Transcript Respiration

• Respiration is the
overall movement
of gases between
the outside
environment and
the internal cells.
• Ventilation is the
movement of air
in and out of the
lungs.
O2
CO2
O2
CO2
• Ventilation should be
matched to
metabolism.
Carbon Dioxide reacts with water!
CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3Carbonic Acid
Bicarbonate
So disturbances in gas exchange or ventilation
are often associated with disruptions of pH.
pH changes with
Hypoventilation &
Hyperventilation
Gas Laws
Dalton’s Law
• Total pressure = sum of
partial pressures
• PATM = P N2 + P O2 + P CO2
• 100% = 79% + 21% + <1%
• P O2 = 0.21 x 760mmHg = 160
• Partial pressure of Oxygen in
atmosphere at sea level is
160 mmHg
• Regardless of elevation, air is
always 21% O2.
•
N2 is physiologically inert; ignore
except for decompression sickness
Henry’s Law
• Gases dissolve in liquids
in proportion to their
partial pressure in the air
in contact with that liquid
air
P O2 =160 mmHg
liquid
P O2 =160 mmHg
Why the difference in partial
pressures in Air and Alveoli?
Ventilation by Bulk Flow
Gas exchange by Diffusion
Where should the receptors be for
the negative feedback loop for
homeostasis?
Gas exchange
Gradient for CO2 is only 6 mmHg;
CO2 is more soluble and permeable than O2
Gas exchange
• All gases move by diffusion. Thus limited by:
– Surface area
– Distance
– Concentration (partial pressure) gradient
• In the lung, gases must move from air to water
and vice versa. The amount is proportional to
– Solubility (CO2 more soluble than O2)
– Temperature (colder fluids dissolve more gas)
– Pressure gradient
Respiratory
Physiology
The physics of
air flow
1) Flow in tubes
2) Ventilation
Poiseulle’s equation
The Structure underlying the function:
Upper
Respiratory
Tract
Lower
Respiratory
Tract
Intercostal muscles
Bronchitis= infection/inflammation of conducting airways
Asthma = smooth muscles contract →increase resistance to
airflow in conducting airways.
Pneumothorax (unilateral due to each lung having its own compartment.
Visceral pleura and parietal pleura
separated by fluid-filled pleural cavity which
allows lung and chest wall to slide relative
to each other but remain adhered unless air
enters the pleural cavity (which leads to
collapse of the lung and outward expansion
of chest wall on that side.)
Greg R. and the story of spontaneous pneumothorax
Upper Tract
Sleep Apnea
a)obstructive,
b)central
&
CPAP
Continuous Positive Airway Pressure
Bronchopulmonary
segments and Surgical
resection
Figure 22.5
Respiratory
Epithelium
of Airway
(Not alveolus!)
Mucus escalator
Smoker’s hack
• What does a
river delta and
your lungs have
in common?
Mixing of
Freshwater (inspired air)
and
Salt water (alveolar air)
Slower velocity of flow in delta (respiratory
airways)
Figure 13-2
Impaction
Sedimentation
Decrease
In Flow
Rate
Brownian Diffusion
Anatomical Dead Space
Particle Filtration:
deposition varies
Pulmonary arterial blood = low in O2
Cartilage prevents collapse of
airways during expiration.
V/Q inequality = imperfect match between air flow and blood flow
Response of pulmonary arterioles to low P O2
Matching blood flow (Q, also called “perfusion” ) to ventilation (V) by
pulmonary arterioles that constrict in response to low O2 and
dilate in response to hi O2
(Note this response to O2 is opposite that of systemic arterioles!)
Thus, poorly ventilated regions of the lung will receive less blood flow.
So…. Q is “matched” to V, but not perfectly.
And low perfusion in a region leads to bronchoconstriction.
V/Q inequality
Figure 22.10
5 liters of blood in
pulmonary capillaries
with surface area
equal to a tennis court
Type I pneumocytes are
simple squamous epithelia
that comprise the majority
of the surface area.
Type II pneumocytes
secrete surfactant.
Gas exchange by diffusion
based on gradients.
Who cares?
Figure
13.17
Respiratory
Distress Syndrome
of the Newborn
Law of LaPlace
Surfactant reduces surface tension which
reduces the mechanical effort of ventilation and
prevents the collapse of smaller alveoli.
Figure 13.19
Tidal inspiration
At end of normal tidal expiration
V = VT x f
VA = (VT – VDS) x f
Anatomic dead space = air remaining in
conducting zone (typically 150 ml.)
What is VA if Tidal Volume is 150 ml?
O2 uptake
CO2 production
CO2 production
O2 uptake
= Respiratory
Quotient
=0.8 for mixed diet
200mlCO2/min
250 ml O2/min
= 0.8 for proteins
= 0.7 for fat
= 1.0 for carbohydrate
C6H12O6 + 6 O2 → 6 CO2 + 6 H2O + energy
Where are receptors for
negative feedback loop?
Gas exchange
Peripheral Chemoreceptors
1) Carotid bodies
(not carotid sinuses
which are baroreceptors)
2) Aortic bodies (not aortic arch
baroreceptors)
Central Chemoreceptors in
medulla (sensitive to H+ in
interstitial fluid of medulla)
To ponder: Why should there
be three sets of
chemoreceptors?
Carbon Dioxide reacts with water!
CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3Carbonic Acid
Bicarbonate
H+ can’t cross Blood Brain Barrier but CO2 does!
Central Chemoreceptors respond to H+ produced by
diffusion of CO2 into brain interstitial fluid.
In what forms are O2 and
CO2 found in the blood?
Gas exchange
Figure 13.27
Partial Pressures are
the same, but total
oxygen content differs!
Bound & Free
CO2 and O2 bound to Hb do not
contribute to partial pressure (no
longer a dissolved gas!)
Peripherial chemoreceptors can detect ONLY dissolved gasses!
Hb can bind
O2, CO2, and H+
Figure 13.31
100
40
100
Increases in CO2 and
H+ decrease the affinity
of Hb for O2
Steep
Flat
Shifting the
Oxyhemoglobin dissociation curve
At 40 Torr,
more DPG,
higher temperature, and
greater acidity
(all indicative of increased
metabolism)
shift dissociation curve down
(Hb has a lower affinity for O2) and thus
more O2 is unloaded into the tissues.
Notice the main affect is on the steep
portion of the curve which means that
there is little influence on the loading of
O2 onto Hb in the lungs
Table 13.09
Figure 13.34
Ventilation is relatively unaffected by
PaO2 until it falls below 60. Explain
why!
carbaminohemoglobin
Chloride
Shift
CA = carbonic anhydrase
Hb is a Buffer
Carbon dioxide transport
40
46
carbaminohemoglobin
46
40
Any deviation from the
set point for CO2
Causes immediate
changes in ventilation!
Why should this be so?
CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3Carbonic Acid
Bicarbonate
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Figure 13.22
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Figure 13.32
Negative feedback loop for
control of blood gases
Cervical
spinal cord
injury
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Name the
components of the
negative feedback
loop
Figure 13.40
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Respiratory Physiology
during Exercise
Blood gases and pH
change very little except
when exercise is intense.
Therefore, changes in
minute ventilation are not
the result of negative
feeback.
How can this be?
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Negative feedback operates! But the changes in
ventilation at the onset and offset of exercise cannot be
explained by negative feedback.
Experience, learning, modification of
motor program, feed forward!
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Figure 13.43
Integrator
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