Respiratory

Huyen Doan Van MD., PhD

1
 TOPICS
1. Organization of the respiratory system
2. Ventilation and lung mechanics
3. Exchange of gases in alveoli and tissues
4. Transport of oxygen in blood
5. Transport of carbon dioxide in blood
6. Transport of hydrogen ion between tissues and lungs
7. Control of respiration
8. Hypoxia
9. Nonrespiratory functions of lungs

2
ORGANIZATION OF THE RESPIRATORY SYSTEM

3
THE AIRWAYS

4
BLOOD VESSELS

5
THE ALVEOLI

6
RELATION OF THE LUNGS TO THE THORACIC WALL

7
 PLEURAE
The pleurae form a thin double-layered serosa. The parietal
pleura covers the thoracic wall and superior face of the
diaphragm. The visceral pleura covers the external surface of the
lung.

The pleura produce fluid that remains in the pleural cavity. This
lubricates the lung to prevent friction while breathing.

Pleurisy is an infection or inflammation of the pleura and often

results from pneumonia. This results in a roughening of the pleura,
which creates friction and a stabbing pain with each breath. As
the disease progresses there is a build-up of fluid, which hinders
breathing.
8
STEPS OF RESPIRATION

9
VENTILATION AND AIR FLOW
Ventilation is defined as the exchange of air
between the atmosphere and alveoli.

F = P/R

Remember that flow (F) is proportional to the

pressure difference ( P) between two points and
inversely proportional to the resistance (R).

10
 VENTILATION
Boyles law: at a constant temperature the pressure of a
gas varies inversely with its volume.

P1V1=P2V2

Remember that gases always fill their container. So in a

large container the molecules in a given amount of gas
will be far apart (low pressure). In a smaller container
that same amount of gas will have molecules close
together (high pressure).

11
 PRESSURE MEASUREMENTS
We measure this in mm Hg or atmospheres (atm).
At sea level this is 760 mm Hg or 1 atm.
If you were to go to higher altitudes (i.e., up in
the Andes Mountains), then the pressures would
be different.

12
VENTILATION AND LUNG MECHANICS

13
 INTRAPLEURAL PRESSURE

Pip is the pressure in the pleural cavity.

It also fluctuates with breathing, but it is always 4

mm Hg less than Palv.

IF Pip = Palv THE LUNGS WILL IMMEDIATELY

COLLAPSE!
14
 TRANSPULMONARY PRESSURE

Transpulmonary pressure = Palv Pip

Transpulmonary pressure is the transmural pressure that

governs the static properties of the lungs.

Transmural means across a wall and is represented by

the pressure in the inside of the structure (Pi) minus the
pressure outside the structure (PO).

15
16
 Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

End Begin
Patm = 0
Inspiration Expiration

No flow
1 End of expiration 1 Beginning of inspiration
8

6 Palv = 0
Ptp
Ptp = 4
4
Various pressures during breathing (mmHg)

Pip = 4
Patm = 0 Patm = 0
2
3 Palv 4 Mid- 2 Mid-inspiration

Airflow
expiration

Airflow
1 Patm 1
0
4

2
2
Patv = 1 Palv = 1

4 Ptp = 6 Ptp = 5
Pip 3 End of Patm = 0
inspiration and
Pip = 6

No flow
Pip = 5 beginning of
6 expiration
Breath volume (L)

0.5
Palv = 0
0
Elastic recoil
Ptp = 7
4 sec force
Time
Inspiratory
muscle force Pip = 7
INSPIRATION

18
EXPIRATION

19
 LUNG COMPLIANCE

Compliance can be considered the inverse of stiffness.

The greater the lung compliance, the easier it is to expand

the lungs at any given change in transpulmonary pressure.

There are two major determinants of lung compliance:

1. The stretchability of the lung tissues
2. The surface tension at the air-water interfaces within the
alveoli

20
21
 LUNG COMPLIANCE AND SURFACTANT
The type II alveolar cells secrete the detergent-like substance
known as surfactant.

Surfactant markedly reduces the cohesive forces between water

molecules on the alveolar surface.

Therefore, surfactant lowers the surface tension, which increases

lung compliance and makes it easier to expand the lungs.

22
 Law of Laplace
No surfactant With surfactant

a a

Ta b b
Airflow Pb
rb
ra Tb ra rb
Pb
Pa Tb
Pa Ta

If Ta = Tb 2T If Tb < Ta (due to unique

=
property of surfactant)
then Pa < Pb then Pa = Pb
ra > rb
and there is no flow from b to a;
and air flows from b to a; smaller alveoli do not
b collapses into a collapse into bigger alveoli
 Clinical Interest
A lack of surfactant is a huge problem for premature babies
whose Type II cells are not mature enough to produce surfactant.
This is known as infant respiratory distress syndrome (IRDS) or as
respiratory distress syndrome of the newborn (RDSN).

Too little surfactant allows the alveoli to collapse and then they
have to re-inflate every time. This is a huge energy drain.

Normally surfactant isnt made until the last two months in utero. If
a baby is being born too early they can now administer some
steroids to help stimulate production. But in most emergency
births this isnt possible so the baby is put on a ventilator.
Artificial surfactant is also available.
24
 AIRWAY RESISTANCE
Airway resistance is normally very small, but changes in airway resistance
follow changes in airway radii.

Airway radii may change in response to physical, neural, and chemical factors.

25
 ASTHMA
Asthma: airway smooth muscle contracts strongly, markedly
increasing airway resistance.

Basic defect: chronic inflammation, the causes of which vary from

person to person and include; allergy, viral infections, and sensitivity
to environmental factors.

The underlying inflammation makes the airway smooth muscle

hyperresponsive and causes it to contract strongly in response to
such things as exercise (especially in cold, dry air), cigarette smoke,
environmental pollutants, viruses, allergens, normally released
bronchoconstrictor chemicals, and a variety of other potential
triggers.
26
 ASTHMA
The first aim of therapy for asthma is to reduce the chronic
inflammation and airway hyperresponsiveness with anti-
inflammatory drugs, particularly leukotriene inhibitors and inhaled
glucocorticoids.

The second aim is to overcome acute excessive airway smooth

muscle contraction with bronchodilator drugs, which relax the
airways.

For example, one class of bronchodilator drugs mimics the normal

action of epinephrine on beta-adrenergic (beta-2) receptors.
Another class of inhaled drugs block muscarinic cholinergic
receptors, which have been implicated in bronchoconstriction.
27
 CHRONIC OBSTRUCTIVE PULMONARY DISEASE

The term chronic obstructive pulmonary disease refers to emphysema,

chronic bronchitis, or a combination of the two.

These diseases cause severe difficulties not only in ventilation, but in

oxygenation of the blood.

Emphysema is caused by destruction and collapse of the smaller

airways.

Chronic bronchitis is characterized by excessive mucus production in

the bronchi and chronic inflammatory changes in the small airways.
The cause of obstruction is an accumulation of mucus in the airways
and thickening of the inflamed airways. 28
EMPHYSEMA

29
LUNG VOLUMES AND CAPACITIES

30
LUNG VOLUMES AND CAPACITIES

31
OBSTRUCTIVE LUNG DISEASES
Forced vital capacity (FVC)
Forced expiratory volume in 1 second (FEV1): the volume
of air that can be expelled from maximum inspiration in
the first second

OBSTRUCTIVE: Tiffeneau: FEV1/FVC > 80% but normal

Vital capacity

RESTRICTIVE lung disease: Normal Tiffeneau: but

VC< 80%

32
ALVEOLAR VENTILATION AND DEAD SPACE
Minute ventilation = Tidal volume x Respiratory rate
VE = VT x f
6000 = 500 12
But dead space is 150 mL so VA = 350 X 12 = 4200 mL

33
ALVEOLAR VENTILATION

34
EXCHANGE OF GASES IN ALVEOLI AND TISSUES
Respiratory Quotient = CO2 produced / O2 consumed

RQ depends on nutrients, Mixed diets= 0.8,

Assumed cells used 250 mL O2 /Min, Produced 200 mL

CO2 (RQ= 0.8)

Minute ventilation: 4000 mL, 21% of gas is O2 so 21% x

4000 = 840 mL O2

In each breath but only 590 mL O2 will be exhaled (840-

250)

35
EXCHANGE OF GASES IN ALVEOLI AND TISSUES

36
PARTIAL PRESSURES OF GASES

Daltons Law: The partial gas pressure of any gas

in a mixture is the fractional concentration of that
gas times the total pressure of all gases.

Po2 = 0.21 x 760 mmHg at sea level

Henrys Law: the gas dissolved will directly

proportional to the partial pressure of the gas with
which the liquid is in equilibrium.

37
PARTIAL PRESSURES OF GASES

38
 150

Alveolar partial pressure (mmHg)

O2

100 Normal resting

values

50

CO2

0
1.0 4.0 8.0
Alveolar ventilation (L/min)

Hypoventilation Hyperventilation
 Increased metabolism: O2 consumption O2 in venous
blood O2 concentration gradient O2 diffusion from
alveoli to blood alveolar Po2 Decreased
Decreased metabolism: increased
GAS EXCHANGE BETWEEN ALVEOLI AND BLOOD

41
MATCHING OF VENTILATION AND BLOOD FLOW IN
ALVEOLI

42
TRANSPORT OF OXYGEN IN BLOOD

Oxygen is transported
in the blood bound to
hemoglobin.

43
WHAT IS THE EFFECT OF P O 2 ON HEMOGLOBIN SATURATION?

44
OXYGEN MOVEMENT IN LUNGS AND TISSUES
OXYGEN MOVEMENT IN LUNGS AND TISSUES

46
EFFECTS OF BLOOD P CO 2 , H + CONCENTRATION, TEMPERATURE, AND DPG
CONCENTRATION ON HEMOGLOBIN SATURATION

47
48
TRANSPORT OF CARBON DIOXIDE IN BLOOD
CO2 dissolved in in water: 10%

25-30 % CO2 : combine Hb

CO2 + Hb Hb CO2

Remaining CO2: 60-65% in form of HCO3 -

49
TRANSPORT OF CARBON DIOXIDE IN BLOOD

50
TRANSPORT OF HYDROGEN IONS BETWEEN TISSUES AND LUNGS

51
 NEURAL GENERATION OF RHYTHMICAL BREATHING

An overdose of
morphine,
barbituates or
alcohol suppresses
the neurons in the
ventral respiratory
group and stops
respiration.

52
PERIPHERAL CHEMORECEPTORS

53
54
LOW ARTERIAL P O2 CAUSES HYPERVENTILATION

55
REFLEXIVELY INDUCED HYPERVENTILATION AND
H+ CONCENTRATION

56
CONTROL OF VENTILATION BY PO2, PCO2, AND H +
CONCENTRATION

57
CONTROL OF VENTILATION DURING
EXERCISE

58
 HYPOXIA
Hypoxia is an inadequate oxygen delivery to tissues.
The pathophysiology of emphysema is a major cause
of hypoxia.
1. Anemic hypoxia: poor O2 delivery because of too few
RBCs or abnormal hemoglobin
2. Ischemic hypoxia: blood circulation is impaired
3. Histotoxic hypoxia: the bodys cells are unable to use O2
(cyanide causes this)
4. Hypoxemic hypoxia: reduced arterial O2
(can be caused by lack of oxygenated air, pulmonary
problems, lack of ventilation-perfusion coupling)
59
 CARBON MONOXIDE POISONING

This is a type of hypoxemic hypoxia. It is the leading

cause of death from fire.

CO is an odorless, colorless gas that competes with O2 for

the binding sites on the hemoglobin. It has a 200-times
greater affinity for hemoglobin than O2 does.

The symptoms are confusion, respiratory distress, the skin

becomes cherry red. NO CYANOSIS is detectable.

To treat it, hyperbaric treatment or 100% oxygen is used.

60
FUNCTIONS OF THE RESPIRATORY SYSTEM

61