THE HUMAN

RESPIRATORY SYSTEM

Laboratory 6

Objectives:
1.Measure static lung volumes with minimally invasive methods
2.Examine the effects of alveolar gases and lung volumes on respiratory mechanics
3.Examine the effects of moderate exercise on ventilation
Procedures/Overview:
4.Use a spirometer to measure lung volumes
5.Try breath holds after re-breathing, hyperventilation, and other procedures to
explore gas and volume effects
6.Use a bicycle and spirometer to measure the effects of exercise on ventilation
Terminology:
Ventilation, Anatomical Dead Space, Internal Respiration, External Respiration,
Alveolar Pressure, Intramural Pressure, Alveolar Pressure, Intrapleural Pressure,
Diaphragm, Phrenic Nerve, Intrapleural Space, Intercostal Muscles/Nerves, Lung
Volumes (TV, IRV, ERV, RV), Lung Capacities (TLC, FRC, VC, IC), Central/Peripheral
Chemoreceptors, Hering-Breuer Reflex, Lung Parenchyma, Hyperpnea, Minute
Ventilation (V-dot-E),

RESPIRATORY ANATOMY
The respiratory system functions
to exchange gases between the
external environment and the
body
During ventilation, air travels into
airways down a pressure
gradient
Pathway:
Entry through nose/mouth
Passage through nasopharynx
and oropharynx, glottis, larynx
Entry into tracheobronchial tree
Exchange at alveoli

AIRWAY ZONES
Airways branch into bronchi
and bronchioles, then
respiratory bronchioles and
alveolar ducts
Conducting Zone:
First 16 generations contain no
alveoli and do not participate in gas
exchange
Anatomical Dead Spaces

Transitional & Respiratory

Zones:
Alveolar ducts and alveoli begin to
appear and gas exchange can
occur.

RESPIRATION
Gas exchange occurs at the AlveolarCapillary Unit = External Respiration
Alveoli are thin walled and highly vascularized
Air is humidified gas is dissolved for diffusion
down its partial pressure gradient

The intracellular metabolic processes of

mitochondria = Internal Respiration
O2 diffuses into cells and tissues down partial
pressure gradients and is used to generate ATP
CO2 is produced and diffuses back out

GAS EXCHANGE
Gases diffuse down partial
pressure gradients
Blood in the pulmonary
circulation flows such that
oxygen will move into the blood
and carbon dioxide will move
out
Venous Blood:
PO2 <40mmHg, PCO2>46mmHg

Alveolar Air:
PO2 ~100mHg, PCO2~40mmHg

OXYGEN TRANSPORT
O2 diffuses into plasma and is
loaded onto hemoglobin
molecules
A conformational shift allows
more O2 to bind up to 4 O2 per
Hb
Arterial O2 saturation is usually
100%
The change in PO2 and pH at the
receiving tissue reduces Hbs
affinity for O2, delivering it to the
tissue

CARBON DIOXIDE
TRANSPORT
Carbon dioxide diffuses from the
cell into capillary blood and can
react in 3 major ways:

1. ~8% will react slowly to form

bicarbonate
2. ~65% will enter red blood
cells and react rapidly with
water and carbonic anhydrase
(CA) to form bicarbonate
3. ~27% will enter the RBC and
react with terminal amine
groups of blood proteins,

MECHANICS OF BREATHING
Air
moves from areas of higher pressure
to lower pressure
(V dot) = flow of air during
ventilation
Palv = Alveolar Pressure
Patm = Atmospheric Pressure
R = Resistance ()
Intrapleural Pressure (Pip): pressure
at the interface of the lung and chest
wall
Transmural Pressure (Ptm): difference
between Palv and Pip (NOT ON EXAM).

INSPIRATION
Inspiratory Muscles:
Diaphragm (primary) innervated by
phrenic nerve, contracts downward to
expand the intrapleural space
external intercostals (for deep breathing)
innervated by intercostal nerves, contract
to raise and enlarge the rib cage

Process:
Muscles are activated to contract
Thoracic volume increases
Intrapleural pressure is reduced
Alveoli enlarge passively and P Alv is reduced
Air flows into lungs

EXPIRATION
Muscles
None required during normal breathing
expiration is passive.
Abdominal wall and Internal intercostals
activate during forced exhalation

Process
Relaxation of inspiratory muscles
Elastic recoil of lungs increases alveolar
pressure
Air moves out of lungs down the pressure
gradient

PART 1: MEASURING STATIC

LUNG VOLUMES

LUNG VOLUMES
Tidal Volume (TV): The volume of air entering and leaving the

lungs with each normal breath. At rest (~12-15 breaths/min)

Inspiratory Reserve Volume (IRV): Additional volume of gas

that can be inhaled above TV during a forced maximal inspiration.
At rest
Expiratory Reserve Volume (ERV): Additional volume of gas
that can be exhaled beyond TV during a forced maximal expiration.
Residual Volume: Volume of gas left after a maximal forced
expiration (due to dead space).

LUNG CAPACITIES
Total Lung Capacity (TLC): total volume of air in the lungs

after a maximal inspiration.

Functional Residual Capacity (FRC): volume of gas

remaining in the lungs at the end of normal tidal expiration.

Vital Capacity (VC): Volume of air expelled from the lungs

after a maximal inspiration and expiration.

Inspiratory Capacity (IC): Maximal volume of air that can

be inspired.

PART 2: EFFECTS OF
INSPIRED GAS COMPOSITION
AND LUNG VOLUME ON
RESPIRATION
Factors that affect ventilation:
Arterial PCO2 and PO2
Blood PH
Temperature
Exercise or anticipation of exercise
Voluntary control

Receptors involved in control:

Central chemoreceptors (medulla
oblongata)
Peripheral chemoreceptors (aortic arch
& carotid body)
Muscle spindle / stretch receptors (lung
parenchyma)

CONTROL OF VENTILATION
Breathing is spontaneously initiated by the
Pons and Medullary respiratory centers
Medullary/Pons respiratory centers:
Dorsal Respiratory Group (DRG) contain
mostly inspiratory neurons (i.e. phrenic nerve)
Ventral Respiratory Group (VRG) contain both
inspiratory and expiratory neurons, but more
important in pacing (exercise)
Pre-Botzinger Complex: contains pacemakers
Pneumotaxic Center: involved in stopping
inspiration
Apneustic Center: involved in initiating
inspiration

Breathing can also be modified by

receptors

HYPOVENTILATION &
HYPERVENTILATION

Hyperventilation is an increase in ventilation achieved by increasing

respiratory rate and/or tidal volume, not related to metabolic drive.
Rate of ventilation is higher than what is needed to remove CO2 from
blood
Leads to a decrease in PCO2 (hypocapnia)
Decreased PCO2 causes decreased inspiratory drive

Prolonged hyperventilation will lead to respiratory alkalosis (increase in

pH)
Leads to vasoconstriction in brain arterioles
Decreases blood flow in the brain -> dizziness

Hypoventilation is a decrease in ventilation, leading to an increase in

arterial PCO2 (hypercapnia)
The increase in PCO2 will cause a decrease in pH (respiratory acidosis)
This activates chemoreceptors to increase respiratory rate

PERIPHERAL
CHEMORECEPTORS

Found in the carotid bodies and

aortic arch
NOT the same receptors as the
CV baroreceptors!
Able to sense decreases in
arterial PO2 (hypoxia) and to
a lesser extent increases in
PCO2, decreases in pH

Activation of receptors will cause

an increase in ventilation rate

CENTRAL
CHEMORECEPTORS
Located in the Medullary
Respiratory Center

Sense increases in PCO2

and decreases in pH by
sensing [H+] in cerebrospinal
fluid
This is a slow reaction but
when the chemoreceptors are
activated it will cause an
increase in ventilation rate

STRETCH RECEPTORS
Stretch receptors are located in the smooth muscle of large and small
airways, also in lung parenchyma (connective tissue around lungs)
Afferent fibers travel through the vagus nerve and project into the
brainstem.
When there is an increase in stretch there will be an inhibition of inspiratory
neurons. The opposite will happen if there is a decrease in stretch. (HeringBreuer Reflex)
This reflex contributes to pacemaking and initiation of inspiration &
expiration. (NOT actually a significant contributor to prevention of
overinflation the ribs do that!)
High levels of inflation = increased stretch = decreased respiratory drive
Low levels of inflation = decreased stretch = increased respiratory drive

PART 3: EXERCISE
HYPERPNEA
Hyperpnea: increase in ventilation
matching an increase in metabolic
activity, such as exercise

Ventilation rate matches need for CO2

removal, so there is no decrease in arterial
PCO2 beyond normal as seen in
hyperventilation

Exercise increases demand for oxygen

and produces more carbon dioxide
Perfusion of upper lungs increases to
increase gas exchange
Larger surface area is needed to make up
for increased pulmonary vascular pressure

MEASURES OF VENTILATION
Minute Ventilation - (V dot E)
Volume of air that was moved in and out of the lungs per minute
TV tidal volume (mL/breath)
RR respiratory rate (breaths/minute)

Dead Space Ventilation Volume of air not participating in gas exchange per minute
- dead space volume (mL/breath)

Alveolar Ventilation Part of the tidal volume that enters or leaves the gas exchange area of the lung
per breath per minute

NOTES FOR LAB

Exercise appropriate clothing can be worn in this lab
If you are sick or have recently had any kind of
upper respiratory infection, you MAY NOT BE A
SUBJECT ON ANY STATIONS. Please do not
contaminate the equipment!
MAXIMAL respiratory efforts are important for parts
1 and 2