Respiratory

Physiology
 Learning Objectives

Describe the three processes of respiration

1.Pulmonary ventilation
2.External respiration
3.Internal respiration

Identify the various lung volumes and capacities

Describe O2 and CO2 transport

Identify the factors that control respiration

Respiratory Function During Anesthesia

 Three Processes of
Respiration
1. Pulmonary ventilation (breathing)
• physical movement of air into and out of lungs
• inspiration - active
• expiration - usually passive
2. Pulmonary (external) respiration
• gas exchange at lung
3. Tissue (internal) respiration
• gas exchange at tissues
 Inhalation
 Inhalation
 Active process
• During quiet breathing
contraction of diaphragm
and external intercostals
expands thoracic cavity

• Decreases pressure (Boyle’s

law – volume inversely
related to pressure)

• air flows down pressure

gradient
 Exhalation
 Exhalation during quiet
breathing is passive
process
• Elastic recoil of chest
wall and lungs

• Due to:
 Recoil of elastic fibres
 Inward pull of surface
tension of alveolar fluid
 Deep Forceful Breathing
 Deep Inhalation
• During deep forceful inhalation accessory muscles of inhalation
participate to increase size of thoracic cavity
 Sternocleidomastoid – elevate sternum

 Scalenes – elevate first two ribs

 Pectoralis minor – elevate 3rd–5th ribs

 Deep Exhalation
• Exhalation during forceful breathing is active process
 Muscles of exhalation increase pressure in abdomen and thorax
• Abdominals
• Internal intercostals
Factors affecting pulmonary
ventilation
 Surface tension of alveolar fluid
• surfactant
 Lung compliance
• Elasticity
• Surface tension
 Airway resistance
The major task of the lung is:

To oxygenate the blood and

Eliminate carbon dioxide from it.

This is accomplished by exchanging gas between alveoli and pulmonary capillary blood

To establish gas exchange in the human lung, there must Be:

Ventilation of the alveoli

Diffusion through the alveolar-capillary membranes,

Circulation or perfusionof the pulmonary capillary bed.

The lung is regularly affected by :

Anesthesia
Mechanical ventilation.
Preexisting lung disease

Knowledge of the functional impairment :

Prevent any disastrous impairment in gas exchange.

Ventilation
Dead Space and Alveolar Ventilation

Normal tidal breath is approximately 0.5 to 0.6 L

Respiratory frequency :16 b/min,
Range : 12 to 22breaths/min.
Magnitude and rate:
Metabolic demand
pulmonary function
If:
Respiratory center is intact and functioning.
Ventilation :approximately 7to 8 L/min.
VDS: 100 to 150 mL
VDS/VT ratio is 0.3
Alveolar ventilation: around 5 L/min .

Ventilation-perfusion ratio accordingly is 1.

 Increased minute ventilation:
Physical exercise,
Reduced inspiredoxygen concentration increased dead space ventilation
Metabolic acidosis.
Increased Dead Space Ventilation

If dead space is increased, ventilation must be raised to account for the

“losses” and to maintain PaCO2 at anormal level

Dead space is increased:

Mouthpiece
Valve
Facemask.
“apparatus dead space” : 25 and a few hundred mL, compared 100 to 150
ml (“anatomic dead space”)

Bronchiectasis : Vds/Vt ratio = 0.8 to 0.9. mv= 30 to 50 L/min

pulmonary embolus (“alveolar dead space”) VDS/VT= 0.7 to 0.8, mv= 20
L/min.
Obstructive lung disease, including asthma, chronic bronchitis, and
emphysema.
Hyperventilation and Exercise

Almost 20-fold higher than resting ventilation,

To above 100 L/min in women and above 150 L/min in men,

But only for a brief period of half a minute or so.

Lower PaCO2 and affect consciousness.

Ventilatory capacity perform during rebreathing of expired gas or add CO2

VT to approximately two thirds of vital capacity (VC) , or 2.5 to 4 L

Frequency to 40 breaths/min or greater.

During maximum physical exercise, minute ventilation increases less, to

Two thirds of maximum capacity = 65 to 100 L/min i

In athletes, ventilation may exceed 150 L/min.

 Lung volumes and capacities

4 lung volumes:
tidal (~500 ml)
inspiratory reserve (~3100 ml)
expiratory reserve (~1200 ml)
residual (~1200 ml)

4 lung capacities
inspiratory (~3600 ml)
functional residual (~2400 ml)
vital (~4800 ml)
total lung (~6000 ml)
Lung Volumes
Functional Residual Capacity

There is a certain amount of air in the lungs after an ordinary expiration.

This volume is called functional residual capacity (FRC)

Approximately 3 to 4 L , dependent on :
Sex Age
Height Weigh
Exercise Asthma
COPD Fibrosis
Pulmonectomy

The balance of the inward force of the lung and the outward force of the
chest wall determines the volume:

Inward force of the lung, or “elastic recoil,”

Outward force of the chest wall is exerted by the ribs, joints, and muscles
Total Lung Capacity and Subdivisions

The gas volume in the lung after a maximum inspiration is called total lung
capacity (TLC).
It is typically 6 to 8 L
COPD increase TLC up to 11 – 12 L
RLD deacrease TLC low to 3-4 L

Residual volume ~ 2-2.5 L

Even after a maximum expiratory effort, some air is left in the lung and no
region normally collapses. This persisting gas volume is called residual volume
(RV)

The maximum volume that can be inspired and expired is called vital capacity.
VC is thus the difference between TLC and RV and is around 4 to 6 L.

It reduced:
Restrictive lung disease
Obstructive lung disease.
normal lungs

restrictive lung disease

chronic obstructive lung

disease
 Respiratory Mechanics

Understanding the mechanics serves two purposes :

1-what governs the distribution of inspired air.

2- recording as a diagnostic and prognostic tool in lung disease.

Compliance of the Respiratory System :

The elastic behavior of the lung is often analyzed in terms of compliance,
which is the inverse of elastance.

Compliance is expressed as change in lung volume divided by the

change
in pressure required tocause the increment in volume

Normal lung compliance is around 0.2 to 0.3 L/cm H2O (2 to 3 L/kPa).

It varies with lung volume, and decreases with an increase in lung

volume.
 Resistance of the Respiratory
System
Pressure is required to overcome :

Resistance to gas flow through the airways during respiration.

Sliding of different components of lung tissue and the chest wall.

Gas flow :
Turbulent - proportional to the square of the pressure
Laminar- linearly related to the pressure.

Airflow resistance :
Normal-1 cm H2O/L/sec.

5 cm H2O/L/sec in mild to moderate asthma and bronchitis

Greater than 10 in more severe cases.

8 endotracheal tube - resistance of 5 cm H2O/L/sec

Size 7 tube -to 8 cm H2O/L/sec

Distribution of Inspired Gas:
Effect of Compliance, Resistance, and Airway Closure
Closing volume (CV) :

The volume above RV atwhich airways begin to close during expiration is called

closing volume (CV)

The sum of RV and CV iscalled closing capacity (CC )

 Airflow resistance :
Can be higher in expiration than inspiration,
Particular forced breathing
Patients with obstructive lung disease
If resistance is increased during inspiration :
probably caused by narrowing of extrathoracic airways
Lung tissue resistance :
Around 1 cm H2O/L/sec ,
can be increased threefold to fourfold in chronic lung disease.
Chest wall resistance

Inertia or Acceleration of Gas and Tissue

One additional component of the total impedance to breathing, is inertance,

Pressure required to accelerate air and tissue during inspiration and expiration.
Is minor under normal breathing
More important:
Very rapid breathing : HFO, yogi exercise, rapid shallow breathing
Can contribute 5% to 10% of the total impedance.
 Gas Distribution

Distribution of Inspired Gas:

Effect of Compliance, Resistance, and Airway Closure

During quiet breathing, most gas goes to the lower, dependent regions :

increasing lung volume= more and more pressure is required to inflate

the lung

transpulmonary pressure todecrease from the top to the bottom of the lung

During inspiration,pleural pressure is lowered, which causes the lower lung

regions to inflate more than the upper ones

What causes the pleural pressure gradient?

Gravity
Closing volume (CV) ?
The volume above RV at which airways begin to close during
expiration
Cosing capacity (CC) ?

The sum of RV and CV is called closing capacity

Secretions, edema, and spasm affect gas distribution:

decreasing or eliminating ventilation

Pursed-lips breathing

Devices available to breathe out through that act as resistance.

Increase in lung volume is the only way of increasin transpulmonary
and transairway pressure, and this stabilizes the airway.

slow expiratory flow move the EPP up to the larger airways

or the mouth, which will prevent floppy airways from
collapsing
 Diffusion in Airways and Alveoli
Total cross-sectional area:

Trachea = 2.5 cm2 to:

70 cm2 in the 14th generation entering the acinus

0.8 m2 in the 23rdgeneration.

The total alveolar surface is approximately 140 m2.

Gas flow velocity will decrease as the area increases:

Trachea = around 0.7 m/sec,

Alveolar surface it is no higher than 0.001 mm/sec.

Transport of O2 and CO2 is therefore accomplished by diffusion in

the peripheral airways and in the alveoli, not by convective flow.

 Diffusion Across Alveolar-Capillary Membranes

Oxygen diffuses passively from the alveolar gas phase into plasma and red
cells, where it binds to hemoglobin.

Carbon dioxide diffuses in the opposite direction, from plasma to the alveoli.

Diffusion over the membranes determined by :

(1)the surface area available for diffusion

(2) the thickness of the membranes

(3) the pressure difference of the gas across the barrier

(4) the molecular weight of the gas, and

(5) the solubility of the gas in the tissues that it has to traverse
 Gas Exchange
Exchange of O2 and CO2 between alveolar air and
blood occurs via passive diffusion
 Governed by
– Dalton’s Law
 Each gas in a mixture exerts own pressure
– Partial pressure

– Henry’s Law
 Quantity of gas that dissolves in liquid proportional to
partial pressure and solubility coefficient
– Solubility of CO2 greater than O2 (24x)
 External and Internal
Respiration
 External respiration
– Diffusion of:
 O2 from alveoli to blood
 CO2 from blood to alveoli
– Blood leaving pulmonary
capillaries mixes with blood
draining lung tissue
 PO2 of blood in
pulmonary veins lower
than in pulmonary
capillaries
 Internal respiration
– Diffusion of:
 O2 from blood to tissues
 CO2 from tissues to blood Jenkins, Kemmitz & Tortora (2007 p. 861)
 Pulmonary Perfusion

Pressure-Flow Relationship

Pulmonary circulation is a low-pressure system.

20 mm Hg systolic and 8 mm Hg diastolic 6 to 10 times lower than systemic

Larger vascular diameter , shorter distance =decreases the demand on driving

pressur.

Pulmonary capillary blood flow is pulsatile

Alveolar walls is very thin, without causing any leakage of plasma ,facilitates

diffusion of O2 and CO2.

ASudden increase pressure to above a mean of 30 mm Hg causes :

effusion of plasma into promoting lung edema.

 A slower increase in pressur=(“vascular remodeling”) :

Edema is prevented better, despite even severe pulmonary

hypertension,but diffusion capacity will be impaired.

Distribution of Lung Blood Flow

Blood flow governed by driving pressure and vascular resistance

Gravitational orientation ? playing only a minor role,

but there is “fractal” distribution

Gravitational Distribution of Blood Flow in the Lung

Nongravitational Inhomogeneity of Blood Flow Distribution
 Hypoxic Pulmonary Vasoconstriction

HPV : a compensatory mechanism aimed at reducing blood

flow in hypoxic lung regions.

The major stimulus is low alveolar oxygen tension

The stimulus of mixed venous PO2 is much weaker

Pulmonary hypertension and pulmonary edema may develop

at high altitude

Chronic lung disease with hypoxemia also causes HPV, but :

Allows time for remodeling of the pulmonary vascular wall:

 Causes of Hypoxemia and Hypercapnia

Causes of hypoxemia classified as :

Hypoventilation,

V/Q mismatch,

Impaired diffusion,

Right-to-left shunt.

Hypercapnia caused by:

Hypoventilation,

V/Q mismatch,

Shunt
In practice hypoventilation is the only cause of real importance
 Hypoventilation

defined as ventilation that results in a PaCO2 above 45 mm Hg (6 kPa)

hypoventilation can be present even when minute ventilation is high :

Metabolic demand increased

Dead space ventilation is increased

Increased alveolar PCO2 reduces the space available for oxygen

Thus, PIO2 of 149 mm Hg (19.9 kPa) , PaCO2 of 40 mm Hg (5.3 kPa):

PAO2 is 99 mm Hg (13.2 kPa)

During hypoventilation ,a PaCO2 60 mm Hg (8 kPa):

PAO2 is 74 mm Hg (9.9 kPa)