Respiratory System

lungs.
he lungs.

paransal sinuses, inhaled air becomes turbulent. The gases in the air are

perature

matter

teeth, lips, and tongue work to produce sound.

l communication

ssolve in the mucus in the nose, the molecules can bind to receptors in the olfactory epithelium.

s glands, lysozyme in the mucus all help defend the body against infection by airborne pathogens.

> primary bronchi ---> secondary bronchi ---> tertiary bronchi ---> bronchioles ---> terminal bronchioles ---> respiratory bronchioles --->

ovides an overview of the respiratory system, including its functions and organs.
ys that serve to warm, moisten, and filter the inhaled air: nose, nasal cavity, pharynx, larynx, trachea,
chi, bronchioles, terminal bronchioles.
ers of branching in the lungs which significantly increases cross sectional area for flow

hioles, alveolar ducts, alveolar sacs, and about 300 million alveoli
s’ volume
area for gas exchange

ut of the lungs.
costals muscles promote ventilation

ween the alveoli and the blood of the pulmonary capillaries.

nd carbon dioxide between the lungs and tissues

ween the blood of the systemic capillaries and cells.

izes internal and external respiration.

ons.

the information that follows on pulmonary ventilation.

r into and out of the lungs

epends on volume changes in the thoracic cavity
sure changes, which lead to the flow of gases in and out of the thoracic cavity to equalize pressure
ation
high pressure to areas of low pressure

ween the pressure and volume of gases is inversely proportional for a gas held at a constant temperature

es, volume increases

, pressure increases
xed
horacic volume increases
oracic volume decreases

cic Cavity

ibed relative to atmospheric pressure

ssure exerted by all of the gases in the air we breathe (760 mm Hg at sea level)
re is less than ATM
e is greater than ATM

60mmHg (when even with ATM )

ys eventually equalizes itself with atmospheric pressure

vity which adheres lungs to thoracic cavity ~ 756mmHg

s less than intrapulmonary pressure and atmospheric pressure
ural pressure fluctuate with the phases of breathing

ose apposition – stretching the lungs to fill the large thoracic cavity

olarity of water attracts wet surfaces

ATM (760mmHg) is greater than intrapleural pressure (756mmHg) so lungs expand
xternal intercostal muscles (inspiratory muscles) contract and the rib cage rises, stretching the lungs and increasing intrapulmonary v
ure drops below atmospheric pressure (1 mm Hg) drawing air flow into the lungs, down its pressure gradient, until intrapleural pressu

d the rib cage descends due to gravity, elasticity.

ases, elastic lungs recoil passively and intrapulmonary volume decreases.
s above atmospheric pressure (+1 mm Hg), gases flow out of the lungs down the pressure gradient until intrapulmonary pressure is 0
 exhalation
ycle = tidal volume

tion

tic source of resistance to airflow

een flow (F), pressure (P), and resistance (R) is

Flow = ΔP /R

ase with which lungs can be expanded due to change in transpulmonary pressure
ors:
ung tissue and surrounding thoracic cage
he alveol
easily
more force
brotic lung diseases and inadequate surfactant production

ebound after being stretched

ssue causes lungs to assume smallest possible size
ar fluid draws alveoli to their smallest possible siz

me when stretching force is released

ecules to one another at a liquid-gas interface, the thin fluid layer between alveolar cells and the air
ar surface is always acting to reduce the alveoli to the smallest possible size
complex secreted by Type II alveolar cells, reduces surface tension and helps keep the alveoli from collapsing

esistance with the greatest resistance being in the medium-sized bronchi,

onchioles: COPD
 educes surface area for gas exchange
veolar membrane slows gas exchange, loss of lung compliance
al space increases diffusion distance
n decreases airway ventilation

nto and out of the lungs with each breath (approximately 500 ml)
air that can be inspired forcibly beyond the tidal volume (2100–3200 ml)
air that can be evacuated from the lungs after a tidal expiration (1000–1200 ml)
e lungs after strenuous expiration (1200 ml)
ount of air that can be inspired after a tidal expiration (IRV + TV)
) – amount of air remaining in the lungs after a tidal expiration

nt of exchangeable air (TV + IRV + ERV)

all lung volumes (approximately 6000 ml in males)

f the conducting respiratory passages (150 ml)

ease to act in gas exchange due to collapse or obstruction
and anatomical dead spaces
s Exchange

oxygen and carbon dioxide across the respiratory membrane

d gas solubilities
on and pulmonary blood perfusion
he respiratory membrane

structure of the alveoli and describes external respiration.

gases is the sum of the pressures exerted independently by each gas in the mixture

ach gas is directly proportional to its percentage in the mixture

ygen (PO2)
en
ir = 760 mmHg
9 mmHg

liquid, each gas will dissolve in the liquid in proportion to its partial pressure

ssolve in a liquid also depends upon its solubility

erent solubilities:
most soluble
soluble as carbon dioxide
insoluble in plasma

re
 s
ressure

wing for efficient gas exchange

les) of about 60 m2 (40 times that of one’s skin)
sed of alveolar and capillary walls
f three types of cells:

ila cells that form a nearly continuous lining of the alveolar wall.
ype of cells.
as exchange.

und between type I alveolar cells

helial cells whose free surfaces contain microvilli
fluid keeps the surface between the cells and the air moist
rfactant a mixture of phospholipids and lipoproteins that lowers the surface tension of the alveolar fluid, which reduces the tendency

lar wall
at remove fine dust particles and other debris in the alveolar spaces. engulf foreign particle

ws the structure of respiratory membranes. Review the first half of the animation.

79% & oxygen ~21%, only 0.03% is CO2

vapor

– oxygen diffuses from the alveoli and carbon dioxide diffuses into the alveoli
ucting passages
at occurs with each breath
ure of alveolar oxygen is 100mmHG and partial pressure of alveolar CO2 is 40mmHg

O2) of venous blood is 40 mm Hg

Hg
to rapidly reach equilibrium (0.25sec)
pulmonary capillary and still be adequately oxygenated
 partial pressure gradient 40 -> 46:
in plasma than oxygen
with oxygen

between systemic capillaries and tissue cells are the same as those acting in the lungs
usion gradients are reversed
than in systemic arterial blood
tissues is 40 mm Hg and PCO2is 45 mm Hg

internal respiration occurs.

hing the alveoli
he alveoli
htly regulated for efficient gas exchange
e changes in the diameters of the pulmonary arterioles
: vasoconstriction
h: vasodilation

r transport in the blood

bound to Hb (HbO2)
O2 not bound to (HHb)

O2 / /g of Hb
s
2/g of Hb
r hemes of the molecule are bound to oxygen
n one to three hemes are bound to oxygen
ases oxygen is regulated by:

cal)

roduces a oxygen-hemoglobin dissociation curve:

turated
erventilation has little effect on arterial O2 levels
pletely saturated at a PO2 of 70 mm Hg
ly small increases in oxygen binding
e is still adequate when PO2 is below normal levels

uration

s 20 ml oxygen per 100 ml blood (20 vol %)

unloaded during one systemic circulation
aries, 5 ml oxygen/dl are released

m hemoglobin and is used by cells

utput need not increase
crease hemoglobin’s affinity for oxygen and enhance oxygen unloading from the blood
ture of Hb - Bohr effect
bolism when environmental O2 levels are low
emic (tissue) capillaries where oxygen unloading is the goal

three forms

0%
obin – 20% is carried in RBCs as carbaminohemoglobin
70% is transported as bicarbonate (HCO3–)

nd combines with water to form carbonic acid (H2CO3), which quickly dissociates into hydrogen ions and bicarbonate ions
bly catalyzes the conversion of CO2 and water to carbonic acid
stem resists blood pH changes

ved by combining with HCO3–

eleasing H+

om RBCs into the plasma

bicarbonate ions from the RBCs, chloride ions (Cl–) move from the plasma into the erythrocytes. This is called chloride shift.

reversed
the RBCs and bind with hydrogen ions to form carbonic acid
carbonic anhydrase to release carbon dioxide and water
from the blood into the alveoli

ability of Hb to pick up CO2 and CO2 generated H+ is called the Haldane effect.
synchrony to facilitate O2 liberation and uptake of CO2 and H+
he blood:
m Hb (Bohr effect)
O2 to combine with Hb (Haldane effect), and more bicarbonate ions are formed
ry circulation
 ry centerscontrol breathing. The centers located in the medulla oblongata set the rate and rhythm of
gulate the rate and depth of breathing.

DRG), or inspiratory center:

sic rhythm “pacemaking” (now believed to be pre-Botzinger complex)

y muscles and sets eupnea(12-15 breaths/minute)
xpiration
VRG) or expiratory center
ry neurons
ng quite breathing
d is high
nspiration and expiration
 Control via phrenic (to the diaphragm) and intercostal(to the external intercostal

muscles) ner ves

y centers to smooth out inspiration and expiration transitions

s the regulator; it coordinates the transition between inhalation and exhalation; it also prevents
lways sending inhibitory impulses to the inspiratory center (DRG)
dinates the transition between inhalation and exhalation by fine-tuning the medullary respiratory centers;
ory impulses to the inspiratory center (DRG) which result in a slower, deeper inhalation; this is necessary
r breath p
s to allow expiration to occur normally

ow actively the respiratory center stimulates the respiratory muscles

how long the inspiratory center is active
medulla are sensitive to both excitatory and inhibitory stimuli

tch reflexes modify pacemaker activity

promote reflexive constriction of air passages

tch receptors in the lungs are stimulated by lung inflation
sent to the medullary inspiration center to end inhalation and allow expiration
the limbic system to modify rate and depth of respiration
occurs in anger
crease respiratory rate
om the cerebral motor cortex that bypass medullary controls
olding, taking a deep breath

by chemoreceptors of the brain stem

nto the cerebrospinal fluid where it is hydrated
releasing hydrogen ions
lting in increased depth and rate of breathing
 and rate of breathing that:
e from the blood
capnia
al stimulus, control of breathing at rest is regulated by the hydrogen ion concentration in the brain
breathing due to abnormally low PCO2 levels
cur until PCO2 levels rise

by the aortic and carotid bodies

60 mm Hg) are needed before oxygen levels become a major stimulus for increased ventilation
., as in emphysema and chronic bronchitis), chemoreceptors become unresponsive to PCO2 chemical stimuli
e principal respiratory stimulus (hypoxic drive)

l pH

spiratory rate even if carbon dioxide and oxygen levels are normal
alling pH is mediated by peripheral chemoreceptors

with diabetes mellitus

mpt to raise the pH by increasing respiratory rate and depth

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This material is based upon work supported by the Nursing, Allied Health
and Other Health-related Educational Grant Program, a grant program
funded with proceeds of the State’s Tobacco Lawsuit Settlement and
administered by the Texas Higher Education Coordinating Board.