Respiratory System

 Internal respiration “cellular”: internal metabolic

process carried out within the mitochondria:
O2+nutrients CO2+energy

 External respiration: all events that are

responsible for the exchange of O2 & CO2
between the external environment and cells, it
occurs in 4 steps:
1-breathing (ventilation)
2-gas diffusion between alveoli and blood
3-transport of gases by blood
4-gas diffusion between capillary & tissue
 Atmosphere Steps of external respiration

1 Ventilation or gas exchange between

the atmosphere and air sacs (alveoli)
in the lungs

O2 CO2
Alveoli of lungs
2 Exchange of O2 and CO2 between air
CO2
in the alveoli and the blood
O2

Pulmonary
circulation

3 Transport of O2 and CO2 between the

lungs and the tissues

Systemic
circulation

CO2
O2
4 Exchange of O2 and CO2 between the
blood and the tissues
Food + O2 CO2 + HO2 + HTP Internal respiration

Tissue cell Fig. 12-1, p. 366

Non-respiratory functions of the system:
1-water loss and heat elimination, also
keeps alveoli wet
2-inhances venous return
3-acid-base balance
4-enables speech
5-defends against foreign inhaled matters.
6-removes, modifies, & activate or
inactivate materials “prostglandins”
7-smelling
8-shape of the chest
9-protects heart & vessels
10-aireate the blood between respiratory
phases
 Respiratory airways
 Nose  pharynx (throat)  trachea
(windpipe)

 Larynx at the entrance of trachea

 Two main branches (bronchi)  branches

 bronchioles
 (continue to next slide)

Nasal
passages

Mouth

Pharynx Terminal
bronchiole
Larynx
Respiratory
Trachea bronchiole
Cartilaginous
ring
Right
bronchus
Alveolar
Bronchiole sac

Terminal
bronchiole Fig. 12-2a, p. 367
 lungs
 Alveoli : clustered thin walled
inflatable grape like sacs ( thin layer
of type I alveolar cells)
 Interstitial space very thin ~ 0.5 Mm
 300 million alveoli, each 300 Mm
diameter, surface area
2
over 75m
 Type II alveolar cells secrete
pulmonary surfactant
 Alveolar macrophages
Terminal
bronchiole Smooth
muscle

Branch of Branch of
pulmonary pulmonary
artery vein

Respiratory
bronchiole

Alveolus Pulmonary
capillaries

Alveolar
Pores of Kohn sac

Fig. 12-2b, p. 367

 Pleural sac
 Double walled, closed, separates
lungs from the thoracic wall and
other surrounding structures

 Pleural cavity, intrapleural fluid

 Respiratory mechanics
 Air moves by pressure gradient:
1-atmospheric (barometric) pressure
760mmHg at sea level
2-intra-alveolar pressure “no air
flow” = atmospheric pressure
3-intrapleural pressure is less than
atmospheric ~ 756 mmHg
Atmospheric pressure
(the pressure Atmosphere
exerted by the 760 mm Hg
weight of the gas in the
atmosphere on objects on Airways
the Earth’s surface—760
mm
Hg at sea level)

Thoracic wall

Intra-alveolar
pressure (the
pressure within
the alveoli—760 mm Plural wall
Hg when equilibrated
with atmospheric
pressure)

Lungs

Intrapleural pressure (the 756 mm Hg

pressure within the pleural sac
—the pressure exerted outside
the lungs within the thoracic
cavity, usually less than
atmospheric pressure at 756
mm Hg) Fig. 12-5, p. 370
 The lungs are stretched to fill the thorax
because:
a- intrapleural fluids cohesiveness
b- transmural pr. Gradient

 Pneumothorax: abnormal condition, air in

the pleura so there’s no transmural pr.
gradient so no force to stretch the lungs
collapse
 760

Puncture wound
in chest wall

760 760 760

760

756 756

Traumatic pneumothorax

(Continue to the next slide)

Numbers are mm Hg pressure. Fig. 12-8a, p. 371

 760

760 760 760 760 760

756

Collapsed lung

(Continue to the next slide)

Numbers are mm Hg pressure. Fig. 12-8b, p. 371

 Air flow
 Boyle’s law at constant temperature :
partial pressure of a gas varies
inversely with the volume of the gas
 Respiratory muscles change the
thoracic cavity volume which causes
lung volume change
 Inspiration & expiration ( one breath)
are the respiratory cycle.
Equilibrated;
no net movement of air

Preinspiratory
size of thorax

760

756 Preinspiratory
size of lungs

Before inspiration
Fig. 12-12a, p. 374
 Respiratory muscels
 Major inspiration muscles:
a- diaphragm b- external
intercostals

 Accessory inspiration muscles:

a- sternocleidomastoid b- scalenus

 Expiratory muscles:
a- abdominal muscles b- internal
intercostals
 Elevation of ribs causes sternum
External Elevated to move upward and outward,
intercostal rib cage which increases front-to-back
muscles dimension of thoracic cavity
(relaxed)
Contraction
of external
intercostal
muscles

Sternum

Contraction
of diaphragm
Diaphragm
(relaxed)
Lowering of diaphragm on
contraction increases vertical
dimension of thoracic cavity
Before inspiration Inspiration

Contractions of external intercostal

muscles causes elevation of ribs,
which increases side-to-side
dimension of thoracic cavity Fig. 12-11a, p. 374
Relaxation Contraction of internal intercostal
of external muscles flattens ribs and
intercostal sternum, further reducing
muscles Contraction side-to-side and front-to-back
of internal dimensions of thoracic cavity
intercostal
muscles

Contraction
of diaphragm

Position of relaxed
Relaxation of
abdominal muscles
diaphragm
Contractions of abdominal
muscles cause diaphragm to
be pushed upward, further
Passive expiration reducing vertical dimension
of thoracic cavity
Return of diaphragm, ribs, and sternum
to resting position on relaxation of Active expiration
inspiratory muscles restores thoracic
cavity to preinspiratory size
Fig. 12-11bc, p. 375
 Elastic behavior of the lung
 Compliance: how much effort is
required to stretch or distend the lung “
how much volume change occurs in the
lung from a given change in the
transmural pr. gradient
 Pulmonary elastic behavior depends on:

1-pulmonary elastic connective tissue:

large quantity of elastin fibers, they
tend to bounce back lungs to their
original shape
2- Alveolar surface tension:
thin liquid film that lines the alveoli
unique attraction between water
molecules at the air-water interface
attraction creates surface tension which
opposes the expansion of the alveoli and
tends to shrink them
pulmonary surfactant: mixture of lipids &
proteins secreted from type II cells, it
lowers alveolar surface tension so it
increases lung compliance & reduces lung
tendency to recoil so no collapse
newborn respiratory distress syndrome is
treated by surfactant and drugs for
maturation process
 Lungs volume & capacities
 Tidal volume -500mL- (TV)
 Inspiratory reserve volume -3000mL- : extra volume
can be maximally inspired over & above TV (IRV)
 Inspiratory capacity -3500mL- : maximum volume
the can be inspired at the end of normal quite
expiration (IC)
 Expiratory reserve volume -1000mL- :extra volume
that can be actively expired by maximally contracting
the expiratory muscles beyond that normally
passively expired (ERV)
 Residual volume -1200mL- : minimum volume
remaining in the lung after maxim expiration (RV)
 Functional residual capacity -2200mL- : volume in
lungs at the end of quite passive expiration
“ERV+RV” (FRV)
 Lungs volume & capacities
 Vital capacity -4500mL- : maximum air that
can be moved after maximum inspiration
(VC)

 Total lung capacity -5700mL- (TLC)

 Forced expiratory volume in 1 sec. (FEV1) :

volume of air in first second of vital capacity
determination , normally = 80% of VC
TV = Tidal volume (500ml)
IRV = Inspiratory reserve volume (3,000 ml)
IC = Inspiratory capacity (3,500 ml)
ERV = Expiratory reserve volume (1,000 ml)
RV = Residual volume (1,200 ml)
FRC = Functional residual capacity (2,200 ml)
VC = Vital capacity (4,500 ml)
TLC = Total lung capacity (5,700 ml) Fig. 12-14b, p. 378
 Alveolar ventilation: volume of air exchanged
between atmosphere & alveoli per minute
 Pulmonary ventilation: volume of air breathed in &
out in one minute = TV x respiratory rate = 500 x
12 = 6000 mL/min.
 Anatomic dead space: volume of airway
conducting channels ~ 150mL
 Alveolar ventilation rate= (TV – DS) x res. rate =

(500-150) x 12 = 4200 mL/min

 Alveolar dead space: ventilated alveoli that do not
participate in gas exchange with blood because
they are inadequately perfused, normally not
significant
 Gas exchange
 Partial pressure of gasses :
 dry atmospheric air contains 79% N,
21% O2, ~0% CO2, ~0% H2O vapor
 the partial pressure of the gas is
directly proportional to the % of that
gas in the mixture
 PN2=600 mmHg PO =160 mmHg
2

PCO2= 0.023 mmHg

 Partial pr. In liquid: the more the gas is
dissolved the more the partial pr. Is in it
 Alveolar air:
PO2=100 mmHg atmospheric=160
mmHg because H2O vapor replaces
some of the O2 and the fresh air is
mixed with old alveolar air
PCO2=40 mmHg through the
respiratory cycle because CO2 diffuses
from blood at the same time removed
continuously out.
 Arterial blood in lungs contains 40
mmHg O2 , 46 mmHg CO2
 Capillary blood equilibrates with alveoli
 PO2= 100 mmHg, PCO2=40mmHg
 Surface area, thickness of membrane,
could change the diffusion rate but
healthy persons have constant surface
area & thickness
 emphysema, pulmonary edema,
pulmonary fibrosis, pneumonia
 Gas transport
 O2 in blood is transported in 2 forms:
physically dissolved & chemically bound to
Hb
 3mL O2 is dissolved in 1L blood at PO2=100
mmHG so total blood has 15mL O2
dissolved equivalent to 1.5% of total O2 in
blood so 98.5% is bound
 PO2 in blood represents the dissolved
portion only
 Reduced hemoglobin (deoxyhemoglobin)
 PO2 is important to determine the % of Hb
saturation of O2
Average resting Normal PO2 at
PO2 at systemic pulmonary
capillaries capillaries

Fig. 12-22, p. 388

 Hb  4 molecules of O2
 O2-Hb dissociation curve is S-shaped

 The significance of the plateau portion:

1- when the alveolar PO2 decreases down
to 60 mmHg it will not affect the amount
of O2 in the blood
2- when breathing pure O2 (600mmHg) 
100% saturation, so the rang between
60mmHg – 100mmHg gives only 10%
difference in saturation
 The significance of the steep portion:
1- at 40mmHg which is the average
PO2 in the capillary blood the Hb
saturation is 75% so 25% leaves
2- if the metabolism is high the PO2
from capillaries to the veins will not
be 40 mmHg it will go down to 20 or
less, at that level the saturation goes
down to 30% so more than 45% O2
is released  a small drop in the
systemic capillary CO2 can make large
amount of O2 diffusion to tissues
 Factors affecting Hb affinity:
1- CO2 : if increases  shift to right
2- pH : if decreases shift to right
3- temp. :if increases  shift to right
4- 2,3 bisphosphoglycerate : if increases
 shift to right
 Factors concentration differ in the
pulmonary circulation from the systemic
circulation
 Hb affinity to CO is 240 times it affinity to
O2  HbCO is called carboxyhemoglobin
 Arterial PCO2 and acidity,
normal body temperature
(as at pulmonary level)

PCO2 (as at
Acid (H+) tissue
level)
Temperature
or
2,3-Bisphosphoglycerate

Fig. 12-24, p. 391

 CO2 is mainly transported as
bicarbonate in 3 forms:
a- physically dissolved 10%
b- bound to Hb 30%
-
c- HCO3 60%

+ -
 H2O + CO2  H2CO3  H + HCO3
 Control of respiration
nervous control:
-respiratory center in brain stem:
1-primary control centre: medullary
respiratory center (aggregation of
neuronal cell bodies)
2-apneustic center & pneumotaxic
centre: in pons and they influence the
output from the primary control center
 Pons

Pons
Pneumotaxic center
respiratory
Apneustic center
centers

Respiratory Pre-Bötzinger
control complex
centers in
brain stem
Dorsal respiratory
Medullary group
respiratory
center Ventral respiratory
group Medulla
Fig. 12-26, p. 396
Medullary center has:
1-dorsal respiratory group (DRG) : contains
only inspiratory neurons “quite breathing”
2-ventral respiratory group (VRG) : has
inspiratory & expiratory neurons “active
inspiration & expiration”

 Generation of respiratory rhythm is by the

pre-botzinger complex located near the
upper end of the medullary centre “as a
pacemaker activity”
 Apneustic & pneumotaxic centers: fine
tuning influences:
-pneumotaxic : switches off inspiratory
neurons limiting the time of inspiration
-apneustic : prevents the switching of
inspiratory neurons so it provides extra
boost to the inspiratory drive

 Hering-breuer reflex: when TV is larger

than 1L, pulmonary stretch receptors within
the smooth muscles of the airways signals
to afferent nerves to the medullary center
to inhibt respiration
 Control of respiration
 Chemical control:
1-decrement of PO2 is sensed by arterial &
peripheral chemoreceptors (carotid bodies &
aortic bodies) which leads to increment in the
+
ventilation.
increment in H concentration in the arterial
blood will stimulate the bodies
the threshold for stimulation is high when
PO2 is higher than 60mmHg because until 60
mmHg the Hb saturation is still 90%
very low PO2 could depress the respiratory
centre instead of increasing ventilation
Sensory Sensory
nerve fiber nerve fiber

Carotid sinus
Carotid bodies

Carotid artery

Aortic bodies

Aortic arch

Heart

Fig. 12-27, p. 397

 2- CO2 generated+ H and arterial PCO2 changes
significantly increase ventilation
 peripheral receptors do not respond
to PCO2 increment
 central receptors in the medulla
monitor [H+] in the ECF
 H+ cannot pass the blood-brain barrier while
the CO2 can so :
+
↑ art. CO-2  ↑ CO2 in ECF ( H2O + CO2  H2CO3
 H + HCO3)

very high CO2 “more than 80 mmHg”

depresses the respiratory center
 Arterial PCO2 Relieves

Brain ECF PCO2

(when
arterial
PCO2
Brain ECF
>70-80
mm Hg)

Brain ECF H+

Weakly
Medullary
Peripheral respiratory Central
chemoreceptors chemoreceptors
center

Ventilation

ca = Carbonic anhydrase
Arterial PCO2 Fig. 12-28, p. 398
The End