RESPIRATORY PHYSIOLOGY

Dr. Okon MRCS

 Lung Pressures

Lung recoil - the inward force created by the
elastic recoil properties of alveoli.

acts to collapse the lung

Chest wall recoil - the outward force of the
chest wall

FRC as counterbalance

Intrapleural pressure (IPP) – pressure
generated by the Pleural cavity
 outward recoil of the chest and inward recoil of the
lung create a negative (subatmospheric) IPP.

Transmural pressure gradient - pressure
gradient across any tube or sphere
 Inside pressure minus outside pressure
 At FRC, IPP is negative, and thus PTM is positive.
This positive outward force prevents alveolar
collapse (atelectasis).

 Before Inspiration

The lung is at FRC

Intrapleural pressure is negative at FRC
because the inward elastic recoil of the lungs is
opposed by the outward-directed recoil of the
chest wall.

Alveolar pressure must be zero
 During Inspiration

Intrapleural pressure becomes more negative.
 The more negative IPP causes PTM (TPP) to increase,
which in turn causes expansion of the lungs. The greater the
contraction, the greater the change in intrapleural pressure
and the larger the PTM (TPP) expanding the lung.
 The expansion of the lung increases alveolar volume.
 the rise in volume causes pressure to decrease, resulting in
a negative (subatmospheric) alveolar pressure.
 Air rushes into the lungs.
 The lung expands until alveolar pressure equilibrates with
atmospheric pressure.
 Expiration

Passive activity

Relaxation of the muscles of inspiration causes
intrapleural pressure increase

Decreased PTM leads to the drop alveolar
volume, which increases alveolar pressure

Intraalveolar pressure - It is slightly negative
during inspiration and slightly positive during
expiration.
 No matter how large a breath is taken, intraalveolar
pressure always returns to 0 at the end of
inspiration and expiration.

Total atmospheric pressure = 0.
CARDIOVASCULAR CHANGES
WITH VENTILATION

Inspiration
 Intrapleural pressure becomes more negative (decreases). Increases
the PTM across the vasculature, causing the great veins and right atrium
to expand.
 This expansion decreases intravascular pressure, thereby increasing the
pressure gradient driving VR to the right heart.

Systemic venous return and right ventricular output are increased. An
increase in the output of the right ventricle delays closing of the pulmonic
valves and typically results in a splitting of the second heart sound.

Pulmonary vessels expand, and the volume of blood in the pulmonary circuit
increases. Pulmonary vascular resistance (PVR) is lowest at FRC, it
increases.

Venous return to the left heart, and the output of the left ventricle is
decreased,

Decreased systemic arterial pressure (drop in systolic most prominent).

Inspiration reduces vagal outflow to the heart resulting in a slight rise in
heart rate (respiratory sinus arrhythmia).
 Expiration

Reverse process

Valsalva maneuver is a forced expiration
against a closed glottis. This forced expiration
creates a positive IPP which compresses the
great veins in the chest. This in turn reduces
VR.
POSITIVE-PRESSURE
VENTILATION

Assisted Control Mode Ventilation (ACMV)
 The inspiratory cycle is initiated by patient or automatically
 Expiration is accomplished in the normal manner

Positive End-Expiratory Pressure (PEEP)
 Positive pressure is applied at the end of the expiratory cycle
to decrease alveolar collapse. It is useful in treating the
hypoxemia of acute respiratory distress syndrome
 Small alveoli have a strong tendency to collapse, creating
regions of atelectasis.
 The larger alveoli are also better ventilated, and
supplementary oxygen is more effective at maintaining a
normal arterial PO2.
 Positive pressure ventilation and accentuated by PEEP
causes a decrease in venous return and cardiac output.

Continuous Positive Airway Pressure
(CPAP)

CPAP, continuous positive pressure is applied
to the airways.

Useful to treat obstructive sleep apnea (OSA)
since the lung and upper airways
(nasopharynx) remain at a larger volume
throughout the respiratory cycle.CPAP is
administered by mask.

The patient breathes spontaneously.
 PNEUMOTHORAX

Traumatic (perforation of chest wall) or spontaneous (rupture of
an alveolus)
 Intrapleural pressure increases from a mean at -5 cm H2O
to equal atmospheric pressure.
 Lung recoil decreases to zero as the lung collapses.
 Chest wall expands. At FRC, the chest wall is under a slight
tension directed outward. It is this tendency for the chest
wall to spring out and the opposed force of recoil that
creates the intrapleural pressure of -5 cm H2O.
 Transpulmonary pressure is negative.

Tension pneumothorax most commonly develops in patients on
a positive-pressure ventilator.
 LUNG COMPLIANCE

Change in lung volume (tidal volume) divided
by the change in surrounding pressure.

Increased compliance means more air will flow
for a given change in pressure.

Reduced compliance means less air will flow for
a given change in pressure
Components of Lung Recoil


Collagen and elastin fibers of the lung

– The larger the lung, the greater the stretch of the tissue and
the greater the recoil force.
 The surface tension forces in the fluid lining the alveoli.
Surface tension forces are created whenever there is a
liquid–air interface.

– Surface tension forces tend to reduce the area of the surface
and generate a pressure.They act to collapse the alveoli;
therefore, these forces contribute to lung recoil.

Surface tension forces are the greatest component of lung
recoil.

Law of LaPlace.

Pressure ∝tension/radius

Surfactant reduces the surface tension and
prevents collapse of the small alveoli

It lowers surface tension forces more in small
alveoli than in large alveoli.
 Respiratory Distress Syndrome
(RDS)

Infant RDS (hyaline membrane disease) is a
deficiency of surfactant.

Adult respiratory distress syndrome (ARDS) is
an acute lung injury
