PHYSIOLOGY (DR. DACANAY)
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 PA progressively increases bec of the effect of gravity to
hydrostatic pressure
 Blood flow is driven by between arterial & alveolar
pressures
Zone 3-blood flow is highest
 PA>Pv>Pa
 Blood flow is driven by the difference between arterial &
venous pressure
VENTILATION/PERFUSION (V/Q) MATCHING
Ventilation/perfusion (V/Q) ratio
 Ratio of alveolar ventilation (V) to pulmonary blood
flow (Q)
 Matching ventilation and perfusion is important to
achieve ideal exchange of O2 and CO2
Normal V/Q ratio
 If frequency, tidal volume, & pulmonary cardiac output
are normal, V/Q ratio is about 0.8
 PO2= 100 mmHg; PCO2=40 mmHg
V/Q ratio in airway obstruction
 Complete obstruction V is zero, Q is normal V/Q=0
 Perfusion without ventilation
 PO2 & PCO2 will approach that of mixed venous blood
 Clinical scenario: foreign body obstruction
V/Q ratio in blood flow obstruction
 Complete pulmonary artery obstruction Q is zero, V
is normal V/Q=infinite
 Ventilation without perfusion (dead space)
 Clinical scenario: pulmonary embolism
V/Q ratios in different parts of the lungs
 Blood flow (Q) is lowest at the apex, highest at the base
 Ventilation (V) is lowest at apex, highest at base (but
regional difference is not as great as for perfusion)
o V/Q is highest at apex (>1)
o V/Q is lowest at base (<0.8)
 At apex- PO2 is highest; PCO2 is
lowest
 At base- PO2 is lowest; PCO2 is
highest
REGULATION OF THE PULMONARY BLOOD FLOW
Hypoxic vasoconstriction
 Hypoxia causes local vasoconstriction; this response is
opposite of that systemic circulation
 Physiologically important bec local vasoconstriction
diverts blood away from poorly ventilated, hypoxic
regions of the lung and toward well-ventilated region
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PULMONARY BLOOD FLOW: SHUNTS

Right-to-left shunts

 Normally, 2% of CO bypasses the lungs

 In congenital abnormalities, as high as 50%.

 Admixture of venous blood to arterial blood results to

decreased PA02 (arterial O2).

 Estimated by breathing 100% O2 and measuring the

degree of equilibrium of PAO2

Left-to-right shunts

 Less common

 Results to increased PO2 in right side of the heart

 Causes:

 congenital anomaly (PDA)

 traumatic injury

V/Q RATIOS AT THE DIFFERENT PARTS OF THE LUNGS

 Blood flow (Q) is lowest at the apex, highest at the base

 Ventilation (V) is lowest at apex, highest at base (but
regional difference is not as great as for perfusion)
o V/Q is highest at apex (>1)
o V/Q is lowest at base (<0.8)
 At apex- PO2 is highest; PCO2 is
lowest
 At base- PO2 is lowest; PCO2 is
highest

PULMO – RESPIRATORY PHYSIOLOGY (DR. DACANAY) CASTILLO, N.P. 3F