Download Energetics/Energy Transfer in the Body

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Gas Exchange and Transport
Gas Exchange and Transport
The driving force for pulmonary
blood and alveolar gas exchange is
the Pressure Differential –
The difference between the partial
pressure of a gas (O2 or CO2) above a fluid
and dissolved in fluid (alveoli or blood)
Gas Exchange and Transport
Pressure Differential
Fig 13.1
Gas Exchange and Transport
Henry’s Law:
The rate of gas diffusion into a liquid
depends on:
1) Pressure differential between the gas
above the fluid and gas dissolved in
fluid
2) Solubility (dissolving power) of the gas in
the fluid
CO2 highly soluble
Gas Exchange and Transport
Saturation with water
vapor - lower PO2
Constant loading and
unloading of CO2 and O2
FRC necessary to prevent
swings in CO2 and O2
concentration in alveoli
PO2 – 100 mm Hg:
regulates breathing
and 02 loading of Hb
Fig 13.2
PCO2 – 40 mm Hg:
chemical basis for
ventilatory control via
respiratory center
Gas Exchange and Transport
Time Required for Gas Exchange
Capillary transit
time is ~0.75 s
During maximal
exercise,
capillary transit
time is ~0.4 s
Gas exchange
during maximal
exercise not a
limiting factor
Fig 13.2
Gas Exchange and Transport
Time Required for Gas Exchange
Pulmonary
disease impacts
this process:
1. Thicker alveolar
membrane
2. Reduced surface
area
Fick's Law-Gas diffuses
at rate proportional to:
Tissue thickness
(inversely)
Tissue area (directly)
Fig 13.2
Gas Exchange and Transport
O2 Transport:
•Dissolved oxygen in blood only sustains life
for about 4 seconds (0.3 mL O2 / dL)
•Small amount establishes PO2 which
regulates breathing and oxygen loading of
hemoglobin
Gas Exchange and Transport
O2 Transport:
•Hemoglobin (Hb) – Protein in red blood cells
that transports 02 bound to iron
•Each Hb has 4 iron atoms (can bind 4 O2)
•Hb transports 19.7 ml/dL (vs 0.3 ml/dL - plasma)
(65 x that in plasma)
Anemia:
Low iron in red blood
cells results in low
oxygen carrying capacity
Fig 13.3
Gas Exchange and Transport
Oxyhemoglobin dissociation curve:
Describes Hb
saturation with
O2 at various
PO2 levels
100 mm Hg:
98% saturation
60 mm HG:
decline in %
saturation
40 mm HG: 75%
of O2 remains with
Hb - 5 ml delivered
to tissues
Athletes?
Fig 13.4
Gas Exchange and Transport
Bohr effect –
•Increased blood acidity
(lactic acid),
temperature, CO2
causes downward shift
to the right
•Facilitates dissociation
of O2 from Hb
•No effect on capillary
blood Hb-O2 binding
Fig 13.4
Gas Exchange and Transport
Oxyhemoglobin dissociation curve:
Myoglobin:
•Intramuscular O2
storage protein
•Transfers O2 to
mitochondria when
PO2 falls
•At 40 mm Hg, Mb
95% saturated
with O2
•No Bohr effect
occurs with
myoglobin
Fig 13.4
Dynamics of Pulmonary
Ventilation
Pulmonary Ventilation
Ventilatory Control – How does our body control
rate and depth of breathing in response to
metabolic need
Medulla –
Inspiratory neurons
activate diaphragm
and intercostals
Expiratory neurons
activated by
passive recoil of
lungs
*Mechanisms maintain constant alveolar
and arterial gas pressures
Fig 14.1
Pulmonary Ventilation
1. At rest, chemical state of the blood controls
ventilation
PO2, PCO2, acidity
(lactate), temperature
PO2 – no effect on medulla
(peripheral chemoreceptors
detect arterial hypoxia,
altitude)
PCO2 – most important
respiratory stimulus to
medulla at rest
Fig 14.2
Pulmonary Ventilation
2. During exercise, no single mechanism explains
increase in ventilation (hyperpnea)
Neurogenic Factors:
Cortical: Motor cortex stimulates respiratory
neurons to increase ventilation
Peripheral: Mechanoreceptors in muscles, joints,
tendons influence ventilatory response
•Peripheral chemoreceptors become sensitive to
CO2, H+, K+, and temperature during strenuous
exercise
Pulmonary Ventilation
Phases of Ventilatory Response During Exercise:
I. Neurogenic – central
command, peripheral
input stimulates medulla
Fig 14.4
II. Neurogenic –
continued central
command, peripheral
chemoreceptors (carotid)
III. Peripheral - CO2, H+,
lactate (medulla),
peripheral chemoreceptors
Recovery – removal of
central, peripheral,
chemical input
Rapid Slower
rise
exponential
rise
Steady
Abrupt
state
decline
ventilation